Psychopathology_ Research, Assessment and Treatment in -- Davey, Graham -- 2014 -- Chichester, West Sussex_ Wiley -- 9781118897324 -- 53ef4810f8f7eecc98b366b0680e518a -- Anna’s Archive (1)

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Psychopathology
Research, Assessment and
Treatment in Clinical Psychology
SECOND EDITION
GRAHAM DAVEY
GEORGE GREEN LIBRARY OF

SCIENCE AND ENGINEERING
BRA the British WI LEY

< i BY olagical Society
Published by British Psychological Society and John Wiley & Sons Ltd
Copyright © 2014 John Wiley & Sons Ltd
Copyright © 2008 Graham Davey A 24 QU 6S
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Library of Congress Cataloging-in-Publication Data
Davey, Graham.
Psychopathology : research, assessment and treatment in clinical psychology / Graham Davey.—Second edition.
pages cm
Includes bibliographical references and index.
ISBN 978-1-118-65933-5 (pbk. : alk. paper)—1. Psychology, Pathological—Textbooks. JI. Title.
RC454.D275 2014
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2014017639
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Brief Contents
Acknowledgements
Preface to Second Edition
Accompanying Online Resources for Instructors and Students
PART! INTRODUCING PSYCHOPATHOLOGY: CONCEPTS, PROCEDURES AND PRACTICES
Chapter 1 An Introduction to Psychopathology: Concepts, Paradigms and Stigma
Chapter 2 Classification and Assessment in Clinical Psychology
Chapter 3 Research Methods in Clinical Psychology
Chapter 4 Treating Psychopathology 101
Chapter 5 Clinical Practice 127
PART Il PSYCHOPATHOLOGY AND PSYCHOLOGICAL DISORDERS 143
Chapter 6 Anxiety and Stressor-Related Problems 145
Chapter 7 Depression and Mood Disorders 195
Chapter 8 Experiencing Psychosis: Schizophrenia Spectrum Problems 235
Chapter 9 Substance Use Disorders 283
Chapter 10 Eating Disorders 331
Chapter 11 Sexual and Gender Problems 363
Chapter 12 Personality Disorders 407
Chapter 13 Somatic Symptom Disorders 449
Chapter 14 Dissociative Experiences 469
Chapter 15 Neurocognitive Disorders 491
Chapter 16 Childhood and Adolescent Psychological Problems 523
Chapter 17 Neurodevelopmental Disorders 561
Index 599
Digitized by the Internet Archive
in 2023 with funding from
Kahle/Austin Foundation
https://archive.org/details/psychopathologyr0000dave_r2q2
Contents
Acknowledgements xvii
Preface to Second Edition xix
Accompanying Online Resources for Instructors and Students XXV
PART! INTRODUCING PSYCHOPATHOLOGY: CONCEPTS, PROCEDURES AND PRACTICES 1
Chapter 1 An Introduction to Psychopathology: Concepts, Paradigms and Stigma 3

Introduction 5
1.1 A Brief History of Psychopathology 6
1.1.1 Demonic Possession 6
1.1.2 The Medical or Disease Model 8
1.1.3 From Asylums to Community Care 9
Self-Test Questions 13
Section Summary 13
1.2 Defining Psychopathology 14
1.2.1 Deviation from the Statistical Norm 14
1.2.2 Deviation from Social and Political Norms 15
1.2.3 Maladaptive Behaviour and Harmful Dysfunction 15
1.2.4 Distress and Disability 17
Self-Test Questions i,
Section Summary 18
1.3. Explanatory Approaches to Psychopathology 18
1.3.1 Biological Models 18
1.3.2 Psychological Models 23
Section Summary 28
1.4 Mental Health and Stigma 30
1.4.1 What Is Mental Health Stigma? 30
1.4.2. Who Holds Stigmatizing Beliefs about Mental Health Problems? 30
1.4.3 What Factors Cause Stigma? 30
1.4.4 Why Does Stigma Matter? 32
1.4.5 How Can We Eliminate Stigma? 32
Section Summary 33
1.5 Concepts, Paradigms and Stigma Revisited 33
Chapter 2 Classification and Assessment in Clinical Psychology 35

Introduction 36
2.1 Classifying Psychopathology BY
2.1.1 The Development of Classification Systems 37
22D SIMS 38
2.1.3. Conclusions 43
Section Summary 44
viii CONTENTS
22, Methods of Assessment 44

2.2.1. The Reliability and Validity of Assessment Methods 44
2.2.2 Clinical Interviews 45
2.2.3. Psychological Tests 47
2.2.4 Biologically Based Assessments 54
2.2.5 Clinical Observation a7
2.2.6 Cultural Bias in Assessment 60
Section Summary 63
23 Case Formulation 64
Section Summary @
2.4 Classification and Assessment in Clinical Psychology Revisited 66
Chapter 3 Research Methods in Clinical Psychology 69
Introduction 70
Bal Research and Science 71
3.1.1 What Is Research? 7
3.1.2 Scientific Method iii
Section Summary 74
3.2 Clinical Psychology Research — What Do We Want to Find Out? 74
3.2.1. How Does Clinical Psychology Research Help Us to Understand Psychopathology? 74
3.2.2 What Questions Do Clinical Psychologists Use Research to Try to Answer? 75
Section Summary 76
249) Research Designs in Clinical Psychology 76
3.3.1 Correlational Designs Ta.
3.3.2 Longitudinal Studies and Prospective Designs 78
3.3.3 Epidemiological Studies 80
3.3.4 Experimental Designs 80
3.3.5 Mixed Designs 84
3.3.6 Natural Experiments 85
3.3.7 Single-Case Studies 86
3.3.8 Meta-Analyses and Systematic Reviews 88
3.3.9 Qualitative Methods 90
Section Summary 94
3.4 Ethical Issues in Clinical Psychology Research 95
3.4.1 Informed Consent 95
3.4.2 Causing Distress or Withholding Benefits 97
3.4.3. Privacy and Confidentiality 98
Section Summary 99
ye) Research Methods in Clinical Psychology Revisited 99
Chapter 4 Treating Psychopathology 101

Introduction 102
4.1 The Nature and Function of Treatments for Psychopathology 103
4.1.1 Theoretical Approaches to Treatment 103
4.1.2 Modes of Treatment Delivery 113
Self-Test Questions Wy
Section Summary 118
. contents [iii
4.2 Evaluating Treatment 118
4.2.1 Factors Affecting the Evaluation of Treatments 119
4.2.2 Methods of Assessing the Effectiveness of Treatments 120
4.2.3 What Treatments Are Effective? 123
Section Summary 125
4.3 Treating Psychopathology Reviewed 125
Chapter 5 Clinical Practice 127

Introduction 128
5.1 The Economic Cost of Mental Health Problems 129
Section Summary 130
5.2 Who Are Mental Health Professionals? 130
Section Summary 133
5.3 Providing Mental Health Services 133
5.3.1 What Facilities are Available? 133
5.3.2 How Are Mental Health Services Structured? 133
5.3.3 The Recovery Model 134
Self-Test Questions 1S5
Section Summary 1295)
5.4 The Role of the Clinical Psychologist 135
5.4.1 Key Capabilities and Competencies iT)
5.4.2 The Reflective Practitioner Model 138
5.4.3 Regulation and Continuing Professional Development 138
5.4.4 Training to be a Clinical Psychologist 139
Section Summary 141
5.5 Clinical Practice Reviewed 142
PART Ii PSYCHOPATHOLOGY AND PSYCHOLOGICAL DISORDERS 143

Chapter 6 Anxiety and Stressor-Related Problems 145
Introduction 146
6.1 Specific Phobias 149
6.1.1 The Aetiology of Specific Phobias 151
6.1.2 The Treatment of Specific Phobias 155:
Section Summary 157
6.2 Social Anxiety Disorder iley/
6.2.1 The Aetiology of Social Anxiety Disorder 158
6.2.2 The Treatment of Social Anxiety Disorder 161
Section Summary 162
6.3. Panic Disorder and Agoraphobia 162
6.3.1 The Aetiology of Panic Disorder and Agoraphobia 165
6.3.2 The Treatment of Panic Disorder 168
Section Summary 169
6.4 Generalized Anxiety Disorder (GAD) 170
6.4.1 The Aetiology of Generalized Anxiety Disorder 171
6.4.2 The Treatment of Generalized Anxiety Disorder 173
Section Summary 175
6.5 Obsessive Compulsive Disorder (OCD) 176
6.5.1 The Aetiology of Obsessive Compulsive Disorder 180
6.5.2 The Treatment of Obsessive Compulsive Disorder 183
Section Summary 185
6.6 Trauma and Stress-Related Disorders 186
6.6.1 The Aetiology of Post-Traumatic Stress Disorder (PTSD) 188
6.6.2 The Treatment of Post-Traumatic Stress Disorder 191
Section Summary 193
6.7. Anxiety and Stressor-Related Problems Reviewed 193
Chapter 7 Depression and Mood Disorders 195

Introduction 196
7.1 Major Depression 198
7.1.1 The Diagnosis and Prevalence of Major Depression 198
7.1.2 The Aetiology of Major Depression 201
Section Summary 214
7.2 Bipolar Disorder 215
7.2.1 The Diagnosis and Prevalence of Bipolar Disorder 216
7.2.2 The Aetiology of Bipolar Disorder PAVE
Self-Test Questions ZS
Section Summary 2S
7.3 The Treatment of Depression and Mood Disorders 2D
7.3.1 Biological Treatments 220
7.3.2 Psychological Treatments 222
Section Summary Way
7.4 Deliberate SelfHarm 227,
Section Summary 229
7.5 Suicide 229
7.5.1 Risk Factors for Suicide 2Gi
7.5.2 Identifying and Preventing Suicide 232,
Section Summary 253
7.6 Depression and Mood Disorders Reviewed 234
Chapter 8 Experiencing Psychosis: Schizophrenia Spectrum Problems 255

Introduction 237,
8.1 The Nature of Psychotic Symptoms 238
8.1.1 Delusions 238
8.1.2 Hallucinations 239
8.1.3. Disorganized Thinking (Speech) 240
8.1.4 Grossly Disorganized or Abnormal Motor Behaviour 240
8.1.5 Negative Symptoms 242
Section Summary 243
contents [Gail
8.2 The Diagnosis of Schizophrenia Spectrum Disorders 243
8.2.1 Delusional Disorder
a2
8.2.2 Brief Psychotic Disorder
aii
8.2.3. Schizophrenia 244
8.2.4 Schizoaffective Disorder 245
Section Summary 245
8.3 The Prevalence of Schizophrenia Spectrum Disorders 245
Section Summary 246
8.4 The Course of Psychotic Symptoms 246
8.4.1 The Prodromal Stage 246
8.4.2 The Active Stage 248
8.4.3 The Residual Stage 248
Section Summary 248
8.5 The Aetiology of Psychotic Symptoms 249
8.5.1 Biological Theories 249
8.5.2 Psychological Theories 257
8.5.3. Sociocultural Theories 264
Section Summary 268
8.6 The Treatment of Psychosis 270
8.6.1 Biological Treatments 270
8.6.2 Psychological Therapies 272
8.6.3 Family Interventions 275
8.6.4 Community Care 276
Section Summary 279
8.7 Experiencing Psychosis Reviewed 280
Chapter 9 Substance Use Disorders 283

Introduction 284
9.1 Defining and Diagnosing Substance Use Disorders 286
Section Summary 288
9.2 The Prevalence and Comorbidity of Substance Use Disorders 288
Section Summary 290
9.3 Characteristics of Specific Substance Use Disorders 290
9.3.1 Alcohol Use Disorder 290
9.3.2 Tobacco Use Disorder 295
9.3.3 Cannabis Use Disorder 298
9.3.4 Stimulant Use Disorders 302
9.3.5 Sedative Use Disorders 306
9.3.6 Hallucinogen-Related Disorders 308
Section Summary 311
9.4 The Aetiology of Substance Use Disorders 312
Experimentation 314
9.4.1
9.4.2 Regular Use 315
9.4.3 Abuse and Dependence 318
Section Summary 320
9.5 The Treatment of Substance Use Disorders
9.5.1 Community-Based Programmes
9.5.2 Behavioural Therapies
9.5.3 Cognitive Behaviour Therapies (CBTs)
9.5.4 Family and Couple Therapy
9.5.5 Biological Treatments
Self-Test Questions
Section Summary
9.6 Substance Use Disorders Reviewed
Chapter 10 Eating Disorders

Introduction
10.1 Diagnosis and Prevalence
10.1.1 Anorexia Nervosa
10.1.2 Bulimia Nervosa
10.1.3 Binge-Eating Disorder (BED)
Self-Test Questions
Section Summary
10.2 Cultural and Demographic Differences in Eating Disorders
10.2.1 Cultural Differences
10.2.2 Demographic Factors within Cultures
Self-Test Questions
Section Summary
10.3 The Aetiology of Eating Disorders
10.3.1 Biological Factors
10.3.2 Sociocultural Influences
10.3.3 Experiential Factors
10.3.4 Psychological and Dispositional Factors
10.3.5 Transdiagnostic Models of Eating Disorders
Self-Test Questions
Section Summary
The Treatment of Eating Disorders
10.4.1 Pharmacological Treatments
10.4.2 Family Therapy
10.4.3 Cognitive Behaviour Therapy (CBT)
10.4.4 Prevention Programmes
Self-Test Questions
Section Summary
10.5 Eating Disorders Reviewed
Chapter 11 Sexual and Gender Problems
Introduction
11.1 Defining Pathological Sexual Behaviour
Self-Test Questions
Section Summary
Sexual Dysfunctions
11.2.1 Diagnosis of Sexual Dysfunctions
11.2.2 The Aetiology of Sexual Dysfunctions
11.2.3 The Treatment of Sexual Dysfunctions
Self-Test Questions
Section Summary
contents [Sati
Paraphilic Disorders
11.3.1 The Diagnosis and Description of Paraphilic Disorders
11.3.2 The Aetiology of Paraphilic Disorders
11.3.3 The Treatment of Paraphilic Disorders
Self-Test Questions
Section Summary
Gender Dysphoria
11.4.1 Diagnosis and Description of Gender Dysphoria
11.4.2 The Aetiology of Gender Dysphoria
11.4.3 The Treatment of Gender Dysphoria
Self-Test Questions
Section Summary
ES) Sexual and Gender Problems Reviewed
Chapter 12 Personality Disorders

Introduction
12.1 Contemporary Issues in the Diagnosis of Personality Disorders
12.1.1 The Categorical Approach to Personality Disorders in DSM-IV-TR and DSM-5
12.1.2 Problems with the Traditional Categorical Model
12.1.3 DSM-5’s Alternative Model
Self-Test Questions
Section Summary
22 Personality Disorders and their Diagnosis
12.2.1 Odd/ Eccentric Personality Disorders (Cluster A)
12.2.2 Dramatic/Emotional Personality Disorders (Cluster B) 415
12.2.3 Anxious/ Fearful Personality Disorders (Cluster C)
Section Summary 423
2S The Prevalence of Personality Disorders 424
Section Summary 426
12.4 The Aetiology of Personality Disorders 426
12.4.1 Odd/Eccentric Personality Disorders (Cluster A) 427
12.4.2 Dramatic/Emotional Personality Disorders (Cluster B) 427
12.4.3 Anxious/Fearful Personality Disorders (Cluster C) 436
Section Summary 439
125) Treating People with a Diagnosis of Personality Disorder 440
12.5.1 Drug Treatments 441
12.5.2 Psychodynamic and Insight Approaches 441
12.5.3 Dialectical Behaviour Therapy 442
12.5.4 Cognitive Behaviour Therapy 443
12.5.5 Schema-Focused Cognitive Therapy 445
Section Summary 446
12.6 Personality Disorders Reviewed 447
Chapter 13 Somatic Symptom Disorders 449

Introduction 450
13m The Diagnosis and Characteristics of Somatic Symptom Disorders 451

13.1.1 Somatic Symptom Disorder 451
13.1.2 Illness Anxiety Disorder 452
GAVE contents
13.1.3 Conversion Disorder
13.1.4 Factitious Disorder
Self-Test Questions
Section Summary
132 The Aetiology of Somatic Symptom Disorders
13.2.1 Psychodynamic Interpretations
13.2.2 Consciousness and Behaviour
13.2.3 Risk Factors for Somatic Symptom Disorders
13.2.4 Learning Approaches
13.2.5 Cognitive Factors
13.2.6 Sociocultural Approaches
Self-Test Questions
Section Summary
13%3 The Treatment of Somatic Symptom Disorders
13.3.1 Psychodynamic Therapy
13.3.2 Behaviour Therapy
13.3.3 Cognitive Behavioural Therapy
13.3.4 Drug Treatments
Self-Test Questions
Section Summary
13.4 Somatic Symptom Disorders Reviewed
Chapter 14 Dissociative Experiences

Introduction
14.1 The Diagnosis and Characteristics of Dissociative Disorders
14.1.1 Dissociative Amnesia
14.1.2 Dissociative Identity Disorder (DID)
14.1.3 Depersonalization Disorder
14.1.4 Dissociative Disorders and PTSD
Self-Test Questions
Section Summary
14.2 The Aetiology of Dissociative Disorders
14.2.1 Risk Factors for Dissociative Disorders
14.2.2 Psychodynamic Theories
14.2.3 The Role of Fantasy and Dissociative Experiences
14.2.4 Cognitive Approaches
14.2.5 Biological Explanations
14.2.6 Dissociative Symptoms as Role-Playing and Therapeutic Constructions
Self-Test Questions
Section Summary
14.3 The Treatment of Dissociative Disorders
14.3.2 Hypnotherapy
14.3.4 Developments in Treatments for Dissociative Disorders
Self-Test Questions
Section Summary
14.4 Dissociative Disorders Reviewed
Chapter 15 Neurocognitive Disorders 491
Introduction 492
15.1 The Diagnosis and Assessment of Neurocognitive Disorders 493
15.1.1 Cognitive Impairments in Neurocognitive Disorders 493
15.1.2 Assessment in Clinical Neuropsychology 495
15.1.3 The Diagnosis of Neurocognitive Disorders 497
Section Summary 510
15.2 Treatment and Rehabilitation for Neurocognitive Disorders IU
15.2.1 Biological Treatments DZ,
15.2.2 Cognitive Rehabilitation Se
15.2.3 Caregiver Support Programmes 518
Section Summary S21)
15.3 Neurocognitive Disorders Reviewed Sy
Chapter 16 Childhood and Adolescent Psychological Problems 523

Introduction 524
16.1 The Diagnosis and Prevalence of Childhood and Adolescent Psychological Problems:
Some General Issues 526
16.1.1 Difficulties Associated With Identification and Diagnosis of Childhood
and Adolescent Psychological Problems 526
16.1.2 Childhood Psychopathology as the Precursor of Adult Psychopathology 526
16.1.3 The Prevalence of Childhood and Adolescent Psychological Disorders 528
Self-Test Questions
Section Summary
16.2 Disruptive Behaviour Problems
16.2.1 Attention Deficit Hyperactivity Disorder (ADHD)
16.2.2 Conduct Disorder
Self-Test Questions
Section Summary
16.3. Childhood and Adolescent Anxiety and Depression
16.3.1 Childhood Anxiety
16.3.2 Childhood and Adolescent Depression
Self-Test Questions
Section Summary
16.4 The Treatment of Childhood and Adolescent Psychological Problems
16.4.3 Family Interventions
16.4.4 Cognitive Behaviour Therapy (CBT)
16.4.5 Play Therapy
Self-Test Questions
Section Summary
16.5 Childhood and Adolescent Psychological Problems Reviewed
Chapter 17 Neurodevelopmental Disorders 561
Introduction 562
17.1. The Categorization and Labelling of Neurodevelopmental Disorders 563
Section Summary 564
17.2 Specific Learning Disabilities 564
17.2.1 Specific Learning Disorder 564
17.2.2 Communication Disorders 566
17.2.3 The Aetiology of Specific Learning Disabilities 567
17.2.4 The Treatment of Specific Learning Disabilities 569
Section Summary 570
17.3 Intellectual Disabilities 57)
17.3.1 DSM-5 Diagnostic Criteria for Intellectual Disability bya
17.3.2 Alternative Approaches to Defining Intellectual Disability 571
17.3.3 The Prevalence of Intellectual Disabilities D772.
17.3.4 The Aetiology of Intellectual Disabilities ebipa
17.3.5 Interventions for Intellectual Disabilities 579
Section Summary 583
17.4 Autistic Spectrum Disorder (ASD) ; 584
17.4.1 The Characteristics of Autistic Spectrum Disorder 585
17.4.2 The Diagnosis of Autistic Spectrum Disorder 587
17.4.3 The Prevalence of Autistic Spectrum Disorder 587
17.4.4 The Aetiology of Autistic Spectrum Disorder 588
17.4.5 Interventions and Care for Individuals with Autistic Spectrum Disorder 593
Section Summary 596
17.5 Neurodevelopmental Disorders Reviewed 597
Index 599
Acknowledgements
This second edition could not have been produced with- http: / /twitter.com/GrahamCLDavey, visit my website at
out a lot of hard work on the part of the Wiley commis- http://www.papersfromsidcup.com, or read my blogs
sioning and production team, including Andrew McAleer, at http://www.papersfromsidcup.com/graham-daveys-
Georgia King, Ellie Wilson, Juliet Booker, Claire Jardine blog.html, and http://www.psychologytoday.com/blog/
and Deborah Egleton, and to them I am particularly why-we-worry.
grateful. I'd also like to continue to thank those people As soon as this book is with the printers, it’s my inten-
who advised me on the first edition, much of which is tion to revisit the cold beers and stunning sunsets offered
still relevant to the second edition. These include Alison by La Trata and Paradise bars on Naxos in the Greek
Brown, Kate Cavanagh, Roger Cocks, Rudi Dallos, Andy Islands, where I wrote the acknowledgements to the first
Field, Daniel Freeman, Theresa Gannon, David Green, edition. I hope you enjoy the second edition as much as
Richard Hastings, Marko Jelicic, Jo Johnson, Fergal Jones, I’m intending to enjoy those cold beers and magnificent
Ruth Mann, Charlie Martin, Lance McCracken, Michael sunsets.
Morgan, Peter Muris, Ben Smith, Helen Startup, Emma
Veitch, Brendan Weekes, and Leonora Wilkinson. More
recently, people who have provided help and advice on
the second edition include Chris Brewin, Kate Cavanagh,
Suzanne Dash, Thomas Ehring, Fergal Jones, Nick Lake,
Fran Meeten, Michael Morgan and Filip Raes, as well as
a number of nameless reviewers of the first edition who
have all helped to shape this revised text.
Writing a book is usually easiest when you start with
a blank sheet of paper and a pen; reshaping a first edi-
tion of a book into its second edition feels much harder —
rather like trying to prepare quail consommé from the
leftovers of a bacon sandwich! So, a big thank you to all
those people who have actively endured my ‘culinary’
frustrations over. the past 18 months — especially Benie,
my daughters Kate and Lizzie, and Emily, Doon, Lucy,
Simon, Cathy, my mother Betty, Owl and Mogg (both of
whom periodically attempted to motivate me with gifts
of rodent body parts), and finally Megan the banana-
eating dog.
If you have time on your hands, you can follow my Graham C, L. Davey
ramblings on mental health and psychology on Twitter at Brighton, July 2014
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Preface to Second Edition
Clinical psychology is a topic that fascinates a majority methods developed to try and eliminate stigma. In addi-
of undergraduate psychology students. This is hardly tion we have continued to provide multiple perspectives
surprising given that a substantial proportion of stu- on mental health problems from a range of psychological,
dents entering degree programmes in psychology do so biological and genetic approaches, and to emphasize the
with a career in applied psychology firmly in mind. For important significance of experimental psychopathology to
these students, clinical psychology offers an understand- good clinical psychology research. We have also expanded
ing of people and their mental health problems, as well our coverage of cross-cultural issues and included an
as a means to research and treat those problems. The expanded Focus Point in Chapter 1 devoted to sociocultural
first edition of this text was designed specifically to pro- factors and psychopathology that draws together some of
vide those students with a comprehensive coverage of the cross-cultural, gender and ethnicity issues discussed
both psychopathology and clinical practice, and we have throughout the book.
attempted to improve significantly on that coverage in Finally, student readers often fail to appreciate the
this second edition. wealth of additional material and resources that are
The main emphases of the second edition are still to provided on the websites that accompany books such as
provide students at undergraduate level with a compre- this. In this second edition these online resources have
hensive and accessible introduction to psychopathology, been significantly expanded. For students we still have
and, in addition, to provide a source book for more our large bank of self-test questions, online glossary and
in-depth study for postgraduate students, researchers and chapter learning objectives, but to this we've added a sig-
clinical psychologists. Conveying the research basis for nificant range of instructional and supplementary videos
clinical psychology is a main theme of this book, as is the covering such topics as descriptions of symptoms and
desire to describe how treatments and interventions work aetiologies, examples of diagnosis and diagnostic inter-
in practice — and many of the latter are described in the views, recounted personal experiences of people with
book’s Treatment in Practice features. This second edition mental health problems and discussions and examples
has specifically focused on updating the research on which of treatment. There are also student learning activities,
an understanding of mental health problems is based, and discussion topics, lists of relevant journal articles (many
rounds off an understanding of research and treatment in of which provide free links to relevant articles published
clinical psychology by introducing a new chapter on clini- in Wiley-Blackwell journals), and topics for discussion
cal provision that describes how mental health services related to clinical research and clinical practice. Instructor
implement the research and development that occurs in resources include essay questions, access to all figures
psychopathology. Perhaps most significantly, this second and plates for inclusion on class handouts or PowerPoint
edition brings to the reader the new diagnostic criteria presentations, template PowerPoint presentations for
published in DSM-5 in May 2013 and we mix a description each chapter, and a separate instructor-only bank of
of these revised diagnostic criteria with a critical discus- multiple-choice questions for student assessments.
sion of how these changes were developed and what their Just like the first edition, the second edition is sup-
significance might be. There are also three important plemented by a range of features designed to facilitate
changes in the early chapters. Chapter 1 now provides effective teaching and learning. These include:
(1) a fuller history of psychopathology, including the
development from asylums to community care; (2) a sig- ¢ Focus Points These provide more in-depth
nificantly expanded section on explanatory approaches discussion of particular topics that are conceptu-
to psychopathology that provides the reader with a ally important, controversial or simply of con-
foundation knowledge of the psychological and biologi- temporary interest. Whenever possible these are
cal substrates that are used to explain psychopathology, linked to everyday examples — such as high-profile
and this includes new material on neuroscience, genetics news items — that allow the reader to consider the
issues in a contemporary, everyday context.
and epigenetics; and (3) an expanded section devoted to
stigma and mental health — in particular what stigma is, ¢ Research Methods Boxes These features con-
who holds stigmatizing beliefs, why stigma matters, and tain detailed descriptions of methods utilized in
re PREFACE TO SECOND EDITION
psychopathology research, and describe the pros and is either described or defined at that point.
and cons of individual methods, their potential Highlighting these terms makes them easy to
uses, and these examples act to supplement the locate, and the list of key terms online can serve
general material provided on research methods in as a revision check-list — especially for students
Chapter 3. Like most researchers, those involved due to take multiple-choice questionnaire
in clinical psychology research are often imagina- assessments.
tive in their use of research methods and many
of the examples provided in research methods Finally, I hope you find this second edition readable,
boxes attempt to convey how methods from accessible and enlightening, and a worthwhile addition
other areas of psychology and science gener- to your teaching and learning activities. It’s been a mon-
ally can be adapted to study issues relevant to ster project for me, and I’ve learnt a lot in the process.
psychopathology. I hope you do, too — good luck!
Graham Davey
Case Histories Most chapters contain exam-
Brighton, July 2014
ple case histories describing the symptoms,
experiences and life circumstances encoun-
tered by individuals experiencing particular
psychopathologies. Each of these examples con- NEW TO THE SECOND
cludes with a clinical commentary that is designed
to link the detail of that specific case history to
EDITION
the general facts to be learnt in the text.
The Client’s Perspective Many chapters also Chapter 1 — An Introduction to Psychopathology:
contain examples of an individual’s own descrip- Concepts, Paradigms and Stigma
tions of the experience of psychopathology.
These are designed to provide the reader with ¢ Begins with a new section covering the history of
an insight into the phenomenology of different psychopathology, including demonic possession,
psychopathologies, and the way that symptoms the medical and disease models, and develop-
affect moods, experiences, and affect everyday ments from asylums to community care.
living — including social, occupational and edu- ¢ Contains a new section dedicated to ‘Mental health
cational functioning. These descriptions are and stigma’, and includes discussion of who holds
also supplemented by the personal accounts of stigmatizing beliefs, what causes stigma, why
psychopathologies that begin each chapter. As with stigma matters, and how we might eliminate it.
case histories, client’s perspective features usually e Expanded sections on explanatory approaches to
conclude with a clinical commentary that links the psychopathology, with new basic material on bio-
personal experiences of the psychopathology to logical approaches, including genetics, epigenetics
the academic content of the text. and neuroscience.
Treatment in Practice Boxes These boxes ¢ Revised with newly featured material, including
attempt to provide the reader with a more detailed sociocultural factors and psychopathology, and a
insight into how individual treatments are con- new, updated mental health quiz.
ducted in practice. It is often difficult fora student
to understand, for example, how a therapy is Chapter 2 — Classification and Assessment in Clinical
conducted in practice from descriptions given Psychology
in academic texts. These boxes will provide some
specific examples of how a practitioner might imple- ¢ This chapter has been expanded to include both
ment the principles of a treatment in a specific case. classification and assessment.
Self-Test Questions Throughout each chap- ¢ The newly revised classification system DSM-5 is
ter the reader will encounter self-test questions. fully described, including the main changes from
These are designed to test the reader’s absorp- DSM-IV-TR, the controversies and criticisms of the
tion of basic factual and conceptual knowledge. new system, and a discussion of issues involved in
Instructors and teachers can also use these ques- the development of classification systems.
tions as a basis for discussing key material in class ¢ All sections of the chapter have been updated
or in small group discussions. with the most recent research and with develop-
Key Terms and Definitions When each term ments in assessment techniques, including neuro-
first appears in the text, it is highlighted in bold imaging techniques and the WAIS-IV.
PREFACE TO SECOND EDITION oxi
Chapter 3 — Research Methods in Clinical Psychology There is a full discussion of the range of mental
health professionals involved in service provi-
Information on research designs has been updated sion for mental health and their roles in that
with examples. delivery.
The section on meta-analyses is expanded to The range and structure of mental health services
include systematic reviews, with examples of how is described.
meta-analyses and systematic reviews should be
The latter part of the chapter focuses on the role
reported.
of clinical psychologists, their key capabilities and
Updated information on ethical issues has been competences, and how they are trained.
added, including informed consent, together with
The chapter also contains examples of how clini-
examples of contemporary consent forms.
cal psychologists work and what their weekly rou-
There are new Focus Points on scientific methods tines might be like.
as a model for clinical psychology research.
Recent developments in the reporting of Chapter 6 — Anxiety and Stressor-Related Problems
research findings are discussed, including the
shift in importance from statistical significance This chapter now includes all the new DSM-5
to effect sizes. diagnostic criteria and covers the distinctions
between anxiety disorders, the inclusion of OCD
Chapter 4 — Treating Psychopathology as a separate diagnostic category, and the develop-
ment of a stressor-related category.
The section on cognitive therapies has been All aetiology discussions have been updated with
expanded to include description and examples of the most recent research.
new ‘waves’ of CBT, including mindfulness-based
cognitive therapy (MCBT) and acceptance and
The section on specific phobias now includes a
commitment therapy (ACT). discussion of the contribution of neuroimaging
studies to understanding phobias.
Sections on drug treatments have been updated
with the most recent research. Genetic factors are included in the coverage of
social anxiety disorder, including the role of
Gestalt therapy is now briefly described in
behavioural inhibition.
a Focus Point.
The section on panic disorder includes fuller
Modes of Treatment Delivery have been
discussion of agoraphobia as a separate disorder
expanded to now include ‘telepsychiatry’
category and includes a discussion of the role of
and a discussion of the ‘Improving Access to safety behaviours.
Psychological Therapies’ (IAPT) programme and
the role of psychological well-being practitioners. Generalized anxiety disorder includes discussion
of some newer theories of GAD and worrying,
The section on evaluating treatment now includes
including a revamped discussion of information
a fuller discussion of the types of ways in which
processing biases and the role of meta-beliefs in
treatments can be measured and evaluated,
pathological worrying.
and what RCTs tell us about the efficacy of a
treatment.
A new Focus Point describes the development of
attention bias modification (ABM) techniques for
A full discussion of the ‘Dodo Bird Verdict’ is
the treatment of anxiety.
included, examining the ways in which different
types of interventions might be more or less effec- Included in the section on OCD are some
tive as each other, and the factors that contribute newly defined OCD-related disorders, includ-
to effective psychological treatment generally. ing hoarding disorder and hair-pulling disorder
(trichotillomania).
Chapter 5 — Clinical Practice The OCD-related disorder body dysmorphic

disorder is now included in this chapter as a new
This is an entirely new chapter covering aspects Focus Point.
of clinical practice and service provision. The aetiology of OCD now includes new discus-
The chapter begins by looking at the scale of sion on mental contamination and a discussion of
mental health problems and what might be the role of clinical constructs in the explanation
required to help people deal with these problems. of OCD.
xxii PREFACE TO SECOND EDITION
¢ Finally a new overarching section entitled Significantly expanded section on cognitive theo-
‘Trauma and stress-related disorders’ discusses ries of psychosis, including sections on cognitive
the definitions of PTSD and acute stress disorder. biases, ‘jumping to conclusions’ and cognitive
The chapter provides a description of the new factors involved in ‘hearing voices’.
diagnostic criteria for these disorders and updates Updated discussion of the latest trials data on
research relevant to the understanding and expla- antipsychotic drugs as treatment for psychotic
nation of stress-related disorders. symptoms.
A new separate section discussing cognitive
Chapter 7 — Depression and Mood Disorders
behaviour therapy for psychosis (CBTp).
This chapter has been restructured to include Section devoted to cognitive remediation
separate main sections on major depression and training (CRT).
bipolar disorder. New Focus Point on the role of early intervention
All mood disorders have been updated with the strategies for dealing with psychosis.
latest diagnostic criteria from DSM-5 as well as Discussion of the relationship between schizo-
more recent prevalence data. phrenia and violence, including recent data and
The sections on the aetiology and explanation of psychological models.
bipolar disorder have been expanded to include Focus Points on (1) schizophrenia and influenza,
recent research, a fuller description of genetic fac- and (2) cannabis use and psychotic symptoms,
tors, and a discussion of the triggers for depres- updated with most recent research.
sion and mania in bipolar disorder.
There is a new Research Methods section discuss- Chapter 9 — Substance Use Disorders
ing the role of experimental psychopathology
methodologies in depression research. Includes updated statistics on prevalence rates
and drug usage rates — both worldwide and in
The section on deliberate self-harm has been
the UK.
updated with recent DSM-5 diagnostic criteria.
Updated with the latest diagnostic criteria for
New Focus Points discuss a range of depression-
substance use disorders in DSM-5.
related problems as well as new research linking
depression with inflammation. New detailed sections on (1) Reward pathways
in the brain, and (2) The nature and role of drug
The section on suicide has been expanded to
“craving.
include discussion of the role of contemporary
living problems, such as the effect of the eco- Discussion of new and controversial treatment
nomic recession on mood disorders. programmes for substance use disorder, including
supervised drug injections and monetary rewards
The research on media contagion and suicide
for abstinence.
among young people is also a new discussion
feature. Detailed descriptions of the characteristics of
drugs of abuse on the book’s website.
Chapter 8 — Experiencing Psychosis: Schizophrenia Newly structured sections dedicated to alcohol
Spectrum Problems use disorder, tobacco use disorder and cannabis
use disorder.
Updated with the most recent DSM-5 diagnostic
criteria, including new disorder categories delu- Discussion of the aetiology of substance use
sional disorder and brief psychotic disorder. disorders updated with the most recent research
findings.
Updated data on prevalence rates.
Discussion of attenuated psychotic symptoms Chapter 10 — Eating Disorders
syndrome.
Updated with the latest research on the genetics ¢ Fuller discussion of CBT and transdiagnostic
of schizophrenia. approaches to eating disorders and their treatment.
Sections on brain neurotransmitters and the neu- Inclusion of the tripartite model and how peer,
roscience of schizophrenia include most recent media and parental influences may lead to eating
research. disorders.
PREFACE TO SECOND EDITION xxiii
Updated with the latest diagnostic criteria for eat- Chapter 14 — Dissociative Experiences
ing disorders in DSM-5, plus description of other
feeding and eating disorders. ¢ All diagnostic criteria updated to be DSM-5
Focus Point on historical examples of eating compliant.
disorders. New section on the relationship between dissocia-
Describes and discusses each of the main eating tive experiences and PTSD, including a descrip-
disorders in separate sections — namely, anorexia tion of complex PTSD.
nervosa, bulimia nervosa and binge eating disorder. Updated with new research on memory processes
Updated with all the latest statistics on eating dis-
in dissociative disorders.
orders and obesity from both the UK and WHO.
All aetiology sections updated with the most recent Chapter 15 — Neurocognitive Disorders
research on the causes of eating disorders — espe-
cially genetic and neurobiological explanations. Categorization of neurocognitive disorders
updated according to the new diagnostic catego-
Chapter 11 — Sexual and Gender Problems ries in DSM-S.
Information on all neurocognitive disorders
Updated with the latest DSM-5 diagnostic criteria updated with the new DSM-5 diagnostic criteria.
for sexual dysfunctions, paraphilic disorders and
New section describing frontotemporal neurocog-
gender dysphoria.
nitive disorder.
All aetiology and treatment sections updated with
All prevalence rates updated with more recently
the latest research.
available data.
Chapter 12 — Personality Disorders All aetiology sections updated with recent
research published up to and including 2013.
Extensive discussion of the issues raised by
New Focus Point discussing the pros and cons of
DSM-5 around the diagnosis of personality
genetic testing for degenerative neurocognitive
disorders.
disorders.
Description of DSM-5 diagnostic criteria and
Treatment and rehabilitation section updated
the alternative model for diagnosis proposed for
with the most recent efficacy and RCT outcome
research in DSM-5.
studies.
Sections on aetiology of personality disorders
updated with the most recent research.
Chapter 16 — Childhood and Adolescent Psychological
New discussion on the problems associated with Problems
estimating the prevalence rates of personality
disorders. All diagnostic criteria updated to be DSM-5
New Focus Point discussing the possible relation- compliant.
ships between ADHD and antisocial personality Greater emphasis on developmental
disorder. psychopathology approaches.
New section on schema therapy for personality
All aetiology sections updated with recent find-
disorders. ings from genetic and epigenetic studies.
Chapter 13 — Somatic Symptom Disorders All prevalence figures for mental health problems
in children and adolescents updated with the
Fully updated to take account of changes to this most recently available figures.
category of disorders published in DSM-5. Section on drug treatments for childhood and
Disorders covered include somatic symptom adolescent psychological problems includes the
disorder, illness anxiety disorder (formerly hypo- most recent evidence on the regulation of drugs
chondriasis), conversion disorder and factitious for childhood conditions and the risks vs. benefits
disorder. of certain types of medication.
e All sections updated with the latest research on Extended section on CBT as applied to childhood
somatic symptom disorders and their aetiology. and adolescent problems.
xxiv | PREFACE TO SECOND EDITION
Chapter 17 — Neurodevelopmental Disorders ¢ New section and Focus Point on the empathizing—
systematizing theory of autistic spectrum
¢ All diagnostic criteria updated to be DSM-5 com- disorder.
pliant, along with changes in the structure of indi-
; ¢ Discussion of the implications of changes to
vidual sections as dictated by changes in DSM-5. 5S
autistic spectrum disorder diagnostic criteria in
¢ Updated research on the genetics of intellectual DSM-5 on prevalence rates.
disorders and autistic spectrum disorders.
Accompanying Online Resources for
Instructors and Students
RESOURCES FOR STUDENTS

An all new student website is available at www. wiley-psychopathology.com.
The website houses all the student resources including video, reading and activities
as well as a live feed into the author blog.
Sample Student Lecturer Further

About Buy Contact Us
Chapters Resources Resources Reading
|Click to view all student resources

| including video, reading and
| activities.
Psychopathology: Research, Assessment and
Treatment in Clinical Psychology
i
2nd Edition
|Click to view all lecturer resources
| including instructors test bank,
|essay questions, PowerPoint slides |
|and additional videos. |
Experimental Psychopathology -
I've just spent a very stimulating 2 i

"/ and enlightening couple of weeks, _| Professor Graham Davey, University of Sussex
|first at the Rome Workshop in Copyright
inten Wey and Same bed 2014
|Experimental Psychopa... }
|The Impact of Impact factors -
|Good
This blog post is about the negative
tiePoel Davey
|effect that journal impact factors
/can have on the progress and
| development of scie...
;
PSYCHOPATHOLOGY
RESEARCH, ASSESSMENT AND Biography
|Swimming in Treacle - Doing SussexUniversity:
| Experimen... TREATMENT IN CLINICAL Psychology Home Page
|Around three years ago Andy Field | PSYCHOLOGY BA, PhD. (Wales)
|and I, with the help of a number of _ | Psychopathology continues to rise in
|very valued friends, created anew | : | popularity as a course of study and Graham C. L. Davey, Ph.D. is Professor
|Experimental Ps... | : many students go on to pursue a of Psychology at the University of
1} B - | f( i in its associated profession
career int es: of Sussex, UK. His research interests
| The F Frigh tening GgConve rgenc e of | me
Clinical psychology. To meet this extend across mental health problems
naarlade 5 4 need, Psychopathology has been generally, and anxiety and worry
I've just spent the last six months | designed to provide students with a specifically. Professor Davey has
researching and writing the second | ESC HTA comprehensive coverage of both published over 140 articles in scientific
|edition of my Psychopathology text ‘ psychopathology... and professional journals and written or
|book — and 11... a aN) Aa Detter edited 16 books including...
The website has been developed in parallel with the textbook and all the online materials relate directly to features
and content from the book.
xxvii | ACCOMPANYING ONLINE RESOURCES FOR INSTRUCTORS AND STUDENTS
CLIENT’S PERSPECTIVE 6.2:

POST-TRAUMATIC STRESS DISORDER
‘I thought | was over it. Just when | think I'm getting bet- what I'll do, and | know they just want me to move on. I
ter and don't have to worry about it anymore, something wish I could but |
just can’t see a way out!
will trigger a memory and I'll be right back there again.
Sometimes it’s just 4 feeling | have, and other times I'll see
something that reminds me of what happened and it feels Clinical Commentary
like it’s happening all over again. It’s been almost a year This description is typical of many PTSO suffer-
now and I'm seeing a therapist three times a week as well ers and highlights feelings of depression, lack of
as taking antidepressants. | can have good days - maybe control and anger. Some theories of PTSD (such
two or three in a row - then my mood will get worse and as ‘mental defeat’) emphasise that those who
the blackness will come back. It feels as if my thoughts develop PTSD after a severe trauma tend to view
aren't my own and my mind is somewhere else while my themselves as a victim, process all information
body is just going through the motions. Every time the about the trauma negatively, and view them-
black moods come it feels harder and harder to get back
from them. It makes me so angry when | feel like this and
my mind becomes full of violent thoughts; this rage takes
over and | can't control it. I'm scared of what | might do
when I'm feeling this angry. | don’t want to tell my friends
or family about
> Specific Phobes > Activity
Bow 6.1
foe a video On post traumatic what I'm think-
stress Gioeder go to > Exposure Treatment for Phobias > Revision flastxards
Ch06 Set A
wwe wiley psychopathology
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video cht > Anxiety > Revision flattkards
ChO06 Set B
> Post Traumatic Stress Disorder > Revision flavkards

ChO6 Set C
> Journal Artie: Cognitivet
for perlormance anxiety > erent rca iene A > Revision flastxards ChOG Set D
> dournsl Zuticle: New insightsin > Revisions flashcards ChOG Set F
cogeitive behavioural therapy as
treatment of pani disorder > Revision fastkards ChO6 Set F
> Author blog on clinical constructs > Revision flashcards

ChOd Set G
Links are embedded
> Author blog on worrying > Research questions Choe
in the text allowing > Gloseary key terms Ch06 > Self-test questions
Ch06 Set A
students to navigate > Clinical issues Ch06 > Sett-test questions Ch06 Set B
directly to the resources. > Unks to journal articles ChO06
All resources are summarized in tables at the end of each chapter and students can navigate to the site via the URL
or using QR codes.
eos To access the online resources for this chapter go to

a www.wiley-psychopathology.com/ch17
Reading Activity
Rosa’s Law Learning and intellectual Activity 17.1

Glossary of key terms disabilities Self-test questions
Clinical issues Autistic spectrum disorder Revision flashcards
Links to journal articles Research questions
References
ACCOMPANYING ONLINE RESOURCES FOR INSTRUCTORS AND STUDENTS xxvii”
The student website houses a huge variety of new digi- The site also contains hundreds of new student
tal material curated especially for the new edition, includ- quizzes, as well as revision flashcards, student learn-
ing more than 50 instructional and supplementary videos ing activities, discussion topics, lists of relevant journal
covering descriptions of symptoms and aetiologies, exam- articles (many of which provide free links to relevant
ples of diagnosis and diagnostic interviews, recounted per- articles published in Wiley Blackwell journals), and top-
sonal experiences of people with mental health problems, ics for discussion related to clinical research and clinical
and discussions and examples of treatment. practice.
Visit www.wiley-psychopathology.com
to view all student resources.
[a]eet
RESOURCES FOR LECTURERS

The online resources for lecturers have all been fully questions. Additional essay questions, exam questions
updated for the new edition and an additional suite of 15 and additional discussion topics are also available along
bespoke videos of diagnostic interviews is now avail- with a full set of PowerPoint presentation slides.
able for lecturers to use in the classroom. All of these resources can be accessed by instructors
A fully updated lecturer test bank has been devel- on our lecturer book companion site at www. wiley.com/
oped for the new edition, including over 1,000 unique college/davey.
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Partl
Introducing Psychopathology:
Concepts, Procedures
and Practices
1. Anlntroduction to Psychopathology: 3 Research Methods in Clinical Psychology

Concepts, Paradigms & Stigma 4 Treating Psychopathology
2. Classification & Assessment in Clinical 5 Clinical Practice
Psychology
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DIANA 2hepsorie >
An Introduction to Psychopathology:
Concepts, Paradigms and Stigma
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resources for this chapter go ie)
www.wiley-psychopathology.com/ch1
ROUTE MAP OF THE CHAPTER CHAPTER OUTLINE
This first chapter introduces the reader to a number of basic

issues concerned with the definition and explanation of 1.1 A BRIEF HISTORY OF PSYCHOPATHOLOGY 6
psychopathology - including the issue of ‘stigma’ that is
often an outcome of how psychopathology is conceptual- 1.2 DEFINING PSYCHOPATHOLOGY 14
ized and portrayed. The first section describes a brief history
of how mental health problems have been conceived and : 1.3 EXPLANATORY APPROACHES
TO
treated. This is followed, in the second section, by a discus- PSYCHOPATHOLOGY 18
sion of how psychopathology can be defined, and how we
identify behaviour that is in need of support andtreatment. : 1.4 MENTALHEALTHAND STIGMA. 30
The third section describes some of the most common
explanatory approaches that have been developed to help : 1.5 CONCEPTS, PARADIGMS AND STIGMAREVISITED 33
us understand psychopathology, and these approaches are
ones that the reader will encounter frequently throughout
this book. Finally, the fourth section takes a close look at
mental health stigma, how it is manifested, why it is impor-
tant, and how stigma can be dealt with.
a PSYCHOPATHOLOGY
LEARNING Ne SP StS
When you have completed this chapter, you should be able to:
1. Discuss the pros and cons of a number 3. Describe and evaluate the nature and causes of
of different approaches to defining mental health stigma.
psychopathology. 4. Compare and contrast approaches to the
2. Describe important developments in the history. explanation of psychopathology, including
of our understanding and response to mental historical approaches, the medical model and
health problems. psychological models.
Am |Crazy?! don’t know what is wrong with me. | did have depression in the past and what |am going through doesn't feel a lot like
what | had before. My moods change every 30 minutes at times. | have been like this for a while. |started out about once a week |
would have a day where | was going from one extreme to the next. In the past few weeks it has gotten worse. It seems like my moods
change for no reason at all. There are times that |will just lay down and cry for what appears to be no reason at all and then 2 hours
later | will be happy. | find myself yelling at my son for stupid reasons and then shortly after | am fine again. | truly feel that |am
going crazy and the more | think about it the worse |get. am not sleeping or eating much and when | do eat | feel like | will be sick.
Joan’s Story
For the past 10 months serving in Iraq I’ve told myself not to think about all that’s going on around me. I've forced myself to go
about my daily activities in some sort of normal manner. | knew that if |thought too much about the fact that mortars could hit
meat any time, or if | laid in bed every night knowing that a mortar could drop through the ceiling while |slept, or if |focused too
much on the randomness of death here, I'd go crazy.
And for the past 10 months, I’ve managed to put these things out of my head for the most part. I’ve managed to try to live a
normal life here while people die around me. But for some reason, since |got back from leave, | can’t seem to shake the jitters, the
nervousness, the just plain uneasiness | feel walking around or driving through the city streets.
Everywhere | walk I’m constantly thinking about where I'm going to go ifa mortar
lands. I’m always looking for the next bunker. When | leave the relative safety of the
For a video on post-traumatic stress . j
disomieroate __ base, I'm constantly running scenarios through my head of the worst case situations.
www.wiley-psychopathology.com/ | There comes a point where living in fear is not living at all.
video/ch1 :
Greg's Story
When | was a child | regularly experienced dreams in which there was an awful buzzing noise; at the same time | could see what
I can only describe as the needle from a machine such as a lie detector test drawing lines. | had a dream where an older alien
cloaked in orange took me on a ship and told me things that | can’t remember yet. He took me over an island (I think it was
Australia) everything was dead and there was a mushroom cloud over it. Then there were five or six aliens, and one was holding
a clear ball. |knew that inside there was an embryo. They put it inside me. About one and a half weeks later |was confirmed preg-
nant. Then, when we were driving on the motorway, | seem to have lost 2 hours before seeing a brilliant flash above the car. |got
pains in my left temple, behind my left eye and in my left cheekbone. There is a scar on my right leg which | can’t explain. Some
people think I’m crazy, but | know it happened.
Betty’s Story
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA ee
| started using cocaine at 13. Before, |was using marijuana and alcohol and it didn’t really work for me, so |wanted to step it up a
level. |started using heroin when | was 15. | began using it to come down from cocaine and get some sleep. But | started liking the
heroin high and started using it straight. Every day, after a while. Along with cocaine, | also began taking prescription drugs when
was 13. They were so easy to get. | never had to buy them or get them from a doctor. | would just get them from friends who had
gone through their parents’ medicine cabinet. |also thought that prescription drugs were ‘safer’ than other drugs. | figured that it
was okay for people to take them, and if they were legal, | was fine. Like | said, prescription drugs were incredibly easy to get from
friends, and it always seemed to be a last-minute thing. Heroin was also easy to get — all |had to do was go into town and buy
it. My heroin use started spiralling out of control. |stopped going to school. | was leaving home for days at a time. My whole life
revolved around getting and using drugs - |felt like |was going crazy.
Erica’s Story
Introduction feels sick when she eats. Greg feels anxious about the dan-
gers of his daily life serving in Iraq. He feels nervous and
We begin this book with personal accounts from four jittery. Betty doesn’t think she’s crazy — but other people
very different individuals. Possibly the only common do. They think that her story about being abducted by
link between these four accounts is that they each use aliens is a sign of psychosis or disordered thinking — she
the word ‘crazy’ in relating their story. Joan questions thinks it seems perfectly logical. Finally, Erica’s behaviour
whether she is going crazy, Greg tells us how he tries to has become controlled by her need for drugs. She feels
prevent himself from going crazy, other people think out of control and all other activities in her life — such as
Betty is crazy, and Erica’s life gets so out of control that her education — are suffering severely because of this.
she too felt like she was ‘going crazy’. We tend to use These four cases are all ones that are likely to be
words like ‘crazy’, ‘madness’ and ‘insanity’ regularly — as encountered by clinical psychologists and although
if we knew what we meant by those terms. However, very different in their detail, they do all possess some
we do tend to use these terms in a number of different commonalities that might help us to define what rep-
circumstances — for example, (1) when someone’s behav- resents psychopathology. For example, (1) both Joan and
iour deviates from expected norms, (2) when we are Greg experience debilitating distress, (2) both Joan
unclear about the reasons for someone’s actions, and Erica feel that important aspects of their life
(3) when a behaviour seems to be irrational, or (4) when (such as their moods or cravings) are out of their
a behaviour or action appears to be maladaptive or control and they cannot cope, (3) both Joan and Erica
harmful to the individual or others. You can try seeing find that their conditions have resulted in them fail-
whether these different uses of the term ‘crazy’ or ‘mad’ ing to function properly in certain spheres of their life
apply to each of our personal accounts, but they proba- (e.g. as a mother or as a student), and (4) Betty’s
bly still won’t capture the full meaning of why they each life appears to be controlled by thoughts and memo-
used the word ‘crazy’ in their vignettes. Trying to define ries which are delusional and are probably not real. As
our use of everyday words like ‘crazy’, ‘madness’ and we shall see later, these are all important aspects of
‘insanity’ leads us on to thinking about those areas of psychopathology, and define to some extent what will
thinking and behaving that seem to deviate from nor- be the subject matter of clinical practice. However,
mal or everyday modes of functioning. For psycholo- deciding what are proper and appropriate examples of
gists the study of these deviations from normal or psychopathology is not easy. Just because someone's
everyday functioning are known as psychopathology, behaviour deviates from accepted norms or patterns
and the branch of psychology responsible for under- does not mean they are suffering from a mental or
standing and treating psychopathology is known as clin- psychiatric illness, and just because we might use the
ical psychology. term ‘crazy’ to describe someone’s behaviour does
Let’s examine our four not mean that it is the product of disordered think-
psychopathology The study of deviations ing. Similarly, we cannot attempt to define psychopa-
personal accounts a little
from normal or everyday psychological or
behavioural functioning. closer. Joan is distressed thology on the basis that some ‘normal’ functioning
because she appears to (psychological, neurological or biological) has gone
‘linical psychology The branch of have no control over her wrong. This is because (1) we are still some way from
»sychology responsible for understanding moods. She feels depressed; understanding the various processes that contribute
ind treating psychopathology. she shouts at her son; she to psychopathology, and (2) many forms of behaviour
Re: PSYCHOPATHOLOGY
that require treatment by clinical psychologists are 1.1.1 Demonic Possession

merely extreme forms of what we would call ‘normal’
or ‘adaptive’ behaviour. For example, we all worry and Many forms of psychopathology are accompanied by
we all get depressed at some times, but these activi- what appear to be changes in the individual's personality,
ties do not significantly interfere with our everyday and these changes in personality or behaviour are some
living. However, for some other people, their experi- of the first symptoms that are noticed. The reserved per-
ence of these activities may be so extreme as to cause son may become manic and outgoing, and the gregarious
them significant distress and to prevent them from person withdrawn and sombre. They may start behaving
undertaking normal daily living. Before we continue in ways that mean they neglect important daily activities
to discuss individual psychopathologies in detail, it is (such as parenting or going.to work), or may be harm-
important to discuss how the way we define psycho- ful to themselves or others. The fact that an individual’s
pathology has evolved over time, and ways in which personality seems to have changed (and may do so very
we can define and classify psychopathology and men- suddenly) has historically tended people towards describ-
tal health problems generally. ing those exhibiting symptoms of psychopathology as
being ‘possessed’ in some way. That is, their behaviour
has changed in such a way that their personality appears
to have been taken over and replaced by the persona of
someone or something else.
1.1 A BRIEF HISTORY OF Explanations of psychopathology in terms of ‘posses-
sion’ have taken many forms over the course of history,
PSYCHOPATHOLOGY and it is a form of explanation that has meant that many
who have been suffering debilitating and distressing psy-
Throughout history, we have been willing to label chological problems have been persecuted and physically
behaviour as ‘mad’, ‘crazy’ or ‘insane’ if it appears abused rather than offered the support and treatment
unpredictable, irrational, harmful, or if it simply devi- they need. Many ancient civilizations, such as those in
ates from accepted contemporary social norms. Egypt, China, Babylon and Greece, believed that those
Characters from history who have been labelled in exhibiting symptoms of psychopathology were pos-
such a way include the Roman Emperor Caligula, sessed by bad spirits (this is
King George III, Vincent Van Gogh, King Saul of known as demonology), demonology Many ancient civilizations,
such as those in Egypt, China, Babylon
Israel, and Virginia Woolf, to name just a few. But the and the only way to exor- and Greece, believed that those exhibiting
term ‘madness’ does not imply a cause — it simply cise these bad spirits was symptoms of psychopathology were
redescribes the behaviour as something that is odd. with elaborate ritualized possessed by bad spirits - known as
Views about what causes ‘mad’ behaviour have ceremonies that frequently demonology.
changed significantly over the course of history, and it involved direct physical
is instructive to understand how the way we attribute attacks on the sufferer’s body in an attempt to force out
the causes of mental health problems have developed the demons (e.g. through torture, flogging or starva-
over time. An historical perspective on psychopathol- tion). Not surprisingly, such actions usually had the effect
ogy and ‘madness’ is important because it helps us to of increasing the distress and suffering of the victim.
understand how our views of the causes of mental In Western societies, demonology survived as an
demonic possession Historical explana-
health problems have explanation of mental health problems right up until the
tions of psychopathology such as ‘demonic changed and developed 18th century, when witchcraft and demonic possession
possession’ often alluded to the fact that Over time, and it also were common explanations for psychopathology. This
the individual had been‘possessed’in contrasts with the Middle Ages in England when indi-
helps us to understand
some way.
how approaches to treat- viduals were often treated in a relatively civilized fashion.
ing and dealing with When someone exhibited symptoms typical of psychopa-
medical model An explanation of psycho- mental health problems thology a ‘lunacy trial’ was held to determine the individ-
pathology in terms of underlying biological
have changed. We will ual’s sanity, and if the person was found to be insane, they
or medical causes.
begin by looking at an were given the protection of the law (Neugebauer, 1979).
historical perspective on Nevertheless, demonic possession is still a common expla-
explaining psychopathology, which is known as nation of psychopathology in some less developed areas
demonic possession. We will then describe how the of the world — especially where witchcraft and voodoo are
medical model of psychopathology developed, and still important features of the local culture such as Haiti
finish with a discussion of the transition from asylums and some areas of Western Africa (Desrosiers & Fleurose,
to community care. 2002). The continued adoption of demonic possession
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA Core
as an explanation of mental health problems (especially accompanied by exorcism as an attempted treatment —

in relation to psychotic symptoms) is often linked to even in individuals with a known history of diagnosed psy-
local religious beliefs (Ng, 2007; Hanwella, de Silva, chotic symptoms (e.g. Tajima-Pozo, Zambrano-Enriquez,
Yoosuf, Karunaratne & de Silva, 2012), and may often be de Anta, Moron, Carrasco, Lopez-Ibor et al., 2011).
et
=
SPIRIT POSSESSION AS A TRAUMA-RELATED
- PHENOMENON IN UGANDAN CHILD SOLDIERS
=
Oo in the so-called Lords g
a. Resistance Army - a group | To read the article by Neuner etal. on
WV Spirit Possession go to
=) that has waged along and : www.wiley-psychopathology.com/
UW brutal campaign to over- | reading/ch1
\e) throw the government of
Bhs
Uganda - with youths who had never been abducted.
Cen is a form of spirit possession where the ‘ghost
of a deceased person visits the affected individual and
replaces his or her identity’ The table below shows that
reporting of spirit possession is significantly higher in
AUBERT/Getty
DOMINIQUE
Images
former abducted child soldiers than in non-abductees.
Even today, many cultures still believe that unusual They also found that reports of spirit possession were
behaviour that may be symptomatic of psychopa- related to trauma exposure (such as sexual assault and
thology is caused by spirit possession — especially in being forced to kill), to psychological distress, and to
some less developed areas of the world where such higher rates of suicide and post-traumatic stress disorder.
beliefs are still important features of the local culture. Neuner, Pfeiffer, Schauer-Kaiser, Odenwald et al.
Interestingly, beliefs about spirit possession are not (2012) conclude that in many ofthe areas of the world
simply used to try and explain the effects of psycho- where beliefs about spirit possession are widely held,
pathology-related experiences, but are also regularly such beliefs are a standard consequence of psycho-
used to control and coerce individuals. logical trauma and may be a way of explaining the
Neuner, Pfeiffer, Schauer-Kaiser, Odenwald et al. dissociative symptoms that often accompany intense
(2012) carried out a study investigating the prevalence traumatic experiences (see Chapter 14). These beliefs
of cen, a local variant of spirit possession, in youths about spirit possession can then be used by various
aged between 12 and 25 years in war-affected regions local agencies to manipulate the behaviour of individ-
of northern Uganda. They compared youths who had uals — even to the extent of coercing them into acts of
been abducted and forced to fight as child soldiers extreme brutality.
Frequencies of characteristics of spirit possession in total and divided by abduction status
Characteristics of spirit possession (%) Total Abductees Non-abductees p
Within the past 4 weeks, were you haunted by ghosts 14.4 Dies 9.2 <.001
of adeceased person?
Within the past 4 weeks, did these spirits enter your 10.3 W733 57 <.001
body and replace your inner self?
Within the past 4 weeks, during the time the spirit 9.0 15.4 3.9 <.001
possessed you, did you show behaviour or make
movements that were not under your control, but
controlled by the spirit?
Within the past 4 weeks, did it occur that you had lack 15.1 23.6 8.8 <.001
of memory for parts of the time or the whole time the
spirit possessed you?
Did you ever seek help because ghosts haunted you? 5 23.6 8.8 <.001
Four or more characteristics (high spirit possession) 8.2 14.3 sy <.001
Source: Neuner, F., Pfeiffer, A., Schauer-Kaiser, E., Odenwald, Elbert T. & Ertl, V. (2012) Haunted by ghosts: Prevalence, predictors
and outcomes of spirit possession experiences among former child soldiers and war-affected civilians in Northern Uganda.
Social Science
& Medicine, 75, 548-554, Table 1. Reproduced with permission.
i: ee PSYCHOPATHOLOGY
«
1.1.2 The Medical or Disease Model congenital risk factors (such as maternal infections dur-
ing pregnancy) (e.g. intellectual disorders, ADHD),
As cultures develop, then so too do the types of causes abnormal physical development (e.g. autism), and the
that they attribute behaviour to. In particular, as we physical effects of pathological activities (e.g. the effect
began to understand some of the biological causes of of hyperventilation in panic disorder) amongst others.
physical disease and illness, then our conception of ‘mad- However, while such biological factors may play a role in
ness’ moved very slowly towards treating it as a disease the aetiology of some psychopathologies, biological
(hence the term ‘mental illness’). The impetus for this explanations are not the only way in which psychopathol-
change in conception came in the 19th century when it ogy can be explained, and nor is biological dysfunction
became apparent that many forms of behaviour typical necessarily a factor underlying all psychopathology.
of psychopathology were the result of physical illnesses, As we shall see later, it is often a person’s experiences that
such as strokes or viral infections. For example, without are dysfunctional, not their biological substrates.
proper treatment, the later stages of the sexually trans- However, despite its obvious importance in develop-
mitted disease syphilis are characterized by the inability ing a scientific view of psychopathology and providing
to coordinate muscle movements, paralysis, numbness, some influential treatments, the medical model of psy-
gradual blindness and dementia — and many of these chopathology has some important implications for the
symptoms cause radical changes in the individual’s per- way we conceive mental health problems. Firstly, an obvi-
sonality. The discovery that syphilis had a biological ous implication is that it implies that medical or biologi-
cause, and was also an important contributor to the cal causes underlie psychopathology. This is by no means
mental disorder known as general paresis, implied that always the case, and bizarre behaviour can be developed
many other examples of by perfectly normal learning processes. For example, in
general paresis A brain disease occurring
mental or psychological Chapter 8 we describe the. example of the schizophre-
as a late consequence of syphilis, charac-
terized by dementia, progressive muscular illness might also have nia sufferer who learnt through perfectly normal learn-
weakness and paralysis. medical or biological ing processes to carry a broom around with them for 24
explanations. This became hours a day (see Focus Point 8.5). Similarly, children with
somatogenic hypothesis The hypothesis |yown as the somato-
that the causes or explanations of psycho-
autism or intellectual disabilities often learn disruptive,
genic hypothesis, which
logical problems can be found in physical challenging or self-harming behaviours through normal
or biological impairments. advocated that the causes learning processes that have nothing to do with their
or explanations of psycho- intellectual deficits (see Treatment in Practice Box 17.1).
logical problems could be found in physical or biological Furthermore, in contrast to the medical model, both
impairments. psychodynamic and contemporary cognitive accounts of
The medical model of psychopathology that was fos- psychopathology argue that many psychological prob-
tered by the somatogenic hypothesis was an important lems are the result of the individual acquiring dysfunc-
development because it introduced scientific thinking tional ways of thinking and acting, and acquiring these
into our attempts to understand psychopathology, and characteristics through normal, functional learning pro-
shifted explanations away from those associated with cul- cesses. In this sense, it is not the individual or any part
tural and religious beliefs. The medical model has given of their biology that is dysfunctional, it is the experiences
rise to a large body of scientific knowledge about psycho- they have had that are dysfunctional and have led to
pathology that is based on medicine, and this profession them thinking and acting in the way they do.
is known as psychiatry. The primary approach of the Secondly, the medical model adopts what is basically
medical model is to iden- a reductionist approach by attempting to reduce the
psychiatry A scientific method of treat- tify the biological causes of
ment that is based on medicine, the pri-
complex psychological and emotional features of psy-
psychopathology and treat chopathology to simple biology. If you look at the per-
mary approach of which is to identify the
biological causes of psychopathology and them with medication or sonal accounts provided at the beginning of this chapter,
treat them with medication or surgery. surgery. As we shall see in it is arguable whether the phenomenology (i.e. the per-
later chapters, there are sonal experience of psychopathology) or the complex
many explanations of psychopathology that allude to cognitive factors involved in many psychological prob-
biological causes, and these attempt to explain symptoms lems can be reduced to simple biological descriptions.
in terms of such factors as brain abnormalities (e.g. in Biological reductionism cannot easily encapsulate
dementia, autism), biochemical imbalances (especially the distress felt by sufferers; nor can it easily explain the
imbalances of brain neurotransmitters) (e.g. major dysfunctional beliefs and forms of thinking that are
depression, bipolar disorder, schizophrenia), genetic fac- characteristic of many psychopathologies. In addition,
tors (e.g. learning disabilities, autism, schizophrenia), complex mental health problems are often not just
chromosome disorders (e.g. intellectual disabilities), biological or even simply reducible to psychological
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA oF
problems and processes, they are influenced by the 1.1.3 From Asylums to
socio-economic situation in which the individual lives,
their potential for employment and education, and the Community Care
support they are given that will provide hope for recov- Prior to the 18th century, hospitals and asylums were few
ery and support for social inclusion (this broad ranging and far between, and those that were established were
approach to understanding and treating mental health often devoted to very specific and often highly infectious
problems is known as the recovery model, and is dis- illnesses (such as leprosy). ‘Madness’ was considered to
cussed in more detail in section 5.3.3). All of these fac- be a local or domestic problem, and individuals suffering
tors arguably contribute to a full understanding and mental health problems would either be cared for by
explanation of psychopathology. their families or by their local parish authorities.
Finally, as we have mentioned already, there is an However, as many traditional infectious diseases became
implicit assumption in the medical model that psycho- less common, many hos-
pathology is caused by ‘something not working prop- pices for these diseases asylums In previous centuries asylums
erly’. For example, this type of explanation may allude were converted into asy- were hospices converted for the confine-
to brain processes not functioning normally, brain or lums for the confinement ment of individuals with mental health
os
body biochemistry being imbalanced, or normal physi- of ind
tas duals wit’ h mental ProPlems
a ivi
cal development being impaired. This ‘something is health problems.
broken and needs to be fixed’ view of psychopathol- Because there was no coordinated government
ogy is problematic for a couple of reasons. First, rather response to mental health issues until the 19th cen-
than reflecting a dysfunction, psychopathology might tury, individual privately funded hospitals or ‘mad-
just represent a more extreme form of normal behav- houses’ began to appear prior to this time, and the
iour. We all get anxious, we all worry, and we all get most famous of these was the Bethlem Hospital in
depressed. Yet anxiety, worry and depression in their Moorfields, London, which in 1676 had a capacity for
extreme form provide the basis of many of the mental 100 inmates (Porter, 2006). Life in these asylums was
health problems we will cover in this book. If we take often cruel and inhumane, and because ‘madhouses’
the example of worry, we can all testify to the fact that were essentially businesses established for financial
we worry about something at some time. However, for profit, many expanded to take more and more suffer-
some of us it may become such a prevalent and regu- ers in conditions that were not subject to inspection
lar activity that it becomes disabling, and may lead to under the relevant legislation of the time (MacKenzie,
a diagnosis of generalized anxiety disorder (GAD; see 1992). Any medical treatments provided were usually
Chapter 6). Nevertheless, there is no reason to suppose crude and often painful (e.g. drawing copious quanti-
that the cognitive mechanisms that generate the occa- ties of blood from the brain, hot and cold baths, mer-
sional bout of worrying in all of us are not the same cury pills, or administration of the opiate laudanum to
ones that generate chronic worry in others (Davey, pacify inmates), and the nature of the inmates often
2003). In this sense, psychopathology can be viewed expanded to include not just those with mental health
as being on a dimension rather than being a discrete problems, but paupers and individuals from poor back-
phenomenon that is separate from normal experience. grounds — especially young pregnant women, who
There is accumulating evidence that important psycho- were considered to be ‘wayward’ or ‘morally degener-
pathology symptoms are on a dimension from normal ate’. This growing hotchpotch of inmates in 18th- and
to distressing, rather than being qualitatively distinct 19th-century asylums gave rise to ad hoc approaches to
(e.g. Haslam, Williams, Kyrios, McKay & Taylor, 2005; mental health care that were based around combating
Olatunji, Williams, Haslam, Abramowitz & Tolin, moral degeneration and ‘social weakness’, and such
2008). A second reason this view is problematic is that, approaches probably represent the roots of the mod-
by implying that psychopathology is caused by a nor- ern-day stigma that is associated with mental health
mal process that is broken, imperfect or dysfunctional, problems. Indeed, in Victorian times, the public could
the medical model may have an important influence on buy tickets to view the inmates of asylums, a process
how we view people suffering from mental health prob- that will have increased the conception that individuals
lems and, indeed, how they might view themselves. At with mental health problems were objects of curiosity
the very least it can be stigmatising to be labelled as excluded from everyday society.
someone who is biologically or psychologically imper- However, in the 19th century there was a gradual
fect, and people with mental health problems are often movement towards more humane treatments for indi-
viewed as second-class citizens — even when their symp- viduals in asylums, and these developments were led by
toms are really only more prominent and persistent a number of important reforming pioneers. Philippe
versions of characteristics that we all possess. Pinel (1745-1826) is often considered to be the first to
Pyle PSYCHOPATHOLOGY
+
Ss
introduce more humane treatments during his time as patients. The first attempts milieu therapies The first attempts to a
the superintendent of the Bicétre Hospital in Paris. He were known as milieu structure the hospital environment for
patients, which attempted to create a ther-
began by removing the chains and restraints that had pre- therapies, which were the
apeutic community on the ward in order
viously been standard ways of shackling inmates, and first attempts to create a to develop productivity, independence, j
started to treat these inmates as sick human beings rather therapeutic community on responsibility and feelings of self-respect.
than animals. Further enlightened approaches to the the ward which would dev-
treatment of asylum inmates were pioneered in the USA elop productivity, independence, responsibility and feel-
by Benjamin Rush of Philadelphia, and by the Quaker ings of self-respect. This included mutual respect
movement in the UK. The latter developed an approach between staff and patients, and the opportunity for
known as moral treatment, which abandoned contem- patients to become involved in vocational and recrea-
moral treatment Approach to the treat- porary medical approaches tional activities. Patients exposed to milieu therapy were
ment of asylum inmates, developed by the in favour of understand- more likely to be discharged from hospital sooner and
Quaker movement in the UK, which aban- ing, hope, moral responsi- less likely to relapse than patients who had undergone
doned contemporary medical approaches
bility, and occupational traditional custodial care (Paul & Lentz, 1977; Cumming
in favour of understanding, hope, moral
responsibility, and occupational therapy. therapy (Digby, 1985). & Cumming, 1962). A further therapeutic refinement of
Even into the 20th cen- the hospital environment came with the development of
tury and up until the 1970s in both the UK and the USA, token economy programmes (Ayllon & Azrin, 1968).
hospitalization was usually the norm for individuals with These were programmes based on operant reinforce-
severe mental health problems, and lifelong hospitaliza- ment, where patients would
tion was not uncommon for individuals with chronic receive tokens (rewards) for token economy A reward system which
involves participants receiving tokens for
symptoms. However, it became clear that custodial care exhibiting desired behavio- engaging in certain behaviours, which at a
of this kind was neither economically viable nor was it urs. These desired behav-. later time can be exchanged for a variety of
providing an environment in which patients had an iours would usually include reinforcing or desired items.
opportunity to improve. Because of the growing num- social and self-help behav-
bers of in-patients diagnosed with mental health prob- iours (e.g. communicating coherently to a nurse or other
lems, the burden of care came to rest more and more on patient, or washing or combing hair), and tokens could sub-
nurses and attendants who, because of lack of training sequently be exchanged for a variety of rewards such as
and experience, would resort simply to restraint as the chocolate, cigarettes and hospital privileges. A number of
main form of intervention. This would often lead to studies have demonstrated that token economies can have
deterioration in symptoms, with patients developing significant therapeutic gains. For example, Gripp & Magaro
what was called social breakdown syndrome, consisting of (1971) showed that patients in a token economy ward
confrontational and challenging behaviour, physical improved significantly more than patients in a traditional
aggressiveness, and a lack of interest in personal welfare ward, and Gershone, Errickson, Mitchell & Paulson (1977)
and hygiene (Gruenberg, 1980). found that patients in a token economy scheme were better
Between 1950 and 1970, these limitations of hospitali- groomed, spent more time in activities and less time in bed,
zation were being recognized and there was some and made fewer disturbing comments than patients on a
attempt to structure the hospital environment for traditional ward. Patients on token economy schemes also
earn discharge significantly sooner than patients who are
not on such a scheme or have been involved in a milieu ther-
apy programme (Hofmeister, Schneckenbach & Clayton,
1979; Paul & Lentz, 1977). However, despite the apparent
success of token economies, their use in the hospital setting
has been in serious decline since the early 1980s (Dickerson,
Tenhula & Green-Paden, 2005). There are a number of rea-
Reproduced
ry.
sons for this decline, and they are discussed in Focus Point 1.2.
Since the 1970s treatment and care of individuals diag-
nosed with severe mental health problems has moved
away from long-term hospitalization to various forms
of community care. However, the psychiatric hospital is
still an important part of the treatment picture for those
Central
Cardiff
© with
Libra
perm Bs. i
displaying severe and distressing symptoms — especially
PHOTO 1.1 This photograph shows a ward in Cardiff City since it will often be the environment in which treatment
Mental Hospital, Whitchurch, UK, in the early 20th century. Beds takes place for an individual's first acute experience (e.g.
are crowded close together allowing little personal space for a first psychotic episode). However, length of stay in hos-
patients, who were often hospitalized for much of their lives. pital for individuals has been significantly reduced as a
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA oe
J
=
THE DECLINE OF THE TOKEN ECONOMY
=
2 Despite its apparent therapeutic advantages, recent scheme return to low baseline levels outside of
surveys indicate that the use of ‘token economies’ in
2) the program (e.g. Ayllon & Azrin, 1968; Walker &
Oo. clinical settings is in serious decline (Corrigan, 1995; Buckley, 1968). However, there are other studies
mM) Hall & Baker, 1973; Boudewyns, Fry & Nightengale, that have shown positive effects of maintenance
=) 1986; Dickerson, Tenhula & Green-Paden, 2005). A
U and generalization (Banzett, Liberman & Moore,
ie) number of reasons have been put forward for this 1984). Nevertheless, it should be pointed out that
ri decline. generalization is not a passive process, and cli-
nicians must actively build into the programme
° There are legal and ethical issues that need to strategies that transfer positive effects to settings
be considered. This is especially so when deci- outside the treatment scheme (Stokes & Baer,
sions have to be made about who will partici- 1977; Stokes & Osnes, 1988).
pate in token economies, for how long, and what 7 Some other proponents of the token econ-
will be made available as positive reinforcers. omy have argued that its decline has been the
Legislation over the past 25 years has sought to result of unfounded misconceptions about the
protect patients’ rights, and treatment staff are nature and efficacy of such programmes (e.g.
severely constrained with regard to the use of Corrigan, 1995). These include such misconcep-
more basic items as reinforcers (Glynn, 1990) - tions as token economies not being therapeuti-
especially when patients now have a legal right cally effective, their benefits do not generalize,
to their own personal property and humane they do not provide individualized treatment,
treatment, including comfortable bed, chair, bed- they are abusive and coercive, and they are
side table, nutritious meals, cheerful furnishings, not practical to implement in the context of
and suchlike. present-day attempts to treat patients in the
* One of the major challenges for token econo- community. Corrigan (1995) argues that these
mies has been maintenance and generalization are all unfounded, and that the token economy
of therapeutic effects. To the extent that patients remains an important and valuable tool for the
can obtain reinforcers outside the programme management of patients and staff in treatment
and avoid punishment by exiting from the pro- settings.
gramme, the therapeutic benefit of token econo-
mies becomes less useful (Glynn, 1990). It is true Source: From Davey G.C.L. (1998). Learning theory. In C.E. Walker
that some studies have shown that behaviours (Ed.) Comprehensive clinical psychology: Foundations of clinical
targeted for improvement in a token economy psychology, Vol. 1. Elsevier. Reproduced with permission.
result of the development of more effective early inter- feeding themselves, managing their money, and coping
vention treatments and supportive community care and with social interactions and life stressors.
outreach programmes. With the development of more In 1963, the US Congress passed a Community
effective pharmacological and psychological treatments Mental Health Act that specified that, rather than be
in the 1950s and 1960s, it became clear that most people detained and treated in hospitals, people with mental
diagnosed with severe mental health symptoms could health problems had the right to receive a broad range
be treated to a point where they were capable of living of services in their communities. These services
at least some kind of life back in the community. This included outpatient therapy, emergency care, preventa-
helped relieve the economic burden of lifelong hospi- tive care, and aftercare. Growing concerns about the
talization and custodial care. However, even when living rights of mental health patients and a change in social
back in their communities, it was clear that many indi- attitudes away from the stigma associated with mental
viduals diagnosed with mental health problems would health problems meant that other countries around the
often need support and supervision. They would need world swiftly followed suit in making mental health
help maintaining their necessary medication regime, treatment and aftercare available in the community
finding and keeping a job or applying for and securing (Hafner & van der Heiden, 1988). These events led to
welfare benefits. They may also have needed help with the development of a combination of services usually
many aspects of normal daily living that others would termed assertive community treatment or assertive
take for granted, such as personal hygiene, shopping, outreach, and, in the US alone, this has led to around a
a PSYCHOPATHOLOGY
THE CLIENT’S PERSPECTIVE 1.1:

THE EXPERIENCE OF HOSPITALIZATION
Janey describes her first experience of a psychiatric ward very comfortable and creaked with every breath. It took a
after exhibiting psychotic symptoms in 1985. She then long time for morning to come.
describes her experiences on being readmitted to the | spent the next few days feeling bored and frustrated
same ward after relapse in 2000. because |was not allowed offthe ward on my own and there
was not a lot to do. The two women went for their treat-
1985 ment. One came back with a headache and one felt sick and
was told to go and lay on her bed. There was intense drama
‘The ward was supposed to be for 24 people but it was my for a while when a man abruptly kicked at one of the doors
bad luck that they were decorating one ofthe other wards and tore it off its hinges. Someone seeing it set an alarm
and we had four extra beds squashed into various corners. off and suddenly there were nurses everywhere. The man
The whole area smelled of smoke, floor cleaner and urine -— (who never spoke the whole time | was there) was given
in that order. | was given a bed - one of five in a four- some medication and order was resumed. The Christmas
person room - and introduced to my two neighbours. decorations were put up — paper chains and plastic baubles
A nurse went through my things, listing my valuables and only. Later another man in black leather silently and inexpli-
in the end confiscating my birth control pills. | argued cably held my hand while we were watching TV:
about that too because | didn’t see how oestrogen and
progesterone could be seen as dangerous. 2000
The other patients terrified me; some seemed to have
strange glassy-eyed expressions or shambling walks. ‘Of course the building hasn't changed and, although there
There were people pacing the ward in silence, someone have obviously been several facelifts within the ward, it
smashed a guitar against the wall, another person wet the still has that lived-in look, with splodges of something-or-
floor. One of my room-mates, an oldish, sleepy-looking other on the floor and walls. The internal structure of the
woman called Amy, told me that she had entered ‘The place has changed a little, so the nurses have a big room,
Brain of Britain’ programme in the past but frankly, | didn’t as compared with a little one (6 years ago) and a nursing
believe her. And there was a young man in a wheelchair, station (15 years ago). | didn’t walk into a sea of smoke this
who, | was informed, had jumped off a building. Most time, all smoking has been confined to one room. We have
people were smoking heavily. carpet in the corridor and there are more single rooms too.
late someone else's dinner (they were on leave) because But other than that, the basic cubicle with bed, wardrobe
food was ordered two days ahead and | had yet to fill in and locker are the same. Drug times, ward rounds and that
menus. Then | retreated onto my bed to hide and to try to sort of thing seem immutable, set in stone. Unfortunately,
read — desperately attempting to act normal so | could go even some of the patients have stayed the same - though
home as soon as possible. Fortunately, my husband came | suppose they can say that of me.
to visit me and | felt happier for a while. The rules of the ward are stricter, with notices pinned up
| heard a weird conversation between two women in to remind us of them.’No visitors until four o'clock’ ‘no mobile
my room who were to have a treatment in the morning. phones, ‘no smoking except in the smoking room; ‘drug and
Both were scared because they didn’t know what to expect alcohol use will result in the police being called; and so on.
and | couldn't imagine what was going to happen to them. And good behaviour is enforced with a‘sin bin; the seclusion
That night | had to queue at the drug trolley for my room (I was threatened with seclusion for kicking the door
birth control pill. The quantity of medication some of the in a moment's temper.) Surprisingly, all of this makes for a
patients were getting surprised and shocked me. The more relaxed, less dog-eat-dog atmosphere.
only drug whose name | recognized was chlorpromazine There is a mission statement on the wall by the new
because | had been given it when | was 15. Some people and bigger nurses’ room now. It contains lots of long words
received a bright orange sticky liquid that had to be meas- like ‘integrity’, ‘confidentiality’ and ‘valuing individuals’ —
ured out carefully, others a large amount of a brown liquid. the shortest is ‘caring’ | guess this is a response to hospi-
Afterwards there was hot milk to make a bedtime tal trusts and The Patients’ Charter, though I’m not sure
drink of chocolate or Ovaltine but | was not quick enough that practically it makes any difference at all. Observation
so | didn’t get any. | spent the night getting up to switch levels are more relaxed: the hell of having a nurse with
the night light off because it was too bright to sleep, only you all the time — even in the loo - seems to have disap-
to have the staff switch it back on again. The bed was not peared. The food is still bad, with little green vegetables.
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA (oa
The queue for medication still takes time to get through, Once more I’m back out in the community, trying to sort
and ECT is still done on Tuesday and Friday. Sadly, the my life and planning not to have to go into hospital again
suicide of those with a mental health problem has not
changed at all. During my three weeks in the ward, one of Source: Adaptedfrom http://www.schizophrenia.co.uk/treatment/
my fellow patients found a way to kill himself. treatment_articles/treatment.
tenfold decrease in the number of people being treated UK, assertive outreach is a way of working with groups
in hospital for mental health problems (Torrey, 2001). of individuals with severe mental health problems who
Assertive community treatment programmes help peo- do not effectively engage with mental health services.
ple recovering from psychotic episodes with their medi- Assertive outreach staff would expect to meet their cli-
cation regimes, psychotherapy, assistance in dealing ents in their own environments, whether that is a
with everyday life and its stressors, guidance on making home, café, park or street, and the aim is to build a
decisions, residential supervision and vocational train- long-term relationship between the client and mental
ing (Bebbington, Johnson & Thornicroft, 2002). In the health services.
SELF-TEST QUESTIONS
° Why was demonic possession such a popular way of explaining psychopathology in historical times?
© What are the pros and cons of the medical model of psychopathology?
® How has care for people with mental health problems developed from the times of asylums to the present day?
SECTION SUMMARY
1.1 ABRIEF HISTORY OF PSYCHOPATHOLOGY
This section has provided an historical perspective on the way in which people have attempted to understand and explain
mental health problems, and also describes how people with mental health problems have been treated over the centuries.
Today, most models of mental health provision espouse compassion, support, understanding, and empowerment for indi-
viduals suffering mental health problems (Repper & Perkins, 2006), but it has been a long journey to get to this point. It has
,
required us to understand that individuals with mental health problems are not ‘possessed, they do not need to have ‘demons
exorcised or driven from their bodies by physical force, they do not need to be incarcerated in asylums, and nor do they need
life-long custodial care in psychiatric institutions. However, while most of the physical constraints and impositions imposed
on individuals with mental health problems have been lifted, attitudes to mental health problems have been slower to evolve,
and the stigma and discrimination associated with mental health problems remain a significant issue in need of resolution
(see section 1.4).
The key points are:

e Historical explanations of psychopathology such as ‘demonic possession’ often alluded to the fact that the individual had
been ‘possessed’ in some way.
e The medical model attempts to explain psychopathology in terms of underlying biological or medical causes.
© Historically individuals with mental health problems were often locked away in asylums or given lifelong custodial care in
psychiatric hospitals.
‘
© Current models of mental health care espouse compassion, support, understanding, and empowerment.
aia PSYCHOPATHOLOGY
. ; -
service user groups (groups of individuals who are end
1.2 DEFINING users of the mental health services provided by, for
PSYCHOPATHOLOGY example, government agencies such as the NHS), chari-
table organizations that champion the rights of mental
health service users, such as Rethink (www.rethink.org),
The personal accounts at the beginning of this chapter and “Time to Change’, a national UK programme aiming
have been chosen to represent rather different and con- to promote awareness of service user groups Groups of individu- f
trasting examples of mental health problems. However, mental health problems als who are end users of the mental health
it is not hard to believe that the experiences reported by and to combat stigma services provided by, for example, govern-
Joan, Greg and even Erica are ones for which they would and discrimination (www » ment agencies such as the NHS.
be happy to receive some structured help and support. .time-to-change.org.uk).
Interestingly, even though her behaviour may seem the So, when considering how to define psychopathology
most bizarre of each of these introductory accounts, we must consider not only whether a definition is useful
Betty is the one who doesn’t believe she has a problem. in the scientific and professional sense, but also whether
So how do we define what is a problem that should it provides a definition that will minimize the stigma
be considered suitable for support and treatment, and experienced by sufferers, and facilitate the support they
what is not? Unlike medicine, we can’t simply base our need to function as inclusive members of society. Let us
definitions on the existence of a pathological cause. bear this in mind as we look at some potential ways of
This is because we have already argued that psychologi- identifying and defining psychopathology.
cal problems often do not have underlying physical or
biological causes; and, secondly, knowledge of the aeti-
ology of many psychopathologies is still very much in 1.2.1 Deviation from the
its infancy, so we are not yet in a position to provide Statistical Norm
a classification of psychopathologies that is based on
causal factors. This leads us to try to define psychopa- We can use statistical definitions to decide whether an
thology in ways that are independent of the possible activity or a psychological attribute deviates substantially
causes of such problems — and, as we shall see, many from the statistical norm, and in some areas of clinical
attempts to do this have important ethical and practical psychology this has been
used as a means of decid- Statistical norm The mean, average
implications.
: : or modal example of a behaviour.
The problems of defining psychopathology not only ing whether a particular
revolve around what criteria we use to define psychopa- disorder meets diagnostic criteria. For example, in the
thology, but also what terminology we use. For exam- area of intellectual disability, if an IQ score is significantly
ple, there are still numerous psychopathology courses below the norm of 100 this has been used in the past as
and text books that use the title abnormal psychology. one criterion for diagnosing intellectual disability (see
Merely using this title Table 17.3). Figure 1.1 shows the distribution of IQ scores
abnormal psychology An alternative implies that people suffer- in a standard population, and this indicates that the per-
definition of psychopathology, albeit with ing from mental health centage of individuals with IQ scores below 70 would be
stigmatising connotations relating to not
being ‘normal:
problems are in some way relatively rare (i.e. around 2-3 per cent of the population).
‘abnormal’ either in the However, there are at least two important problems with
statistical or the functional using deviations from statistical norms as indications of
sense. But the term ‘abnormal’ also has more important psychopathology. Firstly, in the intellectual disability case,
ramifications because it implies that those people suffer- an IQ of less than 70 may be statistically rare, but rather
ing psychopathology are in some way ‘not normal’ or than simply forcing the individual into a diagnostic cate-
are inferior members of society. In this sense, the gory, a better approach would be to evaluate the specific
‘abnormal’ label may affect our willingness to fully needs of individuals with intellectual disabilities in a way
include such individuals in everyday activities and may that allows us to suggest strategies, services and supports
lead to us treating such individuals with suspicion rather that will optimize individual functioning. Secondly, as we
than respect (see section 1.4 for a fuller account of men- can see from Figure 1.1, substantial deviation from the
tal health stigma and how this affects people suffering norm does not necessarily imply psychopathology
with mental health problems). Individuals with mental because individuals with exceptionally high IQs are also
health problems have become increasingly vocal about statistically rare — yet we would not necessarily be willing
how psychopathology and those who suffer from it are to consider this group of individuals as candidates for
labelled and perceived by others, and examples of psychological intervention. We might feel that adopting a
groups set up to communicate these views include definition of psychopathology that is statistically based
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA oa
political dissidents who were active against the commu-

nist regime were regularly diagnosed with schizophrenia
and incarcerated in psychiatric hospitals. At first, we might
think that this is a cynical method of political repression
used to control dissent, but amongst many in the Soviet
Union at the time it represented a genuine belief that
anti-Soviet activity was indeed a manifestation of psycho-
Below Average Average Above Average
pathology (surely, anyone who wanted to protest against
Percentage |= the perfect social system must be suffering from mental
of scores in 13.59 |34.13 |34.13] 13.59| 2.14 health problems!). Soviet psychiatrists even added to the
interval
official symptoms of schizophrenia by including ‘reformist
Stanford-
Binet lQ
8 84 100 116 13 delusions: a belief that an improvement in social conditions
can be achieved only through the revision of people’s atti-
tudes, in accordance with the individual’s own ideas for the
FIGURE 1.1 This figure represents a normal distribution
transformation of reality’ and ‘litigation mania: a convic-
curve for IQ scores. From this distribution it can be seen that
tion, which does not have any basis in fact, that the indi-
68 per cent of people score between 84 and 116 points, while
only 2.27 per cent of people have an IQ score below 68 points.
vidual’s own rights as a human being are being violated
This graph suggests that around 2-3 per cent of the popula-
and flouted’ (Goldacre, 2002). However, since the collapse
tion will have IQs lower than the 70 points that is the diagnos- of the Soviet system, few would suspect that these kinds of
tic criterion for intellectual development disorder. However, beliefs and activities are representative of psychopathology.
the problem for basing a definition of psychopathology on Second, it is difficult to use cultural norms to define
scores that deviate substantially from the norm is that high IQ psychopathology because cultural factors seem to sig-
also is very rare. Only 2.27 per cent of the population have an nificantly affect how psychopathology manifests itself.
IQ score greater than 132 points. For example: (1) social and cultural factors will affect the
vulnerability of an individual to causal factors (e.g. poor
mental health is more prevalent in low-income coun-
lends some objectivity and measurability to our defini-
tries) (Desjarlais, Eisenberg, Good & Kleinman, 1996);
tion. However, where we draw our cut-off points between
(2) culture can produce ‘culture-bound’ symptoms of
normality and abnormality will still be a subjective judg-
psychopathology which seem confined to specific cul-
ment. Finally, emotions such as anxiety and depression
tures and can influence how stress, anxiety and depres-
that underlie the most common mental health problems
sion manifest themselves (two examples of such
are not statistically rare emotions. They are experienced
‘culture-bound’ effects are described in Focus Point
almost daily by most people, and this represents another
1.3, and these are known as Ataque de Nervios, a form
reason why deviation from the statistical norm does not
of panic disorder found in
make a good basis on which to define psychopathology. Ataque de Nervios A form of panic disor-
Latinos from the Caribbean
der found in Latinos from the Caribbean.
(Salman, Liebowitz, Guar-
naccia, Jusino, Garfinkel Seizisman A state of psychological
1.2.2 Deviation from Social etal., 1998), and Seizisman, paralysis found in the Haitian community.
and Political Norms a state of psychological par-

alysis found in the Haitian community (Nicolas, De Silva,
There is often a tendency within individual societies for Grey & Gonzalez-Eastep, 2006)), and (3) society or cul-
the members of that society to label a behaviour or activ- ture can influence the course of psychopathology — for
ity as indicative of psychopathology if it is far removed example, schizophrenia in developing countries has a
from what they consider to be the social norms for that more favourable course and outcome than in developed
culture. We assume (perhaps quite wrongly) that socially countries (Weisman, 1997).
normal and acceptable behaviours have evolved to rep-
resent adaptive ways of behaving, and that anyone who
deviates from these norms is exhibiting psychopathol- 1.2.3 Maladaptive Behaviour
ogy. However, it is very difficult to use deviation from and Harmful Dysfunction
social norms, or even violations of social norms, as a way
of defining psychopathology. It is often tempting to define psychopathology in terms
First, different cultures often differ significantly in what of whether it renders the individual incapable of adapt-
they consider to be socially normal and acceptable. For ing to what most of us would consider normal daily
example, in the Soviet Union during the 1970s and 1980s, living. That is, whether a person can undertake and hold
S16: PSYCHOPATHOLOGY
it PSYCHOPATHOLOGY AND CULTURE

~-
in Psychopathology can manifest itself in different forms by adopting avoidance and withdrawal strategies-
= in different cultures, and this can lead to some disor- hence the common diagnosis of panic disorder with
2)
a. ders that are culture specific (i.e. have a set of symp- agoraphobia.
WV toms which are found only in that particular culture).
ms
U Two such examples are Ataque de Nervios, which is
SEIZISMAN
2) an anxiety-based disorder found almost exclusively
ba amongst Latinos from the Caribbean (Salman et al., The name literally means ‘seized-up-ness’ and refers to a
1998), and Seizisman, a state of psychological paraly- state of paralysis usually brought on by rage, anger, or
sis found in the Haitian community (Nicolas, DeSilva, sadness, and in rare cases happiness. Events that can
Grey & Gonzalez-Eastep, 2006). cause Seizisman include a traumatic event (such as receiv-
ing bad news), a family crisis, and verbal insults from
ATAQUE DE NERVIOS others. Individuals affected by the syndrome become
completely dysfunctional, disorganized and confused,
Its literal translation is ‘attack of nerves, and symp- and unresponsive to their surroundings (Laguerre, 1981).
toms include trembling, attacks of crying, screaming The following quote illustrates how viewing traumatic
uncontrollably, and becoming verbally or physically events while working within a Haitian community that is
aggressive. In some cases, these primary symptoms attuned to the symptoms of this syndrome can actually
are accompanied by fainting bouts, dissociative expe- give rise to these culture-bound symptoms:
riences and suicide attempts.
Research on Ataque de Nervios has begun to show
| remember over and over, when | was a UN Human
that it is found predominantly in women, those over
Rights Monitor and | was down there in Port-au-
45 years of age, and those from low socio-economic
Prince viewing cadaver after cadaver left by the
backgrounds and disrupted marriages (Guarnaccia
Haitian army, people would say, ‘Now go home and
et al., 1989). The symptoms appear to resemble many
lie down or you will have Seizisman’ And | never
| of those found in panic disorder, but with a coexisting
really had a problem, you know? | never threw up
affective disorder characterized by emotional lability
or fainted no matter what | saw, but | started to feel
and anger (Salman et al., 1998).
‘stressed’ which is an American illness defined in an
| From this research, it appears that Ataque de Nervios
American way. After viewing one particularly vile
may be a form of panic disorder brought on by stress-
massacre scene, | went home and followed the cul-
| ful life events (such as economic or marital difficulties),
tural model | had been shown. | lay down, curled
but whose expression is determined by the social and
up, and went incommunicado. ‘Ah-hah! Seizisman!’
cultural norms within that cultural group. In particular,
said the people of my household.
| Latino cultures place less emphasis on self-control and
emotional restraint than other Western cultures, and so
Source: Nicholas, G., De Silva, A.M., Grey, K.S. & Gonzalez-
the distress of panic disorder in Latinos tends to be Eastep, D. (2006), Using a multicultural lens to understand
| externalized in the form of screaming, uncontrolled illness among Haitians living in America. Professional
behaviour and aggression. In contrast, in Western cul- Psychology: Research and Practice, 37, 702-707. American
tures the distress of panic disorderis usually coped with Psychological Society. Reprinted with permission.
down a job, can cope with the demands of being a par- those disorders are defined. The problem with defining
ent, develop loving relationships, and function socially. In psychopathology solely in terms of maladaptive behaviour
its extreme form, maladaptive behaviour might involve is also apparent when we discuss forms of behaviour that
behaving in a way that is a threat to the health and well- we might call maladaptive, but we would not necessarily
being of the individual and to others. It is certainly the want to label as psychopathology. The behaviour of many
case that current diagnostic criteria, such as DSM-5, do use people convicted of murder or terrorist acts, for exam-
deficits in social, occupational and educational functioning ple, is maladaptive in the sense that it is harmful to oth-
as one criterion for defining ers, but it is by no means the case that all murderers or
terrorists commit their crimes because they have mental
/ TY LE EAE ES Oe FELLER TRG Re many psychological disor-
—=| To read more about DSM-5 go to \ d b fareee

http: phoaihes peut j €rs, Dut it 1s Ay no means health problems. On the other side of the coin, it can be
— mmm the only criterion by which argued that many forms of psychopathology may not be
h
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA ar
representative of maladaptive behaviour but instead suffer considerable personal distress — often to the point
serve a protective or adaptive function. For example, a of wanting to take their own lives. Defining psychopa-
case can be made for suggesting that specific phobias such thology in terms of the degree of distress and impair-
as height phobia, water phobia, snake and spider phobia ment expressed by the sufferer is useful in a number of
are adaptive responses which protect us from exposure ways. Firstly, it allows people to judge their own ‘normal-
to potentially life-threatening situations (e.g. Seligman, ity’ rather than subjecting them to judgments about their
1971; see Chapter 6). ‘normality’ made by others in society, such as psycholo-
A similar approach is to assume that mental health gists or psychiatrists. Many people who are diagnosed
problems can be defined as harmful dysfunction with psychological disorders originally present them-
harmful dysfunction Assumption (Wakefield, 1997). This selves for treatment because of the distress and impair-
that psychopathology is defined by the view assumes that psycho- ment caused by their symptoms, and to some degree this
‘dysfu nction’ of a normal process that has pathology is defined by the makes them judges of their own needs. Secondly, defin-
i consequence of being in some way
‘dysfunction’ of a normal ing psychopathology in terms of the degree of distress
armful.
process that has the conse- and impairment experienced can be independent of the
quence of being in some way harmful. For example, type of lifestyle chosen by the individual. This means
‘hearing voices’ during episodes of psychosis may be we do not judge whether someone has a psychopathol-
caused by the brain’s inability to turn off unwanted ogy purely on the basis of whether they are perceived as
thoughts, and these may give rise to potentially harmful productively contributing to society or not, or whether
consequences such as extreme paranoia. The problem they actively violate social norms, but on the basis of
with this type of definition is that we still know very little how they are able to cope with their lifestyle.
about the brain mechanisms that generate psychopathol- As attractive as this definition for defining psycho-
ogy symptoms, so it is very difficult to know what ‘nor- pathology seems, it does have a number of difficulties.
mal’ process might be dysfunctioning. In addition, there Firstly, this approach does not provide any standards by
are now a number of taxometric studies suggesting that which we should judge behaviour itself. For example, in
many common mental health problems are best consid- our introductory personal accounts, Betty’s behaviour and
ered as dimensional rather than categorical (e.g. Haslam, thoughts do not entirely seem to be based in reality,
Williams, Kyrios, McKay & Taylor, 2005; Olatunji, and they could be manifestations of the thought-
Williams, Haslam, Abramowitz & Tolin, 2008). That is, disordered behaviour that is sometimes characteristic
distressing mental health symptoms are just more of those experiencing psychotic episodes (see Chapter
extreme versions of normal emotions and behaviours, 8). But Betty does not express any feelings of distress or
and are not in any way as qualitatively different from nor- impairment. Similarly, in Erica’s story she does admit
mal behaviour as the harmful dysfunction model would that her substance dependency is beginning to cause her
imply. some distress, but should we consider that a teenager’s
drug addiction is in need of treatment only if they express
unhappiness about their situation? Finally, psychopathol-
ogy classification schemes do include so-called ‘disor-
1.2.4 Distress and Disability
ders’ in which diagnosis does not require that the sufferer
Later in this chapter we will look at some of the ways necessarily reports any personal distress or impairment.
in which psychologists and psychiatrists have attempted A good example of this is that group of disorders known
to classify psychopathology, and in order to be diagnosed as personality disorders (see Chapter 12). For example, indi-
as a psychological disorder one of the most common viduals diagnosed with borderline personality disorder or
requirements is that the symptoms must cause ‘clinically antisocial personality disorder frequently exhibit behav-
significant distress or impairment in social, academic, or iour that is impulsive, emotional, threatening, and harm-
occupational functioning’. It is clearly the case that many ful to themselves and others. Yet they are often unwilling
individuals with severe symptoms of psychopathology do to admit that their behaviour is unusual or problematic.
SELF-TEST QUESTIONS
° What are the problems with using the normal curve to define psychopathology?
© How do cultural factors make it difficult to define psychopathology in terms of deviations from social norms?
e Whatare the pros and cons of using maladaptive behaviour or distress and impairment as means ofdefining psychopathology?
RIS PSYCHOPATHOLOGY
SECTION SUMMARY
1.2 DEFINING PSYCHOPATHOLOGY
None of these individual ways of defining psychopathology is ideal. They may fail to include examples of behaviour that we
intuitively believe are representative of mental health problems (the distress and impairment approach), they may include
examples we intuitively feel are not examples of psychopathology (e.g. the statistical approach, the deviation from social
norms approach), or they may represent forms of categorisation that would lead us simply to imposing stigmatising labels on
people rather than considering their individual needs (e.g. the statistical approach). In practice, classification schemes tend
to use an amalgamation of all these approaches with emphasis being placed on individual approaches depending on the
nature of the symptoms and disorder being classified. a
To sum up:
* Potential ways of defining psychopathology include deviation from the statistical norm, deviation from social norms,
exhibiting maladaptive behaviour, and experiencing distress and impairment.
Pereerrrerretrrrrrrrrr iret rr tirr rrr rere eee
Secondly, this view also applies to psychopathology. For

1.3 EXPLANATORY example, symptoms of psychosis might be explained
APPROACHES TO genetically (in terms of the inheritance of genes that give
rise to a predisposition for these symptoms), biologically
PSYCHOPATHOLOGY (in terms of abnormalities in brain function that gener-
ate symptoms), behaviourally (in terms of how sympto-
matic behaviours are learnt through experience), and
Despite the fact that symptoms of mental health prob-
psychologically (in terms of how symptoms might be
lems seemed baffling to many people, there was still a
generated by dysfunctional ways of thinking). In many
strong desire to understand psychopathology, to describe
cases, a specific psychopathology can be explained at all
its causes, and, as a consequence, to develop effective
these different levels. Furthermore, these explanations
interventions. Section 1.1 described some of the impor-
within different paradigms are not mutually exclusive —
tant milestones in the history of psychopathology, and
they supplement each other and provide a fuller, richer
how an understanding of mental health problems has
understanding of that psychopathology.
evolved from the level of primitive beliefs, through an
The following sections introduce you to some exam-
application of medical knowledge, to current models of
ples of these different paradigms and how they each con-
care. This section will now introduce you to the main
tribute to our broad understanding of psychopathology.
contemporary explanatory approaches to psychopathol-
ogy, and these are ones that you will encounter regularly
in the following chapters.
At this point it is important to understand what an
1.3.1 Biological Models
explanatory paradigm is, and why we can explain men- Genetics and neuroscience are two of the most impor-
tal health problems in many different ways within a tant biological paradigms through which researchers
number of different paradigms. Firstly, human beings attempt to understand psychopathology. The discipline
are multifaceted organisms; they consist of a genetically of genetics provides us with a variety of techniques that
propagated biological substrate which serves as a basis allow an assessment of whether psychopathology symp-
for behaviour and a whole range of psychological pro- toms are inherited or not, and neuroscience techniques
cesses, such as thinking, learning, remembering, per- allow us to determine whether psychopathology symp-
ceiving, and so on. These genetic, biological, behavioural toms are associated with abnormalities or differences in
and psychological processes are interdependent and brain or central nervous system functioning.
together make up our conception of the complete
thinking and behaving human being. But genetic, bio-
logical, behavioural and psychological processes can also Genetics
be studied independently; they have their own language Genetics is a fast growing and important branch
of description, and researchers may be skilled in study- of science, and collabora- genetics The study of heredity and the
ing people only within one of these basic paradigms. tions such as the Human variation of inherited characteristics. 2
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA ec
Genome Project are attempting to identify those genes extent to which they are genetically related to
that may be responsible for human characteristics, disor- each other. These studies are known as
ders and diseases (Collins & McKusick, 2001). People are concordance studies, where the probability of
biological organisms who come into the world with a bio- symptoms occur- concordance studies Studies designed
logical substructure that will be significantly determined ring can be related to investigate the probability with which
by the genes they have inherited from their ancestors. to the degree to family members or relatives will develop a
It is therefore almost a truism to say that behaviour — psychological disorder depending on how
which different
closely they are related — or, more specifi-
and mental health problems too — will therefore have family members cally, how much genetic material they have
at least some genetic component. In some cases the share genes in in common.
genetic component may be extremely influential (e.g. common.
in Huntington’s disease — see Focus Box 1.4); in others
2. Twin studies compare the probability with which
it may be a necessary component but may not always
monozygotic (MZ) and dizygotic (DZ) twins both
be sufficient to trigger a mental health problem; in still
develop psychopathology symptoms. MZ twins
other cases the genetic component may be relatively
share 100 per cent of their genetic material,
nonspecific and less important to the development of a
whereas DZ twins share only 50 per cent of their
mental health problem than the experiences that an indi-
genes, so a genetic
vidual may have during their lifetime. twin studies Studies in which researchers
explanation of
The way in which genetics might influence psychopa- have compared the probability with which
psychopathology monozygotic (MZ) and dizygotic (DZ) twins
thology can be studied in a variety of ways:
would predict that both develop symptoms indicative of a
1. By studying psychopathology symptoms across there would be psychopathology in order to assess genetic
greater concordance contributions to that psychopathology.
different family members who may differ in the
ne
—_
THE GENETICS OF INHERITING MENTAL HEALTH PROBLEMS
_
Huntington's disease is a degenerative neurological The gene for Huntington’s disease is dominant, and
= condition that can often give rise to dementia, and it so the disease can be inherited even if only one par-
oO
a. is caused by a dominant mutation in a gene on the ent has the mutant gene. In this case, inheriting the
Wr fourth chromosome. Each person has two copies of mutant gene is the primary factor in the affected indi-
=) this gene (each one called an allele), one inherited vidual developing the disease. In other mental health
U
Le) from each parent. In the case of Huntington's disease problems where genetic factors have been found
Me an individual only needs one copy of the mutant allele to be important (e.g. schizophrenia), inheritance is
to develop the disease. Parents randomly give one of only one of a number of factors that has been found
their two alleles to their offspring, so a child of aparent to contribute to the development of symptoms, and
who has Huntington's disease has a 50 per cent chance this has led researchers to advocate a diathesis—stress
of inheriting the mutant version of the gene from their model in which inherited factors provide a vulnerabil-
parent. A grandchild of aperson with Huntington’s dis- ity to develop symptoms, but these symptoms do not
ease has a 25 per cent chance of inheriting the mutant appear unless the individual encounters stressful life
gene and so developing the disease. experiences.
Parent 1 Parent 2
h=normal allele
H = Huntington's allele
oo) (rs)
possible gametes
a Oe
possible combination
of alleles in offspring
Hh
Huntington's Huntington's
0% PSYCHOPATHOLOGY
ey ‘ %
in the diagnosis of a mental health problem in transmitting psychopathology symptoms. One method
MZ than in DZ twins (see Chapter 8 for some of identifying individual genes that has been particularly
examples of this approach). applied to psychopathology is genetic linkage analysis.
3. Because both families and twins are likely to Linkage analysis works by
share similar environments as well as genes, comparing the inheritance genetic linkage analysis A method of
identifying individual genes by comparing ©
interpretation of family and twin studies can be of characteristics for which
the inheritance of characteristics for which
difficult. However, many of these difficulties of gene location is known gene location is known (e.g. eye colour)
interpretation can be overcome by studying (e.g. eye colour) with the with the inheritance of psychopathology
the offspring of MZ and DZ twins rather inheritance of psychopa- symptoms.
than the twins themselves (Gottesman & Bertelsen, thology symptoms. For
1989). If one MZ twin develops psychopathology example, if the inheritance of eye colour follows the
symptoms and the other does not, any genetic same pattern within a family as particular psychopathol-
element in symptoms should still show up in the ogy symptoms, then it can reasonably be concluded that
children of either of the two MZ twins. That is, the gene controlling the psychopathology symptoms can
the children of the MZ twins should still exhibit probably be found on the same chromosome as the gene
similar rates of risk for the psychopathology controlling eye colour. While such methods are extremely
(because they have inherited the same valuable, it should be pointed out that it is very rare that
predisposition) — even though one of their parents psychopathology symptoms can be traced to an individ-
developed the symptoms and the other did not. ual gene, and very often symptoms are associated with
multiple genes, which testifies to the complex and often
However, in the vast majority of psychopathologies we heterogeneous nature of mental health problems (e.g.
will describe in this book, people do not solely inherit a Badner & Gershon, 2002; Levinson, Lewis & Wise, 2002;
mental health problem through their genes, a mental health Faraone, Doyle, Lasky-Su, Sklar, D’Angelo et al., 2007).
problem develops because of an interaction between a In addition, an alternative means of identifying psychopa-
genetic predisposition and our interactions with the thology-relevant genes is to use non-human animals. For
environment (Shenk, 2010). This is basically what is known example, researchers can manipulate specific genes in ani-
as a diathesis—stress model of psychopathology, where mals with some accuracy, and in mice studies can even
‘diathesis’ refers to an inher- delete individual genes. This then enables the researcher
diathesis-stress model Model that sug- ited predisposition and to determine whether that gene is linked to any changes
gests a mental health problem develops
‘stress’ refers to a variety of in the animal’s behaviour that might be indicative of psy-
because of an interaction between a
genetic predisposition and our interactions experiences that may trig- chopathology (e.g. by observing more anxious behav-
with the environment. ger the inherited predisposi- iour) (Gross, Zhuang, Stark, Ramboz et al., 2002).
tion (this is a model that is Finally, one new area of genetics highly relevant
particularly important in the understanding of psychosis: to psychopathology is epigenetics. We know that
see Chapter 8). This interaction between genes and experi- aspects of psychopathology and mental health can
ences gives rise to the notion of heritability. Heritability is be influenced
; by genetics epigenetics The study of changes in
a measure of the degree to which symptoms can and hereditary factors, and _organisms caused by modification of gene
be accounted for by genetic we also know that personal expression rather than alteration of the
heritability A measure of the degree to factors, and this ranges from experiences can also influ- genetic code. _
which symptoms can be accounted for 0 to 1; the nearer this figure ence psychopathology. However, recent research in the
by genetic factors. It ranges from 0 to 1,
and the nearer this figure is to 1, the more
is to 1, the more important developing area of epigenetics suggests that the way
important are genetic factors in explaining are genetic factors in that parents behaved or what they ate can also affect the
the symptoms. explaining the symptoms. subsequent behaviour of their offspring by influencing
In the case of Huntington’s their offspring’s genetic heritage, either by changing the
disease described in Focus Point 1.4, the heritability of nature of their DNA or triggering or inhibiting the
Huntington's symptoms is very close to 1 because if you expression of genes that may represent risk factors for
inherit the dominant gene for this disorder, that is sufficient psychopathology. Similarly, the early experiences of an
to ensure that the individual will develop the disease. individual may either trigger or inhibit the expression of
Not only do genetic approaches to psychopathology genes they may possess that make them vulnerable to
attempt to estimate the heritability of individual disor- mental health problems such as anxiety or depression,
ders, the area of molecu- and in this way there can be a direct interaction between
molecular genetics Genetic approach
that seeks to identify individual genes lar genetics also seeks to environmental factors and inherited factors. For exam-
that may be involved in transmitting identify individual genes ple, early life stress can enable the expression of genes
psychopathology symptoms. that may be involved in that control the neuroendocrinology of post-traumatic
8
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA eke
stress disorder (PTSD), which then puts such individuals in executive functions such as planning and decision mak-
at higher risk of developing PTSD after highly traumatic ing, error correction and troubleshooting, novel situa-
life experiences (Yehuda, Flory, Pratchett, Buxbaum tions, and inhibiting habitual and impulsive responses
et al., 2010). This has important implications for our (Norman & Shallice, 1980). Given the important func-
understanding of how mental health problems develop tions of the frontal lobes, it is an area of the brain where
and the aetiology of those disorders (Kofink, Boks, deficits or abnormalities have been implicated in many
Timmers & Kas, 2013). types of psychopathology, including attention disorders,
perseveration and stereotyped behaviour patterns, lack
Neuroscience of drive and motivation, inability to plan ahead, and apa-
The neuroscience paradigm seeks an understanding of thy and emotional blunting. Alternatively, because the
psychopathology by identifying aspects of the individu- frontal lobes also control response inhibition, deficits in
al’s biology that may contribute to symptoms. The main this area can also be associated with impulsivity, eupho-
focus of this paradigm is on brain structure and function, ria, and aggressive behaviour — especially in relation to
although the broader activity of the neuroendocrine sys- personality disorders (Brower & Price, 2001; Meyers,
tem has also been implicated in some psychopathology Berman, Scheibel & Hayman, 1992).
symptoms, especially mood disorders (the neuroendo- A further set of brain areas that are often implicated in
crine system involves interactions between the brain and psychopathology are collectively known as the limbic sys-
the endocrine system that produces hormone secretions tem. The limbic system comprises the hippocampus,
in the body). mammillary body, amygdala, hypothalamus, fornix and
thalamus. It is situated
Brain structure and function The brain is the organ beneath the cerebral cortex limbic system A brain system compris-
ing the hippocampus, mammillary body,
that controls and organizes most of a person’s behaviour — (see Figure 1.2b) and is ~amygdala, hypothalamus, fornix and
including their actions and their thoughts, so it is not sur- thought to be critically thalamus. It is situated beneath the cer-
prising that the brain has been a focus for attempting involved in emotion and ebral cortex and is thought to be critically
to understand psychopathol- learning. For example, the involved in emotion and learning.
orpus callosum A set of nerve fibres
which connects the two mirror-image ogy. The brain is divided into hippocampus is involved in spatial learning and the amyg-
hemispheres ofthe brain. two mirror-image hemi- dala is an important region coordinating attention to emo-
spheres that are connected tionally relevant stimuli
by a set of nerve fibres called the corpus callosum. (e.g. threatening or fear-rel- hippocampus A part of the brain which is
é : involved in spacial learning.
The outer convoluted area of the brain is known as the evant stimuli). Because of DeP 9
cerebral cortex, and the large troughs in the convolu- its function in regulating emotional responses, the amyg-
3 A
tions are called fissures
“
dala is an important brain structure in understanding many
cerebral cortex The outer, convoluted
(see Figure 1.2a). The lat- aspects of psychopathology. It is involved in the formation
area of the brain. |
eral and central fissures and storage of emotion- amygdala The region ofthe brain
divide the cerebral cortex relevant stimuli and pro- responsible for coordinating and initiating
) For a brain labelling activity based on ) into four lobes: the frontal, vides feedback to the responses to fear.
é Figure 1.2 go to
www.wiley-psychopathology.com/
| occipital, temporal and pari- thalamus that results in appropriate motor action (Del
activities/ch1 etal lobes, and these areas Casale, Ferracuti, Rapinesi, Serata et al., 2012). Because of
serve various specific func- this role, the amygdala is important in activating phobic
tions. The occipital lobe is fear (Ahs, Pissiota, Michelgard, Frans, Furmark et al., 2009),
occipital lobe Brain area associated with
the area for visual percep- and depressed individuals show more activity in the amyg-
visual perception.
tion, the temporal lobe is dala when viewing emotional stimuli than non-depressed
considered to be a focus for individuals (Sheline, Barch, Donnelly, Ollinger et al., 2001).
temporal lobe The areas of the brain
that lie at the side of the head behind the
memory processes, and the
temples and which areinvolved in hearing, parietal lobe is associated Brain neurotransmitters These are the chemicals
memory, emotion, language, illusions, with visuomotor coordina- that help neurones to communicate with each other and
tastes and smells. tion (Kolb & Whishaw, 2009). thus are essential components of the mechanisms that
However, the frontal lobes regulate efficient and effective brain functioning. During
parietal lobe Brain region associated with are especially important, synaptic transmission, neurones release a neurotransmit-
visuo-motor coordination. and are the areas of the ter that crosses the synapse
brain that are considered and interacts with receptors ff For a brain labelling activity
frontal lobe One of four parts of the cer- to make us_ uniquely on neighbouring neurones, based on Figure 1.3 go to
ebrum that control voluntary movement, www.wiley-psychopathology.com/
human. The frontal lobes and most neurotransmitters | activities/ch1
verbal expressions, problem solving, will
power and planning. are known to be important relay, amplify and modify '
2" PSYCHOPATHOLOGY
(a) The Cerebral Cortex
Axon
Synaptic vesicles
Synapse
Neurotransmitter
Dendrites
Receptor
FIGURE 1.3 Neurons, neurotransmitters and nerve impulses.

The cells in the brain are called neurons and consist of (1) the cell
body, (2) dendrites, and (3) one or more axons of varying length.
When a neuron sends a signal to another neuron, a nerve impulse
travels down the axon to the synapse between the two neurons. The
(b) The limbic system
end of the axon contains synaptic vesicles which are small structures
Thalamus
Fornix filled with neurotransmitters. When the neurotransmitter is released
into the synapse, some of the molecules reach the receptor and a
message is sent to the post-synaptic cell. Once a pre-synaptic neu-
ron has sent its signal, the synapse then has to return to its normal
state by either breaking down any remaining neurotransmitter in
the synapse or taking it back into the axon through a process called
re-uptake.
Hypothalamus
of mood disorders (see Chapter 7); dopamine is central to
Amygdala
important theories of schizophrenia and psychotic symp-
Mammillary body toms (see section 8.5.1); and norepinephrine and GABA may
Hippocampus play a role in anxiety symptoms. Even so, the functions of
neurotransmitters are often not simple or easy to define. For
FIGURE 1.2 The neuroanatomy ofthe brain.
(a) The cerebral cortex
example, dopamine has many functions in the brain, includ-
(b) The limbic system ing important roles in regulating voluntary movement,
motivation and reward, and is critically involved in mood,
brain neurotransmitters Brain neuro- signals between neurones attention and learning. Similarly, early theories of the role
transmitters are chemicals that help neu-
(see Figure 1.3). There are
of neurotransmitters in psychopathology symptoms tended
rones to communicate with each other and to assume that symptoms were caused by either too little
are essential components of the mecha- many different types of
nisms that regulate efficient and effective brain neurotransmitters or too much of a particular neurotransmitter. This picture,
brain functioning. that can be grouped accord- however, is much too simple, and more recent theories sug-
ing to either their chemical gest that symptoms may be associated with much more
dopamine A compound that exists in
structure or to their func- complex interactions between different neurotransmitters
the body as a neurotransmitter and as a
(e.g. Carlsson, Waters, Holm-Waters, Tedroff et al., 2001).
precursor of other substances including tion, and a number of dif-
adrenalin. ferent neurotransmitters
have been implicated in Summary
serotonin An important brain neurotrans-
psychopathology, includ- Most chapters of this book will have a section on bio-
mitter where low levels are associated with
depression. ing dopamine, _ seroto- logical explanations of psychopathology where expla-
nin, norepinephrine, and nations of the causes of symptoms will be discussed
norepinephrine A neurotransmitter gamma-aminobutyric acid in terms of genetics, brain structure and function, and
thought to play a role in anxiety symptoms.
(GABA). Abnormalities in brain neurotransmitters. Because behaviour and thought
gamma-aminobutyric acid (GABA) A levels of serotonin and cannot occur in the absence of a biological substrate, it
neurotransmitter thought to play a role in norepinephrine have been is clear that biological explanations of psychopathology
anxiety symptoms. implicated in the symptoms will be highly relevant. They will tell us whether all or
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA Poke
some of the symptoms of a mental health problem are but during these cases clients often began talking about
inherited or not; they will also provide us with informa- earlier traumatic experiences and highly stressful emo-
tion about whether abnormalities in brain function or tions. In many cases, simply talking about these repressed
neurotransmitter activity are associated with psycho- experiences and emotions under hypnosis led to an eas-
pathology. There are some clear advantages to the bio- ing of symptoms. Freud built on these cases to develop
logical approach — especially in terms of treatments. One his influential theory of psychoanalysis, which was an
prominent example is that if we can identify associations attempt to explain both psychoanalysis An influential psychologi-
between psychopathology and imbalances in neurotrans- normal and abnormal psy- cal model of psychopathology based on
mitters, then we can develop pharmaceutical products chological functioning in the theoretical works of Sigmund Freud.
that might resolve this imbalance — and this has been terms of how various psychological mechanisms help to
particularly the case with mood disorders and psychotic defend against anxiety and depression by repressing
symptoms. However, mental health problems cannot memories and thoughts that may cause conflict and
always be reduced simply to biological descriptions, and a stress. Freud argued that three psychological forces shape
full understanding of the causes and experience of mental an individual’s personality and may also generate psycho-
health problems will require description and explanation pathology. These are the id (instinctual needs), the ego
at other levels (e.g. how a person’s experiences influence (rational thinking), and the superego (moral standards).
their thoughts and behaviour, how their interpretation The concept of the id was used to describe innate
of events affects their emotions, and how distress is expe- instinctual needs — especially sexual needs. He noted that
rienced and manifested). We will discuss some of these from a Mey early ae) chil- ‘id In psychoanalysis, the concept used
alternative — but complimentary — paradigms below. dren obtained pleasure _ to describe innate instinctual needs-
from nursing, defecating, especially sexualneeds,
masturbating, and other
1.3.2 Psychological Models ‘sexually’ related activities and that many forms of behav-
Moving away from the biological model of psychopa- iour were driven by the need to satisfy the needs of the id.
thology, some approaches to understanding and explain- As we grow up, Freud argued that it becomes appar-
ing mental health problems still see mental health ent to us that the environment itself will not satisfy
problems as symptoms produced by an underlying all our instinctual needs, and we develop a separate part
cause (what is known as the pathology model), but hold of our psychology known as the ego. This is a rational
that the causes are psychological rather than biologi- part of the psyche that =?
ego In psychoanalysis, a rational part of
cal or medical. These approaches often view the cause asLeM pleat? control the the psyche that attemptsto control the
as a perfectly normal and adaptive reaction to difficult impulses of the id, and impulses oftheid. ,
or stressful life conditions (such as the psychoanalytic ego defence mechanisms
view that psychopathology is a consequence of perfectly develop by which the ego
attempts to control un- ego defence mechanisms Means by
normal psychodynamic processes that are attempting bleiae 1 d which the ego attempts to control un-
to deal with conflict). As such, psychological models of acceptable 1d Impulses and acceptable id impulses and reduce the
psychopathology tend to view mental health symptoms reduce the anxiety that id anxiety that id impulses may arouse.
as normal reactions mediated by intact psychological or impulses may arouse.
cognitive mechanisms, and not the result of processes The superego devel-
ops out of both the id and SuPerege Key concept in Sigmund Freud's
that are abnormal, ‘broken’ or malfunctioning. psychoanalytic theory. The superego devel-
The following sections describe in brief some of the ego, and represents our ops out of both the id (innate instinctual
main psychological approaches to understanding and attempts to integrate ‘val- needs) and ego (a rational part of the psy-
parents ot soley. Freud, rat cag

explaining psychopathology. ues’ that we learn from our che that attempts to control the impulses
The psychoanalytical or psychodynamic model argued that we will often parents or Society
This approach was first formulated and pioneered by the judge ourselves by these
Viennese neurologist Sigmund Freud (1856-1939). He values that we assimilate and if we think our behaviour
collaborated with the physician Josef Breuer in an attempt does not meet the standards implicit in these values we
to understand the causes will feel guilty and stressed.
Sigmund Freud An Austrian neurologist According to Freud, the id, ego and superego are often
of mysterious — physical
and psychiatrist who founded the psycho-
analytic school of psychology. symptoms such as hysteria in conflict, and psychological health is maintained only
and spontaneous paralysis — when they are in balance. However, if these three factors
symptoms which appeared to have no obvious medical are in conflict then behaviour may begin to exhibit signs
causes. Freud and Breuer first tried to use hypnosis as a of psychopathology. Individuals attempt to control con-
means of understanding and treating these conditions, flict between these factors and also reduce stress and
wa PSYCHOPATHOLOGY
conflict from external events by developing defence There is no doubt that the psychoanalytical model *
mechanisms. Table 1.1 describes some of these defence has been extremely influential, both in its attempts to
defence mechanisms |n psychoanalysis, mechanisms together with provide explanations for psychopathology and in the
the means by which individuals attempt some examples of how treatments it has helped to develop. Psychoanalysis was
to control conflict between the id, ego they are presumed to pre- arguably the first of the ‘talking therapies’ and as many
and superego and also reduce stress and
vent the experience of as 20 per cent of modern practising clinical psychologists
conflict from external events.
stress and anxiety. identify themselves at least in part with a psychoana-
A further factor that Freud believed could cause psy- lytical or psychodynamic approach to psychopathology
chopathology was how children negotiated various (Prochaska & Norcross, 2003). Psychoanalysis was also
stages of development from infancy to maturity. the first approach to introduce a number of perspectives
He defined a number of on psychopathology that are still important today, includ-
stages of development Progressive important stages through ing (1) the view that psychopathology can have its origins
periods of development from infancy
which childhood develop- in early experiences rather than being a manifestation of
to maturity.
ment progressed, and each biological dysfunction, and (2) the possibility that psycho-
of these stages was named after a body area or erogenous pathology may often represent the operation of “defence
zone. If the child successfully negotiated each stage then mechanisms’ that reflect attempts by the individual to
this led to personal growth and a psychologically healthy suppress stressful thoughts and memories (see, for exam-
person. If, however, adjustment to a particular stage was ple, cognitive theories of chronic worrying in Chapter
not successful, then the individual would become fixated 6 and theories of dissociative disorders in Chapter 14).
on that early stage of devel- Theorists in the psychoanalytic tradition have elaborated
oral stage According to Freud, the first opment. For example, on Freud’s original theory, and we will see many exam-
18 months of life are based on the child’s Freud labelled the first 18 ples of psychodynamic explanations applied to specific
need for food from the mother. If the
mother fails to satisfy these oral needs, the
months of life as the oral psychopathologies presented later in this book. However,
child may become fixated at this stage and stage because of the child’s psychoanalytic theory does have many shortcomings,
in later life display ‘oral stage characteristics’ need for food from the and it is arguably no longer the explanation or treatment
such as extreme dependence on others. mother. If the mother fails of choice for most psychological problems; nor is it a par-
to satisfy these oral needs, adigm in which modern day evidence-based researchers
the child may become fixated at this stage and in later life attempt to understand psychopathology. This is largely
display ‘oral stage characteristics’ such as extreme because the central concepts in psychoanalytic theory are
dependence on others. Other stages of development hard to objectively define and measure. Because concepts
include the anal stage (18 months to 3 years), the phallic such as the id, ego and superego are difficult to observe
stage (3 to 5 years), the latency stage (5 to 12 years), and and measure, it is therefore difficult to conduct objective
the genital stage (12 years to adulthood). research on them to see if they are actually related to
TABLE 1.1 Defence mechanisms in psychoanalytic theory
Denial The individual denies the source ofthe anxiety exists (e.g. | didn’t fail my exam, it must be a mistake).
Repression Suppressing bad memories, or even current thoughts that cause anxiety (e.g. repressing thoughts about
liking someone because you are frightened that you may be rejected if you approach them).
Regression Moving back to an earlier developmental stage (e.g. when highly stressed you abandon normal coping strate-
gies and return to an early developmental stage — for instance, by smoking if you are fixated at the oral stage).
Reaction Doing or thinking the opposite to how you feel (e.g. the person who is angry with their boss may go out of
formation their way to be kind and courteous to them).
Projection Ascribing unwanted impulses to someone else (e.g. the unfaithful husband who is extremely jealous of his
wife might always suspect that she is being unfaithful).
Rationalization Finding a rational explanation for something you've done wrong. (e.g. you didn’t fail the exam because you
didn’t study hard enough but because the questions were unfair).
Displacement Moving an impulse from one object (target) to another (e.g. if you've been told off by your boss at work, you
go home and shout at your partner or kick the dog).
Sublimation Transforming impulses into something constructive (e.g. redecorating the bedroom when you're feeling
angry about something).
Each of the Freudian defence mechanisms described above function to reduce the amount of stress or conflict that might be caused by specific
experiences.
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA 2s
symptoms of psychopathology in the way that Freud and adaptive behaviour can be acquired through learning,
his associates describe (Erdelyi, 1992). then so can many forms of dysfunctional behaviour. The
two important principles of learning on which this
The behavioural model approach was based are classical conditioning and
Most psychological models have in common the view operant conditioning. Classical conditioning represents
that psychopathology is caused by how we assimilate the learning of an association between two stimuli, the
our experiences and how this is reflected in thinking first of which (the condi-
and behaviour. The behavioural model adopts the broad tioned stimulus, CS) pre- classical conditioning The learning of an
association between two stimuli, the first
view that many examples of psychopathology reflect dicts the occurrence of the
of which (the conditioned stimulus, CS)
our learnt reactions to life experiences. That is, psycho- second (the unconditioned predicts the occurrence of the second
pathology can be explained as learnt reactions to envi- stimulus, UCS). The proto- (the unconditioned stimulus, UCS).
ronmental experiences, and this approach was promoted typical example of | this
primarily by the behaviourist school of psychology. form of learning is Pavlov’s experiment in which a hungry
During the 1950s and 1960s, many clinical psycholo- dog learns to salivate to a bell (the CS) that predicts subse-
gists became disillusioned by psychoanalytic approaches quent delivery of food (the UCS), and this is represented
to psychopathology and sought an approach that schematically in Figure
was more scientific and 1.4. In contrast, operant operant conditioning The modifi-
learning theory The body of knowledge cation of behaviour as a result of its
=ncompassing principles of classical and
objective. They turned to conditioning represents consequences. Rewarding consequences
operant conditioning (and which is fre- that area of psychology the learning of a specific increase the frequency of the behav-
quently applied to explaining and treating known as learning theory behaviour or response iour, punishing consequences reduce its
osychopathology). and argued that just as because that behaviour has frequency.
FIGURE 1.4 Classical conditioning.

(1) Before conditioning takes place, Pavlov’s dog salivates only to the presentation of food and not to the presentation of the bell;
(2) pairing the bell with food then enables the dog to learn to predict food whenever it hears the bell; and (3) this results in the dog
subsequently salivating whenever it hears the bell. This type of learning has frequently been used to explain psychopathology, and
one such example is the acquisition of specific phobias where the phobic stimulus (the CS) elicits fear because it has been paired with
some kind of trauma (the UCS) (see Figure 6.2).
PSYCHOPATHOLOGY
' a
in this book include learning approaches to understand-
ing the acquisition of bizarre behaviours in schizophre-
nia (Ullman & Krasner, 1975), how the stress-reducing
or stimulant effects of nicotine, alcohol and many illegal
drugs may lead to substance dependency (e.g. Schachter,
1982), how hypochondriacal tendencies and somatoform
disorders may be acquired when a child’s illness symp-
toms are reinforced by attention from parents (Latimer,
1981), and how the disruptive, self-harming or challeng-
ing behaviour exhibited by individuals with intellectual
or developmental disabilities may be maintained by
attention from family and carers (Mazaleski et al., 1993).
The behavioural approach led to the development of
important behavioural treatment methods, including
LIBRARY
PHOTO
RESEARCHERS/SCIENCE
behaviour therapy and behaviour modification. For
PHOTO 1.2 Operant conditioning. example, if psychopathology is learned through normal
In operant conditioning, the rat learns to press the lever learning processes, then it should be possible to use those
in this Skinner Box because it delivers food, and food acts to same learning processes to help the individual ‘unlearn’
reinforce that behaviour so that it occurs more frequently any maladaptive behaviours or emotions. This view ena-
in the future (known as operant reinforcement). Operant
bled the development of treatment methods based on
reinforcement has been used to explain how many behaviours
that are typical of psychopathology are acquired and main- classical conditioning principles (such as flooding, sys-
tained. That is, many bizarre and disruptive behaviours may tematic desensitisation, aversion therapy: see Chapter 4)
be acquired because they actually have positive or rewarding and operant conditioning principles (e.g. functional anal-
outcomes (see Focus Point 8.5 as an example). ysis, token economies: see section 1.1.3 and Chapter 17).
Furthermore, learning principles could be used to alter
psychopathology symptoms even if the original symp-
certain rewarding or reinforcing consequences. A proto- toms were not necessarily acquired through condition-
typical example of operant conditioning is a hungry rat ing processes themselves, and so the behavioural
learning to press a lever to obtain food in an experimental approach to treatment had a broad appeal across a very
chamber called a Skinner Box (see Photo 1.2). wide range of symptoms and disorders.
These two forms of learning have been used to explain As influential as the behavioural approach has been
a number of examples of psychopathology. For instance, over the years, it too has some limitations. For example,
classical conditioning has been used to explain the acqui- many psychopathologies are complex and symptoms
sition of emotional disorders including many of those are acquired gradually over many years (e.g. obsessive
with anxiety-based symptoms (see Chapter 6). For exam- compulsive disorder, substance dependence, somato-
ple, some forms of specific phobias appear to be acquired form disorders, and so on). It would be almost impossi-
when the sufferer experiences the phobic stimulus (the ble to trace the reinforcement history of such symptoms
CS) in association with a traumatic event (the UCS), and across time in an attempt to verify that reinforcement
such experiences might account for the acquisition of processes had shaped these psychopathologies. In addi-
dog phobia (in which dogs have become associated with, tion, learning paradigms may simply not represent the
for example, being bitten or chased by a dog), accident most ideal conceptual framework in which to describe
phobia (in which travelling in cars has become associ- and understand some quite complex psychopathologies.
ated with being in a traumatic car accident), and dental For example, many psychopathologies are characterized
phobia (when being at the dentist has become associ- by a range of cognitive factors such as information pro-
ated with a traumatic dental experience) (Davey, 1989; cessing biases, belief schemas and dysfunctional ways of
Kuch, 1997; Doogan & Thomas, 1992). Classical condi- thinking, and learning theory jargon is probably not the
tioning processes have also been implicated in a num- best framework in which to accurately and inclusively
ber of other forms of psychopathology, including the describe these phenomena. The cognitive approaches we
acquisition of post-traumatic stress disorder (PTSD) (see will describe next are probably more suited to describing
Chapter 6), the acquisition of paraphilias (see Chapter and explaining these aspects of psychopathology.
11), and substance dependency (see Chapter 9). Operant
conditioning has been used extensively to explain why a The cognitive model
range of psychopathology-relevant behaviours may have Perhaps the most widely adopted current psychologi-
been acquired and maintained. Examples you will find cal model of psychopathology is the cognitive model,
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA prs
and one in four of all present-day clinical psychologists limitations. For example, rather than being a cause of
would describe their approach as cognitive (Prochaska & psychopathology, it has to be considered that dysfunc-
Norcross, 2003). Primarily, this approach considers psy- tional thoughts and beliefs may themselves simply be just
chopathology to be the result of individuals acquir- another symptom of psychopathology. For example, we
ing irrational beliefs, developing dysfunctional ways of have very little knowledge at present about how dysfunc-
thinking, and processing information in biased ways. It tional thoughts and beliefs develop. Are they the product of
was an approach first pioneered by Albert Ellis (1962) and childhood experiences? Do they develop from the behav-
Aaron Beck (1967). Albert Ellis argued that emotional ioural and emotional symptoms of psychopathology (i.e.
distress (such as anxiety or depression) is caused primar- do depressed people think they are worthless because of
ily because people develop a set of irrational beliefs by their feelings of depression)? Or are they merely post hoc
which they need to judge their behaviour. Some people constructions that function to help the individual rational-
become anxious, for example, because they make unreal- ize the way they feel? These are all potentially fruitful areas
istic demands on themselves. The anxious individual may for future research.
have developed unrealistic beliefs such as ‘I must be loved
by everyone’, and the depressed individual may believe The humanist-existential approach
‘Iam incapable of doing anything worthwhile’. Judging Some approaches to psychopathology believe that
their behaviour against such ‘dysfunctional’ beliefs insights into emotional and behavioural problems can-
causes distress. Aaron Beck developed a highly success- not be achieved unless the individual is able to gain
ful cognitive therapy for depression based on the view insight into their lives from a broad range of perspec-
that depressed individuals have developed unrealistic dis- tives. People not only acquire psychological conflicts and
tortions in the way they perceive themselves, the world, experience emotional distress, they also have the ability
and their future (see Chapter 7). For example, the cog- to acquire self-awareness, develop important values and
nitive approach argues that depression results from the a sense of meaning in life, and pursue freedom of choice.
depressed individual having developed negative beliefs If these latter abilities are positively developed and
about themselves (e.g. ‘Iam worthless’), the world (e.g. encouraged, then conflict, emotional distress and psy-
‘bad things always happen’), and their future (e.g. ‘I am chopathology can often be resolved. This is the general
never going to achieve anything’), and these beliefs act to approach adopted by humanistic and existential models
maintain depressive thinking. of psychopathology, and the aim is to resolve psycho-
The view that dysfunctional ways of thinking gener- logical problems through insight, personal development,
ate and maintain symptoms of psychopathology has been and self-actualisation.
applied across a broad range of psychological problems, Because such approaches are interested primarily in
including both anxiety disorders and mood disorders, insight and personal growth when dealing with psycho-
and has also been applied to the explanation of specific pathology, they are relatively uninterested in aetiology
symptoms, such as paranoid thinking in schizophrenia and the origins of psychopathology, but more interested
(Morrison, 2001), antisocial and impulsive behaviour in in ameliorating symptoms of psychopathology through
personality disorders (Young, Klosko & Weishaar, 2003), encouraging personal development. An influential exam-
dysfunctional sexual behaviour in sex offenders and pae- ple of the is humanistic-existentialist approach is client-
dophiles (Ward, Hudson, Johnston & Marshall, 1997), centred therapy devel-
and illness reporting in hypochondriasis and somato- oped by Carl Rogers (1951, humanist-existentialist approach A
form disorders (Warwick, 1995) to name but a few. 1987). This approach stres- model of psychopathology which aims to
resolve psychological problems through
The cognitive approach has also been highly successful ses the goodness of human insight, personal development, and
in generating an influential approach to treatment. If dys- nature and assumes that if self-actualization.
functional thoughts and beliefs maintain the symptoms individuals are unrestricted
of psychopathology, then these dysfunctional thoughts by fears and conflicts, they client-centred therapy An approach to
and beliefs can be identified, challenged and replaced will develop into well- psychopathology stressing the goodness
by more functional cognitions. This has given rise to adjusted, happy _ indivi- of human nature, assuming that if individu-
als are unrestricted by fears and conflicts,
a broad-ranging therapeutic approach known as cogni- duals. The client-centred they will develop into well-adjusted, happy
tive behaviour therapy (CBT), and many examples of the therapist will try to create individuals.
use of this approach will be a supportive climate in
cognitive behaviour therapy (CBT) An encountered in this book. which the client is helped to acquire positive self-worth.
intervention for changing both thoughts As successful as the The therapist will use empathy to help them understand
and behaviour. CBT represents an umbrella ne
term for many different therapies that SONS approach Mapes
the client’s feelings and unconditional positive regard, by
share the common aim of changing both to have been in recent which the therapist expresses their willingness to totally
cognitions and behaviour. years, it too also has some accept the client for who he or she is.
oe eam PSYCHOPATHOLOGY
? C %
As we said earlier, this type of approach to psychopa- (Patterson, 2000; Greenberg, Watson & Lietaer, 1998). "
thology does not put too much emphasis on how psy- Similarly, exponents of existential therapies believe that
chopathology was acquired, but does try to eradicate experimental methodologies are. inappropriate for esti-
psychopathology by moving the individual from one mating the effectiveness of such therapies, because such
phenomenological perspective (e.g. one that contains methods either dehumanize the individuals involved
fears and conflicts) to another (e.g. one that enables the or are incapable of measuring the kinds of existential
client to view themself as a worthy, respected and achiev- benefits that such approaches claim to bestow (Walsh
ing individual). Approaches such as humanistic and exis- & McElwain, 2002; May & Yalom, 1995). Nevertheless,
tentialist ones are difficult to evaluate. For example, most such approaches to treatment are still accepted as hav-
controlled studies have indicated that clients undergoing some value and are still used at least in part by
ing client-centred therapy tend to fair no better than clinical psychologists, counselling psychologists and
those undergoing non-therapeutic control treatments psychotherapists.
SELF-TEST QUESTIONS
e What are the main approaches to understanding psychopathology that are advocated by the biological approach?
® Can you describe the basic concepts underlying psychoanalytic and psychodynamic approaches to psychopathology?
© What are the learning principles on which the behavioural approach to psychopathology is based?
° Who were the main founders of the cognitive approach to psychopathology, and what were their main contributions?
® How do humanistic—existential approaches to psychopathology differ from most of the others?
SECTION SUMMARY
1.3 EXPLANATORY APPROACHES TO PSYCHOPATHOLOGY
The four psychological paradigms we have discussed in this section have tended to evolve historically from explanatory
paradigms that have represented different ‘schools’ of psychology generally, but all have a relevant place in explaining
psychopathology - either at different levels of explanation (e.g. cognitive vs. behavioural), or using different philosophi-
cal approaches to explaining human behaviour and psychopathology (e.g. the hypothetical constructs developed by the
psychoanalytical approach vs. the learning paradigm developed by behaviourist approaches). In addition to pure psycho-
logical paradigms, clinical psychologists are continually developing new ways of conceptualising and studying the factors
that influence the development of mental health problems, and one approach of growing importance is to consider how
sociocultural factors might affect the acquisition of psychopathology. Some examples ofthis latter approach are discussed
in Focus Point 1.5.
The key points are:

¢ Psychological models view psychopathology as caused primarily by psychological rather than biological processes.
° Influential psychological models of psychopathology include biological models, the psychoanalytical model, the behavioural
model, the cognitive model, and the humanist-existential model.
¢ Biological models attempt to explain psychopathology in terms of processes such as genetics and brain structure and function.
° Psychoanalytical models attempt to discuss psychopathology in terms ofthe psychological mechanisms that help to defend
against anxiety and depression.
¢ Behavioural models use processes of learning such as classical conditioning and operant conditioning to understand how
psychopathology might be acquired.
e The cognitive model considers psychopathology to be the result of individuals acquiring irrational beliefs, developing dys-
functional ways of thinking, and processing information in biased ways.
° The humanist-existential approach attempts to help the individual to gain insight into their lives from a broad range of
perspectives and develop a sense of meaning in life.
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA er
a
=
=~
There is a growing realization that sociocultural fac-
= tors can influence both the acquisition of mental
another example where prevalence rates are higher in
most Western cultures, but may only be rarely reported
2)
a health problems and the way that psychopathology in less socio-economically developed societies (Keel
Vv) is expressed. These factors include gender, culture, & Klump, 2003). Finally, some combinations of mental
=)
U ethnicity and socioeconomic factors such as poverty health problems may be found only in certain specific
\e) and deprivation, and we will discuss some examples cultures, and be examples ofthe culturally specific ways
fl. of these here. in which stress and trauma are manifested. Two specific
examples of this are provided in Focus Point 1.3.
GENDER
ETHNICITY
Your gender is likely to be a significant factor in whether
youare likely to develop a particular mental health prob- The frequency of diagnosis of many mental health prob-
lem. For example, the prevalence of major depression is lems also differs across different ethnicities. For example,
twice as high in women as it is in men, women are signif- schizophrenia is more frequently diagnosed in indi-
icantly more likely to develop anxiety-based problems viduals of African descent than white European origin.
such as social anxiety disorder, panic disorder or gen- Conversely, specific types of eating disorders — such as
eralized anxiety disorder (see Chapter 6), and women anorexia nervosa — are found more commonly in white
are also significantly more likely to develop eating women than black women (Lovejoy, 2001). In some of
disorders such as anorexia nervosa or bulimia nervosa these cases, there may be a genetic component (e.g.
(see Chapter 10). Alternatively, males are more likely to individuals of Asian descent inherit a gene which makes
develop conduct disorders, attention deficit hyperac- drinking large amounts of alcohol aversive, and so
tivity disorder (ADHD) (see Chapter 16), and antisocial makes them less likely to develop alcohol dependency
personality disorder (Chapter 12). How gender differen- and abuse problems; Wall et a/., 2001), but equally it may
tially affects the acquisition of these various disorders be the case that diagnostic criteria are either wittingly or
is far from clear, and could be linked to gender-based unwittingly applied differently to people from different
biological differences (e.g. men appear to possess a ethnic backgrounds (e.g. it is caused by a cultural bias
gene that imparts risk for alcohol abuse and depend- in assessment — see section 2.2.6). For example, black
ency, and this can be passed on to their sons; Chapter Americans have a higher rate of diagnosis of disorders
9), to factors associated with the gender roles that males such as schizophrenia and alcoholism, whereas white
and females adopt in different societies (e.g. women’s Americans are more likely to be given the less stigma-
roles in society may be more stressful than men’s and tizing diagnosis of major depression (Garb, 1997), and
so increase the risk of mental health problems), or dif- such differential effects may reflect differential diagno-
ferences in gender-based coping practices (e.g. women ses driven by implicit racial and ethnic stereotyping.
ruminate more than men, while men frequently react
to stress by distracting themselves; Just & Alloy, 1997). POVERTY
An interesting discussion of the role of gender in risk for
major depression is provided in Activity 7.1. Finally, the socio-economic conditions in which an
individual is either raised or lives in is an important
CULTURE contributor to the development of psychopathology.
Obvious examples include the development of con-
The culture in which you live can also be a factor that duct disorders, some personality disorders such as anti-
will determine whether you develop a particular mental social personality disorder, and substance abuse and
health problem and also how that problem will mani- dependency problems. However, poverty is also a risk
fest itself. For example, prevalence rates for many com- factor for the development of many common mental
mon mental health problems differ significantly across health problems such as anxiety and depression, pos-
the world. In the case of major depression, prevalence sibly because of the additional stressors and traumas
rates can vary between 1.5 per cent and 19 per cent that accompany poverty, unemployment, substand-
(Weissman, Bland, Canino, Faravelli et a/., 1996), and ard accommodation, and neglect (Evans & Kim, 2012).
may be affected by the stigma associated with report- Indeed, so specific are many of the stressors that afflict
ing symptoms, cultural differences in diagnosing symp- people living in poverty that it may be necessary to
toms, and depression being expressed in more physical develop interventions that are tailored to the spe-
terms in some societies (called somatisation) (Patten, cific sociocultural experiences of low-income families
2003; Compton et al., 1991). Eating disorders are (Goodman etal., 2013).
oe Se PSYCHOPATHOLOGY
mental health problems such as eating disorders and’*

1.4 MENTAL HEALTH substance abuse were self-inflicted, and (3) respond-
AND STIGMA ents believed that people with mental health problems
were generally hard to talk to. People tended to hold
these negative beliefs regardless of their age, regardless
There are still attitudes within most societies that view of what knowledge they had of mental health problems,
symptoms of psychopathology as threatening and uncom- and regardless of whether they knew someone who had
fortable, and these attitudes frequently foster stigma and a mental health problem. More recent studies of attitudes
discrimination towards people with mental health prob- to individuals with a diagnosis of schizophrenia or major
lems. Reactions to people often change when they suffer depression convey similar findings. In both cases, a signifi-
a mental health problem, and this leads to loss of respect cant proportion of members of the public considered that
and consideration. Such reactions are common when peo- people with mental health problems such as depression
ple are brave enough to admit they have a mental health or schizophrenia were unpredictable and dangerous, and
problem, and they can often lead on to various forms of they would be less likely to employ someone with a mental
exclusion or discrimination — either within social circles health problem (Wang & Lai, 2008; Reavley & Jorm, 2011).
or within the workplace. In the following sections we
will look at five key questions: (1) what is mental heaith
stigma?; (2) who holds stigmatising beliefs and attitudes?; 1.4.2 WhoHolds Stigmatizing Beliefs
(3) what factors cause stigma?; (4) why does stigma mat-
about Mental Health Problems?
ter?; and (5) how can we eliminate stigma?
Perhaps surprisingly, stigmatising beliefs about individu-
als with mental health problems are held by a broad range
of individuals within society, regardless of whether they
1.4.1 What Is Mental Health Stigma? know someone with a mental health problem, have a
Mental health stigma can be divided into two distinct types. family member with a mental health problem, or have
The first, social stigma, is characterized by prejudicial a good knowledge and experience of mental health prob-
attitudes and discriminating lems (Crisp et al., 2000; Moses, 2010; Wallace, 2010). For
mental health stigma Mental health
behaviour directed towards example, Moses (2010) found that stigma directed at ado-
stigma can be divided into two distinct lescents with mental health problems came from fam-
types: social stigma is characterized by individuals with mental
prejudicial attitudes and discriminating health problems as a result ily members, peers and teachers. Forty-six per cent of
behaviour directed towards individuals of the psychiatric label they these adolescents described experiencing stigmatisation
with mental health problems. Perceived
have been given. In contrast, by family members in the form of unwarranted assump-
stigma or self-stigma is the internalizing by tions (e.g. the sufferer was being manipulative), distrust,
the mental health sufferer of their percep- perceived stigma or self-
tions of discrimination. This can signifi- stigma is the internalising avoidance, pity and gossip; 62 per cent experienced stigma
cantly affect feelings of shame and lead to by the mental health suf- from peers, which often led to friendship losses and
poorer treatment outcomes. social rejection (Connolly, Geller, Marton & Kutcher,
ferer of their perceptions
of discrimination (Link, 1992); and 35 per cent reported stigma perpetrated by
social stigma Stigma characterized by
prejudicial attitudes and discriminating Cullen, Struening & Shrout, teachers and school staff, who expressed fear, dislike,
behaviour directed towards individuals 1989), and perceived stigma avoidance, and underestimation of abilities. Mental
with mental health problems as a result of
can significantly affect feel- health stigma is even widespread in the medical profes-
the psychiatric label they have been given. sion, at least in part because it is given a low priority dur-
ings of shame and lead
to poorer treatment out- ing the training of physicians and GPs (Wallace, 2010).
perceived stigma/self-stigma The
internalising by the mental health sufferer comes (Perlick, Rosenheck,
of their perceptions of discrimination. Clarkin, Sirey 2001).
This
can significantly affect feelings of shame
In relation to social
1.4.3 What Factors Cause Stigma?
and lead to poorer treatment outcomes.
See also Mental health stigma. stigma, studies have sug- The social stigma associated with mental health problems
gested that stigmatising almost certainly has multiple causes. We've seen in the
attitudes towards people with mental health problems section on historical perspectives that throughout history
are widespread and commonly held (Crisp, Gelder, Rix, people with mental health problems have been treated
Meltzer & Rowlands, 2000; Bryne, 1997; Heginbotham, differently, excluded and even brutalized. This treatment
1998). In a survey of over 1700 adults in the UK, Crisp et may come from the misguided views that people with
al. (2000) found that (1) the most commonly held belief mental health problems may be more violent or unpre-
was that people with mental health problems were dan- dictable than people without such problems, or some-
gerous — especially those with schizophrenia, alcohol- how just ‘different’, but none of these beliefs has any
ism and drug dependence, (2) people believed that some basis in fact (see e.g. Swanson, Holzer, Ganju & Jono,
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA cE.
1990). Similarly, early beliefs about the causes of mental itself implies that people with mental health problems
health problems, such as demonic or spirit possession, are in some way ‘different’ from ‘normally’ functioning
were ‘explanations’ that would almost certainly give rise individuals. Secondly, the medical model implies diag-
to reactions of caution, fear and discrimination. Even nosis, and diagnosis implies a label that is applied to a
the medical model of mental health problems is itself an ‘patient’. That label may well be associated with undesir-
unwitting source of stigmatising beliefs. Firstly, the medi- able attributes (e.g. ‘mad’ people cannot function prop-
cal model implies that mental health problems are on a erly in society, or can sometimes be violent), and this
par with physical illnesses and may result from medical or again will perpetuate the view that people with mental
physical dysfunction in some way (when many may not health problems are different and should be treated with
be simply reducible to biological or medical causes). This caution.
2
=
‘CREATING’ MENTAL HEALTH PROBLEMS THROUGH THE MEDICALISATION
~~ OF EVERYDAY PROBLEMS OF LIVING
=
2) It is worth considering when an everyday ‘problem in sexuality in order to sell their products (Moynihan,
QO. living’ becomes something that should be categorized 2006). Some drug companies claim that sexual desire
va)
= as a mental health problem. It is a fact of life that we problems affect up to 43 per cent of American women
U all have to deal with difficult life situations. Sometimes (Moynihan, 2003), and can be successfully treated
Oo these may make us anxious or depressed, sometimes with, for example, hormone patches. However, others
a
we might feel as though we are ‘unable to cope’ with claim that this figure is highly improbable and includes
these difficulties. But they are still problems that women who are quite happy with their reduced level
almost everyone encounters. Many people have their of sexual interest (Bancroft, Loftus & Long, 2003). Tiefer
own strategies for coping with these problems: some (2006) lists a number of processes that have been used
get help and support from friends and family and in either wittingly or unwittingly in the past to ‘medical-
more severe cases perhaps seek help from their doc- ize’ what many see as normal sexual functioning -
tor or GP. However, at what point do problems of living especially the normal lowering of sexual desire found
cease to be everyday problems and become mental in women during the menopause. These include
health problems? In particular, we must be wary about (1) taking a normal function and implying that there
‘medicalising’ problems in daily living so that they is something wrong with it and it should be treated
become viewed as ‘abnormal’, symptoms of illness or (e.g. implying that there is something abnormal about
disease, or even as characteristics of individuals who the female menopause, when it is a perfectly normal
are ‘ill’or in some way ‘second class’ biological process), (2) imputing suffering that is not
Below are two useful examples of how everyday necessarily there (i.e. implying that individuals who
problems in living might become medicalized to the lack sexual desire are ‘suffering’
as a result), (3) defining
point where they are viewed as representing illness or as large a proportion of the population as possible as
disease rather than normal events of everyday living. suffering from the‘disease; (4) defining a condition as a
First, experiencing depression is the third most com- ‘deficiency’, disease or disease of hormonal imbalance
mon reason for consulting a doctor or GP in the UK (e.g. implying that women experiencing the meno-
(Singleton et al., 2001), and in order for GPs to be able pause have a ‘deficiency’ of sexual hormones), and
to provide treatment for such individuals, there is a (5) taking a common symptom that could mean any-
tendency for them to over diagnose mild or moderate thing and making it sound as if it is a sign of a seri-
depression (Middleton et al/., 2005). This may have con- ous disease (e.g. implying that lack of sexual desire is
tributed to the common view expressed by lay people a symptom of underlying dysfunction). While sexual
that depression is a ‘disease’ rather than a normal con- dysfunctions are sometimes caused by medical condi-
sequence of everyday life stress (Lauber et a/., 2003). If tions, lack of sexual desire and interest is itself often
lay people already view depression as a ‘disease’or bio- portrayed as a medical condition in need of treatment.
logical illness, and GPs are more than willing to diag-' Yet a reduction in sexual interest and desire can be a
nose it, then we run the risk of the ‘medicalisation’ of healthy and adaptive response to normal changes in
normal everyday negative emotions such as mild dis- body chemistry or as a normal reaction to adverse life
tress or even unhappiness (Shaw & Woodward, 2004). stressors or relationship changes. ‘Medicalising’ symp-
Second, some clinical researchers have argued that toms in this way leads to us viewing what are normal
the medical pharmaceutical industry in particular has everyday symptoms and experiences as examples of
attempted to manipulate women’s beliefs about their dysfunction or psychopathology.
by ee PSYCHOPATHOLOGY
; ‘
We will discuss ways in which stigma can be addressed social isolation (Yanos, Roe & Lysaker, 2010). These fac- .
below, but it must also be acknowledged here that the tors alone represent significant reasons for attempting
media regularly play a role in perpetuating stigmatising to eradicate mental health stigma and ensure that social
stereotypes of people with mental health problems. The inclusion is facilitated and recovery can be efficiently
popular press is a branch of the media that is frequently achieved.
criticized for perpetuating these stereotypes, and a par-
ticular example of this is provided in Focus Point 1.7.
Blame can also be levelled at the entertainment media. 1.4.5 How Can We Eliminate Stigma?
For example, cinematic depictions of schizophrenia are
often stereotypic and characterized by misinformation We now have a good knowledge of what mental health
about symptoms, causes and treatment. In an analysis stigma is and how it affects sufferers, both in terms of
of English-language movies released between 1990 and their role in society and their route to recovery. It is not
2010 that depicted at least one character with schizo- surprising, then, that attention has most recently turned
phrenia, Owen (2012) found that most schizophrenic to developing ways in which stigma and discrimination
characters displayed violent behaviour, one-third of can be reduced. As we have already described, people
these violent characters engaged in homicidal behaviour, tend to hold these negative beliefs about mental health
and a quarter committed suicide. This suggests that neg- problems regardless of their age, regardless of what
ative portrayals of schizophrenia in contemporary mov- knowledge they have of mental health problems, and
ies are common and are sure to reinforce biased beliefs regardless of whether they know someone who has a
and stigmatising attitudes towards people with mental mental health problem. The fact that such negative atti-
health problems. While the media may be getting better tudes appear to be so entrenched suggests that cam-
at increasing their portrayal of anti-stigmatising material paigns to change these beliefs will have to be multifaceted,
over recent years, studies suggest that there has been no will have to do more than just impart knowledge about
proportional decrease in the news media’s publication of mental health problems, and will need to challenge exist-
stigmatising articles, suggesting that the media are still ing negative stereotypes especially as they are portrayed
a significant source of stigma-relevant misinformation in the general media (Pinfold, Toulmin, Thornicroft,
(Thornicroft, Goulden, Shefer, Rhydderch et al., 2013). Huxley et al., 2003). In the UK, the Time to Change
campaign is one of the biggest programmes attempting
to address mental health
stigma and is supported Time to Change A national UK
1.4.4 Why Does Stigma Matter?
both by charities and men- programme aiming to promote awareness
of mental health problems and to combat
Stigma embraces both prejudicial attitudes and discrimi- tal health service providers stigma and discrimination.
nating behaviour towards individuals with mental health (www.time-to-change.org
problems, and the social effects of this include exclusion, -uk). This programme provides blogs, videos, TV adver-
poor social support, poorer subjective quality of life, and tisements, and promotional events to help raise aware-
low self-esteem (Livingston & Boyd, 2010). As well as ness of mental health stigma and the detrimental effect
its affect on the quality of daily living, stigma also has this has on mental health sufferers. However, raising
a detrimental effect on treatment outcomes, and so hin- awareness of mental health problems simply by provid-
ders efficient and effective recovery from mental health ing information about these problems may not be a sim-
problems (Perlick, Rosenheck, Clarkin, Sirey et al., 2001). ple solution — especially since individuals who are most
In particular, self-stigma is correlated with poorer voca- knowledgeable about mental health problems (e.g. psy-
tional outcomes (employment success) and increased chiatrists, mental health nurses) regularly hold strong
Bp The popular press can often present mental illness in a ‘Bonkers Bruno Locked Up’, which was later changed to
way which propagates the stigmas attached to mental ‘Sad Bruno in Mental Home’
=
-
illness. In September 2003, the ex-heavyweight cham- Sane chief executive Marjorie Wallace said: ‘It is
= pion boxer, Frank Bruno was treated for depression at both an insult to Mr Bruno and damaging to many
O a psychiatric hospital, and the mental health charity
a. thousands of people who endure mental illness to
Ww Sane (http://www.sane.org.uk) subsequently criticized label him as “bonkers” or “a nutter” and having to be
=) unsympathetic coverage of his illness in the media. “put ina mental home”.mt
U
\o) The BBC News website reported that an early.edi-
Lin tion of the Sun newspaper had the front page headline Source: http://news.bbc.co.uk/1/hi/uk/3130376.stm.
as
CHAPTER 1 AN INTRODUCTION TO PSYCHOPATHOLOGY: CONCEPTS, PARADIGMS AND STIGMA = 337
stigmatising beliefs about mental health themselves! these kinds of intergroup events suggests that they
(Schlosberg, 1993; Caldwell & Jorm, 2001). As a conse- (1) improve attitudes towards people with mental health
quence, attention has turned towards some methods problems, (2) increase future willingness to disclose
identified in the social psychology literature for improv- mental health problems, and (3) promote behaviours
ing intergroup relations and reducing prejudice (Brown, associated with anti-stigma engagement (Evans-Lacko,
2010). These methods aim at promoting events to London, Japhet, Rusch et al., 2012; Thornicroft, Brohan,
encourage mass participation social contact between Kassam & Lewis-Holmes, 2008). A fuller evidence-based
individuals with and without mental health problems evaluation of the Time to Change initiative can be found
and to facilitate positive intergroup contact and disclo- in a special issue dedicated js
sure of mental health problems (one example is the Time to this topic in the British § To read more about facts and myths of
mental health statistics go to
to Change Roadshow, which sets up events in prominent Journal of Psychiatry (vol. | http://tinyurl.com/qeoenzd
town centre locations with high footfall). Analysis of 202, issue s55, April 2013).
SELF-TEST QUESTIONS
° Describe the main characteristics of mental health stigma.

® What kinds of interventions have been developed to try to reduce mental health stigma?
SECTION SUMMARY
1.4 MENTAL HEALTH AND STIGMA

Hopefully, this section has introduced you to the complex nature of mental health stigma and the effects it has on both the
daily lives and recovery of individuals suffering from mental health problems. We have discussed how mental health stigma
: manifests itself, the effect it has on social inclusion, self-esteem, quality of life and recovery. We ended by describing the devel-
; opment of multifaceted programmes to combat mental health stigma and discrimination.
The key points are:
® Social stigma is characterized by prejudicial attitudes and discriminating behaviour directed towards individuals with men-
tal health problems.
° Stigmatising beliefs about people with mental health are held by a broad range of individuals within society, including
family members, peers, teachers, and members of the medical profession.
¢ The popular media often play a role in perpetuating stigmatising stereotypes of people with mental health problems.
® Stigma has a detrimental effect on treatment outcome for people with mental health problems.
¢ Stigma can be addressed by adopting methods described in the social psychology literature for improving intergroup
relations.
of psychopathology, looking at traditional ways in which

1.5 CONCEPTS, PARADIGMS people have tried to understand and explain mental health
problems and how people with mental health problems
AND STIGMA REVISITED have been treated. This has given us a backdrop by which
to discuss the many contemporary ways in which psycho-
This chapter has introduced the reader to the impor- pathology can be defined and the explanatory paradigms
tant concepts and paradigms that surround psycho- that are used in modern day scientific study of psycho-
pathology. We have set the scene with a brief history pathology. Defining exactly what kinds of symptoms or
(oe PSYCHOPATHOLOGY
behaviour should be considered as examples of psycho- imposing stigmatising labels on people suffering from
pathology is also problematic. The four types of defi- psychopathology. In practice, classification schemes end
nition that we discussed (deviation from the statistical up using an amalgamation of these different approaches
norm, deviation from social norms, maladaptive behav- to definition, and we will discuss some of these issues in
iour, and distress and impairment) all have limitations. Chapter 2. Finally, this chapter has introduced the notion
Some fail to cover examples of behaviour that we would of mental health stigma, described what it is and how it
intuitively believe to be representative of mental health affects individuals with mental health problems. Stigma
problems, others may cover examples that we intuitively and discrimination are currently important targets for
feel are not examples of psychopathology, or they may change, and programmes designed to challenge stigma
represent forms of categorisation that would lead us to are a significant part of most mental health services.
ee To access the online resources for this chapter go to

iO) os nae www.wiley-psychopathology.com/ch1.
Reading Activity
DSM-5 Website ° Post traumatic stress Figure 1.2 labelling

Journal article: Spirit disorder Figure 1.3 labelling
possession Self-test questions
Facts and myths of mental Revision flashcards
health statistics
Research questions
Glossary key terms
Clinical issues
Links to journal articles
References
2 Classification and Assessment
in Clinical Psychology
= ira To access the online resources for this chapter go to

f _www.wiley-psychopathology.com/ch2.
This chapter describes the various ways in which clinicians

gather information about a client’s problems. This infor- 2.1 CLASSIFYING PSYCHOPATHOLOGY 37
mation can then be used to help them classify the person’s
problems, understand the causes of those problems, and 2.2 METHODS OF ASSESSMENT 44
to treat their problems. The chapter begins by discussing:
classification of mental health problems and in particular { 2.3 CASEFORMULATION 64
the most recent developments found in the classification
system DSM-5. We then continue by discussing the ben- 2.4 CLASSIFICATION AND ASSESSMENT IN CLINICAL
efits and limitations of clinical interviews, psychological PSYCHOLOGY REVISITED 66
tests, biologically based assessments and clinical obser-
vation, and introduce the reader to the concepts of relia-
bility and validity. The chapter ends by discussing cultural
biases in clinical assessments and the popular use of case
formulations as a means of understanding the client's
problems and developing a strategy for treatment.
Sens PSYCHOPATHOLOGY
LEARNING OUTCOMES
1. Compare and contrast the pros and cons of ~ 4. Critically analyse some of the sources of cultural
DSM as a means of classifying and diagnosing bias that may influence the process of clinical
psychopathology. assessment.
2. Describe a range of clinical assessment methods 5. Explain what a case formulation is, and provide
and evaluate the benefits and limitations of each. some examples from different psychological
3. Describe the concepts of reliability and validity as approaches.
applied to clinical assessment methods.
| saw Mrs Ann Smith, aged 39, in my clinic today. She met criteria for depression, with a 5 month history of low mood. This was
triggered by an argument with her husband during the Christmas period. Despite receiving a lot of support from her husband,
Ann continues to experience ‘black spells; which can go on for5days per episode. In March she expressed some suicidal thoughts,
which precipitated her referral to psychiatric services.
At interview Ann was well presented, clear and articulate. However, both her eye contact and concentration were poor, and she
reported having lost 10Ibs in weight. This is the first time she has been referred to psychiatric services, but has been prescribed anti-
depressant medication on three previous occasions by her GP. She states that she has experienced low times throughout her life.
She is the middle child of three and stated that she missed a lot of schooling due to the combination of having chronic asthma
and an overprotective mother. She left school without qualifications, feeling she has not realized her potential in any area. She
married Michael 14 years ago. Owing to his job as a vicar, they entertain frequently.
For a video on depression go to
She finds the entertaining difficult. |would welcome your assessment of this case,
video/ch2 with a view of taking her on for therapy.
Ann’s Story (as told by Blackburn, James & Flitcroft, 2006)
Introduction of information about the client, and this information is

often gathered using a range of different clinical tools
Ann has low mood. She has been prescribed antidepres- and techniques. Clinical assessment procedures are for-
sant medication by her GP, who subsequently referred mal ways of finding answers to these questions, espe-
her to a psychiatrist. Following an interview with the cially: ‘Precisely what problems does this person have?’
psychiatrist, the latter sent the above referral letter on ‘What has caused their problems?’ “What is the best way
to a clinical psychologist. The referral letter immedi- to treat their problems?’ ‘Did our treatment work?’
ately raises a number of questions, the main one being: Clinicians use a wide range of assessment proce-
‘Can we help this person?’ But this question itself raises dures to gather this information. In many cases, the
a number of other questions that will need answering. types of techniques they use will depend on their theo-
These questions include: (1) Are Ann’s symptoms typi- retical orientation to psychopathology. For example, the
cal of a specific psychological problem (e.g. depression)? cognitive-behavioural clinician may want to find out quite
(2) Do they meet the criteria for formal diagnosis of a different information to a psychodynamic clinician —
mental health problem? (3) What has led this person to largely because their conceptions of the causes of psy-
have these problems? (4) Are there specific events that chopathology are different, and because the kinds of
trigger her symptoms? (5) How can we help this person? therapeutic techniques they employ are different. The
(6) By what criteria will we judge that we have success- cognitive therapist will want to know what kinds of cog-
fully helped this person? These are all questions that the nitions may trigger symptoms so that these cognitions
clinical psychologist must answer by gathering a variety can be addressed in therapy, whereas a psychodynamic
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY vA.
therapist may want to explore the client’s history of disorder or substance dependency are all very different
conflicts and defence mechanisms in order to assess and require different approaches and different means of
their suitability for psychodynamic therapy (Marzillier & support and intervention. We need to have some basis for
Marzillier, 2008). differentiating between these different kinds of problems
In this chapter we will describe the range of assess- and determining the different kinds of support that each
ment techniques available to clinicians that enables them might need, and classification systems provide a common
to answer the basic questions about a case that we have language for reporting and monitoring mental health
just raised. These techniques are an aid to diagnosis, an problems which allows the world to share and compare
aid to determining the best intervention for a client, and data in a consistent way. Thirdly, how do we decide if our
a help in establishing whether treatment has successfully interventions and support for sufferers have been effec-
dealt with the client’s symptoms. We will discuss these tive unless we have some objective way of defining what
assessment types individually, but to gain a complete constitutes the symptoms of psychopathology? One
picture of the client’s condition, the clinician will usu- important and objective way of determining whether an
ally use a range of different assessments (Meyer, Finn, individual is responding to treatment is to see if there has
Eyde, Kay et al., 2001). The chapter begins by discuss- been any improvement in objectively defined and meas-
ing the ways in which we currently classify and diagnose urable symptoms. Classification systems based on clus-
mental health problems, since many forms of assess- ters of symptoms may help us to do this. Finally, whether
ment are structured in ways that enable classification. we like it or not, modern day society requires that we
We then move on to discussing different types of assess- assess and classify people for a number of reasons, and
ment, including the interview, psychological tests, bio- this is also the case with psychopathology. For example,
logically based tests, and observation. Finally we discuss we might want to know whether a person is psychologi-
some issues relating to diagnosis and how diagnosis can cally fit to stand trial for a criminal offence, whether a
be associated with the development of a treatment plan child has disabilities that will require special educational
(known as formulation). needs, or whether financial compensation or damages
should be awarded to an individual because of psycho-
logical symptoms caused by the actions of others. All of
2.1 CLASSIFYING these requirements of modern society necessitate a form
of assessment and classification that can adequately and
PSYCHOPATHOLOGY objectively deal with these kinds of issues.
In Chapter 1 we discussed the difficulties associated with

defining what is and is not a mental health problem. 2.1.1 The Development of
Given the inherent difficulties surrounding this question
Classification Systems
you may be saying to yourself “why try to define and
classify psychopathology at all?’ Nevertheless, there are Arguably the first person to develop a comprehensive clas-
some good reasons for wanting to do this. Firstly, as a sification system for psychopathology was the German
social and biological science, psychology will want to try psychiatrist Emil Kraepelin (1883-1923). He suggested
to understand the causes of mental health problems. This that psychopathology, like physical illness, could be clas-
is important so that we can develop effective treatments sified into different and separate pathologies, each of
that address the root causes of psychopathology and also which had a different cause and could be described by
develop prevention strategies designed to reduce the risk a distinct set of symptoms that he called a syndrome.
of individuals developing symptoms of psychopathology. Kraepelin’s work provided
Most sciences use classification to group phenomena into some hope that mental syndrome Adistinct setofsymptoms.
categories according to their similarities. Categorisation illness could be described
and classification is thus an important first stage in the and successfully treated in much the same way as other
pursuit of knowledge about causes and aetiology, and medical illnesses.
it would be difficult to discuss aetiology in this book if Following on from Kraepelin’s scheme, the first
there were not some form of classification that enabled extensive system for classifying psychopathology was
us to understand how different causes relate to differ- developed by the World Health Organisation (WHO),
ent symptoms. Secondly, classification is necessary if we which added psychologi- International List of Causes of Death
are to effectively organize services and support for suf- cal disorders to the Inter- (ICD) The international standard
ferers. For example, the needs of individuals with intel- national List of Causes diagnostic classification developed by
the World Health Organisation (WHO).
lectual disabilities, major depression, an anxiety-based of Death (ICD) in 1939.
ct ea PSYCHOPATHOLOGY
Despite this development, the mental disorders sec- four basic objectives: (1) it must provide necessary and“
tion in the ICD was not widely accepted, and in 1952 sufficient criteria for correct differential diagnosis, (2) it
the American Psychiatric Association (APA) published should provide a means of distinguishing ‘true’ psy-
its first Diagnostic and Statistical Manual (DSM). chopathology (in the medical or dysfunctional sense)
In 1968 the APA produced a second version of its diag- from non-disordered human conditions that are often
nostic manual (DSM-II) and in 1969 the WHO published labelled as everyday ‘problems in living’, (3) it should
a new classification system, which was more widely provide diagnostic criteria in a way that allows them to
accepted, while in the UKa be applied systematically by different clinicians in dif-
Diagnostic and Statistical Manual
glossary of definitions was ferent settings, and (4) the diagnostic criteria it provides
(DSM) First published in 1952 by the
American Psychiatric Association (APA), produced to accompany should be theoretically neutral, in the sense that they
the DSM extended the World Health the WHO system (General do not favour one theoretical approach to psychopa-
Organisation's (WHO) International Listof Register Office, 1968). thology over another. Whether DSM can achieve these
Causes of Death (ICD) classification system
However, the WHO sys- four objectives will be to some extent the measure of
to include a more widely accepted section
on mental disorders. tem was simply a listing of its success. The breakdown of the chapters in DSM-5 is
diagnostic categories, and shown in Table 2.1.
while DSM-II and the British Glossary of mental disorders
provided more information on which to base diagrio-
ses, the actual practice of diagnosing psychopathology TABLE 2.1 Chapters in DSM-5
varied widely. However, in 1980, the APA produced a
Neurodevelopmental Disorders
substantially revised and expanded DSM-III which has
come to be accepted as the most influential diagnos- Schizophrenia Spectrum and Other Psychotic Disorders
tic system. The most recent version that is used in this Bipolar & Related Disorders
book is DSM-5, which was published in 2013. The ICD
Depressive Disorders
system is currently in its tenth edition (ICD-10), with
ICD-11 under development and due to be published in Anxiety Disorders
2015. Most revisions of the DSM have been coordinated Obsessive-Compulsive and Related Disorders
with the ICD to ensure some consistency of diagnosis
Trauma- and Stressor-Related Disorders
across systems. For convenience and consistency, we will
be using only the DSM diagnostic system in this book Dissociative Disorders
(see Cooper, 1994, for a guide to the ICD-10 classifica- Somatic Symptom Disorders
tion system, and http://www.who.int/ classifications/
Feeding and Eating Disorders
icd/revision/en/index.html for details of the most
recent ICD revision). Elimination Disorders
Sleep—Wake Disorders
Sexual Dysfunctions
2.1.2 DSM-5 Gender Dysphoria
Defining and diagnosing psychopathology Disruptive, Impulse Control and Conduct Disorders
Before attempting to classify psychopathology it was Substance-Related and Addictive Disorders
necessary for DSM to define what it considers to be a
Neurocognitive Disorders
mental disorder. As we have already seen in Chapter 1
this is not a simple matter. However, DSM does make Personality Disorders
some attempt to rule out behaviours that are simply Paraphilic Disorders
socially deviant as examples of psychopathology and
Other Disorders
puts the emphasis on distress and disability as important
defining characteristics. Distress relates to the chronic The number of total disorders in DSM-5 has not increased signifi-
experience of pain or distressing emotions, and dis- cantly, but some disorders have now had their importance recog-
nized by being allocated separate chapter headings (e.g. obsessive
ability refers to the fact that distress can lead to impair- compulsive disorder). The chapter on neurodevelopmental disorders
ment in one or more important areas of functioning, is anew heading containing autism spectrum disorders, intellectual
such as education, employment, and dealing with fam- development disorder, and attention/hyperactivity disorder (ADHD).
ily and social responsibilities. It is also important to try The chapter on substance use and addictive behaviours now includes
gambling disorder. The importance of both bipolar disorder and
to define at this point what exactly the DSM system is depressive disorders is recognized by them being allocated to sepa-
designed to do. Wakefield (1997) argues that DSM has rate chapters.
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY 3
DSM classification systems also provide the following be more extreme versions of everyday behaviour. For
information: (1) essential features of the disorder (those example, at times we all worry about our own life
that ‘define’ the disorder and allow for consistent diag- problems — some more than others. In extreme cases
nosis across clinicians), (2) associated features (i.e. those worry can become so regular and persistent that it will
that are usually, but not always, present), (3) diagnostic interfere with our daily living and may meet DSM cri-
criteria (a list of symptoms that must be present for the teria for diagnosis as a disorder (e.g. generalized anxi-
patient to be given this diagnostic label), and (4) infor- ety disorder, GAD; see Chapter 6). However, chronic
mation on differential diagnosis (i.e. information on how worrying and GAD symptoms appear to be dimen-
to differentiate this disorder from other, similar disor- sional, and range in frequency and intensity across
ders). Finally, as we mentioned earlier, an important fea- the general population (Niles, Lebeau, Liao, Glenn &
ture of DSM is that it avoids any suggestion about the Craske, 2012). In such circumstances, the cut off point
cause of a disorder unless the cause has been definitely for defining an activity such as worrying as a disorder
established. This means that diagnosis is made almost becomes relatively arbitrary. DSM had traditionally
entirely on the basis of observable behavioural symp- attempted to deal with this problem by adding a clini-
toms rather than any supposition about the underlying cal significance criterion to many diagnostic categories
cause of the symptoms. which required that symptoms cause ‘significant dis-
tress or impairment in social, occupational, or other
important areas of functioning’ (Spitzer & Wakefield,
General problems with classification 1999), and the purpose of this was to try and differen-
While classification systems such as DSM attempt to tiate symptoms that reflect normal reactions to stress
provide an objective and reliable set of criteria by which that the individual may be able to cope with from
psychopathology symptoms can be diagnosed, they are those that may require intervention and treatment to
in many senses imperfect. restore functioning. However, with growing evidence
Firstly, we have already mentioned that DSM does that psychopathology symptoms are on a dimension,
not classify psychopathology according to its causes, DSM-5 has included simple dimensional measures of
but does so merely on the basis of symptoms. This disorder severity to accompany more specific diagnos-
can be problematic in a number of different ways. For tic criteria. For example, in the case of GAD, dimen-
example, psychopathologies that look the same on sional measures such as per cent of the day spent
the surface may have different causes, and as a con- worrying can provide an indication of symptom sever-
sequence require different forms of treatment. Also, ity on a dimensional scale.
diagnosis on the basis of symptoms gives the illusion Fourthly, DSM conceptualizes psychopathology as
of explanation, when it is nothing more than a re- a collection of hundreds of distinct categories of disor-
description of the symptoms (Carson, 1996). So, to say ders, but what happens in practice provides quite a dif-
that ‘she hears voices because she has schizophrenia’ ferent picture. For example, the discrete, differentially
sounds like an explanation, but, within DSM, schizo- defined disorders listed in
comorbidity The co-occurrence of two or
phrenia is merely a collective term for the defining DSM regularly co-occur. more distinct psychological disorders.
symptoms. This is known as comor-
Secondly, simply using DSM criteria to label people bidity, where an individual client will often be diagnosed
with a disorder can be stigmatising and harmful. We with two or more distinct disorders (e.g. an anxiety dis-
saw in Chapter 1 that individuals with a mental health order such as obsessive compulsive disorder and major
diagnosis tend to be viewed and treated differently depression). What is interesting is that comorbidity is so
within society. In addition, diagnostic labels actually common that it is the norm rather than the exception.
encourage individuals to adopt a ‘sick’ role and can For example, surveys suggest that up to 79 per cent of
result in people adopting a long-term role as an indi- individuals diagnosed with a disorder at some point dur-
vidual with what they perceive as a debilitating illness ing their lifetime will have a history of more than one
(Scheff, 1975). disorder (Kessler, McGonagle, Zhao, Nelson et al., 1994).
Thirdly, DSM diagnostic classification tends to The frequency of comorbidity suggests that most disor-
define disorders as discrete entities (i.e. after being ders as defined by DSM may indeed not be independent
assessed, you will either be diagnosed with a disorder discrete disorders, but may represent symptoms of either
or you will not). However, much recent evidence has hybrid disorders (e.g. a
begun to suggest that psychopathology may be dimen- disorder that contains ele- hybrid disorders Disorders that con-
sional rather than discrete (Krueger & Piasecki, 2002). ments of a number of dif- tain elements of a number of different
ferent disorders) or a more disorders.
That is, symptoms diagnosed as a disorder may just
hy eee PSYCHOPATHOLOGY
“
disorder spectrum The frequency of broad ranging syndrome disorder (Kessler, Nelson, McGonagle, Liu, Schwartz
comorbidity suggests that most disor- or disorder spectrum that et al., 1996), (2) various anxiety disorders are highly
ders as defined by DSM may indeed not represents a higher order comorbid with each other (Brown, Campbell, Lehman,
be independent discrete disorders, but
categorical class of symp- Grisham & Mancill, 2001), and (3) depression and anxi-
may represent symptoms of a disorder
spectrum that represents a higher-order toms (Krueger, Watson & ety are together both highly comorbid with other
categorical class of symptoms. Barlow, 2005; Widiger & psychopathologies, such as substance abuse, eating dis-
Samuel, 2005). An exam- orders, somatoform disorders and personality disorders
mixed anxiety-depressive disorder An ple of a hybrid disorder is (Mineka, Watson & Clark, 1998; Widiger & Clark, 2000).
example of a hybrid disorder whereby peo- mixed anxiety-depressive Figure 2.1 provides a schematic representation of this
ple exhibit symptoms of both anxiety and disorder, and many people proposed spectrum of emotional disorders, indicating
depression, yet do not meet the thresh-
exhibit symptoms of both its hierarchical structure and showing how individual
old for either an anxiety or a depression
diagnosis. anxiety and depression, yet disorders defined in DSM may only represent the bot-
do not meet the threshold tom level of this hierarchy. Defining psychopathology in
for either an anxiety or a depression diagnosis (Barlow such hierarchical structures rather than defining them as
& Campbell, 2000). Examples such as this suggest that discrete independent entities has the benefit of explain-
because DSM defines disorders as numerous individual ing and predicting comorbidity and it begins to provide
discrete entities, it fails to recognize when combina- some theoretical insight into how different symptoms
tions of discrete symptoms may each not reach a level may be related.
significant enough for diagnosis, but may collectively One final problem with DSM is that it can be con-
be causing significant distress. There is also a broader ceived as a ‘hodgepodge’ collection of disorders, that
theoretical implication to the fact that comorbidity is so have been developed and refined in a piecemeal way
common, and this is that psychopathology may occur across a number of revisions (see Focus Point 2.1) — and
in a spectrum that has a hierarchical structure rather this makes it almost impossible to frame a definition
than consisting merely of numerous discrete disorders. of what a mental health problem actually is. Frances &
For example, Watson (2005) argues that anxiety and Widiger (2012) characterize this ‘hodgepodge’ view in
depression (which are both diagnosed as separate disor- the following quote:
ders in DSM-5) may both be members of a larger spec-
trum of emotional disorders. This is based on the facts The current list of mental disorders certainly consti-
that (1) 58 per cent of individuals with major depres- tutes a hodgepodge collection. Some describe short-
sion also meet DSM criteria for a comorbid anxiety term states, others life-long personality. Some reflect
y Emotional
_ Disorders”
Bipolar Disorders Distress Disorders Fear Disorders
pocatd | Mga So
BPD | BPD Il Gi; MDD DD GAD Panic Agora- Social ~ Specific
Disorder phobia Phobia Phobia
ATER NEGO
FIGURE 2.1 More detailed research on anxiety and depressive disorders can help reveal the way in which individual disorders are
related and why many diagnosable disorders are frequently comorbid. This figure shows a proposed spectrum of emotional disorders
which indicates how anxiety and depression may be related. For example, the fact that MDD and GAD are both classified as ‘distress
disorders’ provides some indication of why these two apparent different DSM disorders are frequently comorbid. Only the bottom line
of the figure represents the individual disorders defined in DSM-5 (after Watson, 2005). BPD | = bipolar | disorder; BPD I = bipolar II
disorder; CT = cyclothymia; MDD = major depressive disorder; DD = dysthymic disorder; GAD = generalized anxiety disorder;
PTSD = post-traumatic stress disorder.
Source: Watson, D. (2005). Rethinking the mood and anxiety disorders: A quantitative hierarchical model for DSM-V. Journal
of Abnormal
Psychology, 114, 522-536. American Psychological Association. Reprinted with permission
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY a
inner misery, others bad behaviour. Some represent involved many years of ae
problems rarely or never seen in normals, others are deliberation and field tri- ii etitad the eee
just slight accentuations of the everyday. Some reflect als to determine What “russesssssmsssssssemsmEs
too little self-control, others too much. Some are quite changes to mental health
intrinsic to the individual; others are defined against classification and diagnosis are essential and empirically
varying and changing cultural mores and stressors. justifiable. The main changes between DSM-5 and its
Some begin in infancy, others in old age. Some affect predecessor (DSM-IV-TR) are listed in Table 2.2. Firstly,
primarily thought; others emotions, behaviors, or previous versions of DSM placed mental health prob-
interpersonal relations; and there are complex combi- lems on a number of different axes representing clini-
nations of all these. Some seem more biological, oth- cal disorders (Axis I), developmental and personality
ers more psychological. disorders (Axis II), or general medical conditions (Axis
—(Frances & Widiger, 2012, p. 111) III). This multiaxial system has been scrapped — largely
because there was not enough evidence to justify the
While DSM is not ideal, it is the most comprehensive differences between them. Instead, in DSM-5, clinicians
classification system we have available, and while we will be encouraged to rate severity of symptoms along
have just listed a number of criticisms of DSM we must continuums developed for each disorder. Secondly, the
also remember that classification in and of itself does also importance of some disorder categories has been rec-
have some advantages (see p. 37). ognized either by allocating them to their own chapter
or by recognising them as new individual diagnostic
Changes in DSM-5 categories. For example, obsessive compulsive disorder
Published in 2013, DSM-5 arguably represents the most (OCD) is recognized as a significant mental health prob-
comprehensive revision of the DSM so far, and it has lem by being allocated its own chapter in DSM-5, and
Peon.
CRITICISMS OF THE DSM DEVELOPMENT PROCESS 8
N
~
DSM regularly undergoes an intensive revision process and simpler to proliferate multiple categories of
i to take account of new research on mental health prob- disorder based on relatively small differences in
\®)
a lems and to refine the diagnostic categories from ear- descriptions of symptoms.
|
fal lier versions of the system. One would assume that this Most experts involved in developing DSM are
ae would be a deliberate and objective process that could primarily worried about false negatives (i.e. the
UW
(e) only further our understanding of psychopathology, missed diagnosis or patient who doesn't fit neatly
and that is certainly the intention of the majority of into the existing categorisations), and this leads
those involved. However, at least some people argue to either more inclusive diagnostic criteria or
that the process of developing a classification system even more diagnostic categories. Unfortunately,
such as DSM can never be entirely objective, free from experts are relatively indifferent to false positives
bias, or free from corporate or political interests. Allen (patients who receive unnecessary diagnosis,
Frances and Thomas Widiger were two individuals who treatment, and stigma) and so are less likely to be
were prominent in the development of the fourth edi- concerned about over-diagnosis.
tion of the DSM, and they have written a fascinating Political and economic factors have also shaped
account of the lessons they believe should be learned the ‘medical model’ view of psychopathology
from previous attempts to revise and develop mental on which DSM is based, and also contributed to
health classification systems (Frances & Widiger, 2012). the establishment and proliferation of diagnostic
They make the following points: categories. For example, the pharmaceutical
industry benefits significantly from the sale of
1. Just as the number of mental health clinicians medications for mental health problems, and its
grows, so too will the number of life conditions profits will be dependent on both (1) conceptions
that work their way into becoming disorders. This of mental health based on a medical model that
is because the proliferation of diagnostic categories implies a medical solution, and (2) a diagnostic
tends to follow practice rather than guide it. system that will err towards over-diagnosis
2. Because we know very little about the true rather than under-diagnosis (see Pilecki, Clegg &
causes of mental health problems, it is easier McKay, 2011).
> aa PSYCHOPATHOLOGY
TABLE 2.2 Summary of changes in DSM-5 more of a number of academic skills, including oral »
language, reading, written language or mathematics
Axes I, Il and II will be combined
(Chapter 17), and the new substance use disorder cat-
— Disorders no longer categorized as acute or life-long.
egory will combine the previous DSM-IV-TR categories
New chapters for OCD and Trauma and Stress-Related of substance abuse and substance dependence into one
Disorders
overarching disorder. Some other important changes
— Confirms the growing importance of these types of
disorder as possibly independent of other anxiety-based
include (1) the elevation of binge-eating disorder from
problems. an appendix to a recognized diagnostic category, (2)
disruptive mood regulation disorder as a new category
Autism Spectrum Disorder will incorporate many previously
for diagnosing children who exhibit persistent irrita-
separate labels (e.g. Asperger's disorder).
bility and behavioural outbursts, and (3) the removal
New Disruptive Mood Dysregulation Disorder of the ‘bereavement exclusion’ from the diagnosis of
— Diagnoses children with persistent irritability.
major depression (which means that depressive symp-
Binge Eating Disorder, Hoarding Disorder and Skin-Picking toms lasting less than 2 months following the death of a
Disorder included loved one can be included amongst the criteria for diag-
— All recognized as new independent disorder categories.
nosing major depression, and reflects the recognition
Personality Disorders retained with added dimensional that bereavement is a severe psychological stressor that
scales. can precipitate major depression).
PTSD included in new chapter on stress
— Emphasizes the importance of trauma-related disorders. Criticisms of changes in DSM-5
Removal of bereavement exclusion in Major Depression While these most recent changes to the DSM have been
— Allows bereavement to be included as a contributor to Major extensively discussed and researched, many of the revi-
Depression. sions have been received critically, and it is worth discuss-
Substance use disorder combines substance abuse and
ingsome of these criticisms ,
substance dependence. because they provide an | For a video on criticism of the changes
insight into the difficulties — www.wiley-psychopathology.com/
to DSM-5 go to
See text for further elaboration.
of developing a mental dis- video/ch2
orders classification system
that is fair and objective.
new diagnostic categories within this chapter include Firstly, many of the diagnostic changes will reduce
‘Hoarding disorder’ (see Chapter 6) and “Excoriation the number of criteria necessary to establish a diagno-
disorder’ (skin-picking disorder). Similarly, DSM-5 has a sis. This is the case with attenuated psychosis syndrome,
new chapter, ‘Trauma and stress-related disorders’, that major depression, and generalized anxiety disorder,
now includes post-traumatic stress disorder (PTSD). and this runs the risk of increasing the number of peo-
DSM-5 focuses more on the behavioural symptoms that ple that are likely to be diagnosed with common men-
accompany PTSD and proposes four distinct diagnostic tal health problems such as anxiety and depression. It
clusters instead of the previous three. Thirdly, major is a debatable point whether increases in the number
changes have been made to the criteria for diagnosing of diagnosed cases is a good or a bad thing, but it is
autistic spectrum disorder (ASD), specific learning dis- likely to have the effects of ‘medicalising’ many every-
orders, and substance use disorders. Autistic spectrum day emotional experiences (such as ‘grief’ following a
disorder has become a diagnostic label that will incor- bereavement, or worry following a stressful life event),
porate many previous separate labels (e.g. Asperger's and creating ‘false-positive’ epidemics (Frances, 2010;
syndrome, childhood disintegrative disorder, pervasive Wakefield, 2013).
developmental disorder) in an attempt to provide more Secondly, DSM-5 has introduced disorder catego-
consistent and accurate diagnosis for children with ries that are designed to identify populations that are
autism (see Chapter 17). DSM-5 will retain the categori- at risk for future mental
cal model for personality disorders outlined in DSM- health problems, and these attenuated psychosis syndrome DSM-5
IV-TR, but rating scales are provided to assess how include mild neurocogni- has introduced disorder categories that are
designed to identify populations that are
well an individual’s symptoms fit within these different tive disorder (which would
at risk for future mental health problems.
types (Chapter 12). The new specific learning disorder diagnose cognitive decline _ Attenuated Psychosis Syndrome is seen
category is broadened to represent distinct disorders in the elderly) and attenu- as a potential precursor to psychotic
which interfere with the acquisition and use of one or ated psychosis syndrome episodes.
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY As
(seen as a potential precursor to psychotic episodes). any criteria defining a diagnostic cut-off point will be
Once again, these initiatives run the risk of medicalis- entirely arbitrary. DSM-5 has attempted to recognize
ing states that are not yet full-blown disorders, and could the importance of the dimensionality of symptoms
facilitate the diagnosis of normal developmental pro- by introducing dimensional severity rating scales for
cesses as psychological disorders. individual disorders. But as we have seen from the dis-
Thirdly, there are concerns that changes in diagnos- cussion above, each iteration change in DSM diagnos-
tic criteria will result in lowered rates of diagnosis for tic criteria changes the number and range of people
some particularly vulnerable populations. For exam- who will receive a diagnosis, and this makes it increas-
ple, applying the DSM-5 criteria for autistic spectrum ingly hard to accept diagnostic categories as valid con-
disorder to samples of children with DSM-IV-TR diag- structs (see e.g. Kendler, Kupfer, Narrow, Phillips &
noses that would no longer be available in DSM-5 sug- Fawcett, 2009).
gested that 9 per cent of this latter group would lose
their autism diagnosis with the introduction of the new
DSM.-5 criteria (Huerta, Bishop, Duncan, Hus & Lord,
2.1.3 Conclusions
2012). Similar concerns
specific learning disabilities Disorders
such as dyslexia and communication have been voiced about Despite its conceptual difficulties and its many critics,
disabilities. changes to specific learn- DSM is still the most widely adopted classification and
ing disabilities diagnostic diagnostic system for mental health problems. Such
dyslexia A persistent, chronic learning criteria in DSM-5, and the a system is needed for a number of reasons, including
disability in which there are developmental
possibility that deletion determining the allocation of resources and support for
eficits in spelling, reading and writing
abilities. of the term dyslexia as a mental health problems, for circumstances that require
diagnostic label will disad- a legal definition of mental health problems, and to pro-
vantage individuals with specific phonologically based, vide a common language that allows the world to share
developmental reading disabilities. and compare data on mental health problems. Having
Finally, two enduring criticisms of DSM generally said this, there are still many significant problems associ-
that have continued to be fired specifically at DSM-5 have ated with DSM, and diagnosing and labelling people with
been that (1) DSM-5 has continued the process of specific psychological disorders raises other issues to do
attempting to align its diagnostic criteria with develop- with stigma and discrimination. Indeed, we should be
ments and _ knowledge clear that diagnostic systems are not a necessary require-
from neuroscience (Regier, ment for helping people with mental health problems
To read about the proposed DSM-5
changes, which continue to spark Narrow, Kuhl & Kupfer, to recover, and many clinical psychologists prefer not
controversy, go to 2011) when there is in fact to use diagnostic systems such as DSM-5, but instead
http://tinyurl.com/pf40d43
very little new evidence prefer to treat each client as someone with a unique
from neuroscience that mental health problem that can best be described and
helps define specific mental health problems, and (2) treated using other means such as case formulation (see
most mental health problems (and psychological dis- section 2.3 for a fuller description and examples of case
tress generally) are now viewed as dimensional, so formulation).
SELF-TEST QUESTIONS
® Can you briefly describe the history of the development of psychopathology classification systems?
® What is the DSM classification system primarily designed to do?
* DSM is not an ideal classification system. Can you describe at least four problems associated with this method of
classification?
° What are the main changes that were implemented in DSM-5?
nic Soe PSYCHOPATHOLOGY
STROSS ME! cciie ylsvlies. veilmmubgery hoodtiqusclieemeslingitinh ozone aaa

2.1 CLASSIFYING PSYCHOPATHOLOGY
e The two most influential classification systems are the American Psychiatric Association (APA) Diagnostic and Statistical
Manual and the World Health Organisation (WHO) International List of Causes of Death (ICD).
® Currently, the most widely adopted classification system is DSM-5.
to which the test will produce roughly similar results

2.2 METHODS OF when the test is given to the same person several weeks
ASSESSMENT or even months apart (as long as no treatments or inter-
ventions have occurred in between). Most psychological
tests are based on the assumption that most traits and
This section describes in some detail a range of personal characteristics are relatively stable and can be
assessment tools that clinical psychologists can use reliably measured (see p. 47). If the test has high test—
to aid diagnosis, determine the best forms of inter- retest reliability, then when an individual is given the
vention for an individual’s problems, and assess their test on two separate occasions, the two scores should be
progress towards recovery. But first, it is important to highly correlated.
be sure that a method of assessment is both reliable Second, inter-rater reliability refers to the degree
and valid. to which two independent clinicians will actually
agree when interpreting
or scoring a particular test. inter-rater reliability The degree to i
:
how or fe Most highly structured Whi¢ich two independent
P cliniciansor
;
2.2.1. The Reliability and Validity desrgesireln gah PENS veg
researchers actually agree when ‘
interpreting or scoring a particular test.
of Assessment Methods ity inventories, will have 4
high inter-rater reliability because the scoring system
In order for assessment methods to provide objec- is clearly defined and there is little room for individ-
tive information about clients we need to be sure ual clinician judgements when interpreting the test.
about two things. First, we need to be sure that the However, some other tests have much lower inter-
reliability The extent that an assess- method has high reli- rater reliability, especially where scoring schemes are
ment method will still provide the same ability; that is, that the not rigidly defined, and projective tests are one exam-
result when used by different clinicians on method will provide the ple of this (see pp. 50-53).
different occasions.
same result when used by Third, many assessment tests have multiple items
different clinicians on dif- (e.g. personality and trait inventories) and internal
validity The extent that an assessment
ferent occasions. Second, consistency within such tests is important. Internal con-
method actually does measure what it
claims to be measuring. we also need to be sure sistency refers to the extent to which all the items in
that the assessment has the test consistently relate to each other. For example, if
validity; that is, that it actually does measure what it
there are 20 items in a test, then we would expect scores
claims to measure (e.g. if it is a test measuring anxi- on each of those 20 items
ety, then scores on the test should correlate well with to correlate highly with internal consistency The extent to which
other ways of measuring anxiety). all the items in a test consistently relate to
each other. If one item one another. :
doesn’t correlate highly
Reliability with the others, then it may lower the internal consist-
Reliability refers to how consistently an assessment ency of the test. The internal consistency of a question-
method will produce the naire or inventory can usually be assessed by using a
test-retest reliability The extent that a same results, and _ reli- statistical test called Cronbach’s &, and this test will also
test will produce roughly similar results
when the test is given to the same person
ability can be affected by indicate whether any individual item in the test is signifi-
several weeks or even months apart (as a number of different fac- cantly reducing the inter- Cronbach'sa Statistical test used to asses:
long as no treatments or interventions tors. First, test—retest reli- nal consistency of the test _the internal consistency of a questionnaire
have occurred in between). ability refers to the extent (Field, 2013a, pp. 708-710). Or inventory.
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY aS
Validity reliable information about childhood abuse and neglect

It is important to be sure that an assessment method will indicate that such individuals are likely to suffer a
actually measures what it claims to be measuring, and range of possible psychopathologies in later life (see
this is covered by the concept of test validity. However, Table 16.1).
validity is a complex concept, and we will begin by dis- Finally, construct validity is also an impor-
cussing some of the more obvious issues surrounding tant concept in clinical assessment. A construct is a
this problem. hypothetical or inferred
To determine whether a test actually measures what attribute that may not construct validity Independent evidence
showing that a measure of a construct is
it claims to measure, we need to establish the concur- be directly observable related to other similar measures.
rent validity of the test. That is, we need to see if or directly measurable.
scores on that test cor- Hypothetical constructs are used frequently in the
concurrent validity A measure of how study of psychopathology to help understand some
relate highly with scores
highly correlated scores of one test are
with scores from other types of assess- from other types of assess- of the cognitive factors that may cause or maintain
s that we know also measure that ment that we know also mental health problems, and so being able to meas-
attribute. measure that attribute. ure them is a useful tool in diagnosis and subsequent
For example, the Spider treatment. For example, individuals with obsessive
Phobia Questionnaire (SPQ) purports to be a meas- compulsive disorder (OCD) tend to have inflated con-
ure of the spider phobic’s anxious reaction to spiders ceptions of their own responsibility for preventing
(Watts & Sharrock, 1984), but in order to establish the harm, and this inflated responsibility appears to be
concurrent validity of this questionnaire, we might an important vulnerability factor in developing OCD
need to be sure that scores actually correlate highly (Salkovskis, 1985; Rachman, 1998; see Chapter 4).
with other measures of spider fear such as the magni- However, inflated responsibility is not directly observ-
tude of physiological anxiety measures taken while the able, but has to be inferred from indirect measures
individual is viewing a spider. of the individual’s behaviour, and so questionnaires
A particular assessment method may appear to be such as the Obsessive Beliefs Questionnaire (OBQ)
valid simply because it has questions which intuitively have been developed to measure beliefs about inflated
seem relevant to the trait or characteristic being meas- responsibility (see p. 49). The more independent evi-
ured. This is known as face validity, but just because dence that can be gathered to show that a measure
a test has items that seem intuitively sensible does not of a construct like inflated responsibility is related to
mean that the test is a other similar measures (e.g. compulsive persevera-
face validity The idea that a particularvalid measure of what it tion at checking tasks, or higher scores in groups
sessment method may appear to be claims to be. For exam- diagnosed with OCD than non-clinical control par-
valid simply because it has questions
ple, a questionnaire meas- ticipants), the greater the construct validity of the
which intuitively seem relevant to the
trait or characteristic being measured. uring health anxiety may measure.
ask about how frequently
the respondent visits a doctor. Although this would
be a characteristic of health anxiety, it is also a char- 2.2.2. Clinical Interviews
acteristic of individuals who are genuinely ill or have
chronic health problems. The nature of clinical interviews
For an assessment method to have high predictive We have all probably been interviewed at some point in
validity it must be able to help the clinician to predict our lives. This may be fora job, a place at university, or by a
future behaviour and doctor enquiring about symptoms of an illness. An inter-
predictive validity The degree to which future symptoms, and so view usually represents el n gtia eietarritler eb
3 assessment method isable to help the
inician predict future behaviour and
be valuable enough to em informal, relatively Z For a video on anxiety go to
future symptoms. help with the planning of unstructured conversa- | www.wiley-psychopathology.com/

video/ch2
care, support or treatment tion between two or more
for that individual. For example, a good measure of people, the purpose of
depression would predict that certain types of antide- which is to gather some information about one or more
pressant medication will help to alleviate the symptoms. of those people in the interview. The clinical interview is
Some assessment measures are predictive in the sense probably the first form of contact that a client will have
that they help us to understand the kinds of factors that with a clinician, and the clinical psychologist will usu-
might pose as risk factors for subsequent psychopathol- ally be trying to gain a broad insight into the client and
ogy. For example, assessments that allow us to gather their problems. Questions may relate to the nature of
BESS PSYCHOPATHOLOGY
» YQ
the symptoms the client experiences, their past history, such structured interview technique is known as the
and their current living and working circumstances. The Structured Clinical Interview for DSM-IV-TR (SCID)
type of questions that will be asked in a clinical interview (Spitzer, Gibbon & Williams, 1986), which can be used
will depend very much on the theoretical orientation of for determining diagnoses. The SCID is a branching,
the clinician. For example, psychodynamic clinicians are structured interview in
structured interview An interview
likely to want to ask questions about the client's child- which the client's response in which questions to be asked, their
hood history, their memories of past events, and to take to one question will deter- sequence and detailed information to be
note of any strong emotional responses that may indicate mine the next question to gathered are all predetermined.
unconscious processes (see Chapter 1). In contrast, the be asked. This enables the
Structured Clinical Interview for DSM-
behavioural interviewer will want to explore any relation- clinician to establish the IV-TR (SCID) A branching, structured
ships between the client’s symptoms and environmental main symptoms exhibited interview in which the client's response t
events, such as the consequences of symptoms that may by a client, their severity one question will determine the next a
tion to be asked. i
reinforce them. Finally, the cognitive clinician will want to (on a scale of 1 to 3), and
try to discover whether the client holds any assumptions whether a combination of
or beliefs that may maintain or influence their problems. these symptoms and severity meet DSM criteria for a
In general, those conducting clinical interviews must particular disorder. The SCID has been shown to pro-
be skilful in guiding the client towards revealing the vide highly reliable diagnoses for many disorders (Segal,
kinds of information they are looking for. They must Herson & Van Hasselt, 1994; Lobbestael, Leurgans &
be able to establish a good rapport with the client, they Arntz, 2011), with one study indicating 85.7 per cent
must gain their trust, they must be able to convince the agreement on diagnosis between different clinicians
client of the value of the theoretical approach they are using the SCID (Miller, Dasher, Collins, Griffiths &
taking, and in most cases they must be able to empathize Brown, 2001).
with their clients in order to encourage them to elabo- Structured interviews can also be used to determine
rate on their concerns and to provide information that overall levels of psychological and intellectual function-
they may otherwise be reluctant to give. The clinical ing, especially in older people who may be suffering from
interviewer can encounter a number of difficulties when degenerative disorders such as dementia. One such struc-
conducting an interview and these will often require all tured interview is the Mini Mental State Examination
their experience and skill to overcome. For example, (1) (MMSB), which is a structured test that takes 10 minutes
many clients will want to withhold information about to administer and can provide reliable information on
themselves, especially if it involves painful or embar- the client’s overall levels of cognitive and mental func-
rassing memories, or if the information concerns illegal tioning. A fuller description of this structured interview
or unsocial activities (such as illegal drug use or is given in Chapter 15 (see Focus Point 15.2).
illegal sexual activities), and (2) clients may well have
poor selfknowledge, and so be unable to answer ques- Limitations of the clinical interview
tions accurately or with any real insight into why they The clinical interview is usually a good way of beginning
behave or feel the way they do. It is the skilled interview- the process of assessment, and it can provide a range of
er’s job to find ways to deal with these problems and to useful information for the clinician. However, there are
reveal the reliable information that they need to form a limitations to this method. First, the reliability of clini-
diagnosis, to understand the causes of the client’s prob- cal interviews is probably quite low. That is, no matter
lems, and to formulate a treatment programme. how skilled they may be, two different clinicians are
quite likely to end up with rather different information
Structured interviews from an unstructured interview. For example, clients
The clinician can also use the interview method to are likely to give different information to an interviewer
acquire the kinds of standardized information they who is ‘cold’ and unresponsive than to one who is ‘warm’
need to make a diagnosis or to construct a case for- and supportive (Eisenthal, unstructured interview A free-flowing
mulation (see section 2.3), but this requires that they Koopman & Lazare, 1983), _interview in which questions to be asked,
conduct the interview in a structured way. The normal anda teenage clientis likely their sequence and detailed information to
clinical interview would probably contain many open to respond differently to a be gathered are not predetermined.
questions such as “Tell me something about yourself young interviewer who is dressed casually than to an
and what you do’, and the direction of the interview older interviewer who is dressed formally. There is also
will be to some extent determined by the client’s significant evidence that an interviewer's race and sex
responses to these open questions. However, struc- will influence a client’s responses (Paurohit, Dowd &
tured interviews can be used to enable the clinician to Cottingham, 1982). As we have already mentioned,
make decisions about diagnosis and functioning. One many clients may have quite poor self-awareness, so only «
&
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY eae
a skilled interviewer will be able to glean the information for a psychological disorder. For example, scores on a test
they require by inferring information from the client’s such as the Clark—Beck Obsessive-Compulsive Inventory
responses. Interviewers are also prone to biases that may (CBOCI) (Clark & Beck, 2003) can be used to estimate
affect the conclusions they draw from an interview. For the probability with which a client might meet diagnos-
example, they may rely too heavily on first impressions tic criteria for OCD; and (4) unlike the ad hoc quizzes
(the primacy effect), or give priority only to negative and questionnaires you might find in popular magazines,
information (Meehl, 1996), and may be influenced by most structured psychological tests are rigorously tested
irrelevant details such as the client’s biological sex, race, to ensure that they are both valid and reliable (see sec-
skin colour or sexual orientation. Finally, there are some tion 2.2.1). That is, they are tested to ensure that they
psychological disorders in which sufferers may inten- are a valid measure of what they claim to be measuring
tionally mislead the interviewer or lie to them, and this (e.g. that scores on a written psychological test claiming
can mean that the client can manipulate the interview to measure anxiety actually correlate with behavioural
or deliberately provide misleading information. This can measures of anxiety) and that the test is reliable in the
often occur with personality disorders, such as border- sense that it yields consistent scores when it is given to
line personality disorder or antisocial personality disor- the same person on different occasions.
der, or in the case of sexual disorders such as paedophilia Most psychological tests are based on the psycho-
(see Chapters 11 and 12). metric approach. That is, the test assumes that there
are stable underlying characteristics or traits (e.g. anxi-
ety, depression, compulsiveness, worry, and so on) that
2.2.3 Psychological Tests exist at different levels in everyone. The psychological
tests we will discuss below can take a number of dif-
Psychological tests represent highly structured ways of ferent forms and serve a psychometric approach The idea that
gathering information about an individual. They usually number of different func- a psychological test assumes that there
take the form of a written questionnaire in which the tions. For example, some are stable underlying characteristics or
client has to respond to a series of questions or stimuli. tests stick rather rigidly traits (e.g. anxiety, depression, compulsive-
ness, worry) that exist at different levels in
However, they can be given verbally by the clinician or to the structured ques- everyone.
completed on a computer. The psychological test is one tion, response and scoring
of the most common forms of assessment in clinical psy- format similar to that shown in Table 2.3 (personality
chology and it is considerably more structured than the inventories, specific symptom inventories), while others
interview method. Psychological tests have a number of (such as projective tests) may closely define the ques-
advantages as methods of assessment: (1) they usually tions or stimuli to be presented to the client, but allow
assess the client on one or more specific characteristics a much wider range of potential responses. The clinical
or traits (e.g. levels of anxiety, depression, IQ, cognitive psychologist will use psychological tests for a variety of
functioning, or individual psychopathology traits such as different purposes, including the assessment of psycho-
hypochondriasis, paranoia, conversion hysteria, and such- pathology symptoms, intelligence, and neurological or
like); (2) they will usually (but not always) have very rigid cognitive deficits.
response requirements so that the questions can be scored
according to a pre-conceived scoring system. Table 2.3 Personality inventories
provides an example of the question format for a meas- The most well-known of the personality inventories
ure of trait anxiety — the State-Trait Anxiety Inventory used by clinical psychologists and psychiatrists is the
(STAI) (Spielberger, Gorsuch, Lushene, Vagg & Jacobs, Minnesota Multiphasic Personality Inventory (MMPI).
1983) — and this is a test format common to many psy- This was originally developed in the 1940s by Hathaway
chometric tests; (3) once data from these tests have been and McKinley (1943), and has been updated by Butcher,
collected from large numbers of participants, statistical Dahlstrom, Graham, Tellegen & Kraemer (1989) (now
norms for the tests can be established. This is known as known as the MMPI-2). The MMPI-2 consists of 567 self-state-
standardisation, and allows the clinician to see where ments to which the client
an individual client’s score on the test falls in relation to has to respond on a three- Minnesota Multiphasic Personality
Inventory (MMPI) A well-known person-
the normal distribution of scores for that test (e.g. see point scale by replying either ality inventory used by clinical psychologists
Figure 1.1). It also means ‘true’, ‘false’ or ‘cannot say’. and psychiatrists.
standardisation The establishment of that the clinician may be The questions cover topics
statistical norms for clinical tests, which able to use the score on a
allows the clinician to see where an individ-
such as mood, physical con-
particular test to estimate cerns, social attitudes, psy- To read more about The Minnesota
Jal client’s score on the test falls in relation Multiphasic Personality Inventory go to
‘0 the normal distribution of scores for whether a client might chological symptoms and http://tinyurl.com/pws65k4
hat test. meet the diagnostic criteria feelings of well-being. The
ae eae PSYCHOPATHOLOGY
TABLE 2.3 Measuring state and trait anxiety using a questionnaire
The STAI is a well-known psychometric test for measuring levels of state and trait anxiety. Its questions take the following format,
and this format is one that is regularly used in psychological tests of this kind (after Spielberger, Gorsuch, Lushene, Vagg, & Jacobs,
1983).
A number of statements which people have used to describe themselves are given below. Read each statement and then
circle the appropriate number to the right of the statement to indicate how you generally feel. There are no right or wrong
answers. Do not spend too much time on any one statement but give the answer which seems to describe how you gener-
ally feel.
1 = Almost never
2 = Sometimes
3 = Often
4 = Almost always
1. | feel pleasant 1
2. | feel nervous and restless 1

3. | feel satisfied with myself 1
4. |wish| could be as happy as others seem to be 1
5. | feel like
a failure 1 Nt
ah
oN
WieeNe
BC
BCU)
(Co)
Coe
CO LH
LH
ff
&
F
The scale of 1 to 4 is known as a ‘Likert scale’ where the client has to specify their level of agreement with each statement. Some items will be
reversed so that the respondent cannot simply endorse each item in the same way (e.g. Q3 is a reversed item in which the anxious individual would
endorse a low number rather than a high number). The clinician can then create a total score for a client by adding together the individual scores
that the client has circled (but remembering to reverse score any reversed items — e.g. on Q3 4 would be scored as 1, 3 as 2, and so on). When data
have been collected from a large number of participants from differing age groups and demographic backgrounds statistical norms for the test can
be established, and this is known as‘standardisation’. This allows the clinician to compare the score of their client with the normal distribution of
scores that occur in the population in general.
original authors asked around 800 psychiatric patients scale), or (4) because they are defensive and want to avoid
to indicate whether the questions were true for them, appearing incompetent (measured by the K scale).
and compared their responses with those from 800 non- Clinical research has indicated that the MMPI has
psychiatric patients. They then included in the inventory good internal reliability, and scores on the MMPI appear
only those questions that differentiated between the two to have excellent clinical validity by corresponding accu-
groups. The test now has four validity scales and ten clini- rately with clinical diagnoses and ratings of symptoms
cal scales, and examples of these are shown in Table 2.4. made by both clinicians and members of the client’s own
The test provides scores for each scale between 0 and family (Ganellan, 1996; Graham, 1990; Vacha-Hasse,
120, and scores above 70 on a scale are considered to be Kogan, Tani & Woodall, 2001). One limitation of the
indicative of psychopathology. The scores from the vari- MMPI is the time that it takes to administer, and answer-
ous scales can be displayed on a graph to give a distinctive ing 567 questions requires some stamina on the part of
profile indicating the client’s general personality features, both the client and the overworked clinician. However,
potential psychopathology, and emotional needs. The shortened versions of the MMPI-2 are available, and these
validity scales are particularly useful, because they allow show both good reliability and validity (Dahlstrom &
the clinician to estimate whether a client has been provid- Archer, 2000).
ing false information on the test. Clients might provide
false information for a number of reasons: (1) because
they want to ‘look good’, and so respond in a socially Specific trait inventories
acceptable way (measured by the lie scale), (2) because While personality inventories such as the MMPI assess
they may want to fake psychopathology symptoms in characteristics of the client across a range of differ-
order to receive attention and treatment (measured by ent traits and domains, other inventories have been
the F scale) (Rogers, Sewell, Martin & Vitacco, 2003), (3) developed simply to measure functioning in one spe-
because they are being evasive or simply having difficulty cific area or one specific psychopathology. Such tests
reading or interpreting the questions (measured by the ? may measure emotional functioning, such as levels
ri
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY aS
TABLE 2.4 Subscales and sample items from the MMPI
Subscale What the scale measures Sample item
? Evasiveness or difficulty interpreting the question (Number of items left unanswered)

L (lie scale) Tendency of respondent to respond in a socially “| approve of every person | meet”
acceptable way i
F Respondent is trying to fake psychopathology “Everything tastes sweet”
symptoms
K Respondent is defensive and trying not to look “Things couldn't be going any better for me”
incompetent
Hypochondriasis (HS) Abnormal concern with bodily sensations “lam often aware of tingling feelings in my body”
Depression (D) Pessimism and hopelessness “Life never feels worthwhile to me”
Conversion Hysteria (Hy) Uses physical symptoms to avoid conflicts and “My muscles often twitch for no apparent reason”
responsibilities
Psychopathy (Pd) Emotional shallowness and disregard for social “| don’t care about what people think of me”
norms
Masculinity-femininity Identifies resoondents with non-traditional gender “| like to arrange flowers”
(Mf) characteristics
Paranoia (Pa) Pathological suspiciousness or delusions of gran- “There are evil people trying to influence my mind”
deur or persecution
Psychasthenia (Pt) Identifies respondents with obsessions, compul- “| save everything | buy, even after | have no use
sions, guilt, and irrational fears for it”
Schizophrenia (Sc) Identifies bizarre sensory experiences and beliefs “Things around me do not seem real”
Hypomania (Ma) Identifies emotional excitement, hyperactivity and “Sometimes | have a strong impulse to do some-
impatience thing that others will find appalling”
Social Introversion (Si) Identifies someone who is shy, modest and prefers “lam easily embarrassed”
solitary activities
of anxiety, depression or anger, or they may measure hypothetical constructs hypothetical constructs Constructs that
aspects of behaviour such as social skills. More recently, that are not necessarily are not necessarily directly observable but
other tests have been developed in an attempt to meas- directly observable but have to be inferred from other data.
ure cognitive functioning or cognitive constructs that have to be inferred from
are relevant to psychopathology. One such example is the answers given to a range of questions. For exam-
the Obsessive Belief Questionnaire (OBQ) (Steketee, ple, the degree to which an individual cannot tolerate
Frost, Bhar, Bouvard et al., 2005) which was designed uncertainty (a factor that has been implicated in the
to assess beliefs and appraisals considered critical to acquisition and maintenance of a number of anxiety
the acquisition and maintenance of obsessions. This disorders) is assessed on the OBQ by asking respond-
measures six cognitive constructs thought to play a ents to endorse statements such as ‘If I am uncer-
role in OCD, including: (1) intolerance of uncertainty, tain there is something wrong with me’ or ‘I should
(2) overestimation of threat, (3) control of thoughts, be 100 per cent certain that everything around me is
(4) importance of thoughts, (5) beliefs about inflated safe’. Taken together, such questions provide an esti-
responsibility, and (6) perfectionism. (You may want mate of how much the individual is able to ‘tolerate’
to look at section 6.5 to understand how these cogni- uncertainty.
tive constructs are relevant to the aetiology of OCD.) Because of their potential diagnostic and theoreti-
Specific tests such as these can be used to measure cal value (such inventories can also be used as research
variables that are directly observable and measurable, tools to help us understand the causes of psychopathol-
such as characteristics found in observable behaviour. ogy), the number of specific trait inventories available
But they are becoming increasingly used to measure to clinicians and researchers has burgeoned in the past
Bal ee PSYCHOPATHOLOGY
; rs
10-15 years. While some are very valuable and have revealed information about the individual’s psychologi-
good face validity, many others are relatively underde- cal condition. Most versions of the Rorschach Inkblot
veloped. For example, unlike the MMPI, a majority of Test now use around 10 official inkblots of which five are
specific trait inventories fail to include any questions black ink on white, two are black and red ink on white,
to indicate whether respondents are faking responses and three are multicoloured. An example of a black-and-
or are merely being careless with their answers, and white and multicoloured inkblot are given in Figure 2.2.
many are not subjected to stringent standardisation, The clinician will have available to them a highly struc-
validation and reliability tests. There is even a view that tured scoring system (e.g. Exner & Weiner, 1995) that
researchers may simply create a specific trait inventory allows them to compare the scores the client provides
to serve their own theoretical purposes and to give their with a set of standardized personality norms, that may
theoretical perspective a facade of objective credibility provide indications of underlying psychopathology.
(i.e. they may create an inventory simply to ‘meas- However, if the test is used as a formal assessment proce-
ure’ a construct that they themselves have invented) dure, it is still heavily dependent on the clinician's inter-
(Davey, 2003). pretation of the client’s responses. For example, if certain
themes keep appearing in the client’s responses they
Projective tests may provide evidence of underlying conflicts, such as
This group of tests usually consists of a standard fixed the repeated perception of ‘eyes’ on the inkblots perhaps
set of stimuli that are presented to the client, but are providing evidence of paranoia the clinician may want to
ambiguous enough for the client to put their own explore further. Nevertheless, the Rorschach test can be
interpretation on what the stimuli represent. This often a valid and reliable test for the detection of thought dis-
allows for considerable variation in responses between orders that may be indicative of schizophrenia or people
clients, and also considerable variation between cli- at risk of developing schizophrenia (Lilienfeld, Wood &
nicians in how the responses should be interpreted. Garb, 2000; Viglione, 1999).
The most widely used of the projective tests are the The Thematic Apperception Test (TAT) is a pro-
Rorschach Inkblot Test, jective personality test consisting of 30 black-and-white
projective tests A group of tests usually the Thematic Apper- pictures of people in vague or ambiguous situations
consisting of astandard fixed set of stimuli ception Test (TAT), and (Morgan & Murray, 1935). The client is asked to create a
that are presented to clients, but which are
the Sentence Completion dramatic story around the
ambiguous enough for clients to put their
Test. Projective tests were picture, describing what Thematic Apperception Test (TAT) A |
own interpretation on what the stimuli
projective personality test consisting of 7
represent. originally based on the they think is happening in
30 black-and-white pictures of peoplein
psychodynamic view that the picture, what events vague or ambiguous situations.
people’s intentions and desires are largely unconscious, preceded it , what the indi-
and must be inferred indirectly (Dosajh, 1996). Most viduals in the picture are saying, thinking or feeling, and
projective tests were designed during the mid-20th cen- what the outcome of the situation is likely to be. Many
tury and were extremely popular for assessment pur- clinicians claim that this test is particularly useful for elic-
poses right up to the turn of the century. However, as iting information about whether the client is depressed,
we shall see below, because they are open-ended tests has suicidal thoughts, or strong aggressive impulses
that allow significant variation in client responding, (Rapaport, Gill & Shaefer, 1968). Clients usually identify
they are significantly less reliable and valid than more with one of the characters in the pictures (known as the
structured tests. Nevertheless, even though their popu- ‘hero’) and the picture then serves as a vehicle for the cli-
larity has declined in recent years (Piotrowski, Belter ent to describe their own feelings and emotions as if they
& Keller, 1998), many clinicians still use these types of were involved in the ambiguous scene. The TAT may also
tests to give them some first impressions of a client’s allow the clinician to determine the client’s expectations
symptoms or as part of a larger battery of assessment about relationships with peers, parents, other authority
procedures. figures, and romantic partners. It can also be a useful
The Rorschach Inkblot Test was originally developed tool after a client has been formally diagnosed in order to
by the Swiss psychiatrist Hermann Rorschach. He cre- match them with a suitable form of psychotherapy, and
ated numerous inkblots by dropping ink onto paper and the TAT has also been used to evaluate the motivations
then folding the paper in half to create a symmetrical and attitudes of individuals who have been accused of vio-
image. He discovered that lent crimes (Kim, Cogan,
Rorschach Inkblot Test A projective
personality test using inkblots created by
everyone he showed them Carter & Porcerelli., 2005). Sentence Completion Test An open-
to saw designs and shapes ended projective personality test that
dropping ink onto paper and then folding Finally, the Sentence
provides clients with the first part of an
the paper in half to create a symmetrical in the blots, and he assu- Completion Test is a use- uncompleted sentence which they com-
image.
med that their responses ful open-ended assessment plete with words of their own.
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY Per
iStock.com/Zmeel
©
Photography
FIGURE 2.2 The Rorschach Inkblot Test.

The Rorschach Inkblot Test usually consists of ten official inkblots. Five inkblots are black ink on white. Two are black and
red ink on white. Three are multicoloured, and the pictures above give examples of ablack-and-white inkblot and a multicol-
oured one. The clinician shows the inkblots in a particular order and asks the client: ‘What might this be?’ (a free association
phase). After the patient has seen and responded to all the inkblots, the clinician then presents them again one by one to study,
(the inquiry phase). The client is asked to list everything they see in each blot, where they see it, and what there is in the blot
that makes it look like that. The blot can also be rotated. The clinician also times the patient, which then factors into the overall
assessment.
Methods of interpretation differ. The most widely used method in the United States is based on the work ofJohn E. Exner (Exner &
Weiner, 1995). In this system, responses are scored systematically with reference to their level of vagueness or synthesis of multiple
images in the blot, the location of the response, which of a variety of determinants is used to produce the response (e.g. whether
the shape of the inkblot, its colour, or its texture is primary in making it look like what it is said to resemble), the form quality of the
response (to what extent a response is faithful to how the actual inkblot looks), the contents of the response (what the respondent
actually sees in the blot), the degree of mental organising activity that is involved in producing the response, and any illogical, incon-
gruous, or incoherent aspects of responses.
test that was first developed in the 1920s, and provides

clients with the first part of an uncompleted sentence,
such as ‘Tlike...’, ‘I think of myself as ...’, ‘I feel guilty
when .. ., which the client then completes with words
of their own. This test allows the clinician to identify
topics that can be further explored with the client, and
can also help to identify ways in which an individual's
psychopathology might bias their thinking and the way
they process information. Research Methods in Clinical
Psychology Box 2.1 shows how the sentence comple-
tion task has been used to identify trauma-relevant
thinking biases in combat veterans with PTSD (Kimble,
LIBRARY
PHOTO
MERRIM/SCIENCE
LEW
Kaufman, Leonard, Nestor et al., 2002). Such thinking
biases help to maintain emotional problems, and using FIGURE 2.3 The Thematic Apperception Test (TAT).
the sentence completion task can help the clinician to The Thematic Apperception Test consists of 30 black-
identify ways of thinking that can be targeted during —and-white pictures similar to the one above. The clientis
treatment. asked to create a dramatic story around the picture. Clients
As we mentioned earlier, the popularity of projec- _ will usually identify with one of the characters in the pic-
tive tests has declined steadily over the years. There are _ tures, which enables them to express their own feelings and
a number of reasons for this: (1) such tests are mainly emotions as if they were involved in the scene.
as y ae PSYCHOPATHOLOGY
THE SENTENCE COMPLETION TEST
The sentence completion task is an open-ended assessment test that,

To read the article by Kimble etal.
provides the client with the first part of a sentence which the client then |
(2002), which reports on sentence
has to complete in their own words. This is a useful projective test that : completion tests, go to
allows the clinician to identify topics that are important to the client, © www.wiley-psychopathology.com/
reading/ch2
and to identify any biases in the way that a client tends to think about “
things. For example, incomplete sentences such as ‘My greatest fear. . .;
‘\ feel. . .;‘l need ../ and so on can give the clinician an insight into some of the :client’s emotional responses.
Similarly, questions such as ‘My father . . .,‘Other pupils . . .;‘Most girls . . . will provide some insight into the cli-
ent’s feelings about others.
The sentence completion task can also be used successfully as an important research tool. For example,
Kimble et al. (2002) used a sentence completion task to assess interpretation biases in combat veterans who
were diagnosed with PTSD (see Chapter 6). They gave their participants 33 sentences to complete. Each item
was generated so that it could be completed with words of military or non-military content. Examples included:
‘He was almost hit bya.. .’
‘The night sky was full of. . .’
‘The air was heavy with the smell of . .’
‘The silence was broken by the. . .’
For instance, ‘He was almost hit by a.. / could be completed with the word ‘rock’ or the word ‘bullet’ The fig-
ure below shows that veterans with PTSD completed sentences with significantly more ‘war’ or trauma-relevant
words than veterans without PTSD. These findings suggest that individuals diagnosed with PTSD have biases in
the accessibility, encoding and retrieval of trauma-relevant information, and that sentence completion tasks of
this kind might help to differentiate individuals with a diagnosable mental health condition from those without.
Military
BOX
PSYCHOLOGY
2.1
METHODS
CLINICAL
IN
RESEARCH Ambiguous
Non-Military
Endings
Word
Final
PTSD No PTSD
Source: Kimble, M.O., Kaufman, M.L., Leonard, L.L., Nestor, P.G. et al. (2002). Sentence completion test in combat veterans with
and without PTSD: Preliminary findings. Psychiatry Research, 113, 303-307. Reproduced with permission.
based on revealing information that is relevant to psycho- low (Lilienfeld, Wood & Garb, 2000), and different cli-
dynamic approaches to psychopathology, and the role of nicians will often interpret the same responses in quite
psychodynamic approaches in the assessment and treat- different ways; (3) even with highly standardized scoring
ment of psychopathology has itself declined over the methods, some projective tests such as the Rorschach
past 30 years; (2) even though standardized procedures Test often result in psychopathology being inferred
for scoring projective tests have developed over recent when other evidence for such a conclusion is sparse. For
years, the reliability of such tests is still disappointingly instance, Hamel, Shaffer & Erdberg (2000) administered:
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY — 330
the Rorschach Test to 100 school children and, although Intelligence tests are used by clinicians in a number of
none of them had any history of mental health prob- contexts. For example, (1) they are used with other meas-
lems, the results of the test were interpreted in almost ures of ability to diagnose intellectual and learning disabili-
all cases as evidence of faulty reasoning that might be ties, and the cardinal DSM-IV-TR diagnostic criterion for
indicative of schizophrenia or mood disorder; (4) projec- ‘mental retardation’ was based primarily on an IQ score two
tive tests such as the TAT have intrinsic cultural biases. standard deviations below the mean (e.g. an IQ score of
For instance, in the traditional set of TAT pictures there less than 70; see Chapter 17); (2) IQ tests are also used to
are no ethnic minority characters even though the cli- try to assess the needs of individuals with learning, devel-
ent is expected to identify with one of the characters in opmental or intellectual disabilities so that support can be
the picture. In some cases, this has been overcome by provided in any specific areas of need. Tests that provide
developing more contemporary TAT pictures that contain scores on a range of different ability scales are best suited
figures from ethnic minorities (Costantino, Flanagan & for this purpose, and one such example is the Wechsler
Malgady, 2001); and (5) most projective tests are labour Adult Intelligence Scale, now in its fourth edition
intensive for the limited amount of objective informa- (WAIS-IV) (Wechsler, 2008). This contains scales that meas-
tion they provide. Clinicians need extensive training in ure vocabulary, arithmetic
order to administer tests such as the Rorschach and TAT, ability, digit span, informa- AIS (Wechsler Adult Intelligence
Scale) A test designed to measure intel-
and they are time-consuming to administer, interpret tion comprehension, letter— ligence in adults and older adolescents. It
and score. Given the development of more objective number sequencing, picture contains scales that measure vocabulary,
and easily scored inventories, this has inevitably led to a completion ability, reason- arithmetic ability, digit span, inforrnation
decline in the popularity of projective tests. ing ability, symbol search comprehension, letter-number sequenc-
ing, picture completion ability, reason-
and object assembly ability. ing ability, symbol search and object
Intelligence tests Tests such as the WAIS-IV assembly ability.
Intelligence tests are regularly used by clinicians in a vari- can also be used as part of a
ety of settings and for a variety of reasons. IQ (intelli- battery of tests to assess whether an individual is eligible
gence quotient) tests, as they are now generally known, for special educational needs, and it will provide informa-
were first devised in the tion that will suggest strategies, services and support that
Q (intelligence quotient) tests Tests
early part of the 20th cen- will optimize the individual’s functioning within society;
Used as a means of estimating a person’s
ntellectual ability. tury as a means of compar- and (3) intelligence tests are frequently used as part of a
ing intellectual ability in battery of assessments used in neurological evaluations
specific groups of people (e.g. army recruits). Arguably (see section 15.1), and can help to detect when a client
the first IQ test was that produced by the French psy- has brain damage caused by traumatic injury or cerebral
chologist Alfred Binet in 1905, and this was a test that infection, or has a degenerative brain disorder such as
purported to measure intelligence across a number of Alzheimer’s disease.
verbal and nonverbal skills. From early tests such as this However, despite their practical benefits across a
there are now over 100 tests of intelligence available, range of clinical contexts, intelligence tests still have
most of which are standardized to have a score of 100 as a number of limitations. Firstly, intelligence is an
the mean and a score of 15 or 16 as the standard devia- inferred construct. That is, it does not objectively exist in
tion (see Figure 1.1). As you can see from Figure 1.1, 68 the same way that physical attributes such as heart rate
per cent of the population will score between 84 and 116 or blood pressure exist, but is a hypothetical construct
(one standard deviation from the mean) on IQ tests, and that has been developed by psychologists to help us try
around 2 to 3 per cent of the population will have IQ to understand how well individuals can adapt to various
scores less than two standard deviations from the mean problems. This has led some sceptical psychologists to
(e.g. less than 70). Because of their continued develop- suggest that there is no clear definition of intelligence
ment over the previous 100 years, IQ tests have high inter- but that ‘intelligence is merely what IQ tests measure’!
nal consistency (i.e. a client will score roughly the same Secondly, if that latter statement is true, then our con-
on different items that measure the same ability), high ception of whether someone is intelligent or not will
test-retest nee os e. a client who takes the same test depend on the reliability and validity of the individual
UJ, twice but some months IQ test we use to measure their intelligence, and this
To read Sparrow & Davies's article on ) or years apart will achieve can raise some difficulties. For example, many IQ tests
assessment of intelligence go to
| roughly the same score are culturally biased, and appear to be based on middle-
reading/ch2 both times), and good valid- class, majority ethnic background views of what is adap-
ity (i.e. the tests are good tive (Gopaul-McNichol & Armour-Thomas, 2002), and
at predicting intellectual ability or future educational so will disadvantage those from lower socio-economic
performance) (Sparrow & Davies, 2000). backgrounds, from ethnic minorities, or from poorer
a) See PSYCHOPATHOLOGY
.
~\
quality educational backgrounds (Walker, Batchelor & PET scans and fMRI scans (see next section), blood tests
Shores, 2009). While attempts have been made over the (to assess potential inherited or genetic components to a
years to eradicate cultural bias of this kind, it is difficult disorder), and chemical analyses of cerebrospinal fluids.
to eliminate it entirely. For instance, a test question may But of equal importance in this overall assessment is the
ask whether a cup goes with a bowl, a spoon or a saucer, use of neurological tests that measure cognitive, percep-
but a child from a low socio-economic background may tual and motor performance as indicators of underlying
never have drunk from a cup with a saucer, and may brain dysfunction (Rao, 2000). The rationale behind the
be more likely to associate a cup or mug with a spoon. use of such neurological tests is that different psychologi-
Even so, because it is widely known that some ethnic cal functions (such as motor skills, memory, language,
minorities perform relatively poorly on IQ tests, this planning and executive functioning) are localized in dif
knowledge alone can interfere with test performance ferent areas of the brain (see Table 15.1), so discovering
in that group (Spencer, Steele & Quinn, 1999). Thirdly, a specific cognitive deficit can help to identify the area of
intelligence tests mainly tend to be rather ‘static’ tests of the brain where any damage may be localized. In addi-
intellectual ability and provide a snapshot of ability at any tion, collecting such information is also crucial for identi-
point in time. What they do not usually appear to meas- fying the focus of rehabilitation strategies and in patient
ure is the individual’s capacity to learn or their poten- care and planning for the client (Veitch, 2008). Tests that
tial to acquire new cognitive abilities (Grigorenko & are commonly used by clinical neuropsychologists in
Sternberg, 1998). Fourthly, many researchers argue that this respect are the Adult Memory and Information Pro-
our current conception of intelligence as measured cessing Battery (AMIPB)
by IQ tests is too narrow. There are many other skills (Coughlan & Hollows, Adult Memory and Information
Processing Battery (AMIPB) A neu-
that are not usually included in our conceptions of, and 1985), the Halstead—
ropsychological test in wide use inthe
measures of intelligence, and these include music abil- Reitan Neuropsychological. UK, comprising
two testsofspeed of
ity, physical skill, the ability to perceive, understand and Test Battery (Broshek & information processing, verbal memory 4
express emotion (known as ‘emotional intelligence’), Barth, 2000), and the pre- tests (list learning and story recall) and
visual memory tests (design learning and
and the ability to implement solutions to real-world viously mentioned Mini
figure recall). ° 3
problems (Gardner, 1998; Mayer, Salovey & Caruso, Mental State Examination
2000). For example, are Lionel Messi’s footballing skills (MMSE). Each of these Halstead-Reitan Neuropsychological i
as much an intelligent skill as arithmetic or verbal ability tests is described in more Test Battery A common neuropsych
(Bishop, Wright, Jackson & Abernethy, 2013)? detail in Chapter 15, and logical test used in the USA, compiled
their administration and to evaluate brain and nervous system
functioning across a fixed set of eight
Neurological impairment tests scoring is an important tests. The tests evaluate function across
Many psychological and cognitive problems are not part of the day-to-day tasks visual, auditory and tactile input, verbal
caused by problematic life experiences or by dysfunc- undertaken by clinical communication, spatial and sequential
neuropsychologists (Veitch, perception, the ability to analyse infor-
tional ways of thinking, but are caused by damage to the
mation, and the ability to form mental
structure and functioning of the brain and the central 2008; see ‘A week in the life concepts, make judgements, control
nervous system. Such damage can be caused by traumatic of a clinical psychologist’, motor output and to attend to and
injury (such as might be received in a car accident), car- Chapter 15). memorize stimuli.
diovascular problems (such as a stroke), cerebral infection
(such as meningitis), a brain tumour, or be the result of a
degenerative brain disorder (such as Alzheimer’s disease). 2.2.4 Biologically Based Assessments
In such cases damage to the brain can cause both changes
in personality (e.g. change someone from a passive into In many cases, information about biological structures
an aggressive individual) and cause deficits in cognitive and biological functioning can help to inform the assess-
functioning depending on the areas of the brain that are ment and diagnosis of psychological problems. There
affected. These issues are discussed more thoroughly in are two main types of biologically based assessment
Chapter 15, but at this point we will mention the value of that we will describe here: psychophysiological tests and
neurological assessment tests in enabling the clinician to brain imaging.
determine the nature of any cognitive deficits (e.g. mem-
ory deficits, deficits in language skills, and so on), to iden- Psychophysiological tests
tify whether such deficits are the result of brain damage, There are a number of psychophysiological tests that can
and in many cases to identify the area of the brain that be used to provide information about potential psycho-
has been affected. Clinicians will usually employ a battery logical problems. For example, anxiety causes increased
of tests when assessing for possible neurological deficits, activity in the sympathetic nervous system and is regu-
and these may include EEG analyses, brain scans such as larly accompanied by changes in physiological measures
such as heart rate, blood pressure, body temperature the use of lie detectors. lie detectors The measurement of
and electrodermal! responding. Similarly, anger is usually Lie detectors use changes changes in autonomic responding used to
associated with physiological changes in blood pressure in autonomic responding identify whether an individual is lying in
response to specific preset questions. This
and heart rate. So, psychophysiological tests can provide in an attempt to identify is a controversial technique that has often
useful information related to emotionally based psycho- whether an individual is been used in criminal prosecutions and
logical problems. lying in response to spe- employment screening.
One important measure of physiological activity is cific preset questions, and
electrodermal responding, sometimes known as the gal- this technique has often been used in criminal prosecu-
vanic skin response (GSR) or skin conductance response tions and employment screening — especially in the USA
(SCR). Emotional responses such as anxiety, fear or (Krapohi, 2002). However, while a polygraph may detect
anger increase sweat-gland anxiety or arousal caused by the participant lying, it is
electrodermal responding A psy- activity, and changes in this also likely to detect changes in arousal caused by factors
-hophysiological measure which uses
2lectrodes attached to the fingers of
activity can be recorded other than lying (e.g. the question simply being a stress-
participants to test emotional responses with the use of electrodes ful or unusual one), and so may represent an anxious —
such as anxiety, fear or anger by measuring that would normally be but innocent — participant as one who may appear to be
changes in sweat-gland activity. attached to the fingers of guilty (Raskin & Honts, 2002). As a result, findings from
the participant. Changes lie detector tests in the USA are now used significantly
in skin conductance caused by sweat-gland activity can less as evidence of criminal guilt (Daniels, 2002).
then be measured as changes on a polygraph — a pen Finally, another important psychophysiological assess-
that records changes in skin conductance on a continu- ment measure is the electroencephalogram (EEG). This
ally moving roll of graph paper (see Photo 2.1). Skin involves electrodes being
conductance measures have been used in a variety of attached to the scalp that electroencephalogram (EEG) A psycho-
contexts: (1) to assess the kinds of stimuli or events that record underlying electri- physiological assessment measure which
elicit anxiety in a client (Cuthbert, Lang, Strauss, Drobes cal activity and can help involves electrodes being attached to the
scalp that record underlying electrical
et al., 2003; Alpers, Wilhelm & Roth, 2005); (2) to assess to localize unusual brain activity and can help to localize unusual
autonomic or physiological reactivity in certain diag- patterns in different areas brain patterns in different areas of the
nostic groups (e.g. individuals diagnosed with antisocial of the brain. Abnormal brain.
personality disorder tend to have less reactive autonomic electrical patterns detected
nervous systems than non-clinical samples) (Lykken, by EEG can indicate a number of problems, includ-
1995); (3) to assess the ability of clients to cope following epilepsy, brain tumours or brain injury (Cuthill &
ing treatment interventions (Bobadilla & Taylor, 2007; Espie, 2005).
Grillon, Cordova, Morgan, Charney & Davis, 2004); and
(4) whether autonomic indices of anxiety or arousal cor-
respond with appropriate changes in behaviour (e.g. in
panic disorder, ayoidance responses may be triggered by
physiological changes indicative of anxiety) (Karekla,
Forsyth & Kelly, 2004). Other useful examples of psy-
chophysiological measurement techniques include the
electromyogram (EMG), which measures the electrical
activity in muscles, and the
electromyogram (EMG) A psycho- electrocardiogram (ECG)
ohysiological measurement technique that for measuring heart rate.
measures the electrical activity in muscles. Although measures such
as electrodermal respond-
alectrocardiogram (ECG) A psychophysi- ing can indicate emotional
dlogical measurement technique used for changes indicative of anxi- LIBRARY
PHOTO
NOVOSTI/SCIENCE
RIA
measuring heart rate. ety, fear or anger, it is not PHOTO 2.1 The polygraph is a device used to measure
always foolproof. Rather changes in physiological responding that may indicate emo-
than specifically indicating the presence of these discrete tional changes such as anxiety, fear or anger. The polygraph
emotions, skin conductance is more properly an indi- works by recording physiological measures (such as skin
cator of general physiological arousal, and this can be conductance or heart rate) on a continually moving roll of
caused by a variety of factors, including simply orient- graph paper. In more recent times, these measures can be
ing towards or attending to an event (Siddle, 1983). This analysed directly by computer and the output displayed on
issue is nowhere better illustrated than in the history of the computer screen.
56 PSYCHOPATHOLOGY
%\
Neuroimaging techniques
Many behavioural, cognitive and psychological prob-
lems may be linked to abnormalities in brain func-
tioning, and while neurological tests can indicate that
possible brain dysfunction may be involved, we will
usually need to use techniques that provide images
of the brain to confirm this. There is an expanding
range of neuroimaging or brain imaging techniques
now available, and some provide the clinician with
anatomical and structural information about the brain
(e.g. whether a brain tumour is present) while others
provide information about brain activity and brain
functioning (e.g. whether specific brain areas are fully iStock.com
©
functioning).
Computerized axial tomography (CAT) machines
are sophisticated versions of X-ray machines, and can
be used to form a three-
computerized axial tomography (CAT) dimensional picture of the
A neuro imaging technique which uses
brain. Figure 2.4 shows a
sophisti cated versions of X-ray machines
and can be used to form a three- CAT scan machine. The
dimensi onal picture of the brain. patient lies down on a plat-
form which then moves
through a large doughnut-like ring. The ring turns so that
with each turn a narrow ‘slice’ of the brain is X-rayed, PHOTO
LTD/SCIEN
IMAGING
MEDICAL
CANE
DU LIBRARY
Credit: SCIENCE PHOTO LIBRARY
and a computer uses this information to construct two-
dimensional cross-sections of the brain and these many FIGURE 2.4 Computerized axial tomography or ‘CAT’ scanning.
separate images can also be combined to provide a three- The top picture shows a CAT scan machine. The client lies
dimensional image of the brain. CAT scan images can down on the platform with their head positioned within the
help to detect abnormal growths in the brain such as large doughnut-like ring. The ring turns to X-ray individual
tumours or enlargement of the ventricles in the brain thin ‘slices’ofthe brain, and a computer is used to turn these
that can indicate tissue degeneration typical of dementia individual images into either a two-dimensional or three-
or schizophrenia. dimensional picture of the brain. The lower pictures show an
Positron emission tomography (PET) scans allow example CAT scan of a ‘slice’ of a normal brain (left) next to
measurement of both brain structure and function. A one that reveals a large brain tumour (right: the darker area).
PET scan can provide pic-
positro n emission tomography (PET) tures of chemical activity
A neuroimaging technique which allows in the brain either at rest
measurement of both brain structure
and fun ction by utilising radiation
or when the participant
emitted from the participant to develop is undertaking cognitive
images. tasks such as language,
learning, remembering or
sensory processing. The PET scanner utilizes radia- 1 month 3 month 6 month 12 month
tion emitted from the participant to develop images.
Each participant is given a minute amount of a radio-
FIGURE 2.5 PET scan ofa developing infant brain.
active drug that closely resembles a natural substance
These images are of PET scans showing the increase in
used by the body. Gamma radiation produced by the
brain activity that accompanies the growth of the brain in the
radioactive drug is detected by the PET scanner and
same infant from the age of 1 to 12 months. This can be used,
shows in fine detail the metabolism of glucose in the
for instance, to pinpoint developmental problems in children
brain. The PET scanner’s computer uses this detail
much earlier than other tests would. Brightly coloured areas
to produce colour pictures of the functioning brain.
represent areas of the brain where metabolic rates are high,
Brightly coloured areas represent areas of the brain
and represent high levels of brain activity.
where metabolic rates are high, and represent high Source: The Crump Institute for Molecular Imaging, Department of
levels of brain activity. Figure 2.5 illustrates a series of Molecular & Medical Pharmacology, University of California at Los
PET scans taken of a human infant’s brain at intervals Angeles. Reproduced with permission.
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY
from 1 to 12 months, and these images clearly show

the increase in brain activity with early development.
Because the PET scan provides images of the brain
indicating both levels of activity and areas of activ-
ity, it is a useful tool for assessing cognitive function-
ing, and provides information about braimfunctioning
in degenerative diseases such as Alzheimer’s disease,
and brain functioning in intellectual disabilities such
as Down syndrome. In Chapter 8, Figure 8.2 also pro-
vides an example of the use of PET scans in assessing
brain functioning in schizophrenia.
One further imaging technique that has been devel-
oped is known as magnetic resonance imaging (MRI).
MRI scanning involves the
magnetic resonance imaging (MRI) A participant being placed
reuroimaging technique which involves inside a large circular mag-
he participant being placed inside a large FIGURE 2.6 Functional magnetic resonance imaging (fMRI).
circular magnet that causes the hydrogen
net which causes the hydro- fMRI scans allow the researcher to measure brain activity while
atoms in the body to move. This produces gen atoms in the body to the participant is completing various behavioural or cognitive
in electromagnetic signal that is converted move. This then produces tasks. In this example, individuals with a diagnosis of PTSD were
oy the scanner’s computer into visual an electromagnetic sig-
asked to recall autobiographical memories that might give rise to
dictures of the brain. .
nal that is converted by distressing ‘flashbacks’ of their trauma, and researchers were able
the scanner’s computer to track the brain activity that accompanied this experience.
For a video on MRI scanning go to into visual pictures of the Source: Whalley, M.G., Kroes, M.C., Huntley, Z., Rugg, M.D., Davis,
www.wiley-psychopathology.com/ _ brain. Pictures of the brain S.W. & Brewin, C.R. (2013). An fMRI investigation of posttraumatic
video/ch2
produced by MRI scan- flashbacks. Brain and Cognition, 81(1), February, 151-159, Figure 1.
Reproduced with permission.
ning are highly detailed
and allow the detection of even the smallest of lesions or
tumours. A more recent development of MRI technol-
ogy is known as functional magnetic resonance imag-
2.2.5 Clinical Observation
ing ((MRI). This allows the clinician to take brain images A further method of collecting useful clinical information
so quickly that tiny changes in brain metabolism can be is by direct observation of a client’s behaviour. This can
detected and can provide minute-to-minute information supplement information from interviews and psychologi-
about actual brain activity. cal tests, and often allows an assessment of behaviour in
functional magnetic resonance imaging This technology can be its natural context, such as the home, school classroom
fMRI) A development of MRI technology used to measure chang- or community setting. Direct observation can provide an
which allows the clinician to take brain
ing brain activity while the objective assessment of the frequency of particular behav-
mages so quickly that tiny changes in
drain metabolism can be detected and can participant is undertaking iours (e.g. aggressive behaviours) when this may not be
rovide minute-to-minute information particular tasks, such as a so easily obtained from reports given by the client them-
bout actual brain activity. memory task or viewing an self, their family or carers. It also allows behaviour to be
emotional film. Figure 2.6 assessed in the context of events that precede the behaviour
provides an example of an fMRI scan of individuals (and so may trigger the problem behaviour) and events
diagnosed with PTSD who are asked to recall an auto- that immediately follow the behaviour (and may represent
biographical memory that gives rise to flashbacks. fMRI the consequences of the behaviour that reinforce its occur-
analyses allow the researcher to identify which areas of rence). Treatment in Practice Box 17.1 provides a detailed
the brain are involved in this activity and the sequential example of how an observational technique can be used to
activation of brain areas that are specific to experiencing identify what factors might be triggering and maintaining
a distressing ‘flashback’. challenging behaviour in an individual with intellectual
As you can see from this section, the use of modern disabilities. This example used an ABC chart that requires
brain imaging technology has been invaluable in provid- the observer to note what
ing detailed evidence of brain abnormalities and dys- happens before the target ABC chart An observation method
that requires the observer to note what
function in relation to a whole range of psychopathology behaviour occurs (A), what happens before the target behaviour
problems. As we shall see in Chapter 3, these techniques the individual did (B), and occurs (A), what the individual did (B), and
are not only valuable for assessment purposes but are what the consequences of what the consequences of the behaviour
were (C).
also a useful research tool. the behaviour were (C).
cos aaa PSYCHOPATHOLOGY
Se OBSERVATIONAL CODING FORMS

N
~
Shown here are four different types of observational system that simply measures the frequency ofselected
= coding forms. Which one a clinician would use would —_behaviours. Figure 3 extends this by providing the fre-
2)
a depend on the type ofdata they want to collect. Figure ©quency of selected behaviours over a period of time.
4) 1 is a simple coding scheme in which the observer This will allow the clinician to see if there is anything
p=) merely describes the behaviours they observe plus the interesting in the sequence or order that behaviours
U
oO antecedents and consequences of these behaviours. are emitted. Finally, Figure 4 provides a coding scheme
LL Because the observer is describing the behaviours in that allows the recording of quite complex informa-
their own words, there is likely to be poor inter-rater — tion, including the behaviour of the client in relation
reliability using this scheme. Figure 2 providesacoding _ to others in the situation, such as teacher and peers.
FIGURE 1 Sample descriptive coding form.
Situation Behaviour Antecedents |
Sitting in circle
time |
9.00 am Slapped peer sitting immedi- None observed Peer and teacher both
ately to his left with open hand ignored
9.03 am Yelled “NO!”at teacher and Teacher gave specific com- Teacher ignored, students
remained seated mand for all students to return | laughed
to their seats
Got up and sat in seat Peer came over to him and Teacher gave specific,
whispered in his ear labeled praise to target child |
| FIGURE 2 Sample checklist for coding child behaviour. |
Fidgeting in seat
Getting out of seat
Running around classroom
Interrupting others
Physical aggression toward peers
Physical aggression toward teachers
Verbal threats of aggression toward peers

Verbal threat of aggression toward teachers
FIGURE 3 Sample interval coding form.
Behaviours S044) ||30m |:

Inappropriate /
| |Movement
| |Inattention WW
Physical
Aggression
oe
Self-Injurious
Behaviour
(continued)
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY 59"
FIGURE 4 Sample interval coding form with antecedents, behaviours, and consequences.
Consequences
Target Teacher
Behaviour Antecedents
a
; +
Teacher left room Child

Physical took his toy
Aggression
None observed
Teacher specifi t
Positive Peeiner ceri
Social
: None observed
Interaction
Source: Nock, M.K. & Kurtz, $.M.S. (2005). Direct behavioural observation in school settings: Bringing science to practice. Cognitive &
Behavioral Practice, 12, 359-370. Reproduced with permission.
Focus Point 2.2 provides some examples of how behay- more time-consuming forms of assessment, not just in
iours and events can be coded when undertaking a clini- terms of the amount of time required to simply observe
cal observation (Nock & Kurtz, 2005), and which type of behaviour, but also in terms of the amount of time needed
coding method you use will depend largely on what you to properly train observers in the use of the various cod-
want to find out (e.g. do you want to just find out how ing systems (see e.g. Abikoff, Gittelman & Klein, 1980;
frequently a behaviour occurs, or do you want to know see also Focus Point 2.2). This is especially so if members
more about the context in which a behaviour is emitted?). of the client’s family need to be trained to make system-
There are a number of advantages to using obser- atic observations in the home setting. Secondly, observa-
vational techniques. First, if the observer is appro- tion will usually take place in a specific setting (e.g. the
priately trained, observation can provide important school classroom or the home), and behaviour in this
objective measures of the frequency of behaviours specific context may not be typical of behaviour in other
and those events that precede and follow them, and contexts (Nock & Kurtz, 2005). Thirdly, the presence of
the latter information will often provide an insight into an observer may lead those involved in the observation
the purpose the problematic behaviour serves (e.g. in setting to behave differently to how they would normally
Treatment in Practice Box 17.1, systematic observa- behave (Kazdin, 1978; Skinner, Dittmer & Howell, 2000),
tion reveals that the purpose of Andy’s self-injurious and this may often be the case with children, who will
behaviour is to enable him to be removed from noisy show dramatic improvements in behaviour when they are
and crowded situations) (Kazdin, 2001; Miltenberger, aware they are being observed. This problem can often
1997). Second, observational data has greater external be overcome by video-recording behaviour without an
or ecological validity than self-reports or other forms observer present and then analysing the recording at a
of testing because such later time. Similarly, the clinician may want to undertake
‘cological validity The extent to which
onditions simulated in the laboratory data provide a measure- analogue observations in
eflect real-life conditions. ment of the behaviour as a controlled environment analogue observations Clinical observa-
tions carried out in a controlled environ-
it is actually occurring in a that allows surreptitious ment that allows surreptitious observation
context. Third, observation of behaviour in a context observation of the client. of the client.
can often suggest workable answers to problem behav- For example, children can
iour as can clearly be seen in Treatment in Practice Box be observed interacting in a playroom while the observer is
17.1. Once it was established that Andy’s self-injurious situated behind a two-way mirror. Fourthly, unless observ-
behaviour was functioning to get him removed from ers are properly trained in the coding methods used, there
a stressful environment, staff could look out for signs may be poor inter-observer reliability (Kamphaus & Frick,
that he was becoming overstimulated and remove him 2002). That is, two different observers assessing the same
from the room before he began to injure himself. participant may focus on quite different aspects of behav-
Having listed these advantages of clinical observation, iour and context, and arrive at quite different conclusions
it also has a number of drawbacks. Firstly, it is one of the about the frequency and causes of behaviour. Fifthly, as in
aa ae PSYCHOPATHOLOGY
‘ .
all observational procedures, the data can be influenced information about clients’ day-to-day experiences, to aid
by the observer's expectations. Observer expectations can diagnosis, to plan treatment, and to evaluate the effec-
cause biases in the way that information is viewed and tiveness of treatment (Piasecki, Hufford, Solhan & Trull,
recorded and this can be caused by the theoretical orienta- 2007). In addition, self-monitoring itself can have ben-
tion of the observer and what they already know about eficial effects on behaviour even prior to any attempts at
the person being observed. intervention. For example, many problematic behaviours
One final form of clinical observation that is frequently (e.g. smoking, illicit drug use, excessive eating) can occur
used is known as self-observation or self-monitoring. without the individual being aware of how frequently
This involves asking the client to observe and record their they happen and in what circumstances they happen, and
own behaviour, perhaps by using a diary or a smart phone self-monitoring can begin to provide some self-knowledge
(see Focus Point 2.3) to that can be acted on by the individual (see Figure 2.7). As
self-observation A form of clinical
observation that involves asking clients tonote when certain behav- a result, selfmonitoring often has the effect of increasing
observe and record their own behaviour, iours or thoughts occur the frequency of desirable behaviours and decreasing the
perhaps by using a diary or a smartphone and in what contexts they frequency of undesirable behaviours (McFall & Hammen,
to note when certain behaviours or
occur. This has the ben- 1971). This is known as reactivity, and clinicians can often
thoughts occur and in what contexts
they occur. efit of collecting data in take advantage of this process to facilitate behaviour
real time and overcomes change.
self-monitoring A form of clinical obser- problems associated with
vation which involves asking clients to poor and biased recall of
observe and record their own behaviour, to
behaviour and events when
note when certain behaviours or thoughts 2.2.6 Cultural Bias in Assessment
occur, and in what contexts they occur. using retrospective recall
methods (Strongman & A majority of the most widely used assessment methods
Russell, 1986). The increasing use of electronic diaries have been developed on populations consisting largely
for self-observation has come to be known as ecological of people from a single cultural background and with
ecological momentary assessment
momentary assessment a limited ethnic profile — that is, most tests have been
(EMA) The use of diaries for self-observation (EMA) (Stone & Shiffman, developed on white European or white American popu-
or self-monitoring, perhaps by using an 1994), and such methods lations. Because of this fact, many tests and assessment
electronic diary or a smartphone. have been used to gather methods may be culturally biased and provide a less than
APPS FOR SELF-MONITORING

Smartphone apps are increasingly used by clinical 100% wi vodafoneUK > 09:32
psychologists and researchers to facilitate patient and MoodPanda Log Out Home How are you, Jake?
participant self-monitoring of behaviours, symptoms MY MY

j DIARY, GRAPHS
and moods. They are convenient to carry and easy to
ANY REASON
use, and provide information that can be sent elec- its my birthday yay! #birthday
WORLD = PANDA
tronically from the smartphone to the relevant data
POINT
FOCUS
2.3 collection point at any time. A commercial example FEED NEWS SHARE
f£nv1.@8 © on@
of an app for self-monitoring is MoodPanda, an app Update Mood To 9
that allows the individual to record their mood wher-

ever they are, post the data to a central collection
point, and — if needs be - collate data into a graphical
format to view progress. However, even with sophis-
ticated apps, self-reporting of mood can still be very
unreliable, and apps are now being developed that
can record mood changes throughout the day by
detecting tell-tale changes in a person’s voice that Source: http://www.newscientist.com/article/mg21729056.600-
moodsensing-smartphone-tells-your-shrink-how-you-feel.html
indicate the emotional state they are in. Miller (2012)
provides a detailed review of previous psychological For further reading on mood-sensing
research using mobile electronic devices, and out- smartphone tells your shrink how you
lines what smartphones can do now and will be able feel go to
www.wiley-psychopathology. com/ch02
to do in the future.
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY Gl.
were significantly more likely to be hospitalized with

80
is © Smoking Reports a diagnosis of schizophrenia than non-immigrants or
3 Random Prompts immigrants from other areas of the world (Cochrane,
<= 60 1977). While this might be considered as an ethnic dif-
iv)
iw) ference in susceptibility to some psychiatric disorders,
[e)
LL subsequent studies suggested that many West Indian
°
rc}
Ww 40 immigrants who had been hospitalized with a diag-
<
|
od nosis of schizophrenia lacked the symptoms com-
2
Ww
— rc
monly regarded as primary indicators of the disorder
© 20 (Littlewood, 1992). Similar studies suggested that alco-
a is
< 4 holism was preferentially diagnosed in Irish immigrants
to the UK- often independently of a proper assessment
0 a? ‘ T
of symptoms — and this suggested that popular ethnic
stereotypes were often carried over into medical and
psychiatric practice (Bagley & Binitie, 1970). As well as
the apparent bias in assessment and diagnosis in eth-
ONGOING STRESSORS SOCIAL CONTACTS
nic minorities, individuals from low socio-economic
FIGURE 2.7 Self-monitoring of smoking behaviour. groups may also experience bias. For example, many
This figure shows the results of a smoking self-monitoring clinicians tend to view clients from lower socio-
task undertaken by a college student. The student was economic backgrounds as more disturbed than those
asked to record what they were doing each time a ciga- from higher socio-economic groups (Bentacourt &
rette was smoked and each time they were given random Lopez, 1993; Robins & Regier, 1991), and this may
prompts by a palm-top computer. Comparing the base rates result from the clinicians’ stereotypes of different socio-
(random prompts) with smoking rates when in various situ- economic groups being able to influence judgements
ations allows the clinician to see whether certain situations made during unstructured interviews (Garb, 1997).
are triggers for smoking. In this case comparisons suggest
that low grades and doing school work represent triggers Causes of cultural anomalies in
for smoking, whereas being with family or partner usually
assessment and diagnosis
elicits no cigarette smoking.
The reasons for cultural differences in assessment and
Source: Piasecki, T.M., Hufford, M.R., Solhan, M. & Trull, T.J. (2007).
Assessing clients in their natural environments with electronic
diagnosis are multifaceted and not simply due to the
diaries: rationale, benefits, limitations, and barriers. Psychological fact that most structured assessment tools were devel-
Assessment, 19, 25-43. American Psychological Association. oped without regard to cultural diversity. We will discuss
Reproduced with permission. some of the factors below, and these include (1) the fact
that mental health symptoms may manifest differently in
different cultures, (2) language differences between cli-
accurate picture of the mental health of individuals from ent and clinician, (3) the effect of cultural differences in
different cultural backgrounds. As we shall see below, religion and spiritual beliefs on the expression and per-
these biases can manifest in many different ways, and cli- ception of psychopathology, (4) the way that cultural dif-
nicians must be aware that such biases may affect both ferences affect client-clinician relationships, and (5) the
their judgements and their diagnoses. role of cultural stereotypes in the perception of ‘normal-
ity and ‘abnormality’ in ethnic groups.
Examples of cultural anomalies in First, we saw in Chapter 1 that stress and mental
assessment and diagnosis health problems can actually manifest quite differently
Cultural anomalies can be identified in a number of dif- in different cultures and Focus Point 1.3 provides two
ferent ways. First, some ethnic groups score differently examples of this. Since the diagnosis of psychopathology
on assessment tests than others. For example, American is based almost entirely on the presence of observable
Asians tend to score significantly higher on most scales symptoms (especially in DSM) then this will complicate
of the MMPI than white Americans (McNulty, Graham, and confuse the process of diagnosis when assessing cli-
Ben-Porath & Stein, 1997). Second, black Americans ents from different cultural backgrounds.
have a higher rate of diagnosis of disorders such as alco- Second, language differences and difficulties can also
holism or schizophrenia whereas white Americans are create biases in assessment and diagnosis. For example, a
more likely to be given the less stigmatising diagnosis number of studies have suggested that the diagnosis that
of major depression (Garb, 1998). Similarly, it was clear a client receives may depend critically on whether they
during the 1970s that West Indian immigrants to the UK are assessed in their first or second language. Interestingly,
S24) PSYCHOPATHOLOGY
when a client is interviewed in their second language and clinicians in such a position need to be flexible in their
their symptoms are often assessed as significantly less approach to assessment and diagnosis and to build a help-
severe than if they are interviewed in their first language ful therapeutic relationship by candidly exploring issues
(Malgady & Costantino, 1998), and this appears to be of apprehension, timidity and distrust (Whaley, 1997).
because undertaking an interview in a second language Finally, just like any other social interaction, a discus-
requires the client to organize their thoughts better and sion between a client and clinician can be influenced by
therefore appear more coherent. However, this is not the racial and ethnic stereotypes. For example, stereotypes
only distortion that can affect assessment and diagnosis. can significantly affect how ambiguous information in an
Some other studies have suggested that undertaking a interview or a case report is interpreted. In an analogue
diagnostic interview in the client’s second language can study, Rosenthal & Berver (1999) gave white American
also result in symptoms being assessed as significantly students a vignette providing unfavourable information
more severe than if it was in their first language, and this about a hypothetical client. For half the participants the
distortion seems to be caused by the client’s misuse of client was described as white American, for the other half
words, hesitations and misunderstanding of questions he was described as African-American. Subsequently,
suggesting a lack of coherent thought (Cuellar, 1998). participants were given more favourable information
Even the misunderstanding of colloquialisms when cli- about the client. For those who believed the client to be
ent and clinician are both using their first language can white American, the more favourable information influ-
affect assessment. For example, Turner, Hersen & Heiser enced their final judgement, but for those who though
(2003) point to the use by African-Americans of the he was a black American, the positive information
phrase “That’s all right’ when asked about their motives failed to change their original negative view. Common
for engaging in certain behaviours. A white American cli- stereotypes held about African-American and Hispanic
nician might see this response as the individual condon- clients by clinicians are that they are violent, hostile and
ing what might be seen as pathological behaviour, but unmotivated for treatment (Pavkov, Lewis & Lyons,
in African-American speech this phrase is used to mean 1989; Whaley, 1998), and these perceptions undoubtedly
‘Although I know exactly how to answer you, I have no affect their clinical judg-
intention of doing so’. ments. Garb (1997) called To read Garb’s article on bias go to
Third, differences in spiritual or religious beliefs this a confirmatory bias,
reading/ch2
between cultures can affect assessment and diagno- whereby clinicians ignore
sis. For example, behaviour that may be considered as information that does
a symptom of psychopathology in one culture may be not support their initial confirmatory bias A clinical bias whereb
seen as relatively normal or to have non-psychological hypotheses or stereotypes, individuals with a mental health problem
causes in other cultures. We saw in Chapter 1 that some and they interpret ambigu- ignore information that does not support
their beliefs interpret ambiguous informa-
cultural beliefs view unusual behaviour as evidence that ous information as sup- tion as supporting their beliefs.
the individual is possessed by evil spirits rather than suf- porting their hypotheses.
fering mental health problems. Similarly, in some other In some cases these biased judgements are the result of
cultures visual or auditory hallucinations with a religious direct racism, but more often they are probably mani-
content may be considered to be a normal part of reli- festations of indirect racism in which the clinicians are
gious experience rather than a sign of psychopathology, unaware of their stereotype biases. Whether direct or
and the clinician may be faced with a client who is not indirect racism is involved, clinicians have a responsibil-
necessarily exhibiting the early symptoms of schizophre- ity to learn about and eradicate their own stereotypes
nia but is merely indulging in religious experiences com- and prejudices, and to provide an honest and unbiased
mon to their culture. assessment process for clients from ethnic minorities
Fourth, when facing a clinician who is a member of an (Hollar, 2001; Adebimpe, 1994).
ethnic majority, the client who is from an ethnic minor-
ity is quite likely to experience apprehension and timidity, Addressing cultural anomalies in
and this can affect the way that the client presents them- assessment and diagnosis
selves at interview and can also affect the clinician’s view Clinicians need to work hard to eliminate cultural bias
of their symptoms (Terrell & Terrell, 1984; Whaley, 1998). from their assessment and diagnostic processes, and this
For example, apprehension and timidity can often make needs to be addressed at a number of levels, including
the client seem incoherent or withdrawn, and this would eradicating bias from existing assessment tools, develop-
need to be disentangled from any similar symptoms that ing new culture-free assessments, adopting assessment
were a true manifestation of psychopathology. In more procedures that minimize cultural bias, and training cli-
extreme examples, the client from an ethnic minority nicians to identify cultural and racial bias in their own
may be distrustful of a clinician from an ethnic majority, thinking and in the assessment processes that they use.
DSM has made some attempt to identify potential of self, their understanding of illness, and their atti-
cultural anomalies in diagnosis by including a specific tudes to mental health provision and medicine in gen-
section on ‘Culture, age and gender’ factors within most eral (Littlewood, 1992). Sadly, clinicians from minority
diagnostic categories. For example, we note in Chapter groups are often as ill-equipped to deal with the diagno-
16 that when diagnosing conduct disorder the clinician sis of clients from minority groups as their non-minority
is asked to take account of the social background of colleagues, largely because they have been trained in the
the client. In certain deprived inner-city areas, behav- same programmes (Turner, Herson & Heiser, 2003).
iours characteristic of conduct disorder may be seen as Finally, we can attempt to aspire to culture-free assess-
being protective and may represent the norm for that ment methods by making tests and assessments more
environment. They may also serve an adaptive function valid and reliable. Aklin & Turner (2006) advocate the
in dealing with poverty and the threatening behaviour development of structured interviews to replace the cur-
of others rather than being symptoms of an underlying rent unstructured interview that is frequently the main
pathology. vehicle for diagnosis, and support for this view comes
In addition to this, clinicians need proper educa- from studies indicating there are fewer problems with
tion and training when required to assess and diagnose the assessment of ethnic minorities when structured
minority persons (Hall, 1997; Aklin & Turner, 2006). rather than unstructured methods of interviewing are
They would need to understand minorities’ construction used (Widiger, 1997).
® Can you define what is meant by test-retest reliability, inter-rater reliability and internal reliability?
® Can you define what is meant by concurrent validity, face validity, predictive validity and construct validity?
® What are the main benefits and limitations of the clinical interview?
° What is a structured interview? Can you provide an example of one?

® What are the advantages of psychological tests as methods of assessment?
* Can you describe a detailed example of a personality inventory?
* How do projective tests differ from other types of psychological test?
® Can you describe the features of at least one projective test?
® What are the benefits and limitations of intelligence tests?
® Can you name and describe at least two psychophysiological tests that might be used for clinical assessment?
® Can you name and describe three different neuroimaging techniques?
© What are the benefits and limitations of clinical observation techniques?
® What is ecological momentary assessment (EMA)?
® Can you provide at least three examples of cultural bias in assessment and diagnosis?
® Can you describe at least two studies that have identified some ofthe causes of cultural bias in assessment and diagnosis?
SECTION SUMMARY
2.2 METHODS OF ASSESSMENT
You can see from the preceding sections that cultural bias in assessment and diagnosis is a complex and pervasive phenom-
enon. The clinician needs to be aware ofthe sources ofany cultural bias in these processes, and should be reflective about their
own potential stereotypes of ethnic minorities and the effect this might have on their clinical judgments. A special issue of the
journal Professional Psychology: Research & Practice (2012, vol. 43, issue 3) is dedicated to discussing multicultural practice in
professional psychology, and provides a valuable summary of contemporary issues and solutions.
PSYCHOPATHOLOGY
The key points introduced in this section are:

the test will provide the same result when used by different clinicians on different occasions.
© Test reliability measures whether
° Test validity measures whether an assessment method actually measures what it claims to measure.
® Anunstructured clinical interview is probably the first contact a client will have with a clinician.
° Structured interviews can be used to help make decisions about diagnosis and functioning. One such example is the
Structured Clinical Interview for DSM (SCID).
¢ Psychological tests are a highly structured way of gathering information about the client.
¢ The most well-known personality inventory is the Minnesota Multiphasic Personality Inventory (MMPI).
¢ Specific trait inventories are used to measure functioning in one specific area (e.g. depression).
¢ Projective tests include the Rorschach Inkblot Test, the Thematic Apperception Test (TAT), and the Sentence Completion Test.
© Both /Q tests and tests of general ability, such as the Wechsler Adult Intelligence Scale (WAIS), are regularly used by clinicians.
° Neurological impairment tests are used to measure deficits in cognitive functioning that may be caused by abnormalities in
brain functioning.
¢ Psychophysiological tests can be used to measure emotional responding.
¢ Neuroimaging techniques generate images ofthe brain that provide information on any abnormalities in brain functioning.
¢ Important neuroimaging techniques include computerized axial tomography (CAT), positron emission tomography (PET),
magnetic resonance imaging (MRI), and functional magnetic resonance imaging (fMRI).
¢ Clinical observation techniques can be used to gather objective information about the frequency of behaviours or the con-
texts in which behaviours occur.
e Because assessment methods have usually been developed on populations from a single cultural background, they often
result in biased assessments when applied to individuals from a different cultural background.
Most practising clinical psychologists will usually

develop a case formulation when dealing with a client, and
this is an attempt to work towards explaining the client’s
The various forms of assessment we have described in problems in established theoretical terms. In most cases,
the previous section are all used by clinicians to gather the explanation developed will also suggest interventions
useful information about the client and their problems. that may be successful in resolving those problems, and it
Some clinicians use this information to establish a psy- will be a precise account of the patient’s problems devel-
chiatric diagnosis (e.g. to determine whether the client’s oped in collaboration with the client, not imposed on the
symptoms meet DSM-5 criteria for a specific disorder), client (as psychiatric diagnosis might be). Persons (1989)
whereas others use this information to draw up a psy- has described case formulation as having six components:
chological explanation of the client’s problems and to (1) creating a list of the client’s problems, (2) identifying
develop a plan for therapy. This latter approach is known and describing the underlying psychological mechanisms
as case formulation, and is an approach that has been that might be mediating these problems (and the nature
increasingly adopted over the past 20 years by clini- of the mechanisms described will depend on the theoreti-
cians who consider that cal orientation of the clinical psychologist — see below),
case formulation The use of clinical each client’s problems are (3) understanding the way in which the psychological
information to draw up a psychological
explanation of the client's problems and to
uniquely different, and so mechanisms generate the client’s problems, (4) identi-
develop a plan for therapy. require an individualized fying the kinds of events that may have precipitated the
approach (Persons, 1989). client’s problems, (5) identifying how these precipitating
It is an approach also championed by those who view events may have caused the current problems through
the psychiatric diagnostic model of psychopathology the proposed psychological mechanisms, and (6) develop-
as unhelpful in practice and stigmatising to clients (e.g. ing a scheme of treatment based on these explanations
Boyle, 2007; May, 2007). and predicting any obstacles to treatment.
CHAPTER 2 CLASSIFICATION AND ASSESSMENT IN CLINICAL PSYCHOLOGY ee
How a case formulation is constructed will depend problems, and it also enables the clinician to clearly
on the theoretical orientation of the clinical psychologist explain the formulation to the client. Activity 2.1 pro-
and, within an individual formulation, explanation of the vides a detailed and structured example of how a formu-
client’s problems will be couched in terms of the psychol- lation based on a cognitive-behavioural approach could
ogist’s own preferred theoretical approach. For example, be attempted, and provides an example of a formula-
those who work within a cognitive or behavioural model tion interview that the reader can attempt to interpret in
of psychopathology (see section 1.3.2) will attempt to terms of the theoretical model provided. This example
find explanations for the client’s problems based on cog- shows how the case formulation for a client suffering
nitive and behavioural causes — sometimes known as panic disorder would be interpreted by a cognitive-
an ABC approach. That is, they will attempt to identify behavioural psychologist in terms of existing cognitive
the antecedents (A) to the problems, describe the beliefs models of panic disorder (see Chapter 6). Once the dia-
(B) or cognitive factors that are triggered by these ante- gram is completed this
cedents, and the consequences (C) of these events. For should suggest some pos-
To complete Activity 2.1 - a case
example, if a client suffers from panic attacks, the case sible targets for interven- | formulation for panic disorder - go to
formulation may discover that (1) these occur in situations (e.g. using CBT to | www.wiley-psychopathology.com/
tions where there are crowds of people (antecedents), change misinterpretations “ activities/ch2
(2) that the client believes that feeling hot, sweaty and of bodily sensations and to
faint are signals for an impending heart attack (beliefs), prevent the use of safety behaviours — see section 6.3).
and (3) the client indulges in certain ‘safety’ behaviours Tarrier (2006) lists the various advantages of the case
designed to keep her ‘safe’ — such as avoiding going out formulation approach: (1) it allows a flexible and idiosyn-
of the house — but which reinforce the symptoms and cratic understanding of each client’s individual problems
beliefs (consequences) (Marzillier & Marzillier, 2008). irrespective of individual diagnoses they may have been
Based on this knowledge, the clinical psychologist can given (i.e. in clinical practice, a client’s problems do not
begin to understand the factors that are causing and usually fall into simple diagnostic categories, but may
maintaining these problems (e.g. the faulty beliefs and reflect a range of problems unique to that individual), (2)
the ‘safety’ behaviours) and develop therapeutic inter- it is collaborative and treats the client with regard, (3) it
ventions to try to deal with these.
In contrast, psychologists who hold a psychodynamic
perspective use formulations to address the way that cur-
rent problems reflect underlying unconscious conflicts
and early developmental experiences, and will couch
their formulations in these kinds of ways. For those psy-
chologists who believe that a holistic or systemic view
of a person’s problems is important (e.g. their problems
can only be fully. understood within a family or social JACK MOTHER AND SISTERS
Tries to help, fails, drinks, takes Helpful and concerned about
context), the formulation will be developed in terms
drugs, feels angry — feels rejected Jack's abuse, but then feel
of the important relationships between the client and so drinks and takes drugs to feel better. let down, angry, rejecting.
important other people in their life. For example, within
the context of the family, someone with a psychologi-
cal problem may be seen as a weak and dependent per-
son, and this may influence how other members of the
family treat the client, and determine what demands
the client may make on their family. Thus, the client’s
problems can be formulated as interactions between var-
FIGURE 2.8 A systemic case formulation.
ious ‘actors’ (the family members) which may maintain
Jack has problems with both drugs and drink. He later
the client’s problems (Marzillier & Marzillier, 2008; Dallos
became involved in petty crime, and was diagnosed as
& Draper, 2005). Figure 2.8 provides a simple example
depressed. He also began to exhibit paranoia and delusional
of a systemic formulation which attempts to explain how ideation. This simple formulation shows how the reactions
a client’s problems are maintained by the relationships of Jack and his mother and sisters reinforce Jack's feelings of
between him and other members of his family. rejection and his abuse of drink and drugs.
In many cases clinicians prefer to represent their for- Source: Dallos, R. & Stedmon, J. (2006). Mapping the family dance.
mulations in a diagrammatic form that permits easy In L. Johnstone & R. Dallos (Eds.) Formulation in psychology and
identification of factors that may be causing the client's psychotherapy. London: Routledge. Reproduced with permission.
66 PSYCHOPATHOLOGY
‘ a
is firmly based on a theoretical understanding of psycho- history, and (5) it allows the development of treatment
pathology (unlike diagnosis which is based entirely on strategies that can be moulded to the specific needs of
a description of symptoms), (4) it can include informa- that individual client, which is especially advantageous
tion about a client’s past history (e.g. their exposure to in treating complex cases that do not easily conform to
risk factors) and the client’s personal, social and family standard diagnostic categories.
SELF-TEST QUESTIONS
° What are the main components of a case formulation?

* Can you describe how a cognitive-behavioural clinician and a psychodynamic clinician might approach case formulation
differently?
SECTION SUMMARY
2.3 CASE FORMULATION
¢ Acase formulation is used by clinicians to draw up a psychological explanation of a client's problems and to develop a plan
for therapy.
¢ The clinician's theoretical approach will determine how they explain the client's problems and what information they
require during the case formulation process.
2.4 CLASSIFICATION AND interview, and this may be entirely unstructured or may
have a very rigid structure depending on the nature of
ASSESSMENT IN CLINICAL the information the clinician wants to gather (Activity
PSYCHOLOGY REVISITED 2.1 provides a good example of a structured interview
designed to gather very specific information about a
client). However, as well as benefits, the clinical inter-
This chapter began by discussing the reasons for wanting view also has many limitations. Its reliability is quite low,
to classify mental health problems — it enables sharing depends on the client’s willingness to provide valid infor-
of knowledge about mental health and it enables suffer- mation about themselves and their problems, and is prone
ers to receive support that is appropriate for their specific to cultural bias when clinician and client are from differ-
problems. However, with classification comes diagnosis, ing ethnic backgrounds. More structured ways of gath-
and there is still a lively debate about whether classifica- ering information include psychological tests, and under
tion and diagnostic systems such as DSM-5 are valid (i.e. this heading we have reviewed personality inventories,
do they define ‘real’ problems or are they merely an arti- specific trait inventories, projective tests, and intelligence
ficial way of arbitrarily classifying symptoms?) or indeed tests. Biologically based assessments such as psycho-
useful (does labelling someone with a psychiatric diagno- physiological tests and brain neuroimaging techniques
sis help or hinder their recovery?) can be valuable for confirming the validity of interview
This chapter has also reviewed the diverse and varied or pencil-and-paper tests, and can often identify whether
ways in which clinicians gather information by which any impairments in brain functioning may be underlying
they can classify, understand and treat the mental health the client’s problems. Finally, we have discussed the use
problems brought to them by their clients. This informa- of case formulations, which have become a popular tool
tion is used to address a number of questions, includ- for clinicians of most theoretical persuasions. The case
ing: “Precisely what problems does this person have?’ formulation allows the clinician to draw up a psychologi-
‘What has caused their problems?’ “What is the best way cal explanation of the client’s problems and to develop a
to treat their problems?’ “Did our treatment work?’ By plan for therapy, and this allows a flexible and personal
far the most common assessment method is the clinical understanding of each client’s individual problems.
ey
x =
To access the online resources for this chapter go to
aad www.wiley-psychopathology.com/ch2
Activity
DSM-5 Website Psychiatric Interviews Activity 2.1

Proposed DSM-5 for Teaching: Self-test questions
changes continue to Depression
Revision flashcards
spark controversy Criticisms of DSM-5
Research questions
The Minnesota Psychiatric Interviews
Multiphasic for Teaching: Anxiety
Personality Inventory MRI scanning
Journal article:
Sentence completion
Journal article: The
assessment of intelli-
gence and cognition
Journal article: Race
bias, social class bias,
and gender bias in
clinical judgment
Mood-sensing smart-
phone tells your
shrink how you feel
Glossary key terms
Clinical issues
Links to journal
articles
References
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3 Research Methods in Clinical
Psychology
[=] a oO
~ To access the online resources for this chapter go to
_www.wiley-psychopathology.com/ch3
This chapter begins by describing what research is, and

RESEARCH AND SCIENCE 71
then discusses a number of ways in which research can be
conducted, with special attention being paid to the role
2 CLINICAL PSYCHOLOGY RESEARCH - WHAT DO WE
of scientific method in clinical psychology research. The
WANTTO FIND OUT? 74
chapter then describes why clinical psychologists might
want training in research, and what kinds of questions
they are interested in addressing. The bulk of the chap- RESEARCH DESIGNS IN CLINICAL PSYCHOLOGY 76
ter is concerned with describing and evaluating a range
of research designs used by clinical psychology research- ETHICAL ISSUES IN CLINICAL PSYCHOLOGY
ers. Finally, a chapter on research would not be complete RESEARCH 95
without a full discussion of the ethical issues that clinical
psychologists are likely to encounter while undertaking tad ul RESEARCH METHODS IN CLINICAL PSYCHOLOGY
research. REVISITED 99
ry ite PSYCHOPATHOLOGY
LEARNING OUTCOMES
1. Describe and evaluate a range of research - 3. Critically evaluate the ethical issues relevant to
methods that can be used in clinical psychology clinical psychology research.
research.
2. Describe the types of research questions that are
central to clinical psychology research.
am a clinical psychologist. Among the healthcare professions, clinical psychology is one of the few to provide extensive research
training, and a clinical psychologist can be involved in both basic and applied research. Because of the breadth of their training in
research methods, clinical psychologists are well suited to design, implement, and evaluate research, and to conduct evaluations
of the services provided by mental health care agencies. When you are a practicing clinical psychologist, finding time to conduct
research of any kind is difficult. But when | am involved it helps me to satisfy my curiosity, to generate new knowledge on which
more effective treatments may be based, and to evaluate whether the current services we offer are effective.
Sarah's Story
world. Indeed, in the UK, almost all clinical psychology

Introduction
training courses are based in university psychology depart-
Why might a profession whose main aim is arguably to ments, and have substantial research training components
alleviate mental health problems want to do research or to them. The current view of the link between research
be involved in research? Why are clinical psychologists and practice that is held in the UK tends to be one in
given such a rigorous training in research methods which scientific method is systematically integrated into
anyway — shouldn't they simply be taught how to help clinical work (Barker, Pistrang & Elliott, 2002). Shapiro
people recover from their mental health problems? The (1985) defines this applied scientist view of clinical psy-
personal account above goes some way to answering chologists as (1) applying the findings of general psychol-
these questions. Even if they are simply offering a ogy to the area of mental health, (2) using only methods
treatment-based service, clinical psychologists should be of assessment that have been scientifically validated, and
able to evaluate whether their services are effective and (3) doing clinical work within the framework of scientific
successful, and to do this with any degree of objectivity method. However, this view of clinical psychologists,
requires a knowledge of scientific method. Sarah’s story their approach to research, and how they use research is
reflects a widely held view that the clinical psychologist not as clear cut as it sounds, and in order to understand
should be thought of as a scientist-practitioner or an how research is used by clinicians and integrated into
applied scientist - someone who is competent as both their role as mental health professionals we need to
a researcher and a practi- spend a little time understanding what is meant by (1)
scientist-practitioner Someone who tioner. This view arose in research and (2) scientific method, and also we need to
is Competent as both a researcher and a
practitioner.
the early 20th century when look at what value research might have within the
psychology was thought of broader scope of psychopathology. For example, some
as an experimental science. researchers simply want to understand what causes psy-
applied scientist Someone who is However, as the discipline chopathology, others want to know whether there is
competent as both a researcher anda
practitioner.
of psychology developed empirical evidence supporting the efficacy of specific
from being a pure research treatments, and others simply want a systematic way of
subject to an applied profession, clinical psychology still understanding and interpreting the symptoms of their
maintained its links with universities and the academic clients.
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY 2a
3.1 RESEARCH AND SCIENCE (usually so that our collecting of facts can be replicated
by others and our conclusions verified by them). Because
the scientific method is used predominantly in psycho-
3.1.1 What Is Research? logical research and clinical psychology research, we will
discuss this approach in detail below.
If you are a psychology student, you have probably
already encountered a course designed to teach you
about research. You will probably have undertaken some
3.1.2 Scientific Method
practical classes designed to teach you about research Scientific method espouses the pursuit of knowledge
methods, and you will also have learnt about the role through systematic and thorough observation. It
that statistics plays in interpreting research data. But did also requires that research findings are replicable and
anyone actually tell you what research is in the first place? testable.
In general, psychology considers itself to be either a bio- By replicable, we mean that the results of the research
logical or a social science, so the emphasis is on using have been collected under controlled conditions that
scientific method to understand human behaviour. But will allow any other researcher to reproduce those exact
research can mean much more than this. In its broadest same findings. Researchers using the scientific method
sense, research is a form of investigation aimed at discov- attempt to achieve this by precise measurement of stim-
ering some facts about a topic or about furthering under- uli and behaviour and accurate and complete descrip-
standing of that topic through careful consideration or tion of the methods by which the data were collected.
study. In this respect, research does not necessarily have Replicability is essential to the progress of scientific
to adhere to scientific principles, and understanding of a knowledge because it means that different researchers
topic may be enhanced in many other ways. For example, can be sure that a research finding is a legitimate fact
we can learn a lot about human behaviour and human that can be relied upon when developing explanations
nature from literature and the way that many classical of a phenomenon. This is especially true in the case of
authors describe everyday experiences and their conse- human behaviour, where the subject matter is often
quences. Many clinicians and psychotherapists claim that complex and may differ significantly from situation to
they gain understanding and knowledge from their own situation. Activity 3.1 provides a discussion of one of the
clinical experiences which they can use systematically seminal research papers in human psychopathology —
and successfully when treating their clients (Morrow- the attempt by Watson & Rayner (1920) to condition a
Bradley & Elliott, 1986). Even historical research can be phobia in an 11-month-old
used to further understanding of psychopathology. In a infant (see section 6.1.1).
To read Watson & Rayner’s article on
systematic search of the historical literature on spiders You will see from this dis- | conditioned emotional reactions go to
and how humans have perceived them over the centuries, cussion that although this / www.wiley-psychopathology.com/
reading/ch3
Davey (1994) found that spiders had been traditionally paper is often considered ‘
linked with the spread of disease and illness — a finding to be one of the found-
which may help us to understand why fear of spiders is ing pieces of scientific research in psychopathology, the
so prevalent in Western societies today. What is common ability of other contemporary researchers to replicate it
to these different approaches is that they are attempts to was limited — largely because Watson & Rayner were less
understand an issue through systematic and careful con- than systematic in the way they collected their data and
sideration of the relevant facts. However, how we collect reported it.
the facts that are relevant to our considerations can vary By testable, we mean that a scientific explanation is
considerably. Literature collects facts usually through couched in such a way that it clearly suggests ways in
the author’s observations of life and everyday living which it can be tested and potentially falsified. Scientific
which are then presented within an unfolding story; his- method often relies on the
torical research collects facts by accumulating evidence construction of theories To complete Activity 3.1 go to
from historical documents or artefacts; and the practic- to explain phenomena, and | www.wiley-psychopathology.com/
activities/ch3
ing clinician gathers facts from their everyday experi- a theory is a set of proposi-
ences with clients. In each case, these facts can then be tions that usually attempt
considered systematically in an attempt to enhance our to explain a phenomenon theory A set of propositions that usually
understanding. by describing the cause— attempt to explain a phenomenon by
describing the cause-effect relationships
In contrast, scientific method advocates that facts are effect relationships that that contribute to that phenomenon.
collected in rather specific ways. Usually this means that contribute to that phenom-
we should collect our facts for consideration in a system- enon. Theories are expected to be able to take into
atic way defined by objectivity and precise measurement account all relevant research findings on a phenomenon,
ay ee PSYCHOPATHOLOGY
' _
and be articulated in such a way that they will also have falsification, and if it is not possible to falsify a theory by
predictive value. That is, they should be able to predict generating testable hypotheses, then that theory is not
what might happen in as yet untested situations. Thus, a scientific, and, in Popper’s view, is of little explanatory
good theory will allow the researcher to generate value. Activity 3.2 provides an example of a psychological
hypotheses about what might happen, and to test theory that attempts to explain why some people develop
these hypotheses in other panic disorder (see section 6.3). This is a theory that can
hypotheses Tentative explanations for a research studies. If the be represented schematically as a series of cause-effect
phenomenon used as a basis for further relationships, and the sequence of cause-effect relation-
hypotheses are confirmed
investigation or predicting the outcome of
a scientific study. in these other studies the ships described in this theory are assumed to precipitate
theory is upheld, but if regular panic attacks in those diagnosed with panic disor-
the hypotheses are disconfirmed then the theory is either der. This relatively simple theory is constructed in such a
wrong or needs to be changed in detail to explain the new way that we can generate a number of testable hypothe-
facts. This process illustrates one of the important distinc- ses from it, andso we could | yr.
tions between science and so-called non-science. Karl potentially falsify the the- {B) To complete Activity 3.2 go to
Popper (1959) proposed that science must be able to for- ory according to Popper's | activities/ch3
mulate hypotheses that are capable of refutation or criteria.
oe
aa: SCIENTIFIC METHOD AS A MODEL FOR CLINICAL
= PSYCHOLOGY RESEARCH: THE PROS AND CONS
=
Le) We have described what the scientific method is, but Hammond, Jones, Watson et al., 2013). However, as we
Q. is it the best model by which to conduct clinical psy- shall see on numerous occasions throughout this book,
WV
a) chology research? In many countries of the world, many forms of therapy are not couched in ways that
U clinical psychology has either explicitly or implicitly make them amenable to assessment through a tradi-
° adopted the scientist-practitioner model described in tional scientific approach (e.g. psychoanalysis). As a
LL.
section 3.1.2, with the implication that practising clin- result, at least some clinicians view processes designed to
ical psychologists are willing to at least call them- scientifically assess treatments (such as those reported
selves scientists by training even if they do not by NICE) as being ways in which those clinicians who sup-
regularly practice as scientists. Nevertheless, in many port therapies derived from traditional scientific
countries there is a growing pressure for mental approaches can impose their own view of what treat-
health services to provide scientific evidence that ments are effective (Elliott, 1998; Roth & Fonagy, 1996).
treatments and therapies are effective and economi- Let us look at some of the benefits and costs of clinical
cal. In the UK, one such agency that attempts to assess psychology adopting the scientific method in its research.
and recommend effective forms of treatment for men- There are several apparent benefits to clinical psy-
tal health problems is the National Institute for Health chology using the scientific method as a model for
and Care Excellence (known as NICE, www.nice.org research. Firstly, there is probably no doubt that clini-
.uk). It does this primarily by recommending treat- cal psychology has used its scientific credentials as a
ments whose efficacy can be labelled as ‘evidence- means of acquiring prestige and establishing its sta-
based’: that is, whose efficacy has been proven tus as an independent discipline within the field of
through research using the sci- mental health (Lavender, 1996). There was no greater
evidence-based Treatments whose
entific method. There is thus proponent of this approach than one of the founders
efficacy has been proven through research
using the scientific method. some pressure from these agen- of British clinical psychology, H.J. Eysenck, who was a
cies for clinical psychologists to vigorous supporter of science and scientific method in
accept the scientific method - at least as a way of clinical psychology research. Secondly, some writers
assessing the effectiveness of therapies - and as a have argued that clinical psychologists often consist-
way of assessing the cost effectiveness of individual ently fail to use research evidence to inform their treat-
interventions, which is an important consideration for ments and instead rely on anecdotal clinical experience
agencies providing psychological services (e.g. Crow, (Dawes, 1994). If this is so, then there becomes a thin
Agras, Halmi, Fairburn et al., 2013; Radhakrishnan, line between clinicians who base their interventions
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY
on unvalidated experience and a bogus psychotherapist on scientific method or not) as irrelevant to their profes-
who invents a so-called therapy whose basic tenets are sional practice (Barlow, Hayes & Nelson, 1984). Thirdly, in
not amenable to objective assessment. Keeping abreast contrast to scientific method, an alternative approach to
of recent developments in evidence-based research is research in clinical psychology is one based on social con-
therefore an important component of good-practice for structionism (Burr, 1995). This approach emphasizes that
clinical psychologists, and scientific method provides reality is a social construction, and so there are no basic
the theoretical and empirical developments by which the ‘truths’ of the kind that we seek to discover using the sci-
clinician can achieve this (Singer, 1980). Thirdly, Belar & entific method. Instead, knowledge consists of multiple
Perry (1992) have argued that scientific method provides realities that are constructed by people and may be his-
a useful framework for theory building that allows clini- torically and culturally specific. It is claimed this approach
cians to test out their clinical observations and assess their has particular relevance in clinical psychology because
efficacy. Otherwise, they argue, clinical experiences are in psychopathology frequently involves individuals creat-
danger of becoming simply a set of random observations ing their own realities (e.g. the paranoid individual cre-
that the clinician is unable to categorize into effective and ates a reality in which everyone is against them, and the
ineffective interventions. depressed individual creates a reality in which they view
In contrast, at least some clinicians have argued that the themselves as worthless). These various realities can be
scientific method in its strictest form may not be suitable accessed through analysing language and social interac-
for clinical psychology research or practice. Firstly, some tions, and so those who advocate a social constructionist
writers claim that to base clinical psychology research on approach argue that the study of language and discourse
strict scientific method aligns it too closely to the medi- is the only means of understanding human experience
cal model of psychopathology and invites many of the and, as a consequence, human psychopathology.
problems associated with a strict medical model of psy- Despite the fact that at least some clinicians have
chopathology (see Chapter 1) (Corrie & Callahan, 2000). adopted alternative frameworks (e.g. the social con-
Secondly, while the scientist-practitioner model is often structionist approach), scientific method is still the most
seen as the model for clinical psychology, it is seldom an favoured model for research in most areas of clinical psy-
ideal that is fulfilled in practice (Barlow, Hayes & Nelson, chology, including research on the causes of psychopa-
1984). For the clinical psychologist, the need to alleviate thology (aetiology), research pursuing the development
a client’s psychological problems is often more press- of new forms of treatment, and research assessing the effi-
ing than the need to be scientifically rigorous. Similarly, cacy and cost-effectiveness of treatments. Even though
the demands placed on overworked clinicians in under- each person may develop their own individual psycho-
resourced mental health services means that they are logical reality, the fact that human beings are evolved
rarely likely to engage in any meaningful research inde- biological organisms means that there are almost certain
pendently oftheir clinical practice (Head & Harmon, 1990) to be general ‘truths’ or processes common to all humans
and will certainly rank research as a priority significantly that can be discovered using scientific method. As a
lower than their service commitment (Allen, 1985; Corrie consequence, there are also likely to be a set of general
& Callahan, 2000). The pressures of their work mean that ‘truths’ or processes common to psychopathology across
they will often view the research literature (whether based all individuals.
® Can you describe the main principles of the scientific meth od?
© What is the difference between a theory and a hypothesis?
® What do we mean when we say that decisions about the effectiveness of an intervention should be evidence-based?
© What are the benefits and drawbacks with clinical psychology using the scientific method as a model for research?
® Whatis social constructionism and how does it offer a different research approach to the scientific method?
od Cae PSYCHOPATHOLOGY
%
SECTION SUMMARY
3.1 RESEARCH AND SCIENCE
© Research is about furthering understanding of a topic through careful consideration or study.

* Scientific method espouses the pursuit of knowledge through systematic observation, and requires that research findings
are replicable and testable.
¢ A theory is a set of propositions that attempt to explain a phenomenon.
»
° There is growing pressure for mental health services to recommend treatments whose efficacy is evidence-based.
© Social constructionism is one research approach in clinical psychology that is an alternative to the scientific method.
3.2 CLINICAL PSYCHOLOGY Once we have been able to describe and categorize
psychopathology then we are one step away from pre-
RESEARCH - WHAT DO WE diction. A logical next stage is to use these descriptions
and categorisations to help prediction A statement (usually quantita-
WANT TO FIND OUT? us
:
predict psychopathol- tive) about what will happen under specific
ogy. For example, we may conditions as a logical consequence of
know that certain child- scientific theories. ’ .
3.2.1 How Does Clinical hood or developmental experiences may increase the
Psychology Research Help Us to risk of developing psychopathology later in life, and one
such list of these risk factors is provided in Table 16.1.
Understand Psychopathology?
This table indicates how various forms of childhood
Clinical psychology researchers use research methods in abuse or neglect can raise the risk of developing a range
a variety of different ways to answer a number of dif- of psychopathologies (as one example, childhood physi-
ferent questions. We will describe the range of research cal and sexual abuse increases the risk of developing ado-
methods available to clinical psychologists in the next lescent eating disorders). However, while research may
section, but first let’s briefly look at how research can have identified such experiences as risk factors, this does
help us understand psychopathology. not imply a direct causal
Research can have a number of immediate goals. relationship between the risk factors Factors that may increase the
risk of developing psychopathology later —
These goals include description, prediction, control and risk factor and the psycho- in life.
understanding (explanation), and a clinical psychology pathology — it merely indi-
researcher may be using research methods to achieve any cates that the early experience in some as yet unknown
one or more of these goals. way increases the possibility that a psychopathology
For example, description involves the defining and will occur.
categorising of events and relationships, and a researcher The next aim of research would move beyond describ-
may simply want to find ing and categorising events to actually trying to control
description The defining and categoris- suitable ways of describ- them in a way that (1) Pro- control Using our knowledge of the
ing of events and relationships relevant to vides us with a clear picture
psychopathology.
ing and categorising psy- causal relationships between events to
chopathology. To some of the causal relationships manipulate behaviour or cognitions.
extent this is what is represented in DSM-5 (the catego- involved, and (2) allows us to develop methods of chang-
rising of psychopathology), but other researchers have ing events for the better. In the case of psychopathology,
used research methods to discover whether different this latter aim would include using our knowledge of the
symptoms are related or co-occur (e.g. Watson, 2005). causal relationships between events to control behaviour
For example, Figure 2.1 provides an example of how so that we could change it — the basic tenet of many forms
research methods have been used to understand how of treatment and psychotherapy. One of the main tools for
symptoms of anxiety and depression are related, and discovering causal relationships between events is the exp-
such categorisation of symptoms is a first step towards erimental method, which we will describe in more detail
defining the biological or psychological mechanisms in section 3.3. For example, numerous studies have indi-
that link anxiety and depression. cated that experimentally inducing a bias to interpret
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY gs
ambiguous events as threatening causes an increase attack that have been identified using controlled research
in experienced anxiety (Wilson, MacLeod, Mathews & methods (Clark, 1986). Clearly, in this model, panic
Rutherford, 2006). As a consequence this research suggests attacks are precipitated by the individual catastrophically
that if we can decrease this interpretation bias in anxious misinterpreting ambiguous bodily sensations. This
individuals, it should significantly reduce the anxiety they implies that attempting to control and change this ten-
experience (e.g. see Treatment in Practice Box-6.4). dency to catastrophically misinterpret bodily sensations
The final aim of research is understanding. That is, should help to reduce the frequency and intensity of
once we have described and categorized psychopathology, panic attacks in panic disorder, and, over the years, inter-
and once we have begun to ventions of this kind have been refined to a point where
inderstanding Afull description of how identify some of the causal they offer successful treatment for many suffering panic
he causal factors affecting psychopathol-
SB iritelce factors affecting psychopa- disorder (Wells, 2006; Fisher, 2008).
thology, we are probably at To be useful in helping to understand psychopathol-
a point where we want to describe how all these factors ogy, research does not necessarily have to be carried out
interact, and this will provide us with a theory (or model) on those who have mental health problems or who dis-
of the phenomenon we are play symptoms of psychopathology. In Chapter 1 we
nodel A hypothetical description of a trying to explain. Activity discussed the possibility that much of what is labelled as
yrocess or mechanism (such as a process .
isle
r psychological mechanism involved in
3.2 provides a useful exam- psychopathology is often just an extreme form of com-
sychopathology). ple of how researchers mon and accepted behaviours. That is, symptoms diag-
believe the various causal nosed as a psychological disorder may just be more
factors involved in panic disorder interact, and it is the extreme versions of everyday behaviour. One good
development of models such as this (describing the inter- example is worrying. Worrying is usually viewed as a
relationships between events) that can add significantly to perfectly normal reaction to the challenges and stressors
our understanding of psychopathology and suggest prac- encountered in daily life and the activity of worrying
tical ways of alleviating and treating symptoms. may often help us to cope with these problems by ena-
bling us to think them through. However, once uncon-
trollable worrying becomes a chronic reaction to even
3.2.2 What Questions Do minor stressors it then begins to cause distress and inter-
Clinical Psychologists Use fere with normal daily living. Because symptoms diag-
nosed as a disorder may just be more extreme versions of
Research to Try to Answer?
everyday behaviour, then what we find out about activi-
Potentially we can use research methods to try to under- ties such as worrying in non-clinical populations will
stand any aspect of psychopathology that might interest probably provide some insights into the aetiology of
us. Arguably, the primary aim of clinical psychology pathological worrying when it is a significant indicator
research is to further our knowledge and understanding of a psychological disorder such as generalized anxiety
of psychopathology and its treatment, and one impor- disorder (GAD). Undertaking research on healthy,
tant aspect of this is an understanding of the causes non-clinical populations in order to shed light on the
of psychopathology, and especially an understanding of aetiology of psychopathology is known as analogue
the aetiology of psychological problems and disorders. research, and such research makes an important contri-
Although the term aetiology is mainly used in medi- bution to the understand-
F f A ; F i ae analogue research Research on healthy,
7 s di h cal settings to reler to the ing of psychopathology ‘non-clinical populationsin orderto shed
etiology A term widely usedinpsycho- causes of diseases or path- (Davey, 2003; Vredenburg, fight on the aetiology of psychopathology.
athology to describe the causes or origins ‘ ne
f psychological symptoms. ologies,
ian it isla
in eeea alsodenen
a term
bal Flett & Krames, 1993).
Another important function of clinical psychology
thology to describe the causes or origins of psychological research is to determine the efficacy of treatments and
symptoms. We will discuss in detail research that has led interventions. This includes testing the effectiveness of
to an understanding of aetiology in sections specifically newly developed drug, surgical or psychological treat-
set aside for this in later chapters. One practical implica- ments. Research may even try to compare the effective-
tion of research into the aetiology of mental health ness of two different types of treatment for a psychological
problems is that understanding the causes of psychopa- disorder (e.g. comparing a drug treatment for depression
thology will inevitably suggest methods of intervention with a psychological treatment for depression). Such
that might be used to alleviate those problems. Once studies are not quite as simple as they may initially seem
again, Activity 3.2 provides a useful example that illus- because the researcher will have to compare those who
trates this. The model of panic disorder displayed in this undergo the treatment with those who do not, and they
Activity describes the causal factors that generate a panic will also have to control for extraneous factors that might
ee PSYCHOPATHOLOGY
+ ~~
influence improvement that are not directly due to the ‘how will we know if the clinical audit The use of research
therapy being tested (e.g. how attentive the therapist is, service has achieved what methods to determine whether existing
clinical knowledge, skills and resources are
or the degree to which the client participating in the study it is trying to achieve?’
effective and are being properly used. Also
‘expects’ to get better). We will discuss therapy outcome (Barker, Pistrang & Elliott, known as evaluation research. sen
research of this kind in more detail in Chapter 4, but 2002). In this sense, clinical
the interested reader may want to have a look at Sloane, audit does not add to the body of knowledge about psy-
Staples, Cristol, Yorkston & Whipple (1975), Shapiro, chopathology, but is an attempt to ensure that current
Barkham, Rees, Hardy, Reynolds et al. (1994) or Clark, knowledge is being effectively used. In particular, clinical
Ehlers, Hackmann, McManus et al. (2006) as examples of audit is intended to influence the activities of a local
how intervention outcome research is conducted. team of clinicians, rather than influencing clinical prac-
Finally, practising clinical psychologists often have tice generally (Cooper, Turpin, Bucks & Kent, 2005), and
pressing questions that, for various reasons, they need to clinical audit uses research methods to assess how much
answer. Very often these are questions of a practical end users value the services on offer, their satisfaction
nature related to their employment as mental health with these services, and what is perceived as good and
professionals working in organisations that provide men- bad about the services offered (for an example, see
tal health services. For example, in the UK, most NHS Tulett, Jones & Lavender, 2006).
service providers will want to ensure that the service These, then, are some of the reasons why clinical psy-
they are offering is effective, and this is known as chologists do research. They include attempts to answer
evaluation research or clinical audit. Clinical audit uses pressing practical problems (e.g. what treatments are
research methods to deter- effective?) and attempts to add to the body of knowledge
evaluation research See clinical audit.
mine whether existing cli- about psychopathology (e.g. what causes specific psycho-
nical knowledge, skills and resources are effective and are pathologies?). The next section introduces you to some
being properly used, and the kind of questions addressed of the research methods that can be used to answer these
will include ‘what is the service trying to achieve?’ and questions.
SELF-TEST QUESTIONS
* Can you name four main goals of research?
° What does the term aetiology mean?
e What is analogue research?
® What is clinical audit?
SECTION SUMMARY
3.2 CLINICAL PSYCHOLOGY RESEARCH - WHAT DO WE WANT TO FIND OUT?
¢ The main goals of research are description, prediction, control, and understanding.
* Clinical psychology research is often aimed at understanding the aetiology, or causes of psychopathology.
e Analogue research involves using healthy non-clinical participants or non-human animal studies to understand
psychopathology.
factors, including (1) the nature of the question you are

3.3 RESEARCH DESIGNS asking (e.g. do you want to find out whether one event
IN CLINICAL PSYCHOLOGY causes another or whether these events are merely cor-
related?), (2) the nature of the population you are study-
ing (e.g. is the psychopathology you are studying rare,
There is a whole range of research designs that are rel- and so you only have access to a few participants?), and
evant to clinical psychology research and the type of (3) whether your research is at an early or advanced stage
method you choose will be determined by a number of (e.g. you may simply want to be able to describe some
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY ee
of the phenomena associated with a psychopathology package such as Statistical Package for the Social
rather than to explain its causes in detail). The follow- Sciences (SPSS) (Field, 2013a). This will compute a cor-
ing represent examples of the main research designs relation coefficient (denoted by the symbol r) which
used in clinical psychology research, and other more spe- measures the degree of
cific examples can be found in the specialized Research relationship between the Statistical Package for the Social
Methods Boxes found in individual chapters. two variables. The correla- Sciences (SPSS) A computer program
specifically developed for statistical
tion coefficient can range analysis for the social sciences.
from +1.00 through 0.00
3.3.1 Correlational Designs to —1.00, with 1.00 denoting a perfect positive correla-
tion between the two variables (i.e. as scores on one vari-
Correlational designs are among those most commonly able increase, then scores on the other variable will
used in clinical psychology research. The aim of this increase) and —1.00 denot- positive correlation A relationship
methodology is to try to ing a perfect negative cor- between two variables in which a high
orrelational designs Research designs determine whether there relation between the two score On one measure is accompanied by a
vhich enable a researcher to determine high score on the other.
is a relationship between variables (i.e. as scores on
‘there is a relationship or association
etween two or more variables. two or more variables. For one variable increase, then
example, is trait anxiety scores on the other varia- negative correlation A relationship
between two variables in which a high
associated with worrying? Is body dissatisfaction associ- bles will decrease). A cor- score on one measure is accompanied by a
ated with excessive dieting in eating disorders? Is the relation coefficient of 0.00 low score on the other.
availability of drugs associated with substance abuse in indicates that the two vari-
adolescents? As long as we have valid and reliable ways ables are completely unrelated. The relationship between
of measuring the variables we want to study (see section two variables can also be represented graphically in what
2.2.1), then we can undertake a correlational analysis. is known as a scattergram, and Figure 3.1 provides three
Basically a correlational analysis will tell you whether examples of scattergrams
scattergram A graphical representation
two variables co-vary. That is, if you increase the value representing three differ- showing the relationship between two
of one measure then does the value of the other also ent types of relationships variables.
increase? In the examples we have just given, a positive between variables. These
correlation between trait anxiety and worrying would scattergrams show how the line of best fit differs with
indicate that as trait anxiety increased, worry would also the nature of the relationship between the two variables
increase, and a positive correlation between body dissat- concerned. The statistical line of best fit A straight line used as a
isfaction and dieting would indicate that as body dissatis- package that calculates the _ best approximation of a summary of all the
faction increased so too would dieting behaviour. Note correlation coefficient and points ina scattergram.
that this does not imply a causal relationship between prints out the scattergram
the two variables and it does not explain why they are for you will also provide you with an indication of the
related; it only indicates that scores on one variable co- statistical significance of your results. A researcher will
vary with scores on the other variable. So, for example, a want to know the degree statistical significance The degreeto
positive correlation between trait anxiety and worrying to which their results occur- which the outcome of a study is greater or
red by chance, and if the smaller than would be expected by chance.
could mean any of the following: (1) that increases in
worrying cause an increase in trait anxiety, (2) that probability of their results occurring by chance is low then
increases in trait anxiety cause an increase in worrying, they can be relatively assured that the finding is a reliable
or (3) that some other variable causes similar changes in one. Traditionally, a correlation is considered statistically
both worry and trait anxiety (e.g. increases in depression significant if the probability of it occurring by chance is
could cause both increases in worrying and increases in less than 5 in 100, and this is written as p < .05 (p stands for
trait anxiety). So a correlational analysis is often a method probability). From the examples given in Figure 3.1 you
that is used at the very beginning of a research pro- can see that the correlations in both Figures 3.1a and 3.1b
gramme to simply try to map out how the relevant vari- are statistically significant (because the p values are less
ables involved in a particular phenomenon interrelate. than .05). However, the correlation in Figure 3.1c is not sig-
To undertake a correlational analysis the researcher nificant (because the p value is higher than .05), meaning
needs to obtain pairs of scores on the variables being there is probably no important relationship between the
studied. For example, if you are interested in whether two variables. (see also Focus Point 3.3 later in the chapter
there is a relationship between trait anxiety and worry- for a discussion of probability levels and effect sizes).
ing, you can ask participants to complete questionnaires Correlational designs are valuable for clinical psy-
measuring worry and trait anxiety. You will then have chology researchers in a variety of ways. First, they
two scores for each participant, and these scores can be allow the researcher to begin to understand what vari-
entered into a spreadsheet for a computer statistical ables may be interrelated and this provides a useful first
PSYCHOPATHOLOGY
+ ~
(a) 80 3 (b) 50 Jit ti
al hin ‘aa cea :

=a: a: me |
60 : 5 Q [ 0 0 ¢ : : .
a wo 2 304|
(S)
SS a te : J a :
Y Sg = Tee
(@}
>) 50 : L > ae: = go ; :
fee : af |= mA A ‘eee «el

(@) ey cl mi 7
= “i = 7 l
40 ai
~~ 10 o
30 | a
i] C
20 + 7 i ae 0) | T T
0 10 20 0 10 20 30
TRAIT ANXIETY BODY DISSATISFACTION
FIGURE 3.1 Correlation scattergrams. () 190

In a questionnaire study, 132 female college student par-
ticipants were asked to fill in valid and reliable questionnaires
measuring (1) the extent to which they worried, (2) their level ISG aa
of trait anxiety, (3) the degree of positive mood they exhibited ;
over the past 6 months, (4) their level of dissatisfaction with FAO + | a cae : =
their body shape, (5) their current level of depression, and 3 pakorecnaee a
(6) their height. a aed eae wig) Uw
(a) This scattergram shows the relationship between worry a Ba
scores and trait anxiety scores for the 132 participants. This oe
exhibits a positive correlation, and the line ofbest fit (the ee
straight line) indicates this by showing an increasing trend.
The correlation coefficient calculated by SPSS was r = .66, and 140
this was significant at p <.001.
(b) This scattergram shows the relationship between 130
measures of positive mood and body dissatisfaction for the 0) 10 20
132 participants. This exhibits a negative correlation, and DEPRESSION
the line ofbest fit (the straight line) indicates this by showing
a decreasing trend. The correlation coefficient calculated by experience of stressful events is associated with depres-
SPSS was r = -.40, and this was significant at p <.001. sion (e.g. Brown & Harris, 1978).
(o) This scattergram shows the relationship between However, as we indicated earlier, correlational designs
measures of height and depression for the 132 participants. are limited. They certainly do not allow us to draw any
This indicates that these variables are unrelated with the line
conclusions about causality, and they usually provide
ofbest fit (the straight line) showing neither an increasing nor
very little insight into the mechanism or process that
decreasing trend. The correlation coefficient calculated by
might mediate the relationship between the two vari-
SPSS was r =.01, with p > .80, and this was non-significant.
ables that are correlated. We need to use other designs
(such as the experimental design) to help us answer the
question of how the two variables are related.
step towards understanding a particular phenomenon.
Second, correlational designs are useful for researching
how individual differences and personality factors may 3.3.2 Longitudinal Studies and
relate to psychopathology. For example, they would Prospective D esign s
allow us to determine whether a personality factor, such
as perfectionism, was related to a psychopathology, An alternative form of cor-. longitudinal study Research that takes _
such as obsessive-compulsive disorder (e.g. Tolin, Woods & _ relational design is known peau rae fom ie Sone Dar tigipagis at
oie wo or more different times in order to
Abramowitz, 2003). Third, they would also allow us to as the longitudinal study specify the time relationships between
determine whether certain experiences were associated or prospective design. In _ variables.
Thismay extend over many years
with specific psychopathologies, such as whether the _ the traditional correlational °F ver 4 participant's whole lifetime...
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY yo
= CORRELATION AND CAUSATION

mM
=
ie mood causes a person to have body piercings? We cer-
tainly can't tell from the correlation alone. However, the
o
Ou significant relationship between these two variables
Vv) may not even represent a causal relationship between
=]
1S) them at all, but that they may both be caused by some
2) other third variable that was not measured in the cor-
Li,
relational study. In_ this third variable A factor that may mediate
case, both having body the relationship between two other meas-
piercings and negative ures that are significantly correlated.
|
mood may be caused by
some other variable, such as (1) being young, and so
© iStock.com/muldoon being more likely to indulge in body piercing and expe-
rience adolescent depression (Caliendo, Armstrong &
Roberts, 2005), (2) having a tendency to indulge in risk-
A significant positive correlation between two vari- taking behaviours, and so being more likely to be less
ables does not imply causation, nor does it provide socially conformist but negatively affected by unusual
any real insight into why or how the two variables are experiences (Carroll, Riffenburgh, Roberts & Myhre,
related. Take the following example. 2002), or (3) being a substance abuser, and so more likely
There is a significant positive correlation between to be drawn to socially nonconformist cultures that
body piercings and measures of negative mood (Skegg, might include body piercing as a fashion statement as
Nada-Raja, Paul & Skegg, 2007). Does this mean that well as experiencing the negative emotions that are
body piercing causes negative mood, or that negative associated with substance abuse (Forbes, 2001).
= =
design, all measures are taken at the same point in time measure of negative attributional style at time 1 was
(known as a cross-sectional design, because the study sim- shown to predict increases in depression scores between
ply takes a sample of measures as a ‘cross-section’ of ongo- times 1 and 2. This type of design enables the researcher
ross-sectional design A research design ing behaviour). However, in to understand the time course of relationships between
jat involves the collection of data from a longitudinal or prospective two variables, and to determine whether one variable
ample at just one point in time. designs, measures are taken predicts changes in a second variable. In the case given in
at two or more different Research Methods Box 7.2, a negative attributional style
times. In a longitudinal study, measures are taken from the predicts future increases in depression, and can therefore
same participants on different occasions usually over be identified as a risk factor for depression.
extended periods of time. This may extend over many years, One example of a longitudinal study is the Dunedin
or, in more long-term studies, over a participant’s whole life- Multidisciplinary Health and Development Study — a longi-
time. Prospective studies take measures of the relevant vari- tudinal investigation of health and behaviour in a complete
ables at a particular point in time (usually called time 1), and birth cohort (http:/ /dunedinstudy.otago.ac.nz). Participants
then go back to the same participants at some future time in the study were born in Dunedin, New Zealand, between
and take the same or similar measures again (usually called April 1972 and March 1973, and over 1000 of these individu-
time 2). Both longitudinal and prospective designs enable als then participated in follow-up assessments at age 3, 5,
the researcher to specify more precisely the time-order rela- 7,9, 11, 13, 15, 18, 21, 26, 32 and 38 years. The study has
rospective designs Research that takes
tionships between variables enabled researchers to understand the time-order relation-
\easures from the same participants at two that are correlated. That is, ships between variables associated with health and psycho-
more different times in order to specify because measures are taken pathology, and to understand how some variables can be
1e time relationships between variables. from the same participant at identified as predictors or risk factors for later behaviour.
both times 1 and 2, the researcher can not only see whether For example, using prospective data from the Dunedin
there are correlations between variables X and Y, but also study, Reichenberg, Caspi, Harrington, Houts, Keefe et al.
whether variable X measured at time 1 predicts changes in (2010) found that children who grow up to develop adult
measures of variable Y that occurred between times 1 and 2. schizophrenia enter primary school struggling with verbal
A detailed example of a prospective design is given in reasoning and lag further behind peers in working memory,
Research Methods in Clinical Psychology Box 7.2 where a attention, and processing speed as they grow older.
VSO PSYCHOPATHOLOGY
; ~\
3.3.3 Epidemiological Studies population at any one point in time). You can see from
these examples that prevalence rates represent incidence X
Epidemiology is the study of the frequency and distribu- duration, and it is important to view prevalence in this way
tion of disorders within specific populations over a speci- because some disorders are of high incidence but low
fied period of time. In this sense, epidemiological research duration (e.g. bouts of depression), and some others are
usually takes the form of a large-scale survey, and tends to of low incidence but long duration (e.g. schizophrenia).
be descriptive in the sense that it attempts to provide details DSM usually provides information on either the lifetime
primarily about the prevalence of psychological disorders. prevalence rates of a disorder or its point prevalence, and
prevalence The number of instances of However, it can also be these are the kinds of statistics we will be using when con-
a given disease or psychopathology ina used to gather information sidering specific disorders in later chapters.
given population at a designated time. about the factors that cor- The benefits of epidemiological studies are that they
relate with psychological disorders, and this can provide provide information about the frequency of mental health
information about how a specific disorder affects people, problems that can be used for planning healthcare services.
whether it is more prevalent in young people or old peo- They may also provide information about the risk factors
ple, men or women, and so on. It can also help us to under- for various psychological disorders, which will help health
stand what some of the risk factors are for a specific service providers to identify those who may be at risk of
psychological disorder, and whether the incidence of a dis- developing a mental health problem and so introduce
orderisincreasing or decreasing overtime. Epidemiological programmes designed to help prevent those problems.
studies are usually large-scale ones, and need to have For example, excessive alcohol consumption in pregnant
enough respondents in the mothers is a risk factor for infant fetal alcohol syndrome in
epidemiological studies Research which
takes the form of a large-scale survey used
survey to ensure that the the offspring, and prevention programmes aim to identify
to study the frequency and distribution of sample is representative of those women at risk of aleohol abuse during pregnancy
disorders within specific populations over all types of person in the and to provide interventions or alcohol-reduction counsel-
a specified period of time. population being studied. ling (Floyd, O’Connor, Bertrand & Sokol, 2006).
One of the largest epidemiological studies in the world is However, like all research approaches, there are some
in the US, and is called the NIMH Epidemiological limitations to epidemiological studies. For example, to
Catchment Area Study (Regier, Myers, Kramer, Robins et provide valid descriptions of the prevalence rates of
al., 1984; Narrow, Rae, Robins & Regier, 2002). This survey psychological disorders in a particular population, the
has interviewed over 20,000 respondents and has collected sample used must be truly representative of that popula-
data on the prevalence rates of an extensive range of mention. This is often difficult to achieve because such stud-
tal health problems, many of which are described in the ies will never attain a 100 per cent response rate, and
prevalence sections of later chapters. many respondents will often refuse to take part. Studies
One of the main uses of epidemiological studies is to suggest that those who are most likely to refuse to take
determine the prevalence rates of various mental health part in an epidemiological survey are men, individuals
problems, and prevalence rates can be described in a of low socio-economic status, and individuals from eth-
number of different ways. nic minority populations (Fischer, Dornelas & Goether,
prevalence rates The representation of inci- For example, respondents
dence by duration of a particular disorder. 2001), and this is likely to mean that the samples used in
in an epidemiological study most epidemiological studies are not fully representative
can be asked: (1) “Have you ever experienced symptoms of the population being studied.
of a specific psychopathology in your lifetime?’ (providing
information on the lifetime prevalence rate of a disor-
der); (2) ‘Have you experi-
lifetime prevalence The frequency of a
enced symptoms of a
3.3.4 Experimental Designs
disorder within a lifetime.
specific psychopathology Arguably one of the most powerful research designs is the
in the past month?’ (providing information on the one- experiment. This is a design
month prevalence rate of a disorder, e.g. Regier, Farmer, in which the researcher For a video on conducting
Rae, Myers et al., 1993); or (3) Are you experiencing symp- manipulates a particular experiments in psychopathology go to
one-month prevalence The frequency
toms of a specific psycho- variable and observes the video/ch3
of occurrence of a disorder in a population pathology at the present effect of this manipulation
within the past month. time?’ (providing informa- on some outcome, such as
tion on what is known as experiment A design in which the
the participant’s behaviour.
researcher manipulates a particular
point prevalence The frequency of a the point prevalence of a For example, if we want to variable and observes the effect of this q
disorder in the population at any one point disorder, i.e. the frequency know whether negative manipulation on some outcome, such as
nas of a disorder in the mood makes people worry, the participant's behaviour.
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY oe
we can experimentally manipulate participants’ moods a mood manipulation that increases positive rather than
and see if this changes the extent to which they worry in negative mood, and perhaps a third group who undergo
the way we predicted. One important advantage of the a similar manipulation that does not change mood at all.
experimental design over many of the other research So, our experimental group may listen to sad music that
designs we will discuss is that it does allow the researcher makes their mood more experimental group A group of partici-
to determine whether there is a causal *relationship negative, our first control pants who experience the independent
between variables, and to identify the direction of the group may listen to happy variable in an experimental study.
causal effect. This is an important step in developing the- music that makes their control group A group of participants
ories and models about the aetiology of psychopatholo- mood more positive, and who experience manipulations other
gies (Field & Davey, 2005). our second control group than the independent variable being
may listen to neutral music investigated.
Basic features of the experimental method that does not change their mood in either direction.
In most experiments the researcher manipulates one par- Suppose now that, after the music manipulation, partici-
ticular variable to assess its effects on a particular out- pants in our experimental group worry more than par-
come. Usually, the experimenter begins with an ticipants in both the positive and neutral control groups.
experimental hypothesis or experimental prediction This allows us to conclude that negative mood causes an
oo 5 ae about what will happen. increase in worrying, and allows us to discount our other
«xperimental hypothesis A prediction
For example, we may pre- potential confounding explanations. For example, the
)bout what the outcome of an experimen-
ialmanipulation might be. dict that if we increase increase in worrying in the negative group is not a result
negative mood, our partic- of (1) a change in mood in any direction (because the
experimental prediction See experimen- ipants will worry more, positive mood group did not show a similar increase in
alhypothesis. and this hypothesis is worrying), (2) simply listening to music (because all
derived either from (1) an three groups listened to music, but only the negative
existing academic theory about worrying, (2) our obser- group showed an increase in worry), or (3) simply being
vations of worrying in everyday life, (3) the existing in an experiment (because our positive and neutral mood
research literature on worrying, or (4) the outcomes of groups did not increase their worrying as much as the
other studies we have conducted on worrying. The negative mood group). It is still possible, however, that
variable we are manipulating (in this case mood) is the differences in worrying between our three groups
known as the independent variable, and the outcome have occurred by chance, and just as much as the
variable we are measuring researcher using correlational designs needs to conduct a
independent variable (IV) The variable (in this case worrying) is statistical analysis to rule this out, so does the researcher
thatismanipulated in an experiment. 5
known as the dependent using experimental designs. This means that we need to
variable. However, imag- have an objective way of measuring the outcome
dependent variable (DV) The outcome
variable that is measured in an experiment. ine that our experiment (dependent variable) so that the data from the experi-
involves simply increasing ment can be subjected to an analysis using inferential sta-
negative mood and finding out that this increases the tistics, and we can then gauge how important the
participants’ tendency to worry. This is not as informa- differences in worry between our groups are (see Focus
tive as it seems because (1) simply changing a partici- Point 3.3). In this case we need to find a way of objec-
pant’s mood in any direction (positive or negative) may tively measuring the amount of worrying that each par-
cause them to worry more, (2) if we use sad music to put ticipant indulges in after the mood manipulation.
our participants into a negative mood, maybe it is just One other feature of designing experiments is in the
listening to music that makes them worry more assignment of participants to the various conditions or
(regardless of whether it is sad music), or, more radically, groups in the experiment. Typically, researchers use ran-
(3) any participant taking part in any experiment dom assignment of partic-
may simply worry more. This clearly indicates that to be ipants to experimental random assignment Assignment of par-
ticipants to different treatments, interven-
able to make some valid conclusions about the effect of conditions. This is to ensure tions or conditions according to chance.
our manipulation, we will have to compare our that, at the outset of the
manipulation with some other conditions that control experiment, all groups have participants with similar char-
for any confounding effects. These comparisons are acteristics. In our example experiment, the findings of our
known as control conditions. For example, suitable study would be compromised if we happened to have par-
control conditions in our ticipants in our negative mood group who naturally worried
control conditions Conditions within
in experiment that control for any effects
example experiment would more than the participants in the other two control
other than that produced by the independ- be to have a group of groups — even before we had completed our experimental
antvariable. participants who undergo manipulations. This can usually be prevented by the random
yy Aaa PSYCHOPATHOLOGY
ae FROM STATISTICAL SIGNIFICANCE TO EFFECT SIZES

is]
-
Traditionally, inferential statistics has used a very specific an experimental effect existed (if p < .05) or it did
= method for testing whether differences between experi- not exist (if p > .05). However, selecting a p level of
Oo .05 by which to reject the null hypothesis is entirely
a. mental groups are statistically significant (and are there-
Vi fore unlikely to have occurred by chance). This is known arbitrary; it merely tells us that the null hypothesis
e) as null hypothesis significance testing (Field, 2013a), and is unlikely — it does not tell us that our experimental
U
Oo the statistical tests we use tell us the degree to which hypothesis is correct. In addition, the p value calcu-
Le the pattern of results we got could have occurred by lated with inferential statistics can be influenced by
chance (the null hypothesis). In an experiment where we many factors that are not directly related to your
decide to look at whether manipulating negative mood manipulation. For example, the more participants
increases worrying and we find that measures of worry you test in your experiment, the more likely you are
are higher in the group that experienced negative mood to get a p of less than .05 - even when the measured
we can create two simple hypotheses: differences between the groups in your experiment
are quite small (Cohen, 1990).
e Null hypothesis: Increased levels of worrying
More recently, less emphasis has been placed on
were nothing to do with negative mood.
the importance of the actual p value (and whether the
e Alternative hypothesis: Increased levels of wor-
null hypothesis might be rejected) and more on effect
| rying were caused by negative mood.
size. An effect size is simply an objective and stand-
| When using statistics, you can only show that the ardized measure of the magnitude of the difference
| null hypothesis is likely to be wrong (you can never between your experimental condition and the control
prove your alternative hypothesis). Traditionally, conditions. The larger thé effect size, the more likely it is
researchers have adopted a significance level ofp < .05 that your results did not occur by chance. This provides
to decide whether the null hypothesis can be rejected. a dimensional scale by which to judge the importance
If p < .05, it means that there is only a 1 in 20 chance of your results rather than an arbitrary categorical “all-
that your experimental results occurred by chance, or-none” decision provided by null hypothesis signifi-
| so they are more likely to have been caused by your cance testing. Many measures of effect size are used
experimental manipulation. in contemporary clinical psychology research, with the
One problem with null hypothesis significance most common being Cohen's d and Pearson’s correla-
testing is that it led researchers to believe that either tion coefficient r (Field, 2013a).
Wistots Wii etsh, ciety iAbs
assignment of participants to groups, and this should nor- conditions a participant is in, and also knows what the
mally ensure that there are no statistical differences experimental predictions are for these conditions, the
between the groups at the outset of the experiment on experimenter may provide subtle cues which lead the
characteristics that may influence the dependent variable. participant to behave in the predicted way. To avoid
Finally, both the experimenter and the participant experimenter bias of this kind a double-blind procedure
may introduce bias into an experiment that can affect the can be used in which neither the experimenter nor
validity of the findings. For example, during an experi- the participant is aware
ment, a participant may begin to think about the pur- of which group the par- double-blind An experimental procedure
pose of the experiment and behave in a way that is ticipant is in (i.e. a second in which neither the experimenter nor the
participant is aware of which experimental
consistent with these thoughts. When this occurs, the experimenter may be emp- condition the participant is in.
participant is said to be responding according to the loyed simply to assign par-
demand characteristics of the experiment (i.e. what ticipants to experimental conditions without the first
they think the experiment experimenter knowing). An eb cdis example of
demand characteristics The features
is about) rather than to the implicit experimenter bias gsm
of an experiment which are the result of
participants acting according to what they stimuli and events in that we encountered in our To read the author's blog on‘An
effect is not an effect until it is replicated
believe is expected of them. the experiment. Equally, the lab when researching the (pre-cognition or experimenter demand
experimenter may unwit- relationship between cogni- effects)’ go to
tingly bias the results of an experiment. Because the tions and OCD symptoms www.wiley-psychopathology.com/
reading/ch3
experimenter may know which of the experimental is recounted in my blog.
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY EBs
, Activity 3.3 introduces discrete. That is, symptoms diagnosed as a psychological

To complete Activity 3.3 go to | you to the kinds of ques- disorder may just be extreme versions of normal, every-
activities/ch3
| tions that someone under- day behaviours and reactions (Krueger & Piasecki, 2002;
/ taking an experimental Olatunji, Williams, Haslam, Abramowitz & Tolin, 2008;
study needs to ask when Niles, Lebeau, R.T., Liao, B., Glenn, D.E. & Craske, 2012).
designing and analysing their experiment, and-you should If so, then what we find out about these behaviours and
ensure you understand the various concepts described in reactions in non-clinical populations will tell us something
this section before attempting this activity. about the processes that cause the more severe reactions
found in clinical populations. Second, in the laboratory we
Uses of the experiment in clinical can use experimental manipulations to create psychopa-
psychology research thology in non-clinical participants. For example, in
Experimental designs are used extensively in research into Chapter 6, the attention bias modification procedure
the aetiology of psychopathology (known as experimen- described in Treatment in Practice Box 6.4 demonstrates
tal psychopathology). This is because the experiment is a how non-clinical participants might be made ‘anxious’ by
powerful technique that allows the researcher to establish establishing in them a threat interpretation bias, which
the direction of causal relationships between events, and can then be used to study how this ‘anxiety’ might be alle-
this is critical for our understanding of the causes of psy- viated (e.g. MacLeod & Mathews, 2012). Third, non-clini-
chopathology. Many research methods do allow us to say cal participants can be selected for an experimental study
that two variables may be significantly associated, but that because they are similar to individuals with psychopathol-
is all—they do not tell us whether there is a causal relation- ogy. For example, a good deal of research has been carried
ship between these events. For example, we know that out on college students who score high on measures of
depression is associated with low levels of the brain neuro- depression but at sub-clinical levels (Vredenburg, Flett &
transmitter serotonin. But do low levels of serotonin Krames, 1993). Such participants do not usually have lev-
cause depression, or does depression cause a reduction els of depression that is clinically significant, but it does
in brain serotonin levels, or is some third factor involved in allow an experimenter to compare how college students
affecting both? Only properly controlled experiments can scoring high or low on measures of depression might
answer some of these questions. However, having said react to an experimental manipulation. Finally, analogue
this, it is often difficult to do experiments with individuals populations do not even have to be human to provide val-
with mental health problems. Experiments involve manip- uable information about psychopathology. Animal studies
ulating critical variables, and this may mean exposing are also a valuable source of information about basic pro-
already vulnerable and distressed individuals to even cesses that might underlie psychopathology, especially
greater distress. Imagine doing our experiment on the when attempting to understand how brain function may
effect of negative mood on worrying with individuals influence psychopathology. Animal models allow
diagnosed with generalized anxiety disorder (GAD). researchers to experimen-
These are people who already suffer chronic uncontrolla- tally investigate such factors animal models The use of laboratory
:
ble worry at distressing levels, and our negative mood as the genetics of a psycho- animals
"Bs in research
its to simulate processes
0 sinulatee
comparable to those occurring in humans.
manipulation could make this even worse. In order to pathology (using intensive
avoid these ethical difficulties, many clinical psychology breeding programmes), changes in brain biochemistry
researchers carry out their research in what are known as associated with specific psychopathologies (such as changes
analogue experiments using analogue populations (see in brain neurotransmitter levels associated with psychotic-
Davey, 2003; Vredenburg, Flett & Krames, 1993). As we like symptoms), and the effects of drugs on psychopathol-
mentioned earlier (section ogy (such as the effect of antidepressants on brain
nalogue populations Populations that 3.2.2), analogue popula- biochemistry and behaviour) (e.g. Porsolt, Lepichon &
articipate in mental health research but _
tions are usually partici- Jalfre, 1977; Lavi-Avnon, Yadid, Overstreet & Weller, 2005).
) not have mental health diagnoses; they
ay be human or non-human animals.
pants without any mental Animal studies offer researchers the advantage of having
health problems and often complete control over the organism’s developmental his-
consist of a normal sample of healthy, student partici- tory (and so controlling genetic factors, and factors affected
pants. However, for experiments on psychopathology by feeding and living experiences), and permit the use of
undertaken with analogue populations to be valuable we some experimental methods that would be considered too
need to consider what makes them valid analogues of psy- intrusive to use with human participants (such as assessing
chopathology processes. There are at least three ways in the effects of electrical stimulation of the brain, and the
which we can argue that analogue studies are valid (see sampling of brain neurotransmitters). Nevertheless, even
also Research Methods Box 7.1). First, it is being increasingly though many types of animal research are legally licensed
argued that psychopathology is dimensional rather than by governments, it is an area of research that has become
Ga-8 PSYCHOPATHOLOGY
: * wy
increasingly controversial because of changing views on given a pill regardless of what is in the pill. Nevertheless,
the ethical implications of using non-human animals in suffice it to say here that the experimental method does
scientific experiments (Rollin, 2006; Rowan, 1997). provide a useful paradigm for assessing the effectiveness
Another important use of the experimental design in of different interventions, but we will discuss the com-
psychopathology research is in studies testing the effec- plexities and limitations of this approach when we discuss
tiveness of treatments for mental health problems. These treatment methods more thoroughly in the next chapter.
types of studies are often known as clinical trials and
clinicaltrials Experimental research attempt to test whether Summary
studies used to test the effectiveness of (1) a treatment is more The experiment is arguably the most powerful research
treatments for mental health problems. effective than no _treat- tool that we have because it allows us to draw conclu-
ment, (2) whether treatment A is more effective than sions about the direction of causality between vari-
treatment B, or (3) whether a newly developed treatment ables, and this is the first step towards putting together
is more effective than existing treatments. In a standard theories and models of how psychopathology is caused.
treatment efficacy experiment, researchers will allocate However, in order to provide valid results, experi-
clients or patients with a specific psychopathology (e.g. ments must be carefully designed and well controlled.
depression) to different experimental conditions. The Experiments are more than just data collection exercises,
experimental group will receive the treatment manipula- and the experimenter needs to manipulate important var-
tion whose efficacy is being tested (e.g. a form of psycho- iables in order to discover causal relationships between
therapy), and control groups will undergo other events and behaviour. This means that in some cases the
manipulations depending on what comparisons need to experiment can be too intrusive for use with clients suf-
be made. For example, if the researchers want to dis- fering psychopathology, and this means that many of
cover if the psychotherapy treatment is more effective our studies investigating psychopathology need to be
than a drug treatment, then a control group will receive conducted on analogue populations such as healthy vol-
the drug instead of psychotherapy. The researchers unteers and non-human animals.
will then measure symptoms at various points in time
after the two treatments to assess which is more effective
(e.g. Ward, King, Lloyd, Bower et al., 2000; Leff, Vearnals,
3.3.5 Mixed Designs
Brewin, Wolff et al., 2000). Sometimes, researchers may
want to assess whether a particular intervention is more One of the basic principles of experimental design is that
effective than simply doing nothing. However, this is not participants must be assigned to different groups on a ran-
as simple a comparison as it sounds. Logically you would dom basis. However, this principle can be set aside if the
imagine that a researcher would subject half the partici- research question being tackled requires a mixed design.
pants to the intervention, and allocate the other half to a For example, suppose we
mixed design Research which uses the
control condition in which they receive no treatment. wanted to see whether neg- non-random assignment of participants to
Suppose the researcher wants to assess the effectiveness ative mood caused anxious groups in an experiment.
of a drug treatment for depression. Just giving the exper- individuals to worry more
imental group a pill containing the drug and giving the than depressed individuals. In an experiment of this kind,
control group nothing has a number of problems. First, we would still be experimentally inducing negative mood
the experimental group may get better simply because (the experimental manipulation), but we would not be
they are being giving a pill and this leads them to expect assigning participants randomly to the experimental
to get better. This is known groups; we would want to ensure that in one experimen-
placebo effect The effect when partici- as a placebo effect, where tal group we only had anxious individuals and in a second
pants in a clinical trial show improvement
even though they are not being given a
a participant may improve experimental group we only had depressed individuals.
theoretically structured treatment. simply because the proce- We would select the participants pre-experimentally
dure they are undergoing on the basis of these attributes and assign them non-
leads them to believe they should or might get better. To randomly to each group. This is known as a mixed design
control for this possibility, a control group should be because (1) we are adopting elements from the experi-
included in which the participants are given a pill that con- mental approach (i.e. we are manipulating an independ-
tains an inactive substance (such as a sugar pill). This is ent variable), but (2) we are assigning our participants
known as a placebo con- non-randomly to the experimental groups. This is a design
placebo control condition A con-
trol group that is included in a clinical trol condition that controls that is used quite frequently in psychopathology research
trial to assess the effects of participant for the possibility that par- because the clinical psychology researcher may often want
expectations. ticipants may improve sim- to know if a particular variable will affect individuals with
ply because they are being different psychopathologies in similar or different ways. «
i
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY 85.
An example of a mixed design is a study by Sanderson, symptoms in individuals diagnosed with social phobia and
Rapee & Barlow (1989) investigating the effects of expec- panic disorder, but not in individuals diagnosed with OCD.
tations on panic disorder. They pre-selected two groups of This example illustrates how useful the mixed design
participants: one group consisted of individuals diagnosed can be when attempting to assess how individuals with
with panic disorder and the other group consisted of indi- different diagnoses or groups of symptoms will react
viduals with no psychiatric diagnosis. They then subjected to an experimental manipulation (such as a treatment
both groups to an experimental manipulation. In this case, intervention). However, we must always be aware of the
they asked all participants to inhale compressed air and fact that one of the variables in a mixed design (in this
but told them they were inhaling CO,, which could induce case the diagnostic groups) is not manipulated, and so
a panic attack. Even though the compressed air itself we cannot infer a direct causal relationship between the
could not have induced a panic attack, participants diag- diagnostic category and the effects of the manipulation.
nosed with panic disorder were significantly more likely to For example, in Figure 3.2 we cannot infer that the fail-
have a panic attack after the manipulation, suggesting that ure of the OCD group to improve after being given a pla-
in such individuals the mere expectation of a panic attack cebo is caused by the specific fact that they are suffering
is likely to induce one. from OCD because we have not explicitly manipulated
Mixed designs are frequently used in treatment outcome that variable. It could be that some other variable related
studies, where the effectiveness of a particular interven- to OCD is causing the failure to respond, such as hav-
tion is being assessed on individuals with different psychi- ing less faith in drug treatments generally, or individuals
atric diagnoses or with different severity of symptoms. with OCD may be more resistant to any treatment than
Figure 3.2 shows the results of a mixed design study carried those in the other groups.
out by Huppert, Schultz, Foa & Barlow (2004) designed to
assess the effects of administering a placebo pill to three
different groups of participants, each diagnosed with a dif- 3.3.6 Natural Experiments
ferent psychiatric disorder. In this study they found that
their experimental manipulation (the administration of a Most experiments are the result of a deliberate manipula-
placebo pill) significantly reduced the severity of reported tion carried out under controlled conditions by an experi-
menter. However, in the case of clinical psychology
research, nature may sometimes provide us with the
opportunity to observe the effects on behaviour of a nat-
ural manipulation. Natural experimentsusually allow us
to collect data on the
effects of events that we natural experiments Research which
allows researchers to observe the effects
would not usually be able on behaviour of a naturally occurring
to manipulate in the labo- ‘manipulation’ (such as an earthquake).
ratory, and such events
include natural disasters such as earthquakes and floods,
traumatic disasters or accidents such as the Kings Cross
tube station fire, or terrorist attacks such as those on the
World Trade Center in New York on 11 September 2001.
For example, van Griensven, Chakkraband, Thienkrua,
Pengjuntr et al. (2006) studied survivors of the 2004 tsu-
SCORE
SEVERITY
SYMPTOM
nami in southern Thailand, and found that the event had
caused elevated rates of symptoms of PTSD, anxiety and
depression in survivors of this event. Other studies have
used naturally occurring disasters as a tool to assess
whether such events increase psychopathology only in
3.0 . 7
individuals with particular characteristics. For instance,
social phobia OCD panic disorder Weems, Pina, Costa, Watts et al. (2007) found that PTSD
GROUP symptoms in children following the devastation caused
by Hurricane Katrina in the southern USA in 2005 was
FIGURE 3.2 Example of a mixed design. highest in those children who had high levels of trait anxi-
Source: Huppert, J.D., Schultz, L.T., Foa, E.B. & Barlow, D.H. (2004).
ety prior to the disaster.
Differential response to placebo among patients with social phobia,
panic disorder, and obsessive-compulsive disorder. American
Other variables that may play a part in the develop-
Journal of Psychiatry, 161, 1485-1487. ment of psychopathology include poverty and social
6 PSYCHOPATHOLOGY
~
deprivation, and these are clearly factors that we could not study was Freud himself, and many important features
easily manipulate in a controlled experiment. However, of psychoanalytic theory were based on Freud's detailed
Costello, Compton, Keeler & Angold (2003) took advan- observation and analysis of individual cases. One such
tage of the opening of a casino in an American Indian example is the famous case of Little Hans, a 5-year-old
reservation to study how poverty and conduct disorder in boy who had a fear of horses. Focus Point 6.1 describes
children might be linked (see section 16.2.2). The introduc- how Freud studied this single case in detail, and how it
tion of the casino provided income that moved many of enabled him to develop his view that many childhood
the local families out of poverty, and Costello et al. found fears were caused by a subconscious Oedipus complex.
that this resulted in a significant decrease in the symptoms In a different example in the 1940s, case studies of dis-
of conduct disorder in local children — but only in those turbed children provided the Austrian psychiatrist Leo
children whose families had benefited financially from the Kanner with a set of observations indicating a consistent
introduction of the casino, suggesting either a direct or set of symptoms that he called infantile autism, and which
indirect link between poverty and symptoms of childhood gave rise to the symptom classification that we currently
conduct disorder. know as autistic spectrum disorder (see Chapter 17).
Case studies are valuable in a number of different cir-
cumstances. First, they are useful when there are only a
few instances of a particular psychopathology available
3.3.7 Single-Case Studies
for study. This was the case when dissociative identity
For a variety of reasons, clinical psychology researchers disorder (DID) (multiple personalities) was first reported
may study just one individual, and gather the information as a specific disorder in the 1950s and 1960s, and an
and knowledge they require from detailed description and example of the use of case histories in the first descrip-
analysis of a single case. This may take the form of a com- tions of this disorder is provided in Case History 14.1.
prehensive case study in which the clinician gathers Second, case studies are also valuable for providing new
detailed information about insights into existing psychopathologies, and the detailed
case study An in-depth investigation of
an individual participant.
the individual, including information that a case study can offer often provides
details of symptoms, fam- new ways of looking at a particular problem and new
ily history, medical history, details of personal experi- facts that can subsequently be subjected to more rigor-
ences, educational background and suchlike, and then ous research methods (Davison & Lazarus, 1995), and
attempts to ascertain what light these details may cast on the example of Kanner’s discovery of infantile autism
an understanding of the individual’s psychopathology. through meticulous case studies of individual children is
In some respects, the case formulation that clinical prac- one such example. Third, the case study can also provide
titioners undertake when conducting therapy is a form detailed information that may disprove existing theories.
of case study in which they attempt to understand the We saw in section 3.1.2 that scientific hypotheses can
causes of an individual client’s symptoms in terms of often be refuted or falsified by a single finding, and case
that person’s cognitions, experiential history or personal histories are capable of providing individual findings that
relationships (see section 2.3). An alternative form of the are inconsistent with existing theories or explanations of
single-case study is the single-case experiment, in which a psychopathology. For example, some theories of eating
single-case experiment A single case a participant’s behaviour is disorders such as anorexia nervosa propose that dissatis-
study in which a participant's behaviour is observed and measured faction with body shape is a critical factor in developing
observed and measured both before and both before and after an an eating disorder. However, it would only take one case
after an experimental manipulation.
experimental manipulation. history describing an individual who developed anorexia
The researcher can then make some assumptions about without exhibiting any body dissatisfaction to question
what is happening by comparing the participant’s behav- the universality of this theory.
iour before the manipulation with their behaviour after Despite these benefits, the case study also has a sig-
the manipulation, and that individual then acts as both nificant number of limitations. First, and most impor-
experimental participant and control participant. tant, case studies lack the objectivity and control provided
by many other research methods. For example, the infor-
Case studies mation collected by a clinical researcher in a case study is
Before the development of sophisticated research likely to be significantly influenced by that clinician’s
designs, the case study was one of the most widely used theoretical orientation. Arguably, the detailed informa-
methods of collecting information about psychopathol- tion on Little Hans collected by Freud was significantly
ogy, and knowledge collected in this way often served influenced by Freud’s own theoretical views on psycho-
as the basis for the development of early theories of pathology, and it was quite likely that he collected and
psychopathology. One famous exponent of the case used only that information that was consistent with his
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY ae
existing views. Freud clearly spent much time finding out control condition) before introducing the experimental
about Little Hans’s childhood whereas more cognitively manipulation (the experimental condition), and behav-
or behaviourally oriented psychologists would focus on iour during baseline can then be compared with
current cognitions or those current environmental fac- behaviour following the manipulation. Most single-case
tors that might be maintaining Little Hans’s behaviour experiments use variations of what are known as the
(see section 1.3.2). Second, case studies are-usually low ABA or ABAB design. In the ABA design, an initial
on external validity. That is, the findings from one case baseline stage involves
are rarely generalisable to the observation and meas- ABA design A single-case experiment
xternal validity The extent to which the other cases. For instance, urement of behaviour which involves an initial baseline stage of
esults of a study can be extrapolated to observation and measurement of behav-
ther situations.
because of the subjective without any intervention
iour without any intervention (A), followed
nature of the information (A); this is then followed by a treatment or manipulation stage
collected by a clinician in a case study, how can we be by a treatment or manipu- where the experimental manipulation is
sure the supposed causes of psychopathology in that lation stage where the introduced and its effect on behaviour
case study will also be true for other individuals with experimental manipulation observed and measured (B). A final return-
to-baseline stage is then introduced (A) in
similar psychopathologies? Finally, we have just argued is introduced and its effect which behaviour is once more observed
that the case study can be valuable in providing evi- on behaviour observed in the absence of the treatment or
dence that could disprove a theory, but because of the and measured (B); subse- manipulation.
uncontrolled way in which case studies are collected it is quently a final return-to-
not particularly useful for providing evidence to sup- baseline stage is then introduced (A), in which behaviour
port theories. For example, a case study may indicate is once more observed in the absence of the treatment or
that a young woman with an eating disorder is dissatis- manipulation. The second baseline stage is included to
fied with her body shape. This is information that is con- ensure that any behaviour change that occurs in stage B
sistent with theories of eating disorders that assume a is caused by the manipulation and not any confounding
role for body dissatisfaction, but it is not evidence that factor such as a natural drift in behaviour over time.
differentially favours that theory because the case study In the ABAB design (sometimes known as a reversal
does not (1) rule out other explanations, or (2) indicate design), a second treatment ABAB design A single-case experiment,
that body dissatisfaction plays a critical role in causing or manipulation stage is similar to the ABA design, with the addi-
the eating disorder. introduced and provides tion of a second treatment or manipulation
extra power in demon- stage, providing extra power in demon-
strating that any changes in behaviour
Single-case experiments strating that any changes are explicitly due to the manipulation or
The single-case experiment has a particular value in psy- in behaviour are explicitly treatment.
chopathology research and is used relatively frequently. due to the manipulation or
The main value of this method is that it enables the treatment. Figure 3.3 provides an example of the use of
researcher (1) to undertake an experimental manipu- an ABAB design. This demonstrates the effectiveness
lation (and so potentially make some inferences about of providing a social story conveying information about
causal relationships between variables), and (2) to use appropriate mealtime behaviour for an individual with
one individual as both experimental and control partic- Asperger's syndrome (Bledisoe, Smith Myles & Simpson,
ipant. There is a particular advantage to using a single 2007). In this example, the effectiveness of the manipula-
participant and subjecting that individual to both experi- tion was demonstrated by the fact that behaviours
mental and control conditions. First, in many psychopa- returned to baseline levels following the withdrawal of
thology studies the use of a control group may mean the manipulation (the second A stage), and across all four
denying individual participants a treatment that they stages the frequency of the measured behaviour fluctu-
need. For example, if a researcher is attempting to assess ated in accordance with whether the experimental
the efficacy of a particular treatment, they would have manipulation was present (B) or not (A).
to compare the treatment with a control group who did One disadvantage to the ABAB design is that it alter-
not receive that treatment. This obviously raises ethical nates periods of treatment with non-treatment, and this
issues about withholding treatment from clients who may be problematic if the study is assessing the effective-
may benefit from it. Second, some psychopathologies are ness of a treatment that has important benefits for the par-
quite rare, and it can be quite difficult to gather enough ticipant (e.g. it prevents self-injurious behaviour or alleviates
participants to form groups of experimental and control distress). This can be overcome by using a multiple-
participants, and conducting an experiment on a single baseline design. There are two variations to this pro-
participant may be a necessity. cedure: (1) using a single multiple-baseline design An experimen-
The single-case experiment allows the experimenter participant, the researcher tal design in which the researcher studies
to take some baseline measures of behaviour (the can select two or more _ several behaviours
ata time.
PSYCHOPATHOLOGY
iP es St a Dl es Fl? 1 6 el Pe ee] can be overcome to some extent by using more than one
A B A B participant. If the treatment or manipulation is effective
67-4 ; ;
\ | | = Spills
across more than one participant then this increases the
5 t ft 7 i} =m= Mouthwipes chances that it will be generalisable to other individuals.
\ f \ ; 1
SS q ‘ 1 |
v \ f \ 1 } \ 1
Sov \4 $/ Ae+e [| \
3 f§ +++ ate 3.3.8 Meta-Analyses and
c y \ FRE 3
\ + AN 9ili es ec Systematic Reviews
2j ¥ O70 an get \ eae,
14 y \ oat Many different researchers frequently conduct studies
/ { \ f investigating the same or similar phenomena, so it is
SSS fas
Ie235 4576078) 9MONT 12 1314 lo 1617 18 [9:20.21
usually the case that we end up with many studies pro-
Days viding information on the same issue. For example, we
may want to know whether cognitive behaviour therapy
FIGURE 3.3 Example of a single-case experimental ABAB design.
(CBT) is a successful treatment for depression, and many
The participant in this study was a 13-year-old male with
different researchers may end up conducting studies and
Asperger's syndrome and attention deficit hyperactivity
experiments to this end. Some of these studies may con-
disorder (ADHD) (see Chapter 17) who exhibited a number of
vincingly demonstrate that CBT is effective, some others
eating-related problems (e.g. talking with mouth full, spilling
food, talking in a loud voice.). Days 1-7 show the baseline
may suggest that its effectiveness is marginal, and still
levels of spills (a ‘bad’ response) and mouthwipes (a ‘good’ others may fail to provide any evidence for its effective-
response) (the first Aphase). The intervention used (phase ness. So how do we decide which studies to believe, and
B) was a social story provided to the participant to help him how do we try to make am informed decision about the
improve his eating habits. The figure shows how good eating effectiveness of CBT in treating depression? Traditionally,
behaviours tended to increase and bad behaviours tended this task would have been undertaken in review articles
to decrease in frequency during the intervention phases, but in which the reviewer would collect together all the rel-
return to normal during baseline phases. evant studies, and try to make an informed judgement
Source: Bledisoe, R., Smith Myles, B. & Simpson, R.L. (2007). Use of across the whole range of studies and their results (e.g.
a social story intervention to improve mealtime skills ofan ado- Brewin, 1996; Marcotte, 1997; Laidlaw, 2001). However,
lescent with Asperger syndrome. Autism 7(3), 289-295. © 2007 by
this approach is likely to be highly subjective, and one
SAGE. Reprinted by permission of SAGE.
reviewer may significantly disagree with another about
the importance of individual studies. In addition, some
researchers with vested interests in particular types of
behaviours to measure and can target the treatment or treatment may consciously or unconsciously bias the
manipulation on one behaviour but allow the other way they interpret findings (e.g. those favouring drug
behaviours to act as control comparisons, or (2) the treatments for depression are likely to be less convinced
researcher can use multiple participants by first taking by studies demonstrating the effectiveness of CBT than
baseline measures from each (stage A), and then intro- others) (Field, 2013b).
ducing the treatment or manipulation (B) successively These problems with subjective reviews have led to
across the participants. The multiple baseline design attempts to develop more objective reviews using standard-
means that each individual within the study can receive ized review procedures and statistical methods. Meta-
the treatment for a maximum amount of time without analyses and systematic reviews are the outcome of this
compromising the experimental balance of the study process, and are now becoming accepted ways of objec-
(e.g. Thompson, Kearns & Edmonds, 2006). tively assessing the strength of findings across different
While the single-case experiment has a number of studies. A systematic review is a review of a clearly
significant benefits, it too also has some limitations. formulated question that
Most importantly, it is still a single-case study, so it may uses systematic and explicit systematic review A review of a clearly
be difficult to generalize the results to other individuals methods to identify, select, formulated question that uses systematic
with similar psychopathologies — just because a treat- and critically appraise rele- and explicit methods to identify, select, and
critically appraise relevant research, and to
ment works for one person does not necessarily mean vant research, and to collect collect and analyse data from the studies
it will work for another. Group designs overcome this and analyse data from the that are included in the review.
problem by using statistical inference across a number studies that are included in
of participants to determine the probability that the the review. Guidelines for collecting and reporting clinically
findings from the study will be generalisable to a larger relevant systematic reviews are provided by groups such as
population. However, the problem of generalisability PRISMA (Preferred Reporting Items for Systematic
s
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY Bo
Reviews & Meta-Analyses: http://www.prisma-statement ardised measure of the effect size An objective and standardized
-org/index.htm), QUORUM (Quality of Reporting Meta- magnitude of the effect measure of the magnitude of the effect
Analyses: Moher, Liberati, Tetzlaff, Altman & The PRISMA observed in a study (i.e. observed in a research study.
Group, 2009), and the American Psychological Association the difference in measured outcome between partici-
(MARS, Meta-Analysis Reporting Standards: Cooper, pants in a treatment or experimental group and those in
Maxwell, Stone, Sher & Board, 2008). Figure 3.4 provides appropriate control conditions), and the fact that it is
an example of a flow-chart provided by PRISMA for record- standardized means that we can use this measure to
ing and reporting how studies for a systematic review were compare the outcomes of studies that may have used
sourced and collated. different forms of measurement. Meta-analyses are now
In addition to a systematic review, a meta-analysis an almost accepted way of overviewing an area of stud-
attempts to detect trends across studies found through ies that address the same or a similar research issue, and
eta-analysis A statistically accepted systematic review that are particularly popular as a statistical tool for assessing
ay of assessing the strength of a particu- may have used different the effectiveness of interventions for psychopathology
|ae across a number of different procedures, different num- (for examples, see Cuijpers, van Straten & Warmerdam,
aS: bers of participants, differ- 2007; Hanrahan, Field, Jones & Davey, 2013; De Maat,
ent types of control procedures, and different forms of Dekker, Schoevers & De Jonghe, 2006).
measurement, and it does this by comparing effect sizes While many meta-analyses have been carried out spe-
across studies. An effect size is an objective and stand- cifically on the effectiveness of individual treatments and
PRISMA 2009 Flow Diagram
<
e}
= Number of records identified Number of additional records
| = through database searching identified through other sources
=
o
a,
aaa) Number of records after duplicates

removed
a
&
<&
5
vi Number of records Number of records
screened excluded
Number of full-text Number of full-text

2 articles assessed articles excluded, with
ir for eligibility reasons
Wes)
|
Number of studies
included in qualitative
Ga synthesis
ov
a] Number of studies
3 3 :
a) included in
= quantitative synthesis
(meta-analysis)
Wag)
FIGURE 3.4 PRISMA flow diagram.
An example of a flow chart for recording and reporting how studies for a systematic review are sourced and selected.
Source: Moher, D., Liberati, A., Tetzlaff, J., Altman, D.G. & The PRISMA Group (2009). Preferred reporting items for systematic reviews and meta-analyses:
The PRISMA statement. PLoS Med, 6(6), e1000097. DOI: 10.137 1/journal.pmed1000097 (for more information, visit www.prisma-statement.org).
90 PSYCHOPATHOLOGY
* ~~
interventions, the basis of comparison can be other factors the raw material for quali- quantitative methods Research methods
such as type of psychopathology being treated or the com- tative research is ordinary that place an important emphasis on accu-
rate and valid measurement of behaviour
parison of drug treatments generally versus psychother- language, and any analy-
and attempt to draw conclusions from
apy interventions. One of the earliest meta-analyses was a sis is verbal rather than sta- their studies on the basis of statistical
large-scale study carried out by Smith, Glass & Miller (1980) tistical. The raw data in inference.
assessing whether psychotherapies were more effective than qualitative studies are usu-
no treatment at all. From the results of their meta-analyses ally the participant’s own qualitative methods. Research methods —
they concluded that (1) a very wide range of psychothera- descriptions of themselves, that rely on the analysis of verbal reports
pies were more effective at reducing symptoms of psycho- their experiences, their feel- rather than on statistical analyses of quan-
pathology than no treatment at all, and (2), perhaps more ings and thoughts, their. table data.
controversially, that effect sizes did not differ significantly ways of communicating with others, and their ways
across different types of psychotherapies — implying that all of understanding the world. Study samples are often
psychotherapies were equally effective! (See Focus Point 4.4.) small, and data are collected using unstructured or semi-
Nevertheless, while a meta-analysis may seem like an structured interview techniques that can be analysed in a
objective solution to the problem of reviewing the findings variety of non-statistical ways. Qualitative methods are
from groups of studies, this method too has its limitations. particularly suited to clinical psychology research
First, meta-analyses frequently rely almost entirely on ana- because they enable the researcher to gain an insight
lysing the results of published studies, and published stud- into the full experience of psychopathology, including
ies are much more likely to have significant results than the sufferer’s feelings, ways of coping, and the specific
non-significant results (Dickersin, Min & Meinert, 1992). ramifications that the psychopathology has on everyday
This means that meta-analyses are likely to overestimate life (see Research Methods in Clinical Psychology Box
mean effect sizes because they are unlikely to include 3.1). In recent years, qualitative methods have provided
unpublished studies that are probably non-significant. information relevant to scale development, informed
The result is that they are probably biased towards claim- theories of psychopathology, and provided explana-
ing that a variable or treatment is effective when it may tions for unusual research findings and unusual case his-
not be (Field, 2013a, 2013b). Second, effect sizes will be tories (Hill, Thompson & Williams, 1997; Rennie,
influenced by the quality of the research (e.g. whether Watson & Monteiro, 2002; Nelson & Quintana, 2005;
the control conditions are adequate or whether outcome Miller & Crabtree, 2000; Harper & Thompson, 2011).
measures are accurate and sensitive), but meta-analyses Barker, Pistrang & Elliot (2002) provide a succinct
include all studies equally, and do not take into account illustration of the difference between qualitative and
the quality of individual studies. The researcher undertak- quantitative research:
ing a meta-analysis can overcome this problem by compar-
ing effect sizes in ‘well-conducted’ and ‘badly conducted’ A simplified illustration of the difference between
studies (Field, 2013a, 2013b), but this then involves the the quantitative and the qualitative approach is
researcher in making some subjective judgements about shown in the differing responses to the question
what is ‘good’ and ‘bad’ research (Eysenck, 1994). There ‘How are you feeling today?’ A quantitative ori-
is even the possibility that meta-analyses might become entated researcher might ask the participant to
a self-perpetuating form of analysis, with at least some respond on a seven-point scale, ranging from 1 =
studies now attempting meta-analyses of meta-analyses ‘very unhappy to 7 = ‘very happy’, and receive an
(e.g. Butler, Chapman, Forman & Beck, 2006)! answer of 5, signifying ‘somewhat happy’. A qualita-
tive researcher might ask the same person the same
question, ‘How are you feeling today?’, but request
3.3.9 Qualitative Methods an open-ended answer, which could run something
like “Not too bad, although my knee is hurting me
So far we have mainly discussed those research methods a little, and I’ve just had an argument with my boy-
that place an important emphasis on accurate and valid friend. On the other hand, I think I might be up for
measurement of behaviour and attempt to draw conclu- promotion at work, so I’m excited about that.’ In
sions from their studies on the basis of statistical infer- other words, the quantitative approach yields data
ence. These methods tend to be collectively known as which are relatively simple to process, but are lim-
quantitative methods, but there is a growing body of ited in depth and hide ambiguities; the qualitative
research methodologies in clinical psychology that do approach yields a potentially large quantity of rich,
place less emphasis on exact measurement and statistical complex data which may be difficult and time con-
analysis, and these are known as qualitative methods. suming to analyse. (Barker, Pistrang & Elliot, 2002,
Instead of emphasising mathematical analyses of data, p.73; reproduced with permission)
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY
re A QUALITATIVE STUDY OF DENTAL PHOBIA

ns.)
x<
0 This example is based on a paper by Abrahamsson et al. (2002) and gives you an insight into how qualitative
fea)
> methods might be used in clinical psychology research. The following sections describe the aims of the study,
UO how it was conducted, and how the results were analysed to provide a theoretical perspective on the experience
Oo of dental phobia.
=
Oo
as
UW> AIMS
>
WV To explore the situation of dental phobic patients and to investigate (1) how their dental phobia interferes with
a.
wal their normal routines, their daily functioning and their social activities and relationships, (2) what factors contrib-
< ute to the maintenance of their phobia, and (3) how they cope with their fear.
bee
==
sl STUDY SAMPLE
U
es Eighteen patients applying for treatment at a specialized dental fear clinic in Goteborg, Sweden. All patients were
WV currently refusing dental treatment because of their phobia.
ja)
\e)
= IN-DEPTH INTERVIEWS
-
La
= Audio-taped, open-ended interviews were conducted with each participant. The purpose of using open-ended
c interviews was to explore the situation of dental phobics as expressed by the participants themselves. An inter-
U view guide was used as a basic checklist to make sure that relevant topics were covered. These included onset of
ce
<x dental fear, family, experiences in dental care, health and effects on everyday life, coping strategies. Interviews
Lu were introduced with questions such as ‘Does your dental fear have an impact on your daily life?’‘In what way?,
Ww
Lud ‘What do you do/feel?’ and so on.
c
ETHICAL ISSUES
It was stressed that participation was voluntary, all data collected would be confidential, and the participant had
the right to end participation at any time. All participants completed and signed an informed consent form.
ANALYSIS OF DATA
Interview transcripts were analysed using grounded theory (see section 3.3). The aim of this method is to focus
on different qualities of phenomena in order to generate a model or a theory. Different qualities of phenomena
might include psychosocial processes, existing problems caused by dental phobia, how participants coped with
their problems, and so on. This process should be conducted with the original aims of the study clearly in mind.
The interviews were analysed line-by-line and broken down into segments reflecting their content. Segments
with similar contents were then grouped together to form more abstract categories.
EXAMPLES OF FORMING ABSTRACT CATEGORIES
One participant expressed the following: ‘What I’m most afraid of is that infections will spread. . . I've had a lot of
colds in the last year. . .|don’t know if it has anything to do with my teeth. | only know that I’ve waited much too
long. Another participant said: ‘The idea of having false teeth at 45, then I'd be at rock bottom. . . |don’t know if |
could handle it psychologically: Similar comments made by a number of participants led the researchers to cre-
ate the abstract category ‘Threat to own health’ to describe this group of responses.
Similarly, participants also provided responses of the following kind: ‘My worries about going to the den-
tist are a matter for me and me alone . . . maybe | could tell someone but they probably wouldn't care at all’
and ‘A friend said he had booked an appointment for me [at the dentist] and | went completely cold. When
PSYCHOPATHOLOGY
the time got nearer [for the appointment), | saw the date couldn't be right and understood that it was a joke’ These
and similar responses were grouped into the abstract category of ‘Lack of social support and understanding’
CONCLUSIONS
This analysis allowed the researchers to construct a model or theory of the experience of dental phobia, which is represented
schematically below. Four main categories of experience were developed: threat to self-respect and well-being, avoidance,
readiness to act, and ambivalence in coping. This provides a rich description of how dental fear affects the daily lives of these
individuals and how social and psychological factors interact to determine how they cope with this fear.
aa ae
AVOIDANCE READINESS TO ACT
Avoidance and suppression AMBIVALENCE Problem solving strategies

Factors preventing problem solving IN COPING Self-strength
Lack of social support and understanding Pee ae Social support
Source: Abrahamsson, K.H., Berggren, U., Hallberg, L.R. & Carlsson, S.G. (2002). Ambivalence in coping with dental fear: A qualitative
study. Journal of Health Psychology, 7,653-664. © 2003 by SAGE. Reprinted by permission of SAGE.
This example shows how qualitative methods are which may lead them to construct hypotheses suitable
non-quantitative, usually open-ended (in the sense that for study using quantitative methods.
the researcher does not know before the study exactly
what data they may collect), and enable the researcher Conducting and analysing qualitative studies
to begin to understand an individual’s lived experiences, Qualitative studies are not entirely unstructured, and
the feelings they have about their experiences, and the qualitative techniques specify ways in which data
perceptions and meaning they give to their experiences should be collected and analysed. First, unlike quan-
(Nelson & Poulin, 1997; Polkinghorne, 1983). Given titative methods that tend to emphasize the random
these characteristics, a typical qualitative study will selection of participants and allocation to experimental
involve detailed interviewing of participants to identify groups, qualitative methods tend to deliberately specify
themes involving feelings and the meaning that those groups of participants for sampling depending on the
participants give to their feelings. phenomenon or psychopathology the researcher is
The advantages of using qualitative methods are: interested in. For example, these may include individu-
(1) some aspects of psychopathology are difficult to als who have suffered childhood abuse, families with a
express numerically, and a qualitative approach allows member who is suffering a mental health problem, par-
data to be collected about more complex aspects of expe- ents of autistic children, and suchlike (Cresswell, 1998).
rience, (2) they permit intensive and in-depth study of Once selected, participants will then usually take part
individuals or small groups of individuals, (3) because in a semi-structured, open-ended interview in a relaxed
interviewing techniques are usually open-ended, the and comfortable interaction (Kvale, 1996). All interview
researcher may discover interesting things about a psy- questions would normally. be related back to the origi-
chopathology that they were not originally looking for, nal research question(s) posed prior to the study. For
and (4) they can be an extremely valuable source of instance, a research question might be ‘How do indi-
information at the outset of a research programme, and viduals with panic disorder cope with day-to-day living?’
provide the researcher with a rich source of information In this example, the interviewer can ask very general
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY Soke
questions or more specific questions that are derived feelings of individuals with dental phobia. The study also
from the original research question. A general ques- provided some higher level theoretical insights by suggest-
tion might be “What problems do you encounter each ing how several psychological and social factors interact to
day because of your panic attacks, and how do you cope determine how dental phobics cope with their fear
with them?’ A more specific question might be ‘How do (Abrahamsson, Berggren, Hallberg & Carlsson, 2002).
you feel about not being able to leave the house because Grounded theory can be used with data collected in a
of the possibility you might have a panic attack?’ In this number of forms, including interviews, focus groups,
kind of structure, the participant has the opportunity to observation of participants, and diary material. It is also an
respond to both general and specific questions. The gen- approach that allows a constant dynamic interaction
eral questions allow the participant to create their own between research and theory. For example, the study
picture of their experiences, and the specific questions reported in Research Methods Box 3.1 provided some the-
allow the researcher to obtain detailed information that oretical insights into how dental phobics coped with their
is relevant to the original research question. fear, and this theoretical
Once detailed responses from the interview have been insight can then provide the To read the article by Abrahamsson
collected, the researcher has the task of making sense of basis of a refined research | et al. on‘Ambivalence
in coping with dental fear’go to
the data, picking out consistent themes that emerge question and a subsequent | www.wiley-psychopathology.com/
in the participant’s responding, and deciding how these qualitative study pursuing | reading/ch3
themes might relate to the original research thisussue mn further details Wier sea eee ee
question that was posed. The first step is to break up the In summary, qualitative methods lend themselves
interview transcript into manageable and meaningful particularly well to understanding and describing many
units. There are a number of ways to do this (Giorgi, 1985; aspects of psychopathology, and are becoming increas-
Merleau-Ponty, 1962), but for simplicity we will describe a ingly used in clinical psychology research (Barker,
commonly used approach known as grounded theory. Pistrang & Elliot, 2002). They are useful for collecting
Grounded theory is an data on everyday feelings and experiences associated
rounded theory An approach to qualita- approach to qualitative with psychopathology, and data collected in this way can
ve analysis which involves identifying analysis that was developed make a significant contribution to theory. In this section
ynsistent categoriesorthemes within the
ata, then building on these to provide
by Glaser and Strauss of the chapter it has not been possible to convey the full
ore abstract theoretical insights into the (1967). It involves identify- range of qualitative methods available to the researcher,
nenomenon being studied. ing consistent categories or nor to convey the important philosophical and episte-
themes within the data, mological underpinnings of many of these techniques
and then building on these to provide more abstract theo- (see Willig, 2001; Henwood & Pidgeon, 1992). However,
retical insights into the phenomenon being studied. qualitative methods are not just an alternative to quanti-
Research Methods Box 3.1 provides a detailed specific tative methods; the two can be combined in a useful and
example of how grounded theory has been used to under- productive way in clinical psychology research. Examples
stand how dental phobics cope with their psychopathol- include using qualitative data to clarify quantitative find-
ogy, and how it affects their day-to-day living. As we can ings, beginning research in a new area with qualitative
see, this study was able to identify a number of consistent research but moving this on using quantitative methods,
themes that emerged from the interview data, and pro- or using qualitative data to develop quantitative meas-
vided a rich insight into the everyday experiences and ures (Barker, Pistrang & Elliot, 2002).
SELF-TEST QUESTIONS
© What are the main aims of correlational designs?

° What is the difference between a positive and negative correlation?
e Can you identify how a scattergram can tell us how two variables are related (see Figure 3.1 )?
© Howdo longitudinal and prospective studies differ from correlational studies?

° Can you describe the different ways in which prevalence rates can be measured?
e Which research design is the most effective for identifying causal relationships between variables?
° Can you describe what an independent variable (IV) and a dependent variable (DV) are?
° Experimental designs use control groups. What are they and how would you design one?
94 PSYCHOPATHOLOGY
e What are the demand characteristics of an experiment?

e What are clinical trials?
° What is a placebo control condition?
* Can you describe what a mixed design is?
® What are the advantages and drawbacks of using case studies in research?
* What is an ABAB design?
° How do multiple-baseline designs differ from ABAB designs?
° How is effect size used to overview studies in a meta-analysis?
* What are the main differences between quantitative and qualitative research methods?
e What is grounded theory?
SECTION SUMMARY
3.3 RESEARCH DESIGNS IN CLINICAL PSYCHOLOGY
This section of the book has reviewed the various research methodologies that are available to the clinical psychology
researcher. All of these methodologies include ways of collecting information and, in many cases, ways of interpreting that
information. As we indicated at the outset of this section, the type of research method you adopt will depend very much on
(1) the nature of the research question you are asking (do | want to discover whether there are causal relationships between
variables, or do |just want to know if two variables are related in some way?), (2) the nature of the population you are studying
(e.g. do you have lots of participants available orjust a few?), and (3) whether your research is at an early or advanced stage (if
it is the former you may want to use qualitative methods; if the latter, then quantitative methods may be more appropriate).
The key points are:
© correlational designs enable the researcher to determine if there is a relationship between two or more variables.
e A correlation coefficient can range from +1.00 through 0.00 to —1.00, with +1.00 referring to a perfect positive correlation
between two variables and —1.00 denoting a perfect negative correlation.
e Both /ongitudinal and prospective studies take measures from the same participants at two or more different times in order
to specify the time-relationships between variables.
e Epidemiological studies provide details about the prevalence of psychological disorders.
e Experiments involve the researcher manipulating one of the variables (the independent variable) and then measuring the
effect of this on behaviour (the dependent variable).
e To be valid, experimental studies need to use appropriately designed control conditions.
¢ Clinical trials are types of experiments that are used to test the effectiveness of treatments.
¢ Aplacebo effect is when a participant in a clinical trial shows improvement even though they are not being given an effec-
tive treatment.
e Mixed designs use the non-random assignment of participants to groups in an experiment.
¢ Natural experiments allow researchers to observe the effects on behaviour of a naturally occurring ‘manipulation’ (such as
an earthquake).
© Single-case studies allow researchers to collect data from just one individual.
¢ The single-case experiment uses ABA, ABAB or multiple-baseline designs to carry out controlled experiments on individual
participants.
¢ Meta-analyses are statistically accepted ways ofassessing the strength of a particular finding across a number of different studies.
° Systematic reviews are reviews that use systematic and explicit methods to identify, select, and critically appraise relevant research.
* Qualitative methods use ordinary language as their raw material, and adopt verbal rather than statistical analyses.
* Grounded theory is one particular example ofaqualitative method that is used extensively in clinical psychology research.
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY 95
3.4 ETHICALISSUES IN (4) who will know about the participant’s involvement in
the study and whether confidentiality will be maintained,
CLINICAL PSYCHOLOGY (5) whether participation is voluntary or a payment is
being offered, and (6) a clear indication to the participant
RESEARCH that they can withdraw from the study at any time and
without prejudice if they so wish. Participants should
also be given the opportunity to ask questions about the
It would be almost impossible to do psychological
study in order to enable them to make an informed deci-
research in general, and clinical psychology research in
sion about participation, and they should also be given
particular, without the individuals who are needed to act
sufficient time to reflect on this information.
as participants. However, the people that we recruit as
All of this information is usually provided in a written
participants have rights that need to be protected, they
informed consent form that the participant must then
have a dignity that needs to be preserved, and their well-
sign to acknowledge that
being needs to be maintained. These all form part of the informed consent form See Informed
they understand what the consent.
ethical deliberations that need to be fully considered
study involves and that
before we begin a particular piece of research. Examples
they formally consent to take part in the study. A simple
of ethical issues that might be encountered in clinical
example of an informed consent form is provided in
psychology research include: ‘Is it harmful to induce
Figure 3.5. Consent forms may be more or less detailed
panic attacks in an experiment?’ “What will be the effect
depending on the complexity of the study and the nature
of inducing a negative mood in my participants, and how
of the participants required for the study. For example, if
can I ensure this doesn’t affect them after the experi-
the study is one that requires the participation of indi-
ment?’ ‘Is giving a participant a placebo pill instead of an
viduals already undergoing treatment for mental health
active drug tantamount to withholding treatment?’ ‘Does
problems, then the participant may need to know how
my experiment involve deceiving the participants in any
their involvement in the study might affect their treat-
way? ‘How can I be sure that my participants’ involve-
ment and whether it might have an adverse effect on
ment in the study is truly voluntary?’ Most organisations
their existing mental health condition. In such circum-
that host clinical psychology research (such as universi-
stances, informed consent forms might also want to
ties or hospitals) now have ethical committees that are
include further details such as (1) the identity of the
required to vet all research proposals to check that they
researchers and their contact details, (2) a clear descrip-
meet basic ethical standards and protect the participants
tion of any complex procedures (e.g. any procedures
in the research. Ethical issues in clinical psychology
that may be invasive), (3) the identity of others who
research fall under three main headings: (1) Informed
might be directly or indirectly associated with the
consent, (2) Causing dis-
formed consent Detailed information research (e.g. organisations that might be funding
out an experiment is given to potential tress or withholding bene-
the research, such as drug companies or mental health
ticipants to enable them to make an fits, and (3) Privacy and
formed decision to participate. oat charities), (4) reasons why the participant has been
' aie contidentality selected (in case the participant may feel stigmatized by
being approached to participate), (5) the possible harms
3.4.1. Informed Consent and benefits of the procedure (especially if the participant
has an existing mental health problem), and (6) details of
Researchers should always properly inform participants any future use of the data that is collected from the study.
about what it is they will be participating in, what they The issue of informed consent becomes problematic
will be asked to do, and what experiences they might have when an individual’s understanding of the information
while taking part in the study. This information needs to provided in a consent form is limited. This is particularly
be detailed enough for the researcher to be sure that the so with children and certain categories of adults — for
potential participant can make a rational and informed example those who have learning disabilities or exhibit
decision about whether to participate or not. This psychotic symptoms (Bersoff & Bersoff, 1999; Fisher,
means that the information provided about the study Cea, Davidson & Fried, 2006). In the case of children and
should be as detailed as possible, and — importantly - adolescents below the age of 17 years, the written con-
it should be couched in a language that the participant sent of the parent or guardian is required as well as either
will understand and not include technical jargon that is the verbal or written agreement of the child.
only likely to be comprehensible to the researcher. This Obtaining full informed consent of a participant also
information should include (1) details of the purpose of becomes somewhat problematic if informing the partici-
the experiment, (2) a description of the procedures the pant of all the details of the study is likely to significantly
participant will encounter, (3) the duration of the study, affect the results. For example, participants in many drug
96 PSYCHOPATHOLOGY
%
Consent Form
STUDY TITLE:
STUDY APPROVAL REFERENCE
This study will take approximately 15-20 minutes and consists of
listening to music, reading vignettes on a computer screen and
taking part ina short task.
Thank you for agreeing to take part in this study. Your formal
consent is required to confirm that your participation is voluntary
and that you have the right to withdraw at any time.
| agree to take part in the above research study. | have had the study explained to me
and | have read and understood the Explanatory Statement, which | may keep for my
records. | understand that agreeing to take part means that | am willing to:
(1) Listen to music
(2) Read vignettes on a computer screen

(3) Take part in short task
| understand that any information | provide is confidential, and that no information

that | disclose will lead to the identification of any individual in the reports on the
study, either by the researcher or by any other party.
| consent to the processing of my personal information for the purposes explained to me. |
understand that such information will be treated in accordance with the terms of the Data
Protection Act 1998.
| understand that my participation is voluntary, that |can choose not to participate in

part or all of the study, and that | can withdraw at any stage ofthe study without being
penalized or disadvantaged in any way.
Sign:
Date:
FIGURE 3.5 Above is an example ofasimple informed consent form that would be used in a study looking at the effect of music-
induced mood changes on a simple written task.
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY eo
treatment studies are given placebo pills to assess what to describe or experience their symptoms during the
improvement might occur if they believe they are receiv- study. In other cases we intentionally try to recreate
ing a drug but in fact are not. This involves some decep- the conditions that cause psychopathology symptoms in
tion on the part of the researcher in the sense that they order to understand the causes of that psychopathology.
aception The act of deceiving. have not told those taking Both of these cases involve the researcher in important
the placebo that it is not an ethical considerations. In clinical psychology research,
active drug. At the very least, this means that the partici- distress to the participant can be caused in a number of
pant is not being given all the information about what is ways, for instance by (1) asking them to relate or relive
happening in a study, and if this is the case, can they then distressing memories or experiences (e.g. in a study
make an informed decision about whether to participate? looking retrospectively at experiences that may have
This is a moot point, and is important because many psy- preceded a psychopathology), (2) subjecting them to
chological studies depend for the validity of their findings experimental manipulations that may cause stress, anxi-
on deceptions of this kind. Many researchers overcome ety or negative feelings generally (e.g. a mood induction
this problem by withholding some information from par- procedure), (3) requiring a participant to reveal infor-
ticipants if providing that information is likely to affect mation about themselves that may be embarrassing
the outcome of the study. They will then offer the partici- or humiliating (e.g. in questionnaire studies investigat-
pant a full debriefing at the end of the study, explaining ing sexual behaviour), (4) presenting physically aversive
any deception and offering any withheld information. If stimuli such as electric shocks or loud noises (e.g. in fear
the participant is unhappy about this, the researcher can conditioning studies), or (5) subjecting the participant
then offer them the opportunity to withdraw their con- to circumstances and situations that may be a threat to
sent to use their data (Bersoff & Bersoff, 1999). their self-image or self-esteem (e.g. in situations where
Finally, it is worth reiterating that all efforts should be participants may be given real or false feedback suggest-
made to ensure that a participant's involvement in a study ing their performance on a task is poor or substandard).
should be truly voluntary. There should be no explicit or Even asking a participant to complete a validated ques-
implicit coercion. How often has a student trying to finish tionnaire measuring trait characteristics such as anxiety
off their undergraduate project gone into the corridor or or depression might be distressing. For example, answer-
coffee bar and tried to per- ing questions about the frequency of suicidal ideation in
oluntary Of one’s own free will or design; suade someone to take a questionnaire such as the Beck Depression Inventory
ot forced or compelled.
part in their experiment — ‘J (BDI) may trigger distressing thoughts for someone who
only need half a dozen more people, they plead! Is any- is either currently depressed or knows someone who has
one approached in this way a genuine volunteer if they attempted suicide.
agree to take part? Probably not, because at least some Because of these potential harms that could affect
will feel obliged to participate in order to ‘help’ the student participants, researchers have an obligation to be vigi-
out. Similar problems in obtaining truly voluntary consent lant throughout a study for any indication that the par-
are found in many other situations, such as studies that ticipant might be experiencing distress. If the researcher
involve hospital in-patients, prisoners, and even under- does notice indications of distress, they should termi-
graduate psychology students who have to take part in nate the study or suspend data collection until the par-
research studies to gain course credits for their degree pro- ticipant feels able to continue. A basic rule is that at the
gramme! Some service providers (such as the NHS) have end of the study the participant should certainly be in no
developed a more imaginative and inclusive way of seek- worse a psychological or physical state than when they
ing participant involvement in clinical research, and this is started it. In experimental studies that are likely to cause
by involving service users (e.g. clients and patients) in the stress (such as fear conditioning studies, negative mood
whole research process, from design, through participa- manipulations, studies involving negative or threatening
tion to the reporting of findings. Also, at a national level, materials) the experimenter should always ask the partic-
INVOLVE is a group dedicated to facilitating public par- ipant at the end of the study how they are feeling. If they
ticipation in research designed to improve well-being and claim they feel distressed, stressed, anxious, sad, or have
reduce social problems generally (www.involve.org.uk). other negative feelings, then the experimenter should be
able to actively offer some means of dealing with these
feelings. This may include offering the opportunity to
3.4.2 Causing Distress listen to a relaxation tape or music designed to induce
positive mood, or in more severe cases the experimenter
or Withholding Benefits may want to provide information about counselling ser-
In many cases it is difficult to do clinical psychology vices that can be made available to the participant (e.g.
research without asking someone with a psychopathology if it is a study taking place on a University campus, the
98 PSYCHOPATHOLOGY
+ ~
experimenter may be able to provide the location and can decide not to provide privacy The right of participants to decid
phone number of the university counselling service). some forms of information not to provide some forms of information |
to the researcher if they so to the researcher if they so wish (e.g. their
Clearly, making people distressed in a research study is
age or sexual orientation).
not an acceptable end in itself, and the researcher must wish (e.g. their age or sex-
always weigh up whether the potential benefits of their ual orientation), and confi-
research (in terms of its contribution to knowledge) out- dentiality means participants in psychological research have
weighs the potential distress that may be caused to some a right to expect that information they provide will be treated
participants. confidentially. For example,
On the other side of the coin, a study may not cause if a piece of research is even- confidentiality The right of participants —
in psychological research to expect that
distress but may involve the active withholding of bene- tually published in a scien-> information they provide will be treated i
fits for the participant. This is especially the case with tific journal, participants confidence. :
studies attempting to assess the effectiveness of treat- who contributed to the
ments for psychopathology. For example, let us assume a study should not be identifiable. In the event that confi-
researcher is attempting to find out if a new psychother- dentiality and/or anonymity cannot be guaranteed, the
apy is effective for treating depression. The study would participant must be warned of this in advance of agreeing
involve participants diagnosed with depression and some to participate. Indeed, according to legislation in many
would be allocated to the experimental condition and countries (such as the Data Protection Act in the UK) infor-
receive the new psychotherapy while for comparison mation obtained about a participant during a study is con-
purposes others would need to be allocated to control fidential unless otherwise agreed in advance. In many
conditions that did not receive the new psychotherapy. cases, such as questionnaire studies, researchers will ensure
This raises a significant ethical issue. Should we withhold that all data collected are anonymous, and participants will
effective treatment for someone suffering depression usually only have to provide basic demographic informa-
simply because we need to allocate them to a no treat- tion (e.g. sex, age, and so on) that will not usually allow
ment control condition? A similar issue is that such them to be identified. In some other circumstances (such as
studies also have very nar- longitudinal studies, where participants may have to be
no treatment control condition The
row inclusion criteria. contacted to provide data on more than one occasion) it
allocation of participants to a control
condition, in which they do not receive the That is, to be able to inter- may be necessary to retain some information that will
treatment under investigation. pret their results clearly, identify the participant over the course of the study, but
the researcher would want this can be erased once all the data are collected. In studies
to ensure that the study only included participants who where personal or sensitive information is being collected
had a simple diagnosis of depression. Interpreting the (such as studies involving participants with mental health
data would be complicated if the study also included par- problems), the informed consent form should clearly state
ticipants who were diagnosed with other disorders that who will have access to the data and the findings of the
were comorbid with depression. This means that those study. If interviews with participants are audiotaped or
with more complex psychopathologies are likely to be videotaped, it should be clear to the participant who will
excluded from treatment outcome studies and so denied hold those tapes and how long they will be retained before
access to the treatment programme associated with the being destroyed.
study. Researchers tend to try to overcome the ethical However, issues of confidentiality and anonym-
issues involved in allocating a patient to a no treatment ity become problematic when the participant discloses
condition by adopting what are called waiting-list con- information about illegal activities or events or circum-
trols. That is, they use patients who are on a waiting list stances that may be detrimental to an individual’s psy-
for treatment as their no treatment control condition. chological or physical health. For example, what should
Such individuals would not be receiving treatment any- a researcher do if a participant tells them about suicidal
way during the time that they are on the waiting list. intentions, serious drug abuse, criminal activities, physi-
This may be a suitable way out of this particular ethical cal or sexual abuse and the like? Certainly, a researcher
dilemma, but as the reader is probably aware, it is a solu- has a legal and moral obligation to consider appropriate
tion that paradoxically is available only as long as service action if they believe a crime has been committed or is
providers are unable to offer immediate treatment! intended, and in some countries it is mandatory by law,
for example, to report information about criminal activi-
ties such as child abuse (Becker-Blease & Freyd, 2006).
Perhaps it is important to be clear that confidentiality is
3.4.3 Privacy and Confidentiality
not the same as secrecy, and is therefore not absolute. If
All participants in psychological research have a right to pri- the researcher believes that a study might reveal infor-
vacy and confidentiality. Privacy means that participants mation about illegal or immoral activities, then they -
CHAPTER 3 RESEARCH METHODS IN CLINICAL PSYCHOLOGY le 99S
might inform participants at the outset of the study that researcher, and no one can morally turn a blind eye
(1) confidentiality is not absolute, and (2) the researcher knowing that others may be harmed or an individual
will inform the participant if confidentiality is broken. is in a state of life-threatening distress. Because of their
However, providing such information at the outset of knowledge of psychopathology and the provision of
a study is likely to mean that participants will be sig- treatments, most clinical psychology researchers are
nificantly less willing to provide sensitive information usually in the privileged position of being able to offer
(Bersoff & Bersoff, 1999). at least some kind of support and guidance to those dis-
Finally, what should a researcher do when a par- closing information indicating serious distress. As a con-
ticipant provides information that they are likely to sequence, a researcher may be able to suggest treatment
harm themselves or others or are seriously distressed? or referral to an appropriate support service immedi-
This obviously requires a judgement on the part of the ately after the study.
SELF-TEST QUESTIONS
e What is informed consent?
° What ethical issues need to be considered when a research study may cause distress to a participant or lead to the with-
holding of benefits?
® What issues of privacy and confidentiality should be considered when designing and conducting a research study?
SECTION SUMMARY
3.4 ETHICAL ISSUES IN CLINICAL PSYCHOLOGY RESEARCH
No description of research using human participants is complete without a thorough discussion of ethical issues. Proper ethi-
cal procedures are designed to protect the rights, dignity and well-being of participants in research, and are a necessary part
of any clinical psychology research project. Ethical issues can be grouped under three broader headings, namely: (1) informed
consent (e.g. ‘are the participants fully informed about the study and can they freely and voluntarily give their informed con-
sent to participate?’); (2) causing distress or withholding benefits (e.g. ‘what is the risk that a research procedure will cause a
‘participant harm or distress, and how can we avoid this?’); and (3) privacy and confidentiality (e.g. ‘are the participants’ rights
to privacy and confidentially being properly respected?’).
The key points are:
e Participants in clinical psychology research have rights that need to be protected, a dignity that needs to be preserved, and
a well-being that needs to be maintained.
© The informed consent of participants should always be obtained before they take part in a study.
© Participation in any research study should be voluntary.
e Researchers have an obligation to be vigilant throughout a study for any indication that the participant might be experi-
encing distress.
e All participants in psychological research have a right to privacy and confidentiality.
3.5 RESEARCH the symptoms of psychopathologies and the feelings

and experiences of those who suffer with mental health
METHODS IN CLINICAL problems, (2) understand the causes of psychopatholo-
gies, (3) assess the efficacy of interventions developed to
PSYCHOLOGY REVISITED treat psychopathology, and (4) assess the effectiveness of
services provided to treat and support those with mental
Research is an important and central feature of clinical health problems (known as evaluation research or clini-
psychology. Research techniques allow us to (1) describe cal audit). Different research methods may be based on
0028, PSYCHOPATHOLOGY
+ %
different theories of knowledge, and a theory of knowl- depend very much on the nature of the research question
edge represents a way of trying to understand the world. being asked. For example, correlational and longitudinal
Many of the research methods we have described in this methods are useful for determining if there is a relationship
chapter are based on the scientific method espoused by between two or more variables, the experimental method
Karl Popper, and require that research results should be is useful for identifying causal relationships between vari-
replicable and that theories should be experimentally test- ables, case studies provide important ways of studying a
able. However, even within the realm of clinical psychol- phenomenon when the number of available participants
ogy there are many who feel that the scientific method is restricted, and qualitative methods are useful for gaining
is not well suited to exploring many of the important an insight into the full experience of psychopathology or
aspects of psychopathology such as the phenomenology beginning new research in an area. The final and essential
of psychopathology. part of a description of research methods in clinical psy-
We have then described in detail a range of research chology is a discussion of ethical issues, and these are vital
methods that are available to the clinical psychology in the protection of the rights, dignity and well-being of
researcher, and the type of method adopted will usually those who participate in clinical psychology research.

Reading Activity
Journal article: Condi- e Conducting Activity 3.1

tioned emotional experiments in Activity 3.2
reactions psychopathology
Activity 3.3
Author blog: An effect is
Self-test questions
not an effect until it is
replicated (pre-cognition Revision flashcards
or experimenter Research questions
demand effects)
Journal article:
Ambivilence in coping
with dental fear
Glossary key terms
Clinical issues
References
4 Treating Psychopathology
To access the online resources for this chapter go to ~

This chapter discusses the reasons for treating psycho-

pathology, the different theoretical approaches to treat- 4.1 THE NATURE AND FUNCTION OF TREATMENTS
ment, and how we attempt to evaluate whether treatment FOR PSYCHOPATHOLOGY 103
is successful or not. The first section describes six differ-
ent theoretical approaches to treatment and the basic 4,2 EVALUATING TREATMENT 118
principles on which each of these approaches are based.
We then discuss some of the modes of treatment deliv- : 4.3 TREATING PSYCHOPATHOLOGY REVIEWED 125
ery, many of which have been developed in recent years.
Finally, we discuss ways of evaluating treatment and cover
issues about what constitutes a therapeutic gain, how
long it may take to achieve a successful outcome, and
how therapeutic gains should be measured. We end the
chapter by describing some of the methodologies that
are currently used to objectively assess the effectiveness
of treatments for psychopathology, and discuss whether
all types of treatment interventions are equally effective
(known as the ‘Dodo Bird Verdict’).
OIE PSYCHOPATHOLOGY
LEARNING OUTCOMES
1. Describe some of the reasons for wanting to treat 3. Describe and evaluate at least three to four
psychopathology. different modes of delivery for treatments of
2. Describe and compare and contrast the basic psychopathology.
theoretical principles on which at least four 4. Critically assess methods for determining the
different types of psychotherapy are based. effectiveness of treatments for psychopathology.
| was a 22-year-old trainee working for a publishing company in London, and | was obsessed with food. |made a pact with myself
to limit myself to less than 700 calories a day. This worked well for awhile, but then | started binge eating, and my fear of gaining
weight led me to make myself sick. Sometimes up to five or six times a day. This left me totally drained — both emotionally and
physically, and my relationship with my partner began to go downhill rapidly. | really hated myself, and | felt fat and disgusting
most days. Ifonly |felt thinner |would feel better about myself. My GP eventually referred me to a clinical psychologist, who helped
me to understand how my thinking was just plain wrong. He explained to me how | evaluated my self-worth purely on the basis
of my weight and body shape. My thinking was also ‘black and white’—| believed that foods were either goodor, if not, they were
‘vad: During therapy|learnt to identify and challenge my irrational thoughts about food and eating, this helped me to begin to
eat relatively normally again, and | began to feel less anxious and worthless. What amazed me most was that eating normally
didn’t mean | put on weight, and |felt in control again - the first time for years. All this was so wonderful that | became anxious
about the possibility of therapy ending and that I'd simply go back to starving and bingeing. But | was encouraged to practise
anumber of coping strategies and learnt what | should do in circumstances where | felt |might relapse back into my old ways.
Elly’s Story
as those involving depression, stress and anxiety-based

Introduction
problems. In most cases, this support will usually be in
Psychopathology can take many forms and involve the form of suitable medication, but it may also take the
anxiety, depression, worthlessness, guilt, and feelings of form of providing access to stress-management courses,
lack of control, amongst others. For many people these short-term counselling or psychotherapy, access to self-
feelings become so intense that they cause personal dis- help information or even computerized CBT (e.g. van
tress and significantly impair normal daily functioning. Boeijen, van Oppen, van Balkom, Visser et al., 2005). In
Some people are able to deploy adaptive coping strate- other cases, it may be necessary for the individual to be
gies that allow them to successfully negotiate such peri- referred for more specific and specialized treatment, and
ods in their life (e.g. by seeking help and support from the nature of this treatment may often depend on the
friends and family, or using problem-solving strategies to nature and severity of that person’s symptoms. This is
deal with life problems that may be causing their symp- a fairly standardized route by which individuals suffer-
toms). Others may be less able to cope constructively, ing psychopathology come into contact with the treat-
and choose less adaptive means of dealing with their ment methods required to alleviate their symptoms and
symptoms, such as resorting to substance abuse and their distress. Others may simply decide to by-pass the
dependency or deliberate self-harm. Whatever route health services available in their community and directly
an individual may take, the distress and disruption that approach an accredited counsellor or psychotherapist
symptoms of psychopathology cause will often lead an who can privately supply the treatment services they
individual to seek professional help and support for their require. Whichever route is followed, the aim is to find
problems. The first port of call is usually the individual’s a suitable specialist who can successfully alleviate the
doctor or GP, and the GP may be able to offer sufficient symptoms of psychopathology and ease the distress that
help to deal with acute bouts of psychopathology such is experienced.
CHAPTER 4 TREATING PSYCHOPATHOLOGY 103
4.1 THE NATURE AND accredited therapists will now also have to demonstrate
that they have periodically engaged in continuing profes-
FUNCTION OF TREATMENTS sional development (CPD). That is, they must demonstrate
that they regularly update their knowledge of recent
FOR PSYCHOPATHOLOGY developments in treatment techniques. If a therapist is
unable to demonstrate that they are actively engaged in
CPD, then they may be in danger of losing their status
Elly’s story provides her personal account of how therapy
as a legally registered practitioner. This has meant that
helped to alleviate her eating problems, provided her
practitioners have become much more eclectic in the
with insight into the thought patterns that gave rise to
types of treatment they will offer as they learn new treat-
her psychopathology, and how she learnt to cope with
ment methods through the need to demonstrate their
situations that might give rise to relapse. Based on the
continuing professional development. While some prac-
example in Elly’s story, treatments for psychopathology
tising therapists may also use the research literature as
will usually possess some, if not all, of the following
a way of updating their therapeutic skills, most rely on
characteristics: (1) they can provide relief from the dis-
information from less formal sources, such as colleagues,
tress caused by symptoms, (2) they can provide the client
professional newsletters, workshops and conferences
with self-awareness and insight into their problems,
(Goldfried & Wolfe, 1996).
(3) they enable the client to acquire coping and problem-
Secondly, treatments may be chosen largely on the
solving skills that will prevent similar problems occur-
basis that they are effective at treating a certain type of
ring in the future, and (4) they attempt to identify and
psychopathology. In the UK, the National Institute for
resolve the causes of the psychopathology, whether
Health and Care Excellence (NICE) recommends treat-
those causes are recognized as problematic ways of
ments for specific psycho-
behaving, problematic ways of thinking, or problematic
pathologies on the basis National Institute for Health and Care
ways of dealing with or assimilating life experiences.
that their effectiveness is Excellence (NICE) An independent UK
Many treatments only possess some of these characteris-
evidence-based and empir- organisation responsible for providing
tics. For example, many drug treatments for psychopa- national evidence-based guidance on
ically supported by scien- promoting good health and preventing and
thology will have a palliative effect (i.e. reduce the
tifically rigorous research treating ill health. \5 >
severity of symptoms and
alliative effect The reduction of the (see also Focus Point 3.1),
so alleviate distress), but
verity of symptoms and alleviation of and we will discuss some of these recommendations in
they may only rarely pro-
stress. ne. e later chapters when we discuss treatment programmes
vide the client with insight
for specific psychopathologies. Nowadays, most types of
into their problems. Some other therapies may serve the
theoretical approach have been adapted to treat most
primary purpose of helping the client to achieve insight
psychopathologies, or at least some aspect of most psy-
into their problems (e.g. psychodynamic psychothera-
chopathologies and these will be discussed in detail in
pies), but it does not always follow that this insight will
the treatment sections of each ensuing chapter.
bring about behaviour change or provide suitable coping
skills (Prochaska & Norcross, 2001). Still other therapies
may provide effective ways of changing behaviour (such
as many behaviour therapies), but do not necessarily 4.1.1 Theoretical Approaches
provide the client with insight into the causes of their to Treatment
problems.
The treatment that is provided for a psychopathol- Traditionally, popular therapies have been developed
ogy will depend on at least two factors: (1) the theo- around a relatively small number of important theo-
retical orientation and training of the therapist, and retical approaches. We discussed these theoretical
(2) the nature of the psychopathology. Firstly, a therapist approaches in some detail in section 1.3 and you may
will tend to adopt those treatment practices that they want to return to this section in order to refresh your
have most experience with and were originally trained memory about how these different theoretical models
to use. This will often involve therapies with a specific conceptualize and explain psychopathology. This sec-
theoretical approach (e.g. a psychodynamic approach, a tion continues with a summary of how these theoretical
client-centred approach, a cognitive approach or a behav- approaches are adapted to treat psychopathology.
ioural approach — see section 1.3.2), and these theoretical
approaches will not just advocate different treatment pro- Psychodynamic approaches
cedures, but will also advocate quite different approaches The aim of most psychodynamic therapies is to reveal
to understanding and explaining psychopathology. Most unconscious conflicts that may be causing symptoms of
104 PSYCHOPATHOLOGY
+ 4
psychopathology. Most psychodynamic approaches underlying conflicts interpretation In psychoanalysis, helpinc

assume that unconscious conflicts develop early in life, and and help the client the client to identify important underlyir
conflicts.
part of the therapy is designed to identify life events that develop ways of
may have caused these unconscious conflicts. Once these dealing with these conflicts.
important developmental
Frosh (2012, p.100) summarizes Freud’s conception
psychodynamic approaches Forms of life events and unconscious
therapy which attempt to reveal uncon-
conflicts have been identi- of psychoanalysis as a therapeutic process in the follow-
scious conflicts that may be causing ing way:
psychopathology. fied, the therapist will help
the client to acknowledge
the existence of these conflicts, bring them into conscious ¢ Psychoanalysis is a way of exploring the uncon-
awareness, and work with the client to develop strategies scious that might have therapeutic effects, but it is
for change. One important form of psychodynamic therapy not solely or necessarily therapeutic in its aims.
is psychoanalysis, and this is a type of therapy based on the ¢ The assumption that psychological conflict arises
theoretical works of Sigmund Freud (1856-1939). The aim from unconscious complexes suggests that if
of psychoanalysis is to bring any unconscious conflicts into psychoanalysis brings unconscious material into
awareness, to help the individual understand the source of consciousness, it will have the effect of lessening
these conflicts (perhaps by identifying past experiences psychological disturbance.
or discussing the nature of important relationships), and ° Freud was cautious about the power of psychoanal-
to help the individual towards a sense of control over ysis to make a significant difference but neverthe-
behaviour, feelings and attitudes. There are several basic less believed that the movement from ‘unconscious
techniques used by psychoanalysts to achieve these goals. to conscious’ was an important step in advancing
For example: individual well-being as well as social life.
¢ Psychological disturbance is caused by a complex
1. Free association: here the client is encouraged to array of phenomena, but at its core is the rela-
verbalize all thoughts, feelings and images that tionship between anxiety and repression, which
come to mind while the produces a variety of strategies aimed at keeping
free association A technique used in ; : : ;
3
psychoanalysis where the client is encour-
analyst
;
is normally seated
i
troubling unconscious material out of awareness.
aged to verbalize all thoughts, feelings and behind them, and this { e The different strategies (defences) adopted by
images that come to mind. process functions to bring
different people and in different circumstances
into awareness any
(see Table 1.1) characterize the various forms of
unconscious conflicts or associations between
psychological disturbance — neurosis, psychosis
thoughts and feelings.
and so on.
2. Transference: Here the analyst is used as a target
¢ Psychoanalysis as a mode of therapy aims at
for emotional responses, and the client behaves or
producing insight. It’s main methods of thera-
feels towards the analyst
peutic activity are focused on interpretation and
transference A technique used in psy- as they would have Peencrente
choanalysis where the analyst is used as behaved towards an
a target for emotional responses: clients
important person in their
behave towards the analyst as they would As a form of treatment, psychoanalysis may take
have behaved towards an important per- lives. This allows the client
up to three to five sessions a week and change is expected
son in their lives. to achieve understanding
to take place at a normal maturational rate, and so may
of their feelings by acting
require anything between 3 and 7 years for the full thera-
out any feelings or neuroses that they have
peutic benefits of the therapy to be recognized. Other
towards that person.
forms of psychodynamic therapy may be briefer and less
3. Dream analysis: Freud believed that unconscious intensive than psychoanalysis, and may draw on techniques
conflicts often revealed themselves in symbolic from other sources, such as family therapy (see the section
forms in dreams, and this below). Primarily, psychoanalysis represents a quest for
dream analysis The analysis of dream
made the analysis of self-knowledge, where an individual’s problems are viewed
content as a means of accessing uncon-
scious beliefs and conflicts. dream content an in the context of the whole person, and in particular, any
important means of conflicts they may have repressed. It can be a helpful treat-
accessing unconscious beliefs and conflicts. ment for many people with moderate to severe anxiety or
4. Interpretation: Finally, the skilled psychoanalyst depression-based problems — especially when other, more
has to interpret information from all of the above conventional, therapies have failed. In studies where the
sources and help the client to identify important effects of long-term psychoanalytic therapy have been -
CHAPTER 4 TREATING PSYCHOPATHOLOGY 105
measurable, it has been shown to only be more effective behaviour analysis. The behaviour analysis An approach to
than control treatments that do not possess a specialized term behaviour therapy is psychopathology based on the principles
psychotherapy component, suggesting that the evidence often used even more of operant conditioning (also known as
behaviour modification).
for the effectiveness of long-term psychoanalytic therapy eclectically nowadays to
for psychopathology is still limited and at best conflicting refer to any treatment that
(Smit, Huibers, Ioannidis, van Dyck et al., 2012). attempts to directly change behaviour (rather than, say,
cognitions), whether the underlying pra a
are based
Behaviour therapy on conditioning or not.
In the 1940s and 1950s there was a growing dissatisfac-
tion with the medical or disease model of psychopathol-
ogy, and also with the unscientific approaches to Therapies based on classical conditioning
psychopathology being generated by many psychody- principles Behaviour therapy effectively originates
namic theories. These dissatisfactions led psychologists from the writings of Wolpe (1958), who argued that
to look towards the developing area of experimental psy- many forms of emotional disorder could be treated
chology for objective knowledge that might be used to using the classical conditioning principle of extinction.
inform treatment and therapy. The body of knowledge The assumption was that
extinction The classical conditioning prin-
that psychologists turned to was that of conditioning if emotional problems ciple which assumes emotional problems
(see section 1.3.2), and this such as anxiety disorders can be’unlearnt’by disrupting the associa-
a. A form of associative learn- gave rise to the develop- were learnt through classi- tion between the anxiety-provoking cues
y on which behaviour therapies
» based.
ment of what came to be cal conditioning, they or situations and the threat or traumatic
outcomes with which they have become
known as behaviour ther- could be ‘unlearnt’ by dis- associated.
apy. Firstly, such therapies rupting the association
haviour therapy A term currently used
all interventions that attempt to change
stressed the need to treat between the anxiety-provoking cues or situations and
2 client's behaviour (and have largely symptoms of psychopa- the threat or traumatic outcomes that they have become
en based on principles from learning thology as bona fide behav- associated with. In practice, this means ensuring that the
ory). ioural problems rather anxiety-provoking stimulus, event or situation is experi-
than the mere symptoms enced in the absence of accompanying trauma so that
of some other, hidden underlying cause. Secondly, at the the former no_ longer
flooding A form of exposure therapy
time, many psychologists believed that numerous psy- comes to evoke the latter.
for the treatment of phobias and related
chological disorders were the result of what was called The most famous behav- disorders in which the patient is repeatedly
faulty learning, and that symptoms were acquired iour therapy techniques to exposed to highly distressing stimuli.
through simple condition- apply extinction principles
ilty learning A view that the symptoms ing processes. For example, are flooding, counter-
counterconditioning A behaviour ther-
psychological disorders are acquired
it was believed that anxiety conditioning and sys- apy technique designed to use condition-
ough the learning of pathological
ponses. symptoms could be acqui- tematic desensitisation, ing techniques to establish a response that
red through classical condi- and they have collectiv- is antagonistic to the psychopathology.
tioning (see Figure 6.2), and behavioural problems might ely come to be known
systematic desensitisation A behaviour
be acquired through processes of operant conditioning — as exposure therapies
therapy based on classical conditioning
e.g. bizarre and inappropriate behaviours might be (Richard & Lauterbach, used in the treatment of phobias and
acquired because they have been reinforced or rewarded in 2007; Craske, Liao, Brown anxiety disorders, during which the client
the past (see Focus Point 8.5). The reasoning here was that, & Vervliet, 2012) because overcomes their fears through gradual and
systematic exposure.
if psychological problems were acquired through learning, they are all based on the
then conditioning principles could be used to develop ther- need to expose the client exposure therapy Treatment in which
apies that effectively helped the individual to ‘unlearn’ to the events and situa- sufferers are helped by the therapist
those problematic associations. Two distinctive strands of tions that evoke their dis- to confront and experience events and
stimuli relevant to their trauma and their
behaviour therapy developed from these assumptions. tress and anxiety — so that
symptoms.
The first was a set of therapies based on the principles of they can learn that they
classical conditioning, and the second based on principles are no longer threatening reciprocal inhibition A principle of
of operant conditioning. While the former group of (see Davey, 1998). Wolpe behaviour therapy in which anxiety is
eliminated not just by extinguishing the
therapies continues to be (1958) also introduced the
relationship between the anxiety-inducing
haviour modification Behavioural known as behaviour ther- principle of reciprocal cue and the threatening consequence,
atment methods based on operant
apy, the latter group has inhibition, in which an but also by attaching a response to the
\ditioning principles, which assume that
rnt psychopathology can be ‘unlearnt’ also come to be known as emotional response is anxiety-inducing cue which is incompat-
eliminated not just by ible with anxiety.
ng normal! learning processes. behaviour modification or
106 PSYCHOPATHOLOGY
: *
extinguishing the relationship between the emotion- therapy than do those of classical conditioning. Operant
inducing cue and the threatening consequence, but also conditioning is concerned with influencing the fre-
by attaching a response to the emotion-inducing cue quency of a behaviour by manipulating the conse-
which is incompatible with anxiety (e.g. relaxation). It quences of that behaviour. For example, if a behaviour
has often been assumed that these techniques can only is followed by rewarding or reinforcing consequences,
be applied to the treatment of emotional problems such it will increase in frequency. If it is followed by punish-
as anxiety disorders, but they have in fact been applied to ing or negative consequences, it will decrease in fre-
a range of disorders including addictive disorders quency (Davey, 1989). Operant conditioning principles
(O’Leary & Wilson, 1975), marital conflict (Jacobson & have mainly been used in therapy in three specific ways:
Weiss, 1978), and sexual dysfunction (Mathews, Bancroft, (1) to try to understand ‘what rewarding or reinforc-
Whitehead, Hackmann et al., 1976). ing factors might be maintaining an inappropriate or
Aversion therapy is another treatment based on maladaptive behaviour — this is known as functional
classical conditioning, but is rather different to the pro- analysis (e.g. trying to understand what factors might
ceeding therapies because be maintaining challenging or aggressive behaviours
aversion therapy A treatment based it attempts to condition in individuals with intellectual disabilities); (2) to use
on classical conditioning which attempts
to condition an aversion to a stimulus or
an aversion to a stimulus reinforcers and rewards to try to establish new or
event to which the individual is inappropri- or event to which the indi- appropriate behaviours (e.g. to establish self-help or
ately attracted. vidual is inappropriately social behaviours in individuals who have become
attracted. For example, withdrawn because of their psychopathology); and (3)
aversion therapy is most widely used in the treatment to use negative or punishing consequences to try to
of addictive behaviours such as alcoholism, and in these suppress or eliminate problematic behaviours in need
procedures the taste of alcohol is paired with aversive of urgent attention (e.g. to eliminate or suppress
outcomes (e.g. sickness-inducing drugs) in order to con- self-injurious behaviours in individuals with intellect-
dition an aversive reaction to alcohol (e.g. Voegtlin & ual disabilities or severe autistic symptoms) (see
Lemere, 1942; Lemere & Voegtlin, 1950) (see Chapters SECHONBIZASIORD))s
9 and 11 for discussion of the use of aversion therapy A functional analysis is where the therapist attempts
in the treatment of substance abuse and paraphilias). to identify consistencies between problematic behaviours
Since the 1950s and 1960s, this type of procedure has and their consequences — : <a .
a functional analysis An observational
been used to treat a wide variety of problems, includ- especially to try to discover method for identifying the consistencies
ing inappropriate or distressing sexual activities (e.g. whether there might be a__ between problematic behaviours and the —
Feldman & MacCulloch, 1965), drug and alcohol consistent event or conse- Consequences that may be reinforcing ther
addiction (McRae, Budney & Brady, 2003), and even quence that appears to be maintaining the behaviour by
obsessions and compulsions associated with anxiety rewarding it. For example, self-injurious or challenging
(Lam & Steketee, 2001). Aversion therapy was popu- behaviours may be maintained by a range of reinforcing
larized in the 1971 cult film A Clockwork Orange where consequences, such as the attention the behaviour may
the lead character’s excessive violence was treated by attract or the sensory stimulation it provides (see
‘conditioning’ him to vomit whenever he saw a violent Treatment in Practice Box 17.1). Identifying the nature of
act. However, while aversion therapy for some prob- the consequence allows the therapist to disrupt the rein-
lems (e.g. alcoholism, sexual offending) has been forcement contingency and, if necessary, reduce the fre-
shown to have some therapeutic gains when used in quency of that behaviour through extinction (Wacker,
conjunction with broader community support pro- Steege, Northrup, Sasso et al., 1990). Functional analysis
grammes (Azrin, 1976) or social skills training (Maletzky, has been adopted across a range of clinical settings, and
1993), substance abuse or sexual offending responses has been successfully applied to controlling aggressive/
are often very resistant to this form of treatment, and challenging behaviour (O'Reilly, 1995), tantrums (Darby,
there is very little evidence that aversion therapy Wacker, Sasso, Steege et al., 1992), ADHD (Northrup
alone has anything other than short-lived effects (e.g. et al., 1995), depression (Ferster, 1985), eating problems
Wilson, 1978), and does not significantly reduce reoff- (Slade, 1982), and self-injurious behaviour (Iwata, Dorsey,
ending in sexual offenders (Marques, Wiederanders, Slifer et al., 1985).
Day et al., 2005). Other influential interventions based on operant con-
ditioning principles include the token economy, response
shaping, and behavioural self-control. In the psychiatric
Therapies based on operant conditioning prin- setting, a token economy involves participants receiving
ciples The principles of operant conditioning offer tokens (a generalized reinforcer) for engaging in behav-
some rather different approaches to treatment and iours defined by the programme, and at a later time these «
CHAPTER 4 TREATING PSYCHOPATHOLOGY 407°
tokens can then be exchanged for a variety of reinforcing (defining appropriate responses), and (7) substituting
or desired items (e.g. access to the hospital grounds, a other activities for between-meal eating (programming
visit to the cinema, and so on). In psychiatric care, the acceptable competing responses). These principles are
token economy was first used to foster prosocial or self- relatively easy to apply to your own behaviour, and Activity
help behaviours (e.g. combing hair, bathing, brushing 4.1 provides some suggestions as to how you might
teeth, and suchlike) in previously withdrawn patients, develop your own behav-
although its use and popularity has declined significantly ioural self-control _ pro- To complete Activity 4.1 go to
over the past 20 years (for a fuller discussion of this gramme to promote an | www.wiley-psychopathology.com/
decline, see Focus Point 1.2). Response shaping is a activity such as studying. activities/ch4
procedure that can be used to encourage new behav-

iours that are not already Cognitive therapies
sponse shaping A reinforcement
ocedure that is used to develop new
occurring at a reasonable
haviours. frequency. This may be The origins of cognitive therapy In the past 40 years,
especially a problem with one of the most impressive developments in our under-
withdrawn individuals or individuals with restricted standing of psychopathology has been our evolving insight
behavioural repertoires (such as those with severe intel- into the cognitive factors that play important roles in caus-
lectual disabilities). However, the technique of response ing and maintaining psychopathology. For example, some
shaping by successive approximations is a way around psychopathologies are caused by dysfunctional ‘ways of
this problem. Here, the therapist will first reinforce a thinking’ — either about the self or the world (e.g. in major
behaviour that does occur quite frequently and is an depression). In other cases, psychopathologies are char-
approximation to the specific target response. Once this acterized by dysfunctional ways of processing and inter-
general response is established, reinforcement is given preting incoming information. For example, many anxiety
only for closer and closer approximations to the target disorders are characterized by a bias towards processing
response. An example of the use of response shaping is threatening or anxiety-relevant information (e.g. general-
provided in Treatment in Practice Box 4.1. Finally, the use ized anxiety disorder, see Treatment in Practice Box 6.4)
of operant conditioning principles for behaviour change or to interpreting ambiguous information negatively (e.g.
purposes does not have to be overseen or administered panic disorder, see Figure 6.5). In both cases these biases act
by a therapist. The principles are quite clear and can be to develop and maintain anxiety. If such cognitive factors
used by any individual to control and manage their own are maintaining psychopathology, then developing treat-
behaviour. This personal use of operant conditioning ments that try to address and change these dysfunctional
principles has come to be known as behavioural self- cognitive features is important. Two early forms of cog-
control (e.g. Thoresen & Mahoney, 1974), and has since nitive therapy based on these assumptions were rational
been developed into multi- emotive therapy (RET) and Beck’s cognitive therapy.
havioural self-control The personal
faceted behavioural pro- How people construe themselves, their life and the
e of operant conditioning principles to
ange or control one’s own behaviour. grammes to deal with a world is likely to be a major determinant of their feel-
variety of personal prob- ings, and rational emotive therapy (RET) developed
lems, including addiction, habits, obsessions, and other by Albert Ellis (1962) was
behavioural problems (Lutzker & Martin, 1981; Stuart & one of the first cognitive rational emotive therapy (RET) A
Davis, 1972). A programme developed by Stuart (1967) therapies to address these cognitive therapy technique developed
by Albert Ellis (1962) which addresses how
provides a good example of a multifaceted behavioural factors. In particular, Ellis people construe themselves, their life and
self-control scheme designed to address obesity by con- believed that people carry the world.
trolling behaviours contributing to overeating. The main around with them a set of
elements of this programme were: (1) recording the time implicit assumptions which determines how they judge
and quantity of food consumption (self-observation), themselves and others, and that many of these implicit
(2) weighing in before each meal and before bedtime (help- assumptions may be irrational and cause emotional
ing the individual to discriminate how eating might have distress. For example, two irrational beliefs include
contributed to weight gain), (3) removal of food from all (1) demanding perfection from oneself and from oth-
places in the house except the kitchen (so that only the ers, and (2) expecting approval from others for every-
kitchen comes to act as a cue for eating), (4) pairing eating thing one does. Clearly, there will be many occasions
with no other activity that might make eating enjoyable, when these goals are not met, and this will cause anxi-
and so reinforce it (e.g. eating should not occur while ety, depression and emotional discomfort. Rational
watching an enjoyable TV programme), (5) setting a emotive therapy attempts to challenge these irrational
weight loss goal of 1-2 pounds/week (setting clearly beliefs and to persuade the individual to set more attain-
attainable goals), (6) slowing down the pace of eating able life goals. As such, RET is a good example of a
dak: PSYCHOPATHOLOGY
CLINICAL PERSPECTIVE - TREATMENT IN PRACTICE BOX 4.1:

AN EXAMPLE OF RESPONSE SHAPING
Response shaping is a useful procedure for strengthen- on the ward and the nursing staff were asked to
ing rarely occurring behaviours or building up complex attend to his needs, but only if he verbalized them.
response repertoires, and this method is utilized regularly
in behaviour modification programmes. An early study by This example demonstrates a number of features of the
Isaacs, Thomas & Goldiamond (1960) serves to illustrate response-shaping procedure in clinical settings. First, it pro-
this method. They attempted to reinstate verbal behav- vides an example of how response shaping can be a power-
iour in a psychiatric in-patient who had been mute for ful and effective means of establishing complex response
over 19 years. In this example, the target behaviour occurs repertoires relatively quickly. Second, it also illustrates the
relatively infrequently, and thus has to be approached via distinction between ‘arbitrary’ and ‘natural’ reinforcers in
the reinforcement of successive approximations to the behaviour modification. In this case, chewing gum was an
behaviour. They discovered that although the patient effective reinforcer for the behaviours being shaped; but it
was withdrawn, he did appear to respond to chewing is an ‘arbitrary’ one in that it is not a normal reinforcer for
gum, which they considered would act as an effective verbal behaviour. Thus, while chewing gum may have acted
reinforcer. They then broke down the target behaviour so as an effective reinforcer during the shaping process, in
that it could be reached by reinforcing a series of approxi- order to be maintained in any way, verbalisations need to
mations to verbal behaviour. The first responses to be be transferred to a more ‘natural’ reinforcer for those behav-
reinforced were fairly simple, discrete responses whose iours. This was the aim of stage 6 in the study, where the
baseline levels were high enough for them to occur spon- patient's needs were met only if he verbalized them.
taneously within a training session. The shaping pro- Finally, there was no apparent follow-up analysis of the
gramme went as follows: gains achieved in this study, and one suspects that, once
back in the unstructured setting of the ward, the patient
1. when the patient moved his eyes towards the in the Isaacs, Thomas & Goldiamond study would have
chewing gum, he was reinforced by being given the reverted to his previous mute state. However, this study
gum - after 2 weeks the probability of this response does still emphasize two things. Firstly, behaviour change
was relatively high; has to be subsequently supported by stable and struc-
2. the experimenters then only gave the patient gum tured changes to the individual's environment which will
when he moved his mouth and lips — by the end of maintain the therapeutic gains achieved in the behaviour
week 3, these behaviours were relatively frequent; modification programme. Secondly, whether the patient in
3. the experimenters then withheld gum until the this study did revert to a mute state still does not deny the
patient made vocalisations of some sort — by the usefulness of response-shaping procedures in swiftly dev-
end of the fourth week the patient was moving his eloping relatively complex
eyes and lips and making audible ‘croaking’ noises; behaviour repertoires - the
4. during weeks 4 and 5, the experimenter asked the problem of response main- | To read Issacs, Thomas & Goldimond’s
article on reinstating verbal behaviour
patient to ‘say gum, repeating this each time the tenance, however, usually | in psychotics go to
patient vocalized — at the end of week 6, the patient requires other considerations | www.wiley-psychopathology.com/
spontaneously said ‘gum please’; (cf. Glynn, 1990; Stokes & Baer, % reading/ch4
5. in later sessions the patient verbally responded to 1977; Stokes & Osnes, 1988).
questions from the experimenters, but only in the
therapeutic situation; Source: From Davey G.C.L. (1998). Learning theory. In C. E. Walker
6. to enable verbal behaviour to generalize beyond the (Ed.) Comprehensive clinical psychology: Foundations of clinical
experimental setting, the patient was placed back psychology. Vol 1. Elsevier. Reproduced by permission.
group of therapies that attempt to change a set of core cognitive therapy is cognitive therapy A form of psychother-
beliefs about the world that may be dysfunctional (i.e. required for successful apy based on the belief that psychological
either fallacious, or a source of conflict and emotional treatment, and this ther- problems are the products of faulty ways c
thinking about the world.
distress). However, make no mistake about it, changing apy will normally go
an individual’s core beliefs — which have been through a process of chal-
developed and refined over a period of many years — lenging existing dysfunctional beliefs, replacing these
is no easy thing. This is why highly structured with more rational beliefs, and then getting the
CHAPTER 4 TREATING PSYCHOPATHOLOGY 109.
individual to test out this new set of beliefs in struc- ‘Waves’ of CBT CBT has not been a static treatment
tured behavioural exercises. innovation, and just like any other knowledge-based
Aaron Beck’s cognitive theory of depression is out- development, new forms of CBT have evolved out of
lined in more detail in Chapter 7, and from this theory earlier ones. These progressive developments have come
he developed a cognitive therapy for depression. Beck to be known as ‘waves’, and at the present time we are
argues that depression results when the individual devel- experiencing what is called the ‘third wave’ of CBT tech-
ops a set of cognitive schemas (or beliefs) which bias the niques. The ‘first wave’ occurred during the 1950s and
individual towards negative interpretations of the self, 1960s and was represented largely by behaviour therapy
the world and the future, and any therapy for depression techniques based on learning theory and conditioning
must therefore address these schemas, deconstruct them principles. The ‘second wave’ developed in the 1970s and
and replace them with more rational schemas that do not 1980s when it became clear that what we do is not just
always lead to negative interpretations. Beck’s cognitive influenced by our learning and conditioning experiences,
therapy does this by engaging the depressed individual in but also by what and how we think (cognitions), and how
an objective assessment of the way we think affects our emotions. This gave rise to
.ck’s cognitive therapy An intervention their beliefs, and requires the traditional forms of CBT initially developed by ther-
rived from Beck’s view that depression
them to provide evidence apists such as Aaron Beck and described in the previous
maintained by a ‘negative schema’ that
a depressed individuals to hold nega- for their biased views of section. However, a ‘third wave’ or ‘third generation’ of
e views about themselves, their future the world. This enables the CBT methods has developed which emphasizes mindful-
d the world (the ‘negative triad’). individual to perceive their ness and acceptance.
existing schemas as biased, Mindfulness-based cognitive therapy (MBCT) is a direct
irrational and overgeneralized (see section 7.3.2). extension of traditional CBT in which treatments
Out of these early pioneering cognitive therapies emphasize achieving a men- mindfulness-based cognitive therapy
developed what is now known as cognitive behaviour tal state characterized by (MBCT) A direct extension of traditional
therapy (CBT), which is an intervention for changing present-moment focus and CBT in which treatments emphasize
both thoughts and behav- non-judgemental aware- achieving a mental state characterized
by present-moment focus and non-
gnitive behaviour therapy (CBT) An iour, and represents an ness (Bishop, Lau, Shapiro, judgemental awareness.
tervention for changing both thoughts umbrella term for many Carlson et al., 2004; Kabat-
d behaviour. CBT represents an umbrella
rm for many different therapies that
different therapies that Zinn, 2003). The purpose of this is to improve emotional
are the common aim of changing both share the common aim of well-being by increasing awareness of how automatic cog-
gnitions and behaviour. — changing both cognitions nitive and behavioural reactions to thoughts, sensations and
and behaviour. A CBT emotions can cause distress. Clients are encouraged to
intervention usually possesses most of the following acknowledge and accept their thoughts and feelings, and by
characteristics: focusing on the present rather than the past or future, the
1. the client is encouraged to keep a diary noting the individual can learn to deal more effectively with life stress-
occurrence of significant events and associated ors and challenges that generate anxiety or depression.
feelings, moods, and thoughts in order to
Mindfulness interventions are considered to reduce symp-
demonstrate how events, moods and thoughts
toms of common mental health problems such as anxiety
and depression by countering avoidance strategies, helping
might be interlinked;
the individual to respond reflectively rather than reflex-
2. with the help of the therapist, the client is urged
ively to stressors, and reducing physical symptoms by
to identify and challenge irrational, dysfunctional
advocating the use of meditation and yoga exercises
or biased thoughts or assumptions;
(Kabat-Zinn, 1982). Since its early development, mindful-
3. clients are given homework in the form of ness has now been successfully applied to a wide range of
‘behavioural experiments’ to test whether their mental health problems, including anxiety, depression,
thoughts and assumptions are accurate and pain relief, post-traumatic stress disorder, and psychosis
rational; and (Williams & Kuyken, 2012; Kocovski, Segal & Battista,
4. clients are trained in new ways of thinking, 2009; Vujanovic, Niles, Pietrefesa et al., 2011; Chadwick,
behaving and reacting in situations that may Hughes, Russell et al., 2009).
evoke their psychopathology. Acceptance and commitment therapy (ACT) is
As an example, Treatment in Practice Box 6.3 dem- another third wave CBT
acceptance and commitment therapy
onstrates how a cognitive behaviour therapist would intervention that has grown (ACT) A’‘third wave’ CBT intervention that
conduct an interview designed to identify and challenge in popularity over recent adopts some aspects of mindfulness, but
irrational and dysfunctional beliefs in an individual diag- years. It is an approach has developed more from the Skinnerian
nosed with panic disorder. that adopts some aspects approach to understanding behaviour.
ORs PSYCHOPATHOLOGY
«
of mindfulness, but has developed more from the behav- Humanistic therapies
iour analysis or Skinnerian approach to understanding Throughout the 20th century, many psychotherapists felt
behaviour (see section 1.3.2). ACT differs from traditional that psychological therapy was becoming too focused on
CBT in that, rather than getting individuals to manage and psychological and behavioural mechanisms, or on psycho-
change their thoughts and the way they think, it teaches logical structures (such as personality), and was losing
them to ‘just notice’, accept, and embrace private events sight of both the feelings of the individual and the indi-
such as thoughts (especially thoughts that may be intrusive, vidual themselves. As a consequence, a number of what
distressing, or unwanted). As such, it aims to help the indi- are called ‘humanistic’ therapies developed, including
vidual clarify their personal values, to take action on them, Gestalt therapy (Perls, 1969), existential therapies (Cooper,
and to increase their psychological flexibility (Zettle, 2005; 2003), primal therapy (Janov, 1973), narrative therapy
Hayes, Luoma, Bond, Masuda & Lillis, 2006). Activity 4.2 (Freedman & Combs, 1996), and transpersonal therapy
provides you with an exam- (Wellings, Wilde & McCormick, 2000) and, arguably the
“\, ple of how ACT attempts most successful among these, client-centred therapy
To complete Activity 4.2 go to
www.wiley-psychopathology.com/ to help you distance your- (Rogers, 1961). These humanistic therapies had a num-
activities/ch4 self from negative or dis- ber of factors in common:
tressing thoughts. (1) they espoused the need humanistic therapies Therapies that
attempt to consider the ‘whole’ person
While ‘new wave’ developments bring new and excit- for the therapist to develop and not just the individual symptoms of
ing ways of delivering CBT across a range of disorders, a more personal relation- psychopathology.
these new approaches are still being evaluated. Studies ship with the client in order
suggest that third wave therapies such as MBCT and to help their clients reach a state of realisation that they
ACT should not be considered as separate from the can help themselves; (2) they were holistic therapies in
growing body of CBT approaches (Hofman, Sawyer that they emphasized the
& Fang, 2010), may have their successful therapeutic holistic therapies Therapies which
need to consider the emphasize the need to consider the ‘whol
effects through similar mechanisms to CBT (Hofman, ‘whole’ person and not just person, not just those ‘bits’ of the person
Asmundson & Beck, 2013), and are generally equally those ‘bits’ of the person that manifest psychopathology. _
effective as each other (Ost, 2008; Gaudiano, 2009). that manifest psychopa-
CBT in general is perceived as an evidence-based and thology; (3) therapy should be seen as a way of enabling
cost-effective form of treatment that can be success- individuals to make their own decisions and to solve their
fully applied to a very broad range of psychopathologies own problems rather than imposing structured treat-
(Butler, Chapman, Forman & Beck, 2006), is equally as ments or ways of thinking on them; (4) humanistic thera-
effective as other forms of psychotherapy, and superior pies espouse the need for the therapist—client relationship
to many other forms of psychotherapy when treating to be a genuine reciprocal and empathetic one, rather
anxiety and depressive disorders (Tolin, 2010). than the limited skilled professional—referred client
a GESTALT THERAPY
J
-
Gestalt therapy is a popular existential humanistic achieving this is by using the role-playing empty-chair
< therapy that was originally developed by Fritz Perls technique, which involves the client addressing the
O and colleagues in the 1940s and 1950s (Perls, 1947;
a. empty chair as if another person was in it and acting
WV Perls, Hefferline & Goodman, 1951). It focuses on an out the two sides of a discussion.
=} individual's experiences in the present moment, the Gestalt therapy is often considered a good method
U
\e) therapist-client relationship, and the contexts in for managing tension, depression and anxiety, and
Li which the individual lives their life. It emphasizes that uncontrolled outcome studies suggest that Gestalt
the most helpful focus of psychotherapy is on what a therapy provides participants with better emotional
person is doing, thinking, and feeling at the present well-being and a heightened sense of hope (Leung,
moment, rather than on what was, might be, or could Leung & Ng, 2013). At least some psychotherapists
be. It is also a method of awareness practice very simi- believe that the methods deployed by Gestalt therapy
lar to mindfulness, discussed above, in which current might be productively integrated with more con-
perceiving, feeling and acting are helpful to interpret- ventional interventions such as cognitive therapy
ing, explaining, and conceptualising experience. Much (Tonnesvang, Sommer, Hammink & Sonne, 2010), and
of the Gestalt approach is about the client exploring might make a useful contribution to modern psychiat-
their relationship with themselves, and one method of ric practice (Clegg, 2010).
CHAPTER 4 TREATING PSYCHOPATHOLOGY on
relationship that exists in many forms of psychological members of the family — especially where communica-
therapy; and (5) increasing emotional awareness is a criti- tion between individuals might be the cause of psycho-
cal factor in alleviating psychological distress, and is neces- pathology in one or more family members; (2) it can
sary before the client can begin to resolve life problems. resolve specific conflicts — for example, between adoles-
Client-centred therapy focuses on the individual's cents and their parents; and (3) it may apply systems
immediate conscious experience, and critical to this form theory (attempting to understand the family as a social
of humanistic therapy is the creation of a therapeutic cli- system) to treatment by
systems theory Approach that attempts
mate that allows the client to progress from a state of rigid trying to understand the to understand the family as a social system.
selfperception to one which encourages the client to complex relationships and
become independent, self-directed, and to pursue self- alliances that exist between family members, and then
growth. For Carl Rogers (1902-1987), empathy (‘putting attempting to remould these relationships into those
yourself in someone else’s expected in a well-functioning family (the latter may usu-
npathy An ability to understand and shoes’) was the central ally involve ensuring that the primary relationship in the
perience a client's own feelings and
rsonal meanings, and a willingness to
important feature of any family — between the two parents — is strong and func-
monstrate unconditional positive regard therapist-client __relation- tional) (Minuchin, 1985).
r the client. ship, and it is this ability that In family therapy, the therapist or family therapy
is essential in guiding the team meets with those members of the family willing
client towards resolving their own life problems. Empathy to participate in discussion about a topic or problem
has at least two main components in this context: (1) an raised by one or more members of the family. In the
ability to understand and experience the client’s own feel- case of an adolescent eating disorder, the parents may
ings and personal meanings, and (2) a willingness to dem- have raised the issue of how their child’s eating disor-
onstrate unconditional positive regard for the client. This der affects family functioning, and this may be explored
latter feature involves valu- with the family over a series of meetings. Family thera-
conditional positive regard Valuing
ing the client for who they pists are usually quite eclectic in the range of approaches
ents for who they are without judging
are and refraining from they may bring to family therapy, and these may include
judging them. Another cognitive-behavioural methods, psychodynamic appro-
important feature of client-centred therapy is that it is not aches, and systemic analyses depending on the nature of
directive. The therapist acts primarily as an understanding the problem and its underlying causes. In many cases,
listener who assists the client by offering advice only when family therapists may focus on how patterns of inter-
asked. The overriding goal is to develop the client through action within the family maintain the problem (e.g. an
empathy, congruence and unconditional positive regard to eating disorder) rather than trying to identify the cause
a point where they are successful in experiencing and (the latter may be seen as trying to allocate blame for the
accepting themselves, and are able to resolve their own problem within the family). Over a period of between 5
conflicts and difficulties. and 20 sessions, the family therapist will attempt to iden-
In much the same way that psychoanalysis has tify family interaction patterns that the family may not
evolved, client-centred therapy has developed not just be aware of, and to suggest to family members different
as a therapy, but also as a process for fostering personal ways of responding to each other. A case example of the
self-growth. The general approach places relatively lit- use of family therapy with an adolescent with an eating
tle emphasis on how the psychopathology was acquired, disorder is provided in Treatment in Practice Box 10.1.
but attempts to eliminate symptoms by moving the cli-
ent from one phenomenological state (e.g. a state of Drug treatments
anxiety, depression, and suchlike) to another (e.g. one Pharmacological or drug treatments are regularly used
that enables the client to view themselves as worthy and to alleviate some of the symptoms of psychopathologies.
respected individuals). They are often the first line of treatment provided by
GPs and doctors to tackle anxiety and mood-based prob-
Family and systemic therapies lems, and may be sufficient to enable an individual to see
Family therapy is a form of intervention that is becoming through an acute bout of anxiety or depression. Some of
increasingly helpful as a means of dealing with psychopa- the most commonly used
antidepressant drugs Drug treatments
thology that may result from the relationship dynamics drug treatments include intended to treat symptoms of depression
within the family (Dallos & antidepressant drugs to and mood disorder.
mily therapy A form of intervention Draper, 2005). Family ther- deal with symptoms of
folving family members that is helpful
apy has a number of pur- depression and mood dis- anxiolytic drugs Drug treatments
a means ofdealing with psychopathol-
y that may result from the relationship poses: (1) it helps to improve order, anxiolytic drugs to intended to treat symptoms of anxiety and
namics within the family. communications between treat symptoms of anxiety stress.
St22°% PSYCHOPATHOLOGY
; fe
antipsychotic drugs Drug treatments and stress, and antipsy- do appear to hasten recovery from an episode of depres-
intended to treat symptoms of psychosis chotic drugs prescribed sion, relapse is extremely common after the drug is dis-
and schizophrenia spectrum disorders. for symptoms of psychosis continued (Reimherr, Strong, Marchant et al., 2001).
and schizophrenia.
Drug treatments for anxiety There are numerous
Drug treatments for depression Drug treatments psychological disorders that are characterized by chronic,
for depression were first successfully developed in the high levels of anxiety. The more prevalent of these include
1960s and the drugs that were first developed were called clinically diagnosable specific phobias, panic disorder, gen-
tricyclic antidepressants (because of their chemical eralized anxiety disorder (GAD), obsessive compulsive dis-
structure). These drugs order (OCD), and post-traumatic stress disorder (PTSD)
tricyclic antidepressants Antidepressant
have their effect by increas- (see Chapter 6). The symptoms of these disorders can
drugs developed in the 1960s which have
their effect by increasing the amount of ing the amount of norepi- usually be treated with anxiolytics (tranquilizers) such as
norepinephrine and serotonin available for nephrine and _ serotonin the benzodiazepines (which include the well-known
synaptic transmission. available for synaptic trans- tranquillizer Valium), and
mission. Other antidepres- they have their effect by benzodiazepines A group of anxiolyt-
ics which have their effect by increasing
sants introduced during this period were monoamine increasing the level of the the level of the neurotransmitter GABA at
oxidase inhibitors (MAOIs) (such as phenelzine and tra- neurotransmitter GABA at synapses in the brain.
nylcypromine). MAOIs are synapses in the brain. Benzo-
monoamine oxidase inhibitors effective for some people diazepines are usually prescribed only for short periods
(MAOIs) Antidepressants which are
effective for some people with major
with major depression who because they can encourage dependence if taken over a
depression who do not respond to other do not respond to other longer period, and can also be abused if available in large
antidepressants. antidepressants. They are doses. However, it is important to be aware that anxiolytics
also effective for the treat- will usually offer only symptom relief, and do not address
ment of panic disorder and bipolar depression. Most the psychological and cognitive factors that may be
recently, we have seen the development of the first maintaining the anxiety. Serotonin—norepinephrine reup-
‘designer drugs’ for depression, and these include fluo- take inhibitors (SNRIs) are a more recently developed class
xetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), and of drugs for anxiety-based
citalopram (Celexa). These newer drugs are collectively symptoms (Hoffman &_ serotonin-norepinephrine reuptake
called selective serotonin reuptake inhibitors (SSRIs) Mathews, 2008). SNRIs inhibitors (SNRIs) A recent group of
: eet . drugs for anxiety-based symptoms which
because they selectively selectively inhibit sak cay selectively inhibit norepinephrine and
selective serotonin reuptake inhibitors affect the uptake of only nephrine and serotonin serotonin reuptake and have been shown.
(SSRIs) A recent group of antidepressant
one neurotransmitter — reuptake and have been to be effective and well tolerated in indi-
drugs that selectively affect the uptake
usually serotonin. SSRIs shown to be effective and viduals with anxiety disorders. |
of only one neurotransmitter — usually
serotonin. can reduce the symptoms well tolerated treatments
of depression as rapidly in individuals with anxiety disorders (Dell’Osso, Buoli,
as tricyclic antidepressants, and have far fewer side effects. Baldwin & Altamura, 2010), making them superior to
SSRIs — especially Prozac — have often been viewed as the benzodiazepines in terms of reduced side effects and less
miracle drug for depression. However, it can also cause likelihood of withdrawal symptoms following discontin-
some side effects (such as a loss of sexual desire in up to uation (Schweizer, Rickels, Case & Greenblatt, 1990).
30 per cent of users - Montgomery, 1995) and is possibly
at the point where it is becoming overprescribed by GPs Drug treatments for psychosis Drug treatments
who are perhaps failing to look further for more struc- for psychosis and schizophrenia have radically revolu-
tured psychological treatment for their patients (Olfson & tionized the way that schizophrenia sufferers are treated
Klerman, 1993). In relation to this latter point, recent and cared for. The use of effective antipsychotic drugs
studies suggest that antidepressants are more effective became common in the 1960s and 1970s, and this had the
than placebos for people with severe depression, but not effect of drastically reducing the number of individuals
for those with mild depression (Fournier, DeRubeis, with psychotic symptoms who needed long-term institu-
Hollon et al., 2010), yet GPs and physicians are often tionalized care, and has enabled many experiencing such
more than ready to prescribe these drugs for people with symptoms to achieve a level of functioning that permits
mild, first-episode depression. This issue is compounded relatively normal day-to-day functioning. Prior to the
by the fact that almost 40 per cent of those who are pre- 1980s, it was estimated that two out of three schizophre-
scribed with antidepressants stop taking the drug within nia sufferers would spend most of their lives in a psychi-
the first month — often because of the side effects (Olfson, atric institution; beyond the 1980s, the average length of
Blanco, Liu et al., 2006). Finally, although antidepressants stay has come down to as little as 2 months (Lamb, 1984). .
CHAPTER 4 TREATING PSYCHOPATHOLOGY Poe,
Antipsychotics (such as chlorpromazine and halop- kinds of beneficial insights into the psychopathology
eridol) have their effects by blocking dopamine recep- that psychological therapies may provide. This account
tors and help to reduce the high levels of dopamine is consistent with the fact that when drug treatments are
in the brain (see Chapter 8). This not only reduces the successful over the longer term, this is more likely to be
major positive symptoms (such as thought disorder and the case if drug treatment is combined with psychologi-
hallucinations), but can also reduce the major negative cal treatment (e.g. CBT) (Hollon & Beck, 1994; Thase,
symptoms (such as social withdrawal). However, while Greenhouse, Frank, Reynolds et al., 1997).
these drugs have had a remarkable effect on reducing
the symptoms of psychosis, and, as a consequence, Summary of theoretical approaches
reducing the burden of institutionalized care for suf- Each of the theoretical approaches to treatment we have
ferers, there are some negative factors to consider. For discussed in this section can be used to treat a range
example, most antipsychotics do have some undesir- of different psychopathologies, and we will look more
able side effects for some people (such as blurred vision, closely at how to evaluate their success later in this chap-
muscle spasms, blood disorders, cardiac problems, and ter. Each of these approaches differs not only in the basic
so on), and these side effects can cause relapse, or make intervention procedures they use, but also in the way
sufferers unwilling to take their medication on a regular they attempt to explain psychopathology (see Chapter 1).
basis (which needs constant monitoring if the individual Contemporary practitioners may well be skilled in using
is being cared for in the community). more than one of these approaches, and, indeed, a com-
bination of approaches may be used to address specific
Problems with drug treatments Despite the fact psychopathologies (e.g. the use of both drug treatment
that appropriate medication can often provide relief and CBT to treat depression).
from the symptoms of psychopathology, there is a view
that interventions using drugs alone may be problem-
atic for a number of reasons. Firstly, prescribing drugs
4.1.2 Modes of Treatment Delivery
for some mild psychopathology symptoms may effec-
tively “‘medicalize’ what are merely everyday problems The standard and traditional mode of psychotherapy
of living, and lead people to believe that acute bouts of delivery is in one-to-one, face-to-face meetings or ses-
anxiety or depression are ‘diseases’ that will not be alle- sions between a therapist and a client, and this is still the
viated until medical treatment has been sought (Shaw & most prevalent mode of delivery today. However, with
Woodward, 2004; see Focus Point 1.6). Similarly, many the pressing need to treat ever increasing numbers of
drugs are tested for their effectiveness on individuals individuals referred with symptoms of psychopathol-
with severe symptoms, and some recent studies sug- ogy, overstretched clinicians and service providers often
gest that they may be ineffective for people with only look to find more cost-effective and efficient ways to
mild symptoms (Fournier, DeRubeis, Hollon et al., 2010; deliver treatment interventions. The following section
Kirsch, Deacon, Huedo-Medina et al., 2008). Secondly, looks briefly at some of the modes of delivery that have
long-term prescription of drugs for a psychopathology been developed to supplement the traditional one-to-one
may lead sufferers to believe that their symptoms are therapist—client model.
unchangeable and that their psychological and social
functioning will depend on them continuing to take Group therapy
their medication. This can often prevent such individu- Therapy can also be undertaken in a group and not just
als from trying to understand their symptoms and from on a one-to-one therapist—client basis. Group therapy
gaining insight into symptoms that may be primarily can be useful (1) when a
group therapy Therapy taken in the form
psychological rather than medical in nature (Bentall, group
se
of individuals share of a group, usually when individuals share
2003; see Activity 8.2 for an example related to drug similar problems or psy- similar problems or psychopathologies.
interventions for psychotic symptoms). Finally, there is chopathologies (e.g. self-
some evidence that while drug treatment of psychopa- help groups), or (2) when there is a need to treat an
thology may alleviate the immediate symptoms, it may individual in the presence of others who might have a
worsen the long-term course of a disorder. For exam- role in influencing the psychopathology (e.g. family
ple, while antidepressant drugs may alleviate the imme- therapy). Group therapies can have a number of advan-
diate symptoms of depression, there is evidence that tages, especially when individuals (1) may need to work
they may also increase vulnerability to relapse over the out their problems in the presence of others (e.g.
longer-term (Fava, 2003). This may be a result of drug in the case of emotional problems relating to relation-
tolerance effects as a result of continued drug use plus ships, feelings of isolation, loneliness and rejection), (2)
the fact that drug treatment alone may not facilitate the may need comfort and support from others, and (3) may
S148 PSYCHOPATHOLOGY
+ ~*~
acquire therapeutic benefit from observing and watching counsellors tend to adopt a range of theoretical
others. There are now many different types of group approaches, with the main ones being psychodynamic,
therapy (Bloch & Crouch, 1987), and these include cognitive behavioural, and humanistic (MacLeod, 2003).
experiential groups and encounter groups (which Counsellors with different theoretical orientations may
encourage therapy and self- often focus on different outcomes. Humanistic counsel-
encounter groups Group therapy which
encourages therapy and self-growth growth through disclosure lors tend to promote self-acceptance and personal free-
through disclosure and interaction. and interaction) and self- dom; psychodynamic counsellors focus primarily on
help groups (which bring insight; and cognitive behavioural counsellors are mainly
self-help groups Group therapy which together people who share a concerned with the management and control of behav-
brings together people who share a common problem in an iour and symptoms of psychopathology (MacLeod,
common problem in an attempt to share
information and help and support one attempt to share informa- 2003). Some counsellors specialize in areas such as mari-
another. tion and help and support tal breakdown, rape, bereavement or addictions, and
each other: e.g. Alcoholics their specialized roles may be recognized by the use of
Anonymous, http: / /www.alcoholics-anonymous.org titles such as mental health counsellor, marriage coun-
.uk/; see Focus Point 9.1). However, interventions that sellor or student counsel-
mental heaith counsellor A counsellor
have traditionally been used only in one-to-one client— lor. Counselling agencies
who specializes in mental health problems
therapist situations are now being adapted to group set- have been established in a
tings, and two of these include CBT and mindfulness range of organisations to
(Arch, Ayers, Baker, Almklov et al., 2013). Adapting inter- supplement community marriage counsellor A counsellor who
ventions for groups is likely to be a cost-effective solution mental health services and specializes in marriage problems. q
for service providers as well as an effective way of help- provide more direct and
student counsellor A counsellor who
ing clients to manage symptoms of psychopathology. immediate access to sup- specializes in students’ problems.
port for vulnerable or
Counselling needy individuals. Counselling services may be directed
Counselling is still a developing and evolving profession towards people with particular medical conditions such
that has burgeoned in the past 20-30 years, and its as AIDS and cancer, and also to the carers of individuals
expansion has partly resul- suffering these illnesses, and these services are often
For a video on the benefits of talking ‘ted from the increasing provided by voluntary and charitable organisations set
therapy go to _ demand for trained spe- up specifically for these purposes. Even individual
activities/ch4
cialists able to provide companies and organisations may have set up their
"immediate support and own in-house counselling services to help people
treatment across a broad through difficulties and anxieties associated with
counselling A profession that aims both to their work.
range of problems and cli-
promote personal growth and productivity
and to alleviate any personal problems that ent groups. Counsellors
may reflect underlying psychopathology. receive specialized train- Computerized CBT (CCBT)
ing in a range of support, Because a treatment such as CBT has a highly organized
guidance and intervention techniques, and their levels of structure, it lends itself well to delivery by other modes
training are monitored and accredited by professional and as a package that might be used independently by the
bodies such as the British Association for Counselling client. In recent years, computerized CBT (CCBT) has
and Psychotherapy (BACP) in the UK, or Division 17 been developed as an alter-
(Counselling Psychology) of the American Psychological native to therapist delivered computerized CBT (CCBT) Developed as-
an alternative to therapist delivered CBT,
Association. Arguably, the primary task for counselling is CBT, and consists of highly CCBT consists of highly developed software
to give the client an opportunity to explore, discover and developed software pack- packages that can be delivered via an
clarify ways of living more satisfyingly and resourcefully ages that can be delivered interactive computer interface on a per-
sonal computer, over the internet or via the
(British Association for Counselling, 1984), and to ‘help via an interactive computer
telephone using interactive voice response
clients to understand and clarify their views of their lifes- interface on a personal com- (IVR) systems.
pace, and to learn to reach their self-determined goals puter, over the internet or
through meaningful, well-informed choices and through via the telephone using interactive voice response (IVR)
resolution of problems of an emotional or interpersonal systems (Moritz, Schilling, Hauschildt, Schrdéder & Treszl,
nature’ (Burks & Stefflre, 1979, p.14). These definitions 2012). Two CCBT packages that have been recommended
indicate that counselling is a profession that aims at both by the UK Department of
promoting personal growth and productivity and allevi- Health are ‘Beating the Beating the Blues® A computer-based
ating any personal problems that may reflect underlying Blues’ and ‘Fear Fighter’: (1) CBT programme used in the management
psychopathology. In order to achieve these aims, Beating the Blues® as an of mild and moderate depression.
CHAPTER 4 TREATING PSYCHOPATHOLOGY aise
option for delivering computer-based CBT in the manage- as CCBT (Ormrod, Kennedy, Scott & Cavanagh, 2010;
ment of mild and moderate depression, and (2) Fear Barazzone, Cavanagh & Richards, 2012).
ar Fighter™ A computer-based CBT Fighter™ as an option for
gramme used in the management of delivering computer-based E-therapy
nic and phobia. CBT in the management The rapid growth of the internet over the past 15-20
of panic and phobia (NICE, years has meant people now have almost immediate
2008). Beating the Blues consists of a 15 minute introduc- access to information about mental health problems and
tory video and eight 1 hour interactive sessions, including email provides another potential form of communication
homework to be completed between sessions. The pro-
between ther apists and cli- e-therapy A treatment method which
gramme helps the client identify thinking errors, chal- ents. As a result more and __ involves the use of email and internet
lenge negative thoughts, and identify core negative more therapists and prac- technology.
beliefs, and provides help and advice on more adaptive titioners are using email as
thinking styles (http://www.ultrasis; see also Treatment an integral part of the treatment they provide and this is
in Practice Box 7.1). Fear Fighter is a CBT-based package often known as e-therapy (Hsiung, 2002). Email is a use-
for phobic, panic and anxiety disorders and is divided into ful adjunct to face-to-face sessions in a number of ways:
nine steps with support available from trained helpers via
telephone calls or emails throughout treatment. The 1. it may be used to enhance weekly sessions,
package helps clients identify specific problems, develop monitor treatment from a distance, monitor
realistic treatment goals, and monitor achievement behaviour daily, communicate with the client’s
through self-exposure (http: / /www.fearfighter.com). family members, or intervene in a crisis
CCBT is recommended by the UK National Institute (Yellowlees, 2002; Yager, 2002);
for Health and Care Excellence as a suitable intervention 2. it allows clients to initiate contact with
for individuals with persistent sub-threshold depressive the therapist more easily and, because the
symptoms or mild to moderate depression (NICE, 2008). communication is online, this may make the
Studies comparing CCBT with other forms of support client feel more secure (Ainsworth, 2002);
and intervention are still in their infancy, but those availa- 3. it allows clients who may be withdrawn or shy
ble are relatively supportive and suggest that CCBT along in personal face-to-face interviews (such as
with other guided self-help programmes can be a valuable adolescents with eating disorders) to be more
and effective way of treating individuals with common open and compliant (Yager, 2002), and
mental health problems (Cuijpers, Marks, van Straten,
4. it enables clients to contact therapists more
Cavanagh et al., 2009; Kaltenthaler, Parry, Beverley &
regularly in areas where resources are more
Ferriter, 2008). For example, Proudfoot, Ryden, Everitt,
difficult to access in person, or when clients are
Shapiro et al. (2004) found that Beating the Blues provided living in remote and inaccessible areas (Gibson,
a more effective treatment for depression and anxiety than
Morley & Romeo-Wolff, 2002).
GP treatment as usual, and in a review of 16 studies explor-
ing the efficacy of CCBT, Kaltenthaler, Parry & Beverley However, at present there is very little research on the
(2004) found that five studies showed CCBT to have effectiveness of online services or the potential beneficial
equivalent outcomes to therapist led CBT, and four stud- effects of email communication between therapists and
ies found CCBT to be more effective than GP treatment clients. There are also some limitations to email commu-
as usual. CCBT offers a number of advantages to both nication, including miscommunication because neither
clients and service providers, including increased flexible party to the communication is able to see the nonverbal
access to evidence-based treatments, reduction of waiting cues being given by the other, it is very difficult to ensure
lists, and savings in therapist time (Learmonth, Trosh, Rai, the confidentiality of online communications, and online
Sewell & Cavanagh, 2008; Titov, 2007). However, there communication makes it very difficult to intervene effec-
are still issues surrounding client engagement with CCBT. tively in severe emergencies, such as when, for example,
Clearly, clients need to have a minimum knowledge of a client may have suicidal intentions.
computers, and may often view CCBT as both mechani-
cal and impersonal (Beattie, Shaw, Kaur & Kessler, 2009). ‘Telepsychiatry’: Therapy by telephone
CCBT may also lack many of the ingredients to successful and videoconferencing
therapy that are a function of the therapeutic relationship Most clients telephone their therapists, if only to schedule
between therapist and client (Dogg-Helgadottir, Menzies, an appointment, but the telephone can also provide a
Onslow, Packman & O’Brian, 2009), but there are recent means of facilitating and
indications that it is possible to incorporate these impor- conducting treatment (which telepsychiatry Therapy facilitated by
is owns elepsychiatry). telephone or videoconference.
tant ‘alliance’ ingredients into self-help programmes such
16K PSYCHOPATHOLOGY
For example, Ludman, Simon, Tutty & Von Korff (2007) Improving Access to Psychological
report an evaluation of a telephone-based CBT pro- Therapies (IAPT)
gramme for depression in which clients were given eight It is now clear that mental health problems are far from
core sessions using standard CBT procedures adapted for uncommon. One in four people will suffer a diagnosable
use over the telephone. This was supplemented by mental health problem in their lifetime (Bebbington,
homework exercises for clients, and regular assessments Brugha, Coid, Crawford et al., 2007), and one in six
also conducted over the phone. Figure 4.1 shows that people in the UK will be diagnosed with either chronic
CBT conducted over the phone was more successful in anxiety or depression. These statistics have implications
reducing depression scores than usual care (clients receiv- for the well-being of those who suffer these disabilities,
ing antidepressants) up to 12-18 months post-treatment, their families, the agencies that are attempting to pro-
and these supplement results of other outcome studies vide services for those with mental health problems,
suggesting that telephone therapy is both acceptable and and also the contribution that sufferers can make to the
effective (Leach & Christensen, 2006; Lynch, Tamburrino economic prosperity of the countries in which they live.
& Nagel, 1997; Mohr, Hart, Julian, Catledge et al., 2005). Mental health is the largest single cause of disability in the
Telephone therapy may prove to be an effective form UK, with the total loss of economic output due to depres-
of intervention when clients live in remote or inacces- sion and anxiety in the UK estimated to be in excess of
sible areas, and it is a mode of delivery that can save time £12 billion a year (London School of Economics &
and reduce travel costs. Furthermore, with continued Political Science, 2006; Department of Health, 2012). It
developments in computer technology, real-time video therefore not only makes good therapeutic sense to
conferencing is also a means by which psychotherapy improve access to mental health treatments, it also
can be delivered to clients who are physically disabled makes good economic sense to help people recover
or live remotely, and comparative studies of face-to- from their problems. Givén the evidence-based success
face, real-time video conferencing, and two-way audio of therapies such as CBT for common mental health
therapy suggest that differences in outcomes among the problems, many countries are now trying to find
three modes of treatment delivery are surprisingly small ways to increase and improve access to these therapies.
(Day & Schneider, 2002; Shore, 2013). This has given rise to large-scale initiatives, comm-
only known as Improving Access to Psychological
Therapies (IAPT), which aim at increasing significantly
=~ == Usual care the availability of evidence-based interventions — such
Vv WeRie Rass stePeeters
UF 3 —»<—= Phone therapy |-- as CBT. To meet these
=
je) goals involves: (1) training Improving Access to Psychological
ac \ Acute-phase
significant numbers of Therapies (IAPT) NHS programme
ne) ) treatment providing services across England for treat-
Al (months 0-6) Continuation or booster- practitioners in psycho- ing people with depression and anxiety
v \ phase treatment Post-treatment phase
eo
oO
1 X
Y
(months 6-12) (months 12-18) logical therapies such as disorders.
aa
U
CBT — known as psycho-
Yn
am logical well-being practitioners (PWPs) (Focus Point
4.2 provides a personal account of someone who was
trained to deliver low-
intensity CBT under the psychological well-being practitioners
(PWPs) People trained under the I|APT
Months since randomisation IAPT scheme); (2) improv- initiative to deliver psychological therapies
ing access and reducing such as CBT.
FIGURE 4.1 /mprovement in depression scores as a waiting times for treat-
function of therapy by telephone (CBT) or care as usual ment; and (3) increasing client choice and satisfaction. A
(pharmacotherapy). CBT by telephone results in a marked consequence of this will be improved social and eco-
improvement in depression scores over pharmacotherapy
nomic participation as those previously suffering com-
in the first 6 months of treatment and gains are maintained
mon mental health problems return to work and normal
up to 18 months after the start of treatment. (HSCL =
social and family functioning. Asa result, the costs of the
Hopkins Symptom Checklist, a measure of the remission of
IAPT programme are considered to be offset by the
depression).
Source: After Ludman, E.J., Simon, G.E., Tutty, S. & Von Korff, M.
increased economic contribution of those who have
(2007). A randomized trial of telephone psychotherapy and recovered from their mental health problems (e.g.
pharmacotherapy for depression: Continuation and durability of Radhakrishnan, Hammond, Jones, Watson et al., 2013).
effects. Journal of Consulting and Clinical Psychology, 75, 257-266. Key successes of the programme in the UK in the first 3
American Psychological Association. Adapted with permission. years include (1) treating more than 1 million people in
CHAPTER 4 TREATING PSYCHOPATHOLOGY va
IAPT services, (2) recovery rates in excess of 45 per cent Verdeli, 2011), where lay and community health workers
(see section 4.2.2 for a discussion of recovery rates for are being trained in evidenced-based practices. However,
psychological therapies), and (3) over 45,000 people mov- the challenges of providing access to psychological thera-
ing off benefits into paid employment (Department of pies for those who need them are still immense, with the
Health, 2012). Schemes for improving access to psycho- ‘treatment gap’ (a term used to describe the shortfall in
logical therapies are now being rolled out in many coun- mental health provision for sufferers) exceeding 75 per
tries, including developing countries such as India, cent in most parts of the world (Kohn, Saxena, Levav &
Pakistan and Uganda (Patel, Chowdhary, Rahman & Saraceno, 2004).
ASHLEY SNOWDON’S EXPERIENCE Teaching people CBT-based skills has meant that
they have been able to take control of their own prob-
Psychological Well-being Practitioner, lems and are more able to manage them in future.
Teeside IAPT Service | have often found that people integrate CBT skills into
their lives and then come back and report that they
Working as a psychological wellbeing practitioner have been teaching them to their friends and family!
POINT
FOCUS(PWP) in Teesside IAPT has been challenging and
4.2 | have also been closely involved in a pilot scheme
rewarding over the past few years. Since completing working with drug and alcohol users, who have
my training, | have seen over 200 people, some with responded really well to the short-term, time-limited
| relatively complex problems who have never accessed work, because they can see quicker results and seem
- mental health treatment before, for whom brief inter- to feel empowered by the guided self-help approach.
ventions have had a huge impact on their functioning.
The range of problems clients have presented with has Source: |APT three-year report: The first million patients,
been surprisingly broad, and has given me excellent November 2012. http://www.hsj.co.uk/Journals/2012/12/04/
development opportunities as well as developing my w/g/m/9265-2900428-TSO-IAPT-3-year-report-pdf.pdf.
| confidence as a clinician. Reproduced with permission.
® What are the main principles of psychodynamic therapy?

® Can you describe some ofthe basic techniques used by psychoanalysts?
® Can you describe the behaviour therapy techniques that are based on classical conditioning?
* Can you describe some of the treatment techniques that have been developed based on principles of operant
reinforcement?
® Can you describe at least two types of cognitive therapy?

© What are ‘third wave’ CBT methods — can you describe at least one ofthese?
® What are the main theoretical principles on which humanistic therapies are based?
® What are the main principles used in client-centred therapy?
® What is family therapy and how is it conducted?
® Can you name the main types of drug treatments for psychopathology?
® Can you describe two to three types of group therapy?
® What are the main characteristics of counselling?
° Can you describe the main features of computerized CBT (CCBT), e-therapy, and therapy by telephone?
© What does IAPT stand for, and what is it trying to achieve?
oa pti PSYCHOPATHOLOGY
SECTION SUMMARY
4.1 THE NATURE AND FUNCTION OF TREATMENTS FOR PSYCHOPATHOLOGY
With the average waiting-time for conventional treatments provided by community mental health services in many parts of
the world often longer than 1-2 years — especially for popular and specialized treatments such as CBT — practitioners and ser-
vice providers are under pressure to provide more cost-effective and immediate forms of interventions for people with mental
health problems (Layard, 2007). We have reviewed some of the modes of delivery that may prove to be more immediate
and cost effective, although most of these modes ofdelivery represent relatively new innovations that have yet to be fully and
properly evaluated.
e The treatment provided for a psychopathology will depend on the theoretical orientation of the therapist and the nature
of the psychopathology.
© Psychodynamic approaches to therapy attempt to reveal unconscious conflicts that may be causing psychopathology.
© Behaviour therapies are mainly based on the principles of classical and operant conditioning.
® Behaviour therapies based on classical conditioning include flooding, counterconditioning, systematic desensitisation, and
aversion therapy.
e Therapies based on operant conditioning include functional analysis, token economy, response shaping, and behavioural
self-control.
¢ Important cognitive therapies include rational emotive therapy (RET), Beck’s cognitive therapy, and cognitive behaviour
therapy (CBT).
¢ ‘Third wave’ cognitive therapies include mindfulness-based cognitive therapy (MBCT) and acceptance and commitment
therapy (ACT).
e Humanistic therapies attempt to consider the ‘whole’ person and not just the symptoms of psychopathology.
¢ Family therapy attempts to deal with psychopathology by addressing relationship dynamics within the family.
e Drug treatments have been developed to alleviate some of the symptoms of psychopathology, particularly in disorders
associated with depression, anxiety and psychosis.
e Important drug treatments include antidepressant drugs, anxiolytic drugs, and antipsychotic drugs.
¢ Recently developed modes of treatment delivery include group therapy, counselling, computerized CBT (CCBT), e-therapy,
‘telepsychiatry’, and the Improving Access to Psychological Therapies (IAPT) programme.
theoretical approaches to treatment use radically differ-

4.2 EVALUATING ent criteria for judging outcomes. Therapists using CBT
TREATMENT typically use elimination of psychopathology symptoms
as the main criterion of success; behaviour therapists
view the modification of maladaptive behaviours as
All of the therapies and treatments we have discussed in important; psychodynamic therapists view the elimina-
previous sections of this chapter have at least some degree tion of unconscious conflicts as critical to therapeutic
of intuitive plausibility as treatments for psychological success; and humanistic psychotherapists see enhance-
problems. Nevertheless, how do we assess how effective ment of personal autonomy as their main therapeutic
a treatment is? This is not as simple as it sounds. Firstly, objective. Erwin concludes that, at the end of the day,
we often have to try to compare the efficacy of therapies what constitutes a successful therapeutic intervention is
that have quite different assumptions about what ‘suc- often a subjective judgement and may boil down to little
cessful therapy’ is (e.g. cognitive therapies would expect more that the outcome was beneficial in some way to the
to see some significant improvement after a few weeks client — or at least to someone!
or months, whereas psychoanalytic and humanistic Despite these difficulties in deciding on a common
therapies are seen as developmental, life-long processes set of criteria for gauging success across different treat-
promoting self-growth). And secondly, we have to decide ment types, there are some good reasons for wanting to
on what constitutes a therapeutic gain (i.e. on what par- try to objectively assess how successful therapies are:
ticular measures are we expecting to see improvement?). (1) psychological disorders are distressing to the indi-
For example, Erwin (2000) describes how different vidual, and we have a moral and professional obligation :
CHAPTER 4 TREATING PSYCHOPATHOLOGY cto
to seek ways of alleviating this distress rapidly and effec- are generally very complex things, and they will often
tively; (2) some treatments may have short-term gains contain many factors that might help (or hinder) recov-
but be significantly less effective over the longer term — ery. Some obvious factors that might help recovery
leaving the individual open to relapse — so we need to be include a sympathetic therapist, a rationale for recov-
sure that therapies have lasting therapeutic effects; and ery that the client understands and believes will help
(3) individuals with psychological problems are a very them, a therapeutic intervention with well thought-out
vulnerable group of people, and we need to ensure that principles that have been tried and successfully tested
they are not exploited financially and psychologically by before. Factors that might hinder recovery include an
what is a growing industry of essentially bogus therapies unsympathetic therapist, an unsupportive home envi-
with shallow — but often beguiling — rationales, and little ronment, or the use of an intervention that is poorly
or no medium-term therapeutic benefit. structured and not soundly based on proven psychother-
apy principles. These are all factors that need to be con-
sidered when evaluating the effectiveness of a therapy,
and we will discuss these in turn below. However, one of
4.2.1 Factors Affecting the the central issues in evaluative research is determining
whether an intervention is effective primarily because of
Evaluation of Treatments
the therapeutic principles in the intervention (e.g. psy-
On what basis do therapists decide whether their treat- choanalytic principles, cognitive-behavioural principles,
ments are successful? Focus Point 4.3 provides an inter- and so on), and determining whether a treatment works
esting example of this (described by Davey, 2002). The because of the principles it _jnternal validity Determining whether a
therapist in this example assumed that her treatment was contains is known as assess- treatment works because of the principles
ing its internal validity. it contains.
being effective because no one ever returned to complain
about it! But there could be many reasons why individ- Because therapeutic interventions are usually a con-
uals may not complain, and the client in this example glomeration of many different factors, assessing the
is quite happy to return for more therapy even though reasons for the efficacy of therapies is difficult, and
her first session was not as successful as she was led to the sections below describe some of the factors that can
believe it should be. The moral of this story is that a cli- confound the assessment of therapeutic effectiveness.
ent simply saying they are satisfied with the outcome of
the therapy does not mean either (1) that any objective Spontaneous remission
therapeutic gain has been achieved, or (2), if some thera- Just because someone exhibits objective improvement in
peutic gain was achieved, that it was due explicitly to the symptoms after treatment does not necessarily mean
type of therapy that was used. Therapeutic interventions that the treatment was the cause of the improvement.
|
sie
oh STOP SMOKING IN ONE SESSION!
Z= As | was passing a local ‘holistic’ health clinic, | noticed

a sign outside which - in large letters — implored “STOP
‘| did not do follow-up calls as | thought this would be
intrusive so, therefore, | do not have stats on my suc-
(e) SMOKING IN ONE SESSION!” (Which session? Surely cess rates. However, | know | have had a high success
a.
wi not the first one?!) Having interests in both clinical rate because people referred others to me and came
> and health psychology areas, | was intrigued to find back to me for help on other issues’ Interestingly, my
WU
eo)
ine
out more. As it turns out, a friend of mine had just
recently visited the clinic and had received a single
friend who had attended the clinic was smoking regu-
larly again within 3 days of the hypnotherapy session,
1 hour session of hypnotherapy in an attempt to stop and — despite having long discussions with me about
smoking — cost £50. Knowing the literature on psy- the validity of the treatment and its lack of success —
chological treatments for smoking and how difficult it said she was thinking of attending again (this time in
is to achieve abstinence, | decided to find out a little relation to other aspects of her life) because the hyp-
more about these treatment claims. | emailed the hypnotherapist had been so caring, understanding and
notherapists offering services at the clinic and asked interested in her problems!
if stopping smoking in one session of hypnotherapy
was achievable, and what their success rates were like. Source: From Davey G.C.L. (2002). Smoking them out. First
| did get a reply from one ofthe practitioners, who had published in The Psychologist, 15(10). Published by The British
worked as a hypnotherapist for 7 years. She replied: Psychological Society (www.thepsychologist.org.uk).
704) PSYCHOPATHOLOGY
: * ey
The famous British psychologist Hans Eysenck argued in making people better, but whether they make people
that many people who have mental health problems will better specifically because of the principles they contain
simply get better anyway over a period of time — even (see above). .
without therapy (Eysenck, 1961), and this can often be Consequently, studies that attempt to evaluate the
the result of an individual’s changing life experiences effectiveness of a therapy’s principles also need to
(e.g. positive life changes) (Neeleman, Oldehinkel & control for other factors such as the amount of atten-
Ormel, 2003). This is known as spontaneous remission, tion or empathy that the client is receiving from the
and the current estimate is therapist. One recently developed form of control
spontaneous remission The fact that condition for attention, understanding and caring is
that around 30 per cent of
many people who have psychological dis-
orders will simply get better anyway over a those diagnosed with anxi- known as befriending. This is a control condition
period of time, even without therapy. ety and depression-based designed to provide par- ; =
Sy t ‘eh ea potore befriending
A form of control condition —
disorders will get better Sear i ae for attention, understanding and caring
without structured treatment (Jacobson & Christenson, mately the same amount sed in treatment outcome studies.
1996). So, if we are assessing the effectiveness of a ther- of therapist contact as
apy we would expect to see improvement rates signifi- the treatment conditions being tested, with sessions
cantly greater than 30 per cent in order to take into spaced at similar intervals. In the befriending condition
account the fact that many of those undertaking the the therapist aims to be empathetic and nondirective and
therapy would show a spontaneous improvement in does not attempt to directly tackle symptoms, and the
symptoms anyway. session is normally focused on discussion of neutral top-
ics such as hobbies, sport, and current affairs (Sensky,
Placebo effects Turkington, Kingdon, Scott et al., 2000; Bendall, Jackson,
If someone suffering with anxiety symptoms is given a Killackey, Allott et al., 2006).
sugar pill but they are told that it is an anxiolytic medica-
tion, they often report significant improvements in those
symptoms. This suggests that individuals will often get 4.2.2 Methods of Assessing the
better because they expect to get better — even though
Effectiveness of Treatments
the actual treatment that they have been given is effec-
tively useless (Paul, 1966). This is known as the placebo We have to begin this section by acknowledging that
effect (Paul, 1966; see also section 3.3.4). Thus, it may be the advocates of some therapeutic approaches do not
the case that many psychological treatments have ben- believe that the success or otherwise of their therapeutic
eficial effects because the client expects them to work — approaches can be assessed using objective or quantita-
and not because they are treatments that are effective tive methods (e.g. Marzillier, 2004). This is because those
in tackling the factors maintaining the psychopathol- therapists view their treatments not as attempts to elimi-
ogy. Unfortunately, the positive gains produced by pla- nate symptoms of psychopathology, but as attempts to
cebo effects are short-lived, and comparative studies of reconstruct a client’s meaning of the world (e.g. Rosen,
placebo effects with actual structured psychotherapies 1996), or to move the client from one phenomenologi-
strongly suggest that structured psychotherapies lead cal state to another (e.g. humanistic approaches). In each
to greater improvement than placebo control condi- case, these are not changes that are easy to objectively
tions (Robinson, Berman & Neimeyer, 1990; Andrews & measure, and nor are there particularly well-defined cri-
Harvey, 1981). teria for when these goals have been reached.
Nevertheless, there are still many compelling reasons
Unstructured attention, understanding for wanting to assess in some formal way whether a
and caring treatment is effective and successful, and we have aired
In addition, we know that people with psychological some of the moral and compassionate reasons for want-
problems also show some improvement in symptoms ing to do this at the beginning of section 4.2. In addition
when they can simply talk about their problems in an to these reasons, mental health service providers have
unstructured way with either a professional therapist or a duty to ensure that the services they are offering are
a friend or relative (Lambert, Shapiro & Bergin, 1986). effective, and they will need some benchmark by which
This suggests that many forms of social support may have to measure whether the treatments they offer are either
a therapeutic effect in and of themselves (Borkovec & successful or at least provide satisfaction for the end-
Costello, 1993), and this factor must be taken into users they are providing for.
account when judging how effective a structured ther- Two popular methodologies for assessing the effec-
apy is. One of the important things that we want to find tiveness of treatments are: (1) randomized controlled
out about therapies is not just whether they are effective trials, and (2) meta-analyses and systematic reviews.
CHAPTER 4 TREATING PSYCHOPATHOLOGY Pan
Randomized controlled trials (RCTs) Problems with RCTs While RCTs do provide an
objective way of assessing the effectiveness of therapies,
What are RCTs? The current methodology of they do have a number of practical limitations: (1) partic-
choice for assessing the effectiveness of therapies is ipants do drop out of these studies, and may do so more
randomized controlled trials (RCTs) (e.g. Barker, from some conditions — e.g. the no treatment conditions —
Pistrang & Elliott, 2002, than others, (2) RCTs are costly and time consuming to
idomized controlled trials pp.153-159; Jadad & undertake, and (3) because participants are assigned ran-
's) Comparison of the effectiveness of
reatment being assessed with a variety
Enkin, 2007). This proce- domly to conditions, it does not take account of the fact
control conditions, and with other forms dure compares the effec- that some participants may prefer some types of therapy
therapy and treatment (if necessary). tiveness of the treatment to others (Brewin & Bradley, 1989).
being assessed (across a Furthermore, to be genuinely objective, RCTs need to
range of objective measures) with a variety of control be free of any form of explicit or implicit bias that might
conditions, and with other forms of therapy and treat- influence the results of a basic comparison between the
ment (if necessary). Participants in the study are intervention being assessed and the control conditions.
assigned randomly to each of these conditions. Apart Unfortunately, this is often not the case. Firstly, those
from the treatment being assessed, the control condi- who carry out the RCT often have an allegiance to the
tions used in RCTs are those that will control for the psychotherapy being tested, and this may be a source
kinds of effects described in section 4.2.1. These will of experimenter bias that favours the effectiveness of
include: (1) a no treatment or a waiting list control that intervention. Meta-analytic reviews suggest that
group of participants who researcher allegiance to a particular intervention does
iting list control Participantsin a ran- _ will receive no treatment indeed substantially bias the results of an RCT (Munder,
mized controlled trial who will receive (to control for the effects Briitsch, Leonhart, Gerger & Barth, 2013). Secondly,
treatment; often difficult to achieve nf
cause of the ethical issues involved
spontaneous remis- there is a significant bias in scientific publication to pub-
withholding treatment from clinically sion), a condition that is lishing findings when there is a significant difference
stressed individuals. often difficult to achieve between experimental interventions and control con-
because of the ethical ditions, but not when this difference is non-significant
issues involved in withholding treatment from clini- (the latter are known as ‘null findings’) (Dwan, Altman,
cally distressed individuals (see section 3.4.2); (2) an Arnaiz, Bloom et al., 2008). Thus, there may well be a
expectancy and relationship control group, to control large number of RCTs that have shown no effect of a
for placebo effects and for the beneficial effects of con- treatment compared with control conditions, but have
tact with a therapist (e.g. ‘befriending’ — see section never been published. This has the effect of biasing RCTs
4.2.1); and (3) a comparative treatment group, in which towards providing published evidence that a treatment
the original therapy can be compared with a plausible ‘works’ rather than ‘doesn’t work’. In addition, commer-
alternative therapy that is known to have beneficial cial interests may be associated with whether an RCT
effects. For the original therapy to be deemed effective is published that reports a positive finding or a nega-
and possess internal validity, participants receiving that tive finding. For example, Yaphe, Edman, Knishkowy &
therapy must show greater improvement than those in Hermand (2001) found that RCTs assessing the effective-
both the no treatment and the expectancy and relation- ness of drug treatments were significantly more likely
ship control conditions, and improvement that is at to report a positive or significant effect if the study had
least equivalent to that exhibited by the comparative been funded by the pharmaceutical industry than if
treatment group. Figure 4.2 provides a schematic exam- funds came from non-industry sources!
ple of one RCT study comparing the efficacy of cogni- Finally, we must remember that RCTs have tradi-
tive therapy and exposure plus applied relaxation tionally only told us whether a particular intervention
treatments for social phobia. This shows how the origi- is significantly better than a control condition or signifi-
nal 116 participants in the study were assessed, the rea- cantly better than an alternative intervention (in terms
sons why 54 were excluded from the study, how they of effect sizes; see section 4.2.3). What they often do not
were randomly allocated to one of three treatment tell us is what percentage of the participants in the study
conditions, how many dropped out of the study before exhibited recovery or clinically significant change to the
completion, and when the outcome assessments were point where they no longer meet the criteria for a clini-
taken. The graph below the flow chart shows that the cal diagnosis (Jacobson
clinical significance The percentage
cognitive therapy condition was significantly more se ‘Ieugng WOOle Wise.
of participants in a study who exhibited
effective at reducing symptoms of social phobia than 2004). The latter is known recovery or clinically significant change to
both exposure and applied relaxation and those in a as clinical significance the point where they no longer meet the
waiting list control condition. and the former reflects criteria for a clinical diagnosis.
Py PSYCHOPATHOLOGY
116 Referrals meeting DSM-IV

criteria for social phobia
barre Die ob pseiy) uss ;
54 Excluded |
Reasons for siclusioh
11 social phobia not main prohient
10 current or past psychosis
8 previous CBT or EXP.
—y» £7toomild
5 alcohol/substance dependence —
4 severe depression requiring
immediate treatment :
2 borderline personality disorder
7 refused to participate
21 Allocated to CT | 21 Allocated to EXP + AR 20 Allocated
49 Cc npleted Treatment,
|
2 ee Out
=o Wait
4— Exp + AR FIGURE 4.2 A random controlled trial comparing the effec-
== CT tiveness of CBT and applied relaxation for social phobia.
The flow chart shows how the 116 participants in the study
were allocated to experimental conditions and assessed.
The graph below the flow chart shows that the CBT condition
(CT) was more effective at reducing the symptoms of social
phobia than exposure and applied relaxation (Exp + AR) and
Phobia
Social
Composite a ‘waiting list’ control (Wait).
Source: Clark, D.M., Ehlers, A., Hackmann, A., McManus, F. et al.
(2006). Cognitive therapy versus exposure and applied relaxa-
tion in social phobia: A randomized controlled trial. Journal
Pre Post 3m FU LYnEU
of Consulting and Clinical Psychology, 74, 568-578. American
Assessment Psychological Association. Reproduced with permission.
&
CHAPTER 4 TREATING PSYCHOPATHOLOGY | 423
recovery rates. Jacobson

-overy rates The percentage of people 4.2.3 What Treatments Are Effective?
& Truax (1991) pointed out
10 are no longer diagnosable once they
ve finished treatment. Although we have identified a couple of objective
that statistical significance
and clinical significance do ways of assessing whether therapies are effective, what
not convey the same kinds of information about an inter- do studies using these methods tell us? Comparative
vention, and that it is important to determiite whether studies tend to suggest that most of the accepted ther-
the intervention ‘moves the client from the dysfunctional apies are more effective than no treatment or expec-
to the functional range during the course of therapy’ tancy control conditions, but that the therapies
(Jacobson, Follette, Revenstorf, Baucom et al., 1984, themselves do not differ in their relative effectiveness.
p.340). While most structured interventions are more For example, in a study of depressed individuals,
effective than no treatment control conditions, a look at Gibbons, Hedeker, Elkin, Waternaux et al. (1993)
recovery rates often suggests a less than perfect picture. found that cognitive therapy, interpersonal therapy,
Even for well-established psychological and pharmaceu- and antidepressant medication were all as effective as
tical interventions, recovery rates for common mental each other, but all more effective than a placebo con-
health problems (the percentage of people that are no trol condition (after 16 weeks of treatment). Similarly,
longer diagnosable once they have finished treatment) the meta-analysis conducted by Smith, Glass & Miller
is normally between 50 and 70 per cent (e.g. Hanrahan, (1980) also indicated that psychotherapies were all
Field, Jones & Davey, 2013; Baldwin, Woods, Lawson more effective than no treatment, but none was sig-
& Taylor, 2011; Craske, Liao, Brown & Vervliet, 2012), nificantly more effective than another. This has come
suggesting that such interventions fail to ‘cure’ between to be known as the Dodo Bird Verdict, which is a
30 and 50 per cent of those being treated. This probably phrase taken from Lewis Carroll’s Alice’s Adventures
testifies more to the complexity of many mental health in Wonderland, implying
problems and the factors that maintain psychopathol- that all psychotherapies Dodo Bird Verdict An expression
ogy than the relative ineffectiveness of our current inter- are winners and produce from Lewis Carroll's Alice’s Adventures in
ventions. But clearly more needs to be done to develop equivalent benefits for Wonderland, implying that all psychothera-
pies are more effective than no treatment,
—— te ee ee interventions-thatwill:help clients. This debate is but produce equivalent benefits.
To read the author's blog on
) larger proportions of suf. considered in more detail
‘The lost 40%’go to
http://tinyurl.com/px4znd5 | ferers to fully recover. in Focus Point 4.4.
Nevertheless, despite Rather than conducting objective and well-controlled
some of these limitations, outcome studies, some others have approached the
RCTs have remained a popular method for assessing the issue of the effectiveness of treatments by viewing
relative effectiveness of treatments and are still consid- the client as a consumer and canvassing their views on
ered to be the main standard by which the effectiveness how satisfied they have been with the treatment ‘prod-
of an intervention is experimentally tested. uct’ that they received. Seligman (1995) reported the
results of a large-scale survey of individuals in the USA
Meta-analyses and systematic reviews who had undergone psychotherapy and concluded that:
We have already discussed meta-analyses and system- (1) respondents claimed they benefited significantly
atic reviews as a research method in section 3.3.8, and from psychotherapy, (2) psychotherapy alone did not
the reader is referred back to this in the first instance. differ in effectiveness from medication plus psychother-
The benefit of meta-analyses is that they can be used apy, (3) psychologists, psychiatrists, social workers and
to compare the effectiveness of studies that may have counsellors did not differ in their effectiveness as thera-
used different procedures, different numbers of partici- pists, and (4) the longer the duration of their treatment,
pants, different types of control procedures, and different the larger the positive gains respondents reported.
forms of measurement, and they do this by comparing While the empirical rigour of this consumer-based
effect sizes across studies. One important use of meta- study falls far short of that expected in well-controlled
analyses has been to try to answer an enduring question outcome studies, it does provide some information
in psychotherapy: are psychotherapies more effective about how the recipients of psychotherapy view their
than no treatment at all? An early large-scale meta- treatment and its effects. But, as we have noted in Focus
analysis carried out by Smith, Glass & Miller (1980) con- Point 4.3, asking a client how satisfied they are follow-
cluded that psychotherapies were more effective than ing treatment may not be the best way to judge the
no treatment, but that effect sizes did not differ across effectiveness of a treatment and may reflect the involve-
different psychotherapies, suggesting that all different ment of psychological factors that extend beyond the
psychotherapies were equally effective. original purpose of the treatment.
Mae) PSYCHOPATHOLOGY
= THE DODO BIRD VERDICT

+
- as therapist-client only. relationship — known as the
= therapeutic alliance (Lambert, 1992; Del Re, Fluckiger,
oO Horvath, Symonds & Wampold, 2012), and Wampold,
a
Wi Minami, Baskin & Tierney (2002) found that 7 per
=) cent of the variability in treatment outcome was due
UV
O
x Can ‘
to the therapeutic alliance compared with only 1 per
f wee a
Li, i"
cent attributable to the principles inherent in the
type of psychotherapy being deployed. Apart from
the therapeutic alliance itself, specific features
of the therapist have also been identified as contrib-
uting to the success of therapy. These include posi-
tive, warm, and caring attitudes towards the client
(Najavits & Strupp, 1994), and providing good feed-
back, helping the client to focus on and understand
their own thoughts, attempting to promote auton-
omy and self-efficacy in their clients, and helping
the client with their existing relationships (Korchin &
Sands, 1983).
However, there is evidence that can be mustered
on both sides of the Dodo Bird Verdict, and this debate
is still very much alive (Wampold, Imel & Miller, 2009;
Siev & Chambless, 2009). Some claim that improve-
A number of influential comparative studies and ments in statistical analyses now allow us to make
early meta-analyses all suggested that although psy- fine-grained distinctions between the effectiveness
chotherapies were more effective in treating mental of different therapies in a way that we could not do
health problems than placebos and other appropri- previously (Chambless & Hollon, 1998; Otte, 2011); we
ate controls, no psychotherapy was more effective can demonstrate that some psychotherapies are more
than any other psychotherapy (Smith, Glass & Miller, effective for some mental health problems than for oth-
1980; Gibbons, Hedeker, Elkin, Waternaux et al., 1993; ers (Siev & Chambless, 2007, 2009); and, indeed, we not
Luborsky, Singer & Luborsky, 1975). As early as 1936 only have to consider whether interventions are effec-
Saul Rosenzweig had labelled this effect the Dodo tive in treating psychopathology symptoms, we also
Bird Verdict (Rosenzweig, 1936) after the bird in Lewis have to consider whether they might aiso be harmful
Carroll's Alice's Adventures in Wonderland. |n that story, in the sense that they may evoke negative responses
a number of animals had become wet and in order to to treatment in Some geeenemusnem=emes
dry themselves ran round the lake to see who could clients or client groups / To read more about the therapist
get dry first. No one measured how far they’d run or (e.g. individuals diag- | effect go to
www.apa.org/monitor/2013/02/
for how long, but when asked who had won, the dodo nosed with substance | therapist.aspx
said ‘Everybody has won and all must have prizes’! dependency) (Dimidjian
Those who agree with the Dodo Bird Verdict & Hollon, 2010).
claim that all psychotherapies are equally effective In conclusion, while there is still lively debate about
because they all contain some important common the relative efficacy of various interventions for psy-
factors that are shared across all psychotherapeutic chopathology, there is no doubt that hundreds of
interventions. This is known as the common factors studies have clearly demonstrated that psychotherapy
theory, and Grencavage & Norcross (1990) identified is effective. The Dodo Bird Verdict has also helped to
up to 35 common factors across psychotherapies focus attention on those aspects of psychotherapy
that influence therapeutic outcome. They divided that are common across a majority of intervention
these into five main groups that included client types (e.g. therapist characteristics, the therapeutic
characteristics, therapist characteristics, the change alliance, and suchlike), and clinical psychologists are
process, treatment structures, and therapist-client currently working to identify some of the important
relationship elements. One of the most important characteristics that make some psychotherapists more
common factors affecting outcome is the ideally split effective than others.
CHAPTER 4 TREATING PSYCHOPATHOLOGY as"
SELF-TEST QUESTIONS
What kinds of factors can affect the evaluation of treatments and need to be controlled for in treatment outcome studies?
* What are the two most popular methodologies for assessing the effectiveness of treatments?
* Are structured treatments for psychopathology effective?
* What is the ‘Dodo Bird Verdict’ in relation to the effectiveness of psychotherapies?
SECTION SUMMARY
4.2 EVALUATING TREATMENT
In this section we have described some of the methods that have been developed to try and evaluate the effectiveness of treat-
ments for psychopathology. Over the past 10-20 years a large number of studies assessing the efficacy of therapies for psy-
chological disorders has been carried out, and there is now good empirical evidence to support the effectiveness and internal
validity of many of these therapies. There are too many to mention here, but the interested reader is referred to Chambless&
Ollendick (2001) for a review and analysis of many of these studies; to Butler, Chapman, Forman & Beck (2006) for a review of
the effectiveness of CBT for a range of psychopathologies; and to Westen, Novotny & Thompson-Brenner (2004) for a review
of the pros and cons of the RCT method for assessing the effectiveness of treatments. The reader is also referred to the treat-
ment sections of individual psychopathology chapters in this book for a review of the most effective treatments for individual
psychopathologies.
e Factors affecting the evaluation of treatments include spontaneous remission, placebo effects, and attentional factors pro-
vided by the therapist’s relationship with the client.
e Popular methods for assessing the effectiveness of treatments are randomized controlled trials (RCTs) and meta-analyses.
¢ Most large-scale studies suggest that treatment in general is significantly more effective than no treatment, but that no
psychotherapy is necessarily more effective than any other (known as the Dodo Bird Verdict).
humanistic therapies, and family or systemic thera-

4.3 TREATING pies. Because of the demands placed on overstretched
clinicians and service providers, several different cost-
PSYCHOPATHOLOGY effective modes of delivery have been developed in
REVIEWED recent years, and these include group therapy, counsel-
ling, computerized CBT (CCBT), e-therapy, ‘telepsychia-
try, and programmes designed for the Improving Access
Treatments for psychopathology have developed sig- to Psychological Therapies (IAPT) programme.
nificantly over the past 50-60 years, and the main aims Evaluating the effectiveness of treatments for psycho-
of treatments are to provide relief from the distress of pathology is still a difficult and disputed process, with
symptoms, equip the client with insight into their disagreements about what constitutes a therapeutic
problems, and provide the client with a means of cop- gain, how long it may take to achieve a successful out-
ing with life problems and psychological distress. Most come, and how therapeutic gains should be measured
treatments for psychopathology consist of either drug (if they can be measured at all). The practical need for
treatments or psychotherapy, and psychotherapy can be objective methods for assessing the relative success of
divided into five main theoretical approaches: psychody- treatments has given rise to the adoption of randomized
namic approaches, behaviour therapy, cognitive therapy, controlled trials (RCTs) and meta-analyses as important
126 PSYCHOPATHOLOGY
; %
methods for assessing treatments. Most large-scale stud- a significant increase in the number of treatment out-
ies indicate that psychotherapies generally are more — come studies published, and many of these indicate that
effective than no treatment, but there is little convinc- certain types of treatments may be more effective than
ing evidence that one psychotherapy method is neces- others at treating individual specific psychopathologies
sarily more effective than another (known as the ‘Dodo (see also the treatment sections in the following chapters
Bird Verdict’). Nevertheless, the past 20 years have seen covering individual psychopathologies).
El To access the online resources for this chapter go to

Reading Activity
Author blog - The Lost 40% e The benefits of talking Activity 4.1
The therapist effect therapy Activity 4.2
Journal article: Application Self-test questions
of operant conditioning to Revision flashcards
reinstate verbal behavior in
Research questions
psychotics
Glossary key terms
Clinical issues
References
5 Clinical Practice
iis
fiz To access the online resources for this chapter goto
atta www.wiley-psychopathology.com/ch5
This chapter starts by taking a broad perspective of clini-

cal practice by describing the scale of mental health prob- i 5-! THE ECONOMIC COST OF MENTAL HEALTH
lems that service providers face. We then discuss the types PROBLEMS 129
of mental health professionals that work in this sector,
how individuals with mental health problems access ser- 5.2 WHO ARE MENTAL HEALTH PROFESSIONALS? 130
vices, and the facilities that are available across mental
health services. We end the chapter by focusing on clini- 5.3 PROVIDING MENTAL HEALTH SERVICES 133
cal psychologists and discussing their key capabilities and ‘
competences, how they are regulated, and how they are 5.4 THE ROLE OF THE CLINICAL PSYCHOLOGIST 135
trained. :
ee AM ONE OM “ 5.5 CLINICAL PRACTICE REVIEWED 142
128 PSYCHOPATHOLOGY
LEARNING OUTCOMES
1. Describe the nature and size of mental health 3. Describe the different types of mental health
problems facing service providers. professionals in the UK together with some of the
2. Describe how mental health services in the UK skills they possess.
are structured. 4. Describe and evaluate the role of clinical
psychologists in the mental health services.
My family came to England from Uganda when | was 4 years old. | found leaving our home behind quite traumatic, and then a
year after we arrived here, my father died. It was difficult, losing him on top of everything else. In some Asian families there are
rigid rules about what can and can't be talked about and intimate things aren't mentioned, so |never spoke to anyone about how
| felt or what it was like growing up. |just pushed the sadness down within myself. |got married to an English guy but | still didn’t
talk about it. But, a bit like holding a ball underwater, there’s only so long you can keep your feelings hidden and by the summer of
2006 | was suffering from what | now know was depression. In the end | went to see my GP because |felt |needed to talk through
what was going on. My GP was able to refer me to an Asian psychologist for cognitive behavioural therapy and psychodynamic
therapy, which involved talking through my problems and finding ways to tackle them. When |saw the therapist |wasn’t worried
about confidentiality any more. | live in a different area from my family now and was assured that all our sessions would be com-
pletely confidential. There were lots of things, which she, as an Asian woman, could relate to. |saw my therapist for 50 minutes
every week or two, over 10 months, and she has helped me a lot. I've started building my own life and learnt not to get so bogged
down with the pressures of having to look after everybody else.
I've been discharged now, but | still go for follow-up sessions to see how I’m doing. | know the service is there for me if |need it
again: alll have to do is contact them if | have a crisis or need a session. It has been great to have support from someone | identify
with. I’ve seen things change since | was younger and now there are services for people when they feel ready to get help. If you
want help, see your GP. They may be able to refer you for confidential counselling, or to a psychologist with a specialist under-
TY % —_—_—_—_—,, standing of cultural issues.
For a video on talking therapy go to
(Adapted from http://www.nhs.uk/Conditions/stress-anxiety-depression/Pages/
video/ch5 . therapy-changed-my-life.aspx)
Hina’s Story
Introduction for their problems. So how do people begin to seek help

for mental health problems? What services are available?
Just like Hina, we all experience life events that cause How are those services structured? These are some of
us distress in some form or another. In many cases this the questions we'll be addressing in this chapter. For
distress is short-lived, but for others the distress stays Hina, her journey for help and support began with a visit
with them for long periods and becomes an overbear- to her local GP who then shepherded her on to more
ing and central feature of their life. Many people cope specialized service providers such as counsellors, psycho-
as best they can by keeping their distress and their feel- therapists or clinical psychologists.
ings to themselves. But, as Hina describes in her personal Clinical psychologists are closely involved in helping
account, there’s only so long you can ‘hold a ball under people to recover from problems similar to those described
water before it pops up on the surface. It is often only by Hina. They attempt to help people understand the
when distress eventually becomes unbearable, affects causes of their distress, provide interventions that can help
social, occupational and family functioning, or is rec- to alleviate specific symptoms, and provide support and
ognized by others, that many people begin to seek help guidance through the recovery process. However, mental’
CHAPTER 5 CLINICAL PRACTICE = 929-
health provision is characterized by the involvement of a health problems that contribute to these figures include
whole range of professionals, all with differing skills and anxiety and anxiety disorders (see Chapter 6) and mood
roles, and we will describe some of these people and their disorders such as major depression (see Chapter 7). More
individual skills later in this chapter. You are only likely to severe mental health problems (such as psychoses) are
meet directly with a clinical psychologist if your problems somewhat less prevalent, at around 5 per cent of the
are relatively severe and enduring, but clinical psycholo- population, and around 3.7 per cent of the population
gists do work within multidisciplinary teams (MDTs) that report having serious thoughts of suicide in the prior
aim at providing the basis for support and recovery from a 12 months (SAMHSA, 2011).
range of mental health problems. As a significant cause of disability, the wider economic
In this chapter we will describe the kinds of profes- cost of mental health problems in the UK is immense. It
sionals who provide mental health services, and what has been estimated at £105.2 billion each year in England
services and facilities are available and how people access alone, including the costs of services, lost productivity at
them. We will then focus on the role of the clinical psy- work, and reduced quality of life. As a result, the cost of
chologist by discussing what they do, what their skills poor mental health to businesses amounts to £1000 per
are, and how they are trained. But, first, it is probably employee per year. So, apart from the personal distress
helpful to begin by looking at the size of the problem fac- and dysfunction caused by mental health problems there
ing those who provide mental health services — namely, is also the broader issue of its economic cost to society,
what is the prevalence of mental health problems across and the combination of these factors makes it essential
a country such as the UK, and why are mental health that governments provide suitable services and a skilled
services so important? workforce trained to help those within that society who
suffer mental health problems. Ironically, in recent years
it has been the need to reduce the economic burden of
mental health problems — rather than aiding individual
5.1 THE ECONOMIC COST OF recovery from distress — that has driven restructuring
MENTAL HEALTH PROBLEMS and training within national service providers such as
the UK’s National Health Service (NHS). For exam-
ple, the Improving Access to Psychological Therapies
In the UK, services for mental health problems need to (IAPT) programme in the
be accessible and robust. As in most developed countries, UK, which provides train- f To read more about IAPT go to
in the UK mental health problems are the single largest ing for large numbers of § www.iapt.nhs.uk
cause of disability, contributing up to 22.8 per cent of the new psychological thera-
total burden (compared with 15.9 per cent for cancer and pies practitioners (known as psychological well-being
16.2 per cent for cardiovascular disease) (World Health practitioners; see section 4.1.2), was launched in 2006 on
Organisation, 2008), and, of this, depression alone the premise that it would be a more cost-effective way of
accounts for 7 per cent of the disease burden (World providing services. Using evidence-based interventions
Health Organisation, 2004). At least one in four people such as CBT for common mental health problems would
in the UK will experience a diagnosable mental health return more people to work more quickly and reduce
problem in any one year (Office for National Statistics the costs of mental health problems caused by loss of
Psychiatric Morbidity Report, 2001), and in most devel- productivity (Layard, 2006; Radhakrishnan, Hammond,
oped countries around one in five have a diagnosable Jones, Watson et al., 2013).
mental health problem at any one time according to Given this background, we now move on to consider
the US Substance Abuse and Mental Health Services in more detail the structure of mental healthcare provi-
Administration (SAMHSA, 2011). Common mental sion and the nature of clinical practice.
SELF-TEST QUESTIONS
° What percentage of people in the UK will experience a mental health problem in any one year?
© What is the estimated annual cost of mental health problems in the UK?
soe | PSYCHOPATHOLOGY
SECTION SUMMARY
5.1 THE ECONOMIC COST OF MENTAL HEALTH PROBLEMS
e Atleast one in four people in the UK will experience a mental health problem in any single year.
e The economic cost of mental health problems in the UK has been estimated at £105.2 billion each year.
health problems such as anxiety and depression) to

5.2 WHO ARE MENTAL administering medication. They may specialize in treat-
HEALTH PROFESSIONALS? ing certain types of patient groups, such as children or
people with substance dependency problems, and may
be attached to GP surgeries or operate from community
Mental health problems are often complex and, as mental health centres.
a result, need to be treated in many different ways by a Once referred for a more detailed assessment of their
range of people with a variety of skills. Chapters 6 to mental health problems, an individual is likely to then be
17 in this book will demonstrate how different the vari- seen either by a psychiatrist or a clinical psychologist.
ous psychiatric disorders are — in the way that symptoms Psychiatrists are qualified medical doctors who have
manifest, how sufferers are affected, and what is required received further training in psychiatrists Medical practitioners spe-
to aid recovery — and highlight why mental healthcare mental health problems. cialising in the diagnosis and treatment o
professionals therefore have many different roles to play Psychiatrists can make ini- mental illness. + a
in the recovery process. tial assessments of a per-
The local general practitioner or physician will usu- son’s condition and needs, and can also prescribe
ally be an individual’s first point of contact with men- medications. Clinical psychologists are normally psychol-
tal healthcare services, and it is estimated that around ogy graduates who have clinical psychologists Psychology gradu-
one-quarter to one-third of the people that GPs see on a completed up to 3 years ates who have completed up to 3 years..
daily basis have either emotional or psychological prob- of intensive postgraduate intensive postgraduate training to learn
lems. GPs can often make an initial assessment, prescribe training to learn the skills the skills required for clinical practice, and
who specialize in the2assessment and treat
medication (such as antidepressants), and make referrals required for clinical prac- ment of mental health problems.
to other more specialized services, such as counselling tice, and they will specialize
or child and adolescent services. Interestingly, although in the assessment and treatment of mental health prob-
they are usually the first port of call for people with lems. Clinical psychologists will often specialize in work-
mental health problems, GPs often do not undergo full ing with only one or maybe two client groups, often
continuing professional development in mental health within a preferred psychological approach (e.g. cognitive,
issues as often as might be required given the percent- behavioural, systemic, psychodynamic or humanistic:
age of their patient base that present with mental health see Chapter 4). Some may work exclusively within child
problems (Lester, 2005). Consequently, 91 per cent of and adolescent services, known in the UK as Children and
people with a mental health problem will be treated Adolescent Mental Health Services (CAMHS) (see
within the primary care system, with only a small per- Treatment in Practice Box 5.1); others may be involved
centage referred on to specialist mental health services in learning disability, with older people, or with sub-
(Airey, Boreham, Erens & Tobin, 2003). stance dependency. Clinical psychologists will often
Once an individual has been referred onwards to work within multidisciplinary teams and are closely
more specialized services, they are likely to come into involved in providing care and interventions for mental
contact with one or more professional mental healthcare health problems, but — unlike psychiatrists — are not able
workers, depending on their individual needs and to prescribe medications.
requirements. Community mental health nurses Others involved in the provision of mental health
community mental health
(CMHNs) or community services include counsellors, psychotherapists, occupa-
nurses Registered nurses with specialist psychiatric nurses (CPNs) tional therapists, social
training in mental health. are registered nurses with workers, and approved counsellors People who are trained to
offer talking therapies that will support
specialist training in men- mental health workers. people with mental health problems and
tal health They have a range of skills, from offering coun- Counsellors are trained help them to cope better with their lives |
selling and psychotherapy (e.g. CBT for common mental to offer talking therapies and their symptoms. s
CHAPTER 5 CLINICAL PRACTICE
TREATMENT IN PRACTICE BOX 5.1:

CHILDREN AND ADOLESCENT MENTAL HEALTH SERVICES (CAMHS)
In the 1990s, the UK NHS Health Advisory Service pub- the cooperation and coordination of all services working
lished a wide-ranging review of children and adolescent with children, whether they are health, education, social
mental health services in the UK. This proposed a four- services or other agencies.
tier model for planning and delivering mental health ser- Details of the four tiers of provision are given below.
vices for children. This four-tier scheme has come to be Most children and adolescents with mental health prob-
known as Child and Adolescent Mental Health Services lems will be seen at Tiers 1 and 2. The following tabie
or CAMHS for short (see www.camhscares.nhs.uk). The provides a rough guide to the services available and the
scheme acknowledges that supporting children and problems treated at each tier although it is not always
young people with mental health problems is not the the case that individual services or individual mental
responsibility of individual specialist services, but requires health problems will fall into one particular tier.
Tier Services and agencies involved Types of problems addressed and services
TIER1 ~=—-Mainly practitioners who are not mental health ° Mental health problems in the initial stages or in mild
specialists: GPs, health visitors, school nurses, teach- forms
ers, social workers, youth justice workers, speech and * Offer general advice
language therapists, voluntary agencies
* Contribute towards mental health promotion
* Refer cases to more specialist services if necessary
TIER2 _—~ Practitioners providing services with some mental ° Problems suchas anxiety, sleep disorders, toileting dis-
health focus: school and GP counsellors, school orders, behavioural difficulties, low mood, adjustment
nurses, paediatricians, family support services, family to adverse life events (e.g. bullying, divorce, illness)
mediation services, educational psychologists, vol- * More complex cases referred to Tier 3 when
untary sector mental health organisations (specialis-
necessary
ing in bereavement, domestic violence, and so on)
TIER3 = Multidisciplinary teams working in community ° Severe and persistent cases referred up from Tier 2
mental health clinics or child psychiatry outpatient * Some cases might come straight to Tier 3, such as psy-
services, providing specialist services for children chosis, bipolar disorder, OCD, anorexia, significant self-
and adolescents with more severe and persistent harm/suicidal ideation, and suchlike
disorders
TIER4 Inpatient services, day units, and highly specialized e Similar mental health problems seen at Tier 3, but at
outpatient teams and inpatient units (e.g. forensic the most severe end of the spectrum
adolescent units, eating disorder units, specialist
neuropsychiatric teams, and other specialist teams)
that will support people with mental health problems blems. Occupational therapists are available to help
and help them to cope better with their lives and people with mental health problems adjust to the
their symptoms (see section 4.1.2). Psychotherapists demands of normal day-to-day living, including
have a similar role to counsellors by providing developing personal independence and achieving lev-
a range of psychotherapy els of functioning required for employment. Social
chotherapists Individuals who are
lved in the treatment of mental health
support to individuals with workers are trained to provide a valuable link
blems by psychological rather than mental health problems. between mental health services and broader social
Jical means. Psychotherapists will often service provision, and they can provide advice and
specialize in a particular support on issues such
social workers Professionals whose main
upational therapists Clinicians who therapeutic approach and as welfare benefits, hous- focus is clients’ social care needs (e.g.
cialize in assessing and training (or
raining) occupational and daily living provide support for longer- ing, day care, and occupa- housing). Approved Social Workers are also
S. term mental health pro- tional training. Finally, involved in Mental Health Act assessments.
hyde PSYCHOPATHOLOGY
: w
approved mental health workers approved mental health this enables professionals to bring a range of skills
Professionals who are trained to offer treat- workers will not normally from health and social care that will provide the basis
ments that will support people with mental have the kinds of profes- for support and recovery for individuals with mental
health problems and help them to cope health problems. MDTs will provide individual cli-
sional clinical qualifica-
better with their lives and their symptoms.
They will not normally have the kinds of tions possessed by other ents with more holistic care and are especially help-
professional clinical qualifications pos- mental health profession- ful for dealing with complex and challenging cases.
sessed by other mental health professionals, but will also have Within this team, the clinical psychologist’s role
als, but will have received special training.
received special training in will be to offer a perspective on each case based on
assessing and helping people who may need to be com- their own professional skills, and this may involve pro-
pulsorily detained because of their mental health viding assessments for diagnosis or the evaluation of
problems. a client’s needs, considering aetiology or causes, or
In many cases, mental suggesting support and conducting suitable inter-
multidisciplinary teams (MDTs) MDTs
include workers from a range of disciplines health provision is char- ventions for the client’s specific problems. Table 5.1
that specialize in different aspects of health acterized by professionals provides the descriptions of members of a typical
and social care, e.g. psychiatrists, clinical working in multidiscipli- MDT offering community mental health services
psychologists, social workers and occupa-
tional therapists.
nary teams (MDTs), and (Jones, 2008).
TABLE 5.1
Clinical psychologists frequently work as members of multidisciplinary teams (MDTs). Part of the rationale for MDTs is that they can
provide clients with more holistic care, since they include workers from a range of disciplines that specialize in different aspects of
health and social care. In community mental health teams (CMHTs), the team members can include:
Team manager Usually a social worker or nurse by background, who is responsible for organising
and managing the team
Psychiatrists Medical doctors specialising in mental health, whose role includes making diagno-
ses, prescribing medication and being involved in assessments under the Mental
Health Act, which can result in clients being involuntarily detained in hospital for
assessment or treatment
Psychotherapists, counsellors, clinical psy- Professionals who can offer psychological assessments and interventions (some of
chologists and counselling psychologists the distinctions between these groups are discussed later)
Mental health nurses Nurses specialising in mental health, whose role includes monitoring clients’ mental
health, administrating medication and providing other support
Social workers Professionals whose main focus is clients’ social care needs (e.g. housing). Approved
social workers are also involved in Mental Health Act assessments
Occupational therapists Clinicians who specialize in assessing and training (or re-training) occupational and
daily living skills
Community support workers An individual with experience in helping people with mental health problems to
build relationships within the community
Secretarial staff Responsible for administering the team (e.g. organising appointments and
documentation)
Source: From Jones, F. (2008). What is clinical psychology? Training and practice. In G.C.L. Davey (Ed.) Clinical psychology. Hodder.
SELF-TEST QUESTIONS
* How do people with mental health problems access mental health services?
* Can you name at least five different types of mental health professionals in the UK?
CHAPTER 5 CLINICAL PRACTICE 933°
SECTION SUMMARY
5.2 >WHO ARE MENTAL HEALTH PROFESSIONALS?
¢ The local general practitioner or physician will usually be an individual's first point of contact with mental healthcare
services.
* Professional mental healthcare workers include community mental health nurses (CMHNs), psychiatrists, clinical psycholo-
gists, counsellors, psychotherapists, occupational therapists, social workers, and approved mental health workers.
* In many cases, mental health provision is characterized by professionals working in multidisciplinary teams (MDTs).
5.3 PROVIDING MENTAL Health Act. It can be found at http://www.rethink.org/

how_we_can_help/our_advice_information/
fact
HEALTH SERVICES sheets_az.html.
In addition to psychiatric hospitals, regional secure
units and secure hospitals regional secure units Facilities avail-
S301 What Facilities are Available? are available to treat individ- able to treat individuals who have been
uals who have been admit- admitted by the courts under the Mental
Mental health problems are both diverse and experienced ted by the courts under the Health Act, transferred from prison under
the Mental Health Act, or have been
by many members of society and so will require services Mental Health Act, trans- transferred from an ordinary hospital ward
that are flexible and geared towards managing symp- ferred from prison under because they may need treatment ina
toms that are varied in type and severity. Some people the Mental Health Act, or more secure setting.
will need specialized short-term help in order to recover; have been transferred from
others will need long-term support and care. an ordinary hospital ward because they may need treat-
As a result, mental health services provide a range of ment in a more secure setting.
facilities geared to helping with a multiplicity of prob- Finally in this section, it should be emphasized once
lems. Most people with a mental health problem can be again that while the range and type of facilities avail-
treated on an outpatient basis and treatment can take able for treating mental health problems is quite varied,
place at a dedicated com- the vast majority of people with a mental health prob-
patient basis Most people with a men-
lealth problem can live in the community munity mental health cen- lem are treated voluntarily on an outpatient basis, usually
‘be treated at a dedicated community tre, a day clinic, or some by a care team of professionals with a range of skills.
ital health centre, a day clinic, or some larger GP or physician sur- Compulsory detention or treatment is extremely rare,
er GP or physician surgeries.
geries. Some people may and the overwhelming majority of people with mental
atient hospital care Treatment pro- need voluntary inpatient health problems are neither violent nor a danger to them-
»d to a client who has voluntarily admit- hospital care — especially selves or others.
himself or herself to hospital. Some if that is agreed between
ple can be compulsorily detained ina
pital under the Mental Health Act if their
the patient and their psy-
ital health problems are severe enough. chiatrist, psychologist or 5.3.2 Howare Mental Health
care plan team. Some peo- Services Structured?
ple can even be detained in a hospital under the Mental
Health Act if their mental health problems are severe Apart from the facilities that are available for treatment,
enough, and they can be compulsorily detained (1) in the services need to be structured so that the different skills
interests of their own health or safety, or (2) for the of healthcare professionals can be focused on the different
protection of other people. In England in 2011-2012, sets of problems that make up mental health problems
48,000 people were detained under the Mental Health generally. Within the UK National Health Service, this is
Act (Health & Social Care Information Centre, 2012), currently achieved by organising services around differ-
and this number has been steadily growing over recent ent'client groups. Very broadly, these client groups are
years. However, the number of people that are compul- likely to include (1) children and young people services
sorily detained under the Mental Health Act is still a (commonly known as CAMHS —- Children and Adolescent
small percentage of the people with diagnosable mental Mental Health Services — see Treatment in Practice
health problems each year (around 0.3 to 0.5 per cent). Box 5.1) for children and adolescents with mental health
The organisation Rethink Mental Illness has a factsheet and physical health problems, (2) working age adults
providing information about detention under the Mental who may experience a range of mental health problems,
Wi3q PSYCHOPATHOLOGY
; , wy
(3) older adults who often have mental health problems Instead, within the mental health sphere a number of
combined with physical health problems, (4) children and countries have adopted the recovery model as a basis for
adults with a learning disability, (5) individuals with sub- their provision of services. recovery model Broad-ranging treatmen
stance misuse problems, and (6) people with brain injuries The National Institute for approach which acknowledges the infl
or neurological deficits. Mental Health in England ence and importance of socio-economi
Most services are also likely to have a secure and foren- (NIMHE) endorsed a recov- status, employment and education and
social inclusion in helping to achieve rec
sic team to deal with mental health problems related to ery model as a guiding ery from mental health problems.
criminal behaviour, and an access team devoted to ensur- principle of mental health
ing that individuals seeking help with mental health provision in 2005, and many NHS Trusts have now actively
problems receive rapid access to appropriate services. implemented this approach. In this model, recovery is
Figure 5.1 provides an example of how the services for viewed as a personal journey rather than a set outcome,
one particular mental health trust are structured, but this and this involves not just individual development but also
may differ from area to area depending on the locality of how the individual relates to their community and their
the trust and the nature of the mental health problems society (Repper & Perkins, 2006).
found in that area. Repper & Perkins (2006) note the following as impor-
tant features of recovery:
5.3.3 The Recovery Model

Hope: Developing an ability to persevere through
As well as the physical structure of mental health services, uncertainty and setbacks and developing a sus-
it is also important to consider the ‘philosophy’ or tainable belief in oneself.
approach to treatment that underpins these services. A secure base: Ensuring appropriate housing,
When someone has a physical illness, it is relatively easy to income, health care and security.
talk about a ‘cure’ and to define criteria by which a treat-
Self: Developing a durable sense of self, a sense of
ment will have been successful or not. If someone has a
social belonging and a set of interests.
broken leg, an X-ray will show that it has mended success-
fully after treatment. If someone has a viral disease, drugs Supportive relationships: The development of sup-
can be shown to have dealt with this when the virus is no portive relationships not just with mental health
longer detected in the body. This is not so easy to do professionals, but with friends, family and the
within mental health because mental health problems will community.
largely be defined by the degree of distress and disability Empowerment and inclusion: Developing the confi-
caused by the symptoms and the individual’s ability to dence for independent decision making and help-
cope with them — and distress and disability tend to be seeking, and challenging stigma and prejudice
relative rather than absolute concepts (see Chapter 2). about mental health problems.
Chief Operating Officers
Assistant Chief Operating Officers Business Manager
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FIGURE 5.1 This figure shows how mental health services provided by an NHS Foundation Trust are structured and managed
around themes that reflect the underlying mental health needs of the local community served by the Trust.
CHAPTER 5 CLINICAL PRACTICE eas
¢ Coping strategies: The development of a range of the original social and economic conditions that might have
coping strategies and problem-solving skills that given rise to those problems in the first place? The recovery
will enable the individual to identify and deal with model attempts to empower people and to provide them
stressors and crisis points. with the hope and skills they might need to cope with and
¢ Meaning: Developing a sense of purpose that may rise above these background conditions. However, in many
be related to a social or work role. ways the recovery model is at odds with the diagnostic
model of mental health problems as enshrined in DSM-5
The recovery model rep- (see Chapter 2). DSM-5 rarely takes account of the causes
For an activity on the features of
recovery go to
| resents a holistic approach of mental problems; it infers that the removal of cardinal
www.wiley-psychopathology.com/ | to mental health provision, diagnostic symptoms alone will imply recovery; and it
activities/ch5 / and embraces the view does not recognize the need for others to change as well as
that good mental health those singled out for the diagnosis (e.g. family and friends
requires more than the treatment of individual symptoms involved in supporting the sufferer) (Compton, 2007). This
but requires the development of the person within society. is an ongoing tension between those who support a more
For example, what is the benefit of treating an individual’s eclectic recovery model of mental health and the more tra-
mental health problems if they are then being sent back to ditional medical model of psychiatric symptoms.
SELF-TEST QUESTIONS ©
e What different types of mental health facilities are available in the UK?
® How are mental health services structured?
e What is the recovery model, and what are its main features?
SECTION SUMMARY
ie .
. ay 4
5. 3 “PROVIDING MENTALHEWLTE SERVICES

: af Qi - ' 4
© Mental health services provide facilities on an pueatent basis, voluntary hospital care, and regional secure units for people
~ who have been ) admitted to psychiatric hospitals by the courts. }
8
Mental health services are » structured so that the skills of different healthcare professionals can befocused on the different
sets of problems that make up mental health problems generally.
e The recovery model represents a holistic approach to mental health provision andem braces the view that recovery requires
~ the development of the person within society.
basis, including working in teams and with families, con-

5.4 THE ROLE OF THE ducting assessments, and providing treatment and sup-
CLINICAL PSYCHOLOGIST port to people with distressing mental health problems.
We have briefly described who clinical psychologists are 5.4.1 Key Capabilities
and offered a sketch of what they do in section 5.2. In this
and Competencies
section we will take a more in-depth look at the role of
clinical psychologists and the skills they deploy as mental Clinical psychologists receive training in a range of dif-
health professionals. Before you begin to read this section ferent approaches, including cognitive-behavioural, psy-
take a look at Focus Point 5.1 in which a clinical psycholo- chodynamic and systemic (see section 4.1.1). However,
gist describes a typical week for her working with people these skills are deployed in a wider framework that
with psychosis. This gives a flavour of the range of roles would normally consist of four stages: assessment, for-
that a clinical psychologist undertakes on almost a daily mulation, intervention and evaluation.
136 PSYCHOPATHOLOGY
de A WEEK INTHE LIFE OF A CLINICAL PSYCHOLOGIST

wy
- |tend to try to consider what people with psychosis have
WORKING WITH PSYCHOSIS: A CLINICAL
= PSYCHOLOGIST’S EXPERIENCE in common with other people rather than what sets
oO them apart. In this way | can draw on my experiences of
.
Vv) ‘| have worked with people with psychosis for the past working in anxiety, depression and trauma when | meet,
=) 5 years. Most of the work that | have done has involved and try to help, someone with psychosis.
U either cognitive behavioural therapy (CBT) or family ‘In my experience cognitive behavioural therapy
Oo
LL intervention (Fl) and has been provided through the can help someone make sense of psychotic experi-
NHS. When | started this work | was anxious about try- ences by helping them make links between emotional
ing out these therapies with people with psychosis. states, thoughts, beliefs, traumatic life events and
| had experience of CBT working well in trauma, anxi- psychotic symptoms. Helping people to make sense
ety and depression but was unsure how the therapy of psychotic and emotional experiences by discussing
would translate into psychosis. psychological formulations can help them make con-
‘A typical week would include a whole variety of nections between seemingly unconnected events or
very different tasks. The main focus of the work is the beliefs and disabling and distressing psychotic symp-
| therapy itself but there is a lot that goes on alongside toms. In order to succeed in this work it is first essen-
that. Usually | attend the Community Mental Health tial to engage well with a client. Engagement in CBT
Team meeting where clinical: cases are discussed for psychosis is a big challenge to therapists. For some
and the team decides on who in the team is best for people, having the time and space to talk through their
an individual to see. The team is made up of nurses, experiences in detail is very liberating and although it is
social workers, occupational therapists, psychiatrists hard work — for all parties — it can be very rewarding too.
and psychologists and each professional group takes a ‘Family interventions make up another large part
slightly different perspective on the case in hand. of my clinical work. They have been designed to mini-
‘In addition there are assessments to conduct. | will mize the negative impact of a client’s symptoms on
usually see three or four people a week for an initial carers and to reduce the risk of client relapse. Central
assessment and then write up this information and importance is given to the task of defusing the large
| take it back to the team meeting for allocation. Some range of difficult emotions that psychosis can often
more time is spent writing letters to clients or to GPs engender in families, such as anger and fear. The inter-
/ andalsoin speaking on the telephone to those people. vention is based on a positive view of individuals with
| ‘The bread and butter of the job is the clinical work psychosis and their caregivers; the strengths of the
itself. Psychosis is often confusing and terrifying for family unit are explicitly recognized and family mem-
those who experience it. This may seem like a self- bers are mobilized as supportive therapeutic allies. |
evident and simplistic statement. However, keeping conduct the Fl work with my colleague - who is also
a focus on the distress that people experience helps a clinical psychologist —- and usually we try to see fami-
me a great deal in my work. It is easy to be blinded lies in their own homes.
by the delusions and hallucinations and to fail to con- ‘There is still a lot to learn about how psychology
sider the confusion, distress and fear that so often goes can help people with psychosis and that is what makes
with them. So, as a start point when working in psychosis this area of work so challenging and rewarding!
Normally, the first stage of clinical work with a client on the theoretical orientation of the professionals
would be to undertake an assessment. Typically this will involved. For example, those with a psychodynamic
involve understanding the approach will want to understand how the client’s prob-
assessment Normally, the first stage of
clinical work with a client, which typically
problems that a client is lems relate to underlying, intrapsychic conflicts, while
involves understanding the problems experiencing, what may those with a cognitive-behavioural approach will want to
that a client is experiencing, what may have caused these prob- explore the importance of cognitions and how they influ-
have caused these problems and be main- lems and be maintaining ence moods and behaviour (Marzillier & Marzillier, 2008).
taining them, and how the client would
like to change.
them, and how the client Professionals with a medical training such as psychiatrists
would like to change. A (and also some clinical psychologists) may want to pro-
full assessment of these factors may be undertaken by a vide a diagnosis, which
team of professionals with different skills (e.g. psychia- will classify the client’s diagnosis Aclassification of the client’s
trists, community health workers as well as clinical psy- symptoms according to symptoms according to current diagnosti
chologists), and the nature of the assessments will depend current diagnostic criteria <rteria. i
CHAPTER 5 CLINICAL PRACTICE ee
AN INITIAL ASSESSMENT OF A CLIENT CARRIED OUT

BY A CLINICAL PSYCHOLOGIST
The client, Peter, was reported to be suffering from an episode of clinical depression and, as a result, was experi-
encing depressed mood for much of thé-week, was struggling to sleep properly, and had stopped doing many of
the things that he used to enjoy.
The assessment began by asking Peter to say something about why he had come along and then focused in
detail on his current difficulties. As the clinical psychologist was taking a cognitive-behavioural approach, this
HISTORY
CASE
5.1 involved being curious about the thoughts and images Peter was experiencing (i.e. the cognitive) and the things
he was doing or not doing (i.e. the behavioural), and how these affected and were affected by his depressed
mood. They went on to explore how his problems had developed, the impact they were having on his life cur-
rently, and his goals for the future. They also used some questionnaires (1) to establish a baseline estimate of the
severity of Peter’s depression and (2) to explore whether Peter was experiencing depression related thoughts
that had not been covered in the interview. Throughout, the clinical psychologist attempted to build a therapeu-
tic relationship with Peter by listening carefully to what he was saying and then summarising the understanding
built up, and also by conveying a sense of positive regard and kindness. Crucially, during the assessment it was
also established that, while Peter sometimes experienced suicidal thoughts, he was at low risk of acting on these.
In addition, for homework, Peter was asked to keep a record of his thoughts when he was feeling depressed,
both because doing so might identify important negative thoughts that he had forgotten in the assessment, and
because the process of recording could help him to become more aware of his thinking and the impact it had
on his mood.
Source: After Jones, F. (2011). Clinical psychology: Training and development. In G. Davey (Ed.) Applied psychology. BPS
Blackwell. Reproduced with permission.
(e.g. DSM-5; see section 2.1.2). A variety of methods can are relevant) but would normally focus on psychological
be used to collect relevant information for an assessment. and social processes. This is the stage in which the clinical
The primary means is the psychologist’s skill in being able to link psychological the-
ical interview Primary means of collect-
relevant information for an assessment, clinical interview (see sec- ory with practice is highlighted. Formulations can often
der to understand the problems that ation 2.2.2), especially for be viewed as a series of hypotheses about what is causing
clients who are able to
nt is experiencing, what may have caused a client’s problems and these can be tested out during the
se problems and be maintaining them,
communicate their prob- intervention stage. A detailed example of formulation
| how the client would like to change.
lems effectively. Validated and how it is undertaken is provided in section 2.3.
psychological tests and tests of cognitive ability can also Once the formulation has been completed, a psycho-
be used when required (see section 2.2.3). Primarily, it is logical intervention can be implemented on the basis
important in this first stage for the clinical psychologist to of this. The intervention intervention Psychological treatment,
establish a good working relationship with the client, may be based on one spe- implemented on the basis of the formula-
and you will have seen in section 4.2 what an important cific theoretical approach tion. May be based on multiple theoretical
approaches and may be co-designed with
contributor this relationship is to the success of any sub- (e.g. CBT), or it may inte-
the client.
sequent therapeutic interventions. Case History 5.1 pro- grate anumber of different
vides an example of how an assessment might progress in approaches and ideas depending on the client’s needs
practice. and strengths. Very often the clinical psychologist will
When the assessment process is complete, the process directly involve the client in the planning of the interven-
will move on to a formulation stage. This combines psy- tion to both help the client to understand what will hap-
mulation The use of clinical informa-
chological theory with pen and to develop some conviction on the part of the
1 to draw up a psychological expla- information gained from client about how the intervention might be successful
ion of the client's problems and to the assessment and enables (Hall & Llewelyn, 2006, pp.91-92). The intervention may
elop a plan for therapy. the clinical psychologist to also need to include the client’s family members, espe-
develop an account of how the client’s problems were cially if the client’s difficulties seem to be linked to family
acquired and how they are being maintained, as well as an relationships and dynamics or if the client has specific
indication of what interventions might be theoretically disabilities such as learning disabilities.
useful in alleviating these problems. A formulation may Once the formulation and intervention stages have
acknowledge biological and genetic influences (if they been completed it is important to evaluate them. What
Lies PSYCHOPATHOLOGY
‘ >
has been the impact of the intervention? Is the interven- clinical psychologists reflect on their own experience
tion having the desired effects? Evaluation can be done in when working with clients, and reflect on the process of
a number of ways, includ- interaction with their client (Hall & Llewelyn, 2006, p.17).
evaluation Stage of treatment that
seeks to ensure any intervention is having ing discussion with the cli- This reflection is considered to have a number of benefits:
the desired effect. Can be achieved ina ent and with the use of (1) it facilitates the process of developing the clinical psy-
number of ways, including discussion with validated questionnaires. chologist as an autonomous, qualified and self-directed
the client and with the use of validated professional, (2) it enables clinical psychologists to develop
Therapeutic change can
questionnaires.
often be very gradual so their practice by overcoming habitualized approaches to
the client might not have good insight into the changes treatment and intervention, and to consider the needs of
that may have begun to occur, and validated question- each individual client, and (3) it encourages self-motivation
naires can often provide a more objective measure of and self-directed learning. Most importantly it is one
change. Indeed, the use of validated means of measuring method by which clinical psychologists can learn from
the effectiveness of interventions is a central feature of their own experiences, and practitioners may also attend
evaluation nowadays — largely because of the need to regular reflective practice groups through which individu-
ensure that interventions can be identified as effective als share experiences, or work with a supervisor who may
using evidence-based criteria that will allow services to use facilitate reflective practice. A more structured way of
objective criteria by which to decide what types of inter- facilitating reflective practice is for the clinical psycholo-
ventions are effective and which are not. gist to receive his or her own psychotherapy. This is often
In summary, a clinical psychologist needs to have the the norm in many forms of psychotherapy practice, but it
competencies to assess, formulate, intervene and evalu- is an issue of disagreement within clinical psychology
ate, and to be able to do this in collaboration with other practice (Macran & Shapiro, 1998).
mental health professionals. In addition to these core Finally, it must be pointed out that the reflective prac-
competencies, clinical psychologists will also need to be titioner and scientist-practitioner approaches are not
able to communicate effectively with their clients — both entirely mutually exclusive, and no matter which philo-
verbally and in writing (Hall & Llewellyn, 2006, pp.22— sophical approach you take to your clinical practice, it
25), and these are all skills that will be taught during the will almost certainly be beneficial to regularly reflect on
clinical psychologist’s extensive period of training (see that practice.
Davey, 2011, chapter 6).
5.4.3 Regulation and Continuing

5.4.2 The Reflective Professional Development
Practitioner Model
Because clinical psychologists provide services to vulner-
In Chapter 3 we discussed the widely held view that clin- able groups of people their practice needs to be properly
ical psychologists should be thought of as scientist- regulated to protect the public from malpractice and
practitioners who are competent as both researchers exploitation from untrained individuals. Since 2009, clini-
and practitioners. Many clinical psychologists are happy cal psychologists in the UK have been regulated by an
with this label — especially given the shift towards mental agency known as the Health and Care Professions
health professionals being seen to provide evidence- Council (HCPC) (www.hpc-uk.org), and its role is to pro-
based interventions. However, not all clinical psycholo- tect the public by ensuring Health and Care Professions Council
gists readily accept this conception of themselves. For that clinical psychologists (HCPC) Agency responsible since 2009
example, some prefer to adopt alternative philosophical (amongst other groups of for regulating and maintaining a register —
approaches that place less emphasis on traditional practicing healthcare pro- of clinical psychologists in the UK,ensur-
ing that they meet specified standards of
science (such as social constructionist approaches that fessionals) meet specified training, professional skills, behaviour and
are described in Focus Point 3.1). Nevertheless, despite standards of training, pro- health. | fy
differences in agreement about the importance of fessional skills, behaviour
science in professional clinical psychology practice and health. The HCPC maintains a register of clinical psy-
(e.g. Lilienfeld, Ritschel, Lynn, Cautin & Latzman, chologists who meet these required standards, and it has
2013), clinical psychologists are generally expected to also specified that ‘clinical
adopt a reflective practi- psychologist’ is a protected protected title A job title that can only b
reflective practitioner model Key
competency in which clinical psycholo- tioner model in their work _ title that can only be used used if the individual has received appro-
priate training and is registered with the
gists reflect on their own experience when (Sch6n, 1983). This is con- if the individual has
relevant regulatory body. The title of clin’
working with clients, and reflect on the sidered to be animportant received appropriate train- cal psychologist is protected and regulate
process of interaction with their client.
key competency in which ing and is registered with by the HCPC. =
CHAPTER 5 CLINICAL PRACTICE eee
the HCPC. The HCPC has the authority to take out crimi- (BPS). Once they have this qualification they can apply
nal prosecutions against anyone who uses this protected for a place on a clinical training course, and these courses
title and is not trained or registered to do so. In addition, will be looking for evidence of experience and capability
the HCPC can take action against any clinical psychologist in three areas: academic, clinical and research. In terms
who does not meet their standards of conduct, perfor- of the academic experience, most training courses will
mance and ethics. In such circumstances, further actions require either a first or a good upper-second class degree,
taken by the HCPC may include recommendations for with some additional weight given to postgraduate
further training and supervision, preventing a clinical psy- degrees such as relevant taught master’s degree courses
chologist from practising for a specific period of time, or or a PhD. Candidates are also expected to have some
striking that person off the register for life (see Davey, clinical experience in mental health areas by working as
2011, ch. 1 for further details of HCPC and standards of interns or volunteers in mental health settings, or alter-
conduct, performance and ethics). natively working as an assistant psychologist — the latter
The way that clinical psychologists are regulated dif- usually within the NHS mental health services. Possessing
fers from country to country. In the USA and Canada a good research skills is also an important quality preferred
licence is required to practise as a clinical psychologist, by many clinical training courses. One of the features of
and the terms of this licence often differ between states. clinical psychologists that differentiates them from many
But, in general terms, all states require: (1) graduation other types of mental health professionals is their research
from an accredited training institution with an appropri- skills. These research skills are important for a number of
ate degree, (2) completion of supervised clinical experi- reasons. They provide clinical psychologists with the abili-
ence, and (3) passing a written exam and, in some cases, ties necessary for understanding, critically appraising and
an oral exam. evaluating the clinical literature. Clinical psychologists can
Once they have qualified, clinical psychologists are also use their research skills to evaluate existing services
expected to undertake continuing professional develop- and interventions and conduct research that might lead to
ment (CPD) throughout their career in order to develop the development of new psychological theories and inter-
tinuing professional development their professional compe- ventions. Since much of the time during clinical training
D) The demonstration by accredited tencies. This can include is taken up learning clinical skills, many clinical course
rapists that they regularly update their reading about the latest admissions tutors prefer to take applicants with an existing
ledge of recent developments in
% rn research, attending confer- good knowledge of research methodology, and so some
tment techniques. _
ences and training work- courses are taking an increasing number of candidates
shops, carrying out new activities (e.g. supervising trainee who have successfully completed a research PhD.
clinical psychologists or applying for a research grant) and Applications for clinical training courses in the UK are all
undertaking further qualifications (e.g. specialist training managed through the Clearing House for Postgraduate
in a particular type of psychological therapy). Courses in Clinical Psychology (CHPCCP) (http://www
leeds.ac.uk/chpecp/). However, applications are assessed,
interviews conducted, and
5.4.4 Training to be a Clinical final decisions on accept- Clearing House for Postgraduate
Courses in Clinical Psychology
ance made by members of (CHPCCP) The CHPCCP manages all appli-
Psychologist faculty at each of the rele- cations for clinical training coursesin the
Training to become a clinical psychologist requires skill vant training institutions UK (see http://www.leeds.ac.uk/chpccp/).
and dedication. This section describes some of the pre- that a student has applied
training qualifications and attributes required to become to. Apart from evidence of academic and research ability
a clinical psychologist followed by a brief overview of and clinical experience, courses are usually also looking for
clinical psychology training. a good interpersonal manner, strong communication skills,
and self-awareness. Competition for places on clinical
Pre-training qualifications and experiences training courses in the UK is intense, with applications
Training to become a clinical psychologist is a challenging increasing significantly between 2009 and 2012 (see
and competitive experience. Once a student has decided Figure 5.2), and in 2012 there were 3857 applicants for
that clinical psychology is the career for them, they need 586 places — an applications-to-places ratio of 6.5:1!
to obtain the necessary qualifications and experience to
become eligible for a place on a clinical psychology train-
ing course. In the UK, students will need a first degree in Clinical training
psychology or an equivalent (e.g. a conversion course) that Clinical training courses in the UK are usually 3 year
will make them eligible for graduate basis for chartered programmes that lead to a doctorate in clinical psychol-
membership (GBC) of the British Psychological Society ogy. This doctorate confers eligibility to register as a
140 | PSYCHOPATHOLOGY .
4500 ih
3857
4000 5 mmmet Applicants —@=— Places
3528
3500 |
2969
2000
1500
1000
2006 2007 2008 2011 2012
FIGURE 5.2 Applications vs. places for UK clinical training.

This chart shows the number of applications and actual places for UK clinical training courses between 2006 and 2012. Note that in
2012 the applications: places ratio was 6.5:1
© Clearing House for Postgraduate Courses in Clinical Psychology. Reproduced with permission.
chartered psychologist with the BPS and as a practitioner a week for as long as 6 months, and a trainee
psychologist with the HCPC. Training usually takes will gain experience by taking placements across
place in service with the NHS, with the latter covering a range of settings and client groups, the latter
the trainee’s training fees. Training can be divided into of which will normally include working-age
three components: adults with mental health problems, people
with learning disabilities, children with mental
1. An academic component that takes place in a health problems, and older adults. During
university setting and consists of conventional their placements, trainees receive support and
teaching and learning practices covering such guidance from at least one supervisor who will
topics as human development and interaction, be a practising clinical psychologist.
psychological problems and mental well-being, A research component, in which research skills are
and some skills learning associated with different developed through both teaching and the trainee
psychological approaches to mental health conducting their own research projects. The
problems. Students will learn about the main research projects usually consist of small-scale
approaches to alleviating mental health problems, service-based research such as an evaluation
including cognitive-behavioural, psychodynamic of an intervention, and the most substantial of
and systemic, and a key part of training is these projects will form the trainee’s doctoral
concerned with integrating concepts and dissertation.
interventions from different models to develop
interventions that best suit an individual’s needs. Table 5.2 provides some examples of what a clinical
2. A clinical placement component, in which the psychology trainee will experience during their training
trainee learns how to apply these different and covers the nature of the placements they encounter,
approaches to different client groups, usually the types of psychological models they will learn about,
within the NHS. These placements take up 3 days and some of the key competencies they will acquire.
CHAPTER 5 CLINICAL PRACTICE ay.
TABLE 5.2 Some examples to illustrate the range of client groups, models and competencies typically covered in clinical psychology training
Core clinical placements
Working age adults with mental health problems

Children with mental health problems and their families
People with learning disabilities
Older people with mental health problems
Possible supplementary placements
Further experience in one of the ‘core’ areas

Adults with brain injury
Children with physical health problems
Adults with physical health problems
Classes of models
Cognitive-behavioural
Psychodynamic
Systemic
Developmental
Neuropsychological
Key competencies
The ability to communicate effectively with a range of different clients.

The ability to build and maintain effective relationships with others.
The ability to conduct assessments appropriate to different settings.
The ability to develop ‘formulations’, by forming theory-practice links.
The ability to facilitate interventions appropriate to particular clients and problems.
The ability to evaluate clinical work.
Sufficient self-awareness to be able to reflect on and learn from clinical work.
The ability to understand, conduct and apply the findings of psychological research.
Source: Jones, F. (2011). Clinical Psychology: Training & Development. In Davey, G. (Ed.), Applied Psychology. BPS Blackwell. Reproduced with permission.
| SELF-TEST QUESTIONS _
® What are the four key capabilities and competencies ofclinical psychologists?
® What is the reflective practitioner approach to clinical practice?
® Can you describe how clinical psychologists in the UK are regulated?
e What pre-training qualifications and experiences would someone need before applying for a clinical training place
in the UK?
° What are the three main components of a clinical training programme in the UK?
SECTION SUMMARY
a e i .
: 5.4 THE ROLE OF THE CLINICAL PSYCHOLOGIST
e Key capabilities and competences of clinical psychologists include their ability to conduct assessments, create formulations
of anindividual’s problems, prescribe and conduct interventions, and carry out evaluations of services.
* Clinical psychologists tend to adopt a reflective practitioner approach to their work, reflecting on their own experience
when working with clients.
® Clinical psychologists in the UK are regulated by the Health and Care Professions Council (HCPC).
© Training to becomea clinical psychologist usually consists of three components: an academic component, a clinical compo-
nent, and a research component.
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area PSYCHOPATHOLOGY
.
5.5 CLINICAL PRACTICE mental health problems account for 40 per cent of all
illness but only 13 per cent of NHS funds are devoted to
REVIEWED their treatment.)
Because of their complexity, rictieal health problems
require a range of mental health professionals with a
This chapter has covered a number of important aspects variety of skills, and we have discussed who these profes-
of clinical practice and service provision. We began by sionals are, what skills they possess, how they work, and
looking at the scale of mental health problems in terms where they work. Finally,
of both personal suffering and economic cost, and it is we focused on the role of To read ‘It is inexcusable that mental
health treatments are still
clearly an immense task faced by service providers to the clinical psychologist underfunded’ go to
deal with the high prevalence rates of mental health and covered their role in http://tinyurl.com/cbaz2w9
problems — especially when mental health services are the treatment and recovery
relatively underfunded compared with funding for other of people with mental health nrotiletts he key skills
health problems (In 2012, The Guardian reported that and competencies, and how they are trained.
el: nel To access the online resources for this chapter go to

oe
Reading Activity
Improving Access to ¢ Talking therapy The features of recovery

Psychological Therapies Self-test questions
Website
Revision flashcards
Article on mental health
treatment funding Research questions
Glossary key terms

Clinical issues
References
maa
_- Psychepathoiog and
_ Psychological Disorders
Anxiety and Stressor-Related Problems 12 Personality Disorders
Depression and Mood Disorders 13 Somatic Symptom Disorders

Experiencing Psychosis: Schizophrenia 14 Dissociative Experiences
Spectrum Problems - 15 Neurocognitive Disorders
Substance Use Disorders 16 Childhood & Adolescent Psychological
10 Eating Disorders Problems
11 Sexual & Gender Problems 17 Neurodevelopmental Disorders

ie
+t
Anxiety and Stressor-Related
Problems

This chapter describes some of the main anxiety-based

problems. It discusses contemporary accounts of their
causes (aetiology) and describes a range of relevant and
: 6.2 SOCIAL ANXIETY DISORDER 157
effective treatments for each. It is divided into six main
sections covering specific phobias, social anxiety disor-
: 6.3 PANICDISORDERAND AGORAPHOBIA 162
der, panic disorder, generalized anxiety disorder, obses-
sive compulsive disorder, and trauma and stress-related
6.4 GENERALIZED ANXIETY DISORDER (GAD) 170
disorders such as post-traumatic stress disorder. These
topics are chosen because they represent some of the
: 6.5 OBSESSIVE COMPULSIVE DISORDER(OCD) 176
most prevalent anxiety and stress-based problems (e.g.
panic disorder, generalized anxiety disorder), and they
6.6 TRAUMA AND STRESS-RELATED DISORDERS 186
consist of some of the most thoroughly researched disor-
ders where our understanding of their causeshas become _ ;
relatively well developed. i 6.7 ANXIETY AND STRESSOR-RELATED PROBLEMS
Ri Beas tte ncaa anes a eS a REVIEWED 193
SM eI Vk is Be als
(146 PSYCHOPATHOLOGY
LEARNING OUTCOMES
Pree eee ere Hee H PORTH SOPH HE OH REE PE ress HED HH EEE EE POOH HEH RE DG EH ESO HELE SHS E DH OE EES
1. Describe the kinds of presenting symptoms 4, Distinguish between biological and psychological
that are associated with individual anxiety and explanations of anxiety-based problems.
stressor-based problems. 5. Describe the relevance of research methodologies
2. Describe the characteristics and diagnostic criteria of that have contributed to the understanding of the
six of the important anxiety and stressor disorders. acquisition of anxiety and stress-related disorders.
3. Describe, compare and contrast at least two 6. Describe, compare and contrast at least two
contemporary theories of the aetiology of each therapeutic procedures used for each individual
disorder. anxiety disorder or stress-related disorder.
REET EELS ETE ADDER EAD ERED EEE A AES ADEE EAE ETE EEE AREER ERE DY EEE EE EADIE TIAA ETIAI AA AA EAA AAA GG
ye
I'm 26 years old and experience severe anxiety. I've had on and off panic attacks since | was 17. I’ve really worked hard to manage
it using breathing, daily exercise and diet. | thought I'd beaten it. . . two years pretty symptom free. But shortly after becoming
engaged, the panic attacks started and anxiety came back with a vengeance. | can barely manage my days at work, | have little
appetite and I'm terrified of negative thoughts I've been having. My scariest thought in the past was having a heart attack. But
knowing I'm in such good physical shape | know this isn’t a possibility. My scary thought for the past few weeks has been what if
| kill myself. . . so scary |try not to be alone. My doctor has given me some medication, but |don’t know if it’s working. My friends
who know about psychology say I’m fine and those thoughts are my anxiety.
Michellie’s Story
OEE TNE T EE EET E EEE TTT EEE ETE TE ETE EET EEE TET ELE TEER EE TEED EEE EEE EEE EEE EEE EEE EEE
Introduction need to urinate, sexual problems, and nightmares. In

contrast, the cognitive features of anxiety include a feel-
Anxiety and stress are common features of everyday ing of apprehension or fear, usually resulting from the
living, and will be experienced by us all in one form or anticipation of a threatening event or situation. Usually
another. As an adaptive emotion anxiety can help us pre- accompanying anxiety are intrusive thoughts about the
pare to deal effectively with anticipated threats and chal- threat, catastrophic bouts of worrying about the possible
lenges by increasing our arousal and reactivity, focusing negative outcomes associated with the threat, and — in
our attention, and helping us to problem solve. However, some specific types of problems — uncontrollable flash-
we can often find there will be times in our lives when we backs about past traumas and anxiety-provoking expe-
have difficulty managing our anxiety, and it starts to feel riences. Overly anxious people also find it hard to stop
uncontrollable and distressing. Michelle’s story provides thinking negative and threatening thoughts, and this is in
an example of how anxiety can come to feel distressing part due to the cognitive biases that have developed with
and her commentary gives us a real insight into some the experience of anxiety.
of the more debilitating symptoms of an anxiety prob- We all experience feelings of anxiety quite naturally
lem. These include panic attacks, lack of appetite, scary, in many situations — such as just before an important
uncontrollable thoughts, thoughts about physical illness, exam,while making a presentation at college or work, at
even suicidal ideation. Anxiety generally has both physi- an interview, or on a first date. Most anxiety reactions are
cal and cognitive attributes. First, there are the physi- perfectly natural, and they have evolved as adaptive
cal symptoms of anxiety — such as muscle tension, dry responses that are essential for us to perform effectively
mouth, perspiring, trembling and difficulty swallowing. in challenging circumstances. However, anxiety can
In its more chronic form, anxiety can also be accompa- often become so intense or attached to inappropriate
nied by dizziness, chronic fatigue, sleeping difficulties, events or situations, that it becomes maladaptive and *
rapid or irregular heartbeat, diarrhoea or a persistent problematic for the individual (Lepine, 2002). This is
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS ae
when an anxiety disorder expensive than any other psychological problem (Rovner,
t terized by an excessiveoraroused
ty disorder A psychological disorder
may develop. In a sufferer 1993; Greenberg, Sisitsky, Kessler, Finkelstein et al., 1999).
ea nd feelir s of apprehension, uncer-
of an anxiety disorder, the These economic costs include psychiatric, psychological,
ity and fear.
anxiety response may: and emergency care, hospitalization, prescription drugs,
reduced productivity, absenteeism from work, and sui-
1. be out of proportion to the threat posed by the
cide (Lepine, 2002).
situation or event (e.g. in specific phobias);
In this chapter we will discuss in detail six of the main
2. be a state that the individual constantly finds anxiety and stress-related disorders. The details of these
themselves in and may not be easily attributable disorders can be reviewed online in the table ‘Anxiety
to any specific threat (e.g. in generalized anxiety Disorders — Summary’, which is available on the web-
disorder, or some forms of panic disorder); site at www.wiley-psychopathology.com/ch6. Readers
persist chronically and be so disabling that may want to refer back to this table when they have read
it causes constant emotional distress to the and digested the information on each separate disorder.
individual, who is unable to plan and conduct Throughout this book we have summarized the DSM-5
their normal day-to-day living. This can result in diagnostic criteria for the disorders discussed to give the
an inability to hold down a regular job, maintain student reader a briefer overview, and ok oy
long-term relationships with friends, partners and cannot be read as full diag- _—
family, and so forth. nostic criteria. Please refer § To read the anxiety disorders
summary table go to
to your library’s copy of | www.wiley-psychopathology.com/ch6
Anxiety-based problems are relatively common, DSM-5 for full criteria and
and around 30-40 per cent of individuals in Western aetiology.
societies will develop a problem that is anxiety related The six main anxiety and stress-related disorders are:
at some point in their lives (Shepherd, Cooper, Brown
et al., 1996; NIMH, 2005) (see Figure 6.1). As a result, specific phobias
pathological anxiety imposes a high individual and social social anxiety disorder
burden, tends to be more chronic than many other psy-
panic disorder
chological problems, and can be as disabling as physical
illness. In both Europe and the US, the cost of treat- generalized anxiety disorder (GAD)
ing anxiety-based problems runs into many billions of obsessive compulsive disorder (OCD)
pounds annually, making them more economically bh
wu
nA
-—
NK
& post-traumatic stress disorder (PTSD).
Anxiety as a comorbid condition

Anxiety disorders are diagnosed when subjectively expe-
rienced anxiety is present and recurs on such a regular
and chronic basis that it is distressing and disrupts normal
daily living. However, many of the symptoms of anxiety
are common to a number of different anxiety disorders,
and so it is relatively common for an individual to suffer
from more than one anxiety disorder (Hofmeijer-Sevink,
Batelaan, Harold, van Megen et al., 2012). When anxiety
disorders are comorbid with each other in this way they
of
adult
Per
US
population
cent
have an earlier age of onset, a higher rate of chronicity,
a 1
and are also likely to be associated with depression, and
Lifetime 12-month 12-month with greater social disability. Anxiety symptoms may
prevalence prevalence prevalence be particularly prone to comorbidity because many of the
classified
as severe physiological and cognitive components of anxiety can be
found across different disorders, and so these vulnerabil-
FIGURE 6.1 Prevalence rates for diagnosed anxiety disorders ity factors may trigger the development of multiple anxi-
in the US population. ety problems. Some common cross-disorder phenomena
Lifetime prevalence rates shows that 28.8 per cent of adults that may lead to anxiety—anxiety comorbidity include:
will be diagnosable with an anxiety disorder in their lifetime
(NIMH, 2005). The study also showed that the average age of 1. Physiological symptoms of panic are found not
onset is 11 years. only in panic disorder, but also in the reactions to
Source: National Institute of Mental Health phobic stimuli in specific phobias.
148 PSYCHOPATHOLOGY
; a
2. Cognitive biases — such as information processing increase an individual’s risk of developing several
biases that tend to cause anxious people to anxiety-based problems.
selectively attend to threatening stimuli (Mathews &
Anxiety disorders are also commonly comorbid with
MacLeod, 2005) — are common to almost all anxiety
other psychological disorders (Rodriguez, Weisberg,
disorders.
Pagano, Machan et al., 2004; McLean, Asnaani, Litz &
3. Anumber of prominent psychopathologies Hofmann, 2011), which means that a range of symptoms
are characterized by the dysfunctional and associated with psychological problems can also co-occur
uncontrollable perseveration of certain thoughts, with anxiety (e.g. depression, substance abuse and eat-
behaviours or activities (e.g. pathological worrying ing disorders are commonly experienced with anxiety).
in generalized anxiety disorder, perseverative Table 6.1 shows prevalence rates and comorbidity figures
compulsions in obsessive compulsive disorder, for a number of anxiety and stress-related disorders from
and rumination during periods of depression), a survey by McLean et al. (2011). In this recent survey,
and the psychological mechanism that underlies lifetime prevalence rates for developing an anxiety disor-
dysfunctional perseveration may be similar across der that was comorbid with another psychological disor-
all these disorders (Davey, 2006). der was 44 per cent for women and 34 per cent for men.
4. Certain specific early experiences can be found In particular, anxiety disorders were highly comorbid
in the aetiology of a number of different anxiety with mood disorders and with substance use disorders.
disorders (e.g. physical or sexual abuse during Let’s look at each of the anxiety diagnostic categories
childhood), and experiences such as these may in turn, starting with a closer look at specific phobias.
TABLE 6.1 Lifetime and 12-month prevalence rates of comorbid disorders among individuals diagnosed with an anxiety disorder
12-Month Lifetime
Disorder Women (%) Men (%) Woimen (%) Men (%)
Mood disorders
Major depressive disorder 23a), 19.1 38.3 30.0
Dysfunctional beliefs U2 8.9 129 10.6

Bipolar 1 2.4 3h.) 3.0 3.3
Bipolar 2 38) 3.9 3.4 Sy

Substance use disorders
Alcohol abuse 43 8.2 15.0 Bo
Alcohol dependency 2.9 48 79 16.7
Drug abuse 1.4 4.5 10.0 21.8

Drug dependency 1.0 DD 4.9 9.3
Eating disorders
Anorexia nervosa 0.0 0.0 0.6 0.2

Bulimia nervosa 1.0 0.0 ep 0.5
Binge-eating disorder 2.0 les! 247, 2.3
Other
Attention deficit/hyperactivity disorder 6.9 7.6 7.8 Wet
Intermittent explosive disorder 9.4 12.5 11.6 19.3
Anxiety disorder
Any additional BMS 27.9 44.8 34.2
Source: McLean, C.P,, Asnaani, A., Litz, B.T. & Hofmann, S.G. (2011). Gender differences in anxiety disorders: Prevalence, course of illness, comorbidity
and burden of illness. Journal of Psychiatric Research, 45, 1027-1035.
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS 149,
6.1 SPECI] FIC PHOBIAS TABLE 6.2 The phobic beliefs of spider phobics
- oh SR ae I A ae A NE ee ee tr A Phobics develop a set of dysfunctional beliefs about their
: : phobic stimulus or event. These beliefs are very rarely chal-
For a video on specific phobias go to ‘ Specific phobias are defi- jenged because the phobic avoids all circumstances where
www.wiley-psychopathology.com/ | ned as a ‘marked fear or such beliefs might be disconfirmed. These beliefs maintain
video/ch6 } anxiety about a specific phobic fear and serve to motivate responses designed to
object or situation (e.g. avoid contact with the phobic stimulus. Below are some exam-
flying, heights, animals, ples of phobic beliefs held by spider phobics. Such beliefs are
cific phobias An excessive, unreason- =. PES the kinds that are challenged in both exposure therapy and
e, persistent fear triggered by aspecific TCeiving an injection, see- cognitive therapy procedures.
ect or situation. ; ing blood)’, and the DSM
criteria for specific phobia armbeliefs: mH .
are presented in DSM-5 Summary Table 6.1. The pho- When a spider is in my vicinity | believe that the spider will:
bic trigger usually elicits extreme fear and often panic, ve Bite me
i Ea (b) crawl towards my private parts
which usually means that the phobic individual devel... g¢ things on purpose to tease me
ops avoidance strategies designed to minimize the pos- (4) get on to parts of me that | cannot reach.
sibility of contact with that phobic trigger. Phobics are
Chaser and prey beliefs:
normally aware that their fear of the phobic situation or Wh eet weet
; : ‘ ‘ ( en | encounter a spider it will:
event is excessive or unreasonable (in comparison either (.) un towards me
with the actual threat it represents or with the less (4) stareatme
fearful responses of other people), but they do acquire a_ (c)_ settle on my face
strong set of phobic beliefs that appear to control their (cd) not be shaken off once it is on me.
fear (Thorpe & Salkovskis, Unpredictability and speed beliefs:
obic beliefs Beliefs about phobic 1997). These beliefs nor- Whenlencountera spider:
nuli that maintain
the phobic’s fear and ah. : PO ; ; ;
pane a Hen an ee mally contain information (a) its behaviour will be very unpredictable
. about why they think the (5) it will be very quick
phobia is threatening and how to react when they are in (©) it will run in an elusive way.
the phobic situation (e.g. avoid contact, and so on) (see __/nvasiveness beliefs:
Table 6.2). Many contemporary psychological treat- When! encounter
a spider it will:
ments for specific phobias are designed to challenge (@) crawl into my clothes
these dysfunctional phobic beliefs and replace them ‘°) walk over me during the night
with more functional beliefs that foster approach and fe) hide ym places Ido not wat rsuc tiger ed
contact with the phobic stimulus instead of avoidance. Response beliefs:
When | encounter a spider | will:
f
\ a) feel faint
(
\ b) lose control of myself
Prevalence
(c) go hysterical
Specific phobias are extraordinarily common, withsurveys (©) scream.
suggesting that a clear majority of the general population — source: Adapted from Arntz, Lavy, van den Berg & van Rijsoort (1993)
(60.2 per cent) experience ‘unreasonable fears’ (Chapman, and Thorpe & Salkovskis (1997).
1997) — although in most cases these fears are rarely severe
enough to result in impairment or distress. Recent sur- diagnosable with a specific phobia in their lifetime (Kessler,
veys suggest that as many as 20 per cent of adults will be Avenevoli, Costello, Green et al., 2012), which suggests
that severe and disruptive phobic symptoms can be quite
common. Table 6.3 shows the prevalence rates for some
of the more common forms of specific phobia. There is
DSM-5 SUMMARY TABLE 6.1 Criteria for specific phobia
also a clear gender difference in the prevalence of specific
¢ Disproportionate and immediate fear relating to a specific phobias, with women being twice as likely as men to be
object or situation diagnosed with a specific phobia (Kessler, McGonagle,
e Objects or situations are avoided, or are tolerated with Zhao, Nelson, Hughes, et al., 1994).
intense fear or anxiety
e Symptoms cannot be explained by other mental disorders Common phobias
and persist for at least six months
Interestingly, common phobias tend to focus on a rel-
e Phobia causes significant distress and difficulty in per-
atively small group of objects and situations, and the
forming social or occupational activities
main ones are animal phobias (including fear of snakes,
150 PSYCHOPATHOLOGY
' + Ay
TABLE 6.3 Lifetime prevalence rates for common specific phobias phobias which are (1) animal phobias (e.g. spiders,
insects, dogs), (2) natural environment phobias (e.g.
Lifetime prevalence rates
heights, storms, water), (3) blood—injection-injury pho-
Social phobia 3.2% bias (BID) (e.g. needles, invasive medical procedures), (4)
Blood-injury-injection phobia 3.5%?
situational phobias (e.g. airplanes, elevators, enclosed
spaces), and other phobias (e.g. situations that may lead
Animal phobias generally 1.1%! to choking or vomiting; in children, loud sounds or cos-
Dental phobia 3-5%? tumed characters!). There is some evidence that if you
Water phobia 3.3%! suffer from a specific phobia in one of these categories,
you are more likely to suffer a phobia of one or more
Height phobia 4.7%'
of the other phobias in that category (e.g. Davey, 1992b;
Claustrophobia/enclosed spaces 2.4%! Fredrikson, Annas, Fischer & Wik, 1996) and, thus, pho-
'Taken from the Epidemiologic Catchment Area (ECA) study (see bias within each category can have a higher incidence of
Chapman, 1997). comorbidity (Kendler, Myers, Prescott & Neale, 2001).
*Kent (1997). There are also important cultural differences in the
*Bienvenu & Eaton (1998).
kinds of stimuli and events that can become the focus
of clinical phobias. For example, Taijin-kyofusho (TKS)
spiders, rats, mice, creepy-crawlies such as cockroaches, is a common Japanese syndrome characterized by a fear
invertebrates, such as maggots and slugs), social phobia, of embarrassing or offending other people (Prince &
dental phobia, water phobia, height phobia, claustro- Tcheng-Laroche, 1987). This is different to the Western
phobia, and a cluster of blood, injury and inoculation syndrome of social phobia, where the fear is based on
fears (known as BII). Most other types of phobias are the public embarrassment experienced by the phobic
less common and can be thought of as quite unusual individual himself or herself. Davey et al. (1998) also
given the degree of threat they might realistically found a number of important cross-cultural differences
pose — such phobias include fear of cotton wool, but- in animal fears. For example, while fear of spiders is a
tons, chocolate, dolls and vegetables (McNally, 1997) (see common phobic reaction in most Western cultures, spi-
Photo 6.1)! DSM-5 specifies five subgroups of specific ders were significantly less feared in the Indian sample
>i
Ss
35)
x=
iS
S
o
© |
Nneirda
©
Gallinago_media
©
Image
PHOTO 6.1 Small animal phobias are very common and consist of creepy-crawlies, insects, mollusks, rodents, spiders, snakes and
lizards, etc. Interestingly, ifyou are fearful of one of these types of animals you are more likely to be fearful of others in this group. Fear
of such animals may be related more to the emotion of disgust rather than anxiety.
All images used under license from Shutterstock.com.
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS ei
used in the study. This kind of cross-cultural variabil- fears of things that usually pose little if any realistic
ity suggests that ‘fear-relevance’ may at least in part be threat, and their acquisition more often than not cannot
determined and developed by factors that are specific to be explained by recourse to simple learning experiences
individual cultures, and this should be contrasted with such as a specific traumatic event. This has led at least
more biologically oriented views which argue that fear- some approaches to psychopathology to view phobias as
responses have been universally pre-wired by evolution- symbolic of other, more deep-rooted psychological diffi-
ary selection pressures (Davey, 1995; see the section on culties. For example, psychoanalytic theory as developed
‘The role of evolution’ below). by Freud saw phobias as a defence against the anxiety
produced by repressed id impulses, and this fear became
associated with external events or situations that had a
6.1.1 The Aetiology of Specific Phobias symbolic relevance to that repressed id impulse. Focus
Point 6.1 describes the classic case of ‘Little Hans’, a
Attempts to explain specific phobias have a long history 5-year-old boy who developed a severe phobia of horses.
and date back to the early days of the psychoanalytic Within Freud’s psychoanalytic theory, the function of
approaches pioneered by Freud and the condition- phobias was to avoid confrontation with the real, under-
ing views developed by the behaviorist J.B. Watson. lying issues (in this case, a repressed childhood conflict).
Originally, there was a tendency to try to explain all However, because of the nature of psychoanalytical the-
types of phobias with just one explanatory theory (e.g. orising, there is little in the way of objective evidence to
classical conditioning), but this approach has now given support such accounts of phobias. Nevertheless, there is
way to the view that different types of phobias might often an element of insight that can be drawn from the
be acquired in quite different ways (a multifaceted symbolic interpretations of case histories provided by
approach). Over the years, an intriguing debate has taken psychoanalysis, and many anxiety disorders may indeed
place about whether phobias are biologically determined function for the sufferer as a way of avoiding confronta-
through evolutionary processes or whether they are tion with more challenging life issues and difficulties.
responses learnt during the lifetime of the individual.
This debate will be an important feature of what follows. Classical conditioning and phobias
Attempts to explain phobias in terms of classical condi-
Psychoanalytic accounts tioning (see section 1.3) date back to the famous ‘Little
Phobias have intrigued psychologists for more than a Albert’ study reported by Watson & Rayner in 1920.
century. This may be because they manifest as irrational Albert was an 11-month-old infant, and Watson & Rayner
Roe LITTLE HANS: THE PSYCHOANALYTIC INTERPRETATION

Xe)
- OF A SPECIFIC PHOBIA
=
2) One of the most famous cases in the history of psy- psychoanalyst, still another aspect of Hans’ uncon-
| On choanalysis is that of‘Little Hans, a 5-year-old who scious fantasies, namely that the falling-down horse
A stood not only for his father, but also for his mother
revealed many of his perceptions, fantasies, and
=)
UW fears to his physician father, who, in turn, reported in childbirth, the box-like carts and vehicles repre-
Le) them to Sigmund Freud. Hans began to have a fear senting the womb. All these complicated, repressed
Li,
of horses, which eventually grew to the point that feelings and perception were thus incorporated in a
he refused to leave the house. The immediate event single phobia.
that precipitated this phobia was seeing a big, heavy It is important to note that Little Hans was basically
horse fall down. Freud interpreted this to mean that a straightforward, cheerful child who experienced nor-
Hans at that moment perceived his own wish that his mal psychosexual development marred only by the
father would fall down. Then Hans, a little Oedipus, episode of the phobia, from which he recovered rather
could take his father’s place with his beautiful mother. promptly. Fourteen years iater, 19-year-old Hans went
Another part of the fear derived from the large size to see Freud. He had continued to develop well and
of horses, which Hans unconsciously identified with had survived without unusual difficulty the divorce
the great power of his father. He expressed the fear and remarriage of both parents. The problems of his
that a horse would come into his room. He also childhood were used by Freud to illustrate the normal
became afraid not only of horses biting him, but of process of psychosexual development - the complex,
carts, furniture vans, and buses. This revealed, to the intense, erotic drama of early childhood.
sas PSYCHOPATHOLOGY
~“
attempted to condition in him a fear to his pet white rat. Incubation is a phenomenon that is frequently
They did this by pairing the rat — the conditioned stimulus observed clinically, but according to conditioning
(CS) — with the frightening event of a loud noise produced theory it should lead to extinction rather than
by striking an iron bar — the unconditioned stimulus (UCS), enhancement of the fear response.
which distressed Albert (the unconditioned response, UCR).
After several pairings of the rat with the noise, Albert Due to these features it is problematic for a classical
began to cry (the conditioned response, CR) whenever the conditioning account to explain the acquisition of all pho-
rat was introduced into the room. This type of explana- bias as resulting from traumatic conditioning episodes,
tion has been popular over the past 50 years, and more but there is strong evidence that traumatic conditioning
sophisticated contemporary conditioning models of spe- experiences are responsible. for the acquisition of at least
cific phobias have been developed (Davey, 1992a, 1997). some phobias. These include dental phobia (Davey, 1988),
However, it is difficult to explain generally the range of choking phobia (Greenberg, Stern & Weilburg, 1988),
features possessed by specific phobias with conditioning accident phobia (Kuch, 1997), and most dog phobias
theories. These criticisms include: (DiNardo, Guzy & Bak, 1988; Doogan & Thomas, 1992).
1. Traumatic experiences are essential for Biological accounts of phobias:

conditioning accounts, yet many phobics The role of evolution
appear unable to recall any trauma or aversive The fact that phobias tend to be focused on a limited
conditioning experience at the time of the onset set of fears that have evolutionary significance has led
of their phobia (Rachman, 1977; Marks, 1969; some researchers to suggest that we may be biologically
Emmelkamp, 1982). This appears to be particularly prepared or pre-wired to acquire certain phobias. For
true of some animal phobics such as snake and instance, clinical phobias tend to cluster around things
spider phobics (Davey, 1992b; Murray & Foote, such as heights, water, spiders, snakes, blood, injury and
1979), and also water and height phobics (Menzies so on, all of which can be considered to have a real life-
& Clarke, 1993a, 1993b). threatening significance that has been present for many
2. Not all people who have pain or trauma paired thousands of years. In contrast, we rarely develop clini-
with a situation develop a phobia. For example, cal phobias of life-threatening stimuli that have only
not everyone who has a traumatic experience appeared more recently in our phylogenetic past, such as
undergoing dental treatment acquires a dental guns and electricity. There are two predominant evolu-
phobia (Lautch, 1971), not everyone who tionary theories of phobias.
experiences a violent thunderstorm acquires a First, Seligman (1971) argued that evolutionary selec-
thunderstorm phobia (Liddell & Lyons, 1978), tion pressures have evolved in us a biological predisposi-
and not all fliers who experience a traumatic tion to learn to associate fear with stimuli that have been
flying accident express a subsequent anxiety of hazardous for our pre-technological ancestors. That is,
flying (Aitken, Lister & Main, 1981; Goorney,
1970). This suggests that a potential conditioning
experience is itself insufficient to cause a phobia.
3. Simple conditioning models treat all stimuli
as equally likely to enter into association with
aversive consequences, yet fears and phobias
are not evenly distributed across stimuli and
experiences. People appear to develop phobias
of animals (snakes, spiders), heights, water,
death, thunder, and fire more readily than fears
of hammers, electric outlets, knives, guns, and
suchlike, even though the latter group of stimuli
seem to have a high likelihood of being associated
with pain or trauma (Seligman, 1971).
4. Asimple conditioning model does not appear to
UCR
account for the common clinical phenomenon of
incubation. Incubation is where fear increases in FIGURE 6.2 The ‘Little Albert’ classical conditioning study
magnitude over successive encounters with the by Watson & Rayner (1920) demonstrated the acquisition of
phobic stimulus — even though it is not followed a phobia by pairing Albert's pet rat (the conditioned stimulus,
by a traumatic consequence (Eysenck, 1979). CS) with a loud noise (unconditioned stimulus, UCS).
is
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS 153.
we tend to have a built-in predisposition to learn to fear evidence in retrospective studies for phobias such as
things such as snakes, spiders, heights, and water because water and height phobia being caused by specific trau-
these have been life-threatening to our ancestors, and matic experiences (Menzies & Clark, 1993a, 1993b). This
those of our ancestors that evolved a biological predispo- account then goes on to explain adult phobias as instances
sition to fear these kinds of stimuli will have been more where these developmental phobias have failed to habit-
likely to survive and pass that fear predisposition on to uate properly.
future generations. This While evolutionary accounts are appealing and appear
logical preparedness A theory which
ues that we have a built-in predisposi-
account is known as bio- to have at least some face validity, we must be cautious
1tolearn to fear things such as snakes, logical preparedness, and about accepting them on the basis of existing evidence
ders, heights and water because these has been supported by two (Delprato, 1980). Firstly, such accounts depend on the fact
fe been life-threatening to our ancestors. lines of evidence: that current phobic stimuli have actually acted as impor-
tant selection pressures over our evolutionary past. But
* If participants in a classical conditioning experi- this is very difficult to empirically verify. For example,
ment are shown pictures of ‘fear-relevant’ stimuli do we tend to have phobic reactions to spiders because
such as snakes and spiders (conditioned stimuli, they once constituted an important life-threatening pres-
CSs) paired with electric shock (unconditioned sure on our pre-technological ancestors? There is no con-
stimuli, UCSs), they develop fear of the CSs more vincing evidence to suggest this. Secondly, evolutionary
quickly and show a greater resistance to extinc- accounts can be constructed in a post hoc manner and are
tion than if pictures of fear-irrelevant stimuli are at risk of being either ‘adaptive stories’ (McNally, 1995)
used as CSs (e.g. pictures of houses) (Ohman, or ‘imaginative reconstructions’ (Lewontin, 1979) (cf.
Erixon & Lofberg, 1975). Merckelbach & de Jong, 1997). This view argues that it is
¢ Also, Cook & Mineka (1990) found that possible to construct, post hoc, an adaptive scenario for
laboratory-reared rhesus monkeys that had never the fear and avoidance of almost any stimulus or event
before seen a snake rapidly acquired fear reactions (McNally, 1995) — see Activity 6.1. This does not mean
to snakes after being shown a demonstration of that evolutionary accounts are wrong (see Ohman &
another monkey being frightened in the presence Mineka, 2001, for a contemporary evolutionary account
of a snake. They did not acquire fear reactions of phobias), merely that
after watching a demonstration of another mon- they are tantalisingly easy
To complete Activity 6.1 go to
key being frightened in the presence of a stimulus to propose, but very diffi- | www.wiley-psychopathology.com/
such as a rabbit or a flower. Both studies suggest cult to substantiate. On my | activities/ch6
that humans and primates such as rhesus mon- blog, there is an informal
keys have an unlearnt predisposition to rapidly discussion on the ‘Mystery ,
To read the author's blog on
acquire fear responses to some types of stimuli of the origins of phobias’ | phobias go to
and not others (see Ohman & Mineka, 2001). that you might find useful | http://tinyurl.com/lyz2mof
and informative.
Second, Poulton & Menzies (2002) have argued for the
existence of a limited number of innate, evolutionary- Biological accounts of phobias:
relevant fears. This non-associative fear acquisition Neuroimaging studies
model argues that fear of a set of biologically relevant An alternative way to try to understand specific phobias
stimuli develops naturally is by investigating the brain neurocircuitry that under-
n-associative fear acquisition A after very early encounters, lies specific phobias, and we can do this using functional
del that argues that fear of a set of given normal maturational neuroimaging techniques (see section 2.2.4). The key
logically relevant stimuli develops
urally after very early encounters given
processes and normal back- brain structure that mediates fearful responding to pho-
‘mal maturational processes and normal ground experiences, and no bic stimuli is the amygdala, an almond-shaped group of
-kground experiences, and no specific specific traumatic experi- nuclei located within the medial temporal lobes (see
umatic experiences with these stimuli ences with these stimuli are Figure 6.3). The amygdala plays a significant role in the
necessary to evoke this fear.
necessary to evoke this fear. formation and storage of memories associated with
Following repeated exposure to these stimuli, the innate emotionally relevant events, and acts as a neural centre
fear reaction will habituate and should eventually disap- that identifies emotional input and then coordinates this
pear. Poulton & Menzies (2002) claim that this account with information from higher cortical areas and subcor-
explains why most children go through a discrete develop- tical nuclei; it next provides feedback to the thalamus
mental period when they appear to be frightened of that results in appropriate motor action (Del Casale,
potential life-threatening stimuli such as heights and Ferracuti, Rapinesi, Serata et al., 2012). The importance
water (Graham & Gaffan, 1997), and why there is little of the amygdala in activating phobic fear is indicated
154 PSYCHOPATHOLOGY
‘ %
Ventral PFC le— increase in heart rate and blood pressure but then ca
Moker YMPEC let»! oFe result in decreased parasympathetic responding that
Pha iPevLPRC Sq causes fainting. Accounts of specific phobias in terms of
CTle_| brain neurocircuitry are not in conflict with other types
of explanations of phobias (e.g. conditioning, evolution-
as Se aa rene ary accounts), but help to specify how the conditions
stumult
— through which specific phobias are acquired are stored
and activated in the brain.
Hippocampus
Multiple pathways to phobias

Brain Stem There is no reason why the acquisition of all phobias
Nuclei
should be explained by just a single process — and evi-
dence is now accumulating to suggest that different types
of phobias are acquired in quite different ways
(Merckelbach, de Jong, Muris & van den Hout, 1996).
We have already suggested that some phobias, such as
dog phobia, dental phobia, choking phobia and accident
phobia, are caused by traumatic conditioning experi-
ences. In contrast, many other common phobias do not
appear to be characterized by a traumatic experience at
their outset — in fact, sufferers often cannot recall the
exact onset of their phobia, which suggests that the onset
may be gradual and precipitated by factors that are not
immediately obvious to the individual. Phobias that fit
this description include most animal phobias (including
snake and spider phobia) (Murray & Foote, 1979;
Merckelbach, Muris & Schouten, 1996), and water and
height phobia (Menzies & Clarke, 1993a, 1993b).
Recent evidence suggests that at least some phobias
Amygdala
are closely associated with the emotion of disgust.
FIGURE 6.3 The amygdala at the crossroads of fear-related
High levels of disgust sensitivity have been found to
information processing. be associated with small
disgust A food-rejection emotion whose
Phobic stimuli enter the amygdala through the thalamus and animal phobias in general purpose is to prevent the transmission of
are then processed by the amygdala, which provides connections (Ware, Jain, Burgess & illness and disease through the oral incor-
to both higher brain function-related cortical areas (light grey) Davey, 1994; Davey, 1994a), poration of contaminated items.
and subcortical nuclei (darker grey). On receiving their output, spider phobia specifically
the amygdala integrates messages, thus providing feedback to (Mulkens, de Jong & Merckelbach, 1996), and has been
the thalamus to generate a motor output. (DLPFC = dorsolateral hypothesized to play a role in mediating blood-injury—
prefrontal cortex; OFC = orbitofrontal cortex; ventral PFC = injection phobia and contamination fears (Page, 1994;
ventral frontopolar prefrontal cortex; VLPFC = ventrolateral Olatunji, Sawchuk, Lohr & de Jong, 2004). Disgust is a
prefrontal cortex; VMPFC = ventromedial prefrontal cortex). food-rejection emotion whose purpose is to prevent the
Source: After Del Casale A., Ferracuti S., Rapinesi C., Serata D. et transmission of illness and disease through the oral
al. (2012). Functional neuroimaging in specific phobia. Psychiatry
incorporation of contaminated items (Davey, 1994b;
Research: Neuroimaging, 202, 181-197.
Rozin & Fallon, 1987), and elevated disgust sensitivity
implies increased avoidance of disgust-relevant objects
(such as faeces or mucus). In the case of animal pho-
by the fact that there is a linear relationship between bias, Davey (1994a) has argued that many animals that
subjective experience of fear and amygdala activation become the focus for phobic responding do so because
(Goossens, Schruers, Peeters, Griez et al., 2007; Ahs, they have disgust relevance. Specifically, they may have
Pissiota, Michelgard, Frans et al., 2009). acquired a disgust relevance (1) by directly spreading
Functional neuroimaging studies have also demon- disease and being a source of contamination (e.g. rats,
strated that blood-injury—injection phobia and dental cockroaches), (2) by possessing features which mimic
phobia are functionally different to other phobias, in that primary disgust relevant stimuli (by resembling, for
they can lead to a biphasic response that begins with an instance, faeces or mucus; e.g. slugs or animals that are:
&
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS — 155_
perceived as slimy such as snakes, snails or lizards), or factors and psychological processes. This being so, spe-
(3) by having contemporary or historical significance as cific phobias are a coherent category only on the basis
stimuli that signalled disease, illness or contamination of their defining symptoms, and therapists may need to
(e.g. maggots, spiders; cf. Davey, 1994a). This look more closely at the different aetiologies to construct
disease-avoidance model of animal phobias (Matchett successful treatments.
& Davey, 1991 is sup-
2ase-avoidance model The view
ported by the findings that
tfsome animal phobias are related to
having a high level of dis-
mpts to avoid disease or illness that 6.1.2 The Treatment of Specific Phobias
gust sensitivity is a vulner-
ht be transmitted by these animals.
ability factor for animal Traditionally, successful treatment for specific phobias
phobias (such as spider phobia), and can mitigate has tended to revolve around some form of exposure to
against successful therapy if it is not directly addressed the phobic stimulus or situation, and, in the past, behav-
in treatment (de Jong, Andrea & Muris, 1997; Mulkens, ioural treatments of choice for specific phobias have
de Jong & Merckelbach, 1996). tended to include systematic desensitisation, flooding
Alternatively, there is evidence that factors closely and counterconditioning (see section 4.1.1). One impor-
associated with panic and panic disorder (see section 6.3) tant issue in therapy for specific phobias is to address the
are also linked to a number of specific phobias. First, there phobic beliefs that sufferers hold about their phobic event
is a fairly high comorbidity rate between panic disorder or situation (see Table 6.2 above). These beliefs are often
and some specific phobias. Studies have identified comor- dysfunctional in that they do not match with the reality
bidity rates of between 40 per cent and 65 per cent (de of the threat (or lack of it) posed by the phobic stimu-
Ruiter, Rijken, Garssen, van Schaik & Kraaimaat, 1989; lus, and they also maintain fear and avoidance responses.
Starcevic, Uhlenhuth, Kellner, & Pathak, 1992), suggest- Because of their strong avoidance of any contact with
ing that panic is common in people suffering from many their phobic situation, sufferers rarely find themselves
different types of specific phobia. Second, some catego- in a situation where they encounter evidence that dis-
ries of specific phobia — especially situational phobias — confirms their phobic beliefs (e.g. continually avoiding
share important characteristics in common with panic spiders never helps the spider phobic to disconfirm their
disorder. For example, situational phobias appear to have belief that, for example, ‘I would come to physical harm
a preponderance of spontaneous onsets typical of panic in the presence of a spider’) (Thorpe & Salkovskis, 1995,
disorder (Himle, Crystal, Curtis & Fluent, 1991), have a 1997). One important feature of exposure therapy is that
significantly higher rate of comorbidity with panic disor- it does put the phobic in situations where they can expe-
der than do other types of phobias, such as animal pho- rience evidence that is contrary to their dysfunctional
bias (Starcevic & Bogojevic, 1997), and frequently have
uncontrollable panic attacks as one of the symptoms of
phobic responding (e.g. height phobia, Antony, Brown
& Barlow, 1997; flying phobia, McNally & Louro, 1992;
claustrophobia, Mclsaac, 1995). Similarly, both claustro-
phobia and height phobia share aetiological factors in
common with panic disorder. For instance, subjective
fear in claustrophobia is focused not just on external
dangers but on anxiety expectancies and bodily sensa-
tions (Craske, Mohlman, Yi, Glover & Valeri, 1995), and
spontaneous panic attacks are found significantly more
often in claustrophobics than in other types of phobias
(Rachman & Levitt, 1985; Craske & Sipsas, 1992). Height
phobia is associated not only with heightened discrimi-
nation of bodily sensations, but also with a bias towards Hoffman
Hunter
Dr.
Courtesy
interpreting ambiguous bodily sensations as threaten- PHOTO 6,2 Exposure therapy is one of the most successful
ing — a characteristic which is central to the aetiology treatments for specific phobias. For many sufferers, however,
of panic disorder (Davey, Menzies & Gallardo, 1997) (see the thought of having to encounter a real spider is severely
section 6.3.1). distressing. Instead, therapists have developed virtual reality
These examples suggest that specific phobias may exposure treatments, in which the client can first encounter
have a number of different causes — depending on the spiders in a controlled virtual environment. This and various
nature of the phobic stimulus or event — and the aeti- other forms of treatment for specific phobias are discussed in
ologies appear to involve quite different vulnerability Choy, Fyer & Lipsitz (2007).
156 PSYCHOPATHOLOGY
~
beliefs. More recently, specific behavioural treatments sub-clinical in intensity or their fears are so specific that
have been combined with cognitive therapy techniques they do not interfere substantially with their daily lives.
to produce integrated short-term therapies that involve So, only those with the most distressing or disabling pho-
cognitive restructuring, intensive exposure to the phobic bias are the ones who seek treatment. In general, recently
event or stimulus, and modelling, and these can be effec- developed therapies for specific phobias have been shown
tive in as little as one 3 hour session (Ost, 1997). to be extremely effective and successful (Ost, 1997). These
In conclusion, it must be remembered that many peo- therapies are usually multifaceted and combine aspects
ple can live with their phobias — either because they are of exposure therapy with cognitive restructuring.
THE CLINICAL PERSPECTIVE - TREATMENT IN PRACTICE BOX 6.1:

ONE SESSION RAPID TREATMENT OF SPIDER PHOBIA
One-session treatments for specific phobias were deavel- be tested by the therapist who then touches the spider.
oped during the 1990s and are remarkably successful as This is repeated up to 10 times to show the client that
effective and long-lasting treatments for many specific the spider's reaction is almost always to run away. This is
phobias (Ost, 1997; Koch, Spates & Himle, 2004; Ost, Alm, followed by the client touching the spider — usually with
Brandberg & Breitholtz, 2001). One-session treatments some physical guidance from the therapist.
usually include a combination of graduated in vivo expo-
sure and modelling. Below is an example of a one-session STEP 3: HOLDING THE SPIDER IN THE HAND
treatment procedure for spider phobia.
The therapist takes the spider on his or her hand, letting it
STEP 1: CATCHING A SMALL SPIDER IN A PLASTIC walk from one hand to another. The client is then encouraged
BOWL to put their index finger on the therapist's hand so that the
spider can walk across the finger and back to the therapist's
The therapist first models how the client should pick up hand. This is repeated a number of times until the spider
the spider by putting a bowl over it and then sliding a card walks across all the client's fingers. Gradually, the thera-
underneath to trap the spider and then picking the bowl pist withdraws physical support and the client allows the
up using the card as a lid. This is repeated three or four spider to walk from one hand to another.
times and on the last occasion the client is instructed to These three steps are then repeated with spiders of
hold the bowl in the palm of his or her hand. At this point increasingly larger size. Throughout the session, the client
a brief role-play can be carried out by having the therapist is taught that he/she can acquire control over the spider
play the part of a person born blind, and the client has by gradually being able to predict what the spider will do.
to describe what is happening (thus forcing the client to The goal of the therapy is to ensure that at the end ofthe
look at the spider in the bowl). session the client can handle two spiders with low or no
anxiety and no longer believe his/her catastrophic cogni-
STEP 2: TOUCHING THE SPIDER tions about spiders.
The therapist asks the client what they think will happen Source: Ost, L.G. (1997). Rapid treatment of specific phobias. In
if they touch the spider. Most spider phobics say the spi- G.C.L. Davey (Ed.) Phobias: Ahandbook of theory, research and treat-
der will climb up their arm. This is a prediction that can ment. Chichester. John Wiley & Sons. Reproduced with permission.
SELF-TEST QUESTIONS
° What are the main diagnostic criteria for specific phobias?

* What are the most common phobias, and what are the kinds of phobic beliefs that accompany them?
* How do classical conditioning and evolutionary theories attempt to explain the acquisition of phobias? What are their
similarities and differences?
* What is the role of brain areas such as the amygdala in the formation of specific phobias?
* Why is exposure such an important feature of treatment for specific phobias?
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS sz
SECTION SUMMARY
6.1 SPECIFIC PHOBIAS
° Specific phobias are defined as an excessive, unreasonable, persistent fear triggered by a specific object or situation.
e Around 10 per cent of people will meet DSM-5 criteria for a specific phobia within their lifetime.
* Common phobias include small animal phobias (insects, rodents, spiders, snakes), social phobia, dental phobia, water pho-
bia, height phobia, claustrophobia, and blood-injury—inoculation (Bll) phobia.
¢ The famous ‘Little Albert’ study by Watson and Rayner (1920) is an example of how phobias can be acquired through clas-
sical conditioning.
¢ Evolutionary accounts of phobias suggest that we have an inbuilt biological predisposition to fear certain stimuli and events
(e.g. heights, water, snakes), because these stimuli were life-threatening to our pre-technological ancestors. Evolutionary
accounts of phobias include biological preparedness theory and the non-associative fear acquisition model.
¢ The amygdala is a brain area that plays a significant role in the formation and storage of memories associated with specific
fears and phobias.
e There is now strong evidence that different phobias may be caused by quite different processes: some involve classical
conditioning, some are caused by high disgust sensitivity, while others appear to be caused by processes similar to those
that cause panic disorder.
e Successful treatment for phobias tends to depend on some kind of exposure to the phobic stimulus or situation, and
exposure therapies that are combined with cognitive behaviour therapy can be effective in as little as one 3 hour
session.
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6.2 SOCIAL ANXIETY their hands shake. Individuals with social anxiety disor-
der almost always experience symptoms of anxiety (e.g.
DISORDER palpitations, tremors, sweating, gastrointestinal discom-
fort, diarrhoea, muscle ten-
sion, blushing, confusion) social anxiety disorder A severe and
Social anxiety disorder is distinguished by a severe and in the feared social situa- persistent fear of social or performance
persistent fear of social or performance situations. The situations. ’
tions, and, in severe cases,
social phobic tries to avoid any kind of social situation these symptoms may turn into a full-blown panic attack.
in which they believe they may behave in an embarrass- As a result of their reluctance to engage with social situa-
ing way or in which they believe they may be negatively tions, sufferers of social anxiety disorder also tend to
evaluated, and these types of situation can range from underperform in education and in the workplace, have
something as simple as having a conversation, eating or impaired social and romantic relationships, and reduced
drinking in front others, or performing in front of others productivity (Moitra, Beard, Weisberg & Keller, 2011;
(e.g. giving a speech). So pervasive is anxiety of these Kessler, 2003). Social anxiety disorder is as common in
socially based situations that it is also a predictor of sev- adolescence as it is in adulthood (Chavira, Stein, Bailey &
eral other debilitating problems such as depression and Stein, 2005), is a common reason for school refusal in
substance abuse (Rapee & Spence, 2004). young children, and is the only mood or anxiety disorder
DSM-5 describes some of the defining features of that has consistently been associated with dropping out
social anxiety disorder, which include situations in which of school early (Stein & Kean, 2000). DSM-5 Summary
the sufferer believes he or she will show anxiety symp- Table 6.2 lists the DSM criteria for the diagnosis of social
toms that will be negatively evaluated (e.g. they will be anxiety disorder.
humiliated, embarrassed, or rejected) or will offend oth-
ers. They may fear public speaking because of concern
that others will notice their trembling hands or voice. Or Prevalence
they may experience extreme anxiety when conversing Social anxiety disorder has a lifetime prevalence rate of
with others because of fear they will appear inarticulate. between 4 and 13 per cent in Western societies and, with a
They may avoid eating, drinking, or writing in public gender prevalence of 3:2 females to males, afflicts females
because of fear of being embarrassed by having others see significantly more often than males (Wittchen & Fehm,
ee PSYCHOPATHOLOGY
: ~%
DSM-5 SUMMARY TABLE 6.2 Criteria for social anxiety disorder it is not clear how specific this genetic component might
be. For example, children with social anxiety disorder
* Distinct fear of social interactions, typified by anxiety
are more likely to have parents with the disorder than
around receiving negative judgment or of giving offense
non-phobic children (Lieb, Wittchen, Hoefler, Fuetsch,
to others
et al., 2000; Mancini, Van Ameringen, Szatmari, Fugere
* Social interactions are avoided, or are experienced with
et al., 1996), and twin studies also suggest that there is a
intense fear or anxiety
significant but moderate genetic influence on the devel-
¢ The avoidance, fear or anxiety often lasts for 6 or more opment of social anxiety disorder (Beatty, Heisel, Hall,
months and causes significant distress and difficulty in
Levine & La France, 2002; Ollendick & Hirshfeld-
performing social or occupational activities
Becker, 2002). While indicating the importance of
e Anxiety cannot be explained by the effects of other men- genetic influences, such studies do beg the question
tal or medical disorders, drug abuse or medication of what aspect of social anxiety disorder is inherited.
Some studies have been able to identify specific con-
structs related to social anxiety disorder that appear to
2003; Xu, Schneier, Heimberg, Princisvalle et al., 2012;
have a genetic component, and these include submissive-
Memik, Yildiz, Tural & Agaoglu, 2011). Age of onset is
ness, anxiousness, social avoidance and behavioural inhi-
considerably earlier than for many of the other anxiety dis-
bition (Warren, Schmitz & behavioural inhibition A construct
orders, with a typical age of onset in the early to middle
Emde, 1999; Robinson,
teens, and usually prior to 18 years of age (Rapee, 1995;
Kagan, Reznick & Corley,
used to define thecharacteristic in som
children of seeming quiet, isolated and 7
Otto, Pollack, Maki, Gould et al., 2001). It is also a particu- anxious when confronted either with -
1992). Other studies indi-
larly persistent disorder, and has the lowest overall remis- situations or with novelty.
cate that social anxiety dis-
sion rate of the main anxiety disorders (Massion, Dyke,
order contains an inherited component that is shared
Shea, Phillips et al., 2002; Hirshfeld-Becker, Micco. Simoes
with other anxiety disorders — and this suggests that what
& Henin, 2008). Cross-cultural studies have shown that
might be inherited is a vulnerability to anxiety disorders
prevalence rates are significantly lower in South-East Asian
generally rather than social phobia specifically (Kendler,
countries (e.g. Korea and Taiwan), than in Western socie-
Walters, Neale, Kessler et al., 1995; Nelson, Grant,
ties (Furmark, 2002), but this may be due at least in part to
Bucholz, Glowinski et al., 2000). Several genes have been
the fact that the expression of social anxiety differs across
associated with socially anxious traits such as shyness
cultures. For example, inJapan, Taijin-kyofusho (TKS) is a
and introversion, although these studies have been far
form of social phobia in which the main fear is of offending
from consistent in their findings (Gelernter, Page,
others (see section 6.1). In Western cultures, social anxiety
Stein & Woods, 2004; Stein & Stein, 2008; Arbelle,
manifests itself primarily as fear of embarrassing oneself.
Benjamin, Golin, Kremer et al., 2003). Nevertheless,
there may still be a modest inherited element that is spe-
6.2.1 The Aetiology of Social cific to social anxiety disorder, and this has been esti-
mated to account for as much as 13 per cent of the
Anxiety Disorder variance in social fears generally (Kendler, Myers,
Although it is a phobia in its own right, social anxiety Prescott & Neale, 2001). Inherited components that are
disorder is considered separately from specific phobias not specific to social anxiety, but related more to the
in DSM-5. There are several reasons for this. Firstly, it is inheritance of anxiety characteristics generally, may be
a highly prevalent disorder, and compares with general- as high as 30-50 per cent (Kendler, Karkowski & Prescott,
ized anxiety disorder (GAD) as one of the most common 1999; Kendler, Neale, Kessler, et al., 1992).
of the anxiety disorders. Secondly, as we will see below,
theories of social anxiety disorder suggest that factors Familial and developmental factors
specific to social anxiety are important in the aetiology of Family studies have indicated that offspring with social
social anxiety disorder. In particular, social phobics pos- anxiety disorder are also more likely to have parents
sess a range of information processing and interpretation (and particularly mothers) with social anxiety disorder
biases that cause them to make excessively negative pre- (Merikangas, Lieb, Wittchen & Avenevoli, 2003; Lieb,
dictions about future social events, and we discuss these Wittchen, Hofler, Fuetsch et al., 2000), and offspring of
various types of bias in the following sections after we parents with an anxiety disorder are marginally more
have first discussed genetic and developmental factors. likely to have social anxiety disorder than offspring of par-
ents with depression (Hirshfeld-Becker, Micco, Simoes &
Genetic factors Henin, 2008), suggesting there is a specific familial link
There is evidence accruing that there is an underlying between anxiety generally and an offspring developing
genetic component to social anxiety disorder, although social anxiety disorder. Because social anxiety appears at
&
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS 159.

SOCIAL ANXIETY DISORDER
‘Fear and anxiety have plagued me for as long as | can day, and I'd walk ,
For a video on social anxiety
remember. If you don’t suffer from SAD you can’t begin to home on my own :
disorder go to
imagine whatit’s like to wake up every day feeling an intense instead: it was a | www.wiley-psychopathology.com/
dread ofjust getting out of bed and going to school or get- 4 mile walk and | video/ché
ting on a bus full of people. It’s as if I'm living in a nightmare took me almost 2
where everyday things become terrifying and confusing. hours.
‘My SAD started when | was about 10 and | had to per- ‘Eventually | dropped out of school altogether and |
form in our school play. The teacher wanted everybody to spend most days now at home by myselforout walking on
join in and, because she knew | was shy, | was given a minor my own. I'm too scared to get a job or to try and go to col-
role along with some other kids. |woke up every morning in lege, as |know my SAD will make it so hard, and |don’t want
tears, terrified of going to school and dreading the moment to fail again. Since being diagnosed with SAD | have started
when | would have to line up in front of everyone. The idea to understand my behaviour and my fears more and I’m
that all the children and teachers would be looking at me hoping to begin a distance learning course next year:
made me so scared | would shake all over and my hands
trembled so much | couldn't even get into my costume. Clinical Commentary
When | was in the rehearsals | would turn bright red and I'd
This client’s perspective highlights the extreme fear
stutter so much | couldn't speak. | could feel everyone look- experienced by many social phobics in a range of
ing at me and | was so self-conscious | would try and hide social and performance situations, and the impact
behind the other kids, thinking if nobody could see me | it can have on social functioning specifically and life
would be safe. When it came to the day of the performance planning more generally. This description highlights
| hid in the toilets and cried the whole way through. a number of important features of social anxiety dis-
‘When | moved into secondary school my SAD got so order, including (1) the biased interpretations that
bad. | couldn't talk aloud in class and when the teachers social phobics have of the reactions of others to them
asked me questions | would stammer and blush. | knew (e.g. ‘| knew everybody noticed how embarrassed
everybody noticed how embarrassed | was and | felt that | was and | felt that they were laughing at how red
my face would go’), (2) the belief that there are obvi-
they were laughing at how red my face would go. |became
ous physical signs of their nervousness which observ-
really self-conscious about my blushing and | couldn't
ers interpret judgmentally (e.g. ‘| was convinced that
stop thinking about how much | would sweat when | was people could smell how sweaty | was and that they
scared in class. | was convinced that people could smell thought |was disgusting’), and (3) the tendency of social
how sweaty | was and that they thought | was disgust- phobics to focus their attention on themselves and
ing. | became obsessed with putting on deodorant, I'd go their own reactions to the possible detriment of their
into the toilets at least five times each day to put more own performance (e.g. ‘Eventually | dropped out of
on. At lunchtime | would hide in an empty classroom and school altogether and | spend most days now at home
eat on my own. Thinking about getting on the school bus by myself’).
scared me so much | had panic attacks at the end of each
a relatively early age compared with other anxiety disor- disorder — so childhood behavioural inhibition is not a
ders, it has been argued that various developmental fac- sufficient condition for social anxiety disorder (Schwartz,
tors and early experiences may precipitate the disorder Snidman & Kagan, 1999) (see Focus Point 6.2). Early
(Neal & Edelmann, 2003). For example, there is consid- parent-child interaction styles may also play a role in
erable evidence that children who exhibit a behaviour- the development of social anxiety. Studies of parent—
ally inhibited (BI) temperament style are at increased risk child interactions suggest that the parents of children
for subsequent social anxiety disorder (Neal, Edelmann with social anxiety disorder exert greater control over
& Glachan, 2002; Kagan, Reznick, Clark, et al., 1984). their children, show less warmth, are less sociable than
However, it is also the case that a significant propor- the parents of individuals without social anxiety disor-
tion of children who are highly behaviourally inhibited der, and also use shame as a method of discipline (Rapee
in early life do not subsequently develop social anxiety & Melville, 1997; Siqueland, Kendall & Steinberg, 1996;
160 PSYCHOPATHOLOGY
Be BEHAVIOURAL INHIBITION (BI) AND SOCIAL ANXIETY DISORDER

oO
- unfamiliar or novel situations. They are also reluctant to
Many children seem quiet, isolated and anxious when
& confronted either with social situations or with nov- approach novel objects, peers, and adults. Preschoolers
oO with BI seem quiet and are reticent to speak or play
a elty, and this characteristic has come to be defined by
W the construct called behavioural inhibition (BI) (Kagan spontaneously, and by age 7 the reluctance to socialize
=) Reznick, Clark, Snidman et al., 1984). Bl represents ‘a is found mainly in group contexts. Blis estimated to have
U
eo) consistent tendency to display extreme fearfulness, quite a high level of inheritability - between 50 and
hu withdrawal, reticence, and restraint in the face of nov- 70 per cent (Smoller & Tsuang, 1998) — and BI is con-
elty’ (Hirschfeld-Becker, 2010), and toddlers exhibiting sidered to be a specific risk factor for social anxiety
BI will show overt distress and cling to their mothers in disorder (Hirschfeld-Becker, 2010).
fhe
Pac aLSte!
Bruch & Heimberg, 1994). While these factors seem to

be important predictors of subsequent social anxiety dis-
order, it is impossible to determine at present whether Negative Observers
™ Neutral Observers
they represent actual causal factors.
~ Positive Observers
Cognitive factors
There appear to be a number of cognitive processes that
are characteristic of social anxiety disorder and which
may all act in some way to maintain fear of social situa-
tions (Stravynski, Bond & Amado, 2004). Firstly, individ-
uals diagnosed with social anxiety disorder possess an
information processing and interpretation bias in which
they make excessively negative predictions about future
social events (Heinrichs & Hofmann, 2001; Hirsch &
Clark, 2004). For example, individuals with social anxiety
disorder rate the probability of negative social events
occurring as higher than either non-clinical controls or Audience’s
Speech
of
Participants’
Rating
Enjoyment
individuals with other anxiety disorders (Foa, Franklin,
Perry & Herbert, 1996; Gilboa-Schechtman, Franklin & Low Social Anxiety High Social Anxiety
Foa, 2000), and this negative evaluation is likely to main-
FIGURE 6.4 High and low socially anxious participants were
tain their avoidance of social situations. Secondly, indi-
asked to give a speech to a group of observers. After giving the
viduals with social anxiety disorder interpret their
speech, the high socially anxious participants rated the observers’
performance in social situations significantly more criti-
enjoyment of their speech significantly lower than low socially
cally than non-sufferers and independent assessors who
anxious participants. The high socially anxious participants even
have observed their behaviour (Stopa & Clark, 1993;
do this when the observers have been instructed to provide posi-
Rapee & Lim, 1992) and also underestimate their own tive feedback, suggesting that socially phobic individuals do not
social skills (Dodd, Hudson, Lyneham, Wuthrich et al., attend to positive feedback cues given by an audience.
2011). Social phobics also find it very difficult to process Source: After Perowne S. & Mansell W. (2002). Social anxiety,
positive social feedback (see Figure 6.4) (Alden, Mellings self-focused attention and the discrimination of negative, neutral
& Laposa, 2004). This focus on negative aspects of the and positive audience members by their non-verbal behaviours.
social situation, and the relative inability to take anything Behavioural and cognitive psychotherapy, 30, 11-23.
‘good’ from a social performance are likely to maintain

the social phobic’s dysfunctional beliefs that social situa-
tions are threatening and that their own performance is known as self-focused attention (Spurr & Stopa, 2002;
likely to be flawed. Thirdly, some theories of social anxi- Bogels & Mansell, 2004), self-focused attention A theory of socia
ety disorder argue that sufferers show a strong tendency and has the effect of lead- anxiety disorder arguing that sufferers
to shift their attention inwards onto themselves and their ing socially anxious indi- show a strong tendency to shift their
own anxiety responses during social performance — espe- viduals to believe they may attention inwards onto themselves and
their own anxiety responses during social
cially when they fear they will be negatively evaluated look as anxious as they performance - especially when they fear
(Clark & Wells, 1995; Rapee & Heimberg, 1997) This is feel inside. This prevents they will be negatively evaluated. *
wh
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS 6
objective processing of the social situation, leads them to 6.2.2 The Treatment of Social
engage in critical self-evaluation, and may well adversely
affect their actual performance in the social situation Anxiety Disorder
(e.g. see Kley, Tuschen-Caffier & Heinrichs, 2011). Both pharmacological treatments and cognitive behav-
Studies have shown that social phobics do indeed display iour therapy (CBT) have been shown to be effective
higher levels of self-reported self-focused attention than in alleviating the symptoms of social anxiety disorder
nonclinical populations (Bogels & Lamers, 2002), and (Rodebaugh, Holaway & Heimberg, 2004; Davidson,
that they recall social memories more often from an 2003), and both are used widely to treat the disorder.
observer perspective than a personal perspective (sug- Successful CBT treatments include elements of the
gesting that they do indeed ‘observe’ themselves while following:
performing socially) (Wells, Clark & Ahmad, 1998). Self-
focused attention therefore appears to have the effect of e Exposure therapy (where the client remains in a
reinforcing the individual’s perception of their own anxi- feared social situation despite distress) — either in
ety in the social situation, can distract the individual vivo, or through the therapist taking on the role
from focusing on the social task at hand and lead to of a stranger in a social situation (Heimberg &
unskilled performance, and result in avoidance of future Becker, 2002).
social situations (Alden, Teschuk & Tee, 1992). Finally, ¢ Social skills training (consisting of modelling, behav-
individuals with social anxiety disorder also indulge in ioural rehearsal, corrective feedback and positive
excessive post-event processing of social events that reinforcement) — this training addresses the social
includes critical self-appraisal of performance and assess- skills deficits usually characteristic of social phobics.
ment of symptom severity. Such post-event rumination e Cognitive restructuring (designed to challenge and
has the effect of maintaining negative appraisals of per- replace the negative biases in information process-
formance over time and maintaining social anxiety ing and the dysfunctional negative self-evaluations
(Abbott & Rapee, 2004; Rachman, Gruter-Andrew & of social performance, and to reduce self-focused
Shafran, 2000). attention) (Rodebaugh & Chambless, 2004).

COGNITIVE THERAPY FOR SOCIAL ANXIETY DISORDER
The following provides a step-by-step account of the own responses and identify key safety behav-
cognitive therapy for social anxiety disorder devised by iours. The client will then attempt to drop
Clark & Wells (1995). The aims of this procedure are (1) these safety behaviours during subsequent
to decrease self-focused attention, (2) to reduce the level role-playing.
of negative interpretations of internal information (e.g. STEP 3 Clients are trained to shift their attention
sweating as a sign of poor performance), (3) eliminate the externally and away from their own internal
use of safety behaviours, which maintain negative beliefs responses and cognitions.
(e.g. if the phobic believes they are trembling and this STEP 4 Video feedback of performance can be used
may be visible, they may grip objects tightly in order to to modify distorted self-imagery.
conceal it, and this response merely maintains the pho- STEP 5 The client is provided with some behavioural
bic’s belief that they are anxious and trembling), and (4) experiments in which they specify their fears
reduce negative post-event processing (see section 6.2). of particular social situations and then test out
whether they occurred during role-play sessions.
STEP 1 The initial phase is designed to inform the cli- STEP 6 Problematic post-event processing is identi-
ent about those factors that are maintaining fied and modified using focused cognitive
their social phobia (see above), and that these restructuring techniques.
are the factors that the therapy is specifically
designed to target. Source: Stangier, U., Heidenreich, T., Peitz, M., Lauterbach, W. &
STEP 2 The second phase attempts to manipulate Clark, D.M. (2003). Cognitive therapy for social phobia: Individual
safety behaviours. Here the client has to role- versus group treatment. Behaviour Research and Therapy, 41(9),
play a social situation and observe his or her 991-1007. Reproduced with permission.
Each of these elements used alone do show therapeu- Schneier, Schmidt, Blanco-Jerez et al., 2003; Van der birdene
tic gains, but an integrated CBT programme appears to Stein & van Balkom, 2000), as have benzodiazepines and
result in maintenance of gains over 6-12 month follow- beta-adrenergic blockers (Schneier, 2011). Comparative
up periods (Feske & Chambless, 1995). Recent reviews outcome studies have suggested that both pharmaco-
of treatments for social anxiety disorder in youth suggest logical and CBT treatments are more effective than non-
that CBT might be more efficacious if integrated with treatment controls (Gould, Buckminster, Pollock, Otto &
specific social skills training (Scharfstein & Beidel, 2011). Yap, 1997), but that the two types of therapy may offer
Drugs such as monoamine-oxidase inhibitors (MAOIs), complementary benefits — drug therapy offering a more
and more recently selective serotonin reuptake inhibi- immediate benefit than CBT, but CBT helping patients
tors (SSRIs) (see section 4.1.1), have been shown to cause to maintain their therapeutic gains over time (Liebowitz,
improvement in measures of social anxiety (Blanco, Heimberg, Schneier, Hope etal., 1999).
SELF-TEST QUESTIONS
e What are the main diagnostic criteria for social anxiety disorder and how does this disorder manifest itself?
® Can you describe the various cognitive factors that appear to play an important role in maintaining social anxiety disorder?
e How do cognitive behaviour therapies and drug treatments complement each other in the treatment of social anxiety
disorder?
SECTION SUMMARY
6.2 SOCIAL ANXIETY DISORDER
¢ Social anxiety disorder is distinguished by a severe and persistent fear of social or performance situations. ao
7. :
® Social anxiety disorder has a lifetime prevalence rate of between 4 and 13 per cent in Western societies.a“— baad
a
:
© There is evidence for a genetic component to social anxiety disorder, but this may bea predisposition to develop anxiety
disorders generally rather than social anxiety disorder specifically. ty
¢ There are a number of cognitive factors that are characteristic of social anxiety disorder, and these include a tendency (1)
to make excessively negative predictions about future social events, (2) to over-critically evaluate their own social perfor-
mance, (3) to shift their attention inwards on to themselves, and (4) to indulge in post-event critical appraisal of their own
performance.
¢ Both monoamine-oxidase inhibitors and selective serotonin reuptake inhibitors fave been shown to be eee ft phar-
macological treatments for social anxiety disorder, as well as cognitive behaviour therapy.
Fane n ene e etme eens ee eH see EEE ES ERG E Eee este aE eE EEE SEES EESSEESSEESEESSEOSEOEEEEEEEDEEDEEEESEEESEE SEEDED EEE OEER HEED Cane een meee nanan nearest ees enseeEee EEE ee ee seeEeeEEeEeaestbeseees Cee mice?
ee eee eee ees
6.3 PANIC DISORDER fearing the consequences of having a panic attack in

public. However, there is still a substantial number of
AND AGORAPHOBIA people who suffer agoraphobia symptoms without panic
attacks, and who appear to fear what might happen if
other anxiety symptoms develop.
Panic disorder and agoraphobia are related — but separable —
anxiety-based problems. Panic disorder is the more
prevalent of the two, but around one-third of those suf- Panic disorder
fering panic disorder also suffer agoraphobia. In those As the name suggests, panic disorder is characterized by
with agoraphobic symptoms, around half will experi- repeated panic or anxiety attacks. These attacks are asso-
ence regular panic attacks but the remainder will not ciated with a variety of
(Andrews, Charney, Sirovatka et al., 2009). Furthermore, physical symptoms, includ- panic disorder An anxiety disorder cha a
terized by
repeated panic or anxiety attack:
for a majority of those people who develop agorapho- ing heart palpitations,
bic symptoms, these symptoms will begin within a year perspiring, dizziness, hyp- panic A sudden uncontrollable fear or
of an initial panic attack, and are usually the result of erventilating, nausea and anxiety. 7
PANIC DISORDER
Marilyn is a 33-year-old single woman who works at a local telephone company and lives alone in her apartment.
She has panic disorder with agoraphobia and her first panic attack occurred 3 years ago when driving over a
bridge on a very rainy day. She experienced dizziness, pounding heart, trembling and difficulty breathing. She
was terrified her symptoms meant she was about to pass out and lose control of her car. Since that time she has
experienced eight unexpected panic attacks during which she feared she was about to pass out and lose control
of herself. She frequently experiences limited symptom attacks (e.g., feels dizzy and fears she may pass out). As
HISTORY
CASE a result
6.1 of her intense fear of having another panic attack she is avoiding the following situations: waiting in
line, drinking alcohol, elevators, movie theatres, driving over bridges, driving on the freeway, flying by plane,
and heights (e.g., will not go out on her tenth-floor balcony). She is often late for work because of taking a route
that doesn’t require her to take the freeway. She is also finding herself avoiding more and more activities. She
frequently feels tearful and on guard. Sometimes she gets very angry at herself as she does not understand why
she has become so fearful and avoidant.
Sharon is a 38-year-old single mother of two teenage daughters who works as a fitness instructor at a local
gym. She experienced her first panic attack during her teens when watching a horror movie with friends at a
local movie theatre. Since that time she has experienced one to two full panic attacks per year that come out of
the blue in a variety of situations (e.g., while waiting in line at the bank, at a shopping mall, walking alone at the
park). The panic attacks reoccurred out of the blue when she was 29 while eating a hot and spicy meal at a local
restaurant. Her panic attacks always include dizziness, feeling of choking, dry mouth, unreality, feeling detached
from her body, and feeling as if she may lose bowel control. Her main fear is that she is dying due to a stroke
although medical problems have been ruled out. Sharon does not avoid anything to prevent the panic attacks
and there has not been a huge negative impact of the panic attacks upon her work, family or social functioning.
Source: http://www.anxietybc.com/disorders/PANIC.html.
Clinical Commentary
Both Marilyn and Sharon exhibit a number of physical symptoms typical of panic attacks, although these
examples show that not everyone experiences similar symptoms. Panic attacks often come ‘out of the blue’
and are unpredictable, and this adds to their frightening nature. In both examples, the individual believes
that the symptoms are signs of impending physical illness or loss of control (catastrophic misinterpretation).
The pervasive fear of further attacks means that Marilyn has developed avoidance responses in an attempt
to minimize future attacks. These avoidance responses interfere with her normal daily life (causing further
stress), and inadvertently help to maintain dysfunctional catastrophic beliefs.
trembling. In addition, the individual may experience individual must experience recurrent panic attacks, and
real feelings of terror or severe apprehension, and in addition they must develop a persistent concern that
depersonalization (a feeling of not being connected to your future panic attacks will occur (see DSM-5 Summary
own body or in real contact with what is happening Table 6.4). The frequency of panic attacks in panic disorder
around you). Most people will experience at least one
DSM-5 SUMMARY TABLE 6.3 Criteria forapanic attack
panic attack in their lifetime, but panic disorder is diag-
nosed when recurrent, unexpected panic attacks keep —_A sudden feeling of extreme fear or distress, which can originate
occurring, and are followed by at least 1 month of per- _ from eitheracalm oran anxious state. Symptoms intensifyina
sistent concerns about having a further attack. For some short space of time and will include a range of sensations such as:
individuals panic attacks are unpredictable, but for oth- —« “fuctuations in heart rate
ers they may become associated (perhaps through clas- e shortness of breath or chest pain
sical conditioning; see section 1.3.2) to specific situations
or events (e.g. riding on public transport). ® nausea
DSM-5 defines a panic attack as an abrupt surge of —¢ dizziness

intense fear or discomfort in which four or more of alist =, shaking
of symptoms develops suddenly (see DSM-5 Summary
The person may fear they are dying or ‘going crazy’
Table 6.3). The criteria for panic disorder state that the
6A: PSYCHOPATHOLOGY
DSM-5 SUMMARY TABLE 6.4 Criteria for diagnosis of panic disorder DSM-5 SUMMARY TABLE 6.5 Criteria for diagnosis of
agoraphobia
Repeated panic attacks followed by at least 1 month of:
° Distinct fear of situations where the individual is outside,
e worrying about further panic attacks and/or the conse- in a crowd or an open space, or in public spaces such as
quences of a panic attack, such as loss of control shops, cinemas or buses
® significant, non-beneficial modification of behaviour(s), e Situations are avoided, or are experienced with intense
designed to avoid future attacks, such as avoidance of fear that help will be unavailable, or that panic or other
triggering situations resultant symptoms will occur
e The individual experiences fear in at least two different
situation types and symptoms of anxiety or avoidance will
can vary considerably between individuals, from one last for 6 months or more
attack per week to frequent daily attacks. Panic disorder e Fear causes difficulty in performing social or occupational
is associated with a number of fears and apprehensions activities and cannot be explained by the effects of other
that the sufferer develops. These include fears that the mental or medical disorders
attacks indicate an underlying serious medical condi-
tion (e.g. cardiac disease, seizure disorder) — even though
repeated medical tests indicate no life-threatening illness.
Others feel they are losing control or simply ‘going crazy’. Prevalence
Sufferers often make significant changes to their behaviour The 12-month prevalence rate for panic disorder is
and their lifestyles as a result of the disorder. For example, around 1.5—3 per cent and between 0.4 per cent and 3
they may ensure that there is always a ‘safe’ place available per cent for agoraphobia (e.g. see Goodwin, Faravelli,
in case they have an attack, and this may cause them to Rosi, Cosci et al., 2005) and both are experienced more
avoid social situations and even quit their jobs. Concerns by women than men (Kessler et al., 1994). Onset is com-
about future attacks often result in the development of mon in adolescence or early adulthood, and can often be
avoidant behaviour; sufferers may find it difficult to leave associated with a period of stress in the individual’s life
the ‘safety’ of their own homes, in which case panic disor- (Pollard, Pollard & Corn, 1989). There is some evidence
der with agoraphobia is a common diagnosis. for culturally determined variance in both the preva-
lence of panic disorder and in the way that panic disorder
Agoraphobia may manifest itself. For example, in some Asian societies,
Agoraphobia is a fear or anxiety of any place where the prevalence is particularly low — possibly because of the
sufferer does not feel safe or feels trapped, and is accom- stigma related to admitting and reporting psychological
panied by a strong urge disorders (e.g. in Taiwan: see Weissman, Bland, Canino,
agoraphobia Afear or anxiety of any place to escape to a safe place Faravelli, Grenwald et al., 1997). However, in other cul-
where the sufferer does not feel safe or feels
trapped, and is accompanied by a strong (e.g. home). Very often, tures, panic disorder may be expressed in the form of
urge to escape to a safe place (e.g. home). this urge to escape or avoid quite different symptoms. For example, Ataque de Nervios
‘unsafe’ places is associated is an anxiety-based disorder found almost exclusively in
with the fear of having a panic attack, and the embarrass- Latinos in the Caribbean. This appears to be a form of
ment that might cause. Agoraphobia is typically associ- panic disorder brought on by stressful life events (such
ated with fear of specific types of places or situations, as economic or marital difficulties), but whose expres-
including public transport, open spaces such as car parks sion is determined by the social and cultural norms
and bridges, or being in shops, supermarkets, theatres or within that cultural group (see Focus Point 1.3). In
cinemas, standing in a queue or being in a crowd, or sim- particular, Latino cultures place less emphasis on self-
ply being alone away from home. As a result of these control and emotional restraint than Western cultures,
fears, many individuals with a diagnosis of agoraphobia and so the distress of panic disorder in Latinos tends
(DSM-5 Summary Table 6.5) rarely venture far from to be externalized in the form of screaming, uncon-
home, and when they do, they may do so only with a trolled behaviour and aggression (Salman, Liebowitz,
trusted friend or relative. Thus, agoraphobia can be a Guarnaccia, Jusino et al., 1998). In contrast, in Western
severely disabling condition that often confines sufferers cultures the distress of panic disorder is usually coped
to their homes for many years, rendering them unable to with by adopting avoidance and withdrawal strategies —
work or to socialize. Sufferers also come to rely heavily hence the common diagnosis of panic disorder with
on friends and relatives to help them with even basic agoraphobia.
activities like shopping or trips to the doctor. This will It is important to remember that panic attacks may be
often put a severe strain on those family members who a feature of the symptoms in a number of the anxiety dis-
care for individuals suffering from agoraphobia. orders (e.g. specific phobias and social phobia). However, «
is
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS — 165—
panic disorder itself is characterized by frequent uncon- lack of oxygen in the cells, and in turn can produce the
trollable panic attacks, and an important aspect of this symptoms of panic attacks that are recognized as anxi-
anxiety-based problem is the individual's intense fear of ety (Zvolensky & Hifert, 2001). This type of explana-
experiencing panic attacks. As we shall see, it is this lat- tion has been partially supported by evidence from
ter feature of panic disorder that plays a central role in what are called biological challenge tests, where panic
theories of the disorder. attacks have been induced by administering carbon
dioxide (CO,) enriched air or by encouraging hyper-
ventilation (Ley & Walker, biological challenge tests Research in
6.3.1 The Aetiology of Panic Disorder 1973). Similarly, sensitiv-
which panic attacks are induced by admin-
ity to increases in CO, istering carbon dioxide (CO,) enriched air
and Agoraphobia havcwincdem suggested as aie by encouraging hyperventilation.
Agoraphobia has only just been recognized as a spe- risk factor for panic disorder (Papp, Klein & Gorman,
cific and distinct disorder in DSM-5, so its aetiology has 1993), and have given rise to what are known as suffo-
rarely received the kind of attention that has been given cation alarm theories of panic disorder, where a com-
to panic disorder. In addition, because agoraphobia is bination of increased CO, intake may activate an
often preceded by panic attacks and full-blown panic dis- oversensitive suffocation
suffocation alarm theories Models of
order, much of the research on the aetiology of these alarm system and give panic disorder in which a combination
two anxiety problems has been focused on panic disor- rise to the intense terror of increased CO, intake may activate an
der. However, agoraphobia can occur independently of and anxiety experienced oversensitive suffocation alarm system and
panic attacks and panic disorder so its origins cannot during a panic attack give rise to the intense terror and anxiety
experienced during a panic attack.
always be traced to panic, and this has given rise to a (Klein, 1993). In support
view that agoraphobia might be a disorder with multiple of this account, panic disorder patients do report sig-
causes, some of which might be genetic in nature — in nificantly more symptoms of shortness of breath when
terms of a genetic vulnerability to anxiety (Wittchen, anxious, and more frequent frightening suffocation
Gloster, Beesdo-Baum, Fava et al., 2010) — and others experiences than other anxiety patients. However,
which are more cognitive — in which agoraphobic avoid- when panic disorder patients are asked to participate in
ance is acquired through the development of negative periods of breath-holding, they do not report any
thoughts about the consequences of experiencing anxi- greater levels of anxiety than non-anxious controls,
ety in public (Goldstein & Chambless, 1978). Because of suggesting that they do not necessarily possess a more
this dearth of research on the causes of agoraphobia, the sensitive suffocation alarm system (Roth, Wilhelm &
remainder of this section focuses on the causes of panic Trabert, 1998). One further intriguing feature of the
disorder. hyperventilation account is that, while biological chal-
lenge tests produce physiological changes that often
The aetiology of panic disorder provoke full-blown panic attacks, they only tend to do
Because of the intense nature of the physical symptoms so in individuals with a history of panic attacks or
of panic disorder, many researchers have looked towards panic disorder (Margraf, Ehlers & Roth, 1986). This is
biological causes. However, it has become clear that the case even though the physiological changes caused
there are also important psychological and cognitive fac- by biological challenge tests are the same in people
tors that contribute to the aetiology and maintenance of diagnosed with panic disorder and those that have no
panic disorder. anxiety disorder (Gorman, Kent, Martinez et al., 2001).
This evidence quite strongly suggests that an impor-
Biological theories of panic disorder tant causal factor in panic disorder is the way that the
The role of hyperventilation Hyperventilation is a individual interprets the physiological changes caused
common feature of panic attacks, and Ley (1987) has by the biological challenge, and this gives rise to the
suggested that dysfunctional breathing patterns may psychological accounts of panic disorder that have
trigger a series of autonomic reactions that precipitate been developed over the past 25 years.
a full-blown panic attack. Hyperventilation is defined
as ‘alveolar ventilation that exceeds metabolic demand’ Noradrenergic overactivity A further account of
and has an end result of raising blood pH level. Oxygen panic disorder that alludes to biological differences
is then delivered less effi- between those that suffer panic disorder and those that do
erventilation A rapid form of breath- not is that the disorder may be caused by overactivity in
ciently to body cells, and
that results in ventilation exceeding
abolic demand and has an end result this can lead to cardiovas- the noradrenergic neurotransmitter system (Redmond,
ising blood pH level. A common fea- cular changes that try to 1977). There is certainly evidence that the noradrenaline
of panic attacks. help compensate for the network may mediate the effects of biological challenges
166 PSYCHOPATHOLOGY
%
in producing panic attacks (Bailey, Argyropoulos, this subsequently leads to a full-blown panic attack.
Lightman & Nutt, 2003), and that norepinephrine is Individuals who do not suffer panic disorder report a
implicated in the symptomatology of panic disorder number of interoceptive and affective responses in bio-
(Sand, Mori, Godau, Stober et al., 2002). One particular logical challenge tests, but they are only rarely made anx-
view related to putative overactivity in the noradrener- ious by these symptoms and hardly ever panic (Bass &
gic system is that patients with panic disorder are defi- Gardner, 1985; Starkman, Zelnik, Nesse & Cameron,
cient in the gamma-aminobutryic (GABA) neurons that 1985). So, what determines whether someone will panic
inhibit noradrenergic activity, and PET scan studies have in response to unusual bodily sensations? Reiss & McNally
tended to support this view (Malizia, Cunningham, Bell, (1985) proposed that some individuals have pre-existing
Liddle et al., 1998). Nevertheless, it is still unclear whether beliefs that bodily sensations may predict harmful conse-
the role of the noradrenergic system is to mediate the quences. They developed the construct of anxiety sensi-
symptoms of panic attacks when they occur, or whether tivity, which refers to fears of anxiety symptoms that are
noradrenergic overactivity represents a vulnerability fac- based on beliefs that such anxiety sensitivity Fears of anxiety symp
tor in the aetiology of panic disorder. symptoms have harmful toms based on beliefs that such symptom:
consequences (e.g. that a have harmful consequences (e.g. that a .
Psychological theories of panic disorder rapid heart beat predicts an rapid heartbeat predicts an impending q
heart attack).
Classical conditioning Goldstein & Chambless impending heart attack). In
(1978) were the first to suggest that an important fea- order to measure this construct, Reiss, Peterson, Gursky
ture of panic disorder was the sufferer’s ‘fear of fear’. & McNally (1986) developed the Anxiety Sensitivity
That is, when they detected what they thought were Index (ASI) (e.g. Table 6.4) (see also the Revised Anxiety
any internal signs of a panic attack (e.g. mild dizziness), Sensitivity Index, ASI-R, Anxiety Sensitivity Index A measure,
they would immediately become fearful of the possible Taylor & Cox, 1998), and developed by Reiss, Peterson, Gursky &
consequences. This would then precipitate a full-blown this contains items such as McNally (1986), to measure anxiety
attack. Goldstein & Chambless (1978) interpreted this as ‘Unusual body sensations sensitivity. g
a form of interoceptive classical conditioning, in which scare me’ and ‘It scares me when | feel faint’. Studies have
the internal cue (such as dizziness) had become estab- shown that individuals with panic disorder score signifi-
lished as an internal conditioned stimulus (CS) predict- cantly higher on the ASI than either non-clinical controls
ing a panic attack (the unconditioned stimulus, UCS). or individuals diagnosed with other anxiety disorders
However, while this account has intuitive appeal, it is not (Taylor & Cox, 1998; Rapee, Ancis & Barlow, 1988).
clear in conditioning terms what is the CS and what is Furthermore, in a prospective study, high ASI scores pre-
the UCS. For example, is a skipped heartbeat a CS that dicted the occurrence of subsequent panic attacks in
precipitates a panic attack, or is it a symptom of the army recruits undergoing a stressful period of training
panic attack itself (the UCS) (McNally, 1990)? Bouton, (Schmidt, Lerew & Jackson, 1997), and this suggests that
Mineka & Barlow (2001) have attempted to address these elevated anxiety sensitivity may be a risk factor for panic
conceptual difficulties by suggesting that anxiety and and perhaps panic disorder (McNally, 2002).
panic are separable aspects of panic disorder. They sug-
gest that anxiety is anticipatory and prepares the system Catastrophic misinterpretation of bodily sensations
for a trauma, whereas panic deals with a trauma that is Based on the fact that panic disorder sufferers are clearly
already in progress. In this conditioning account, anxiety anxious about the possible consequences of bodily symp-
is the learned reaction, called conditioned response (CR) toms, Clark (1986, 1988) developed an influential model
to the detection of cues conditioned stimulus (CS) that of panic disorder in which he hypothesized that panic
might predict a panic attack, and once conditioned anxi- attacks are precipitated by the individual catastrophi-
ety develops it will exacerbate subsequent panic attacks cally misinterpreting their bodily sensations as threaten-
and lead to the development of panic disorder. As pre- ing. Many body sensations are ambiguous: for instance,
dicted by this model, studies confirm that panic attacks the heart skipping a beat could mean either an imminent
are regularly preceded by anxiety in individuals with heart attack (negative interpretation) or that someone
panic disorder (Barlow, 1988; Kenardy & Taylor, 1999). you like has just walked into the room (positive interpre-
tation). However, individuals who tend to develop panic
Anxiety sensitivity What is clear about the phenom- disorder appear to exhibit catastrophic misinterpreta-
enology of panic disorder is that sufferers become tion of bodily sensations;
extremely anxious when they detect any cues (internal or that is, they have a cognitive catastrophic misinterpretation of bodil
sensations A feature of panic disorder
external) that may be indicative of a panic attack. So any bias towards accepting the where there is a cognitive bias towards
theory of panic disorder needs to explain why sufferers more threatening interpre- accepting the more threatening interprete
are made anxious by the detection of these cues, and how tation of their sensations tion of an individual's own sensations.
CHAPTER6 ANXIETY AND STRESSOR-RELATED PROBLEMS
/—— TRIGGER STIMULUS

TABLE 6.4 Example items from the anxiety sensitivity index (ASI-R)
The ASI-R measures anxiety sensitivity, and this is a measure of

an individual's fear of anxiety. Anxiety sensitivity is one of the
_ (INTERNAL OR EXTERNAL)
best predictors of future panic attacks and may be a risk factor
for panic disorder.
|. When | feel like I’m not getting enough air, | get scared
PERCEIVED THREAT
that | might suffocate
2. When my chest feels tight, |get scared | won't be able to

breathe properly
3. It scares me when | feel faint
4, When my throat feels tight, |worry that | could choke to INTERPRETATION OF

ir AS
SENSATIONS APPREHENSION -
death CATASTROPHIC oo
5. It scares me when my heart beats rapidly
6. It scares me when | feel shaky (trembly)
7. When | have trouble swallowing, | worry that | could
choke
8. It scares me when my body feels strange or different in
some way
9. | think it would be horrible for me to faint in public FIGURE 6.5 Clark’s (1986) model of panic disorder.
Perception of a threat triggers apprehension and then bodily sensa-
10 When | tremble in the presence of others | fear what tions associated with that apprehension are interpreted catastrophi-
people might think of me cally. This causes further anxiety which feeds into a vicious cycle that
11. When |feel a strong pain in my stomach, | worry it could triggers a full-blown panic attack.
be cancer Source: Clark, D.M. (1986). A cognitive approach to panic.
Behaviour Research and Therapy, 24 (4), 467-470. Reproduced with
12. When my heart is beating rapidly, |worry that | might be permission.
having a stroke
13. When | feel dizzy, |worry there is something wrong with

my brain Ottaviani & Beck, 1987). In addition, individuals with
panic disorder will experience a panic attack when they
14. When my stomach is upset, | worry that | might be seri-
ously ill
have been told they will receive a CO, challenge, but in
fact are given only compressed air (Sanderson, Rapee &
15. It scares me when | feel tingling or prickling sensations in
Barlow, 1989), suggesting that just the expectancy of an
my hands
attack is enough to trigger one.
16. When | feel ‘spacey’or spaced out | worry that | may be
mentally ill The role of safety behaviours What is intriguing
Source: Taylor, S. & Cox, B.J. (1998). Anxiety sensitivity: Multiple dimen- about panic disorder is that, while some sufferers may
sions and hierarchic structure. Behaviour Research and Therapy, 36(1), have experienced hundreds of panic attacks over a period
37-51. Reproduced with permission. of years, they still misinterpret the physical symptoms in a
catastrophic way — even though nothing catastrophic has
(Clark, Salkovskis, Ost, Breitholz et al., 1997; see Austin & happened to them following a panic attack. So the person
Richards, 2001, for a review). Clark argues that this leads who believes that a slight sensation in the chest signals an
to a vicious cycle where any apprehension is interpreted imminent heart attack still interprets this sensation in this
threateningly and increases the perceived threat, which catastrophic way, even though they have never had a heart
leads to an escalation of anxiety symptoms that then attack following many previously similar panic attacks.
precipitate a panic attack, and this is represented sche- The reason for this is that individuals suffering panic disor-
matically in Figure 6.5. There is a good deal of evidence der tend to develop safety behaviours. Safety behaviours
to support this psychological account. Individuals with are activities that the sufferer will deploy as soon as
panic disorder have been shown to attend to and discrimi- they think they are having a
safety behaviours Activities deployed by
nate their bodily sensations more closely than individu- panic attack, and they dev-
sufferers of panic disorder as soon as they
als without panic disorder (Ehlers & Breuer, 1992), and elop the belief that this acti- think they are having a panic attack, devel-
panic disorder sufferers report that thoughts of imminent vity has saved them from oped in the belief that this activity has
danger typically accompany their attacks (Hibbert, 1984; the catastrophic outcome saved them from a catastrophic outcome.
168 PSYCHOPATHOLOGY
%
they thought would happen (Salkovskis, Clark & Gelder, appears to trigger anxiety, which in turn triggers a panic
1996; Helbig-Lang & Petermann, 2010). Examples of attack. The issues that remain to be resolved in these
safety behaviours include: seeking support by holding on accounts are (1) exactly how the anxiety elicited by cata-
to objects if the believed catastrophic outcome is fainting; strophic misinterpretation of bodily sensations leads to
sitting down if the outcome is a supposed heart attack; or panic, and (2) why some individuals have acquired high
moving slowly and looking for an escape route if the cata- levels of anxiety sensitivity and catastrophic beliefs in the
strophic outcome is losing control or acting foolishly. first place.
Safety behaviours are effectively avoidance responses,
which maintain both the anxiety that gives rise to the
panic attacks and the dysfunctional catastrophic beliefs 6.3.2 The Treatment of Panic Disorder
that make the attacks so distressing. Because of their role
in maintaining panic disorder, safety behaviours are a pri- Because of the distressing physical symptoms experi-
mary target for manipulation and elimination in both enced in panic disorder, psychoactive medication is usu-
behavioural and cognitive therapies for panic disorder ally the first line of treatment provided for sufferers,
(Rachman, Radomsky & Shafran, 2008). and both tricyclic antidepressants and benzodiazepines
may be effective in controlling symptoms (Roy-Byrne &
Summary All of these accounts suggest there is likely Cowley, 1998) (see section 4.1.1).
to be an important psychological component to the However, there is good evidence that structured
development of panic disorder that involves a negatively exposure therapy or cognitive behaviour therapy (CBT)
valenced bias in how the individual interprets and reacts is as effective, if not superior, to drug treatments over the
to their own bodily sensations. This interpretation bias longer term (e.g. Craske, Brown & Barlow, 1991).

COGNITIVE THERAPY FOR PANIC DISORDER
The following transcript gives an example of how a cogni- T: Yes, that’s right: stress can cause some problems in
tive therapist (T) would try to challenge the catastrophic some people. It tends to be people who have some-
beliefs of a panic disorder sufferer (P) who believes that thing wrong with their hearts in the first place. But
signs of an impending panic attack are signals for an stress is not necessarily the same as sudden anxiety
imminent heart attack. or panic. When you panic your body releases adrena-
lin which causes the heart to speed up and your body
P: When I'm panicking, it’s terrible. | can feel my heart to work faster. It's a way of preparing you to deal
pounding; it’s so bad | think it could burst through better with danger. If adrenalin damaged the heart
my chest. or body, how would people have evolved from dan-
T: What thoughts go through your mind when your gerous primitive times? Wouldn't we all have been
heart is pounding like that? wiped out?
P: Well, I’ll tell you what | think: it’s so bad that | think I’m P: Yes, | suppose so.
going to have a heart attack. It can’t be good for your T: So maybe panic itself doesn’t cause heart attacks;
heart to be beating like that. there has to be something physically wrong for that
T: So, are you concerned that anxiety can damage your to happen. When people have had heart attacks they
heart or cause a heart attack? are often given an injection of adrenalin directly into
P: Yes, it must do you some damage. You hear of people the heart in order to help start it again. Do you think
dropping down dead from heart attacks caused by they would do that if it damaged the heart even
stress. more?
T: Do you think more people have stress in their lives P: Nol’m sure they wouldn't.
than die of heart attacks? T: So, how much do you now believe that anxiety and
P: Yes, | suppose so. panic will damage your heart?
= How can that be if stress causes heart attacks? Source: Wells, A. (1997). Cognitive therapy of anxiety disorders: A
P: Well, | suppose it doesn’t always cause problems. practical manual and conceptual guide. Chichester: John Wiley &
Maybe it does only in some people. Sons, pp. 123-124. Reproduced with permission.
In exposure-based treatments, the client is persuaded Telch, Lucas, Schmidt, Hanna, Jaimez & Lucas, 1993;
to experience the conditions that precipitate a panic Luermans, De Cort, Scruers & Griez, 2004). A typical
attack in the controlled environment of the therapy situ- treatment programme would include:
ation (Barlow & Craske, 1994; Craske & Barlow, 2001).
For example, someone whose attacks are preceded by 1. Education about the nature and physiology of
bouts of dizziness may be asked to spin around in a chair, panic attacks,
or if hyperventilation is a trigger, the individual will be 2. Breathing training designed to control
asked to breathe rapidly for a period of time. At the first hyperventilation,
bodily signs of the symptoms associated with panic, the 3. Cognitive restructuring therapy to identify and
client is then asked to apply cognitive and physical tech- challenge faulty threat perceptions,
niques designed to manage the attack (such as applying 4. Interoceptive exposure to reduce fear of harmless
relaxation techniques). This enables the client to manage bodily sensations, and
the attack under relatively ‘safe’ conditions, and to learn 5. Prevention of safety behaviours that may
to exercise control over the cues that would normally maintain attacks and avoid disconfirmation of
predict panic (Craske, Maidenberg & Bystritsky, 1995). maladaptive threat beliefs.
Clearly, an important distinguishing feature of individ-
uals with panic disorder is their fear of bodily sensations, Such programmes have been shown to produce a
their catastrophic misinterpretation of these sensations, durable reduction in symptoms and a significant increase
and the effect these cognitions have in triggering a panic in quality of life for panic disorder sufferers (Barlow,
attack. The development of CBT for panic disorder has Gorman, Shear & Woods, 2000; Telch, Schmidt, Jaimez,
therefore focused specifically on providing clients with Jacquin & Harrington, 1995). More recent studies have
challenges to these beliefs in the form of both correc- also suggested that CBT programmes may be effec-
tive information and experiences designed to eliminate tive specifically because they significantly reduce the
faulty emotional responding (e.g. Clark, Salkovskis, tendency to react fearfully to benign bodily sensations
Hackmann, Middleton, Anastasiades & Gelder, 1994; (Smits, Powers, Cho & Telch, 2004).
SELF-TEST QUESTIONS _
® Can you describe the main symptoms of a panic attack, and the diagnostic criteria for panic disorder?
® What is the relationship between symptoms of panic disorder and agoraphobia?
® How does hyperventilation cause a panic attack?
e What role does the catastrophic misinterpretation of bodily sensations play in the acquisition and maintenance of panic
disorder?
® Can psychological explanations of panic disorder explain more of the facts of panic disorder than biological explanations?
e What is the role of safety behaviours in maintaining panic disorder?
© What are the important features of cognitive behaviour therapy for panic disorder?
SECTION SUMMARY
’
6.3 PANIC DISORDER AND AGORAPHOBIA
© Panic disorder is characterized by repeated panic or anxiety attacks associated with a variety of physical symptoms, includ-
ing heart palpitations, dizziness, perspiring, hyperventilation, nausea, trembling, and depersonalization.
® Agoraphobia is a fear or anxiety of any place where the sufferer does not feel safe or feels trapped, and is accompanied by
a strong urge to escape to a safe place (e.g. home).
e The lifetime prevalence rate for panic disorder is between 1.5 and 3 per cent, although prevalence rates do differ between
different cultures.
PSYCHOPATHOLOGY
Hyperventilation is a common feature of panic disorder, and some theorists have argued that the effect of hyperventilation
on body CO, levels is a causal factor in the development of a panic attack. .
Individuals with panic disorder have high levels of anxiety sensitivity, which is a fear of anxiety symptoms.
Individuals who develop panic disorder tend to catastrophically misinterpret bodily sensations, and interpret them as signs
of an imminent physical threat (e.g. an imminent heart attack signalled by a missed heartbeat). This cognitive bias leads to
a vicious cycle which increases the anxiety symptoms that precipitate a panic attack. :
Safety behaviours are activities that a panic disorder sufferer will deploy during a panic attack and will maintain the belief
that panic attacks might have catastrophic consequences.
Tricyclic antidepressants and benzodiazepines are an effective first-line treatment for panic disorder, but structured expo-
sure therapy or cognitive behaviour therapy (CBT) is as effective, if not superior, to drug treatments over the longer term.
“Cee ceecceecvereseveceeseeeseceseec cece sete ene e ee nee rece eee sees eeu See NOSE OCeE ese cee cee Eeeeceee eee eeeHTeEseeeueETseerEe TONES SEES One eee reseeeeeereeeeueeuereneveresseHesereeserOs HOU SeeeseeHoeereeneererssvoserensseeseeesetee weore®
6.4 GENERALIZED ANXIETY the cardinal diagnostic feature of GAD it may also
be accompanied by physical symptoms such as
DISORDER (GAD) fatigue, trembling, muscle tension, headache,
and nausea.
Generalized anxiety disorder (GAD) is a pervasive

condition in which the sufferer experiences continual Diagnosis and prevalence
apprehension and anxi- The DSM-5 criteria for diagnosis of GAD are shown in
generalized anxiety disorder A perva- DSM-5 Summary Table 6.6 and include:
sive condition in which the sufferer experi- ety about future events,
ences continual apprehension and anxiety and this leads to chronic
about future events, and this leads to and pathological worry- e Excessive anxiety and worry about two or more
chronic and pathological worrying about
ing about those events. domains of activities or events on more days than
those events. not for 3 months or more,
We all worry about
things to some degree — and, indeed, many people ¢ Anxiety and worry are associated with physical
find it beneficial to think about how they might deal symptoms such as restlessness or muscle tension,
with challenging future events. However, worrying e Anxiety and worry are accompanied by one or
for the individual with GAD has a number of features more of: avoidance of events with possible nega-
that make it disabling and a source of extreme emotive outcomes; excessive time and effort spent
tional discomfort. For example, for the individual suf- preparing for events with negative outcomes;
fering GAD: procrastination; or repeated reassurance-seeking
about worries
1. Worrying is a chronic and pathological activity
that is not only directed at major life issues (e.g. e Finally, a consequence of these symptoms will
health, finances, relationships, work-related be clinically significant distress or impairment in
matters), but also to many minor day-to-day social, occupational, or other important areas of
issues and hassles that others would not perceive functioning.
as threatening (Craske, Rapee, Jackel & Barlow,
GAD is twice as common in women as in men, and
1989; Tallis, Davey & Capuzzo, 1994);
can often persist from adolescence to old age (Barlow,
2. Worrying is perceived as uncontrollable — the Blanchard, Vermilyea, Vermilyea & DiNardo, 1986).
individual with GAD feels they cannot control either Over 5 per cent of the population will be diagnosed with
the onset or termination of a bout of worrying;
GAD at some point in their lifetime (Wittchen & Hoyer,
3. Worrying is closely associated with the 2001), and over 12 per cent of those who attend anxi-
catastrophising of worries — that is, worry bouts ety disorder clinics will present with symptoms typical
persist for longer in GAD, they are associated of GAD (Kessler, Keller & Wittchen, 2001). Comorbidity
catastrophising An example of magni- with increasing levels of is also highly prevalent in sufferers of GAD, with rates
fication in which the individual takes a anxiety and distress as the ranging from 45 per cent to 98 per cent (Goisman,
single fact to its extreme, one example bout continues, and Goldenberg, Vasile & Keller, 1995), and individuals diag-
being catastrophic worrying.
worrying seems to make nosed with GAD are also likely to suffer other mental
the problem worse rather than better (see Table health problems, such as depression and eating disorders:
6.5). While pathological and chronic worrying is (Brown, O'Leary & Barlow, 2001). In addition, GAD is
th
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS rae
TABLE 6.5 Catastrophising in worriers and non-worriers TABLE 6.5 (Cont‘d)

These catastrophising sequences generated by a chronic worrier (top) Discomfort Likelihood
and a non-worrier (bottom) were generated using the catastrophic
interview procedure in which the individual is first asked ‘What is your Non-worrier topic: Getting good
main worry at the moment?’In this case both participants replied, grades in school
‘Getting good grades in school! The interviewer then passes this Catastrophising step
response back to the participant by saying ‘What is it that worries
you about getting good grades in school?! Each time the participant I'd end up in a bad job 2 80
responds, the interviewer passes that response back by asking what it I'd get a low salary 2 100
is about the response that worries them. The interview continues until
I'd have less money to spend on what 2 100
the participant can no longer think of any reasons.
| want
By looking at the catastrophising sequences above, we can deduce I'd be unhappy 2 35
a number ofthings about chronic worriers: (1) they produce
significantly more catastrophising steps than non-worriers, (2) they It would be a strain on me 2 10
experience increasing emotional distress as catastrophising contin- I'd worry more 2 5
ues, as evidenced by their ‘discomfort’ scores, and (3) the content
Source: Vasey, M.D. & Borkovec, T.D. (1992). A catastrophizing assessment
of their catastrophising steps becomes more and more threatening
of worrisome thoughts. Cognitive Therapy and Research, 16(5), 505-520.
and catastrophic, as evidenced by their increasing ‘likelihood’ scores
as catastrophising progresses.
Discomfort Likelihood DSM-5 SUMMARY TABLE 6.6 Criteria for diagnosing

Chronic worrier topic: Getting good generalized anxiety disorder
grades in school
e Disproportionate fear or anxiety relating to areas of activ-
Catastrophising step
ity such as finances, health, family, or work/school life
| won't live up to my expectations 50 30
e The individual experiences fear relating to at least two :
I'd be disappointed in myself 60 100 different areas of activity and symptoms of intense anxiety
I'd lose my self-confidence 70 50 or worry will last for 3 months or more, and will be present
for the majority of the time during this period
My loss of self-confidence would 70 50
spread to other areas of my life e Feelings of anxiety or worry will be accompanied by symp-
| wouldn't have as much control as I'd like 75 80 toms of restlessness, agitation or muscle tension
I'd be afraid of facing the unknown WS 100 e Anxiety or worry are also associated with behaviours such
I'd become very anxious 75 100 as frequently seeking reassurance, avoidance of areas of
activity that cause anxiety, or excessive procrastination or
Anxiety would lead to further loss of 75 80
effort in preparing for activities
self-confidence
| wouldn't get my confidence back 75 50 e Symptoms cannot be explained by other mental disorders
such as panic disorder
I'd feel like |wouldn't have any control US 80
over my life
I'd be susceptible to things that nor- 75 80 associated with significant impairments in psychosocial
mally wouldn't bother me
functioning, role functioning, work productivity and
I'd become more and more anxious 80 80
health-related quality of life (Revicki, Travers, Wyrwich,
I'd have no control at all and I'd become 85 30 Svedsater et al., 2012)
mentally ill
I'd become dependent on drugs and 50 30
therapy
I'd always remain dependent on drugs 85 50
6.4.1 The Aetiology of Generalized
They'd deteriorate my body 85 100 Anxiety Disorder
I'd be in pain 85 100
The challenge in explaining GAD is to understand why
I'd die 90 80
some individuals worry chronically and pathologically,
I'd end up in hell 95 80 while many other individuals — often with more stressful
Non-worrier topic: Getting good lifestyles — worry significantly less. Theories will there-
grades in school fore have to explain why GAD sufferers persist with their
Catastrophising step worrying even when it causes them significant distress.
| might do poorly on a test 3 20
I'd get a bad grade in the class 3 100 Biological theories
That would lower my grade-point 2 100 There is some evidence for a genetic component in
average both anxiety generally and GAD specifically (Noyes,
I'd have less of a chance of getting a 2 60 Woodman, Garvey, Cook, Suezer et al., 1992), which
good job suggests that GAD has an inherited component. Twins
FAS PSYCHOPATHOLOGY
ww
studies estimate the heritable component at around 30 of information processing biases which appear to
per cent (Dellava, Kendler & Neale, 2011; Hettema, Neale maintain their hypervigilance for threat, create
& Kendler, 2001), but what appears to be inherited more further sources for worry, information processing biases Biases
than anything else is a vulnerability to anxiety disorders and maintain anxiety. For interpreting, attending to, storing or recal
generally, and less an inherited vulnerability to a specific example, experimental evi- ing information which may give rise to
dysfunctional thinking and behaving.
disorder such as GAD (Tambs, Czajkowsky, Roysamb, dence has demonstrated
Neale et al., 2009). Neuropsychological perspectives on that individuals with GAD preferentially allocate att-
GAD are still in their infancy, with neuroimaging stud- ention to threatening stimuli and threatening informa-
ies of worry implicating prefrontal brain regions in this tion (Mogg & Bradley, 1998; Mathews & MacLeod,
activity (Hoehn-Saric, Schlund & Wong, 2004; Paulesu, 2005). Highly anxious individuals also exhibit a threat-
Sambugaro, Torti, Danelli et al., 2010), but such studies interpretation bias. That is, they resolve ambiguity by
have not yet provided any convincing reasons why wor- selecting the more negative or threatening interpretation
rying in GAD sufferers should be so extreme and dis- of ambiguous information (Blanchette ®& Richards,
tressing. Other neuroimaging studies have focused on 2010). Anxious individuals also have a bias towards
possible abnormalities in emotional regulation in GAD expecting negative outcomes following predictive cues
sufferers (Mennin, Holaway, Fresco, Moore & Heimberg, in classical conditioning studies (Davey, 1992), and they
2007). Etkin, Prater, Hoeft, Menon & Schatzberg (2010) also exhibit reasoning biases that maintain threate-
found reduced regulatory activity in pregenual anterior ning interpretations of events (de Jong, Weertman,
cingulate and parietal cortices in patients with GAD, sug- Horselenberg & van den Hout, 1997; de Jong, Haenen,
gesting a reduced capacity for emotional regulation that Schmidt & Mayer, 1998). Many of these threat-related
might be a risk factor for GAD. information processing biases co-occur in individuals
with anxiety and increase the anxious individual's vul-
Psychological theories nerability to interpreting daily events as threatening
information processing biases in GAD A good and challenging. It is easy to conceive of ways in which
deal of research has now indicated that anxious individ- this interpretational bias might maintain anxiety by
uals, and especially those suffering GAD, have a series maintaining the range of potential threats perceived by

ATTENTION BIAS MODIFICATION (ABM)
Because highly anxious individuals have attentional and words have appeared a‘probe’ appears (e.g. a colon) and the
interpretational biases towards threat that are known to participant has to respond as quickly as possible by indicat-
cause anxiety, a practical way of reversing these biases is ing where the probe appeared. However, in the ABM task,
to use experimental procedures that will neutralize them. the probe always appears in the position where the non-
This training procedure is known as attention bias modi- threatening word had been presented. This process trains
fication (ABM) and has been the individual to attend more rapidly to the non-threat-
GSS ISIS SEAN UU RS
used successfully to modify ening than the threatening word, and so ameliorates any
To read a journal article on attention
bias modification go to both attentional and inter- attentional bias to threat that the participant possessed.
www.wiley-psychopathology.com/ pretation biases in anxious
reading/che ; individuals, and to reduce
ES a ee ee
anxiety vulnerability and lev-
els of dysfunctional anxiety (MacLeod & Mathews, 2012;
Hakamata, Lissek, Bar-Haim, Britton et al., 2010).
The procedure uses the classic dot probe task that has
traditionally been used to measure attentional biases. Dishwasher
Stimuli are presented on a computer screen. First, the par-
ticipant sees a focus point (+), and this is followed by two Humiliated
words presented simultaneously for a very short duration

(usually 500 milliseconds). One will be threatening, (e.g.
‘Humiliated’) and the other with be non-threatening (e.g.
‘Dishwasher’). In the ABM procedure, immediately after the
CHAPTER6 ANXIETY AND STRESSOR-RELATED PROBLEMS 73
the individual (Davey, 2006). Indeed, recent studies have metacognitive beliefs that worrying will be uncontrolla-
shown that these biases causally contribute to worrying ble or harmful. It is the apparent contradiction between
in anxious individuals typically diagnosed with GAD these two sets of beliefs that causes the worry-related dis-
(Hirsch, MacLeod, Mathews, Sandher et al., 2011). tress in GAD according to this model, and metacognitive
Furthermore, there appears to be an important recipro- therapy is a specific form of intervention developed to
cal relationship between experienced anxiety and deal with these GAD-causing beliefs (Wells, 2010).
threat-interpretation biases. Early research indicated Secondly, there is growing evidence that worrying
that anxiety gave rise to threat-interpretation biases may indeed be reinforced because it distracts the worrier
(Mathews & MacLeod, 1994; Mogg & Bradley, 1998; from experiencing other negative emotions and process-
Butler & Mathews, 1983), but more recent research has ing even more stressful phobic images. That is, worry is
indicated that forced learning of threat-interpretation an internal narrative process that prevents the individual
biases also increases the individual’s reported experience from processing other — often more stressful — infor-
of anxiety (Mathews & MacLeod, 2002; Hertel, Mathews, mation (Borkovec, 1994; Borkovec & Lyonfields, 1993).
Peterson & Kintner, 2003; Mathews & Mackintosh, Evidence to support this view comes from the fact that
2000; Wilson, MacLeod, Mathews & Rutherford, 2006). worry produces very little physiological or emotional
This has given rise to interventions for anxiety and arousal (Hoehn-Saric & McLeod, 1988) and appears to
GAD that attempt to correct the attentional bias to block the processing of emotional images (Borkovec,
threat found in anxious Lyonfields, Wiser & Diehl, 1993).
ition bias modification individuals (MacLeod &
Highly anxious individuals have Mathews, 2012). This is
Dispositional characteristics of worriers While
tional and interpretational biases
rds threat that are known to cause known as attention bias there is still some way to go in understanding the psycho-
ty. ABM is a practical way of reversing modification (ABM) and logical and developmental processes that lead to individu-
» biases and uses experimental proce- is described in Treatment als becoming pathological worriers, there is a good deal
5 that will neutralize them. in Practice Box 6.4. of knowledge available about what kinds of psychological
features they possess. For example, worriers are intolerant
Beliefs, meta-beliefs and the function of worry- of uncertainty (Ladoucer, Talbot & Dugas, 1997; Birrell,
ing We mentioned earlier that individuals with GAD Meares, Wilkinson & Freeston, 2011), are high on perfec-
persist chronically with their worrying even though it tionism (Pratt, Tallis & Eysenck, 1997), and have feelings
causes them considerable distress and generates symp- of responsibility for negative outcomes (Startup & Davey,
toms that disrupt normal day-to-day living. This suggests 2003; Wells & Papageorgiou, 1998), which suggests they
that worrying may serve a particular function for such indi- possess characteristics that will drive them to attempt to
viduals, and this functionality may outweigh the negative think about resolving problematic issues. However, wor-
effects of their worrying. Some theories of GAD empha- riers also have poor problem-solving confidence (Davey,
size this functional aspect of worrying. Firstly, both path- 1994d), and couch their worries in ways that reflect per-
ological worriers and individuals diagnosed with GAD sonal inadequacies and insecurities (Davey & Levy, 1998).
hold strong beliefs that worrying is a necessary process This contrasting combination of characteristics appears
that must be undertaken fully and properly in order to to drive the individual to try to resolve problems, but the
avoid future catastrophes (Davey, Tallis & Capuzzo, 1996; process is thwarted by their personal doubt about their
Wells, 1995; Borkovec, Hazlett-Stevens & Diaz, 1999), own ability to solve them successfully (Davey, 1994c).
and these dysfunctional beliefs about the utility of wor-
rying appear to motivate the worrier to persist with their
worrying. A similar view is taken by metacognitive theo- 6.4.2 The Treatment of Generalized
ries of GAD (e.g. Wells, 1995, 2010). Metacognitions are
Anxiety Disorder
overarching cognitive processes that are responsible for
appraising, monitoring and controlling thinking, and so As with most of the anxiety disorders, GAD can be treated
have an important influence on what we think about and either with drugs or with structured psychological therapy
how long we will persist in thinking about something. such as CBT, or with a combination of both. However,
Metacognitive theories of worry argue that the individ- deciding what type of treatment to use is often the most
ual with GAD engages in worrying in response to nega- important decision for service providers and therapists —
tive thoughts (e.g. “What if I lose my job?’) as a means especially for a disorder that is as prevalent as GAD.
of trying to anticipate problems, avoid them or find a Medication might be a suitable first step if immediate
solution. However, individuals with GAD have developed management of the problem is important (for instance, if
metacognitive beliefs about worry that drive their worry- the patient is experiencing extreme distress or has suicidal
ing and also make that worry process distressing. These ideation). Otherwise, longer term structured psychologi-
include positive metacognitive beliefs that worrying will cal therapy (such as CBT) or self-help programmes should
help them solve or avoid problems, as well as negative be offered. Some self-help options are outlined in my blog
.
, on ‘10 tips to manage your of behaviour therapy principles for dealing with worry
To read more about why we worry go to
http://tinyurl.com/clclwfd } worrying and in Chapter
behaviours, while a number of effective variants of CBT
——mmmmmmme 6 Of OUT CBI self-help are now available for dealing with the pathological wor-
guide for managing anxiety rying found in GAD (e.g. cognitive restructuring and
(Davey, Cavanagh, Jones, Turner & Whittington, 2012). metacognitive therapy).
Stimulus controltreatment One of the earliest behav-

Pharmacological treatments ioural interventions for worry in GAD adopted the princi-
Because GAD involves chronic daily anxiety and emo-
ple of stimulus control. This is based on the conditioning
tional discomfort, we might expect that anxiolytics — such
principle that the environments in which behaviours are
as the benzodiazepines — would be the first line of treat-
enacted come to control their future occurrence, and can
ment for sufferers. However, at least 50 per cent of GAD
act to elicit those behaviours (the principle of stimulus con-
sufferers receive initial treatment with antidepressants
trol). Because worrying can occur almost anywhere, and
such as selective serotonin reuptake inhibitors (SSRIs) or
so come under the control of a vast range of contexts, the
serotonin-norepinephrine reuptake inhibitors (SNRIs)
first aim of stimulus control treatment is to limit the con-
on the basis of their proven effectiveness in treating the
texts in which worrying occurs. This is achieved by telling
symptoms of GAD in clinical trials, while only around
clients that they can worry — but only for a specific period
35 per cent are treated with benzodiazepines (Berger,
in a particular location each day (Borkovec, Wilkinson,
Edelsberg, Bollu, Alvir et al., 2011). Treatment with anti-
Folensbee & Lerman, 1983). For example, as outlined in
depressants is justified in many cases because GAD is
Treatment in Practice Box 6.5, they are instructed to worry
regularly comorbid with depression and SSRIs tend to be
at a specific time (e.g. between waking and the end of
better tolerated than benzodiazepines. Nevertheless, the
breakfast) or in a particular location (the living room).
long-term effectiveness of pharmacological treatments
for GAD is questionable given the relative lack of longitu- Cognitive behaviour therapy In the previous section
dinal outcome studies and poor identification of patient we have reviewed a number of psychological theories of
groups who are likely to respond positively to medica- GAD which suggest that cognitive biases and dysfunctional
tion-based interventions (Baldwin, Ajel & Garner, 2010). beliefs about the function of worrying may be central to
the development and maintenance of the disorder. This
Psychological treatments being so, integrated cognitive behavioural therapy seems
stimulus control treatment An early Psychological treatments a suitable method to tackle GAD. CBT for GAD normally
behavioural intervention for worry in GAD for GAD have developed consists of a number of elements, the main ones being:
which adopted the principle of stimu- using both behavioural
lus control, based on the conditioning ¢ self-monitoring
and cognitive methodolo-
principle that the environments in which ¢ relaxation training
behaviours are enacted come to control gies. For example, stimu-
their future occurrence and can act to elicit lus control treatment was : cognitive restructuring
those behaviours. originally developed out ° behavioural rehearsal.

STIMULUS CONTROL TREATMENT FOR GENERALIZED ANXIETY DISORDER
Stimulus control treatment for GAD is an effective treat- 2. Establish a half-hour worry period to take place at
ment for reducing the frequency of worry by controlling the same time and in the same location each day.
the range of contextsinwhich the activity occurs (see sec- 3. When you catch yourself worrying, postpone the
tion 6.4.2). worry to the worry period and replace it with
There are four basic instructions underpinning this attending to present-moment experience.
procedure: 4. Make use of the half-hour worry period to worry
about your concerns.and to engage in problem
1. Learn to identify worrisome thoughts and other solving to eliminate those concerns.
thoughts that are unnecessary or unpleasant.
Distinguish these from necessary or pleasant Source: From Borkovec (2005); Borkovec, Wilkinson, Folensbee &
thoughts related to the present moment. Lerman (1983).
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS ys
Self-monitoring involves making the client aware of of the event with subsequent reality (Borkovec,
their fixed patterns of behaviour and the triggers that Hazlett-Stevens & Diaz, 1999). Other types of cogni-
may precipitate worry. These triggers are often thoughts tive restructuring involve the challenging and replace-
about future events that have very low probabilities of ment of dysfunctional metacognitive beliefs about
happening (e.g. the accidental death of a loved one while worrying — known as metacognitive therapy (Wells,
driving to work), and the client’s attention is drawn to the 1999, 2010) — or the belief held by pathological worri-
fact that these are cognitively constructed rather than real ers that uncertainty has to be resolved by thinking
events. Relaxation training is an obvious way of dealing through every possible scenario (Dugas, Ladouceur,
with the chronic stress experienced by GAD sufferers. Leger, Freeston et al., 2003). Finally, behavioural
ation training A method of dealing
The specific technique rehearsal involves either the actual or imagined
the chronic stress experienced by psy- of progressive muscular rehearsal of adaptive cop- behavioural rehearsal A coping strategy
thology sufferers. A specific technique relaxation is often used ing responses that need that involves either the actual or imagined
ogressive muscular relaxation is often (Bernstein, Borkovec & to be deployed when a rehearsal of adaptive coping responses
,and relaxation is found to be as effec-
Hazlett-Stevens, 2000), and worry trigger is encoun- that need to be deployed when a worry
is some forms of cognitive therapy. trigger is encountered.
relaxation is found to be as tered. These coping strat-
effective as some forms of cognitive therapy (Arntz, egies may involve the deployment of relaxation
2003). Cognitive restructuring methods are used to exercises or pleasant distracting activities designed to
challenge the biases that GAD sufferers hold about how avoid worry (Butler, Fennell, Robson & Gelder, 1991).
litive restructuring Methods used frequently bad events might CBT for GAD has been shown to be effective with or
allenge the biases that a client might happen (Beck, Emery & without the use of pharmacological treatments (Lang,
about how frequently bad events
1t happen and to generate thoughts
Greenberg, 1985), and to 2004), and has long-term effectiveness for a significant
are more accurate. generate thoughts that are proportion of clients (Durham, Chambers, MacDonald,
more accurate (Borkovec, Power & Major, 2003). However, recent meta-analyses
2005). One way of doing this is by using an outcome suggest that while CBT treatments for GAD have
diary in which the client writes down on a daily basis improved over the past 10-15 years, there is still a sig-
their worries and how likely they think the focus of nificant percentage of sufferers who fail to recover
their worries will actually happen. Clients can then fully following cognitive treatments for GAD
compare their own inflated estimate of the likelihood (Hanrahan, Jones, Field & Davey, 2013).
‘SELF-TEST QUESTIONS
® What is the cardinal diagnostic feature of GAD?
© What are the features of worry in GAD that make it a distressing experience for the sufferer?
* How do information processing biases and cognitive factors contribute to the acquisition, maintenance and experience of
anxiety in GAD?
* How do psychological treatments of GAD attempt to bring the activity of worrying under control?
SECTION SUMMARY
6.4 GENERALIZED ANXIETY DISORDER (GAD)
¢ The cardinal diagnostic characteristic of GAD is chronic uncontrollable worrying, which is accompanied by physical symp-
toms such as irritability, muscle tension, fatigue, poor concentration, restlessness, and disturbed sleep.
¢ Over 5 per cent of the population will be diagnosed with GAD in their lifetime, and 12 per cent of those who attend anxiety
disorder clinics will present with GAD.
e Individuals with GAD possess an information processing bias which appears to maintain their hypervigilance for threat
and create the opportunity to catastrophically worry about events. There is evidence that these information processing
biases may actually cause anxiety generally, and can be manipulated therapeutically using attention bias modification
techniques.
FG PSYCHOPATHOLOGY
° Worrying in GAD appears to be maintained by dysfunctional beliefs about the utility of worrying, which appear to motivate
the individual with GAD to persist with their worrying. \
° Anxiolytics are useful for dealing with the anxiety symptoms exhibited by individuals with GAD, but treatments based on
controlling the process of worrying and challenging dysfunctional beliefs about worrying appear to have a more long-term
benefit.
fears. While the main compulsions are usually related to

6.5 OBSESSIVE COMPULSIVE checking or washing, compulsions can also manifest less
DISORDER (OCD) regularly as compulsive hoarding (Steketee, Frost &
Kyrios, 2003), compulsive hair-pulling or skin picking,
superstitious ritualized movements, or the systematic
We have all occasionally gone back to check whether we arranging of objects (Radomsky & Rachman, 2004). In
locked a door, and we have all experienced a sudden, most cases, compulsions are clearly excessive, and are
intrusive thought that we find disturbing and out of place usually recognized as so by the sufferer. Rituals can
(e.g. harming our own child). However, for the person become rigid, stereotyped sequences of behaviours that
with obsessive compulsive disorder (OCD) such the individual is driven to perform as a result of cognitive
obsessive compulsive disorder (OCD) A thoughts and actions are triggers such as intrusive thoughts related to the individ-
disorder characterized either by obsessions repeated often and result ual’s specific fears. For example, individuals distressed by
(intrusive and recurring thoughts that the in a distressing and disa- unwanted immoral or blasphemous thoughts can attempt
individual finds disturbing and uncon-
bling way of life. OCD has to suppress the thought and reduce anxiety by indulging
trollable) or by compulsions (ritualized
behaviour patterns that the individual feels two important and some- in compulsive acts such as counting backwards from a
driven to perform in order to prevent some times independent charac- number until the thought has gone.
negative outcome happening). teristics. Obsessions are
intrusive and _ recurring Diagnosis and prevalence
obsessions Intrusive and recurring
thoughts that the individual In DSM-5, the importance of OCD was recognized by
thoughts that an individual finds disturb-
ing and uncontrollable. finds disturbing and uncon- including OCD and its related disorders as a separate
trollable. These obsessive chapter independent of anxiety disorders generally, and
thoughts frequently take the form of causing some harm this acknowledges some of the special features that OCD
or distress to oneself or to some important other person and related disorders possess. DSM-5 Summary Table 6.7
(such as a partner or offspring). Common obsessions also shows the main diagnostic criteria for OCD. Diagnosis
take the form of fear of contamination (i.e. contaminating is dependent on the obsessions or compulsions causing
oneself or important others), and thoughts about harm, marked distress, being time consuming, or significantly
accidents, and unacceptable sex (Rowa & Purdon, 2005; interfering with the person’s normal daily living. This
Berry & Laskey, 2012). Obsessive thoughts can also take latter diagnostic criterion delineates OCD compulsions
the form of pathological doubting and indecision, and this
may lead to sufferers developing repetitive behaviour pat-
terns such as compulsive checking or washing. Very often, DSM-5 SUMMARY TABLE 6.7 Criteria for obsessive compulsive
obsessive thoughts can be ‘autogenous’ — that is, they seem disorder
uncontrollable and ‘come out of the blue’ — and it is this e Presence of obsessions such as repeated and unwanted
autogenous characteristic that helps to make obsessive thoughts, urges or images that the individual tries to
thoughts distressing. Compulsions represent repetitive or ignore or suppress, and/or
compulsions Repetitive or ritualized ritualized behaviour pat-
e Presence of compulsions where the individual feels com-
behaviour patterns that an individual feels terns that the individual pelled to repeat certain behaviours or mental activities
feels driven to perform in
driven to perform in order to prevent some
negative outcome happening. ¢ The individual believes that the behaviours will prevent a
order to prevent some neg-
catastrophic event but these beliefs have no realistic con-
ative outcome happening. This can take the form of ritu- nections to the imagined event, or are markedly excessive
alized and persistent checking of doors and windows (to
° Obsessions and compulsions consume at least 1 hour per
ensure that the house is safe), or ritualized washing activi-
day and cause difficulty in performing other functions
ties designed to prevent infection and contamination.
Ritualized compulsions such as these also act to reduce ¢ Symptoms cannot be explained by the effects of other
the stress and anxiety caused by the sufferer’s obsessive mental or medical disorders, drug abuse or medication
CHAPTER6 ANXIETY AND STRESSOR-RELATED PROBLEMS
OBSESSIVE COMPULSIVE DISORDER

Luke was 21 years old and attending university, living a considerable distance from his family with whom he
had always been close. It was 2 months before his final year exams and his alarm went off at 8.30 a.m. Turning to
switch off his alarm, Luke was immediately overwhelmed by the feeling of dread that had been with him con-
stantly since the beginning of term.
He quickly got out of bed and went to the bathroom. Luke washed his hands and brushed his teeth before
washing his hands twice more. Stepping into the shower Luke scrubbed himself all over with shower gel,
HISTORY
CASE and washed his hands several more times in between cleaning the rest of his body. After rinsing his hair through
6.2
Luke washed his hands again and got out of the shower; by now it was 9.30.
Luke began to dry his hair but he felt that his hands were still dirty, though by now they were red raw. He
washed them again, rapidly rubbing the backs of his hands and cleaning repeatedly under his nails. They still felt
dirty. Telling himself not to be stupid, Luke moved to the door of the bathroom but felt a strong urge to go back
and clean his hands once more. The feeling was too strong to resist so he quickly rinsed his hands again, dousing
them in sanitizer gel and rushed out of the bathroom, knowing he would be late for his lecture.
Before he could leave the house, Luke checked that the back door was locked and all his housemates’ win-
dows were securely closed, then he went back to the bathroom to wash his hands twice more. Grabbing a clean
towel from the wash, Luke carefully wrapped up his hand so he could open the front door without touching the
dirty handle. Once the door was open, Luke ran back inside to check that he had remembered to secure the win-
dows in all his friends’ rooms and to close all the doors.
Pulling the front door shut with his foot, Luke tested it was firmly shut and then ran towards the bus stop. It
was now 10.15 and he was already 15 minutes late. A bus was arriving just as he reached the stop, hot and out
of breath. Sitting on the bus, Luke felt the sweat on the palms of his hands and wiped them clean on a tissue,
repeatedly cleansing them with the sanitizer gel he always carried with him.
Halfway through thejourney, Luke began to panic that he hadn't locked up the house and imagined coming
home to find he had been burgled and all his housemates’ belongings had been ransacked. Luke got off at the
next stop and took another bus back home, only to find that the doors and windows were locked. Cursing himself
for his irrationality, Luke turned to leave the house once more but, looking at his watch, saw it was now 11.30 and
his lecture was almost over.
Later on, when Luke was diagnosed with obsessive compulsive disorder, 6 months after failing his exams, he
felt a huge sense of relief and was pleased that he could now give his friends and family a logical explanation for
his behaviour. Luke is now receiving treatment for his OCD and, when he explained his condition to the univer-
sity, they agreed he could return and re-sit his exams.
Clinical Commentary
This example shows how obsessions and compulsions in OCD are often compelling and difficult for the suf-
ferer to resist - even when the individual is aware that these thoughts and actions are ‘stupid’ or irrational.
Luke’s compulsions are fueled by the ‘feelings of dread’ that he experiences most mornings when he wakes
up, and this provides the highly anxious state under which compulsions (such as compulsive washing) are
performed. ‘Doubting’ is also a common feature of OCD, and Luke experiences this on his way to university in
the form of doubting whether the doors and windows are locked. The high levels of inflated responsibility usu-
ally possessed by OCD sufferers mean that Luke is driven to continually check that his doubts are unfounded.
from other urges, such as the uncontrollable desire to symptoms are also a common way for anxiety to mani-
eat, drink or gamble, because these are often engaged in fest'itself in childhood, and this is discussed further in
with pleasure (see Chapters 9 and 10 for discussions of Chapter 16. Lifetime prevalence is around 2.5 per cent
these alternative types of compulsions). with a 1-year prevalence rate of between 0.7 and 2.1 per
OCD onset is usually gradual and frequently begins cent, and affects women marginally more frequently
to manifest itself in early adolescence or early adulthood than men (Stein, Forde, Anderson & Walker, 1997;
following a stressful event such as pregnancy, childbirth, Adam, Meinlschmidt, Gloster & Lieb, 2012). Few stud-
relationship or work problems (Kringlen, 1970). OCD ies have investigated the effect of cultural factors on
BIE Ss PSYCHOPATHOLOGY
’ Ww
the prevalence and manifestation of OCD symptoms. mirror checking, and reassurance seeking (see
However, a cross-cultural study reported by Fontenelle, Focus Point 6.3).
Mendlowicz, Marques & Versiani (2004) concluded that 2. Hoarding disorder: Hoarding disorder centres
universal characteristics of sufferers regardless of cul- around a difficulty discarding or parting with
tural background included a predominance of females, possessions to the hoarding disorder Difficulty discard-
a relatively early age of onset, and a preponderance of point where the ing or parting with possessions to the
mixed obsessions and compulsions. The exception to individual’s living area point where the individual's living area is
this was the apparent content of obsessions, which in is severely congested severely congested by clutter.
Brazilian and Middle Eastern samples exhibited a pre- by clutter (see Focus Point 6.4).
dominance of aggressive or religious obsessions (com-
3. Hair-pulling disorder (trichotillomania): the individual
pared with North America, Europe and Africa).
compulsively pulls trichotillomania Hair-pulling disorder in }
out their own hair which the individual compulsively pulls out
OCD-related disorders their own hair resulting in significant hair loss
DSM-S5 has divided OCD-type problems into a number resulting in signi-
of separate diagnostic categories. The main OCD diag-
ficant hair loss.
nostic category is described in DSM-5 Summary Table 4. Skin-picking disorder: Skin-picking disorder is the
6.7, but other OCD-related diagnostic categories include: recurrent picking of
the skin that results skin-picking disorder Recurrent picking
1. Body dysmorphic disorder: This is a pre-occupation : , :
in skin lesions.
of the skin that results in skin lesions.
with perceived defects or flaws in physical
appearance that are not usually perceived by See Davey, Dash & Meeten (2014) for a fuller description
others. This gives rise to compulsive grooming, of OCD-related disorders.
BODY DYSMORPHIC DISORDER

One OCD-related disorder described in DSM-5 is body
dysmorphic disorder (BDD). This is a preoccupation
ie. with assumed defects in appearance that are often
imaginary, but if there is a physical anomaly, those suf-
WU fering from BDD will greatly exaggerate its importance.
ae) Common complaints include flaws in facial features or
Lh facial asymmetry, hair thinning, acne, wrinkles, scars,
vascular markings, irregular complexions, or exces-
sive facial hair. Other common preoccupations include
body shape generally (e.g. preoccupations with being
obese or overweight), and dissatisfaction with specific
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body parts, such as breasts, genitals, buttocks. Sufferers
will often be so embarrassed about their supposed one particular repetitive behaviour is known as ‘mirror
appearance defects that they will often only talk about gazing’ (Windheim, Veale & Anson, 2011). Studies have
them in general terms, and may simply refer to them- shown that about 80 per cent of individuals with BDD
selves as being ‘ugly: The way in which BDD overlaps will repetitively check their appearance in mirrors —
with OCD is in the obsessive thoughts that sufferers often for considerable periods oftime. Interestingly, the
have about their appearance, and sufferers can also remaining 20 per cent tend to avoid mirrors altogether
develop ritualistic compulsions around their defects, (Veale & Riley, 2001). Mirror gazing can be construed as
spending many hours a day viewing themselves in a‘safety seeking behaviour’ which briefly acts to reduce
mirrors or attempting to deal with their problems with distress. However, for individuals with low body-image
excessive grooming behaviour (e.g. skin picking, hair satisfaction mirror gazing for more than 3.5 minutes
combing, applying cosmetics, dieting, and suchlike), results in a more negative opinion about their attrac-
with such behaviours usually adding to the distress that tiveness (Mulken & Jansen, 2009), and mirror gazing
is experienced. Concerns about appearance in BDD are behaviour in the longer term increases distress, main-
frequently accompanied by a host of repetitive and tains negative beliefs about appearance, and reinforces
time-consuming behaviours, aimed at verifying, cam- repetitive appearance-checking behaviours (Veale &
ouflaging, or enhancing the person's appearance, and Riley, 2001).
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS
Individuals with body dysmorphic disorder also develop deliberate self-harm and suicide attempts (Phillips, 2001).
|
dysfunctional beliefs about their appearance, and are quite In addition, adolescents with body dysmorphic disor-
convinced that their own perceptions are correct and undis- der experience high levels of impairment in school and
torted. As a result they may regularly seek cosmetic surgery work functioning, with studies reporting attempted sui-
in orderto correct their‘defects: In a study ofindividuals seek- cide rates of around 45 per cent (Phillips, Didie, Menard,
ing cosmetic surgery, Aouizerate, Pujol, Grabot, Faytout et al. Pagano et al., 2006).
(2003) found that 9.1 per cent of applicants were diagnos- The exact prevalence rates of BDD disorder are unclear,
able with body dysmorphic disorder. In fact, in those appli- although a nationwide German study suggested that the
cants who had no defects or only a slight physical defect, 40 point prevalence of BDD was 1.8 per cent (Buhlmann,
per cent were diagnosable with body dysmorphic disorder. Glaesmer, Mewes, Fama et al., 2010). This study also indi-
A preoccupation with apparent physical defects often cated that those diagnosable with BDD had high rates of
leads to the catastrophising of these characteristics, and previous cosmetic surgery (15.6%), and higher rates of
sufferers will frequently comment on their appearance suicidal ideation (31%). BDD is also relatively common in
to others in negative ways (e.g. ‘| am ugly’, ‘| am fat’). individuals who already have a diagnosis of OCD, with a
Nevertheless, regular reassurance from others fails to lifetime prevalence rate for BDD of 12.1 per cent in indi- |
change these views, and the sufferer can slip into a nega- viduals with OCD (Costa, Assuncao, Ferrao, Conrado et |
tive decline that incurs further psychopathology such al., 2012), reinforcing the view that OCD and BDD may be |
a
as major depression, anxiety, social anxiety disorder,
otfail fina Bass st
related disorders.
all
|
HOARDING DISORDER
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safety risks. Initial epidemiology studies suggest that
s hoarding disorder afflicts around 5.8 per cent of the cur-
| O rent population, and affects men and women equally
a
W (Timpano, Exner, Glaesmer, Rief et a/., 2011).
>
W. Individuals with hoarding disorder may often try to
|
9tl organize their possessions, but their lack of organisa-

tional skills simple makes the chaos worse. The disorder
is particularly associated with an inability to throw away
even normally disposable items such as food and sweet |
wrappings. If the individual has other, more classic, OCD
symptoms this can compound the problem. For exam- |
ple, fear of contamination and superstitious thoughts

(e.g. ‘throwing something away will result in a catastro-
phe of some kind’) may prevent the sufferer from touch-
ing or throwing away items. However, the accumulation
of clutter in hoarding disorder is not simply something
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that is tolerated by the individual, the hoarding causes |
Hoarding Disorder is anew diagnostic category included clinically significant distress and has a significant impact
in DSM-5 (Frost, Steketee & Tolin, 2012; Pertusa, Frost, on social and occupational functioning.
Fullana, Samuels et al., 2010). It is a complex problem Hoarding appears to begin in childhood or adoles-
made up of three specific attributes: (1) collecting too cence, with a chronic and progressive course through-
many items (some sufferers will actually actively collect out the lifespan. This means that many sufferers of
or steal more items to hoard), (2) difficulty parting with hoarding disorder are elderly, and it is often comorbid
or getting rid of hoarded items, and (3) general problems with dementia and other psychiatric diagnoses such
with organising their possessions, probably as a result of as major depression, social anxiety disorder and inat-
problems with more fundamental cognitive processes tentive ADHD (Frost, Steketee & Tolin, 2011). Hoarding
such as information processing, attention, categorisa- disorder can also be restricted to collecting and hoard-
tion, and decision making (e.g. Tolin & Villavicencio, ing individual types of items. Animal hoarding is one |
2011). The result of this hoarding is large piles of clutter recently identified example that can lead to considera- |
that make living spaces impassable, home utilities (such ble animal suffering and neglect (Patronek, 1999; Frost,
as a toilet) unusable, and this can pose both health and Patronek & Rosenfield, 2011).
“sods PSYCHOPATHOLOGY
6.5.1 The Aetiology of Obsessive initiation (Greisberg & McKay, 2003; Rao, Reddy, Kumar,
Kandavel & Chandrashekar, 2008). An alternative view
Compulsive Disorder of brain dysfunction and OCD is based on findings from
When considering the aetiology of OCD, the reader neuroimaging studies. For example, Rapoport (1989)
should be aware that it represents a psychological prob- has argued that obsessions and compulsions are geneti-
lem that possesses a number of quite different, and often cally stored and learnt behaviours that are involuntarily
independent, features. For example, obsessions do not triggered by the brain. Baxter, Ackermann, Swerdlow,
always occur with compulsions, and the two main types Brody et al. (2000) have developed this approach by sug-
of compulsions (i.e. washing and checking) rarely occur gesting that uncontrollable compulsions in OCD result
together in the same individual. This means that many from the brain being unable to inhibit these genetically
theories of the aetiology of OCD have been developed stored behaviours. In particular, they use evidence from
to address only some of its features (e.g. thought sup- neuroimaging studies to argue that OCD compulsions
pression accounts are relevant to explaining only obses- result from the failure of inhibitory pathways project-
sive thoughts), and they are not meant to be universal ing via the basal ganglia to inhibit innate behaviour pat-
explanations of OCD. Bear this in mind when reading terns (Saxena, Brody, Schwartz & Baxter, 1998). While
through the following sections. this hypothesis can account for the rather restricted set
of behaviours that manifest as compulsions (i.e. it is
Biological factors argued that only certain behaviours have been geneti-
As with other anxiety disorders, there is evidence of an cally stored) it still represents an oversimplification of
inherited component to OCD. Twin studies have found how brain structures such as the basal ganglia might be
high concordance for OCD in monozygotic twins (80- involved in OCD (Frampton, 2003).
87 per cent) compared with dizygotic twins (47-50 per
cent) (Carey & Gottesman, 1981). Furthermore, family Psychological factors
relatives of individuals with OCD are also more likely Memory deficits ‘“Doubting’ is a central feature of
to have a diagnosis of OCD than non-family controls OCD, and especially the compulsions associated with the
(Lenane, Swedo, Leonard, Pauls et al., 1990; Hanna, disorder. As a result, it has been suggested that OCD may
Veenstra-VanderWeele, Cox, Boehnke et al., 2002), with be characterized by memory deficits that give rise to the
some studies concluding that familial transmission of doubting that, for example, doors have been locked or
OCD is a result of genetic rather than environmental hands have been washed properly. Memory deficit mod-
factors (Nestadt, Samuels, Riddle, Bienvenu et al., 2000). els take a number of different forms. It has been sug-
More recent genetic linkage studies have also begun to gested that OCD sufferers may have:
identify some of the candidate genes for the transmis-
¢ a general memory deficit (Sher, Mann & Frost,
sion of the inherited component to OCD (e.g. see Wang,
Samuels, Chang, Grados et al., 2008).
1984):
Onset of OCD can also be associated with traumatic ¢ less confidence in the validity of their memories
brain injury or encephalitis (Jenike, 1986), which suggests (Watts, 1993); or
that there may be a neuropsychological deficit in some ¢ a deficit in the ability to distinguish between the
forms of OCD. This neuropsychological deficit may give memory of real and imagined actions (Brown,
rise to the ‘doubting’ that things have been done prop- Kosslyn, Breiter, Baer & Jenike, 1994).
erly, which is a central feature of many forms of OCD.
Areas of the brain that have been identified as impor- However, evidence supporting the role of these mem-
tant in this respect include the frontal lobes and the basal ory deficits in OCD is equivocal (Hermans, Engelen,
ganglia. When sufferers are shown stimuli representa- Grouwels, Joos et al., 2008), and recent theoretical views
tive of their obsession or compulsion (e.g. an unlocked suggest that the deficits that give rise to OCD ‘doubting’
door) blood flow increases in both the frontal lobes may not be problems with memory or working memory
and the basal ganglia, suggesting that these areas may per se, but are the result of a deficit in executive func-
have at least some role in OCD (Rauch, Jenike, Alpert, tioning in general (Harkin & Kessler, 2011). For example,
Baer et al., 1994). In other neuropsychological studies, if OCD sufferers spend a lot of time checking both rel-
OCD sufferers appear to demonstrate a variety of basic evant and irrelevant things on a daily basis, this will over-
information processing and executive functioning defi- load executive processes and result in poor encoding of
cits (the latter referring to processes that are involved information and poor attention to relevant information,
in planning and attentional control), and these include which in turn will cause memory deficits. This is con-
deficits in spatial working memory, spatial recognition, sistent with another body of evidence which suggests
visual attention, visual memory, and motor response that lack of confidence in recall may be a consequence of:
compulsive checking or washing rather than a cause of preventing harm, and this inflated responsibility
it (van den Hout & Kindt, 2003; Harkin & Kessler, 2009; appears to be an important vulnerability factor in
Radomsky & Alcolado, 2010). In effect, the more some- developing OCD (Salkovkis, 1985; Rachman, 1998).
one checks, the less confident they will be about what
they have checked. Salkovskis, |Rachman, inflated responsibility The belief that
Ladouceur, Freeston, et al. one has power to bring about or prevent
Clinical constructs and OCD Clinical psychology (1996) have defined inflated subjectively crucial negative outcomes.
researchers regularly use their clinical experience as a start- responsibility as ‘the belief These outcomes are perceived as essential
to prevent. They may be actual: that is, hav-
ing point for understanding the causes of a disorder; from that one has power which ing consequences in the real world, and/or
this experience they develop what are known as clinical is pivotal to bring about or at a moral level.
constructs, and the purpose of these constructs is to link prevent subjectively cru-
thoughts, beliefs and cognitive processes to sub- cial negative outcomes. These outcomes are perceived
.
al constructs Clinical psychology sequent symptoms. These as essential to prevent. They may be actual, that is hav-
| ae develop constructs in order constructs can be develo- ing consequences in the real world, and/or at a moral
escribe the combination of thoughts, ped in such a way that they level.’ There is considerable evidence that inflated respon-
efs, cognitive processes and symptoms sibility is a characteristic that is a central causal feature
erved in individual psychopathologies.
can be objectively meas-
ured (e.g. with question- of obsessive compulsive disorder generally (Salkovskis,
naires) and in many cases manipulated experimentally. Shafran, Rachman & Freeston, 1999; Salkovskis, Wroes,
This then provides an insight into how symptoms are Gledhill, Morrison, Forrester et al., 2000) and compul-
affected by the cognitive factors that clinicians observe in sive checking specifically (Rachman, 2002; Bouchard,
their everyday practice. In Rheaume & Ladouceur, 1999). Experimental studies that
this section we will briefly have manipulated inflated responsibility have shown that
To read the author's blog about
clinical constructs go to look at the role of three it causes increases in perseverative activities such as com-
http://tinyurl.com/k9xx9g2
clinical constructs that have pulsive checking (Lopatka & Rachman, 1995; Bouchard,
helped us to understand Rheaume & Ladouceur, 1999).
OCD. These are inflated responsibility, thought—action fusion,
and mental contamination. A critical view of clinical con- Thought-action fusion It is a common clinical expe-
structs can be found in my blog. rience that many individuals with OCD believe that their
unpleasant, unacceptable thoughts can influence events
Inflated responsibility Everyone experiences uncon- in the world. For example, if they have an intrusive
trollable intrusive thoughts on almost a daily basis thought about an airplane crashing, they believe this may
(Rachman & DeSilva, 1978). However, what differenti- cause an airplane to crash. If they have a thought about
ates these normal intrusive thoughts from the distressing becoming ill, they believe this makes it more likely that
and obsessive thoughts experienced in OCD is the mean- they will become ill. This is known as thought—action
ing attached to them by OCD sufferers. Individuals diag- fusion (TAF) (Shafran & Rachman, 2004), and it is a
nosed with OCD appear to have developed a series of belief that simply having thought-action fusion A dysfunctional
dysfunctional beliefs about their obsessional thoughts. thoughts can in some way assumption held by OCD sufferers that
For example: directly affect what hap- having a thought about an action is like
pens in the world. If the performing it.
1. Because they had the thought, they feel
supposed consequences of thoughts are aversive or nega-
responsible for its content — so, if a sufferer
tive, then this will cause the sufferer to try and suppress
thinks of murdering their child, they believe they
these thoughts (see section below on thought suppres-
may be going crazy and will murder their child
sion), and it will generate considerable distress and
(Salkovskis, 1985).
anxiety. Interestingly, TAF will be related to the degree to
2. Sufferers appraise obsessional thoughts as having which an individual assigns importance to thoughts, and
potentially harmful consequences and this causes this is something that in many cases has been shown to be
intense anxiety and triggers compulsive actions closely related to religiosity. For example, the degree to
designed to eradicate the thought or to make sure which individuals assign importance to thoughts is also
the perceived harm does not occur (e.g. compulsive related to Christian religiosity (Abramowitz, Deacon,
thought suppression strategies such as counting Woods & Tolin, 2004), and Christian groups have been
backwards or checking and re-checking locks and shown to score higher on measures of TAF than other
windows to ensure that the home is safe). religious groups (Siev & Cohen, 2007). However, the
3. Individuals with OCD tend to have inflated relationship between religiosity, TAF and OCD symp-
conceptions of their own responsibility for toms is less straightforward, and recent studies suggest
F822 PSYCHOPATHOLOGY
! ;
30 -/] ] of OCD contamination fear that is caused by quite spe-
cific experiences, it is possible to ameliorate the symp-
toms using adaptations of standard CBT interventions
(Warnock-Parkes, Salkovskis & Rachman, 2012).
Thought suppression Because individuals with

cy . . . .
20
obsessive thoughts find these intrusions aversive and dis-

tressing, they may try to actively suppress them (using
either thought suppression or distraction techniques).
However, there is good thought suppression A defence mecha
About
Thoughts
Tape
Percent evidence that actively sup- nism used by individuals with obsessive
pressing an unwanted thoughts to actively suppress them (usin
thought will actually cause either thought suppression or distraction
: techniques).
it to occur more frequently
Yes No No once the period of suppression or inhibition is over
(Group A) (Group B) (Group C)
(known as a ‘rebound’ effect), and this may account to
Prior Suppression
some degree for the fact that OCD sufferers experience
FIGURE 6.6 After listening to a tape of arecorded story, par- significantly more intrusions than non-clinical popula-
ticipants were then asked to verbalize their stream of conscious tions (Wenzlaff & Wegner, 2000). Wenzlaff, Klein &
thoughts. However, participants in one group (Group A) were Weener (1991) have also argued that suppressing an
asked to suppress their thoughts of the tape during this period, unpleasant thought induces a strong negative emotional
while other participants were not (Groups B and C). In the final state that results in the suppressed thought becoming
period, all participants were asked to think about anything. associated with that negative mood state. Whenever that
The figure shows that participants in the suppression condition negative mood state occurs in the future, it is therefore
subsequently reported more thoughts about the tape than more likely to elicit the unwanted and aversive thought,
participants in the other groups (a ‘rebound effect). and this may also contribute to the OCD sufferer experi-
Source: After Clark, D.M., Ball, S. & Pape, D. (1991). An experimen-
encing regular, uncontrollable intrusions.
tal investigation of thought suppression. Behaviour Research and
Therapy, 29(3), 253-257.
Perseveration and the role of mood OCD is one
that moral TAF translates into OCD symptoms only in example of a number of perseverative psychopatholo-
religious groups for whom the importance of thoughts is gies, each of which is characterized by the dysfunctional
not the norm (Siev, Chambless & Huppert, 2010). perseveration of certain thoughts, behaviours or activi-
ties (others include pathological worrying and chronic
Mental contamination While there are a significant rumination in depression). In almost all examples of
number of OCD sufferers who fear actual contamination these psychopathologies the perseveration (e.g. compul-
(e.g. by contact with dirt, germs, and suchlike), there is sive checking, washing) is viewed as excessive, out of pro-
also another group for whom comparable feelings of portion to the functional purpose that it serves, and a
dirtiness can be provoked without any physical contact source of emotional discomfort for the individual con-
with a contaminant, and this has come to be called men- cerned. In this context, some theories have attempted to
tal contamination (Rachman, 2004, 2006). Mental con- explain why OCD sufferers persevere at an activity for sig-
tamination can be caused by images, thoughts, and nificantly longer than non-sufferers. One such account is
memories, and tends to be the mood-as-input hypothesis (Meeten & Davey, 2011;
mental contamination Feelings of dirti-
ness can be provoked without any physical
caused by a violation of Davey, 2006; MacDonald & mood-as-input hypothesis A hypothesis
contact with a contaminant. Mental some kind by another per- Davey, 2005a). This model claiming that people use their concurrent -
contamination can be caused by images, son, such as degradation, states that OCD sufferers mood as information about whether they
thoughts, and memories and may be asso- betrayal, emotional abuse, persevere with their com- have successfully completed a task or not.
ciated with compulsive washing and even
physical abuse or humilia- pulsive activities because (1) they use an implicit ‘stop
betrayal experiences.
tion, which gives rise to rule’ for the compulsive activity which says they must
feelings of dirtiness or pollution, and in many cases may only stop when they are sure they have completed the
be associated with compulsive washing or cleansing task fully and properly (known as an ‘as many as can’ stop
(Rachman, 2010; Zhong & Liljenquist, 2006). In addition rule); and (2) they undertake the task in a strong negative
to these feelings of contamination, individuals also expe- mood (usually an anxious mood). The mood-as-input
rience anxiety, disgust, shame, anger, guilt, and sadness account claims that OCD sufferers use their concurrent
(Rachman, Radomsky, Elliot & Zysk, 2012). While men- mood as ‘information’ to assess whether they have met .
tal contamination seems to represent a very specific form their strict stop rule criteria. However, their endemic
ra)
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS oes
negative mood is interpreted as providing information prevention, which involves g¢#@™°"™="===""

; mae & For a video on exposure treatment for
that they have not completed the task properly — so they strategies such as practising | phobias go to
persevere (i.e. a negative mood implies all is not well and competing behaviours, | www.wiley-psychopathology.com/
the criteria have not been met). This model is supported habit reversal, or modifica- video/ch6
by the fact that the inflated responsibility that OCD suf- tion of compulsive rituals
ferers possess is likely to give rise to deployed ‘as many as (again, see Treatment in Practice Box 6.6). Preventing the
can’ stop rules (to ensure that, for example, checking or client from engaging in their rituals:
washing is done properly so that no harm will ensue).
Interestingly, and consistent with the mood-as-input 1. Allows anxiety to extinguish by habituating the
account, inflated responsibility is not a sufficient condition links between obsessions and their associated
for an individual to persevere at a compulsive activity — it distress;
has to be accompanied by negative mood (MacDonald & 2. Eliminates ritualistic behaviours that may
Davey, 2005b). This is because a negative mood is con- negatively reinforce anxiety (Steketee, 1993);
tinually being interpreted as providing feedback that the 3. Contributes to the disconfirmation of
important goals of the compulsive activity have not been dysfunctional beliefs (e.g. ‘I will catch an
met, so the activity needs to be continued. infectious disease if I touch a dirty cup’) by
forcing the client to encounter feared situations
Summary As we mentioned at the outset of this sec- and experience the reality of the outcomes
tion on aetiology, many of these theories are designed to associated with that action.
address only specific features of OCD rather than repre-
sent universal explanations of the disorder. For example, ERP is a highly flexible therapy that can be adapted to
some theories try to explain why ‘doubting’ is a central group, self-help, inpatient, outpatient, family therapy, and
feature of OCD (these include both neurophysiologi- computer-guided interventions (Fischer, Himle & Hanna,
cal and memory deficit models), others address why 1998; Grayson, 1999; Wetzel, Bents & Florin, 1999; Hand,
intrusive thoughts become so aversive and uncontrolla- 1998; Grunes, 1999; Nakagawa, Marks, Park Bachofen
ble (e.g. inflated responsibility and thought suppression et al., 2000). Controlled outcome studies suggest that
accounts), and yet others try to explain why individuals ERPisalong-term effective _..
with OCD show dysfunctional perseveration at activi- treatment for around 75 For a video on obsessive compulsive
ties such as checking or washing (e.g. the mood-as-input per cent of clients treated disorder go to
model). Undoubtedly, a full account of OCD will contain with ERP (Franklin & Foa, | video/ché
at least some, if not all, of these different elements of 1998; Kyrios, 2003).
explanation.
Cognitive behaviour therapy (CBT)

6.5.2 The Treatment of Obsessive Although ERP has been the treatment of choice for OCD
Compulsive Disorder for over 20 years, it is often a difficult treatment for many
sufferers to enter. This is because sufferers may feel una-
Exposure and ritual prevention (ERP) ble to expose themselves to their fear triggers and find it
treatments impossible to prevent themselves acting out their rituals.
The most common, and arguably the most successful, As many as 30 per cent of clients drop out of ERP before
therapy for OCD is exposure and ritual prevention treat- completing treatment (Wilhelm, 2000). An alternative
ment (also known as exposure and response prevention form of therapy for such individuals is cognitive behav-
treatment) (Meyer, 1966; iour therapy (CBT) based on targeting and modifying
yosure and ritual prevention treat- Kyrios, 2003). This therapy the dysfunctional beliefs that OCD sufferers hold about
nt A means of treatment for obsessive
npulsive disorder (OCD) which involves
consists of two compo- their fears, thoughts, and the significance of their rituals
ded exposure to the thoughts that trig- nents. The first is graded (Abramowitz, Brigidi & Roche, 2001; Salkovskis, 1999;
distress, followed by the development exposure to the situations Wilhelm, 2000; Marks, 2003; see the section ‘Inflated
yehaviours designed to prevent the and thoughts that trigger responsibility’ above). Dysfunctional beliefs that are usu-
ividual’s compulsive rituals.
distress — e.g. for someone ally challenged in cognitive therapy for OCD include:
with compulsive washing this may involve touching a
dirty dish or imagining touching a dirty dish (the latter is ¢ responsibility appraisals, where the sufferer believes
called imaginal exposure) (see Treatment in Practice they are solely responsible for preventing any
Box 6.6). Clients will encounter their triggers in a graded harmful outcomes;
and planned way until distress levels have significantly ¢ the over-importance of thoughts, where sufferers
decreased. The second component is ritual or response believe that having a thought about an action
Pisa PSYCHOPATHOLOGY

EXPOSURE HIERARCHIES AND RESPONSE PREVENTION IN ERP TREATMENTS OF OCD
Arguably the most effective therapies for OCD are expo- regime for fear of contamination from germs, and dis-
sure and ritual prevention treatments (ERP) (see sec- tressing thoughts about sexual abuse. Table 2 provides
tion 6.5.2). Table 1 gives examples of a graded exposure some examples of response prevention techniques.
Table 1
Example 1: Fear of contamination Example 2: Teacher's distressing intrusive thoughts about sexually abusing
(distress level/100) students (distress level/100)
tle Touch rim of own unwashed le Watch video or listen to audio tape of expert discussing sexual abuse of
coffee cup (30) children (40)
2. Touch rim of partner’s unwashed 2. Listen to tape of expert while looking at class photo (50)
coffee cup (40)
3. Eat snack from dish in cupboard 3. Listen to loop tape of own distressing thoughts about sexually abusing
after touching partner's unwashed students in general (60)
coffee cup (45)
4. Drink water from partner's glass (55) 4. Listen to loop tape about students in general looking at class photo (65)
5. Eat snack straight from unwashed 5. Listen to loop tape ofdistressing thought about sexually abusing specific
table top (65) student (70)
6. Have coffee at a café (70) 6. Listen to loop tape about specific student looking at class photo (75)
7. Have meal at a restaurant (80) 7. Listen to loop tape holding specific student’s homework (80)
8. Touch toilet seat at home without 8. Stand in front of class repeating statement on loop tape to self (90)
washing hands for 15 minutes (85)
9. Touch toilet seat at home without 9. Stand close to specific student repeating statement on loop tape to self (95)
washing hands for 30 minutes (90)
10. Using public toilet (100) 10. Stand next to specific student repeating statement on loop tape to self (100)
Table 2
OCD Symptom Response Prevention Strategy
Hand-washing or cleaning rituals Response delay (i.e. extending period between ‘contamination’ and cleaning or
washing); use of ritual restrictions (e.g. decreasing cleaning or washing time);
clenching fists; extension strategies to undermine avoidance (e.g. touch self,
clothes, and suchlike)
Checking lights, switches, oven, appli- Response delay; use of ritual restrictions (e.g. restrict number of checks); turning
ances, and so on and walking away; extension strategies (whistle a happy tune)
Counting (e.g. bricks, words) Refocusing techniques; singing a song; going ‘blank’; meditation
Source: Kyrios, M. (2003). Exposure and response prevention for OCD. in R.G. Menzies & P. de Silva (Eds.) Obsessive-compulsive disorder:
Theory, research and treatment. Chichester: John Wiley & Sons. Reproduced with permission.
is like performing the action (thought—action An integrated cognitive therapy for OCD would thus
fusion) (see Treatment in Practice 6.6); consist of:
° exaggerated perception of threat, where the * educating clients that intrusive thoughts are
sufferer has highly inflated estimates of the quite normal, and that having a thought about
likelihood of harmful outcomes (Van Oppen & an action is not the same as performing it
Arntz, 1994). (Salkovskis, 1999);
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS BS?
¢ focusing on changing the client’s abnormal risk effect on dysfunctional brain circuits. Tricyclic antidepres-
assessment — perhaps by working through the sants can have beneficial effects across some specific
probabilities associated with feared outcomes symptoms of OCD (such as reducing the persistence and
(Van Oppen & Arntz, 1994); frequency of compulsive rituals), but seem to have their
* providing the client with behavioural exercises effect only when OCD is comorbid with depression
that will disconfirm their dysfunctional beliefs (Hohagen, Winkelmann, Rasche-Ruchle, Hand et al.,
(e.g. a client who fears shouting out blasphemous 1998). Comparative studies have suggested that both
thoughts in church would be asked to go to SSRIs and tricyclic drugs are less effective than standard
church and see if this happens) (Salkovskis, 1999). psychological therapies such as exposure and ritual pre-
vention (ERP) (Rauch & Jenike, 1998; Greist, 1998). In
general, ERP is equally as effective as drug treatments in
Pharmacological and neurosurgical the short term, free from physical and psychological side
treatments effects, and associated with greater long-term gains
Pharmacological treatments have proved to be a short- (Greist, 1998; Marks, 1997). When pharmacological and
term, effective and cheap way of treating OCD, although psychological treatments have failed, neurosurgery has
relapse tends to be common on discontinuation of the become an intervention of last resort in OCD. The most
drug treatment (McDonough, 2003; Pato, Zohar- common procedure is cingulotomy, which involves
Kadouch, Zohar & Murphy, 1988). Serotonin and selec- destroying cells in the cingulum, close to the corpus cal-
tive serotonin reuptake inhibitors (SSRIs) are the most losum. These treatments cingulotomy A neurosurgical treatment
commonly prescribed drug and have the effect of increas- do report some improve- of OCDinvolving destroying cells in the
ment in OCD symptoms cingulum, close to the corpus callosum.
ing brain serotonin levels (see section 4.1.1). However,
there is still no consensus view on a model of serotonin (Dougherty, Baer, Cosgrove, Cassem et al., 2002), but
dysfunction in OCD (Delgado & Moreno, 1998), and it there is a lack of evidence on the longer term gains of
has been suggested that the beneficial effects of SSRIs neurosurgical treatments and their possible side-effects
may be restricted simply to its nonspecific ameliorative (McDonough, 2003).
SELF-TEST QUESTIONS
® Can you describe what obsessions and compulsions are, and provide some examples of each?
© How have biological theories attempted to explain the obsessions and compulsions found in OCD?
© How does the construct of inflated responsibility help to explain how OCD is acquired and maintained?
® What are the similarities and differences between exposure and ritual prevention treatment (ERP) and cognitive behaviour
therapy (CBT) for OCD?
SECTION SUMMARY
6.5 OBSESSIVE COMPULSIVE DISORDER (OCD)
© OCD is characterized by either obsessions, which are intrusive and recurring thoughts that the individual finds disturbing
and uncontrollable, or compulsions, which are ritualized behaviour patterns that the individual feels driven to perform in
order to prevent some negative outcome happening.
* Common compulsions include washing, checking, and the systematic arrangement of objects. Related compulsions
include hoarding, hair-pulling (trichotillomania) and skin-picking.
¢ OCD onset is usually gradual and has a lifetime prevalence rate of around 2.5 per cent.
© Biological theories of OCD argue that there may be neurological deficits underlying OCD which either give rise to the typical
‘doubting’ behaviour common in the disorder, or result in an inability to inhibit certain behaviour patterns (such as checking).
© OCD tends to be associated with a number of dysfunctional beliefs, and the most prominent is the sufferer’s inflated con-
ception of their own responsibility for preventing harm, and this ‘inflated responsibility’ appears to be an important vulner-
ability factor in developing OCD.
6 4 PSYCHOPATHOLOGY
® Exposure and ritual prevention (ERP) treatments are the most common, and arguably the most successful, means of treat-
ment for OCD. These involve graded exposure to the thoughts that trigger distress, followed by the development of behav-
iours designed to prevent the individual's compulsive ritual.
® Pharmacological treatments for OCD can also be effective (e.g. serotonin and selective serotonin reuptake inhibitors), and
psychosurgery is sometimes a treatment of last resort (e.g. cingulotomy).
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precipitating cause is a traumatic experience has led to

6.6 TRAUMA AND STRESS- PTSD being placed in its own broader diagnostic cate-
RELATED DISORDERS gory (Friedman, Resick, Bryant, Strain et al., 2011).
In this section we will explore trauma and stress-related Diagnosis and prevalence of trauma and
disorders. In DSM-5 these forms of disorder are now stress-related disorders
listed separately from anxiety disorders, but the major The DSM diagnostics criteria for PTSD and acute stress
diagnostic category in this section remains post- disorder are provided in DSM-5 Summary Table 6.8
post-traumatic stress disorder (PTSD)
traumatic stress disorder and 6.9. PTSD is one of the few disorders in DSM-5 in
A set of persistent anxiety-based symp- (PTSD). There is still con- which the cause of the disorder is a defining factor.
toms that occurs after experiencing or siderable debate about In this case, diagnosis of PTSD is considered only if the
witnessing an extremely fear-evoking or whether PTSD should be individual has experienced an extreme trauma prior
life-threatening traumatic event.
considered an anxiety dis- to symptoms. They may have (1) directly experienced
order, a stress-induced fear response, a dissociative the trauma (e.g. been involved in a natural disaster
disorder (see Chapter 14), or a trauma and stressor- such as an earthquake or fire, or been subjected to life-
related disorder, but acknowledgement that its primary threatening physical abuse such as rape), (2) witnessed a

POST-TRAUMATIC STRESS DISORDER
‘| thought | was over it. Just when | think I’m getting bet- what Ill do, and | know they just want me to move on. |
ter and don't have to worry about it anymore, something wish | could but |just can’t see a way out!
will trigger a memory and I'll be right back there again.
Sometimes it’s just a feeling | have, and other times I'll see
something that reminds me of what happened and it feels Clinical Commentary
like it’s happening all over again. It’s been almost a year This description is typical of many PTSD suffer-
now and I’m seeing a therapist three times a week as well ers and highlights feelings of depression, lack of
as taking antidepressants. | can have good days - maybe control and anger. Some theories of PTSD (such
two or three in a row - then my mood will get worse and as ‘mental defeat’) emphasize that those who
the blackness will come back. It feels as if my thoughts develop PTSD after a severe trauma tend to view
aren't my own and my mind is somewhere else while my themselves as a victim, process all information
body is just going through the motions. Every time the about the trauma negatively, and view them-
black moods come it feels harder and harder to get back selves as unable to act effectively. Such individu-
from them. It makes me so angry when | feel like this and als believe they are unable to influence their own
my mind becomes full of violent thoughts; this rage takes fate and do not have the necessary skills to pro-
over and | can’t control it. I’m scared of what | might do tect themselves from future trauma. Ehlers & Clark
when I'm feeling this angry. |don’t want to tell my friends (2000) suggest that such individuals only partially
» or family about process their memory of the trauma because of
For a video on post-traumatic \ what I'm think- their perceived lack of control over it, and so they
stress disorder go to | ing because they do not integrate that event fully into their own
video/ch6 |: might be fright- autobiographical knowledge.
mete SEVNEO MOCO Or
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS 187:
DSM-5 SUMMARY TABLE 6.8 Criteria for diagnosing post- DSM-5 SUMMARY TABLE 6.9 Criteria for the diagnosis of acute
traumatic stress disorder stress disorder
¢ The individual has been exposed to or threatened with The individual has been exposed to or threatened with death,
death, serious injury or sexual violation: by direct experi- serious injury or sexual violation: by direct experience or by wit-
ence or by witnessing a traumatic event; upon learning nessing a traumatic event; upon learning about a violent or acci-
about a violent or accidental death of a close friend or dental death of a close friend or family member; or by extreme
family member; or by extreme or repeated exposure to the or repeated exposure to the effects of a traumatic event. At least
effects of a traumatic event, such as emergency workers nine of the following symptoms will be displayed:
encountering human remains
e Recurrent, intrusive and involuntary memories of the
¢ Intrusive symptoms associated with the traumatic event traumatic event
will be experienced, such as: disturbing dreams or feeling
e Repeated distressing dreams related to the traumatic
that the event is recurring while awake; uncontrolled
event, or feeling that the event is recurring while awake
memories of the event; extreme physical reactions or
mental distress upon being reminded of the trauma e Extreme physical reactions or mental distress upon being
reminded ofthe trauma
e Individuals will avoid internal and/or external reminders of
the trauma e Numbness or detachment from others
e Atleast two changes to mood or thought processes e Changes in the individual’s sense of reality and an altered
will occur, such as: feelings of disconnection; continual perspective of oneself or one’s surroundings
negative emotions and ongoing difficulty in experiencing
e Difficulty in remembering aspects of the traumatic event
positive emotions; extreme and disproportionate negative
expectations; reduced interest in activities; being unable e Avoidance of internal and/or external reminders of the trauma
to remember certain aspects of the traumatic event e Difficulties in sleeping
e Changes to reactive behaviour will occur, and individuals e Hypervigilance
will display two or more of the following symptoms: reck-
lessness, aggression, hypervigilance, inability to concen- e Irritability or aggression
trate, difficulty sleeping, an exaggerated startle response e Difficulty in concentrating
e Symptoms began or worsened after the traumatic event(s) e Exaggerated startle response
and continued for at least 1 month, causing significant
difficulty in functioning Symptoms may begin within 3 days to 1 month of the trauma
taking place and will persist for at least 3 days or up to 1 month
e Symptoms cannot be explained by the effects of other
mental or medical disorders, drug abuse or medication Symptoms cannot be explained by the effects of other men-
tal or medical disorders, drug abuse or medication
Symptoms cause difficulties in performing important func-
traumatic event in which others may have suffered (e.g. tions and cause clinically significant distress
witnessing the 9/11 terrorist attacks on New York),
(3) learnt that a severe traumatic event has happened to
a close family member or friend, or (4) been subjected substance abuse, suicidal thoughts, and stress-related
repeatedly to distressing details of trauma (e.g. the kind violence (Jacobsen, Southwick & Kosten, 2001; Zatzick,
of regular exposure to details of trauma that might be Marmer, Weiss, Browner et al., 1997; Hobfoll, Spielberger,
experienced by police officers or emergency workers). Breznitz, Figley et al., 1991), as well as suicidal thoughts
The symptoms typical of PTSD are grouped into (Bernal, Haro, Bernert, Brugha et al., 2007) and self-harm
four categories. These are (1) intrusive symptoms such (Weierich & Nock, 2008). The kinds of traumatic events
as flashbacks, intrusive thoughts, or physiological reac- that precipitate PTSD are often life-threatening in their
tions, (2) avoidance responding such as active avoidance of severity. Studies suggest that PTSD symptoms are devel-
thoughts, memories or reminders of the trauma, (3) nega- oped by up to 90 per cent of rape victims (Rothbaum,
tive changes in cognition and mood such as persistent fear, Foa, Riggs, Murdock et al., 1992), between 70 and 90 per
horror, anger, guilt or shame, persistent negative beliefs cent of torture victims (Moisander & Edston, 2003), over
about themselves, others or the world (e.g. ‘no one can 50 per cent of prisoners of war (Engdahl, Dikel, Eberly
be trusted’, ‘I’ve lost my soul for ever’), or dissociative & Blank, 1997), between 20 and 25 per cent of earth-
feelings of detachment or estrangement from others, and quake and flood survivors (Basoglu, Kilic, Salcioglu &
(4) increased arousal and reactivity such as hypervigilance Livanou, 2004; North, Kawasaki, Spitznagel & Hong,
and exaggerated startle responses. Once symptoms 2004), and around 15 per cent of motor vehicle accident
develop, PTSD is often a chronic condition that can last victims (Bryant & Harvey, 1998). DSM-5 also emphasizes
for years (Perkonigg, Pfister, Stein, Hofler et al., 2005). that PTSD symptoms can be acquired in cases where
It is also associated with depression, guilt, shame, anger, the stressor has not been life-threatening to the sufferer
marital problems, physical illness, sexual dysfunction, (e.g. suffering PTSD after the loss of a loved one), or has
188 PSYCHOPATHOLOGY
+ ~
involved simply viewing stressful images of life-threaten- shifting significantly towards that of PTSD, it remains to
ing traumas (e.g. watching images of the 9/11 terrorist be seen whether fewer post-trauma survivors are diag-
attacks on TV — Piotrowski & Brannen, 2002), and this nosed with ASD as were with DSM-IV-TR criteria.
extension of the diagnostic criteria for PTSD has gener-
ated controversy, either because it makes the symptoms of
PTSD easier to fake in those who might benefit financially 6.6.1 The Aetiology of Post-
from a diagnosis (Rosen, 2004), or because it confuses Traumatic Stress Disorder (PTSD)
PTSD with merely experiencing stress (McNally, 2003a).
The lifetime prevalence rate for PTSD is between 1 and The diagnostic criteria for PTSD specify either a life-
3 per cent (Helzer, Robins & McEvoy, 1987). However, prev- threatening trauma or severe stress as a causal factor in
alence rates are significantly higher for groups who are at the disorder. However, not everyone who has these kinds
risk of experiencing severe trauma. These include a 12-33 of experiences develops PTSD. This is the main challenge
per cent prevalence rate for civilians living in war zones for any theory of the aetiology of PTSD — why do some
(Farhood & Dimassi, 2012; Charlson, Steel, Degenhardt, people develop PTSD symptoms after these experiences,
Chey et al., 2012), 10 per cent for rescue workers (Berger, but not others? The answer must lie either in psychologi-
Coutinho, Figueira, Marques-Portella et al., 2012), and 13.2 cal or biological vulnerability factors, or in the psychologi-
per cent for members of operational infantry in the recent cal strategies that individuals have developed to deal with
Iraq and Afghanistan conflicts (Kok, Herrell, Thomas & events like trauma and stress (e.g. differences in learnt
Hoge, 2012). Around 50 per cent of adults experience coping strategies). Also, because PTSD has many different
at least one event in their lifetime that might qualify as a symptom features, some theories address specific features
PTSD-causing trauma (Ozer & Weiss, 2004). Following such of the symptomatology (e.g. the flashbacks), and others
events, women are significantly more likely than men to address the time course of the disorder and how it is emo-
develop PTSD (by a factor of 2.4:1), and this is not explained tionally experienced (Brewin & Holmes, 2003). We will
simply by differences in the perceived threat to life from the explore these various possibilities below when we look at
experience (Holbrook, Hoyt, Stein & Sieber, 2002). Apart some of the main models of the aetiology of PTSD.
from gender differences in prevalence rates, there is also
some emerging evidence on the role that cultural variables Biological factors
play in PTSD. Ethnic groups can differ quite significantly in Studies carried out on war veterans have suggested that
the prevalence of PTSD — Caucasian disaster victims show PTSD has a genetic element to it, and a heritability compo-
lower prevalence rates than Latinos or African Americans — nent of 30 per cent has been estimated (True, Rice, Eisen,
and these differences cannot be entirely explained simply Heath et al., 1993). This has led some to suggest that PTSD
by differences in the frequency of exposure to traumatic develops as a result of gene x environment vulnerability
experiences (Perilla, Norris & Lavizzo, 2002; Norris, Perilla, factors interacting, and the combination of an extreme
Ibanez & Murphy, 2001). The fact that around 50 per cent of trauma experience and a genetic predisposition to PTSD
the population will experience at least one event in their life are required to generate PTSD symptoms (Mehta & Binder,
that could be classified as a PTSD-relevant trauma means 2012). What the biologically conferred vulnerability factor
that many people experience trauma but do not develop might be is still as yet unclear. Some possibilities are:
PTSD. It is understanding these individual differences in
susceptibility to PTSD that will give us some insight into 1. A relatively small or under-developed
the mechanisms that give rise to PTSD. hippocampus. The hippocampus is that
The symptoms of acute stress disorder (ASD) are very region of the brain that plays a critical role in
similar to those of PTSD, but the duration is much shorter memories related to emotion, and studies have
(3 days to 1 month after indicated that this region is significantly smaller
acute stress disorder (ASD) A short-term
psychological and physical reaction to trauma exposure). DSM-5 in individuals who develop PTSD (Bremner,
severe trauma. Symptoms are very similar criteria have been explicitly Vythilingam, Vermetten, Southwick et al., 2003)
to those of PTSD, but the duration is much
modified to make ASD and a smaller hippocampus represents a real risk
shorter (3 days to 1 month after trauma
symptoms much more factor for the development of PTSD following
exposure).
compatible with PTSD, and a traumatic experience (Gilbertson, Shenton,
so ASD may well be a diagnostic category that predicts Ciszewski, Kasal et al., 2002).
subsequent PTSD — but that remains to be determined. 2. Failure of brain centres such as the ventromedial
There has been some prior debate about whether ASD frontal cortex to dampen activation of the brain’s
actually represents a psychological disorder as such, or fear coordinating centre, the amygdala (Koenigs
whether it is a normal short-term psychological and physi- & Grafman, 2009), which means that the
cal reaction to severe trauma (Harvey & Bryant, 2002). individual is unable to control the activation of
However, with the diagnostic criteria for ASD in DSM-5 fear following trauma.
CHAPTER6 ANXIETY AND STRESSOR-RELATED PROBLEMS 189 —
3. Genetically endowed heightened startle responses for coping or confronting painful or stressful memories.
and fear-relevant endocrine secretion (Broekman, In particular, dissociation seems to be an important risk
Olff & Boer, 2007; Segman & Shalev, 2003). factor for PTSD. Individuals who experience dissociation
either just before or during the trauma are more likely to
Vulnerability factors develop PTSD (Ehlers, Mayou & Bryant, 1998); using dis-
As not everyone who experiences a life-threatening trauma sociation as a coping strategy after the trauma, they are at
develops PTSD, there must be factors that make some risk of chronic long-term PTSD symptoms (Briere, Scott
people more vulnerable than others. A number of factors & Weathers, 2005). Dissociative symptoms immediately
have been identified that characterize those individuals after rape also predict the development of PTSD (Brewin
likely to develop PTSD after trauma, which include: & Holmes, 2003). (See section 14.1.2 for a discussion of the
relationship between PTSD and dissociative experiences.)
e A tendency to take personal responsibility for the
traumatic event and the misfortunes of others Conditioning theory
involved in the event (Mikhliner & Solomon, 1988); Because there is always an identifiable traumatic experi-
¢ Developmental factors such as early separation ence in the history of PTSD, it is quite reasonable to sup-
from parents or an unstable family life during early pose that many of the symptoms of PTSD may be due
childhood (King, King, Foy & Gudanowski, 1996); to classical conditioning (see section 1.3). That is, trauma
(the unconditioned stimulus, UCS) becomes associated at
¢ A family history of PTSD (Foy, Resnick, Sipperelle &
the time of the trauma with situational cues associated
Carroll, 1987);
with the place and time of the trauma (the conditioned
e Existing high levels of anxiety or a pre-existing stimulus, CS) (Keane, Zimering & Caddell, 1985). When
psychological disorder (Breslau, Davis, Andreski these cues (or similar cues) are encountered in the future,
et al., 1997). they elicit the arousal and fear that was experienced dur-
ing the trauma. For example, seeing a pile of bricks on the
Interestingly, low intelligence is also a vulnerability factor ground may elicit strong arousal, fear and startle responses
(Vasterling, Duke, Brailey et al., 2002), and high IQ is the for an earthquake survivor, because such cues had become
best predictor of resistance to the development of PTSD associated with the fear experienced during the traumatic
(Silva, Alpert, Munoz et al., 2000). This may be because earthquake experience. The conditioning model would
there is a link between IQ level and the development of further argue that such conditioned fear responses do not
coping strategies to deal with experienced trauma or extinguish because the sufferer develops both cognitive and
stress. Other important predictors of PTSD development physical avoidance responses which distract them from
are the experiences reported by trauma victims at the fully processing such cues and therefore does not allow the
time of the trauma. These include the reporting of disso- associations between cues and trauma to extinguish. The
ciative symptoms at the time of the trauma (see below), reduction in fear resulting from these avoidance responses
and a belief that one is about to die (McNally, 2003b). reinforces those responses and maintains PTSD symptoms.
These types of experiences may be important in that they There is probably an element of classical conditioning in
may relate to how the individual processes and stores the development of PTSD, largely because formally neu-
information about the trauma at the time, and this is tral cues do come to elicit PTSD symptoms. There is also
important in some specific theories of PTSD symptoms. evidence that individuals suffering PTSD will more readily
develop conditioned responses in laboratory-based experi-
Avoidance and dissociation ments than non-sufferers (Orr, Metzger, Lasko, Macklin
After any distressing and traumatic experience, how the et al., 2000). However, classical conditioning does not pro-
individual copes with that experience will be critical to vide a full explanation of PTSD. It does not explain why
the subsequent psychological health. One coping style some individuals who experience trauma develop PTSD
that is not conducive to a beneficial outcome is avoid- and others do not, and it cannot easily explain the range
ance coping, and individuals who avoid thinking about of symptoms peculiar to PTSD but rarely found in other
their trauma are more likely to develop PTSD following a anxiety disorders, such as re-experiencing symptoms, dis-
traumatic experience (Sharkansky, King, King, Wolfe et al., sociative experiences, and so on.
2000). One psychological process that seems to be used to
enable individuals to detach and distance themselves from Emotional processing theory
trauma is dissociation (see Chapter 14). Dissociation is the Foa, Steketee & Rothbaum (1989) have suggested that the
feeling that one is detached from both mind and body, intense nature of the trauma in PTSD creates a represen-
and is associated with an inability to recall important per- tation of the trauma in memory that becomes strongly
sonal information of a stressful nature. In the context of associated with other contextual details of the event (e.g.
PTSD, dissociation may represent an avoidant strategy if a person has been badly injured in a serious traffic
vison: PSYCHOPATHOLOGY
+ *
accident, cues to do with roads, cars, hospitals, and even This negative approach to the traumatic event and its con-
travelling generally will come to selectively activate the sequences simply adds to the distress, influences the way
fear network in memory). The avoidance of any contexts the individual recalls the trauma, and may give rise to mal-
that might activate this fear network means that there is adaptive behavioural and cognitive strategies that main-
little opportunity for the PTSD sufferer to weaken these tain the disorder. In effect, these individuals believe they
associations between fear and the everyday cues that will are unable to influence their own fate and do not have the
activate that fear. This account has elements in common necessary skills to protect themselves from future trauma.
with classical conditioning models of PTSD, but it differs Ehlers & Clark (2000) suggest that such individuals only
in some significant ways. Firstly, emotional processing partially process their memory of the trauma because of
theory claims that severe traumatic experiences are of their perceived lack of control over it, and so they do not
such major significance to the individual that they lead to integrate that event fully into their own autobiographical
the formation of represen- knowledge. This leads to symptoms such as re-experienc-
emotional processing theory Theory
that claims that severe traumatic experi- tations and associations in ing the trauma in the present (outside of a temporal con-
ences are of such major significance to an memory that are quite dif- text), difficulty in recalling events from the trauma, and
individual that they lead to the formation ferent from those formed dissociation between the experience of fear responses and
of representations and associations in
as a result of everyday their meaning. The ‘mental defeat’ model is supported by
memory that are quite different to those
formed as a result of everyday experience. experience. For example, if evidence suggesting that PTSD sufferers do indeed have
severe trauma has become negative views of the self and the world, including nega-
associated with certain cues (e.g. after being assaulted in tive interpretations of the trauma (Dunmore, Clark &
an alleyway), this experience will now override any other Ehlers, 1999), negative interpretations of PTSD symptoms
positive associations formed as a result of previous experi- (Clohessy & Ehlers, 1999; Mayou, Bryant & Ehlers, 2001),
ence with that cue (the alleyway). Secondly, severe trauma negative interpretations of the responses of others
not only results in cues eliciting very strong fear responses, (Dunmore, Clark & Ehlers, 1999), and a belief that the
it also changes the individual’s previous assumptions trauma has permanently changed their life (Dunmore,
about how safe the world is, so many more cues than pre- Clark & Ehlers, 1999; Ehlers, Maercker & Boos, 2000).
viously will come to elicit responses related to fear, startle
and hypervigilance (Foa & Rothbaum, 1998).
The emotional processing theory is an example of those Dual representation theory
theories of PTSD that have attempted to include explana- A rather different approach to explaining PTSD, called dual
tions about how fear responses are learnt, stored and trig- representation theory, is that it may be a hybrid disorder
gered, and about how the traumatic event changes the consisting of the involve- dual representation theory An appro
individuals assumptions and beliefs about themselves and ment of two separate mem- to explaining post-traumatic stress
the world. These types of theories have come to be known ory systems (Brewin, 2001; disorder (PTSD) suggesting that it may b
as information-processing models because they specify Brewin, Dalgleish & Joseph, a hybrid disorder involving two separate
memory systems.
how fear memories are laid down and activated in fear net- 1996). The verbally accessible
works. They have also given rise to some successful thera- memory (VAM) system registers memories of the trauma
peutic procedures for PTSD which address how the fear that are consciously processed at the time. These memo-
network resulting from traumatic experience can be modi- ries are narrative in nature and contain information about
fied (Foa & Rothbaum, 1998). In addition, this account of the event, its context, and personal evaluations of the expe-
PTSD has been elaborated more recently to take account rience. They are integrated with other autobiographical
of the fact that individuals who prior to the trauma have memories and can be readily retrieved. The situationally
relatively fixed views about themselves and the world are accessible memory (SAM) system, however, records informa-
actually more vulnerable to PTSD (Foa & Riggs, 1993). tion from the trauma that may have been too brief to
apprehend or take in consciously, and this includes infor-
Mental defeat mation about sights and sounds, and extreme bodily reac-
Ehlers and Clark (2000) have suggested that there is a spe- tions to trauma. The SAM system is thus responsible for
cific psychological factor that is important in making an the vivid, uncontrollable flashbacks experienced by PTSD
individual vulnerable to PTSD. This is a specific frame of sufferers which are difficult to communicate to others
mind called mental defeat, in which the individual (because these memories are not stored in a narrative
sees themselves as a victim: form). There is good neuropsychological evidence for the
mental defeat A specific frame of mind in
which the individual sees themselves as a
they process all informa- existence of these two separate memory systems and their
victim. This is a psychological factor that is tion about the trauma neg- links with the brain centre associated with fear (the amyg-
important in making an individual vulner- atively, and view themselves dala) (Brewin, 2001). There is also evidence that is consist-
able to PTSD. as unable to act effectively. ent with predictions from the dual representation theory.
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS fot
For example, Hellawell & Brewin (2004) found that, when may all be equally effective in treating PTSD symptoms
describing their memories, PTSD sufferers characterized (Benish, Imel & Wampold, 2008).
flashback periods with greater use of detail, particularly
perceptual detail, by more mentions of death, more use of Psychological debriefing
the present tense, and more mention of fear, helplessness, Over the past 20 years or so there has been a growing
and horror. In contrast, ordinary memories were charac- belief amongst mental health professionals that PTSD
terized by more mention of secondary emotions such as can be prevented by immediate and rapid debriefing of
guilt and anger. These findings are consistent with the view trauma victims within 24-72 hours after the traumatic
that flashbacks are the result of sensory and response infor- event (Caplan, 1964; Bisson, 2003). The exact form of
mation stored in the SAM system. the intervention can vary, with the most widely used
techniques referred to as crisis intervention or critical
incident stress management (CISM) (Everly, Flannery
Summary & Mitchell, 2000). The purpose of these interventions
Once again, it is clear that PTSD has a number of differ- is to reassure the participants that they are normal
ent features, each of which requires explanation. Some people who have experienced an abnormal event, to
theories have tried to explain some of the specific features encourage them to review what has happened to them,
of PTSD (such as dual representation theory’s attempt to express their feelings about the event, and to discuss
to explain specific features such as flashbacks), while oth- and review support and coping strategies in the imme-
ers have tried to identify the dispositional features that diate post-trauma period. Psychological debriefing
make some individuals vulnerable to developing PTSD has been used with survi- psychological debriefing A structured
while others do not (e.g. mental defeat). Others attempt vors, victims, relatives, way of trying to intervene immediately
to describe why severe trauma causes the symptoms that emergency care workers, after trauma in order to try to prevent the
it does, and why these anxiety-based symptoms persist and providers of mental 4¢velopment
ofPTSD.
for such long periods (e.g. conditioning theory and emo- health care (Bisson, 2003). The scale of this type of
tional processing theory). intervention can be gauged by reactions to the terrorist
attacks on the World Trade Center on September 11,
2001, when more than 9000 counsellors went to
6.6.2 The Treatment of Post- New York to offer immediate aid to victims and fami-
lies of the attack (McNally, Bryant & Ehlers, 2003).
Traumatic Stress Disorder
Critical incident stress debriefing includes a number of
The treatment of PTSD has two main aims. The first is components, including:
to try to prevent the development of PTSD after an indi-
vidual has experienced a severe trauma. The second is to ¢ explanation of the purpose of the intervention
treat the symptoms of PTSD once these symptoms have ¢ asking participants to describe their experiences
developed. Rapid psychological debriefing has usually ¢ discussion of the participant’s feelings about the
been the accepted way of trying to intervene immedi- event
ately after trauma in order to try to prevent the devel-
e discussion of any trauma-related symptoms the
opment of PTSD, although there is now some doubt
participant may be experiencing
about whether this kind of rapid intervention provides
any therapeutic gains. Once symptoms have developed, * encouraging the participant to view their symp-
most psychological therapies either rely on some form of toms as normal reactions to trauma
exposure therapy (usually involving the client imagining e discussing the participant’s needs for the future
events during their traumatic experience) in an attempt (Mitchell & Everly, 1993).
to extinguish fear symptoms, or adopt other treatments
that focus on the patient’s trauma memories or their As laudable as immediate professional help may
meanings, and international treatment guidelines rec- seem in these circumstances, there is much criticism of
ommend trauma-focused psychological treatments as psychological debriefing and its value as an intervention
the first-line treatment for PTSD (Ehlers, Bisson, Clark, for PTSD. Firstly, it is not clear whether victims will
Creamer et al., 2010). Therapies that possess this expo- gain any benefit from being counselled by strangers and
sure element include imaginal flooding, eye movement possibly ‘coerced’ into revealing thoughts and memo-
desensitisation and reprocessing (EMDR), and cogni- ries that in the immediate wake of the trauma may be
tive restructuring, but there is an ever-expanding set of difficult to reveal. Secondly, many of the survivors of
emerging treatments for PTSD (see Cukor, Spitalnick, severe trauma do not display symptoms of psychologi-
Difede, Rizzo et al., 2009), which meta-analyses suggest cal disorders, nor will they develop PTSD. Psychological
Cpa PSYCHOPATHOLOGY
$ %
debriefing techniques make little attempt to differenti- or memory while simulta- eye movement desensitisation and
neously visually following reprocessing (EMDR) A form of exposur
ate these survivors from those who may genuinely
therapy for PTSD in which clients are
need longer term guidance and treatment. Thirdly, con- the therapist’s finger that required to focus their attention on a
trolled comparative studies that have attempted to eval- is moving backwards and traumatic image or memory while simul-
uate the effects of psychological debriefing techniques forwards in front of their taneously visually following the therapis
suggest there is little convincing evidence that debrief- eyes. This continues until finger moving backwards and forwards
ing reduces the incidence of PTSD — and indeed it may the client reports a signifi- befor thsllesyees
in some cases impede natural recovery following trauma cant decrease in anxiety to the image or memory. The
(Bisson, 2003; McNally, Bryant & Ehlers, 2003). Most therapist then encourages the client to restructure the
recent reviews of early psychological interventions for memory positively, by thinking positive thoughts in rela-
the prevention of PTSD suggest that no psychologi- tion to that image (e.g. ‘I can deal with this’). The ration-
cal intervention can be recommended for routine use ale for this procedure is that combining eye movements
following traumatic events, and early psychological with attention to fearful images encourages rapid decon-
intervention may even have an adverse effect on some ditioning and restructuring of the feared image (Shapiro,
people (Roberts, Kitchiner, Kenardy & Bisson, 2009). 1995, 1999). There is evidence that EMDR is more effec-
tive than no treatment, supportive listening and relaxa-
Exposure therapies tion (McNally, 1999), but some studies have shown that
Arguably the most effective form of treatment for PTSD is it has a higher relapse rate than cognitive behaviour
exposure therapy, in which the sufferer is helped by the therapy (Devilly & Spence, 1999). Nevertheless, recent
therapist to confront and experience events and stimuli rel- reviews suggest that EMDR is one of the most effec-
evant to their trauma and their symptoms. The rationale tive treatments for PTSD, despite its controversial sta-
behind exposure therapy is that (1) it will help to extinguish tus (Bradley, Greene, Russ et al., 2005). Critics of EMDR
associations between trauma cues and fear responses (Foa argue that, although it does have some success in treating
& Rothbaum, 1998), and (2) it will help the individual to the symptoms of PTSD, it is little more than just another
disconfirm any symptom-maintaining dysfunctional beliefs form of exposure therapy. However, experimental stud-
that have developed as a result of the trauma (e.g. ‘I can’t ies have demonstrated that the eye movement compo-
handle any stress’) (Foa & Rauch, 2004). For the individual nent of EMDR is essential for successful treatment no
suffering PTSD, exposure to their fear triggers is often a dif- matter how this might be achieved (e.g. up and down eye
ficult step to take, and exposure may even make symptoms movements are as effective as side to side movements)
worse in the early stages of treatment (Keane, Gerardi, (Lee & Cuijpers, 2013). What does appear to be impor-
Quinn & Litz, 1992). This being the case, exposure can be tant is that the eye movement task — however achieved —
tackled in a number of different forms — especially in vari- should tax working memory and so weaken traumatic
ous imaginal forms. This can be achieved (1) by asking the memories (van den Hout & Engelhard, 2012).
client to provide a detailed written narrative of their trau-
matic experiences (Resick & Schnicke, 1992), (2) with the Cognitive restructuring
assistance of virtual reality technology using computer- There are various forms of cognitive restructuring
generated imagery (Rothbaum, Hodges, Ready, Graap & therapy for PTSD, but most attempt to help clients do two
Alarcon, 2001), or (3) by simply asking the client to visual- things: evaluateandreplace intrusive ornegativeautomatic
ize feared, trauma-related scenes for extended periods of thoughts; and evaluate and change dysfunctional beliefs
time (known as imaginal flooding) (Keane, Fairbank, about the world, themselves and their future that have
imaginal flooding A technique whereby Caddell & Zimering, 1989). developed as a result of the trauma (Marks, Lovell,
a client is asked to visualize feared, trauma- Such imaginal treatments Noshirvani & Livanou, 1998; Foa & Rothbaum, 1998).
related scenes for extended periods of time. are usually then supple- For example, Foa & Rothbaum (1998) suggested that
mented with subsequent in vivo exposure that would two basic dysfunctional beliefs mediate the develop-
require graded exposure to real trauma-related cues. ment and maintenance of PTSD. These are (1) ‘the
Comparative studies generally indicate that exposure-based world is a dangerous place’, and (2) ‘I am totally incom-
therapies provide therapeutic gains that are superior to petent’. Foa & Cahill (2001) argued that immediately
medication and social support (Foa & Meadows, 1997; after a severe trauma, all victims develop a negative
Marks, Lovell, Noshirvani, Livanou et al., 1998). view of the world and themselves, but for most indi-
A recently developed, and somewhat controversial viduals these beliefs become disconfirmed through daily
form of exposure therapy for PTSD is known as eye experience. However, those who avoid trauma-related
movement desensitisation and reprocessing (EMDR) thoughts will also avoid disconfirming these extreme
(Shapiro, 1989, 1995). In this form of treatment, the client views and this will foster the development of chronic
is required to focus their attention on a traumatic image PTSD. While exposure therapy alone may encourage’
CHAPTER 6 ANXIETY AND STRESSOR-RELATED PROBLEMS 193 —
experiences that disconfirm these dysfunctional beliefs, analysed treatments that contain both exposure and cog-
cognitive therapists have proposed that procedures that nitive restructuring components suggest that cognitive
directly attempt to alter PTSD-related cognitions should restructuring does not significantly augment exposure
also be included in the treatment (Resick & Schnicke, therapy in producing changes in dysfunctional cogni-
1992; Steil & Ehlers, 2000). However, studies that have tions (Foa & Rauch, 2004).
SELF-TEST QUESTIONS
* Can you describe the main symptoms of PTSD and how they may differ from the symptoms found in other anxiety disorders?
® What are the diagnostic differences between PTSD and acute stress disorder?
® Can you list some of the important risk factors for PTSD, and describe how they might contribute to the development of PTSD?
° We discussed the main theories of the aetiology of PTSD (conditioning theory, emotional processing theory, ‘mental defeat’,
and dual representation theory). Can you describe the main features of at least two of these and discuss their similarities
and differences?
° What are the main treatments for PTSD, and how have these been derived from theories ofthe aetiology of PTSD?
SECTION SUMMARY
6.6 TRAUMA AND STRESS-RELATED DISORDERS
@ The diagnosis of PTSD is based on identifying exposure to a specific fear-evoking, and usually life-threatening, event (e.g.
being involved in a natural disaster, serious physical assault and suchlike).
¢ Acute stress disorder is a short-term psychological and physical reaction to severe trauma.
e The main symptoms of PTSD include increased arousal, numbing of emotions, flashbacks and the re-experiencing of the trauma.
e The lifetime prevalence rate for PTSD is between 1 and 3 per cent (even though around 50 per cent of adults experience at
least one event in their lifetime that might qualify as a PTSD-causing event).
e Vulnerability factors for PTSD include a tendency to take personal responsibility for the event, developmental factors such as
an unstable early family life, a family history of PTSD, and existing high levels of anxiety or a pre-existing psychological disorder.
® There is no consensus on a specific psychological model of PTSD, and current explanations include: (1) classical condition-
ing, (2) emotional processing theory, (3)’mental defeat’, and (4) dual representation theory.
e Attempting to prevent the development of PTSD through the rapid and immediate debriefing of trauma victims (critical
incident stress debriefing) is now generally acknowledged to be ineffective and even counterproductive.
¢ The most effective forms of treatment for PTSD are exposure therapies, where the sufferer is helped by the therapist to
confront and experience events and stimuli relevant to their trauma. These may include imaginal flooding or eye move-
ment desensitisation and reprocessing (EMDR); and graduated exposure treatment can be supplemented with cognitive
restructuring designed to evaluate and change dysfunctional beliefs about the world.
stressor-related problems such as post-traumatic stress

6.7 ANXIETY AND disorder (PTSD). Common to all of these disorders
STRESSOR-RELATED is the intense experience of anxiety that the individual
finds distressing and which causes significant impair-
PROBLEMS REVIEWED ment in social, occupational, or other important areas
of functioning. At this point it is worth referring back
to the table given on the website in which we began by
In this chapter we have reviewed six of the main anxiety- summarising some of the important features of these
based problems — specific phobia, social anxiety disor- problems. This table shows that anxiety manifests itself
der, panic disorder, generalized anxiety disorder (GAD), in many different ways in these different disorders — as
obsessive compulsive disorder (OCD), and trauma and pathological worrying in GAD, as compulsive ritualized
ose PSYCHOPATHOLOGY
. 1%
thoughts and actions in OCD, as physical panic attacks of anxiety-based problems generally. However, there are
in panic disorder, and the re-experiencing of trauma in some features that are common to these different prob-
PTSD. Many of these anxiety problems are precipitated lems and these may provide some insight into how dif-
by periods of stress in a person’s life (e.g. panic disorder, ferent anxiety-based problems develop. These features
GAD, OCD), yet we do not yet know why an individual include the information-processing and interpretational
who has experienced a period of life stress will develop biases that accompany most anxiety disorders, and also
one particular disorder (e.g. OCD) rather than another the dysfunctional beliefs that anxiety sufferers seem to
(e.g. panic disorder). This will be an important issue for form and which maintain their symptoms (e.g. the spider
future clinical research. phobic’s beliefs that spiders are threatening and harmful,
Just as the symptoms of these anxiety-based problems and the GAD sufferer’s belief that worrying is an impor-
are often quite different, so are the theories that try to tant and necessary activity to engage in). These phenom-
explain them, and there is certainly no single, unified ena may eventually form the basis of a unified theory of
theory that can convincingly explain the development anxiety-based problems.
Reading Activity
Anxiety disorders summary Specific phobias Activity 6.1

table Social anxiety disorder Self-test questions
Author blog — phobias Exposure treatment for Revision flashcards
Why we worry phobias Research questions
Author blog - clinical Obsessive compulsive
constructs disorder: A client’s
Journal Article: Attention bias perspective
modification Post traumatic stress
Glossary key terms disorder
Clinical issues
References
7 Depression and Mood Disorders

This chapter describes depression and mood disorders,

their symptoms, theories of their aetiology, and the main 7.1 MAJOR DEPRESSION 198
forms of treatment for these problems. The two main mood
disorders covered are major depression (sometimesknown : 7-2 BIPOLAR DISORDER 215
as unipolar depression), and bipolar disorder (characterized
by periods of mania alternating with periods of depres- : 7.3 THETREATMENT OF DEPRESSION AND MOOD
sion). The chapter covers a range of theories of depression DISORDERS 219
and mood disorders including biological theories and
psychological theories. The section on treatment looks at 7.4 DELIBERATE SELF-HARM 227
the way in which antidepressant drugs help to alleviate the
symptoms of depression, and how anumber of psychologi- : 7.5 SUICIDE 229
cal therapies have been developed to address the cogni-
tive biases that characterize major depression. The chapter 7.6 DEPRESSION AND MOOD DISORDERS REVIEWED 234
ends by discussing two phenomena associated with mood
disorders and depression in particular, namely deliberate
self-harm and suicide.
196 PSYCHOPATHOLOGY
LEARNING OUTCOMES
1. Describe the characteristics and main 4. Distinguish between biological and psychological
diagnostic criteria of depression and bipolar theories of depression.
disorder. 5. Describe and evaluate the role of cognitive factors
2. Compare and contrast at least two biological in explaining the development of depression.
theories of the aetiology of depression and mood 6. Compare and contrast biological, behavioural
disorders. and cognitive therapies for depression and mood
3. Compare and contrast at least two psychological disorders.
theories of the aetiology of depression and mood 7. Summarize the main psychological characteristics
disorders. of suicide and deliberate self-harm.
The overwhelming sadness — to me, it’s my menace. My menace was with me in the shower, on the phone, in class. Everywhere.
| would become lost in a thoughtless stretch on blank - where distraction to nothing in particular would take over. Consumed
by nothing - thinking of nothing, but my mind was locked down - stuck - paralysed. Studying was difficult if not impossible.
! was becoming overwhelmed, and not understanding what | was dealing with - no relatable experience. It made things almost
intolerable. A good day was sleeping until 10 - getting up - maybe going to a morning lecture. Taking another nap in the
afternoon - skipping class — reading books to pass the time that seems inescapable. Your mind gets into internal conflicts. Plenty
of time for that. Time seems to always stretch in front of you — you can’t bear thinking of doing anything to fill the time, but are
beaten up by the fact the routine will exist the next day, and the next day, and the next, and why at all bother? What is it all for?
Joe’s Story (The Menace of My Own Life)
are losses and failures. Experiences such as losing a job or

Introduction
the death of a loved one are likely to trigger periods of
In Joe’s Story, his account of the experience of depres- sadness, lethargy, and rumination. Similarly, failures —
sion gives considerable insight into the various disabling such as failing an exam or failing to persuade someone
features of this psychological problem. These include you like to date you — can also lead to periods of hopeless-
the overwhelming feelings of sadness and lethargy. Each ness and the fostering of negative cognitions associated
day is as miserable as the next in an unrelenting cycle with pessimism and self-doubt. Nevertheless, most of us
of emptiness, and Joe hardly ever experiences pleasure or can shake off these feelings within a few days or weeks,
any positive emotion. Those suffering depression lack and get on productively with our life. For others, how-
initiative, and often move and speak more slowly than ever, the symptoms of depression may linger on and
non-sufferers (Sobin & Sackheim, 1997), they spend spread to all aspects of their lives — emotional, behav-
more time alone and may stay in bed for long periods — ioural, cognitive, and physical — and this can result in diag-
especially delaying getting out of bed in the mornings. nosable bouts of depression that are debilitating enough
Beck (1967) described depression as a ‘paralysis of will’ in to prevent an individual from living a normal day-to-day
which individuals experience only pessimism and hope- life. In extreme cases, the symptoms of depression can
lessness about their lives. This can often lead to suicidal develop even without the occurrence of a precipitating
thinking, and suicide often feels like the only solution for life event, such as a loss or a failure, and will often persist
many individuals suffering depression. for much longer than would be expected following a loss
We all experience periods of depression in our lives, such as a bereavement.
and we can usually attribute these periods of depression . Depression is the prom- depression A mood disorder involving -
to specific events. Two types of events are particularly inent emotion in mood dis- emotional, motivational, behavioural,
important in triggering periods of depression, and these orders, but it can often be Physical and cognitive symptoms.«,
CHAPTER 7 DEPRESSION AND MOOD DISORDERS Ane
ia An emotion characterized by associated with its opposite — where they are and to be left alone), and appetite and
\dless, frenzied energy and feelings
namely mania. Mania is an sexual desire can also be significantly reduced. Depressed
phoria.
emotion characterized by individuals exhibit a number of behavioural symptoms,
boundless, frenzied energy and feelings of euphoria. As including a slowness of speech and behaviour generally
we shall see later, individuals who have a bipolar disorder (Joiner, 2002). They become physically inactive, stay in
frequently oscillate between deep depression’ and fre- bed for long periods, and reports of decreased energy,
netic mania. tiredness and fatigue are common. Even the smallest of
Depression involves emotional, motivational, behav- tasks seem to require substantial physical exertion.
ioural, physical and cognitive symptoms. The emotional Depression also has an embodied element to it. People
experiences of depressed individuals are usually restricted who experience depression also exhibit characteristic
to negative ones and these are often described as ‘sad, postures and movements that are an integral feature of
hopeless, miserable, dejected, and discouraged’. Such their depression experience, and the role of these embod-
individuals are often close to tears and have frequent cry- iments is discussed more fully in Focus Point 7.1. Physical
ing episodes. Only very rarely do depressed individuals symptoms also include sleep disturbance such as middle
report experiencing pleasant or positive emotions; they insomnia (waking up during the night and having diffi-
exhibit a complete loss of sense of humour, and rarely culty getting back to sleep) and terminal insomnia (wak-
display positive facial expressions (Sloane, Strauss & ing early and being unable to return to sleep). In some
Wisner, 2001). Anxiety is also commonly experienced cases, depression can be associated with oversleeping
with depression, which suggests that many sufferers may (hypersomnia), where the individual indulges in
experience simultaneously a range of negative emotions increased daytime sleeping. Depressed individuals also
(Bakish, 1999) that may be reflective of a single underly- complain of regular headaches, indigestion, constipa-
ing symptomatology. Depressed individuals exhibit a tion, dizzy spells, and general pain (Fishbain, 2000).
range of motivational deficits, and these include a loss of Arguably the most disabling of the symptoms of depres-
interest in normal daily activities or hobbies. They exhibit sion are its cognitive features, and, as we shall see later,
a lack of initiative and spontaneity, and frequently report many theories of depression view these cognitive symp-
‘not caring anymore’, and not getting pleasure from toms as central and as factors that need to be addressed
activities that they previously enjoyed. This lack of initia- in order to complete effective treatment. In particular,
tive may manifest itself initially in social withdrawal depressed individuals tend to have developed extremely
(depressed individuals regularly report wanting to stay negative views of themselves, the world around them, and
DEPRESSION, EMBODIMENT AND THE ROLE OF EXERCISE

Most people will associate depression with an internal mindfulness therapy to normalize gait patterns in
feeling that they would describe as sad, lethargic or depressed patients also helped to relieve their depres-
empty, but recent evidence suggests that the experi- sion experiences.
ence of ‘depression’ also has an embodied component. Many studies have also found that exercise can
That is, there is a reciprocal relationship between bod- reduce depression severity in people with a diagnosis
ily expression and how an emotion is experienced of major depression (Rimer, Dwan, Lawlor, Grieg et al.,
POINT
FOCUS
7.1 and processed. For example, a report by Michalak, 2012) - including even treatment-resistant forms of
Troje, Fischer, Vollmar et al. (2009) describes how depression (Mota-Pereira, Silverio, Carvalho, Ribeiro
depressed patients exhibit embodied components et al., 2011), and exercise has also been shown to
of their experience in the form of reduced walking be beneficial for older people suffering depression
speed and smaller amplitude of vertical movements (Bridle, Spanjers, Patel, Atherton & Lamb, 2012). There
of the upper body. Similarly, hunched postures also are many reasons why a regular exercise programme
elicit feelings of depression (Riskind & Gotay, 1982). may help alleviate depressive symptoms. For example,
These embodiments are not just reflections of inner exercise may help to eliminate poor postures that con-
feelings, they comprise an integral part of the depres- tribute to the embodied depression experience; it can
sion experience because attempts to directly modify also decrease the incidence of cardiovascular disease,
these postural features of depression also relieve the hypertension and type 2 diabetes (Powers, 2002) - all
experience of depression. In such an intervention, of which may enable better psychosocial functioning
Michalak, Troje & Heidenreich (2010) found that using and increase quality of life.
198 PSYCHOPATHOLOGY
t >N oy
their own future (Beck, 1987; Gable & Shean, 2000), and It specifies the criteria for major depressive episode Episode of maj
this generates pessimistic thinking where sufferers believe a major depressive epi- depression, defined by the presence of fiv 0
more depressive symptoms during the same
nothing can improve their own lot. This in turn leads to a sode (which is not a cod-
2-week period, as stated by the DSM-5.
lack of initiative, with individuals reporting impaired able disorder), which can
ability to think, concentrate or make decisions. This be found in DSM-5 Summary Table 7.1. Major depres-
inability to affect the future also generates other prob- sive disorder is defined by the presence of five or more
lematic beliefs, such as a sense of worthlessness, shame depressive symptoms during the same 2-week period
and guilt. Because of this, many depressed individuals (DSM-5 Summary Table 7.1). However, depression is
develop the dysfunctional belief that others would be often a normal reaction to a number of life events (such
better off if they were dead, and this can often lead to as bereavement, financial problems, natural disasters,
transient but recurrent suicidal thoughts (see section 7.5). and suchlike), and for depression to become clinically
There are two main problematic a diagnosis of major depressive disorder
major depression A psychological prob-
lem characterized by relatively extended types of clinical depression. requires the presence of dysfunctional symptoms such as
periods of clinical depression which cause The first, and most com- feelings of worthlessness, suicidal ideation, and impair-
significant distress to the individual and mon, is major depression, ment of daily functioning. In addition, there has been
impairment in social or occupational func-
and the second is bipolar much discussion about whether depression in response
tioning. See also unipolar depression.
disorder. The main features to bereavement should be included as one of the criteria
bipolar disorder A psychological disorder of these two types of mood
characterized by periods of mania that disorder can be reviewed
alternate with periods of depression.
online in the depression and
ipolaea
unipolar ion
depression A Psycnologi
psychologicalcal dis-als mood disorders summary DSM-5 SUMMARY TABLE 7.1 Criteria for amajor depressive
episode
order characterized by relatively extended table, which is available on
periods of clinical depression that causethe website at www e At least five of the following are present, including either
significant distress to the individual and
-wiley-psychopathology. depressed mood or loss of interest:
impairment in social or occupational func-
tioning. See also major depression.
com/ch7. Readers may ¢ Depressed mood most of the time
want to refer back to this
table when they have read and digested the information e Less interest or enjoyment of most activities
in this chapter. Major depression (sometimes known as e Significant weight change not associated with dieting
unipolar depression) is one of the most common of all
e Insomnia or excessive sleep
the psychological problems, and is characterized by rela-
tively extended periods of clinical depression that cause e Excessive increase or reduction in physical movement
significant distress to the individual and impairment in ° Substantial fatigue or lack of energy
social or occupational functioning. Bipolar disorder is
¢ Feelings of worthlessness or excessive or inappropriate
characterized by periods of mania that alternate with
guilt
periods of depression, and this leads individuals with
bipolar disorder to describe their lives as an “emotional ¢ Lack of concentration or ability to think or make decisions
roller-coaster. Sufferers experience the extremes of e Recurrent thoughts of death and suicide or suicide attempt
these emotions in ways that cause emotional discomfort
e The symptoms are not better accounted for by schizoaffec-
and distress.
tive disorder or other mental disorder or due to the effects
This chapter now continues by discussing the diag- of a substance or other medical condition
nosis, prevalence and aetiology of major depression,
and then — in section 7.2 — the diagnosis, prevalence and
aetiology of bipolar disorder.
DSM-5 SUMMARY TABLE 7.2 Criteria for major depressive

disorder
7.1 MAJOR DEPRESSION Major depressive disorder

e Presence of a single major depressive episode (not attrib-
utable to normal and expected reactions to bereavement,
7.1.1 The Diagnosis and Prevalence etc.) without previous manic or hypomanic episode where
symptoms are not better.accounted for by other disorders
of Major Depression ° The symptoms must cause clinically significant distress
DSM-5 has introduced a number of changes to the way or impairment in social, occupational or other forms of
functioning.
in which major depression is categorized and diagnosed.
CHAPTER 7 DEPRESSION AND MOOD DISORDERS 199
contributing to a diagnosis of major depressive disorder Secondly, depression is one of the most prevalent of
and bereavement symptoms had been excluded prior all psychological problems and is experienced in some
to DSM-5. However, recent research has indicated that form or other by almost everyone at some time in their
bereavement-related depression is not significantly differ- life. Indeed, experiencing depression is the third most
ent from major depressive disorder that presents in other common reason for consulting a doctor or GP in the
contexts; it is most likely to occur in individuals with past UK (Singleton, Bumpstead, O’Brien, Lee et al., 2001).
histories of major depressive disorder; and is also likely In order for GPs to be able to provide treatment for
to be chronic and recurrent (Zisook, Corruble, Duan, such individuals, there is a tendency for them to over-
Iglewicz et al., 2012). For these reasons, bereavement- diagnose mild or moderate depression (Middleton,
related symptoms are now no longer excluded from the Shaw, Hull & Feder, 2005). This raises a number of
diagnostic criteria. issues, including the possible stigmatisation that such
Chronic mood disturbances primarily characterized a label might incur for the patient. In addition, lay
by depressive symptoms can also be diagnosed, although beliefs about depression suggest that many people
these conditions must have been apparent for at least already view depression as a ‘disease’ that is a conse-
2 years, and would normally not be severe enough to quence of everyday life stress (Lauber, Falcato, Nordt
disrupt normal social and occupational functioning and & Rossler, 2003). If lay people already view depression
warrant a diagnosis of major depression. The most as a ‘disease’ or biological illness, and GPs are more
significant of these is dysthymic disorder, in which than willing to diagnose it, then we run the risk of the
the sufferer has experi- ‘medicalisation’ of normal everyday negative emotions
sthymic disorder A form of depression enced at least 2 years of such as mild distress or even unhappiness (Shaw &
which the sufferer has experienced at
ast 2 years of depressed mood for more depressed mood for more Woodward, 2004).
ys than not. days than not (see DSM-5 Thirdly, depression occurs in a variety of different
Summary Table 7.3). Indivi- guises within psychopathology and is commonly comor-
duals diagnosed with this disorder experience many of bid with other important disorders (Kessler, Nelson,
the behavioural and cognitive characteristics of major McGonagle, Liu et al., 1996; Table 7.1). This has given
depression, but these are less severe (meeting only two or rise to a range of different diagnosable disorders that
more of the symptom criteria for major depression). have depression as a central feature within them. As a
However, diagnosing depression is a controversial result, major depressive disorder is a relatively ‘pure’
issue for a number of reasons. Firstly, DSM-5 requires diagnosis where the cause of depression cannot be attrib-
the identification of five symptoms for a period of uted either to some other disorder (such as the conse-
2 weeks for a diagnosis of major depression. But are such quences of substance abuse) or to specific biological,
people any different in their experiences and their func- environmental factors or other life events (such as
tioning from someone who exhibits only three symp- post-natal depression). Prominent examples of dia-
toms? Studies have suggested that individuals with three gnosable problems which premenstrual dysphoric disorder
symptoms exhibit similar levels of distress and problems have depression as a signif- A condition in which some women
with day-to-day living as individuals with five symptoms icant core element include experience severe depression symptoms
(Gotlib, Lewinsohn & Seeley, 1995). premenstrual dysphoric between 5 and 11 days prior to the start
of the menstrual cycle. Symptoms then
disorder, seasonal affec-
improve significantly within a few days
tive disorder (SAD) and after the onset of menses.
chronic fatigue syndrome
DSM-5 SUMMARY TABLE 7.3 Criteria for dysthymic disorder (CFS) (or myalgic enceph- Jauebnabathective ditorder (GAD)
¢ Depressed mood most of the time for at least 2 years alomyelitis, ME), and these A condition of regularly occurring
depressions in winter with a remission
are discussed briefly in
e Presence of at least two of the following: the following spring or summer.
Focus Point 7.2.
e Poor appetite or overeating Finally, depression is
e Lack of or excessive sleeping highly comorbid with chronic fatigue syndrome (CFS)
A disorder characterized by depression and
anxiety problems and
e Low levels of energy or fatigue mood fluctuations together with physical
around 60 per cent of symptoms such as extreme fatigue, muscle
e Low self-esteem people with depression pain, chest pain, headaches and noise and
e Poor concentration or decision-making abilities will also experience an light sensitivity.
anxiety disorder (Mofft,
e Feelings of hopelessness
Caspi, Harrington, Milne et al., 2007). This has given
e The symptoms are not due to the effects of a substance or rise to a diagnostic category called mixed anxiety/
other medical condition depressive disorder that is used to describe a significant
008: PSYCHOPATHOLOGY :
' 2
TABLE 7.1 Comorbidity of major depressive disorder with other (Zinbarg, Barlow, Liebowitz et al., 1994). This has
DSM disorders led some researchers to suggest that depression and
anxiety are not truly independent disorders but rep-
Lifetime 12-month
comorbidity (%) comorbidity (%) resent subcategories of a larger group of emotional
disorders with symptoms that can often intermix (e.g.
Anxiety disorders Watson, 2005).
Generalized anxiety 17.2 15.4 Depression is arguably the most prevalent of the psy-
disorder (GAD) chopathologies that are covered in this book. Estimates
Agoraphobia 16.3 12.6
of lifetime prevalence rates for major depression in
American community samples range from 5.2 per cent
Specific phobia 24.3 23.7
to 17.1 per cent (Kessler, McConagle, Zhao, Nelson et al.,
Social phobia DTA 20.0 1994; Weissman, Bland, Canino, Favarelli et al., 1996), and
Panic disorder 9.9 8.6 depression is now so commonly recognized that it contrib-
utes 12 per cent to the total burden of nonfatal global dis-
Post-traumatic stress 19°5 1/52
ease (Ustun, Ayuso-Mateos, Chatterji, Mathers et al., 2004).
disorder (PTSD)
The lifetime risk for major depression may be
Any anxiety disorder 58.0 Sile2 as high as 20 per cent for men and 30 per cent for
Substance use disorders women (Kruijshaar, Barendregt, Vos, de Graaf et al.,
2005), and the World Health Organisation estimates
Alcohol dependence 23.5 13.0
that 350 million people worldwide of all ages suf-
Drug dependence ISS, IS fer from depression (WHO, 2012). However, gauging
Alcohol abuse w/o 4.1 1.4 the prevalence of depressive symptoms has been diff-
dependence cult because (1) prevalence rates appear to differ sig-
Drug abuse w/o 6.5 1.1 nificantly across different cultures, (2) the incidence of
dependence the diagnosis of depression has increased steadily over
the past 90 years, and (3) different studies have tended to
Any substance use 38.6 ish
disorder use different diagnostic tools when assessing prevalence.
For example, studies conducted by the Crossnational
Other disorders
Collaborative Group reported very large cultural vari-
Dysthymia 6.7 4.0 ations in the prevalence of major depression. These
Conduct Disorder 16.2 = ranged from 1.5 per cent in Taiwan to 19.0 per cent in
Lebanon. Lifetime prevalence rates for Puerto Rico and
Aggregate number of disorders
Korea were relatively low at 4.3 per cent and 2.9 per
One 24.7 58.9 cent respectively, compared with 10.2 per cent for the
>One 74.0 26.9 US (Weissman, Bland, Canino, Favarelli et al., 1996).
There appear to be a number of reasons for these large
Two 17.4 15.4
international variations in lifetime prevalence rates.
>Three Sik9 16.5 These include (1) the stigmatising of psychopathology
Note that the lifetime comorbidity rate of major depression with another in many non-Western societies such as Taiwan, indi-
anxiety disorder is 58 per cent and with more than one other DSM cating that many individuals in those societies will be
disorder is 74 per cent, suggesting that individuals with depression tend
unwilling to report symptoms of major depression
to experience a range of negative emotions and comorbid disorders.
(Compton, Helzer, Hwu, Yeh et al., 1991), (2) higher
Source: After Kessler, R.C., Nelson, C.B., McGonagle, K.A., Liu, J.,Swartz, M. &
Blazer, D.G. (1996). kill of DSMIII-R major depressive disorder in levels of somatisation (the expression of psychologi-
UC, a the general population: Results cal distress in physical terms) in non-Western countries
To see the Summary table on depres- ‘\, from the US national comorbidity (Simon, VonKorff, Piccinelli, Fullerton et al., 1999),
) survey. British Journal of Psychiatry,
sion and mood disorders go to
(3) the fact that — unlike many other conditions (such
www.wiley-psychopathology.com/ » 168(1), 17-30. Reproduced by
reading/ch7 : permission of the Royal College of as obesity and hypertension) — depression cannot be
Psychiatrists. observed or measured directly, so there will always
be an element of subjectivity in the way the sympt-
oms are measured and recorded (Patten, 2003a), and
number of people who experience a mix of anxi- (4) lifetime prevalence rates will always be affected by
ety and depression (around 8 per cent of people recall problems, and recall failure with age appears
with either depression or anxiety symptoms meet to account for the fact that lifetime prevalence rates
the criteria for mixed/anxiety depressive disorder decrease with increasing age cohorts (Patten, 2003b).
s
S
—
SEASONAL AFFECTIVE DISORDER (SAD)
= although theories have argued for the involvement of
viral or immunological factors (Behan, More & Behan,
Oo
a. Seasonal affective disorder (SAD) is a condition of reg- 1991) and environmental stressors such as pollution
WV) ularly occurring depressions in winter with a remission or organophosphates (Jason, Wagner, Taylor, Ropacki
=) the following spring or summer, and is a relatively
U et al., 1995). Other researchers have pointed out that
2) common condition affecting 1-3 per cent of adults in depression can be identified as a risk factor in CFS,
Lt, temperate climates (Westrin & Lam, 2007). The main with a predisposition among CFS sufferers to develop
symptoms include depressed mood, lack of energy, depression and to exhibit frequency of depression
hypersomnia, craving for carbohydrates, overeating, prior to CFS onset at twice the level of controls (Straus,
and weight gain (Blehar & Rosenthal, 1989). There is Dale, Tobi, Lawley et al., 1988). Interestingly, stud-
some evidence that individuals who develop SAD do ies that have provided cognitive behaviour therapy
so because the longer periods of darkness in winter for adolescents with CFS have resulted in significant
increase their secretion of the hormone melatonin, decreases in fatigue severity and functional impair-
which acts to slow organisms ment, suggesting that addressing psychological fac-
alatonin A hormone that acts to slow down, making them sleepy and tors in CFS may play a significant role in successfully
ganisms down, making them sleepy less energetic (Wetterberg, treating the syndrome (Stulemeijer, de Jong, Fiselier,
d less energetic. 1999). The answer to this is to Hoogveld & Bleijenberg, 2005).
provide individuals suffering
from SAD with light therapy or photo therapy in which
they are exposed to periods ofartificial sunlight during PREMENSTRUAL DYSPHORIC
the darker winter months (Magnusson & Boivin, 2003; DISORDER (PMDD)
Reeves, Nijjar, Langenberg, Johnson et al., 2012).
PMDD is a condition in which some women will expe-
rience severe depression symptoms between 5 and
CHRONIC FATIGUE SYNDROME (CFS) 11 days prior to the start of the menstrual cycle, but
these symptoms then improve significantly within
Chronic fatigue syndrome (CFS) is characterized by a few days after the onset of menses. DSM-5 notes
depression and mood fluctuations together with phys- that such symptoms can cause significant distress
ical symptoms such as extreme fatigue, muscle pain, and disruption to normal daily living and include
chest pain, headaches, and noise and light sensitiv- symptoms such as mood swings, irritability or anger,
ity (Yancey & Thomas, 2012). Its causes are unclear at feelings of hopelessness, decreased interest in usual
present, and this may be the reason why it is given a activities, disruption of normal sleep patterns, leth-
variety of names, including ‘yuppie flu’ because of its argy, and food cravings. PMDD affects between 2 and
tendency to afflict predominantly successful young 5 per cent of women during the years they experi-
people - especially women — struggling with stress- ence menstrual periods (Epperson, Steiner, Hartlage,
ful work and family responsibilities (Ho-Yen, 1990). Eriksson et al., 2012), but can be successfully treated
About 75 per cent of reported cases are adult white using healthy lifestyle management (e.g. adopting a
females (Showalter, 1997), but this may simply reflect balanced diet and taking regular exercise), antide-
the reluctance of males to report such symptoms. pressant medication, or CBT (Kleinstauber, Witthoft &
The causes of CFS have not been clearly identified, Hiller, 2011).
The incidence of major depression has stead- 7.1.2 The Aetiology of Major
ily increased since 1915 and median age of onset has Depression
decreased to around 27 years in the US (Kessler, 2002).
Women are almost twice as vulnerable to periods of Biological theories
major depression as men
To complete Activity 7.1 go to i (Nolen-Hoeksema, 2002), Genetic factors There is good evidence that
activities/ch7
_ and this is independent of depressive symptoms run in families, and this sug-
cultural background. gests the possible existence of an inherited or genetic
202 PSYCHOPATHOLOGY
component to major depression, and first-degree relatives neurones, their abnormally low levels in depressed indi
of major depression sufferers are around two to three viduals may account for the cognitive, behavioural and
times more likely to develop depressive symptoms than motivational deficits found in major depression. In addi-
are individuals who are not first-degree relatives of suffer- tion to abnormalities in serotonin and norepinephrine
ers (Gershon, Hamovit, Guroff, Dibble et al., 1982; Maier, levels, it is also believed that low levels of the neurotrans-
Lichtermann, Minges, Heun et al., 1992). In addition, her- mitter dopamine might be involved in major depression
itability based on twin studies is moderate and estimated (Naranjo, Tremblay & Busto, 2001). Dopamine is sig-
to be between 30 and 40 per cent (Kendler, Gardner, nificantly involved in the reward systems in the brain,
Neale & Prescott, 2001; Sullivan, Neale & Kendler, 2000; and so depleted dopamine levels may be responsible for
Agrawal, Jacobson, Gardner, Prescott & Kendler, 2004), deficits in this system in depression giving rise to a lack
with adoption studies suggesting that this is a genu- of motivation, initiative, and pleasure (Treadway &
ine inherited effect rather than a familial one (Wender, Zald, 2011).
Kety, Rosenthal, Schulsinger et al., 1986; Cadoret, 1978). The tricyclic drugs that are often prescribed for people
However, after two decades of genetic research the spe- suffering major depression have their beneficial effects by
cific genes contributing to this inherited component are preventing the reuptake by the presynaptic neurone of
still largely unknown. Candidate genes include the sero- neurotransmitters serotonin and norepinephrine. This
tonin transporter gene (SLC6A4) that can enhance or ter- results in higher levels of these neurotransmitters in the
minate the action of the brain neurotransmitter serotonin synapse, and this facilitates the transmission of impulses
(see next section on Neurochemical factors) (Clarke, Flint, to the postsynaptic neurone — thus facilitating brain
Attwood & Munafo, 2010; Levinson, 2006), although activity (see Figure 7.1). More recently, the development
recent reviews have cast some doubt on the critical role of
this gene in mediating the inherited component of major
depression (Munafo, 2012).
Neurochemical factors Depression and mood dis-

Electrical stimulus
orders have been shown to be reliably associated with from the brain cell
abnormalities in the levels of certain brain neurotrans-
mitters, and three neurotransmitters are particularly
significant — namely, serotonin, norepinephrine and
dopamine (Delgardo & Moreno, 2000), and major Re-uptake
i : cn Neurotransmitters
depression is often associated with low levels of these
ee ie ® o blocked by SSRI
neurotransmitters. A number of factors led to findings
d Released
about the importance of serotonin and norepinephrine
aVy me vo Bee. neurotransmitters
levels in particular. First, in the 1950s it was noticed ere
4 A
> «4
Vv J
=
14
ES v <4 >
a ioe)
| Receptors
that many medications for high blood pressure also
caused depression (Ayd, 1956), and this effect was Brain cell
found to be the result of such medications decreasing
brain serotonin levels. The 1950s also saw the develop-
ment of drugs that significantly alleviated the symp-
toms of depression. The main ones were tricyclic
drugs (such as imipramine) and monoamine oxidase
FIGURE 7.1 Neurones release the neurotransmitters sero-
(MAO) inhibitors (such as
tricyclic drugs Drugs which block tonin and norepinephrine from their endings when they fire
tranylcypromine). Both
the reuptake of both serotonin and and these help transmission between brain cells. Some of the
norepinephrine. of these drugs have their
neurotransmitter molecules are recaptured by the neurone
effects by increasing levels using a reuptake mechanism, and this can occur before they
of both serotonin and norepinephrine in the brain. These are received by the receptor neurone, thus weakening the
findings led to the development of neurochemical theo- transmission between neurones. Both tricyclic drugs and SSRIs
ries of depression that argued that depression was caused have their effect by blocking the reuptake of these neuro-
by either low norepinephrine activity (Bunney & Davis, transmitters and so ensure that neural transmission is more
1965) or low serotonin activity (Golden & Gilmore, effective. Tricyclic drugs block the reuptake of both serotonin
1990). Because these neurotransmitters are necessary and norepinephrine, while SSRIs selectively block the reuptake
for the successful transmission of impulses between only of serotonin.
&
of selective serotonin reuptake inhibitors (SSRIs) (such as

Prozac) has allowed researchers to assess the specific role
of serotonin in depression, and researchers now believe
that serotonin levels play a central role in major depres-
sion. However, this picture is relatively simplistic, and the
most recent neurochemical theories of mood disorders
suggest that interactions between different neurotrans-
mitters may be important. Some researchers suggest that
depression is associated more with an imbalance in neu-
rotransmitters than with deficits in specific neurotrans-
mitters (Rampello, Nicoletti & Nicoletti, 2000; Ressler
& Nemeroff, 1999). Other theorists have suggested that
low levels of serotonin interact with levels of norepineph-
rine in rather complex ways, such that combinations of
low levels of both serotonin and norepinephrine produce
depression, but low levels of serotonin and high levels of
norepinephrine result in mania (Mandell & Knapp, 1979).
Brain abnormalities and depression Recent devel-

opments in cognitive neuroscience together with the FIGURE 7.2 Key brain regions involved in affect and
evolution of new technologies for scanning and photo- mood disorders: (a) orbital prefrontal cortex (green) and the
graphing the brain (e.g. magnetic resonance imaging ventromedial prefrontal cortex (red), (b) dorsolateral prefrontal
(MRI); see section 2.2.4) have led to a greater understand- cortex (blue), (c) hippocampus (purple) and amygdale (orange),
ing of the brain areas involved in depression and mood (d) anterior cingulated cortex (yellow).
disorders (Davidson, Pizzagalli, Nitschke & Putnam, Source: After Davidson, R.J., Pizzagalli, D., Nitschke, J.B. & Putnam, K.
(2002). Depression: Perspectives from affective neuroscience. Annual
2002). Studies have identified dysfunction or abnormali-
Review of Psychology, 53, 545-574. Annual Review of Psychology by
ties in a number of brain areas that appear to be associ-
Stone, Calvin Perry. Reproduced with permission of ANNUAL REVIEWS
ated with depression. These areas are the prefrontal in the format Republish in a book via Copyright Clearance Center.
cortex, be anteriories cortex, the hippocampus,
TT, and the amygdala, and
To read ‘Depression: perspectives from
these areas are illustrated
affective neuroscience’ go to
www.wiley-psychopathology.com/ _ in Figure 7.2. This raises
reading/ch7 / the question of the role deficit in the ‘will-to-change’ that is also characteristic of
that such areas may play in depressed individuals. Third, individuals with depression
relation to depression, and Davidson et al. (2002) have and mood disorders also show signs of dysfunction in
attempted to address these issues. First, depression is the hippocampus (Mervaala, Fohr, Kononen, Valkonen-
associated with significantly lower levels of activation in Korhonen et al., 2000). The hippocampus is important in
the prefrontal cortex (Drevets, 1998), and this area is adrenocorticotropic hormone secretion and is also criti-
important in maintaining representations of goals and cal in learning about the context of affective reactions
the means to achieve them. Decreased activation in this (Fanselow, 2000). Thus, deficits in hippocampus function
area may result in the failure to anticipate incentives, in depression may result in the individual dissociating
which is a common feature of depression. Second, affective responses from their relevant contexts. In
decreased anterior cingulate cortex (ACC) activation is depression, this may manifest itself as feelings of sadness
also reported in major depression (Beauregard, Leroux, occurring independently of contexts in which we would
Bergman, Arzoumanian normally expect such emotions (i.e. sadness is experi-
terior cingulate cortex (ACC) Thefron- et al., 1998). Evidence enced in all contexts, not just following relevant life
part of the cingulate
cortex resembling suggests that ACC activa- events such as a bereavement). Finally, major depression
collar’ form around the corpus callo-- a
m, used for the relay ofneural signals petionns paereme when effort-
has also been found to be associated with structural and
tween the right and fe bale Pisce ful emotional regulation functional abnormalities in the amygdala, and especially
the brain. is required in situations with increased amygdala activation (Abercrombie,
where behaviour is failing Schaefer, Larson, Oakes et al., 1998). A role of the amyg-
to achieve a desired outcome (Ochsner & Barrett, 2001), dala is in directing attention to affectively salient stimuli
and Davidson et al. (2002) suggest that this may reflect a and prioritising the processing of such stimuli. The effect
of raised levels of activation in the amygdala may there- the cognitive, behavioural and motivational symptoms
fore result in the depressed individual prioritising threat- of depression (see also Focus Point 7.3 describing how
ening information for processing and interpreting such inflammation might affect the experience of depression
information negatively. through its affect on neurotransmitters).
These explanations of
To complete a brain labelling activity depressive symptomatology Summary of biological theories The preceding
based on Figure 7.2 go to
in terms of dysfunction in evidence suggests that biological factors may play an
activities/ch7 specific brain areas are not important role in the development and maintenance
necessarily inconsistent with of mood disorders such as major depression. There is
those theories that attempt to explain depression in terms clearly an inherited component (which accounts for
of neurotransmitter imbalances. It is quite possible that about one-third of the variance in measures of depres-
the functional brain deficits reported in depression may sion), and imbalances in specific brain neurotransmitters
indeed result from imbalances in specific neurotransmit- such as serotonin, norepinephrine and dopamine have
ters such as serotonin, dopamine and norepinephrine been clearly linked to symptoms of depression. Recent
(e.g. Kupfer, Frank & Phillips, 2012). developments in brain scanning technology have also
allowed researchers to identify abnormalities in specific
Neuroendocrine factors Depression is regularly areas of the human brain that are associated with depres-
associated with problems in the regulation of body corti- sion. These are all impressive and important findings, but
sol levels — a hormone that is secreted in times of stress. we must remember that depression and mood disorders
We mentioned earlier that the hippocampus is important almost certainly do not stem solely from biological dys-
in adrenocorticotropic hormone secretion, and that function. As we shall see in the next section, psychologi-
depressed individuals frequently exhibit hippocampal cal and cognitive factors are equally important in the
abnormalities (Mervaala, Fohr, Kononen, Valkonen- aetiology and maintenance of mood disorders, and sup-
Korhonen et al., 2000). These hippocampal abnormali- plement our knowledge of biological factors. Biological
ties are regularly linked with high levels of cortisol (an and psychological explanations are not mutually exclu-
adrenocortical hormone), sive and they attempt to explain phenomena at different
cortisol An adrenocortical hormone.
and patients receiving levels of description. Indeed, it is still not clear whether
chronic corticosteroid therapy for endocrine problems many of the biological factors we have described in this
have smaller hippocampal volumes and higher depres- section are truly causal factors in depression, or whether
sion ratings than nonpatient controls (Brown, Woolston, they simply represent biological changes that reflect the
Frol, Bobadilla et al., 2004). In addition, the hypothalamic— experience of depression. That is, biological factors may
pituitary—adrenocortical (HPA) network is the biological give rise to many of the symptoms of depression, but
system that manages and reacts to stress, and triggers the psychological processes may in turn trigger these bio-
secretion of cortisol in response to stress. It is the lack of logical factors.
inhibitory control over cortisol secretion that is linked
with depression, and around 80 per cent of individuals Psychological theories
who are hospitalized because of their depressive symp-
toms show poor regulation of the HPA network (Heuser, Psychodynamic explanations There are numer-
Yassourides & Holsboer, 1994) and are more likely to be ous different psychodynamic views of depression (see
prone to future bouts of depression (Aubry, Gervasoni, Blatt & Homann, 1992), but the most well-established
Osiek, Perret et al., 2007). is the psychoanalytic account pioneered by Freud
Cortisol may influence depressive symptoms by (1917/1963) and Abraham (1916/1960). This view
causing enlargement of the adrenal glands and in turn argues that depression is a response to loss, and, in par-
lowering the frequency of serotonin transmitters in the ticular, a response to the loss of a loved one such as a
brain (Roy, Virkkunen & Linnoila, 1987). We saw ear- parent. The first stage of response to this loss is called
lier that low levels of the neurotransmitter serotonin introjection, where the individual regresses to the oral
in the brain have been established as an important fac- stage of development, and introjection A response to a loss where
tor in depression. As noted above, cortisol is also a hor- this allows them to inte- individuals regress to the oral stage of
mone that is released by the body during times of stress grate the identity of the development, which allows them to inte-
(Holsboer, 2001), and it is no coincidence that periods of person they have lost with grate the identity of the person they have
lost with their own.
depression are often preceded by stressful life events. So, their own. Introjection also
according to this account, life stressors raise levels of the allows them to direct all of the feelings they would have
adrenocortical hormone cortisol that in turn lowers levels for the loved one onto themselves. These include anger
of the brain neurotransmitter serotonin, which results in if they feel that the loved one has ‘deserted them’ and,
CHAPTER 7 DEPRESSION AND MOOD DISORDERS
ms DEPRESSION AND INFLAMMATION

Ss
me
Zz As we mentioned at the beginning of this chapter, dysfunction, and impaired sleep (Miller, Maletic &
fe)
a.
depression is a widely experienced mental health
problem. It has significantly high prevalence rates;
Raison, 2009; Meyers, Albitar & Estey, 2005).
So, how might inflammation and symptoms of
WV it is highly comorbid with other psychopathologies; it
> is also commonly experienced during many physical
depression be causally linked? Animal studies suggest
administration of cytokines can profoundly affect the
a
fe)
i,
illnesses (such as cardiac illnesses, cancer, diabetes, metabolism of the neurotransmitters implicated in
rheumatoid arthritis, and multiple sclerosis); and it depression, including serotonin, norepinephrine and
is also experienced during degenerative brain disor- dopamine (Anisman, Merali & Hayley, 2008; Felger,
ders such as Parkinson's disease and Alzheimer’s dis- Alagbe, Hu, Mook et al., 2007). Cytokines also gener-
ease (see Chapter 15). However, depression is not just ate behaviours strikingly similar to symptoms found in
a consequence of physical illness, it is also in many depression, such as listlessness, loss of appetite, lack of
cases a predictor of future illness. For example, depres- interest in socialising and sex, and increased sensitivity
sion is known to be a risk factor for coronary artery to pain. From an adaptive viewpoint, it makes sense for
disease (Stewart, Rand, Muldoon & Kamarck, 2009; an organism that is fighting disease and infection to
Suls & Bunde, 2005) and for strokes (May, McCarron, restrict activity generally and eat less to allow available
Stansfield, Ben-Shlomo et al., 2002). resources to be focused on the area that is under physi-
This link between depression and physical _ill- cal attack from illness.
nesses has led to the development of theories arguing There is still much more research required before
that inflammation may contribute to the experience we can be confident that inflammation is a process that
of depression. Central to this view are cytokines - contributes significantly to the experience of depres-
proteins made by immune cells that control responses sion, but the current arguments seem compelling
to foreign antigens and germs, generating inflam- and logical. It remains to be seen whether inflamma-
mation and fever. Consistent with this is the fact that tion is an explanation for all depression experience, or
depression also seems in be associated with changes whether some other causes of depression and depres-
in the immune system, especially those changes that sion experience are independent of inflammation.
involve cytokines. Studies have also shown that both However, if inflammation and depression are insepara-
medically ill and medically healthy individuals with bly bound together, then one implication of this is that
major depression exhibit all the cardinal features of treatment for depression will also need to take account
inflammation, including elevations in inflammatory of those medical processes that can alleviate inflam-
cytokines and symptoms such as fatigue, cognitive mation and relieve physical illness.
guilt if they experience any positive emotions in the are viewed as equivalent to losing a loved one. These
wake of the loss. The individual begins to experience losses then cause the individual to regress to the oral
self-hatred that develops very rapidly into low self- stage of development and may trigger memories of
esteem, and this adds to feelings of depression and inadequate parental support during childhood. In addi-
hopelessness. Because such losses return the individual tion, parental loss is no longer seen as a necessary condi-
to the oral stage of development, psychoanalysis argues tion for the development of depression, and poor
that depression has a functional role to play, in that it parenting is a more significant risk factor (Lara & Klein,
returns the person to a period in their life when they 1999). Support for this view comes from studies that
were dependent on others (their parents). During their have shown a relationship between risk for depression in
depressed state, this regression to the oral stage allows adulthood and having experienced a particular kind of
the individual to become dependent on their relation- parenting style known as affectionless control (Garber
ships with others in order to utilize the support that & Flynn, 2001). This type
this will offer. One problem with this psychoanalytic of ‘parenting is character- affectionless control A type of parenting
interpretation is that not everyone who experiences ized by high levels of over- characterized by high levels of overprotec-
tion combined with a lack of warmth
depression has lost a loved one, and this led Freud to pro- protection combined with and care.
pose the concept of sym- a lack of warmth and care.
nbolicloss A Freudian concept
ereby other kinds of losses within one’s bolic loss in which other There is some empirical support for this psychoana-
(e.g. losing a job) are viewed as equiva- kinds of losses within lytic view of depression. For example, individuals who
t to losing a loved one. one’s life (e.g. losing a job) report that their childhood needs were not adequately
met by their parents are more likely to become depressed be an active contributor to their lack of reinforcement ~
after experiencing a loss (Goodman, 2002). Also, especially social reinforcement. For example, depressed
there is evidence for a link between parental loss individuals are significantly more likely than non-
and depression. Women whose mothers either died or depressed individuals to elicit negative reactions in
abandoned them during their childhood are more likely others (Joiner, 2002) — perhaps because they do not enter
to develop depression than women who have not had into the reciprocal reinforcing activities that social inter-
these kinds of experiences (Harris, Brown & Bifulco, action requires. Depressed individuals are also less skilled
1990). Nevertheless, there are difficulties with the psy- at interacting with others than non-depressed individu-
choanalytic view. Firstly, much of the empirical evidence als (Joiner, 2002; Segrin, 2000). In particular, they will
that is consistent with this view is also consistent with usually communicate negative attitudes, appear with-
many other theories of depression, so the evidence does drawn and unresponsive, and tend to demand reas-
not help to differentiate between theoretical approaches. surance. Indeed, when interacting with depressed
Secondly, many individuals who do experience parental individuals, non-depressed control participants exhibit
loss or poor parenting do not go on to develop depres- less positive social behaviour, are less verbal, and are
sion. Psychoanalytic approaches do not clearly explain less positive than when interacting with a non-depressed
why this is the case. Finally, because of the way that individual (Gotlib & Robinson, 1982).
psychodynamic theories are formulated, many of the The frequent failure of depressed individuals to elicit
key aspects of the theory are difficult to test. Concepts reinforcing reactions from individuals with whom they
such as introjection, fixation at the oral stage of develop- are communicating has led to interpersonal theories of
ment and symbolic loss are all difficult to operationalize ression. These theories interpersonal theories
: Theories
: that
Gen
and measure, and so verify empirically. This difficulty is argue that depression is argue that depression is maintained by a
compounded by the Freudian belief that such processes maintained by a cycle Qf cycle of reassurance-seeking by depresse
are thought to operate at the unconscious level. excessive reassurance seek- individuals that is subsequently rejected b
ing faanmde presse duadinade family and friends because ofthe negative
, way in which depressed individuals talk
Behavioural theories The most obvious characteris- uals that is subsequently about their problems.
tics of depressed individuals include their lack of motiva- rejected by family and friends
tion and initiative, a considerably diminished behavioural because of the negative and repetitive way in which the
repertoire, and a view of the future that lacks positive depressed individual talks about their problems (Joiner,
and fulfilling experiences. Some theorists have suggested 1995). Excessive reassurance seeking is defined as ‘the
that these characteristics provide evidence that depres- relatively stable tendency to excessively and persistently
sion results from a lack of appropriate reinforcement for seek reassurances from others that one is lovable and
positive and constructive behaviours (Lewinsohn, 1974). worthy, regardless of whether such assurance has already
This leads to the extinction of existing behaviours, and been provided’ (Joiner, Metalsky, Katz & Beach, 1999),
to a behavioural vacuum’ in which the person becomes and the negative beliefs about themselves, their world and
inactive and withdrawn. It is certainly the case that their future leads depressed individuals to doubt any
periods of depression follow life ‘losses’ such as bereave- reassurances they are given by friends and family, and this
ment, retirement, or redundancy, and each of these continual doubting may come to annoy friends and family
events represent the loss of important sources of reward who try to provide reassurance (Joiner & Metalsky, 1995).
and reinforcement for social and occupational behaviours Interestingly, excessive reassurance seeking in depressed
(see also Figure 7.5 showing how suicide rates increase individuals predicts future depressive symptoms (Joiner,
during a financial recession). In support of this account, Metalsky, Katz et al., 1999; Haeffel, Voelz & Joiner, 2007),
it has been shown that depressed individuals report fewer and roommates of depressed college students report
rewards in their life than non-depressed individuals, and greater hostility to them than to non-depressed room-
introducing rewards into the lives of depressed individu- mates (Joiner, Alfano & Metalsky, 1992). Excessive reas-
als helps to elevate their mood (Lewinsohn, Youngren & surance seeking by depressed individuals is also associated
Grosscup, 1979; Jacobson, Martell & Dimidjian, 2001). with motivation to obtain self-confirming negative feed-
The fact that life ‘losses’ are likely to result in the reduc- back, which is another risk factor for depressive symp-
tion of reinforcing events for the depressed individual toms and interpersonal rejection that creates a vicious
also leads to a vicious cycle that can establish depres- cycle of rejection and depression (Davila, Stroud & Starr
sion as a chronic condition. For example, once the indi- et al., 2009). Evidence such as this appears to support the
vidual becomes depressed, then their lack of initiative view that the behaviour and attitudes displayed by
and withdrawal is unlikely to lead to the development depressed individuals elicits negative responses in others,
of other alternative sources of reinforcement. Indeed, and this in turn can exacerbate the symptoms of depres-
the demeanour of the depressed individual is likely to sion (Evraire & Dozois, 2011).
CHAPTER 7 DEPRESSION AND MOOD DISORDERS 207°
However, we must be cautious about how we inter- that leads to a vicious cycle of depressive affect and symp-
pret this evidence as a causal factor in depression. tomatology. Beck argued that these negative schema are a
Firstly, much of the research on the link between lack relatively stable characteristic of the depressed individual’s
of reinforcement and depression has been retrospec- personality, and develop as a result of early adverse child-
tive in nature, and it is quite reasonable to suppose that hood experiences — especially concerning loss (such as the
depressed individuals may underestimate the extent of loss of a parent figure). In later life, a stressful experience will
the actual rewards in their life. Secondly, we need to reactivate this negative schema and give rise to the biased
understand whether excessive reassurance seeking and thinking that generates depressive symptoms such as deficits
seeking negative feedback are dispositional factors that in motivational, affective, cognitive and behavioural
create a risk for depressive symptoms or whether depres- functioning.
sive symptoms themselves elicit these characteristics Beck argued that the depressed individual’s negative
(Evraire & Dozois, 2011). schema maintained some interrelated aspects of nega-
tive thinking that Beck called the negative triad. In
Negative cognitions and self-schema_ One of the particular, depressed peo- negative triad Atheory of depression
most influential of all the theories of depression is Beck’s ple hold negative views of in which depressed people hold negative
cognitive theory (Beck, 1967, 1987). This theory intro- themselves (e.g. ‘I am unat- views of themselves (e.g.'l am unattractive’),
duced the idea that depression could be caused by biases tractive’), negative views of their future (e.g.‘Iwill never achieve any-
thing’) and of the world (e.g. ‘The world is a
in ways of thinking and processing information. We of their future (e.g. ‘I will dangerous and unsupportive place’).
know that depressed individuals indulge in a good deal never achieve anything’),
of ‘negative thinking’, and that they experience more and of the world (e.g. ‘the world is a dangerous and
negative intrusive thoughts than non-depressed individu- unsupportive place’). This set of negative beliefs eventu-
als (Reynolds & Salkovskis, 1992). Facts such as this have ally generates self-fulfilling prophecies. That is, the
led Beck (1987) to claim that depressed individuals have depressed individual interprets events negatively, fails to
developed a broad-ranging negative schema that tends take the initiative, and then inevitably experiences fail-
them towards viewing the ure. The negative triad of beliefs leads to a number of
gative schema A set of beliefs that world and themselves in a systematic biases in thinking, including arbitrary infer-
ds individuals towards viewing the
negative way (see Figure 7.3).
rid and themselves in a negative way.
ence, selective abstraction, overgeneralization, magnifi-
Ks
In turn, these negative cation and minimization, personalization, and all-or-none
schema influence the selection, encoding, categorisation, thinking (see Table 7.2).
and evaluation of stimuli and events in the world in a way There is considerable evidence that depressed indi-
viduals do show the negative cognitive biases that
Beck’s theory predicts. First, some studies have shown
attentional biases to negative information in depressed
Negative triad
individuals that results in them prioritising that nega-
tive information. In the emotional Stroop procedure,
depressed individuals are slower at naming the colour of
negative words than positive words, suggesting that their
attention is drawn towards the meaning of such words
(Gotlib & Cane, 1987; Epp, Dobson, Dozois & Frewen,
2012). Also, in a dichotic listening procedure, depressed
individuals have greater difficulty ignoring negative words
that are presented as distractors than do non-depressed
Failures and losses participants (Ingram, Bernet & McLaughlin, 1994).
(the individual fails to take initiatives, and opportunities are lost) The exact nature of this attentional bias is unclear, and
some studies have failed to replicate these experimental
effects (e.g. Mogg, Bradley, Williams & Mathews, 1993).
Nevertheless, there is sufficient evidence to suggest that
there is a bias towards processing negative information
in depression — especially if it is information that is
specifically relevant to depression (rather than general
FIGURE 7.3 Beck’s negative schema in depression. negative words) (Gotlib, Gilboa & Sommerfeld, 2000).
This figure shows how the negative biases in the think- Second, memory biases are also apparent in depression,
ing of depressed individuals leads to a vicious cycle in which with depressed individuals able to recall more nega-
depression becomes a self-fulfilling prophecy. tive words than positive words in explicit memory tests
208 PSYCHOPATHOLOGY
TABLE 7.2 Thinking biases in Beck's model of depression interpreting ambiguous events negatively or to judge
events more negatively. There is considerable evidence,
Arbitrary inference Jumping to a conclusion when
for example, that depressed affect is associated with
evidence is lacking or is actually
contrary to the conclusion more critical selfjudgement and a raising of personal
performance standards (Forgas, Bower & Krantz, 1984;
Selective abstraction Abstracting a detail out of context
Scott & Cervone, 2002). More recent theories suggest
and missing the significance of the
that the combination of biases in attention, interpreta-
total situation
tion, memory and cognitive control and their interaction
Overgeneralization Unjustified generalization on the may be a better predictor of depressive symptoms than
basis ofa single incident (e.g. making
any of these biases alone (Hirsch, Clark & Mathews, 2006;
a single mistake and concluding
‘| never do anything right’)
Everaert, Koster & Derakshan, 2012), and this is a poten-
tially fruitful direction for future research in this area.
Magnification and Perceiving events as either totally
In addition to the evidence supporting the existence
minimization bad or neutral or irrelevant.
of negative information processing biases in depres-
Catastrophising is an example of
magnification, in which the individual sion, there is also evidence that supports specific predic-
takes a single fact to its extreme tions from Beck’s theory. For example, studies using the
(e.g. a scratch on a new car means the Dysfunctional Attitude Scale (DAS) — which measures
car is wrecked and needs replacing) dysfunctional negative beliefs — have shown that nega-
Personalization The propensity to interpret events tive thinking in combination with a recent negative life
in terms of their personal meaning to event can trigger depression (Lewinsohn, Rohde, Seeley
the individual rather than their & Baldwin, 2001). Further research has suggested that
objective characteristics (e.g. believ- depressed individuals may have two different types of neg-
ing that a frown on another person's ative schema — one related to dependency and the other
face means they are annoyed specifi-
related to criticism (Nietzel & Harris, 1990). In the case of
cally with you)
a dependency self-schema, losses would trigger depres-
All-or-none thinking Events are labelled as black or white, sion (e.g. bereavement), but in the case of the criticism
good or bad, wonderful or horrible
self-schema, depression would be triggered by failures
(e.g. assuming that everyone will
(e.g. failing an interview) (Coyne & Whiffen, 1995).
either accept you or reject you)
Finally, we tend to associate depression, and Beck's
cognitive theory of depression in particular, with pessi-
mistic thinking caused by negative self-schemas.
(Mathews & MacLeod, 1994), but this again seems to However, evidence sug-
apply predominantly to depression-relevant material gests that what depressed pessimistic thinking A form of dysfunc-
tional thinking where sufferers believe F
rather than threat-relevant material generally (Watkins, individuals may actually nothing can improve their lot.
Mathews, Williamson & Fuller, 1992). Furthermore, lack is the positive inter-
recent studies have indicated that depressed individu- pretation bias possessed by non-depressed individuals. It
als will remember more negative than positive infor- turns out that depressed individuals are much more
mation about themselves (Alloy, Abramson, Murray, accurate in experimental studies at evaluating (1) how
Whitehouse & Hogan, 1997), and of particular inter- much control they may have over a situation (Alloy &
est is the biased recall of autobiographical memories by Abramson, 1979), and (2) the impression they made on
depressed individuals. Not only do they recall fewer posi- others in a social situation (Lewinsohn, Sullivan &
tive autobiographical experiences than non-depressed Grosscup, 1980). In contrast, non-depressed individuals
individuals, but those positive memories that are are unduly optimistic in their estimates. This suggests
retrieved are more general and less detailed (Williams & that depressed individuals may be much more objective
Scott, 1988; Raes, Hermans, Williams & Eelen, 2006). about the judgements they make, and it is non-depressed
Subsequent studies have suggested that there may be individuals who possess a positive bias that may act to
an association between experiencing early life trauma ‘make them feel good about themselves’ (Lewinsohn,
(such as childhood abuse) and reduced autobiographical Sullivan & Grosscup, 1980).
memory specificity (Raes, Hermans, Williams & Eelen, In summary, Beck’s cognitive theory of depression
2005), and that poorly detailed autobiographical mem- has been significantly influential in determining the
ories may be linked to the deficits in problem-solving way we conceptualize, research and treat depression. It
ability that are characteristic of depressed individu- has generated a range of research on cognitive biases in
als (Pollock & Williams, 2001). Third, there is experi- depression and has contributed substantially to cognitive-
mental evidence that depressed individuals exhibit based treatments of depression (see section 7.3.1).
the interpretational bias that would lead them to However, it is still unclear whether the negative cognitive
CHAPTER 7 DEPRESSION AND MOOD DISORDERS 209%
USING EXPERIMENTAL PSYCHOPATHOLOGY METHODS

TO UNDERSTAND DEPRESSION
Theories of depression that allude to biases in thinking and dysfunctional beliefs (such as Beck's cognitive theory
of depression) need to be empirically tested to find out whether such biases do mediate depression. One impor-
tant way of doing this is to use experimental psychopathology to study the psychological processes that
underlie basic mental health problems such as depression (Vervliet & Raes, 2012).
experimental psychopathology
One aim of experimental psychopathology is to mimic in healthy individuals Experimental field of psychological science
those processes thought to underlie the cognitive or neurological mechanisms that aimed at understanding the processes
give rise to psychopathology, and so either increase our understanding of those underlying psychopathology.
mechanisms, or to confirm that such mechanisms do indeed lead to increases in symptoms. There are many ways
7.1
METHODS
RESEARCH
in which this can be achieved. One is by re-creating in the experimental lab the conditions thought to give rise to
symptoms, and testing these out on healthy individuals (e.g. by using negative mood inductions to generate sad
mood in healthy participants, and see if this affects attentional and memory biases in ways predicted by Beck's
theory — see section 7.1.2); an alternative is to create animal models of individual psychopathologies that can be
tested in experimental studies on animals such as rats or mice (e.g. testing the inflammation model of depression
on laboratory rats by experimentally investigating the effects of administered cytokines on the metabolism of
neurotransmitters implicated in depression; see Focus Point 7.3).
Vervliet & Raes (2012) point out that when conducting experimental psychopathology methods on healthy
participants, we need to be sure that such methods have external validity and are able to bridge what is called the
‘translational gap’ from healthy individuals to clinical cases. Up to four criteria need to be met for external validity:
(1) face validity - where there is at least a degree of phenomenological similarity between the behaviour of the
model and the symptoms in the disorder, (2) predictive validity - where performance in the model predicts per-
formance in the disorder, (3) construct validity - where the experimental psychopathology procedure accurately
recreates the aetiological processes or mechanisms known to operate in the disorder, and (4) diagnostic validity -
where the procedure shows that any experimental manipulations produce behavioural or cognitive outcomes
that can be properly extrapolated to those found in diagnosed patients (e.g. in intensity or frequency).
One example of the use of experimental psychopathology methods in the study of depression is a study by
Hepburn, Barnhofer & Williams (2006). They studied the effect of experimentally induced positive and negative
mood in healthy participants on the cognitive processes underlying future thinking. They found that partici-
pants induced into a negative mood (equivalent to depression) rated positive future events as more negative
than those in a positive mood and became less fluent at generating future positive events. They conclude that
increased negative or depressed mood may significantly reduce the accessibility of positive future events, and
also lead to the assessment of those events when retrieved as less positive than when in a neutral or positive
mood. This may have significant relevance to the processes underlying hopelessness (see section 7.1.2) and may
be a risk factor for suicidality.
biases defined by Beck’s theory actually cause depres- belief that negative life events will happen whatever they
sion, or whether these biases are simply a consequence do. Seligman (1974) first derived this hypothesis from
of experienced depression. Further research will be animal learning experiments in which dogs were first
needed to clarify issues such as this. given unavoidable electric shocks, and then subsequently
taught to learn a simple avoidance response that would
Learned helplessness and attribution During a avoid the shocks. He found that dogs that were given
person’s lifetime they may experience a number of una- prior unavoidable electric shocks were subsequently
voidable and uncontrollable negative life events. These unable to learn the avoidance response and simply lay
may include the sudden death of a close friend or rela- down in the apparatus and ‘quietly whined’. One exam-
tive, or being made redundant from a job. Seligman ple of how learned help-
(1975) proposed that depression could be linked specifi- lessness theory has been learned helplessness A theory of depres-
cally to these kinds of experiences, and that they give rise applied to depression is in sion that argues that people become
depressed following unavoidable negative
to a ‘cognitive set’ that makes the individual learn to the case of battered women. life events because these events give rise
become ‘helpless’, lethargic and depressed. It is the per- Walker (2000) has suggested to a cognitive set that makes individuals
ceived uncontrollability of these negative life events that that a pattern of repeated learn to become ‘helpless; lethargic and
partner abuse leads battered depressed.
is important, and leads the individual to the pessimistic
Ries PSYCHOPATHOLOGY
women to believe that they are powerless to change their be manipulated or are unlikely to change. In particular
situation. As a result, such women come to exhibit all the people who are likely to become depressed attribute neg-
symptoms of depression and display the ‘passivity’ found in ative life events to (1) internal rather than external factors
battered woman syndrome. (e.g. to personal traits rather than outside events),
However, while animal (2) stable rather than unstable factors (e.g. things that
battered woman syndrome The view experiments on learned are unlikely to change in the near future), and (3) global
that a pattern of repeated partner abuse rather than specific factors (e.g. causes that have an effect
helplessness do appear to
leads battered women to believe that they
have a formalistic similar-
are powerless to change their situation.
over many areas of their life rather than being specific to
ity to human depression, one area of functioning). Table 7.3 provides an exam-
there are a number of reasons for believing that it is not ple of the range of attributions that someone might
a full or comprehensive account of depression. Firstly, make in relation to failing a maths exam. In this case,
some studies with humans have suggested that prior the global, stable, and internal attribution is ‘I lack intel-
experience with uncontrollable negative events may ligence’, and this attribution is likely to have a number
actually facilitate subsequent performance (Wortman & of negative consequences. First, it is the kind of cause
Brehm, 1975). Secondly, many depressed individuals see that is not easily changed so that future failures might
themselves as being responsible for their failures and be avoided. Second, it reflects negatively on the individ-
losses — yet someone who perceives himself or herself as ual’s self-concept, and so is likely to reduce self-esteem.
helpless should not blame themselves for these events. Third, it is a global attribution, and so the individual is
Thirdly, in the specific case of battered woman syn- likely to believe that they will fail at many other things,
drome, passivity may not be the result of the woman and not just a maths exam, and this is likely to lead to the
learning that she is helpless, but it may be a learned adap- kinds of pessimistic thinking typical of depression.
tive response to abuse. This may take the form of the In contrast, if the student had attributed their failure to
woman thinking, ‘If I do not make requests and acqui- specific, unstable factors, such as ‘I am fed up with
esce to his demands, he is less likely to hit me’ (Peterson, maths’ or ‘my maths test was numbered 13’, they would
Maier & Seligman, 1993). have been less likely to experience helplessness (because
These difficulties and inconsistencies in the original these are factors that could change quite easily or
learned helplessness theory led to the development of a reduced self-esteem).
revised theory that included the important concept of In order to test the attributional account of depression,
attribution (Abramson, Seligman & Teasdale, 1978). Peterson, Semmel, von Baeyer, Abramson et al. (1982)
Attribution theories of depression argue that people developed the Attributional Style Questionnaire (ASQ)
learn to become helpless, which measures tendencies to make the particular kinds
attribution theories Theories of or more specifically “hope- of causal inference that are hypothesized to play a causal
depression which suggest that peoplewho Jeo’ because they possess role in depression (see Table 7.4). Several studies have
are likely to become depressed attribute : 3 :
ae :
negative life events to internal, stable and
certain attributional styles subsequently found that use of the global/stable attri-
global factors. that generate pessimistic butional style is a vulnerability factor for future depres-
thinking. Attributions are sion (Butters, McClure, Siegert & Ward, 1997; Chaney,
the explanations that individuals have for their behaviour Mullins, Wagner, Hommel et al., 2004) — especially fol-
and the events that happen to them. In particular, lowing negative life events (Hankin & Abramson, 2002).
Abramson, Seligman & Teasdale (1978) argue that A study by Metalsky, Joiner, Hardin & Abramson (1993)
people become depressed when they attribute negative gave students the ASQ prior to a midterm exam and then
life events primarily to factors that either cannot easily measured depressive symptoms over the subsequent
TABLE 7.3 Why! failed my GCSE maths exam
Internal External
(personal) (environmental)
Degree Stable Unstable Stable Unstable
Global | lack intelligence | am exhausted These tests are unfair It’s an unlucky day
Specific | lack mathematical ability (lam fed up with maths The test is unfair My maths test was numbered 13
People who become depressed tend to attribute negative life events to internal, stable global causes (in this example‘Ilack intelligence’ is an exam-
ple of this). In contrast, had the individual attributed their failure to specific, unstable factors (such as‘l am fed up with maths’ or‘My maths test was
numbered 13’), they would have been less likely to experience helplessness.
és
TABLE 7.4 The Attributional Style Questionnaire (ASQ)
The ASQ contains a number of hypothetical situations designed to measure the individual's bias towards making certain kinds
of attributions for both positive and negative events. Abramson, Seligman & Teasdale (1978) argued that people who attribute
negative events to internal, stable and global events are most likely to develop helplessness and depression.
Sample situation and items:
You have been looking for a job unsuccessfully for some time.
|. Write down the one major cause.
2. Is the unsuccessful job search due to something about you or to something about other people in the circumstances?
TOTALLY DUE TO
OTHER PEOPLE OR TOTALLY

CIRCUMSTANCES 1 2 3 4 5 6 DUE TO ME
3. In the future when looking for a job, will this cause be present?
WILL NEVER AGAIN WILL ALWAYS

BE PRESENT 1 2 3 4 5 6 BE PRESENT
4. |s the cause something that just influences looking for a job or does it also influence other areas of your life?
INFLUENCES JUST INFLUENCES

THIS PARTICULAR ALL SITUATIONS
SITUATION 1 2 3 4 56 IN MY LIFE
5. How important would this situation be if it happened to you?
NOT AT ALL EXTREMELY

IMPORTANT 1 2 3 4 See 6 IMPORTANT
Item 2 measures internality, item 3 measures stability, and item 4 measures globality
5 days. They found that the students’ enduring depressive Abramson, Metalsky & Alloy (1989) suggested that the
reactions during this period were predicted by a global/ tendency to attribute negative events to global/stable
stable attributional style together with low self-esteem causes represents a diathesis which, in the presence of
and exam failure. This suggests that the global/stable negative life events, increases vulnerability to a group
attributional style in the context of a negative life event of depressive symptoms, including retarded initiation of
(e.g. exam failure) is a good predictor of subsequent voluntary responses, apathy, lack of energy and psycho-
depression. Finally, a computer-based cognitive bias mod- motor retardation. This cluster of symptoms is known as
ification task (see Treatment in Practice Box 6.4) can be hopelessness, which is an expectation that positive out-
used to create either negative or positive attributional comes will not occur, negative outcomes will occur, and
styles, and individuals in which the positive attributional that the individual has no responses available that will
style is induced subsequently report less depressed mood change this state of affairs. Hopelessness theory is very
in response to a stressor than individuals in which a neg- similar to attributional/
hopelessness theory A theory of depres-
ative attributional style is induced (Peters, Constans & helplessness accounts in sion in which individuals exhibit an expec-
Mathews, 2011). Experimental studies such as this sug- that negative life events tation that positive outcomes will not
gest a direct causal link between attributional style and aré viewed as interacting occur, negative outcomes will occur, and
depressed mood. with a global/stable attri- that the individual has no responses avail-
able that will change this state of affairs.
butional style to generate
Hopelessness theory The attributional/helplessness depressed symptomatology. However, hopelessness
account of depression has been further refined to account theory also predicts that other factors, such as low self-
for the fact that attributional style appears to interact esteem, may also be involved as vulnerability factors
with a number of other factors to cause depression. (Metalsky, Joiner, Hardin & Abramson, 1993). Many
ay ae PSYCHOPATHOLOGY
- * %
studies have supported the hopelessness theory by con- (1) many of the studies claiming to support hopeless:
firming that depression can be predicted by a combina- ness theory have been carried out on healthy or only
tion of negative attributional style, negative life events, mildly depressed participants who are not representa-
and low self-esteem (Alloy, Lipman & Abramson, 1992; tive of individuals who are clinically depressed (Coyne,
Metalsky & Joiner, 1992; Metalsky, Joiner, Hardin & 1994), (2) a majority of studies testing the model are
Abramson, 1993; Bohon, Stice, Burton, Fudell et al., correlational in nature, and so cannot provide any evi-
2008), and that the negative attributional style is signifi- dence on the possible causal role of hopelessness cogni-
cantly more related to hopelessness depression symp- tions in generating depression (Henkel, Bussfield, Moller
toms (e.g. lethargy, hopelessness, difficulty making & Hegerl, 2002), (3) the model does not explain all of
decisions) than endogenous depression symptoms (e.g. the depressive symptoms-required for a DSM-5 diagno-
loss of interest in sex, loss of appetite, loss of weight) sis, only those related to hopelessness, and (4) there is
(Joiner, 2001). In addition to predicting many symptoms some evidence that the negative attributional style dis-
of depression, hopelessness is also a construct that has appears during remission or recovery from depression
been shown to predict suicidal tendencies and, in par- (Hamilton & Abramson, 1983), and this suggests that it
ticular, completed suicide (Conner, Duberstein, Conwell, may not be a universal or enduring feature of individu-
Seidlitz & Caine, 2001). als who experience depression. This latter fact raises the
Nevertheless, despite the enhanced ability of the question of what comes first, the negative attributional
evolved model to predict depressive episodes, there are style or symptoms of depression? (But see Research
still a number of limitations to hopelessness theory: Methods 7.2.)
2 PROSPECTIVE STUDIES
Ss
Vv)
(a) Questionnaire studies are usually designed to see whether there are any relationships (i.e. correlations) between
Le) different measures. This is a very useful first step in researching a topic because it tells us what measures or
25 constructs appear to be strongly associated. For example, measures of negative attributional style (attribut-
-
La ing negative events to global/stable causes) are found to be highly correlated with measures of depression
= (Alloy, Lipman & Abramson, 1992).
- Theorists who support the hopelessness theory of depression would say that these kinds of correlations
U
c provide support for that theory (i.e. support for the view that a negative attributional style is a causal factor in
x developing depression). However, when two measures are highly correlated we must be cautious for at least two
ud
WV) reasons:
Lu
ce
1. We cannot infer that there is a causal relationship between these measures, because their association might
be mediated by some third variable that has not been measured. For example, negative attributional style
and depression might be highly correlated because they are both related to the number of negative life
events the people have experienced
Negative Attributional
Negative
Lite Events
ne ee Depression
2. Similarly, if there is a causal relationship between two variables that are highly correlated, we do not know
the direction of that causal relationship. While hopelessness theory predicts that negative attributional
style should cause depression, a correlation between these two variables is just as likely to imply that
depression causes a negative attributional style.
Negative Attributional
|
Depression
One way to overcome some of these difficulties in interpreting results from correlational studies is to conduct
what are known as prospective studies.
Prospective studies take measures ofthe relevant variables at a particular point in time (usually called Time 1),
and then go back to the same participants at some future time or times and take the same measures again
(usually called Time 2). Using this method a researcher can see if measures of a variable at Time 1 (e.g. negative
attributional style) predict, or are correlated with, measures of variables taken at Time2 (e.g. depression). In addi-
tion, because the researchers will have taken measures of depression at both Time 7 and Time 2, they can also
see if levels of negative attributional style predict changes in depression scores between Time 1 and Time 2. This
procedure allows the researcher to make much stronger statements about the possible causal direction of a
relationship between two variables, and whether one variable is a risk factor for the other (i.e. whether negative
attributional style is a risk factor for increased depression over time).
Such a prospective study was undertaken by Robinson & Alloy (2003). Using undergraduate students as
participants, they took measures of negative attributional style (using the Cognitive Style Questionnaire) and
depression (using the Beck Depression Inventory) at Time 1. Regular prospective assessments then took place
every 6 months for 2.5 years (Time 2, Time 3. . . and so on). Even when the level of depressive symptoms at
Time 1 was taken into account, they found that measures of variables such as negative attributional style pre-
dicted the incidence and number of future depressive episodes. They concluded that negative cognitive style
(including negative attributional style) was a risk factor for future depression.
Rumination theory Depressed individuals spend a Rumination in depressed individuals appears to be driven
good deal of time indulging in ruminative activities, which by meta-cognitive beliefs that rumination is a necessary
may either increase the risk of depression or increase the process to undertake in order to resolve depression
probability of relapse following recovery from depression. (Papageorgiou & Wells, 2001), and these beliefs appear to
Rumination is a tendency to repetitively dwell on the contribute to the repetitive or perseverative nature of
experience of depression or depressive rumination (Hawksley & Davey, 2010; Chan,
umination The tendency to repetitively
its possible causes, either in Davey & Brewin, 2013). Other studies have indicated that
well on the experience of depression or
s possible causes. a repetitive or ‘brooding’ rumination is associated with overgeneral autobiographi-
fashion (Crane, Barnhofer & cal memory (Sumner, 2012), which is a common charac-
Williams, 2007) or in an analytical way that attempts to teristic of depressed individuals. Rumination is also a
seek explanations for the experience (Watkins, 2008). vulnerability factor for depression during the transition
Tendency to ruminate has been shown to predict the onset from early to middle adolescence (Abela & Hankin, 2011),
of depressive episodes (Morrow & Nolen-Hoeksema, and is higher in women than men — possibly contributing
1990; Nolen-Hoeksema, 2000), and relapse back into to the significantly higher depression rates in women than
bouts of depression (Michalak, Holz & Teismann, 2011). men (Nolen-Hoeksema, 2000).
_
SELF-TEST QUESTIONS
e What are the two main mood disorders?
e Name at least five of the symptoms that must be present during a 2-week period for a diagnosis of major depressive
disorder?
e Why has it been difficult to gauge the prevalence of depressive disorders?
° Can you describe some of the problems involved in diagnosing major depressive disorder?
° Can you describe some of the main features of seasonal affective disorder (SAD) and chronic fatigue syndrome (CFS)?
® Describe the evidence that suggests there is a genetic component to major depression.
® What role do the neurotransmitters serotonin, dopamine and norepinephrine play in depression?
° How have abnormalities in certain brain areas been linked to the experience of depression?
e Howare cortisol levels supposed to be involved in the development of depression?
® Why is the individual’s response to loss so important in psychodynamic theories of depression?
214 PSYCHOPATHOLOGY
%
Can you describe how behavioural theories and interpersonal theories explain the development of depression?
What is Beck's ‘negative triad’? ;
What is the evidence that depressed individuals hold negative beliefs about themselves and the world?
What are the benefits and the limitations of learned helplessness as an explanation of depression?
What kinds of attributions are likely to lead to depressed thinking?
What are the important features of hopelessness theory of depression?
SECTION SUMMARY
7.1 MAJOR DEPRESSION
Major depression (or unipolar depression) and bipolar depression are the two main types of clinical depression.
Depression is the third most common reason for consulting a doctor or GP in the UK.
The lifetime comorbidity rate of major depression with another anxiety disorder is 58 per cent and with more than
one other DSM disorder is 74 per cent suggesting that individuals with depression experience a range of negative
emotions.
Premenstrual dysphoric disorder, seasonal affective disorder (SAD), and chronic fatigue syndrome (CFS) are three promi-
nent disorders with depression as a significant element.
Estimates of lifetime prevalence rates for major depressive disorder range from 5.2 to 17.1 per cent.
Major depression is almost twice as common in women as in men.
The incidence of major depression has increased since 1915 with a median onset age of around 27 years.
There is good evidence for a genetic component to major depression.
Abnormalities in the levels of the brain neurotransmitters serotonin, dopamine and norepinephrine are associated with
depressed mood.
Depressed mood has been shown to be associated with abnormal activity in a number of brain areas, including the
prefrontal cortex, the anterior cingulate cortex, the hippocampus, and the amygdala.
High levels of cortisol may lead to depression by causing enlargement of the adrenal glands and in turn lowering
the frequency of serotonin transmitters in the brain.
Psychoanalytic theory argues that depression is a response to loss, and the loss of aloved one such as a parent.
Behavioural theories claim that depression results from a lack of appropriate reinforcement for positive and constructive
behaviours, and this is especially the case foliowing a ‘loss’ such as bereavement or losing a job.
Interpersonal theories of depression claim that depressed individuals alienate family and friends because of their
perpetual negative thinking, and this alienation in turn exacerbates the symptoms of depression.
Beck's cognitive theory of depression argues that depression is maintained by a ‘negative schema’ that leads depressed
individuals to hold negative views about themselves, their future and the world (the ‘negative triad’).
Learned helplessness theory argues that people become depressed following unavoidable negative life events because
these events give rise to a cognitive set that makes individuals learn to become ‘helpless’ lethargic and depressed.
Attributional accounts of depression suggest that people who are likely to become depressed attribute negative life events
to internal, stable, and global factors.
Hopelessness is a cluster of depression symptoms that are characterized by an expectation that positive outcomes
will not occur, negative outcomes will occur, and the individual has no responses available that will change this state
ofaffairs.
Depressive rumination can increase the risk of depression or increase the risk of relapse.
&
7.2 BIPOLAR DISORDER conversations to talk about something that has just
caught their attention. Individuals in a manic phase may
spontaneously start conversations with strangers, and
, Bipolar disorder is a mood indulge in inappropriate or imprudent sexual interactions.
For a video on bipolar disorder go to
www.wiley-psychopathology.com/ | disorder characterized by These behaviours are usually recognized as excessive
video/ch7 | alternating periods of dep- by those who know the sufferer, but any attempt to quell
ression and mania. Often these excesses is usually met with anger and annoyance.
the swings between these two states can be very rapid, As a result, irritability and lability of mood is often one of
taking the individual from an extreme ‘high’ to an extreme the significant features of the manic individual. Periods
‘low’ very quickly. The personal accounts of experiences of mania can last for days or even weeks, and onset can
of bipolar disorder described in Client’s Perspective 7.1 occur rapidly over the course of a single day. DSM-5
provide some insight into the desperation generated by Summary Table 7.4 provides the criteria for a manic
periods of depression and the frightening confusion that episode (although this is not a codable disorder). Because
can be experienced during periods of sustained mania. of these symptoms, bipolar disorder is a severely
Someone who suffers bipolar disorder and is in a manic debilitating condition that can limit functioning and
phase can be recognized by many characteristics, includ- workplace productivity; it is associated with increased
ing the expression of a constant, sometimes uncon- mortality andrelativelyhigh SE EDDIE
nected, stream of thoughts and ideas; attention span rates of relapse (Newberg, For a video on mania go to
may be limited and the person shifts rapidly from topic Catapano, Zarate & Manji, | video/ch7
to topic. They will be loud and often interrupt ongoing 2008).
CLIENT’S PERSPECTIVE 7.1

THE EXPERIENCE OF BIPOLAR DISORDER
Descriptions offered by people with bipolar disorder give MANIA

valuable insights into the various mood states associated
with the disorder: ‘The fast ideas become too fast and there are far too
many... overwhelming confusion replaces clarity... you
stop keeping up with it -memory goes. Infectious humour
DEPRESSION ceases to amuse. Your friends become frightened . . .
everything is now against the grain. . . you are irritable,
‘| doubt completely my ability to do anything well. It angry, frightened, uncontrollable, and trapped.
seems as though my mind has slowed down and burned
out to the point of being virtually useless . . . [I am]
haunt[ed] . . . with the total, the desperate hopelessness
Clinical Commentary
of it all... Others say, “It’s only temporary, it will pass, you
can get over it”, but of course they haven't any idea of how This provides an insight into how the different
| feel, although they are certain they do. If | can’t feel, mood states in bipolar disorder are experienced,
move, think or care, then what on earth is the point?’
and how the transition from a depressive episode
moves through the mild manic episode called
hypomania to full blown mania. Typical of the
HYPOMANIA transition from depression to full-blown mania
are (1) the overwhelming flow of thoughts and
‘At first when I'm high, it’s tremendous . . . ideas are ideas that lead to the sufferer seeming incoher-
fast. . . like shooting stars you follow until brighter ones ent and interrupting ongoing conversations,
appear. . . All shyness disappears, the right words and (2) the temptation to indulge in inappropriate
gestures are suddenly there . . . uninteresting people, sexual interactions as everyone around becomes
things become intensely interesting. Sensuality is perva- a focus of interest and shyness is lost, and (3) the
sive; the desire to seduce and be seduced is irresistible. inevitable drift by the sufferer into irritability, frus-
Your marrow is infused with unbelievable feelings of ease, tration and anger as friends and acquaintances
power, well-being, omnipotence, euphoria. . . you can try to quell the excesses of thought and behaviour.
do anything. . . but, somewhere, this changes:
216 | PSYCHOPATHOLOGY
®
DSM-5 SUMMARY TABLE 7.4 Criteria fora manic episode 7.2.1. The Diagnosis and Prevalence
Unusual and continual elevated, unreserved or irritable of Bipolar Disorder
mood and unusual and continual increase in energy levels
lasting at least a week DSM-5 defines two main types of bipolar disorder,
Presence of at least three of the following:
namely ‘bipolar disorder I’ and ‘bipolar disorder IV’.
DSM-5 Summary Table 7.5 illustrates the main diagnos-
e Inflated self-esteem or grandiosity
tic features of these two definitions. The most common
e Less need for sleep of these two diagnoses is bipolar disorder I, where indi-
e Increased talkativeness viduals exhibit full manic and major depressive episodes
e Racing thoughts in alternating sequences. In bipolar disorder II, major
depressive episodes alternate with periods of hypomania
e Easily distractible
(mild manic episodes — see DSM-5 Summary Table 7.6
e Increase in goal-directed activity or unintentional and for a definition of hypoma-
purposeless motions hypomania Mild episodes of mania.
nia). While the symptoms
e Unnecessary participation in activities with a high of bipolar disorder II must be sufficiently severe to cause
potential for painful consequences distress or impairment, individuals with this disorder can
as MOOD DISORDERS AND CREATIVITY

=
— Brian Wilson, T.S. Eliot, Mark Twain and Vincent Van to have suffered childhood sexual abuse. In addition
Gogh. These artists are a few of many that have all suf- to this evidence that psychological problems may
2)
a fered from symptoms of bipolar disorder, and thereisan precede creativity, some studies have found that indi-
WwW enduring belief that creativity in the arts is associated viduals with bipolar disorder score higher on measures
>
with psychological disturbance and even ‘madness: Is of creativity than do non-clinical control participants
this just a myth or is there some truth in this belief? (Richards, Kinney, Lunde et al., 1988).
a Kay Jamison (1992), a psychiatrist, spent some years In contrast to this evidence, it could be argued that
studying the lives of famous contributors to the arts, artistic communities, where emotional expression is
including poets, artists and musicians. She concluded a valued commodity, are welcoming places for indi-
that there did seem to be a link between mood disor- viduals with psychological or mood disorders (Ludwig,
ders such as bipolar disorder and creativity and artis- 1995). We must also remember that psychological dis-
tic achievement. She found that British poets during order is not a prerequisite for creative achievement, and
the 18th century were significantly more likely than (1) many people make significant artistic and creative
members of the general population to have suffered contributions without exhibiting any signs of mental
symptoms of bipolar disorder, have been committed health problems, and (2) those artists suffering psycho-
to a lunatic asylum, or have committed suicide. This logical problems often continue to make impressive
_ view has been reinforced by a recent large-scale study contributions to their art even after successful treat-
showing that bipolar disorder is more prevalent in ment of their disorders JIamison, 1995; Ludwig, 1995).
groups of people with artistic or scientific professions, Even so, it is worth considering how psychological
such as dancers, researchers, photographers and problems such as bipolar disorder might contribute
| authors (Kyaga, Landén, Boman, Hultman et al., 2013). to creativity. First, mania gives individuals the energy
| But what exactly might this link between bipolar disor- and sharpened thinking that may be required for
_ der and creativity be? creative achievement, and it also gives the individual
The first question to ask is ‘what comes first — the confidence and feelings of inspiration that may not
creativity or the psychological disturbance?’ There otherwise be experienced. Second, there is evidence
| is some evidence that creative individuals do have a that depressed mood can also make a contribution
family history of psychological problems, suggesting to creativity by raising performance standards. For
that their psychological difficulties may precede their example, Martin & Stoner (1996) found that nega-
| creativity. For example, creative individuals often had tive moods lead to lower Ronficlence inmaneeadeguacy
| parents who suffered from psychological disorders, of creative effort, and ===
_ and may have suffered the kind of childhood abuse this spurs individuals in To read more on bipolar disorder
and creativity go to
that might give rise to psychological problems later in negative moods on to http://tinyurl.com/9jg2q7m
life. For instance, the author Virginia Woolf was known greater efforts.
CHAPTER 7 DEPRESSION AND MOOD DISORDERS ag
DSM-5 SUMMARY TABLE 7.5 Criteria for bipolar disorder | and DSM-5 SUMMARY TABLE 7.7 Criteria for cyclothymic disorder
bipolar disorder II
e For at least 2 years there have been many periods with
Bipolar disorder | hypomanic symptoms that do not meet the criteria for a
¢ Presence or history of at least one manic episode(s) hypomanic episode and many periods with depressive
° The manic episode may have been preceded by and may symptoms that do not meet the criteria for a major depres-
be followed by hypomanic or major depressivé-episodes. sive episode. These symptoms have not been absent for
more than 2 months at a time
e Symptoms are not better accounted for by schizoaffective
disorder or other disorders ¢ No major depressive episode, manic episode or hypomanic
episode has been present during the first 2 years of the
Bipolar disorder Il disorder
e Presence or history of at least one major depressive episode(s)
e The episode is not due to the use of medication, drug
e Presence or history of at least one hypomanic episode(s)
abuse or other treatment
* No history of manic episode(s)
¢ Symptoms are not better accounted for by schizoaffective
disorder or other disorders
DSM-5 SUMMARY TABLE 7.6 Definition of hypomania 35
3 —@ Point prevalence
e Unusual and continual elevated, unreserved or irritable
mood and unusual and continual increase in energy levels S 25 )— 6/12-month prevalence
lasting at least a week fo)
e Presence of at least three of the following:

& “| &
e Inflated self-esteem or grandiosity
a
e Less need for sleep } tl

e Increased talkativeness
e Racing thoughts
e Easily distractible
Woy x
Ce :
eS~Y i ~ SS
e Increase in goal-directed activity or unintentional and
\\ Now @W&
purposeless motions Zo teRS
e Unnecessary participation in activities with a high ~
potential for painful consequences
FIGURE 7.4 Prevalence of bipolar disorder across various
e Anoted change in functionality which is not usually seen
in the individual and changes in functionality and mood regions of the world.
Source: Ferrari, A.J., Baxter, A.J. & Whiteford, H.A. (2011). A system-
are noticeable by others
atic review of the global distribution and availability of prevalence
e The episode is not due to the use of medication, drug data for bipolar disorder. Journal ofAffective Disorders, 134(1), 1-13,
abuse or other treatment Figure 2. Reproduced with permission.
often be relatively productive during their periods of suggest a lifetime prevalence rate of around 1 per cent
hypomania (Jamison, 1995). (Merikangas, Akiskal, Angst, Greenberg et al., 2007).
Cyclothymic disorder is a mild form of bipolar disor- This appears to be supported by a systematic review of
der in which the sufferer global prevalence data showing a 12-month prevalence
peotnymic dis disorder A form of depres-
has mood swings over a rate of 0.8 per cent when data are compared across 20
on characterized by at least 2 years of
pomania symptoms that do not meet period of years that range geographic regions of the world (see Figure 7.4) (Ferrari,
Ie criteria for a manic episode and in from mild depression to Baxter & Whiteford, 2011).
hich the sufferer experiences alternating euphoria and excitement. It
eriods of withdrawal then exuberance, is characterized by at least 2
adequacy and then high self-esteem.
years of hypomania symp- 7.2.2 The Aetiology of Bipolar Disorder
toms that do not meet the criteria for a manic episode,
and the sufferer will experience alternating periods of Biological theories
withdrawal then exuberance, inadequacy and then high
self-esteem, and so on (see DSM-5 Summary Table 7.7). Genetic factors There is good evidence that bipo-
Bipolar disorder is much less common than major lar disorder has an inherited component. For example,
depressive disorder, and epidemiological studies family studies have indicated that 10-25 per cent of
218% PSYCHOPATHOLOGY
TABLE 7.5 Concordance rates in selected twin studies of can have a significant effect on both mania and depres»
bipolar disorder sion symptoms within a 7-8 week period compared with
placebo controls, but it is still unclear how the beneficial
Monozygotic Dizygotic twins
Study twins (MZ) (%) (DZ) (%)
effects of this drug combination might act through their
effects on specific brain neurotransmitters (Deeks &
Rosanoff et al. (1935) 69.6 16.4 Keating, 2008).
Kallman (1954) 92.6 23.6
Bertelsen (1979) 58.3 73 Triggers for depression and mania

Kendler et al. (1993) 60.7 34.9 in bipolar disorder
Bipolar disorder consists of two quite different symp-
TOTAL 69.6 29.3
tom types in depression and mania, and what interests
Source: Kelsoe, J.R. (2003). Arguments for the genetic basis of the bipolar
clinical researchers is the triggers for these two differ-
spectrum. Journal ofAffective Disorders, 73, 183-197. Reproduced with
permission.
ent types of symptoms. The triggers for a depressive
episode in bipolar disorder appear to be very similar to
the factors that instigate depression generally, namely
first-degree relatives of bipolar disorder sufferers have experiences such as losses, failures, and negative life
also reported significant symptoms of mood disorder events generally (Johnson, Cuellar & Miller, 2010).
(Gershon, 2000), and it has been estimated that approxi- The triggers for bouts of mania also appear to be var-
mately 7 per cent of the first-degree relatives of sufferers ied and include an increased responsiveness to rewards
also have bipolar disorder (Kelsoe, 2003) — this is com- (e.g. mania can be a reaction to a positive life event such
pared with a lifetime prevalence rate in the general pop- as passing an exam) (Meyer, Johnson & Winters, 2001),
ulation of between 0.4 and 1.6 per cent. Twin studies reactions to antidepressant medication, disrupted sleep
also suggest a significant inherited component in mood patterns and circadian rhythms, seasonality (bouts of
disorders. For example, Table 7.5 shows the concord- mania increase in either spring or summer), stressful life
ance rates for bipolar disorder in sets of MZ twins and events generally, and exposure to high emotional expres-
DZ twins (Kelsoe, 2003). Concordance rates average sion in family members or caregivers (Proudfoot, Doran,
69 per cent and 29 per cent for MZ and DZ twins respec- Manicavasagar & Parker, 2011).
tively, suggesting that sharing all genes as opposed to Study of some of these triggers has resulted in
half of genes more than doubles the risk for developing a number of models of mania. Firstly, the study of
bipolar disorder. how mania is triggered by goal attainment (e.g. pass-
ing an exam) suggests that mania may be associated
Neurochemical factors Bipolar disorder has also with dysregulation in the behavioural activation sys-
been shown to be reliably associated with abnormalities tem (BAS) that regulates sensitivity to rewards, and
in levels of brain neurotransmitters. Like major depres- the goal-directed behaviours that are facilitated by
sion, bipolar disorder seems to be associated with dopa- the BAS are very similar to those behaviours exhibited
mine and norepinephrine irregularities, but serotonin by bipolar sufferers during a manic phase (e.g. physi-
does not appear to play such a central role in bipolar ological arousal, increased sociability and incentive-
symptoms, and this is evidenced by the fact that sero- reward motivation) (Depue & Iacono, 1989). Secondly,
tonin reuptake is not a sufficient condition for antide- the fact that mania is associated with disruption to
pressant efficacy in bipolar depression (Fountoulakis, sleep and circadian rhythms suggests that this may
Kelsoe & Akiskal, 2012). In addition, the mania found in be an important cause of mania. Not only does sleep
bipolar disorder is found to be associated specifically duration predict hypomanic symptoms the follow-
with high levels of norepinephrine (Bunney, Goodwin & ing morning (Leibenluft, Albert, Rosenthal & Wehr,
Murphy, 1972; Altshuler, 1996), but disruption to normal circadian rhythms (e.g.
olanzapine An antipsychotic drug com- Curran, Hauser, Mintz et driving through the night, long airplane journeys,
monly prescribed in combination with the al., 1995). A common pop- working night shifts) also results in a shift to hypomania
antidepressant SSRI drug fluoxetine as a
treatment for bipolar disorder.
ular form of treatment for within 24 hours. The close relationship between sleep/
bipolar disorder is a combi- circadian rhythm disruption and manic episodes has led
fluoxetine (Prozac) A selective serotonin
nation of the antipsychotic some theorists to suggest that sleep deprivation may
reuptake inhibitor (SSRI) which reduces drug olanzapine and the be the final common pathway through which a variety
the uptake of serotonin in the brain and is antidepressant SSRI drug of other factors precipitate episodes of bipolar mania
taken to treat depression. fluoxetine (Prozac). This (Wehr, Sack & Rosenthal, 1987).
&
SELF-TEST QUESTIONS
* What are dysthymic disorder and cyclothymic disorder?

* What is the distinction between bipolar disorder | and bipolar disorder II?
* Describe the evidence that suggests there isagenetic component to bipolar disorder.
* What are the main types of pharmacological treatment for bipolar disorder?
* What factors trigger either periods of depression or periods of mania in bipolar disorder?
SECTION SUMMARY
7.2 BIPOLAR DISORDER
* Bipolar disorder is characterized by periods of mania that alternate with periods of depression.
© Hypomania are defined as mild manic episodes.
® Cyclothymic disorder is a mild form of bipolar disorder which ranges from mild depression to mania.
© The lifetime risk for bipolar disorder is 0.4 to 1.6 per cent.
° There is good evidence for a genetic component to bipolar disorder. Generally, 10 to 25 per cent of first-degree relatives
of bipolar disorder sufferers also report symptoms of mood disorder, as do 5-10 per cent offirst-degree relatives of major
depression sufferers.
¢ Two significant triggers for mania in bipolar disorder include goal attainment and sleep disruption.
often adopted, and these models advise that the type of

7.3 THE TREATMENT treatment provided for depression should be tailored
to the severity of the symptoms and the personal
OF DEPRESSION AND and social circumstances of the sufferer. An example
MOOD DISORDERS of a stepped-care model would be one where (1) GPs
and physicians — who are normally the first port of call
for many people experiencing depression — are advised
The previous sections illustrate the broad range of to ensure that proper assessment is made of individu-
theories addressing the aetiology of mood disorders, als who might present with symptoms of depression,
and these theories have each given rise to a variety of and they should not simply respond by providing medi-
different treatments for these disorders. These include cation, (2) medication would not normally be recom-
a number of biological-based treatments such as drug mended for the initial treatment of depression but should
therapy and electrocon- be reserved for the treatment of moderate to severe
lectroconvulsive therapy (ECT) A vulsive therapy (ECT) depression where there is more evidence for its effective-
1ethod of treatment for depression or
which address the known ness, and (3) mild depression should be treated primarily
sychosis, first devised in the 1930s, which
wolves passing an electric current of neurochemical imbalances with brief behavioural and cognitive interventions, and
round 70-130 volts through the head of in depression, and a wide these include structured exercise (e.g. three sessions per
1e patient for around half a second. range of psychological week, of moderate duration, for 10-12 weeks), guided
therapies including psy- self-help and computerized CBT sean pass (an exam-
tepped-care models Treatments for chodynamic, behavioural ple of which is “Beating the Blues™’ — see Treatment
sychopathology that emphasize that the in Practice Box 7.1 and g# ;
and cognitive behavioural
spe of treatment provided for those indi- To read more about ‘Beating the
duals should be tailored to the severity therapies. Stepped-care section 4.1.2) (Scogin,
Blues’go to
ftheir symptoms and their personal and models for the treat- Hanson & Welsh, 2003; | www.beatingtheblues.co.uk
cial circumstances. ment of depression are NICE, 2008).
PSYCHOPATHOLOGY
TREATMENT IN PRACTICE 7.1

BEATING THE BLUES USING COMPUTERIZED CBT
The UK National Institute for Health & Care Excellence programme driven by their current needs, including
(NICE) guidelines for treating depression recommend homework projects to complete between sessions, and
that computerized CBT (CCBT) is considered for persistent clinical outcomes are monitored on a session-by-session
sub-threshold depressive symptoms or mild to moderate basis.
depression (NICE, 2008). The programme helps the user to identify thinking
One particular programme that has been devel- errors, challenging negative automatic thoughts, modi-
oped for this purpose is ‘Beating the Blues’. The pro- fying attributional style, and identifying core negative
gramme uses interactive multimedia techniques to beliefs. It also provides guidance on behavioural tech-
maximize user-friendliness and patient engagement. niques (including graded exposure, sleep management,
It provides role-models in the form of case study vid- problem solving, task breakdown, activity scheduling
eos that guide the patient’s progress at each stage of and so forth) that are designed to promote more helpful
therapy. Patients follow a unique pathway through the thinking styles and behavioural repertoires.
THE TOUR > SETTINGS >
BEATING THE BLUES © MY PROJECTS

Session 1
> As you work through Beating the Blues,
smail projects for you to do between
modules will appear here
START
MODULE >
REVIEW PREVIOUS SESSIONS >
A sample page from the CCBT programme ‘Beating the Blues’™

Source: Reproduced by permission of Ultrasis Plc.
7.3.1 Biological Treatments to address these imbalances and deal with the symptoms
of depression. The three main types of medication for
Drug therapy depression are (1) trycyclic drugs (such as imipramine),
We saw earlier that depression is commonly associated (2) monoamine oxidase (MAO) inhibitors (such as
with deficits or imbalances in the neurotransmitters ser- tranylcypromine), and (3) selective serotonin reuptake
otonin, norepinephrine and dopamine and over the past inhibitors (SSRIs such as Prozac). The first two types
50 years various drugs have been developed that attempt of drug have their effect by increasing levels of both
CHAPTER 7 DEPRESSION AND MOOD DISORDERS aa
TABLE 7.6 Side effects of drugs used to treat major depression rapid relief from symptoms in around half of those
and bipolar disorder
treated, and are effective not only with bouts of major
Category Side effects depression, but also with chronic depressive disor-
ders such as dysthymic disorder (Hellerstein, Kocsis,
Tricyclic drugs Blurred vision, anxiety, fatigue, Chapman, Stewart & Harrison, 2000). Meta-analyses
dry mouth, increased risk suggest that both tricyclic drugs and SSRIs are more
of heart attack and stroke,
effective than placebo controls, and generate significant
constipation, gastric disorders,
hypotension, sexual dysfunc- improvement in around 55-60 per cent of those treated,
tion, weight gain with both tricyclic drugs and SSRIs being equally effective
(Arroll, Macgillivray, Ogston, Reid et al., 2005). However,
Monoamine oxidase inhibitors Hypertension, dry mouth, diz-
(MAOIs)
relapse is a common occurrence after drug treatment
ziness, headaches and nausea
for depression has been withdrawn (Reimherr, Strong,
Selective serotonin reuptake Anxiety, fatigue, gastric dis- Marchant, Hedges & Wender, 2001), and a more effective
inhibitors (SSRIs) orders, headaches, dizziness,
treatment may be to combine drug therapy with psycho-
sleeping difficulties
logical therapies such as CBT (Kupfer & Frank, 2001).
Lithium Cardiac arrhythmia, fatigue, In contrast to those drugs prescribed for major
blurred vision, tremors, on
depression, the drug therapies of choice for bipolar dis-
overdose can cause delirium,
order are rather different. The traditional treatment for
convulsions and fatalities
bipolar disorder has been lithium carbonate. Around
80 per cent of bipolar dis-
lithium carbonate A drug used in
order sufferers who take
the treatment of bipolar disorder.
serotonin and norepinephrine in the brain, while SSRIs lithium benefit from it,
act selectively on serotonin and prevent its reuptake by and the drug can provide relief from symptoms of both
the presynaptic neurone (see Figure 7.1). All of these manic and depressive episodes (Prien & Potter, 1993).
drugs act by facilitating the transmission of impulses There is some debate about how lithium actually moder-
between neurones. Treatment outcome studies have ates the symptoms of bipolar disorder. Early views sug-
generally indicated that depressed individuals given gested that lithium stabilizes the activity of sodium and
these forms of medication benefit when compared with potassium ions in the membranes of neurones, and it is
individuals taking placebos. Around 60-65 per cent the instability of these ions that give rise to the symp-
of individuals taking trycyclic drugs show improve- toms of bipolar disorder (Swonger & Constantine, 1983).
ment (Gitlin, 2002) along with around 50 per cent tak- Other accounts argue that it changes synaptic activity in
ing monoamine oxidase inhibitors (Thase, Trivedi & neurons in such a way as to help neurotransmitters to
Rush, 1995). Although these forms of drug treatment bind to a receiving neuron, thus helping to facilitate and
are relatively effective, they often have significant physi- stabilize neuronal transmission (Ghaemi, Boiman &
cal and psychological side effects and these are listed in Goodwin, 1999). More recently, it has been suggested
Table 7.6. The most recently developed of these drugs, that lithium modulates neuronal transmission by affect-
SSRIs, do have some benefits over trycyclic drugs and ing the expression of genes that govern these activities
MAO inhibitors in that they produce fewer side effects (Lenox & Hahn, 2000). However, treatment of bipolar
(Enserink, 1999) and it is harder to overdose on them symptoms with lithium carbonate does have some disad-
(Isbister, Bowe, Dawson & Whyte, 2004). However, vantages. Firstly, discontinuation often increases the risk
SSRIs such as fluoxetine (Prozac) take around 2 weeks of relapse (Suppes, Baldessarini, Faedda & Tohen, 1991),
to begin to have an effect on symptoms (which is and, secondly, an added disadvantage of lithium treat-
roughly the same as trycyclics), and also have their own ment is the difficulty in prescribing a suitable dosage on
side effects such as headache, gastric disorders and sex- an individual basis. Lithium is a toxic substance and the
ual dysfunction (Rosen, Lane & Menza, 1999). There is effective dose for alleviating symptoms is often close to
also controversy about whether SSRIs such as Prozac the toxic level. As a consequence, an overdose can cause
increase the risk of suicide. Recent meta-analyses sug- delirium, convulsions and, in rare cases, can be fatal.
gest that increased risk of suicide with the use of SSRIs More recently, combinations of antipsychotic drugs and
cannot be ruled out, but these risks should be balanced SSRIs have been used successfully to address symptoms
against the effectiveness of SSRIs in treating depres- of bipolar disorder. (e.g. a combination of the antipsy-
sion (Gunnell, Saperia & Ashby, 2005). Nevertheless, chotic drug olanzapine and the antidepressant SSRI drug
despite these cautions, the drugs that have been devel- fluoxetine), and this combination has been shown to
oped to treat depression do help to alleviate symptoms have significant effects on both mania and depression
in a significant number of cases, they provide relatively symptoms (Deeks & Keating, 2008).
93293) PSYCHOPATHOLOGY
; %
Electroconvulsive therapy (ECT) accounts is the view that depression is a response to loss
This method of treatment was first discovered in the (perhaps of a loved one) and may manifest as symbolic
1930s (Bini, 1938) and involves passing an electric current loss, in which other kinds of losses (such as losing a
of around 70-130 volts through the head of the patient for job) are seen as equivalent to losing a loved one.
around half a second. It was first used as an experimental Psychodynamic theories (such as those developed by
means of inducing brain seizures, but was subsequently Freud and Abraham) argue that the individual's response
found to have beneficial effects on symptoms of severe to loss is to turn their anger at the loss inwards, and this
depression. Today, ECT is used primarily with individu- in turn can develop into self-hate resulting in low self-
als suffering severe depression who have not responded esteem (Frosh, 2012, ch.13). The aim of psychodynamic
well to other forms of treatment (Cohen, Taieb, Flament, therapy, therefore, is to help the depressed individual
Benoit et al., 2000). While it can provide effective short- achieve insight into this repressed conflict and to help
term relief from symptoms of severe depression, it also release the inwardly directed anger. Psychodynamic
has a number of controversial features. Firstly, it has a therapy will do this by using various techniques to help
number of side effects, the most common of which is people explore the long-term sources of their depression
memory loss that affects the ability to learn new material (see section 4.1.1), and this will involve exploring con-
(anterograde amnesia) and the ability to recall material flicts and problematic relationships with attachment fig-
learnt before the treatment (retrograde amnesia). These ures — such as parents — and discussing long-standing
effects can last for up to 7 months following ECT (Lisanby, defensive patterns. For example, the psychodynamic
Maddox, Prudic, Devanand & Sackeim, 2000; Sackeim, therapist may use free association or dream interpreta-
Prudic, Fuller, Keilp, Lavori et al., 2007). Secondly, many tion to help the individual recall early experiences of
people find the idea of having a strong electric current loss that may have contrib-
passed through their brain frightening, and will be resist- uted to repressed conflicts dream interpretation The process
and symptoms of depres- of assigning meaning to dreams. _
ant to the use of this kind of therapy. Indeed, many view
the physical nature of ECT as a form of ‘assault’ on the sion. In this way, psycho-
patient, and a means of managing unruly inpatients dynamic therapies attempt to bring meaning to the
rather than a form of therapy. This was a view that was symptoms of depression, and help the individual under-
strikingly portrayed in the 1975 film One Flew Over The stand how early experiences may have contributed to
Cuckoo’s Nest starring Jack Nicholson. Thirdly, no one is their symptoms and affected their current interpersonal
clear how ECT does work in alleviating the symptoms of relationships.
severe depression, but it has been suggested that shock Evidence for the therapeutic efficacy of psycho-
affects the levels of serotonin and norepinephrine in the dynamic therapies in the treatment of depression is
brain (Mann & Kapur, 1994). However, this beneficial meagre. This is in part because processes within psycho-
effect may be short-term and limited to as little as 4 weeks dynamic therapies are difficult to objectify and study ina
(Breggin, 1997), and the relapse rate is high (Royal College controlled way. Psychodynamic therapists also differ sig-
of Psychiatrists, 2002). Other researchers have argued nificantly in the way they interpret psychodynamic prin-
that the short-term beneficial effects of ECT are nothing ciples in practice. A controlled study by the American
more than would be expected following any trauma to the Psychiatric Association (APA, 1993) reported that there
brain — with immediate symptoms being confusion, head- was no evidence for the long-term efficacy of psycho-
ache and nausea followed by a period of emotional shal- dynamic treatment of depression, although some more
lowness, denial and artificial euphoria that may last for a recent studies have indicated that short-term psychody-
few weeks (Breggin, 1997). namic interventions may be as effective as CBT in signifi-
Nevertheless, despite these criticisms, ECT may still cantly reducing symptoms of depression (Leichsenring,
have a role to play in the treatment of severe depression 2001; Lemma, Target & Fonagy, 2011).
in both Major and bipolar depression when symptoms
are resistant to pharmacological treatment (Medda, Social skills training
Perugi, Zanello, Cuiffa & Cassano, 2009), and the almost It was Lewinsohn and his colleagues (e.g. Lewinsohn &
immediate beneficial effects of ECT may be helpful in Shaw, 1969) who first drew attention to the fact that
alleviating depression when suicide is a real possibility. depressed individuals (1) have deficits in the general
social skills that are required for efficient and effective
interactions, and (2) possess a demeanour that others
7.3.2 Psychological Treatments (e.g. other family members) find aversive. These two
features of the depressed individual will act to accen-
Psychoanalysis tuate depression by reducing the frequency of social
In section 7.1.2 we discussed some of the psychody- interactions and reducing the rewards that the individ-.
namic explanations of depression. Central to these ual might obtain from these interactions. The kinds of |
CHAPTER 7 DEPRESSION AND MOOD DISORDERS pay vl
interpersonal social skills deficits possessed by depressed vicious cycle where this lack of reward generates depres-
individuals range from negative self-evaluation of their sive symptoms, and in turn, the individual’s depressive
own skills to deficits in behavioural indicators of social behaviour may ultimately lead to aversive social conse-
skills such as eye contact, relevant facial expressions, and quences in the form of negative social reactions from
speed of response in conversations (Segrin, 2000). friends and family (Coyne, 1976). This view has led to the
In response to these deficits, social skills training development of behavioural activation therapy for
therapy for depression was developed (Becker, Heimberg depression that attempts
behavioural activation therapy A
& Bellack, 1987). Social skills training assumes that to increase the client’s therapy for depression that attempts to
cial skills training A therapy for
depression in part results access to pleasant events increase clients’ access to pleasant events
2pression that assumes that depression in from the individual’s ina- and rewards and decrease and rewards and decrease their experience
art results from an individual's inability to bility to communicate their experience of aver- of aversive events and consequences.
ymmunicate and socialize appropriately, and socialize appropri- sive events and consequences (Lewinsohn, Sullivan &
1d that addressing these skill deficits
ould help to alleviate many of the
ately, and that addressing Grosscup, 1982; Turner & Leach, 2012). Early behav-
mptoms of depression. these skill deficits should ioural activation programmes attempted to achieve
help to alleviate many of these goals through daily monitoring of pleasant/
the symptoms of depression. This may involve training unpleasant events and the use of behavioural interven-
assertion skills, conversational interaction skills, dating tions that developed activity scheduling (e.g. scheduling
skills, and job interview skills, and can involve proce- reinforcing activities so that they will reinforce less
dures such as modelling, rehearsal, role-playing, and attractive activities). They also include social skills
homework assignments out of the therapeutic setting and time management training (Lewinsohn & Shaffer,
(Jackson, Moss & Solinski, 1985; Becker, Heimberg & 1971; Zeiss, Lewinsohn & Munoz, 1979). The use of
Bellack, 1987). behavioural activation therapy was given a further
An example of one particular social skills training boost by the fact that a number of studies demon-
programme for depression is that designed by Herson, strated that cognitive change is just as likely to occur
Bellack and colleagues (Hersen, Bellack & Himmelhoch, following purely behavioural interventions as after cog-
1980; Thase, 2012). This involved 1-hour sessions for nitive interventions (Jacobson & Gortner, 2000; Simons,
12 weeks and began by focusing on skills appropriate Garfield & Murphy, 1984). That is, reductions in nega-
for interactions with family, friends, work colleagues, tive thinking and negative self-statements in depression
and strangers respectively. Particular features of this can be decreased by behavioural interventions that con-
programme included (1) role-playing tasks, feedback, tain no explicit cognitive change components. Recent
modelling and positive reinforcement for appropri- developments of behavioural activation therapy
ate behaviours, and (2) attention to the specific details include the self-monitoring of pleasant/unpleasant
of social interactions such as smiles, gestures, use of experiences and the identification of behavioural goals
eye contact and so on. Clients were subsequently given within major life areas (e.g. relationships, education)
homework tasks requiring them to practise their skills that can be targeted for development and reinforce-
outside of the therapy situation. As a result of this pro- ment, and behavioural activation therapy has also been
gramme, clients showed not only improvements in their shown to be beneficial for individuals suffering chronic
social skills but also a decrease in symptoms of depres- depression (Erickson & Hellerstein, 2011). Treatment
sion that were still apparent 6 months after the end of in Practice Box 7.2 gives an example of how a brief
the programme. Studies evaluating the efficacy of social behavioural activation therapy programme is struc-
skills training for depression have shown that such pro- tured and executed (Lejuez, Hopko, LePage, Hopko &
grammes result in an improvement in a range of social McNeil, 2001).
skills and a decrease in reported symptoms of depression Outcome studies suggest that behavioural activa-
(Zeiss, Lewinsohn & Munoz, 1979). They also suggest tion therapies are at least as effective as supportive psy-
that social skills training is equally as effective as other chotherapy in reducing the symptoms of depression
psychological therapies commonly employed for depres- (Hopko, Lejuez, LePage, McNeil & Hopko, 2003), and
sion (Fine, Forth, Gilbert & Haley, 1991; Miller, Norman, equally as effective as CBT in preventing relapse after
Keitner, Bishop & Dow, 1989). 24 months (Gortner, Gollan, Dobson & Jacobson, 1998).
Behavioural activation therapy Cognitive therapy

Behavioural theories of depression emphasize that As we saw in section 7.1.2, dysfunctional cognitions
depression may be triggered by a life-event loss (such as a appear to play an important part in the maintenance of
bereavement), and this event may represent the loss of depressive symptoms. Beck’s cognitive theory of depres-
important sources of reward and reinforcement for the sion (Beck, 1967, 1987) argues that depression is main-
individual. This leads the depressed individual into a tained by a systematic set of dysfunctional negative
PSYCHOPATHOLOGY
TREATMENT IN PRACTICE 7.2

BRIEF BEHAVIOURAL ACTIVATION TREATMENT FOR DEPRESSION (BATD)
BATD is conducted over 8 to 15 sessions, and sessions education, employment, hobbies and recreational
progress through the following stages: activities, physical/health issues, spirituality.
4. Following goal setting, an activity hierarchy is
1. Assessing the function of depressed behaviour; constructed in which 15 activities are rated ranging
weakening access to positive reinforcement (e.g. from ‘easiest’ to ‘most difficult’ to accomplish.
sympathy) and negative reinforcement (e.g. escape With progress being monitored by the therapist,
from responsibilities); establishing rapport with the over a period of weeks the client progressively
client and introducing the treatment rationale. moves through the hierarchy from easiest to most
2. Increasing the frequency and subsequent reinforce- difficult. Patients are urged to identify weekly
ment of healthy behaviour; clients begin a weekly rewards that can be administered if activity goals
self-monitoring exercise that serves as a baseline are met.
assessment of daily activities and orientates clients to
the quantity and quality of their activities, and generates Source: Hopko, D.R., Lejuez, C.W., Ruggiero, K.J. & Eifert, G.H. (2003).
ideas about activities to target during treatment. Contemporary behavioural activation treatments for depression:
3. Emphasis is shifted to identifying behavioural Procedures, principles, and progress. Clinical Psychology Review,
goals within major life areas, such as relationships, 23, 699-717. Reproduced with permission.
beliefs that form a negative schema though which the allows them to link the automatic thoughts to particular sit-
depressed individual views themselves, their world, and uations and outcomes, and to think through possible
their future. From this theory Beck developed one of rational alternatives to the negative automatic thought
the most successful and widely adopted therapeutic (see Table 7.7). The overall philosophy of cognitive therapy
approaches for depression, and this has come to be for depression is to correct the negative thinking bias pos-
known by various names including cognitive therapy, sessed by depressed individuals, and in some cases this aim
cognitive retraining or cognitive restructuring. The can be supplemented with the use of reattribution train-
thrust of this approach is (1) to help the depressed indi- ing (Beck, Rush, Shaw & Emery, 1979). Reattribution train-
vidual identify their negative beliefs and negative thoughts, ing attempts to get the reattribution training A technique used
(2) to challenge these thoughts as dysfunctional and irra- client to interpret their in the treatment of depression which
tional, and (3) to replace difficulties in more hope- attempts to get clients to interpret their
cognitive retraining An approach to these negative beliefs with ful and constructive ways difficulties in more hopeful and construc- _
treating depression developed by Aaron tive ways rather than in the negative,
more adaptive or rational rather than in the negative, global, stable ways typical of depressed q
Beck. Also known as cognitive therapy or
cognitive restructuring. beliefs. For example, global, stable ways typical individuals.
depressed individuals tend of depressed individuals
to hold beliefs and attributional styles that are overgeneralized. (see Tables 7.3 and 7.4).
They will respond to a specific failure (such as failing their Outcome studies have shown that cognitive therapy is
driving test) with statements such as ‘Everything I do ends in usually at least as effective as drug therapy in treating the
failure’ or “The world is against me’. The cognitive therapist symptoms of depression (Rush, Beck, Kovacs & Hollon,
will attempt to identify these overgeneralized beliefs and 1977), and some have shown that it is superior to drug
challenge them as irrational — using, if at all possible, rele- therapy at 1-year follow-up (Blackburn & Moorhead,
vant examples from the client’s own experiences. In addition 2000; Hollon, Shelton & Davis, 1993). DeRubeis, Hollon,
to this, the client will be asked to monitor the negative Amsterdam, Shelton et al. (2005) compared cognitive
automatic thoughts that therapy with drug therapy (paroxetine) and a placebo-
negative automatic thoughts Negatively give rise to negative beliefs control condition. After 8 weeks they found improve-
valenced thoughts that the individual finds and depressive symptoms, ment in 43 per cent of the cognitive therapy group,
difficult to control or dismiss. often using a form which 50 per cent of the drug treatment group, against
és
CHAPTER 7 DEPRESSION AND MOOD DISORDERS nas:
TABLE 7.7
Below is an example of a thought record form used to record the negative automatic thoughts (‘hot thoughts’) experienced
by depressed individuals. This form relates these thoughts to possible situational triggers and attempts to get the depressed
individual to think up evidence that might be contrary to that ‘hot thought’
3. Automatic » 4. Evidence that 5. Evidence that 6. Alternative/

thoughts supports the does not support balanced 7. Rate moods
1. Situation 2.Moods (images) hot thought the hot thought thoughts now
Who? What do you What was going Write an Re-rate

What? feel? through your alternative moods listed
When? Rate each mood Mind just before or balanced in column 2
ieee (0-100%) you started to thought. as well as any
SIE feel this way? Ratehowmuch) new moods
Any other you believe in (0-100%)
oe Nee each alterna-
Images? tive or bal-
anced thought
(0-100%)
In hotet Depressed 100% I need something ‘The hurt made When Tin with other
room — Lonely 100% celeste ts unbearable A SOA
alone — Y NUM Kill. myseY, 5 begin to
Sunday Empty 100% take away the pain CE feet better
10pe C ee 100% Nothing
ee 19189 peoplehavetried —_‘U¥*
; ft like
Ly thes
thy before
Unmotwated right for me to help meand and have managedto
100% lin worthless — I've been given get myself through it
Stressed I can never many drugs, none Some mornings Iwake
anything differently, so there may

ae
My friends tel me
that I have something
to offer
What ts there to
look forward to in Ido laugh when Tim
life? with others
I feet like an empty

hell
Source: After Greenberger, D. & Padesky, C. (1995). Clinician’s guide to mind over mood. New York: Guilford Press.
only 25 per cent in the placebo group, and these levels the sufferer with medication compliance, mood moni-
of improvement were maintained at 16 weeks. Cognitive toring, anticipating stressors, interpersonal functioning
therapy also appears to have longer term beneficial and problem solving (Scott, Garland & Moorhead, 2001;
effects by preventing relapse compared with medication Danielson, Feeny, Findling & Youngstrom, 2004).
(Hensley, Nadiga & Uhlenhuth, 2004; Dobson, Hollon, While there is no doubt that cognitive therapy is suc-
Dimidjian, Schmaling et al., 2008), but a combination of cessful in helping to treat depression, there is still some
cognitive therapy with drug treatment appears to be supe- debate about how it achieves these effects. We have seen
rior to either treatment alone (Kupfer & Frank, 2001). earlier that cognitive change is just as likely to occur fol-
Cognitive therapy has also been successfully adapted to lowing purely behavioural treatments as they are after
treat individuals with bipolar disorder in conjunction cognitive treatments. Cognitive therapy contains both
with appropriate medication (Newman, Leahy, Beck elements of cognitive restructuring, which aims at
et al., 2002) in both individual (da Costa, Range, Malagris, changing cognitions directly, and behavioural exercises
Sardinha et al. (2010) and group (Gomes, Abreu, Brietzke, designed to establish new cognitions — so, is the cognitive
Caetano et al., 2011) settings. These interventions help restructuring element entirely necessary? In addition,
226%: PSYCHOPATHOLOGY
’ :
there is evidence that cognitive therapy not only changes onset of negative thinking, and it aims at getting indi-
negative cognitions, but also results in improvements in viduals to take a ‘decentred’ perspective by being aware
abnormal biological processes (Blackburn & Moorhead, of negative thinking patterns and viewing them purely
2000). This raises the question of whether cognitive as mental events rather than accurate reflections of real-
therapy has its effects by changing cognitions or biologi- ity (Teasdale, 1988; Teasdale, Segal & Williams, 1995).
cal processes. Nevertheless, regardless of how it works, MBCT is based on an integration of aspects of CBT and
cognitive therapy certainly does work, and recent evi- components of the mindfulness-based stress reduction
dence suggests that it not only reduces the occurrence programme that contains elements of meditation and
of negative cognitions in depression, but it also helps to provides training in the deployment of attention (Kabat-
dissociate negative cognitions from the symptoms Zinn, 1990). Clients are taught to become more aware
of depression better than other treatments (Beevers & of, and relate differently to, their thoughts, feelings and
Miller, 2005). bodily sensations, and treat thoughts and feelings as
passing events in the mind rather than identifying with
Mindfulness-based cognitive them. It also teaches skills that allow individuals to dis-
therapy (MBCT) engage from habitual dysfunctional cognitive routines
A critical issue in the treatment of depression is how to and depression-related patterns of ruminative thought.
predict and eliminate possible relapse after remission or Studies suggest that MBCT can: (1) significantly reduce the
successful treatment. In the case of major depression, probability of future relapse (Ma & Teasdale (2004) found
it appears that the risk of relapse increases with every that MBCT reduced relapse from 78 per cent to 36 per
consecutive bout of depression, and this increased risk cent, and in participants who had experienced four or more
also means that depression can reoccur with less and bouts of depression only 38 per cent of those receiving
less external provocation (such as a stressful life event) MBCT relapsed compared. with 100 per cent in the treat-
(Kendler, Thornton & Gardner, 2000). This increased ment-as-usual control group); and (2) significantly reduce
risk of relapse in recovered depressed individuals symptoms of mood disorders (Hofman, Sawyer, Witt &
appears to be caused by periods of negative mood Oh, 2010). These findings suggest that teaching previously
(dysphoria) activating patterns of negative or depres- depressed individuals to adopt a detached, decentred rela-
sogenic thinking, such as self-devaluation and hopeless- tionship to their depression-related thoughts and feelings
ness (Ingram, Miranda & Segal, 1998; Segal, Gemar & can have significant therapeutic gains. Included in the online
Williams, 1999). That is, as soon as the recovered resources: ismam Science Jer =
depressed individual begins to feel depressed again, this Oxford Live lecture on ff For a video on the science
reactivates negative thinking that leads to a downward the science of mindful- | of mindfulness go to
spiral to relapse. MBCT was developed to try to com- ness by Professor Mark | video/ch7
bat this linkage between periods of dysphoria and the Williams.
SELF-TEST QUESTIONS
° What is a stepped-care model for the treatment of depression?

° What drugs are important in controlling brain neurotransmitter levels, and how do they have their effect?
° What are the important components of social skills training for depression?
° What is the rationale behind behavioural activation therapy for depression?
* How does cognitive therapy attempt to eradicate negative thinking?
® What is reattribution training?
* What is mindfulness-based cognitive therapy and what role does it play in the management of depression?
° What are the main types of pharmacological treatment for bipolar disorder?
CHAPTER 7 DEPRESSION AND MOOD DISORDERS rye
SECTION SUMMARY
7.3. THE TREATMENT OF DEPRESSION AND MOOD DISORDERS
e Drug treatments have been developed that. attempt to address the imbalance in neurotransmitters such as serotonin,
dopamine and norepinephrine.
e Three main types of medication for depression are trycyclic drugs, monoamine oxidase (MAO) inhibitors, and selective
serotonin reuptake inhibitors (SSRIs).
¢ Lithium carbonate is the main drug prescribed for bipolar disorder.
¢ Symptoms of bipolar disorder have also been treated successfully with a combination of antidepressant and antipsychotic
drugs (e.g. olanzapine and fluoxetine).
e Electroconvulsive therapy (ECT) is sometimes used with individuals suffering severe depression who have not responded
well to other forms of treatment.
e Psychodynamic therapy uses a range of techniques (e.g. free association, dream analysis) to help the individual to explore
the long-term sources oftheir depression.
e Social skills training assumes that depression results from the depressed individual's inability to communicate and socialize
appropriately, and addresses this deficit using social skills training programmes.
® Behavioural activation therapies attempt to increase the individual’s access to pleasant events and rewards and decrease
their experience of aversive events.
® Cognitive therapy for depression attempts to help the depressed individual identify negative beliefs and thoughts, chal-
lenge these beliefs as irrational, and replace them with positive rational beliefs.
¢ Outcome studies suggest that cognitive therapy is at least as effective as drug therapy.
¢ Mindfulness-based cognitive therapy (MBCT) has been developed to prevent relapse in recovered depressed individuals by
making them aware of negative thinking patterns that may be triggered by subsequent bouts of depression.
© Computerized CBT is also an effective treatment for milder forms of depression.
to the surface of the body that is likely to induce bleeding

7.4 D E LI B E RATE or bruising’ (see DSM-5 Summary Table 7.8). This phe-
SELF-H ARM nomenon has previously been labelled in many ways,
including ‘self-mutilation’, ‘self-harm’, ‘cutting’, and
parasuicide, but it is important to distinguish deliberate
Deliberate self-harm is self-harm from both suicide and parasuicide. The large
For a video on self-harm go to
defined as direct and delib- majority of people who indulge in deliberate selfharm
video/ch7 erate bodily harm in the donot have suicidal intentions and nor are they at risk for
absence of suicidal intent suicide (Greydanus & Shek, 2009).
(Nock, 2010), and most As noted in Client’s Perspective 7.2, deliberate self-
eliberate self-harm A parasuicidal frequently takes the form harm is predominantly an adolescent activity, with
wi, of cutting and carving the surveys suggesting that between 13 and 45 per cent of
1g or burning oneself, taking overdoses, j ; 2. ;
tting oneself, pulling hair or picking skin, Skin with a knife or similar adolescents may have deliberately self-harmed at some
‘self-strangulation. sharp instrument (usually time (e.g. Plener, Libal, Keller, Fegert & Muehlenkamp,
on arms, legs and stom- 2009) but only 4-5 per cent of adults (Briere & Gil,
ach), burning, taking overdoses, pulling hair or picking 1998; Klonsky, 2011). People typically engage in self
skin. Deliberate self-harm is included under a new harm when they are alone and experiencing negative
DSM-5 diagnostic category thoughts and feelings (e.g. having a bad memory, feel-
on-suicidal self-injury The act of called non-suicidal self- ing angry, experiencing self-hatred or numbness) (Nock,
sliberately causing injurytoone's body injury that covers ‘inten- Prinstein & Sterba, 2009). This suggests that self-injury
ithout conscious suicidal intent. tional self-inflicted damage is performed as either a means of self-soothing or of
yl PSYCHOPATHOLOGY
DSM-5 SUMMARY TABLE 7.8 Criteria for non-suicidal injury are more at risk of developing self-harm activities, and*
these include depressed adolescents (Hawton & James,
* Over the previous year on at least five occasions the indi-
2005) — especially those going through interpersonal cri-
vidual has intentionally self-inflicted damage to the surface
of their body to induce bleeding, bruising or pain with ses, or individuals with existing mental health problems
the anticipation that the injury will lead to only minor or such as eating disorders (Wedig & Nock, 2010), excessive
moderate physical injury alcohol intake (Hussong, 2003), substance abuse (Koob &
° Presence of at least two of the following:
Kreek, 2007; Greydanus & Shek, 2009), and psychosis
(Gerard, de Moore, Nielssen & Large, 2012). In par-
° Negative feelings or thoughts such as depression,
ticular, adolescents at risk of deliberate selfharm show
anxiety, and suchlike immediately prior to the self-injury
intrapersonal vulnerabilities such as higher physiologi-
° Prior to the self-injury a period offixation with the cal arousal in response to frustrating tasks and stressful
intended self-injury which is hard to resist
events (Nock & Mendes, 2008; Nock, Wedig, Holmberg &
¢ Preoccupation with self-injury occurs frequently even Hooley, 2008), and poor verbal communication and
when not acted upon social problem-solving skills (Nock & Mendes, 2008;
¢ The self-injury is carried out with the expectation that it Nock & Photos, 2006).
will relieve a negative feeling or induce a positive feel- Preventing selfharm can be difficult because acts of
ing during or directly after the self-injury self-harm are often impulsive, carried out in secret, and
e The self-injury does not occur only during states of denial is a common feature of those who self-harm —
psychosis, delirium or intoxication especially when the self-harm may have a positive
e There is no suicidal intent effect by providing temporary relief from their difficul-
ties. Similarly, most self-injurers also report feeling lit-
tle or no pain during self-harming, and this also makes
help-seeking (e.g. with the end goal of enlisting others the activity difficult to detect (Favazza, 1996; Nock &
to help the individual cope with their negative feelings Prinstein, 2004). However, it may be possible to target
or negative self-image) (Muehlenkamp, Engel, Wadeson, vulnerable groups and to ensure that they have access
Crosby et al., 2009). Many adolescents who self-harm do to mental health services and support services. As we
not usually suffer any long-term psychological effects have noted above, vulnerable groups that have been
from doing so, but there are groups of individuals who identified include (1) depressed adolescents, (2) those

DELIBERATE SELF-HARM
Comments from an adolescent self-harmer posted on an and 45 per cent of adolescents have deliberately self-
internet message board: harmed at some time (e.g. Plener, Libal, Keller, Fegert &
Muehlenkamp, 2009). Self-harm usually occurs when the
‘Hello. . . Um where to start. The thing is self-harm is
person is alone and experiencing negative thoughts or
the only way | can deal with things. lve tried every-
feelings, and appears to serve a self-soothing or help-
thing in the book and yeah, none of it even comes
seeking function (Nock, 2010). The most common forms
close to cutting. | tried the rubber-band thing and
of deliberate self-harm are cutting or carving the skin
ended up with huge welts that actually bruised
with a sharp instrument, usually on the arms, legs and
and thats just anouther form of self-harm. | tryied writ-
stomach, but can also include burning, taking overdoses,
ing, doing other things. . . None of it helps. My scars are
pulling hair and picking skin. Many adolescents who
another thing about self-harm that | cant draw myself
self-harm do not suffer any long-lasting psychological
away from. | like them in some odd way. . .| know. Your
effects from doing so, but there are vulnerable groups of
probably thinking im insane or an attention-getter or
adolescents for whom self-harm may be a more endur-
somthing. . . But is there ANYONE who feels the same?
ing problem. These include depressed adolescents, those
| mean likes the way it feels and honestly doesnt want
with interpersonal crises, or individuals with some exist-
to stop even though its bad and all. . .?’
ing mental health problems such as psychosis, substance
Deliberate self-harm is primarily an adolescent abuse problems, or eating disorders (Hawton & James,
phenomenon, and estimates suggest that between 13 2005; Greydanus & Shek, 2009).
&
CHAPTER7 DEPRESSION AND MOOD DISORDERS 229°
with interpersonal crises, such as those who have lost a of treatment for deliberate self-harm appears to be prob-
partner or have run away from home, and (3) those who lem-solving therapy. This is often used with adolescents
have previously self-harmed (especially in conjunction and enables them to bring new coping strategies to the
with substance misuse and conduct disorder) (Hawton & difficulties in their lives, and, when extended to the indi-
James, 2005). vidual’s family, this can facilitate the sharing and expres-
There are at present no evidence-based psychological sion of feelings. CBT for depression can also be used if
or pharmacological treatments for deliberate self-harm depression and low self-esteem are major underlying fac-
(Nock, 2010). However, one of the more effective forms tors in an individual’s self-harm.
SELF-TEST QUESTIONS __
° How is deliberate self-harm defined and what kinds of problems lead adolescents in particular to self-harm?
© What are the most common forms of deliberate self-harm?
* What psychological functions is deliberate self-harm thought to serve?
SECTION SUMMARY
7.4 DELIBERATE SELF-HARM
® Deliberate self-harm is common in adolescence, and commonly includes cutting and carving the skin, burning, taking
overdoses, pulling hair or picking skin.
® Deliberate self-harm can be performed as a form of self-soothing or as help-seeking.
© One of the more effective treatments
for deliberate self-harm includes problem-solving therapy.
See en even cence rene renveresree reese eesreesen sees eneseeeesseeseesssesasesassessersersnnsseusensrensussessastensceneete”
(Isacsson & Rich, 1997), and the cognitive construct of

‘hopelessness’ is probably one of the best single predic-
tors of suicide (Beck, Steer, Kovacs & Garrison, 1985) (see
The World Health Organisation estimates that 1 million section 7.1.2). Recent estimates of suicide rates indicate
people commit suicide each year (WHO, 2012), but the that the 12-month prevalence rate for suicide attempts
number of people who attempt suicide is 20 times higher. for developed countries is 0.4 per cent and for suicidal
The WHO report also described other sobering facts ideation is 2 per cent (Borges, Nock, Kessler, Haro Abad,
about suicide. Suicide is the second highest cause of Hwang et al., 2010). Studies that have investigated the
death worldwide amongst lifetime prevalence rates for suicide suggest that 13.5
icide The action of killing oneself
entionally. — 15- to 19-year-olds, and per cent of people report lifetime suicidal ideation, 3.9
suicide rates continue to per cent have planned a suicide, and 4.6 per cent have
be a serious problem in high-income countries, but attempted suicide in their lifetime (Kessler, Borges &
are increasing significantly in middle- and low-income Walters, 1999). The likelihood of an individual commit-
countries. ting suicide tends to increase with age, although there
Suicide attempts often occur in the context of mental has been an alarming increase in the number of younger
health problems (especially depression), and it has been people attempting suicide in recent years, with a rise in
estimated that 90 per cent of suicide victims may have the US of 200 per cent since 1960 reported by the US
a diagnosable psychiatric disorder at the time of their National Center for Health Statistics. Women are around
death (Isometsa, Henriksson, Marttunen et al., 1995). three times more likely to attempt suicide than men, but
Over half of those that successfully commit suicide are the rate for successful suicide is around four times higher
usually significantly depressed before the fatal attempt in men than women (Peters & Murphy, 1998), and this
23045 PSYCHOPATHOLOGY
TABLE 7.8 Characteristics that define suicide attempters and completers -
Characteristics Attempters Completers
Gender Mainly female Mainly male
Age Mainly young Increased risk with age
Method Pills, cutting More violent (guns, jumping)
Common diagnoses Mild depression, borderline personality Major depression, alcoholism

disorder, schizophrenia
Dominant affect Depression with anger Depression with hopelessness
Motivation Change in situation, cry for help Death, self-annihilation
Source: Fremouw, W., Callahan, T. & Kasden, J. (1993). Adolescent suicide risk: Psychological, problem-solving and environmental factors. Suicide and
Life-Threatening Behaviour, 23(1), 46-54. Reproduced with permission.
is because men will tend to adopt more lethal methods probably exposed to many of the life stressors experi-
than women (such as guns and jumping, see Table 7.8). enced by adults, yet may lack the coping resources to
Suicidal phenomena have become more common in deal with them effectively (Reynolds & Mazza, 1994);
teenagers and adolescents, and suicide is reported to be (2) suicide is also a sociological as weil as a psychological
the second or third most frequent cause of death among phenomenon, and media reports of suicide often trig-
15- to 24-year-olds in many countries (Commonwealth ger a significant increase in suicides (Gould, Jamieson &
Department of Health and Family Services, Australia, Romer, 2003), which is especially true in the case of ado-
1997). Up to 15 per cent of American high-school stu- lescents and teenagers, where news of celebrity suicides
dents have been reported as attempting suicide at least are often associated with increases in the rate of teenage
once (King, 1997), and suicidal phenomena in adoles- suicide attempts (see Focus Point 7.5); and (3) there is a
cents include suicide attempts, deliberate self-harm, and strong relationship between depression, substance abuse
suicidal plans, threats and thoughts (Hawton, Rodham, and suicide, and the increasing use of drugs and alcohol
Evans & Weatherall, 2002). The reasons for the increase in young teenagers may well provide one of the reasons
in adolescent suicide rates is unclear, but a number for increased rates of suicide and deliberate self-harm in
of factors may be relevant: (1) modern teenagers are this group (Gould & Kramer, 2001).
ei MEDIA CONTAGION AND SUICIDE AMONG THE YOUNG

Ss
=
When Nirvana lead singer Kurt Cobain committed any effect. In particular, Martin & Koo (1997) inves-
= suicide in April 1994 it had a significant impact on tigated the effect of the suicide of Kurt Cobain on
oO young people, who saw Cobain as the spokesman
a. Australian adolescent suicide rates for the 30-day
Vv) for their troubled generation. The sudden deaths period after his suicide. They found no evidence for
=) of celebrities in this way have given prominence to a ‘suicide contagion’ effect, with suicide rates for the
U
Le) social factors that may influence suicide — especially 30-day period after Cobain’s death being lower than
Li amongst the young. That is, reporting of suicide in the rates for the same period in some previous years.
media may trigger ‘contagion’ effects in which young Nevertheless, a recent systematic review of the effects
people imitate their idols. However, the evidence for of media reporting on suicide rates concludes that
media contagion effects on suicide rates is equivocal. media reporting and suicidality are probably related,
Some studies have found evidence for increased rates suggesting that the media need to be responsible
of adolescent suicide after high-profile media stories about the way they report celebrity suicides in order
about suicide (Motto, 1970; Phillips & Carstensen, to minimize imitation by vulnerable groups (Sisask &
1986; Littman, 1985), while others have failed to find Varnik, 2012).
CHAPTER7 DEPRESSION AND MOOD DISORDERS ste
7.5.1 Risk Factors for Suicide physical disability are also predictors of suicide (Dubow,
Kausch, Blum, Reed & Bush, 1989; Wagman Borowsky,
One of the best predictors of future suicide attempts Resnick, Ireland & Blum, 1999); and (4) low socio-eco-
is a history of at least one previous suicide attempt nomic status is also a significant risk factor (Li, Page,
(Leon, Friedman, Sweeney et al., 1990). However, since Martin & Taylor, 2011), and the impact of the recent
only 20-30 per cent of those who attempt suicide have worldwide economic recession has resulted in a sig-
made a previous attempt, it is important to look at nificant 3.8 per cent increase in the suicide rate since
other risk factors. Suicide is a complex phenomenon, its onset (Reeves, Stuckler, McKee, Gunnell et al., 2012)
and risk factors encompass a broad range of domains (see Figure 7.5). In a large-scale study of risk factors
such as psychiatric, psychological, physical, personal, carried out for the World Health Organisation, Borges,
familial and social factors (Evans, Hawton & Rodham, Nock, Kessler, Haro et al. (2010) found that risk factors
2004). For example: (1) suicide is related to diagnoses for suicidal behaviours in both developed and develop-
of depression, schizophrenia, borderline personality dis- ing countries included being female, being young, lower
order, panic disorder, alcoholism, and substance abuse education and income, unmarried status, unemploy-
(e.g. Isometsa, Henriksson, Marttunen et al., 1995), ment, parent psychopathology, childhood adversities,
Nordentoft, Mortensen & Pedersen (2011) found that and a current DSM psychiatric diagnosis. A combination
absolute risk of suicide was highest for those with a of these risk factors was able to predict suicide attempts
diagnosis of bipolar disorder (6-10 per cent) and major with some accuracy. Perhaps not surprisingly, life stress is
depression (5—7 per cent), but all psychiatric disorders one of the most significant predictors of suicide, and sui-
studied resulted in an increase in suicide risk of between cide attempts are often preceded by a significant negative
2 and 8 per cent compared with the rate of less than life event. The types of life events that may trigger sui-
1 per cent found in the control group of individu- cide can differ across age groups. For adolescents and
als without a psychiatric diagnosis; (2) psychological teenagers these are more likely to be relationship issues,
predictors of suicide include the cognitive construct of separations and interpersonal conflicts; in middle age
‘hopelessness’ (Alloy, Abramson, Hogan, Whitehouse they are more likely to be financial issues; and in later life
et al., 2000), and also low self-esteem (Fergusson & they tend to be related to disability and physical health
Lynskey, 1995); (3) both poor physical health and (Rich, Warsadt, Nemiroff et al., 1991).
125:—
PAO)
: ‘Excess deaths: 4750

11.54
Suicide
100000
rate
per 1180.5)
ia el
*F
0 lawl T == Syl =I mal <== sa a ne fm
1999 2000 2001 2002 2003 2004 #=+.2005 2006 2007 2008 #2009 2010
Year
FIGURE 7.5 Suicide and the economic recession.

Time trend analysis of suicide rates in 50 US states between 1999 and 2010. Vertical line shows onset of the economic recession.
Source: After Reeves, A., Stuckler, D., McKee, M., Gunnell, D., Chang, S. & Basu, S. (2012). Increase in state suicide rates in the USA during
economic recession. Lancet, 380(9856),1813-1814. Reproduced with permission.
iy li PSYCHOPATHOLOGY
Finally, there is also a genetic element to suicidal behav- 7.5.2 Identifying and
iour. Both twin studies and adoption studies support the
view that suicidality has an inherited component that may Preventing Suicide
be as high as 48 per cent (Joiner, Brown & Wingate, 2005) It is notoriously difficult to pick up the signs that an indi-
and which is independent of the heritability of other psy- vidual is seriously contemplating a suicide attempt. Prior
chiatric disorders (Rujescu, Zill, Rietschel & Maier, 2009). to an attempt, suicidal individuals will often seem calm,
This may be related to factors controlling low levels of rational, and even show signs of improvement in their psy-
serotonin metabolites in the brain which have been found chological condition. This calm and rationality may sim-
to be associated with suicidal behaviour in individuals suf- ply reflect the period of thought and planning that many
fering major depression (Van Praag, Plutchik & Apter, who decide to attempt suicide go through. Individuals
1990; Winchel, Stanley & Stanley, 1990). planning suicide will often meticulously dispose of their
This diversity of risk factors has led researchers to possessions, plan how their family will be cared for, and
argue that suicide probably results from a complex inter- take time to plan the act itself — often choosing a time
play between sociocultural factors, traumatic events, and place where they cannot be disturbed. According to
psychiatric history, personality traits and genetic vul- Kessler, Borges & Walters (1999), a national survey of sui-
nerability (e.g. Rujescu, Zill, Rietschel & Maier, 2009; cide in the USA suggested that about 39 per cent of those
Balazic & Marusic, 2005), all of which will need to be who attempt suicide are determined to die, while 47 per
included in a comprehensive model of suicide aetiology. cent do not wish to die but are communicating a ‘cry for

SUICIDE NOTES
individuals who are no longer around to explain why

they took their own life.
e This suicide note was written by an individual who
committed suicide by jumping under a moving train
in the UK, and it is typical in that it is short, expresses
guilt at the action, but also emphasizes the extreme
pain and hopelessness that the victim experiences.
e Most suicide notes are addressed to specific indi-
viduals, usually in an attempt by the victim tojustify
their actions to family and friends. However, they
can often be as confusing as they are enlightening -
especially since those taking their own lives may be
in such a confused and desperate state that they do
not fully understand their own reasons for commit-
ting suicide (Shneidman, 1973).
e Research on the content of suicide notes has not
particularly enlightened us to why some people
commit suicide, but there are age differences in the
content of such notes. Young people usually point
to interpersonal relations as the reason for their
suicide; middle-aged people tend to report simply
being unable to cope with life stressors; and older
individuals are more likely to report being driven to
suicide by health problems and physical disabilities
(Lester, 1998).
e Around one in three people who commit suicide
leave a suicide note, and analysis of such notes can Note © 2000/7 Forensics Linguistics Institute (FLI). All rights
provide an insight into the feelings and motives of reserved,
CHAPTER 7 DEPRESSION AND MOOD DISORDERS 23s"
help’ to friends and relatives in an attempt to convey their care for at-risk individuals, and (3) restricting access to
pain and hopelessness. Their survey also suggested that means of suicide (van der Feltz-Cornelis, Sarchiapone,
around 72 per cent of those who had constructed a sui- Postuvan, Volker et al., 2011). Related to this last point,
cide plan went on to make a suicide attempt, and they awareness of methods used to commit suicide and
suggest that prevention is best focused on those who plan attempts to reduce the lethality of those methods is also
suicide attempts and identifying those factors that indi- important in reducing the number of successful sui-
cate that a suicidal individual is drawing up a plan. cides. For example, an Australian study found that lethal-
The fact that around half of those attempting suicide ity rates for suicide attempts involving motor vehicle
do not want to die, but need to convey their pain and exhaust fumes and hanging had decreased sharply over
despair, means that intercepting these individuals before the previous 10 years (Spittal, Pirkis, Miller & Studdert,
they make a successful suicide attempt is important. The 2012). This appeared to be a consequence of the intro-
main forms of intervention include 24-hour helplines duction of catalytic converters on car engines that signif-
and telephone support lines such as those provided icantly reduced lethal carbon monoxide emissions, and
by the Samaritans in the UK (http://www.samaritans systematic removal of ligature points from institutional
.org.uk/). School-based educational programmes are settings in which those at risk of suicide might be living.
also being developed, and these are aimed at warning Finally, both psychological and pharmacological
teenagers about the early signs of suicidal tendencies in treatments can be helpful for individuals who are at high
their peers and providing them with appropriate support risk for repeated suicide attempts. Medications for mood
information. However, while these prevention schemes disorders (see section 7.3.1) can reduce the risk of sui-
have some success with some groups of users (e.g. young cide significantly, and these may include antidepressants
females), they are less effective in preventing suicide in (Bruce, Ten Have, Reynolds, Katz et al., 2004) and antip-
other groups (e.g. adolescent boys) (Gould & Kramer, sychotics (Meltzer, Gatwood, Goodman & Ford, 2003).
2001). Multilevel interventions for suicide preventions CBT can also be used successfully to reduce suicide risk
are also being developed, and best practices that have and suicide behaviours in particular client groups, such
been identified as effective are (1) training general practi- as adolescents (Stanley, Brown, Brent, Wells et al., 2009)
tioners (GPs) or family physicians to recognize and treat and individuals suffering psychosis (Tarrier, Haddock,
depression and suicidality, (2) improving accessibility of Lewis, Drake & Gregg, 2006).
SELF-TEST QUESTIONS
© Can you name the main risk factors for suicide?

e What are the best ways ofidentifying and preventing suicide?
SECTION SUMMARY
7.5 SUICIDE
e Over half of those that successfully commit suicide are significantly depressed before the fatal attempt.
® Suicidal ideation is reported by 13.5 per cent of people during their lifetime.
e Women are three times more likely to attempt suicide than men, but the rate for successful suicide is four times higher in
men than women.
e Risk factors for suicide include an existing psychiatric diagnosis, low self-esteem, poor physical health and physical
disability, and experiencing a significant negative life event.
e There is an inherited component to suicide which may be as high as 48 per cent.
e The main forms of intervening to prevent suicide include 24-hour helplines and telephone support lines (e.g. the
Samaritans), and school-based educational programmes warning about the early signs of suicidal tendencies.
© Both medications for mood disorders and CBT can be helpful in reducing suicide risk in vulnerable people.
34s PSYCHOPATHOLOGY
. /.
7.6 DEPRESSION AND in neurotransmitter imbalances in the brain (section
7.2.2). Alook back at the online ‘Summary’ table reminds
MOOD DISORDERS us of the various theories that have been developed to
try to explain all or parts of the symptoms of depression.
REVIEWED These theories range from biological theories covering
inherited factors, brain neurochemical imbalances and
Depression is arguably the most prevalent of all the main brain abnormalities, to a full spectrum of psychologi-
psychopathology symptoms we will cover in this text cal theories attempting to explain both the behavioural
(lifetime prevalence rates between 5.2 and 17.1 per cent), and cognitive features of depression. Drug treatments,
it afflicts women twice as frequently as men, and it is such as trycyclic drugs, monamine oxidase inhibitors,
estimated that it contributes 12 per cent to the total bur- and, more recently, selective serotonin reuptake inhibi-
den of non-fatal global disease (Ustun, Ayuso-Mateos, tors (SSRIs), have been shown to alleviate many of the
Chatterji, Mathers & Murray, 2000). It is an emotion symptoms of severe depression (section 7.3.1). However,
that all of us experience at some point — especially in both behavioural and cognitive therapies appear to have
relation to losses and failures in our lives. However, for promise as long-term effective treatments for depression,
some it is a sustained, crippling and distressing problem and these therapies help the sufferer by enabling them
(see the personal description given at the beginning of to identify and challenge ingrained negative views of
this chapter), and may even lead to suicidal ideation, themselves and the world. Finally, two important clinical
and suicide attempts (section 7.5). Bipolar disorder is the phenomena related to mood disorders and depression
other main mood disorder covered in this chapter, and are deliberate self-harm and suicide. Deliberate self-
this is characterized by alternating periods of depression harm is an increasingly recognized problem that mainly
and mania (see Client’s Perspective 7.1). This is a signifi- afflicts adolescents, while mental health problems
cantly less prevalent disorder (lifetime prevalence rate generally — and mood disorders specifically — are a signifi-
between 0.4 and 1.6 per cent) that appears to have a basis cant risk factor for suicide.
Bl To access the online resources for this chapter go to

Reading Activity
Depression and mood Bipolar disorder: A personal Activity 7.1

disorders summary account
Brain areas and depres-
Journal article: Depression — Mania: Diagnostic interview sion labelling
Perspectives from affective The science of mindfulness Self-test questions
neuroscience
Self harm: A personal Revision flashcards
Article on bipolar disorder account Research questions
and creativity
Beating the Blues
Glossary key terms
Clinical issues
References
Experiencing Psychosis:
Schizophrenia Spectrum Pro
To access the online resources for this chapter goto |

This chapter describes the symptoms of psychosis and

examines the heterogeneous diagnostic categories within THE NATURE OF PSYCHOTIC SYMPTOMS 238
DSM-5. We begin by describing the main symptoms of
2 THE DIAGNOSIS OF SCHIZOPHRENIA SPECTRUM
psychosis and then cover the main diagnostic categories
DISORDERS = 243
within schizophrenia spectrum disorder. We also consider
the stages through which psychotic symptoms develop.
THE PREVALENCE OF SCHIZOPHRENIA SPECTRUM
We then describe and evaluate a range of explanations
DISORDERS 245
of psychosis, and these theories often attempt to explain
symptoms at a number ofdifferent levels, such as biologi- THE COURSE OF PSYCHOTIC SYMPTOMS 246
cal, psychological and social levels. We finish by describ-
ing a variety of biological and psychological treatments 8.3 THE AETIOLOGY OF PSYCHOTIC SYMPTOMS 249
for psychotic symptoms, and end by discussing the role of
8.6 THE TREATMENT OF PSYCHOSIS 270
community care as a means of long-term supervision and
management for those suffering from psychosis. §.7 EXPERIENCING PSYCHOSIS REVIEWED 280
M2364 PSYCHOPATHOLOGY
LEARNING OUTCOMES
1. Describe the main clinical symptoms of psychosis, 3. Describe, evaluate and compare the main
and the key features of the main diagnostic psychological and sociocultural theories of the
categories defining schizophrenia spectrum aetiology of psychosis.
disorders in DSM-5. 4. Describe and evaluate the role of familial and
2. Describe and evaluate the main biological psychological factors in relapse following remission.
theories of the aetiology of psychosis — especially 5. Describe a range of treatments for psychotic
the role of brain neurotransmitters and brain symptoms, including biological, psychological,
abnormalities. familial, and community care interventions.
Trying to look at the lead up to an illness is difficult. Before |had any symptoms, | was generally feeling like |couldn't cope, but |didn’t
know how to go about getting any help. | was in a bad relationship and it ended, but |dearly wanted something to take its place.
| moved to Birmingham, to do a post-graduate diploma in housing. | recognized that | wasn't really feeling together, but |just
hoped that things would improve. | lived on my own ina bedsit and generally became antagonistic towards others.
| had passed my first-year exams and was working as a student placement for Warwick District Council. By about October of
1992, | believed that DJs on the radio were talking directly to me. When | told other people this they just laughed. But these DJs
started to become very important to me, so | continued to believe it was happening, despite what other people were saying. |just
kept it as my secret, until eventually when | was not at work |would listen to the radio 24 hours a day.
| believed that a radio DJ wanted a relationship with me, and throughout the course of our courtship — over the airwaves — the
DJ and myself would actually discover the meaning of life. Everything had a meaning and eventually | had a sort of vision: God,
he spoke to me and said ‘No matter what happens, | will always love you’ | felt special and chosen and at the same time | thought
that other people were telepathic and could read my mind.
| was still working and started a 2-week placement at Newtown neighbourhood office. By now the world looked very different,
with people being able to read my mind. Whenever names were said, such as Lorraine or Pat, it had something to do with the state
of my relationship with the radio DJ. Lorraine meant sorrow or floods of tears like rain; Pat meant that someone was patronis-
ing me, orl them, depending on the context; Jackie meant that | was being chucked or that | was chucking him. | used to ring up
the radio station under different names, all of which had a hidden meaning, such as Dawn - meaning that something had just
dawned on me. Maureen meant that |was marooned.
Whilst on this placement - | was only there for 2 days — | began to get physical or tactile hallucinations. | thought that | had
been shot in the head to remove a blood clot. Then, as | was working with one of my colleagues, |actually felt my brain crack open,
then masses of blood came out of one of my ears, then a small trickle from the other. This for me meant that | was dead or dying
in spirit, which | believed in more than the mortal body. At this point | started crying. My colleague went to put his hands on my
arm, which he quickly removed as my arms were red hot. | asked to go home early, which was allowed.
That night, | thought that the devil was after me: |saw him come through one of the speakers of my stereo system. | was also
probably hearing voices, but they were mixed in with the talk of the radio DJs. Suddenly, | became frustrated and ran out of the
house into the middle of the road and started screaming. My neighbour came out and told me to come inside. He told me he had
called the police and | started thumping him thinking he was the devil.
The experiences of the illness left me socially inept, mainly because | couldn't think to speak and engage in interpersonal relation-
ships. | tried very hard to overcome the symptoms of the illness, including lack of motivation, but | was also conscious not to do too
much. | did voluntary work and finished off my course. But, | was generally feeling different and less capable than everyone else. |
tended to sleep an awful lot, but always tried to keep going, although many times |felt like giving up. But, this time |had come so far
away from my delusions that there seemed like no going back. Eventually, |found employment and!am currently working part-time.
Sophie's Story
&
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS ey yes
Introduction felt that she had been shot in the head and her brain had
cracked open. Sophie’s story ends with her experiences
Psychotic symptoms can be crippling and are often leaving her feeling socially inept and affecting her longer
characterized by disturbances in thought and language, term ability to be productive and motivated.
sensory perception, emotion regulation, and behaviour. Psychosis is a collective name given to an extensive
Sufferers may experience sensory hallucinations and range of disparate symptoms that can often leave an indi-
also develop thinking biases that may lead to pervasive vidual feeling frightened and confused, and the presence of
false beliefs or delusions about themselves and the world different combinations Of ve
around them. Individuals with psychotic symptoms may these symptoms may lead / For a video on psychosis go to
often withdraw from normal social interaction because to a diagnosis of any one of www.wiley-psychopathology.com/
video/ch8
of these disturbances of perception and thought, and this a number of schizophre-
can result in poor educational performance, increasing nia spectrum disorders.
schizophrenia spectrum disorders The
lack of productivity, difficulties in interpersonal relation- DSM-5 has moved away
name for separate psychotic disorders
ships, neglect of day-to-day activities and a preoccupa- from a single overriding that range across a spectrum depending
tion with a personal world to the exclusion of others. As diagnostic category (schiz- on severity, duration and complexity of
a result, many individuals exhibiting psychotic symptoms ophrenia) split into a series symptoms.
fall to the bottom of the social ladder or even become of subtypes (paranoid, disor-
homeless because they cannot hold down a job or sustain ganized, catatonic, undifferentiated), and now lists a
a relationship — a phenomenon known as downward drift number of separate psychotic disorders that range across
(Hollingshead & Redlich, 1958) (see section 8.5.3). a spectrum depending on severity, duration and com-
Sophie’s story is a particularly severe example of how plexity of symptoms. The main diagnostic categories in
psychotic symptoms can manifest themselves. Her story DSM-5 are schizophrenia, schizotypal personality disor-
starts with a stressful life —exemplified by being ina difficult der, delusional disorder, brief psychotic disorder, and
relationship — and an overwhelming feeling of inability to schizoaffective disorder, and we will discuss these indi-
cope. Whilst living alone she finds maintaining relation- vidually later in this chapter. But first we will discuss
ships with others difficult. The developing symptoms of the key cognitive and behavioural features that define
psychosis include delusions (that the DJ is talking directly psychosis — combinations of which give rise to the differ-
to her and that others were developing telepathic powers ent diagnoses. These key features include delusions, hal-
that enabled them to read her mind) and she begins to lucinations, disorganized thinking, abnormal motor
feel that she possesses special powers. Eventually Sophie behaviour, and negative symptoms (indicative of dimin-
begins to experience sensory hallucinations in which she ished emotional expression).
ie HISTORY OF SCHIZOPHRENIA AS A DIAGNOSTIC CATEGORY

ie'6]
~
The symptoms of psychosis have been reported which there was no recovery. In contrast to Kraepelin,
“s throughout history, but because the symptoms can the Swiss psychiatrist Eugen Bleuler (1908) believed
o)
a. be so varied and wide ranging, ‘schizophrenia’ has only that the onset of dementia praecox was not simply
4) gradually been isolated as a single diagnostic category restricted to adolescence and early adulthood and also
pa to cover these heterogeneous characteristics. believed that it did not inevitably lead to dementia.
U
2) The European psychiatrist, Emil Kraepelin (1896), He preferred to use the term schizophrenia (from the
tele was the first to distinguish schizophrenia from a range Greek schiz, to spilt, and phren, the mind), because he
of other psychiatric symptoms (such as manic depres- felt that it properly described the splitting of different
sive illness). He did this by bringing together a number psychological functions within a single personality.
of contemporary diagnostic concepts including para- Unfortunately, this term has also had its problems,
noia, catatonia and hebephrenia (symptoms indicative with the popular belief that the term schizophrenia
of incoherence and fragmentation of personality) refers to a split- or double-personality. In order to try to
under the general term dementia praecox. He unify the various symptoms under a single diagnostic
assumed that dementia praecox category, Bleuler used the concept of the ‘breaking of
mentia praecox An early, general
m for a number of diagnostic concepts was a single disease that mani- associative threads’as being central to all of the symp-
luding paranoia, catatonia and hebe- fested itself in late adolescence toms of schizophrenia. That is, effective thinking, com-
‘enia (symptoms indicative of incoher- or early adulthood and had a munication and action were not possible if the ability
-e and fragmentation of personality). deteriorating prognosis from to associate things together was disrupted. In this
PSYCHOPATHOLOGY
respect, it is interesting to note that in later sections in this inevitably meant that people could receive a diagnosis of
chapter we will see that there is evidence that at least schizophrenia but exhibit quite different symptoms. The
some of the clinical symptoms of schizophrenia may be latest diagnostic manual, DSM-5, has moved away from
determined by dysfunctions in associative and attentional defining a single overriding diagnostic category with a
processes (see section 8.5.2). series of subtypes towards considering schizophrenia as
Recent diagnostic criteria recognize the complexity a spectrum disorder. The important diagnostic categories
of schizophrenia as a diagnostic category, and up until in this spectrum are schizophrenia, schizotypal personality
the publication of DSM-5, diagnosis was not dependent disorder, delusional disorder, brief psychotic disorder, and
on one essential symptom, but on the basis of the pres- schizoaffective disorder, and these will be discussed later in
ence of at least two or three of five basic symptoms. This this chapter.
absurd beliefs with logical thought has led some clini-

8.1 THE NATURE OF cians to suggest that delusions may be the result of an
PSYCHOTIC SYMPTOMS inability to integrate perceptual input with prior knowl-
edge even though rational thought processes are still
intact (Frith, 1996; Frith & Dolan, 2000). For other clini-
DSM.5 lists five important characteristics for diagnosing cians it is suggestive of the development of biased infor-
schizophrenia spectrum disorders. The first four of these mation processing and the development of dysfunctional
characteristics are traditionally known as positive symp- beliefs about the world (e.g. Freeman, Garety, Kuipers,
toms, because they tend to reflect an excess or distortion Fowler & Bebbington, 2002; Morrison, 2001), or decision-
of normal functions (e.g. developing inappropriate making processes that lead the individual to ‘jump to
beliefs or perceiving things conclusions’ on the basis of minimal evidence (e.g.
positive symptoms Characteristics of that are not there), and the Moritz & Woodward, 2005; Garety & Freeman, 1999).
psychotic symptoms which tend to reflect final category represents The main types of delusion found in those experienc-
an excess or distortion of normal functions. what are known as nega- ing psychosis are: (1) Persecutory delusions (paranoia),
tive symptoms, and these in which the individual
negative symptoms Symptoms charac- reflect symptoms charac- believes they are being persecutory delusions Delusions in q
teristic of adiminution or loss of normal teristic of a diminution or persecuted, spied upon, which the individual believes they are
functions. loss of normal functions. being persecuted, spied upon, or are in
or are in danger (usually danger (usually as the result of a conspir-
as the result of a cons- acy of some kind).
piracy of some kind); (2)
Grandiose delusions, in which the individual believes
8.1.1 Delusions
they are someone with fame or power or have excep-
Delusions are firmly held but erroneous beliefs that tional abilities, wealth or
grandiose delusions Delusions in which
(1) usually involve a misinterpretation of perceptions fame (e.g. Jesus Christ,
the individual believes they are someone
or experiences, and (2) or a famous music star); with fame or power or have exceptional
delusions Firmly held but erroneous
become fixed beliefs that (3) Delusions of control, abilities, wealth or fame.
beliefs that usually involve a misinterpreta-
tion of perceptions or experiences. are not amenable to change where the person believes
in light of conflicting or that their thoughts, feel- delusions of control Delusions where the
contradictory evidence. Such delusions are commonly ings or their actions are person believes that his or her thoughts, —
feelings or actions are being controlled
experienced by around 75 per cent of those individuals being controlled by external by external forces (e.g. extraterrestrial or
hospitalized because of their psychotic symptoms (Maher, forces (e.g. extraterrestrial supernatural beings).
2001), and while some delusions may be clearly bizarre or supernatural beings), and
(e.g. the individual may believe that their entire internal this is often associated with the belief that control is
organs have been taken out and replaced by those of being exerted through devices (such as the radio) which
someone else), others may not (e.g. a paranoid belief that are sending messages directly to the person’s brain; (4)
the individual is constantly under surveillance by the Delusions of reference, where the individual believes
police). Regardless of how bizarre a delusion is, the suf- that independent external delusions of reference Delusions where
ferer is often able to bring reason and logic to support events are making specific the individual believes that independent
their delusion — even though the underlying belief itself is reference to them (e.g. in external events are making specific refer-
clearly absurd (Maher, 2001). This ability to support Sophie’s Story, she believes ence.to him or her. :
s
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS 239°
rilistic delusions Delusions where indi- that the DJ on the radio is self-generated actions could be attributed to an external
luals believe that some aspect of either talking directly to her); (5) source. They found that such erroneous beliefs gener-
> world or themselves has ceased to exist
Nihilistic delusions, where ated higher than normal levels of activation in the pari-
g. the person may believe that they are
fact dead). the individual believes that etal cortex and cerebellum and they suggest that these
some aspect of either the areas of the brain may be altered during psychotic epi-
otomanic delusions Relatively rare world or themselves has sodes so that self-produced actions and thoughts are
ychotic delusions, where an individual ceased to exist (e.g. the per- experienced as external.
s a delusional belief that a person of son may believe that they
yher social status falls in love and makes are in fact dead) or a major
1orous advances towards them.
catastrophe will occur; and
8.1.2 Hallucinations
_ (6) Erotomanic delusions,
For an activity on types of
) when an individual falsely People suffering psychotic symptoms regularly report
delusions go to
www.wiley-psychopathology.com/ | believes that another per- sensory abnormalities across a broad range of sensory
activities/ch8 son is in love with him or modalities, and this is usually manifested as perceiving
her (see Focus Point 8.2). things that are not there. Hallucinations can occur in
One common feature of psychotic thought is that any modality (e.g. audi-
touveniacton Staton hallucinations A sensory experience in
sufferers frequently believe that their thoughts are being y ey y which a person can see, hear, smell, taste or
interfered with or controlled in some way, either by and tactile), but the most fg something that isn’t there.
being openly broadcast to others or by having thoughts common are auditory hal-
planted into their mind by external forces. This type of lucinations that are reported by around 70 per cent of
delusion is so common that it may offer some insight sufferers (Cleghorn, Franco, Szechtman, Kaplan et al.,
into the cognitive deficits underlying a majority of psy- 1992). Auditory hallucinations are usually manifested
chotic thought. For example, in an experimental study, as voices, and these can be experienced as external
Blakemore, Oakley & Firth (2003) used hypnosis to voices commanding the individual to act in certain
generate beliefs in non-clinical participants that their ways, two or more voices conversing with each other,
a EROTOMANIA AND STALKING

0
=
One form of psychotic delusion is called erotomania. eventually come to have a relationship with their vic-
~ This is a relatively rare disorder where an individual has tim. An example ofthis is the case of Agnetha from the
\o) Swedish pop group ABBA, who was stalked for some
o a delusional belief that a person of higher social sta-
nn tus falls in love and makes amorous advances towards years by a Dutch man who believed he was destined
=] them. As a result of these delusions, the individual suf- to be with her.
VU
Oo fering erotomanic delusions may often end up stalk- Stalking appears to be on the increase in many
fi ing their target by regularly visiting their home in an Western countries (Pathe, 2002), causes substantial
attempt to meet and talk with them or by following distress to its victims, and can be caused by a range of
them as they go about their daily business. There are psychopathologies (e.g. erotomanic delusions, severe
two types of erotomanic delusion. The first is where personality disorder, obsessive compulsive disorders).
the individual believes their victim loves them. In this Studies of individuals with erotomanic delusions
case the individual believes they are having a rela- indicate that they are usually isolated loners with-
tionship with their victim, and they will make regular out a partner or full-time occupation and around half
attempts to try to contact and meet their victim in have a first-degree relative with a delusional disorder
order to substantiate the relationship. The American (Kennedy, McDonough, Kelly & Berrios, 2002). Many
actress Rebecca Schaeffer was tragically shot in 1989 also develop fantasies in which they are driven to pro-
by a stalker who was rebuffed by her when attempt- tect, help or even harm their victims (Menzies, Federoff,
ing to talk to her about their ‘relationship. The second Green & Isaacson, 1995). One example is the German
form of erotomanic delusion is when the individual stalker who was obsessed with tennis star Steffi Graf,
believes that they are destined to be with their victim, and this drove him to attack and stab her tennis rival,
even though they are aware they may never have met Monica Seles, during a tournament in Hamburg in 1993
them. So, if they pursue them long enough, they will in a deluded attempt to try to further Graf's career.
‘RAGS PSYCHOPATHOLOGY
or a voice commentating on the individual's own 8.1.3 Disorganized Thinking (Speech)

thoughts. In all cases these voices are perceived as being
distinct from the individual’s own thoughts. Research Disorganized thinking will normally be inferred from the
into brain areas involved in speech generation and the individual’s speech, and there are a number of common
perception of sounds suggests that when sufferers features displayed by individuals experiencing psychotic
claim to hear ‘voices’ this is associated with neural acti- symptoms. The most common are derailment or loose
vation in these areas of the brain (Keefe, Arnold, Bayen, associations, where the individual may drift quickly
McEvoy & Wilson, 2002; McGuire, Silbersweig, Wright, from one topic to another derailment A disorder of speech wher
Murray et al., 1996), and the sufferer attributes them to during a conversation. Their the individual may drift quickly from o
external sources. Visual hallucinations are the second answers to questions may topic to another during a conversation.
most common type of hallucination and can take either be tangential rather than
a diffuse form as in the perception of colours and relevant (‘tangentiality), loose associations Disorganized think-
ing in which the individual may drift
shapes that are not present, or they can be very specific and in some cases their
quickly from one topic to another during <
such as perceiving that a particular person (e.g. a part- speech may be so disorgan- conversation.
ner or parent) is present when they are not. Other hal- ized that it is neither struc-
lucinations can be tactile and somatic (e.g. feeling that tured nor comprehensible. tangentiality A disorder of speech in g
one’s skin is tingling or burning) or olfactory and gusta- Instances of the latter are which answers to questions may be tan-
‘clanging’, the use of neol- gential rather than relevant. 3
tory (e.g. experiencing smells that are not present or
foods that taste unusual). ogisms, and ‘word salads’:
clanging A form of speech pattern in a
For those who believe that their hallucinations are Focus Point 8.3 provides
schizophrenia where thinking is driven
real, such experiences can be extremely frightening. examples of the confused by word sounds. For example, rhyming or
However, while some individuals suffering psychosis are speech generated by some alliteration may lead to the appearance
convinced their hallucinations are real, many others individuals exhibiting psy- of logical connections where none in fact
exists. 4
are aware that their hallucinations may not be real. This chotic symptoms. These
suggests that psychotic episodes may be associated with loose associations that
neologisms Made up words, frequently
a reality-monitoring deficit. That is, individuals suffer- appear to govern psychotic constructed by condensing or combining
ing psychotic symptoms may have difficulty identifying speech suggest that suffer- several words. |
the source of a perception and difficulty distinguishing ers (1) have difficulty inhib-
whether it is real or imagined. In support of this possi- iting associations between word salads When the language of the
bility, Brebion, Amador, David, Malaspina et al. (2000) thoughts (Titone, Holzman person experiencing a psychotic episode
appears so disorganized that there seem
found that when individuals diagnosed with schizophre- & Levy, 2002) and so tend
to be no link between one phrase and th
nia and non-clinical controls were asked to remember to follow the track of the next. Zz
words that had either been generated by themselves or first association that comes
been generated by the experimenter, schizophrenic indi- to mind, and (2) have difficulties understanding the full
viduals differed in three important ways from non- context of a conversation (Cohen, Barch, Carter & Servan-
clinical controls. Firstly, they were more likely to identify Schreiber, 1999), and so cannot distinguish the full mean-
items as having been in the generated list of words ing of a conversation or sentence from its detail. The
when they were not (false positives); secondly, they result of these loose associations is that psychotic speech
were more likely to report that words they had gener- can be very detailed in terms of number of words, breadth
ated themselves were generated by the experimenter; of ideas, and grammatical
poverty of content A characteristic of J
and thirdly, they were more likely to report that correctness, but it will usu- the conversation of individuals suffering
spoken items had been presented as pictures. These ally convey very little (pov- psychosis in which their conversation has
results suggest that individuals diagnosed with schizo- erty of content). very little substantive content. :
phrenia have a reality-monitoring deficit (i.e. a problem

distinguishing between what
reality-monitoring deficit Where an actually occurred and 8.1.4 Grossly Disorganized
individual has a problem distinguishing what did not occur), and a
between what actually occurred and what
self-monitoring deficit (ie. or Abnormal Motor Behaviour
did not occur.
they cannot distinguish Grossly disorganized or abnormal motor behaviour may
between thoughts and manifest itself in a variety of ways. Behaviour may be child-
self-monitoring deficit Where individu-
ideas they generated them- like and silly (and inappropriate for the person's chronologi-
als cannot distinguish between thoughts
and ideas they generated themselves selves and thoughts or cal age), or inappropriate to the context (e.g. masturbating
and thoughts or ideas that other people ideas that other people in public). It may be unpredictable and agitated (e.g. shout-
generated. generated). ing and swearing in the street) and the individual may have.
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS 2a
o DISORGANIZED SPEECH INDICTATIVE OF DISORGANIZED THINKING

oo
=
Psychotic symptoms frequently exhibit a range of
= attributes that indicate disordered thinking. Below are
or combining several words. Some examples given by
individual sufferers are the following:
\e)
a. examples of some of the more common of these disor-
V) ganized speech symptoms. SPECTROAUTOROTATION Circling in everywhere, as with
p>)
U checkers or a bat in baseball
Oo WORD SALAD SNIGGERATION A giggle or sniggering. | do it
Lobe
sometimes
In many cases, the language of the person experienc- RELAUDATION Praising over and over
ing a psychotic episode appears so disorganized that
there seems to be no link between one phrase and the CIRCLINGOLOGY Study of a rolling circle; a fruit
can in the form of a cylinder
next, and this is known as a ‘word salad’. Some word
rolling
salads simply do not seem to be attempts to commu-
nicate anything structured and appear to drift without
substance from one unconnected sentence to the next:
CLANGING
‘Everything is going around in slow motion. The
boxes are clanging and chattering to be let out. People exhibiting psychotic symptoms often try to
Behind my forehead the past is surfacing, mixing a communicate using words that rhyme, and this isknown
bottle of acid solution. A stake jams a door that leads as‘clanging’ lf you go back to look at Sophie’s story at the
to a mirage of broken appearances. Inside a box, beginning of this chapter, you will see that she used a
pounding fists try to pull down my imagination. The series of names to denote the state of her mind or how
ground work is split into hundreds of pieces; each she was feeling. These names rhymed with words that
fragment is separate as if it had some kind of indi- described her feelings (e.g. Lorraine — Tears like rain;
vidual purpose. The truth is locked up ina unit! Pat — Patronising; Jackie - Being Chucked; Maureen —
Marooned). In other cases, sufferers only appear able
In other cases, word salads appear to be sets of to construct sentences if the words in them rhyme —
| phrases or words linked by association to the previous and this communication may begin with a sensible
| phrase. For example, in answer to the question ‘What response but then degenerate into nonsense because
colour is your dress?’ a sufferer answered ‘red... Santa of the urge to ‘clang’as the following transcript shows:
Claus... flying through the sky... God‘ This is known
as loose association or derailment and makes it very dif-
ficult to follow the conversation of an individual when Therapist: ‘What colour is your dress?’
a single, often unimportant word from the previous Client: 'Red.... Likea bed!
sentence becomes the focus of the next sentence.
Therapist: ‘Why is it like a bed?’
Client: ‘Because it’s dead’
NEOLOGISMS
Therapist: ‘Why is a bed like being dead?’
Totryand communicate, many individuals suffering psy-— Cjjant: ‘1dunno... maybe it’s a med’
chotic symptoms often make up words and use them in Sete frre a
their attempts to communicate. These are called neolo- Tse Rit HAE SST ICE
gisms, and are frequently constructed by condensing _ Client: ‘A bled?
difficulty completing any goal-directed activity (e.g. anina- environment (catatonic catatonic motor behaviours
bility to focus on or complete basic day-to-day tasks such stupor), maintaining rigid, Characterized by a decrease in reactivity
immobile postures (cata- and maintaining rigid, immobile postures.
as cooking or maintaining personal hygiene). The person’s
appearance may be dishevelled and they may well dress tonic rigidity), resisting
in an inappropriate manner (e.g. wearing heavy, thick cloth- attempts to be moved (catatonic negativism), or pur-
ing in hot weather or walking around in public in only poseless and excessive motor activity that often consists
their underwear). Catatonic motor behaviours are of simple, stereotyped movements (catatonic excitement
characterized by a significant decrease in reactivity to the or stereotypy) (see Photo 8.1).
* ~
8.1.5 Negative Symptoms

Negative symptoms are common within a diagnosis of
schizophrenia, but less so in the other schizophrenia spec-
trum disorders. Negative symptoms include diminished
emotional expression, avolition, alogia, anhedonia, and aso-
ciality. Diminished emotional expression (also described
as affective flattening)
diminished emotional expression A Gg
includes reductions in facial reduction in facial expressions of emotion,
expressions of emotion, lack of eye contact, poor voice intonation,
lack of eye contact, poor and lack of head and hand movements
voice intonation, and lack of that would normally give rise to omotioll
expression.
head and hand movements
that would normally give affective flattening Limited range and —
rise to emotional expres- intensity of emotional expression; a negag
sion. Avolition represents tive’ symptom ofschizophrenia. 4
an inability to carry out or
complete normal day-to- avolition An inability to carry out or
complete normal day-to-day goal-orientec
day goal-oriented activities, activities, and this results in the individual
and this results in the indi- showing little interest in social or work 3
vidual showing little interest activities.
in social or work activities.
Alogia is characterized by a alogia A lack of verbal fluency in which q
the individual gives very brief, empty
lack of verbal fluency in
replies to questions.
which the individual gives
very brief, empty replies to anhedonia Inability to react to enjoyable
with
Reproduced
Library.
Photo
Studio/Science
Grunnitus
permission.
questions. Anhedonia is the or pleasurable events.
PHOTO 8.1 /n some very severe cases of psychosis, the decreased ability to expe-
individual may lapse into a catatonic stupor. Those who rience pleasure from posi- asociality A lack of interest in social
interactions, perhaps brought about by a
lapse into this state become withdrawn and inactive for long tive stimuli or an inability
gradual withdrawal from social interaction
periods. In extreme cases this may take the form of catatonic to recall pleasurable events generally.
rigidity, in which the individual will adopt a rigid, often awk- (Kring & Neale, 1996). Fin-
ward posture for many hours. Others exhibit what is known ally, asociality refers to a lack of interest in social interac-
as waxy flexibility, and will maintain a posture into which tions, perhaps brought about by a gradual withdrawal
they have been placed by someone else. from social interactions generally.
SELF-TEST QUESTIONS
* What is the difference between the positive and negative symptoms of schizophrenia?
® Can you name some of the different types of delusional states found in delusional disorder?
* What are the most common forms of hallucination experienced in schizophrenia and approximately what percentage of
sufferers report hallucinations?
* Can you name the different forms of disordered speech and communication exhibited by individuals diagnosed with
schizophrenia and provide some examples of each?
° What are the characteristics of catatonic motor behaviours?
* Can you describe some of the specific symptoms that are collectively known as negative symptoms?
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS
SECTION SUMMARY
8.1 THE NATURE OF PSYCHOTIC SYMPTOMS
° The first four characteristics are known as positive symptoms, and the fifth category represents negative symptoms.
e Roughly 75 per cent of people hospitalized with a diagnosis of schizophrenia experience delusions.
e The main types of delusions are (1) persecutory delusions, (2) grandiose delusions, (3) delusions of control, (4) delusions of
reference, and (5) nihilistic delusions.
e Around 70 per cent of individuals diagnosed with schizophrenia report auditory hallucinations.
e Individuals suffering hallucinations may have a reality-monitoring deficit (distinguishing between what actually occurs
and what does not).
¢ The most common forms of disorganized speech are derailment, loose associations, clanging, neologisms and word salads.
® Grossly disorganized or abnormal motor behaviour is usually behaviour inappropriate to a context (e.g. masturbating in
public). Catatonic motor behaviours are characterized by a decrease in reactivity and maintaining rigid, immobile postures.
e Negative symptoms are characterized by flat affect, lack of interest in social or work activities, poverty of speech (alogia)
and apathy (avolition).
8.2 THE DIAGNOSIS DSM-5 SUMMARY TABLE 8.1 Criteria for delusional disorder
e One or more delusions lasting at least 1 month

OF SCHIZOPHRENIA
e Apart from the impact of the delusions, normal function-
SPECTRUM DISORDERS ing is not markedly impaired and behaviour is not bizarre
e Any manic or major depressive episodes which have

occurred have been brief in relation to the delusional
DSM-5 has organized schizophrenia spectrum disorders episode
along a gradient of psychopathology and impairment —
from less severe to more severe and disabling. Clinicians e The disorder is not directly attributable to the use of a
substance or medication and is not better explained by
are asked to consider diagnosis along this continuum,
other mental disorder
taking into account the number of diagnosable symp-
toms, the severity of those symptoms, and the time
period over which symptoms have been manifested.
We will describe the diagnostic criteria for four of these conspired against, cheated, spied on, followed, poisoned,
spectrum disorders, namely delusional disorder, brief maliciously maligned, harassed, or obstructed in the pur-
psychotic disorder, schizophrenia, and schizoaffective suit of long-term goals. Other common subtypes are ero-
disorder. Although DSM-5 considers schizotypal person- tomanic type (see Focus Point 8.2) and the grandiose type
ality disorder to be within the schizophrenia spectrum, (where the individual has a strong conviction that they
it is normally considered as a personality disorder, and have some great talent or insight). Grandiose delusions
so its diagnostic criteria and description can be found in may often have a religious content or consist of beliefs
Chapter 12, Personality Disorders. that the individual has a special relationship with a prom-
inent person. Apart from the direct impact of the delu-
sions, psychosocial functioning in such individuals may
seem quite normal. However, depending on the type of
8.2.1 Delusional Disorder delusional belief held by the individual, this may often
The diagnostic criteria for delusional disorder are given give rise to social, marital or work problems. Many also
in DSM-5 Summary Table 8.1. Subtypes of delusional exhibit mood problems associated with their delusional
disorder include the most common which is the persecu- beliefs, especially anger outbursts or antagonistic behay-
tory type, where the individual believes they are being iour when their beliefs are not taken seriously.
8.2.2 Brief Psychotic Disorder phase and can be a significant indicator of later full:
blown symptoms of psychosis (Lencz, Smith, Auther,
The core feature of brief psychotic disorder is the sudden Correll & Cornblatt, 2004). Additional symptoms dis-
onset of at least one of the main psychotic symptoms — played by individuals with a diagnosis of schizophrenia
namely, delusions, hallucina- may include inappropriate affect (e.g. laughing inappro-
brief psychotic disorder The sudden tions, disorganized speech, priately), depressed mood, anxiety or anger, disturbed
onset of at least one of the main psychotic or grossly abnormal psych- sleep patterns and lack of interest in eating. Individuals
symptoms, with this change from a non-
omotor behaviour (see sec- with a diagnosis of schizophrenia may often show a lack
psychotic state to the appearance of
tion 8.1.4), with this change
symptoms occurring within 2 weeks and of insight into their symptoms, and may be hostile and
from a non-psychotic state
being associated with emotional turmoil ageressive. However, aggression is more common in
or overwhelming confusion. to the appearance of symp- younger males and for individuals with a past history of
toms occurring within 2 violence, non-adherence to treatment, substance abuse
weeks and being associated with emotional turmoil. or and impulsivity (DSM-5, p.101). It must, however, be
overwhelming confusion. The diagnostic criteria are pro- emphasized that the vast majority of people with a diag-
vided in DSM-5 Summary Table 8.2. nosis of schizophrenia are not aggressive and are more
likely to be the victims of violence and aggression than
be the perpetrators.
8.2.3 Schizophrenia DSM-5 SUMMARY TABLE 8.3 Criteria for schizophrenia
A diagnosis of schizophrenia is given when there is range
e Atleast two of the following must be present for a signifi-
of symptoms covering cognitive, behavioural and emo- cant period of time during a one month period:
tional dysfunction and also
schizophrenia The main diagnostic impaired occupational or e Delusions
category for psychotic symptoms. The five social functioning — but no e Hallucinations
central characteristics are delusions, hal-
single symptom is charac-
lucinations, disorganized speech, grossly e Disorganized speech
disorganized or catatonic behaviour and teristic of this diagnosis.
flattened affect, poverty of speech and DSM-5 Summary Table 8.3 e Highly disorganized or catatonic behaviour
apathy. shows the diagnostic crite- e Negative symptoms such as diminished emotional
ria for schizophrenia and expression
two or more of the five symptoms in the first point must
e The ability to function in one or more major areas such as
be present for a significant proportion of time during a work, self-care or interpersonal relationships is markedly
1-month period or longer. The following point is also diminished
important as it recognizes that symptoms must be asso-
¢ Continuous signs of the disturbance last for at least
ciated with impaired functioning across areas such as
6 months
work, interpersonal relations, or self-care. Prodromal
symptoms often precede the active phase, and residual symp- ¢ The disorder is not directly attributable to the use of a
toms may follow it (see below). Similarly, negative symptoms substance or medication and is not better explained by
other mental disorder
or social isolation are common during the prodromal
DSM-5 SUMMARY TABLE 8.2 Criteria for brief psychotic

disorder
e Presence of at least one of the following: DSM-5 SUMMARY TABLE 8.4 Criteria for schizoaffective
disorder
¢ Delusions
e Hallucinations ¢ Acontinuous period of illness during which there is a

major mood episode (major depressive or manic)
e Disorganized speech
e Delusions or hallucinations for 2 or more weeks without
e Highly disorganized or catatonic behaviour the occurrence of a major mood episode
e The disturbance lasts between 1 day and 1 month with ¢ Symptoms for a major mood episode are present for the
eventual return to normal behaviour majority of the duration of the illness
¢ The disorder is not directly attributable to the use of a ¢ The disorder is not directly attributable to the use of a
substance or medication and is not better explained by substance or medication and is not better explained by
other mental disorder other mental disorder
&
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS 245,
8.2.4 Schizoaffective Disorder episode reflecting either depression or mania that are
present for the majority of the duration of the illness
Schizoaffective disorder is diagnosed when an (DSM-5 Summary Table 8.4). Schizoaffective disorder
individual displays symptoms that meet the criteria will frequently impair occupational functioning and
hizoaffective disorder Characterized for schizophrenia (see may be associated with restricted social functioning,
y schizophrenia symptoms plus a period above), but where there is difficulties with self-care, and an increased risk for
flecting either depression or mania. also a significant mood suicide.
SELF-TEST QUESTION
° What are the four main schizophrenia spectrum disorder diagnostic categories in DSM-5?
SECTION SUMMARY
8.2 THE DIAGNOSIS OF SCHIZOPHRENIA SPECTRUM DISORDERS
¢ DSM-5 has organized schizophrenia spectrum disorders along a gradient of psychopathology and impairment — from less
severe to more severe and disabling.
¢ The most common forms of delusional disorder are persecutory type and grandiose type.
¢ Brief psychotic disorder is typified by the sudden onset of one of the main psychotic symptoms.
© Schizophrenia is the main diagnostic category in schizophrenia spectrum disorders, and occurs when there is range of symp-
toms covering cognitive, behavioural and emotional dysfunction and also impaired occupational or social functioning.
e Schizoaffective disorder is characterized by schizophrenia symptoms plus a period reflecting either depression or mania.
Cee encereeceressenccesseenseneesenesreseeseseesssstesesssnesensstessessseseesessesssseeteesteseresteeseesseeseeeesees Seen ee area reerees eres tees ease e esse eet P ESE HESEE ESE Ets EeEs EEE EeEEOEEaEsTEESEeeseEssressessseesseesesessessensssssseer”
8.3. THE PREVALENCE with over 80 per cent continuing to have problems with
social functioning and 79 per cent undertaking no work
OF SCHIZOPHRENIA of any kind (Thornicroft, Tansella, Becker, Knapp et al.,
2004). The World Health Organisation found the preva-
SPECTRUM DISORDERS lence of schizophrenia roughly similar across the world.
However, interestingly, the course of schizophrenia tends
When precise methods for its diagnosis are applied, the to be less severe in developing countries than in devel-
lifetime prevalence rate for a diagnosis of schizophrenia oped nations (Thara, Henrietta, Joseph, Rajkumar &
is between 0.3 and 0.7 per cent — around 24 million people Eaton, 1994). The reasons for this difference in prog-
worldwide (van Os & Kapur, 2009), and mostly in the age nosis are unclear, although the central support role of
group 15-35 years. The World Health Organisation has the family and differences in beliefs about the origins
recognized that schizophrenia is one of the top 10 medi- of psychological disorders in developing countries may
cal disorders causing disability (WHO, 1990), and the be important (Lin & Kleinman, 1988).
mortality rate among people with a diagnosis of schiz- Some studies have identified some consistent cultural
ophrenia is around 50 per cent higher than normal. In differences in the prevalence of schizophrenia within
addition, sufferers tend to die around 10 years earlier than individual countries. For example, in a UK-based study,
individuals who have never been diagnosed with schizo- King, Nazroo, Weich, McKenzie et al (2005) found that
phrenia (Jeste, Gladsjo, Lindamer et al., 1996). Around the reporting of psychotic symptoms was higher in eth-
10 per cent die by suicide (NICE, 2010). While treatments nic minority groups than in ethnic white individuals. This
and interventions for psychosis are continually improv- increase in the reporting of symptoms was twice as high
ing, a significant number of people with a diagnosis of in people of African-Caribbean origin as in whites. There
schizophrenia continue to suffer lifelong impairment, have been a number of hypotheses that have attempted
246 PSYCHOPATHOLOGY
bs
to explain this apparent cultural difference, and there is unemployment, poor housing, and low socio-economic
at least some evidence that the higher symptom levels in status (Hjern, Wicks & Dalman, 2004). Finally, the inci-
black American men than white American men may be dence of schizophrenia is similar for males and females,
the result of racial disparities in mental health treatment although females tend to have a later age of onset and
between blacks and whites in the USA (Whaley, 2004). fewer hospital admissions, and this may be the result of
In other within-country studies, immigrants have been females attaining higher levels of social role functioning
shown to have significantly higher rates of schizophrenia before illness, which confers a better outcome (Hafner,
diagnosis than members of the indigenous population. A 2000; Murray & van Os, 1998; Angermeyer, Kuhn &
personal or family history of migration is an important Goldstein, 1990).
risk factor, and immigrants from developing countries Finally, delusional disorder and brief psychotic disor-
are at greater risk than those from developed countries der are new diagnostic categories within schizophrenia
(Cantor-Graae & Selten, 2005). At least part of the expla- spectrum disorders, but DSM-5 estimates that the life-
nation for the higher incidence in immigrants can be time prevalence rate for delusional disorder is around 0.2
traced to the stress caused by many of the initial con- per cent, and that brief psychotic disorder may account
sequences of immigration, such as language difficulties, for 9 per cent of cases of first-onset psychosis.
SELF-TEST QUESTIONS
e What is the estimated lifetime prevalence rate for a diagnosis of schizophrenia?

® Some ethnic and cultural differences in the prevalence rates of schizophrenia have been found within individual countries.
Can you describe some of these differences?
SECTION SUMMARY
8.3 THE PREVALENCE OF SCHIZOPHRENIA SPECTRUM DISORDERS
° The lifetime prevalence rate for a diagnosis of schizophrenia is between 0.5 and 0.7 per cent, and is similar across different
countries and cultures.
¢ Rates of diagnosis of schizophrenia do tend to be higher in some ethnic groups (e.g. people of African-Caribbean origin in
the UK), and in immigrant populations generally.
¢ Estimates for the lifetime prevalence rate for delusional disorder is around 0.2 per cent.
8.4 THE COURSE OF late adolescence or early adulthood. A study of nine

countries by the World Health Organisation found that
PSYCHOTIC SYMPTOMS 51 per cent of individuals diagnosed with schizophrenia
were between 15 and 25 years of age (Sartorius, Jablensky,
Korten, Ernberg et al., 1986), and over 80 per cent are
\, Psychotic symptoms usu-
For a video on schizophrenia go to between 15 and 35 years of age. For some individuals,
www.wiley-psychopathology.com/ | ally develop through a
the onset of psychotic symptoms can be rapid and dra-
video/ch8 / well-defined succession of
matic, but for most it represents a slow deterioration
stages. The three predomi-
from normal functioning over an average period of
nant phases are (1) the prodromal stage, (2) the active stage,
around 5 years (Hafner, Maurer, Loffler, van der Heiden
and (3) the residual stage.
et al., 2003). This slow deterioration is known as the
prodromal stage, and is
first exhibited as slow prodromal stage The slow deterioration —
8.4.1 The Prodromal Stage from normal functioning to the delusional -
withdrawal from normal and dysfunctional thinking characteristic
The large majority of those who develop psychotic life and social interaction, of many forms of schizophrenia, normally
symptoms show the first signs of these symptoms during shallow and inappropriate taking place over an average of 5 years.
emotions, and deterioration in personal care and work or adolescents appear to be linked to normal development,
school performance, with some evidence that grey mat- and that psychotic symptoms may emerge from a trou-
ter loss may occur in those brain areas mediating social bled teenage state that has failed to cope with normal
cognition (Bhojraj, Sweeney, Prasad, Eack et al., 2011). maturation. This leaves the adolescent unable to cope
That psychosis initially develops during late adolescence with a majority of the life challenges that they will have
is one of the basic facts of this psychopathology, but why to deal with at this stage of development, and the result-
should onset occur during this rather specific point in an ing response is a withdrawal from social interaction and
individual's lifespan? The course of psychosis is best a fall in educational performance. Eventually such ten-
understood in terms of a stress-diathesis model, in which dencies will become noted by family and friends, and the
psychotic symptoms are caused by an underlying inher- development of disordered thoughts, delusions and
ited biological vulnerability, but this vulnerability fre- erratic and bizarre behaviour mark the onset of the
quently manifests as specific symptoms if the individual active stage.
has certain critical and stressful life experiences. There is a During the development of DSM-5, a case was made
good deal of evidence that over 70 per cent of individuals for including what was to be called attenuated psychotic
who first show symptoms of psychosis have experienced symptoms syndrome (also known as ‘psychosis risk syn-
stressful life events in the previous 3 weeks (Brown & drome’) (Woods, Walsh, Saksa & McGlashan, 2010).
Birley, 1968), and the transition from adolescence This would have been characterized by mild psychotic
to adulthood is arguably one of the most stressful symptoms that don’t meet the diagnostic criteria for
periods of an individual’s life. In addition, Harrop & full-blown schizophrenia, but would enable clinicians
Trower (2001) argue that prodromal-like signs in normal to identify at least some individuals who were in the
THE PRODROMAL STAGE - IDENTIFYING THE EARLY SIGNS

‘Fifteen-year-old Caitlin was an excellent student with many friends when she entered the ninth grade. One
year later, she suddenly became restless in school, stopped paying attention to her teachers, and eventu-
ally failed all of her subjects. At home she appeared increasingly withdrawn and isolated, spending hours
sleeping or watching television. The previously even-tempered adolescent became angry, anxious, and sus-
picious of those around her, and was occasionally seen talking to herself while making repetitive, odd hand
motions. Several years later, hearing voices and insisting that the CIA was hatching an elaborate plot to
HISTORY
CASE
8.1 murder her and her family, she was diagnosed with schizophrenia:
Source: Can we prevent or delay schizophrenia? Retrieved from http://www.med.nyu.edu/content?ChunklID=14245
Clinical Commentary
This description of the development ofCaitlin’s symptoms is typical of the prodromal stage ofschizophrenia.
She became withdrawn, ill-tempered, anxious and suspicious, and showed a marked decline in academic
performance. Unfortunately, these signs are often difficult to differentiate from many of the behavioural
changes exhibited by normal individuals as they progress through adolescence, so diagnosis at an early
stage is often difficult. These difficulties with early diagnosis are unfortunate because evidence suggests that
the earlier treatment begins after the development of actual psychosis, the more rapid the immediate recov-
ery and the better the overall outcome (see Focus Point 8.9 on Early Intervention Services).
Some more specific prodromal features associated with schizophrenia include:
Peculiar behaviours
Impairment in personal hygiene and grooming
Inappropriate affect (e.g. laughing when talking about something sad)
Vague, overly elaborate, or circumstantial speech
Poverty of speech
Odd beliefs or magical thinking
Unusual perceptual experiences.
prodromal state for subsequent schizophrenia spectrum disordered speech). However, during the residual stage »
disorders. However, the final decision was to omit this they may well still exhibit negative symptoms, such as
category from DSM-5 because of the poor diagnostic blunted affect, withdrawal from social interaction, and
reliability revealed in an earlier clinical trial (Carpenter & find it difficult to cope with normal day-to-day activi-
van Os, 2011). ties such as holding down a job. Long-term studies have
suggested that around 28 per cent of sufferers will
remit after one or more active stage, 22 per cent
8.4.2 The Active Stage will continue to show positive symptoms over the
longer term, and around 50 per cent will alternate
In the active stage, the individual begins to show unam-
between active and residual stages (Wiersma, Nienhuis,
biguous symptoms of psychosis, which may manifest
Slooff & Giel, 1998). These statistics indicate that
as delusions, hallucina-
active stage The stage in which an relapse is relatively common, and relapse can often be
tions, disordered speech
individual begins to show unambiguous traced to either (1) stressful life events or return to a
and communication, and a
symptoms of psychosis, including delu- stressful family environment after a period of hospitali-
sions, hallucinations, disordered speech range of full-blown symp-
6 sees zation or care (see section 8.5.3), or (2) non-adherence
and communication, and a range of full- toms that are outlined in
blown symptoms. to medication. It is estimated that around 40-50 per
section 8.1.
cent of those diagnosed with schizophrenia fail at some
point to adhere to their course of medication (Lacro,
Dunn, Dolder, Leckband & Jeste, 2002), and partial
8.4.3 The Residual Stage
compliance is likely to result in significantly higher lev-
Recovery from the symptoms of psychosis is usually els of relapse and re-hospitalization (Eaddy, Grogg &
gradual, but many sufferers may still retain some symp- Locklear, 2005). The factors most associated with non-
tomatology over the longer term. The residual adherence or non-compliance with medication include
stage is reached when the poor insight, negative attitudes to medication, a history
residual stage The stage of psychosis
when the individual ceases to show promi-
individual ceases to show of non-adherence, substance abuse, inadequate dis-
nent signs of positive symptoms (such as prominent signs of posi- charge or aftercare planning, and poorer therapeutic
delusions, hallucinations or disordered tive symptoms (such as relationships between patient and service providers
speech). delusions, hallucinations, (Lacro et al., 2002).
SELF-TEST QUESTIONS
° What are the main stages through which psychotic symptoms normally develop?
* What are the factors that may contribute to relapse following recovery from an acute psychotic episode?
SECTION SUMMARY
8.4 THE COURSE OF PSYCHOTIC SYMPTOMS
° The large majority of those who develop psychotic symptoms show the first signs of symptoms during late adolescence or
early adulthood. This is known as the prodromal stage.
¢ Around 70 per cent of those who show first signs of psychotic symptoms have experienced stressful life events in the
previous 3 weeks.
¢ Around 28 per cent of those diagnosed with schizophrenia will remit after 1 or more active stages, 22 per cent will continue
to show positive symptoms over the long term, and 50 per cent will alternate between active and residual stages.
is
8.5 THE AETIOLOGY OF delusions, and disordered thought and communication —

many of which do have their origins in normal psycho-
PSYCHOTIC SYMPTOMS logical processes. Others have attempted to identify the
nature of the stressors that might trigger psychotic symp-
toms in vulnerable individuals. Finally, sociocultural
The evidence we have reviewed so far portrays psychosis views of psychosis take an entirely different perspective
as a broad range of loosely associated symptoms. It can and argue that the course of psychotic symptoms may
manifest as disordered thinking and communication, dis- be determined by the simple act of diagnosing someone
ordered perceptions, hallucinations and delusions, and as with schizophrenia or by the fact that they are born into
behavioural deficits. In addition, no one single clinical a disadvantaged socio-economic group, and factors such
symptom is the cardinal feature by which the main as these may be enough to promote the development of
DSM-5 diagnostic category of schizophrenia is charac- psychotic symptoms. We will explore all of these differ-
terized. This being the case, theories of the aetiology of ent approaches in the following sections.
psychosis are also diverse and include biological, psycho-
logical and sociological approaches to understanding
this psychopathology. The overarching approach to
understanding psychosis is a diathesis-stress perspec- 8.5.1 Biological Theories
tive. That is, psychosis is Genetic factors
athesis-stress The perspective that thought to be caused by a It has always been known that psychotic symptoms
sychopathology is caused by a combina-
combination of a geneti- appear to run in families, and this suggests that there may
yn of a genetically inherited biological
athesis (a biological predisposition) and cally inherited biological well be some form of inherited predisposition. That psy-
wironmental stress. diathesis (a biological pre- chosis has an inherited component has been supported
disposition to schizophre- by the results of concordance studies. If an individual is
nia) and environmental stress. This means that even if diagnosed with schizophrenia, Table 8.1 shows the prob-
you have a genetically pre-programmed disposition to ability with which a family member or relative will also
psychosis, you may well not develop any symptoms develop the disorder. This shows that the probability with
unless you experience certain forms of life stressors. which the family member or relative will develop schizo-
Such stressors might involve early rearing factors phrenia is dependent on how closely they are related —
(Schiffman, Abrahamson, Cannon, LaBrie et al., 2001), or, more specifically, how much genetic material the
dysfunctional relationships within the family (Bateson, two share in common (Gottesman, McGuffin & Farmer,
1978), an inability to cope with the stresses of normal 1987; Cardno, Marshall, Coid, Macdonald et al., 1999).
adolescent development (Harrop & Trower, 2001), or Recent studies have suggested that an individual who has
with educational or work demands. In addition, recent a first-degree relative diagnosed with schizophrenia is 10
research on the diathesis-stress approach to schizophre- times more likely to develop psychotic symptoms than
nia suggests that stress may worsen symptoms in those
with a genetic vulnerability to psychosis through its
effect on cortisol production in the body (Jones &
TABLE 8.1 Concordance rates for individuals with a diagnosis
Fernyhough, 2007).
of schizophrenia
Because of the heterogeneous nature of schizophre-
nia as a diagnostic category and the range of diverse % diagnosed with
symptoms that accompany psychosis, the study of the Relation to proband schizophrenia
causes of these symptoms has focused on explaining Spouse 1.00
specific features of psychosis rather than attempting to
Grandchildren 2.84
elaborate an all-inclusive explanation. This is sometimes
known as a ‘complaint-oriented approach’ (Bentall, Nieces/nephews 2.65
2006), which not only argues that there is a need to study Children 935
individual symptoms, but also that individual symptoms
Siblings 7.30
may have their origin in psychological mechanisms that
underlie normal experience (Bentall, 2004). For example, Dizygotic (fraternal) twins 12.08
some theories have attempted to identify the inherited Monozygotic (identical) twins 44.30
component of individual symptoms; others the abnor-
Source: Gottesman, |.l, McGuffin, P. & Farmer, A.E. (1987). Clinical genetics
malities in brain biochemistry or brain functions that as clues to the real genetics of schinzophrenia (a decade of modest
accompany psychotic symptoms. Still others have tried gains while playing for time). Schizophrenia Bulletin, 13(1), 23-47.
to understand the cognitive processes that underlie By permission of Oxford University Press.
250.4 PSYCHOPATHOLOGY
«
someone who has no first-degree relatives diagnosed psychotic symptoms. This suggests that a genetic risk
with schizophrenia (Schneider & Deldin, 2001). factor has been passed on to offspring, even though one
However, simply because psychotic symptoms tend set of parents did not develop schizophrenia themselves.
to run in families does not establish a genetic basis for Another way of tackling the problems of separating
this psychopathology. For example, some family envi- out the influence of genetic inheritance and environmen-
ronments may have dysfunctional elements (e.g. dif tal experience is to look at the incidence of schizophrenia
ficulties in communication between family members) in children who are biologically similar but have been
that may give rise to the development of psychosis. In reared apart (adoptions studies). If there is an important
order to examine the genetic basis more carefully, many genetic element to psycho-
researchers have undertaken twin studies, in which they sis, then we would expect _adoption studies Research conducted .
on children who have been reared by indi-
have compared the probability with which monozygotic the children of a mother viduals other than their biological parent
(MZ) and dizygotic (DZ) twins both develop symptoms diagnosed with schizophre-
indicative of schizophrenia. MZ twins share 100 per cent nia to have similar probabilities of developing schizophre-
of their genetic material, whereas DZ twins share only nia regardless of whether they had been reared with their
50 per cent of their genes, so a genetic explanation of mother or not. A seminal study by Heston (1966) com-
psychotic symptoms would predict that there would be pared 47 adopted children who were reared apart from
greater concordance in the diagnosis of schizophrenia in their schizophrenic biological mothers with 50 control
MZ than in DZ twins. This can clearly be seen in Table adopted children whose mothers were not diagnosed with
8.1 where the concordance rate for MZ twins is 44 per schizophrenia. He found symptoms of psychosis in 16.6
cent, but falls to only 12 per cent in DZ twins. Twin per cent of the adopted children of the schizophrenic
studies have indicated that the heritability estimate for mothers, and no symptoms in the adopted children of
schizophrenia is approximately 80 per cent (Cardno & mothers without schizophrenia. Studies of adopted chil-
Gottesman, 2000; Sullivan, Kendler & Neale, 2003), dren conducted in Denmark have shown similar results.
which makes schizophrenia one of the most heritable Kety (1988) and Kety, Wender, Jacobsen, Ingraham et al.
of psychiatric disorders (Gejman, Sanders & Kendler, (1994) found that adopted children who develop psychotic
2011). As convincing as these data may seem, there are symptoms are significantly more likely to have had bio-
still problems in interpreting twin studies. For example, logical relatives with a diagnosis of schizophrenia (21.4
(1) MZ twins will always be the same sex whereas DZ per cent) than adoptive relatives with a diagnosis of schiz-
twins may not be, (2) MZ twins are usually physically ophrenia (5.4 per cent). These types of studies provide
identical, unlike DZ twins, and this may lead to family strong evidence for a genetic component to schizophrenia
and friends treating MZ twins more similarly than they and psychosis. However, some more recent adoption stud-
would DZ twins (i.e. MZ twins could experience more ies suggest that genetic liability still interacts with environ-
similar environmental factors than DZ twins), and (3) mental factors to predict the development of psychotic
MZ twins are likely to have shared the same placenta symptoms. Wahlberg, Wynne, Hakko, Laksy et al. (2004)
prior to birth whereas DZ twins do not, and this would found that in adopted children, inherited genetic factors
mean that any interuterine abnormalities would be more were an important predictor of a diagnosis of schizophre-
likely to affect both MZ twins through the shared pla- nia but only in combination with certain environmental
centa (Davis & Phelps, 1995). However, many of these factors found in the adopted home environment. In this
difficulties of interpretation can be overcome by study- particular study, an adopted child was more likely to be
ing the offspring of MZ and DZ twins rather than the diagnosed with schizophrenia if they had a biologically
twins themselves (Gottesman & Bertelsen, 1989). If one inherited predisposition and they were also brought up in
MZ twin develops psychotic symptoms and the other an adopted home environment where there were dys-
does not, any genetic element in psychosis should still functional communication patterns (see section 8.5.3).
show up in the children of either of the two MZ twins. While genetic inheritance is an important predictor of
That is, the children of the MZ twins should still exhibit psychotic symptoms, this is further evidence that genetic
similar rates of risk for schizophrenia (because they have factors interact with environmental factors in a way pre-
inherited the same predisposition) — even though one of dicted by diathesis-stress models.
their parents developed schizophrenia and the other did Not only are these kinds of genetic studies important
not. This is exactly what Gottesman & Bertelsen (1989) in determining whether a diagnosis of schizophrenia has
found: 16.8 per cent of the offspring of the MZ twins a significant inherited component, they are also begin-
that were diagnosed with schizophrenia were likely to ning to show that individual symptoms associated with
develop psychotic symptoms themselves, and 17.4 per a diagnosis of schizophrenia may also have an important
cent of the offspring of the MZ twins that were not diag- inherited component, and these include factors such
nosed with schizophrenia were also likely to develop as experiencing hallucinations (Hur, Cherny & Sham, |
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS Oat
2012), volume of grey matter in specific brain regions effort has been directed at attempting to identify the spe-
(van Haren, Rijsdijk, Schnack & Picchioni, 2012), and cific genes through which the risk for psychosis may be
catatonia (Beckmann & Franzek, 2000). However, for transmitted (Harrison & Owen, 2003), the chromosomes
some other psychotic symptoms there is less evidence on which these genes are located (Kendler, Myers, O’Neill,
for overriding genetic determination, and these include Martin et al., 2000), and how these genes and their possible
some negative symptoms such as anhedonia (Craver & defects may give rise to psychotic symptoms (Andreasen,
Pogue-Geile, 1999) and delusions (Cardno & McGuffin, 2001). These endeavours have primarily involved genetic
2006; Varghese, Wray, Scott & Williams, 2013). Finally, linkage analyses, in which blood samples are collected in
recent genetic studies of schizophrenia and its related order to study the inheritance patterns within families that
disorders have begun to show that there are genetic over- have members diagnosed with schizophrenia. Linkage
laps between schizophrenia and some other psychiatric analyses work by comparing the inheritance of character-
disorders, such as bipolar disorder and autism, suggesting istics for which gene location is well known (e.g. eye col-
Sawa
that variation in a specific our) with the inheritance of psychotic symptoms. If the
To read the article on ‘The heritability “\ gene or set of genes may inheritance of, for example, eye colour follows the same
of delusional-like experiences’ by : simultaneously affect the pattern within the family as psychotic symptoms, then it
Varghese et al. go to
_ development of these dif- can reasonably be concluded that the gene controlling psy-
reading/ch8 | ferent diagnoses (Gejman, chotic symptoms is probably found on the same chromo-
LEIS
"Sanders & Kendler, 2011). some as the gene controlling eye colour, and is probably
genetically linked to that ‘marker’ characteristic in some
Molecular genetics way. Research Methods Box 8.1 illustrates an example of
If, as seems likely, there is a genetic component to psycho- how a particular trait of those diagnosed with schizophre-
sis, how is it transmitted between related individuals, and nia, in this case poor eye-tracking of a moving object, can
how does this inherited component influence the devel- be used as a genetic marker to track other psychotic symp-
opment of psychotic symptoms? In recent years, much toms that may be linked genetically to this characteristic.
SMOOTH-PURSUIT EYE-TRACKING AS A MARKER

FOR THE INHERITANCE OF PSYCHOSIS
Smooth-pursuit eye-tracking is the ability to follow a moving object in a smooth continuous movement with
your eyes while keeping your head still. However, many individuals with a diagnosis of schizophrenia are unable
to do this, and can only follow a moving object with jerky movements of the eyes (known as saccadic move-
ments) (Schneider & Deldin, 2001). This may seem like a relatively innocuous symptom, but it has importance
because it is a characteristic that can be used as a genetic marker for schizophrenia. That is, unlike the broader
symptoms of schizophrenia (such as thought disorder, delusions, and hallucinations), abnormalities in smooth-
pursuit eye-tracking are probably related to a rather specific neurological abnormality which may be directly
linked to abnormalities in individual genes. If this is so, then the gene responsible for specific eye-tracking
METHODS
RESEARCH
8.1 deficits may also be associated with many of the more disabling symptoms of schizophrenia. So, by tracing the
gene responsible for eye-tracking deficits we may also locate the gene or genes responsible for other psychotic
symptoms.
There is now a large body of evidence indicating that around 30-45 per cent of first-degree relatives of indi-
viduals diagnosed with schizophrenia exhibit poor performance in smooth pursuit eye-tracking tasks — even
when those first degree relatives have not been diagnosed with schizophrenia (Karoumi, Saoud, d’Amato,
Rosenfeld et al., 2001; Louchart-de la Chapelle, Nkam, Houy, Belmont et a/., 2005), and this suggests that deficits
in eye-tracking performance are likely to be an indicator of an inherited predisposition to schizophrenia. In addi-
tion, studies of twins in which only one of the pair has developed psychotic symptoms (discordant twins) show
that concordance of eye-tracking abnormalities are twice as high in monozygotic twins (MZ) than dizygotic (DZ)
twins (Levy & Holzman, 1997) (see section 8.5.1 for an explanation of concordance studies in twins), providing
more evidence for the involvement of inherited genetic factors. Studies have still been unable to track down
the specific gene associated with this eye-tracking abnormality, although there is some evidence that it may be
linked with a number of genes that are also responsible for interfering with dopamine metabolism (Trillenberg,
Lencer & Heide, 2004), and this may be the important connection between eye-tracking deficits and the broader
symptoms of schizophrenia.
252 PSYCHOPATHOLOGY
%
Using analyses such as these, genes associated with surprising, therefore, that many researchers have sus-
the development of psychotic symptoms have been pected that the thought disorders, hallucinations and
identified on a number of chromosomes including 8 and behaviour problems characteristic in the diagnosis of
22 (Kendler, Myers, O'Neill, Martin et al., 2000), 2, 3, 5, schizophrenia may be caused by malfunctions in these
6, 11, 13 and 20 (Badner & Gershon, 2002; Levinson, brain neurotransmitters. The biochemical theory of
Lewis & Wise, 2002), and 1 and 15 (Gejman, Sanders & schizophrenia that has been most prominent over the
Kendler, 2011). Also, other techniques, such as genome- past 50 years is known as the dopamine hypothesis, and
wide association studies (GWAS) allow researchers this account argues that the symptoms of schizophrenia
to identify rare mutations in genes that might give rise to are importantly related to
psychotic symptoms -— excess activity of the neu- _dopamine hypothesis A theory which
argues that the symptoms of schizophre
genome-wide association studies especially those mutations rotransmitter dopamine. are related to excess activity of the neur
(GWAS) Technique which allows research-
that give rise to ‘copy There are a number of fac- transmitter dopamine.
ers to identify rare mutations in genes
that might give rise to psychopathology number variations’ (CNVs), tors that have led to the
symptoms. a term that refers to an implication of excess dopamine activity.
abnormal copy of DNA in First, the discovery of antipsychotic drugs that helped
a gene (either a deletion or a duplication). Mutations to alleviate the symptoms of psychosis (such as the phe-
resulting in DNA deletions (International Schizophrenia nothiazines) led to the discovery that such drugs acted
Consortium, 2008) as well as mutations causing DNA by blocking the brain’s
duplications (Levinson, Duan, Oh, Wang et al., 2011; dopamine receptor sites phenothiazines A group of antipsychotic
drugs that help to alleviate the symp-
Kirov, Grozeva, Norton, Ivanov et al., 2009) have been and so reduced dopamine
toms of psychosis by blocking the brain’s
found to be associated with schizophrenia. However, activity (Schneider & Deldin, dopamine receptor sites and so reduce
while many studies have shown associations between 2001). Interestingly, while. dopamine activity.
individual genes and schizophrenia symptoms, there the administration of anti-
have also often been failures to replicate these findings psychotic drugs alleviated many of the positive symp-
(Kim, Zerwas, Trace & Sullivan, 2011). This probably toms of schizophrenia, such as thought disorder and
testifies to the heterogeneity of schizophrenia as a diag- social withdrawal, they also had the side effect of pro-
nostic category, and that different people with a diagno- ducing muscle tremors very similar to those seen
sis of schizophrenia may not have the same underlying in Parkinson’s disease, and it was already known that
genetic factors contributing to their symptoms. For Parkinson’s disease was caused by low levels of dopa-
example, many of the mutations causing the CNVs men- mine. In contrast, when people suffering Parkinson’s dis-
tioned above are very rare, and so schizophrenia symp- ease were given the drug L-dopa to raise brain dopamine
toms may be caused by many different and very rare levels, they often began to exhibit psychotic symptoms
gene mutations. Secondly, some of the gene factors asso- (Grilly, 2002). This evidence strongly suggests that either
ciated with schizophrenia may have their impact on quite high levels of brain dopamine or excess dopamine activ-
specific aspects of psychological functioning. For exam- ity is responsible for many of the symptoms of psychosis.
ple, deficits in executive functioning (planning, working Subsequent research has suggested that many antipsy-
memory, problem solving) are known to be characteris- chotic drugs have their effect by binding specifically to
tic of schizophrenia, and some genes have been identi- dopamine receptors and reducing brain dopamine activ-
fied which are associated specifically with executive ity (Burt, Creese & Snyder, 1977).
functioning deficits in schizophrenia (Harrison & Second, during the 1970s it was noticed that there was
Weinberger, 2004; Owen, Williams & O’ Donovan, 2004). a strong link between excessive use of amphetamines and
But executive functioning deficits are also associated a syndrome known as amphetamine psychosis. When
with many other psychiatric disorders, such as autistic taken in high doses for long periods of time, ampheta-
spectrum disorder and intellectual disabilities, and so this mines produce behavioural
particular gene mutation may not be purely a risk factor symptoms in humans and amphetamine psychosis A syndrome in f
for schizophrenia and we might predict it to be present animals that closely resem- which high doses of amphetamines taken
without an individual necessarily developing psychotic ble symptoms of psycho- for long periods of time produce behav-
ioural symptoms in humans and animals
symptoms. sis. These include paranoia that closely resemble symptoms
and repetitive, stereotyped of psychosis.
Brain neurotransmitters behaviour patterns (Angrist,
Cognition and behaviour are very much dependent on Lee & Gershon, 1974). Subsequently we have learnt that
the efficient working of brain neurotransmitters, which amphetamines produce these disturbed behaviour pat-
enables effective communication between brain cells and terns by increasing brain dopamine activity, and giving
functionally different parts of the brain itself. It is not amphetamines to those diagnosed with schizophrenia .
&
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS 253
actually increases the severity of their symptoms consistent with the fact that antipsychotic drugs only
(Faustman, 1995). appear to attenuate positive symptoms and have little
Third, brain imaging studies have indicated that indi- or no effect on negative symptoms (the behavioural
viduals diagnosed with schizophrenia show excessive lev- symptoms associated with flattened affect), and this effect
els of dopamine released from areas of the brain such as of excess dopamine appears to be localized in the mes-
the basal ganglia — especially when biochemical precur- olimbic dopamine pathway (Davis, Kahn, Ko & Davidson,
sors to dopamine, such as dopa, are administered to the 1991). However, the mesocortical pathway begins in the
individual (Carlsson, 2001; Goldsmith, Shapiro & Joyce, ventral tegmental area but projects to the prefrontal
1997), cortex, and the dopamine neurons in the prefrontal cor-
Finally, post-mortem studies have found increased tex may be underactive. This has important implications
levels of dopamine and significantly more dopamine for cognitive activity because the prefrontal cortex is
receptors in the brains of deceased schizophrenia the substrate for important cognitive processes such as
sufferers — especially in the limbic area of the brain working memory, and these cognitive processes contrib-
(Seeman & Kapur, 2001). ute to motivated and planned behaviour (Winterer &
So, how might dopamine activity be involved in the Weinberger, 2004). In this way, dopamine activity might
production of psychotic symptoms? Figure 8.1 illustrates account for both the positive and the negative symptoms
two important dopamine pathways in the brain, the observed in schizophrenia, but because antipsychotic
mesolimbic pathway and the mesocortical pathway. drugs block dopamine receptors only in the mesolimbic
nesolimbic pathway One of two impor- These two pathways begin pathway, this accounts for why such drugs only affect
ant dopamine pathways in the brain, in the ventral tegmental positive symptoms.
vhich may be impaired during schizophre- area of the brain, but may While the dopamine hypothesis has been an influen-
ia. The other pathway is the mesocortical
have quite different effects tial biochemical theory of schizophrenia for more than
athway.
on the appearance of psy- 30 years, there is still some evidence that does not fit
nesocortical pathway One of two impor- chotic symptoms. First, an comfortably within this hypothesis. First, while antip-
ant dopamine pathways in the brain, excess of dopamine recep- sychotic drugs are usually
vhich may be impaired during schizophre-
tors only seems to be related effective in dealing with g For a brain labelling activity based on
ia. The other pathway is the mesolimbic
athway. to the positive symptoms many of the symptoms | Figure 8.1 go to
associated with schizophre- of schizophrenia, they do | activities/ch8
nia (hallucinations, delusions, disordered speech). This is not start having an effect
Cingulate gyrus
Mesocortical pathway
Prefrontal cortex
Ventral tegmental
Hypothalamus area
Hippocampus
Mesolimbic pathway
Amygdala
FIGURE 8.1 Abnormalities in dopamine activity may be linked to the brain's mesocortical pathway and the mesolimbic path-
way. Both begin in the ventral tegmental area, but the former projects to the prefrontal cortex and the latter to the hypothalamus,
amygdala, hippocampus and nuclear accumbens. The dopamine neurons in the prefrontal cortex may be underactive (leading to the
negative symptoms of schizophrenia), and this underactivity may then fail to inhibit dopamine neurons in the mesolimbic pathway
causing an excess of dopamine activity in this pathway (resulting in positive symptoms) (see e.g. Davis, Kahn, Ko & Davidson, 1991).
254 PSYCHOPATHOLOGY
on symptoms until about 6 weeks after treatment has (the areas in the brain containing cerebrospinal fluid) ®
commenced. This is unusual, because antipsychotic and this is associated with overall reduction in cortical
drugs are known to start blocking dopamine receptors grey matter (Andreasen, Flashman, Flaum, Arndt et al.,
in the brain within hours of administration, so we would 1994). In cases of chronic schizophrenia, the enlarge-
expect improvement to be immediate (Sanislow & ment of the ventricles is a continuous on-going process
Carson, 2001; Davis, 1978). Second, many new antip- (Mathalon, Sullivan, Lim & Pfefferbaum, 2001), and this
sychotic drugs are effective despite having only a mini- may suggest that enlarged ventricles are a consequence
mal effect on brain dopamine levels (e.g. clozapine) of schizophrenic symptoms rather than a cause of it.
or appear to be effective because they not only block However, enlarged ventricles are found even in individu-
dopamine receptors, but also block other neurotrans- als who have just experienced their first psychotic epi-
mitters (Nordstrom, Farde, Nyberg, Karlsson et al., sode, implying it may be a feature that is present prior to
1995). Other neurotransmitters that have been impli- the first symptoms developing (Cecil, Lenkinski, Gur &
cated in psychotic symptoms include serotonin, gluta- Gur, 1999),
mate and GABA neurons (Stone, Morrison & Pilowsky, Second, schizophrenia is associated with reduced vol-
2007), and this is perhaps not so surprising given that ume of grey matter in the prefrontal cortex (Buchanan,
serotonin neurons regulate dopamine neurons in the Vladar, Barta & Pearlson, 1998). This area plays an impor-
mesolimbic pathway, and glutamate and dopamine dlys- tant role in a number of cognitive processes, the most
regulation may interact with each other. A full under- important being executive functioning, which enables
standing of the role of neurotransmitters in psychotic planning, goal-directed behaviour, and decision making; it
symptomatology will only result from a full underst- also mediates speech and coordinates working memory.
anding of how these brain neurotransmitters affect Deficits in executive functioning would encompass poor
each other, and how this interaction influences brain performance on cognitive tasks associated with speed and
processes that give rise to both positive and negative accuracy, abstraction/categorisation, memory and sus-
symptoms. tained attention, and they are also associated with nega-
tive symptoms of schizophrenia such as blunted affect
The neuroscience of schizophrenia and social withdrawal (Antonova, Sharma, Morris &
The brains of individuals with a diagnosis of schizophre- Kumari, 2004; Artiges, Martinot, Verdys, Attar-Levy et al.,
nia show a number of structural differences to those of 2000; Pinkham, Penn, Perkins & Lieberman, 2003). In
non-sufferers, and these differences can often be linked to particular, individuals with a diagnosis of schizophrenia
the nature of the symptoms displayed by sufferers. These who exhibit negative symptoms show significantly lower
differences appear to continue to develop throughout prefrontal cortex metabolic rates than non-sufferers
the lifetime of the individual displaying psychotic symp- (Potkin, Alva, Fleming, Anand et al., 2002), and they have
toms, and are usually apparent at the time of the first psy- reduced prefrontal cortex blood flow when undertaking
chotic episode — suggesting that they may play a causal decision-making card sorting tasks such as the Wisconsin
role in symptoms rather than simply being a conse- Card Sort Test (WCST) (Weinberger, Berman & Illowsky,
quence of psychotic symptoms (Cecil, Lenkinski, Gur & 1988). All of this is consistent with the fact that the meso-
Gur, 1999; Olabi, Ellison-Wright, McIntosh, Wood et al., cortical dopamine pathway extends to the prefrontal cor-
2011). The most important of these structural differ- tex, and that dopamine neurons in the prefrontal cortex
ences are (1) enlarged ventricles (the spaces in the brain are relatively less active in individuals with schizophrenia.
filled with cerebrospinal fluid), (2) reduced grey matter Most recent evidence suggests that these deficits in pre-
in the prefrontal cortex, and (3) structural and functional frontal cortex functioning in schizophrenia are not neces-
abnormalities in the temporal cortex and its surround- sarily due to a reduction in the number of neurons in this
ing areas, including reduced volume in the basal ganglia, area, but to disrupted synaptic connections between neu-
hippocampus, and limbic structures. rons in the glutamatergic, GABAergic, and dopaminergic
First, the brains of individuals with schizophrenia pathways (Seshadri, Zeledon & Sawa, 2013) and to a
tend to be smaller than those of non-diagnosed controls, reduction in the dendritic spines of neurons which
and this is also the case in first-degree relatives of suffer- reduces the connectivity between these cells (Paspalas,
ers who have not developed psychotic symptoms (Ward, Wang & Arnsten, 2013; McGlashan & Hoffman, 2000).
Friedman, Wise & Schulz, 1996; Baare, van Oel, Pol, This reduced connectivity
Schnack et al., 2001). This suggests that smaller brain size between neurons in an area dendritic spines Small protrusion froma _
neuron’s dendrite that receives input from
may be determined by genetic rather than environmen- of the brain responsible for a single synapse of an axon.
tal factors. This is consistent with the most frequently executive functioning may
enlarged ventricles Enlargement of the confirmed finding that well give rise to the disordered speech and behavioural
areas in the brain containing cerebrospinal schizophrenia is associated disorganisation often found in schizophrenia. Figure 8.2
fluid, associated with schizophrenia. with enlarged ventricles shows how a PET scan reveals decreased frontal lobe ©
which are disrupted in schizophrenia and could give rise

to spurious associations, chaotic speech, and hallucina-
tions (Tamminga, Stan & Wagner, 2010).
These findings tend to suggest that abnormalities
in different areas of the brain may each be associated
with different symptoms of psychosis. Some individu-
als with a diagnosis of schizophrenia show abnormali-
ties in some of these brain areas, but many others show
abnormalities in all of them — which explains why many
exhibit both positive and negative symptoms (Kubicki,
Westin, Maier, Frumin et al., 2002).
One final issue, of course, it what causes these struc-
FIGURE 8.2 These pictures show ventricular enlargement
tural and functional differences in the brains of individu-
in the brains of an individual diagnosed with schizophrenia als with a diagnosis of schizophrenia? One factor we have
(right) and a healthy control (left). Ventricular enlargement is already mentioned is genetic mutation in genes that con-
a common feature of the brains of individuals diagnosed with trol the development of the brain and its associated cog-
schizophrenia, and is indicated by differences in the dark areas nitive processes. Many of the neurological defects found
shown in these MRI scans. in schizophrenia research are ones that could only have
Source: Reig, S., Penedo, M., Gispert, J.D., Pascau, J., Sanchez- occurred during early brain development when the com-
Gonzalez, J., Garcia-Barreno, P. and Desco, M. (2007). Impact of plex structure of the brain is developing, and this sug-
ventricular enlargement on the measurement of metabolic activity gests that prenatal factors may be important in causing
in spatially normalized PET. Neurolmage 35, 742-758, Figure 5.
subsequent brain abnormalities (Allin & Murray, 2002).
Reproduced with permission of Elsevier.
In particular, individuals diagnosed with schizophrenia
do not show the normal hemispheric asymmetry in brain
development that occurs during the second trimester of
activity in a schizophrenia sufferer compared with a pregnancy (4-6 months), and this may give rise to deficits
healthy control participant, as well as the enlarged ventri- in those areas of the brain concerned with language and
cles in the brain of the schizophrenia sufferer. associative learning (Sommer, Aleman, Ramsey, Bouma
Third, brain imaging studies have also shown abnor- & Kahn, 2001). In addition, brain damage or abnormali-
malities in the temporal cortex, including limbic ties that occur after the third trimester of pregnancy are
structures, the basal ganglia and the cerebellum normally self-repairing through a process known as glial
(Shenton, Dickey, Frumin & reactions. That such repair is not found in post-mor-
smporal cortex Abnormalities in this
rain area are associated with symptoms of McCarley, 2001; Gur, Cowell, tem studies of the brains of individuals diagnosed with
hizophrenia. 5 Latshaw, Turetsky et al., schizophrenia suggests that brain areas must have been
2000; Gur, Turetsky, Cowell, damaged or suffered abnormal development prior to the
asal ganglia A series of structures Finkelman et al., 2000). third trimester (Brennan & Walker, 2001).
cated deep in the brain responsible for Abnormalities in neural Another important consideration is that environmen-
jotor movements.
activity in the temporal tal factors may influence the early development of the
lobe-limbic system are brain either during gestation or at birth. Two particular
2rebellum The part of the brain at the
ack of the skull that coordinates muscular more associated with the risk factors that have been postulated include birth com-
tivity. positive symptoms of schiz- plications and maternal infections. Birth complications —
ophrenia, such as halluci- such as reduced supply of oxygen to the brain — appear
nations and symptoms of thought disorder (McCarley, to occur at a higher rate in individuals who eventually
Salisbury, Hirayasu, Yurgelun-Todd et al., 2002), and display symptoms of psychosis (Brown, 2011; Walker,
auditory hallucinations have been shown to be associ- Kestler, Bollini & Hochman, 2004), but, of course, not
ated with neural activation in the temporal lobes—limbic everyone who suffers birth complications then develops
system (Shergill, Brammer, Williams, Murray & McGuire, psychosis, so other factors must be involved. The prob-
2000). These deficits are also associated with reduced vol- ability of an offspring developing schizophrenia is also
ume in the temporal cortex and hippocampus in individ- significantly higher in mothers who have suffered an
uals with a diagnosis of schizophrenia (Steen, Mull, infection during pregnancy (Brown & Derkits, 2010), and
McClure et al., 2006; Fischer, Keller, Arango, Pearlson, one particular infection that has been widely studied in
et al., 2012). Furthermore, impaired hippocampal func- this respect is influenza. For example, one recent study
tion in schizophrenia could underlie a range of symp- suggested that a mother’s exposure to influenza during
toms because of the role of the hippocampus in memory the first trimester of pregnancy resulted in a sevenfold
for events and facts and in pattern completion, all of increase in the probability of their offspring developing
256 PSYCHOPATHOLOGY
psychotic symptoms (Brown, Begg, Gravenstein et al., this. First, we have argued that many of the symptoms of
2004). However, the effect sizes in studies such as these schizophrenia — and especially the negative symptoms —
are small, and there have been many failed attempts to can be traced to abnormalities in the prefrontal cortex,
demonstrate that maternal influenza is a risk factor for the area that controls many complex cognitive activi-
offspring psychosis, so the jury is still out on this issue. ties. However, the prefrontal cortex is a brain structure
Some of the evidence for a role of maternal influenza that only fully matures in adolescence and early adult-
on offspring psychosis is discussed in Focus Point 8.4. hood, so any developing deficits in that brain region are
Finally, if the causes of schizophrenia can be traced to only likely to manifest in an obvious way at maturation
early brain development, then why don’t at-risk individu- (Giedd, 2004), and this is consistent with adolescents at
als develop psychotic symptoms until they are usually well risk for psychosis showing prodromal symptoms such as
into adolescence? There may be at least two reasons for social withdrawal, shallow emotion, and deterioration
~ VIRAL INFECTIONS AND PSYCHOTIC SYMPTOMS

wa
= likely to have been exposed to influenza during preg-
= nancy than the mothers of individuals who are not
oO diagnosed with schizophrenia, and recent systematic
a.
WV reviews strongly suggest that prenatal exposure to
=) a number of infections and inflammatory responses
U
may be associated with increased risk of adult schizo-
\e)
Li. phrenia (Khandaker, Zimbron, Lewis & Jones, 2013).
In particular, exposure to the influenza virus appears
to be important during the first trimester (Brown,
Begg, Gravenstein, Schaefer et a/., 2004) and the third
trimester (de Messias, Cordeiro, Sampaio, Bartko &
Kirkpatrick, 2001) - and the latter is a prenatal period
which is known to be connected to the possible
development of brain abnormalities associated with
schizophrenia.
Source: Dr R. Dourmashkin/Science Photo Library. Reproduced with permission.
Most viral infections have their effects relatively
One interesting hypothesis is that psychotic symp- immediately, so how might viral infections prenatally
toms may be triggered by viral infections experi- or in early childhood lead to the development of psy-
enced either prenatally or postnatally (Torrey, 1991; chotic symptoms in later adolescence? One possibility
Mednick, Machon, Huttunen & Bonnett, 1988). There is that viral infections — especially prenatally - might
is a range of converging, but largely circumstantial, disrupt brain development and lead to the kinds of
evidence for the involvement of viral infections in the brain abnormalities that are typical in individuals
aetiology of psychosis. First, epidemiological studies diagnosed with schizophrenia. To this extent, animal
have shown that people diagnosed with schizophre- research is currently providing some useful information
nia are significantly more likely than others to have suggesting that rats or mice prenatally infected with
been born in the winter, and so were more likely to viruses such as influenza experience developmental
have been exposed to viruses prenatally or during the abnormalities that result in permanent changes in brain
first 6 months of their lives (Torrey, Miller, Rawlings & structure and function (Pearce, 2001; Fatemi, Pearce,
Yolken, 1997). Second, there also appears to be a Brooks & Sidwell, 2005; Kneeland & Fatemi, 2013).
relationship between the outbreak of epidemics, However, we must remember that not everyone who is
such as influenza epidemics, and the development of exposed to viruses at a critical age develops psychotic
psychotic symptoms. Individuals who were exposed symptoms and we need to be able to explain this fact.
prenatally to influenza are significantly more likely to For example, it may be that if viruses do cause develop-
develop psychotic symptoms in later life (Mednick, mental abnormalities leading to psychotic symptoms,
Machon, Huttenen & Bonett, 1988). Third, mothers of this may only happen in those who already have an
individuals diagnosed with schizophrenia are more inherited vulnerability to these symptoms.
is
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS 5 257
in school work during their early teens. Second, late of the oral stage of development. This regression is thought
adolescence is also a period associated with increased tobe caused by cold and unnurturing parents, and the reg-
stress, and especially exposure to stressors that the ression to a state of primary narcissism gives rise to a
individual will not have experienced before (e.g. sex- loss of contact with reality. Freud described the symp-
ual relationships, and social and educational respon- toms of thought disorder, communication disorder and
sibilities). Stress increases cortisol levels which in turn withdrawal typical of psychosis as evidence of a self-cen-
activates brain dopamine activity, and any factor that tred focus, and he argued that any attempts to re-establish
stimulates brain dopamine activity in at-risk individu- contact with reality give rise to the hallucinations and
als is likely to trigger the onset of psychotic symptoms delusions characteristic of psychosis.
(Walker, Mittal & Tessner, 2008). In the 1950s and 1960s, many psychodynamic expla-
In summary, there is now good evidence that psy- nations of psychosis were related to dysfunctional family
chotic symptoms are associated with deficits in impor- dynamics, and championed by such contemporary psy-
tant brain areas. These deficits manifest as lower brain chodynamic theorists as Gregory Bateson and R.D.
volume, neurotransmitter imbalances — especially in Laing. Prior to this, Fromm-Reichmann (1948) had
dopamine, glutamate and GABA pathways — and poorer developed the concept of the ‘schizophrenogenic
performance on cognitive neuropsychological tasks. mother’ — literally a mother who causes schizophrenia!
Particularly important brain areas exhibiting deficits are According to Fromm-Reichmann, schizophrenoge-
the prefrontal cortex, the temporal cortex and the hip- nic mothers were cold,
pocampus, and deficits in functioning in the prefrontal rejecting, distant and dom- _schizophrenogenic mother A cold,
cortex and temporal cortex can be clearly associated with inating. Such mothers rejecting, distant and dominating mother
who causes schizophrenia according to
both negative and positive symptoms respectively. The demanded dependency and -Fromm-Reichmann. ‘ a ,
causes of these structural and functional brain deficits emotional expressions from
in schizophrenia are unclear, although gene mutations, their children, but simultaneously rejected displays of
environmental factors influencing prenatal develop- affection and even criticized the dependency that they
ment, and maternal infections are all possibilities that are implicitly attempted to foster in their children. This
being currently researched. account suggests that when subjected to such conflicting
messages and demands from a dominant close relative, the
child withdraws and begins to lose touch with reality — at
least in part as a way of avoiding the stresses and conflicts
8.5.2 Psychological Theories
created by the mother.
Over the past 30 years or so, most research has been The empirical evidence supporting these psycho-
focused on genetic and biological theories of schizophre- dynamic theories of psychosis is meagre. First, genetic
nia, and psychological models have generally received accounts of psychosis are now largely accepted as impor-
less attention. However, there has recently been a resur- tant contributors to psychosis — even by psychodynamic
gence of interest in psychological models of psychosis — theorists, and have been incorporated in some way into
especially cognitive models that view psychotic symptoms psychodynamic theories. In some cases it is argued that
as the result of cognitive biases in attention, reasoning and inherited biological predispositions may facilitate regres-
interpretation (Savulich, Shergill & Yiend, 2012). We will sion to earlier psychological states (Willick, Milrod &
begin this section by discussing some traditional psycho- Karush, 1998), while others suggest biological predis-
logical interpretations of psychosis — especially psychody- positions may prevent the individual from developing
namic and behavioural accounts. We will then move on to an ‘integrated self’, and this gives rise to the disrupted
consider cognitive accounts of psychosis, including both behaviour patterns exhibited in individuals diagnosed
cognitive deficits (impairments in cognitive functioning) with schizophrenia (Pollack, 1989). Second, there is very
and cognitive biases (the tendency to attend to a certain little evidence that mothers of individuals displaying
type of stimulus or interpret ambiguity in just one par- psychotic symptoms actually possess the characteristics
ticular direction). of the schizophrenogenic mother described by Fromm-
Reichmann (Waring & Ricks, 1965).
Psychodynamic theories
Freud (1915, 1924) hypothesized that psychosis is caused Behavioural theories
by regression to a previous ego state which gives rise to a There are a number of views that suggest a role for
preoccupation with the self — this is known in psychoana- learning and conditioning in the development of psy-
lytic terminology as regres- chotic symptoms — if not as a full theory of psychosis,
imary narcissism Regression to a then as an explanation of why unusual behaviour pat-
sion to a state of primary
evious ego state which gives rise toa
narcissism characteristic terns are typical of many forms of psychosis. Ullman &
eoccupation with the self.
258 PSYCHOPATHOLOGY
%
Krasner (1975) argued that the bizarre behaviours of established, it was transferred from a continuous to an
individuals diagnosed with schizophrenia developed intermittent reinforcement schedule until the patient
because they are rewarded by a process of operant was carrying the broom around for a considerable part
reinforcement. That is, because of the disturbed fam- of the day. This study suggests that what look like quite
ily life often experienced by individuals diagnosed with bizarre and inappropriate behaviours can be developed
schizophrenia and the attentional difficulties that are a by simple contingencies of reinforcement. Further
central feature of the psychopathology, such individuals support for a learning view comes from evidence that
tend to find it difficult to attend to normal social cues extinction procedures can be used to eliminate or to
and involve themselves in normal social interactions. significantly reduce the frequency of inappropriate
Instead, their attention becomes attracted to irrelevant behaviours simply by withdrawing attention or with-
cues, such as an insect on the floor, an unimportant holding rewards when these inappropriate behaviours
word in a conversation, a background noise, and so are emitted. Allyon (1963) describes the behaviour of
forth. Attention to irrelevant cues such as these makes a 47-year-old female diagnosed with schizophrenia who
their behaviour look increasingly bizarre, and as a result insisted on wearing around 25 pounds of excess cloth-
it gets more and more attention, which acts as a rein- ing, even in hot weather. This individual’s bizarre
forcer to strengthen such behaviours. clothing habits were, however, soon returned to normal
There is some limited evidence to support the view when a weight limit was set each time she tried to enter
that inappropriate reinforcement may generate some the hospital dining room. On each day she was allowed
bizarre behaviours, and it may account for the frequency into the dining room only if she weighed 2 pounds less
of inappropriate behaviour emitted by an individual than the previous day. This could only be achieved by
diagnosed with schizophrenia. For example, Focus discarding some of the excess clothing and within 14
Point 8.5 describes a study conducted some years ago weeks she was down to wearing quite normal clothing.
by Ayllon, Haughton & Hughes (1965). They reinforced The fact that inappropriate behaviours can be eliminated
a female resident in a psychiatric hospital for carry- and acceptable social and self-care behaviours developed
ing a broom. Whenever she was observed holding the using operant reinforcement procedures does suggest
broom nurses were asked to approach her, offer her a that at least some of the unusual behaviours emitted by
cigarette or give her a token which could be exchanged individuals diagnosed with schizophrenia may be under
for a cigarette. Eventually, when this behaviour was the control of contingencies of reinforcement.
a CAN PERFECTLY NORMAL PROCESSES CAUSE BIZARRE BEHAVIOUR?

0
=
A revealing study by Ayllon, Haughton & Hughes in 1965 a ritualistic procedure, a magical action. . . Her
= provides insight into some of the processes that might broom would be then: (1) a child that gives her
O generate the kinds of bizarre and apparently irrational love and she gives him in return her devotion,
Qa
— behaviour that make up some forms of psychopathology. (2) a phallic symbol, (3) the scepter of an omnipo-
=) They used operant reinforcement methods (see tent queen... this isa magical procedure in which
U
2) section 1.3.2) to reward a female patient diagnosed the patient carries out her wishes, expressed in a
La with schizophrenia for carrying a broom. way that is far beyond our solid, rational and con-
Whenever she was observed holding the broom a ventional way of thinking and acting’
nurse would approach her, offer her a cigarette, or give
her a token which could be exchanged for a cigarette. (Ayllon, Haughton & Hughes, 1965, p.3)
After a period of this reinforcement, the patient was
carrying the broom around for most of the day, and
First, this psychodynamic explanation given by one
even taking it to bed with her when she slept.
of the psychiatrists is a good example of how easy it is
At this point, the researchers called in two psy-
to overspeculate about the causes and meaning of a
chiatrists (who were unaware of the reinforcement
behaviour when the real causes are unknown. Second,
schedule) to give their opinions on the nature of the
it shows how behaviour that is viewed as representa-
behaviour. One of them gave the following reply:
tive of psychopathology can be acquired through a
‘Her constant and compulsive pacing, holding a perfectly normal learning mechanism (in this case
broom in the manner she does, could be seen as operant reinforcement).
s
Cognitive theories and may well be a contributing factor to the disordered

thought and communication exhibited by individuals diag-
Cognitive deficits One of the most obvious character- nosed with schizophrenia. These attentional deficits and
istics of psychosis is the individual’s seeming inability on high distractibility appear to be related to the fact that indi-
some occasions to make simple associations between rele- viduals with a diagnosis of schizophrenia typically demon-
vant events (e.g. sticking to the theme of a conversation), strate impairments in working memory and executive
but on other occasions to make associations that are irrel- functioning (Reichenberg, 2005; Verdoux, Liraud, Assens,
evant (e.g. being unable to prevent themselves from ‘clang- Albalan & van Os, 2002; Gopal & Variend, 2005), and these
ing or emitting words that rhyme). These opposing deficits are likely to be a consequence of impaired
tendencies seem to reflect deficits in attentional processes, neurological functioning in the prefrontal cortex (see
where the individual seems unable to focus attention on section 8.5.1).
relevant aspects of the environment (underattention), or
overattends to irrelevant aspects of the environment Cognitive biases Of specific interest to cognitive the-
(overattention). One characteristic of normal attentional orists are the delusional beliefs that are regularly devel-
processes is the orienting response, which is a physiologi- oped during psychotic episodes, and over 50 per cent of
cal reaction consisting of changes in skin conductance, individuals diagnosed with schizophrenia are diagnosed
brain activity, heart rate and blood pressure. These with paranoid schizophrenia (Guggenheim & Babigian,
responses naturally occur 1974). This raises the issue of why so many sufferers
ienting response A physiological reac- when the individual is pre- should develop these par-
yn to a stimulus consisting of changes in
sented with a novel or
in conductance, brain activity, heart rate
ticular kinds of delusions. paranoid schizophrenia A sub-type of
schizophrenia characterized by the pres-
\d blood pressure. prominent stimulus, and Amongst individuals diag- ence of delusions of persecution.
they indicate that the stim- nosed with schizophrenia
ulus is being attended to and processed. However, around who are living in the community, Harris (1987) found that
50 per cent of individuals diagnosed with schizophrenia they were 20 times more likely than non-sufferers to
show abnormalities in their orienting reactions, suggesting report intrusive or confrontational experiences, such as
that they are not attending to or processing important threats from landlords, police enquiries, burglaries and
environmental stimuli (Olbrich, Kirsch, Pfeiffer & Mussgay, unwanted sexual propositions, so there may be some
2001). While we might expect such difficulties in atten- basis in experience to the development of persecutory
tional processing to give rise to disordered thinking and beliefs. However, researchers have pointed out that para-
responding to environmental stimuli, deficits in orienting noid delusions may also be the result of cognitive biases
responses have also been found to be correlated with the that have been developed by the sufferer (in much the
negative symptoms of schizophrenia such as withdrawal same way that cognitive biases may underlie the experi-
and blunted affect (Slaghuis & Curran, 1999). In contrast, ence of anxiety and its related disorders, see section 6.4.1).
overattention is when an individual attends to all aspects In the following section, we will consider the evidence for
of their environment and is unable to filter out irrelevant four types of biased cognition: attentional biases, attribu-
stimuli. Studies have shown that individuals with a diagno- tional biases, reasoning biases, interpretational biases,
sis of schizophrenia are highly distractable, and perform and then consider theory of mind impairments. In par-
poorly at cognitive tasks when they are also presented with ticular, these types of accounts have led to a greater
irrelevant, distracting stimuli or information (Wielgus & understanding of how individuals develop paranoid idea-
Harvey, 1988). Interestingly, such individuals actually per- tion in delusional disorder, and why ‘hearing voices’ is
form better than non-diagnosed control participants at such a prominent feature of psychotic delusions.
tasks where attending to distracting stimuli can improve
performance. For example, the negative priming effect is Attentional biases Anxiety disorders are typically
when a non-clinical participant shows an increased reac- associated with attentional biases towards threatening
tion time when asked to name a target word they have pre- stimuli (see Section 6.4.1) and individuals suffering psy-
viously been asked to ignore. However, participants chotic symptoms also show some similar attentional
diagnosed with schizophrenia fail to exhibit this negative biases. There is preliminary evidence that individuals
priming effect, and perform just as well whether they have with delusional disorder selectively attend to pathology
been asked to ignore the relevant prime or not (Peters, congruent information. For example, individuals with
Pickering, Kent, Glasper et al., 2000). This inability to screen persecutory delusions exhibit attentional biases towards
out irrelevant stimuli or to ignore distractions correlates stimuli that have emotional meaning or are paranoia rel-
highly with many of the positive symptoms of schizophre- evant (Fear, Sharp & Healy, 1996; Bentall & Kaney, 1989).
nia (Cornblatt, Lenzenweger, Dworkin & Kimling, 1985) Interestingly, individuals prone to persecutory delusions
260 PSYCHOPATHOLOGY
be CANNABIS USE AND PSYCHOTIC SYMPTOMS

ioe)
= In addition, further studies have demonstrated that
There has long been a view that regular psycho-
re tropic drug use may be related to the development cannabis use increases the risk of psychotic symptoms,
\e) of psychotic symptoms, and this has recently focused but has a greater impact on those that already have a vul-
a.
WV on the relationship between cannabis use and sub- nerabilitytoschizophrenia
=) sequent diagnosis of schizophrenia (Arsencault, (Verdoux, Gindre, Sorbara,
WU For a video on cannabis and
Le) Cannon, Witton & Murray, 2004). Apart from legal Tournier, Swendsen, 2003; psychosis go to
be substances such as alcohol and tobacco, cannabis is Henquet, Krabbendam, www.wiley-psychopathology.com/
video/ch8&
the most widely used illicit drug used by schizophre- Spauwen, Kaplan et Gi
nia sufferers, and substance use disorder generally 2005). Finally, meta-anal-
is estimated to be 4.6 times higher in schizophrenia yses suggest that the mean age of onset of psychotic
sufferers than the general population (Regier, Farmer, symptoms among cannabis users is almost 3 years ear-
Rae, Locke et al., 1990). lier than that of non-cannabis users — even when other
Cross-sectional studies have shown that individu- factors such as tobacco use are controlled for (Myles,
als diagnosed with schizophrenia use cannabis sig- Newall, Nielssen & Large, 2012), and pea ae
with schiz-
nificantly more often than other individuals in the ophrenia using cannabis 4
general population (Degenhardt & Hall, 2001). Some are more regularly hospi- { To read the article on ‘Causal linkages
between cannabis use and psychotic
have argued that this relationship between cannabis talized than non-cannabis | symptoms’ by Fergusson etal. go to
use and schizophrenia reflects a form of ‘self medi- users (van Dijk, Koeter, www.wiley-psychopathology.com/
cation’, in which individuals may start using canna- Hijman, Kahn & van den reading/ch8
bis because of a predisposition for schizophrenia Brink, 2012). :

(Khantzian, 1985). However, others have argued for a So if there is a causal link between cannabis use
direct causal link between cannabis use and schizo- and schizophrenia, what is the mechanism that
phrenia, and case history studies frequently describe mediates this link? First, there may be a neurological
psychotic episodes being preceded by the heavy use explanation. Research suggests that cannabis has an
of cannabis (Wylie, Scott & Burnett, 1995), and canna- important effect on brain chemistry, and the com-
bis use being associated with earlier onset of symp- pound tetrahydrocannabinol (THC) that is found in
toms (Buhler, Hambrecht, Loffler, an der Heiden & cannabis can release the neurotransmitter dopamine
Hafner, 2002). (Tanda, Pontieri & DiChiara, 1997; Arnold, Boucher &
Prospective studies that have monitored can- Karl, 2012). Excess dopamine activity has been identi-
nabis use and psychotic symptoms in individuals fied in the aetiology of schizophrenia, and heavy can-
over a lengthy period of time appear to indicate nabis use may therefore raise brain dopamine activity
that there is indeed a causal link between cannabis to levels triggering psychotic episodes. In addition,
and the development of psychotic symptoms. First, regular cannabis use may also affect the course of
Andreasson, Allebeck, Engstrom & Rydberg (1987) brain maturational processes associated with schizo-
found a dose-response relationship between canna- phrenia, and has been shown to result in smaller cer-
bis use at 18 years and later increased risk of psychotic ebellar white-matter volume in schizophrenia patients
symptoms. Subsequent prospective studies have who use cannabis regularly (Solowij, Yucel, Respondek,
found that 18-year-olds meeting the criteria for can- Whittle, Lindsay et a/., 2011). Alternatively, Freeman,
nabis dependence had rates of subsequent psychotic Garety, Kuipers, Fowler & Bebbington (2002) have
symptoms that were twice the rate of young people argued that anomalous experiences (that do not have
not meeting these criteria (Fergusson, Horwood & a simple and obvious explanation) are one of the fun-
Swain-Campbell, 2003). Also, this relationship could damental factors contributing to the development
not be explained by high cannabis use being asso- of delusional thinking, and psychoactive street drugs
ciated with any pre-existing psychiatric symptoms such as cannabis are likely to increase the frequency
(Fergusson, Horwood & Ridder, 2005). Statistical mod- of such anomalous experiences. If the individual is
elling of these longitudinal data show that the direc- in an anxious state and already feeling isolated, then
tion of causality appears to be from cannabis use to these anomalous experiences are likely to be inter-
psychotic symptoms and not vice versa (Fergusson preted threateningly and give rise to the persecutory
et al., 2005). and paranoid ideation often found in schizophrenia. |
are slower to locate angry faces than control partici- experimenter hides the jars from view and then, one by
pants (Green, Williams & Davidson, 2001), and make one, draws a series of beads from one of the jars and asks
fewer fixations and show reduced attention to the salient the participant to say which jar the beads are being drawn
information of facial features than controls (Loughland, from. The fewer the number of beads drawn before the
Williams & Gordon, 2002; Phillips & David, 1998). This is participant reaches a decision indicates a greater jump-
particularly interesting given that potentially. angry facial ing to conclusions bias. Typically, individuals with a delu-
expressions would have added significance for someone sional disorder witness the drawing of three beads or
with a persecutory delusion, and suggests that although fewer before making a decision (Fine, Gardner, Craigie
they may be initially attentive to threat, they then adopt & Gold, 2007; Peters & Garety, 2006), and this jumping
an avoidance strategy that involves avoiding fixating on to conclusions bias has been shown in individuals that are
threatening stimuli (Green, Williams & Davidson, 2003). delusion-prone (Colbert & Peters, 2002), are at high risk
for psychosis (Broome, Johns, Valli, Woolley et al., 2007),
Attributional biases A good deal of research has and are suffering a first episode of psychosis (Falcone,
indicated that individuals with delusional beliefs (par- Wiffen, O’Connor, Kolliakou et al., 2010). These studies
ticularly persecutory beliefs) have a bias towards attribut- collectively suggest that jumping to conclusions may cre-
ing negative life events to external causes (Bentall, 1994; ate a biased reasoning process that leads to the formation
Bentall & Kinderman, 1998, 1999; Bentall, Corcoran, and acceptance of delusional beliefs and eventually to
Howard, Blackwood & Kinderman, 2001). For example, delusional symptoms (Savulich, Shergill & Yiend, 2012).
using the Attributional Style Questionnaire (see Table However, it’s not clear whether jumping to conclusions
7.4), Kaney & Bentall (1989) found that patients with is symptomatic of all delusional beliefs (e.g. delusions of
paranoid delusions made excessively stable and global grandeur or reference), or whether it is restricted to per-
attributions for negative events (just like depressed indi- secutory delusions (Startup, Freeman & Garety, 2008).
viduals), but also attributed positive events to internal One final issue with reasoning biases in psychosis is
causes and negative events to external causes. A subse- what causes these reasoning biases — especially jump-
quent study by Bentall, Kaney & Dewey (1991) found ing to conclusions — and how might these biases interact
that this tendency of individuals with paranoid delusions with the experiences of psychosis-prone individuals to
to attribute negative events to external causes was only cause persecutory symptoms? One particular model that
evidenced when there was a perceived threat to the self — attempts to deal with these issues is the threat-anticipation
they did not necessarily attribute negative events to model of persecutory delusions (Freeman, Garety,
external sources when describing the experiences of Kuipers, Fowler & Bebbington, 2002). This model argues
others. These studies all suggest that individuals exhibiting that four factors are important in contributing to the
paranoid delusions have had significantly more negative, development of cognitive biases involved in persecutory
threatening life events than control individuals without a ideation. These are: (1) anomalous experiences (such as
diagnosis, and have also developed a bias towards attribut- hallucinations) that do not appear to have a simple and
ing negative events to external causes. At the very least, obvious explanation (and are therefore open to biased
this attributional bias will almost certainly act to maintain interpretations); (2) anxiety, depression and worry that
paranoid beliefs, and maintain their delusions that some- would normally cause a bias towards negative thinking
one or something external is threatening them. and threatening interpretations of events (see section
6.4.1); (3) reasoning biases on the part of the individual
Reasoning biases _ Over the past 15 years or so, con- which lead them to seek confirmatory evidence for their
siderable evidence has accrued to suggest that individ- persecutory interpretations rather than question them
uals with delusional disorders have a reasoning bias in (e.g. jumping to conclusions); and (4) social factors, such
the form of jumping to conclusions. That is, such indi- as isolation and trauma, which add to feelings of threat,
viduals make a decision about the meaning or impor- anxiety and suspicion. Of particular importance is the
tance of an event on the relationship between anxiety and jumping to conclu-
mping to conclusions The process of
daking a decision about the meaning or basis of significantly less sions, where anxiety is known to increase the tendency
portance of an event on the basis of evidence than someone to jump to conclusions even in a healthy population, and
sufficient evidence. without a delusional disso. to generate and reinforce paranoid ideation (Lincoln,
order. This has been demonstrated using the classic Peters, Schafer & Moritz, 2009). In addition, there is now
‘jumping to conclusions’ task (Huq, Garety & Hemsley, a growing body of evidence showing that there is a sig-
1988; Westermann, Salzmann, Fuchs & Lincoln, 2012). nificant association between state anxiety and jumping
In this task, participants view two jars each containing to conclusions in individuals with a diagnosis of schizo-
100 beads: Jar A with 85 red beads and 15 yellow beads, phrenia (Ellett, Freeman & Garety, 2008; Lincoln, Lange,
and Jar B with 85 yellow beads and 15 red beads. The Burau, Exner & Moritz, 2009) (Photo 8.2).
2623-4 PSYCHOPATHOLOGY
PHOTO 8.2 People vulnerable to paranoid thinking try to make sense of unusual
internal experiences by using those feelings as a source of evidence that there is a
threat, and they then incorporate other evidence around them to substantiate that
belief (e.g. interpreting the facial expressions of strangers in the street as additional
evidence that they are threatened). Freeman (2007) argues that these paranoid
interpretations often occur in the context of emotional distress, are often preceded by
stressful events (e.g. difficult interpersonal relationships, bullying, isolation), and hap-
pen against a background of previous experiences that have led the person to have
beliefs about the self as vulnerable, others as potentially dangerous, and the world as
bad. In addition, living in difficult urban areas is likely to increase the accessibility of
Shutterstock.com
from
license
under
Used
Vlad.
Axente
© such negative views about others.
ie ABDUCTION BY ALIENS - A RECIPE FOR CREATING UNUSUAL BELIEFS?

co
-
Many people worldwide have claimed to have been room. While many people interpret these post-
= abducted by aliens, been taken against their will to sleep paralysis experiences as dreaming, some
oO an alien spacecraft or enclosed place, questioned people interpret these experiences as seeing
a
7a) or physically examined, and they remember these figures, ghosts, or aliens.
=) experiences either consciously or through methods Tendency to recall false memories: In an
U
Le) such as hypnosis. Indeed, many of those people who elegant set of experimental studies, McNally and
LL claim to be alien abductees are seemingly sincere, colleagues found that individuals who claimed
psychologically healthy, nonpsychotic people. So, to have been abducted by aliens were prone
are their experiences real or have they developed a to what is known as ‘false memory syndrome’
rather unusual set of beliefs to try and give mean- (McNally, 2012). That is, alien abductees regularly
ing to their anomalous experiences — in much the claimed to recall words, items, sentences, and so
same way that people with psychotic delusions are on in memory tests that they had never actually
thought to do? (Freeman, Garety, Kuipers, Fowler & seen before. If this ‘false memory’ effect can be
Bebbington, 2002). generalized to autobiographical memories, then
Professor Rich McNally and his colleagues at Harvard individuals who claim to have been abducted
University have spent over 10 years researching the by aliens would be twice as likely to ‘falsely
psychology of alien abductees remember’ things that had never happened to
(McNally, 2012), and in particu- them than would non-abductees.
To read about alien abductions and
psychology go to
4 lar why it is that some people High levels of ‘absorption’: Alien abductees
http://tinyurl.com/omdimoq » embrace the identity of ‘alien also score significantly higher than most
AAAS
abductee’ His research has iso- people on the mental characteristic known
lated a number of traits pos- as ‘absorption’ This is a trait related to fantasy
sessed by ‘alien abductees’ each of which he argues proneness, vivid imagery, and susceptibility to
contributes to the experiences they recall when ‘being hypnosis and suggestion. Because of this it is
abducted’ and to the desire to cling on to their belief probably not surprising that many alien abductees
that aliens were responsible for their abduction experi- recall their experiences under hypnosis, where
ences. Let’s look at each of these five traits in turn. memories of abduction can be induced through
suggestibility — especially if the person leading the
|. Regularly experiencing sleep paralysis and hypnosis session asks particularly leading questions
hallucinations when awakening: Many people about abduction.
who have reported alien abduction suffer New Age beliefs: Being whisked up into space
episodes of early morning sleep paralysis. On ships by tractor beams or light sources is not some-
awakening from this paralysis, their terror gives thing that happens every day — nor is it something
rise to hallucinations of flashing lights and that is easily explainable within our existing
buzzing sounds. Some experience feelings of knowledge of physics. Similarly, being subjected
‘floating’ around the room or seeing figures in the to imaginative medical procedures requires a
s
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS 263.
tendency to accept unusual and non-mainstream by a set of experiences that the individual tries to give
ideas. This is also a trait possessed by ‘alien abductees’ meaning to. As McNally (2012) points out, it is still unclear
They score highly on measures of magical ideation and whether all these characteristics are necessary ingredi-
endorse New Age ideas that encompass beliefs about ents in the recipe for ‘alien abduction’ or whether some
alternative medicines and healing, astrology, and are more necessary than others. Other researchers have
fortune telling. Such beliefs would certainly allow the also identified some other characteristics, such as para-
individual to accept things happening to them that noid thinking and weak sexual identity (Clancy, 2005).
would be dismissed by existing scientific knowledge. As McNally shrewdly points out, ‘alien abduction’ beliefs
5. A familiarity with the cultural narrative of alien often deepen spiritual awareness and give shape to the
abduction: As a cultural phenomenon, alien abd- identities of abductees and provide a basis for their beliefs
uction has entered folklore and the images and about the world and the universe. Whether the experi-
descriptions of aliens and their spacecraft have ences of abduction were real or not, the experiences and
become familiar to many people. Alien abductees interpretations adopted by ‘alien abductees’ are often
tend to be very familiar with this cultural narrative, psychologically helpful and can be spiritually comforting.
which is one possible reason why their descriptions It may be that the delusional beliefs developed by
of aliens and their spaceships are so similar — being individuals suffering psychosis also play a similar psycho-
fuelled as they are by sci-fi films and numerous books logical role.
about aliens and alien abduction.
This piece was first published at http://www.psychologytoday
This example gives you some idea of how complex, .com/blog/why-we-worry/201207/five-traits-could-get-you-
/ enduring and highly unusual beliefs might be developed abducted-aliens
Interpretational biases In addition to attentional, Williams, Cooke & Kuipers (2012) found a link between
attributional and reasoning biases, accounts of psychotic beliefs about voices and both emotional and behavioural
delusions have been supplemented by findings that a responses to voices. Beliefs about the omnipotence of
number of other information processing biases may be voices was significantly associated with measures of dis-
involved in the development of delusions. For example, tress, and beliefs about the intent of voices (e.g. malevo-
Morrison (2001b) has argued that many individuals diag- lence vs. benevolence) was associated with resistance to
nosed with schizophrenia have a bias towards interpret- or engagement with voices respectively. However, what
ing cognitive intrusions such as hearing voices as is not yet fully clear is why individuals suffering psychosis
threatening in some way. In this case, a perfectly normal develop the negative interpretations of voices that they
auditory hallucination may then be interpreted as threat- do — such as them being uncontrollable, external, domi-
ening (e.g. ‘I must be mad’, nating, distressing. Waters, Allen, Aleman, Fernyhough
a voices Auditory hallucinations, et al. (2012) have provided one theory. They argue that
‘The Devil is talking to
snerally associated with psychotic
elusions. ; me’, ‘If I do not obey the the aberrant voices heard by both healthy and psychosis-
voices they will hurt me’), suffering individuals are generated by hyperactivation of
and this misinterpretation causes anxiety, negative mood auditory neural networks that may be triggered by envi-
and physiological arousal which produces more auditory ronmental or internal factors, and it is failures in signal
hallucinations, which are in turn interpreted negatively, detection that lead the individual to accept these voices
and so on (Baker & Morrison, 1998). Interestingly, hear- as real and meaningful but not self-generated. In addi-
ing voices is not restricted to individuals suffering psy- tion to this, the deficits in working memory and execu-
chosis, and around 13 per cent of healthy individuals tive functioning exhibited by individuals suffering
report hearing voices (Bevan, Read & Cartwright, 2011). psychosis means that they in particular may be unable to
However, what characterizes hearing voices in individu- suppress these voices using deliberative, top-down pro-
als suffering psychosis is the distress that these voices cessing, and nor are they able to distract from them eas-
induce. Individuals with a diagnosis of schizophrenia ily. The distress this will cause is likely to be one source
report the voices they hear as more unacceptable, uncon- of interpretational bias, which will lead the individual
trollable, and distressing than healthy individuals increasingly to interpret the voices as threatening, and
(Morrison, Nothard, Bowe & Wells, 2004), and interpret- the voice content as malevolent.
ing voices as dominating or insulting is associated with Finally, as individuals suffering psychosis increasingly
distress (Vaughan & Fowler, 2004). In addition, Peters, come to interpret the voices they hear as external and
264 — PSYCHOPATHOLOGY
uncontrollable, they will develop a ‘relationship’ with Olesek et al., 2011). TOM deficits have also been identi>
these voices, and the nature of this relationship may fied in the prodromal stages of psychosis (Bora &
determine the level of distress and disability, and control Pantelis, 2013). The fact that TOM deficits appear to be
the nature of the responses that the voices elicit in the a feature of a number of schizophrenia spectrum disor-
individual. Hayward, Berry & Ashton (2011) have iden- ders and can be detected at various stages of their devel-
tified a number of different types of relationships that opment suggests that TOM deficits may be indicative of
individuals with a diagnosis of schizophrenia have with more global cognitive dysfunction, including deficits in
their voices. Often this is a ‘power’ struggle, in which the executive functioning and working memory.
sufferer is constantly engaged in trying to regain power
over their voices. It can lead some individuals to become
8.5.3 Sociocultural Theories
socially isolated as they withdraw into the world of their
voices. But for others who are already socially with- The overarching diathesis-stress model of schizophre-
drawn, it may lead to the generation of hallucinations nia emphasizes that a biological predisposition interacts
and delusions to make sense of the world of their voices with environmental or life stressors to trigger psychotic
(Hoffman, 2007). symptoms. Sociocultural views of schizophrenia attempt
to supplement this view by identifying social, cultural or
Theory of mind (TOM) Another cognitive account familial factors that generate stressors that could precipi-
of psychotic delusions alludes to the possible inability of tate psychotic symptoms. First, we will look at general
individuals diagnosed with schizophrenia to understand social factors that have been implicated in the aetiology
the mental state and intentions of others. Individuals of psychosis, and then look more closely at how the fam-
who cannot infer the beliefs, attitudes and intentions of ily environment can influence the development of psy-
others are said to lack a theory of mind (TOM), and this chotic symptoms.
is a deficit that is known to be prominent in autistic indi-
viduals (see section 17.4.4). Frith (1992) has argued that Social factors
TOM deficits may also be an important factor in the The highest rates of diagnosis of schizophrenia are usu-
development and mainte- ally found in poorer inner city areas and in those of low
theory of mind (TOM) The ability to
nance of psychotic delu- socio-economic status, and this has given rise to two
understand one’s own and other people's
mental states. sional beliefs. If individuals rather different sociocultural accounts of schizophrenia.
diagnosed with schizophr- The first is known as the sociogenic hypothesis.
enia are unable to infer the intentions or mental states of This claims that individuals in low socio-economic
others, then they may begin to believe that others are classes experience signifi-
either hiding their intentions or their intentions are hos- cantly more life stressors sociogenic hypothesis The theory that —
tile. In one study, Corcoran, Cahill & Frith (1997) tested than individuals in higher individuals in low socio-economic classes
experience significantly more life stressor:
the ability of individuals diagnosed with schizophrenia socio-economic classes, and than individuals in higher socio-economic
to understand different types of jokes. In one set of these stressors are associ- classes, and these stressors are associated
jokes, the participant needed to infer the mental state of ated with unemployment, with unemployment, poor educational
one of the characters in order to understand the joke; in poor eduicationalt levels levels, crime and poverty generally.
the other set of jokes, only interpretation of the physical crime and poverty gener-
events in the cartoon was needed (see Figure 8.3). They ally. Having to endure these stressors may trigger
found that individuals with persecutory delusions found psychotic symptoms in vulnerable people. A study con-
the first type of joke more difficult to understand. ducted in Denmark indicated that factors associated with
However, individuals without persecutory delusions low socio-economic status may be risk factors for psy-
found both types of jokes equally easy to understand. chosis, and these include unemployment, low educa-
Furthermore, in tasks designed to test the ability of indi- tional attainment, lower wealth status, low income,
viduals to understand situations in which individuals parental unemployment and parental lower income
hold false beliefs or intend to deceive, individuals with (Byrne, Agerbo, Eaton & Mortensen, 2004). Studies con-
persecutory delusions performed significantly worse ducted on immigrants have also indicated that such
than non-clinical control participants (Frith & Corcoran, groups have a higher incidence of the diagnosis of schiz-
1996). However, TOM deficits are not specific to para- ophrenia, and this has been attributed to the stress caused
noid delusions and have subsequently been described in by many of the initial consequences of immigration,
individuals with a diagnosis of schizophrenia (Bora, such as language difficulties, unemployment, poor hous-
Yucel &Pantelis, 2009), and have been found to be a sta- ing, and low socio-economic status (Hjern, Wicks &
ble marker for the condition across time (Lysaker, Dalman, 2004). However, while this evidence provides
MO. HO! FANCY

BEING AFRAID OF
A ltée CAA!
“It'sno wonder we're an endangered species, really”
FIGURE 8.3 Two typical cartoons taken from the study by Corcoran, Cahill & Frith (1997). In type (a) jokes the participant needs to
infer the mental state of one of the characters to understand the joke, and if individuals with persecutory delusions lack a ‘theory of
mind’ they will find these jokes difficult to understand. The type (b) joke is an example from their physical/behavioural joke, where
only interpretation of the physical events in the cartoon is needed to understand the joke. Corcoran et al. found that individuals with
persecutory delusions found type (a) jokes more difficult to understand, whereas people without persecutory delusions were equally
able to understand both types (a) and (b).
Source: Corcoran, R., Cahill, C. & Frith, C.D. (1997). The appreciation ofvisual jokes in people with schizophrenia: A study of ‘mentalising’ ability.
Schizophrenia Research, 24(3), 319-327. Reproduced with permission.
some support for the sociogenic hypothesis, there is little schizophrenia have indicated that, although they may be
evidence that socio-economic class per se increases the of low socio-economic status, they are as likely to have
risk of psychotic symptoms. In particular, parental socio- parents from a higher socio-economic class as from a low
economic class is not a significant risk factor for a diagno- one (Turner & Wagonfeld, 1967).
sis of schizophrenia (Byrne, Agerbo, Eaton & Mortensen, An alternative explanation for the fact that individuals
2004), and studies of individuals with a diagnosis of diagnosed with schizophrenia appear to have low
266 ~~ PSYCHOPATHOLOGY
; ra
socio-economic status is that the intellectual, behavioural vulnerable to acquiring psychotic symptoms. As we have
and motivational problems afflicting individuals with psy- already seen, some psychodynamic views believed it was
chotic symptoms mean they will suffer a downward drift certain characteristics possessed by the mother that
into unemployment, pov- was important in precipitating psychosis (the schizophre-
downward drift A phenomenon in erty and the lower socio- nogenic mother; section 8.5.2). However, more recently,
which individuals exhibiting psychotic economic classes as a result attention has turned from the characteristics of individ-
symptoms fall to the bottom of the social of their disorder. This is known ual family members to the patterns of interactions and
ladder or even become homeless because
as the social-selection the- communications within the family.
they cannot hold down a job or sustain a
relationship. ory, and claims that indi- Some approaches suggest that the risk factor within
viduals displaying psychotic families for the development of psychotic symptoms lies
social-selection theory Argues that symptoms will drift into in the nature of the way that parents and children com-
there are more individuals diagnosed lifestyles where there is less municate. In the 1950s, Bateson, Jackson, Haley &
with schizophrenia in low socio-economic social pressure to achieve, Weakland (1956) argued that psychosis may develop in
groups because after they have devel- families where communication is ambiguous and acts to
no need to hold down a
oped psychotic symptoms they will drift
downwards into unemployment and
regular job, and they can double-bind the child. This double-bind hypothesis
low-achieving lifestyles. cope with their difficulties claims that the individual is subjected within the family
on a simple day-to-day to contradictory messages
basis. This hypothesis is supported by the fact that many from loved ones (e.g. a double-bind hypothesis Theory advoce
individuals diagnosed with schizophrenia may have par- mother may both request ing that psychotic symptoms are the resu
of an individual being subjected within |
ents with high socio-economic status, even though they displays of affection, such the family to contradictory messages fron
themselves are living in poverty-ridden areas of towns as a hug, and then reject loved ones.
and cities (Turner & Wagonfeld, 1967). them as being a sign of
One final sociocultural view of schizophrenia is known weakness). This leaves the individual in a conflict situa-
as social labelling, in which it is argued that the develop- tion in which they may eventually withdraw from all
ment and maintenance of social interaction. Focus Point 8.8 offers some examples
social labelling The theory that the devel- psychotic symptoms is influ- of double-bind situations and conversations, and it is
opment and maintenance of psychotic
enced by the diagnosis itself clear from these examples that, whichever of the themes
symptoms are influenced by the diagnosis
itself.
(Modrow, 1992). In particu- the child reads into the ambiguous message, they are in a
lar, if someone is diagnosed no-win situation.
as ‘schizophrenic’ then it is quite possible (1) that others will The double-bind hypothesis has subsequently been
begin to behave differently towards them, and define any superseded by more empirical research which has identi-
deviant behaviour as a symptom of schizophrenia, and (2) fied a construct called communication deviance (CD) in
that the person who is diagnosed may themselves assume families, and which is related to the development of psy-
a ‘role’ as someone who has a disorder, and play that role chotic symptoms. CD is a
to the detriment of other — perhaps more adaptive — roles. general term used to communication deviance (CD) A gener;
At the very least this is likely to generate a self-fulfilling describe communications term used to describe communications
that would be difficult for ordinary listen
prophecy, in which a diagnosis leads to the individual, their that would be difficult for ers to follow and leave them puzzled ant
family and friends behaving in ways that are likely to main- an ordinary listener to fol- unable to share a focus of attention with
tain pathological symptoms. Evidence for such an effect low and leave them puz- the speaker.
can be found in the classic study by Rosenhan (1973) in zled and unable to share a
which eight individuals without any symptoms of psycho- focus of attention with the speaker. Such communica-
pathology presented themselves at psychiatric hospitals tions would include (1) abandoned or abruptly ceased
complaining of various psychotic symptoms. Not only remarks or sentences, (2) inconsistent references to events
were these ‘normal’ individuals immediately diagnosed or situations, (3) using words or phrases oddly or wrongly,
with schizophrenia, they were subsequently treated in an or (4) use of peculiar logic. Studies have demonstrated
authoritarian and uncaring manner by hospital staff, began that CD isa stable characteristic of families with offspring
to feel powerless, bored and uninterested, and even had who develop psychotic symptoms (Wahlberg, Wynne,
great difficulty being viewed and treated as ‘normal’ once Keskitalo, Nieminen et al., 2001). When children with a
they had left the hospital! biological predisposition to schizophrenia have been
adopted and brought up in homes with adopted parents
Familial factors who do not have a biological predisposition for schizo-
There is a general belief across most theoretical perspec- phrenia, CD has been found to be an independent predic-
tives on schizophrenia that the characteristics of the fam- tor of the adopted child developing psychotic symptoms
ily are in some way important in making an individual (Wahlberg, Wynne, Hakko, Laksy et al., 2004). This.
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS -267—
sae
fe]
DOUBLE BIND AND PARADOXICAL COMMUNICATION te
=
Below are some visualisations inspired by Double Bind theory where the verbal message may contradict the
= implied message therefore invalidating both.
oe)
a. a
VI
=) With paradox there is essentially no choice
U but there is the illusion of choice.
oe)
Li.
A sign which reads ‘Do not read ‘Be independent’. ‘Do something spontaneous’
this sign. Paradoxically you cannot do You can neither obey nor disobey because
what it asks and implies whatever you do will be wrong.
simultaneously.
You Know
IT love you
I CAN'T TAKE
DoPEERIREARLY. IT ANYMORE
VERY HAPPY
suggests that CD is a risk factor for a diagnosis of schizo- Since its development, EE has been shown to be a
phrenia that is independent of any biological or inherited robust predictor of relapse (Kavanagh, 1992) and, in
predisposition, and that CD is not simply the product of particular, relapse involving positive psychotic symp-
a shared genetic defect between parents and offspring. toms. Families high in EE tend to be intolerant of the
Another construct that has been closely linked to the patient's problems and have inflexible strategies for
appearance and reappearance of psychotic symptoms is dealing with their difficulties and symptoms. High
known as expressed emotion (EE). The importance of the EE families also have an attributional style that tends
family environment in contributing to psychotic symp- to blame the sufferer themselves for their condition
toms was first recognized and the consequences of their symptoms (Weisman,
pressed emotion (EE) A qualita- when it was found that indi- Nuechterlein, Goldstein & Snyder, 2000; Barrowclough,
€ measure of the ‘amount’ of emotion
viduals who left hospital Johnston & Tarrier, 1994). It is not clear how high EE
splayed, typically in the family setting,
ually by a family member or caretakers. following treatment for psy- within a family might influence tendency to relapse,
chosis were more likely to but a recent 20-year prospective study suggests that EE
relapse if they returned to live with parents or spouses than is a valid predictor of relapses and re-hospitalizations
if they went to live in lodgings or to live with siblings (Cechnicki, Bielanska, Hanuszkiewicz & Daren, 2013).
(Brown, Carstairs & Topping, 1958). From this it was dis- One mechanism by which EE may trigger relapses is
covered that many of the discharged patients were through a high sensitivity to stress in psychosis suf-
returning to environments where communications were ferers. The stress caused by EE may trigger cortisol
often hostile and critical. This led to the development of release in the hypothalamic—pituitary—adrenal system,
the construct of EE, which refers to high levels of criti- and this is known to increase dopamine activity and so
cism, hostility and emotional reactivate symptoms in vulnerable individuals (Walker,
~, involvement between key Mittal & Tessner, 2008). The link between EE and psy-
To complete Activity 8.1 go to )) members of a family. Some chotic symptoms is further supported by the fact that
activities/ch8
examples of high EE are some studies have shown that interventions to moder-
shown in Activity 8.1. ate the high EE levels in a family may actually have a
268 PSYCHOPATHOLOGY
beneficial effect on relapse, suggesting a possible causal in Mexican immigrants to the US than in the indigenous
link between high EE and relapse (Hogarty, Anderson, population. However, as immigrants became more famil-
Reiss, Kornblith et al., 1986; Tarrier, Barrowclough, iar with American culture (language and media), EE
Vaughn, Bamrah et al., 1988). Finally, cultural factors became increasingly related to relapse, which suggests
also appear to moderate the effect of EE on symptoms that the EE-schizophrenia relapse link may be mediated
and relapse. Aguilera, Lopez, Breitborde, Kopelowicz & by cultural differences in warmth, mutual interdepend-
Zarate (2010) found that EE was less likely to cause relapse ence and kin relationships (Singh, Harley & Suhail, 2013).
SELF-TEST QUESTIONS
° What is the diathesis-stress perspective that is used to explain the aetiology of psychotic symptoms?
® Concordance studies, twin studies and adoption studies are used to determine the extent of genetic factors in psychosis.
Can you give examples of these types of methods?
° What are genetic linkage analyses and how are they used to identify the specific genes through which the risk for psychosis
may be transmitted?
® What is the dopamine hypothesis and how did the role of dopamine in psychosis come to be discovered?
e What abnormalities can be found in the brains of individuals diagnosed with schizophrenia, and which brain areas are most
affected by these abnormalities?
® Can you describe the evidence supporting the view that brain abnormalities in individuals diagnosed with schizophrenia
may result from abnormal prenatal development?
e What are the main features of psychodynamic explanations of psychosis?
® Can you describe some of the attentional deficits that are characteristic of psychosis and explain how they might contrib-
ute to the clinical symptoms?
° A number of cognitive biases have been implicated in the development of some psychotic symptoms. What are these
biases and how might they contribute to factors such as delusional thinking?
e What is a sociocultural theory of psychosis? Can you describe and evaluate the significance of at least two sociocultural
accounts of psychosis?
e What is double-bind hypothesis and how does it try to explain the development of psychotic symptoms?
* What are (1) expressed emotion, and (2) communication deviance, and what is the evidence that they constitute a risk fac-
tor for the development of psychotic symptoms?
SECTION SUMMARY
8.5 THE AETIOLOGY OF PSYCHOTIC SYMPTOMS
The overarching explanation of psychosis is one of diathesis-stress. That is, individuals who develop psychotic symptoms have
an inherited vulnerability to develop these symptoms (diathesis) that are likely to be triggered by experiencing environmental
stressors. We have discussed a mixture of biological, psychological (cognitive) and sociocultural theories of psychosis, and
these rather different types of explanation are by no means mutually exclusive. They all aim to explain different features of psy-
chosis often at different levels of description. For example, it is pretty much established that psychosis has an inherited compo-
nent and that the development of psychotic symptoms is associated with abnormalities in brain neurotransmitter activity (e.g.
excess dopamine activity) and abnormalities in specific brain areas (particularly the frontal lobes and the mesolimbic system).
These biological abnormalities in turn appear to give rise to deficits in cognitive functioning, such as problems in attention,
executive functioning and working memory. Psychological explanations of delusional thinking have received considerable
attention in recent years, and these have identified biases in attention, attributional processing, reasoning, and ambiguity
interpretation, in ways that are likely to give rise to delusional thinking and delusional beliefs about the world. Finally, sociocul-
tural theories of psychosis try to explain the uneven distribution of schizophrenia diagnosis across socio-economic and ethnic
groups, and have sought to identify sources of life stressors that may trigger psychotic symptoms. These may include dysfunc-
tional family structures and deviant forms of family communication. All of these views are relevant to a full picture of psychosis.
The key points covered in this section are: =
¢ The overarching approach to understanding psychosis is a diathesis-stress perspective in which a combination of geneti-
cally-inherited predisposition (diathesis) and environmental stress are thought to cause psychotic symptoms.
* Concordance studies suggest that an individual who has a first-degree relative diagnosed with schizophrenia is 10 times
more likely to develop psychotic symptoms than someone who has no first-degree relatives diagnosed with schizophrenia.
¢ The concordance rate for schizophrenia in MZ twins is 44 per cent but falls to 12 per cent in DZ twins.
¢ Adoption studies show that the probability ofanadopted child developing psychotic symptoms is linked to the probability
of the biological mother developing psychotic symptoms, and not to the probability of the adoptive mother developing
psychotic symptoms.
® Genetic linkage analyses have helped to identify some of the specific genes through which the risk for psychosis might be
transmitted.
® Genome-wide association studies (GWAS) allow researchers to identify rare mutations in genes that might give rise to
psychotic symptoms.
¢ The main biochemical theory of schizophrenia is the dopamine hypothesis, which argues that psychotic symptoms are
related to excess activity of the neurotransmitter dopamine.
e¢ Two important dopamine pathways in the brain, the mesolimbic pathway and the mesocortical pathway may be impaired
during psychosis.
e Psychotic symptoms are associated with brain abnormalities, including smaller brain size and enlarged ventricles (the areas
in the brain containing cerebrospinal fluid).
® Schizophrenia is specifically associated with reduced volume of grey matter in the prefrontal cortex which affects executive
functioning, decision making and working memory.
® Brain imaging studies have also shown abnormalities in the temporal cortex, including limbic structures, the basal ganglia
and the cerebellum.
e Evidence suggests that schizophrenia may also be associated with birth complications and maternal infections during pregnancy.
© Psychodynamic theories of psychosis have claimed that it is (1) due to regression to a state of primary narcissism, or (2) develops
because of a‘schizophrenogenic mother who fosters psychotic symptoms in her offspring (psychodynamic theories).
e Atleast some inappropriate behaviour patterns exhibited by individuals diagnosed with schizophrenia may be developed
and maintained through processes of operant reinforcement (behavioural theories).
e¢ Around 50 per cent of individuals diagnosed with schizophrenia show abnormalities in their attentional processes suggest-
ing an inability to attend to and process relevant stimuli.
® Delusional disorder is often associated with cognitive biases in attention, attribution, reasoning, and interpretation.
® Delusional disorders are associated with a reasoning bias called ‘jumping to conclusions’ where the individual infers mean-
ing on the basis of very little evidence.
e There is evidence that individuals diagnosed with schizophrenia may not be able to understand the mental states of others
(a‘theory of mind’ deficit), and this may be a factor in the development of delusions — especially delusions of persecution.
© The sociogenic hypothesis claims that individuals in low socio-economic classes experience significantly more life stressors
than those in higher socioeconomic classes, and this is more likely to contribute to the increased prevalence of the diagno-
sis of schizophrenia in low socio-economic groups.
® Social-selection theory argues that there are more individuals diagnosed with schizophrenia in low socio-economic groups because
after they have developed psychotic symptoms they will drift downwards into unemployment and low-achieving lifestyles.
® Social labelling theory claims that once an individual has been diagnosed with schizophrenia, such labelling is likely to give
rise to circumstances which will tend to maintain psychotic symptoms.
® High levels of expressed emotion (high levels of criticism, hostility and emotional involvement between family members) and
communication deviance (poorly structured means of communication between family members) within the families of individ-
uals diagnosed with schizophrenia have been shown to be associated with relapse and the development of positive symptoms.
“2708. PSYCHOPATHOLOGY
* ~
8.6 THE TREATMENT found in section 1.1.3. But

the advent of antipsychotic
hospitalization To admit someone toa
hospital for treatment. |
OF PSYCHOSIS medications in the 1950s

significantly reduced the need for hospitalization, and we
begin our discussion of the treatment of psychotic symp-
With appropriate medication, care and supervision, toms by discussing various forms of biological interven-
most people who have suffered psychotic symptoms can tion (e.g. psychosurgery and drug therapy), followed by
eventually cope with many aspects of day-to-day liv- psychological interventions (social skills training, cogni-
ing, but others may still find it difficult to hold down tive behaviour therapy, cognitive remediation therapy, and
a job or make lasting relationships. Supervision and family therapy interventions), and finally we will discuss
care is often necessary because relapse is a common the role of early intervention programmes and then the
feature of psychosis. A systematic review of remission role of community care (e.g. assertive community treat-
rates in schizophrenia suggests that remission rates vary ment and assertive outreach programmes) in addressing
between 17 and 78 per cent in first-episode schizophre- the longer term needs of those with a diagnosis of
nia, and 16 to 62 per cent in multiple-episode schizo- schizophrenia.
phrenia, with remission rates highest in those taking
second-generation antipsychotics and early response to
treatment, and early treatment intervention (AlAqeel & 8.6.1 Biological Treatments
Margolese, 2012). However, after recovery from a first ;
episode, studies have shown that around 81 per cent will Electroconvulsive ther apy (ECT)
relapse within the following 5 years, and 78 per cent and psychosurgery
will also have a second relapse within that time. Even Early forms of intervention for psychosis seem particu-
10 years after the first episode, around 50 per cent of larly barbaric in retrospect. Between the 1930s and 1950s,
sufferers will have relapsed at least once and been hos- invasive interventions such as ECT (Bini, 1938) and pre-
pitalized as a result (Moilanen, Haapea, Miettunen, frontal lobotomy (Moniz, 1936) were used on thousands
Jaaskelainen et al., 2013). Discontinuing antipsychotic of schizophrenia sufferers. ECT involves inducing brain
drug therapy increases the risk of relapse by almost five seizures by passing an electric current through the head
times (Robinson, Woerner, Alvir, Geisler et al., 1999), of the patient for around half a second (see section 7.3.1),
and illegal drug dependence is another risk factor (San, and tends to be used today to treat psychotic symptoms
Bernardo, Gomez & Pena, 2013). These are important when they are comorbid with depression that has failed
problems for the management and treatment of psycho- to respond to other forms of treatment. Prefrontal
sis, and, in addition, individuals diagnosed with schizo- lobotomy is a surgical procedure that involves severing
phrenia often lack insight into their disorder, deny they the pathways between the frontal lobes and lower brain
are ill, or are too distracted and disabled to respond either areas. Lobotomy was used frequently for patients who
to reflective therapies or to the requirements of care were disruptive or violent,
programmes. In part as a consequence of this, reviews and the procedure did prefrontal lobotomy A surgical proce-
dure that involves severing the pathways
of medication non-adherence among patients diag- appear to have the effect of between the frontal lobes and lower brair
nosed with schizophrenia have been found to be as high making such individuals areas. 4
as 49 per cent (Lacro, Dunn, Dolder, Leckband & Jeste, more passive and many
2002), and predictors of non-adherence include use of were able to be discharged from hospital. However, dur-
illegal substances, alcohol and poor insight (Jonsdottir, ing the 1950s the wisdom of the procedure came to be
Opjordsmoen, Birkenaes, Simonsen et al., 2013). Factors questioned. Fatality rates from the procedure were unac-
such as these often impose intolerable burdens on the ceptably high (between 1.5 and 6 per cent) and loboto-
families and carers of those diagnosed with schizophre- mies significantly affected the patient’s intellectual
nia. The sufferers’ frequently disturbed and disruptive capacities and emotional responsiveness (Tierney, 2000).
behaviour and denial of illness often leaves families with While lobotomies had seemed to be a good way of
little alternative than to seek involuntary hospitalization reducing overcrowding in hospitals in the 1930s, the
for the individual and the prescription of antipsychotic development of effective antipsychotic drugs in the 1950s
drugs at the earliest opportunity. provided a more acceptable and less invasive means of
Traditionally, custodial care and hospitalization were controlling psychotic symptoms.
custodial care A form of hospitalization
the main forms of inter-
or restraint for individuals with psycho- vention for psychosis, and Antipsychotic drugs
pathologies whose behaviour is thought of some characteristics of Specially developed antipsychotic drugs and medications
as disruptive or harmful. early custodial care can be are the first line of intervention for psychotic symptoms,
is
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS vac
and arguably are the most effective treatment for the posi- & Deniker, 1952). They found a marked and consistent
tive clinical symptoms. The main classes of drugs used for drop in psychotic symptoms in such patients with the use
the treatment of psychotic symptoms are known as antip- of these drugs, and by the late 1950s such drugs had been
sychotics or neuroleptics (because some of these drugs widely adopted for use with individuals diagnosed with
produce undesired motor behaviour effects similar to the schizophrenia. These drugs were revolutionary in their
symptoms of neurological effects, and were the first form of treatment that
uroleptics One of the main classes of
ugs used for the treatment of psychotic
diseases such as Parkinson’s appeared to successfully and reliably reduce the positive
mptoms. disease). Nowadays, antip- symptoms of schizophrenia (such as hallucinations, and
sychotic drugs can be disordered thought and communication). These tradi-
divided into two broad groups usually labelled first- and tional antipsychotic drugs appear to have their therapeu-
second-generation drugs (see Table 8.2). First-generation tic effects by blocking excessive dopamine activity in the
antipsychotics (sometimes also called typical antipsychot- brain (Grilly, 2002). However, there are a number of
ics) consist of the traditional drugs that have been devel- problems with the use of antipsychotic drugs. First, they
oped over the past 50 years (such as chlorpromazine and are not a ‘cure’ for psychosis, and tend to act to suppress
haloperidol), and second-generation antipsychotics rather than eliminate symptoms. As a result sufferers
(sometimes called atypical antipsychotics) refer to those usually need lifelong medication to control their symp-
that have been developed in recent years. In the years toms. Second, these types of drugs also have a number
after their development, it was originally thought that of undesirable side effects. These include tiredness, lack
second-generation drugs were more effective over a of motivation, dry mouth, blurred vision, constipation,
broader range of symptoms than first-generation drugs impotence, and dizziness resulting from lowered blood
(Citrome, Bilder & Volavka, 2002) and were associated pressure. Most importantly, between 20 and 25 per cent
with less risk of relapse (Leucht, Barnes, Kissling, Engel et of people who take typical antipsychotic drugs for any
al., 2003), and with less risk of involuntary motor behav- period of time will develop disorders of motor move-
iour side effects (Csernansky & Schuchart, 2002). (But see ment such as tardive dyskinesia (Grilly, 2002). Typical
more recent research described below.) symptoms include movement disorders that resemble
The first-generation antipsychotic drugs were symptoms of Parkinson’s
tardive dyskinesia A disorder of motor
developed in the 1940s and 1950s, when a number of disease, including limb movement.
st-generation antipsychotic researchers discovered that tremors, involuntary tics,
tugs Developed in the 1940s and 1950s, antihistamine drugs used lip-smacking and chin-wagging, shuffling gait, and emo-
hen a number of researchers discovered to combat allergies — such tionless expressions. These symptoms appear to result
at antihistamine drugs used to combat
as phenothiazines and from the lowering of brain dopamine activity that is a
lergies also helped to calm patients
fore surgery. chlorpromazines — also consequence of typical antipsychotic drug use. Such
helped to calm patients problematic side effects cause around 50 per cent of
before surgery. This led to these drugs being used with those treated with typical antipsychotic drugs to quit
individuals, such as those with psychotic symptoms, who medication after less than a year, with a resulting signifi-
showed signs of extreme psychological disorder (Delay cant increase in the probability of relapse.
TABLE 8.2 First- and second-generation antipsychotic drugs
Category Generic name Trade name Usual daily dose (mg)
First generation Chlorpromazine Largactil 75-300

Haloperidol Haldol 3-15
Pimozide Orap 4-20
Trifluoperazine Stelazine 5-20
Sulpiride Dolmatil 200-800
Second generation Amisulpride Solian 50-800

Aripiprazole Abilify 10-30
Clozapine Clozaril 200-450
Olanzapine Zyprexa 10-20
Quetiapine Seroquel 300-450
Risperidone Risperdal 4-6
Sertindole Serdolect 12-20
Zotepine Zoleptil 75-200
QIDS PSYCHOPATHOLOGY
~~
Second-generation antipsychotic drugs (such as 8.6.2 Psychological Therapies

clozapine, resperidone and olanzapine) were developed
in the 1980s and were Social skills training .
second-generation antipsychotic thought to have a number So far in this chapter we have seen ample evidence that
drugs Drugs developed in the 1980s, of benefits over traditional there are deficits in the behavioural, cognitive and emo-
thought to be an improvement on tradi- antipsychotics: (1) their tional responses of individuals diagnosed with schizo-
tional antipsychotics. However, we now phrenia. This may lead their friends and family to view
know that they can cause significant
neurological effects selec-
side effects. tively target certain types their behaviour as inappropriate, their thoughts as con-
of dopamine receptors fused, and their emotional responses as erratic. An obvi-
and also influence serotonin receptors in ways that make ous consequence of these characteristics is that it will
their therapeutic effects more specific (Worrell, Marken, make it difficult for sufferers to interact socially with
Beckman & Ruehter, 2000); (2) they are associated with others, to live normal lives in which they can readily
significantly less risk of relapse than traditional antipsy- negotiate normal day-to-day activities, and to develop
chotics (Leucht, Barnes, Kissling, Engel et al., 2003); (3) close relationships with others. In fact, the inappropriate
they produce significantly fewer major side effects, such responses of individuals displaying psychotic symptoms
as involuntary motor behaviour disturbances may generate a vicious cycle in which inappropri-
(Csernansky & Schuchart, 2002); (4) sufferers taking the ate behaviour causes others to back off from contact
atypical antipsychotics are more likely to comply with with the sufferer, and this in turn is likely to exacer-
and persevere with their medication regimes than those bate symptoms and generate feelings of alienation and
taking traditional antipsychotics (possibly because of worthlessness.
fewer disturbing side effects) (Dolder, Lacro, Dunn & One obvious way to intervene in this cycle is to pro-
Jeste, 2002); and (5) while being highly effective with pos- vide the sufferer with training in the appropriate social
itive symptoms, atypical antipsychotics also help to skills they will need to deal with basic everyday inter-
reduce the frequency and magnitude of negative symp- actions. Social skills training consists of a combination
toms (Grilly, 2002). of role-playing, modelling and positive reinforcement,
However, recent research has cast some doubt on and the individual is taught how to react appropriately
the benefits of second-generation drugs over their in a range of useful social situations. Such training will
first-generation predecessors. First, some second- provide the client with a range of transferable social
generation drugs such as clozapine have their own seri- skills, such as conversational skills, appropriate physi-
ous side effects and can affect immune functioning in a cal gestures, eye contact, and positive and appropriate
small percentage of individuals, plus they can be asso- facial expressions (Smith, Bellack & Liberman, 1996).
ciated with weight gain, and produce extrapyramidal In addition, the client will be asked to role play in cer-
side effects resembling the Parkinson’s disease symp- tain specific scenarios (e.g. how to respond to someone
toms also found with first-generation antipsychotics who has just done them a favour). They are also posi-
(Meltzer, Cola, Way et al., 1993; Young, Niv, Cohen, tively rewarded for appropriate reactions. Such training
Kessler & McNagny, 2010; Rummel-Kluge, Komossa, may have other tangential benefits in helping the client
Schwarz, Hunger et al., 2010). Second, large, independ- to maintain contact with outreach or community super-
ent randomized controlled trials comparing first- and visors, and help them to find work (e.g. teaching them
second-generation drugs found no difference in effec- how to behave in job interviews) and find accommoda-
tiveness between the two types of drug, and the section (Pratt & Mueser, 2002). Randomized controlled tri-
ond-generation drugs produced as many unpleasant als have provided good evidence for the effectiveness of
side effects as the first-generation ones (Lieberman, social skills training on skills acquisition, assertiveness,
Stroup, McEvoy, Swartz et al., 2005; Jones, Barnes, social functioning, and a reduction in general psycho-
Davies, Dunn et al., 2006). pathology (Pfammatter, Junghan & Brenner, 2006), and
The development of new drug treatments for psy- providing coping skills and social support can reduce the
chosis is an important ongoing process, and it is still effects of stress on relapse and help individuals achieve
unclear what biochemical mechanisms many of these their social goals (Addington, Piskulic & Marshall, 2010).
drugs influence to have their successful therapeutic A more focused form of social skills training is
effects. However, antipsychotic drugs have become a supported employment.
central feature of treatment for psychotic symptoms This was developed as supported employment A special pro-
and significantly more independent research is needed an alternative to other gramme designed with a built-in suppor
mechanism to help people with physical,
to improve their effectiveness, reduce their unpleasant vocational rehabilitation
mental or developmental disabilities reac
side effects, and improve patient adherence to medica- schemes such as sheltered and maintain their customized vocation
tion regimes. workshops, which had goals and objectives.
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS 2 27a
generally been viewed as unsuccessful (Bond, 1992). One delusional beliefs (O’Connor, Stip, Pélissier, Aardema et
example of supported employment is the individual al., 2007); (2) to develop non-psychotic meaning for symp-
placement and support (IPS) model, which focuses on toms such as hearing voices (Trower, Birchwood, Meaden,
the search for jobs in integrated community settings Byrne et al., 2004); and (3) to reduce negative symptoms
with the provision of follow-along to help the individual by challenging low expectations (Rector, Beck & Stolar,
optimize work performance support. Supported employ- 2005). In addition, cognitive therapy methods generally
ment has been found to lead to significantly higher rates have also been found to be effective in other areas of treat-
of work and more wages earned than comparative pro- ment, and these include: (1) helping the sufferer to adjust
grammes (Bond, Drake & Becker, 2012). to the realities of the outside world after dehospitalization
(known as personal therapy), and (2) helping with medica-
Cognitive behaviour therapy tion compliance. CBT can
for psychosis (CBTp) also be extended to psychotic reattribution therapy A treatment used
Because of their confused thinking, their frequent lack of symptoms in the form of in helping individuals with paranoid symp-
toms to reattribute their paranoid delu-
insight into their disorder, and the potential difficulties reattribution therapy. We sions to normal daily events rather than
in communicating with individuals exhibiting psychotic have already noted that para- the threatening, confrontational causes
symptoms, cognitive therapies were previously thought noid individuals make they believe underlie them.
to be inappropriate and ineffective for the treatment of more attributions for neg-
psychotic symptoms. This view was strengthened by the ative events that are of an external rather than internal
belief that most of the disordered thinking in schizophre- nature, and this appears to maintain their delusions that
nia was the result of dysfunctional brain neurotransmitter someone or something external is threatening them
mechanisms rather than psychological factors. However, (Lee, Randall, Beattie & Bentall, 2004). Reattribution
as we have seen in the section on aetiology, there is a therapy can be used to challenge these dysfunctional
developing body of evidence to suggest that some psycho- attributions, and the client is encouraged to consider
logical processes may be involved in generating and main- more normal causes for their hallucinations than the dys-
taining psychotic thought, particularly hearing voices, functional or delusional ones that they may hold.
delusions and paranoid views of the world (Bentall, Treatment will usually involve monitoring the frequency
Corcoran, Howard, Blackwood & Kinderman, 2001; of delusional beliefs, attempting to generate alternative
Morrison, 2001b), and it is becoming clear that CBT can explanations for delusional beliefs, and then providing
be adapted to effectively target and challenge these types behavioural experiments that will enable the client to
of psychotic symptoms (and is currently labelled as cogni- test out the reality of their beliefs (Alford & Beck, 1994;
tive behaviour therapy for psychosis (CBTp)) (Kingdon Chadwick & Lowe, 1994). Frequently, a verbal challenge
& Turkington, 2004; Haddock & Slade, 1995; Morrison, will be enough to get the client to reject their dysfunc-
Renton, Dunn, Williams & tional belief (e.g. the therapist may simply ask whether it
g itive behaviour therapy for Bentall, 2003; Fowler, makes sense for things to be the way the client says they
y
ychosis (CBTp) Form of CBT which Garety & Kuipers, 1995). are, and a logical discussion of evidence may be sufh-
lps toaddress any abnormal attribu- For example, Morrison cient), in other cases a ‘reality test’ in the form of a
nal processes and information process-
J and reasoning biases that may ae rise (2001b) has argued that
behavioural experiment may be necessary. For example,
delusional thinking. many individuals diag- in the case of a client who maintained they could tell
nosed with schizophrenia what was going to be said on television before it was
have a bias towards interpreting cognitive intrusions as actually said, a video recording was put on ‘pause’ at pre-
threatening in some way (e.g. ‘If I do not obey the voices arranged times, and the client was asked to say what was
they will hurt me’) and this misinterpretation causes a coming up (Chadwick & Lowe, 1990).
vicious cycle which produces more hallucinations, which Finally, there is currently vigorous debate about the
are in turn interpreted negatively, and so on. Having inter- success of CBTp in alleviating psychotic symptoms and
preted an hallucination as threatening, many individuals enabling recovery. Early randomized controlled trials
may then indulge in what are known as ‘safety behaviours’ indicated that CBTp was effective in helping to reduce
which effectively prevent the individual from disconfirming hallucinations and delusions, and decreased both positive
their belief that the hallucination is threatening. Safety and negative symptoms while lifting mood and improv-
behaviours include things like lying down, drinking alco- ing life functioning (Bustillo, Lauriello, Horan & Keith,
hol, or shouting at the voices to go away (Frederick & 2001; Wykes, Steel, Everitt & Tarrier, 2008). However,
Cotanch, 1995), and they may actually have the effect of effect sizes were often modest, and while CBTp is more
increasing the frequency of the hallucinations (Nayani & effective than either usual treatment or attentional con-
David, 1996). Clinicians can use CBTp methods in a vari- trol conditions, it does not appear to perform significantly
ety of ways: (1) to help the sufferer challenge their better than other forms of therapy for treating psychosis
S974) 2) PSYCHOPATHOLOGY
7 ; i.
(Newton-Howes & Wood, gaining and maintaining employment and
To read the article on ‘CBT and the
psychopathology of schizophrenia’ by
2013, but see Hutton, 2013, accommodation);
Newton-Howes & Wood go to for a critical commentary on 4. identifying inappropriate cognitions and
this meta-analysis). However, dysfunctional thinking biases that might foster
reading/ch8
it is clear that CBTp does catastrophic and deluded thinking (and so help the
provide a useful adjunct client to prevent intrusive catastrophic thinking);
to treatment for psychotic 5. learning to deal with negative feedback from
To read the article on ‘CBT for schizo-
phrenia’ by Hutton go to symptoms, is well tolerated others and to resolve interpersonal conflicts
www.wiley-psychopathology.com/ _ by sufferers, and can be
reading/ch8 (known as ‘criticism management and conflict
used in conjunction with
resolution’); and (6) learning how to comply
medication or other forms
with medication regimes (Hogarty, Greenwald,
of psychosocial intervention (e.g. Sommer, Slotema,
Ulrich, Kornblith et al., 1997; Hogarty, Kornblith,
Daskalakis, Derks et al., 2012).
Greenwald, DiBarry et al., 1997).
Personal therapy
When individuals diagnosed with schizophrenia are dis- Cognitive remediation training
charged from hospital after an acute episode, they usually In earlier sections of this chapter we've described how
find themselves in a challenging environment in which schizophrenia is associated with a number of important
their cognitive skills and their ability to cope leave a lot to be cognitive deficits, especially those relating to attention,
desired. As a consequence, relapse rates are usually high. memory and executive functioning. These cognitive
Personal therapy is a broad-based cognitive behaviour pro- deficits negatively affect psychosocial functioning
personal therapy A broad-based cogni- gramme that is designed to (Heaton, Paulsen, McAdams, Kuck et al., 1994) and
tive behaviour programme that is designed help such individuals with impair the impact of psychiatric rehabilitation
to help individuals with the skills needed the skills needed to adapt to programmes such as social skills training and vocational
to adapt to day-to-day living after dis-
day-to-day living after dis- rehabilitation (Mueser & McGurk, 2004). Because of
charge from hospital.
charge. Clients are taught a this, it makes sense to try to find ways to improve
range of skills in either a group setting or on an individual the basic cognitive functioning of individuals with a dia-
basis, and these include: gnosis of schizophrenia,
because this will inevita- cognitive remediation training (CRT) f
1. learning to identify signs of relapse (e.g. social treatment programme for clients designe
bly have positive knock-on
withdrawal) and what to do in such circumstances; to develop and improve basic cognitive
effects on other rehabili- skills and social functioning generally.
2. acquiring relaxation techniques designed to help tation programmes. This
the client deal with the anxiety and stress caused by has given rise to what are cognitive enhancement therapy (CET)
challenging events (e.g. to reduce levels of anger called cognitive reme- form of intervention which addresses
deficits in both social cognition (the abil-
that might give rise to unnecessary aggression); diation training (CRT) ity to act wisely in social situations) and
3. identifying inappropriate emotional and or cognitive enhancement neurocognition (basic abilities in cognitiv
behavioural responses to events, and learning therapy (CET) program- functioning, such as memory
and attention).
new and adaptive responses (e.g. to help with mes, most of which employ
e EARLY INTERVENTION SERVICES

i>]
ra
It has been known for some time that the sooner psy- has been shown to produce better clinical outcomes
= chotic symptoms are detected and treated, the better than standard service treatment (Garety, Craig, Dunn,
O the long-term prognosis (Marshall, Lewis, Lockwood,
a. Fornells-Ambrojo etal., 2006), to be cost effective (Singh,
V) Drake et al., 2005). In the UK, this has led to the estab- 2010), and to significantly reduce the risk of second
=] lishment of multiple discipline clinical teams whose relapse (Alvarez-Jimenez, Parker, Hetrick, McGorry &
U
Oo purpose is to provide an intensive case management Gleeson, 2011). However, it is still unclear whether
fh of at risk individuals and to educate GPs and physi- these services might merely be delaying psychosis
cians in recognition and response to subclinical symp- and not necessarily reducing long-term risk (Preti &
toms. The aims of this team are to reduce the duration Cella, 2010). Even so, early intervention services have
of untreated psychosis to less than 3 months, and the been established in a number of countries world-wide,
team will then provide intensive case management for including the UK, Australia and New Zealand, Norway
the patient over the next 3-5 years. Early intervention and Denmark, and Canada and the USA.
s
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS 75a
computer-based or pencil-and-paper tasks to improve contribute to both the development of symptoms and
attention, memory and problem solving (Krabbendam to the risk of relapse. In particular, expressed emotion
& Aleman, 2003), and an example exercise is described in (EE) and communication deviance (CD) within families
Treatment in Practice Box 8.1. Cognitive remediation are factors that have been shown to be associated with
training varies in length and intensity, with most relapse and the development of positive symptoms.
programmes providing two training sessions per week Families with high levels of CD and EE have difficulty
that can last for up to 6 months or 80 hours of training with effective communication between family members,
(Hogarty, Flesher, Ulrich, Carter et al., 2004). Meta- high levels of criticism, a tendency to blame the sufferer
analyses report significant effects of cognitive remediation for their symptoms and the family consequences of those
training on attention, verbal memory, problem solving, symptoms, and possess inflexible strategies for dealing
verbal working memory, processing speed, and social with difficulties. Clearly, if these characteristics can be
cognition, but rather modest effects on symptom addressed and modified, then this should be reflected in
reduction (McGurk, Twamley, Sitzer, McHugo & Mueser, lower risk for positive symptoms and relapse.
2007; Wykes, Huddy, Cellard, McGurk & Czobor, 2011). Family interventions can take many forms, but the
However, cognitive remediation is particularly effective main features of a majority of these types of interven-
when combined with social skills training and supported tion are that they are designed to educate the family
employment (McGurk, Mueser & Pascaris, 2005; about the nature and symptoms of psychosis and how
Silverstein, Spaulding, Menditto, Savitz et al., 2008), and to cope with the difficulties that arise from living with
can result in improvement in social and cognitive skills someone with a diagnosis family psychoeducation Family interven-
up to 24 months after entering such training programmes of schizophrenia (some- tion designed to educate the family about
(Hogarty, Flesher, Ulrich, Carter et al., 2004). times known as family the nature and symptoms ofpsychosis and
psychoeducation). More how to cope with the difficulties that arise
from living with someone with a diagnosis.
specifically:
8.6.3 Family Interventions
In section 8.5.3 we discovered that the family environ- 1. families learn about the diagnosis, prevalence and
ment for someone diagnosed with schizophrenia may aetiology of psychotic symptoms,
CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 8.1:

COGNITIVE ENHANCEMENT THERAPY
Cognitive enhancement therapy is a developmental ambiguous to require abstraction. Many clients will ini-
approach that attempts to provide individuals diagnosed tially group items such as iron, wood, glass and steel
with schizophrenia with cognitive exercises that will into a category of ‘building materials, and ink, paper,
help them develop cognitive functions that have been clay, sand and nylon into ‘art supplies: However, with
impaired by their disorder. These include such skills as some subtle coaching, clients are encouraged to seek
attention, memory, and problem solving. a more abstract basis for sorting (e.g. ‘Does nylon really
The following ‘categorisation exercise’ is designed to have anything in common with sand?’). Success can then
help develop working memory and abstraction skills. be achieved when patients reason that ink, paper, glass,
Patients are asked to group the following words into four steel and nylon are all ‘fabricated materials: The skills
coherent categories: that clients require to complete this task successfully
include remembering previous failed attempts, remem-
love iron air home bering the words that require further categorisation, and
remembering individual words within the context of
nylon human spider sand
categories that have already been established. As such,
stone food clay wood the task provides the client with training in memory and
steel water pig paper abstraction skills that they can take to other problem-
solving situations.
virus flower ink glass
Source: After Hogarty, G.E. & Flesher, S. (1999). Practice prin-

The categories of‘living things’ and ‘things one needs ciples of cognitive enhancement therapy for schizophrenia.
to live’ are fairly obvious but the last two are sufficiently Schizophrenia Bulletin, 25,693-708.
S276 PSYCHOPATHOLOGY
: 7
2. they learn about the nature of antipsychotic interventions without accompanying behavioural train:
medication and how to help the sufferer to ing components may be less effective at achieving some
comply with their medication regime, goals, such as medication adherence (Zygmunt, Olfson,
3. they are taught how to recognize the signs of Boyer & Mechanic, 2002).
relapse and to identify and deal with stressors that
could cause relapse,
8.6.4 Community Care
4. through social skills training, they will learn how
to identify problems, to solve them and to achieve With the development of relatively effective antipsychotic
family goals, and drugs in the 1950s and 1960s, it became clear that most
people diagnosed with schizophrenia could be treated to
5. families will also learn how to share experiences
a point where they were capable of living at least some
and avoid blaming either themselves or the
kind of life back in the community. This helped relieve
sufferer for their symptoms and the consequences
the economic burden of lifelong hospitalization and
of their symptoms.
custodial care. However, even when living back in their
These educational targets are achieved in a variety of communities, it was clear that individuals diagnosed with
ways. For example, high EE families may be asked to schizophrenia would often need support and supervision.
watch videos of how low EE families interact (model- They would need help maintaining their necessary medi-
ling) (Penn & Mueser, 1996). Counselling can be pro- cation regime, finding and keeping a job or applying for
vided to help family members interact in less emotional and securing welfare benefits. They may also have needed
ways, and group discussions where families share their help with many aspects of normal daily living that others
experiences can help to provide reassurance and a net- would take for granted, such as personal hygiene, shop-
work of social support (known as supportive family ping, feeding themselves, managing their money, and
management). A more intensive form of family inter- coping with social interactions and life stressors.
vention is known as applied family management, and In 1963, the US Congress passed a Community Mental
this goes beyond educa- Health Act, which specified that, rather than be detained
supportive family management A tion and support to include and treated in hospitals, people with mental health prob-
method of counselling in which group
discussions are held where families share active behavioural training lems had the right to receive a broad range of services in
their experiences and which can help to elements. Communication their communities. These services included outpatient
provide reassurance and a network of and coping skills can be therapy, emergency care, preventative care, and aftercare.
social support.
taught with the active Growing concerns about the rights of mental health
applied family management An inten-
involvement of members patients
4 and ;a change in social attitudes away from the
sive form offamily intervention which goes of the family by using stigma associated with mental health problems meant
beyond education and support to include modelling, role playing, that other countries around the world swiftly followed
active behavioural training elements. providing positive and cor- suit in making mental health treatment and aftercare
rective feedback, and using available in the community (Hafner & van der Heiden,
homework assignments. For example, families may be 1988). These events led to the development of a combina-
taught to have one member chair a problem-solving tion of services usually termed assertive community treat-
meeting (leading the family through the steps) and ment or assertive outreach, and, in the US alone, this has
another as secretary (recording information on a prob- led to around a tenfold decrease in the number of people
lem-solving form). As homework, families may be asked being treated in hospital for
to meet weekly to practise problem solving without the mental health problems assertive community treatment
presence of a therapist or facilitator (Mueser, Sengupta, (Torrey, 2001). Assertive Programmes to help people recovering —
from psychotic episodes with their medic
Schooler, Bellack et al., 2001). community treatment pro- tion regimes, offering psychotherapy, ass
Outcome studies have indicated that family inter- grammes help people tance in dealing with everyday life and its
ventions significantly reduce the risk of relapse, reduce recovering from psychotic stressors, guidance on making decisions,
symptoms, and improve the sufferer’s social and voca- episodes with their medi- residential supervision and vocational
training.
tional functioning for periods up to 2 years (Huxley, cation regimes, psychother-
Rendall & Sederer, 2000; Pharoah, Mari, Rathbone & apy, assistance in dealing
Wong, 2010), and family interventions that are con- with every-day life and its stressors, guidance on making
ducted for longer than 9 months appear to be particu- decisions, residential supervision and vocational training
larly effective (Kopelowicz & Liberman, 1998). Recent (Bebbington, Johnson &
assertive outreach A way of working wi
studies have suggested that no one form of family inter- Thornicroft, 2002). In the groups of individuals with severe mental
vention is necessarily more effective than others (Huxley, UK, assertive outreach health problems who do not effectively
Rendall & Sederer, 2000), but family psychoeducation is a way of working with engage with mental health services.
cal
CHAPTER 8 EXPERIENCING PSYCHOSIS: SCHIZOPHRENIA SPECTRUM PROBLEMS Vea
groups of individuals with severe mental health problems TABLE 8.3 Theaims and characteristics of assertive outreach
who do not effectively engage with mental health ser- programmes
vices. Assertive outreach staff would expect to meet
AIMs:
their clients in their own environments, whether that is a Assertive outreach services aim at helping clients to:
home, café, park or street, and the aim is to build a long-
* Reduce their number of hospital admissions, in terms of
term relationship between the client and mental health
both frequency and duration
services. Table 8.3 provides a list of some of the main
aims and characteristics of assertive outreach pro- * Find and keep suitable accommodation
grammes in the UK, and these emphasize teaching basic
° Sustain family relationships
living skills, providing support and guidance, and pre-
venting relapse and hospitalization. ° Increase social network and relationships
There is good evidence that community care pro- * Improve their money management
grammes help to stabilize the condition of individuals
diagnosed with schizophre- ° Increase medication adherence
mmunity care Care that is provided
itside a hospital setting. nia, ensure that they inte- ° Improve their daily living skills
grate more effectively into
° Undertake satisfying daily activities (including
their local communities, comply with their medication
employment)
regimes, and stay out of hospital longer than sufferers who
are not part of a community care programme (Madianos e Improve their general health
& Madianou, 1992; Hansson, Middelboe, Sorgaard, ° Improve their general quality of life
Bengtsson-Topps et al., 2002; Bebbington, Johnson &
Thornicroft, 2002). However, community care services are ° Stabilize symptoms
often difficult to resource and to coordinate, and it has ° Prevent relapse
been estimated that in any one year in the USA, between
© Receive help at an early stage
40 and 60 per cent of all people experiencing symptoms of
psychosis receive no treatment at all (Wang, Demler & CORE CHARACTERISTICS:
Kessler, 2002). In addition, long-term studies of commu- Assertive outreach involves targeting clients with severe
nity care in the UK suggest that it helps to maintain clinical and enduring mental health problems who have difficulty
and social functioning at a stable level, but does not neces- engaging with services:
sarily help to improve these aspects of the sufferer’s life
* \Itis multidisciplinary, comprising a range of professional
(Reid, Johnson, Bebbington, Kuipers et al., 2001).
disciplines (nurses, psychiatrists and social workers at
The community care approach has also given rise to
a minimum; also, depending on user needs, support
concerns for the physical safety of individuals with men- workers, workers who have also been service users,
tal health problems who are exposed to the stresses and psychologists, occupational therapists, housing
rigours of everyday life, and for the safety of others in the workers, substance misuse specialists and vocational
communities in which they live. For example, studies in the specialists)
UK have suggested that 41 per cent of people with mental ° There is alow ratio of service users to workers; often around
health problems living in the community suffer physical 10 clients per caseload
and verbal harassment, compared with 15 per cent in the
° There is intensive frequency of client contact compared
general population, and this abuse is usually carried out
with that of standard community mental health teams
by teenagers and neighbours (Berzins, Petch & Atkinson, (ideally an average of four or more contacts per week with
2003). There is also concern about the role of individuals each client)
diagnosed with schizophrenia as victims or perpetrators of
» Anemphasis on engaging with clients and developing a
violent crime such as homicide. A Danish study discovered
therapeutic relationship
that the risk of being a victim of homicide was increased
sixfold for people diagnosed with a mental illness such as © Offers or links to specific evidence-based
schizophrenia compared with individuals without a psy- interventions
chiatric diagnosis (Hiroeh, Appleby, Mortensen & Dunn, ° Time unlimited services with a no drop-out policy
2001). They argued that individuals diagnosed with schizo-
e Work with people in their own environment, often their
phrenia may be at such increased risk of a violent death
own home; engages with the users’ support system of fam-
because of a number of factors, including: ily, friends and others
A team approach that provides flexible and creative sup-

1. they are likely to live in places such as inner cities
port to the individual case coordinators
where crime is more prevalent;
PSYCHOPATHOLOGY
2. they may have behavioural characteristics such as used to imply that the community care approach to men:
alcohol or drug abuse that increases the risk; tal health care is dangerous and has failed. However, the
3. they might provoke the hostility of others because evidence to support this view is mixed and more com-
of their psychotic symptoms (such as paranoia); plex than it looks at first sight (Bo, Abu-Akel, Kongersley,
Haahr & Simonsen, 2011). First, one body of evidence
4. because of their symptoms, they may be less aware
reaching back to the 1980s implied that having a major
of their own safety needs;
mental health problem, such as schizophrenia, was not a
5. they may be killed by others with mental health risk factor for violence (Teplin, 1985; Elbogen & Johnson,
problems that they are in contact with; and 2009) and did not predict increased levels of violence in
6. they may be more likely to be victims of those exhibiting psychotic symptoms (Quinsey, Harris,
motiveless killings because of their appearance, Rice & Cormier, 2006). However, other evidence has
which might be unkempt and dirty. suggested a link between schizophrenia and violent
behaviour, including increased aggressive behaviour
In contrast, tragic and high-profile murders carried out and an increased risk for violent and non-violent crimes
by people with mental health problems have often been (Hodgins, 2008; Soyka, Graz, Bottlender, Dirschedl &
Violence in Schizophrenia
os
Antisocial behaviour prior to No antisocial behaviour prior to
illness onset illness onset
| FaRGEr |
Primary explanation Primary explanation
Psychopathic traits Positive psychotic symptoms:
Antisocial personality disorder - Threat/Control Override
(Fear of being threatened)
- Command hallucinations
- Persecutory ideation
- Delusions/hallucinations
ja with threatening content
Secondary concerns
Positive psychotic symptoms Secondary concerns
Substance abuse Substance abuse
Mentalising disabilities Delinquent personality features
!
Mentalising disabilities
|
Ses
ates
Target intervention Target intervention

Personality features related to Positive psychotic symptoms
psychopathy Substance abuse
|
——————_
Treatment method Treatment method

Not available Cognitive behavioural therapy (CBT)
hal Es
FIGURE 8.4 The occurrence of violence in schizophrenia as a consequence of two developmental trajectories stemming from anti-
social or violent behaviour prior to onset of the disorder, and no violent behaviour prior to disorder onset. Note the different types of
primary explanations for these two different trajectories.
Source: Sune, B., Bo, S., Abu-Akel, A., Kongerslev, M., Haahr, U.H. & Simonsen, E. (2011). Risk factors for violence among patients with schizophre-
nia. Clinical Psychology Review, 31(5), 711-726. Reproduced with permission.
Schoech, 2007). Volavka, Laska, Baker et al. (1997) found schizophrenia would not commit serious violence in any
that approximately 20 per cent of individuals with a diag- one given year (Walsh, Buchanan & Fahy, 2002).
nosis of schizophrenia were involved in some kind of What is of some concern, however, is the apparent
violent behaviour prior to contact with the health sys- prevalence of substance and chemical abuse by indi-
tem — suggesting that any increase in risk for violence viduals suffering psychosis and living in the commu-
after the onset of psychotic symptoms may be due to a nity. The lifetime prevalence rate for substance abuse
prior history of violence, or, perhaps more importantly, among people diagnosed with schizophrenia is around
to the poorer socio-economic living conditions that 50 per cent, and may be significantly higher in those
many schizophrenia sufferers experience. Bo, Abu-Akel, who are homeless (Kosten & Ziedonis, 1997). In an
Kongerslev Haahr & Simonsen (2011) proposed a two- Australian study, Wallace, Mullen & Burgess (2004)
trajectory model for violence in patients with schizo- found that between 1975 and 1995, substance abuse
phrenia, and this is shown schematically in Figure 8.4. problems for individuals diagnosed with schizophre-
One trajectory describes violence in schizophrenia suf- nia increased from 8.3 per cent to 26.1 per cent, and
ferers with a prior history of violence, and argues that significantly higher rates of criminal conviction were
violence in this group may be due to pre-existing person- found for those with substance abuse problems (68.1
ality disorders such as psychopathic traits and antisocial per cent compared with 11.7 per cent). We know that
personality disorder. The other trajectory describes vio- regular use of some substances (such as cannabis — see
lence in sufferers who had not previously shown antiso- Focus Point 8.6) can directly increase the risk of devel-
cial tendencies, and ascribes the onset of violence in this oping positive symptoms, and that the use of others
group to positive symptoms such as ‘hearing voices’ and (such as cocaine and amphetamines) can exacerbate
persecutory delusions. Nevertheless, while many epide- these symptoms (Laruelle & Abi-Dargham, 1999). The
miological studies would lead us to believe that there is challenge for community care programmes is to tackle
a link between schizophrenia and violence, only a very what appears to be increasing levels of substance abuse
small proportion of violence in society is accounted in individuals with psychotic symptoms living in the
for by individuals with a diagnosis of schizophrenia, community, and, in so doing, to decrease the risk of
and studies indicate that 99.97 per cent of those with relapse and hospitalization.
| SELF-TEST QUESTIONS __
© What are antipsychotic drugs, how are they thought to deal with the psychotic symptoms, and how are they categorized?
® What problematic side-effects do antipsychotic drugs have?
® What are the important characteristics of social skills training for individuals diagnosed with schizophrenia?
® What is CBTp and how is it used to treat individuals diagnosed with schizophrenia? With what particular types of symptoms
is it most effective?
® What is cognitive remediation training (CRT)?

® Can you describe a typical family-based intervention for psychosis and the factors that such interventions are designed to
address?
° Whatare the different types of community care programmes provided for individuals diagnosed with schizophrenia, and is
there any evidence for their effectiveness in controlling psychotic symptoms?
SECTION SUMMARY
8.6 THE TREATMENT OF PSYCHOSIS
Treating psychotic symptoms is a relatively long-term process. This will often begin with sub-clinical symptoms being picked
up by an early intervention team, and may require immediate and urgent treatment with antipsychotic drugs to deal with the
positive symptoms found during early psychotic episodes. Psychological therapies may be required to deal with the longer
term cognitive and behavioural deficits that may restrict full social and occupational functioning, and family based interven-
tions will help to maintain a stable, stress-free environment in which the risk of relapse is minimized. Long-term community
PSYCHOPATHOLOGY '
SS
care is often overseen by a case manager who will help the sufferer with their medication regimes, residential supervision,
vocational training, and regular access to mental health services. NICE recommends that various different interventions are
considered in planning for recovery from a first episode of schizophrenia - and these can include case manager Oversees long-term com-
both medications and psychotherapy (NICE, 2010). However, there are a range ofdiffering views munity care and helps the client with the’
across the medical, psychological and social spectrum about what is the best approach to take medication regimes, residential supervi-
for the long-term treatment of individuals with schizophrenia. Some of these views are contro- sion, vocational training, and regular
versial, but are worth discussing. Activity 8.2 provides you with an opportunity to consider some access to mental health services.
of these alternative views.
The key points covered in this section are:
® Remission rates vary between 17 and 78 per cent in first-episode schizophrenia, and 16 to 62 per cent in multiple-episode
schizophrenia.
e Electroconvulsive therapy (ECT) and psychosurgery were common forms of treatment for psychosis prior to the develop-
ment of antipsychotic drugs.
psychosurgery Brain surgery used to
e Antipsychotic drugs are relatively successful for treating the positive symptoms of schizo-
treat symptoms of psychopathology.
phrenia, and are thought to be effective because they reduce excessive levels of dopamine
activity in the brain.
© Social skills training can be used to help psycnosis sufferers to react appropriately in a range of useful social situations.
¢ Personal therapy is a broad-based cognitive-behaviour programme designed to help individuals diagnosed with schizo-
phrenia with the skills required to adapt to day-to-day living after discharge from hospital.
® Cognitive behaviour therapy for psychosis (CBTp) helps to address any abnormal attribu-
tion processes and information processing and reasoning biases that may give rise to abnormal attribution processes The
delusional thinking. view that paranoid delusions may be the
result of a bias towards attributing nega-
© Cognitive remediation training (CRT) is designed to help the individual diagnosed with schiz-
tive life events to external causes.
ophrenia to address deficits in social cognition (the ability to act wisely in social situations)
and neurocognition (memory and attention).
° Family interventions are designed to educate the family about the nature of psychotic symp-
toms and how to cope with difficulties that arise from living with someone with a diagnosis To complete Activity 8.2 go to
of schizophrenia. www.wiley-psychopathology.com/
activities/ch8
e Assertive community treatment and assertive outreach are forms of community care that help \
the individual recovering from psychotic symptoms with their medication regimes, psycho-
therapy, decision making, residential supervision and vocational training.
8.7 EXPERIENCING These combinations of symptoms also frequently result

in a marked inability to undertake normal social and
PSYCHOSIS REVIEWED occupational functioning. The prominent approach
to explaining the development of psychotic symptoms
is a diathesis-stress one. That is, there is clear evidence
Psychosis is a name given to a collection of disparate for a genetic predisposition to psychotic symptoms, but
symptoms, and has led DSM-5 to redefine its diagnostic the symptoms appear to be triggered by experiencing
categories into what are known as schizophrenia spectrum environmental stress. The genetic predisposition does
disorders. The main categories include schizophrenia, not appear to be a specific one, and is not transmitted
schizotypal personality disorder, delusional disorder, through a single gene (Kendler, Myers, O’Niell, Martin
brief psychotic disorder and schizoaffective disorder. et al., 2000). Nor is the nature of the environmental
Symptoms are classified as either positive symptoms stressors that may trigger psychotic symptoms fully
(because they reflect an excess or distortion of normal understood. These may range from stressful life experi-
functions, e.g. hallucinations, delusions, disordered ences (such as unemployment) (Brown & Birley, 1968), to
speech, and disorganized motor behaviours) or negative dysfunctional family environments (where intra-family
symptoms (which reflect the loss or diminution of nor- communication may be problematic) (Goldstein, 1987),
mal functions, e.g. diminished emotional experience). to the hassles and challenges encountered in normal.
adolescent development (Harrop & Trower, 2001). There normal lives without experiencing the disabling positive
is, however, good evidence that many of the symptoms symptoms that appear to be linked to imbalances in brain
of psychosis are associated with imbalances in brain neu- neurotransmitter activity (e.g. disordered speech and
rotransmitters such as dopamine, serotonin, glutamate thought, hallucinations). However, after an initial psy-
and GABA (Stone, Morrison & Pilowsky, 2007), and chotic episode, relapse is the norm rather than the excep-
this occurs mainly in the mesolimbic and mesocortical tion and around 50 per cent of sufferers will rarely fully
pathways of the brain. This leads to cognitive deficits recover from the effects of their symptoms (Wiersma,
in important brain areas such as the prefrontal cortex, Nienhuis, Slooff & Giel, 1998). Because of this, long-
where attention, memory and executive functioning are term care and supervision are required, and this means
all impaired. In addition, recent years have seen a resur- that individuals diagnosed with schizophrenia will often
gence in interest in cognitive theories of psychotic symp- require (1) lifelong medication, (2) individual therapies
toms, and especially the development of cognitive biases to deal with their specific cognitive and behavioural defi-
in attention, attributional processes, reasoning and ambi- cits (e.g. social skills training, CBTp), (3) family inter-
guity interpretation (Savulich, Shergill & Yiend, 2012). ventions designed to ensure a family environment that
These processes have been shown to contribute to the minimizes stressors, maintains a medication regime and
development of delusional beliefs as well as the way in can recognize early signs of relapse, and (4) longer term
which many people with psychotic symptoms hear and community care to provide guidance on decision mak-
react to auditory hallucinations or ‘voices’. ing, residential supervision, vocational training, and to
The development of antipsychotic drugs over the past ensure a long-term relationship between the individual
50 years has meant than many sufferers can lead relatively and mental health services is maintained.

Activity
Journal article: The heritability Psychosis: Diagnostic Types of delusions

of delusional-like experiences interview Brain areas labelling
Journal article: Tests of causal Schizophrenia Activity 8.1
linkages between cannabis Cannabis and psychosis Activity 8.2
use and psychotic symptoms
Self-test questions
Alien abductions: The real
Revision flashcards
deal?
Research questions
Journal article: Cognitive
behavioural therapy and
the psychopathology of
schizophrenia
Journal article: Cognitive-
behavioral therapy for
schizophrenia
Glossary key terms
Clinical issues
References
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Stance Use Disorders

‘www.wiley-psychopathology.com/ch9
This chapter begins by discussing substance use disorders

generally, including general diagnostic criteria and preva- 9.1 DEFINING AND DIAGNOSING SUBSTANCE
lence rates. We then look at the specific characteristics of USEDISORDERS 286
a number of drugs whose use regularly gives rise to addic-
tion and dependency. We look in detail at alcohol, nicotine 9.2 THE PREVALENCE AND COMORBIDITY OF SUBSTANCE
and cannabis use, and then continue by looking at a range USE DISORDERS 288
of stimulant, sedative and hallucinogenic drugs. In par-
ticular, we review the physical and psychological effects of 9.3 CHARACTERISTICS OF SPECIFIC SUBSTANCE
these drugs, their prevalence of use, the nature of abuse =: USE DISORDERS 290
and dependency on these substances, and the costs of
dependency in psychological, physical health and eco- : 9.4 THE AETIOLOGY OF SUBSTANCE USE DISORDERS 312
nomic terms. The chapter then continues by reviewing a
developmental model of substance use disorders in which 9.5 THE TREATMENT OF SUBSTANCE USE DISORDERS 321
we consider the risk factors that contribute to experimen-_:
tation, regular use and, in some cases, abuse and depend- 9.6 SUBSTANCE USE DISORDERS REVIEWED 329
ency. Finally, we cover the various types of treatment for
substance use disorders and evaluate their success.
284-5) PSYCHOPATHOLOGY
~
LEARNING OUTCOMES
1. Describe the main diagnostic criteria for 4. Describe a developmental model of substance
substance use disorders and be able to define key dependency and evaluate the risk factors that
terms such as craving, tolerance and withdrawal. contribute to the different stages in this model.
2. Describe the specific characteristics of a range 5. Describe and evaluate the efficacy of a range of
of substances that give rise to dependency and psychological and biological treatment methods
abuse, including specific stimulants, sedatives, and for treating substance use disorders.
hallucinogenic drugs.
3. Describe and evaluate the psychological, physical
health and economic costs of specific substance
use disorders.
My name is Tim and!am from Yorkshire. |hada normal life untill was 12 years old, and then my mother and father started to fight.
The fights were very violent and quite frightening; | have since learnt that this was mostly my mother’s fault. It became apparent that
we were left outside pubs a lot but it seemed normal. My two brothers and |suffered a terrible few-years — the scars are still with us.
Our house was sold and we ended up on a bad council estate in Sheffield which has since been knocked down. The violent
drinking bouts got worse and | left home although | was just 15. | still found a job but suffered terribly over leaving my younger
brothers. |found a bedsit and a job and the peace was heavenly. | then moved to Derby to live with my uncle’s family and eventu-
ally got married to a lovely lady and had two daughters.
My drinking started in Derby. No one thing made me drink but | gradually drank more and more over the years. | started my
own catering business and was extremely successful. |employed 65 staff and enjoyed all the benefits of being my own boss. | had
money, cars and plenty of time to drink! | did not know then what would happen because of my drinking. My wife told me about
my behaviour but | ignored her and her advice. | would not listen to anyone. Worst of all! was out on the road driving to my cater-
ing sites and drinking all day. | still functioned but | do not know how to this day; nor do! know how | kept my licence.
| sold my Company and borrowed £100,000 from the bank to buy — yes, you guessed — a pub/restaurant. What a nightmare —
my own ‘booze’
on tap! Needless to say the venture was doomed from the start. |drank morning, noon and night and had plenty
of friends - or so | thought. Eventually my wife left me and went back to her parents, and! do not blame her.
| went bankrupt and moved to a bedsit once again. | then went on cider and anything else | could get. | had defrauded the
Customs & Excise while | was drinking so | ended up in prison for 12 months, which was a disaster. They put me in charge of
the officers’ mess and bar! Needless to say |was in seventh heaven. | came out of prison a complete wreck and moved from city to
city for 10 years. |was sacked from numerous chefs’ jobs and was in and out of several mental hospitals all over the country. |did
stay dry for a while but when my father died |started to drink again and went back to prison as | wanted the peace and friendship
| found the first time. However this was not meant to be and! found it very hard to cope without the booze second time around.
! was begging in Soho when! decided to try to turn my life around. |moved to Leicester where - through Alcoholics Anonymous
cumin, —/ Stopped drinking. |did have relapses but, following hepatitis, jaundice and a bleeding
© For a video on alcohol misuse go to } throat, | stopped four and a half years ago. | could not suffer those terrible withdrawals
\ (re Cem tee ded __againand |still have the scars of drinking - epilepsy and digestive problems. But |am dry.
Tim’s Story
Introduction moods. They can, of course, have these effects either for
better or for worse, and the short-term benefit of a substance
A drug can be very loosely defined as any substance, other may lead to longer term physical and mental costs (as the
than food, that affects either our bodies or our minds in experience of Tim, above, clearly demonstrates). Never-
drug A substance that has aphysiological SOme way. Such substances _ theless, in most Westernized cultures, drugs are almost a
effect when ingested or otherwise intro- may give us energy, relax normal part of daily life. We use drugs to wake up in the
duced into the body. us when nervous, change morning (caffeine in tea and coffee), to stay alert during
our ways of thinking, distort our perceptions, or change our _ the day (nicotine in cigarettes), to reduce pain (aspirin and
CHAPTER 9 SUBSTANCE USE DISORDERS Bice
paracetamol), to control our physical shape (dieting pills), illicit substance at least once in the previous year, (2) there
and to relax (alcohol, sleeping pills). While the use of drugs were between 99,000 and 253,000 deaths globally in 2010 as
in this way may seem to provide benefits to daily living, there a result of illicit drug use, with drug-related deaths account-
are a number of problems that arise out of this culture: ing for between 0.5 and 1.3 per cent of all-cause mortality
among those aged 15-64, (3) with estimated annual prev-
1. while many of these substances have short-term alence of cannabis use in 2010 ranging from 2.6 to 5 per
benefits they may have longer-term negative cent of the adult population (between 119 million and 224
physical and psychological effects with persistent million estimated users aged 15-64), cannabis remains the
use (e.g. alcohol) world’s most widely used illicit substance, and (4) in terms
2. many people either become psychologically or of prevalence, amphetamine-type stimulants (ATS) (exclud-
physically addicted to a drug, and continue to ing ‘Ecstasy’) remain second only to cannabis, with an esti-
use the drug when it no longer has the original mated prevalence of 0.3—-1.2 per cent in 2010 (between 14.3
benefits (e.g. sleeping pills and dieting pills); and million and 52.5 million users) (see Figure 9.1).
3. many people move on from taking legal drugs to
taking illegal substances, many of which are
physically damaging, highly addictive, and
frequently blight social, educational and
occupational performance (e.g. cocaine, heroin,
solvents, and hallucinogens such as LSD).
Furthermore, in addition to traditional illicit drugs

such as cocaine and Ecstasy, recent years have been char-
acterized by a dramatic rise in the number of newer
classes of psychostimulants — usually known as synthetic
th salts ‘Bath salts’ is the name for cathinones, but more fre-
sce group of drugs containing quently referred to as ‘bath
etic chemicals related to cathinone, salts’ (Fass, Fass & Garcia,
ichisan amphetamine-like stimulant _ 2012) (see Focus Point 9.5
in the khat plant. :
si . later in the chapter). Images
Getty
©
The abuse and misuse of drugs has become one of PHOTO 9.1 Paul Gascoigne was well known as a talented
society's biggest problems. Substance abusers often pay a footballer throughout Europe, having played for teams such as
high personal cost for their dependency in terms of failed Newcastle United, Tottenham Hotspur, Lazio, and Rangers. But since
relationships, ruined careers, poor health and premature retiring from professional football, his life has become dominated by
death (Photo 9.1). Society also pays a high cost in terms of his dependency on alcohol and its associated mental health prob-
lost productivity and the strain such abuse puts on national lems. Like most people with a substance use disorder, his health has
health resources. In 2012, the World Health Organisation suffered, his problems curtailed a promising coaching career, and he
(WHO, 2012) estimated that (1) in 2010 between 153 mil- has had numerous run-ins with the law. Despite a willingness to enter
lion and 300 million people aged 15-64 (3.4-6.6 per cent rehabilitation, his many relapses are well known, and such relapses
of the world’s population in that age group) had used an are a common feature of treatment for severe substance use disorder.
6.0
5.0
(percentage)
Annual
prevalence
f= 2008 2009 2010 2008 2009 2010 2008 2009 2010 2008 2009 2010 2008
bbEge
2009 2010 2008 2009 2010
Cannabis ATS (excluding Ecstasy-group Cocaine Opioids Opiates
‘Ecstasy’)
FIGURE 9.1 Estimates of the annual prevalence of illicit drug use worldwide among people between 15 and 64 years of age, 2008-2010.
Source: World Drug Report 2012, Figure 1. Retrieved from http://www.unodc.org/documents/data-and-analysis/WDR2012/WDR_2012_web_small.pdf
286 PSYCHOPATHOLOGY
Even legal drugs such as tobacco and alcohol are prob- and these factors can be reviewed at the outset in thé
lematic and usage regularly leads to death, illness and ‘Summary table’ on the book’s website at www.wiley-
impoverishment. There are more than 1 billion tobacco psychopathology.com/ch9. But first, it is necessary to
smokers worldwide, of which around 80 per cent live describe some of the terminology commonly used in
in low- and middle-income countries. Approximately this area of psychopathology, and to look at the more
one person dies every 6 seconds due to tobacco and general criteria for diagnosing and describing substance
this accounts for 1 in 10 adult deaths (WHO, 2013). The abuse and dependence.
world’s population consumes an average of 6.13 litres
of alcohol per year per person, and the harmful use of
alcohol results in 2.5 million deaths a year and contrib- 9.1 DEFINING AND
utes directly to 60 types of injuries and diseases (WHO,
2011). In the UK, the percentage of the population that DIAGNOSING SUBSTANCE
reported smoking cigarettes had declined to 21 per cent
in 2008 (down from 39 per cent in 1980) (The Health &
USE DISORDERS
Social Care Information Centre, 2011), but alcohol con-
sumption in the UK has been steadily increasing over the Traditionally, pathology associated with substance and
past 45 years, as can be seen later in Figure 9.4. drug use had fallen into two categories: substance abuse
Equally alarming is the frequency of drug use in ado- and substance dependence. Substance abuse was defined
lescents and school children. Usage and dependence at as ‘a maladaptive pattern of substance abuse A pattern of drug
such an early age may well lead to life-long dependency substance use manifested or substance use that occurs despite 4
and health problems. In the US, over 50 per cent of ado- by recurrent and _ signifi- knowledge of the negative effects of the
drug, but where use has not progressed 4
lescents have tried illegal drugs at least once (Johnston, cant adverse consequences
full-blown dependency.
O’Malley & Bachman, 2001). In the UK, surveys indicate related to repeated use of
that 38 per cent of 15-year-olds have used an illegal drug the substance’, and substance dependence as ‘a cluster of
in the year prior to the survey, and 23 per cent in the pre- cognitive, behavioural and physiological symptoms indi-
vious month (Department of Health, National Report, cating that the individual substance dependence A clusterof
2004), and in 2009 as many as three in ten secondary continues use of the sub- cognitive, behavioural and Physiologica
school pupils (29 per cent) had tried smoking at least stance despite significant symptoms indicating that the individual —
continues use of the substance despite
once (The Health & Social Care Information Centre, substance-related problems’.
significant substance-related problems. —
2011). However, in a reassuring recent report, the num- However, these two catego-
ber of school pupils who reported taking drugs in the ries have been combined into a single “Substance Use
UK had dropped from 42 per cent in 2001 to 29 per cent Disorder’ category in DSM-5. The reason for this is two-
in 2011 (National Foundation for Educational Research, fold. Firstly, most individuals who exhibited the criteria for
2011). Nevertheless, once an individual has used one ille- substance abuse rarely go on to develop substance depend-
gal drug, a majority will go on to abuse more than one ence (Schuckit, Smith, Danko et al., 2001), and, secondly,
(e.g. cocaine, cannabis, crack cocaine) (Tsuang, Lyons, detailed analysis of the diagnostic criteria for substance
Meyer, Doyle et al., 1998), and multiple drug abuse signif- dependence and substance abuse indicated that they
icantly increases other risks to well-being such as being represented one and not two disorder categories. As a
in a car crash, mental health problems, violent behav- result DSM-5 has defined the general criteria for just
iour, and promiscuous sexual behaviour (Greenwood, a single substance use disorder (SUD) category, and the
White, Page-Shafer, Bein et al., 2001). broad criteria for this cate-
The significant risk to physical health, mental health, gory fit within four overall substance use disorder (SUD) Where
social integration, and productivity posed by substance groups covering impaired an individual has at least one substance
disorder diagnosis, whether it is a general
abuse and dependence makes it quite a suitable subject control, social impairment,
diagnosis of substance dependency or —
for prevention and treatment. If we look at Tim’s story at risky use and pharmaco- abuse, or a more specific substance cat-
the beginning of this chapter, we can see that his alco- logical criteria. These group- egory disorder.
hol abuse and dependence resulted in failed relation- ings and their associated
ships, a ruined career and business, criminality, physical criteria are listed in Table social impairment When persistent sub:
health problems such as hepatitis, jaundice and epilepsy, 9.1. In DSM-5, these broad stance use results in failure to fulfil major
and mental health problems requiring hospitalization. criteria for substance use role obligations at work, school, or home.
The remainder of this chapter will look at some of the disorder are then applied to
physical and psychological factors that lead to depend- individual substances to pro- risky use Recurrent substance use in
ence on, and abuse of, a range of substances, and how duce specific diagnostic cri- situations in which it is physically and
these problematic behaviour patterns can be treated, teria for the use of different psychologically hazardous.
CHAPTER 9 SUBSTANCE USE DISORDERS 287
TABLE 9.1 General criteria for substance use disorders TABLE 9.2 Basic terminology in the study and treatment of
substance use disorders
Impaired control »* Substance taken for longer than originally
intended Terminology Definition
* Reports desire to cut down, but with Addiction* Drug use to the point where the body’s
multiple unsuccessful efforts to quit ‘normal’ state is the drugged state (so the
* Individual spends a significant amount body requires the drug to feel normal).
of time obtaining the substance and *Addiction is a term that is rarely used nowa-
recovering from its effects days because it implies that drug dependence
* In severe cases, virtually all the individual's is primarily a physical one, whereas in reality
daily activities revolve around the substance it is a complex mix of physical and psychologi-
cal dependence
* Craving is manifested by an intense desire
or urge for the substance that may occur Psychological The user’s tendency to alter their life
at any time dependence because of the drug, and to centre their
activities around the drug
Social ° Substance use results in failure to fulfil major
impairment role obligations at work, school or home Craving A strong subjective drive to use the substance
® Individual persists with substance use Tolerance The need for greater amounts of the drug
despite recurrent social and interpersonal or substance to achieve intoxication (or the
problems caused by the substance desired effect) or a markedly diminished
effect with continued use of the same
° The individual may withdraw from family
amount ofthe drug or substance
activities and hobbies in order to use the
substance Withdrawal A maladaptive behavioural change, with
physiological and cognitive concomitants,
Risky use ° Recurrent substance use in situations in
that occurs when blood or tissue concentra-
which it is physically hazardous
tions of asubstance or drug decline in an
° The individual continues to take the sub- individual who has previously maintained
stance despite knowledge of persistent prolonged heavy use of the substance or drug
or recurrent physical or psychological
Substance A drug of abuse, a medication, or a toxin
problems caused by the substance
Pharmacological ° Tolerance is signalled by requiring

criteria increasing doses of the substance to
achieve the desired effects clear that the individual has changed their life to ensure
° The individual experiences withdrawal
continued use of the drug, that all their activities are cen-
symptoms, and continues to take the tred on the drug and its use, and this leads to neglect of
substance in order to relieve these with- other important activities such as work, social and family
drawal symptoms commitments. While the physical consequences of sub-
stance use disorders can be devastating (in terms of their
negative effects on physical health and longevity), the chal-
substances (e.g. alcohol, amphetamines, cannabis, cocaine, lenges for psychopathology are arguably to prevent sub-
hallucinogens, opioids, and stimulant- and tobacco-related stance abuse, to develop interventions to help alleviate
disorders), and some of these specific diagnostic criteria abuse and dependence, and to understand the conditions
are discussed later in this chapter. under which some individuals develop substance use disor-
Some other terms used in the diagnosis and treatment ders. This understanding will result not only from a knowl-
of substance use disorders are listed in Table 9.2. For exam- edge of the physical effects of individual substances, but
ple, when the person’s ‘normal’ body state is the drugged also from a knowledge of how the individual uses the drug
diction When a person's ‘normal’ body state (so that the body and the negative effect it has on their daily lives.
teisthe drugged state (so that the body requires the substance to Tolerance refers to the
tolerance The need for increased
Juires the substance to feel normal). feel normal), this is known need for increased amounts amounts of a substance in order to achieve
Res APY). 5 as addiction, and craving is of the substance in order similar effects across time.
ving The strong subjective drive that
dicts have to use a particular substance. the term used for the strong to achieve similar effects
subjective drive that addicts across time. Withdrawal withdrawal Where the body requires
ychological dependence When indi- the drug in order to maintain physical
have to use the substance indicates that the body
uals have changed their life to ensure stability, and lack of the drug causes a
\tinued use of a particular drug such (see Focus Point 9.8). The requires the drug in order range of negative and aversive physical
t all their activities are centred on the term psychological depen- to maintain physical stabil- consequences (e.g. anxiety, tremors and, in
ig and its use. dence is used when it is ity, and lack of the drug extreme cases, death).
288 PSYCHOPATHOLOGY
: ‘
causes a range of negative and aversive physical conse- work), and (4) abandoning or neglecting important life
quences (e.g. anxiety, tremors and, in extreme cases, death). activities because of the drug (e.g. failing to go to work
As outlined in Table 9.1 behavioural features of depend- because of persistent hangovers; neglecting friendships,
ence include (1) unsuccessful attempts to cut down on use relationships, child care, and educational activities). It is
of the drug, (2) a preoccupation with attempts to obtain also important to emphasize at this early stage that sub-
the drug (e.g. theft of money to buy illegal drugs, driving stance use disorder is a chronic relapsing condition, in which
long distances late at night to buy alcohol, multiple visits substance users find their habits hard to eliminate, and it is
to doctors to obtain prescription drugs), (3) unintentional almost normal following treatment for substance depend-
overuse, where people find they have consumed more of ence to be associated with multiple relapses.
the substance than they originally intended (e.g. ending up We will discuss the conditions that lead to this syn-
regularly drunk after only going out for a quick drink after drome in more detail in section 9.4.
SELF-TEST QUESTIONS
® Can you define the terms craving, tolerance and withdrawal?
® What is craving?
SECTION SUMMARY
9.1 DEFINING AND DIAGNOSING SUBSTANCE USE DISORDERS ot ti te
e Substance dependence is characterized by both tolerance and withdrawal effects.

. aty
e Substance abuse is a pattern of substance use that occurs despite knowledge of the negative effects of the substance, but :
where it has not yet progressed to full-blown dependence.
© Craving is the term used for the strong subjective drive that addicts have to use a substance.
¢ Tolerance refers to the need for increased amounts of a drug to achieve the same effects across time.
¢ Withdrawal indicates that the body requires the drug in order to maintain physical stability.
9.2 THE PREVALENCE Kessler, Hughes, Anthony & Nelson, 1995; Compton,
Thomas, Stinson & Grant, 2007). Of those individuals
AND COMORBIDITY OF aged between 15 and 54 years, 51 per cent had used ille-
SUBSTANCE USE DISORDERS gal drugs, non-medical prescription drugs (e.g. sedatives,
tranquilizers), or inhalants at some point in their lives,
and 15.4 per cent had done so in the previous 12 months.
Drug use and dependence is highly prevalent in the In the US, the Substance Abuse and Mental Health
general populations of many countries, although rates Services Administration’s 2004 National Survey on Drug
of substance use disorders will vary markedly across Use and Health estimated that 22.5 million persons
countries depending on the legal, moral and religious aged 12 or older met criteria for substance dependence
attitudes to drugs in those countries. The lifetime prev- or abuse in the foregoing year (SAMHSA, 2005), and a
alence rate for substance dependence has been calcu- majority of those with substance abuse and dependency
lated in the US at between 2.6 and 5.1 per cent (Warner, problems rarely seek help, with as few as 8.1 per cent of
CHAPTER 9 SUBSTANCE USE DISORDERS
TABLE 9.3 Comorbidity of substance use disorders with other

psychiatric disorders*
Percentage of individuals also

diagnosed with a substance use
Psychiatric disorder disorder (SUD)
Bipolar disorder 60.7%
Major depression 18%

Obsessive compulsive 32.8%
disorder (OCD)
Panic disorder 35.8%
Schizophrenia 47%
Bulimia nervosa 28%
FIGURE 9.2 Lifetime prevalence of drug disorders among Personality disorders 42%
persons with mood and anxiety disorders. *Rate of substance use disorders in the general population is
Source: Data from Conway, K.P., Compton, W., Stinson, F.S. & Grant, around 5%.
B.F. (2006). Lifetime comorbidity of DSM-IV mood and anxiety dis- Source: Data taken from Brooner, King, Kidorf, Schmidt & Bigelow
orders and specific drug use disorders: Results from the National (1997); Cuffel, 1996; Regier, Farmer, Rae, Locke et al., 1990; Zanarini,
Epidemiologic Survey on Alcohol and Related Conditions. Journal Frankenburg, Dubo, Sickel et a/., 1998; Lacey, 1993.
ofClinical Psychiatry, 67(2), 247-257. Reproduced by permission of
Physician's Postgraduate Press, Inc.
those diagnosed with substance abuse claiming to have is that substance abuse and dependence may be a risk
sought help or treatment (Compton, Thomas, Stinson & factor for the later development of a psychiatric illness
Grant, 2007). (e.g. Wylie, Scott & Burnett, 1995). For example, panic
A particularly important aspect of substance use dis- attacks may result from cocaine use and persist even after
orders is that they are highly comorbid with a range of cocaine abstinence has been achieved (Rosen & Kosten,
other psychological disorders. Community epidemio- 1992), with the latter possibly increasing the likelihood
logical studies suggest that, amongst individuals with of relapse back to cocaine or another drug to cope with
substance dependence, 53-76 per cent have at least one these panic attacks. However, the majority of current
other co-occurring psychiatric disorder (Zilberman, evidence is consistent with the view that psychiatric and
Cao & Jacobsen, 2003), and there is an especially strong psychological disorders usually pre-date substance abuse
association of lifetime mood and anxiety disorders with and dependence (Merikangas, Mehta, Molnar, Walters
substance use disorders (Merikangas, Mehta, Molnar, etal., 1998; Abraham & Fava, 1999), anda recent UK study
Walters et al., 1998) (see Figure 9.2). Other studies have indicated that the risk for substance abuse attributable
indicated significantly higher levels of substance use dis- to prior psychiatric illness was 14.2 per cent, compared
orders in individuals with bipolar disorder, major depres- with a risk for psychiatric illness attributable to substance
sion, anxiety disorders — such as obsessive compulsive abuse of only 0.2 per cent (Frisher, Crome, MacLeod,
disorder and panic disorder — schizophrenia, bulimia Millson & Croft, 2005). This suggests a ‘self-medication’
nervosa and personality disorders than in the general effect, in which individuals with an established psychiat-
population (see Table 9.3). The high level of comorbid- ric disorder start using substances to alleviate the nega-
ity between substance use disorders and other mood and tive emotional and behavioural effects of the disorder
anxiety disorders has generated a number of hypotheses (Mueser, Drake, & Wallach, 1998; but see Focus Point 7.7
about why substance use disorders occur so regularly in for an account of a causal relationship between cannabis
the context of other psychological disorders. One view use and psychotic symptoms).
SELF-TEST QUESTION
® How are substance use disorders and other psychiatric disorders related? Is one a risk factor for the other?
SECTION SUMMARY
9.2 THE PREVALENCE AND COMORBIDITY OF SUBSTANCE USE DISORDERS
° The lifetime prevalence rate for substance dependence in the US is between 2.6 and 5 per cent.
¢ Substance use disorders are highly comorbid with a range of other Axis | and Axis II disorders.
STIMULANTS ~ DEPRESSANTS
9.3 CHARACTERISTICS
OF SPECIFIC SUBSTANCE Alcohol
|
Amphetamines — Barbiturates
Cocaine | Opiates
USE DISORDERS Caffeine _ Heroin
| Benzodiazepines
In this chapter we need to look closely at the nature of

different substance dependencies. These will cover alco-
hol and nicotine — because of the close links that use
of these substances have with normal everyday life —
then three specific groups of substances: stimulants
(e.g. cocaine, ampheta-
stimulants Substances that increase cen- mines and caffeine), seda-
tral nervous system activity and increase tives (e.g. opiates, such as
blood pressure and heart rate.
heroin, and barbiturates), HALLUCINOGENS
and hallucinogens (e.g.
sedatives Central nervous system depres- LSD and other halluci- FIGURE 9.3 A drug chart showing how the different sub-
sants which slow the activity of the body, stances described in this chapter overlap across categories.
nogenics, cannabis, and
reduce its responsiveness, and reduce
pain tension and anxiety. This group of MDMA, better known as
substances includes alcohol, the opiates Ecstasy). It is important 9.3.1 Alcohol Use Disorder
and their derivatives (heroin, morphine, to be aware that relatively
methadone and codeine), and synthesized Alcohol is one of the most 4
few of the drugs we will
tranquillizers such as barbiturates.
discuss fit simply and eas- commonly used drugs in a | To calculate your level of alcohol con-
sumption, use the Drinkaware
ily into any one of these very large number of coun- | Unit Calculator at
hallucinogens Psychoactive drugs which drug categories and many tries worldwide. In most | www.drinkaware.co.uk/unitcalculator
affect the user's perceptions. They may
either sharpen the individual's sensory
have multiple effects, with countries it is also legal and
abilities or create sensory illusions or some overlap between cat- can be easily purchased
alcohol A colourless volatile liquid com-
hallucinations. egories. That is why each and consumed. In the US pound which is the intoxicating ingredier
textbook you read on this over 65 per cent of people in drinks such as wine, beer and spirits. q
topic appears to have a different form of categorisation. will at some time consume
Figure 9.3 provides you with a drug chart that maps a drink that contains alcohol (Centers for Disease Control
how the different substances described in this chap- and Prevention, 2002), and in the UK this figure rises to 92
ter overlap across categories. This shows that nicotine per cent of males and 86 per cent of females (WHO, 2004).
can act as both a stimulant and a depressant; hallu- However, patterns of alcohol consumption appear to have
cinogenic drugs such as LSD and MDMA have both become ever more problematic, with surveys in 2000
hallucinogenic and stimu- suggesting that 26 per cent of the UK population could
For an activity based on Figure 9.3
lant properties; and cannabis be labelled as hazardous drinkers — that is, they have
regarding the different substances is probably the most difficult five or more standard drinks
hazardous drinkers Individuals who hai
discussed in this chapter go to to categorize because it can (males) or three or more five or more standard drinks (males) or
activities/ch9
_ have a variety of psychologi- standard drinks (females) three or more standard drinks (females) o
cal and physical effects. on a typical drinking day a typical drinking day.
(WHO, 2004) and the overall amount of alcohol drunk per units on at least one day of the week: 24 per cent of
individual in the UK has been steadily increasing over the those aged 16-24, but just 2 per cent of those aged 65
past 45 years (see Figure 9.4). and over. However, the prevalence of binge drinking
What is known as ‘heavy episodic’ drinking or binge among young men and women in the UK has fallen
drinking has also reached epidemic levels in many since 1998. In 2010 the prevalence among young men,
European countries. Binge drinking refers to a high according to the ONS, remained at 24 per cent while
intake of alcohol in a among young women it fell to its lowest recorded level
ge drinking A high intake of alcohol in
ngle drinking occasion. single drinking occasion. at 17 per cent (Office for National Statistics, 2010) (see
There is no single defini- Figure 9.5).
tion of binge drinking but, in the UK, it is normally Alcohol has its physical and psychological effects when
defined as taking at least 8 units (males) or 6 units its main constituent, ethyl alcohol, is absorbed into the
(females) of alcohol in a single day. One-fifth (20 per bloodstream through the
ethyl alcohol The intoxicating constituent
cent) of men drink more than 8 units on at least one day lining of the stomach and of alcoholic drinks.
of the week: the proportion ranges from 24 per cent of intestine. Alcohol then
men aged 16-24 to only 5 per cent of those aged 65 and reaches the brain and central nervous system via the
over. Thirteen per cent of women drink more than 6 bloodstream. At first, alcohol acts to relax the individual,
Change in data
source from 2002
of
alcohol
Litres
pure
eT
1961 1966 1971 1976 1981 1986 WE IS 2001 2006

Year
FIGURE 9.4 Annual alcohol consumption per person over 15 years of age in the UK, 1961-2006.
Source: Management of substance abuse in UK http://www.who.int/substance_abuse/publications/global_alcohol_report/profiles/gbr.pdf
(accessed 20th December 2013). © World Health Organization. Reproduced with permission.
30
% 25
=n
20
=
(55
Os Sy ae T maw T i= pa he
ae
1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010
FIGURE 9.5 Prevalence of binge drinking among 16- to 24-year-olds in the UK, 1998-2010.
Source: From House of Commons Library (2012). Statistics on alcohol. Reproduced with permission.
and it does this by influencing the receptors associated effects. The long-term physical effects of heavy alcohols
with the neurotransmitter GABA. This facilitates this consumption include withdrawal symptoms when the
neurotransmitter’s inhibitory function by preventing body is deprived of alcohol, and these include restless-
neurons firing and making the drinker feel more ness, inability to sleep, anxiety and depression, muscle
relaxed (Harvey, Foster, MacKay, Carroll et al., 2002). tremors, and rises in blood pressure and temperature.
Initially, this makes the drinker more talkative, friendly, Following withdrawal after extended heavy drinking
confident and happy. As more alcohol is absorbed over a number of years, the drinker may experience
into the central nervous system, the second stage delirium tremens (DTs), where the drinker becomes
of intoxication makes the drinker become less able to delirious, experiences unpleasant hallucinations, and
make judgements; they talk less coherently, memory exhibits shaking and mus-
is affected, and they may switch from being relaxed cle tremors. Longer-term delirium tremens (DTs) A severe form of
alcohol withdrawal that involves sudden
and happy to emotional and aggressive. Finally, the negaue physical effects of and severe mental or nervous system
physical effects of alcohol intoxication include motor heavy alcohol consump- changes.
coordination difficulties (in balance and walking), tion include hypertension,
slowed reaction times, and blurred vision. This course heart failure, stomach ulcers, cancer, cirrhosis of the
of the effect of alcohol is known as biphasic, because liver, brain damage (including shrinkage of the frontal
the initial effects act as lobes), and early dementia. Furthermore, many of the
biphasic Where the initial effects of a drug : ,
may act as a stimulant (e.g. alcohol making a stimulant (making the
effects of long-term alcohol dependence are similar to
the drinker reactive and happy), but the drinker reactive and happy), malnutrition. This is because alcohol contains calories,
later effects act as a depressant (making but the later effects act as but is entirely devoid of any required nutrients. This
the drinker sluggish and experience nega- 2) depressant (making the leads drinkers to feel full but take in little or no nutrition.
tive emotions).
drinker sluggish and expe- The consequence is vitamin and mineral deficiencies
rience negative emotions). We can see how drinking which can lead to dementia and memory disorders, such
alcohol can be appealing to many people because of its as Korsakoff’s syndrome. One indirect physiological
initial effects (i.e. it helps alleviate stress after a busy risk associated with heavy 7
day at work, increases sociability, reduces inhibitions, drinking in women is fetal Korsakoff’s syndrome A syndrome
involving dementia and memory disorde
and so on). However, many of the so-called effects of alcohol
:
syndrome,
ei
in cole
which is caused by long-term alcohol
alcohol are actually mythical, and result from a drinker’s which heavy drinking by a abuse and dependency.
expectations about the effects of alcohol rather than its mother during pregnancy
real effects. For example, in a couple of classic studies, can cause a whole range of
fetal alcohol syndrome Physiological ris
Lang, Goeckner, Adessor & Marlatt (1975) and Wilson & physical and psychological associated with heavy drinking in wom
Lawson (1976) gave participants a disguised non- abnormalities in the child, in which heavy drinking by amother
alcoholic beverage when they were expecting alcohol. including physical defor- during pregnancy can cause physical and
They subsequently reported increases in sexual arousal mities, heart problems, psychological abnormalities in the child.
and aggression, even though they had become less stunted growth, hyperac-
physiologically aroused. Expectations about the effects tivity and learning difficulties (Hankin, 2002). Finally, the
of alcohol appear to play an important role in drinking important physical effects of alcohol abuse and depend-
behaviour, with positive expectancies about the effects of ence discussed in this section substantially reduce lon-
alcohol being a significant predictor of its use (Sher, gevity in drinkers, and the number of alcohol-related
Wood, Wood et al., 1996). deaths in the UK has more than doubled between 1979
and 2000 (Baker & Rooney, 2003), suggesting that long-
Alcohol abuse and dependence term drink-related disorders are a significant cause for
Because of its short-term positive psychological and concern.
physical effects, and probably equally as much because The diagnostic criteria for alcohol use disorder are
of the positive cognitive expectations that have built up provided in DSM-5 Summary Table 9.1. The disor-
around the consumption of alcohol in many societies, it der is defined by a cluster of behavioural and physical
has come to be seen by many as a way of enduring life’s symptoms such as evidence of tolerance effects and
problems and relieving tension. However, because of its withdrawal symptoms that develop within 4-12 hours
availability, many come to use alcohol to the point where of restricted consumption. However, many individuals
it begins to have significant negative effects on both phys- with alcohol dependence may never experience with-
ical and psychological health. With increased use, the drawal once a pattern of compulsive drinking develops
body begins to show tolerance to alcohol and the drinker in which their whole life centres around obtaining and
has to consume ever larger amounts to achieve the same consuming alcohol. Work performance and child care or
household responsibilities may be significantly affected DSM-5 SUMMARY TABLE 9.1 Criteria for alcohol use disorder
either by the after-effects of drinking (e.g. hangovers) or
A pattern of alcohol use causing impairment or distress lead-
by being intoxicated while trying to perform these func-
ing to at least two of the following within a 12 month period:
tions. Interestingly, a US national survey indicated that
e Alcohol is taken in greater amounts or for longer than
workplace alcohol use and impairment directly affected
was intended
an estimated 15 per cent of the US workforce, with
1.6 per cent working under the influence of alcohol, and e Acontinuing desire or unsuccessful efforts to control
9.2 per cent working with a hangover (Frone, 2006), alcohol use
and lost productivity features as the dominant economic e Alot of time is spent in acquiring, using and recovering
cost of alcohol consumption in many countries around _ from the effects of alcohol
the world (Rehm, Mathers, Popova, Thavorncharoensap ° Craving, or a strong desire to use alcohol
et al., 2009). Alcohol abuse is also characterized by the e Alcohol use results in a failure to fulfil major life roles at
drinker putting themselves at physical risk while intoxi- work, home and so forth
cated, including drink driving and becoming engaged
e Persistent alcohol use despite the effect on interper-
in violent arguments (see “The costs of alcohol use dis- sonal, recreational or social interactions or despite hav-
orders’ below). Such individuals will also continue to ing an ongoing physical or psychological problem that
drink when they know that their drinking is a cause of is likely to have been caused or made worse by alcohol
significant social or interpersonal problems (such as ° Tolerance symptoms associated with high alcohol use
their physical abuse of family members, or by causing
e Withdrawal symptoms associated with high alcohol use
problems in their relationship with a partner).
TREATING ALCOHOL DEPENDENCE

Like most of the substance use disorders, alcohol depend- that alcoholics should achieve during the recovery pro-
ence is difficult to treat successfully. This is because of a cess and the 12-step programme has been shown to
-« number of factors: achieve long-term absti-
: WV
nence in around 25 per
> 1. many people dependent on alcohol use it as a centof participants, plus
To read about the AA’s 12-step
programme go to
way of coping with life stresses and difficulties, a significant decrease in http://tinyurl.com/om2w7u3
and this can easily lead to relapse when stress is alcohol consumption in 78
experienced during or after treatment; per cent (Ouimette, Finney & Moos, 1997). Many of the
2. alcohol dependence is often comorbid with other beneficial effects of self-help groups such as AA may be
psychological disorders, which makes treatment attributable to the client replacing social networks ofdri-
of the dependence more problematic; and nking friends with other AA members.
3. alcohol is often part of polydrug abuse, where those
dependent on alcohol also abuse other drugs as
MOTIVATIONAL-ENHANCEMENT THERAPY
well, and the use of one drug (e.g. nicotine) is likely
to trigger the use of another (e.g. drinking alcohol).
This form of cognitive behaviour therapy places the
responsibility for change on the client, and attempts to
Treatments for alcohol dependence take a variety
provide them with a range of skills to deal with their
of different forms, and we will describe some of them
drinking (Miller & Rollnick, 2002). The therapist pro-
here. The most successful forms of treatment, however,
vides individual feedback to the client on the effects of
are usually multifaceted approaches that combine a
their drinking (such as the effects on other family mem-
number of individual therapies into a single coherent
bers), explores the benefits of abstinence, and then
programme for the client.
designs a treatment programme specifically tailored to
the individual's own needs. Motivational-enhancement
SELF-HELP GROUPS therapy (MET) is one of the most successful and cost-
effective therapeutic approaches for alcohol depend-
The most commonly sought source of help for alcohol- ency, and studies suggest around 50 per cent of clients
related problems are community self-help groups such report that both levels of drinking and alcohol-related
as Alcoholics Anonymous (AA) (http://www.alcoholics- problems decreased significantly in the 12-months fol-
anonymous.org.uk/). AA describes what it calls 12 steps lowing treatment (UKATT Research Team, 2006).
PSYCHOPATHOLOGY
SOCIAL BEHAVIOUR AND NETWORK THERAPY that acamprosate enabled twice as many clients to remain
abstinent 1 year later than did psychosocial therapy alone
This is a treatment aimed at mobilising and developing a (Swift, 1999). In addition, some drugs, such as ondanse-
positive social network for the client that will facilitate a tron, have been shown to be effective with early-onset
change in drinking behaviour (Copello, Orford, Hodgson, alcoholics who began drinking heavily before 25 years of
Tober & Barrett, 2002). The therapist works with both the cli- age (Johnson, Roache, Javors, DiClemente et a/., 2000).
ent and with those in the client's social network who are
willing to support the client’s efforts to change (such as fam- BRIEF INTERVENTIONS
ily, friends, work colleagues), and the aim is to create a sup-
portive social network that will sustain abstinence beyond Many people with alcohol-related problems frequently
the therapy period. Controlled receive brief periods of treatment, such as counsel-
social behaviour and network therapy outcome studies suggest that ling (five or fewer sessions). Such treatments are usually
(SBNT) A treatment aimed at mobilising social behaviour and _net- conducted by GPs, nursing staff or trained counsellors,
and developing a positive social network work therapy (SNBT) has and consist mainly of communicating alcohol-relevant
for the client that will facilitate a change in health advice, providing information on the negative
similar success rates to MET
drinking behaviour.
(UKATT Research Team, 2006). consequences of drinking, and practical advice on com-
munity resources that might help achieve moderation or
PHARMACOTHERAPY abstinence. Controlled trials in the US and Canada have
demonstrated that this approach significantly reduced
Drugs have been developed that attempt to block alcohol-related problems and increased use of healthcare
alcohol-brain interactions that might promote alcohol services (Fleming, Barry, Manwell, Johnson & London,
dependency. One of these is the drug naltrexone, which 1997; Israel, Hollander, Sanchez-Craig, Booker et al., 1996).
helps prevent relapse in those recovering from alcohol Brief interventions are particularly valuable for helping
dependency. Acamprosate has also been shown to be suc- those in the early stages of alcohol use who are at risk of
cessful as a treatment, with outcome studies suggesting developing full-blown alcohol use disorders.
Prevalence of use some individuals develop such problematic dependencies.

The lifetime prevalence rate for alcohol dependence is Alcohol use disorders are predicted by factors including:
around 12.5 per cent, and around 17.8 per cent for alcohol 1. a family history of alcoholism, suggesting that
abuse. Dependence is more prevalent among men than there may be a genetic component to the disorder
women, in younger and unmarried adults, and those in (see section 9.4.3), or that the offspring model
lower socio-economic groups (Hasin, Stinson, Ogburn & their drinking behaviour on those of their parents,
Grant, 2007). There are some ethnic differences in preva- or that parental drinking gives rise to stressful
lence rates, with white Americans being more likely to be childhood experiences that precipitate drinking in
diagnosed than black Americans, and rates of diagnosis the offspring (Sher, 1991; Windle & Searles, 1992),
are also inversely related to educational level. Alcohol
2. long-term negative affect, including neuroticism and
dependence and abuse is frequently associated with abuse
depression (Sher, Trull, Bartholow & Vieth, 1999),
of other drugs, and is highly comorbid with other psychi-
atric disorders. For example, heavy alcohol use is often 3. a diagnosis of childhood conduct disorder
part of polydrug abuse, or abuse of more than one drug (Johnson, Arria, Borges, Ialongo & Anthony,
at a time, and over 80 per cent of alcohol abusers are smok- 1995; Rohde, Lewinsohn & Seeley, 1995),
polydrug abuse Abuse of more than one

ers (Shiffman, Fischer, Paty, 4. experiencing life stress and particularly childhood
drug at atime. Gyns et al., 1994). life stressors (Wilsnack, Vogeltanz, Klassen &
Harris, 1997), and
The course of alcohol use disorders 5. holding beliefs that drinking alcohol will have a
Alcohol use disorders often pass through stages of favourable outcome (e.g. that it reduces tension
heavy and regular drinking, then on to alcohol abuse, and or makes social interactions easier) (Greenbaum,
finally end up in many Brown & Friedman, 1995),
alcohol use disorders Problematic cases as alcohol depend-
patterns of alcohol use leading to clinically
significant impairment or distress.
ence (Jellinek, 1952), and The costs of alcohol use disorders
these stages can be fairly In economic terms, alcohol-related problems cost the
clearly defined in Tim’s story given at the beginning of this US economy around $185 billion in 1998 in terms of
chapter. There are also several risk factors for alcohol use lost productivity, healthcare and other costs (National
disorders, and these might give us some insight into why Institute on Alcohol Abuse and Alcoholism, 2000).
Annual alcohol-related costs of crime and public disorder cigarettes, chewing tobacco, snuff, and in pipes and
in the UK in 2001 were estimated at £1.5 billion and work- cigars. Smoking tobacco actually delivers nicotine to
place costs to employers in 2007 were estimated at £7.3 the brain faster than if it were intravenously injected,
billion per year. Costs to the UK National Health Service and so is a highly efficient and effective way of expe-
alone are £2.7 billion per annum, including 1 in 26 NHS riencing the drug. Nicotine has a number of physical
bed days for alcohol-related health problems and up to 35 effects. First, it acts as a stimulant by increasing blood
per cent of all accident and emergency attendance costs pressure and heart rate. But, paradoxically, it also has
(WHO, 2004; Department of Health, 2008). Accidents a calming effect by reducing self-reported stress lev-
and crime are two of the biggest social problems associ- els and reducing the smoker’s feelings of anxiety and
ated with alcohol misuse. Drink driving accounts for 20 anger (Warburton, 1992). In survey studies, smokers
per cent of all driver road deaths in the UK, and a sig- usually endorse statements such as ‘Smoking relaxes
nificantly higher percentage in the US (Kennedy, Isaac & me when I am upset or nervous’ and ‘Smoking calms
Graham, 1996), and level of alcohol use is one of the best me down’ (Ikard, Green & Horn, 1969). However,
predictors of an individual being involved in recurrent nicotine does have a number of important negative
motor vehicle crashes (Fabbri, Marchesini, Dente, Iervese effects, and smokers regularly report adverse moods
et al., 2005). Alcohol also increases the risk of death from when they have not smoked recently, and periods of
boating accidents (Smith, Keyl, Hadley, Bartley et al., stress and irritability are commonly experienced in the
2001), and drownings (Bell, Amoroso, Yore, Senier periods between cigarettes or when attempting to quit
et al., 2001). In a review of the relationship between smoking (Hughes, Higgins & Hatsukami, 1990). These
drinking and health in a range of countries worldwide, characteristics suggest that nicotine is an addictive
Norstrom & Ramstedt (2005) found that per capita alco- drug that develops physical and psychological depend-
hol consumption in a country significantly predicted (1) ence. First, there is growing evidence to suggest that
mortality from liver cirrhosis and other alcohol-related nicotine has rewarding sensory effects caused by releas-
diseases, (2) mortality from accidents and homicide, and ing dopamine in the mesolimbic system of the brain
(3) death from suicide. (Stahl, 1996), and which acts through nicotinic recep-
Finally, alcohol use has come to be closely associ- tors to increase the firing rate of midbrain dopamine
ated with criminal and illegal activities, and violence neurons (Dani & De Biasi, 2013). The effects of dopa-
and abuse. In particular, alcohol consumption has mine release in this brain region are to elevate mood,
been found to be significantly related to violent crime decrease appetite, and enhance cognitive functioning
(Friedman, Glassman & Terras, 2001), rape and sexual generally, and these are consequences that are similar
assault (Merrill, Thomsen, Gold & Milner, 2001), and to the effects of other addictive drugs such as cocaine
child molestation (Aromacki & Lindman, 2001). (Stein, Pankiewicz, Hanch, Clo et al., 1998). Second, the
reported calming effect of nicotine may be mediated
Summary by more basic psychological processes representing the
Alcohol use disorders cause significant short-term and reversal of the unpleasant abstinence or withdrawal
long-term impairment, including impairment to occupa- effects experienced if the smoker has not taken nico-
tional, educational and social functioning, and they have tine in the recent past (known as the nicotine depriva-
important detrimental long-term effects on health. Alcohol tion model; Parrott, 1999). Interestingly, when asked to
use disorders are also closely associated with a range of report their moods over a normal day, smokers report
social problems, such as drink driving, violent crime, and significant fluctuations in moods, with reports of
criminal activities generally. It is still unclear why some normal moods during smoking and increased stress-
people acquire an alcohol dependence, although alcohol ful and irritable periods between cigarettes (Parrott,
use disorders are highly comorbid with other psychiatric 1994). Smokers’ stress levels appear to be similar to
disorders — including other substance abuse disorders. This non-smokers’ only just after having smoked, and become
suggests that, for many people, alcohol use may become worse than non-smokers during periods of abstinence
a means of coping with adverse or challenging life experi- or between cigarettes (Parrott 2006). This suggests that
ences because most alcohol users have an expectancy that smokers need to smoke simply to experience positive
drinking alcohol will have beneficial effects (e.g. reduce mood levels similar to non-smokers, and that the stress
tension, make social interactions easier). and irritability they experience between cigarettes are
withdrawal symptoms caused by their dependence on
nicotine (Schachter, 1978; Parrott & Murphy, 2012).
9.3.2 Tobacco Use Disorder
otine The addictive agent found in

Nicotine is the addictive Prevalence of use
acco; it acts as a stimulant by increasing agent found in tobacco, After alcohol, nicotine is the second most widely used
od pressure and heart rate. and is normally taken as drug worldwide, and kills up to half of its users (WHO,
+ ~
Wever OF
60 7 casionally
Percentages moked oe preinno =
be aa ;
50 44 = Aa
Ae =e
- — dk
aise
an
40
& 30-7 < AES

Pras
—i—- TS & _— 8 me <
. = is — _3—__-__¢-—4—»— 2 =
20 he seems
] X-SMOKe
10 7
0 + —y ait ea) a (a a Se. (ea Dara Fe et Me

i Granpe a earl
1982 1990 1992 1994 1996 1998 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010
Year
FIGURE 9.6 Cigarette smoking status among adults in England, 1982 and 1990-2010.
Source: From The Office for National Statistics (2012). General Lifestyle Survey 2010. Copyright © 2012, re-used with permission of The Office of
National Statistics.
2013). About one-third of the adult global population in many countries across the world, and was introduced
smokes and among teenagers aged 13-15 years world- in England in 2007. The effect of this legislation has been
wide, about one in five smokes. While the rate of smoking to significantly reduce exposure to second-hand smoke
is gradually falling in developed nations, it is rising by 3.4 (SHS exposure among children declined by nearly 70 per
per cent per year in the developing world (WHO, 2004), cent), to decrease the number of hospital admissions for
and nearly 80 per cent of the world’s 1 billion smokers cardiac problems, and it is associated with a statistically
live in low- and middle-income countries (WHO, 2013). significant increase in the number of smokers making an
Evidence suggests that around 50 per cent of those who attempt to quit (Bauld, 2011).
start smoking in their adolescent years will go on to smoke
for at least a further 15-20 years. Figure 9.6 shows that in Tobacco use disorder
England the number of smokers has decreased steadily The diagnostic criteria for tobacco use disorder are
since 1982, with around 20 per cent of adults still report- given in DSM-5 Summary Table 9.2, and associated fea-
ing smoking regularly in 2010. The level of use in those tures supporting diagnosis
tobacco use disorder A problematic
people who do smoke is also still unacceptably high, with include smoking within
pattern of tobacco use leading to clinical
male smokers reporting an average 13.3 cigarettes a day, 30 minutes of waking, significant impairment or distress.
compared with 12.1 a day for women (UK Government smoking daily, smoking
Statistics, 2010) — and these figures are worrying when more cigarettes per day, and waking at night to smoke.
we come to look at the adverse long-term health conse- When taken for the first time, nicotine may cause nau-
quences of smoking (see below). The overall decrease sea and dizziness, and it may have a more intense effect
in smoking prevalence since 1980 seems to be mainly when taken first thing in the morning. However, with
due to the increase in people who have never smoked or repeated use, these effects become significantly weaker
only occasionally smoked, with the proportion of adults as a tolerance to the drug builds up. Abstinence or
who have never smoked rising from 43 per cent in 1982 restricted access to nicotine produces a well-defined
to 55 per cent in 2010 (UK Government Statistics, 2010). withdrawal syndrome. This consists of dysphoric or
A quarter of children in the UK aged between 11 and 15 depressed mood, insomnia, irritability, frustration,
have tried smoking at least once and, in 2011, 5 per cent anger, anxiety, difficulty concentrating, restlessness and
of children were regular smokers. impatience, decreased heart rate, and increased appe-
It is worth noting that almost two-thirds of smokers tite or weight gain. A heavy smoker can exhibit these
in the UK said they wanted to give up, but over half said symptoms after only a few hours voluntary or enforced
it would be difficult to go without a cigarette for a day, abstinence (such as on an airplane journey).
and one of the main DSM-5 criteria for substance use dis- Using the DSM-IV nicotine dependence criteria, it is
order is repeated unsuccessful attempts to control use of estimated that the 12-month rate for tobacco use disor-
the substance. Finally, legislation prohibiting smoking in der in the US is around 13 per cent in adults, and has
workplaces and enclosed public areas is being introduced different prevalence rates in different ethnic groups,
DSM-5 SUMMARY TABLE 9.2 Criteria for tobacco use disorder with Native Americans being highest (23 per cent) and
Hispanics lowest (6 per cent) (DSM-5, 2013). Tobacco
° A pattern of tobacco use causing impairment or distress lead-
ing to at least two of the following within a 12 month period: use disorder is also found to be comorbid with a range
of other psychiatric disorders, with the most common
¢ Tobacco is taken in greater amounts or for longer than
being alcohol/substance use disorder, depressive, bipo-
was intended
od lar, anxiety and personality disorders, and ADHD (DSM-
e Acontinuing desire or unsuccessful efforts to control 5, 2013), with comorbidity ranging from 22 to 32 per
tobacco use
cent in these cases.
¢ Alot of time is spent in acquiring and using tobacco
¢ Craving, or a strong desire to use tobacco The costs of nicotine use
Like many addictive drugs, arguably the main costs
¢ Tobacco use results in a failure to fulfil major life roles at
work, home and so on of nicotine dependence are those to physical health.
Smoking is the single largest preventable cause of dis-
e Persistent tobacco use despite the effect on interper-
ease and premature death in the world and kills nearly 6
sonal, recreational or social interactions or despite hav-
ing an ongoing physical or psychological problem that
million people each year (WHO, 2013), and it is a signifi-
is likely to have been caused or made worse by tobacco cant factor in heart disease, stroke and chronic lung can-
cer, cancer of the larynx, oesophagus, mouth, bladder,
¢ Tolerance symptoms associated with high tobacco use
cervix, pancreas, and kidneys. In the UK, over 300,000
e Withdrawal symptoms associated with high tobacco use patients are admitted to NHS hospitals every year due to
vi QUITTING SMOKING
ry
=
Z As we have already noted, smokers find it extremely NICOTINE REPLACEMENT THERAPY (NRT)
hard to quit the habit - even though they may be fully
ire)
a aware of the health implications of their habit, and This aims to replace the nicotine from cigarettes by
m,) even when they themselves are already suffering from means of skin patches, chewing gum, lozenges, inhala-
=) smoking-related diseases. Since around 80-90 per tors or nasal sprays. Preliminary studies suggest that
UW
\@) cent of all smokers would meet DSM-IV-TR criteria for nicotine replacement therapy is significantly more
Eh substance dependence, successfully treating nicotine effective than a placebo, eeee
ee
Se
nicotine replacement therapy Aims

dependence is likely to need a range of approaches, and around 17 per cent
to replace the nicotine from cigarettes
including psychological and pharmaceutical. of people using NRT have by means of skin patches, chewing gum,
Smoking is difficult to treat because (1) smokers are fully abstained for 12 lozenges, inhalators or nasal sprays.
constantly suffering nicotine withdrawal symptoms months following the
when not smoking, and this drives the craving for further treatment (NICE, 2002).
cigarettes, and (2) smokers come to use cigarettes as a
way of dealing with any negative mood (not just those
associated with withdrawal), so any life problems that BUPROPION
cause negative affect will also trigger the desire to smoke.
For these reasons, treatment programmes for This is a mild antidepressant drug that acts as a selec-
smokers tend to have poor success rates and high tive inhibitor of dopamine and noradrenalin reuptake,
relapse rates, and only around 10-20 per cent of those and is thought to act directly on the brain pathways
who try to quit on their own are still abstinent a year involved in dependence and withdrawal. Bupropion
later (Lichtenstein & Glasgow, 1992). There are some is significantly more effective than a placebo con-
important predictors of whether an attempt to quit trol, and 19 per cent of those taking the drug had not
will fail, and these include (1) a diagnosis of major smoked in the 12 months following the treatment
depression (Glassman, 1993) - 50 per cent of smokers
who make repeated unsuccessful attempts to quit can
be diagnosed with major depression, (2) regular bouts
of negative mood which increase cigarette cravings, AVERSION THERAPY
and (3) whether the person has to spend periods of
time in environments where smoking is common and This treatment attempts to replace the pleasant feel-
cigarettes are readily available (e.g. pubs and bars). ings associated with smoking a cigarette with negative
Some of the main forms of intervention for smok- consequences such as feeling ill or nauseous. One form
ing are the following: of aversion therapy is known as rapid smoking, where |
PSYCHOPATHOLOGY
the smoker puffs on a cigarette roughly every 4-5 seconds COMPLEMENTARY THERAPIES
until they feel ill and cannot take another puff (Spiegler &
Guevremont, 2003). This type of treatment is known to Two forms of complementary therapy frequently used
reduce craving, but has had limited success at controlling by smokers in order to try and quit are hypnotherapy and
actual smoking behaviour (Houtsmuller & Stitzer, 1999). acupuncture. There is some evidence that hypnotic
and suggestion-based approaches do yield higher rates of
COGNITIVE BEHAVIOUR THERAPY (CBT) abstinence relative to waiting list and no treatment con-
trols, but there is little systematic evidence to suggest that
Because depression and negative mood appear to be fac- hypnotherapy is more effective than equivalent placebos
tors that are regularly associated with failure to quit smok- (Green & Lynn, 2000; Villano & White, 2004) — so those ‘stop
ing, recent treatments have adapted CBT of depression for smoking in one session’ signs outside your local holistic
use in smoking cessation programmes. In this case, CBT health centre might be somewhat misleading! There is
| is used to help smokers develop alternative strategies for some evidence that compared with control participants,
dealing with depression and negative mood that do not acupuncture can help smokers to reduce their levels of
involve a return to smoking. Such interventions have been smoking over a number of years (He, Medbo & Hostmark,
shown to produce higher rates of abstinence than stand- 2001). However, there is little more than anecdotal evi-
ard health education interventions (Hall, Reus, Munoz, dence that acupuncture is an effective means of quitting
Sees et al., 1998). smoking (Villano & White, 2004).
smoking-related diseases (Royal College of Physicians, respiratory infections and,asthma attacks (Cowley, 1992;
2002), and in the UK around 85,000 deaths were caused Skorge, Eagen, Eide, Gulsvik & Bakke, 2005). Across the
by smoking between 1998 and 2002. In 2011, around world it is estimated that 603,000 premature deaths
18 per cent of all deaths in the UK were estimated to occurred in 2004 as a result of passive smoking (WHO,
be attributable to smoking (The Health & Social Care 2010), although in the UK the introduction of legislation
Information Centre, 2011). It is also estimated that in 2007 banning smoking in workplaces and enclosed
around half of all teenagers who are currently smok- spaces has significantly reduced exposure to second-hand
ing will die from diseases caused by tobacco if they con- smoke (Bauld, 2011).
tinue to smoke. One-quarter will die before they reach
70 years of age and will lose, on average, 21 years of Summary
life (Peto, 1994). The economic cost of tobacco-related A significant number of regular smokers meet the diag-
health problems is staggering. In the UK, the treatment nostic criteria for nicotine dependence, which makes it
of smoking-related disorders was estimated to cost the an activity of concern for both clinical psychologists and
NHS around £5.2 billion in 2005/6 (The Health & Social medical doctors. In part, the smoking habit appears to be
Care Information Centre, 2011), including £127 million developed by the effect of nicotine on dopamine reward
to treat lung cancer alone (Parrott, Godfrey, Heather, pathways and maintained by the smoker’s need to reverse
Clark & Ryan, 2006). the unpleasant nicotine withdrawal effects that are expe-
Finally, the health hazards associated with smoking rienced between cigarettes or during abstinence. Tobacco
extend beyond those who smoke. Cigarettes give off use disorder does not have many of the short-term costs
smoke that contains a complex mix of thousands associated with alcohol dependence (such as impairment
of chemicals - many of which can have toxic effects if of occupational and social functioning), but it does have
inhaled. This, of course, represents a health risk to those significant medium- to long-term health costs, and is the
non-smokers who share environments with smokers, single largest cause of premature death worldwide.
and this is known as passive smoking from second-hand
passive smoking The breathing in ofair smoke. Just 30 minutes of
9.3.3 Cannabis Use Disorder
that contains other people's smoke. exposure to second-hand
smoke is enough to reduce The drug cannabis is derived
second-hand smoke A person's exhaled cannabis A natural drug derived from the
smoke, inhaled by another person. blood flow to the heart, from the hemp plant canna- hemp plant, cannabis sativa.
and non-smokers who are bis sativa. The most power-
exposed to second-hand smoke in the home have a 25 per ful of the cannabis group hashish The most powerful of the can-
nabis group ofdrugs.
cent increased risk of heart disease. In particular, passive of drugs is hashish, and
smoking is a substantial danger to health in the case a weaker derivative — known marijuana A derivative of cannabis consis
of babies and young children, causing increases in as marijuana — consists of ing of dried and crushed cannabis leaves.
. dried and crushed cannabis cannabinoid brain receptors CB1 and CB2 found in the
For a video on cannabis go to
www.wiley-psychopathology.com/ ) leaves. Cannabis is normally hippocampus, cerebellum and striatum (Ameri, 1999).
video/ch9 | smoked after being rolled These receptors appear to influence levels of dopamine
into a cigarette known as a in those brain areas known to play a role in mediating
‘joint’. However, it can also reward and pleasure experiences, and this seems to be
be eaten. The effects of cannabis are to produce feelings of the route by which cannabis has its most important posi-
relaxation (at low doses), euphoria, sociability and sharp- tive psychoactive effects.
ened perceptions that sometimes result in mild sensory Cannabis was used in the mid-20th century for its sup-
hallucinations (known as being ‘spaced out’), but it can also posed medicinal properties, which included its analgesic
cause difficulties in concentration and impairment of mem- effects (see Focus Point 9.3), but it was smoked mainly for
ory. Although it is primarily classified as a sedative /depres- pleasure. It is now an illegal drug in most countries even
sant because of its relaxing effects, it can sometimes also though its effects on behaviour and health are less severe
have stimulant effects, and make some individuals agitated than many other illicit drugs. There is some concern, how-
and paranoid. For example, when larger doses are taken, ever, that regular cannabis use may have permanent effects
cannabis may exacerbate an already frightened, stressed or on cognitive functioning, and psychological and physi-
paranoid state, causing anxiety and distress. Sensory distor- cal health (Kalant, 2004;
tions may also give the user feelings of depersonalization Iversen, 2005; Johns, 2001), For a video on the medical use of
similar to those experienced during panic attacks (see sec- but we will discuss the rel- | cannabis go to
tion 6.3), and some cannabis users become gripped by feel- evant evidence on these | video/ch9
ings of panic and anxiety. issues later in this section.“
The main active ingredient in cannabis is THC
(A’-tetrahydrocannabinol), and the amount of THC in Prevalence of use
cannabis will determine the strength of its psychoactive Cannabis remains the most widely used illicit substance
effects. THC is generally believed to have low addic- globally, with an estimated annual prevalence in 2010 of
tive properties, although it is still possible for regular 2.6-5.0 per cent of the adult population (between 119
cannabis users to become dependent on the drug (see million and 224 million users aged 15-64 years), and the
below). THC has a mild stimulant effect by increasing use of cannabis has increased significantly since the 1960s—
heart rate, and has its psychoactive effects by influencing especially in developed countries in North America,
. THE MEDICAL APPLICATIONS OF CANNABIS om

toy)
-
Long before it became an illegal drug, cannabis was studies that have employed double-blind randomized
= used primarily for medicinal purposes. It was known to controlled trials and placebo controls in patients with
o neuropathic pain or multiple sclerosis have demon-
Oo. have relaxing and analgesic effects, and was used in
Ww the 1970s to reduce the nausea and lack of appetite strated that cannabis reduced the severity of reported
=) caused by chemotherapy in cancer patients (Sallan, pain significantly more in the cannabis treated than in
U
2) Zinberg & Frei, 1975). Neurophysiological studies have the placebo group (Berman, Symonds & Birch, 2004;
ui, shown that cannabis has moderate analgesic effects, Zajicek, Fox, Sanders, Wright et al., 2003).
and these are caused by the active ingredient in can- Problems with the medical application of cannabis
nabis, THC, helping to block pain signals reaching the are (1) that it is still an illegal drug in most developed
brain (Richardson, Kilo & Hargreaves, 1998). These countries, and (2) smoking cannabis may not be the
analgesic effects are more powerful than codeine and healthiest way to take the drug given the potential
of longer duration. health risks associated with smoking (Mather, 2001).
Because of the potential medical applications of However, many governments are now licensing the
cannabis as a powerful analgesic, there have been sig- use of cannabis-based drugs for use with specific
nificant lobbies in many countries to legalize cannabis patient groups. For example, in 2005, the UK Home
for medical use. In a UK survey, individuals reported the Office licensed the drug Sativex for individual patient
medicinal use of cannabis with chronic pain, multiple use (such as those with multiple sclerosis, where can-
sclerosis, depression, arthritis, and neuropathy (Ware, nabis has been shown to ease stiffness, muscle spasms
Adams & Guy, 2005). Cannabis has also been involved and pain). Sativex avoids the problems of smoking by
in the treatment of patients with seizures, glaucoma, providing the active ingredients THC and cannabidol
asthma and anxiety (Mather, 2001). Recent outcome in a mouth spray.
300 PSYCHOPATHOLOGY
: > x
Western Europe and Australasia. In 2010, the annual DSM-5 SUMMARY TABLE 9.3 Criteria for cannabis use disorder
prevalence rate for cannabis use was highest in Oceania ¢ A pattern of cannabis use causing impairment or distress
(Australia and New Zealand) at 9.1-14.6 per cent, fol- leading to at least two of the following within a 12 month
lowed by North America (10.8 per cent), Western and period:
Central Europe (7 per cent), and West and Central Africa
e Cannabis is taken in greater amounts or for longer than
(5.2-13.5 per cent) (WHO, 2012). In the UK, cannabis has was intended
around 2-5 million regular users, with around 15 million
e Acontinuing desire or unsuccessful efforts to control
having admitted to using it (Atha, 2005). In the US and
cannabis use
Europe, cannabis use increased dramatically in the 1970s
and early 1980s, increased again during the 1990s, but has ¢ A lot of time is spent in acquiring, using and recovering
from the effects of cannabis
remained fairly stable since then (Johnston, O’Malley &
Bachman, 2001). However, cannabis use is concentrated ¢ Craving, or a strong desire to use cannabis
mainly among young adults (aged 15-34 years), with 20 ¢ Cannabis use results in a failure to fulfil major life roles
per cent of this age range in the UK admitting to can- at work, home and so on
nabis use in the previous 12 months (Department of e Persistent cannabis use despite the effect on interper-
Health, 2004). sonal, recreational or social interactions or despite hav-
ing an ongoing physical or psychological problem that is
Cannabis use disorder likely to have been caused or made worse by cannabis
Over the past few decades, the cannabis available on the ¢ Tolerance symptoms associated with high cannabis use
street has become stronger and in many cases THC con-
¢ Withdrawal symptoms associated with high cannabis use
tent has risen from 1—5 per cent to 10-15 per cent. As a
result, there is increasing evidence for a cannabis abuse
and dependence syndrome in many users. For example,
cannabis intoxication are often reported and the symp-
tolerance and withdrawal effects have been reported in
toms of intoxication after recent use of cannabis begin
some individuals who use cannabis regularly. Objective
with a ‘high’ feeling fol-
studies have indicated that cannabis can cause toler-
lowed by symptoms that cannabis intoxication Symptoms of
ance effects, and individuals who use cannabis daily over
include euphoria with inap- intoxication after recent use of cannabis
months or years may develop a need for more potent begin with a ‘high’ feeling followed by
propriate laughter and gran- symptoms that include euphoria with ina
forms of cannabis that would be toxic to most non-users
diosity, sedation, lethargy, propriate laughter and grandiosity, seda-
(Nowlan & Cohen, 1977). In heavy users, dependence
impairment in short-term tion, lethargy, impairment in short-term
is indicated by withdrawal during periods of absten-
memory, difficulty carrying memory, impaired judgment, distorted
tion, and these include flu-like symptoms, restlessness sensory perception and impaired motor
out complex mental pro- performance.
and irritability (Kouri & Pope, 2000). Symptoms usually
cesses, impaired judgement,
begin within 1-3 days after cessation of use and peak
distorted sensory perceptions, impaired motor perfor-
between days 2 and 6, and usually last a maximum of 14
mance, and the feeling that time is passing slowly (DSM-5,
days (Budney, Moore, Vandrey & Hughes, 2003).
2013, p.516). Occasionally, cannabis intoxication can be
Individuals who regularly use cannabis can develop
associated with severe anxiety, dysphoria and social with-
all the general diagnostic features of a substance use dis-
drawal. Cannabis use disorder usually develops over a
order, and DSM-5 provides a specific set of diagnostic
criteria for cannabis use disorder (see DSM-5 Summary period of time that is characterized by continuing
increased use and reduction in pleasurable effects.
Table 9.3). Cannabis use
cannabis use disorder Disorder usually
disorder is often the only
Studies have identified a number of risk factors for
develops over a period of time that is
developing cannabis dependence, and these include
characterized by continuing increased use substance use disorder
of cannabis and reduction in pleasurable experienced by an individ- 1. age of onset — the earlier that first use is recorded
effects.
ual, and they will often the higher the likelihood of cannabis dependence
report that it’s being used to cope with mood, sleep, (Taylor, Malone, Iacono & McGue, 2002),
pain, or other physiological and psychological prob-
2. tobacco smoking and regularity of cannabis use are
lems. In the US, the 12-month prevalence rate of can-
both independent predictors of cannabis dependence
nabis use disorder is approximately 3.4 per cent among
(Coffey, Carlin, Lynskey, Li & Patton, 2003),
12- to 17-year-olds, and 1.5 per cent amongst adults
(DSM-5, 2013). 3. impulsiveness and unpredictability of moods
An individual diagnosed with cannabis use disorder (Simons & Carey, 2002),
can spend much of their time daily acquiring and 4. a diagnosis of conduct disorder and emotional
smoking the drug and this may severely interfere with disorders during childhood (Meltzer, Gatwood,
family, school, work or recreational activities. Signs of Goodman & Ford, 2003), and
5. dependence on alcohol and other drugs accuracy are significantly affected after smoking canna-
(Degenhardt, Hall & Lynskey, 2001). bis (Kurzthaler, Hummer, Miller, Sperner-Unterweger et
al., 1999). Other studies have looked at the role of canna-
Like many substance use disorders, cannabis use dis-
bis use in drivers involved in accidents. For example, the
order is a risk factor for a number of other psychiatric active ingredient in cannabis, THC, is found in the blood
diagnoses, and these include anxiety and panic disorder of impaired or accident-involved drivers with a frequency
(Thomas, 1996), major depression (Chen, Wagner &
that significantly exceeds that in the general population
Anthony, 2002), increased tendency for suicide (Beautrais, (Kalant, 2004), and Scandinavian studies have indicated
Joyce & Mulder, 1999), and schizophrenia (Degenhardt & that 1 in 10 of drivers arrested for impaired driving tested
Hall, 2001). This once more begs the question of whether positive for cannabis (Christophersen, Ceder, Kristinsson,
individuals suffering psychological problems are likely Lillsunde et al., 1999; Steentoft, Muller, Worm & Toft,
to resort to cannabis use as a form of self-medication, 2000). However, we must still be cautious about what
or whether cannabis use is linked to a future increase in we conclude from these findings, because many of those
psychiatric diagnoses (Di Forti, Morrison, Butt & involved in car accidents are young risk-taking males who
Murray, 2007). The evidence on this is far from clear, are more likely to be using cannabis and other substances
although prospective studies indicate that (1) there is a (such as alcohol), so cannabis use may not necessarily be
causal link between regular cannabis use and the devel- the main cause of accidents in these groups.
opment of psychotic symptoms typical of schizophrenia We know that cannabis causes cognitive deficits while
(Fergusson, Horwood & Ridder, 2005; see also Focus the individual is under the influence of the drug, but does
Point 7.7), and (2) daily cannabis users may double their regular cannabis use cause long-term, permanent damage
risk of subsequently developing symptoms of anxi- to cognitive skills and achievement generally? First, canna-
ety and depression (Patton, Coffey, Carlin, Degenhardt bis use is associated with a syndrome of underachievement,
et al., 2002). Also, in a longitudinal New Zealand study, in which regular users exhibit lower IQ (Fried, Watkinson,
McGee, Williams, Poulton & Moffitt (2000) found that James & Gray, 2002), lower educational achievement
mental health problems at age 15 years were a predictor (Gruber, Pope, Hudson & Yurgelun-Todd, 2003), and moti-
of cannabis use at age 18 years, but that cannabis use at vational deficits (Lane, Cherek, Pietras & Steinberg, 2005).
age 18 predicted increased risk of mental health prob- However, there is very little evidence for permanent neu-
lems at age 21 years. While these studies tend to suggest ropsychological deficits in cannabis users (Gonzalez, Carey
that regular cannabis use indeed predicts increased risk & Grant, 2002), and any cognitive deficits found during
for subsequent mental health problems, the causal rela- cannabis use do not appear to persist after the individual
tionship may not be direct. For example, both heavy can- stops using the drug (Iversen, 2005). However, regular
nabis use and mental health problems are also associated heavy users are likely to have lower educational achieve-
with factors like low socio-economic status, childhood ment and lower income than non-users, but this may be
behavioural problems, parental neglect, and suchlike, due to a number of factors, including
and it may be these factors that act as causes of both can-
nabis use and subsequent mental health problems. 1. use of cannabis during school and college
years impairing educational performance and
The costs of cannabis use disorder subsequent career prospects,
We have just discussed the possibility that regular heavy 2. heavy cannabis use being associated with depri-
cannabis use may be associated with increased risk for a vation and poor educational opportunities, or
number of mental health problems such as anxiety, depres- 3. an amotivational syndrome in cannabis users, in
sion and schizophrenia. Such use is also associated with a which those who take amotivational syndrome A syndrome in
range of cognitive deficits and with health problems. up regular cannabis which those who take up regular cannabis
Regular cannabis use is associated with a range of cog- use are more likely to uSe are more likely to be those who exhibit
nitive deficits while individuals are under the influence be those who exhibit 2 athy loss of ambition and difficulty
; oe : , concentrating.
of the drug, and these include deficits in reaction time, apathy, loss of
decreased attention span, deficits in verbal ability, slower ambition and difficulty concentrating (Maugh, 1982).
problem-solving ability, and loss of short-term memory
(Lundqvist, 2005; Kalant, 2004). This has important impli- There is also some debate about whether regular can-
cations for cannabis users when complex psychomotor nabis use has long-term physical health consequences.
skills are required while engaging in potentially danger- First, cannabis generally contains more tar than nor-
ous activities. One such activity is driving, and there is mal cigarettes, and so presents a significant risk for
evidence that cannabis use does affect both driving skills smoking-related diseases such as cancer. Studies have
and driving safety (Smiley, 1999). Laboratory studies suggested that cannabis smoke can cause mutations
have demonstrated that perceptual and motor speed and and cancerous changes (Marselos & Karamanakos,
302 PSYCHOPATHOLOGY
1999), but there is only modest epidemiological evi- develop conditioned responses to drug-related stimuli
dence suggesting that cannabis users are more prone to (e.g. craving when seeing white powder) which contrib-
cancer than non-users (Sidney, Quesenberry, Friedman utes to relapse and treatment difficulties (Volkow, Wang,
& Tekawa, 1997; Zhang, Morgenstern, Spitz, Tashkin Telang, Fowler et al., 2006). The estimated 12-month
et al., 1999). Second, regular cannabis use does appear to prevalence of amphetamine-type stimulant disorders in
be associated with a reduction in the male hormone tes- the USA is 0.2 per cent among 12-17 year-olds and 0.2
tosterone (Grinspoon, Bakalar, Zimmer et al., 1997), and per cent among adults (DSM-5, 2013, p.564). Risk factors
there is a possibility that this could cause impaired sexual for developing stimulant use disorder include comorbid
functioning in the young males who are the main users bipolar disorder, schizophrenia, and antisocial personality
of cannabis. Third, chronic cannabis use does appear disorder. Childhood conduct disorder is also associated
to impair the efficiency of the body’s immune system with later development of stimulant-related disorders.
(Nahas, Paton & Harvey, 1999), although as yet there has
been no obvious effect of this found on the rate of physi- Cocaine
cal illnesses in cannabis users. Overall, the most probable Cocaine is a natural stimu-
adverse effects of cannabis on health generally include a lant derived from the coca For a video on cocaine go to
dependence syndrome, increased risk of motor vehicle plant of South America. video/ch9
crashes, impaired respiratory function, cardiovascular After it has been processed,
disease, and adverse effects on psychosocial development cocaine is an odourless,
and mental health (Hall & Degenhardt, 2009). white powder that can be injected, snorted or, in some
purer forms (e.g. crack cocaine), smoked (which is known
as free-basing). When used crack cocaine Free-based cocaine boiled
9.3.4 Stimulant Use Disorders for recreational purposes jit down into crystalline balls. q
is usually snorted and
Stimulants are substances that increase central nervous absorbed into the blood- free-basing The inhalation of cocaine b
system activity and increase blood pressure and heart rate. stream through the mucus smoking.
As a result, they facilitate alertness, provide feelings of membrane of the nose. The ‘rush’ caused by a standard
energy and confidence, and speed up thinking and behav- dose of cocaine takes approximately 8 minutes to take
iour. One of the drugs we have already discussed has stim- effect, and lasts for about 20 to 30 minutes. The ‘rush’ often
ulant effects, and that is nicotine. In this section, we will brings feelings of euphoria, and has its initial effects on the
discuss three more stimulant drugs, namely cocaine, brain to make users feel excited and energized. After these
amphetamine and caffeine. The popular recreational initial effects, the drug then affects other parts of the central
drug MDMA (3, 4-methyl- nervous system to produce increased alertness, arousal and
cocaine A natural stimulant derived from
the coca plant of South America which, enedioxymethampheta- wakefulness. The main effects of cocaine are caused by the
after processing, is an odourless, white mine) — better known as drug blocking the reuptake of dopamine in the brain. This
powder that can be injected, snorted or, in Ecstasy — is also a stimulant facilitates neural activity and results in feelings of pleasure
some forms (e.g. crack cocaine), smoked.
similar to amphetamine, and confidence (Volkow, Wang, Fischman, Foltin et al.,
but it also has hallucino- 1997) (see Focus Point 9.7 later in the chapter).
genic effects and will be dis-
amphetamines A group of synthetic
drugs used primarily as a central nervous
cussed later in this chapter. Prevalence of use The lifetime prevalence rate of
system stimulant. Common forms are Stimulant use is most cocaine use in developed countries is between 1 and 3
amphetamine itself (benzedrine), dextro- common among individu- per cent (WHO, 2006). In European countries this varies
amphetamine (dexedrine) and metham-
als aged 12-25 years, and between 0.5 and 6 per cent, with Spain and the UK being
phetamine (methedrine).
first regular use occurs at the upper end of this range (Department of Health,
on average at age 23 years 2004), and this rises to 14.4 per cent in the USA accord-
caffeine A central nervous system stimu-
lant that increases alertness and motor (DSM-5, 2013). Stimulants ing to the US National Household Survey of 2002. Use
are often first used for pur-
activity and combats fatigue; found in a of powder cocaine in the UK was stable at around 2.2
number of different products, includingposes such as controlling per cent between 2010 and 2012. Use by young adults
coffee, tea, chocolate and some over-the-
weight or to improve work aged 15-34 is around 4 per cent in the UK, with users
counter cold remedies and weight-loss
aids. or school performance, either discontinuing use after a brief period of experi-
and can be used daily or in mentation, or continuing to use it at weekends and in
‘binges’ in which high doses are used every hour or so. recreational settings (such as bars and clubs).
Addiction can occur very rapidly, and individuals using
amphetamines or cocaine can develop a stimulant use Cocaine use disorder Because the effects of cocaine
disorder as rapidly as in 1 week, and sufferers can often last only for around 30 minutes, there is a need for
frequent doses to maintain the ‘rush’ caused by the drug. dopamine neurons in the brain, leaving the casual user
This means the user may spend large sums of money on vulnerable to longer-term drug dependence (Ungless,
the drug in relatively short periods of time, and may even Whistler, Malenka & Bonci, 2001). Tolerance occurs with
resort to theft and fraud to obtain funds to buy the drug. repeated use, requiring larger doses and greater expense
Cocaine dependence occurs when the individual finds it for similar effects. When not taking cocaine, severe with-
difficult to resist using the drawal symptoms can occur, particularly hypersomnia,
caine dependence Occurs when the drug whenever it is availa- increased appetite, negative and depressed mood, and
vidual finds it difficult to resist using
» drug whenever it is available and leads
ble (the diagnostic criteria these increase the craving for further use or relapse dur-
neglect of important responsibilities. for cocaine use disorder ing abstinence. Erratic behaviour, social isolation and
are based on those in Table sexual dysfunction are regular characteristics of long-
9.1), and this in turn leads to neglect of important respon- term cocaine dependence, and the long-term user may
sibilities such as those associated with work or child care. well develop symptoms of other psychological disorders,
There is even some evidence from animal studies that a such as major depression, social phobia, panic disorder,
single exposure to cocaine induces long-term changes in generalized anxiety disorder, and eating disorders.

COCAINE DEPENDENCY
It all began in 1983 when | first starting doing cocaine. At it. It was a real social drug. |
For a video on cocaine: risk
first it was something that | did about once a week, usu- stopped doing it at bars, and
and recovery go to
ally on a Friday night and into Saturday. | would use it to would go back to the flat www.wiley-psychopathology.com/
go out to the bars and go drinking. | would buy a gram, and just lay around doing video/ch9
and usually there would be a little left over for Saturday coke all the time. My friend
morning. This went on for several months and as | came in shot his, | snorted mine. In desperation to make more
contact with more people who liked coke, | would start to money | expanded the territory that | was working and
split grams with people during the week. This increased would drive 80 miles to do service calls. |was doing about
until |was doing that every day. This took about a year to a gram a day; my friend was doing the same in his veins.
develop. | was fixing business machines and would col- My attitude in life became one of giving up and thinking
lect a little money every day. By the second year | would that | would die eventually, but that was OK, as long as |
buy coke at least once a day. | thought that | would try could do coke till | did.
selling it, to help with the costs, which were starting to
stack up. But, the coke | would buy would always end up Alan’s story
being snorted by myself and a couple of close friends. By

the third year nearly all of my money was going for coke.
Food became secondary to me and | would skip days’ eat- Clinical Commentary
ing to be able to afford coke. | started to hang out with a Like many people, Alan began using cocaine as a
guy who shot his coke up with needles. We became best recreational drug, taking it mainly at weekends
friends. |would fix a machine and he would be waiting for and when socialising in bars. Because the drug has
me in my car. We would instantly go and buy coke with a relatively brief ‘high’ (around 30 minutes), users
the money that | had just made, occasionally stopping require more and more regular doses in order to
somewhere for a sandwich, which was all that | would be maintain the euphoria generated by cocaine,
eating by that time. and the cost of this leads to significant financial
This went on until | was made homeless but we man- problems. As is typical of individuals with cocaine
aged to get a cheap flat to share. | started to get con- dependency, Alan began to neglect his responsi-
cerned that | had a habit that | could not kick. |saw many bilities, including failing to pay bills and losing his
people wreck their lives during this period. In fact my busi- home. Eventually, psychological dependency was
ness was in serious trouble as | never paid my bills. Part of complete when his life revolved entirely around
the problem was that coke was really ‘the’ thing to do in acquiring and taking the drug.
this town at the time. Seemed everyone | knew was into
304 PSYCHOPATHOLOGY
The costs of cocaine use disorder Apart from the forms are amphetamine itself (benzedrine), dextroam:
negative effects of regular use on occupational, social phetamine (dexedrine), and methamphetamine (meth-
and educational functioning, cocaine also has a num- edrine). These are highly addictive drugs that are used
ber of adverse cognitive and health effects. For exam- primarily to generate feelings of energy and confidence,
ple, cocaine abusers regularly show evidence of deficits and to reduce feelings of weariness and boredom. They
in decision making, judgement and working memory were originally synthesized in the 1920s as an inhalant
(Simon, Domier, Sim, Richardson et al., 2002; Pace- to aid breathing, but came to be used later as a means of
Schott, Stickgold, Muzur, Wigren et al., 2005), and there appetite control and to combat feelings of lethargy and
is evidence from animals studies that regular cocaine use depression. When used in small doses, amphetamines
also disrupts learning — although it is still unclear whether enable individuals to feel alert, confident and energised.
these effects are permanent deficits caused by cocaine They also help motor coordination but, contrary to pop-
use (Kantak, Udo, Ugalde, Luzzo et al., 2005). There is ular belief, do not help intellectual skills (Tinklenberg,
also accumulating evidence that cocaine use by pregnant 1971). They also have a number of physical effects, such
mothers can also cause significant developmental defi- as increasing blood pressure and heart rate, but can cause
cits in their newborn offspring, and this is manifested as headaches, fevers, tremors and nausea.
retarded development in the first 2 years of life (Singer, Amphetamines have their effects by causing the
Arendt, Minnes, Farkas et al., 2002), a higher incidence release of neurotransmitters norepinephrine and dopa-
of attention deficit hyperactivity disorder (ADHD) at age mine, and simultaneously blocking their reuptake. They
6 (Linares, Singer, Kirchner, Short et al., 2006), and defi- are normally taken in a pill or capsule form, but in the
cits in visual motor development (Arendt, Short, Singer, case of methamphetamine it can be taken intravenously
Minnes et al., 2004). At least a partial cause of these effects or by ‘snorting’. In its clear, crystal form, the latter is
may be the role of cocaine in causing irregularities in pla- known as ‘ice’, ‘crank’ or.‘crystal meth’, and dependence
cental blood-flow during pregnancy. Finally, because of on methamphetamine can be particularly rapid. With
its effects on blood pressure and cardiovascular function- the use of higher doses, and during withdrawal, users
ing, high doses of cocaine can cause heart problems and experience a range of negative symptoms, including
brain seizures, although it is unusual for death to be solely anxiety, paranoia, irritability, confusion and restlessness
attributed to cocaine abuse. However, cocaine may be an (Kaplan & Sadock, 1991).
important contributor to death by aggravating existing
cardiovascular problems (e.g. arrhythmias, heart attacks, Prevalence of use Amphetamine use in the UK
cerebral haemorrhages). In a UK study, 30.4 per cent of is around 2 per cent, and has fallen significantly since
112 regular male cocaine users with an average age 1996 (Home Office, 2012). Worldwide, amphetamine-
of 44 years showed evidence of coronary artery aneu- type stimulants (excluding Ecstasy) had an estimated
rysms, compared with only 7.6 per cent of non-cocaine prevalence of 0.3-1.2 per cent, and is the second most
users (Satran, Bart, Henry, Murad et al., 2005), indicating widely used group of drugs (WHO, 2012). According
an important and significant increase in cardiovascular to DSM-IV-TR, the lifetime prevalence of amphetamine
disease in regular cocaine users. use disorders is around 1.5 per cent. The World Health
Organisation estimates that there are between 14 million
Amphetamines and 52.5 million estimated global users, and ampheta-
Amphetamines are a group of synthetic drugs used pri- mine-type stimulants account for around 16 per cent of
marily as a central nervous system stimulant. Common worldwide illicit drug abuse.
e .
boy)
-
On December 11,2002,The Who bassist John Entwistle
= died after taking cocaine that caused his already dis-
Oo Clinical Commentary
a. eased heart to fail. The 57-year-old was found dead in
WV There are few deaths that are directly attributa-
a hotel room in Las Vegas when the band was about
ee} to embark on a US tour. Doctors reported evidence of
ble to cocaine use, but cocaine is known to exac-
U erbate already existing cardiovascular problems
o high blood pressure and high cholesterol, which had
because of its effect on blood-pressure levels and
LL. been compounded by smoking. The coroner recorded
heart rate.
that cocaine in his body had compounded heart dis-
ease that was already present.
wy ‘BATH SALTS’
Or
-
= The stimulant effects of bath salts are thought to
occur by raising dopamine levels in the brain circuits
2)
a that regulate reward and movement. Until recently,
VW) bath salts were cheap and legal in many countries,
==)
U but they were placed under an emergency ban by the
Oo US Drug Enforcement Administration in 2011, and all
LL. cathinone substitutes were made illegal in the UK in
2010. They have been linked to a surge in visits to acci-
dent and emergency units with common complaints
being cardiac symptoms (chest pains, high blood pres-
Images
Association
AP/Press
©
sure) and psychiatric symptoms such as paranoia, hal-
‘Bath salts’is the name for an emerging group ofdrugs lucinations and panic attacks.
containing synthetic chemicals related to cathinone - Being such anew group ofdrugs, it is difficult to esti-
which is an amphetamine-like stimulant found in mate the prevalence of bath salts use, but retrospec-
the khat plant. These synthetic cathinone’s can pro- tive hair sample studies of individuals who had tested
duce euphoria and increased sociability and sex drive positive for amphetamines or MDMA in 2009/10 found
(Prosser & Nelson, 2012). Typically they are in the form psychoactive substances similar to cathinone synthet-
of a white or brown crystalline powder, and are taken ics in 37 per cent of these samples (Rust, Baumgartner,
orally, inhaled or injected. Dally & Kraemer, 2012).
Amphetamine use disorder Although the effects of followed by stereotyped, repetitive behaviour, anger,
amphetamine are longer lasting than other stimulants, physically aggressive behaviour, and impaired judge-
such as cocaine, tolerance to amphetamine occurs rap- ment. Physical symptoms of intoxication include pupil-
idly and higher and higher doses are needed to achieve lary dilation, perspiration or chills, nausea or vomiting,
similar stimulant effects (Comer, Hart, Ward, Haney chest pains and, in extreme cases, seizures or coma.
et al., 2001). Once high dose usage is achieved, the stimu- Withdrawal symptoms can appear within a few hours or
lant effects of amphetamine also become associated with a few days of ceasing use of amphetamine, and is associ-
intense, but temporary, psychological symptoms such as ated with depression, fatigue, vivid and unpleasant
anxiety, paranoia, and psychotic episodes resembling dreams, insomnia, and increased feelings of agitation.
schizophrenia (see below). Those who are dependent on
methamphetamine (so-called ‘speed freaks’) will often The costs of amphetamine use disorder A num-
use the drug continuously ber of studies using both human and non-human partici-
thamphetamine Methedrine, a com-
for a number of days, pants have suggested that regular use of amphetamines
n form of amphetamine.
experiencing a continuous (especially methamphetamine) may cause long-term
‘high’ without eating or sleeping. This will then be fol- central nervous system damage (Frost & Cadet, 2000;
lowed by a few days feeling depressed and exhausted, but Volkow, Chang, Wang, Fowler et al., 2001). Volkow et al.
then the cycle starts again. Speed freaks who behave in (2001) found that chronic methamphetamine use inhib-
this way become unpredictable, anxious, paranoid and ited the production of the neurotransmitter dopamine in
aggressive, and may be a danger to themselves and oth- the orbitofrontal cortex, and this may play a significant
ers. Dependence is indicated by regular use of the drug role in maintaining addictive behaviours. For example,
whenever it is available, neglect of normal responsibili- the orbitofrontal cortex is associated with compulsive
ties associated with work or family, and continuing use behaviour and with resistance to extinction of a behav-
when the individual is aware that using the drug is caus- iour even when rewards are withdrawn. These effects
ing family or employment problems. Amphetamine are very similar to those reported by drug addicts who
intoxication normally claim that once they start using a drug such as metham-
phetamine intoxication begins with a ‘high’ fol- phetamine they cannot stop — even when the drug is no
phetamine use, which normally lowed by feelings of longer pleasurable. There is also evidence from animal
jins with a ‘high’ but is equally likely studies showing that chronic use of methamphetamine
e followed by stereotyped, repetitive
euphoria, energy, talka-
laviour, anger, physically aggressive tiveness, and alertness — damages both dopamine and serotonin neurotransmit-
laviour, and impaired judgement. but is equally likely to be ter systems in the brain (Frost & Cadet, 2000), and this
: :
effect appears to be reflected in slow or poor decision- substances includes alcohol (see section 9.3.1), the opi.
making in individuals with methamphetamine use disor- ates and their derivatives (heroin, morphine, methadone
der (Paulus, Tapert & Schuckit, 2005). and codeine), and synthesized tranquilizers such as bar-
biturates. This group of
barbiturates A class of sedative drugs
Caffeine drugs has a number of det- related to a synthetic compound (barbitu
Most readers of this book are probably familiar with rimental effects on regular ric acid) derived from uric acid.
taking caffeine in one form or another — as are around users, including rapid tol-
85 per cent of the population of the world. Caffeine erance effects, severe withdrawal symptoms, and high
can be found in a number of different products, includ- doses can cause disruption to vital bodily functions.
ing coffee, tea, chocolate, and some over-the-counter
cold remedies and weight-loss aids. Caffeine is a central Opiates
nervous system stimulant that increases alertness and The opiates consist of opium — taken from the sap of the
motor activity and combats fatigue. However, it can also opium poppy — and its derivatives, which include mor-
reduce fine motor coordination and cause insomnia, hine, heroin, codeine and
ee ‘ Opiates Opium, taken from the sap of the
headaches, anxiety and dizziness (Paton & Beer, 2001). methadone. In the 1800s, opium poppy. Its derivatives include mor-
Caffeine enters the bloodstream through the stomach opium was used mainly to _ phine, heroin, codeine and methadone.
and increases brain dopamine levels in a similar way to treat medical disorders,
amphetamine and cocaine. Caffeine in the body reaches because of its ability to relax the patient and reduce both
its peak concentration within an hour, and has a half-life physical and emotional pain. Both morphine and heroin
of 6 hours, which implies that if you have a cup of coffee were new drugs derived from opium during the late 1800s
at 4 p.m. that contains 200mg of caffeine, you will still and early 1900s. Both were used as analgesics, but over
have around 100mg of caffeine in your body 6 hours later time it became apparent that both were highly addictive,
at 10 p.m. So while caffeine may have beneficial short-term and even after having been successfully treated with mor-
effects on alertness, it may have detrimental longer phine or heroin, patients were unable to give up using
term effects which may prevent you from sleeping. The them. Finally, a synthetic form of opium, called metha-
average caffeine intake per day in most of the developing done, was developed by the Germans during World War
world is less than 50mg, compared with highs of 400mg in II. Unlike the other opiates,
methadone A synthetic form of opium.
the UK and other European countries. It is taken more by methadone can be taken
men than women, and caffeine intake usually decreases orally (rather than injected) and is longer lasting. Heroin
with age, with older people showing more intense reac- is currently the most widely abused of the opiates. It is
tions and reporting greater interference with sleep. purchased in a powder
heroin A highly addictive drug derived }
Although caffeine consumption is almost a daily form and is normally taken from morphine, often used illicitly as a
occurrence for most people, it can have both positive by injection usually directly narcotic. 4
and detrimental effects. On the positive side, the bene- into a vein (known as
fits of moderate caffeine intake are increased task focus ‘mainlining’). In contrast, ,
For a video on heroin go to
through alertness, attention and cognitive function, and methadone is frequently | www.wiley-psychopathology.com/
also elevated mood and fewer depressive symptoms used as a replacement drug § video/ch9
and lower risk of suicide. However, high doses of caf- for heroin abusers because
feine can induce psychotic and manic symptoms, and, of its slow onset and weaker effects.
most commonly, anxiety (Broderick & Benjamin, 2004). In the 1990s, heroin became the recreational drug of
These anxiety-generating effects of high doses of caf- choice for many in Europe and the USA. Most opiates
feine make individuals with panic disorder and social and their derivatives cause drowsiness and euphoria.
anxiety disorder particularly vulnerable to their effects In addition, heroin gives a feeling of Ecstasy immedi-
(Lara, 2010). Research on the effects of regular caffeine ately after injection (known as a ‘rush’, which lasts for
intake has increased significantly in recent years, and has 5-15 minutes). For about 5—6 hours after this rush, the
led to the inclusion of caffeine use disorder as a research user forgets all worries and stresses and experiences feel-
diagnosis in DSM-5 (DSM-5, 2013, pp.792-793). ings of euphoria and heightened well-being, and loses all
negative feelings. However, as with many other drugs,
individuals who regularly use heroin rapidly develop tol-
9.3.5 Sedative Use Disorders erance effects and experience severe withdrawal symp-
toms that begin about 6 hours after they have injected
Sedatives are a central nervous system depressant, and the dose.
slow the activity of the body, reduce its responsiveness, Opiates have their effects by depressing the central
and reduce pain, tension and anxiety. This group of nervous system, and the drug attaches to brain receptor,
CHAPTER 9 SUBSTANCE USE DISORDERS 307°
sites that normally receive endorphins and stimulates found that use of heroin controlled drug user A long-term drug
these receptors to produce more endorphins (Gerrits, in this subgroup had user who has never been in specialized
Wiegant & Van Ree, 1999). Endorphins are the body’s relatively few health risks, treatment and who displays levels of
occupational status and educational
natural opioids, and release and suggested the terms achievement similar to the general
dorphins The body’s natural opioids. of these neurotransmitters controlled drug user or population.
> release of these neurotransmitters acts
acts to relieve pain, reduce unobtrusive heroin user
elieve pain, reduce stress and create
asurable sensations. stress, and create pleasura- to describe them. There is unobtrusive heroin user A long-term
ble sensations. other evidence that opiate heroin user who has never been in special-
ized treatment and who displays levels
use need not necessarily of occupational status and educational
Prevalence of use The estimated worldwide annual lead to long-term dep- achievement similar to the general
prevalence of opiate use in 2010 was 0.3-0.5 per cent endency. Some theorists population.
of the population aged between 15-64 (around 13 to 21 believe that opiate drug
million people). North America (3.8-4.2 per cent), use is linked to life stressors, and if these stressors are
Oceania (2.3-3.4 per cent), and Eastern and South- temporary, then so will be the drug use (Alexander &
Eastern Europe (1.2-1.3 per cent) are the regions with Hadaway, 1982). In support of this view, many US sol-
the highest prevalence rates (WHO, 2012). In the UK diers became regular heroin abusers during the Vietnam
there has been a decrease in opiate drug use in recent War, but relatively few continued to use the drug once
years, but in 2009/10 there were an estimated 306,000 they had returned home Geen pelleapie noes is
opiate or crack cocaine users aged 15 to 64 in England. undoubtedly a dangerous ne . }
For a video on opioid use
drug, it does appear that | disorder go to
Opioid use disorder Most opiate users build up a some people, in some cir- www.wiley-psychopathology.com/
tolerance to the drug quickly, and have to use larger and cumstances, can effectively video/ch9
larger doses to experience equivalent physical and psy- manage and regulate their
chological effects. Also associated with repeated use are use of the drug without problems (Warburton, Turnbull
severe withdrawal effects. In the case of heroin, with- & Hough, 2005).
drawal symptoms will begin around 6 hours after injec-
tion, and without further doses the user will experience The costs of opioid use disorder Apart from the
a range of aversive withdrawal symptoms. These will severe withdrawal symptoms experienced after drug
begin with feelings of anxiety, restlessness, muscle aches, use, there are a number of risks that regular opiate users
increased sensitivity to pain, and a renewed craving for face. These include (1) the risk of accidental overdose if
the drug. More severe withdrawal is associated with inexperienced users fail to properly dilute pure forms of
muscle aches, insomnia and fever. Acute withdrawal heroin for use, (2) being sold street heroin that contains
symptoms for heroin usually peak within 1-3 days and potentially lethal additives, such as cyanide or battery
will subside over a period of 5—7 days. Opioid use disor- acid, and (3) the risk of contracting human immunodefi-
der is often difficult to treat because of the severe with- ciency virus (HIV) or hepatitis from sharing unsterilized
drawal symptoms experienced by sufferers. It is also needles. The number of deaths from opiate overdoses in
frequently associated with the UK more than doubled between 1993 and 2000, and
ioid use disorder The development of
erance to opiates, in which the user has
a history of drug-related in a long-term US study of heroin addicts, 28 per cent
use larger and larger doses to experi- crimes (e.g. possession or had died before the age of 40. Interestingly, only one-
ce equivalent physical and psychological distribution of drugs, third of these deaths were from overdose, and over half
ects. Also associated with severe with- forgery, burglary). Marital were from homicide, suicide or accident (Hser, Anglin &
wal effects.
difficulties and unemploy- Powers, 1993). The high cost of opiate drugs such as her-
. ment are often associated oin also leads regular users into illegal activities to raise
To read the article on heroin use by
i with opioid use disorder at money for their dependence, and the most common of
Shewan & Delgarno go to
www.wiley-psychopathology.com/ _ all socio-economic levels these are theft, fraud and prostitution. Heroin use is also
reading/ch9 (DSM-5, 2013). However, highly associated with crime generally, with regular drug
many users seem able to users being three to four times more likely to commit
use opiates such as heroin as a periodic recreational drug a criminal offence than non-users (Bennett, Holloway
and continue to lead reasonably functioning lives in the & Farrington, 2008), and the Home Office estimated
interim. For example, a Scottish study of long-term her- that, in the mid-1990s, around 20 per cent of all peo-
oin users who had never been in specialized treatment ple arrested in the UK were taking heroin. So while we
revealed that they had levels of occupational status and reported earlier that it is possible for some heroin users
educational achievement similar to the general UK popu- to live reasonably normal lives, there are still significant
lation (Shewan & Dalgarno, 2005). Shewan & Delgarno risks to the life and health of many opioid users.
308 PSYCHOPATHOLOGY
9.3.6 Hallucinogen-Related Disorders focus their attention on very small details in their envi-
ronment. Advocates of the drug claim that this height-
Psychoactive drugs, or hallucinogens, have their effects by ened perception can open up. new states of awareness
changing the user’s perceptions. They may either and allow the user to become more enlightened about
sharpen the individual’s sensory abilities or create sen- the world and themselves. However, because of its sen-
sory illusions or hallucinations. Unlike stimulants and sory enhancing properties, LSD can also cause hallucina-
sedatives, they have less significant effects on arousal lev- tions, including distorted perceptions of space and time
els, and are less addictive than these other two classes of (Kaplan & Sadock, 1991), perceiving people and objects
substances. In this section we will discuss in detail that are not present, and enabling the user to believe
two hallucinogen drugs — they have attributes that they in fact do not possess. On
lysergic acid diethylamide (LSD) A hal-
lucinogenic drug that produces physical
namely, lysergic acid a number of occasions, this latter effect has had danger-
effects including dilated pupils, raised diethylamide (LSD) and ous consequences when users who believe they have the
body temperature, increased heart rate the combined hallucino- power of flight have thrown themselves out of upper-
and blood pressure, sweating, sleepless- gen and stimulant MDMA,
ness, dry mouth and tremors.
storey windows.
or Ecstasy as it is better The awareness-enhancing properties of LSD can
known, a substance that also have negative consequences. If the user is feeling
MDMA MDMA (3,4-methylenedioxymeth-
amphetamine), the drug Ecstasy. has become an important anxious or stressed after having taken LSD, these feel-
recreational drug over the ings can be exaggerated to the point where the indi-
past two decades. Other common hallucinogenic drugs vidual can experience extreme terror or panic. Such
include the phencyclidines, which include PCP, ‘angel experiences are known as ‘bad trips’, and these feelings
phencyclidines Group of common hallu- dust’, and less potent com- subside as the dose wears off. However, regular users
pounds such as ketamine,
cinogenic drugs, which includes PCP, ‘angel can come to experience what are known as ‘flashbacks’.
dust’ and less potent compounds such as cyclohexamine and dizo- These are a vivid re-experiencing of a ‘trip’ that can
ketamine, cyclohexamine and dizocilpine.
cilpine. The phencycli- occur days, months or even years after the actual LSD
dines produce feelings of separation from mind and trip (Abraham & Wolf, 1988).
body in low doses, and stupor and coma at high doses, LSD appears to have its affects by influencing neu-
and the rising use of some phencyclidines, such as keta- rons in the brain that normally control visual informa-
mine, has led to the inclusion of ‘Phencyclidine Use tion and emotion, and it does this by affecting the levels
Disorder’ as a diagnostic category in DSM-S5. of the neurotransmitter serotonin in these brain areas
(Goodman, 2002).
EYSEEGIC acid
Ss e.dhethylamine (LSD)
_ LSD is an hallucinogenic
For a video on LSD go to
drug that was first synthe- Prevalence of use In the US and Europe, use of
video/ch9 sized by the Swiss chemist LSD peaked during the 1960s and 1970s and has been
. Albert Hoffman in 1938. gradually declining ever since as stimulant drugs such
LSD was sustain first of the widely used psyche- as cocaine and amphetamines became the recreational
delic drugs, and came to be fashionable as a ‘mind- drug of choice. In the UK, the use of LSD has declined
expanding’ drug associated with the social changes from 4 per cent in 1996 to 0.5 per cent in 2011/12
and experimentation dur- (Home Office, 2012). In the USA, the 12-month preva-
psychedelic drugs Consciousness-
ing the 1960s and 1970s. lence rate for LSD use in adults was 0.3 per cent in
expanding or mind-expanding drugs.
LSD, commonly referred 2011, a figure that has also been declining significantly
to as ‘acid’, is sold on the street in tablets, capsules and, over the past 20 years (National Institute on Drug
occasionally, liquid form. It is odourless, colourless, has a Abuse, 2012).
slightly bitter taste and is usually taken orally. Often LSD
is added to absorbent paper, such as blotting paper or to
sugar cubes. The drug starts to take effect around 30 LSD abuse and dependence While LSD is not
to 90 minutes after taking it, and physical effects include generally considered to be a physically addictive drug,
dilated pupils, raised body temperature, increased heart its regular use can still foster dependence. Hallucinogen
rate and blood pressure, sweating, sleeplessness, dry use (such as LSD or MDMA) is normally restricted to
mouth, and tremors. just two to three times per week in regular users, but
LSD produces sharpened perceptions across a variety cravings for the drug have been reported after individu-
of senses. Colours can be enhanced and users come to als have stopped using it. Because most hallucinogens
have an extended duration of action and a long half-life, Prevalence of use Global use of Ecstasy-group
individuals with hallucinogen use disorder can spend many substances is estimated at 0.2-0.6 per cent of the adult
hours and even days recovering from the effects of the population (between 10.5 and 28 million users) and is at
drug, and some hallucinogens — such as MDMA - are comparable levels to cocaine use (WHO, 2012). There
often associated with physical ‘hangover’ symptoms that was some evidence that usage was declining, but most
occur the day after use. recent evidence suggests a possible resurgence of Ecstasy
use in Europe and the USA. In the UK, there were esti-
mated to be around 0.2 million Ecstasy users in 2011/12,
The costs of LSD use The effects of LSD are gener-
ally unpredictable and prior to use the individual will not although the number of users had fallen from 1.8 per
know whether or not they will experience a ‘bad trip’. If cent of the population in 2000 to 1.4 per cent in 2011/12.
a large dose is taken, this can cause hallucinations and
sensory changes that can make the user frightened, can
Ecstasy regular use Regular users of Ecstasy can
cause panic, and can make the individual think they are
spend many hours and even days recovering from the
going crazy. Although LSD is not considered an addictive
effects of the drug, and hallucinogens such as MDMA
drug, it can have tolerance effects, where regular users
are often associated with physical ‘hangover’ symptoms
have to take larger and larger doses to achieve similar
that occur the day after use. Symptoms of MDMA hang-
effects. In a small number of individuals, regular use can
overs include insomnia, fatigue, drowsiness, headaches,
be associated with psychiatric disorders such as psychotic
and sore jaw muscles resulting from teeth clenching.
symptoms or chronic depression. However, it is unclear
Such symptoms will inevitably interfere with normal
whether such individuals already had underlying psy-
occupational and social functioning for some time after
chiatric problems prior to their regular use of the drug,
drug use. There are no recent figures for Ecstasy-related
and, as we have described elsewhere, regular drug use
substance abuse disorders, but Ecstasy users do appear
can tend to become heavy and regular in individuals with
to be at high risk of substance use disorders — if not with
pre-existing psychiatric problems.
MDMA, then with other substances such as cannabis,
opioids and sedatives (Wu, Parrott, Ringwalt, Patkar
Ecstasy et al., 2009).
Most readers will by now be aware of the drug MDMA
(3,4-methylenedioxymethamphetaime) — better known
as the ‘clubbing drug’ Ecstasy. Over the past two dec- The costs of Ecstasy use There are also a number
ades, Ecstasy has become of dangers associated with regular Ecstasy use, and
For a video on Ecstasy go to ) the drug of choice for these include the following: (1) the drug causes severe
| those regularly attend- dehydration and this can cause heat stroke in hot envi-
video/ch9
' ing dance parties, raves ronments such as raves or nightclubs. Even trying to
or nightclubs. It is usually counteract these effects by increasing fluid intake can
tasy An illegal amphetamine- taken in pill form and acts cause hyponatremia or water intoxication (Braback
ed synthetic drug with euphoric
as both a stimulant and hal- & Humble, 2001); (2) as a stimulant, Ecstasy increases
acts. Also known asMDMA r
L-methylenedioxymethamphetamine). lucinogen. It gives the user heart rate and blood pressure, and this can be poten-
added energy to continue tially dangerous for users with existing cardiovascular
partying, and elevates mood. Ecstasy has its effects by problems; and (3) Ecstasy is known to be a selective
releasing the neurotransmitters serotonin and dopamine neurotoxin that destroys the axons to which serotonin
(Malberg & Bronson, 2001). Elevated levels of serotonin would normally bind (Ricaurte, Yuan & McCann, 2000).
generate feelings of euphoria, well-being and sociability, Because of this, Ecstasy is thought to cause a range of
and sounds and colours are experienced more intensely long-term problems including memory deficits, verbal-
(high levels of brain serotonin are also found in individu- learning deficits, sleep problems, lack of concentration
als with bipolar disorder experiencing a manic phase). and increased depression and anxiety (Reneman, Booij,
Effects can be experienced within around 20 minutes of Schmand, Brink et al., 2000; Jansen, 2001). More recent
taking the dose and will last for around 6 hours. However, research and reviews have supported this, with evidence
high levels of brain dopamine can cause psychotic in particular that Ecstasy users score lower on measures
symptoms, such as paranoid thinking and confusion, of executive functioning and working memory, particu-
and these are symptoms often experienced by regular larly updating, attention shifting and access to long-term
Ecstasy users. memory (Verbaten, 2010).
‘3108 PSYCHOPATHOLOGY
SELF-TEST QUESTIONS
Can you name the main groupings into which drugs of abuse are categorized?
9.3.1 Alcohol Use Disorder

How is binge drinking defined, and how prevalent is it amongst young people?
How does alcohol make the drinker feel relaxed and less stressed?
What are the main symptoms of withdrawal from alcohol in heavy drinkers?
Can you name the main criteria for alcohol use disorder?
What are the main risk factors for alcohol use disorder, and can any of them be identified as causal factors?
Can you name three physiological risks associated with heavy alcohol drinking?
Can you list the economic and health costs of alcohol use disorders?
9.3.2 Nicotine Use Disorder

What are the main physical effects of nicotine?
Can you describe the main features of the nicotine withdrawal syndrome?
Can you explain why people start and continue to smoke even though smoking has important negative health
consequences?
What are the main risks of smoking to physical health?

What are the physical and cognitive effects of cannabis?
What is the main active ingredient in cannabis? What are the main features of cannabis dependence, cannabis abuse, and
cannabis intoxication?
What are the main risk factors for cannabis use disorder?
What are the cognitive deficits that some clinicians argue are associated with regular cannabis use?
9.3.4 Stimulant Use Disorder

What are the main stimulant drugs of abuse?
Can you describe the main effects of a standard dose of cocaine?
What are the different forms of cocaine, how are they administered and what different effects do they have?
How does cocaine cause feelings of euphoria and Ecstasy?
What are the main cognitive and health effects of regular cocaine use?
What are ‘bath salts’?
What are the main symptoms of amphetamine intoxication?
Can you describe the main features of caffeine intoxication and caffeine withdrawal?
9.3.5 Sedative Use Disorder

Can you name the different types of opiates that are the main drugs of abuse?
To which receptor sites do opiates normally attach to create their pleasurable effects?
What are the health risks faced by individuals with opiate use disorder?
9.3.6 Hallucinogen-Related Disorder

What are the main cognitive and behavioural effects of lysergic acid diethylamide (LSD), and how does it have these
effects?
What are some ofthe negative psychological and physiological effects of Ecstasy (MDMA)?
CHAPTER 9 SUBSTANCE USE DISORDERS eS
SECTION SUMMARY
9.3 CHARACTERISTICS OF SPECIFIC SUBSTANCE USE DISORDERS
e Substances of abuse can be categorized in three broad groups, namely stimulants (e.g. cocaine), sedatives (e.g. heroin) and
hallucinogenic drugs (e.g. LSD).
9.3.1 Alcohol Use Disorder

e Alcohol has its effects by binding to the neurotransmitter GABA, preventing neurones firing and making the drinker feel
more relaxed.
° Many of the so-called ‘positive’ effects of alcohol are mythical, and result from the drinker’s expectations about the effects
of alcohol.
e Longer-term negative physical effects of alcohol include hypertension, heart failure, stomach ulcers, cancer, cirrhosis of the
liver, brain damage, and early dementia.
e Delirium tremens (DTs), Korsakoff’s syndrome and fetal alcohol syndrome are physiological risks associated with heavy drinking.
° The lifetime prevalence rate for alcohol use disorder is between 12.5 and 17.8 per cent
e Alcohol use disorders cost the UK an estimated £1.5 billion in 2001.
9.3.2 Nicotine Use Disorder

e Nicotine has its effects by releasing dopamine in the brain, which acts to elevate mood.
° Regular smokers need to smoke simply to experience positive mood levels similar to non-smokers.
¢ The number of smokers in the UK has declined steadily in the past 15-20 years to around 20 per cent ofadults.
¢ Mood manipulation is an important part of nicotine dependence, and smoking a cigarette may eventually become a con-
ditioned response to any form of stress.
e There are substantial health risks to smoking, and passive smoking or second-hand smoke is also an important health risk
for non-smokers.

e The drug cannabis is derived from the hemp plant cannabis sativa, and is also known as hashish and marijuana.
e@ The main active ingredient in cannabis is THC (A?-tetrahydrocannabinal), the amount of which determines the strength of
it psychoactive effects.
© |tis estimated that 2.6 to 5 per cent of the world’s population use cannabis at least once a year.
© Risk factors for developing cannabis use disorder include early age offirst use, tobacco smoking, impulsiveness and unpre-
dictability of moods, diagnosis of childhood conduct disorder, and dependence on alcohol and other drugs.
® Cannabis use disorder is a risk factor for a number of psychiatric diagnoses including anxiety, panic disorder, major depres-
sion, and schizophrenia.
® Regular cannabis use predicts lower educational achievement and lower income than non-use.
9.3.4 Stimulant Use Disorders

@ Stimulant drugs include cocaine, amphetamine and caffeine.
© Cocaine causes feelings of euphoria by blocking the reuptake of dopamine in the mesolimbic areas of the brain.
e Cocaine is usually snorted, but can also be inhaled by smoking, which is known as free-basing.
© The lifetime prevalence rate of cocaine use in developed countries is between 1 and 3 per cent.
® Cocaine can be an important contributor to death by aggravating existing cardiovascular problems.
e Amphetamines are a group of synthetic drugs used primarily as a central nervous system stimulant.
e Amphetamines have their effects by causing the release of the neurotransmitters norepinephrine and dopamine, and
simultaneously blocking their reuptake.
PSYCHOPATHOLOGY
e Amphetamine use in the UK is around 2 per cent and has fallen significantly since 1996.
° Caffeine enters the bloodstream through the stomach and increases brain dopamine levels in a similar way to ampheta-
mine and cocaine.
® Caffeine Use Disorder has been included in DSM-5 as a new research diagnosis.
9.3.5 Sedative Use Disorders

® Sedatives are a central nervous system depressant, and slow the activity of the body, and reduce pain, tension and anxiety,
and include opiates (such as heroin) and barbiturates.
® Opiates (such as heroin) attach to brain receptor sites that normally receive endorphins, encourage the receptors to pro-
duce more endorphins that relieve pain, reduce stress, and create pleasurable sensations.
e The estimated annual prevalence rate for opiate use in 2010 was 0.3-0.5 per cent of adults.
® Some heroin users, known as controlled drug users or unobtrusive heroin users, seem able to use the drug without it affect-
ing their social and occupational functioning.
9.3.6 Hallucinogen-Related Disorders

¢ Hallucinogenic drugs have their effects by changing the user’s perceptions, and include cannabis, lysergic acid diethyla-
mide (LSD), phencyclidines (e.g. PCP) and MDMA (better known as the ‘clubbing drug’ Ecstasy).
e Lysergic acid diethylamide (LSD) is an hallucinogenic drug first synthesized in 1938.
e LSD has both awareness enhancing properties and occasional negative consequences known as‘bad trips’
e LSD appears to have its effects by influencing neurons in the brain that normally control emotion and visual information,
and it does this by affecting levels of the neurotransmitter serotonin.
e Around 0.3 per cent of Americans claim to have used LSD in the previous 12 months.
e Global use of Ecstasy-group drugs is estimated at 0.2-0.6 per cent of the adult population.
e Ecstasy is known to be a selective neurotoxin that destroys the axons to which serotonin would normally bind.
progress to the next stage unless the factors that mediate

9.4 THE AETIOLOGY OF that transition are present. For example, many substance
SUBSTANCE USE DISORDERS users experience only stages 1 and 2 (experimentation and
regular use), and do not nec-
experimentation A period when an indi-
essarily go on to become vidual may try out different drugs. In some
We have so far described the characteristics of some of dependent on the drug in a cases this period of experimentation may
the main substances of abuse, and in some cases dis- way that significantly affects lead to regular drug use.
cussed factors that may lead to abuse of and dependence their occupational, social and family functioning. There
on that substance. In this section we will look in more may be some overlap between mediating factors and stages
general terms at processes that lead some individuals to (e.g. believing that smoking won't harm you may not only
become substance dependent and why it is that these lead to regular use but can also be a factor leading to nico-
individuals differ from those who may simply experi- tine use disorder), but Figure 9.7 gives you a reasonable
ment with drugs without it significantly interfering with overview of how risk factors may influence substance use
their daily lives (e.g. Shewan & Delgarno, 2005). at different stages of development.
The aetiology of substance use disorders has to be In addition to this developmental view, we will also
viewed in developmental terms because most individuals need to look at some of the neurological and behavioural
who become dependent will go through a series of stages processes that underlie substance use disorders. These
that leads to their disorder. At each stage there may be quite include the neurocircuitry
different risk factors that influence transition to the next of addiction (i.e. the reward For an activity based on Figure 9.7,
stage. Figure 9.7 shows a representation of three important pathways in the brain that regarding the developmental model of
stages that individuals go through towards substance use make substance use pleas- substance abuse and dependence, go to
disorder, together with the risk factors that can influence urable), and the psychology activities/ch9
this transition at each stage. Individuals do not necessarily of ‘craving’ (ie. the way
3
CHAPTER 9 SUBSTANCE USE DISORDERS CoB
= DOES TAKING ‘SOFT’ DRUGS LEAD TO USING ‘HARDER’ DRUGS?

OO
=
= Because cannabis use is prevalent amongst teenagers
and young adults, there has long been some concern
such as cocaine, heroin and amphetamines —- manage
to successfully confine their use to recreational pur-
2)
[oe
that early cannabis use may be the first-step that leads poses only, and use the drug only when socialising or
Wi young people to experiment with ‘harder’, more addic- at weekends. This controlled use does not appear to
=) tive drugs, such as cocaine and heroin. This supposed
UU interfere substantially with occupational, social or edu-
\e)
Li
progression from less addictive drugs, such as canna- cational functioning (e.g. Shewan & Delgarno, 2005).
bis, to more addictive drugs may then trap the individ- So, why do some people appear to progress from
ual into a cycle of substance dependency. softer drugs during adolescence to substance depend-
So, is there any truth to this theory? Certainly there ency during adulthood? One theory is that progression rs
is evidence that regular users of addictive drugs such to long-term dependency is found primarily in those
as cocaine and heroin did start out by using cannabis, who have either psychological problems at the outset
and cocaine use, for example, is significantly predicted oftheir drug use or are suffering life stress (Alexander &
by earlier cannabis use (Kandel, Murphy & Karus, 1985). Hadaway, 1982). Indirect support for this theory comes
Another relevant fact is that cannabis users are more from studies showing that drug abuse often stops
likely than non-users to go on and try cocaine or heroin when life stressors disappear (Bourne, 1974), and that
(Miller & Volk, 1996). However, these findings do not many users of addictive drugs such as cocaine and
imply in any way that cannabis users will always go on heroin are capable of kicking their habit and turning to
to use more addictive drugs, and 40 per cent of regular softer drugs, such as cannabis, as a safer option. Also,
cannabis users do not go on to experiment with cocaine in a recent study, Smith, Jones, Bullmore, Robbins &
or heroin (Stephens, Roffman & Simpson, 1993). Ersche (2014) found that there is a select subset of
Because much drug use is associated with depend- cocaine users who are able to use the substance rec-
ency, we tend to assume that individual users will auto- reationally without developing dependence, and that
matically be dragged along a path of ever-worsening this was due to their lack of attentional preference for
abuse, and that cannabis use will inevitably lead down cocaine-related stimuli compared with dependent
a slippery slope to dependency. However, we must users. This lack of attentional preference significantly
remember that many regular substance users — even reduces attention to cues that elicit ‘craving’ (see Focus
those who use potentially highly addictive drugs Point 9.8).
|
_ ~ ~ —-—-- + - =
. ‘ Abuse and
Experimentation Regular use Dependence
Availability Mood alteration effects Genetic predisposition

(e.g. legality of the drug) (e.g. tension relief) (e.g. inherited physical
Familial factors Self-medication tolerance to the drug)
(e.g. use by family members) (e.g. to deal with life stressors) Long-term substance-
Peer group influences Long-term expectations induced cognitive deficits
(e.g. using drug as a form of (e.g. beliefs that substance has (e.g. brain deficits that affect
group identity) beneficial effects) cognition and decision
Media influences Cultural variables making)
(access to adverts and role (e.g. social norms relating to use) Concurrent psychiatric
model associations with the diagnoses
drug) (e.g. concurrent mood or
anxiety disorders)
Poverty
(e.g. stressful living
conditions and
hopelessness)
FIGURE 9.7 The developmental model ofsubstance abuse and dependence.

in which liking and wanting a drug becomes conditioned conforming to group norms, so an adolescent will start
to external cues which trigger the desire for that drug). using a substance in order to self-categorize themselves as a
These two processes are highlighted and described later in member of a particular group (Schofield, Pattison, Hill &
Focus Points 9.7 and 9.8. Borland, 2001). There is clear evidence that young
We will continue by describing some of the risk fac- people are socially motivated to become drug users
tors that influence substance use at different develop- (Allbutt, Amos & Cunningham-Burley, 1995), but this only
mental stages. rarely takes the form of deliberate ‘pressure’ or ‘persua-
sion’ by others (Lucas & Lloyd, 1999; Schofield, Pattison,
Hill & Borland, 2001). In most cases, young people appear
to take up activities like smoking in order to conform with
9.4. 1 Experimentation
group norms — that is, they can make themselves appear
Availability more like others in the group by conforming to behaviours
Whether an individual can readily get access to the that are typical in the group, such as smoking (Schmitt,
substance is an important factor in the early stages Branscombe & Kappen, 2003). Schofield, Pattison, Hill &
of substance use, and factors such as whether the drug Borland (2001) found that particular group labels (such
is legally available (e.g. alcohol and cigarettes) and its as ‘rebels’, ‘illegal drug users’, ‘motor bike riders’) were
cost are important determinants of initially experiment- associated with extensive smoking, and the degree of
ing with the drug. For example, there is evidence for an smoking determined how strongly an individual identi-
inverse relationship between the use of a drug and its fied with that group. In such groups, in-group favouritism
cost — especially amongst young adolescents. This is true is also expressed by the sharing of cigarettes, and smok-
for alcohol and for cigarettes (Stead & Lancaster, 2005; ing is used to cement friendships, and to indicate commit-
Room, Babor & Rehm, 2005), and suggests that strate- ment to the group (Stewart-Knox, Sittlington, Rugkasa,
gies such as enforcing the minimum age for purchase of Harrisson et al., 2005). This suggests that social networks
tobacco and alcohol, and increasing the price of these can have a strong influence on an individual’s initial sub-
commodities may be effective means of controlling early stance use, and identifying as part of a group that uses
use (Ogilvie, Gruer & Haw, 2006). legal drugs, such as cigarettes and alcohol, also predicts
increased use of other drugs in late adolescence (Chassin,
Familial factors Curran, Hussong & Colder, 1996). Apart from the impor-
Two important factors that can influence early substance tance of social groups determining substance use, it is also
use are (1) whether the substances are regularly used by the case that substance use will determine the kinds of
other family members, and (2) whether the family envi- social groups that an individual will mix in. For example,
ronment is problematic. For example, if a child’s parents once an individual becomes a regular drinker, they begin
both smoke then the offspring is significantly more likely to to choose social groups with similar drinking patterns,
smoke at an early age, and if both parents regularly drink and drinking in a social group environment that supports
alcohol, then the child is also more likely to drink at an alcohol consumption can act to consolidate regular use
early age (Hawkins, Graham, Maguin, Abbott et al., 1998). (Bullers, Cooper & Russell, 2001).
Similarly, having older siblings and spouses that abuse drugs
significantly increases the risk of drug abuse (Kendler, Media influences
Ohlsson, Sundquist & Sundquist, 2013). Neglectful parent- Substance use in young adolescents is significantly
ing also increases the use of alcohol, cigarettes and canna- influenced by advertising and exposure to the product
bis by the child (Cadoret, Yates, Troughton, Woodworth & in media contexts such as television programmes and
Stewart, 1995), and the negative background factors that pre- magazines. Exposure to advertising has been shown to
dict longer term substance use include (1) substance use in be an important factor in encouraging children to take
the childhood home, (2) extreme poverty in the childhood up smoking (While, Kelly, Huang & Charlton, 1996), and
home, (3) marital or legal problems in the household, (4) a US study found that exposure to in-store beer displays,
childhood neglect and abuse — especially childhood sexual magazines with alcohol advertisements, and television
abuse (Sartor, Waldron, Duncan, Grant et al., 2013), and beer advertising predicted drinking in school-age chil-
(5) serious psychiatric illness in the household (Alverson, dren (Ellickson, Collins, Hambarsoomians & McCaffrey,
Alverson & Drake, 2000; Wills, DuHamel & Vaccaro, 1995). 2005). While banning direct advertising of a product has
been shown to produce a significant fall in adolescent
Peer group influences use of that product (Saffer, 1991), substance use (such
Adolescents often begin drug use because of peer group as smoking) is still linked to indirect exposure to images
influences. These influences are not necessarily direct found in fashion, entertainment and gossip magazines
pressure to use the substance but take the form of (Carson, Rodriguez & Audrain-McGovern, 2005).
CHAPTER 9 SUBSTANCE USE DISORDERS “3.
9.4.2 Regular Use feelings of Ecstasy, feelings of well-being and loss of neg-
ative emotions; and hallucinogens — such as cannabis —
Mood alteration effects produce feelings of relaxation, euphoria, sociability and
One of the main reasons for using drugs is that they sharpened perceptions. Interestingly, most of the drugs
have important mood altering effects. Alcohol makes the that we've discussed in this chapter have their pleasur-
drinker friendly, confident and relaxed (Harvey, Foster, able effects by activating a common brain circuitry that
MacKay, Carroll et al., 2002); smokers claim that smoking governs reward and pleasure, and a full discussion of this
cigarettes has a relaxing and calming effect (Ikard, Green & circuitry is provided in Focus Point 9.7.
Horn, 1969); stimulants — such as cocaine and ampheta- Given these rewarding effects of drug use, it makes
mines — affect reward path- sense to assume that regular use can develop as a result
yard pathways The brain neuro- ways in the brain causing of drug use being reinforced by these pleasurable conse-
uitry that make substance use
asurable.
feelings of euphoria, energy quences. Furthermore, if taken regularly enough, many
and confidence (Volkow, drugs can cause permanent changes to the brain reward
Wang, Fischman, Foltin et al., 1997; Taylor, Lewis & Olive, system in such a way as to facilitate addiction (Taylor,
2013); opiates — such as heroin — generate immediate Lewis & Olive, 2013).
8 REWARD PATHWAYS IN THE BRAIN AND DRUG ADDICTION

OV
-
With most of the drugs of abuse that we've discussed 2013). Drugs achieve their pleasurable effects by influ-
= earlier in this chapter, you'll notice that they all either encing the dopamine system, and in particular, the
2) have pleasurable effects on mood or they help people dopaminergic neurons in the ventral tegmental area
ou
4) to feel less bad (e.g. by alleviating negative moods (VTA) of the midbrain and subsequent areas in the lim-
=) or withdrawal symptoms) (Koob & Le Moal, 2008). bic forebrain — especially
U ventral tegmental area (VTA) Part of the
\e) Research on both humans and animals suggests that a the nucleus accumbens midbrain associated with the dopamine
Li broad range of drugs have their pleasurable effects by (NAc). ThisVTA—NAc path- system.
activating the natural reward pathways in the brain way is arguably the most
| by converging ona common circuitry in the brain’s lim- important reward path- nucleus accumbens (NAc) Part of the
limbic forebrain and dopamine system.
bic system (Feltenstein & See, 2008), and many of these way in the brain and
drugs also cause permanent adaptive effects on this gives rise to the pleasurable effects caused not only by
common pathway that contribute to the progression drug use, but also by food, sex and social interactions
and maintenance of addiction (Taylor, Lewis & Olive, (Kelley & Berridge, 2002; Tobler, Fiorillo & Schultz,
Nicotine +
Alcohol 4
Glutamate inputs
(e.g. from cortex)
VTA Opiates
interneuron
Alcohol a
eee
Nicotine
Glutamate +f Cannabinoids 4
inputs
(e.g. from
amygdala VIA NAc
PPT/LDT)
Source: Nestler, E.J. (2005). Is there a common molecular pathway for addiction? Nature |
Neuroscience, 8, 1445-1449, Figure 1. Reproduced with permission.
316 PSYCHOPATHOLOGY
+ >:
2005), and it has also been implicated in other addictive directly increase dopaminergic transmission (DA) in
behaviours such as pathological overeating, gambling the NAc. Opiates do the same indirectly by inhibiting
and sex addictions (Nestler, 2005). GABAergic interneurons in the VTA, which disinhibits
Several additional brain areas have been shown to dopamine neurons in the VTA. Opiates also directly act
interact with this VIA-NAc pathway and are implicated on opiate receptors in the NAc. Nicotine seems to acti-
in drug addiction. These include regions in the amygdala, vate VTA dopamine neurons directly. Alcohol appears to
hippocampus, hypothalamus, and several regions of the have a number of different effects at different points in
frontal cortex (Koob & Le Moal, 2008; Nestler, 2001). the pathway, and the effects of cannabis are also com-
The figure shows the converging actions that a num- plex but may act directly on NAc neurons themselves.
ber of different drugs of abuse have by affecting different Finally, phencyclidine (PCP) may act directly on neurons
components in the VTA-NAc reward pathway. Stimulants in the NAc.
In addition to the intrinsic pleasurable effects of some means of coping with stress (Schacter, 1982; Parrott, 1998,
substances, a good deal of research has been carried out 1999). This begins when the smoker lights a cigarette in
on the putative tension or stress-reducing effects of drugs order to alleviate nicotine withdrawal symptoms, but after
such as nicotine and alcohol. There is some evidence that regular use, many smokers come to associate smoking
alcohol may reduce tension, even in individuals who are with tension relief generally, and so become conditioned
not alcohol dependent (Sher & Levenson, 1982), and this to having a cigarette during or after any stressful experi-
is consistent with the drinker’s everyday belief that drink- ence (Kassel, 2000). This gives feelings of relaxation and
ing is a good way to unwind, such as after a demanding improved concentration as nicotine levels increase,
day at work. However, the picture is not quite that simple. and functions to reinforce the act of smoking. Consistent
Alcohol appears to reduce responding in the presence of with this view is the longitudinal finding that increases in
both negative and positive affect, and so may simply have negative affect and stressful life events are associated with
an arousal-dampening effect regardless of the valency of increases in smoking (Wills, Sandy & Yaeger, 2002).
the drinker’s emotional state (Stritzke, Patrick & Finally, many drugs are powerful reinforcers that can
Lang, 1995). Subsequent studies have indicated that condition the effects of drugs to stimuli and cues asso-
alcohol has its apparent arousal-dampening effects by ciated with the drug (e.g. seeing a cigarette packet, or
altering perception and attention. The alcohol-intoxi- a white powder), and this gives rise to the concept of
cated individual has less cognitive capacity available to ‘craving’ (Robinson & Berridge, 2003). Individuals who
process all ongoing information, and so alcohol acts acquire learnt cravings for a drug are more likely to con-
to narrow attention and means that the drinker pro- sume more of that drug and to have a significantly higher
cesses fewer cues less well. This is known as alcohol rate of relapse following abstention. The role of craving
myopia (Steele & Josephs, 1990), and means that the is discussed more fully in Focus Point 9.8.
drinker’s behaviour is likely In summary, there is clear evidence that many sub-
alcohol myopia The situation where an
alcohol-intoxicated individual has less
to be under the influence stances appear to have mood altering effects — often
cognitive capacity available to process all of the most salient cues caused by their affects on a common brain reward cir-
ongoing information, and so alcohol acts in the situation. In lively, cuitry in the limbic system, and so substance use may
to narrow attention and means that the friendly environments this be maintained by these effects. However, in many cases,
drinker processes fewer cues less well.
will result in the drinker these affects are more complicated than they appear to
processing only these types of cues, and as a consequence the user. For example, alcohol appears not to have a
will feel happy, sociable and will not have the capacity to simple mood enhancing effect, but has an attentional-
simultaneously process worries or negative emotions. focusing effect which makes drinkers feel relaxed and
However, in drinking situations where there are no happy, happy only when there are happy cues for them to focus
lively cues (such as in the case of the unhappy, lone drinker), on. In addition, drugs can often have important con-
the reduced cognitive processing can result in attentional- ditioned effects that will generate craving for the drug
focusing on negative thoughts, experiences and emotions, when drug-related cues are encountered.
and means that the drinker experiences more negative
affect than if they had abstained. Self-medication
In the case of nicotine, we saw in section 9.3.2 that Rather than simply being used as a means of reducing
there is evidence that regular smokers use nicotine as a the effects of everyday tensions-and stressors, substance
ss
CHAPTER 9 SUBSTANCE USE DISORDERS a 31z.
ESRD
STETal
oa CRAVING
Ov
=
The pleasurable effects of drug use can also act as reward centres (Filbey & DeWitt, 2012). In addition, crav-
= potent stimuli that will generate ‘craving’ responses ing can induce attentional biases that enhance process-
2) to cues associated with the drug. This occurs through
a. ing of drug cues, as well as drug anticipatory responses
a] a process of conditioning in which the drug acts as a that exacerbate the craving (Field, Mogg, Mann, Bennett
=) powerful unconditioned stimulus (UCS) that reinforces & Bradley, 2013). Although generated by non-conscious
UW
\e) conditioned responses to drug cues (see section 1.3.2 classical conditioning process, craving is often charac-
LL, for a discussion of classical and operant conditioning) terized as a conscious state that intervenes between the
(Robinson & Berridge, 2003). This means that cues such unconscious cues and consumption (Andrade, May &
as the sensory features of the drug (e.g. a white powder), Kavanagh, 2012). Craving has significant effects on those
the environment in which it is taken (e.g. a pub), or the suffering substance abuse disorders. People who crave a
people the user socializes with when taking the drug substance do use that substance more than people who
can all become cues which elicit craving for the drug. don't crave it (Berkman, Falk & Lieberman, 2011), and, as
Cues for a particular drug can actually trigger responses you can imagine, craving is a significant obstacle to suc-
in the user that are very similar to those associated with cessful treatment and frequently leads to relapse (Evren,
actual use of the drug, and these include pleasurable Durkaya, Evren, Dalbudak & Cetin, 2012; Paliwal, Hyman
Hiesmnireser toto
feelings, physiological arousal, and activation of brain & Sinha, 2007).
use can become regular as a means of self-medication 3. the drug may not only reduce tension and
when the individual is suffering more severe adjustment negative affect, it may have other positive
--medication Self-administration of
difficulties such as those consequences such as helping the individual to
2n illicit drugs by an individual to allevi- caused by diagnosable psy- cope in social situations.
perceived or real problems, usually of a chiatric disorders. This
chological nature. view is supported by the Finally, if substance abusers do genuinely use drugs to
fact that substance use disorders are highly comorbid self-medicate, then their choice of drug should be con-
with a range of other psychiatric disorders, including sistent with their psychiatric symptoms. For example, we
bipolar disorder, depression, eating disorders, schizo- would expect someone with ADHD to prefer ampheta-
phrenia, personality disorders, and anxiety disorders such mines to alcohol due to its stimulating properties, but
as obsessive compulsive disorder, post-traumatic stress individuals with anxiety would prefer alcohol to amphet-
disorder and panic disorder (Regier, Farmer, Rae, Locke amines because of the anxiolytic effects of alcohol.
et al., 1990; Brooner, King, Kidorf, Schmidt et al., 1997) However, there is relatively little evidence in support of
(see Table 9.2), and self-medication is frequently reported these more detailed predictions from the self-medication
by substance users as a motive for using the substance account (Lembke, 2012).
(Sbrana, Bizzarri, Rucci, Gonnelli et al., 2005). There is
evidence that anxiety disorders and depression pre-date Long-term expectations and beliefs
the onset of substance use disorders such as alcohol Substance users can also become regular users because they
dependency (Merikangas, Mehta, Molnar, Walters et al., develop expectations that the substance will have positive
1998; Liraud & Verdoux, 2000), which is again consistent effects. For example, young adolescents who believe that
with the view that drugs are used for medication pur- alcohol affects behaviour in positive ways (e.g. by increas-
poses after a psychiatric disorder has already developed. ing physical pleasure, enhancing sexual performance,
However, if individuals who use drugs for self-medica- facilitating socially assertive behaviour) are significantly
tion purposes are aware of the longer term negative more likely to begin drinking than adolescents who do
effects of these drugs, why do they continue to use them? not hold these beliefs, and are also more likely to become
Drake, Wallach, Alverson & Mueser (2002) suggest a problem drinkers (Goldman, Brown & Christiansen,
number of reasons for continued use: 1987; Christiansen, Roehling, Smith & Goldman, 1989).
In many cases these beliefs appear to be culturally gener-
1. the drug has intrinsic rewarding effects and leads ated, because empirical studies suggest that alcohol does
to physical dependence, not increase levels of sexual arousal or aggression, but
2. the lives of individuals with psychiatric disorders in fact reduces physiological arousal (Lang, Goeckner,
are so miserable that the medicinal effects of the Adessor & Marlatt, 1975; Wilson & Lawson, 1976). Many
drug offset its negative effects, and regular substance users also develop erroneous beliefs
318th PSYCHOPATHOLOGY
that the substance they use is harmless, and these beliefs been found in twin studies of cannabis abuse (Kendler &
help to maintain regular use. For example, the increase Prescott, 1998), nicotine dependency (True, Xian, Scherrer,
in cannabis use during the 1990s was mainly confined to Madden et al., 1999), and drug abuse generally (Tsuang,
those individuals who considered cannabis to be harm- Lyons, Meyer, Doyle et al., 1998). Adoption studies also
less (US Department of Health and Human Sciences, support a role for genetic inheritance in alcohol use
1994), and many regular smokers believe that smoking disorders and drug abuse generally (Cadoret, Troughton,
may cause cancer and illness in other smokers, but not in O’Gorman & Heywood, 1986; Kendler, Sundquist,
themselves (Ayanian & Cleary, 1999). Ohlsson, Palmer et al., 2012).
So how might genetic factors put some individuals
Cultural variables more at risk for substance abuse and dependence than
There are some cultural factors that will influence the others? There are a number of different possibilities.
transition from first use to regular use. For example, Firstly, a genetic predisposition for alcohol dependence
alcohol consumption differs significantly across differ- may interact with environmental factors such as stress
ent countries, and is most prevalent in wine-drinking (a diathesis-stress model). For example, Dick, Pagan,
societies (such as France, Italy and Spain) where drink- Holliday, Viken et al. (2007) found that heritability for
ing alcohol is widely accepted as a social and recrea- alcohol problems in adolescents was higher amongst
tional activity (deLint, 1978). Increased use in these those who had peers who drank alcohol than those
countries may be caused by the regular availability of with peers who didn’t drink alcohol. Cloninger (1987)
alcohol in a range of situations, such as drinking wine has also argued that a genetic predisposition for alco-
with meals and the availability of wine and alcohol in hol dependence will be activated only by experiencing
a broad range of social settings. There are also some environmental stress (e.g. low socio-economic status).
culturally determined differences in beliefs about the However, other studies have indicated that there may be
effects of drugs which appear to affect the frequency of a more general genes—environment interaction, where a
use, and Ma & Shive (2000) found that white Americans genetic predisposition for alcohol dependence will only
reported significantly less risk associated with a range cause alcohol abuse if other environmental factors are
of drugs (alcohol, cigarettes, cocaine and cannabis) than present. These environmental factors are not necessar-
African or Hispanic Americans. The former group was ily stressors, but include factors which might facilitate
found to use all of these drugs significantly more than alcohol use, such as living in places where there are large
the latter groups. numbers of young people (Dick, Rose, Viken, Kaprio &
Koskenvuo, 2001) or peer pressure or parental model-
ling (Rose, 1998). These environmental factors seem to
be important because they are likely to initiate drinking.
9.4.3 Abuse and Dependence
Once drinking has started, genetic factors then appear to
Regular use of a substance is not sufficient to give rise to play a significant role in determining regular use, abuse
a substance use disorder. This latter stage will be subject and dependence (Heath, 1995).
to the diagnostic criteria provided in Table 9.1, and to Secondly, genetic factors may influence tolerance
the regular use causing significant disruption to daily liv- levels to drugs such as alcohol, or affect central nervous
ing in the form of inability to fulfil major obligations at system responses to the drug (Schuckit, 1983). Alcohol
work, school or home, and a failure to deal with family dependence requires that the user has to drink a lot and
responsibilities. In this section, we look at some of the to do this regularly, and many individuals who develop
factors that might cause a shift from regular use to abuse alcohol use disorders appear to have inherited a strong
and dependence. tolerance for alcohol. That is, they report low levels of
intoxication after a drinking bout and they show fewer
Genetic predisposition signs of physical intoxication (such as body sway)
Based on twin, adoption and family studies, the herit- (Schuckit, 1994; Schuckit & Smith, 1996), and these
ability component for substance use disorders could higher thresholds for intoxication may permit heavier
be as high as 0.78 for alcohol and nicotine dependence and heavier bouts of drinking that are typical of alcohol
(Kendler & Prescott, 1998; Merikangas et al., 1998), and use disorders. Thirdly, there is considerable evidence that
around 0.46 for substance use disorders generally (Grove, certain genes influence sensitivity to alcohol, and it is
Eckert, Heston, Bouchard et al., 1990). Twin studies have the inheritance of these genes that determines whether
indicated that the concordance rates for alcohol abuse in a drinker will become dependent. The main candidate
MZ and DZ twins respectively are 54 per cent and 28 per is a gene known as ALDH2 (Wall, Shea, Chan & Carr,
cent (Kaji, 1960), indicating a strong genetic component 2001). Alcohol metabolism in the liver goes through two
in alcohol abuse, and a similar genetic predisposition has main stages, and these are the conversion of alcohol into
a toxic substance called acetaldehyde followed by conver- such as dopamine and serotonin (Nestler, 2001; Heinz,
sion of acetaldehyde into nontoxic acetic acids. ALDH2 Mann, Weinberger & Goldman, 2001), and that meth-
is thought to affect the rate at which acetaldehyde is amphetamine abuse causes at least mild cognitive decline
metabolized — if it is metabolized more slowly, then the observed in early to middle adulthood (Dean, Groman,
individual will begin to feel the negative effects of its tox- Morales & London, 2013). In post-mortem studies of the
icity, such as nausea, headaches, stomach pains,and phys- brains of regular cocaine users, Little, Krolewski, Zhang
ical signs of intoxication. Interestingly, many Asians are & Cassin (2003) found damage to striatal dopamine fibres
known to have a mutant allele for ALDH2 which slows resulting in neuronal changes causing disordered mood
acetaldehyde metabolism and allows it to build up after and disruption to motivational processes. So, this illus-
a drinking bout, and makes drinking large amounts of trates one possible route through which regular use could
alcohol aversive. This appears to be an important factor develop into long-term dependence as changes in brain
in explaining why Asians develop alcohol use disorders structures caused by the drug affect mood and motiva-
at only about half the rate of non-Asians (Tu & Israel, tion to such an extent that the user has significantly fewer
1995). Other mutant forms of this gene which allow cognitive resources available to fight dependence.
rapid metabolism of acetaldehyde may be the inherited
factor that causes tolerance effects in some individuals Concurrent psychiatric diagnoses
and leads to regular alcohol use and dependence. That We have already discussed the role that comorbid psy-
such a tolerance is inherited is supported by the fact that chiatric disorders can play in turning first time users into
sons of heavy alcohol users report being less intoxicated regular users because of the medicating properties the
than others after a standard amount of alcohol and show drug has on the psychiatric symptoms. However, comor-
fewer physical signs of intoxication (Schuckit, Tsuang, bid psychiatric problems appear to play an important
Anthenelli, Tipp et al., 1996). Recent studies have iden- role throughout the developmental process to full abuse
tified a form of the ALDHz2 allele in white American and dependence. For instance, once a user has entered
college students that is associated with lower rates of treatment for their dependence, treatment outcomes are
alcohol use disorder, lower levels of drinking, and with significantly poorer for users with comorbid psychiatric
alcohol-induced headaches (Wall, Shea, Luczak, Cook & disorders, and this is usually due to increased tendency
Carr, 2005), and suggests that variations in the form of to relapse after treatment (Grella, Hser, Joshi & Rounds-
this gene can have an important influence on alcohol Bryant, 2001). There are at least two factors that contrib-
consumption and alcohol use disorders. ute to this poor treatment outcome:
Long-term substance-induced 1. individuals with comorbid psychiatric disorders

are likely to face more life stressors after
cognitive deficits
treatment (e.g. negative emotional states) and are
As you will have read earlier in this chapter, there is much
less likely to have the coping resources required
speculation about whether regular substance use causes
to deal with these stressors than those without
long-term brain damage and permanent deficits in cogni-
psychiatric comorbidity (Ramo, Anderson, Tate
tive processes. Evidence for most of these claims is still
& Brown, 2005), which returns them to drug self-
fairly equivocal — especially in the case of substances such
medication as a way of coping, and
as cannabis or MDMA (Iversen, 2005; Cole, Sumnall &
Grob, 2002). However, most substance use disorders tend 2. users with a psychiatric comorbidity are less likely
to be associated with a syndrome of underachievement, to consider that drugs are problematic compared
with abusers often exhibiting lower IQ, lower educational with their peers and tend to relapse very soon after
achievement, and motivational deficits compared with treatment (Ramo, Anderson, Tate & Brown, 2005),
non-users. This may be a consequence of individuals who which suggests that they lack the motivation
have these intellectual and motivational deficits prior to to abstain, even though their difficulties are
drug use lacking the necessary coping skills to pull them- compounded by the psychiatric comorbidity.
selves out of the vicious downward spiral of abuse and In summary, psychiatric comorbidity is a real risk fac-
dependence. However, an alternative explanation is that tor for both transition from first use to regular use, and
regular substance use may cause these intellectual and from regular use to abuse and dependence, and it is an
motivational deficits, resulting in poorer judgement important factor in determining relapse from treatment.
and decision-making skills, and making such individu-
als more prone to fall into a pattern of long-term abuse. Poverty
For example, there is growing evidence that regular sub- Without doubt there are important socio-economic fac-
stance abuse can have long-term effects on the balance tors at work in determining whether individuals will use
and availability of important brain neurotransmitters drugs and develop from being regular users into being
320 PSYCHOPATHOLOGY
drug dependent. One such factor is poverty. There is evi- to represent circumstances in which the individual will
dence that an individual’s first experience with an illicit have poor access to treatment services and long-term psy-
drug increases in probability if they live in or near an chiatric support (Cook & Alegria, 2011). Endemic drug
economically poor neighbourhood (Petronis & Anthony, use in poor communities fosters other problems, includ-
2003). This is perhaps not surprising given that such indi- ing infections such as HIV and hepatitis C contracted
viduals may well be unemployed, have no other forms through injecting drugs intravenously (Rosenberg,
of recreation available to them, have little hope of occu- Drake, Brunette, Wolford & Marsh, 2005). Finally, sub-
pational or educational fulfilment, and already live in stance dependence in poor areas also fosters crime in the
subcultures that revere drug dealing as a high-status pro- form of robbery, fraud and prostitution as the only means
fession. Such conditions are perfect for the downward of securing money to buy drugs, and violent crime and
spiral into drug abuse and dependence, and are likely racketeering as dealers battle to sell their illicit products.
SELF-TEST QUESTIONS —
° Is there any evidence that using ‘soft’ drugs leads to the use of ‘hard’ drugs?
° What factors lead young people to experiment with drugs?
° How do peer group influences affect whether a young person will try a new drug?
e What factors lead individuals to become regular users of asubstance?
° In what ways do different drugs such as alcohol, nicotine, cocaine, heroin and cannabis alter the user’s mood?
° Research suggests a broad range of drugs have their effects by activating the natural reward pathway in the brain — what
areas of the brain are involved in this pathway?
*® How does craving develop, and how does it contribute to relapse?
e What is the evidence that regular drug use can become a form of self-medication when the user has severe adjustment
difficulties?
° What are the main factors that maintain substance abuse and dependence?
° How have twin and adoption studies shown that there is an inherited component to alcohol use disorder?
° How does the gene ALDH2 influence whether a drinker is likely to become alcohol dependent?
° What kinds of long-term cognitive deficits can regular substance use cause, and how might they be implicated in maintain-
ing substance use disorders?
e What is the link between poverty and substance use disorders?
SECTION SUMMARY
9.4 THE AETIOLOGY OF SUBSTANCE USE DISORDERS
The acquisition of substance abuse and dependency has to be viewed as a developmental process that progresses through a
number of well-defined stages, and different factors are involved in establishing substance use at these different stages. The
main stages of development that we have highlighted are experimentation (what influences first use of a substance?), regular
use (what factors influence the move from experimentation to regular use?), and abuse and dependence (what makes some
people continue to use drugs even though this activity is having significant negative effects on their lives and their health?). It is
important to understand that use may be confined to any one of these stages, and many regular users can often function rela-
tively successfully in their social, work and family environments. However, in terms of understanding psychopathology, it is the
development from regular use to abuse and dependence that is of most interest to us as practitioners and clinical psychologists.
The key points in this section are:
° The aetiology of substance dependence has to be viewed in developmental terms as individuals go through stages of
experimentation, regular use, and then substance abuse and dependence.
CHAPTER 9 SUBSTANCE USE DISORDERS a
9.4.1 Experimentation
e Early use is influenced by the availability of the drug and its economic cost.
° Whether substances are regularly used by family members and whether the family environment is problematic can also
hasten experimentation with drugs.
° Peer groups influence first substance use as individuals start using a substance in order to self-categorize themselves as
members of a particular group.
° Substance use in young adolescents is significantly influenced by advertising and exposure to substances (such as ciga-
rettes and alcohol) in the media.
9.4.2 Regular Use

¢ Almost all substances of dependence have mood altering effects by either creating states of euphoria or Ecstasy or reduc-
ing tension or stress. These factors may contribute to regular use.
e Drugs achieve their pleasurable effects by influencing the dopamine system in the brain — especially the dopaminergic
neurons in the ventral tegmental area (VTA) of the midbrain and the nucleus accumbens (NAc).
® Craving is a conditioned response to cues associated with individual drugs, and increases consumption and risk of relapse.
e Substance use can become regular as a means of self-medication when the individual is suffering severe adjustment
difficulties such as those caused by psychiatric disorders.
e Substance users can become regular users because they develop expectations that the substance will have positive effects.
9.4.3 Abuse and Dependence

¢ There is a significant inherited component to substance use disorders as shown by twin, adoption and family studies.
® A gene known as ALDH2 affects the rate at which alcohol is metabolized, and will influence the individual's tolerance of
alcohol.
e Regular users may become drug dependent because they lack the motivation and the coping skills to pull themselves out
of adownward spiral into abuse and dependence.
® Psychiatric comorbidity is a risk factor for both transition from first use to regular use, and from regular use to abuse and
dependency.
e Endemic drug use is associated with poverty and poor communities, which also fosters health problems such as HIV, crime
and prostitution.
Cece pecnevcnesececeueveensecesereeneesen een seeee sence en eeeeeeeeeee eee eseeeeseeneee ese eneEe eee eneeDeeneeeeEeneneeNSeeneES eee Eee eee ene EeDee eee eDOC Oe UEeEe Re Hee eeee eee eenane nn eeeeee een en eseneee een eeeeeeeereeeeceenesceneseneceneeeeeanceuene®
with most severe dependencies live miserable and unful-

9.5 THE TREATMENT OF filled lives. They may be homeless or living in poverty, and
SUBSTANCE USE DISORDERS the relief from these conditions provided by the drug may
be the individual's only solace. In the UK, the Centre for
Social Justice has recently published a report proposing a
Treating individuals with substance use disorders is not a series of reforms of treatments for substance use disorders,
simple or easy process. At the point where a user reaches most notably arguing that many treatment programmes
the stage of abuse and dependence they are usually physi- are doomed to failure without effectively addressing
cally addicted to the drug, suffer severe withdrawal symp- the poverty, unemployment
toms when abstaining from the drug, and probably mix in and poor living conditions | To read Breakthrough Britain:
social circles that will provide regular temptations to use in which many drug addicts | Addictions, a report on substance abuse
treatments, go to
the drug. In addition, substance use disorders are often exist’ "(Centre tors Social | http://tinyurl.com/ogefosv
associated with other comorbid psychiatric disorders that Justice, 2010).
will need addressing in a full intervention plan. Many Because of these difficulties, treatment interventions
younger individuals with substance use disorders also do with clients suffering substance use disorders are usually
not see their drug taking as dangerous or problematic multifaceted and address the client’s problems at a range
(Ramo, Anderson, Tate & Brown, 2005), and so have a high of different levels. As a consequence, many national treat-
risk of relapse after treatment. It is often the case that those ment programmes provide healthcare advice, general
WR22 ee PSYCHOPATHOLOGY
community support, easy-access drop-in facilities for (e.g. http://talktofrank.com/). Prevention schemes are
drug abusers, and structured treatment programmes — often local and tailored to the specific needs of the com-
both community-based and residential, depending on munity. They aim at educating schoolteachers and par-
the severity of the dependence. Treatment programmes ents on how to deal with specific drug-related incidents
are usually multifaceted, in that they will combine a and how to provide drug advice to young people. Many
range of specific intervention procedures designed to schemes train young people themselves to deliver drug
make the client aware of the circumstances and envi- education information to their peers. Particular strategies
ronmental stimuli that trigger substance use, deal with that drug prevention schemes use are (1) peer-pressure
any comorbid disorders, develop motivation to change, resistance training, where students learn assertive refusal
and teach the social and coping skills needed to deal skills when confronted
peer-pressure resistance training A
with life without drugs. These may also be combined with drugs, (2) campaigns
i
strategy used by drug prevention sche
with detoxification procedures designed to address the to counter the known where students learn assertive refusal sk
physical dependence that drug use has developed. In effects of the media and when confronted with drugs.
the following sections, we will begin by looking briefly advertising (e.g. by com-
at some community care practices, and then turn to bating tobacco advertising with anti-smoking messages),
specific psychological and detoxification approaches. (3) peer leadership, where young people are trained
to provide anti-drugs messages to their peers, and
(4) changing erroneous
9.5.4 Community-Based Programmes beliefs about drugs (e.g. peer leadership A strategy used by druc
prevention schemes where young peo
that use is more prevalent are trained to provide anti-drugs messag
Community-based services come in a number of forms. than it is, or that a drug’s to their peers.
They can be self-help groups, such as Alcoholics effects are relatively harm-
Anonymous (AA) (see Focus Point 9.1), which tries to less). The evidence on the effectiveness of these types of
help the alcoholic replace networks of drinking friends schemes is difficult to gauge because they take place across
with other AA members. different types of communities characterized by different
Alcoholics Anonymous (AA) A support
At least some studies have risk factors and employ a range of different strategies over
group for individuals who are alcohol
dependent and are trying to abstain. suggested that AA partici- different timescales. However, some studies have indi-
pation can have positive cated that at the very least such schemes do appear to
outcomes, and may be an effective form of long-term delay the onset of drug use — even if longer-term effects
abstinence up to 8 years after joining the self-help group are difficult to evaluate (Sussman, Dent, Simon, Stacy et
(Timko, Moos, Finney & Lesar, 2000). However, a sys- al., 1995; Faggiano, Galanti, Bohrn, Burkhart et al., 2008).
tematic review of the eight randomized outcome studies Residential rehabilitation centres are also important
available at the time found that AA was no better than in the treatment and longer term support of individuals
any other kind of structured treatment (Ferri, Amato & with substance use disor-
Davoli, 2008), and AA has notoriously high drop-out ders. Such centres allow residential rehabilitation centres
rates, which are often not factored into the results of people to live, work and Centres that allow people to live, work
and socialize with others undergoing
controlled clinical trials. socialize with others treatment in an environment that offers
Drug-prevention schemes are now widespread and undergoing treatment in advice, immediate support, and group ar
take many forms. Their purpose is to try to prevent first an environment that offers individual treatment programmes enabli
use of a drug or to prevent experimentation witha drug advice, immediate sup- cllentscoJeanmtltesseclal anicle@pimg ski
A , anlr see necessary for the transition back to a
' developing into regular port, group and individual jormal life
drug-prevention schemes Community- Teche masiall through treat -
based services whose purpose is to try to ’ , ay 8 PEAT ERE PROS TAM eS?
prevent firstuse of atdrugiorto prevent information about the and they enable the client to learn the social and coping
experimentation with a drug develop- effects of drugs and by skills necessary for the transition back to a normal life. In
ing into regular'use= usually through developing communica- such centres, detoxification programmes can be moni-
information about the effects of drugs and
tion and _ peer-education tored and supported with the help of peripatetic key
through developing communication and
peer-education skills. skills. In the UK, govern- workers. Residential rehabilitation programmes usually
ment-sponsored schemes combine a mixture of group work, psychological inter-
have a number of elements, which focus respectively ventions, social skills training, and practical and voca-
on young people (especially in schools), communities tional activities. In the UK, clients would normally begin
(targeting young people and their parents who may residential rehabilitation after completing inpatient
be specifically at risk), treatment, and availability. detoxification. Despite the support offered by residential
Twenty-four-hour telephone helplines and internet rehabilitation centres, the percentage of clients in such
websites also provide constant advice and information centres who do not complete their treatment programme
CHAPTER 9 SUBSTANCE USE DISORDERS = 3968
is often unacceptably high (Westreich, Heitner, Cooper, (Wilson, 1978), and outcomes are significantly less
Galanter & Guedj, 1997) and, perhaps not surprisingly, favourable when clients with long-standing substance
non-completers fare significantly less well than com- dependence are treated in this way (Howard, 2001).
pleters (Aron & Daily, 1976; Berger & Smith, 1978). Nevertheless, aversion therapy can be used as part of a
However, a number of studies have clearly indicated that broader treatment package involving community sup-
longer stays in residential rehabilitation centres are con- port, detoxification and social skills training.
sistently associated with better outcomes, with a mini-
mum stay of 3 months recommended (Simpson, 2001). Contingency management therapy
This is a treatment procedure that teaches the client how
to restructure and control their behaviour and environ-
9.5.2 Behavioural Therapies
ment in order to prevent drug use. This approach is also
There is a tradition of using behavioural therapies with based on conditioning principles, and these can include
many substance use disorders, and these are mainly adapta- (1) stimulus control, where the client learns to identify
tions of conditioning principles to the practical difficulties environmental situations that trigger drug use and avoid
involved in controlling and preventing substance abuse and or minimize them (e.g. identifying a stressful day at work
dependence. Behavioural therapies have a number of aims: as a trigger for drinking, and so avoiding pubs or bars),
(2) using rewards to reinforce abstinence (e.g. being given
1. to change substance use from a positive or
vouchers for not using a substance, which can be
pleasurable experience to a negative or aversive
exchanged for desired activities such as a trip to the cin-
one (e.g. aversion therapy) (Weins, Montague,
ema or the theatre), (3) learning to be aware of when and
Manaugh & English, 1976);
how frequently drug taking occurs (e.g. by keeping a
2. to help the individual identify environmental stimuli diary noting all times that drinking occurs), and (4) setting
and situations that have come to control substance attainable goals in a structured step-by-step approach to
use (e.g. contingency management therapy) (Miller, treatment (e.g. by setting non-abstinence goals that are
Leckman, Delaney & Tinkcom, 1992); achievable) (Hester, 1995). Contingency management
3. to reinforce abstinence by rewarding the user therapy continues to be a valuable tool for therapists in
when they provide drug-free urine specimens (e.g. this area, with a number of contingency management therapy
contingency management) (Petry, 2000); and new variations on this Behavioural therapy which aims to help the
methodology being devel- individual identify environmental stimuli
4. to teach the user alternative behaviours that are and situations that have come to control
likely to compete with substance use behaviours oped over the years such as
symptoms such as substance use.
(e.g. relaxation, meditation, social skills and anger teaching job-seeking, asser-
management) (Azrin, Acierno, Kogan, Donohue tiveness and social interaction skills.
et al., 1996). A particularly important variant of behavioural
self-control therapy (BSCT) is known as controlled
Aversion therapy drinking. Traditionally, it has been assumed that a
This treatment has been regularly used in the context of ‘cure’ for a substance controlled drinking A variant of BSCT in
a number of substance disorders, but most notably with use disorder entails com- which emphasis is put on controlled use
plete abstinence, but pro- rather than complete abstinence.
alcohol dependence. Using a classical conditioning para-
digm, clients are given their drug (the conditioned stimu- grammes have been developed more recently that put
lus) followed immediately by another drug (the aversive the emphasis on controlled use rather than complete
unconditioned stimulus) that causes unpleasant physio- abstinence. This has been a particularly useful approach
logical reactions such as nausea and sickness (Lemere & to treating alcohol dependency, and has been pio-
Voegtlin, 1950). The assumption here is that pairing the neered by Sobell & Sobell (1993). The assumptions
favoured drug with unpleasant reactions will make that here are that (1) in modern day Western societies it is
drug less attractive. In addition, rather than physically difficult to avoid alcohol altogether, and so it is better
administering these drugs in order to form an aversive to have the aim of controlling drinking rather than
conditioned response, the whole process can be carried avoiding alcohol completely, and (2) teaching clients to
out covertly by asking the client to imagine taking their have control over their drinking behaviour has other
drug followed by imagining some upsetting or repulsive benefits, such as improved self-esteem, a sense of
consequence. This variant on aversion therapy is known responsibility, and feelings of control over particular
as covert sensitisation (Cautela, 1966). However, there
domains in their life. Absence of these latter character-
is limited evidence that istics often drives the individual to alcohol dependence
ert sensitization The association of
versive stimulus with a behaviour the aversion therapy has any- in the first place. Clients undergo social skills training in
it wishes to reduce or eliminate. thing but short-lived effects order to negotiate situations in which they would
24S PSYCHOPATHOLOGY
= STIGMA AND CONTROVERSIAL TREATMENT PROGRAMMES

OV
- FOR SUBSTANCE USE DISORDERS
=
.e) There is stigma associated with drug abuse and sub- give a crack-free urine sample, and can be tested up
a stance use disorders — to the point where there is often to three times a week. Such programmes are signifi-
4) cantly more effective at establishing abstinence than
a public outcry if treatment programmes propose con-
=)
U troversial interventions that seem counterintuitive to control treatments (Lussier, Heil, Mongeon, Badger &
\e) the non-drug user. Recent examples include (1) treat- Higgins, 2006).
LL.
ing heroin addicts by giving them supervised heroin Despite the success of these types of programmes,
injections and (2) giving drug addicts financial rewards and despite the fact that people will rarely criticize
for staying ‘clean’ rewarding people for losing weight or giving up
In the first example, addicts are given daily injec- smoking, there is often a public reluctance to endorse
tions of heroin in supervised clinics in an attempt to programmes that appear to ‘reward’ individuals who
wean them off the drug. A study of this intervention have an illegal substance use disorder, and there have
based in London, Darlington and Brighton in the UK been problems establishing clinics that use these
divided heroin addicts into three groups, giving one types of programmes in countries such as Germany,
group heroin and giving the other two intravenous the Netherlands, Canada and the UK because of pub-
methadone and oral methadone. All three groups lic criticism. It is clear that many people still believe
showed improvement, but the heroin-using group that drug addiction is solely the ‘fault’ of the addict
| fared much better than the other two, with 75 per and as such is self-inflicted (Crisp, Gelder, Rix, Meltzer &
cent having stopped using street heroin and also Rowlands, 2000). Until we can heepengs this as
having significantly reduced their involvement in ful and discriminating gs -
| crime (Strang, Metrebain, Lintzeris, Potts et a/., 2010). view of those with sub- | To read about a controversial proposal
to create ‘drug rooms for addicts go to
Giving drug addicts monetary rewards for staying stance use disorders, it | anesdtioh coming
clean also has a significant effect on the success of may continue to be dif-
treatment. In the ‘Harbour Steps’ trial run in Lambeth ficult to propose, develop and aWenee tesa tre of
|
in London, addicts earn a small credit each time they interventions.
]
otherwise drink excessively, relaxation training to pre- 9.5.3 Cognitive Behaviour

vent stressors that might trigger drinking, and are
Therapies (CBTs)
encouraged to think positively about other domains in
their life (e.g. to eat healthily). Clients are also taught CBT has been used in the treatment of substance
to believe that they have real control over their drink- use disorders in at least two different ways. The first is to
ing, and the BSCT methods outlined above are regu- use CBT to correct dysfunctional beliefs about relapse,
larly used to provide the client with adaptive strategies and the second is to deal with substance use disorder
for control. Finally, controlled drinking also teaches when it is comorbid with other psychiatric symptoms
the client to be aware that a lapse is not catastrophic such as depression and psychosis.
but is often inevitable and natural, and that they can First, as we mentioned earlier, substance abuse disor-
use the self-control and social skills they have learnt to ders are notoriously difficult to treat over the longer
overcome lapses. Outcome studies suggest that con- term. Individuals can usually quit the substance in the
trolled drinking is achievable, can be as effective over short term, but relapse is common in up to 90 per cent
the longer term as treatments that require total absti- of those receiving treatment for substance dependency
nence (Foy, Nunn & Rychtarik, 1984), and can help (Brownell, 1986). As a result, a successful treatment pro-
individuals to moderate their intake and to live more gramme has to deal as effectively with relapses as it does
fulfilled and healthier lives (Sobell & Sobell, 1995). in getting the client to quit in the first place. Two factors
Controlled drinking is also an accepted treatment appear to be important in determining whether a
strategy for a majority of substance abuse services in relapse will lead to regular use again. These are (1) the
the UK (Rosenberg & Melville, 2005). client’s beliefs about relapse, and (2) experiencing
HAIR SAMPLE ANALYSIS

Many methods of collecting data about substance abuse are relatively unreliable. Self-report is obviously prob-
lematic, because users will often have reason to lie about their drug use (if it involves legal issues such as child
custody), or their recall of drug use may be affected by the changed states of consciousness caused by regular
use ofcertain substances. Even blood and urine samples can be very variable in the data they provide (Spiehler &
Brown, 1987), and are certainly not suitable for estimating longer term drug use.
However, one relatively reliable method of collecting data about drug use is through hair sample analysis
(e.g. Uhl & Sachs, 2004). Small amounts of the drug will accumulate in hair after use and, because head hair
grows at approximately 0.8-1.3cm per month, a record of drug use is available over
a period of weeks or months after intake. A hair sample of only 3-5cm in length is hair sample analysis A method of col-
lecting data about previous drug use by
required
METHODS
RESEARCH
9.1 to provide a record of drug use over the previous 3-4 months, and high- analysing the small amounts of the drug
performance chromatography is used to identify the concentrations of any drugs that accumulate in the hair.
taken up into the hair sample.
Hair sample analysis is not only used as a more reliable way of collecting research data about previous
drug use, it is becoming widely used for medico-legal purposes where the user needs to prove long-term
abstinence (especially in cases related to rehabilitation and legal custody). It is also used to provide a longer
term record ofdrug use in the case of individuals who may have died from overdose (Tagliaro, Battisti, Smith &
Marigo, 1998), and has been used to detect the use ofopiates, cocaine, cannabis, and amphetamines (Jurado &
Sachs, 2003).
Nevertheless, hair sample analysis is not a foolproof way of estimating drug use, and it does have its own
drawbacks as a methodology. For instance, it is not suitable as a measure of current drug use, but only as a
method of estimating previous medium-term use. It also cannot be used on those who present with very short
hair or no head hair!
stressful emotional states, such as anxiety, depression, developed that help the client to deal effectively
anger, and frustration, and these states are responsible with negative emotions, stress, and the factors that
for around 30 per cent of all relapses after treatment might give rise to stress. This is also known as
(Cummings, Gordon & Marlatt, 1980). In order to coun- motivational-enhancement intervention (MET) and
ter these relapse factors, therapists have developed vari- provides communication i a a
ants of CBT that address dysfunctional beliefs about training, work-andschool- tien (MET) An intervention for substance
relapse, and can also provide help in coping with stress-related skills, problem- abuse and dependency involving commu-
ful emotions. In the first case, individuals will often hold solving skills, peer refusal nication training, work- and school-related
dysfunctional beliefs about relapse that facilitate further skills, |negative |mood PA UA ERSMEK
skills, negative mood management, social
regular use. These may include beliefs such as ‘If I lapse, management, social sup- support and general relapse prevention.
then my treatment has failed’, ‘If I lapse, then I am a port, and general relapse
worthless individual who doesn’t deserve to get better’, prevention methods (Miller & Rollnick, 1991). Both
or ‘I’ve had one drink, so I may as well get drunk’ forms of CBT have been shown to be more effective in
(Marlatt & Gordon, 1985). These are what are known as establishing long-term abstinence and effective drug
abstinence violation beliefs that contribute to the tran- avoidance behaviours than traditional aftercare or con-
sition from relapse ‘slips’ to full relapse. CBT attempts trol conditions (McAuliffe, 1990; Farabee, Rawson &
tinence violation Dysfunctional to identify such dysfunc- McCann, 2002) and are particularly effective if com-
efs about relapse following treatment tional beliefs, to challenge bined with family therapy (Waldron, Slesnick, Brody,
them (e.g. relapse doesn't
substance dependency that facilitate Turner & Peterson, 2001).
her regular substance use. Interestingly, recent UK NICE guidelines for treat-
inevitably mean total loss
of control), and to provide the client with the skills ments for substance use disorder recommend CBT
required to negotiate a relapse successfully. To deal with primarily when substance use disorder is comorbid
the second factor, CBT programmes have been with another psychiatric disorder such as anxiety or
: —
depression (see http://www.nice.org.uk/nicemedia/ and improvements in the quality of the couple’s rela-
live /11812/35973/35973.pdf). However, systematic reviews tionship (Fals-Stewart, Birchler & O'Farrell, 1996).
indicate only moderate support for CBT when treat-
ing comorbid depression and substance dependency
(Hides, Samet & Lubman, 2010), with the implica-
tion that more potent
Tovead Inearticie ¢n CBT and forms of CBT still need
Drugs are used to treat substance use disorders in a vari-
substance use by Hides, Samet &
Lubman goto to be developed to deal ety of ways. Collectively these are known as detoxifica-
www.wiley-psychopathology.com/ with substance use disor- tion, and are often used in conjunction with psychological
reading/ch9 eaeats
iz der comorbidity. treatments or as a precur-
sor to psychological treat- detoxification A process of systematic f
and supervised withdrawal from substa
ments (to wean heavy use that is either managed ina residentia
9.5.4 Family and Couple Therapy users off regular substance setting or on an outpatient basis. q
use and make them ame-
Because many regular drug abusers are young people, nable to other forms of therapy). Detoxification is a pro-
they often live with their families and, because of this, cess of systematic and supervised withdrawal from
family members can often provide support during treat- substance use that is either managed in a residential set-
ment on a day-by-day basis. However, family therapy ting or on an outpatient basis. Drug use during detoxifi-
is important for a number of other reasons. Firstly, cation can take a number of forms: (1) to help reduce
many of the parents of substance abusers are also abus- withdrawal symptoms (e.g. anxiolytic drugs), (2) to pre-
ers themselves, and as such may constitute part of the vent relapse by using antagonistic drugs to make subse-
problem that needs to be addressed. Secondly, individu- quent substance use aversive (e.g. Antabuse — a drug that
als with substance abuse problems (such as problem causes vomiting if alcohol is consumed), (3) to block the
drinkers) will often physically and sexually abuse mem- pleasurable CNS effects of a substance (e.g. naxolone —
bers of their family, and so therapy may often need to used with individuals who methadone maintenance - g
involve those who have regular close contact with the are opiate dependent in programmes Adetoxification progranil
abuser. Family therapy is an effective way of identify- order to prevent opiates Where users take
aless virulent opiateir
peeand ae ees family patterns that may having their usual effects order to wean themselves off heroin.
an contribute to adolescent on reward centres in the
To read Rowe's article on family | substance abuse (Rowe
3 > brain), and (4) to wean a user onto a weaker substance
therapy go to 5
www.wiley-psychopathology.com/ 2012), and can often be an (e.g. methadone maintenance programmes, where the
reading/ch9 ) effective brief interven- user takes a less virulent opiate in order to wean them-
—ennmnnee” FiOr for adolescent sub: selves off heroin).
stance abuse when whole families are involved in the Those drugs that help reduce withdrawal symptoms
programme (Szapocznik, Zarate, Duff & Muir, 2013). include clonidine, which reduces noradrenergic activity
Family therapists will attempt to engage members of in the brain (Baumgartner & Rowan, 1987), and acam-
the family in the treatment process and to reduce blam- prosate, a drug that helps to reduce the cravings asso-
ing behaviour. Subsequently, the therapist will use con- ciated with withdrawal (Mason, 2001). Basic anxiolytic
tingency management and behavioural contracting and anti-depressant drugs can also be used to improve
procedures, and teach communication and problem- mood and alleviate negative emotions experienced dur-
solving skills in order to facilitate more adaptive patterns ing withdrawal (Cornelius, Salloum, Mezzich, Cornelius
of interaction within the family. This approach has been et al., 1995).
shown to be particularly successful in dealing with ado- Antabuse (disulfiram) has been used for over 60
lescent substance use problems, and is generally as effec- years in the detoxification of individuals with alcohol
tive in the long term as individual psychotherapies such dependency. It affects the
as CBT (Waldron, Slesnick, Brody, Turner et al., 2001). metabolism of alcohol so antabuse (disulfiram) A drug used in th
that the normal process of caer of individuals with scchol
Specifically involving a client’s spouse or partner in ther-
ependency.
apy also has important beneficial effects. The partner can converting toxic alcohol
offer support when required, but it is also important in products into nontoxic acetic acids is slowed, and this
identifying specific problems in a relationship that may causes the individual to feel nauseous or vomit when-
be contributing to substance abuse. Outcome studies ever they take alcohol. However, the use of Antabuse
have indicated that, when compared with no treatment, does have some problems. It is rarely effective when
couples therapy produces longer periods of abstinence patients are given the drug to take unsupervised, and
CHAPTER 9 SUBSTANCE USE DISORDERS ae
non-compliance and drop-out from such programmes (O’Brien, 2005). The reason why such drugs may be
are high (Fuller, Branchey, Brightwell, Derman et al., effective over a range of substances that have their
1986). Secondly, it does have a number of side effects, psychoactive effects across different brain neurotrans-
and in some rare cases causes liver disease and hepati- mitter pathways is because they suppress the release
tis (Mohanty, LaBrecque, Mitros & Layden, 2004). of endorphins, and endorphin receptors are closely
However, when taken in properly supervised pro- associated with the brain’s reward centres (Leri &
grammes, Antabuse has been shown to be more effec- Burns, 2005).
tive at reducing drinking behaviour than placebo Finally, drug replacement treatment involves treat-
controls (Chick, Gough, Falkowski, Kershaw et al., 1992; ing severe cases of substance abuse and dependence by
Fuller & Gordis, 2004), including having a beneficial effect substituting a drug that drug replacement treatment Involves
on short-term abstinence and days until relapse (Jorgensen, has less damaging effects. treating severe cases of substance abuse
Pedersen & Tonnesen, 2011). Indeed, some long-term For example, many heroin and dependency by substituting a drug
studies of alcohol treatment have suggested that absti- users put themselves at that has lesser damaging effects.
nence rates of 50 per cent are achievable up to 7 years after risk from overdoses, contaminated street heroin, and
initial treatment with the supervised and guided use of using unsterilized needles. To try to address these issues
alcohol deterrents such as Antabuse (Krampe, Stawicki, as rapidly as possible, users can be switched from heroin
Wagner, Bartels et al., 2006), and that Antabuse to the less virulent opium derivative methadone.
can increase treatment Methadone has a slower onset and weaker effects, and
To read an article on ‘The efficacy of effectiveness when com-
disulfiram’ by Jorgensen, Pedersen &
can be taken orally rather than injected. Initial outcome
Tonnesen go to bined with CBT (Pettinati, studies suggested that methadone treatment was helpful
www.wiley-psychopathology.com/ Oslin, Kampman, Dundon in enabling heroin addicts to withdraw from the drug.
reading/ch9
et al., 2010). However, we must remember that methadone is still an
A further set of drugs addictive drug itself and it can be difficult to withdraw
used to treat substance use disorders are those that influ- from (Kleber, 1981), and because of this methadone
ence brain neurotransmitter receptor sites and prevent maintenance therapy can last for many years — and for
the neuropsychological effects of stimulants, opiates and some, for their whole lifetime (Smyth, Barry, Lane,
hallucinogens. For example, drugs such as naltrexone, Cotter et al., 2005; Arora & Williams, 2013). Most recent
naxolone and the more recently developed buprenorfine outcome studies suggest that methadone maintenance
attach to endorphin recep- therapy is most effective when part of a multifaceted
rexone An opioid receptor antagonist tor sites in the brain. This structured therapy programme that includes psycho-
1 primarily in the management ofalco- prevents opioids from hav- therapy, drug education, skills training, and contingency
Jependence and opioid dependence.
ing their normal effect of management (O’Brien & McKay, 2002), and when the
stimulating these sites to client includes non-drug-using family members and
plone One of a set of drugs used to produce more endorphins friends in the treatment (Kidorf, King, Neufeld, Stoller
t substance usedisorders which influ- ‘ Pees rg
> brain neurotransmitter receptor sites BBN CSS he 1S ay
et al., 2005). As well as contributing to the success of
prevent the neuropsychological effects euphoria when drugs such treatment in a multifaceted approach, methadone main-
imulants, opiates and hallucinogens. as heroin are taken. tenance therapy has the added benefits of increasing the
Such drugs do appear to likelihood of entering into longer term comprehensive
renorfine An opioid drug used in the reduce craving for opiates treatment, reducing heroin use and criminal behaviour,
‘ment of opioid addiction. and they help the thera- and reducing health risks (e.g. the number of HIV cases)
peutic process when com- (Schwartz, Highfield, Jaffe, Brady et al., 2006; Farrell,
bined with other forms of psychological therapy Gowing, Marsden, Ling & Ali, 2005; Arora & Williams,
(Streeton & Whelan, 2001). However, such drugs do 2013). While drug maintenance therapies have been
come with a cost. Dosage has to be properly regulated, largely confined to treating drug maintenance therapies Drug treat-
otherwise the client may be thrown rapidly into an opiate dependency, there ment programmes in which severe cases
aversive withdrawal (Roozen, de Kan, van den Brink, have been recent attempts of substance abuse and dependency are
Kerkof & Geerlings, 2002), and narcotic antagonists to develop substitute drugs treated by substituting a drug that has less
damaging effects.
such as naltrexone and naxolone are only effective for for other dependencies.
as long as the client is taking them. However, because One such example is Sativex, an aerosol that combines
these drugs affect the release of endorphins, they have THC and non-psychoactive cannabis ingredients for the
been used to help treat a number of substance use treatment of cannabis dependency. Savitex has the ben-
disorders, including alcohol (O’Malley, Krishnan-Sarin, efit of having weaker effects than cannabis and is taken
Farren & O’Connor, 2000), cocaine and opiate dependence orally rather than smoked (Kleber, 2005).
26: PSYCHOPATHOLOGY
* Why are substance use disorders particularly hard to treat?

* Can you describe the different kinds of community-based programmes that help to prevent or treat substance use
disorders?
* How successful is residential rehabilitation in treating substance use disorders?
® How have the principles of behaviour therapy been adapted to treat substance use disorders?
® Can you name the main features of aversion therapy; contingency management therapy, and controlled drinking?
* What are some ofthe benefits of using controlled drinking goals rather than complete abstinence?
° What are abstinence violation beliefs and how do cognitive behaviour therapies (CBTs) attempt to treat them?
® What is meant by the term detoxification, and how are drugs used in detoxification programmes?
® How have drugs such as naltrexone, naxolone and buprenorfine proved to be useful in the treatment of substance use
disorders?
SECTION SUMMARY
9.5 THE TREATMENT OF SUBSTANCE USE DISORDERS
The treatment of substance use disorders is inevitably a multifaceted one, with most mental health services providing a
range of treatments (detoxification, skills training, behavioural and cognitive therapies, and family and couple therapies) in
a variety of settings (e.g. individual, community-based or residential). Treatments usually involve a combination of drug-based
detoxification, psychological therapy, and skills training, and will usually attempt to involve the client's family and friends in
the therapeutic process. Substance use disorders are difficult to treat and we described some of the difficulties at the outset
of this section on treatment. Nevertheless, outcomes are often good, and total abstinence is an achievable goal — even with
severely addictive substances such as opiates and stimulants. For example, a long-term study of heroin dependence in a
small town in the south-east of England 33 years after initial treatment found that 42 per cent of those treated had been
abstinent for 10 years (Rathod, Addenbroke & Rosenbach, 2005). This suggests that long-term dependence is not inevitable
after exposure to addictive drugs, and individuals can often control their use as well as receive effective treatment for their
dependency when required.
The key points discussed in this this section are:
¢ Treatment of substance use disorders is difficult because of the physical effects of dependence, the probability of comorbid
psychiatric disorders, and high rates of relapse.
¢ Treatment interventions are usually multifaceted and address the individual client’s problems at a range of different
levels.
* One form of community-based service is self-help groups such as Alcoholics Anonymous (AA).
e Drug-prevention schemes are used with young people to try and prevent first drug use.
° Residential rehabilitation centres provide a controlled environment for detoxification and longer term support for individu-
als with substance use disorders.
e Behaviour therapies adapted to treat substance use disorders include aversion therapy and contingency management
therapy.
* Controlled drinking can be used as a non-abstinence approach to treating alcohol abuse and dependency.
&
* Cognitive behaviour therapy (CBT) is used primarily to change individuals’ beliefs about their substance use, but are best
employed when a sufferer has a psychiatric disorder comorbid with substance use disorder.
° Motivational-enhancement training (MET) provides communication training, work- and school-related skills, problem-
solving skills, peer-group refusal skills, relapse prevention methods, and negative mood management.
° Family and couple therapy is useful for ensuring that family members understand the reasons for the substance use and can
provide help and support during and after treatment.
¢ Detoxification is a process of systematic and supervised withdrawal from substance use that often uses the controlled use
of drugs to combat the physical problems of withdrawal and dependence.
¢ Antabuse (disulfiram) causes alcohol to produce toxins which make the individual feel unwell and has been used for over 60
years as a means of controlling alcohol dependency.
¢ Drug maintenance therapies involve treating severe cases of substance use (e.g. heroin dependence) by normally substitut-
ing a drug that has a lesser effect (e.g. methadone).
drugs regularly even though this activity has significant

9.6 SUBSTANCE USE negative effects on their health and social and occupa-
DISORDERS REVIEWED tional functioning?).
Some people do seem to move down a slippery slope
from experimentation to abuse and dependence, but
Substance use disorders are an important social and we have to be clear that many other people do not, and
health problem, as well as also raising many mental health people can be regular substance users without this affect-
issues. Substance use disorders are associated with crimi- ing their family, social and occupational functioning.
nal behaviour (often violent crime), short- and long-term However, when the stage of substance abuse and depend-
health problems, disruption to social and occupational ence is reached, this is often associated with comorbid
functioning, and with increased risk of psychiatric comor- psychiatric problems or simply with poverty, unemploy-
bidity. The main substances of abuse can be grouped ment and poor housing. In the former case, many who
into stimulants (e.g. cocaine, amphetamine), sedatives are substance dependent use their drug to self-medicate
(e.g. opiates, barbiturates), and hallucinogenic drugs (e.g. against the negative effects of their comorbid psychopathy
LSD). Legal drugs such as alcohol and nicotine can also (e.g. depression, eating disorders, anxiety disorders and
foster dependence and can cause significant long-term suchlike). In the case of poverty, the mood altering effects
health problems. of the drug may provide relief from miserable and unful-
Most of the drugs associated with abuse and depend- filled lives.
ence have important mood altering effects that make the Treatment of substance use disorders is usually mul-
user feel confident, relaxed (alcohol, cannabis), euphoric tifaceted, and many health services provide a tiered
(heroin, cocaine), or energized (amphetamines, MDMA). approach by providing a range of treatments, advice and
More importantly, these effects also alleviate any negative training facilities in a variety of settings (e.g. individual,
or stressful mood the user may be feeling prior to use. community-based or residential). Substance use disor-
Most of these substances also have addictive properties as ders can be difficult to treat because of the difficulties
users quickly develop a tolerance to the drug and experi- of dealing with withdrawal symptoms, the fact that the
ence worsening withdrawal symptoms during abstinence. drug has probably been the user’s main method of cop-
Substance use disorders can be seen as developing ing with emotional and life stressors, frequent comorbid-
through a number of different stages, with different fac- ity of other mental health problems, and temptation to
tors affecting transition from one stage to the next (see relapse after treatment. However, outcome studies sug-
Figure 9.7). The three stages highlighted here are experi- gest that with appropriate support and aftercare, treat-
mentation (what determines first use?), regular use, and ment can result in long-term abstinence in a significant
abuse and dependence (what makes some people use proportion of clients.
2aR To access the online resources for this chapter go to

[=]Cae www.wiley-psychopathology.com/ch9
Reading Activity
~
Alcoholics Anonymous Alcohol misuse: A Different sub-

12-step programme personal account stances discussed in
Journal article: Cannabis this chapter
Heroin use Medical use of Alcohol unit con-
Breakthrough Britain: cannabis sumption calculator
Addictions Cocaine Developmental
Debate rages over model of substance
Cocaine: Risk and
experts’ proposal to abuse and
recovery
create ‘drug rooms for dependence
Heroin
addicts in Brighton and Self-test questions
Hove Opioid use disorder
Revision flashcards
Journal article: CBT and LSD
Research questions
substance use Ecstasy
Journal article: Family
therapy
Article: The efficacy of
disulfiram
Glossary of key terms
Clinical issues
References
10 Eating Disorders
This chapter covers the description, aetiology and treat-

ment of the three main eating disorders, namely anorexia 10.1 DIAGNOSIS AND PREVALENCE 333
nervosa, bulimia nervosa, and binge-eating disorder. The

chapter begins by describing the main symptoms and 10.2 CULTURAL AND DEMOGRAPHIC DIFFERENCES IN
diagnostic features of these disorders, and then explores EATING DISORDERS 341
their cultural and demographic distribution. Eating dis-
orders have their origins in a range of psychological, 10.3 THE AETIOLOGY OF EATING DISORDERS 343
sociological and biological processes, and all these are :
explored in the section on aetiology. Finally, eating disor- : 10.4 THE TREATMENT OF EATING DISORDERS 354
ders are often complex and difficult to treat, and the final
section discusses those treatments which have so far proved 10.5 EATING DISORDERS REVIEWED 360
most effective — namely, pharmacological treatments, fam-
ily therapy and cognitive behaviour therapy (CBT).
33255 PSYCHOPATHOLOGY j
“
LEARNING OUTCOMES
1. Describe the characteristics and main 3. Compare and contrast a range of risk factors
diagnostic criteria of the three main eating for eating disorders, covering risk factors at
disorders. different levels of explanation (such as genetic,
2. Describe the cultural and demographic developmental, cultural, and psychological).
distribution of eating disorders, and evaluate why 4. Describe, compare and contrast at least two
this information is important in understanding interventions commonly used in the treatment of
eating disorders. eating disorders.
For as long as | can remember, I've wanted to do everything under the sun — and be the best at it. If! got a C, I'd be really hard on
myself, and my parents made it pretty clear they wanted me to get a scholarship, since paying for college would be a challenge.
Plus, things weren't so great at home..I'd always had a terrible relationship with my dad. |felt like he ignored me most of the
time. He could be pretty scary. Screaming at me for little things — like leaving crumbs on the kitchen table after making a snack.
I'd tell him when he hurt my feelings, but he’d just walk away and slam the door. On top of it all, he and my Mum were fighting a
lot, too.
It was hard to be at school and even harder to be at home. As a result, | began eating less. Starving myself wasn’t my actual
goal at first — just more of a response to everything going on in my life. But | started to lose weight.
Soon, my clothes got looser. Then | became a vegetarian, also cutting out all foods with chemicals and preservatives. | lost
even more weight. | felt | had finally found something | could completely control — my weight. Even though my life felt crazy,
| could do this one thing very well and, initially, |got a high from this accomplishment. Gaining or losing a single pound deter-
mined my mood for the whole day.
| remember watching a film in health class about the dangers of anorexia. |even hung warning posters around school dur-
ing Eating Disorders Awareness Week. But | never connected my own weight loss to anorexia. Denial, of course, is a symptom
of the disease. A voice in my head kept telling me the less food | let touch my lips, the more stable and safe | would be. My fiends
and family kept telling me | was too skinny, but no one could force me to eat. And, to be honest, it made me feel powerful that |
could ignore pleas and starve myself. Even as my bones poked out from under my skin, | could not admit to anyone — including
myself — how incredibly sick | was.
Amy’s Story
Introduction these media-portrayed ideals of a slim body — ideals

which are usually underweight. Given these pressures,
Disorders of eating are complex and have their roots in and the psychological factors that accompany them, it
psychological, sociological and cultural phenomena. In _ is not surprising that eating patterns can become path-
many of today’s cultures, individuals are torn between ological and result in disorders of both under-eating
advertising that implores them to eat a range of foods (anorexia nervosa) and over-eating (bulimia nervosa and
high in calories, and campaigns designed to promote _ binge-eating disorder).
selective and healthy eating, because being overweight Amy’s story above illustrates what a slippery slope
is closely associated with an increase in certain illnesses the descent into an eating disorder can be. The story
and higher death rates. Eating behaviour is also influ- starts with someone who is troubled in various spheres
enced by media representations of ideal body shapes. _ of her life, including school life and home life. In Amy’s
aa These prompt appearance- case, this leads more by accident than design to a reduc-
é RO comple DemibKUALGOS | conscious individuals .to tion in eating. Eventually, controlling eating becomes a
Q ila aah _i control and restrict their goal in itself, and a source of satisfaction when even the
‘Sq eating in order to achieve smallest of dietary goals are met. The obvious physical
CHAPTER 10 EATING DISORDERS 3384
Le WARNING SIGNS OF ANOREXIA NERVOSA

=
(=)
= ° Is she losing a lot of weight? Has she fallen ° Has she started to become obsessive about exer-
Z 7 pounds below the normal weight range for cise, or any other daily routine (e.g. homework)?
fe)
a.
someone of her height? e Is she suffering unusually from infections, consti-
e Isshe becoming an obsessive counter of calories? pation, dizzy spells, insomnia, or does she com-
WV)
> Does she eat only very low-calorie foods, like plain of the cold?
UW salad and fruit?
)tL. ° Isshe becoming secretive or evasive about her eat- From http://www.annecollins.com/eating-disorders/anorexia
ing habits? Does she eat out of sight or in private? .Atm.
consequences of lack of nutrition then become exhaus- eating patterns leading to either underweight or over-
tion and lack of concentration, menstrual irregularities, weight (McBride, McManus, Thompson, Palmer &
and proneness to infections, insomnia, dizzy spells, and Brugha, 2013). Apart from the cultural pressures that
sensitivity to cold. Amy’s story also highlights some of the can trigger over-eating and under-eating, psychological
risk factors that have been found to predict the develop- factors also represent both risk factors and outcomes of
ment of an eating disorder such as anorexia, and these disordered eating. As we shall see later in this chapter,
include high levels of perfectionism, and parents who developmental and psychological processes appear to
exhibit coercive parental control, or who are hostile and act as vulnerability factors in the development of eating
unresponsive to the individual’s needs. Also characteristic disorders, and eating disorders themselves can result in
of the disorder, and featured in Amy’s story, are the need psychological symptoms such as low self-esteem, sub-
to control eating as a central feature of eating disorders stance misuse, and suicidal ideation (Neumark-Sztainer,
generally, the development of very durable and resist- Hannan, 2000).
ant beliefs about the need to diet and control eating, and This chapter will cover the three main eating dis-
the use of denial as a means of avoiding confronting the orders, namely anorexia nervosa, bulimia nervosa and
disorder and challenging dysfunctional beliefs about eat- binge-eating disorder, and for each discuss diagnosis
ing. Focus Point 10.1 summarizes some of the warning and prevalence, the role of sociocultural factors, aetiol-
signs of anorexia nervosa, many of which will have been ogy, and treatment.
apparent as Amy developed her own eating disorder.
Many women consider themselves to be overweight
despite having a BMI in the normal range. Studies of
college women suggest that 43 per cent were currently 10.1 DIAGNOSIS AND
dieting despite 78 per cent of them having a healthy BMI
(Fayet, Petocz & Samman, 2012), while community stud-
PREVALENCE
ies indicate that between 25 and 30 per cent of females
claim to be dieting or actively attempting to lose weight
10.1.1 Anorexia Nervosa
(McVey, Tweed & Blackmore, 2004; Wardle & Johnson,
2002). Dieting is often a significant precursor to anorexia The main symptoms of anorexia nervosa (AN) are self-
nervosa symptoms (Patton, Carlin, Shao, Hibbert et al., starvation and a refusal to maintain a minimally normal
1997) and can become an entrenched habit that is resistant body weight, and examples resembling anorexia have
to both psychological and pharmacological treatment, been reported throughout history (see Focus Point 10.2).
and dieting may contribute to the persistence of symp- It is a disorder that afflicts
anorexia nervosa (AN) An eating disor-
toms in some anorexia nervosa sufferers (Walsh, 2013). mainly adolescent women, der, the main features of which include a
Similarly, recent figures suggest that obesity is increas- and tends to have an onset refusal to maintain a minimal body weight,
ing significantly in Western cultures. In the UK, obesity in the early to middle teen- a pathological fear of gaining weight and a
rates have almost doubled between 1993 and 2011, with age years following either distorted body image in which sufferers
continue to insist they are overweight.
24 per cent of men and 26 per cent of women currently a period of life stress or an
rated as obese, with a BMI in excess of 30 kg/m/* (Health & intense period of dieting. Ten times more females than
Social Care Information Centre, 2011). This suggests males are afflicted by the disorder (Walters & Kendler,
that both under-eating and over-eating have reached 1994), and in recent years there appears to be an increas-
almost epidemic proportions, with surveys suggesting ing trend towards early-onset anorexia in girls between 8
that 6.3 per cent of the UK population exhibit disordered and 13 years of age (Lask & Bryant-Waugh, 2000), with
"334.45 PSYCHOPATHOLOGY
%
surveys indicating that almost 30 per cent of 8- to 3. a distorted body image in which, even when
13-year-olds report avoidant or restrictive eating behav- clearly emaciated, sufferers continue to insist they
iour (van Dyck, Bellwald, Kurz, Dremmel et al., 2013). are overweight.
Important features of anorexia nervosa include:
Weight loss is often viewed as an important achieve-
1. a refusal to maintain a minimal body weight, ment (see the example of Amy at the beginning of this
2. a pathological fear of gaining weight, and chapter), and weight gain as a significant loss of
& HISTORICAL EXAMPLES OF EATING DISORDERS

°
~=
= There is a tendency to think of eating disorders as for their refusal to eat. This may also be true of the his-
Fa modern ailments driven by cultures obsessed with torical examples we have reviewed here.
(°) projecting ideal body shapes to impressionable young Historical examples resembling bulimia nervosa are
a. people. However, examples of disordered eating much rarer than those resembling anorexia nervosa.
“n behaviour can be found throughout history, and many Most examples taken from classical times through to
=)
UY bear resemblance to the eating disorders we find the 19th century report individuals exhibiting periods
(eo) today (Keel & Klump, 2003). Cases of self-starvation of fasting followed by a binge-purge cycle, which sug-
iri have been reported in classical and medieval times, gests that bingeing and purging was rarely found out-
often as a means of achieving heightened spiritual- side of the context of fasting or self-starvation (Keel &
ity amongst religious devotees. Bell (1985) called this Klump, 2003). However, in the 17th century, Silverman
holy anorexia, and cited the example of St. Catherine (1987) reports a description of fames canina - a dis-
of Siena who began self-starvation at the age of order characterized by large food intake followed by
16 years and continued until her vomiting (Stein & Laakso, 1988). Interestingly, however,
holy anorexia Self-starvation reported
in classical and medieval times, often as a
death in 1380 (at the age of 32). when symptoms similar
fames canina An eating disorder charac-
means of achieving heightened spirituality Like modern-day anorexics, St. to bulimia are reported
terized by large food intake followed by
amongst religious devotees. Catherine portrayed herself as in historical writings, most vomiting reported in the 17th century.
| being afflicted by an inability to cases involve adult men.
|
| eat, and all attempts by peers and superiors to induce This is quite unlike the current day disorder of bulimia,
| eating in such fasting saints usually failed. From the which is primarily an affliction of females.
16th to 18th centuries, reports of self-starvation were This brief review suggests that disordered eating
relatively common (McSherry, 1985), with the case of (especially self-starvation) has been around as long
Mary, Queen of Scots (1542-1587) being a prominent as people have been able to write about it and report
one. During the 19th century, study of self-starvation it. In different periods of history, the motivations for
became more systematic within the medical profes- self-starvation appear to be different, although the
sion, with Marce describing a form of hypochondria in symptoms remain remarkably similar. One implica-
which ‘young girls, who at the period of puberty and tion of this is that disordered eating symptoms simi-
after a precocious physical development, become sub- lar to modern-day disorders have been around for
ject to inappetency carried to the utmost limits’ (1860, a considerable period of history. However, changes
p.264). Probably the first use of the term anorexia ner- in contemporary sociocultural factors may influence
vosa was by Imbert (1840), who characterized anorexie the frequency and prevalence of such disorders by
nerveuse by loss of appetite, refusal to eat, and ema- providing a motivation for disordered eating (e.g. reli-
ciation (Vandereycken & Van Deth, 1994). However, gious fasting would have provided a suitable trigger
while these historical examples bear a formalistic for self-starvation in vulnerable individuals in classical
similarity to modern-day eating disorders, the issue of and medieval times). In addition, sociocultural factors
the motivation behind self-starvation in these histori- can also provide socially acceptable means of hiding
cal examples is important. At least some of the earliest the psychological reasons for self-starvation and loss
examples of self-starvation appear to be motivated by of appetite. For example, when fasting became an
religious and spiritual factors, while examples from the acceptable form of convalescence from illness in the
18th and 19th century were justified as either forms 18th and 19th centuries, this may have provided a
of convalescence or hysterical paralysis (Habermas, suitable means of hiding the anorexic individual's sim-
1996). However, Habermas (1989) quite rightly points ple desire to restrict and control their eating (just as
out that individuals with eating disorders tend to hide the trend to diet to achieve a media-driven thin ideal
their goal of losing weight and give other explanations serves the same purpose today).
CHAPTER 10 EATING DISORDERS 335°
self-control. Even when individuals suffering anorexia do DSM-5 SUMMARY TABLE 10.1 Criteria for anorexia nervosa
admit they may be underweight, they often deny the
e A significantly reduced calorie intake relative to the
important medical implications of this, and will continue
requirements of the body leading to a considerably low
to focus on reducing fat in areas of their body that they body weight
still believe are too ‘fat’. DSM-5 Summary Table 10.1 sets
out the main diagnostic criteria for anorexia nervosa. e Intense fear of gaining weight or becoming fat
DSM-5 stresses objective levels for judging the severity of e A disruption in the way that the patient evaluates their
the symptoms based on body mass index (BMI). DSM-5 body or shape, increasing undue influence of body weight
has also adopted the World or shape on self-evaluation
ly mass index (BMI) A way of
Health Organisation lower
asuring a healthy weight range,
ived by using both height and weight limit for ‘normal’ body
asurements. weight of a BMI of 18.5 life event, such as leaving home (Tozzi, Sullivan, Fear,
kg/m?’ as a level below McKenzie & Bulik, 2003), and is often preceded by a
which body weight should be considered as low enough period of changed eating patterns, such as self-imposed
to trigger the possibility of a diagnosis of anorexia ner- dieting. Fortunately, most individuals with a diagnosis
vosa if other criteria are met. The criteria also emphasize of anorexia nervosa will remit and be symptom-free
the pathological fear of weight gain in sufferers, and the within 5 years. However, for others, hospitalization may
distortions in self-perception that accompany anorexia. be required to restore weight and address other medical
DSM-5 also distinguishes two types of anorexia nervosa. complications caused by self starvation.
These are the restricted type AN, in which self-starvation DSM-5 cites the 12-month prevalence rate for anorexia
is not associated with con- nervosa among young females as around 0.4 per cent, with
tricted type AN A type of anorexia
vosa in which self-starvation is not
current purging (e.g. self- a female-to-male ratio of around 10:1, making anorexia
ciated with concurrent purging (e.g. induced vomiting or use of primarily a female disorder. Lifetime prevalence rate for
-inducing vomiting or use of laxatives). laxatives), and the binge- females by the age of 20 years is 0.8 per cent, with a peak
eating/purging type AN, onset age of 19-20 years (Stice, Marti & Rohde, 2013). There
ge-eating/purging type AN A type
where the sufferer regu- is some evidence that cultural and societal factors can affect
ating disorder in which the sufferer
Jlarly engages in purging activities to larly engages in purging the frequency of anorexia, so that prevalence rates may dif-
) control weight gain. activities to help control fer across cultures and across time (see section 10.2 below)
weight gain. (Miller & Pumariega, 2001). However, recent analysis sug-
Because of the severe physical effect of this disorder gests that anorexia may represent a similar proportion of
on the body, anorexia nervosa is usually associated with the general psychiatric population in several Western and
a number of biological symptoms that are effects of the non-Western nations (examples of the latter include Korea,
self-imposed starvation regime. These include (1) tired- Iran, Hong Kong, Japan, Malaysia, and Egypt), and there is
ness, cardiac arrhythmias, hypotension, low blood pres- growing evidence that it is not just a disorder of affluent
sure and slow heartbeats resulting from altered levels of Western cultures (Keel & Klump, 2003).
body electrolytes, such as sodium and potassium, (2) dry High rates of comorbidity exist between anorexia
skin and brittle hair, (3) kidney and gastrointestinal prob- and other psychiatric disorders. For example, studies
lems, (4) the development of lanugo (a soft, downy hair) suggest between 50 and 68 per cent of anorexia suffer-
on the body, (5) the absence of menstrual cycles (amenor- ers also have a lifelong diagnosis of major depression
rhoea), and (6) hypothermia, often resulting in feeling cold (Halmi, Eckert, Marchi, Sampugnaro et al., 1991), and
even in hot environments between 15 and 69 per cent of anorexia sufferers also
snorrhoea The abnormal failure to
istruate.
(Bryant-Waugh, 2000). In meet diagnostic criteria for OCD or obsessive compul-
many cases, starvation has sive personality disorder (OCPD) at some time during
the effect of severely weakening the heart muscles as the their lifetimes (Hudson, Pope, Jonas & Yurgelun-Todd,
body uses these muscles as a source of protein. As a 1983; Wonderlich, Swift, Slotnick & Goodman, 1990).
result, mortality rates (including suicides) in anorexia Most recent surveys suggest significant levels of comor-
nervosa and bulimia nervosa are still unacceptably high, bidity between anorexia nervosa and anxiety disorders
ranging from 5 to 8 per cent (Herzog, Greenwood, suchas OCD (21 percent), panic disorder and agoraphobia
Dorer, Flores et al., 2000; Steinhausen, Seidel & Metzke, (25 per cent), social anxiety disorder (30 per cent) and spe-
2000), with one in five of those deaths the result of sui- cific phobias (25 per cent),
cide (Arcelus, Mitchell, Wales & Nielsen, 2011). and with substance abuse To read an article on comorbidity in
Anorexia nervosa begins to develop usually around

anorexia nervosa by Jordan et al. go to
disorders (34 per cent)
adolescence. It rarely begins before puberty or after (Jordan, Joyce, Carter, Horn reading/ch10
40 years of age. Onset can be associated with a stressful et al., 2008). SE
10.1.2 Bulimia Nervosa 1995), and this suggests that they have lost control over
their eating patterns. Because of this lack of control
Like anorexia nervosa, bulimia nervosa (BN) is also a over an area of their life that is important to them, suf-
disorder that is characterized by fear of weight gain and ferers usually become ashamed of their binges and try to
a distorted perception of conceal them. Consequently, binges tend to occurin secret,
For a video on bulimia go to
body shape. The main fea- and take in foods that are normally quick and easy to con-
video/ch10 ture of bulimia is recur- sume, such as sweets, ice cream, cakes, bread and toast.
rent episodes of binge Binge episodes are often well planned in advance, and can
eating (often eating more be triggered by periods of dysphoric or depressed mood,
bulimia nervosa (BN) An eating disorder,
than a normal person’s interpersonal stressors, or intense hunger following an
the main features of which are recurrent
episodes of binge eating followed by full daily intake of food extended period of dietary restraint. Perhaps, at least in
periods of purging or fasting. in one episode), recurrent part, as a result of this perceived lack of control over their
inappropriate compensa- eating behaviour, individuals with bulimia report high
tory behaviours to prevent weight gain (such as self- levels of self-disgust, low self-esteem, feelings of inad-
induced vomiting or the misuse of laxatives, diuretics, or equacy, and high levels of depression (Shisslak, Pazda &
enemas; vomiting is the most common form of purging Crago, 1990; Vanderlinden, Norre & Vandereycken, 1992;
and occurs in 80-90 per cent of those who present for Carroll, Touyz & Beumont, 1996). However, purging
treatment), and a self-evaluation that is unduly influ- tends to confer relief from the physical discomfort of
enced by body shape and weight. The diagnostic criteria binge eating and also reduces the fear of gaining weight.
for bulimia nervosa are provided in DSM-5 Summary Because of these reinforcing effects of purging, the act of
Table 10.2. purging (e.g. vomiting) may become a goal in itself that
Most bulimia sufferers are not usually overweight reduces anxiety and depression.
compared with the norm for their height (Gordon, 2001); Bulimia displays significantly fewer physical symptoms
nor do they usually become underweight as a result of than anorexia, but the most common physical sign of
their purging — and this distinguishes them from those bulimia is permanent loss of dental enamel as a result
suffering from the binge eating/purging anorexia nervosa of regular induced vomiting. In some cases, swollen
subtype. Bulimia nervosa has a typical onset in late ado- parotid glands can produce a typical puffy face appear-
lescence or early adulthood, with peak onset age between ance, and extreme eating patterns caused by regular
16 and 20 years (Stice, Marti & Rohde, 2013). Disturbed binging and purging can produce menstrual irregularity.
eating behaviour persists in many individuals diagnosed Bulimia is significantly more common than ano-
with bulimia nervosa for several years, although long-term rexia and the lifetime prevalence rate among women is
follow-up studies suggest that approximately 75 per cent between 1 and 3 per cent (Gordon, 2001; Hoek & van
of women with bulimia nervosa were in remission 20 years Hoeken, 2003; Stice, Marti & Rohde, pn In men, the
after being diagnosed (Keel, Gravener, Joiner & Haedt, prevalence rate is approxi- |
2010). About 90 per cent of those suffering bulimia are mately ten times lower. ( To read Hoek & van Hoeken’s review
female (Gotestam & Agras, 1995). Bulimia is frequently Epidemiological — stud- | of the prevalence and incidence of eating
disorders go to
triggered by concerns about weight and body shape, and ies suggest that the inci- | www.wiley-psychopathology.com/
may have its origins in a period of dieting. What is perplex- dence of bulimia nervosa reading/ch10
ing about bulimia is that individuals with strong concerns might have decreased
about their weight and body shape should indulge in since the 1990s (Smink, van Hoeken & Hoek, 2012),
such regular bouts of excessive over-eating (between two but this is in contrast to a perceived increase in occur-
and 12 bouts per week, Garfinkel, Kennedy & Kaplan, rence in the decades prior to 1990. Interestingly, in a
study of bulimia nervosa incidence in the UK from 1988
to 2000, Currin, Schmidt, Treasure & Jick (2005) found
DSM-5 SUMMARY TABLE 10.2 Criteria for bulimia nervosa
that rates of bulimia rose to a peak in 1996 but then sub-
e Repeated incidents of binge eating sequently declined (see Figure 10.1). They relate these
e Frequent inappropriate compensatory behaviours in order fluctuations in incidence to the press coverage given to
to avoid weight gain, such as self-induced vomiting, Princess Diana’s battle with bulimia during the early
fasting or excessive exercise 1990s, and note that the decline in bulimia incidence in
the UK appears to coincide with her death in 1997 (Photo
¢ Binge eating and compensatory behaviours both occur on
average at least once a week for 3 months 10.1). Much fewer cases of bulimia have been reported
in women who have not been exposed to some extent
e View of oneself is overly influenced by body shape and
to Western ideals and influences (Keel & Klump, 2003).
weight
This suggests that bulimia may be a disorder very closely
CHAPTER 10 EATING DISORDERS an
75
Bulimia nervosa
50
25
Incidence
100,000
rate
per
Anorexia nervosa
0 jl
|Se a aL (a
ca.ele. a
1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000
Year
FIGURE 10.1 /n the UK between the years 1988 and 2000,

the incidence of anorexia nervosa remained relatively stable,
Graham/Getty
Tim
©Images
but incidence of bulimia nervosa increased from 1988 to 1996
and then subsequently decreased. PHOTO 10.1 The increase in rates of bulimia nervosa in
Source: Currin, L., Schmidt, U., Treasure, J. & Jick, H. (2005). Time the UK up to 1996 has been attributed to the publication of
trends in eating disorder incidence. British Journal
of Psychiatry, Princess Diana's battle with bulimia during the early 1990s. A
186, 132-135, Figure 1. Reproduced by permission of the Royal decline in the incidence of bulimia after 1996 also appears to
College of Psychiatrists. coincide with her death in 1997.
linked to Western cultural ideals surrounding body including eating and the use of alcohol and drugs (Lacey,
shape and eating behaviours, and so prevalence is likely 1993; Brietzke, Moreira, Toniolo & Lafer, 2011).
to be influenced by changes in social conditions. A case history of the development of bulimia is
Bulimia nervosa is often found to be comorbid with described in Case History 10.1.
other psychiatric disorders. Major depression is the most
commonly diagnosed comorbid disorder; with between
36 and 63 per cent of bulimia sufferers being diagnosed
10.1.3 Binge-Eating Disorder (BED)
with depression (Brewerton, Lydiard, Herzog, Brotman Binge-eating disorder is characterized by recurrent epi-
et al., 1995). Increases in bulimia during winter months sodes of binge eating (see DSM-5 Summary Table 10.3),
also appear to be linked to symptoms of seasonal affec- but without the associated purging or fasting associated
tive disorder (SAD) (Lam, Lee, Tam, Grewal & Yatham, with bulimia. As a result those suffering binge-eating
2001), suggesting that dysphoric mood disorder is a com- disorder tend to be overweight, and usually have a long
mon concurrent symptom of bulimia. There is also evi- history of failed attempts binge-eating disorder (BED) An eating
dence for a strong link between bulimia and borderline to diet and lose weight. As disorder characterized by recurrent epi-
personality disorder (BPD). Studies have suggested that a result, individuals with sodes of binge eating without the purging
between 33 and 61 per cent of women with bulimia binge-eating disorder feel a or fasting that is associated with bulimia
nervosa.
meet the criteria for a personality disorder (Schmidt & lack of control over their
Telch, 1990; Carroll, Touyz & Beumont, 1996). There eating behaviours and this causes them significant dis-
is also strong evidence for a link between the bulimic tress. Individuals with binge-eating disorder are typically
behaviours of bingeing and purging and substance abuse, ashamed of their eating problems and usually attempt to
and with bipolar disorder (Jordan, Joyce, Carter, Horn conceal their symptoms or eat in secrecy. Triggers for
et al., 2008). This includes heavy alcohol use (Lacey, 1993), binge eating can include interpersonal stress, dieting,
increased incidence of the use of soft and hard drugs when negative body image, and boredom. Differentiating
compared with anorexia sufferers and non-clinical controls between a diagnosis of binge-eating disorder and bulimia
(Corbridge & Bell, 1996), and abuse of laxatives, diet pills, nervosa is often difficult and depends on how frequently
diuretics and emetics (Bulik, Sullivan, Epstein, McKee et al., the individual indulges in compensatory behaviours such
1992). The frequent comorbidity of bulimia with person- as purging. Because of the overlap in symptoms, some
ality disorders, bipolar disorder and substance abuse has view binge-eating disorder only as a less severe form of
led to the proposal that bulimia is part manifestation of a bulimia (Hay & Fairburn, 1998; Striegel-Moore, Cachelin,
broader ‘multi-impulsive’ syndrome in which the individual Dohm, Pike et al., 2001). Binge-eating disorder can often
finds it difficult to control many aspects of their behaviour, be found in children and is associated with excessive
Rae se PSYCHOPATHOLOGY
BULIMIA NERVOSA
Sara was the youngest child in her family, with two brothers several years older than her who both left home
before she entered high school. Sara tried hard to please her older brothers even though they teased her and
would often call her names, telling her she was stupid and ugly.
Her father worked long hours as a salesman and was often away from home travelling or staying late in the
office. When Sara was 13 she discovered that her father had been having an affair, and that her mother had
known of this for some years. Sara was very angry with her father and also with her mother for allowing him to
‘get away with it’ She tried to be supportive of her mother but felt hurt and confused, and their close relationship
HISTORY
CASE was damaged. Sara didn’t feel able to confide in her mother anymore and felt strong resentment towards her
10.1
father, who she could not forgive.
Over the next 2 years Sara felt increasingly isolated and unhappy at home and spent as little time there as
possible. When Sara was 16 she met her first boyfriend, Kyle, who was four years older than her. At first Sara was
very happy in the relationship and after 4 months she moved out of home to live with Kyle. Soon, the relationship
became difficult and they often argued about money and household chores, as well as about Sara's belief that
Kyle flirted with other women.
Two years into their relationship Sara discovered that Kyle had been cheating on her with one of her close
friends. When Sara confronted him, Kyle confessed what he had done but blamed Sara for being ‘boring’ and
‘a nag’. He told her that he had never found her attractive and had always wanted to be with her friend instead.
Sara was angry and upset but blamed herself fornot making more ofan effort to be attractive.
Sara reluctantly moved back into her parents’ house, although her relationship with them had not improved
in recent years. Feeling isolated and unhappy she began a crash diet and lost some weight quickly. Her father
often ridiculed her weight loss efforts while her mother encouraged her to ‘make more of herself: Sara became
increasingly unhappy after her initial weight loss and became tired, irritable and preoccupied with food. One
evening she saw a Facebook update telling her that Kyle and her friend were now engaged, and that her friend
was pregnant. She felt jealous and angry that all her efforts to lose weight and ‘improve herself’ had been for
nothing. Sara stuffed herself with food until she couldn't eat any more. Feeling out of control and ashamed she
made herself vomit.
The next day she resolved to eat even less but a week later she binged again. Although she tried to stop, Sara
felt caught in a pattern and was soon bingeing several times a week. Her eating became wildly erratic but her
weight stayed much the same. Her parents didn't realize that anything was wrong and regularly chastised her for
not making more of her life, while Sara began to feel increasingly desperate and alone, and even thought oftry-
ing to kill herself. Although she still saw her friends and was able to hold down a job, Sara was now locked into a
cycle of bingeing and vomiting known as bulimia nervosa.
Clinical Commentary
Sara’s case contains anumber of elements that are typical of individuals who develop bulimia. She had a difficult
home environment and experienced teasing about her weight and appearance, as well as having to adjust to
significant changes in parental relationships. Her subsequent relationship was difficult and when it came to an
end she probably felt that she had little control over her life, and she had no obvious means ofescape from her
situation. Arguments with her boyfriend had reinforced her belief that she had ‘let herself go; and she resolved to
diet to lose weight. Dieting then triggered feelings of extreme hunger which led to binge eating following anger
at her boyfriend's infidelity. Following the binge, feelings of self-disgust and shame lead to purging. This starts a
vicious cycle in which, after each binge, Sara resolves to eat less but inevitably ends up bingeing again.
weight gain, and is common in adolescents and college general population is around 3.0 per cent and has a
students (Napolitano & Himes, 2011). peak onset age of 16-20 years (Stice, Marti & Rohde,
Binge-eating disorder is associated with high levels 2013); the disorder can be as high as 30 per cent among
of major depression, impaired work and social function- individuals seeking weight loss treatment (Dingemans,
ing, low self-esteem, and dissatisfaction with body shape Bruna & van Furth, 2002). While the majority of suffer-
(Striegel-Moore, Cachelin, Dohm, Pike et al., 2001). ers are women, the incidence of binge-eating disorder in
The lifetime prevalence of binge-eating disorder in the women is only one and a half times higher than in men
CHAPTER 10 EATING DISORDERS Sa
(Stice, Telch & Rizvi, 2000; Striegel-Moore & Franko, DSM-5 SUMMARY TABLE 10.3 Criteria for binge-eating disorder
2003). A cross-cultural study by Pike, Dohn, Striegel-
e Repeated incidents of binge eating
Moore, Wifley & Fairburn (2001) found that the inci-
dences of the disorder in white and black American ° Binge eating is accompanied by at least three of the
women were very similar, following:
To read Striegel-Moore & Franko's
article on the epidemiology of
although black. American ¢ Eating quicker than usual
binge-eating disorders go to women appeared to show
e Eating until uncomfortably full
www.wiley-psychopathology.com/ less concern about the dis-
reading/ch10 order than white American e Eating sizable amounts of food when not feeling
women. The case of Rosa pungry
is outlined in Case History 10.2, and this example illus- ¢ Eating alone due to being embarrassed by the amount
trates many of the behavioural and cognitive traits exhib- of food eaten
ited by individuals suffering from binge-eating disorder. ° Feeling disgusted, depressed or guilty after binge
Finally, in this section we have discussed the three eating
most clinically important eating disorders, namely ano-
e Distress regarding binge eating
rexia nervosa, bulimia nervosa and binge-eating disorder.
However, DSM-5 also specifies other feeding and eating ° Binge eating is not accompanied by inappropriate
disorders that may cause distress (e.g. see Table 10.1). compensatory behaviour as seen in bulimia nervosa
BINGE EATING DISORDER

Rosa was a binge eater, but had not had a food binge for over three-and-a-half years when she travelled to attend
the wedding of her friend's daughter. Rosa was normally a confident, professional woman, who enjoyed her
work, and had just successfully completed an important project, which often left her feeling down and empty.
She had spent three years attending Overeaters Anonymous (OA), and knew she needed to avoid
food — especially when she was feeling low.
Rosa managed to keep herself occupied during the day of the wedding, but as the night-time came, the
bluster of the after wedding party made it easy for her to disappear — physically and emotionally — into a binge.
HISTORY
CASE She started with a plate of what would have been an ‘abstinent’ meal (an OA concept for whatever is included
10.2
on one’s meal plan): pasta salad, green salad, cold meats, and lots of bread. The food was plentiful, but Rosa
still wanted more, and spent the next three-and-a-half hours eating. Very soon she started to feel guilty and
ashamed, and began to surreptitiously steal food from plates out of the gaze of the other guests.
When most of the guests had left the dining room she began helping herself to the cakes and desserts. Then,
beginning to feel desperate, Rosa began to pile the food high on her plate, so that if other guests saw her she
could always escape with a large amount offood. By now, the food tasted of nothing to her, but she couldn't stop
eating it. Eventually she realized what she had been doing, felt that she was out of control, and ran crying back
to her room.
This event was the beginning of a six-month relapse into binge eating for Rosa. During the relapse, she binged
on foods and refined carbohydrates, started smoking cigarettes in an attempt to control the binging and was
driven to excessive exercise after each binge.
Throughout the relapse, Rosa went to therapy and to OA. Finally, a combination of antidepressants and a
structured food plan that excluded refined sugars, breads, crackers, and similar carbohydrates helped her to
bring her bingeing under control and manage her eating. Rosa was eventually able to stop taking the antidepres-
sants and continued to be active in OA.
Clinical Commentary
Rosa’s case history is a good example of how a person can lose control of their own eating patterns and eating
behaviour. Features that are typical of binge-eating disorder include (1) eating significantly more than a normal
meal portion in one session; (2) an uncontrollable urge to continue eating despite the situation and surround-
ings; (3) forcing oneself to eat food that is unpalatable or contaminated; (4) a desire to conceal her overeating
from others; and (5) subsequent shame, self-disgust and depression when the binge episode is over.
340 PSYCHOPATHOLOGY
TABLE 10.1 Other feeding and eating disorders in DSM-5
Pica
The persistent eating of non-nutritive, non-food substances on a persistent basis. These might include paper, soap, cloth, hair, ash,
clay, starch, ice, wool, soil, talcum powder, paint, gum, pebbles, coal, and so on
Rumination disorder
Repeated regurgitation of food

Avoidant/restrictive food intake disorder
Avoidant or restriction of food intake resulting in failure to meet requirements for nutrition or insufficient energy intake. This
eating disturbance may manifest as a lack of interest in food, avoidance based on the sensory characteristics of food, or concerns
about the aversive consequences of eating
SELF-TEST QUESTIONS
© What are the three main eating disorders defined by DSM-5?

® Can you describe the main diagnostic criteria for anorexia nervosa, bulimia nervosa, and binge-eating disorder?
° What are the prevalence rates for the main eating disorders, and how do incidence rates compare between males and
females?
® Both anorexia nervosa and bulimia nervosa are highly comorbid with other psychiatric disorders — which ones?
* Can you describe some examples of eating disordered behaviour that has been reported throughout history? How do
these reports resemble the modern-day symptoms ofanorexia and bulimia?
SECTION SUMMARY
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10.1 DIAGNOSIS AND PREVELANCE
¢ There are three important eating disorders defined by DSM-5. These are anorexia nervosa, bulimia nervosa, and binge-eating
disorder.
¢ Examples of disordered eating can be found throughout history, but examples of bulimia are much rarer than the self-
starvation typical of anorexia.
¢ The important features of anorexia nervosa are a refusal to maintain a minimal body weight, a pathological fear of gaining
weight, and a distorted body image in which sufferers continue to insist they are overweight.
e Lifetime prevalence rates for anorexia nervosa are around 0.4 per cent.
e There are high rates of comorbidity between anorexia nervosa and other psychiatric disorders such as major depression
and OCD.
¢ The main features of bulimia nervosa are recurrent episodes of binge eating followed by periods of purging or fasting.
¢ Bulimia nervosa is characterized by high levels of self-disgust, low self-esteem, feelings of inadequacy, and high levels of
depression.
e The lifetime prevalence rate for bulimia nervosa among women is between 1 and 3 per cent.
¢ Bulimia nervosa is often comorbid with major depression, borderline personality disorders and substance abuse.
° Binge-eating disorder is characterized by recurrent episodes of binge eating without the purging or fasting that is associ-
ated with bulimia nervosa. ‘
*° Binge-eating disorder is associated with high levels of major depression, impaired work and social functioning, low self-
esteem, and dissatisfaction with body shape.
wh
CHAPTER 10 EATING DISORDERS oa
10.2 CULTURAL 2000), and more recent studies have indicated more
similarities than dissimilarities in body dissatisfaction
AND DEMOGRAPHIC between ethnic groups in the US (Grabe & Hyde, 2006).
Despite these within-culture ethnic differences in
DIFFERENCES IN vulnerability to eating disorders, symptoms indicative
of anorexia nervosa have been reported in every non-
EATING DISORDERS ~— Western region of the world, and epidemiological stud-
ies suggest that its prevalence may be very similar to that
in Western nations (Keel & Klump, 2003). This may well
10.2.1 Cultural Differences be because most countries in the world are nowadays
Numerous studies have suggested that cultural differences subject to at least some Western influence. An exam-
and cultural change may be associated with differences in ple of this is a study of eating disorders in Hong Kong,
vulnerability to eating disorders, and indeed may rep- in which incidences of anorexia and bulimia doubled
resent direct risk factors for eating disorders (Miller & between 1987 and 2007, along with 25 per cent more
Pumariega, 2001). The cultural differences in eating disor- women reporting body dissatisfaction and fear of gain-
ders are most striking in relation to bulimia. In an exhaus- ing weight (Lee, Ng, Kwok & Fung, 2010). However,
tive study of the literature available at the time, Keel & anorexia symptoms have still been reported in individu-
Klump (2003) found no studies reporting the presence of als who could not have been exposed to Western cultural
bulimia in individuals without exposure to Western ideals, influence. For instance, Abou-Saleh, Younis & Karim
and concluded that there does not appear to be a form of (1998) report a case of anorexia nervosa in an 18-year-old
bulimia that is not related to the weight concerns generated nomadic woman from the Empty Quarter in the United
by exposure to Western cultural ideals. That is, when indi- Arab Emirates. The fact that cases of anorexia are reli-
viduals from non-Western countries such as Iran, Pakistan, ably reported in areas of the world where Western influ-
Egypt and Malaysia have exhibited symptoms of bulimia, ences and ideals are almost nonexistent has led Keel &
they have usually been exposed to Western standards Klump (2003) to suggest that contemporary Western ide-
through learning English, being of high socio-economic als may determine some aspects of anorexia (e.g. weight
status, or being educated beyond secondary level. concern and body dissatisfaction), but are not necessary
The role of culture in the development of anorexia for producing the self-starving syndrome typical of ano-
nervosa is complex. Even within individual Western soci- rexia. In effect, the presence of weight concerns or body
eties (such as the USA) individual ethnic groups show dissatisfaction does not appear to be a universal motivat-
differences in the prevalence of eating disorders, and this ing factor for food refusal in anorexia.
can often be traced to differences in cultural ideals and prac- This summary suggests that cultural factors do appear
tices. For example, African-American women are less likely to influence the prevalence of eating disorders, and the
than white women to have eating disorders (Lovejoy, 2001), emphasis placed on weight concern and body shape in
but both African-American women and children have Western cultures is a potentially important contribu-
larger ideal physiques than their white counterparts, and tor to the development of an eating disorder. As both
are more satisfied with their own body shapes (Powell & non-Western countries and ethnic minorities within
Kahn, 1995; Thompson, Corwin & Sargent, 1997; Western countries become more and more influenced
Neumark-Sztainer & Hannan, 2000). As a result, African by Western ideals, rates of eating disorder appear to rise
American women are more likely to develop an eating in these communities. However, such Western ideals do
disorder that does not involve a drive towards thinness, not appear to be a necessary condition for anorexia.
and so tend to develop bulimia rather than anorexia
(Striegel-Moore & Smolak, 1996). Interestingly, a study of
white Latina and black American college women found 10.2.2 Demographic Factors
that white and Latina women had slimmer personal body within Cultures
shape ideals than black women, and this difference pre-
dicted scores on eating disorder inventories (Gordon, Females are 10 times more likely to develop an eat-
Castro, Sitnikov & Holm-Denoma, 2010). However, ing disorder than males (Striegel-Moore, 1997) and the
exposure of ethnic minorities to the dominant thin ideal reason for this sex-linked effect appears to be the ide-
of American culture seems to be leading to increases in alisation of female weight, size and body shape by the
eating disorder prevalence in minority ethnic groups. In Western media (Harrison, 2001). This results in female
the USA, rates of eating disorders in immigrant Asian thinness becoming an important social value that is
females and Hispanic American women are significantly associated with social acceptance and social rewards
on the increase (Wax, 2000; Chamorro & Flores-Ortiz, (Spitzer, Henderson & Zivian, 1999). Interestingly, at a
342 PSYCHOPATHOLOGY
: : %
time when the populations of both Europe and the USA and importance is placed on body shape, size and weight,
are becoming heavier, studies have suggested that men the rate of eating disordered behaviour is likely to rise
would prefer their body shape to be around 30 pounds within that subgroup. The fact that the media often cre-
heavier than their current weight (McCreary & Sadava, ate body shape, size and weight ideals that are somewhat
2001) — presumably because they believe their body is extreme in comparison to the average or norm — even
not muscular enough. In contrast, females identify their within these subgroups — is simply more grist to this mill.
ideal body weight as an average of around 40 pounds
less than their weight (Irving, 2001). These differences in
culturally determined ideal weight expectations appear
to be largely responsible for the sex-related difference
in prevalence rates for eating disorders, and may be
related to the fact that sexual differences between men
and women are related to women being more likely
to be defined by their bodies and men more likely to
be defined by their accomplishments (Frederickson &
Roberts, 1997). These differences in how the genders are
defined seem to dissipate with age, and long-term studies
have shown that at around the age of 40 years women
diet less, have fewer concerns about their body image,
and fewer eating disorders than when they were 20 years
younger. One fact that reflects the importance of shape
ideals is that eating disorders in males are significantly
higher in groups of males whose body weight and shape
is of more significance and importance to them. For
example, compared with the general adult male popu-
lation, the prevalence rates for eating disorders are sig-
nificantly higher in male body-builders (Holbrook &
Weltzin, 1998), athletes (Byrne & McLean, 2002), and
ballet dancers (Ravaldia, Vannacci, Zucchi, Mannucci
Khayat-Nebinger
Images.
Association
et al., 2003). Also, the instance of eating disorders is sig-
nificantly higher amongst gay men than heterosexual PHOTO 10.2 Western media regularly portray female role
men (Strong, Williamson, Netemeyer & Geer, 2000), models as either naturally thin (and therefore representative
reflecting the relative greater importance placed on male of only a minority of the female population) or unnaturally
physical appearance and attractiveness by gay subcul- thin. Young adolescent females then strive to achieve these
ture. Thus, even within cultures, whenever an emphasis relatively unattainable, or simply unhealthy, ideals.
SELF-TEST QUESTIONS _
* How do demographic factors and cultural aspects of eating disorders help us to understand these disorders?
* How do the symptoms and incidences of eating disorders differ across cultures and ethnic groups?
* What evidence would you cite that shows the importance of body shape ideals as a risk factor for eating disorders?
SECTION SUMMARY
10.2 CULTURAL AND DEMOGRAPHIC DIFFERENCES IN EATING DISORDERS
° Some of the origins of eating disorders lie in the values and ideals defined by cultures.
e Changes in sociocultural factors may influence the frequency and prevalence of eating disorders.
° There is little evidence for examples of bulimia in individuals who have not had exposure to Western ideals.
CHAPTER 10 EATING DISORDERS gag
° Eating disorders are less prevalent in ethnic minorities in the USA, but their incidence is increasing as these minorities are
exposed to the dominant thin ideal espoused by American culture.
° Examples of the self-starvation typical of anorexia nervosa can be found in cultures where Western ideals are nonexistent
and this suggests than anorexia may not simply be a disorder caused by exposure to Western body-image ideals.
¢ Females are 10 times more likely to develop an eating disorder than males.
e The importance of body shape ideals as arisk factor for eating disorders is reflected in the fact that eating disorders in males
are significantly higher in groups of males whose body weight and shape is of more significance and importance to them
(e.g. body-builders, athletes, ballet dancers).
10.3 THE AETIOLOGY OF anorexia and bulimia often have identical risk factors, and
it is not clear why an individual ry no) one of these
EATING DISORDERS disorders rather than the gs SNOT
other. As a consequence | To read Lindberg & Hjern’s article on
the risk factors for anorexia nervosa goto —
it is often difficult to sepa- | www.wiley-psychopathology.com/
Like so many other psychological disorders, eating disor- rate out theories of the | reading/ch10
ders do not appear to be caused by one single factor, but aetiology of anorexia and
have their origins in a range of psychological, sociological bulimia, and many of the following theories are addressed
and biological processes, all of which appear to converge at understanding eating disorders generally rather than
to generate the different eating disorder profiles. So broad individual eating disorders specifically.
is the range of influences that has been identified in this We have already described how the occurrence of eat-
aetiology that many researchers have limited themselves ing disorders appears to be linked to culture and ethnic-
simply to defining the risk factors that underlie eating ity, and this alone should give us some insight into the
disorders (e.g. Polivy & Herman, 2002; Jacobi, Hayward, sociological influences linked to eating disorders. In
de Zwaan, Kraemer & Agras, 2004; Ghaderi & Scott, the following section, we will look at risk factors in
2001). Because of this complexity, theories of the aetiol- more detail, and try to elaborate how these risk factors
ogy of eating disorders based on the description of either might have their effects on the development of eating
psychological or biological processes are relatively under- disorders.
developed. So we tend to have a good idea of what factors
are involved in eating dis-
orders (i.e. what represent
To read Ghaderi & Scott's article on the
prevalence, incidence and prospective risk factors), but relatively
risk factors for eating disorders go to little insight into how they Biological approaches to the aetiology of eating disorders
reading/ch10 are involved. Figure 10.2 centre around genetic influences and neurobiological
illustrates a recent attempt factors.
to classify the risk factors
for anorexia and bulimia across a developmental time-
frame, and this shows how important risk factors are at Genetic influences
a number of different levels of description. These include There is clear evidence that eating disorders do run in
‘prenatal’ risk factors (such as gender and ethnicity), early families, and this is consistent with there being a genetic
developmental influences that generate eating difficulties component to these disorders. First-degree relatives of
(such as infant sleeping and eating patterns), early expe- females with both anorexia and bulimia are significantly
riences (such as sexual abuse and physical neglect), dis- more likely to develop these disorders than relatives of a
positional factors (such as low self-esteem, perfectionism group of females who have never been diagnosed with an
and negative self-evaluation affect), familial factors (such eating disorder (Strober, Freeman, Lampert, Diamond &
as parental obesity and parental attitudes to weight), ado- Kaye, 2000; Kassett, Gershon, Maxwell et al., 1989).
lescent attitudes to dieting and exercise, and comorbid Community-based twin studies have also contributed
psychological disorders (such as OCD and social phobia) to the view that there is an inherited component, and
(see also Lindberg & Hjern, 2003). What you will also see these indicate that genetic factors account for approxi-
from Figure 10.2 is that different eating disorders such as mately 40-60 per cent of liability to anorexia nervosa,
4a ee PSYCHOPATHOLOGY
OCD
Dieting (bingeing)
Preterm birth/
Birth trauma BDD |
Pregnancy
complications/ |
H
Adolescent age |
Gestational age
Genetic Acculturation |
factors
Sexual abuse/Adverse life events |

a: :
gender — pepe
;intestinal problems
Childhood anxiety ~e Negative

Ethnicity Infant sleep pattern aifcuties
disorders pubertal self-evaluation
— Se
High concern parenting
Sy. Se 10y.
OCPD
=
15y.
7
20y.
S|
[high [LL ]medium []low [_]notspecified [__] specific factor
L J
potency
Social phobia
Negative self-evaluation
Parental variables: e.g. critical

comments on weight /
low contact/high expectations
Parental obesity
Adverse
family experiences SSS)
Genetic
Acculturation
effects
Female — Sexual abuse/Childhood adversities

gender
"a Overanxious
Ethnicity disorder Adolescent age
=e d & ae ys Zh Prodromal
Childhood obesity Pubertal timing -Dietir j
‘ Di irsPar Onset
oe T T T T T T a. 7 — T
Sy 10y. 15y. 20y.
[high [-]medium [_]low [___]notspecified Eps tt

ha J
potency
FIGURE 10.2 Classification of the known risk factors for anorexia and bulimia across a developmental timeframe. This shows how
important risk factors are at anumber of different levels of description.
Source: Jacobi, C., Hayward, C., de Zwaan, M., Kraemer, H.C. & Agras, W.S. (2004). Coming to terms with risk factors for eating disorders:
Application of risk terminology and suggestions for a general taxonomy. Psychological Bulletin, 130, 19-65. American Psychological Association.
CHAPTER 10 EATING DISORDERS B45
bulimia nervosa and binge eating disorder (Trace, Baker, 1966). However, there is good reason to believe that lat-
Penas-Lledo & Bulik, 2013). However, while twin studies eral hypothalamus deficits are not a central causal factor
indicate a moderate genetic influence, such studies also in anorexia. Firstly, animal studies show that lateral
suggest a significant impact of unique environmental fac- hypothalamus lesions result in a lack of hunger — but
tors, such as interactions with parents (Baker, Mitchell, anorexia sufferers usually experience intense hunger
Neale & Kendler, 2010), and this implies that eating even though they are starving themselves. Secondly,
disorders are developed through a complex interaction while there are hormonal imbalances found in anorexia
between inherited characteristics and individual experi- that are similar to those in animal studies of lateral hypo-
ences. Molecular genetic studies have also attempted to thalamus lesions, these imbalances appear to be the result
identify the gene loci of these genetic effects, and poten- of the disorder rather than a cause of it (Stoving,
tial target genes have been identified that may influence Hangaard & Hansen-Nord, 1999).
appetite regulation (e.g. serotonergic genes), feeding and Combinations of brain mechanisms and reward path-
food intake (e.g. dopaminergic genes), food reward sen- ways in the brain may also be involved in generating eat-
sitivity (e.g. genes that influence opioid receptors), and ing disorders as a result of their role in triggering either
weight regulation (Trace, Baker, Penas-Lledo & Bulik, satiation or food ‘craving’ or ‘liking’ (Berridge, Ho,
2013). However, molecular genetic studies of eating dis- Richard & DiFeliceantonio, 2010), and we have already
orders are largely in their infancy and have been plagued indicated that there may be some genetic influence on
by underpowered sample sizes and failed replications the strength of these effects. For example, self-starvation
(Sullivan, Daly & O’Donovan, 2012; Wang, Zhang, Bloss, and maintaining a low body weight may be reinforced by
Duvvuri et al., 2011). the endogenous opioids that the body releases during
There may also be a shared familial factor across eat- starvation to reduce pain sensation (Hardy & Waller,
ing disorders suggesting that if an individual has bulimia, 1988). In anorexia, starva-
. ; : endogenous opioids A compound that
this may raise the chances of a related individual not just tion may directly increase the body releases to reduce pain sensation.
developing bulimia, but also either anorexia or bulimia the levels of opioids, thus
(Kendler, MacLean, Neale, Kessler et al., 1991; Wade, producing a state of euphoria; however, because bulimia
Bulik, Sullivan, Neale & Kendler, 2000). However, Keel & sufferers are not necessarily overweight, this disorder
Klump (2003) have argued that the genes contributing may be accompanied by low levels of opioids, and this is
to anorexia may well differ from those contributing to known to promote craving. In support of this latter
bulimia. This is because bulimia appears to be a culture- hypothesis, Brewerton, Lydiard, Laraia, Shook &
bound syndrome whereas anorexia is not (see section Ballenger (1992) did find low levels of the opioid beta-
10.2), and the universal nature of anorexia suggests that endorphin in bulimia sufferers. Nevertheless, it is still dif-
there may be an important genetic component to the ficult to interpret the significance of this finding because
self-starvation that is the central feature of anorexia. low opioid levels may be a consequence of the cravings
Nevertheless, while there appears to be a significant that accompany bulimia rather than a cause of them.
inherited component, this research has yet to determine Also, low levels of serotonin metabolites have been
exactly how inherited dispositions increase the likeli- found in individuals with serotonin metabolites The products pro-
hood of developing an eating disorder. For example, a diagnosis of anorexia duced by the breakdown of serotonin.
does the genetic component to anorexia simply increase and bulimia (Kaye, Ebert,
the tendency to self-starve, or does it increase the vulner- Raleigh & Lake, 1984; Carrasco, Dyaz-Marsa, Hollander,
ability to other risk factors (such as depression or low Cesar & Saiz-Ruiz, 2000). Serotonin promotes satiety,
self-esteem)? and so people with low levels of serotonin metabolites
may be prone to binge eating; low levels of serotonin are
Neurobiological factors also associated with depression, so this might also be a
Because eating disorders involve appetite, a number of reason why eating disorders are so often comorbid with
theories of both anorexia and bulimia allude to the role mood disorders such as depression. The problem
of those brain areas involved in regulating appetite with this as a cause of binge-eating problems is that ani-
(namely the hypothalamus), and to the neurotransmit- mal studies have shown that enforced dieting tends to
ters associated with changes in appetite. Animal research reduce serotonin functioning, so low levels of serotonin
has shown that lesions to the lateral hypothalamus cause metabolites in individuals with either anorexia or bulimia
appetite loss resulting in may have been caused by any prior dieting behaviour
ral hypothalamus A part of the (Chandler-Laney, Castaneda, Pritchett, Smith et al., 2007).
a self-starvation syndrome
othalamus. Lesions to the lateral hypo-
that is behaviourally simi- Finally, dopamine is a brain neurotransmitter involved in
amus cause appetite loss resulting ina
starvation syndrome which is behav- lar to that found in anore- the pleasurable and rewarding consequences of food,
ally similar to that found in anorexia. xia (Hoebel & Teitelbaum, and women diagnosed with anorexia and bulimia exhibit
346 PSYCHOPATHOLOGY
greater expression of the dopamine transporter gene This media influence has resulted in young women
DAT, suggesting that they might be more susceptible adopting ideal body-shape goals that are achievable for
to the rewarding and pleas- only around 5 per cent of
dopamine transporter gene A trans- media influence A term describing a pe
urable effects of eating the female population son's changes in or temptations to changé
porter gene allows drugs to enter cells or, in
some cases, acts to keep them out. Women (Frieling, Romer, Scholz, (Irving, 2001). There is some attitude, behaviour and morals as directly
diagnosed with anorexia and bulimia Mittelbach et al., 2010; evidence that exposure influenced by the media.
exhibit greater expression of the dopamine Thaler, Groleau, Badawi, to these media-portrayed
transporter gene DAT suggesting that they extreme ideals is related to a drive for thinness in young
Sycz et al., 2012).
might be more susceptible to the reward-
ing and pleasurable effects of eating. While most of the evi- adolescent girls. For example, Tiggemann & Pickering
dence seems to suggest that (1996) found that body-shape dissatisfaction and a drive
various brain areas and neurotransmitters are involved in for thinness was significantly associated with watching
eating disorder symptoms, we still cannot be sure that certain types of TV show that portrayed idealized female
these are genuine causal factors or whether they are con- images. Further studies have shown that body dissatisfac-
sequences of behaviours associated with eating disorders tion is directly correlated with the amount of time young
such as dieting or bingeing. female undergraduates spend reading magazines that
expose them to idealized female body shapes (Tiggemann,
2003), and also with the amount of time young women
spend watching music television channels such as MTV
10.3.2 Sociocultural Influences (Tiggemann & Slater, 2004). The more that young adoles-
Section 10.2 described how the incidence of eating dis- cents (between the ages of 14 and 16 years) indulge in
orders appears to be importantly affected by factors ‘celebrity worship’ of a media personality and perceive
associated with culture and ethnicity. Rates of both ano- that personality as having a ‘good’ body shape, the more
rexia and bulimia are higher in cultures that have expe- that adolescent views their own body image as poor
rienced contemporary Western ideals and standards, (Maltby, Giles, Barber & McCutcheon, 2005). Some exper-
and, indeed, it is arguably the case that bulimia is only imental studies that have manipulated the viewing of vid-
found in societies that have been exposed to Western eos with either idealized body images or control images
cultural influences (Keel & Klump, 2003). This suggests have suggested that the relationship between media pres-
that Western cultural factors are a risk factor for eat- entations of idealized body images and eating disorder
ing disorders, and it is important to identify specifically symptoms — such as reduced body dissatisfaction,
what these factors are and how they might trigger an decreased self-esteem, dieting and depression — is a causal
eating disorder. one (e.g. Jett, LaPorte & Wanchisn, 2010). However, the
overall effect sizes for these causal effects are small, sug-
gesting that the influence of watching such media is rela-
Media influences, body dissatisfaction tively modest (Hausenblas, Campbell, Menzel, Doughty
and dieting et al., 2013).
As already pointed out, both anorexia and bulimia are Another socially relevant factor that may have con-
disorders that are largely restricted to females (Strieigel- tributed to the increase in eating disorder symptoms
Moore, 1997) and there is growing acknowledgement over the past 30-40 years is food and eating fashions.
that the general increase in the incidence of eating disor- The more that low-calorie diets become fashionable, the
ders over the past 20-30 years is associated with changes more they are likely to promote restricted eating, which
in the ideal female body shape that is communicated to is a risk factor for developing eating disorder symptoms.
the female populations of Westernized societies. For For example, individuals with an eating disorder are con-
instance, the media are regularly accused of distorting siderably more likely to have been vegetarian compared
reality by portraying female body images that are either to controls (52 per cent vs. 12 per cent) (Bardone-Cone,
naturally thin (and therefore representative of only a Fitzsimmons-Craft, Harney, Maldonado et al., 2012),
minority of the female population) or are unnaturally and the low-carbohydrate diets fashionable over the past
thin (Polivy & Herman, 2002). This is supported by stud- 20-30 years will have contributed to increases in the
ies showing that the BMI (body mass index — see Activity prevalence of restrictive eating practices.
10.1) of Playboy centrefolds between 1985 and 1997 had As well as the exaltation of thinness, Western cul-
continued to fall to a point where almost 50 per cent tures disparage obesity and both implicitly and explicitly
of the centrefolds had a BMI of less than 18 — which is associate it with negative characteristics — even though
considered to be severely underweight (Owen & Laurel- obesity is significantly on the increase in most Western
Seller, 2000). societies. Obese individuals are rated by others as less
CHAPTER 10 EATING DISORDERS -B47-
smart, and more lazy and worthless than non-obese indi- (Polivy & Herman, 1987; Stice, 2001). Figure 10.3 pro-
viduals (DeJong & Kleck, 1986) — even by health profes- vides a schematic representation of one model describ-
sionals who specialize in obesity (Schwartz, Chambliss, ing how body dissatisfaction might be generated through
Brownell, Blair & Billington, 2003)! Jokes and cartoons media, peer and parental influences, and then this itself
that ridicule obesity are commonplace, and this preju- will affect dieting behaviour and eating disorder symp-
dice appears to be deep-rooted and more acceptable than tomatology such as bulimia (e.g. Rodgers, Chabrol &
jokes about race and disability. This will inevitably give Paxton, 2011). There is no doubt that body dissatisfac-
rise to a fear of being fat or obese, which is further grist tion and dieting are important predictors of all eating
to the mill of dieting and body dissatisfaction. disorders (Joiner, Heatherton, Rudd & Schmidt, 1997;
While the preceding evidence suggests that media Steiger, Stotland, Trottier & Ghadirian, 1996; Stice, Shaw
images of idealized thin body shapes are relevant in & Nemeroff, 1998), but it is important to note that they
determining attitudes towards body shape — the question are not sufficient conditions for an individual to develop
we need to ask is how this media-based pressure is con- an eating disorder. For example, (1) many individuals
verted into the eating problems that meet DSM-5 criteria may believe that their actual body shape is quite dispa-
for a psychological disorder. The most obvious route is rate from their ideal (Figure 10.4), yet be quite happy
that idealized media images generate dissatisfaction with with that fact (Polivy & Herman, 2002), and (2) many
the individual’s own body shape (especially in compari- individuals who express real body dissatisfaction do not
son to extreme ideals). Body dissatisfaction (BD) is usu- necessarily go on to develop an eating disorder. Similarly,
ally defined as the gap between one’s actual and ideal while dieting is usually an activity that precedes an eat-
weight and shape (Polivy & ing disorder, many individuals who diet regularly do not
ty dissatisfaction (BD) The gap
ween one’s actual and ideal weight and Herman, 2002), and most
go on to develop an eating disorder. This suggests that
pe. theories of eating disor- additional psychological factors are necessary for body
ders implicate body dissat- dissatisfaction and dieting to develop into an eating dis-
isfaction as an important component of the aetiology order, and we will discuss some of these factors in
(e.g. Stice, 2001; Vohs, Bardone, Joiner, Abramson & section 10.3.4. Nevertheless, body dissatisfaction and
Heatherton, 1999; Polivy & Herman, 1985; van den dieting are vulnerability factors, and this is demonstrated
Berg, Thompson, Obremski-Brandon & Coovert, 2002). in part by the fact that occupations that require an indi-
Body dissatisfaction is likely to trigger bouts of diet- vidual to control and monitor their weight (usually
ing in order to move towards the ideal body shape, and through either exercise or dieting) have higher inci-
ting A restricted regime of eating, regular or excessive die- dences of eating disorders. These include fashion mod-
owed in order to lose weight or for ting is also a common pre- els (Santonastaso, Mondini & Favaro, 2002), actors,
dical reasons. cursor to eating disorders athletes (Sudi, Ottl, Payerl, Baumgartl et al., 2004), figure
Media Self-
influence esteem
Internalisation
Body
dissatisfaction
Parental
influence Appearance
comparison
Peer
influence
FIGURE 10.3 This is one model of how body dissatisfaction might mediate eating disorder symptoms and is known as the tripartite
model (van den Berg, Thompson, Obremski-Brandon & Coovert, 2002; Yamamiya, Shroff & Thompson, 2008). In this model, the effect
of influences from media, parents and peers is mediated by in ternalisation of social ideals and social comparison, leading to body dis-
satisfaction, disordered eating and negative affect.
YC g PSYCHOPATHOLOGY
mala k Al
4
matches your own? :

Which body type closely
"Which body type would youmost like to have? :
women like to have?
Which body type would most
Which body type do so. believe mea like best? -
FIGURE 10.4 Research on female body shape dissatisfaction has demonstrated that females consistently overestimate their own
body size compared with (1) the body size that they thought that men would like most, and (2) the body size they think that most
women would like to have. Interestingly, women rated the body size they thought men would like most as significantly slimmer than
the body size that men themselves rated as most attractive.
Source: Forbes, G.B., Adams-Curtis, L.E., Rade, B. & Jaberg, P. (2001). Body dissatisfaction in women and men: The role of gender-typing and self-
esteem. Sex Roles, 44(7-8), 461-484. Reproduced with permission of Springer.
skaters (Monsma & Malina, 2004) and ballet dancers found that the use of unhealthy weight-control behav-
(Ravaldia, Vannacci, Zucchi, Mannucci et al., 2003). iours (e.g. self-induced vomiting, laxatives, diet pills, or
fasting) was significantly influenced by the dieting behav-
Peer influences iour of close friends, and this influence was effective in
Just like the media, peer attitudes and views can seriously generating unhealthy weight-control behaviours regard-
influence an adolescent’s view of their body, their weight, less of whether the individual was overweight, normal
and their eating and dieting activities, and adolescent weight or underweight. Despite these findings, it is diffi-
girls tend to learn their attitudes to slimness and dieting cult to determine whether peer influences (1) determine
through their close contact with their peers (Levine, attitudes towards eating
Smolak, Moodey, Shuman & Hessen, 1994). Peer pres- and body shape (it is possi- peer influences A term describing ap Y
son’s changes in or temptations to chan
sure can influence attitudes to body shape and eating ina ble that peer groups recruit attitude, behaviour and morals as directl
variety of ways. In some cases, attitudes to eating and members on the basis of influenced by his or her peer group.
body shape within a peer group converge towards those shared concerns rather
that are socially valued (such as dieting or restricted eat- than directly changing the attitudes of their members),
ing) (Meyer & Waller, 2001), and this convergence also or (2) have a significant role in the development of eating
results in the group adopting psychological characteris- disorders (while peer pressure can increase the tendency
tics that may facilitate pathological eating behaviours, to diet or to be dissatisfied with one’s body shape, these
such as perfectionism. A study of adolescent schoolgirls factors do not automatically lead to the development of
by Eisenberg, Neumark-Sztainer, Story & Perry (2005) eating disorders).
CHAPTER10 EATING DISORDERS 349
Familial factors psychological characteristics in the child that play an

We have noted earlier that eating disorders have a ten- active role in the acquisition and maintenance of the dis-
dency to run in families, and while this may in part be order (Polivy & Herman, 2002).
due to inherited characteristics, it may also be a result of As an important part of the family, mothers may have a
the direct influence of family attitudes and dynamics specific influence on the development of eating disorders
on the behaviour of those in the family. In particular, in their children. Mothers of individuals with an eating
Minuchin (Minuchin, Baker, Rosman, Lieberman et al., disorder are themselves more likely to have dysfunctional
1975; Minuchin, Rosman & Baker, 1978) has argued that eating patterns and psychiatric disorders (Hill & Franklin,
eating disorders are best understood by considering the 1998; Hodes, Timimi & Robinson, 1997) and these prob-
family structure of which the sufferer is a part. This fam- lematic maternal eating patterns appear to produce feed-
ily systems theory view argues that the sufferer may be ing problems in their offspring at an early age (Whelan &
embedded in a dysfunctional family structure that actively Cooper, 2000) some of which may give rise to weight gain
promotes the development of eating disorders. The family and disordered eating in their offspring later in life (Easter,
structure may inadvertently, but actively, reinforce a child’s Naumann, Northstone, Schmidt et al., 2013). Mothers
disordered eating, and this can function to distract from of sufferers also tend to excessively criticize their daugh-
dealing with other conflicts within the family (such as ters’ appearance, weight and attractiveness when com-
a deteriorating relationship between the child’s mother and pared with mothers of non-sufferers (Hill & Franklin,
father). In Minuchin’s view, the families of individuals with 1998; Pike & Rodin, 1991), and there is a significant
eating disorders tend to show one or more of the following inverse relationship between a mother’s critical com-
characteristics: (1) enmeshment, in which parents are intru- ments and her daughter's chances of successful recov-
sive, overly involved in their children’s affairs and dismissive ery following treatment (van Furth, van Strien, Martina,
of their children’s emotions and emotional needs Vanson et al., 1996).
(Minuchin, Rosman & While this research strongly implicates the involve-
eshment A characteristic of family
2ms theory in which parents are intru- Baker, 1978), (2) overpro- ment of familial factors in the aetiology of eating disor-
over-involved in their children’s affairs, tection, where members ders, Polivy & Herman
(2002) quite rightly point familial factors The idea that certain
dismissive of their children’s emotions of the family are overly
emotional needs. disorders may be a result of the direct influ-
concerned with parenting out that most of the studies
ence of family attitudes and dynamics on :
and with one another’s wel- are retrospective and cor- the behaviour of those in the family.
protection A characteristic of family relational in nature, and so
fare, and this can often be
2ms theory where members ofthe
ly are overconcerned with parenting viewed by the child as do not imply causation. There may indeed be some form
with one another's welfare, and this coercive parental control of intra-familial transmission of disordered eating pat-
often be viewed by the child as coer- (Shoebridge & Gowers, terns within families, but it is quite likely that some other
parental control. factor (biological, psychological or experiential) may be
2000; Haworth-Hoeppner,
2000), (3) rigidity, where necessary to trigger the severe symptoms typical of a
lity A characteristic of family systems clinically diagnosable disorder (Steiger, Stotland, Trottier
there is a tendency to main-
ry where there is a tendency to main-
tain the status quo within & Ghadirian, 1996).
the status quo within the family.
the family, and (4) lack of
conflict resolution, where families avoid conflict or are
in a continual state of conflict. How these characteristics 10.3.3 Experiential Factors
of conflict resolution A characteris-
of the sufferer’s family
f family systems theory where families influence the development There is some evidence that adverse life experiences may
d conflict or are in a continual state of of an eating disorder is act as a vulnerability factor for eating disorders and as
lict. unclear, although the fam- a precipitating factor for the onset of an eating disor-
ily may focus on the disorder once it has developed in der. For example, Rastam & Gillberg (1992) found that
order to avoid dealing with other difficult and important 14 per cent of anorexia sufferers (compared with 0 per
problems within the family. The disorder may serve a cent of healthy controls) had experienced a negative life
functional purpose for both the parents (by distracting experience (e.g. the loss of a first-degree relative) within
attention away from other family difficulties, such as a 3 months prior to the onset of the disorder. Similarly,
problematic relationship between mother and father) individuals with bulimia report significantly more adverse
and the eating disordered child (as a tool for manipulat- life events prior to symptoms than age-matched healthy
ing the family) (Minuchin, Rosman & Baker, 1978). As controls (Welch, Doll & Fairburn, 1997; Carretero-
we shall see later, the issue of how a dysfunctional fam- Garcia, Planell, Doval, Estragues et al., 2012).
ily environment may generate an eating disorder is Individuals with eating disorders report significantly
still unclear, but it may do so by generating specific more premorbid life stresses and difficulties than do
a
healthy controls (Raffi, Rondini, Grandi & Fava, 2000), bingeing (and then purging). Eating disorders also allow
and the number of adverse life events has been shown the individual to construct a coherent sense of self by
to differentiate between individuals with anorexia and focusing attention on one limited aspect of their lives.
healthy controls (Horesh, Apter, Ishai, Danziger et al., This in turn provides them with rewards that may other-
1996). Like the research on the role of familial factors, wise have been missing from their lives (by attaining self-
such studies are difficult to interpret because they are determined weight control goals), and also provides a
both retrospective and correlational in nature. very narrow life focus that may help them to avoid deal-
However, one particular form of adverse life experi- ing with more deep-seated psychological issues (Polivy
ence that has been implicated as a risk factor in eating & Herman, 2002). Therefore, this rather interesting view
disorders is childhood sexual abuse. There is some evi- of eating disorders views them as means of coping with
dence for higher levels of other, more global psychopathology. More research is
childhood sexual abuse The sexual
maltreatment of a child. childhood sexual abuse in needed to verify this view.
the history of bulimia suf-
ferers than in healthy controls (Steiger, Leonard, Kin et
al., 2000; Garfinkel, Lin, Goering, Spegg et al., 1995;
Welch & Fairburn, 1994), and in anorexia sufferers than 10.3.4 Psychological and
healthy controls (Brown, Russell, Thornton & Dunn,
Dispositional Factors
1997), but not in binge-eating disorder sufferers (Dansky,
Brewerton, Kilpatrick & O’Neal, 1997). One longitudinal Individuals who develop eating disorders do appear to
study of a large community-based sample of mothers have particular personality and dispositional character-
and offspring has indicated that children who had experi- istics that have been variously implicated in the aeti-
enced sexual abuse or physical neglect during childhood ology of those disorders. We have so far identified a
were also at elevated risk for eating disorders (Johnson, number of risk factors for eating disorders, but none of
Cohen, Kasen, Smailes & Brook, 2002). Given that child- these risk factors appears to be a sufficient condition for
hood sexual abuse is now largely accepted as a risk factor developing anorexia, bulimia or binge-eating disorder.
for eating disorders (Polivy & Herman, 2002), it is diffi- It may therefore be the case that specific risk factors
cult to determine how such early experiences facilitate interact with personality traits to generate an eating
the risk of developing an eating disorder. This is compli- disorder.
cated by the fact that childhood sexual abuse is a risk fac- Various studies have identified personality traits that
tor for a wide range of psychiatric disorders (Chou, are characteristic of individuals with diagnosed eating
2012), so we need to discover why some people with this disorders. These traits include:
history specifically develop eating disorders. One possi-
bility is that adverse early experiences generate other ° perfectionism
forms of psychopathology that mediate the develop- e shyness
ment of eating disorders (Casper & Lyubomirsky, 1997). * neuroticism
For example, Steiger, Leonard, Kin et al. (2000) found
¢ low self-esteem
that childhood sexual abuse only facilitated bulimia in
the presence of borderline personality disorder, and ¢ high introspective awareness (awareness of bodily
other researchers have argued that eating disorders are a sensations)
means of coping with the more generalized psychopa- * negative or depressed affect
thology (such as major depression) that results from sex- * dependence and non-assertiveness (Vitousek &
ual abuse (Rorty & Yager, 1996). This latter view sees the
Manke, 1994; Leon, Fulkerson, Perry & Early-
development of an eating disorder as a way of helping Zald, 1995).
the individual to cope with emotional and identity prob-
lems (which may have been caused by earlier adverse life It is worth looking in more detail at some of the more
experiences). For example, anorexia enables the individ- important of these characteristics.
ual to exert some control over at least one aspect of their Eating disorders are very much associated with nega-
life (i.e. their eating), in circumstances where they may tive affect (usually depressed mood), and mood disor-
have experienced very little control over many other ders are often comorbid
negative affect Refers to the full spec-
aspects of their life (Troop, 1998). Similarly, bulimia may with both anorexia and trum of negative emotions.
also serve as a way of coping with the negative affect bulimia (Braun, Sunday &
caused by earlier life difficulties. Bulimia sufferers will Halmi, 1994; Brewerton, Lydiard, Herzog, Brotman
gain emotional relief, which is otherwise elusive, by et al., 1995). While negative mood and stress is a
CHAPTER10 EATING DISORDERS 3s
commonly reported antecedent of eating disorders (Ball A second prominent characteristic of individuals with
& Lee, 2000), there is some disagreement about whether eating disorders is low self-esteem. This low self-esteem
negative affect is a cause or just a consequence of the
my simply be a derivative low self-esteem A person's negative,
disorder. Nevertheless, negative affect has been proposed of the specific negative subjective appraisal of himself or herself.
to play a number of discrete roles in the aetiology of eat- views that those with eat-
ing disorders. Experimental studies have indicated that ing disorders have of themselves (such as being ‘fat’, hav-
induced negative mood does increase body dissatisfac- ing an unattractive body, or, in bulimia, having a lack of
tion and body-size perception in bulimia sufferers control over their eating behaviour). However, there is
(Carter, Bulik, Lawson, Sullivan & Wilson, 1996), and it some evidence to suggest that low self-esteem may have
may contribute in part to eating disorders through this a role to play in the development of eating disorders.
route. Negative mood states have also been shown to Firstly, it is a significant prospective predictor of eating
increase food consumption in individuals who are diet- disorders in females (suggesting that it is not just a conse-
ing or who have distorted attitudes about eating, and this quence of eating disorders) (Button, Sonugabarke,
may represent a role for negative mood in generating the Davies & Thompson, 1996). Secondly, eating disorders
bingeing and purging patterns typical of bulimia suffer- such as anorexia are viewed by some researchers as a
ers (Herman, Polivy, Lank & Heatherton, 1987). For means of combating low self-esteem by demonstrating
example, individuals with bulimia try to alleviate their control over one specific aspect of the sufferer’s own
negative mood by eating, and purging allows them life — namely, their eating (Troop, 1998). In this sense,
to use eating as a mood regulation process without gain- self-esteem may be implicated in the development of eat-
ing weight. However, when the bulimia sufferer begins ing disorders because controlled eating is the individual's
to realize that their eating is out of control, this activity way of combating their feelings of low self-esteem.
no longer provides relief from negative mood, and purg- Individuals diagnosed with anorexia and, to a lesser
ing may take over as a means of relieving guilt, self- extent, those diagnosed with bulimia both score high
disgust and tension (Johnson & Larson, 1982). This is on measures of perfectionism, and this personality
consistent with laboratory-based studies that report that characteristic has regularly been implicated in the
bulimia sufferers show reduced anxiety, tension and guilt aetiology of eating disor-
perfectionism The setting of excessively
following a binge-purge episode (Sanftner & Crowther, ders (Garner, Olmsted &
high standards for performance accompa-
1998). Studies such as these suggest that the negative Garfinkel, 1983; Bastiani, nied by overly critical self-evaluation.
mood possessed by individuals with eating disorders Rao, Weltzin & Kaye, 1995).
may not simply be a consequence of the disorder, but Perfectionism is multifaceted and can be either self-ori-
may play an active role in generating symptoms by ented (setting high standards for oneself) or other-ori-
increasing body dissatisfaction and being involved in pro- ented (trying to conform to the high standards set by
cesses of mood regulation which act to reinforce disor- others). It can also be adaptive (in the sense of trying to
dered eating behaviours. achieve the best possible outcome) or maladaptive (in
FOOD PRELOAD TESTS
Laboratory procedures have been developed that provide an objective behavioural measure of the tendency to
‘binge’ eat, and one of these is the food preload test (Polivy, Heatherton & Herman, 1988).
This test begins by asking participants to eat a filling preload (e.g. a 150z food preload test Laboratory proce-
chocolate milkshake or a large bowl of ice cream) under the pretence of rating its dure developed to provide an objective
palatability. behavioural measure of the tendency to
After eating the preload and making their ratings, participants are then told they binge eat.
can eat as much of the remaining milkshake (or ice cream) as they wish.
The real measure of interest is the amount of milkshake or ice cream that the participant eats by the end of
the study — this is a measure of how willing the individual is to continue eating after having already had a full,
filling portion of food.
METHODS
RESEARCH
10.1 This experimental procedure has shown that willingness to continue eating is a function of a number of fac-
tors, including whether the individual (1) is a restrained eater (i.e. has a tendency to dieting or has distorted atti-
tudes about eating), (2) has low self-esteem, and (3) is in a negative mood. Restrained eaters will even eat more
food than non-dieters, even if they rate the food as relatively unpalatable.
hey ce PSYCHOPATHOLOGY
terms of striving to attain what may well be unachiev- This has led some researchers to suggest that there are some
able goals) (Bieling, Israeli & Antony, 2004). processes or maintaining factors that are common across all
Perfectionism is a predictor of bulimic symptoms in eating disorder diagnostic categories, and one such model
women who perceive themselves as overweight (Joiner, is the transdiagnostic cognitive-behavioural model
Heatherton, Rudd & Schmidt, 1997), and both self- (Fairburn, 2008; Fairburn, Cooper & Shafran, 2003). This
oriented and other-oriented perfectionism have been model argues that a dysfunctional system of self-evaluation
found to predict the onset of anorexia (Tyrka, Waldron, is central to the maintenance of all eating disorders, and
Graber & Brooks-Gunn, 2002). Perfectionism is also that self-worth is defined in
transdiagnostic cognitive-behavioura
one of the few personality traits that predicts the main- terms of control over eating, model A model of eating disorders that
tenance of eating disorders at 10-year follow-up weight and shape, which argues that a dysfunctional system ofa
(Holland, Bodell & Keel, 2013). Other research has sug- in turn leads to dietary evaluationis central to the maintenance
gested that the perfectionist characteristics displayed by restraint. Other subsidiary of all eating disorders, and that self-wor
is defined in terms of control over oat
individuals with eating disorders may actively contrib- mechanisms that operate to
weight and shape, which in turn leads to
ute to their disordered eating. For example, Strober maintain eating disorders in dietary restraint. yee .
(1991) has argued that self-doubting perfectionism pre- this model include low self-
disposes individuals to eating disorders. Perfectionism esteem (which motivates people to pursue achievement in
is highly associated with measures of body dissatisfac- the domain of weight and body shape), clinical perfection-
tion and drive for thinness (Ruggiero, Levi, Ciuna & ism (which projects achievement in dietary restraint as an
Sassaroli, 2003), and so it is not difficult to see how per- important goal), interpersonal problems (which may lead
fectionism may be an indirect causal factor in the aetiol- people to control their weight in order to facilitate inter-
ogy of eating disorders; it drives the dieter to achieve personal issues), and mood intolerance (which encourages
the perfect body shape or the stringent dieting goals binge eating and purging.as a way of coping with negative
they set themselves (Keel & Forney, 2013). Interestingly, mood states). These four additional maintaining factors
perfectionism is a characteristic of many psychological will differ across individuals with different forms of eating
disorders (Egan, Wade & Shafran, 2011), and is the disorder. For example, mood intolerance will be impor-
best predictor of comorbidity across the anxiety distant for bulimia sufferers,
orders (Bieling, Summerfelt, but less so for anorexia suf- To read an evaluation of the trans-
To read Keel & Forney’s article on Israeli & Antony, 2004). So, ferers. Some recent stud- diagnostic cognitive-behavioural model
by Lampard etal. go to
if perfectionism does play a
psychosocial risk factors go to ies have provided evidence www.wiley-psychopathology.com/
reading/ch10
causal role in eating disor- supporting this model. For reading/ch10
ders, we need to ask why it example, Lampard, Byrne,

was an eating disorder that McLean & Fursland (2011) found that low self-esteem was
developed and not any one of a number of other disor- associated with overevaluation of weight and shape which
ders that have perfectionism as a prominent feature. in turn was associated with dietary restraint, and interper-
sonal difficulties were also associated with dietary restraint.
As predicted by the model, Lampard, Tasca, Balfour &
10.3.5 Transdiagnostic Models Bissada (2013) found that the processes of low self-esteem,
overevaluation of weight and shape, and mood intoler-
of Eating Disorders ance were transdiagnostic maintaining factors across all the
In this section on aetiology, we have seen that many of the main eating disorders. This cognitive-behavioural model of
factors that might give rise to eating disorders can often be eating disorders has also provided the basis for the develop-
found as risk factors or causes across all of the eating dis- ment of CBT interventions for eating disorders, which we
orders (e.g. anorexia, bulimia, and binge eating disorder). will discuss later (Fairburn, 2008).
SELF-TEST QUESTIONS
* Can you name some ofthe important risk factors for anorexia and bulimia?
* Can you describe some of the biological factors that might be involved in the development of an eating disorder?
° What role might brain neurotransmitters play in the acquisition and maintenance of eating disorder symptoms?
CHAPTER 10 EATING DISORDERS B53.
* Can you name some of the important sociocultural factors that influence the development of eating disorders? What
evidence is there that these factors influence body dissatisfaction and attitudes to dieting?
* What are the important dispositional factors associated with eating disorders? Do they have a causal role to play in the
development of an eating disorder?
° What are the main features of the tripartite model of eating disorders?
SECTION SUMMARY
10.3. THE AETIOLOGY OF EATING DISORDERS
This section on aetiology has concluded that a number of psychological and cognitive processes may be important common
factors in the acquisition and maintenance ofall eating disorders, and these psychological factors include the defining of self-
worth in terms of control over eating, low self-esteem, clinical perfectionism, interpersonal problems and intolerance of nega-
tive moods such as depression. Many of these psychological factors may be influenced by exposure to media ideals of body
shape, peer attitudes to controlled eating, and familial factors — such as intra-family conflict or dysfunctional mother-daughter
interactions. Traumatic life events also appear to be risk factors for eating disorders, and childhood sexual abuse has been one
specific form in which trauma has been researched in relation to eating disorders. There is an inherited component to eating
disorders, although this is modest and twin studies have tended to emphasize that unique environmental experiences are
equally as important as genes in the aetiology of eating disorders. Finally, eating disorder symptoms have been found to be
associated with a number of brain mechanisms and reward pathways, including opioid, serotonin and dopamine pathways,
but it is still unclear whether these neurobiological processes are causes of eating disorder symptoms or are themselves con-
sequences of those symptoms.
The key points discussed in this section are:
e There is evidence of an inherited component to eating disorders that may account for up to 50 per cent of the variance in
factors causing these disorders.
@ Maintaining a low body weight may be reinforced by the endogenous opioids that the body releases during starvation to
reduce pain sensation.
e The neurotransmitters serotonin and dopamine may be involved in eating disorders by affecting satiety and the pleasur-
able consequences of eating.
e Exposure to media-portrayed extreme body shape ideals has been shown to increase body dissatisfaction in young adoles-
cent females, and to increase their tendency to either diet or purge after overeating.
® Body dissatisfaction and dieting are important vulnerability factors for eating disorders.
® Peer attitudes and views are an important factor in determining an adolescent girl’s attitudes to slimness and
dieting.
e Eating disorders have a tendency to run in families, and family systems views of eating disorders suggest that a dysfunc-
tional family structure may reinforce a child’s disordered eating.
¢ Mothers may have a specific influence on the development of an eating disorder by producing eating problems in their
offspring and criticising their child’s appearance.
e Adverse life experiences (such as childhood sexual abuse) may act as a vulnerability factor for eating disorders.
° Negative affect, low self-esteem and perfectionism are all dispositional factors that have been shown to exert a possible
causal influence on the development of an eating disorder.
e The tripartite model argues that the effect of influences from media, parents and peers is mediated by internalisation of
social ideals and social comparison, leading to body dissatisfaction, disordered eating and negative affect.
remedial medical treatment is often necessary to increase

10.4 THE TREATMENT OF weight, rectify body electrolyte imbalances and, in many
EATING DISORDERS cases, prevent death by self-starvation before some of the
significant psychological factors can be addressed.
Third, eating disorders are often highly comorbid
Eating disorders are complex and difficult to treat but with other psychological disorders, which may make tre-
clinical psychologists have been actively developing a atment difficult and complex. For example, anorexia and
range of treatments, many of which show promising bulimia are often comorbid with major depression
results. However, before we discuss some of these treat- and OCD, and some psychological treatments for ano-
ment methods, it is important to describe some of the rexia have included components used to treat obsessions
challenges that face any intervention for eating disor- and compulsions (such as response prevention and expo-
ders. First, many individuals with eating disorders regu- sure methods; see section 6.5.2) (e.g. Wilson, Eldredge,
larly deny they are ill or have a disorder. Indeed, many Smith & Niles, 1991). Similarly, treatments for eating dis-
individuals with bulimia see their bingeing and purging orders sometimes work better with a concurrent antide-
eating patterns as a positive way of controlling weight, pressant drug (Agras, Rossiter, Arnow, Schneider et al.,
and there has been a recent burgeoning of websites 1992). In addition, there is growing evidence that ano-
extolling the virtues of bingeing and purging as a way rexia and bulimia may be conta withseaisie dis-
of life (Table 10.2). Similarly, individuals with anorexia orders such, as OCPD, 2nd. as
To read the NICE guidelines go to
regularly deny they are pathologically underweight, BPD (Schmidt & Telch,
http://tinyurl.com/orr7xzh
and the fact that they may view their controlled eating 1990; Carroll, Touyz & |
as a way of coping with more general psychopathology Beumont, 1996; O’Brien &
means that it is often viewed as an activity that has ben- Vincent, 2003), and personality disorders of this kind are
efits rather than costs (Rorty & Yager, 1996). Because of themselves quite resistant to treatment (see Chapter 12).
these factors as many as 90 per cent of individuals with In January 2004, the UK’s National Institute for Clinical
diagnosable eating disorders tend not to be in treatment Excellence (NICE) issued clinical guidelines for the treat-
(Fairburn, Welch, Norman, O’Connor & Doll, 1996). ment of eating disorders (these guidelines were retained
Second, individuals with severe eating disorders usu- following a review in 2011), and rated these interventions
ally need medical as well as psychological treatment, and according to the evidence that supported their effectiveness
in the case of anorexia, hospitalization and a period of (Wilson & Shafran, 2005). Table 10.3 shows a summary of
TABLE 10.2
Treating bulimia can be difficult because many individuals with bulimia see their bingeing and purging patterns of eating as a
positive way of controlling weight, and there has been a burgeoning of websites extolling the virtues of bingeing and purging as
a way of life. Below are some examples that illustrate how bulimia sufferers will actively swap experiences, information about the
best ways of purging, and how best to conceal their activities.
° Okay, so last night | was purging, ya know, and it kinda came out with more force than | was expecting. Well, anyway, | leaned
closer and actually only go half in the toilet. The other half goes down the side and on my sock and the floor. | spent for ever
cleaning up but my mum found the left overs and asked if|was sick. | said no. | think she bought it but she'll be on the look out.
So, how can | hide it better? Seriously | need help!
° |really don’t want you to become bulimic because it makes you feel awful, you get headaches, light-headness, irregular heart-
beats and you can rip your throat and you burst blood vessels and all this bad stuff. However, if you do start, to save you a lot of
pain, make sure you drink lots of water with everything, and diet coke is good too. Don't try and purge orange juice because it
hurts like hell. Make sure you chew everything thoroughly too, otherwise it can get stuck in your throat. And if you see blood
when you purge, it is not a good sign and you should stop for a while.
* l'mso sure someone would have to have an answer for me. . . okay, so I’m really good at making myself sick . . . but for the last
2 days | can’t get anything up. .. it’s nasty tho, bc | definitely get dry heaves and | gag for about 10 minutes at atime... and
the last time | tried it |was choking. . . |could still breath but | was gasping . . . | freaked myself out... and | know to chew
really well and all that, so | know thats the problem . . . u think it’s because my oesophagus is irritated or something like that?
Please give mea bit of advice. . . thanks
* Why is it that | can go without food for most of the day and then when it comes to the evening |go totally crazy and binge,
then afterwards |feel really bad and hate myself and vow never to eat that much again, but | always do. Can somebody please
give me some ideas on how to stop binging? I'd really appreciate it.
* After you eat would you go to the bathroom? | am relatively new at it but have had some luck but just not as much coming up
as | thought. How soon after and how long would you do it for?
s
CHAPTER 10 EATING DISORDERS B55
TABLE 10.3 NICE guidelines for the treatment of eating disorders (2004)
PHYSICAL MANAGEMENT OF WEIGHT GAIN IN ANOREXIA NERVOSA

Managing weight gain
* In most patients, the aim should be average weekly weight gain of 0.5-1.0 kg as inpatient and 0.5 kg as outpatient
* Regular physical monitoring, and oral multivitamin/multimineral supplement in some cases, is recommended for inpatients
and outpatients
° Total parenteral nutrition should not be used, unless there is significant gastrointestinal dysfunction
Managing risk
° Healthcare professionals should monitor physical risk. If risk increases, frequency of monitoring and nature of investigations
should be adjusted accordingly
° Pregnant women with current or remitted anorexia should be considered for more intensive care to ensure adequate prenatal
nutrition and fetal development
* Oestrogen should not be given for bone-density problems in children and adolescents, because such treatment may lead to
premature fusion of epiphyses
Feeding against will of patient:
e This should be an intervention of last resort
RECOMMENDED TREATMENT FOR EATING DISORDERS
Anorexia nervosa
Pharmacological Psychological
* Drugs should not be used as sole or primary treatment for ° Consider cognitive analytic or cognitive-behavioural therapies,
anorexia interpersonal psychotherapy, focal dynamic therapy, or family
: : é ; , interventions focused on eating disorders
© All patients with anorexia should have alert placed in their g
prescribing record about risk of side effects ° Family interventions that directly address the eating disorder
should be offered to children and adolescents
Bulimia nervosa
* To be offered trial ofan antidepressant as alternative to,or ° Dietary counselling should not be provided as sole treatment
tec eo progtatttie ° Asapossible first step, patients with bulimia should be

e Patients should be informed that antidepressant drugs encouraged to follow evidence-based self-help programme
can reduce frequency of binge eating and purging, but
® Consider direct encouragement and support to patients under-
long-term effects are unknown 9 PP P
taking evidence-based self-help programme, which may improve
e Selective serotonin reuptake inhibitors (specifically fluox- outcomes and be sufficient for limited subset of patients
etine) are drugs offirst choice for bulimia in terms of accept- ,
Specifically adapted CBT should be offered to adults with bulimia;
ability, tolerability and reduction of symptoms. No drugs
16-20 sessions over 4—5 months. Interpersonal psychotherapy
other than antidepressants are recommended
should be considered as alternative to CBT, but patients should
be informed it takes 8-12 months to achieve similar results
Binge-eating disorder
e Patients should be informed that selective serotonin * Specifically adapted CBT should be offered to adults with
reuptake inhibitors can reduce binge eating, but long-term binge-eating disorder
effects are unknown; antidepressants may be sufficient for
some patients
Source: Wilson, G.1. & Shafran, R. (2005). Eating disorders guidelines from NICE. Lancet, 365, 79-81. Reproduced with permission.
these recommendations for both the physical management found good evidence for the effectiveness of cognitive
of patients with anorexia and the psychological and phar- _behaviour therapy for both bulimia and binge-eating disor-
macological treatment of all eating disorders. No specific _der. In the following sections, we will describe and discuss
recommendations were made for anorexia, but the report _the main forms of treatment that have been used for eating
356 PSYCHOPATHOLOGY
x
disorders. These are pharmacological treatments, family core dysfunctional beliefs in bulimia (see below), and anti-
therapy, and cognitive behaviour therapy (CBT). In addi- depressant drug treatment appears to reduce the tendency
tion to these treatments, clinicians have also advocated the to relapse following cognitive behavioural treatment
use of self-help and alternative delivery systems, and you (Agras, Rossiter, Arnow, Schneider et al., 1992). CBT plus
can see from Table 10.3 that self-help programmes are an antidepressants can also be effectively used in a stepped-
important component of the treatment provision for both care approach in which CBT comprises the initial step with
bulimia and binge-eating disorder. Bulimia self-help groups the addition of fluoxetine for non-responders after six ses-
that use structured manuals and require minimum prac- sions (Mitchell, Agras, Crow, Halmi et al., 2011).
titioner management can show significant treatment Pharmacological treatments with anorexia have tended
gains — especially when these help the patient to identify to be significantly less successful than with bulimia, but the
triggers for bingeing and develop preventative behav- studies assessing drug treatment with anorexia have been
iours for purging (Cooper, Coker & Fleming, 1994), and relatively limited in number (Pederson, Roerig & Mitchell,
can be equally or more effective than CBT in establishing 2003; Claudino, Hay, Lima, Bacaltchuk et al., 2006).
remission from bingeing and purging symptoms (Bailer, Nevertheless, outcome studies so far have found very little
de Zwaan, Leisch, Strnad et al., 2004). Alternative effect of antidepressants on either weight gain in anorexia
delivery systems do allow access to services for sufferers or significant changes in other core features of the disorder,
who might, for whatever reason, not receive other forms such as depression, eating attitudes, or body-shape percep-
of treatment. These include treatment and support via tions (Attia, Haiman, Walsh & Flater, 1998; Biederman,
alternative delivery systems Treatment
telephone therapy, e-mail, Herzog, Rivinus, Harper et al., 1985). Pharmacological
methods that allow access to services for the internet, computer- treatments of eating disorders also have the added dis-
sufferers who might not receive other software CD-ROMs, and advantage of higher drop-out rates from treatment than
forms of treatment. These include treat- virtual reality techniques psychological therapies (Fairburn, Agras & Wilson, 1992),
ment and support via telephone therapy,
email, the internet, computer-software
(see section 4.1.2), and an and also have a number of physical side-effects.
CD-ROMs and virtual reality techniques. initial assessment of the
effectiveness of these meth- 10.4.2 Family Therapy
ods is encouraging (Myers,
To read an article by Myers et a/. about
the use of new technologies in the treat- Swan-Kremeier, Wonderlich, One of the most common therapies used with eating dis-
ment of eating disorders go to Lancaster & Mitchell, 2004; order sufferers — and particularly anorexia sufferers — is
reading/ch10
Wagner, Penelo, Wanner, family therapy. This stems mainly from the theories
Gwinner et al., 2013). of Minuchin (Minuchin, Baker, Rosman, Lieberman
et al., 1975; Minuchin, Rosman & Baker, 1978), whose
family systems theory view argues that the sufferer
10.4.1 Pharmacological Treatments may be embedded in a dys- family systems theory A theory which.
functional family structure argues that the sufferer may be embedd
Because both anorexia and bulimia are frequently comor- that actively promotes the in a dysfunctional family structure that
bid with major depression, eating disorders have tended development of eating dis- actively promotes psychopathology.
to be treated pharmacologically with antidepressants orders (see section 10.3.2). In particular, this view argues
such as fluoxetine (Prozac) (Kruger & Kennedy, 2000). that the eating disorder may be hiding important con-
There is some evidence that pharmacological treatments flicts within the family (such as a difficult relationship
can be effective with bulimia between the sufferer’s parents), and the family may be
pharmacological treatments Drug-based
treatments for psychopathology.
when they are compared implicitly reinforcing the eating disorder in order to avoid
with placebo conditions, confronting these other
but this evidence is still far conflicts. As we noted in To read Dallos’s article on attachment
narrative therapy go to
from convincing (e.g. Grilo, Pagano, Skodol, Sanislow section 10.3.2, the families www.wiley-psychopathology.com/
et al. 2007). Some studies have indicated a modest reduc- of individuals with eating reading/ch10
tion in the frequency of bingeing and purging with such disorders exhibit the char-
antidepressants compared with placebo controls (e.g. acteristics of enmeshment, overprotectiveness, rigidity,
Wilson & Pike, 2001; Bellini & Merli, 2004), but drop-out and lack of conflict resolution, and family therapy can be
rates can still be unacceptably high (Bacaltchuk & Hay, used to unpack and address these dysfunctional family
2003). More significant treatment gains are reported if characteristics. In Treatment in Practice Box 10.1 is an
antidepressant medication is combined with psychologi- example of how family therapy is applied in the context of
cal treatments such as CBT (Pederson, Roerig & Mitchell, an adolescent family member with anorexia. This example
2003). The benefits with joint drug and CBT programmes shows how family therapy can be used to explore concerns
appear to be reciprocal in that CBT helps to address the about relationships and emotional expression within the
CHAPTER 10 EATING DISORDERS 357)
CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 10.1

FAMILY THERAPY FOR EATING DISORDERS
Sandy is 17 and for 2 years had been suffering with ano- Mrs Sinclair a more relational and emotional one. Through
rexia of such severity as to require two brief stays in hospi- the use of a genogram (family tree) it was revealed that
tal. She was living with her parents and older brother. Two both parents had themselves had very negative experi-
older brothers had left home. ences of being parented that made it hard for them to
Though all were invited only Sandy and her parents know how to comfort and help their children. It also tran-
attended for family therapy which took place at intervals spired that their marriage was in serious difficulty. Sandy
of between 3 and 4 weeks over 18 months. The sessions, commented that her parents’ conflicts upset her and she
with the full permission ofall of the family, were of 1 hour felt caught in the middle in trying to meet the emotional
in length, with the therapist in the room with them anda needs of both of her lonely parents. In effect she felt like
team observing from behind a one-way mirror. The team she was a therapist for her own family. (Interestingly, she
usually joined the family and the therapist after 40-50 has gone on to study psychology at university.)
minutes and held a reflective discussion with each other in The therapist and the reflecting team discussed the
front of the family in which they shared their ideas about possible impacts that the parents’ own experiences may
the family’s problems, ideas, understandings and feelings. have had on how they acted towards Sandy. Along with
The family were then invited to comment and then held this there were discussions of a variety of related issues,
a closing discussion with the therapist when the team such as the pressure on young women to confirm to stere-
had left the room. The core idea of family therapy is that otypes ofthinness and self-starving as an attempt to exert
problems such as anorexia are not simply, or predomi- control in one’s life. Some marital work was done sepa-
nantly, individual but are related to wider stresses and rately with the parents to look at their childhoods, their
distress the family is experiencing. In addition it is recog- marriage, their own needs and how these had an impact
nized that the sense of failure and blame associated with on Sandy. Mrs Sinclair in particular felt she had failed as a
conditions such as anorexia can paralyse families’ abilities mother but was relieved to hear that the team did not see
to help each other. it in this way. Sandy gained considerable insight into how
Initially each member of the family was asked to the family dynamics across the generations had had an
describe what they saw as the main problems and invited impact on her and her parents. She became independent
to offer their explanations of the causes of the problem. enough to go to university but initially struggled, as did
This was followed by a focus on two broad areas: her parents, to separate. Some struggle with her weight
(1) the impact of the problems on each of them and their continues but she is confident that she will cope in the
relationships with each other, and, in turn, (2) the influ- long term.
ence that they could exert on the nature of the problems.
Source: Case history provided by Dr Rudi Dallos, Consultant
Initially the parents indicated that the distress caused by Clinical Psychologist (Somerset Partnership Trust) and Director
Sandy's anorexia was the main problem for all of them. of Research, Clinical Psychology Teaching Unit, University of
However, it quickly emerged that the parents had very dif- Plymouth. Davey, G.C.L. (Ed.) (2004) Complete Psychology (Hodder,
ferent ideas about what caused the problems and what to 9780340967553). Focus Point 34.4, p.521. Reproduced by permis-
do to help. Mr Sinclair had a medical and practical view and sion ofTaylor and Francis.
family, as well as individual feelings of failure, shame, disorder symptoms, and a third stage that develops family
and guilt. Exploring these issues throws up other con- relations and activities once recovery from eating disorder
flicts and difficulties within the family, and how the ano- symptoms has occurred (Eisler, 2005; Lock, Le Grange,
rexia sufferer may see themselves as trapped within these Agras, Moye et al., 2010).
existing relationships and conflicts (Dallos, 2004). However, while there is significant support for the use
A more recent family-based therapy for eating disorders of family therapy in eating disordered individuals — especially
is the Maudsley approach, which has a number of stages those with a diagnosis of anorexia nervosa (e.g. Rosman,
beginning with a stage that focuses on how the family can Minuchin & Liebman, 1975), SLES ELE LENO EIDE Gp
help and solve the problems well-controlled treatment To read Downs & Blow’s review of
dsley approach Family based, staged they are facing, a second outcome research remains family-based therapy go to
py for eating disorders. stage that helps the fam- somewhat limited (Cottrell, reading/ch10
ily to challenge the eating 2003; Downs & Blow, 2013). OTE
é
358 PSYCHOPATHOLOGY
; D %
10.4.3 Cognitive Behaviour restrict eating, which leads to an ever-increasing vicious

cycle of bingeing and purging (see Figure 10.5).
Therapy (CBT) Treatment in Practice Box 10.2 shows the three stages
The treatment of choice for bulimia is generally consid- of CBT that are required to deal with both the symp-
ered to be cognitive behaviour therapy (CBT). The UK toms of bulimia and the dysfunctional cognitions that
NICE guidelines for the treatment of eating disorders underlie these symptoms. These cover:
makes its strongest recommendation for the use of CBT
1. meal planning and stimulus control,
with bulimia, usually for 16-20 sessions over a period of
4-5 months (Wilson & Shafran, 2005; see Table 10.3).
2. cognitive restructuring to address dysfunctional
beliefs about shape.and weight, and
CBT for bulimia is based on the transdiagnostic cognitive
model developed by Fairburn and colleagues (Fairburn, 3. developing relapse prevention methods.
Shafran & Cooper, 1999, see section 10.3.5). According
In stage 1, individuals are taught to identify the stim-
to this model, individuals with bulimia have a long-
standing pattern of negative self-evaluation that interacts
uli or events that may trigger a binge episode (such as a
with concerns about weight, shape and attractiveness.
period of stress or after an argument with a boyfriend or
Such individuals come to evaluate their worth solely in parent), and are also taught not to indulge in extremes
terms of their weight and shape — largely because this is of eating behaviour (e.g. dieting and bingeing), and
often the only area of their lives that they can control. that normal body weight can be maintained simply by
They develop idealized views of thinness that are often planned eating. In stage 2, dysfunctional beliefs about
unachievable, and as a result end up in a constant state
weight, body shape and eating are identified, challenged
of dissatisfaction with their body shape and their weight. and replaced with more adaptive cognitions. For exam-
This leads them to excessive dieting, and as a result of
ple, beliefs that relate eating and weight to self worth,
this dietary restriction they lapse into episodes of binge- such as ‘No one will love me if Iam a single pound heav-
ing. This in turn invites the use of weight compensation ier are challenged. In stage 3 relapse prevention is often
methods such as vomiting encouraged with the use of behavioural self-control pro-
) and laxative abuse. Each cedures that enable the individual to structure their daily
For an activity on Fairburn’s Cognitive
Model go to | episode of bingeing and activities to prevent bingeing and purging, and rewarding
| purging is followed by a oneself for ‘good’ behaviours (e.g. sticking to a planned
activities/ch10
" more determined effort to eating programme) (see section 4.1.1).
An ‘enhanced’ form of CBT has been developed for
use with all forms of eating disorder, and this can be
helpful with sufferers who are significantly underweight
Low Self-Esteem (e.g. anorexia nervosa sufferers) by increasing their
motivation to change and then helping them to regain
weight while at the same time addressing psychological
Extreme Concerns about
issues relating to shape and weight (Cooper & Fairburn,
Shape and Weight 2011). Preliminary outcome studies with anorexia suf-
ferers suggest that a majority were able to complete
this enhanced programme with a substantial increase
Strict Dieting in weight and reduction in eating disorder symptoms
(Fairburn, Cooper, Doll, O’Connor et al., 2013).
Outcome studies indicate that CBT of bulimia is suc-
cessful in reducing bingeing, purging and dietary restraint,
‘Binge-Eating’ ;
and there is usually an increase in positive attitudes
towards body shape (Compas, Haaga, Keefe, Leitenberg &
Williams, 1998; Richards, Baldwin, Frost, Clark-Sly et al.,
Self-Induced Vomiting
2000). In addition, follow-up studies suggest that thera-
FIGURE 10.5 Fairburn’s (1997) cognitive model of the
peutic gains can be maintained for up to five years fol-
maintenance ofbulimia, and on which contemporary CBT lowing treatment (Fairburn, Norman, Welch, O’Connor
for bulimia is based. Low self-esteem leads to concerns about et al., 1995). Importantly, when CBT is effective it has
weight, followed by dietary restriction, which —- when such been found to significantly reduce not only the behav-
dieting fails — leads to binge eating and subsequent purging. ioural aspects of bulimia such as bingeing and purging
Following purging, individuals become more determined (Agras, 1997; Wilson, Fairburn & Agras, 1997), but also
to restrict eating, and a vicious cycle is established that has beneficial effects on core ‘cognitive’ aspects of bulimia
maintains the bingeing—purging pattern. such as beliefs about dietary restraint and low self-esteem
CHAPTER 10 EATING DISORDERS

THE THREE STAGES OF CBT FOR BULIMIA NERVOSA
STAGE 1 (3-9 WEEKS) binge eating and purging usually follow the regulari-
sation of eating patterns.
° The cognitive model is explained to clients, and they
learn to control eating and reduce dietary restraint. STAGE 2 (ABOUT 8 WEEKS)
° Clients learn to control eating by discovering what
factors trigger bingeing (e.g. periods of stress ° Clients are taught to identify their thoughts and
or arguments with partners or parents). This is beliefs about eating and their weight, and to chal-
achieved with the use of a diary that allows the cli- lenge dysfunctional and inappropriate beliefs and
ent to discover consistencies between life events thinking patterns.
and bingeing. e The therapist will help to foster healthy ways of think-
¢ Clients are taught techniques such as stimulus con- ing about eating and will also address issues about
trol and meal planning. low self-esteem, and how dysfunctional attitudes that
¢ Stimulus control is where the client is allowed to eat, might link weight and self-worth are irrational (e.g.
but only in certain specified environments (such as ‘No one will love me if |am a single pound heavier’).
their kitchen) or at specific times (e.g. after work).
Eventually eating behaviour is controlled only by these STAGE 3 (ABOUT 4 WEEKS)
stimuli, and is not triggered at all times in all places.
e Meal planning involves ensuring that small, acceptable e Clients are taught various techniques to help pre-
meals are planned and eaten every day. Reductions in vent relapse.
(Anderson & Maloney, 2001). CBT has also been shown 1. educate vulnerable populations about eating
to be a more comprehensive treatment of bulimia than disorders, their symptoms and their causes;
antidepressant drugs (Whittal, Agras & Gould, 1999), and 2. help individuals to reject peer and media pressure
other psychotherapeutic interventions such as psychody- to be thin; and
namically oriented therapy (Walsh, Wilson, Loeb, Devlin
3. target risk factors for eating disorders such as dieting,
et al., 1997) and interpersonal psychotherapy (Wilson,
dissatisfaction with body image, and so forth.
Fairburn, Agras, Walsh & Kraemer, 2002). When effec-
tive, CBT also reports immediate improvement, including
76 per cent of clients showing an improvement in the fre- In a review of effective prevention programmes,
quency of binge eating and 69 per cent showing improve- Stice, Becker & Yokum (2013) identified two contempo-
ment in the frequency of purging within 3 weeks of the rary prevention programmes whose effectiveness could
start of treatment (Wilson, Loeb, Walsh, Labouvie et al., be empirically verified. These were the Body Project inter-
1999). Much of this rapid improvement can be put down vention, in which young women critique the thin-ideal
to the behavioural homework assignments that are a in a series of exercises (Stice, Rohde, Durant & Shaw,
unique feature of CBT and which appear to help alleviate 2012; http://www.bodyprojectsupport.org), and the
depression and enhance self-efficacy (Burns & Spangler, Healthy Weight intervention, which attempts to improve
2000; Fennell & Teasdale, 1987). dietary intake and physical activity (Stice, Trost & Chase,
2003). The most effective prevention programmes have
been found to be those that are the most interactive and
selectively target individuals at high risk for eating disor-
10.4.4 Prevention Programmes ders (Stice, Shaw & Marti, 2007). Future developments
Finally, clinicians are aware in prevention programmes will probably need to extend
ention programmes Intervention
‘ammes that attempt to prevent theof the importance of the number of risk factors that they target (i.e. not just
prevention
-of a psychopathology before the first programmes body dissatisfaction but also dieting and negative affect),
toms are detected. that put eating disorders into and also consider ways in which they can incorporate the
a social context, and try to prevent eating disorders occur- _prevention of both eating disorders and obesity into indi-
ring. School-based prevention programmes attempt to: vidual programmes.
360 PSYCHOPATHOLOGY
“
SELF-TEST QUESTIONS
® Can you name the three main forms of treatment for eating disorders? Which ones are more suited to bulimia or to ano-
rexia, and why?
° What is the rationale for adopting a CBT approach to the treatment of bulimia nervosa, and what are the important stages
ofthis treatment?
® How successful are pharmacological interventions in the treatment of eating disorders?

® What are the main features of family therapy for eating disorders?
SECTION SUMMARY
10.4 THE TREATMENT OF EATING DISORDERS
¢ Eating disorders are often difficult to treat because of the denial by sufferers that they have a disorder, the medical implica-
tions of the symptoms, and comorbidity with other psychological disorders.
¢ There is evidence that self-help groups, alternative delivery systems, and school-based prevention programmes may be helpful
in lowering the prevalence of eating disorders.
¢ The major depression that is often comorbid with eating disorders can be treated pharmacologically with antidepressants
such as fluoxetine.
* One of the most common treatments for eating disorders is family therapy, in which the family’s role in developing and
maintaining an eating disordered individual is explored.
® Cognitive behaviour therapy (CBT) is often an effective treatment for bulimia and attempts to deal with the symptoms of
bulimia, the dysfunctional cognitions associated with disordered eating, and provide prevention against relapse.
with their own body shape, and other comorbid psycho-

10.5 EATING DISORDERS pathology symptoms such as major depression. The sec-
REVIEWED tion on aetiology shows that these three eating disorders
often share similar risk factors (see Figure 10.2), and that
sociocultural values relating to body-shape ideals may
This chapter has reviewed the three main eating disor- play a role in initiating weight-regulating behaviours in
ders — anorexia nervosa, bulimia nervosa, and binge- vulnerable individuals. However, we still know very little
eating disorder. All of these disorders are characterized about why one vulnerable individual will become ano-
by dysfunctional eating patterns. Anorexia represents an rexic and another bulimic, but there are some theories,
extreme form of self-starvation while bulimia and binge- such as the transdiagnostic behavioural model, that are
eating disorder are characterized by the individual’s loss attempting to understand these developmental processes.
of control over their own eating patterns. In the case of Treatments for eating disorders are still at early stages of
bulimia, the individual attempts to compensate for fre- development and refinement. Some forms of CBT have
quent binge eating by purging and fasting. The individual been adapted to treating bulimia with some moderate
with binge-eating disorder binges without compensatory success, and family therapy has been shown to be of par-
behaviour and so frequently ends up overweight or obese. ticular help to individuals with anorexia. But success rates
All these disorders share some common factors, these are still modest. In the meantime antidepressants, such as
include a predominance of female rather than male suf- SSRIs, may provide some short-term relief for the depres-
ferers, fear of weight gain, the individual’s dissatisfaction sion that is often comorbid with eating disorders.
ro
CHAPTER10 EATING DISORDERS 361"
Reading
Journal article: Specificand | ¢ Bulimia: A personal account Activity 10.1

nonspecific comorbidity in | Fairburn’s Cognitive Model
anorexia nervosa activity
Journal article: Review of Self-test questions
the prevalence and inci-
Revision flashcards
dence of eating disorders
Research questions
Journal article:
Epidemiology of binge-
eating disorder
Journal article: Prevalence,
incidence and prospec-
tive risk factors for eating
disorders
Journal article: Risk factors
for anorexia nervosa: A
national cohort study
Journal article: Psychosocial
risk factors for eating
disorders
Journal article: An evalua-
tion of the transdiagnostic
cognitive-behavioural
model of eating disorders
NICE Clinical Guidelines on
Eating Disorders
Journal article: The use of
alternative delivery systems
and new technologies in the
treatment of patients with |
eating disorders
Journal article: Attachment
narrative therapy
Journal article: A substan-
tive and methodological
review of family-based treat- |
ment for eating disorders
Clinical issues
References
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11 Sexual and Gend
Problems

This chapter covers the topics of sexual dysfunction,

paraphilic disorders, and gender dysphoria. The section 11.1 DEFINING PATHOLOGICAL SEXUAL BEHAVIOUR 365
on sexual dysfunctions describes the various disorders of
the sexual cycle, and considers aetiology and a range i '!-2 SEXUALDYSFUNCTIONS 366
of treatment options. Paraphilic disorders are largely dis- :
orders of male sexual function, and are often associated 11.3 PARAPHILIC DISORDERS 383
with sexual offending. The various paraphilic disorders
are described and evidence for theories of aetiology is 11.4 GENDER DYSPHORIA 399
assessed before we cover some of the aspects of treating
paraphilic disorders, including treating those whoaresex- : 11.5 SEXUALAND GENDER PROBLEMS REVIEWED 405
ual offenders. The final section covers gender dysphoria,
and discusses its characteristics and what evidence there
is for aetiology. It also assesses gender reassignment and
pychological treatments for gender dysphoria.
364 PSYCHOPATHOLOGY
“
LEARNING OUTCOMES
ae eLxvalp elm) ©ialeae teas apalele, ©)8 Sasivheledes eee cae eas
.G-w uleverkrelerovatpiece'aie sivie,o.e'ele)nielefe te siulspuis. o wtaleirie. piviwisiets ele sialeleleleleiulatp;uis tae stetule gic.«.s74\s (eleimia/e\ein ein)eime disle| alas ee miaiato ini
1. List the various types of sexual dysfunction, 6. Describe and evaluate behavioural, cognitive and
their place in the sexual cycle, and describe their biological treatments for paraphilic disorders.
diagnostic criteria. 7. Describe the basic features of gender dysphoria
2. Compare and contrast various theories of the and list the diagnostic criteria.
aetiology of sexual dysfunctions. 8. Describe and evaluate treatments for gender
3. Describe and evaluate both psychological and dysphoria.
biological treatments for sexual dysfunctions. 9. Discuss some of the conceptual and ethical issues
4. Describe the basic characteristics of paraphilic involved in defining and diagnosing sexual and
disorders and their diagnostic criteria. gender identity problems.
5. Describe and evaluate both psychological and
biological explanations for the aetiology of
paraphilic disorders.
‘So, | have kind of a weird problem here. Normally, getting an erection is no problem for me. | wake up with one every morning,
masturbate all the time, sometimes pop them up at inopportune moments. I’m 21, by the way. Also in most sexual encounters
there’s no problem; Id say 90 per cent of the time. However, the problem arises — or fails to arise! - when I’m in bed with someone
I'm extremely attracted to and very interested in. To date this has only happened with two men, but it is happening with the
second of those two people right now and it’s driving me crazy. Things will start out fine (i.e. erect) and! can be rolling around in
bed with an erection for an hour, but it seems that as soon as it’s time for my penis to do its duty (that is when foreplay ends and
penetration commences), it deflates and vehemently refuses to be resuscitated. | don’t know what to do! It’s unendingly embar-
rassing, but the worst is that it only occurs with people | really like.’
James's Story
‘1am sure lam not the first cross-dresser to feel this way but when | get the chance to dress, at first |am excited: | can hardly wait
to put on the stockings, skirt and get all dolled up and once | am fully dressed|feel so good — almost like this is the way | am sup-
posed to be. But that feeling does not last. . . Sometimes it will last an hour to hours but | have actually had it diminish within 15
minutes before | feel guilty and then undress and go back to my guy clothes. For some reason a light goes on in my head that tells
me,lamaguy... why am!wearing a skirt?! And then | quickly undress.
But then when | am dressed as a guy|will admire women in skirts and dresses and wish that could be me and all |want to do is
rush home and dress — when my wife is not home. |would love to tell my wife about my CD’ing but Ineed to come to terms with it first’
Chris's Story
Introduction about the nature of sexual behaviour and develop our

own personal likes and dislikes about sexual activities.
Sexual behaviour plays a central role in most of our lives. Furthermore, during adolescence and early adulthood,
It is a very personal and individual topic that we very sexual performance is often related to self-esteem, and
rarely discuss openly with others. Sexual development so becomes an important contributor to psychological
is also an important part of our lives, where we learn development. The importance: of sexual behaviour and
CHAPTER 11 SEXUAL AND GENDER PROBLEMS -365_
the critical role it may play in many of our relationships urges or fantasies. However, two factors are important
means that it can regularly affect psychological function- when attempting to identify psychopathology in both
ing and quality of life generally. There is no definition of sexual behaviour and gender identity. Firstly, a sexual
what is sexually ‘normal’, but clinical psychologists may activity or a gender problem may be considered a suit-
become involved when an individual becomes distressed able case for psychological treatment if it is frequent,
by their sexuality or their sexual activities or when these chronic, causes the individual significant distress, and
cause interpersonal difficulties. We began this chapter affects interpersonal relationships and other areas of
with two quite distinct personal accounts, each of which functioning. Such examples include the personal distress
illustrates in their different ways how an individual’s sex- and strain on interpersonal relationships caused by prob-
ual performance or their feelings of gender may cause lems associated with completion of the normal sexual
them conflict or distress. James’s story is one of problem- cycle (see section 11.2, Sexual dysfunctions, below).
atic sexual performance, where his normally active libido Similarly, the cross-dressing behaviour of Chris in our ear-
fails him just prior to intercourse with men he particu- lier example caused him to experience guilt and anxiety,
larly likes. Chris’s cross-dressing provides excitement that and individuals with gender identity problems (known
quickly gives way to guilt. It is also something he feels as gender dysphoria in DSM-5) also experience consider-
he needs to communicate to his wife, but at present can- able distress, anxiety and depression at being ‘trapped’
not. Both provide examples of the kinds of cases that in what they consider to be a body of the wrong bio-
clinical psychologists are likely to encounter when sexual logical sex. Clearly, such distress is certainly the subject
performance and gender identity have an impact on psy- matter of psychopathology. Secondly, some individuals
chological well-being, causing anxiety and distress, and persistently direct their sexual activity at individuals who
feelings of guilt, shame and depression. do not consent to the activity or who cannot legally give
consent (e.g. children). Such activities include exhibition-
ism (exposing of the genitalia to a stranger), paedophilia,
and rape, and DSM-5 includes some of these activi-
11.1 DEFINING ties (e.g. exhibitionistic disorder, paedophilic disorder)
even though the diagnostic criteria do not require that
PATHOLOGICAL the individual committing these acts should experience
SEXUAL BEHAVIOUR distress. Whether such categories of activity should be
labelled as psychopathologies is a debatable point, and in
many cases they may be more suitably characterized as
As you can imagine, what constitutes a sexual dysfunc- illegal criminal activities outlawed by particular societies.
tion is not a simple matter. Opinions about what is mor- The disorders of sexual functioning and gender iden-
ally and socially acceptable and unacceptable change tity that we will cover in this chapter can be found in
within societies over time, and there are significant dif- three separate chapters of DSM-5: (1) sexual dysfunctions —
ferences between cultures in the implicit rules that con- which represent problems with the normal sexual
stitute acceptable public behaviour (see Chapter 1). For response cycle (e.g. lack of sexual desire or pain during
example, until 1973 the DSM listed homosexuality as a intercourse); (2) paraphilic disorders — which represent
sexual disorder, along with paedophilia, sadism and such- sexual urges or fantasies involving unusual sources of
like, but it is now considered a perfectly normal form of gratification (e.g. non-human objects or non-consenting
sexual activity in most Western societies, and is even con- individuals); and (3) gender dysphoria — where the individ-
sidered a proper form of sexual activity for adolescent ual is dissatisfied with his or her own biological sex and
boys in some societies (Herdt & Stoller, 1990). The actual has a strong desire to be a member of the opposite sex.
nature of the sexual activity per se does not constitute In the case of each of these categories of disorders we
grounds for labelling it as pathological, and people differ will now discuss the nature of the disorders, diagnostic
significantly in the range of stimuli that trigger sexual criteria, prevalence, aetiology and treatment.
T E S T Q U E S T I O NS —
SELF-
® What are the sociocultural problems involved in defining pathological sexual behaviour?
© What are the three main groups of sexual and gender identity disorders?
SECTION SUMMARY
11.1 DEFINING PATHOLOGICAL SEXUAL BEHAVIOUR
* Asexual activity or a sexual problem can be considered a suitable case for treatment if it is frequent, chronic, causes the
individual significant distress, and affects interpersonal relationships and other areas of functioning.
© Some individuals direct their sexual actives at non-consenting others, and these can be described as both paraphilic disor-
ders and sexual offences (e.g. paedophilic disorders).
homosexual relationship. Frequency of sexual activity

11.2 SEXUAL was also significantly higher in 2000 than 1990, with 72
per cent of men and 76 per cent of women reporting
DYSFUNCTIONS having had vaginal intercourse in the previous month; 78
per cent of men and 76 per cent of women also reported
Sex is mainly a private subject, and many people rarely having oral sex in the previous year. These increases in
talk with anyone other than their partner about intimate sexual activity were also accompanied by significant rises
sexual matters. During the 1960s and 1970s, a greater in sexually transmitted infections — a 20 per cent rise in
openness about sex and sexual activities developed as part men and 56 per cent rise in women between 1990 and
of the liberalising climate of the time. Changes in lon- 1999 (Johnson, Mercer, Erens, Copas et al., 2001). A third
gevity, available leisure time, employment, child-rearing wave of the National Survey was completed in 2010
practices, and media coverage of leisure activities led to and was published in November 2013. A summary of the
increased interest in sexual practices. Similarly, effective findings can be found in a special issue of the Lancet at
oral contraceptives and treatments for venereal disease at http://www.thelancet.com/themed/natsal. It shows
helped to remove sexual inhibitions. Finally, changes that the upward trend in sexual activity found between
in obscenity laws permitted sexual explicitness in the 1990 and 2000 has in some respects continued up to 2010.
mass media in a way never previously broadcast. All this The figures available suggest there has been a signifi-
led to increased interest in sexual activity generally and cant change in behaviour and attitudes towards sex in
sexual satisfaction in particular (Tiefer, 2006). At around Western societies over recent decades. There has been
this time, Masters & Johnson (1966) were beginning to an increase in the rate at which both men and women
publish their pioneering research on what they called take sexual partners and a drop in the age at which ado-
the ‘human sexual response’, and the earlier Kinsey lescents report having their first sexual experience. This
ms «=m reports (Kinsey, Pomeroy, is accompanied by a relaxation of attitudes to homosex-
To read about the Kinsey reports goto 5 Martin & Gebhard, 1953) ual behaviour, non-exclusive sexual relationships and sex
) provided hitherto unava-
http://tinyurl.com/8bgygsl outside of marriage. Although sexual activity appears to
ilable statistical informa- have increased over the past 20 years, it is difficult to esti-
tion on the frequency with which Americans engaged mate whether this increase has also given rise to increased
in various sexual activities. To most people’s surprise, sexual performance problems. However, the fact that
these reports revealed that sexual activities were signifi- research on sexual activity can nowadays proceed openly
cantly more widespread than most people were willing and without stigma has meant that significant develop-
to believe at that time. They showed that 90 per cent of ments have been made in how we conceptualize sexual
males had masturbated and oral sex was a common sex- activity and categorize potential dysfunctions. For exam-
ual activity. In addition, the studies revealed that around ple, the normal sexual cycle has been divided into four
80 per cent of men and 50 per cent of women had stages, and sexual dysfunctions can occur at any one of
indulged in premarital sex. More recent data from the these distinct stages. Table 11.1 lists the stages and the
UK National Survey of Sexual Attitudes and Lifestyles specific diagnosable disorders that have been identified
suggested that sexual activity in both males and females with each. The four stages of the sexual response cycle
in the UK increased over the period between 1990 and are: (1) desire (relating to the desire to have sex), (2) arousal
2000. In 2000, men and women between the ages of (a subjective sense of sexual pleasure and accompanying
16 and 44 years reported having had an average of 12.7 physical changes in the genitalia — e.g. penile erection
and 6.5 sexual partners respectively in their lifetime, and in the male, and vaginal swelling and lubrication in the
2.6 per cent of men and women reported having had a female), (3) orgasm (the peaking of sexual pleasure), and
CHAPTER 11 SEXUAL AND GENDER PROBLEMS
TABLE 11.1 Stages of the sexual cycle and their associated DSM-5 disorders
Stage of the
sexual cycle Description Disorders Main diagnostic symptom
Desire Sexual thoughts and fantasies Male hypoactive sexual Persistent or deficient sexual/erotic
and the desire to have SEX, desire disorder thoughts and desire for sexual activity
Arousal Subjective sense of sexual Female sexual interest/ Absent/reduced interest in sexual activity
pleasure and accompanying arousal disorder or erotic/sexual thoughts
physical changes in the geni-
Erectile disorder In males, marked difficulty in obtaining
talia (e.g. penile erection in the
or maintaining an erection during sexual
male, and vaginal swelling and
activity
lubrication in the female)
Orgasm Peaking of sexual pleasure Female orgasmic In females, a marked infrequency of

(including ejaculation in the disorder orgasms or reduced intensity of orgasms
male and vaginal contractions
Delayed ejaculation In males, a marked delay in ejaculation
in the female)
or marked infrequency or absence of
ejaculation
Early ejaculation A persistent onset of orgasm and ejacula-

tion with minimal sexual stimulation and
before the individual wishes it
Sexual pain disorders Genito-pelvic pain/ Persistent difficulties with vaginal

penetration disorder penetration/vaginal or pelvic pain/fear or
anxiety about pain during intercourse
(4) resolution (a post-coital sense of muscular relaxation example, sexual activity and performance usually decline
and well-being). There are no DSM-5 disorders specifi- with age, and in females may do so after the menopause
cally associated with the resolution stage, but there is an (Hayes & Dennerstein, 2005) — and often this is a perfectly
additional set of disorders known as sexual pain disorders normal developmental process rather than a dysfunction.
that can occur at different stages during the sexual cycle The clinician also needs to take into account the client’s
and significantly affect the normal sense of well-being ethnic, cultural, religious and social background — factors
experienced during the resolution stage. We will discuss that may influence desire, expectations and attitudes about
the disorders relating to each stage in more detail later, performance. As we mentioned earlier, diagnosis of a dys-
after we have considered general diagnostic issues. function is given only when the symptoms are persistent,
cause the individual significant psychological distress, and
impair general day-to-day functioning and cause interper-
11.2.1 Diagnosis of sonal distress. In many cases, distress occurs in cases of
sexual dysfunction because it is associated with diagnosa-
Sexual Dysfunctions ble mood disorders or anxiety disorders (especially obses-
sive compulsive disorder, panic disorder, social anxiety
In general terms, sexual dysfunctions are a heterogenous
disorder and specific phobia), and sexual dysfunction can
group of disorders characterized clinically by the individ-
ual’s inability to respond often be a frequent complication of these latter disorders
al dysfunctions Problems with the (Figueira, Possidente, Marques & Hayes, 2001).
sexually or to experience
Jal sexual response cycle (e.g. lack of
al desire or pain during intercourse). sexual pleasure (DSM-5,
p.423). The specific dys- Specific sexual dysfunctions
function must also cause In DSM-5, sexual dysfunction disorders have been cat-
) To read Hayes & Dennerstein’s article
the individual subjective egorized around the stages of the sexual cycle, namely
on the impact of ageing go to
www.wiley-psychopathology.com/ | distress, affect areas of fun- desire, arousal, orgasm and resolution (see Table 11.1),
reading/ch11 ctioning such as relation- and also include a category relating to pain experienced
ships, and be persistent or during the sexual cycle.
recurrent. In each case, the clinician needs to exercise
considerable judgement about what might and might not Disorders of desire and arousal The first two
constitute a diagnosable problem in this area. The age and phases of the sexual response cycle are the desire and
experience of the client needs to be considered. For arousal stages, which consist of the urge and desire to
368 PSYCHOPATHOLOGY
; en
have sex, to indulge in sexual thoughts and fantasies, DSM-5 SUMMARY TABLE 11.1 Criteria for male hypoactive
the experience of sexual attraction to others (all defined sexual desire disorder
by desire), and a subjective sense of sexual pleasure and ¢ Incessantly or recurrently deficient sexual/erotic thoughts
accompanying physical changes in the genitalia (arousal). or desire for sexual activity for a period of at least
DSM-5 identifies three disorders that span these two 6 months, causing significant distress to the patient
phases of the sexual cycle and these are male hypoactive e The sexual dysfunction is not better accounted for by a
sexual desire disorder, erectile disorder and female sexual non-sexual mental disorder or as a consequence of rela-
interest/arousal disorder. tionship or other significant stressors and is not attribut-
able to the effects of amedication/substance or other
Male hypoactive sexual desire disorder ‘This disor- medical condition 5
der is characterized by a persistent and recurrent defi-
ciency or absence of desire for sexual activity and absence
of sexual fantasies that cause the individual marked dis- DSM-5 SUMMARY TABLE 11.2 Criteria for erectile disorder
tress or interpersonal difficulty (DSM-5 Summary
e Atleast one of the following occurs during at least 75
Table 11.1). Low sexual desire may be general or it may
per cent of sexual activity for a period of at least
be focused on sexual activity with one individual (such as 6 months causing significant distress to the patient:
the client’s partner) or on a particular sexual activity
itself (such as oral sex). Male hypoactive sexual desire ¢ Difficulty in obtaining an erection during sexual activity
disorder may be frequently associated with erectile and/ e Difficulty in maintaining an erection until the comple-
or ejaculation concerns, tion of sexual activity
male hypoactive sexual desire disorder and it may be an inability : Decrease in erectile rigidity
Absent/reduced interest in sexual activity
to obtain an erection that
or erotic/sexual thoughts. ° The sexual dysfunction is not better accounted for by a
leads to the man’s loss of
non-sexual mental disorder or as a consequence of rela-
interest in sexual activity. The prevalence of male hypo- tionship or other significant stressors and is not attribut-
active sexual desire disorder depends very much on the able to the effects of a medication/substance or other
individual’s nationality and country of origin, although 6 medical condition
per cent of younger men (age 18-24 years) and 41 per
cent of older men (age 66-74 years) have problems with
sexual desire, and overall prevalence rates vary from 12.5 pressure, diabetes and heart disease are associated with
per cent in Northern European men to 28 per cent in erectile disorders (Berman, Berman, Werbin, Flaherty
Southeast Asian men (DSM-5, p.442). Mood and anxiety et al., 1999) as are activities such as smoking and exces-
symptoms appear to be strong predictors of low sexual sive alcohol consumption (Westheimer & Lopater, 2002).
desire in men, and alcohol may increase this risk. Psychological factors that may affect the ability to
achieve and maintain erection include severe depression
Erectile disorder ‘The basic feature of erectile disor- (Seidman, 2002) and marital, financial and occupational
der is the repeated failure to obtain or maintain erection stress (Morokoff & Gillilland, 1993).
during partnered sexual activities, on all or almost all
occasions over a significant period of time (DSM-5 Female sexual interest/arousal disorder This disor-
Summary Table 11.2). This is often associated with low der is characterized by combinations of the following char-
self-esteem, low self-confidence and a decreased sense of acteristics: significantly reduced sexual interest or arousal
masculinity. Male erectile disorder is one of the most related to lack of interest in sexual activity, absence of
common of the sexual dys- erotic thoughts, unreceptiveness to sexual approaches,
erectile disorder The inability to maintain
an adequate erection during sexual functions in men, is usu- reduced sexual excitement, and reduced sexual sensations
activity. Around 10 per cent of males report ally the disorder that is during sexual activity (DSM-5 Summary Table 11.3). For a
erection problems, but this increases to most commonly referred diagnosis of female sexual interest/arousal disorder to
20 per cent in the over 50s.
for treatment, and is likely be made, clinically significant distress must also be associ-
to have a significant impact on the sexual satisfaction of ated with these symptoms.
both the sufferer and his partner. Approximately 13-21 This disorder is frequently female sexual interest/arousal disorde
per cent of men aged 40-80 years experience occasional associated with problems in Characterized by combinations of signifi
problems with erections, but only 2 per cent of men experiencing orgasm, and cantly reduced sexual interest or arousal
related to lack of interest in sexual activit
younger than 40 years (DSM-5, p.427). The causes of may be associated with pain
absence of erotic thoughts, unreceptive-
male erectile disorder are complex, and appear to range during sexual activity. It is ness to sexual approaches, reduced sexu
across physical, psychological and sociocultural factors. important to recognize that excitement, and reduced sexual sensati
Hormonal and vascular problems such as high blood there are many women during sexual activity.
“
&
CHAPTER 11 SEXUAL AND GENDER PROBLEMS 369°
DSM-5 SUMMARY TABLE 11.3 Criteria for female sexual who experience normal sexual desires, but who — for their
interest/arousal disorder
own reasons — decide not to engage in sexual activities.
¢ Significant reduction or lack ofinterest in sexual arousal/ Such individuals should not be diagnosed with female sex-
receptiveness as marked by at least three of the follow- ual interest/ arousal disorder, and the discussion found in
ing for a period of at least 6 months causing significant Focus Point 11.1 provides some insight into the issues
distress to the patient: By behind the use of the label ‘female sexual dysfunction’.
¢ Lack of/reduced interest in sexual activity
Disorders of orgasm Orgasm is the third stage of
e Lack of/reduced interest in sexual/erotic thoughts or the sexual cycle, when sexual stimulation has been suffi-
fantasies cient to enable the individual’s sexual pleasure to peak. In
e No/reduced initiation of sexual activity and unreceptive both males and females this involves a rhythmic muscu-
to partner's attempt to initiate sexual activity lar contraction of the genitals which results in a release
¢ No/reduced excitement or pleasure during sexual activ- of sexual tension, and in the male is accompanied by
ity in at least 75 per cent of sexual encounters ejaculation of semen. There are three DSM-5 defined
disorders of this stage, and these are female orgasmic disor-
e Lack of/reduced sexual interest in response to any
internal or external sexual cues der, delayed ejaculation, and early ejaculation.
e Lack of/reduced genital or non-genital sensations Female orgasmic disorder ‘This is a persistent or
during sexual activity in at least 75 per cent of sexual recurrent delay in or absence of orgasm following nor-
encounters
mal sexual excitement that causes the individual marked
The sexual dysfunction is not better accounted for by a distress or interpersonal difficulty (DSM-5 Summary
non-sexual mental disorder or as a consequence of rela- Table 11.4). Once again, the clinician has to exercise
tionship or other significant stressors and is not attribut- judgement about whether a diagnosis is relevant in indi-
able to the effects of a medication/substance or other vidual cases. Prevalence rates for female orgasmic prob-
medical condition
lems range from 10 per cent to 42 per cent depending on
CONSTRUCTING FEMALE SEXUAL DYSFUNCTION

eS
Sexual dysfunction is not diagnosed simply on the those in the feminist movement that was developing |
basis of problems in sexual desire and performance, at the time - believe that menopausal symptoms as_ |
but is dependent on the condition also causing described by Wilson were not a medical deficiency, but |
marked distress and interpersonal difficulty. Clearly, the creation of a sexist society (Houck, 2003).
i many people may only rarely experience sexual desire More recently, other writers have argued that the
eh and very rarely indulge in sexual activity — but a siz-

able proportion of those people are quite happy with
pharmaceutical industry has also attempted to manip-
ulate women’s beliefs about their sexuality in orderto |
this state of affairs, and indeed may even advocate and sell their products (Moynihan, 2006). Some drug com-
seek sexual abstinence. But what happens if attempts panies claim that sexual desire problems affect up to
are made to make such people feel inadequate or in 43 per cent of American women (Moynihan, 2003) and
some way ‘abnormal’? can be successfully treated with, for example, hormone
In 1966, a New York gynaecologist called Robert A. patches. However, others claim that this figure is highly |
Wilson published a best-selling book called Feminine improbable and includes women who are quite happy
| Forever,in which he argued that the menopause robbed with their reduced level of sexual interest (Bancroft, |
women of their femininity, their sexuality and ruined Loftus & Long, 2003). |
the quality of their lives. He labelled postmenopausal Tiefer (2006) lists a number of processes that have
women as ‘castrates’ and described the menopause been used either wittingly or unwittingly in the past to
as a ‘deficiency disease’ that should be treated phar- ‘medicalize’ what many see as normal sexual function-
macologically with hormone replacement therapy. ing. These include:
The book and its ensuing publicity had two effects -
it made some postmenopausal women begin to e Taking anormal function and implying that there
believe they were inadequate and had a disorder that is something wrong with it and it should be
needed treatment. It made many others - especially treated.
8370; 4 PSYCHOPATHOLOGY
“\
* Imputing suffering that is not necessarily there. While sexual dysfunctions are sometimes caused
e Defining as large a proportion of the population as by medical conditions (see ‘Biological causes’ in section
possible as suffering from the disease. 11.2.2), lack of sexual desire and interest is itself often por-
* Defining a condition as a ‘deficiency’, disease or dis- trayed as a medical condition in need of treatment. Yet a
ease of hormonal imbalance. reduction in sexual interest and desire can be a healthy
e Taking a common symptom that could mean any- and adaptive response to normal changes in body chem-
thing and making it sound as if it is a sign of aserious istry or as a normal reaction to adverse life stressors or
disease. relationship changes.
DSM-5 SUMMARY TABLE 11.4 Criteria for female DSM-5 SUMMARY TABLE 11.5 Criteria for delayed
orgasmic disorder ejaculation
¢ Delay, infrequency or absence of orgasm or reduced ¢ Delay, infrequency or absence of ejaculation in at

intensity of orgasmic sensations in at least 75 per cent of least 75 per cent of partnered sexual activity for a period
sexual activity for a period of at least 6 months causing of at least 6 months causing significant distress to the
significant distress to the patient patient
¢ The sexual dysfunction is not better accounted for by a ¢ The sexual dysfunction is not better accounted for by a
non-sexual mental disorder or as a consequence of rela- non-sexual mental disorder or as a consequence of
tionship or other significant stressors and is not attribut- relationship or other significant stressors and is not
able to the effects of amedication/substance or other attributable to the effects of amedication/substance
medical condition or other medical condition
factors such as age, culture, duration and severity of Delayed ejaculation This is a persistent or recurrent
symptoms (DSM-5, p.431). Women exhibit significant delay in, or absence of, ejaculation following a normal
differences in the type and intensity of stimulation that sexual excitement phase that causes the individual
triggers orgasm, and as many as 10 per cent of adult marked distress and interpersonal difficulty (DSM-5
women may never have experienced an orgasm Summary Table 11.5). Delayed ejaculation is the least
(Anderson, 1983). In addition, whether a woman achieves common of the male sex-
orgasm or not may be a significant factor in her partner's ual complaints and less delayed ejaculation Persistent or recur-
rent delay in ejaculation following a norm
attitude to sex. Female orgasmic disorder is one of the than 1 per cent of men will sexual excitement phase.
female orgasmic disorder Marked most frequent female sex- complain of problems in
absence, delay or infrequency of orgasm ual disorders referred for reaching ejaculation over a period of 6 months or longer
and markedly reduced intensity of orgas- treatment, and it is experi- (DSM-5, p.425). The clinician must make judgements
mic sensations.
enced by around one in about whether ejaculation is problematically delayed by
four women at some point in their lives, and more sig- taking into account the client’s age and the degree of
nificantly in the postmenopausal period (Heiman, 2002), sexual stimulation. The problems can be caused by phys-
but women who are assertive and who experienced mas- ical factors such as low testosterone levels (Stahl, 2001),
turbatory orgasm prior to becoming sexually active are alcohol consumption, and prescription drugs such as
significantly less likely to be diagnosed with female antidepressants and anxiolytic drugs, all of which can
orgasmic disorder (Hite, 1976). Early sexual experiences affect the response of the sympathetic nervous system
may be important in determining whether a woman (Segraves, 1995; Altman, 2001).
develops female orgasmic disorder. For example, positive
early sexual encounters fostering emotional involvement Early ejaculation This is the persistent or recurrent
are directly related to the probability of reaching orgasm onset of orgasm and ejaculation with minimal sexual stim-
in later sexual encounters (Heiman, Gladue, Roberts & ulation, within 1 minute of penetration, and before the
LoPiccolo, 1986). In contrast, an upbringing that implies person wishes it to happen (DSM-5 Summary Table 11.6).
the woman should deny her sexuality is more likely to Early or premature ejaculation is not unusual when aspects
lead to orgasmic dysfunction, as are the experiences of of the sexual activity are novel (e.g. the person is indulging
being punished for childhood masturbation and receiv- in novel sex acts, with new partners, or has sex only rarely),
ing little or no advice or information about menstruation and this must be taken into account by the clinician when
(LoPiccolo, 1997). making a diagnosis. Most young males learn to delay
; CHAPTER 11 SEXUAL AND GENDER PROBLEMS 87
DSM-5 SUMMARY TABLE 11.6 Criteria for premature (early) DSM-5 SUMMARY TABLE 11.7 Criteria for genito-pelvic pain/
ejaculation penetration disorder
° Continual or recurring pattern of ejaculation occurring in v Persistent or recurring difficulties with at least one of the
least 75 per cent of partnered sexual activity with approxi- following over a period of at least 6 months:
mately one minute of vaginal penetration and before the
e Sexual vaginal penetration
patient desires it for a period of at least six months causing
significant distress to the patient ° Vulvovaginal or pelvic pain during vaginal penetration
e The sexual dysfunction is not better accounted for by a ° Distress about vulvovaginal or pelvic pain during or in
non-sexual mental disorder or as a consequence of rela- anticipation of vaginal penetration
tionship or other significant stressors and is not attribut-
e Tensing or tightening of the pelvic floor muscles during
able to the effects of a medication/substance or other
vaginal penetration
medical condition
e The sexual dysfunction is not better accounted for by
a non-sexual mental disorder or as a consequence of
orgasm with continued sexual experience and age, but relationship or other significant stressors and is not
some continue to have premature ejaculation problems attributable to the effects of amedication/substance or
and so may seek treatment for the disorder, but these are other medical condition
typically men under the age of 30 years (Bancroft, 1989). In
men between the ages of 18-70 years, 20-30 per cent
express concern about premature ejaculation, but in
practice only around 1 per cent of men would meet the stress. Often the causes of genito-pelvic pain/penetration
new DSM-5 diagnostic criteria for early ejaculation sexual pain are physical, disorder Refers to four commonly occur-
(DSM-5, p.444). Early ejaculation has been linked to infre- and may relate to gyn- ring symptoms, namely difficulty having
intercourse, genito-pelvic pain, fear of pain
quent climactic sex (Spiess, eacological or urological or vaginal penetration, and tension of the
y ejaculation The onset of orgasm
‘minimal sexual stimulation. Treatment Geer & O’Donohue, 1984), problems in women, or to pelvic floor muscles.
nis disorder is typically sought by men over-responsiveness to tac- allergic reactions to sub-
=r the age of 30 years.
tile stimulation (Rowland, stances in contraceptive creams, condoms or diaphragms
(see e.g. Brown & Ceniceros, 2001). Because this is a new
Cooper & Slob, 1996), anxiety caused by hurried sexual
experiences in early adulthood (Dunn, Croft & Hackett, disorder, prevalence rates are unknown, but up to 15 per
1999), and, in some cases, with physical or biological
cent of women in North America report recurrent pain
causes (Metz, Pryor, Nesvacil, Abuzzhab & Koznar, 1997).
during intercourse (DSM-5, p.438).
Sexual pain disorders Pain can become a common Summary of specific sexual
experience that is associated with sexual activity. It can dysfunction disorders
occur prior to, during or after sexual intercourse, and sig- The specific disorders that we have discussed can be asso-
nificantly affect the feeling of well-being that is an impor- ciated with individual stages of the sexual cycle. However,
tant feature of the resolution stage of the sexual cycle. In there is clearly a good deal of overlap between these differ-
DSM-5, pain during sexual activity has been included in ent disorders, and a disorder in one particular stage of the
a single new diagnostic category called genito-pelvic pain/ sexual cycle may well affect performance in other stages
penetration disorder. (e.g. disorders of arousal and orgasm may subsequently
affect sexual urges and desires). Diagnosing a sexual dys-
Genito-pelvic pain/penetration disorder This dis- function is not as simple as referring to a list of criteria
order refers to four commonly co-occurring symptoms, symptoms because the clinician has to make judgements
namely difficulty in having intercourse, genito-pelvic pain, about what is dysfunctional in the light of the client’s
fear of pain or vaginal penetration, and tension of the sexual experience, age, religious views, cultural norms,
pelvic floor muscles (DSM-5 Summary Table 11.7). This ethnicity, and upbringing. The clinician also has to decide
disorder is often associated with other sexual dysfunc- whether the sexual problems that are referred are caused
tion disorders such as reduced sexual desire and interest, primarily by physical or medical conditions, and, if so,
and pain is often associated with behavioural avoidance whether the client might be better referred for medical
and an unwillingness to attend gynaecological examina- treatment, perhaps by a pain specialist or a gynaecologist.
tions despite medical advice. Factors that are relevant to Finally, it is important to remember that many people
aetiology in the case of genito-pelvic pain/penetration may not be particularly satisfied with their own sexual
disorder include partner’s sexual problems, relationship performance or that of their partner, but manage to live
problems, individual vulnerability factors (such as poor their daily lives quite happily. For example, older women
body image, history of sexual or emotional abuse), and are less likely to be distressed by low sexual desire than
younger women (Derogatis & Burnett, 2008) (see Focus and symptoms of sexual dysfunction (Najman, Dunne,
Point 11.1), and it is relatively common for many people Purdie, Boyle & Coxeter, 2005). Sexual trauma and child-
to have sexual symptoms for a month without this causing hood sexual abuse has been found to be a significant risk
undue distress. As a consequence, DSM-5 has specifically factor in specific disorders such as female sexual interest/
introduced some minimum arousal disorder (Stuart & Greer, 1984) and sexual pain
To complete Activity 11.1 go to durations for symptoms disorders (Binik, Bergeron & Khalife, 2000; Westheimer &
www.wiley-psychopathology.com/ before a diagnosis can be Lopater, 2002). Finally, sexual dysfunction is more preva-
activities/ch11
made, and a sexual dys- lent in women than in men (43 per cent and 31 per cent
function is diagnosed only respectively) and is more likely among those experiencing
when the condition is persistent, causes the client con- poor physical and emotional health generally (Laumann,
siderable distress, and causes significant interpersonal Paik & Rosen, 1999). However, we must remember that
difficulty. this gender difference may be due at least in part to men
being more embarrassed by sexual dysfunction than
women, and so reporting disorders significantly less. For
11.2.2 The Aetiology example, a study of male erectile disorder found that
two out of three men suffering erectile dysfunction were
of Sexual Dysfunctions embarrassed when discussing this problem with a doc-
In describing the various sexual disorders in the previous tor, and only 25 per cent subsequently sought medical
section we have hinted in some cases about factors that advice (Droupy, 2005).
might cause these specific disorders to develop. This sec-
tion will provide a more thorough review of the aetio- Theories of the aetiology
logy of sexual dysfunction by looking first at the kinds of of sexual dysfunction
risk factors that are associated with the development
of specific disorders, and then looking in more detail at Psychoanalytic theory Much of the psychoanalytic
theories that attempt to explain in more general terms approach to understanding behaviour revolves around
how people might acquire sexual dysfunctions. repressed emotions and desires, and_ specifically
around repressed sexual desires, so it is not unusual that psy-
Risk factors for sexual dysfunctions chodynamic theorists have had something to say about the
Risk factors for individual sexual dysfunctions will usually factors underlying sexual dysfunction. Thus, vaginismus
be to some extent gender related, because many of the may be seen as a women
disorders apply only to a specific gender. So, for example, expressing hostility towards vaginismus The involuntary contraction
of the muscles surrounding the vagina
experiencing the menopause is an important risk factor men; premature ejaculation when vaginal penetration is attempted
for female sexual interest/arousal disorder, and surgi- as men expressing repressed all women who seek treatment for sexual
cally menopausal women (who have undergone hyster- hostility towards women; dysfunctions, around 15-17 per cent are
ectomy) are at significantly greater risk (Dennerstein, and female orgasmic disor- suffering from vaginismus. _
Koochaki, Barton & Graziottin, 2006). For specific male der as a function of enduring penis envy. Because sexual
dysfunctions such as erectile disorder, risk factors include activity is usually pleasurable — yet often frowned upon by
ageing, a diagnosis of depression, cigarette smoking, and society — many psychodynamic views see sexual dysfunc-
medical conditions such as diabetes, cardiovascular tion as resulting from this conflicting state of affairs. Still
and urogential disease (Korenman, 2004; Droupy, 2005). others view male sexual dysfunctions, such as male erectile
For early ejaculation, risk factors include being young, havy- disorder, as a result of an unresolved Oedipus complex
ing experienced divorce, and being more educated (Fasolo, based on a continual sexual attachment of the male to his
Mirone, Gentile, Parazzini & Ricci, 2005). Educational mother (Fenichel, 1945). Regardless of the theoretical valid-
level in men has a complex relationship to sexual dys- ity of these analyses, these views gave psychoanalysis an
function: men who are more educated are more likely to important therapeutic function prior to the development of
report early ejaculation than less educated men (Fasolo, therapies based on more objective and more detailed know!-
Mirone, Gentile, Parazzini & Ricci, 2005), but less edu- edge of sexual dysfunctions such as those pioneered by
cated men are more likely to report erectile disorder than Masters and Johnson in the 1970s.
better educated men (Lyngdorf & Hemmingsen, 2004).
Childhood sexual abuse is also a significant risk factor for The Two-Factor Model of Masters and Johnson
sexual dysfunction in later life. In a large-scale Australian Masters and Johnson were the first researchers to collect
study, more than one in three women and one in six men detailed information about sexual dysfunctions, and to
reported a history of childhood sexual abuse, and there develop a model of sexual dysfunction based on this
was a significant association between childhood abuse empirical evidence. Their model had two important
CHAPTER 11 SEXUAL AND GENDER PROBLEMS 373
components, both of which contributed to sexual dys- sexual and interpersonal problems, and that the latter
function. The first component consisted of a learnt or may be an important cause of the former (e.g. Rosen &
conditioned factor where adverse early sexual experi- Leiblum, 1995). For example, there is an inverse relation-
ences had given rise to a learnt fear or anxiety response ship between a woman’s sexual desire and their level of
whenever the individual was engaged in sexual activity. concern about their partner’s affection (Nobre & Pinto-
Adverse experiences include (1) psychosexual trauma, Gouveia, 2006), and individuals who are angry with their
such as rape or childhood sexual abuse, (2) religious and partners are less likely to desire sexual activity (Beck &
social taboos that give rise to feelings of shame and guilt Bozman, 1995). If negative emotion is a central feature
about sex, (3) embarrassing or belittling early experi- of a couple’s relationship, then emotions such as resent-
ences with sex (e.g. appearing unknowledgeable or inex- ment, disgust, anxiety, anger, distrust, and depression are
perienced to a sexual partner), or (4) excessive alcohol likely to significantly interfere with the development of
use in men, which can affect the ability to achieve and positive feelings required in the desire and arousal stages
maintain erection. Once these factors have begun to gen- of the sexual cycle. If general communication is poor
erate anxiety about sexual performance, the second within a couple, then this is likely to have an important
component of this model is the spectator role that indi- impact on talk about intimate activities such as sex.
viduals adopt in response to their fears and anxieties. Studies have indicated that interpersonal difficulties are
Instead of taking a relaxed attitude to sex, the fearful apparent in sexual dysfunctions diagnosed in both men
individual constantly monitors their own sexual perfor- and women, and are associated with early ejaculation and
mance and the responses of their partner. Their focus of erectile disorders in men (Patrick, Althof, Pryor, Rosen et
attention is therefore directed away from the stimuli that al., 2005; Swindle, Cameron, Lockhart & Rosen, 2004)
provide sexual arousal and sexual pleasure, and on to fac- and sexual dysfunctions generally in women (Clayton,
tors that provide feedback about how well the individual 2003). Men are also significantly more likely to seek
is performing. There are some important similarities help for their sexual dysfunction if it is associated with
between this theory of sexual dysfunction and self- interpersonal difficulties (Papaharitou, Athanasiadis,
focused attention accounts of social anxiety disorder (see Nakopoulou, Kirana et al., 2006). However, we must
Chapter 6) where self-focused attention prevents objec- still be cautious about how to interpret these findings
tive processing of the social situation, which leads the because they only indicate that there is an association
social phobic to engage in critical self-evaluation and between sexual dysfunction and interpersonal difficul-
may well adversely affect their actual performance in the ties and we do not know the direction of any causal
social situation. Because of these similarities, many of relationship.
the processes involved in self-focused attention may also Apart from general difficulties that may have arisen
apply to sexual dysfunction. Although Masters and in a relationship, sexual dysfunction may result from
Johnson’s theory was the first attempt to develop an specific deficiencies in sexual knowledge or sexual
empirical model of sexual dysfunction based on objec- expertise in one or both of the couple. For example,
tively collected data about sexual performance, we must women who suffer female orgasmic disorder often
still be cautious about how the two components of their have partners who are awkward or inexperienced lov-
model interact. For example, while it is clear that many ers (LoPiccolo, 1997; Kaplan, 1974), and individuals
people suffering sexual dysfunction experience perfor- who develop sexual dysfunctions often lack the knowl-
mance anxiety, it is still not clear whether this anxiety is edge and skills required to fully stimulate their part-
a cause or a consequence of ner or satisfy themselves (LoPiccolo & Hogan, 1979).
lormance anxiety The fear of failing
the dysfunction. We have Sexual problems can also develop if one member of
chieve an acceptable level of sexual
ormance, causing an individual to already noted that many a couple is overly anxious about pleasing the other,
yme distanced from the sexual act and specific sexual disorders giving rise to performance anxiety that may inhibit
o become aroused. can be caused by physical sexual feelings and responsiveness to sexual stimuli
or medical conditions, and it may be that anxiety about (Kaplan, 1974).
sexual performance is a consequence of sexual perfor- Finally, untangling the role that interpersonal difficul-
mance being impaired by these conditions rather than a ties may play in causing sexual dysfunction is problem-
cause of the condition per se. atic. This is because interpersonal difficulties are very
often a central outcome of sexual dysfunction anyway.
Sexual dysfunction and interpersonal problems However, therapies for sexual dysfunction that focus
Sex is usually an interpersonal activity, and it may be on the relationship between couples are often success-
that interpersonal problems may be a cause of at least ful, and this suggests that at least some of the causes of
some of the sexual dysfunctions. Many clinicians believe some sexual dysfunctions lie in the details of individual
that individuals with sexual dysfunctions have both relationships.
raya Ss PSYCHOPATHOLOGY
The role of negative emotion and _ psycho- Remote vs. immediate causes One view of the
pathology Satisfying sexual experiences are usually causes of sexual dysfunction is that chronic sexual dys-
dependent on the individual being open to positive pleas- function is caused by a combination of immediate causes
urable emotions and being attentive to those stimuli and remote causes (Kaplan, 1974). Immediate causes are
during sexual activity. Because of this, chronic negative factors that may directly influence sexual performance,
emotions such as depression or anxiety are likely to inter- such as performance anxiety, communication problems
fere significantly with sexual performance, and depression between partners, lack of sexual knowledge, clumsy tech-
and anxiety are significant risk factors for sexual dysfunc- nique. However, many of these are factors that may influ-
tion (Hayes, Dennerstein, Bennett & Fairley, 2008). Studies ence the sexual performance of many people at one time
suggest that 62 per cent of those people with depression or another, and are not necessarily chronic features of a
are also likely to have a sexual dysfunction, compared with person’s lovemaking. However, these immediate perfor-
only 26 per cent of people without depression (Angst, mance problems may arise because of longer term remote
1998), and depression appears to have a bidirectional rela- causes of sexual dysfunction, and these refer to more
tionship with sexual dysfunction — both causing sexual deep-rooted psychological and psychodynamic factors
dysfunction and being a significant outcome of sexual dys- that incline someone to be anxious about their sexual per-
function (Atlantis & Sullivan, 2012). In women, depressive formance. Remote causes include feelings of shame and
symptoms have been shown to be associated with deficits in guilt about sexual activity ‘remote causes Include feelings of shame
sexual desire, sexual fantasy, (which may vary with cul- and guilt about sexual activity, general
To read Atlantis & Sullivan's article on )} sexual arousal, and orgas- ture; see e.g. Woo, Brotto & feelings of inadequacy, feelingsof confli
the association between depression and
mic function (Cyranowski, Gorzalka, 2011), and general brought
: about by long-term life a
sexual dysfunction go to
www.wiley-psychopathology.com/ Frank, Cherry, Houck & feelings of inadequacy and suchlike. : os
reading/ch11 Kupfer, 2004), and men feelings of conflict brought about by long-term life stress
with depression are almost (Kaplan, 1979). In particular, while men may worry dur-
twice as likely to experience erectile dysfunction as non- ing sex about their performance, women worry about
depressed men, and the degree of erectile dysfunction their attractiveness, and may experience intrusive thoughts
increases with increasing degree of depression (Araujo, about their weight (Pujols, Seal & Meston, 2010).
Durante, Feldman, Goldstein & McKinlay, 1998).
Anxiety is another negative emotion that can poten- Biologicalcauses There is considerable debate about
tially have a significant effect on sexual functioning. We whether sexual dysfunctions are the result of psychologi-
have already discussed the role that performance anxiety cal or organic (biological) causes. In the period following
may play in causing sexual dysfunction, and anxiety dis- the pioneering work of Masters and Johnson, research-
orders themselves are associated with sexual dysfunction. ers began to focus on the importance of psychological
These include panic disorder, social anxiety disorder, spe- factors in the aetiology of sexual dysfunction. However,
cific phobia and obsessive compulsive disorder (Figueira, nowadays, there is a belief that organic or biological fac-
Possidente, Marques & Hayes, 2001), and, for example, tors may be an underlying factor in many cases, and that
anxiety disorders can be diagnosed in almost 20 per cent these may combine with psychological factors to gener-
of men suffering from erectile disorder (Mallis, Moysidis, ate a chronic disorder.
Nakopoulou, Papaharitou et al., 2005). High levels of anxi- Biological causes can be classified into three broad
ety may lead to sexual dysfunction simply because it is a categories: (1) dysfunction caused by an underlying
negative emotion that may inhibit the development of medical condition, (2) dysfunction caused by hormonal
pleasurable emotions associated with sexual pleasure. It abnormalities, and (3) changes in sexual responsiveness
may also prevent allocation of attention to stimuli likely caused by ageing.
to provide sexual stimulation and pleasure. Specific anxi- A whole range of medical conditions can give rise to
ety disorders may influence sexual performance in quite sexual desire and performance problems. For example,
specific ways. For example, panic disorder is associated male erectile and orgasmic disorders are associated with
with a fear of bodily sensations, and so the increases in high blood pressure, diabetes, heart disease, cigarette
heart rate and perspiration caused by sexual activity may smoking, and alcoholism. Dysfunctions are also associ-
be interpreted negatively by someone with panic disorder ated with a variety of medications such as antidepressants
(Sbrocco, Weisberg, Barlow & Cater, 1997). Similarly, fear and anxiolytic drugs, and with treatments for hyperten-
of contamination associated with some forms of OCD sion and renal problems (Berman, Berman, Werbin,
may make the individual fearful of bodily contact and sex- Flaherty et al., 1999; Altman, 2001). Medical conditions
ual secretions. Finally, social anxiety disorder is known to that reduce blood flow to the penis (such as blocked arter-
be associated with a self-critical attitude, which may well ies or heart disease) will influence the ability to reach and
give rise to performance anxiety during sexual activity. maintain an erection (Stahl, 2001), and other medical
conditions may cause central nervous system damage that age. For example, reports of erectile problems in men
affects sexual performance and desire, and these include increase significantly after 50 years of age (Laumann,
diabetes, multiple sclerosis, and renal problems (Frohman, Gagnon, Michael & Michael, 1994), and a study of
2002). Female arousal and orgasm is also affected by medi- Australian men over the age of 40 years indicated that
cal conditions in much the same way that these conditions 34 per cent of those men surveyed reported one repro-
influence erection and ejaculation in men. Female arousal ductive health disorder or more, including erectile
and orgasmic disorder has been linked to multiple sclero- dysfunction (21 per cent), lower urinary tract symptoms
sis and diabetes, and both antidepressant (e.g. SSRIs such (16 per cent) and prostrate disease (14 per cent) (Holden,
as Prozac) and anxiolytic medications can affect sexual McLachlan, Pitts, Cumming et al., 2005). Such findings
desire in women in much the same way that they do in may indicate that levels of male hormones generally
men (Hensley & Nurnberg, 2002). Similarly, sexual pain decrease with age, or that reproductive health disorders
disorders may have an organic or medical origin, and these may significantly affect sexual functioning. Sexual desire
may range from painful allergic reactions to contraceptive and performance also decreases with increased age in
creams, condoms or diaphragms (e.g. in the case of female women, and the menopause has a significant influence
dyspareunia) to gynaecological diseases and infections here. Menopause is associated with decreases in oestro-
yareunia A genital pain that can occur of the vagina, bladder or
gen and testosterone levels that can exacerbate female
1g, before or after sexual intercourse. Uterus (which may cause sexual dysfunction (Graziottin & Leiblum, 2005). Studies
e clinicians believe this isa pain disor- symptoms of vaginismus) suggest that around one in four women report a loss of
ather than a sexual dysfunction. (Brown & Ceniceros, 2001; sexual desire after the menopause, and this is associated
McCormick, 1999). Nevertheless, although these forms of with fluctuations in levels of oestrogen and testosterone.
organic disorder may be an underlying cause of sexual However, menopause is associated not only with physical
desire and performance problems, it is quite likely that changes but also with psychological changes, and loss of
they will often generate associated psychological prob- sexual desire in postmenopausal women has been shown
lems that give rise to a diagnosable sexual dysfunction. For to be associated with physical factors such as lower hor-
example, sexual pain or disability caused by disease or monal levels and vaginal dryness and psychological fac-
medical conditions can give rise to anxiety about sexual tors such as depression and living with children (Gracia,
performance or to relationship difficulties. Sammel, Freeman, Liu et al., 2004).
Sexual desire and subsequent arousal and orgasm are One final biological factor that has been researched
dependent on levels of the sex hormones testosterone, in the aetiology of sexual dysfunctions is genetics, and
oestrogen and prolactin, recent epidemiology and candidate gene studies have
osterone A steroid hormone stimulat-
evelopment
of male secondary sexual and imbalances in these suggested a strong genetic influence on female sexual
acteristics. hormones can cause sex- functioning, with the hope that successful identification
ual desire problems in of biomarkers and novel
rogen Any of agroup of steroidhor- both men and women. In genes underlying female To read Burri, Cherkas
& Spector's
es which promote the development women, either high Glow sexual dysfunction will article on the genetics and epidemiology —
maintenance of female characteristics help to improve diagno- of female sexual dysfunction go to
E body. levels of oestrogen can i www.wiley-psychopathology.com/
cause sexual desire prob- sis and treatment (Burri, reading/ch11
actin A hormone from the pituitary | lems, and oestrogen levels Cherkas & Spector, 2009).
d stimulating milk production after can be affected if a woman
pith: is taking the birth control Sociocultural causes The level of sexual dysfunc-
pill, which will artificially raise her oestrogen levels, or is tion within a society can change depending on a range
being given anti-oestrogen therapy for breast cancer that of cultural and economic factors within that society. For
will lower oestrogen levels (Amsterdam, Wheler, Hudis & example, the stress caused by poverty, financial prob-
Krychman, 2005). High prolactin levels have the effect of lems or unemployment have all been linked to erectile
suppressing the hormones responsible for the normal dysfunctions in men (Morokoff & Gillilland, 1993) and
functioning of the ovaries and testes, and high prolactin this effect has been identified during the recent eco-
levels can therefore lead to menstrual irregularity and/or nomic downturn in European countries (Christensen,
fertility problems. In men, erectile dysfunction is associ- Gronbaek, Osler, Pedersen et al., 2011). Many cultures
ated with high levels of prolactin, and erectile problems also specify implicit rules about sexual behaviour, and in
can be eased with the use of drugs that lower prolactin many cases these rules can cause conflict and sexual dys-
levels (Spollen, Wooten, Cargile & Bartztokis, 2004). function. For example, the religious and cultural views
Finally, one of the important variables that affect of many societies require that women should repress
sexual functioning is age, and the prevalence of sexual or deny their sexuality, and so any expression of sexual
dysfunction in both males and females increases with desire or indulgence in sexual activity is likely to cause
376 PSYCHOPATHOLOGY
‘ , %
personal conflict and feelings of shame and guilt. This as these developments in psychological treatment, there
view is supported by the fact that many women who have been significant advances in biological treatments for
have received a strict religious upbringing are more likely sexual dysfunctions. Treatments available today include
to suffer from arousal and orgasmic dysfunction, and drug and hormone treatments for problems of desire,
may have been punished for any sexual activity during arousal and orgasm, and mechanical devices for aiding
childhood and adolescence (Masters & Johnson, 1970). penile erection in men. In the following sections we will
cover some of these treatments in more detail, begin-
Summary We can see from this subsection that the- ning in Treatment in Practice Box 11.1 with an overview
ories of sexual dysfunction are quite wide ranging and of the general structure of sex therapy. The following
encompass both psychological and biological explana- sections then cover a range of psychological and behav-
tions. There is no doubt that many cases of sexual dys- ioural therapies in more detail, followed by a description
function have an organic or biological basis, and these and evaluation of biologically based treatments.
can range from dysfunctions caused by medical condi-
tions, hormone imbalances, and changes in biology with Psychological and behavioural treatments
age. However, since the pioneering work of Masters and
Johnson, psychological factors have also been identified Direct treatment of symptoms Direct treatments
in the aetiology of sexual dysfunction, and these include are techniques targeting the specific sexual performance
performance anxiety, underlying interpersonal prob- deficit. For example, there are two specific techniques
lems, existing psychopathology such as depression and used to help clients with early ejaculation. These are the
anxiety, and a variety of life experiences, such as child- stop-start technique and the squeeze technique. In
hood abuse, psychosexual trauma and exposure to reli- the former, the client’s partner stimulates the penis until
gious and social taboos. close to ejaculation, at which
point the partner is sig- stop-start technique A technique used
to help clients with premature ejaculatio
nalled to stop by the client where the client's partner stimulates the
11.2.3 The Treatment (Semans, 1956). This pro- penis until close to ejaculation, at which 4
cess continues once the point the partner is signalledto stop bya
of Sexual Dysfunctions desire to ejaculate subsides. the client. .
Over the past 60-70 years the treatment of sexual dys- This acts to increase the
functions has developed through a number of distinct amount of — stimulation squeeze technique A technique used to
stages. Prior to the 1950s, psychodynamic therapy was required to achieve ejacula- help clients with premature ejaculation —
where the client's partner firmly squeeze
probably the only structured form of treatment avail- tion. The ‘squeeze’ tech- below the head of the penis just prior to
able to those courageous enough in the existing social nique is very similar, where ejaculation.
climate to admit sexual problems. With its emphasis on the client’s partner will
underlying conflicts and tensions tied to repressed sexual firmly squeeze below the head of the penis just prior to
desires, psychoanalytic theory seemed ideally suited to ejaculation. This has the effect of reducing the erection,
treat sexual dysfunctions. However, the liberating social and can be repeated several times in order to help the cli-
climate of the 1960s and 1970s allowed freer discussion of ent control ejaculation (St Lawrence & Madakasira, 1992).
sexual problems, and with this came the pioneering early The ‘squeeze’ technique has been shown to significantly
work of Masters and Johnson published in their book increase ejaculation latency, and is comparable to the ther-
Human Sexual Inadequacy (1970). This led to the devel- apeutic effects of a number of drugs used to treat prema-
opment of what are now known as direct treatments for ture ejaculation (Abdel-Hamid, El Nagger & El Gilany,
sexual dysfunction. These are often behaviourally based 2001). A direct treatment method designed to deal with
treatments for the specific symptoms of the disorder. So, symptoms of erectile disorder or male and female orgas-
rather than consider erectile dysfunction to be a mani- mic disorder is the tease technique. This involves the part-
festation of underlying psychological problems, thera- ner caressing the client’s
genitals bit stopping siahiet tease technique A direct treatment
pists would provide the client with specific training on
method designed to deal with symptoms
how to achieve and maintain an erection (e.g. the ‘tease’ the client becomes aroused of erectile dysfunction or male and femal
technique). Most modern-day treatment programmes (e.g. achieves an erection) orgasmic disorder. It involves the ae
now include some components designed to directly or approaches orgasm. This caressing the client’s genitals, but stop-
ping when the client becomes aroused —
address the main symptom of the disorder (such as lack enables couples to experi-
(e.g. achieves an erection) or approaches
of desire, erectile problems, or premature ejaculation) as ence sexual pleasure with- orgasm.
well as components designed to deal with accompany- out the need to achieve
ing psychological problems (such as performance anxi- orgasm, and as a result may reduce any performance
ety, related depression, or relationship problems). As well anxiety that may have been contributing to erectile
CHAPTER 11 SEXUAL AND GENDER PROBLEMS 377"
CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE BOX 11.1

WHAT IS SEX THERAPY?
Current forms of sex therapy involve a number of com- CHANGING DYSFUNCTIONAL BELIEFS
ponents, and these different components are designed to
identify specific sexual problems, to address these specific Sex is associated with a whole range of myths and false
problems with direct treatment, to deal with associated beliefs (e.g. ‘too much masturbation is bad for you; ‘nice
psychological and relationship issues, and to provide cli- women aren't aroused by erotic books or films’ and so on)
ents with sexual knowledge and sexual skills. Sex therapy (Bach, Wincze & Barlow, 2001), and if a client holds these
usually treats the couple rather than the individual who false beliefs they may be preventing full sexual arousal
manifests the dysfunction, and couples are urged to share and satisfaction. Using a range of methods, such as those
the responsibility for the sexual problem. Below are some used in CBT (see section 4.1.1), the therapist will attempt
of these separate components which form the important to identify any dysfunctional beliefs, challenge them, and
core stages of sex therapy. replace them with more functional beliefs.
ASSESSMENT DIRECT INTERVENTION AND

BEHAVIOURAL TRAINING
Through interview, the therapist will collect information
about specific sexual problems (e.g. lack of desire by one Depending on the specific sexual dysfunction that has
been referred for treatment, the therapist will advise the
partner, or erectile problems in a male partner), and dis-
cuss current life issues and past life events that may be clients on the use of a range of behavioural techniques
designed to help their specific problem. These techniques
contributing to the problem. This stage will usually
are discussed more fully in section 11.2.3, but include the
be accompanied by a medical examination to determine
‘tease technique’ for erectile dysfunction, ‘stop-start tech-
whether there are organic factors contributing to the
nique’ and ‘squeeze technique’ for premature ejaculation
problems.
(Semans, 1956; LoPiccolo, 1997), and directed masturba-
tion training for arousal and orgasmic disorders (Heiman,
DEALING WITH ORGANIC DYSFUNCTION 2002). Therapists may also teach clients a technique
known as non-demand pleasuring, which involves a cou-
If there are clearly organic or medical factors contrib- ple exploring and caressing each other's body to discover
uting to the dysfunction (such as low hormone levels, sexual pleasure rather than achieving orgasm. This allows
medical conditions such as diabetes or high blood pres- couples to learn how to give and receive sexual pleasure
sure, or other medications, such as antidepressants or without the pressure of needing to achieve orgasm.
anxiolytics), then these may be addressed early in the
programme (e.g. by reducing levels of antidepressant DEALING WITH RELATIONSHIP AND
drugs). LIFESTYLE ISSUES
SEXUAL SKILLS TRAINING Sexual dysfunction is often related to conflict within the
relationship and to stressful lifestyles (e.g. one partner
Many types of sexual problem arise through lack of may be dominating and controlling or the demands of
knowledge about the physiology of sex and a lack of basic factors such as family and work may be causing unneces-
technique during lovemaking. The therapist can address sary stress). The therapist will usually attempt to identify
these factors by providing the clients with educational any factors that may be contributing to the disorder and
materials such as booklets and videos. advise clients on how to improve these.
problems or arousal and orgasmic problems (LoPiccolo, and — in some cases — erotic materials, a woman can be
1997). For individuals with arousal or orgasmic taught step-by-step to achieve orgasm — even in cases
problems, directed mas- where she has never previously experienced an orgasm.
pec masturbation training A turbation training is often This method has been shown to be highly effective, and
Bako tacgcantiona a helpful (Heiman, 2002). over 90 per cent of women treated with this method learn
rial, videos, diagrams and - in some With the use of educational how to achieve orgasm during masturbation (Heiman &
— erotic materials. material, videos, diagrams, LoPiccolo, 1988).
378 PSYCHOPATHOLOGY
.
Couples therapy As we have mentioned several These experiences may simply be embarrassing ones,
times in this chapter, sexual dysfunction may be closely where the individual has been severely embarrassed by
associated with relationship problems. If sexual dysfunc- their lack of sexual knowledge or prowess during an early
tions are a manifestation of broader problems within a sexual encounter. Or they may be more severe and trau-
relationship, then the latter need to be effectively matic experiences, such as sexual abuse or assault (see
addressed. For example, a lack of sexual desire in one section 11.2.2). Appropriate counselling, where the client
partner may be a way that the partner can exert some is encouraged to recall these experiences and talk about
control within the relationship — especially if there are them can help to alleviate the associated sexual prob-
conflicts over power and control. In such cases, underly- lems. This approach acts in a similar way to exposure and
ing sexual dysfunction may entail some implicit reward imaginal flooding therapies for PTSD (see Chapter 6) by
for both partners, one partner gaining reward from their extinguishing the fear that had become associated with
ability to control sex, and the other gaining reward by these memories.
viewing their partner's lack of desire as a weakness,
which enables them to see themselves as controlling. Summary of psychological interventions for
During couples therapy, a therapist will explore these sexual dysfunction ‘There are very few compara-
issues with a couple and try to identify if there are any tive studies of the relative effectiveness of psychologi-
implicit payoffs within the cal therapies for sexual dysfunction. However, a recent
couples therapy A treatment intervention
for sexual dysfunction that involves both relationship for maintain- meta-analysis suggests that psychological-based treat-
partners in the relationship. ing the sexual dysfunction. ments (e.g. sexual skills training, CBT, couples therapy)
are effective options for sexual dysfunction — with out-
Sexual skills and communication training For comes being particularly good for female sexual interest/
many couples, sexual dysfunction is simply another arousal disorder and female orgasmic disorder (Fruhauf,
manifestation of the couple’s inability to communicate Gerger, Schmidt, Munder & Barth, 2013).
effectively with one another. They may be unable to tell
each other what stimulates and pleasures them, or they Biological treatments
may be nervous, shy or unknowledgeable about sexual Many cases of sexual dysfunction may have biological
matters. Such people can be helped using sexual skills or organic causes such as medical conditions, hormone
and communication training. With the use of edu- imbalances, changes in biology with age, or are a reac-
cational materials and videos, a therapist can help clients tion to other medications being taken by the client. This
to acquire a more knowledgeable perspective on sexual indicates that a biological or medical treatment may be
sexual skills and communication activity, begin to communi- appropriate for the disorder. Biological treatments fall
training A treatment method in which a cate to each other effec- into three broad categories: (1) drug treatments, includ-
therapist can help clients to acquire a more tively about sex, and reduce ing medications that directly influence the organic nature
knowledgeable perspective on sexual
any anxiety about ind- of the disorder, (2) hormone treatments designed to cor-
activity, communicate to partners effec-
tively about sex, and reduce any anxiety ulging in sexual activity rect any hormonal imbalances caused by age or illness,
about indulging in sexual activity. (McMullen & Rosen, 1979). and (3) mechanical devices, designed to aid mechanical
functioning during sex (such as achieving erection).
Self-instructional training This is a technique that has
been used across a range of psychopathologies in order to Drug treatments Perhaps the most well-known drug
establish adaptive behaviour patterns. In the context of sex- treatments for sexual dysfunction are Viagra (sildenafil
ual dysfunctions, self-instructional training is used to citrate) and Cialis (tadafil), both phosphodiesterase
teach the client to use positive self-instructions at various type 5 (PDE-5) inhibitors,
Viagra (sildenafil citrate) A drug treat-
points during sexual activity which are used primarily
self-instructional training A procedure ment for sexual dysfunction which is usec
used in the intervention for executive in order to guide their to treat erectile dysfunc- primarily to treat erectile dysfunction in
functioning deficits where individuals learn behaviour and to reduce tion in men. Viagra acts men.
a set of instructions for talking themselves anxiety. In particular, nega- directly on the tissue of
through particular problems.
tive statements (such as ‘T the penis itself. It causes Cialis (tadafil) A drug treatment, used p|
marily to treat erectile dysfunction in met
am never going to maintain an erection’) can be replaced relaxation of the smooth
with positive statements (such as ‘I can allow myself to muscle of the penis that increases blood flow and encour-
enjoy sex, even if my performance is not perfect’), and this ages erection. Studies suggest that 75 per cent of men
helps to distract the client from anxiety-provoking ideation. taking Viagra can achieve erection within 60 minutes of
administration (Goldstein, Lue, Padma-Nathan, Rosen
Dealing with remote causes Many cases of sexual et al., 1998), and in clinical trials Viagra results in sig-
dysfunction have their origins in earlier life experiences. nificantly more erections and successful intercourse
attempts than a placebo control (Moore, Edwards & Hormonetreatments Atleast some sexual dysfunc-
McQuay, 2002) (see Figure 11.1). Viagra has also proved tions may result from imbalances in hormone levels,
to be an effective treatment for male erectile disorder, and disorders can result from either high or low levels
with over 95 per cent of client’s treated with Viagra over of oestrogen in women, low levels of testosterone in
a 1-3 year period expressing satisfaction with their erec- men, and high levels of prolactin in men. These hor-
tions and their ability to effectively engage in sex monal imbalances can be caused by medical conditions
(Carson, Burnett, Levine & Nehra, 2002). In addition, or ageing. Hormone replacement therapy can be used
Viagra has been considered to be an effective treatment to treat disorders of sexual desire — especially in older
for male erectile disorder in cases where this is due to a women or women who have undergone hysterectomy —
medical condition (such as diabetes or cardiovascular and sexual pain disorders such as genito-pelvic pain/
disorder) or as a result of ageing (Salonia, Rigatti & penetration disorder can also be helped with oestro-
Montorsi, 2003). However, Viagra may not be the treat- gen treatment, which can improve vaginal lubrica-
ment of choice for many clients because it also has a tion in postmenopausal women (Walling, Andersen &
number of side effects, such as headaches, dizziness and Johnson, 1990).
facial flushing, and may interact badly with some medi-
cations for cardiovascular disease (Bach, Wincze & Mechanical devices Because an erect penis is such
Barlow, 2001). an important contributor to successful sexual penetra-
Other drugs that have proved useful in treating sexual tion, a number of mechanical devices have been devel-
dysfunctions include yohimbine for erectile dysfunc- oped that can help the male with an erectile dysfunction
tions, which facilitates nor- achieve erection.
;
bine A drug treatment for sexual
epinephrine excretion in
ction which is used primarily to treat The first of these is known as a penile prosthesis,
the brain. This appears to
ile dysfunction in men byfacilitating and an example of this device is shown in Figure 11.2.
pinephrine excretion in the brain.
have the effect of correct- Use of these devices is
ing any brain neurotransmitter problems that are causing normally reserved for Penile prosthesis A mechanical device
normally reserved for non-reversible
the erectile dysfunction (Mann, Klingler, Noe, Roschke non-reversible organic-based organic-based
. . ee
erectile problems.
et al., 1996). Interestingly, both Viagra and yohimbine erectile problems. The pro-
have also been shown to be effective in treating female sthesis consists of a fluid pump located in the scrotum
sexual desire problems (Hernandez-Serrano, 2001). and a semi-rigid rod that is surgically inserted in the
Finally, antidepressant SSRIs such as Prozac are also penis. A discrete squeeze of the pump releases fluid into
an effective treatment for early ejaculation, and delayed the rod that causes the penis to erect. Studies suggest
orgasm is a known side-effect of SSRIs in depressed indi- that the penile prosthesis is a safe and effective means of
viduals who are taking these medications (Assalian & dealing with erectile dysfunction caused by organic or
Margolese, 1996). medical conditions, and 7 years after the implant, the
Erections/week |
| Successful/week
Placebo 25mg fixed 50mg fixed 100mg fixed 200mg fixed Dose optimized
Dosing schedule
FIGURE 11.1 Mean number of erections per week (blue) and erections resulting in successful intercourse (red) with placebo and
different doses of Viagra (sildenafil citrate).
Source: Moore, R.A., Edwards, J.E. & McQuay, HJ. (2002). Sildenafil (Viagra) for male erectile dysfunction: A meta-analysis of clinical trial reports.
BMC Urology, 2(6), Figure 4.
380 PSYCHOPATHOLOGY
; %
penile prosthesis was found to be still successfully deal-
ing with erectile dysfunction in 82 per cent of patients
(Zermann, Kutzenburger, Sauerwein, Schubert &
Loeffler, 2006).
An alternative to the penile prosthesis is a vacuum
erection device (VED). This is a hollow cylinder that is
placed over the penis. The .
client then draws air out vacuum erection device (VED) A
mechanical device normally reserved fo
the cylinder using a hand non-reversible organic-based erectile
pump, and this has the problems.
effect of drawing blood
into the penis and causing an erection. As cumbersome
as this may seem, many clients prefer the VED to
other more conventional treatments for erectile dysfunc-
tion such as Viagra. Of those given a choice between
FIGURE 11.2 The penile prosthesis consists of a fluid pump
equally effective VED or Viagra treatments, 33 per cent
located in the scrotum and a semi-rigid rod surgically inserted preferred the VED -— largely because they disliked the
in the penis. Squeezing the pump releases fluid into the rod adverse side-effects of Viagra (Chen, Mabjeesh &
making the penis erect. Greenstein, 2001).
ERECTILE DYSFUNCTION
R.K., 47, a senior corporate executive had been happily married for 20 years and had three children, but com-
plained of declining erections. Over the preceding 6 months, his erections had become so weak that he could not
penetrate. He stopped trying 3 months ago.
He thought that this was due to his highly stressful lifestyle and pressures at the workplace. He even took a
vacation with his wife hoping that this would improve matters. It only made them worse. His wife, at first very
co-operative, eventually began to feel rejected and there was a palpable friction in their marriage.
When first seen at the clinic, R.K. was defensive. ‘How can this happen to someone like me? | could do it all
HISTORY
CASE
11.1 night, several times a night, night after night. My family doctor says that this kind of thing is quite common these
days and it’s probably the stress.
It turned out that R.K. was a diabetic of 8years’ standing. He also had high blood pressure for which he was on
beta blockers. He was obese (175cm in height; weight 96kg) and smoked 40 cigarettes a day. He partied 7 days
a week and drank heavily. He had never exercised in his life. Sadly, his family doctor had never connected any of
these to his sexual problem.
Tests revealed that his overall rigidity levels were well below normal and that he had problems both with his
arteries and his veins. He was eventually cured with an inflatable penile prosthesis.
Source: Adapted from http://www.testosterones.com/.
Clinical Commentary
R.K. was quick to link his erectile problems with a stressful lifestyle, and his defensive reaction is typical of a
man who values his own sexual performance as an indicator of his own worth. However, once R.K’s medi-
cal history was investigated, it became clear that there were various organic and lifestyle factors that were
probably contributing to his erectile dysfunction, including a history ofdiabetes, high blood pressure, medi-
cations that can interfere with sexual arousal, heavy smoking and heavy drinking. Because many of the
important causes were organic (e.g. diabetes and cardiovascular problems), the best long-term solution in
this case was to implant a mechanical device, such as a penile prosthesis, to aid erection.
Summary oftreatments of sexual dysfunction as well as any underlying psychological, behavioural

This section has discussed the range of treatments and relationship issues. These are supplemented by a
available for sexual dysfunctions. Multifaceted psy- variety of drug and biological based treatments that
chological and behavioural based treatments are now _ help to address any physiological, organic or hormonal
used to deal with the specific symptoms of the disorder deficits.
SELF-TEST QUESTIONS
* Can you describe the four stages of the normal sexual response cycle?
11.2.1 Diagnosis of Sexual Dysfunctions

* Can you name the disorders of desire and their main diagnostic characteristics?
° What are the main disorders of sexual arousal and how are they defined?
* Roughly what percentage of men report erection problems, and how does this change with age?
* What are the main disorders of orgasm and how are they defined in DSM-5?
* What is the main sexual pain disorder described in DSM-5 and how is it defined?
® What kinds of decisions does a clinician have to make when diagnosing a sexual dysfunction?
11.2.2 The Aetiology of Sexual Dysfunctions

* Can you list some of the risk factors that have been associated with sexual dysfunctions?
© How have repressed emotions and desires been used by psychoanalytic theorists to explain sexual dysfunctions?
° What are the two factors in Masters and Johnson's theory of sexual dysfunction?
® How is performance anxiety important in explaining some forms of sexual dysfunction?
© In what ways might interpersonal difficulties be associated with sexual dysfunctions?
e Is there evidence to suggest that negative emotions such as depression and anxiety are outcomes or causes of sexual
dysfunctions?
° What is the difference between remote and immediate causes of sexual dysfunctions? Can you give some examples of both?
® Can you name the three broad categories into which the biological causes of sexual dysfunctions can be classified?
* In what ways does age affect sexual functioning?

® What are direct treatments for sexual dysfunctions?
® Can you name and describe at least three direct treatments for sexual dysfunctions?
e Why is couples therapy an important form of treatment for sexual dysfunction?
e What are the main drug treatments for sexual dysfunctions, and what is the evidence that they are successful?
* What are the main mechanical devices used to treat male sexual dysfunctions?
SECTION SUMMARY
11.2 SEXUAL DYSFUNCTIONS
Sexual dysfunction has an unusual history in the context of psychopathology. In the first half of the twentieth century, sexual
problems were rarely admitted and discussed, let alone treated. With the liberating social climate of the 1960s and 1970s this
attitude changed, and the pioneering research work of a few dedicated clinicians (such as Masters and Johnson) provided
a database of evidence on these kinds of disorders, as well as the first integrated sex therapies for sexual dysfunctions. The
causes of sexual dysfunctions range across the biological and organic, psychological factors such as performance anxiety and
negative cognitions about sex, to interpersonal problems, and an equally broad range of treatments have been developed to
PSYCHOPATHOLOGY
address this array of possible causes. Given all this, it is important to remember that not everyone with less- than-adequate
sexual performance is suffering a sexual dysfunction. The DSM-5 criteria clearly state that any performance deficits must be
accompanied by distress and interpersonal difficulties, and it is these latter two factors that define sexual dysfunction disorders.
The main points are:
e The four stages of the sexual response cycle are desire, arousal, orgasm and resolution, and sexual dysfunctions can be
diagnosed in any of these individual stages.
11.2.1 Diagnosis of Sexual Dysfunction

e Sexual dysfunctions are a heterogeneous group of disorders characterized clinically by Hatesindividual's inability to respond
sexually or to experience sexual pleasure.
° Male hypoactive sexual desire disorder is characterized by a persistent and recurrent deficiency or absence of desire for
sexual activity.
° Erectile disorder is the inability to maintain an adequate erection during sexual activity. Around 10 per cent of males report
erection problems, but this increases to 20 per cent in the over 50s.
¢ Female sexual interest/arousal disorder is characterized by significantly reduced, or absence of, interest in sexual activity,
erotic thoughts, and reduced sexual sensations during sexual activity.
e Female orgasmic disorder is characterized by a delay or absence of orgasm during sexual activity, and around 10 per cent of
adult women may never have experienced an orgasm.
® Delayed ejaculation is a persistent or recurrent delay in ejaculation following a normal sexual excitement phase.
° Early ejaculation is the onset of orgasm with minimal sexual stimulation. Treatment for this disorder is typically sought by
men under the age of 30 years. c
® Genito-pelvic pain/penetration disorder refers to four commonly occurring symptoms, namely difficulty having intercourse,
genito-pelvic pain, fear of pain or vaginal penetration, and tension ofthe pelvic floor muscles.
11.2.2. The Aetiology of Sexual Dysfunctions

® Sexual dysfunction is more prevalent in women than in men (43 per cent and 31 per cent respectively), and is more likely
amongst those experiencing poor physical and emotional health.
e Psychoanalytic theory attempts to account for sexual dysfunctions in terms of repressed sexual desires or hostility to the
opposite sex.
e Masters and Johnson developed a two-factor model of sexual dysfunction where (1) early sexual experiences give rise to
anxiety during sex, and (2) this anxiety leads the individual to adopt a spectator role during sexual activity, which directs
attention away from stimuli providing sexual arousal.
e Interpersonal difficulties may be both a cause and an outcome of sexual dysfunctions.
¢ Anxiety and depression are closely associated with sexual dysfunctions, and these negative emotions may interfere with
sexual performance.
° The causes of sexual dysfunctions can sometimes be defined in terms of immediate causes (e.g. lack of sexual knowledge)
and remote causes (e.g. feelings of shame and guilt that are a result of a specific upbringing).
* Biological causes of sexual dysfunctions can be classified as (1) dysfunctions caused by an underlying medical disorder,
(2) dysfunction caused by hormonal abnormalities, and (3) changes in sexual responsiveness with age.

° Direct treatments attempt to deal with the specific symptoms of the disorder (e.g. the squeeze technique for premature
ejaculation).
° The stop-start technique, squeeze technique and the tease technique are all specific behavioural treatments designed to treat
premature ejaculation and orgasmic disorders.
e If sexual dysfunctions are a manifestation of broader problems then couples therapy can be adopted.
* Biological treatments can be categorized into (1) drug treatments, including medications that directly influence the organic
nature of the disorder, (2) hormone treatment designed to correct hormone imbalances caused by age or sickness, and
(3) mechanical devices, designed to aid mechanical functioning during sex.
* Of the men who take Viagra, 75 per cent can achieve erection within 60 minutes of administration, and over 95 per cent of
clients treated with Viagra over a 1-3 year period express satisfaction with their ability to effectively engage in sex.
* Mechanical devices to aid penile erection and penetration include the penile prosthesis and the vacuum erection device (VED).
11.3 PARAPHILIC These paraphilias have been listed in three groups.

The first group includes fetishistic disorder and trans-
DISORDERS vestic disorder, where the individual experiences sexual
desire towards inanimate objects or derives sexual grati-
fication from cross-dressing. However, to be diagnosed
Sexual dysfunctions are one side of the sexual disorders with either of these disorders, these tendencies must
coin, where individuals complain of deficiencies or inade- cause the individual significant distress or social and/or
quacies in their sexual desire and performance. On the occupational impairment.
other side of the coin are those psychopathologies that are The second group consists of exhibitionistic disorder,
associated with high frequencies of sexual activity or unu- voyeuristic disorder, frotteuristic disorder and paedophilic
sual sexual activities that are often directed at inappropri- disorder. These disorders have been grouped together
ate targets. Sexual experience is normally highly valued in because they usually involve sexual fantasies, urges and
Western cultures, but there is now a good deal of evidence activities directed at non-consenting persons. The exhi-
that high rates of sexual behaviour can be problematic, bitionist will expose himself to unsuspecting victims; the
interfere with personal happiness and social adjustment, voyeur will take sexual pleasure from watching unsuspect-
and be channelled into unusual sexual activities (Kafka, ing others either naked or in the process of undressing;
1997, 2003). When high rates of sexual behaviour are chan- the frotteurist is sexually aroused by rubbing themselves
nelled into unusual or very specific sexual activities, these against a non-consenting person; and the paedophile has
are known collectively as paraphilic disorders. In sexual urges towards and indulges in sexual acts with pre-
DSM-5, the term paraphilia denotes ‘any intense and per- pubescent children, who — by their very age — are unable
philic disorders Represent sexual sistent sexual interest other to legally consent to these activities. This second group
5 or fantasies involving unusual than sexual interest in gen- of paraphilic disorders is defined by the fact that the indi-
es of gratification (e.g. non-human ital stimulation or pre- vidual does not have to experience distress or social or
‘ts or non-consenting individuals). paratory fondling with occupational impairment to be diagnosed with these dis-
phenotypically normal psychically mature, consenting orders, but merely has to have acted on these urges with
human partners’ (DSM-5, p.685). Some paraphilias con- non-consenting persons (Hilliard & Spitzer, 2002).
cern the individual's own erotic activities while others pri- The final group consists of sexual masochism disorder
marily concern the individual’s erotic targets, and a and sexual sadism disorder, where individuals experience
paraphilic disorder is one that currently causes distress or sexual arousal from either (1) the desire to be humili-
impairment to the individual or whose satisfaction has ated or made to physically suffer (masochism) or (2)
entailed personal harm, or risk of harm, to others. A list of inflict physical suffering on others (sadism). Most often
the paraphilias included in DSM-5 is provided in Table 11.2. sado-masochistic acts are performed with a consenting
TABLE 11.2 Paraphilic disorders
Fetishistic disorder Recurrent sexual arousal involving non-animate

Sexual urges that are not directed at objects
another person
Transvestic disorder Recurrent, intense sexual arousal from cross-dressing
Exhibitionistic disorder Sexual arousal from the exposure of one’s genitals to

an unsuspecting person
Voyeuristic disorder Recurrent sexually arousing fantasies involving acts

of observing an unsuspecting person who is naked
Sexual urges directed at non-consenting or in the act of undressed
other persons (in many societies these
Frotteuristic disorder activities represent sexual offences) Recurrent sexual arousing from touching or rubbing
against a non-consenting person
Paedophilic disorder Recurrent, intense sexually arousing fantasies or

urges involving sexual activity with a prepubescent
child
Sexual masochism disorder Sexual arousal from being humiliated or otherwise

Sexual arousal from inflicting or experi- forced to suffer
Sexual sadism disorder encing suffering Sexual arousal from the psychological or physical
suffering of others
384 PSYCHOPATHOLOGY
‘ ‘a
partner, but even in such circumstances, the individual DSM-5 SUMMARY TABLE 11.8 Criteria for fetishistic disorder
may be bothered or distressed by these tendencies and © Over a period of 6months, recurring and strong sexual
acts, and personal distress is an important contributor to arousal from the use of non-living objects or a highly
diagnosis of these disorders. specific focus on non-genital body parts as part of fanta-
From these categorisations it is clear that some para- sies, urges or behaviours, causing significant distress or
philic disorders are victimless (e.g. fetishistic disorder and impairment in social, occupational or other areas of life
transvestic disorder), while others will be defined in law ¢ The fetish is not limited to the clothing used in cross-
as sexual offences (e.g. exhibitionistic disorder, voyeuris- dressing or objects such as vibrators and other genital
tic disorder, frotteuristic disorder, paedophilic disorder, simulators
and those acts of sexual sadism where harm is inflicted
on others without consent). Some require these activi-
ties to cause personal distress to be diagnosed, while oth-
ers do not. This leads to an issue of where the line is rubbing or smelling these articles. A fetish will usually
drawn between acceptable sexual activity and a psycho- have developed by adolescence, and may have developed
pathology. Clearly, many of the urges and fantasies as a result of specific experiences during childhood or
defined in the diagnostic criteria for paraphilias are expe- early adolescence. Some individuals exhibit a phenome-
rienced by many people, and there is a growing industry non known as partialism, which is fascination with an
willing to cater for these urges in films, magazines and individual object or body part to the point where normal
internet sites. However, (1) most people are unwilling to sexual activity no longer partialism A phenomenon inwhich the
act on their fantasies, and are quite happy to restrict their occurs. Note that fetishistic _ is a fascination with an individual objec
sexual interest in paraphilic activities to viewing erotic or disorder is not diagnosed the point where normal sexual activity
longer occurs. as
pornographic material, and (2) it is only when a person’s if the object concerned. is
sexual urges become linked to just one specific type of for the purpose of tactile genital stimulation (such as a
stimulus or act thataes begins to deem that behav- vibrator). However, Focus Point 11.2 provides some case
_ DL jour as abnormal’. We reports of penile injuries from the British Medical Journal
To complete Activity 11.2 go to must bear these issues in and illustrates the lengths that some individuals will go to
activities/ch11 | mind when discussing the gain sexual excitement. While the injuries incurred were
se sans individual paraphilias. obviously not amusing for the victims, the reader may be
The pilcwaeee sectionfidescubes the diagnostic criteria amused by the reasons given for these injuries!
and main characteristics of each of the paraphilic disor-
ders. We will then progress to discuss some of the theo- Transvestic disorder
ries of the aetiology of paraphilic disorders, and finally A diagnosis of transvestic disorder is given when a hetero-
describe and evaluate forms of treatment. sexual male experiences recurrent, intense sexual arousal
from cross-dressing in women’s attire, and this causes sig-
nificant distress or impairment in social or occupational
11.3.1 The Diagnosis and functioning (DSM-5 Summary Table 11.9). A Swedish
Description of Paraphilic Disorders study has indicated that 2.8 per cent of men and 0.4 per
cent of women report at least one episode of transvestic
Fetishistic disorder behaviour during their life, and risk factors for this disor-
A diagnosis of fetishistic disorder is given when a person der include same-sex sexual experiences, being easily sex-
experiences recurrent, intense sexually arousing fantasies ually aroused, pornography use and relatively high
and urges involving non- masturbation frequency (Langstrom & Zucker, 2005). In
fetishistic disorder Recurrent, intense
sexually arousing fantasies and urges animate objects, and this this particular disorder, sexual excitement is achieved
involving non-animate objects, and this causes them personal dis- primarily because female clothes are a symbol of the indi-
causes them personal distress or affects tress or affects social and vidual’s femininity rather than because the garments
social and occupational functioning.
occupational functioning trigger sexual arousal per se (as would be the case
(DSM-5 Summary Table 11.8). Often fetishes are restricted with a simple fetish). In addition, this diagnosis should not
to articles associated with sex, such as women’s clothing be given if the individual has a diagnosis of gender dys-
or undergarments (bras, stockings, shoes, boots, and so phoria (see section 11.4).
on) or to body parts such as feet, toes, or hair. The indi- The person with transves- transvestic disorder When a hetero-
vidual with fetishistic disorder may experience strong sexual male experiences recurrent,
tic disorder will often keep
intense sexual arousal from cross-dressi
desires to obtain or touch these items (e.g. by stealing a collection of women’s in women’s attire, and this causes signif
them from washing lines), may ask a sexual partner to clothes, and sexual arousal cant distress or impairment in social or
wear them during sex, or may masturbate while holding, is normally caused by the occupational functioning.
PENILE INJURIES RESULTING FROM A VACUUM CLEANER |

The following are four cases of penile injury incurred CASE 3
when using a vacuum cleaner in search of sexual
excitement. At least two of these injuries-were caused A 49-year-old man was vacuuming his friend’s stair-
by a‘Hoover Dustette’ which has fan blades only 15cm case in a loose-fitting dressing gown when, intending
from the inlet. to switch the machine off, he leaned across to reach
the plug; ‘At that moment his dressing gown became
_POINT
FOCUS
11.2 CASE1 undone and his penis was sucked into the vacuum
cleaner’ He suffered multiple lacerations to the fore-
skin as well as lacerations to the distal part of the shaft
A 60-year-old man said that he was changing the plug
of the penis.
of his Hoover Dustette vacuum cleaner in the nude
when his wife was out shopping. It ‘turned itself on’
and caught his penis, causing tears around the exter- CASE 4
nal meatus and deeply lacerating the side of the glans.
This patient was aged 68, and no history is available
except that the injury was caused by a vacuum cleaner.
CASE 2
The injury extended through the corpora cavernosa
and the corpus spongiosum and caused complete |
| A 65-year-old railway signalman was in his signal box
division of the urethra proximal to the corona.
when he bent down to pick up his tools and ‘caught
his penis in a Hoover Dustette which happened to be Source: Reproduced from Citron, N.D & Wade, PJ. (1980).
switched on’ He suffered extensive lacerations to the Penile injuries from vacuum cleaners. British
Medical
glans, which were repaired with cat gut with a good Journal, 281(6232), 26. With permission from BMJ Publishing
result. Group Ltd.
DSM-5 SUMMARY TABLE 11.9 Criteria for transvestic disorder DSM-5 SUMMARY TABLE 11.10 Criteria for exhibitionistic
disorder
e Continuing and powerful sexual arousal from cross-
dressing as part of fantasies, urges or behaviours, over a ¢ Continuing and powerful sexual arousal from expos-
period of at least 6 months, causing significant distress or ing one’s genitals to an unsuspecting audience, over a
impairment in social, occupational or other areas of life. period of at least 6 months, as part of fantasies, urges or
behaviours
2 The patient has acted on these urges with a non-
man having thoughts or images of himself as a female. consenting person or the urges cause significant distress
Chris’s story at the beginning of this chapter is a typical or impairment in social, occupational or other areas of life
example of transvestic behaviour. Like Chris, most indi-
viduals diagnosed with transvestic disorder are relatively
happily married men, but are worried what others Table 11.10). These fantasies are usually strong and
(including their wives) may think of their behaviour. As a recurrent to the point where the individual feels a com-
result, over half of those who admit to cross-dressing usu- pulsion to expose himself or herself, and this compulsion
ally seek counselling at some stage because of its effects often makes the individual oblivious of the social and
on their intimate relationships (Doctor & Prince, 1997). legal consequences of what they are doing (Stevenson &
Most men with transvestic disorder have been cross- Jones, 1972). The onset of exhibitionistic disorder usu-
dressing for many years, usually since childhood or early ally occurs before 18 years of age, and is often found in
adolescence (Doctor & Fleming, 2001), and many women individuals who are imma-
are happy to tolerate their husbands’ cross-dressing or ture in their relationships exhibitionistic disorder Involves sexual
even incorporate it into their own sexual activities. with the opposite sex, and fantasies about exposing the penis to a
stranger.
many have problems with
Exhibitionistic disorder interpersonal relationships generally (Mohr, Turner &
This paraphilic disorder involves sexual fantasies about Jerry, 1964). The sufferer’s urge to expose himself/her-
exposing the genitals to a stranger (DSM-5 Summary self will often lead them to find a victim in a public place,
: :
often a park or a side street, where they expose DSM-5 SUMMARY TABLE 11.11 Criteria for voyeuristic disorder
themselves — usually to a single victim. The victim’s ® Continuing and powerful sexual arousal from the obser-
response of shock, fear or revulsion often forms part of vance of an unsuspecting person who is naked, undress-
the gratification that reinforces this behaviour, and the ing or engaging in sexual activity, over a period of at least
exhibitionist may sometimes masturbate while exposing 6 months, as part of fantasies, urges or behaviours
himself/herself (especially if he finds the victim’s reac- e The patient has acted on these urges with a non-
tion to his behaviour sexually arousing) or may return consenting person or the urges cause significant distress
home to masturbate while fantasising about the encoun- or impairment in social, occupational or other areas of life
ter. Exhibitionists will usually expose themselves to
e The individual experiencing the arousal is at least 18 years
women or children, and while no physical harm is usu- of age :
ally involved, the experience for the victim is often trau-
matic and may have lasting psychological consequences.
DSM-5 SUMMARY TABLE 11.12 Criteria for frotteuristic
A significant percentage of individuals with a diagnosis
disorder
of exhibitionistic disorder are non-disclosing, deny any
urges or fantasies related to exposing themselves, and ¢ Continuing and powerful sexual arousal from touching or
report that incidents of exposure were either accidental rubbing against a non-consenting person, over a period of
or non-sexual. Men are significantly more likely to be at least 6 months, as part of fantasies, urges or behaviours
diagnosed with exhibitionistic disorder than women, and e The patient has acted on these urges with a non-
the prevalence rate of exhibitionist acts in men is esti- consenting person or the urges cause significant distress
mated to be between 2 and 4 per cent (DSM-5, p.690). or impairment in social, occupational or other areas of life
Voyeuristic disorder This is usually a male activity, and manifests as a sexual

A diagnosis of voyeuristic disorder is given when an indi- urge to rub the genitalia against the victim’s thighs and
vidual experiences recurrent, intense sexually arousing buttocks or to fondle the victim’s genitalia or breasts
fantasies or urges involving with his hands. This behaviour is usually undertaken in a
voyeuristic disorder When an individual
experiences recurrent, intense sexually
the act of observing an surreptitious way in order to try to make it appear unin-
arousing fantasies or urges involving the unsuspecting person who tentional or as if someone else in the crowded environ-
act of observing an unsuspecting person is naked, in the process of ment is the culprit. Like exhibitionism and voyeurism,
who is naked, in the process of undressing,
undressing, or engaging in this activity usually begins in adolescence, but may sub-
or engaging in a sexual activity.
a sexual activity (DSM-5 side in frequency by the time the individual is in their late
Summary Table 11.11). Sexual arousal normally comes 20s. Frotteurism is considered by many to be a form of
from the act of looking (‘peeping’) and the individual may sexual assault, and at least part of the excitement for frot-
masturbate while in the act of observing others. However, teurs is the feeling of power it gives them over their vic-
the individual rarely seeks sexual activity with those being tim — a feeling that is relatively common in those who
observed. Voyeurism usually begins in early adolescence indulge in sexual assault generally. Around 10-14 per
and may often constitute that individual’s sole sexual cent of adult males seen in outpatient settings for para-
activity in adulthood (Kaplan & Krueger, 1997). The risk philic disorders meet the frotteuristic disorder Intense, recurrent
of being discovered while indulging in voyeuristic behav- criteria for frotteuristic sexual urges to touch and rub up against
iours may also add to the excitement that this behaviour disorder (DSM-5, p.693). __ non-consenting people. |
engenders. However, we must be clear that voyeurism
can be a perfectly acceptable sexual activity when prac- Paedophilic disorder
tised between consenting individuals, but is clearly prob- Paedophilic disorder is defined as sexual attraction
lematic when the voyeur begins seeking non-consenting towards prepubescent children, normally 13 years old or
victims and violates their privacy. Voyeuristic acts are the younger. To be diagnosed with paedophilic disorder,
most common of the potentially illegal paraphilic behav- the individual must be at least 16 years of age and at least
iours, with estimates of the possible lifetime prevalence 5 years older than the vic-
of voyeuristic acts being as high as 12 per cent in males tim. Recent studies sug- paedophilic disorder Sexual attraction
towards prepubescent children, normally
and 4 per cent in females (DSM-5, p.688). gest that up to 9 per cent of 13 years or younger.
of men have described
Frotteuristic disorder having at least one sexual fantasy involving a child, and
This involves intense, recurrent sexual urges to touch so such fantasies are not that uncommon in the general
and rub up against non-consenting people — usually in population (Seto, 2009). However, DSM-5 does highlight
crowded places such as underground trains, buses or the fact that paedophilic disorder is only diagnosed if the
supermarket queues (DSM-5 Summary Table 11.12). individual acts on these fantasies or is distressed by them.
CHAPTER 11 SEXUAL AND GENDER PROBLEMS -387—
The extensive use of pornography depicting children DSM-5 SUMMARY TABLE 11.13 Criteria for paedophilic
is usually an indicator of paedophilic disorder, and the disorder
condition often becomes apparent as a sexual interest e Continuing and powerful sexual arousal from fantasies,
in children around puberty. Those who report paedo- urges or behaviours involving sexual activity with a prepu-
philic sexual urges, usually report a preference for males bescent child or children (aged 13 years or younger)
or females, or sometimes for both. Those attracted to
e The patient has acted on these urges or the urges cause
females usually prefer 8-10 year olds, whereas those significant distress or impairment in social, occupational or
attracted to males usually prefer older children (DSM- other areas of life
IV-TR, p.571). Paedophilia generally, appears to be a life-
e The patient is at least 16 years old and at least 5 years
long condition, in which many with a sexual interest in
older than the child or children involved
children will often deny attraction to children despite
¢ Does not include an individual in late adolescence in an
multiple sexual approaches to them. Paedophilic dis-
ongoing sexual relationship with a 12- or 13-year-old
order, however, is defined by other elements that may
change over time, such as guilt, shame, or feelings of
isolation. The highest likely prevalence for paedophilic may show sexual interest in a daughter only when the
disorder in males is around 3-5 per cent (DSM-5, p.698). daughter begins to become sexually mature), and (2) by
The central feature of the psychopathology is sexual having a relatively normal heterosexual sex life outside of
attraction to children, but this is not equivalent to ‘child the incestuous relationship. In contrast, non-incestuous
sexual abuse’, ‘incest’ or ‘child molestation’ because the paedophiles will normally only become sexually aroused
latter represent criminal acts. It is important to make this by sexually immature children and are sometimes known
distinction because not all who sexually abuse children as preference molesters (Marshall, Barbaree & Christophe,
are diagnosable with paedophilic disorder — for example, 1986). Second, most paedophiles rarely intend to physi-
many who sexually abuse children may opportunistically cally harm their victims preference molesters Non-incestuous
select children simply because they are available; such (even though they may paedophiles who normally only become
people do not necessarily have specific fantasies about threaten their victims in sexually aroused by sexually immature
having sex with children (Fagan, Wise, Schmidt & Berlin, order to prevent disclo- children.
2002). Girls are three times more likely than boys to be sure), but some may only get full sexual gratification from
sexually abused, and children from low-income families harming and even murdering their victims. This latter
are 18 times more likely to be sexually abused (Sedlak & group are probably best described as child rapists, and
Broadhurst, 1996). The paedophile’s sexual activity with appear to be fundamen- child rapists A group of paedophiles who
children is usually limited to acts such as undressing the tally psychologically differ- only get full sexual gratification from harm-
child, exposing themselves, masturbating in the presence ent to other paedophiles ing and even murdering their victims.
of the child, or gently touching or fondling the child and and often have comorbid diagnoses of personality disor-
their genitalia. However, in more severe cases, this activ- der or sexual sadism (Groth, Hobson & Guy, 1982).
ity can extend to performing oral sex acts with the child, Because their behaviour is illegal and socially out-
or penetrating the child’s vagina, mouth or anus with lawed, and because they need to gain the trust of their
fingers, foreign objects or their penis. In general, paedo- child victims in order to indulge in their sexual activi-
philes rarely believe that what they are doing is wrong ties, most individuals diagnosable with paedophilic
and avidly deny their sexual attraction to children. They disorder develop elaborate ways of gaining access to
will also often use egocentric forms of rationalisation to children. This can involve taking jobs in environments
justify their acts (e.g. the acts had ‘educational value’ or where children are frequently found (e.g. schools, resi-
that the child was consenting or gained pleasure from dential children’s homes, and suchlike), gaining the
the activity). Because of this, they often fail to experi- confidence of the parents or family of a child, or more
ence distress or remorse, and so experiencing distress recently by ‘grooming’ children in internet chat-rooms
or psychological impairment is not a necessary part of by pretending to be someone of a similar age to the
the diagnostic criteria for paedophilic disorder (DSM-5 victim. Focus Point 11.3 provides an example of how
Summary Table 11.13). paedophiles may ‘groom’ and ‘lure’ children for sexual
There are numerous unofficial subtypes of paedo- purposes on the internet. In a qualitative study of the
philia. First, some paedophiles limit their activities to their modus operandi of male paedophiles, Conte, Wolf &
immediate family (e.g. children, step-children, nieces and Smith (1989) were able to describe a standard process
nephews) and incest is listed as a specifying factor in through which many paedophiles operated to attract
DSM-5. Men who indulge in incest tend to differ from and isolate their victims and desensitize them to their
other paedophiles (1) by indulging in sexual activity with sexual advances. This process included: (1) choosing an
children of a slightly older age (e.g. an incestuous father open, vulnerable child who would be easily persuaded
388 PSYCHOPATHOLOGY
PAEDOPHILE ‘GROOMING’ OVER THE INTERNET: HOW DO ONLINE

PREDATORS WORK?
Predators establish contact with kids through con- predatory paedophiles don’t usually pose as teen-
versations in chat-rooms, instant messaging, e-mail agers, but do look for signs of a kid who is attention
or discussion boards. Many teens use ‘peer support’ starved or whose parents don’t seem to care much
online forums to deal with their problems. Predators, about them. He will then begin to discover where
however, often go to these online areas to look for vul- they might live by asking questions about their school
11.3 nerable victims.
POINT
FOCUS | or their locality.
Online predators try to gradually seduce their tar- Some predators work faster than others, engag-
gets through attention, affection, kindness, and even ing in sexually explicit conversations immediately.
gifts, and often devote considerable time, money This more direct approach may include harassment
and energy to this effort. They are aware of the lat- or stalking. Predators may also evaluate the kids they
est music and hobbies likely to interest kids. They lis- meet online for future face-to-face contact.
ten to and sympathize with kids’ problems. They also
try to ease young people’s inhibitions by gradually Source: Adapted from http://www.bewebaware.ca/ and http://
introducing sexual content into their conversations www.child-safety-for-parents.com/internet-pedophiles
or by showing them sexually explicit material. Older AAtml#.UIfh2xYQi04.
and would remain silent after the abuse, (2) using non- DSM-5 SUMMARY TABLE 11.14 Criteria for sexual
sexual enticements such as purchases or flattery on masochism disorder
early encounters with the child, (3) introducing sexual ¢ Continuing and powerful sexual arousal from the act of
topics into the conversation, and (4) progressing from being humiliated, tied up, beaten or made to suffer, over
non-sexual touching to sexual touching as a means of a period of at least 6 months, as part of fantasies, urges or
desensitising the child to the purpose of the touching. behaviours
After the abuse, the paedophile would use his adult e The urges cause significant distress or impairment in
authority to isolate the child and their ‘shared behav- social, occupational or other areas of life
iour from family and peers.
Finally, it is important to remember that by their very
age, the victims of paedophilia are non-consenting vic- from being humiliated, beaten, bound or otherwise
tims, and that sexual activity with prepubescent children made to suffer, and these urges cause significant distress
is illegal in most societies. In a general population study or social and occupational impairment (DSM-5 Summary
in the US, 12 per cent of men and 17 per cent of women Table 11.14). In contrast, sexual sadism disorder is when
reported being touched sexually by an older person the person gains sexual arousal and satisfaction from the
when they were children (Laumann, Gagnon, Michael & psychological or physical suffering of others. A diagnosis
Michael, 1994). Furthermore, it is also important to note of sexual sadism disorder
that the victims of paedophilia can suffer long-term psy- is given if these symptoms sexual sadism disorder Whena person
gains sexual arousal and satisfaction fron
chological problems as a result of their experiences, and cause distress or significant the psychological or physical sufreringl
these can manifest as eating disorders, sleep disorders, social or occupational imp- others, and this diagnosis is given if the
depression, anxiety disorders such as panic attacks and airment to the individual, symptoms cause the individual signifi- _
phobias, self-harm, and dissociative disorders, all perse- or if the individual acts on cant distress or if the person acts on thel
impulses with a non-consenting person.
vering well into adulthood. These psychological prob- these urges with a non-
lems are more intense and more enduring if the abuse consenting person (DSM-5 Summary Table 11.15). Sado-
occurred at an early age and the victim knew their abuser masochistic acts are often performed between consenting
well (Kendall-Tuckett, Williams & Finkelhor, 1993). mutual partners, one who gains satisfaction from sadistic
acts and the other who enjoys being humiliated. Sadistic
Sexual masochism disorder and or masochistic activities include acts that emphasize the
sexual sadism disorder dominance and control of one person over the other.
sexual masochism disorder When an
A diagnosis of sexual mas- These may include restraint, blindfolding, spanking,
individual gains sexual arousal and satis- ochism disorder is given whipping, pinching, beating, burning, rape, cutting, stab-
faction from being humiliated, and this if the individual gains sex- bing, strangulation, torture and mutilation. Acts of
causes the individual significant distress. ual arousal and satisfaction dominance (or submission) may include forcing the
DSM-5 SUMMARY TABLE 11.15 Criteria for sexual sadism disorders that involve sexual offending (e.g. paedophilia,
disorder
exhibitionism). Traditionally, psychodynamic explana-
* Continuing and powerful sexual arousal from the physi- tions had been popular but these have now tended to
cal or psychological suffering of another person, over a be superseded by cognitive and, to a lesser degree, bio-
period of at least 6 months, as part of fantasies, urges or logical explanations. We begin this section by looking
behaviours .” at some of the risk factors associated with the develop-
e The patient has acted on these urges with a non-con- ment of paraphilic disorders to give you an indication of
senting person or the urges cause significant distress or some of the experiential and psychological factors asso-
impairment in social, occupational or other areas of life ciated with paraphilias.
Risk factors for paraphilic disorders

submissive partner to crawl on the floor, or keeping It may not have escaped the reader that most of the
them restrained in a cage. Sexual masochists can often DSM-5 diagnosable paraphilias are mainly male activi-
cause their own suffering, and one prominent example is ties, so being male is in itself a risk factor for paraphilic
known as hypoxyphilia, which involves the individual disorders. For example, surveys have suggested that 89
using a noose or plastic bag to induce oxygen deprivation per cent of acts of child sexual abuse are perpetrated by
yphilia An act performed by sexual during masturbation. In men, and only 11 per cent by women (Sedlak &
ists which involves the individual contrast, when they are Broadhurst, 1996), and male masochists outnumber
unable to obtain consent-
a noose or plastic bag to induce oxy-
females by 20:1. It is by no means clear why paraphilias
2privation during masturbation.
ing partners, sexual sadists should be such a male preserve, but this may in part be
may resort to rape, mutilation and murder to satisfy their due to female sexuality being repressed more than male
sexual desires (Dietz, Hazelwood & Warren, 1990), and sexually — especially during socialisation. There is some
there is a high rate of comorbidity between sexual sad- evidence of a link between high rates of sexual activity
ism disorder and impulse disorders. For example, in indi- generally, and anxiety and depression, and paraphilias
viduals with a diagnosis of sexual sadism disorder, 31 per (Kafka, 1997: Raymond, Coleman & Miner, 2003). High
cent were also diagnosed with borderline personality dis- rates of highly sexual activity is known as hypersexual-
order, and 42 per cent with antisocial personality disor- ity, and it was itself considered for inclusion as a disorder
der (Berger, Berner, Bolterauer, Gutierrez & Berger, in DSM-5, although it was
1999). It is estimated that around 5-10 per cent of the hypersexuality The occurrence of high ©
omitted from the final rates of sexual activity. sll
population indulge in some kind of sado-masochistic published version (Walters,
activity at some time in their life (Baumeister & Butler, Knight & Langstrom, 2011). One implication of the link
1997), and most are heterosexual, reasonably affluent, between hypersexuality and paraphilias is that high rates
well-educated, indulge in these activities with a consent- of sexual activity may lead individuals to evolve specific
ing partner, and are not unnecessarily distressed or dis- sexual inclinations and urges that are characteristic of
turbed by their sexual predilections (Moser & Levitt, paraphilia. Hypersexuality is found more often in men
1987). If this is so, then most sado-masochistic activity who are young, have experienced separation from par-
does not involve either psychological distress or imposi- ents during childhood, live in major urban areas, have
tion of a sexual urge on non-consenting persons, and so had sexual experiences at an early age, frequently experi-
would not meet the DSM-5 criteria for a disorder. ence same-sex sexual behaviour, pay for sex, and are
Because sado-masochism is enjoyed by many individuals relatively more dissatisfied with sexual life than non-
who incorporate these activities into their normal sexual hypersexual men (Langstrom & Hanson, 2006). The
relationships, there is a growing market for such activi- study by Langstrom & Hanson also identified a strong
ties catered for by sex shops, underground newspapers association between hypersexuality and exhibitionism,
and websites. Indeed, over the years, sado-masochism voyeurism and sexual masochism and sexual sadism.
(known as S&M) has become a significantly accepted Hypersexual men were also characterized by their will-
subculture within homosexual circles. ingness to indulge in a range of risky behaviours, includ-
ing tobacco smoking, heavy drinking, using illegal drugs,
and gambling. These initial studies do suggest some kind
11.3.2 The Aetiology of important link between hypersexuality and paraphilia,
and further research in this area may help to clarify the
of Paraphilic Disorders risk factors and causes of individual paraphilias. Given
To date there is relatively little research on the causes of that we now know some of the factors that predict
paraphilia disorders, and what research is available has hypersexuality, then these might also play a significant
mainly been confined to the study of those paraphilic role in predicting the development of paraphilias.
390 PSYCHOPATHOLOGY
Numerus studies have also identified some of the risk as sexual sadism, where the sadist is seen as feeling relief
factors involved in paedophilia. These can be categorized from castration anxiety by taking on the role of castrator
as either remote factors (i.e. factors from the individual's rather than the castrated.
developmental history) or precipitant factors (i.e. factors Because of the way in which psychodynamic theory
that lead directly to the expression of paedophile behav- is couched, it is difficult to find objective evidence to sup-
iour). Remote risk factors for paedophilia include being port these explanations of paraphilias. If such factors
a victim of childhood sexual abuse (Cohen, Forman, do underlie paraphilia behaviour, then exploring them
Steinfeld, Fradkin et al., 2010) or possessing an inade- in psychoanalysis should help to alleviate these diverse
quate attachment style that results from being brought sexual activities. However, there is only modest evidence
up in a dysfunctional family (Hanson & Slater, 1988). that psychoanalysis is successful in the treatment of para-
Precipitating risk factors include depression, psychoso- philias (Cohen & Seghorn, 1969), and it is usually entirely
cial stress (for example, as a result of losing a relationship ineffective in treating sexual offenders (Knopp, 1976).
or a job), and alcohol abuse (Fagan, Wise, Schmidt &
Berlin, 2002). Psychiatric comorbidity is also highly Classical conditioning
associated with paedophilic disorder, with 93 per cent One very simple explanation for paraphilic disorders is
of paedophiles being diagnosed with at least one other that unusual sexual urges are the result of early sexual
psychopathology during their lifetime, such as major experiences (such as masturbation) being associated with
depression or anxiety disorders. In addition, 60 per cent an unusual stimulus or behaviour through associative
of paedophiles are diagnosed with a substance abuse dis- learning (classical conditioning). For example, an adoles-
order, and 60 per cent meet the diagnostic criteria for a cent boy’s first sexual experiences may be masturbating
personality disorder (Raymond, Coleman, Ohlerking, to pictures of women dressed in fur or leather (resulting
Christensen & Miner, 1999). The statistics support the in a fur or leather fetish), or masturbating after acciden-
view that psychopathology may be a precipitating factor tally seeing a neighbour undressing (resulting in voyeur-
in triggering paedophile behaviour. ism). Such early experiences may determine the route an
adolescent’s sexual development will take, and this condi-
The psychodynamic perspective tioning account is consistent with the fact that many of
Psychodynamic theorists take a range of views about the the paraphilias first manifest in early adolescence. Support
causes of paraphilias. They can be viewed either as (1) for the classical conditioning account also comes from an
defensive reactions that are attempting to defend the ego early experiment that attempted to develop a fetish for
from repressed fears, or (2) as representing fixation at a women’s knee-length leather boots in a group of male
pregenital stage of development (usually the Oedipal volunteers. Rachman (1966) showed participants slides
stage). For example, fetishism and paedophilia can be of a pair of black, knee-length woman’s leather boots
viewed as the behaviour of individuals who find normal (the conditioned stimulus, CS) followed immediately by
heterosexual sex with women too threatening — perhaps a slide of an attractive female nude (the unconditioned
because of a castration anxiety — and voyeurism is a stimulus, UCS). After a number of pairings of the CS
behaviour that protects the individual from having with the UCS, participants showed an increase in penis
to deal with the relation- volume (as measured by a phallo-plethysmograph) when-
castration anxiety A psychoanalytic term ships that are often an ever the CS slide was shown. One participant even gener-
referring to a psychological complex in
inherent part of sexual life. alized this sexual response to pictures of other forms of
males with a fear of being castrated.
In this respect, psychody- female footwear! Nevertheless, while the conditioning of
namic approaches view those with paraphilias as individu- a sexual fetish can be experimentally demonstrated under
als whose sexual development is immature or who are controlled conditions, it is unlikely that conditioning is
unable to deal with the complexity of relationships that the cause of all paraphilias. It may account for the initial
usually surround normal heterosexual behaviour. (Lanyon, development of some fetishes, and may also account for
1986). Alternatively, paraphilias may be associated with a why sexual urges initially become associated with specific
fixation at the Oedipal stage of development, which is activities such as voyeurism and frotteurism. However, as
itself associated with castration anxiety. For example, normal sexual activities become experienced during ado-
transvestic fetishism is seen as a denial of the mother’s cas- lescence and early adulthood, conditioning theory would
tration. Dressing in a woman’s clothes but still having a predict sexual urges to become associated with these
penis underneath the clothing is seen as reassuring the normal sexual activities and links between sexual urges
transvestite that his mother has not been castrated and he and early, learnt paraphilia behaviour should extinguish.
should not therefore worry about himself being castrated Nevertheless, paraphilias frequently persist — even when
(Nielson, 1960). Castration anxiety again crops up in the sufferer finds them distressing and even when they are
psychodynamic interpretations of other paraphilias such also concurrently indulging in normal sexual behaviour.
CHAPTER11 SEXUAL AND GENDER PROBLEMS 391
Childhood abuse and neglect Dysfunctional beliefs, attitudes and schemata

As we have seen many times in this book, childhood Many problematic behaviours that are central to psycho-
abuse and neglect is an important predictor of psychopathology are often maintained by dysfunctional beliefs
logical problems later in life, and this is no less true for or biases in information processing that lead the individual
the development of paraphilic disorders. However, the to think and behave in the way they do (see Chapters 6 and
way in which negative early experiences may facilitate 7 for examples). This also appears to be true of some of
the development of paraphilic disorders is probably the paraphilic disorders, and especially those that are
complex. First, physical and sexual abuse is a feature of either illegal or involve behaviours towards a non-
the history of many individuals with paraphilias, as is a consenting victim (e.g. paedophilic disorder, exhibitionis-
history of disturbed and neglectful parenting (Mason, tic disorder, voyeuristic disorder). A considerable body of
1997; Murphy, 1997). However, childhood abuse and research suggests that cognitive distortions, dysfunctional
neglect is not a prerequisite for developing a paraphilic beliefs and information processing biases play an impor-
disorder or becoming a sexual offender, and less than 30 tant role in facilitating paraphilias that involve sexual
per cent of sexual offenders have a history of childhood offending in males (Abel, Gore, Holland, Camp et al.,
sexual abuse (Maletzky, 1993). Nevertheless, the level 1989; Ward, Hudson, Johnston & Marshall, 1997; Shruti,
of childhood abuse experienced by sexual offenders is Ward& Gannon, 2008) and ress
almost double the level found in the general population females (Gannon & Alleyne, § To read Shruti, Ward & Gannon’s article
on cognitive distortions in child
(Laumann, Gagnon, Michael & Michael, 1994), so child- 2013). For example, incest |
sex offenders go to
hood abuse may presumably contribute to paraphilia in offenders hold beliefs that | www.wiley-psychopathology.com/
some as yet unspecified way. Problematic parent-child children are both sexually | reading/ch11
relationships may also play a significant role in the devel- attractive and sexually moti-
opment of specific paraphilic disorders. For example, vated (Hanson, Lipovsky & Saunders, 1994), and paedo-
neglectful or abusive parenting can leave the child with philes believe that children want sex with adults, and see
low self-esteem, poor social skills, a lack of effective cop- contact as being socially acceptable and not harmful to the
ing strategies, and an inability to form lasting relation- child (Stermac & Segal, 1989). Abel, Gore, Holland, Camp
ships (Marshall & Serran, 2000). These psychological et al. (1989) labelled these beliefs cognitive distortions
and behavioural deficits may lead the individual to find and argued that, for paedophiles, they serve to legitimize
sexual satisfaction in ways that do not require them to or justify sexual involve-
ment with children and cognitive distortions Beliefs held by
ag se
deal with the consensual relationships required by nor-

sexual offenders that enable them to justify
mal sexual activity (e.g. transvestism, voyeurism, exhibi- function to maintain the their sexual offending. ‘a
tionism, frotteurism), or may lead them to seek sexual behaviour. These beliefs
satisfaction with others, such as children, with whom not only act as reasons why the paedophile should
their underdeveloped social and emotional skills do not sexually offend, they also function as excuses for the behav-
put them at a disadvantage. iour and a means of diffusing responsibility for the beha-
In conclusion, childhood abuse and neglect is certainly viour after the act. They also appear to be a means by
a factor that can be found in the history of some indi- which the paedophile can maintain their self-esteem after
viduals who develop paraphilias, but it is as yet unclear offending (Pollock & Hashmall, 1991; Ward, Hudson,
how these experiences might lead to the development of Johnston & Marshall, 1997). Table 11.3 provides examples
problematic sexual urges. of the cognitive distortions found in the post-offending
TABLE 11.3 Cognitive distortions found in the post-offending statements of paedophiles and exhibitionists
Function of statement Paedophilia Exhibitionism
Misattributing blame ‘She would always run around half-dressed’ ‘The way she was dressed, she was asking for it’
Denying sexual intent ‘| was just teaching her about sex’ ‘| was just looking for a place to pee’
Debasing the victim ‘She always lies’ ‘She was just a slut anyway’
Minimising consequences ‘She's always been really friendly to ‘| never touched her — so | couldn’t have
me - even afterwards’ hurt her’
Deflecting criticism ‘This happened years ago. Why can't ‘It’s not like | raped anyone’
everyone forget about it?’
Justifying the cause ‘If |hadn’t been molested as a kid, I'd never have ‘If |knew how to get dates, | wouldn't have to
done this’ expose myself’
Source: Adapted from Maletzky (2002).

392 PSYCHOPATHOLOGY
statements of paedophiles and exhibitionists, together that underlie the development and purpose of cognitive
with the putative functions that these cognitive distortions distortions in sex offenders (Gannon, Ward & Collie, 2007).
serve. However, there is still some debate about whether The cognitive distortions that many sex offenders hold
sexual offenders such as paedophiles genuinely hold these are often the products of more dynamic cognitive pro-
beliefs or whether they are faked in order to diffuse cesses. For example, Stermac & Segal (1989) found that
responsibility after the offence. Using a procedure in sexual offenders interpret sexual information in a biased
which child molesters believed their responses were being way, usually in a manner consistent with their underlying
monitored by a lie detector, Gannon (2006) found that beliefs about the acceptability of their behaviour. They
participants endorsed fewer cognitive distortions than found that child molesters differed from other respond-
when they believed their responses were unmonitored. ent groups by having a predisposition to interpret infor-
This suggests that at least some cognitive distortions may mation as implying benefits could be gained from sexual
be faked in order to provide post-offence excuses for the contact with children and there was greater complicity on
paedophile’s behaviour, and more experimental techniques the child’s part, with less responsibility on the adult’s part.
may need to be developed to understand the mechanisms Finally, research has suggested that sex offenders — and
E THE BOGUS PIPELINE PROCEDURE TO INCREASE HONEST

=
= ~ RESPONDING IN PAEDOPHILES
>
UO
Le) Sexual offenders such as paedophiles appear to possess a set of cognitive distortions that serve to legitimize
a orjustify sexual involvement with children and function to maintain the behaviour (Abel, Gore, Holland, Camp
12)
G>
et al., 1989) (see Table 11.3). These beliefs may well act as reasons why the paedophile should sexually offend, but
there is still some debate about whether sexual offenders genuinely hold these beliefs or whether they are faked
4) in order to diffuse responsibility after the offence. So how might psychologists find out whether these beliefs are
a real or faked? A study by Gannon (2006) used what is known as a bogus pipeline procedure with child molesters.
=!
<< In this procedure, participants are wired up to apparatus that measures skin conductance through electrodes
2 attached to the fingers. Some participants are then told to refrain from answering dishonestly because skin con-
=
==!
ductance may be related to dishonest responses (as if they were wired up to a ‘lie detector’, but in fact the evi-
dence that skin conductance can reliably indicate lying is modest).
U
The study has the following stages:
=
WV
a) STAGE 1
12)
=
- Convicted paedophiles are asked to say whether they agree or disagree with statements related to cognitive
ae
distortions in sexual offenders. Example items are the following:
=
-
U Some children know more about sex than adults AGREE/DISAGREE
c An 8-year-old can enjoy a good sex joke AGREE/DISAGREE
<—
Li Children are not as innocent as most people think AGREE/DISAGREE
Vv)
La
c
STAGE 2
One week later the same participants had to respond to the same statements (but they were not told it was the
same questionnaire). Half were simply asked to fill out the questionnaire for a second time. The other half were
connected to the bogus pipeline and given instructions that skin conductance could detect dishonest responses.
RESULTS
The results show that, compared with control participants, those attached to the bogus pipeline showed a sig-
nificant reduction in agreeing with the cognitive distortion statements between Time 1 (when they were not
connected to the bogus pipeline) and Time 2 (when they were connected to the bogus pipeline).
—4— Bogus Pipeline

-*-- Control
Strongly
Disagree
Time 1 Time 2
FIGURE 1 Mean cognitive distortion endorsement (+SE) for the bogus pipeline and control groups
Source: Gannon, T.A. (2006). Increasing honest responding on cognitive distortions in child molesters: The bogus pipeline procedure.
Journal ofInterpersonal Violence, 21(3), 358-375. © 2006 SAGE. Reprinted by permission of SAGE publications.
CONCLUSIONS
This imaginative empirical approach to this problem indicates that sexual offenders may to some extent be faking
the cognitive distortions they hold in order to justify their sexual offending. However, we must also note that (1) this.
study does involve some deception, so it is important to ensure that such studies comply with normally accepted
ethical guidelines (such as the BPS guidelines on ethical principles for conducting research with human participants,
http://www.bps.org.uk/), and (2) to ensure a proper balanced design, at Time 2 both experimental and control par-
_ ticipants should have been connected to the bogus pipeline, but only the experimental group told that it may detect
dishonesty - for instance, simply being connected to the bogus pipeline may itself influence responding.
rapists in particular — may have developed integrated cog- Implicit cognitive theories such as these can provide
nitive schemata that guide the offender’s interactions with the sex offender with a justification for both impulsive
their victims and justify their behaviour. Polaschek & and premeditated sexual offences, and can be used as a
Ward (2002) called these implicit theories. Offenders use way of denying both the significance of the offence and
cit theories In sexual offending, inte- these schemata as causal the offender’s responsibility for the offence.
1 cognitive schemas that guide sexual theories about themselves,
Jers’ interactions with their victims their victims and broader
istify their behaviour. Biological theories
categories of people (such As we mentioned earlier, the vast majority of those diag-
as women or children). Polaschek & Gannon (2004) iden- nosed with a paraphilia are male, and so it has been hypoth-
tified five types of implicit theory held by rapists. These esized that paraphilia is caused by abnormalities in male sex
included the beliefs that: hormones or by imbalances in those brain neurotransmit-
1. women are unknowable (i.e. ‘sexual encounters ters that control male sexual behaviour. For example,
will end up being adversarial because a woman’s androgens are the most important of the male hormones,
intentions are unknowable’), and it may be that unusual sexual behaviour, such as
impulsive sexual offending
2. women are sex objects (i.e. “women are
involving non-consenting androgens The most important of the
constantly sexually receptive, and so will enjoy male hormones. Unusual sexual behaviour,
others, may be due to imbal-
sex even when it is forced on them), such as impulsive sexual offending involv-
ances in these hormones. ing non-consenting others, may be due to
3. the male sex drive is uncontrollable (i.e. “a man’s sex However, there is relatively imbalancesinthese hormones.
levels will build up to a dangerous level if women do little ‘convincing evidence
not provide them with reasonable sexual access’), that abnormal androgen levels play a significant role in the
4. men are naturally dominant over women (i.e. ‘men development of paraphilic behaviour, although androgen
are more important in society than women, and a levels may help to maintain paraphilic behaviour once it has
woman should meet a man’s needs on demand’), and been acquired (Buvat, Lemaire & Ratajczyk, 1996), and
5. the world is a dangerous place (ie. ‘it is a dog-eat-dog anti-androgen drugs that reduce testosterone levels are reg-
world and a man needs to take what he can from it’). ularly used to reduce the sexual urges of those with
394 PSYCHOPATHOLOGY
: + aN
paraphilia disorders (Bradford & Pawlak, 1993; Jordan, 20th century when castration was a popular method of
Fromberger, Stolpmann & Muller, 2011). Abnormalities in treating paraphilias such as paedophilia. However, cas-
brain neurotransmitter metabolism — such as serotonin — tration was often reserved for repeated paraphilic behav-
have also been associated with paraphilia (Maes, De Vos, iour that was a criminal act and involved non-consenting
van Hunsel, van West et al., victims (such as paedophilia and, in earlier times, homo-
To read an article on the role of testos- 2001), although it is unclear sexual behaviour when this was deemed illegal). In many
terone in paraphilia by Jordan etal. go to
whether such abnormalit- of these cases, castration was seen more as a criminal
reading/ch11 ies are a cause of paraphi- punishment than a method of treatment, and its effec-
lic, or whether they are a tiveness was often doubted because up to 30 per cent of
consequence of acquiring paraphilic behaviour and the men treated in this way.were still capable of erections
anxiety and depression that is frequently comorbid with and ejaculation up to 10 years after surgery (Grubin &
paraphilia. Mason, 1997).
Finally, there is a small number of studies that have Treatment of paraphilic disorders is further compli-
identified abnormalities or deficits in brain functioning cated by several factors that make successful treatment
with paraphilias. First, abnormalities in the brain’s tem- difficult to achieve. First, many paraphilic disorders
poral lobe have been associated with a number of para- involve criminal behaviour (e.g. paedophilia, exhibi-
philias, including sadism, exhibitionism and paedophilia tionism and voyeurism), and this will often mean that
(Mason, 1997; Murphy, 1997; Mendez, Chow, Ringman, sufferers are reluctant to be wholly truthful about their
Twitchell & Hinkin, 2000). However, these may account activities or to honestly disclose their sexual activities.
for a minority of cases and appear to be related to dysfunc- Second, to many people with paraphilias, their sexual
tion in the temporal lobes leading to sexual disinhibition inclinations involve doing things that they particularly
of previously controlled behaviour. More recent stud- enjoy and which provide sexual satisfaction. If they
ies (albeit based on a small sample of participants) have have been indulging in these activities since early ado-
identified deficits in cognitive abilities in paedophiles that lescence, then their behaviours may seem to them as
are mediated by striato-thalamically controlled areas of normal as conventional sexual behaviour is to a non-
the frontal cortex (Tost, Vollmert, Brassen, Schmitt et al., sufferer (Laws & O’Donohue, 1997). Third, with many
2004). These areas are associated with neuropsychological of the paraphilias that involve a non-consenting victim,
functions that include response inhibition, working mem- the sufferer will often develop a rigid set of beliefs about
ory and cognitive flexibility, and deficits in these domains their activities that enables them to diffuse responsibility
are consistent with the finding that paedophiles frequently for their behaviour and to blame others (e.g. the victim)
have lower than expected IQ scores — often as much as two- (Abel, Gore, Holland, Camp et al., 1989; Shruti, Ward &
thirds of a standard deviation below the population mean Gannon, 2008). Because of this, the individual with a
(Cantor, Blanchard, Robichaud & Christensen, 2005). paraphilic disorder will often deny there is a problem
with their behaviour, lack motivation to change, and
Summary of the aetiology may even fake compliance with therapy simply because
of paraphilic disorders it may allow them to continue their paraphilic activi-
Research on the aetiology of paraphilic disorders has ties subsequently (e.g. if treatment is a requirement for
largely been restricted to understanding the causes of release from prison for sexual offences). And, fourth, as
those paraphilias that involve sexual offending (e.g. we mentioned earlier, paraphilic disorders are highly
paedophilia) — mainly because of the desire to understand comorbid with a number of other psychopatholgies,
and prevent criminal activity. However, the research that including substance abuse, anxiety, depression and per-
is available has identified some risk factors for paraphilia sonality disorders, and these comorbid disorders may
(e.g. hypersexuality, childhood abuse and neglect) and have to be tackled before treatment for the paraphilic
has also indicated that some paraphilias are associated disorder itself can be attempted.
with cognitive biases and dysfunctional beliefs that act We will continue this section by describing some of
to maintain sexual offending and serve to legitimize or the main treatment methods for paraphilic disorders.
justify sexual activities. However, many therapists currently use multifaceted
approaches to treatment and you should bear this in mind
when reviewing these specific treatment methods. For
11.3.3 The Treatment example, a multifaceted approach might involve (1) treat-
of Paraphilic Disorders ing the individual behavioural problem (e.g. shifting sexual
arousal and satisfaction away from specific or inappropri-
Attempts to treat paraphilic disorders have a long ate stimuli and associating it with more acceptable stim-
and complex history, dating back to the first half of the uli), (2) dealing with any dysfunctional beliefs or attitudes
CHAPTER 11 SEXUAL AND GENDER PROBLEMS 395,
that are maintaining the paraphilic behaviour (see Table Satiation is an important conditioning principle in
11.3), and (3) because many paraphilic disorders are asso- which the unconditioned stimulus (in this case sexual sat-
ciated with social skills deficits, the therapist may provide isfaction) comes to be ineffective because it is experi-
social skills training that will help the individual function enced in excess, and this leads to extinction of the sexual
more appropriately with consenting partners. urges that had been conditioned to stimuli or events
associated with that unconditioned stimulus (e.g. fet-
Behavioural techniques ishes). This has led to the development of masturbatory
In section 11.2.2 we discussed a number of early theo- satiation as a treatment for paraphilic disorders, in which
ries of paraphilic disorders that viewed these problems the client is asked to masturbate in the presence of arous-
as resulting from classical conditioning processes. In ing stimuli (e.g. women’s
these accounts, unconventional stimuli or events (such underwear if the client has masturbatory satiation A treatment for
as specific stimuli in fetishes, watching others naked in an underwear fetish) and paraphilias in which the client is asked to
masturbate in the presence ofarousing
voyeurism and suchlike) have become associated with to simultaneously verbal- stimuli.
sexual experiences, such as masturbation, during early ize his fantasies on a tape
adolescence. The assumption of behaviour therapy is recorder. Immediately after he has ejaculated, the client
that if these behaviours are learnt through conditioning, is instructed to masturbate again, no matter how una-
then they can also be ‘unlearnt’ through the use of basic roused or uninterested he feels, and continue for at least
conditioning procedures. Three types of technique will an hour (Marshall & Barbaree, 1978). After a number of
be described here. These are aversion therapy, masturba- these sessions, the client often reports that the stimuli
tory satiation and orgasmic reorientation. that previously sexually aroused them has become bor-
Aversion therapy is based on the assumption that inap- ing or even aversive (LoPiccolo, 1985). Latency to ejacu-
propriate stimuli have become positively associated with lation increases, and the number of sexual fantasies
sexual arousal and sexual satisfaction, and in order to elicited by the paraphilic stimulus significantly decreases
break this association, those stimuli must now be paired (Marshall & Lippens, 1977).
with negative or aversive experiences. For example, treat- An important task for anyone treating paraphilic dis-
ment of a fur fetish may involve pairing pictures of fur or orders is not only to suppress inappropriate or distressing
women wearing fur clothing with aversive experiences sexual activities (perhaps using the methods described
such as an electric shock or drug induced nausea. above) but also to replace these with acceptable sexual
Alternatively, a paedophile may be given electric shocks practices. Orgasmic reorientation is a treatment
when shown pictures of naked children. An avoidance method that aims at mak-
orgasmic reorientation A treatment
component can be added to this treatment in which the ing the client sexually method to replace inappropriate or
client can avoid the negative outcome by pressing a but- aroused by more conven- distressing sexual activities. It aims to
ton which changes the picture from their preferred sexual tional or acceptable stim- make the client sexually aroused by more
stimulus (e.g. fur, naked child) to an acceptable one (e.g. uli. This is a more explicit conventional or acceptable stimuli.
an attractive female). Aversion therapy can also be used in attempt to recondition sexual urges to more conven-
a covert conditioning form, where the client does not tional stimuli, and it can be used as an extension of the
actually experience the pairing of sexual stimuli with masturbatory satiation technique. For example, the cli-
aversive outcomes, but ent is first asked to masturbate while attending to con-
t conditioning Using the client's imagines these associations ventionally arousing stimuli (such as pictures of nude
/ to imagine events in order to condi-
during controlled treat- females), but if they begin to feel bored or lose their erec-
ssociations between events.
ment sessions. For exam- tion, they are asked to switch to attending to pictures
ple, the client may be asked to imagine one of their sexual associated with their paraphilia. As soon as they feel sex-
fantasies and then to vividly imagine a highly aversive or ually aroused again, they must switch back to attending
negative outcome, such as his wife finding him indulging to the conventional stimulus, and so on. Although there
in his paraphilic sexual activities, or being arrested are numerous individual case studies suggesting that
(Barlow, 1993). Aversion therapy has been used to treat some variations of orgasmic reorientation might be suc-
fetishes, transvestism, exhibitionism and paedophilia, and cessful in helping clients to control their paraphilic
there is some evidence that it may have some treatment behaviour, there are no controlled outcome studies avail-
benefit when combined with other approaches such as able to evaluate the success of this method over the
social skills training (Marks, Gelder & Bancroft, 1970). longer term (Laws & Marshall, 1991).
However, as we have reported elsewhere in this book,
aversion therapy rarely achieves long-term success when Cognitive treatment
used alone — and high rates of relapse are associated with We saw in the section on aetiology that dysfunctional
the sole use of aversion therapy (Wilson, 1978). beliefs play a central role in developing and maintaining a
number of paraphilic disorders — especially those para-

(] Treatment group
philias that involve sexual offending with non-consenting
Control group
victims. Cognitive treatment for these paraphilias often
involves cognitive behaviour therapy (CBT), which is
adapted to help the client
cognitive treatment Treatment approach
to identify dysfunctional
intended to help the client identify and Recidivism
(%)
challenge dysfunctional beliefs.
beliefs, to challenge these
beliefs and then replace
them with functional and adaptive beliefs about sexual
behaviour and sexual partners. Table 11.3 shows a list of Sexual offences. All offences
the kinds of dysfunctional beliefs held by paedophiles and
FIGURE 11.3 Effect of sex offender treatment
exhibitionists. These beliefs act as justifications for sexual
Integrated treatment programmes for medium to high-risk
offending and are part of a belief system that effectively
sex offenders in prisons (such as the Core SOTP scheme) are help-
‘gives them permission’ to carry out their offences.
ful in reducing future reconviction rates by up to 3.4 per cent.
Challenging dysfunctional beliefs includes: Source: Based on Schmucker & Losel (2008).
1. demonstrating to clients that their dysfunctional

beliefs are based on their deviant sexual behaviour of sexual offenders. Relapse- relapse-prevention training In —
rather than being justifiable reasons for the prevention training consists paraphilias, a treatment which consists
behaviour, primarily of helping clientsto identify
primarily of helping clients
circumstances, situations, moods and |tyE
2. helping clients to see how they might to identify circumstances, of thoughts that might trigger pore
misinterpret the behaviour of their victims to be situations, moods and types behaviour. fu
consistent with their dysfunctional beliefs, and of thoughts that might trig-
3. discussing dysfunctional beliefs within existing ger paraphilic behaviour. For example, a mood trigger
individual and broader social norms in order might be a period of stress, anxiety or alcohol abuse that
to demonstrate that the client’s beliefs are not precipitates sexual offending, or close contact with children
shared by most other members of society (e.g. to that might activate paedophile behaviours. Sexual offend-
establish that women are not merely objects for ers are also taught to identify the distorted cognitions that
sexual gratification). might lead to offending (e.g. ‘that child is running around
half dressed, so she must be interested in sex’) and are
The UK Home Office has developed a number of inte- taught self-management skills that will enable them to
grated treatments for sexual offenders (Ministry of Justice, interrupt sequences of thoughts that lead to offending or
2010) and Figure 11.3 shows the most recent data, which to avoid situations that place them at risk (e.g. in the case
indicate that the reconviction rate for treated sex offend- of paedophilia, to avoid taking jobs that involve working
ers was up to 3.4 per cent lower than for untreated indi- with or near children, or living near a school). Relapse pre-
viduals (Schmucker ®& Losel, 2008). One integrated vention programmes have been shown to be successful in
treatment for sexual offenders is called the Sex Offender reducing subsequent offending (Marshall & Pithers, 1994)
Treatment Programme (SOTP) and this extensively and are important components of many national treat-
adopts CBT methods for treating imprisoned sex ment programmes for sexual offenders.
offenders (Beech, Fisher & Beckett, 1999), targeting
risk factors for reoffending Hormonal and drug treatments
Sex Offender Treatment Programme
(SOTP) An integrated treatment for sexual
such as sexual preoccupa- As we mentioned earlier, castration was the radical form of
offenders which adopts CBT methods for tion, sexual preferences for treatment for dangerous sex offenders during periods of the
treating imprisoned sex offenders and children, offence-support- 20th century — especially in parts of Europe, and was often
targets risk factors for reoffending such as
ing attitudes, lack of emo- offered as an alternative to imprisonment (Abel, Osborn,
sexual preoccupation, sexual preferences
for children, offence-supporting attitudes, tional intimacy with adults, Anthony & Gardos, 1992). The aim here was to curb the
lack of emotional intimacy with adults, impulsive lifestyle, poor sexual appetite of persistent offenders who were unable to
impulsive lifestyle, poor coping skills and coping skills and problem- respond to any other form of treatment. An arguably
poor problem-solving abilities.
solving abilities. more acceptable way of curbing sexual appetite in
those paraphilics who persistently offend is to use anti-
Relapse-prevention training androgen drugs that significantly decrease the levels
Rather than focusing on an all-embracing ‘cure’ for para-
of male hormones such anti-androgen drugs A group of drugs.
philias, many forms of treatment focus specifically on as testosterone. Currently that significantly decrease the levels of
relapse prevention, and this is especially relevant in the case used testosterone- -lowering male hormones such as testosterone.
oxyprogesterone acetate (MPA) An drugs include medroxypro- Summar y of the treatment

ndrogen, testosterone-lowering gesterone acetate (MPA) of paraphilic disorders
and cyproterone acetate The treatment of paraphilic disorders is generally a dif-
yterone acetate (CPA) An anti- (CPA), and both have been ficult process, not least because many diagnosed with
en, testosterone-lowering drug. shown to reduce the fre- paraphilia will also be sexual offenders (e.g. paedo-
quency of erection and ejac- philes, exhibitionists, voyeurs), and this can lead clients
ulation, inhibit sexual arousal, and to reduce the rate of to be less than truthful about their sexual activities and
reoffending in sexual offenders (Hall, 1995; Bradford & approach treatment with a relatively ingrained set of
Pawlak, 1993; Maletzky & Field, 2003). However, such a beliefs about their activities. Paraphilic disorders are
form of treatment tends to depend very much on the com- also highly comorbid with other psychopathologies —
pliance of the client or offender in taking such drugs regu- such as substance abuse, anxiety, depression and person-
larly. This is particularly important because evidence ality disorders — and this makes treatment additionally
suggests that offenders will often revert to paraphilic behav- complex. Most programmes of treatment adopt a mul-
iour when they cease taking the drug — even after many tifaceted approach that can involve behaviour therapy
years of medication (Berlin & Meinecke, 1981). techniques to address the specific sexual behaviour
An alternative to anti-androgens is the use of antide- problem (e.g. aversion therapy, masturbatory satiation,
pressant drugs such as SSRIs (e.g. fluoxetine) and there orgasmic reorientation) and use CBT to deal with the
is some modest evidence that such drugs will help the dysfunctional beliefs that underlie many paraphilias,
individual control sexual urges — especially if depres- and sexual offending in particular. Finally, social skills
sion is a trigger for indulging in paraphilic behaviour training and relapse-prevention procedures can be used
(Kafka & Hennen, 2000). However, despite encourag- in an attempt to ensure that the individual is able to
ing short-term effects of treatment with SSRIs, there cope with the demands of normal sexual relationships
are as yet no long-term follow-up studies (Maletzky & and to identify situations and circumstances that might
Field, 2003). trigger relapse.
SELF-TEST QUESTIONS
11.3.1 The Diagnosis and Description of Paraphilic Disorders
® How are paraphilic disorders defined in DSM-5?
© What are the main categories of paraphilic disorders described in DSM-5?
° Can you differentiate between those paraphilic disorders that can be labelled ‘victimless’
and those that in many societies
would be labelled ‘sexual offences’?
® Can you list the main diagnostic criteria for fetishistic disorder, transvestic disorder, voyeuristic disorder, frotteuristic disor-
der, paedophilic disorder, sexual masochistic disorder and sexual sadism disorder?

© Can you list some of the main risk factors for paraphilic disorders?
© Paraphilic disorders are highly comorbid with which other psychopathologies?
® What is castration anxiety and how is it used by psychoanalytic theorists to explain paraphilic disorders?
© Howis associative learning thought to be involved in the acquisition of some paraphilic disorders?
e |s childhood abuse and neglect an important factor in the development of paraphilic disorders?
° What are cognitive distortions and how are they used by sexual offenders to justify their actions?
e |s there any substantial evidence that sex hormone imbalances are involved in the development of paraphilic disorders?
e What brain area abnormalities have been associated with paraphilic disorders and how might they cause paraphilic
behaviour?
11.3.3. The Treatment of Paraphilic Disorders

e Why are paraphilic disorders so difficult to treat?
® How have aversion therapy and covert conditioning been utilized to treat paraphilic disorders?
x
* What are masturbatory satiation and orgasmic reorientation techniques, and is there any evidence that they can be suc-
cessfully used to treat paraphilic disorders?
* How has CBT been adapted to help treat paraphilic disorders?
* Can you name the basic principles and stages of the UK SOTP initiative used to treat sexual offenders?
® What are the main drug treatments that have been used to treat paraphilic disorders, and what is the evidence that such
treatments prevent relapse?
® Whatare the main principles of relapse-prevention treatments for paraphilic disorders?
SECTION SUMMARY
11.3. PARAPHILIC DISORDERS
When high rates of sexual behaviour are channelled into unusual or very specific sexual activities, these are known as para-
philias. They range from sexual activities that are victimless (e.g. fetishes and transvestic fetishism) to others that are defined
in law as sexual offences (e.g. paedophilia, exhibitionism, voyeurism). Many paraphilias are diagnosed on the basis of unusual,
recurrent sexual urges that cause personal distress or affect social and occupational functioning (e.g. fetishism, transvestic
fetishism), but others do not require that the individual experiences distress — merely that they have acted on their urges with
non-consenting victims (e.g. paedophilic disorder, exhibitionistic disorder, voyeuristic disorder). Research on the aetiology of
paraphilic disorders has identified some risk factors (e.g. hypersexuality, childhood abuse and neglect) and has also indicated
that dysfunctional beliefs may play an important role in maintaining those paraphilic disorders that are linked to sexual offend-
ing (e.g. paedophilia, exhibitionism). Finally, treatments for paraphilic disorders are still relatively underdeveloped, and adopt
behaviour therapy or CBT techniques to change dysfunctional behaviour and cognitions. Relapse prevention is an important
component of treatment for many paraphilic disorders — especially those related to sexual offending.
The key points are:
¢ Paraphilic disorders tend to be associated with problematic high-frequency sexual behaviours or unusual sexual urges and
activities that are often directed at inappropriate targets.
© Some paraphilic disorders are victimless (e.g. fetishistic disorder, transvestic disorder) while others will be defined in law as
sexual offences (e.g. exhibitionistic disorder, voyeuristic disorder, frotteuristic disorder, paedophilic disorders).
11.3.1 The Diagnosis and Description of Paraphilic Disorder

e Fetishitic disorder involves sexually arousing fantasies and urges directed at non-animate objects.
¢ Transvestic disorder is when a heterosexual male experiences sexual arousal from cross-dressing in women’s clothing.
¢ Sexual masochism is when an individual gains sexual arousal and satisfaction from being humiliated.
¢ Sexual sadism is when a person gains sexual arousal and satisfaction from the psychological or physical suffering of others.
¢ Exhibitionistic disorder involves sexual fantasies about exposing the genitalia to a stranger.
° Voyeuristic disorder involves experiencing intense sexually arousing fantasies or urges to watch an unsuspecting person
who is naked, in the process of undressing or engaging in sexual activity.
° Frotteuristic disorder involves recurrent sexual urges to touch and rub up against other non-consenting people — usually in
crowded places.
¢ Paedophilic disorder is defined as sexual attraction towards prepubescent children, normally 13 years or younger.
¢ Some paedophiles limit their activities to their immediate family (e.g. children, step-children, nieces) and incest is listed as
a specific sub-type of paedophilia in DSM-5.
° Non-incestuous paedophiles will normally only become sexually aroused by sexually immature children, and will often
develop elaborate ways ofgaining access to children through ‘grooming’ activities.
° Sexual masochism disorder is when an individual gains sexual arousal and satisfaction from being humiliated, and this
causes the individual significant distress.
CHAPTER11 SEXUAL AND GENDER PROBLEMS 399°
° Sexual sadism disorder is when a person gains sexual arousal and satisfaction from the psychological or physical suffering
of others, and this diagnosis is given if the symptoms cause the individual significant distress or if the person acts on the
impulses with a non-consenting person.

Most of the DSM-5 diagnosable paraphilic disorders are male activities, and many are also sexual offences (e.g. paedophilic
disorder, exhibitionistic disorder).
Both hypersexuality and childhood abuse and neglect are risk factors for paraphilic disorders.
Psychodynamic theory views paraphilic disorders either as (1) defensive reactions that are attempting to protect the ego
from repressed fears, or (2) as representing fixation at a pregenital stage of development (e.g. the Oedipal stage).
Many paraphilic disorders develop during early adolescence, and inappropriate sexual urges may have been developed
through the association of sexual activities such as masturbation with inappropriate stimuli or activities (the process of
classical conditioning).
The level of childhood abuse experienced by sexual offenders is almost double the level found in the general population.
However, childhood abuse and neglect is not a sufficient condition for committing a sexual offence, because it is reported
by only 30 per cent of sexual offenders.
Sexual offenders, including paedophiles, develop a set of beliefs or cognitive distortions that serve to legitimize or justify
their sexual activities.
Even though anti-androgen drugs are regularly used to treat some paraphilic disorders, there is little convincing evidence
that abnormal androgen levels play a significant role in the development of paraphilic behaviour.
11.3.3 The Treatment of Paraphilic Disorders

Many paraphilic disorders are difficult to treat because (1) they involve criminal behaviour that will make individuals reluc-
tant to be truthful about their activities, and (2) paraphilic disorders are highly comorbid with other psychiatric disorders,
which significantly complicates treatment.
Behavioural treatments for paraphilic disorders include aversion therapy, covert conditioning, masturbatory satiation, and
orgasmic reorientation.
CBT has been adapted to treat paraphilic disorders (especially those involving sexual offending) by addressing the dysfunc-
tional beliefs or cognitive distortions that many sexual offenders develop to legitimize their behaviour.
Anti-androgen drug treatments for paraphilic disorders include medroxyprogesterone acetate (MPA) and cyproterone acetate
(CPA) which reduce the frequency of erection and inhibit sexual arousal.
Because many paraphilic disorders are also sexual offences, relapse-prevention training helps clients to identify circum-
stances that may trigger paraphilic behaviour.
Once eceererernetreseneeen cess seen sense eneee eee Hneesee sense seebesOHSEEHeH sees enssenssnssenesenessnerssneatvensensreees
This disparity can cause gender dysphoria A gender identity

them significant distress disorder in which an individual has a sense
or impairment. In such of gender that is opposite to his or her
biological sex.
Most of us take our sexual identity for granted. We do not circumstances, the individ-
question that we are the sex we were born as, and we ual may see themselves biologically developing as a
find that behaving as either man or a woman (e.g. growing a beard, or developing
For a video on gender dysphoria go to a male or a female is natu- breasts), but cannot shake off the belief that underneath
video/ch11
ral and effortless. Our the physical appearance they are of the opposite gender.
gender identity seems to This may lead them to cross-dress or even seek
have been determined for surgery or take hormones to develop physical features
ar identity The internal sense
ng either male or female. Usually as long as we have lived, of the opposite sex. When this kind of gender
uent with biological gender, but not and we think, act and dress dysphoria becomes problematic and causes significant
5, as in gender dysphoria. accordingly. However, some personal distress and social and occupational impair-
individuals develop a sense of gender dysphoria (unhap- ment, then it may be diagnosed as gender dysphoria
piness with their own gender) and feel that their gender (previously known as ‘gender identity disorder’ in
is the opposite of the biological sex they were born with. DSM-IV-TR).
Forms of gender dysphoria can also be found in child- per cent of boys explicitly express a desire to be of the
hood and are associated with cross-gender behaviour that opposite gender (Zucker & Bradley, 1995), but we must
can be easily recognized by parents and carers (Green & remember that the significant majority of these do not
Blanchard, 1995). These include playing with toys typi- grow up to be adults with diagnosable gender dysphoria.
cally enjoyed by the opposite sex (e.g. boys playing with There is very little epidemiological evidence available
dolls), dressing in clothes of the opposite sex, and prefer- on which to base the prevalence rates of gender dys-
ring friends and playmates of the opposite sex. phoria. However, DSM-5 estimates that the prevalence
rate of gender dysphoria for natal adult males is around
0.005—0.014% and for natal females from 0.002-0.003%
11.4.1 Diagnosis and Description (DSM-5, p.454). Estimates from some European studies
suggest that roughly 1 per 30,000 adult males (0.003%)
of Gender Dysphoria and 1 per 100,000 adult females (0.001%) seek gender
The main components of the diagnosis are that (1) the reassignment surgery. Gender dysphoria can also be
individual exhibits a strong and persistent cross-gender comorbid with a number of other psychiatric diagno-
identification, and that this is not simply because of the ses, especially anxiety, depression and impulse-control
cultural advantages that might be associated with being disorders. Studies suggest that 71 per cent of a sample
the opposite sex, and (2) there must be clear evidence with gender dysphoria fulfilled the criteria for a comor-
of clinically significant distress or impairment caused by bid current and/or lifetime psychiatric diagnosis (Hepp,
their gender dysphoria. Kraemer, Schnyder, Miller & Delsignore, 2005), and
Individuals with a diagnosis of gender dysphoria usu- 17.8 per cent of individuals with the DSM-IV-TR diag-
ally exhibit a strong preoccupation with their wish to live nosis of gender identity disorder have also been found
as a member of the opposite sex and this may lead them to have another comorbid psychiatric disorder (Terada,
to acquire the physical appearance of a member of the Matsumoto, Sato, Okabe et al., 2012).
opposite sex (by cross-dressing or adopting manner-
isms typical of the opposite sex). For example, men may
undergo electrolysis to remove body hair or submit them- 11.4.2 The Aetiology
selves to hormone treatments to develop female physical
of Gender Dysphoria
characteristics such as breasts. Those who have strong
feelings of gender dysphoria may have problematic sex Gender dysphoria is a problem that persists for many
lives. For example, men with gender dysphoria who are individuals over a substantial period of their lives, sug-
married may frequently fantasise about being a lesbian gesting the causes of these problems are not trivial.
lover when they have sex with their wife. Those with However, there is relatively little research on the aetiol-
same-sex partners often prevent their partner from seeing ogy of gender dysphoria. Some risk factors have been
or touching their genitals. Client’s Perspective 11.1 pro- identified, with males suffering gender dysphoria report-
vides a personal account given by one man who had had ing distant relationships with their fathers, and females
feelings of gender dysphoria from a very early age, and often reporting a history of childhood abuse (Bradley &
how — despite having what appeared to others to be a suc- Zucker, 1997). However, such childhood experiences are
cessful marriage, family and business — these feelings were by no means universal across individuals with gender
persistent enough to encourage him to seek treatment. In dysphoria. Neither can we assume that gender dyspho-
many cases the feelings of gender dysphoria are so strong ria results from parents and family reinforcing children
that they drive the individual to seek gender reassignment during childhood for behaving in cross-gender ways.
surgery which culminates in changing the individual physi- For example, when a child dresses up in clothes of the
cally into their preferred gender (see section 11.4.3). opposite sex, they may be rewarded by the attention they
A diagnosis of gender dysphoria can also be given receive, but it is relatively rare for children treated in this
in children. In boys, this may manifest by adopting way to grow into adults with gender dysphoria (Zucker,
female roles during play (such as playing with dolls, tak- Finegan, Deering & Bradley, 1984). Similarly, neither do
ing ‘mother’ roles, avoiding rough-and-tumble play), the prenatal hopes and expectations of a parent appear to
by exhibiting disgust at their penis, or adopting female influence the development of gender dysphoria. Zucker,
activities such as always insisting on sitting on the toi- Wild, Bradley & Lowry (1993) found that mothers of
let when urinating. Girls may exhibit strong aversion to boys with feminine characteristics were just as likely to
their parents’ gender role expectations of them, avoid have wanted a boy as a girl. These findings suggest that
wearing dresses, insist on having short hair, and may also evidence that social development may play a role in the
prefer male playmates and contact sports such as football development of gender dysphoria is equivocal. Let us
and rugby. In childhood, about 3 per cent of girls and 1 now turn our attention to biological factors.
&
CHAPTER11 SEXUAL AND GENDER PROBLEMS SS AOT

GENDER DYSPHORIA
On 1 June 1994, when this journal began, | was living bolder as | gained confidence in my ability to ‘pass’ with-
entirely as Dan - father, husband and small businessman. out being ‘read’
| had been married for 13 years to Alice, with a 10-year-old Throughout this period, | was constantly ‘purging’
son and a 6-year-old daughter. My family life was good, myself of this ‘awful’ desire. Full of guilt | would throw
my business growing, my future bright, but still some- away all my pills, wigs, clothes and any other female
thing was missing. accoutrements, only to be driven to rebuild my collection
| had first felt ‘different’ in infant school, where all the scant days later.
other boys seemed to know instinctively how to act, but Finally, | came to the decision that this secret side, if
| had to struggle to learn the male role by rote: it did not not dealt with openly, would lead to self-destruction and
come naturally. |never considered the possibility |had the the loss of not only my self-respect, but the love of those |
instincts of afemale; | simply thought | had none at all. loved. So, at the end of July 1994, | mustered the courage
By age 7, | was regularly sneaking off to dress in the to calla gender‘hotline’ and get a referral to a doctor who
girls’ clothes my mother brought in as part of her short- provided hormone therapy to transsexuals.
lived ironing business. This was well before puberty and
was not an erotic experience, but rather a feeling of com-
pleteness and contentment. Clinical Commentary
Throughout my teenage years, the need to dress as Dan’s case is typical of a majority of men who
a female came and went in waves, sometimes intense, suffer gender dysphoria. Even though his family
sometimes absent for years at a time. life is settled and happy, and his financial situa-
| was non-agressive in school, both in sports and dat- tion is secure and promising, he is still unable to
ing, and excelled at neither. My only erotic interests were reconcile his gender identity with his biological
not in what | could do to or with a woman, but what it sex, and the urge to act and dress as a woman
would be like to be one. becomes overwhelming in adult life. His feelings
|married asa virgin in 1981,and the longings to be female of gender dysphoria began in childhood when
vanished more than they were there. But, gradually, as | pro- playing the male role did not come naturally.
gressed through adult life, the waves became stronger and However, it is unusual for someone with child-
more frequent. Only twice in my life (both times in my early hood gender dysphoria to carry those feelings
teen years) had | ventured out as a female, both with such into full adulthood as Dan did. His attempts to
tension from fear of discovery that | did not attempt this cross-dress and take on female gender identity
again until three years before this journal began. at first made him feel guilty and finally led him
Suddenly, the need to move in society as a woman to take the decision to make a full transition to
became overwhelming and within 2 months | had made becoming a woman.
nearly a dozen outings, tentative at first, then growing
Biological factors One study has suggested that gender dysphoria may
One view is that gender identity may be influenced by be associated with abnormalities in those areas of the
hormonal factors. In particular, when mothers have brain that regulate sexual behaviour. The bed nucleus of
taken sex hormones during pregnancy (e.g. to prevent the stria terminalis (BSTc) is a brain area that is essential
uterine bleeding), the behaviour of their offspring has for sexual behaviour and is normally larger in males
subsequently been affected in ways consistent with the than in females. However, in autopsies carried out on six
type of hormone used. When pregnant mothers have men who had undergone gender reassignment surgery
taken medications related to male sex hormones, the to become women, Zhou, Hofman, Gooren & Swaab
early behaviour of girls is often more tomboyish than (1995) found a female-sized BSTc in all cases. They
in mothers who had not taken such drugs (Ehrhardt & concluded that males with gender dysphoria appear to
Money, 1967). Similarly, the male offspring of mothers possess female brain structures that may either have a
who took female hormones during pregnancy often dis- genetic origin or may have been influenced by abnor-
play less athletic behaviour than boys whose mothers did malities in early brain development. However, these
not take such hormones (Yalom, Green & Fisk, 1973). early findings have not received convincing support in
B02 aes PSYCHOPATHOLOGY
recent fMRI studies of the brains of male-to-female psychologically adjusted to becoming someone of the
transsexuals, where no evidence was found that the opposite biological sex. The progressive stages of gen-
brains of male-to-female transsexuals were ‘feminized’ der reassignment surgery start with at least 3 months of
(Savic & Arver, 2011). counselling or psychotherapy to ensure the client fully
There have been relatively few studies of the herit- understands the process of treatment and to ensure
ability of gender dysphoria, but a well-controlled child they are fully committed to it. This is usually followed
and adolescent twin sample study by Coolidge, Thede & by hormone treatment to initiate physical changes such
Young (2000) suggested that gender dysphoria is highly as reducing body hair and developing breasts in those
heritable. While this implies a genetic component to men seeking to become biological women, and beard
gender dysphoria, it is not clear from these studies how growth and muscle development in those women seek-
that genetic component is either transmitted or through ing to become men. The next stage is a crucial real-life
what aspect of gender dysphoria or its related psycho- test in which the client must live as the preferred gender
pathology it is manifested. Genetic transmission may for at least 1 year, dressing and presenting themselves as
be through the influence of genes on the development the preferred sex in a way that will lead them to under-
of brain substrates relevant to gender development and stand what this means over the longer term. If the first
identity, or to their effect on hormonal action, but to three stages are completed successfully, the client may
date no convincing candidate genes have been identified then proceed to the fourth stage — surgery, where their
(Klink & Den Heijer, 2014). genitalia are surgically altered to resemble those of
their preferred biological sex.
Despite the radical nature of gender reassignment
therapy, outcome studies tend to indicate that a large
11.4.3 The Treatment majority of clients who undergo the full treatment
of Gender Dysphoria are generally satisfied with the outcome and express
no regrets about their decision (Smith, van Goozen &
Individuals diagnosed with gender dysphoria feel that Cohen-Kettenis, 2001). In a Dutch study of 188 gender
they have a sense of gender that is opposite to the bio- dysphoria sufferers who completed gender reassign-
logical sex they were born with, and gender dysphoria ment surgery, only two expressed any regret at their
involves profound feelings of conflict between gender decision. More importantly, the study found that such
identity and biological sex. There are two important procedures tended to significantly reduce gender dys-
ways in which this imbalance can be corrected — either phoria, and enabled clients to function well psycho-
by (1) attempting to change an individual’s biological sex logically, socially and sexually (Smith, van Goozen,
to be congruent with their feelings of gender identity, or Kuiper & Cohen-Kettenis, 2005). Nevertheless, while
(2) using psychological methods to change their gender such studies seem to indicate that gender reassign-
identity to be congruent with their biological sex. Most ment surgery has a largely positive outcome, we must
individuals with gender dysphoria are usually adamant still be cautious about it as a treatment that solves all
that their biological sex is ‘wrong’ and opt for a the problems associated with gender dysphoria. First,
process that ends in gender reassignment surgery — while many suffering gender dysphoria do go through
a process that involves progressive hormone treatment all four stages of the treatment, a substantial minority
and eventually SuTgeTY drop out of gender reassignment schemes at an early
gender reassignment surgery The pro- to change their basic bio- stage. Smith, van Goozen, Kuiper & Cohen-Kettenis
cess of changing biological sex which ends logical features to be Se : ‘ E
in changing the person's basic biological (2005) report that of 325 individuals who applied for
congruent with their gen-
features to be congruent with his or her gender reassignment surgery, 103 dropped out before
gender identity. der identity. We will dis- starting hormone treatment, and a further 34 dropped
cuss this radical treatment out before surgery (a drop-out rate of 42 per cent).
option first and then look at more psychologically ori-
Indeed, many decide not to continue with the treat-
ented attempts to modify gender identity itself.
ment during the real-life test, when they discover
that the realities of living as someone of the oppo-
Gender reassignment surgery site biological sex are not what they imagined. The
This involves a relatively irreversible process of chang- longer the client is kept in the real-life test phase of
ing the body’s physical characteristics to be consist- the process, the greater the likelihood of a successful
ent with the individual’s feelings of gender. Because it outcome (Botzer & Vehrs, 1997). But if the individual
involves major changes to the person’s anatomy, it is with gender dysphoria already has significant comor-
a treatment option that is approached in a graduated bid psychological problems, then these are unlikely
way in order to ensure that the client is fully aware to be alleviated by gender reassignment surgery
of the long-term implications of the treatment and is (Botzer & Vehrs, 1997).
CHAPTER11 SEXUAL AND GENDER PROBLEMS 403.
DSM-5 SUMMARY TABLE 11.16 Criteria for Gender Dysphoria For example, if an individual feels they are basically
in Adolescents and Adults female but are biologically male, one approach is to
¢ Amarked discrepancy between an individual's expressed use behavioural and cognitive techniques to try to
gender and assigned gender, over a period of at least change their female thoughts and cognitions to male
6 months, as expressed by at least two of the following: ones. However, a vast majority of those with gen-
e Adiscrepancy between expressed gender and sex
der dysphoria approach treatment adamant that it is
characteristics. their biological sex that is wrong and not their gen-
der identity beliefs, so gender identity change proce-
e Anintense desire to be without existing sex charac-
dures tend to be used relatively infrequently. In one
teristics due to a discrepancy between expressed and
assigned gender. early study, Barlow, Reynolds & Agras (1973) report
using behaviour therapy techniques with a 17-year-
e An intense desire for the sex characteristics of another
old gender dysphoric male who wanted to change his
gender or to be treated as another gender.
gender identity rather than his biological sex. They
e An intense belief that one has the typical feelings and used operant reinforcement methods to shape up
reactions of another gender. male-related mannerisms and behaviours, and also
e Symptoms cause significant distress or impairment in used classical conditioning techniques such as aver-
performing major occupational, social or interpersonal life sion therapy to reduce the sexual attractiveness of
functions. men. Even though these techniques were primar-
ily behaviour-oriented (rather than using methods
aimed at directly changing cognitions and beliefs),
Psychological treatments they did appear to have some success — at a 5-year
An alternative approach to the treatment of gen- follow-up the client had acquired a male identity and
der dysphoria is to try to modify the client’s gender sexually preferred women to men (Barlow, Abel &
identity to be consistent with their biological sex. Blanchard, 1979).

GENDER REASSIGNMENT SURGERY
WHAT DOES MALE-TO-FEMALE GENDER and blood vessels remain largely intact. Tissue from the
REASSIGNMENT INVOLVE? scrotum is then used to create the labia, and the urethra is
shortened and repositioned appropriately.
For aman wishing to become a woman, treatment would
mean taking female hormones for at least 1 year before WHAT DOES FEMALE-TO-MALE GENDER
any irreversible surgery would take place. The hormones REASSIGNMENT INVOLVE?
reduce body hair, cause breast development and gener-
ally make the body shape and skin texture more feminine. For a woman wanting to become a man, taking the male
The person would also have to live as a woman, full- hormone testosterone leads to beard growth and mus-
time, for a minimum of 1 year before any surgery can be cle development. On the whole, these changes can’t be
authorized. During this period, some transsexuals may reversed later. As early as 6 months into this programme,
choose to have facial hair removed by electrolysis, it may be possible to have a mastectomy (breast removal).
may undergo cosmetic surgery to make their face more This makes it much easier for the person to appear as a
feminine or learn to raise the pitch of their voice. When a man in public. After at least a year of hormone treatment,
patient feels ready, they may apply for medical approval the ovaries and uterus are removed.
of reassignment surgery. The clinical team will review the For many female-to-male transsexuals, this is as far as
patient’s progress to see how well they’ve adapted to they will go with surgery. Going further is more complex,
their new role, and depending on the results of this evalu- costly and difficult to achieve. For those who do continue,
ation, surgery may then be approved. phalloplasty (penis construction) and testicle implants are
Gender reassignment involves major surgery. Under available. It is also possible to create a male urethra and to
general anaesthetic, the testicles and erectile tissue of move the clitoris to the head of the penis.
the penis are removed. An artificial vagina is then created
and lined with the skin of the penis, where the nerves Source: Adapted from http://www.mind.org.uk/.
404 PSYCHOPATHOLOGY
: , %
Studies such as this suggest that a gender identity that outlined at the beginning of this section, the vast major-
is inconsistent with biological sex might be successfully ity of individuals with gender dysphoria are adamant
changed, and supplementing behaviour therapy meth- that it is their biological sex that they want to change
ods with CBT approaches designed to directly challenge and not their gender identity — so the opportunities to
and change dysphoric gender identity beliefs may make develop more integrated therapies for gender identity
such treatments even more effective. However, as we may be limited.
SELF-TEST QUESTIONS :

° What is gender dysphoria?
e What are the main DSM-5 diagnostic criteria for gender dysphoria?
© What is the evidence that gender dysphoria exhibits in children?

® Is there any evidence that hormonal imbalances might play a role in the development of gender dysphoria?
® What is the evidence that abnormalities in certain brain areas may be associated with gender dysphoria?
© What is the evidence that there is an inherited component to gender dysphoria?

° What is gender reassignment surgery, and what are the progressive stages of this treatment?
e What is the evidence that gender reassignment surgery is a successful treatment for gender dysphoria?
e What techniques are available for changing a client’s gender identity (rather than their biological sex)?
SECTION SUMMARY
11.4 GENDER DYSPHORIA
Many individuals have a sense of gender dysphoria, in which they feel they have a gender identity that is incompatible with
their biological sex. When this gender dysphoria causes significant distress and affects social, occupational and other impor-
tant areas of functioning, DSM-5 provides a series of criteria for the diagnosis of gender dysphoria. Only a modest amount of
research is available on the aetiology of gender dysphoria but there is a known inherited element to the disorder, although it is
far from clear how this inherited component is transmitted and manifested. Treatment for gender dysphoria is largely through
a structured procedure ending in gender reassignment surgery, which attempts to alter the individual’s biological sex. There
are a few successful attempts in the literature to change gender identity beliefs, but gender dysphoria sufferers usually prefer
to change their biological sex rather than their gender identity beliefs.
The key points are:
* Some people develop a sense of gender dysphoria in which they feel that their gender is the opposite to their biological sex.
® Gender dysphoria is found in both adults and children.

¢ Individuals with gender dysphoria exhibit a strong desire to live as a member of the opposite biological sex, and this may
lead them to acquire the physical appearance and mannerisms of the opposite sex. :
¢ Prevalence rates for gender dysphoria are estimated to be around 0.005-0.014% in natal males and 0.002-0.003% in natal
females.
CHAPTER 11 SEXUAL AND GENDER PROBLEMS 405,

* Gender dysphoria does appear to be highly heritable, but it not clear yet how the genetic component is either transmitted
or how it is manifested.

¢ Many individuals with gender dysphoria want to resolve their conflict between gender identity and biological sex by
changing their biological sex rather than vice versa.
¢ Changing biological sex is usually undertaken through a process of gender reassignment surgery, which ends in changing
the person's basic biological features to be congruent with their gender identity.
e While the vast majority of those who complete gender reassignment surgery are satisfied with the outcome, up to 42 per
cent of those who apply for gender reassignment surgery drop out before completing the treatment.
ee rr teri t titer iirriret rrr errr rer errr Terre Ter errr rrr rrr rr rrr rrr
11.5 SEXUAL AND GENDER paedophilic disorder, exhibitionistic

disorder). Some of these activities
disorder, voyeuristic
acquire their status
PROBLEMS REVIEWED as psychopathologies because they are associated with
personal distress or impairment of normal daily activi-
ties (e.g. fetishistic disorders). Others are not necessar-
Sexual behaviour is usually a central feature of our psy- ily associated with personal distress but are diagnosed
chology. A satisfying sex life is an important contributor as disorders because they are activities directed at non-
to quality of life, and our sexual urges and attractions consenting others. As such, these latter examples tend
can determine how we view ourselves and construct our to represent criminal behaviours as well as diagnosable
self-identity. This being the case, it is not surprising that psychopathologies (e.g. paedophilic disorder, exhibition-
when we encounter problems related to sexual activity istic disorder). Much of the research on the aetiology of
it can be an important source of psychological distress. paraphilic disorders has centred on those disorders that
Sexual dysfunctions represent a set of diagnosable represent criminal activities or sexual offences — largely
disorders of the normal sexual cycle, and can be identi- because of the need to help identify and treat such offend-
fied as problematic at various points in this cycle (namely ers. Treatments for paraphilic disorders are also rela-
disorders of desire, arousal, orgasm and resolution). The tively underdeveloped, largely because of the problems
causes of sexual dysfunctions are diverse and include involved in treating people whose behaviour represents
biological and organic factors, psychological factors, and sexual offending. Because a number of the paraphilic
interpersonal problems. At one time, the open discus- disorders are sexual offences, much effort has been chan-
sion and treatment of sexual problems was considered nelled into developing relapse-prevention procedures
taboo, but over the past 50 years the liberalisation of atti- designed to reduce the probability of reoffending.
tudes towards sex has meant the development of a range Finally, many individuals feel they have a gender
of treatments for such disorders. identity that is incompatible with their biological sex,
In contrast to those who report problems with nor- and this is known as gender dysphoria. Gender dyspho-
mal sexual performance, there are those who exhibit ria can be experienced in both childhood and adulthood.
high frequencies of sexual activity that is triggered by or Because a large majority of those with gender dyspho-
directed at inappropriate targets. These are collectively ria are adamant that it is their biological sex they want
known as paraphilic disorders, and some reflect sexual to change (and not their incompatible gender identity),
behaviour that becomes centred on unusual objects or many opt for gender reassignment surgery in a radical
stimuli (e.g. fetishistic disorder, transvestic disorder), attempt to make their biology compatible with their
while others may involve non-consenting persons (e.g. gender identity.
Reading i Activity
Findings in the Kinsey e Gender dysphoria: Activity 11.1

reports A personal account Activity 11.2
Journal article: The Self-test questions
impact of aging on
Revision flashcards
sexual function and
sexual dysfunction in Research questions
women
Journal article:
Bidirectional association
between depression and
sexual dysfunction
genetics and epidemiol-
ogy of female sexual
dysfunction
Journal article: Cognitive
distortions in child sex
offenders
Journal article: The role
of testosterone in sexu-
ality and paraphilia -
A neurobiological
approach
Clinical issues
References
Personality Disorders

This chapter begins by discussing some of the issues sur-

rounding diagnosis of personality disorders raised during the 12.1 CONTEMPORARY ISSUES IN THE DIAGNOSIS
development of DSM-5. It then moves on to describe the 10 OF PERSONALITY DISORDERS. 409
diagnostically independent personality disorders listed by
DSM-5. We then move on to discuss the diagnostic criteria i 12.2 PERSONALITY DISORDERS AND THEIR
for these disorders and describe studies that have provided : DIAGNOSIS 413
data on their prevalence. The section on aetiology reviews
the available evidence on how the different personality : 12.3 THE PREVALENCE OF PERSONALITY DISORDERS 424
disorders are thought to develop and what childhood and
adolescent predictors and risk factors might help ustofore- i 12.4 THE AETIOLOGY OF PERSONALITY DISORDERS 426
cast personality disorders in adulthood. The chapter then
describes and reviews methods of treating people with a 12.5 TREATING PEOPLE WITH A DIAGNOSIS OF
diagnosis of personality disorder, and the range of difficul- PERSONALITY DISORDER 440
: ties involved in these treatments.
eer asa le URE AS A EN i Be a Sc “42.6 PERSONALITY DISORDERS REVIEWED 447
408 PSYCHOPATHOLOGY
%
LEARNING OUTCOMES
1. Discuss contemporary issues in the diagnosis of disorders, antisocial personality disorder,

personality disorders. borderline personality disorder and Cluster C
2. Describe the main diagnostic criteria for the disorders.
DSM-5 listed personality disorders and evaluate 4. Describe and evaluate the factors that make
some of the controversial issues concerning both the treatment of people with a diagnosis of
diagnosis and comorbidity. personality disorder problematic.
3. Describe and evaluate the main theories of 5. Describe and evaluate three or four psychological
the aetiology of a number of personality therapies that have been developed to treat people
disorders, particularly Cluster A with a diagnosis of personality disorder.
nee aaennenccncecccsnsercccecsnncensseecsnnsensressenceesareererenearenseseeeeshassanseeseereenseessenssneeeeseeseeseasereseensensaneseasenseesenssnasresenssessererasesneessesseesersersescencnscassanscasenersenasaasarreeenssernesersereeeree,
My name is Claire, and | am a 28-year-old female. | have always known that something wasn’t right with me, but over
time | learnt the survival technique called denial. | made my first suicide attempt at age 16 and was quickly yanked out
of the hospital by a mother who undoubtedly knew that | was just ‘putting on an act! | had explosive rages at friends, fam-
ily and even strangers. My first ‘tantrums; as my mother called them, began at age 1. | was never happy, never satis-
fied, always looking for that adrenaline rush to try to fill the void in my life. There was always - and to a certain degree, still
is — that missing piece of me. My pattern of unstable relationships was unbearable, love/hate, attracted/disgusted, happy/
miserable... all or nothing. For a long time, | blamed my problems on other people. | would have times where | would dissoci-
ate during a rage when | was of school age only to be told in the office that | hit my best friend for no reason. After time my rages
were only directed at strangers and my family. | only have two basic emotions —- mad and madder. The consequences of anyone
knowing that the pretty, talented, rich girl wasn’t perfect were too steep. My mother made sure of that. |have had a few major
depressive episodes and | have had only one more suicide attempt in adulthood. | have been on antidepressants for 5 years for
help with depression but they haven't helped with my intense mood swings in my interpersonal relationships. | consider myself
now to be a low-functioning ‘borderline’ because | haven't worked a steady job in about 4 years and | began to self-mutilate last
year. | really didn’t think that picking at my skin with pins and tweezers — until |had gaping holes all over my body, including my
face — was anything but a nervous habit.
Claire’s Story
(Claire is diagnosed with borderline personality disorder and bipolar disorder)
Introduction is something that we inwardly experience ourselves and

outwardly project to others. While personalities tend
We all have personalities. Personalities tend to be endur- to be relatively enduring in their main features, most
ing features of individuals that determine how we people will learn and evolve with their experiences,
respond to life events and experiences, and they also pro- and they will learn new and effective ways of behav-
vide a convenient means by which others can label and ing that will enable them to adapt with increasing suc-
react to us. To this extent, a personality is a global term cess to life’s demands. In contrast, some others possess
that describes how you cope with, adapt to, and respond an ingrained and unchanging way of dealing with life’s
to a range of life events, including challenges, frustra- challenges. They rarely learn to adapt their responses or
tions, opportunities, successes and failures. A personality learn new ones. They develop a form of dealing with
CHAPTER 12 PERSONALITY DISORDERS 409
life events that are fixed and unchanging — despite the

fact that they may have maladaptive consequences. They 12.1 CONTEMPORARY
can also introduce disruption and hardship into the lives ISSUES IN THE DIAGNOSIS
of others, and frequently cause emotional distress to
onality disorders A group of
themselves and those they OF PERSONALITY
interact with. Such char-
x marked by persistent, inflex-
naladaptive patterns of thought and acteristics are typical of DISORDERS
iour that develop in adolescence or those individuals who are
| woe andsignificantly impair an
idual’s ability to function. diagnosed with personal- There have been numerous concerns about how person-
ity disorders. ality disorders have been traditionally categorized and
For the purposes of diagnosed, and while DSM-5 has retained the categorical
clinical diagnosis, DSM-5 defines a personality disorder approach to diagnosis outlined in its predecessor, DSM-
(PD) as ‘an enduring pattern of inner experience and IV-TR, DSM-5 also includes an alternative model that
behaviour that deviates markedly from the expectations could be used to generate research on other diagnostic
of the individual’s culture, is pervasive and inflexible, approaches. To fully explain these issues, we will (1)
has an onset in adolescence or early adulthood, is stable briefly describe the traditional diagnostic categories in
over time, and leads to distress and impairment’ (DSM- DSM-IV-TR (also the ones retained in DSM-5 — see sec-
5, p.645). They are often associated with unusual ways tion 12.2 below), (2) explain the important problems that
of interpreting events, unpredictable mood swings, or surround this traditional approach, and (3) describe the
impulsive behaviour. Two of the most well-known of alternative model proposed in DSM-5.
these disorders are borderline personality disorder (BPD),
characterized by major and regular shifts in mood,
impulsivity and temper tantrums, and an unstable self-
image, and antisocial personality disorder (APD), which 12.1.1 The Categorical Approach
is characterized by a chronic indifference to the feel- to Personality Disorders in
ings and rights of others, lack of remorse, impulsivity,
and pursuit of the individual’s own goals at any cost.
DSM-IV-TR and DSM-5
Individuals with APD are often labelled as ‘sociopaths’ DSM-IV-TR listed 10 diagnostically independent per-
or ‘psychopaths’. sonality disorders and these were organized into three
Individuals diagnosed with a personality disorder will primary clusters (and this is still the way that DSM-5
frequently deny their psychopathology, will often be categorizes personality disorders in its main diagnostic
unable to comprehend that their behaviour is contrary section): (1) odd/eccentric personality disorders, (2) dra-
to conventional and acceptable ways of behaving, and matic/emotional personality disorders, and (3) anxious/
will not associate their own psychological difficulties fearful personality disorders.
with their own inflexible ways of thinking and behaving. Those personality disorders grouped in Cluster A all
As a consequence, such disorders are very difficult to have characteristics that resemble many of the symp-
treat because they represent ingrained ways of thinking toms of schizophrenia (see Chapter 8) but, unlike schizo-
and acting. phrenia sufferers, there is no apparent loss of touch with
Claire’s story describes the experiences and feelings reality, nor the experiencing of sensory hallucinations.
of an individual with borderline personality disorder. However, people with Cluster A disorders may behave in
This account displays features that are common to a ways that are indicative of delusional thinking (e.g. para-
number of personality disorders. Claire exhibits frequent noid personality disorder) or exhibit rambling or poorly
mood changes (mood lability), impulsive and aggres- organized speech (e.g. schizotypal personality disorder).
sive reactions to situations, chronic depression, self- The three subtypes of Cluster A are (1) paranoid person-
harm and suicide attempts, impaired occupational and ality disorder, (2) schizotypal personality disorder, and
social functioning, and an enduring disruptive pattern of (3) schizoid personality disorder.
behaviour that has been apparent from childhood into Cluster B includes people diagnosed with dramatic/
adulthood. As we will see later, many personality disor- emotional personality disorders who tend to be erratic in
ders are also associated with poor or unstable self-image their behaviour, self-interested to the detriment of oth-
and are frequently comorbid with other mental health ers, emotionally labile and attention-seeking. These are
problems — particularly depression (both major depres- arguably the most problematic of the personality disor-
sion and bipolar disorder) and many of the anxiety disorders in terms of the extremes of behaviour that they gen-
ders (Ehrt, Brieger & Marneros, 2003; Johnson, Cohen, erate, and the emotional and personal distress that they
Skodol, Oldham et al., 1999). inflict on others. This category includes (1) antisocial
BIOS PSYCHOPATHOLOGY
personality disorder (APD), (2) borderline personality (e.g. impulsivity, poor self-image), and so there is a real
disorder (BPD), (3) narcissistic personality disorder, and temptation for clinicians to diagnose more than one per-
(4) histrionic personality disorder. sonality disorder in a single individual (Grilo, Sanislow &
Finally, as the name suggests, people with an anxious/ McGlashan, 2002). Indeed, perhaps paradoxically, DSM-
fearful personality disorder (Cluster C) exhibit anxious IV-TR often defined personality disorders in ways which
and fearful behaviour. However, unlike the main anxiety either (1) allowed a very heterogeneous group of indi-
disorders, the anxious and fearful behaviour exhibited viduals to be diagnosed under a single diagnostic label,
will have been a stable feature of their behaviour from and for borderline personality disorder (BPD) in par-
late childhood into adulthood, and it is usually not pos- ticular there were almost 100 different permutations of
sible to identify a specific experience or life event that symptoms that would result in a diagnosis of BPD, or (2)
might have triggered this fear and anxiety. Anxious/ allowed clinicians to diagnose multiple comorbidity of
fearful personality disorders may be comorbid with personality disorders in a single individual.
some anxiety disorders (e.g. social anxiety disorder, Thirdly, a number of the existing personality disor-
panic disorder), where triggers for the latter can be iden- der categories are particularly rare in the general popu-
tified. But the pattern of behaviour exhibited by individ- lation (e.g. histrionic personality disorder, dependent
uals with anxious/ fearful personality disorders generally personality disorder) and may therefore not represent
tends to represent ingrained ways of dealing and coping useful independent disorder categories (Samuels, Eaton,
with many of life’s perceived threats. The three disorders Bienvenu, Brown et al., 2002; Trull, Jahng, Tomko et al.,
described in Cluster C are (1) avoidant personality disor- 2010).
der, (2) dependent personality disorder and (3) obsessive Finally, personality disorders may not be as stable
compulsive personality disorder. over time as the definitions in both DSM-IV-TR and
DSM-5 might imply. Studies suggest that as many as
half of the individuals diagnosed with a personality
disorder, do not receive the same diagnosis two years
12.1.2 Problems with the later (Shea, Stout, Gunderson, Morey et al., 2002; Grilo,
Shea, Sanislow, Skodol et al., 2004). They may still
Traditional Categorical Model
be high on measures of those personality traits, but not
Many clinicians and researchers have argued that per- high enough to meet the strict diagnostic criteria set by
sonality disorders do not exist as ‘categories’ — that is, DSM-IV-TR. This suggests that a dimensional approach
they are not discrete disorders that an individual either to measuring and diagnosing personality disorders
possesses or does not possess, but they are in fact dimen- might be more appropriate than the traditional all-or-
sional extensions of ‘normal’ personality traits (e.g. none approach.
Costa & MacRae, 1990). This is problematic in a number
of ways for the all-or-none approach to diagnosis of per-
sonality disorders that DSM-IV-TR had taken.
12.1.3 DSM-5’s Alternative Model
Firstly, there is evidence for a dimensional approach
to personality disorders from the finding that extreme The alternative diagnostic model proposed as a basis for
scores on conventional measures of personality, such further research in DSM-5 has three discrete types of per-
as the ‘five-factor’ model are highly associated with sonality ratings that contrib- level of personality functioni
‘ :
personality disorders (Trull, Widiger, Useda, Holcomb ute to a diagnosis (Skodol, ey
Disturbances in self os
and interpersonal
et al., 1998; Costa & MacRae, 1990; Samuel & Widiger, Clark, Bender, Krueger functioning are at the core of personality
2008). This finding probably resonates with our own et al., 2011). These are level disorders, with the severity of impairment
indicating whether the individual may
intuitive view that we ourselves and many of the people of personality function-
have more than one personality disorde
we know exhibit to some extent and in some circum- ing, personality disorder
stances the traits that we might associate with person- types and personality trait personality disorder types Each of six
ality disorders (e.g. mood swings, impulsive behaviour, domains and facets. This personality disorder traits specified in th
alternative diagnostic schemes publishe
paranoia, lack of social conscience). This suggests that system is designed to pro- in DSM-5.
personality disorders may not be disorders as such, but vide ratings of an individ-
simply represent extreme cases on conventional person- ual’s personality on a series personality trait domains and facets |!
the alternative classification of personali
ality dimensions. of personality dimensions disorders published in DSM-5, there are
Secondly, another conceptual difficulty with the tra- (rather than diagnosing five personality trait domains covering
ditional diagnostic model of personality disorders is in an all-or-none categori- negative affectivity, detachment, antago:
that many of them contain characteristics that overlap cal way) and reduces the nism, disinhibition, and psychoticism.
ss
CHAPTER 12 PERSONALITY DISORDERS AIL
Personality functioning Severity of impairment

+ Impaired sense of self-identity, Client evaluated on five-point scale from
or failure to develop effective ‘no impairment’ to ‘extreme impairment’
interpersonal functioning
FIGURE 12.1 Steps in evaluating personality

In the alternative diagnostic model for personality disorders described in DSM-5, diagnosis progresses through three relatively
independent steps: (1) assessing personality functioning to determine whether there is impairment typical of psychopathology;
(2) amore comprehensive analysis of personality traits rated along a series of dimensions; and (3) determining whether the informa-
tion collected in steps 1 and 2 meet the diagnostic criteria for any of six specific personality disorders.
number of personality disorder categories from 10 down in these areas predicts the presence of a personality dis-
to six. This model also provides information about per- order, with the severity of this impairment indicating
sonality functioning (i.e. do an individual's personality traits whether the individual may have more than one person-
allow them to function adequately at both an emotional ality disorder. Impairments to one’s sense of self include
and behavioural level?) and whether they possess patholog- inability to regulate emotions and self-esteem, and dis-
ical personality traits. These various assessment processes turbances of interpersonal functioning include inability
are shown schematically in Figure 12.1. to empathize and lack of desire and capacity for intimacy
(Bender, Morey & Skodol, 2011).
Level of personality functioning Pathological personality traits

Disturbances in both self and interpersonal functioning Once impairments in personality functioning have
are at the core of personality disorders, and functioning been established, a more comprehensive analysis of
Ai) PSYCHOPATHOLOGY
%
personality trait domains can be made. Scores on each of TABLE 12.1 Definitions of DSM-5 personality disorder trait
these dimensions will help the clinician to decide which domains and facets
specific personality disorders should be diagnosed. There
Domain Facets
are five personality trait domains, covering negative
affectivity, detachment, antagonism, disinhibition and Negative affectivity Emotional lability
psychoticism, and each of these domains is then supple- Anxiousness
mented by a further 25 trait facets which will help the Separation insecurity
Submissiveness
clinician to provide a more detailed rating within each
Hostility
domain (see Table 12.1). Perseveration
Depressivity
Suspiciousness
Specific personality disorders Restricted affectivity
The alternative diagnostic model in DSM-5 has
reduced the number of individual diagnosable person- Detachment Withdrawal
: : ; : Intimacy avoidance
ality disorders from 10 down to six. These are antiso- teeter
ies se nhedonia
cial personality disorder, avoidant personality disorder, Depressivity
borderline personality disorder, narcissistic personality Restricted affectivity
disorder, obsessive compulsive personality disorder, Suspiciousness
and schizotypal personality disorder. Each individual Aneagonism Maniputuvences
personality disorder then has its own set of criteria by Darcieutides
which it can be diagnosed and these criteria are depend- Grandiosity
ent on the presence of high scores on the measures of Attention seeking
personality functioning and high scores on specified Callousness
personality traits. For example, under this proposed Hostility
scheme, a diagnosis of antisocial personality disorder _ Disinhibition Irresponsibility
would be dependent on high ratings on two of the four Impulsivity
elements of personality functioning, and six or more Distractibility
of the following seven pathological personality traits: Risk taking
Rigid perfectionism
manipulativeness, callousness, deceitfulness, hostility
(all aspects of antagonism), risk taking, impulsivity Psychoticism Unusual beliefs and experiences
and irresponsibility (all aspects of disinhibition) (see Eccentricity
Table 12.1). Cognitive and perceptual dysregulation
‘SELF-TEST QUESTIONS
e What are the problems associated with the current categorical approach to diagnosing personality disorders?
e What is the process for diagnosing personality disorders in DSM-5’s alternative model?
SECTION SUMMARY
12.1 CONTEMPORARY ISSUES IN THE DIAGNOSIS OF PERSONALITY DISORDERS
Hopefully this discussion has given you an insight into how the diagnosis of personality disorders may develop in the imme-
diate future and has provided you with some of the reasons why diagnosis might need to change. However, the American
Psychiatric Association decided against introducing these changes with the publication of DSM-5 and agreed to provide more
time for further research on the alternative, dimensional approach. If you are interested in the proposed diagnostic criteria for
DSM-5’s alternative model, these can be found on the book's website at www.wiley-psychopathology.com.
The key points are:
¢ DSM-5 retains previous diagnostic criteria by defining personality disorders on a categorical rather than dimensional basis.
* DSM-5 also discusses a dimensional approach to diagnosing personality disorders, which it hopes will generate further research.
CHAPTER 12 PERSONALITY DISORDERS can
12.2 PERSONALITY disorders (see Table 12.2). The following sections describe
each of these clusters and the diagnosable personality
DISORDERS AND disorders listed in each.
THEIR DIAGNOSIS
12.2.1 Odd/Eccentric Personality
The diagnostic approach adopted in the main body of Disorders (Cluster A)
DSM-5 is the traditional categorical one also found in
Those personality disorders grouped in Cluster A all have
DSM-IV-TR (as opposed to the dimensional alterna-
characteristics that resemble many of the symptoms of
tive described in section 12.1.3) and the categorical per-
schizophrenia (see Chapter 8) but, unlike schizophrenia
spective is the one we will use here. According to this
sufferers, there is no apparent loss of touch with reality,
approach, only when personality traits are inflexible and
nor the experiencing of sensory hallucinations. However,
maladaptive and cause significant functional impair-
people with Cluster A disorders may behave in ways
ment or distress are they diagnosed as personality dis-
that are indicative of delusional thinking (e.g. paranoid
orders. To help the clinician identify when personality
personality disorder) or exhibit rambling or poorly
traits have become maladaptive in this way, DSM-5 pro-
organized speech (e.g. schizotypal personality disorder).
vides a set of general criteria, which is shown in DSM-5
The three subtypes of
Summary Table 12.1. The main criterion is that a per-
odd/eccentric personal- odd/eccentric personality disorders
son's inner experience and behaviour must differ mark- Personality disorders grouped in Cluster A,
ity disorders are (1) para-
edly from expectations of the individual’s culture and the three subtypes of which are (1) para-
noid personality disorder, noid personality disorder, (2) schizotypal
be reflected in at least two of the following four areas:
(2) schizoid personality dis- personality disorder and (3) schizoid
cognition (e.g. ways of perceiving the self and other personality disorder.
order, and (3) schizotypal
people), affectivity (e.g. the range, intensity and change-
personality disorder.
ability of emotions), interpersonal functioning and
impulse control. Further criteria stress that the patterns
Paranoid personality disorder
of behaviour and inner experience must be inflexible
Those with paranoid personality disorder exhibit an
and pervasive, and lead to distress or social, occupa-
enduring pattern of distrust and suspiciousness of oth-
tional or other forms of impairment.
ers (DSM-5 Summary Table 12.2). They will interpret
Apart from these general criteria, DSM-5 then speci-
innocent remarks as threat-
fies criteria for 10 separate types of personality disorder.
ening and will interpret paranoid personality disorder A person-
These are grouped into clusters which cover (1) odd/
the intentions of others ality disorder characterized by an enduring
eccentric personality disorders, (2) dramatic/emotional pattern of distrust and suspiciousness of
as malevolent. They find others.
personality disorders, and (3) anxious/ fearful personality
‘threatening’ hidden mean-
ing in everything and their distrust of others is pervasive
DSM-5 SUMMARY TABLE 12.1 Criteria for general and unchanging. If someone points out to them that their
personality disorder paranoid interpretation of events may be wrong, they
e Anongoing rigid pattern of thought and behaviour that is will inevitably begin to distrust the person who brought
significantly different from the expectations of the person's
culture, displaying manifestation in two or more of the TABLE 12.2 The three clusters of personality disorders in DSM-5
following areas:
Cluster A
¢ Cognition Odd/eccentric Paranoid personality disorder
personality disorders Schizoid personality disorder
e Affectivity
Schizotypal personality disorder
e Interpersonal functioning
Cluster B
¢ Impulse control Dramatic/emotional Antisocial personality disorder (APD)
personality disorders Borderline personality disorder (BPD)
e The pattern is constant and long-lasting and can be traced
Narcissistic personality disorder
back to adolescence or early childhood
Histrionic personality disorder
e The pattern leads to distress or impairment in social, occu-
Cluster C
pational and other areas of life
Anxious/fearful Avoidant personality disorder
e The symptoms are not better accounted for by another personality disorders Dependent personality disorder
mental disorder or due to the effects of a substance or Obsessive compulsive personality
other medical condition disorder (OCPD)
414 PSYCHOPATHOLOGY
DSM-5 SUMMARY TABLE 12.2 Criteria for paranoid personality DSM-5 SUMMARY TABLE 12.3 Griteria for schizoid
disorder personality disorder
¢ Auniversal distrust and suspicion of others to the extent e Apersistent pattern of separation from social relation-
that their motives are seen as malicious, as indicated by at ships and a restricted range of expression of emotions in
least four of the following: relational situations, as indicated by at least four of the
following:
¢ Suspicions that others are misusing, hurting or mislead-
ing him/her © Does not like or want close relationships
¢ Fixation with unjustifiable doubts about the trustwor- e Prefers solitary activities
thiness of friends and suchlike
¢ Take little or no pleasure in sexual experiences with
¢ Unwilling to confide in others because of fear that the another person
information will be used against him/her
e Takes pleasure in few, if any activities
¢ Sees hidden threats in non-threatening words or events
e Lacks close friends or confidents other than immediate
° Bears persistent grudges relatives
e Sees attacks on their character or status that are not ¢ Indifferent to the praise or criticism of others
apparent to others and is quick to react angrily
¢ Displays emotional coldness, detachment or flat
¢ Has ongoing suspicions about the faithfulness of their expression
sexual partner or spouse
e Symptoms do not occur exclusively during the course of
¢ Symptoms do not occur exclusively during the course of any other psychotic disorder
any other psychotic disorder
Those suffering with schizoid personality disorder fail

this to their attention. As a result, individuals with para- to express a normal range of emotions and appear to get
noid personality disorder avoid close relationships, are little sensory or intellectual
often spontaneously aggressive to others, become pre- reward from any activi- schizoid personality disorder A person
ality disorder in which individuals are "
occupied with their mistrust of others to the point of it ties (DSM-5 Summary
described as ‘loners’ who fail to express a
severely disrupting their work performance, and often Table 12.3). They prefer to normal range of emotions and appear to
feel that they have been deeply and irreversibly betrayed spend most of their time get little reward from any activities.
by others — even when there is no objective evidence for by themselves and choose
this. Individuals with paranoid personality disorder will jobs and pastimes that do not involve them in interactions
even misinterpret well-intentioned and complimentary with others (e.g. jobs such as a road sweeper or night
statements as criticism, such as interpreting an offer of watchman) and they can be quite successful and efficient
help as implying that they are not doing a job or task well at their jobs if relatively little social contact with others is
enough. Because such individuals are hypervigilant for involved. However, they seem to be largely unaffected by
the potential malevolent intentions of others, they will both praise and criticism, and prefer mechanical abstract
bear grudges, be quick to attack others for what are seen activities — such as computer or mathematical games — to
as critical comments, and gather trivial and often circum- real-life experiences. It has been suggested that there may
stantial evidence to support ‘jealous’ beliefs — especially be some link between the symptoms of autism and a diag-
about partners and colleagues. Because of their perceived nosis of schizoid personality disorder. For example, the
need to constantly defend themselves against malevolent lack of emotional responsiveness and the tendency to be
others, individuals with paranoid personality disorder withdrawn and uncommunicative resembles the symp-
feel a need to have a high degree of control over those toms of autism, and there is some evidence that there
around them and are frequently involved in litigious dis- may be a modest genetic link between autism and schiz-
putes. They also appear to deploy an attributional style oid personality disorder (Wolf, 2000).
that blames others for everything that goes wrong in their
life (Fenigstein, 1996) and this external locus of control Schizotypal personality disorder
is very similar to the attributional style found in schizo- Individuals with schizotypal personality disorder usu-
phrenics with paranoid delusions (Bentall, 1994). ally exhibit ‘eccentric’ behaviour marked by odd patterns
of thinking and communi-
Schizoid personality disorder cation, and discomfort with schizotypal personality disorder A pet
Individuals with this disorder are often described as ‘lon- close personal relationships. sonality disorder characterized by ‘eccen-
ers’ who have very few, if any, close relationships with In particular, they often tric’ behaviour marked by odd patterns o
exhibit’ uinusdalerereeenn thinking and communication.
others (except perhaps a single first-degree relative).
CHAPTER 12 PERSONALITY DISORDERS aS
reference: they believe that unrelated events pertain to exhibit the positive symptoms typical of magical thinking
them, that they have extrasensory abilities, or that they and ideas of reference while males tend to show more
can influence events external to them in a ‘magical’ way. negative symptoms such as emotional withdrawal (DSM-5
For example, they may believe that their partner taking Summary Table 12.4). Finally, one persistent problem
the dog for a walk was a result of them thinking earlier with the diagnosis of schizotypical personality disorder is
that this needed to be done; or they may indulge in ritual- that it tends to be highly comorbid with the other person-
ized, superstitious behaviour such as walking back and ality disorders, in particular paranoid personality disorder
forth past a lamppost five times in an attempt to prevent and avoidant personality disorder (Morey, 1988), which
harm from occurring to a friend or relative. Because of suggests there may be some common aetiological factors
these magical beliefs, they will often become involved across these different disorders.
with unconventional groups interested in such topics as There is some evidence that the schizotypal disorder
astrology and extraterrestrial phenomena, such as alien may be very closely related to schizophrenia. Firstly, schi-
abduction, and fringe religious groups. Their speech may zotypal personality disorder is found to be significantly
have eccentric characteristics, be excessively rambling, more common in individuals who have biological relatives
and they may use words in unusual ways — but they are with schizophrenia than those who do not (Nicolson &
able to communicate information and do not exhibit the Rapoport, 1999), suggesting a possible inherited link
incomprehensible ‘word salads’ and derailment typical of between the two. Secondly, schizotypal personality
schizophrenia (see section 8.1.3). Individuals with schizo- disorder is significantly more likely to be found in the
typal personality disorder find it very difficult to interact offspring of individuals with schizophrenia than in
in normal social situations; they become anxious, and may the offspring of individuals diagnosed with anxiety dis-
even develop paranoid symptoms. As a result they often orders or no mental disorder (Hans, Auerbach, Styr &
have few, if any, close friends, they are often viewed by Marcus, 2004). Thirdly, some of the symptoms of schi-
others as ‘loners’, and they tend to drift aimlessly and lead zotypal personality disorder can be successfully treated
unproductive lives (Skodol, Gunderson, McGlashan, Dyck with antipsychotic drugs also used to treat schizophre-
et al., 2002). Like all of the personality disorders, these nia (Schulz, Schulz & Wilson, 1988). Fourthly, cognitive
characteristics appear to develop in early adulthood and studies have shown that many of the attentional and
persist over much of the individual’s lifetime. There is a working memory deficits found in schizophrenia are
tendency for schizotypal personality disorder to manifest also apparent in individuals diagnosed with schizotypal
differently in males and females, with females tending to personality disorder (Barch, Mitropoulou, Harvey, New
et al., 2004). Finally, neuroimaging studies show that schi-
zotypal personality disorder shares many forms of brain
DSM-5 SUMMARY TABLE 12.4 Criteria for schizotypal pathology in common with schizophrenia, suggesting it
personality disorder may be a schizophrenia spectrum condition (Fervaha &
¢ Apersistent pattern of social and relational shortfalls, Remington, 2013). This kind of evidence suggests that
evidenced by a lack of ease with, and reduced ability for, schizotypal personality disorder is closely related in many
close relationships, as well as distortions and peculiarities ways to schizophrenia and may even represent a risk fac-
of behaviour as shown by at least five of the following: tor for schizophrenia (Nigg & Goldsmith, 1994).
e Beliefs or perceptions which are irrelevant, innocuous or
unrelated
e Odd beliefs that influence behaviour and are not within
12.2.2 Dramatic/Emotional
subcultural norms Personality Disorders (Cluster B)
e Strange perceptions of what is occurring around them
People diagnosed with dramatic/emotional personality
e Vague or other odd thinking and speech disorders tend to be erratic in their behaviour, self-interested
e Suspicious or paranoid ideas
to the detriment of others, emotionally labile and attention-
seeking. These are arguably the most problematic of the
e |nappropriate or constricted emotional expression
personality disorders in terms of the extremes of behaviour
e Odd, eccentric or strange behaviour or appearance that they generate and the emotional and personal distress
e Lacks close friends or confidents other than immediate
that they inflict on others.
In this category we will dramatic/emotional personality
(clots
describe the symptoms of disorders Personality disorders grouped
in Cluster B, including (1) antisocial person-
¢ High levels of social anxiety despite familiarity
(1) antisocial personality dis- ality disorder, (2) borderline personality dis-
e The pattern does not occur during the course of order (APD), (2) borderline order, (3) narcissistic personality disorder,
schizophrenia or other psychotic disorder personality disorder (BPD), and (4) histrionic personality disorder.
416 PSYCHOPATHOLOGY
SCHIZOTYPAL PERSONALITY DISORDER

lan is 23 and lives at home with his parents. He is unemployed. He spends most of his time watching TV and often
simply sits and stares into space. He says he just feels ‘out of it’a lot of the time. He reports that he seems to see
himself from outside, as if watching himself in a film and reading from a script. He has tried a few jobs but never
manages to persist at one for very long. At his last job, which was ina DIY store, several customers complained to
the manager about lan talking to them in a rambling and vague way - often about irrelevant things. This led
to lan being sacked from this job. lan doesn’t understand why people don't seem to like him and get along with
CASE him. He notices that people move away from him on public transport or avoid talking to him in queues, but noth-
HISTORY
12.1
ing he seems to do or say changes this and he now tries to avoid interactions with others because they make him
anxious. He has no close relationships and complains of feeling lonely and isolated.
Clinical Commentary
lan shows many of the diagnosable symptoms ofschizotypal personality disorder, including unusual ideas
of reference (feeling he is in a film), vague and circumstantial speech in conversations, suspiciousness and
paranoia about others, a lack of close relationships, and feelings of anxiety in interactions with others.
Currently, these characteristics have led to lan being unemployed and leading the life of a relatively uncom-
municative ‘loner’ who shows little emotion.
(3) narcissistic personality disorder, and (4) histrionic per- (5) lack of remorse. The sociopath A person with a personality —
sonality disorder. term ‘sociopath’ — or disorder manifesting itselfinextreme —
‘psychopath’ — is some- antisocial attitudes and behaviour. |
Antisocial personality disorder times used to describe this

psychopath A term often used to
The fundamental feature of antisocial personality dis- type of personality disor-
describe individuals diagnosed with ve
order (APD) is an enduring disregard for, and violation der, and such people are social personality disorder.
antisocial personality disorder (APD) A
of, the rights of others. compulsive and persistent
personality disorder, the main features of This begins in childhood liars (Seto, Maric & Barbaree, 2001) who are self-centred to
which are an enduring disregard for, and (with a history of symp- the point of happily gaining profit at the expense of others.
violation of, the rights of others. It is char- toms of conduct disorder; Some researchers have distinguished different types of
acterized by impulsive behaviour and lack
of remorse, and is closely linked with adult
see section 16.2.2) and con- APD and there appear to be those whose antisocial behav-
criminal behaviour. tinues into adulthood. The iour is a result of unresolved emotional conflicts resulting
behaviour of individuals from adverse early experiences (e.g. childhood neglect or
with APD deviates substantially from what we would abuse), and those antisocial behaviours stem primarily
consider to be normal standards of social behaviour, from impulsivity in reaction to negative emotions
morality and remorse, and is very closely linked with (Karpman, 1941; Poythress, Edens, Skeem, Lilienfeld et al.,
adult criminal behaviour. For example, a survey of prison 2010). Individuals with APD show a disregard for the safety
populations in 12 Western countries found that 47 per of themselves and others, and this is evidenced by their
cent of male inmates and 21 per cent of female inmates impulsive, often aggressive, behaviour and failure to plan
met the diagnostic criteria for APD, and this is around 10 ahead. Such individuals are frequently involved in motor
times the prevalence rate found in the general population accidents as a result of reckless driving (McDonald &
(Fazel & Danesh, 2002). Similarly, a DSM diagnosis of Davey, 1996) or commit physical and sexual assaults (includ-
APD has also been shown to be a significant predictor of ing spouse beating or child beating). Impulsivity and irre-
subsequent criminal behaviour (Fridell, Hesse, Jaeger & sponsibility can be identified in the daily lives of individuals
Kihlhorn, 2008). To be diagnosed with APD, an individ- with APD - they frequently may quit a job without a realis-
ual must be at least 18 years of age and display some of tic plan for getting another one, or default on debts, fail to
the following characteristics: (1) failure to conform to provide child support, or fail to support other dependents
social and legal norms, (2) deceitfulness and impulsivity, on a regular basis.
(3) irritability and aggressiveness, (4) consistent irrespon- Prior to 1980, APD or psychopathy was defined pri-
sibility (e.g. repeated failure to honour obligations), and marily by personality traits such as egocentricity, deceit,
CHAPTER 12 PERSONALITY DISORDERS a7
DSM-5 SUMMARY TABLE 12.5 Criteria for antisocial DSM-5 SUMMARY TABLE 12.6 Criteria for borderline
personality disorder (APD) personality disorder (BPD)
e Pattern of indifference to and violation of the rights of e¢ Along-term display of instability of relationships, self-
others as shown by at least three of the following since the image and behaviour, as well as high levels of impulsivity
age of 15 years old: beginning in early adulthood and indicated by at least five
° Lack of conformity to social norms and regularly indulg- pi otohaeing:
ing in unlawful behaviours e Desperate attempts to avoid real or imagined
e Lying, pretending to be someone else or deceiving sageaaleiea
others for personal gain e A pattern of unstable and intense interpersonal relation-
* Failure to plan ahead or impulsiveness ships, fluctuating between adulation and deprecation
* Irritability and aggressiveness leading to physical fights ° Constantly unstable self-image and identity disturbance
and assaults e Potentially self-damaging impulsivity in at least two
ee areas such as sex, substance abuse and reckless drivin
e Reckless indifference to own and other's personal safety : :
© Consistent irresponsible behaviour e Repeated suicidal behaviour or self-mutilation
Sack ot vemorse e Emotional instability due to reactivity of mood
¢ The person is at least 18 years old e Unsuitable, intense anger or difficulty controlling anger
e Stress-related paranoid idealisation or severe dissocia-
¢ The antisocial behaviour is not associated with symptoms
tive symptoms
of schizophrenia or mania
shallow affect, manipulativeness, selfishness and lack of personal relationships, a borderline personality disorder (BPD) A
empathy. However, with the introduction of DSM-IV, lack of a well-defined and personality disorder, the main features of
APD has been defined more in terms of violations of stable self-image, regular which are instability in personal relation-
ships, a lack of well-defined and stable self-
social norms. The reason given for this shift in emphasis and predictable changes
image, regular and unpredictable changes
is that personality traits are difficult to measure, and it is in moods, and impul- in moods and impulsive behaviour.
easier to agree a diagnosis on the basis of well-defined sive behaviour (DSM-5
behaviours (such as breaking laws or aggressive behav- Summary Table 12.6). These characteristics are perva-
iours) (Widiger & Corbitt, 1993) —and these well-defined, sive and will have endured from childhood into adult-
antisocial behaviours are well-represented in the DSM-5 hood, and can all be seen in the personal account given
diagnostic criteria for APD (DSM-5 Summary Table 12.5). by Claire at the beginning of this chapter.
This shift in the diagnostic criteria has meant that APD In particular, individuals with BPD appear to have a
has become very closely associated with criminal activ- significant fear of abandonment and rejection. This leads
ity rather than being purely a psychopathology requiring them to fall into close and conflict-ridden relationships
treatment. Studies that have surveyed prison populations after as little as a single meeting with someone; but they
have indicated that the number of males in prisons that are just as likely to fall out with that person if they inter-
meet DSM-III-R or DSM-IV-TR criteria for APD range pret the person’s behaviour as uncaring or not attentive
from 50-70 per cent (Fazel & Danesh, 2002; Widiger, enough — and this may often be the case, because the feel-
Cadoret, Hare, Robins et al., 1996). This indicates that ings of the individual with BPD may not be shared by
the changes to the diagnostic criteria for APD over the the other person (Modestin & Villiger, 1989). Although
years have moved this category more towards identifying their behaviour becomes unpredictable and emotional
criminals and criminal behaviour and away from identi- when their expectations for a relationship are not met,
fying psychological factors that might give rise to such they are also riddled with fear about being rejected and
behaviour (such as lack of empathy, superficial interper- losing that relationship. This leads to rapid, ill-tempered
sonal style, inflated sense of self-importance, and so on). mood changes if the individual does not feel that things
There is a real possibility that this move towards defining ‘are going their way’. The results of this emotional
APD in terms of antisocial activities could fudge the dis- roller-coaster and fear of abandonment and rejection are
tinction between psychopathology in need of treatment (1) regular and unpredictable shifts in self-image char-
and criminal behaviour in need of restraint. acterized by changing personal goals, values and career
aspirations, (2) prolonged bouts of depression (Luca,
Borderline personality disorder Luca & Calandra, 2012), deliberate selfharm (Sansone,
The cardinal features of borderline personality dis- Wiederman & Sansone, 2000), suicidal ideation and actual
order (BPD) are an enduring pattern of instability in suicide attempts (Venta, Ross, Schatte & Sharp, 2012),
418 PSYCHOPATHOLOGY
and (3) impulsive behaviour such as drug abuse (Trull, DSM-5 SUMMARY TABLE 12.7 Criteria for narcissistic et
Sher, Minks-Brown, Durbin & Burr, 2000), physical personality disorder

violence, and inappropriate promiscuity (Sansone & e Anongoing pattern of grandiosity, need for adoration
Wiederman, 2009). Because of its close association with and lack of empathy, beginning in early adulthood and
mood disorders, depression and suicide, some researchers indicated by at least five of the following:
have argued that BPD may well be a form of depression e Has a highly exaggerated sense of self-importance and
(Gunderson & Elliott, 1985), but in fact it is just as likely self-achievement
to be comorbid with anxiety disorders or with depressive
e Preoccupied with illusions of unlimited success, power,
symptoms (Grant, Chou, Goldstein, Huang et al., 2008).
beauty or ideal love
Zanarini, Frankenburg, Dubo, Sickel et al., (1998) found
that 96.3 per cent of individuals diagnosed with BPD ° Believes that they are special and can only be under-
stood by people of similar speciality
met the criteria for a mood disorder (major depression,
dysthymia, bipolar II disorder), but 88.4 per cent also met * Commands excessive admiration
the criteria for an anxiety disorder, with panic disorder e Has unreasonable expectations of favourable treatment
(47.8 per cent) and social phobia (45.9 per cent) being
e Exploits others for personal gain
the most prevalent. Interestingly, 64.1 per cent met the
criteria for substance use disorder — reaffirming the link ¢ Lacks compassion and cannot identify with the needs
between BPD and impulsive behaviour — whereas 53 per and feelings of others
cent met the criteria for eating disorders. Another impor- ° Often jealous of others and believes that others are
tant finding is that BPD is often comorbid with PTSD, jealous of them
with 30.2 per cent of those with a diagnosis of BPD also e Shows conceited, self-important behaviour or attitudes
having a diagnosis of PTSD, and 24.2 per cent of those
with PTSD also having a diagnosis of BPD (Pagura,
Stein, Bolton, Cox et al., 2010), a finding that is consistent bragging about their achievements and their talents is a
with the view of some clinicians that BPD may be a form very fragile self-esteem and individuals with narcissistic
of PTSD — especially since many individuals with BPD personality disorder constantly need to seek reassurance.
report a history of traumatic experience related to physi- When this is not forthcoming, they become angry and
cal and sexual child abuse (Heffernan & Cloitre, 2000). At ageressive. Because of the apparent lack of empathy and
the very least, these data suggest that BPD represents a the tendency to exploit others for self-benefit, narcissistic
behavioural style that may put an individual at severe risk personality disorder has been compared to antisocial per-
for a wide range of other psychopathologies. sonality disorder (APD), and it may be a subtype of APD
in that some features of the disorder (such as a grandiose
Narcissistic personality disorder self-image) predict future criminal or delinquent behav-
The individual with narcissistic personality disorder iour (Calhoun, Glaser, Stefurak & Bradshaw, 2001).
routinely overestimates their abilities and inflates their
accomplishments, and_ is Histrionic personality disorder
narcissistic personality disorder A characterized by a perva- Individuals with histrionic personality disorder are
personality disorder in which individuals sive need for admiration attention-seeking and uncomfortable or unhappy when
overestimate their abilities, inflate their
and a lack of empathy with they are not the centre of attention (DSM-5 Summary
accomplishments, have a pervasive need
for admiration and show a lack of empathy the feelings of others. Such Table 12.8). Their behaviour is often dramatic and
with the feelings of others. people believe they are their language theatrical and exaggerated. For example,
superior to others, and they may always seek to
expect others to recognize this. They will constantly fish be the centre of attention histrionic personality disorder A per-
for compliments, and are likely to become angry when at a party, and, if not, may sonality disorder in which anindividual i
such compliments are not forthcoming (Gramzow & suddenly do something attention-seeking and uncomfortable or
unhappy when not the centre of attention
Tangney, 1992). In their relationships, they will expect dramatic to gain attention
great dedication from others and may often exploit (such as make up an intrigu-
others for their own gain. They also have a lack of empa- ing story about themselves or someone else, or create a
thy and either cannot recognize, or simply ignore, the scene). Similarly, they will make extravagant expressions of
desires and feelings of others. Because of this, they tend emotion towards friends and colleagues and have a style
to have a history of problematic relationships and of speech that is excessively impressionistic but lacking in
Campbell (1999) found that individuals with narcissistic detail. For example, they may describe someone as a ‘won-
personality disorder tend to prefer partners that are derful person’ but then be unable to describe any features
openly admiring rather than openly loving (DSM-5 that contribute to this assessment. As a result, such indi-
Summary Table 12.7). However, beneath the facade of viduals are often viewed as shallow, self-dramatising and
CHAPTER 12 PERSONALITY DISORDERS — A19°
DSM-5 SUMMARY TABLE 12.8 Criteria for histrionic Anxious/fearful personality disorders may be comor-
personality disorder bid with anxiety disorders (e.g. social phobia, panic dis-
e Acontinuous pattern of high levels of emotionality and order), where triggers for the latter can be identified. But
attention-seeking, beginning in early adulthood and indi- the pattern of behaviour exhibited by individuals with
cated by at least five of the following: anxious/fearful personality disorders generally tends to
e Unhappy in situations where they are not the centre of
represent ingrained ways
attention of dealing and coping with anxious/fearful personality disorders
The exhibition of persistent anxious and
many of life’s perceived fearful behaviour which is not usually
¢ Shows high levels of inappropriate sexually suggestive
threats. The three disor- linked to a specific trigger experience or
or provocative behaviour in interactions with others
ders to be described in life event.
e Displays rapidly shifting and shallow demonstrations of Cluster C are (1) avoidant
emotion
personality disorder, (2) dependent personality disorder,
¢ Frequently uses personal appearance to draw attention and (3) obsessive compulsive personality disorder.
to self
e Has an excessively impressionistic and detail-lacking Avoidant personality disorder

style of speech The main features of avoidant personality disorder are
e Is self-dramatic, over-theatrical and uses exaggerated persistent social inhibition (characterized by avoidance of
expressions of emotion a wide range of social situa- avoidant personality disorder A per-
tions), feelings of inade- sonality disorder the features of which
e ls easily influenced by others
quacy, and hypersensitivity are avoidance of a wide range of social
e Feels that relationships are more intimate than they to negative evaluation and situations, feelings of inadequacy, and
actually are hypersensitivity to negative evaluation
criticism (DSM-5 Summary and criticism.
Table 12.9). These tenden-
cies appear in late childhood or early adolescence and are
easily influenced. They will draw attention to themselves exhibited across a range of different contexts, including
by exaggerating their illnesses (Morrison, 1989) or dressing occupational and social contexts and in interpersonal
provocatively or seductively. Because of their shallow and interactions generally. Individuals with avoidant personal-
flirtatious nature, individuals with histrionic personality ity disorder are fearful of criticism, disapproval and rejec-
disorder often find it difficult to make lasting relationships tion, and they automatically assume that others will be
and this is frequently a main reason why such individu- critical and disapproving. They will avoid school, work
als seek therapy. Although there was traditionally a bias and all group activities because of these fears, and are una-
towards diagnosing this disorder more often in women ble to form close relationships unless there is an assurance
than in men (Anderson, Sankis & Widiger, 2001), surveys
suggest that it is equally distributed across men and women
(Mattia & Zimmerman, 2001). The prevalence rate of his- DSM-5 SUMMARY TABLE 12.9 Criteria for avoidant
trionic personality disorder is low (0.4 per cent) and it is personality disorder
highly comorbid with other personality disorders such
e A persistent pattern of social reticence, feelings of inad-
as BPD, narcissistic and dependent personality disorders equacy and hypersensitivity to criticism, beginning in early
(Bakkevig & Karterud, 2010). This poor construct validity adulthood and indicated by at least four of the following:
may mean that is it likely to be excluded from future ver-
e Avoiding occupational activities that involve high levels
sions of DSM, although the characteristics of exhibitionism
of interpersonal contact due to fears of criticism or
and attention-seeking may be ones that might be included rejection
in any reformulation (Bakkevig & Karterud, 2010).
e Unwilling to engage with others unless certain of
approval and being liked
12.2.3 Anxious/Fearful Personality e Shows restraint in intimate relationships for fear of

ridicule or shame
Disorders (Cluster C) e Fixation with disapproval or rejection in social situations
As the name suggests, people with a personality disor- e Inhibited in new relationships due to feelings of
der in this cluster exhibit anxious and fearful behaviour. inadequacy
However, unlike anxiety disorders, the anxious and fear- e Feels that they are socially incompetent, unappealing or
ful behaviour exhibited will have been a stable feature of inferior to others
their behaviour from late childhood into adulthood and it
e Highly reluctant to take part in any new activities
is usually not possible to identify a specific experience or
because ofthe potential for embarrassment
life event that might have triggered this fear and anxiety.
420 PSYCHOPATHOLOGY
of uncritical acceptance. They are generally shy, and can- anxious by social situations where particular levels of perfor
not easily talk about themselves for fear of being ridiculed mance might be required (e.g. making a work presentation
or shamed. They also have a clear bias for interpreting or having a job interview) whereas the personality disorder
ambiguous information and comments in a negative way is more associated with (1) fear of personal interactions and
(e.g. someone saying ‘I was surprised by the quality of social relationships generally, (2) the criticism and rejection
your work’ would be interpreted as being critical or disap- that they believe will be associated with these types of expe-
proving, even though their comments could equally be riences, and (3) difficulties in being open with people they
interpreted as praise). Individuals with avoidant personal- are close to (Turner, Beidel, Dancu & Keys, 1986; Marques,
ity disorder are particularly ill at ease with strangers and Porter, Keshaviah, Pollack et al., 2012). In addition, there is
will usually avoid interactions with strangers at all costs. some evidence that avoidant personality disorder is associ-
As a result they are reluctant to take risks, engage in new ated with avoidance behaviour generally, and individuals
activities or even accept job promotions that might involve diagnosed with the disorder show greater avoidance of
greater responsibility and interaction with others. emotion, novelty and other non-social events than non-
People with avoidant personality disorder generally have sufferers (Taylor, Laposa & Alden, 2004). However, some cli-
low self-esteem and will frequently feel angry at themselves nicians believe that avoidant personality disorder and social
for being withdrawn and not enjoying the apparent social anxiety disorder are both components of a broader social
rewards and intimate relationships experienced by others anxiety spectrum (Tillfors & Ekselius, 2009) and there is
(Lynum, Wilberg & Karterud, 2008). As you can imagine, evidence to suggest that (1) the severity of the symptoms of
avoidant personality disorder has many features in common antisocial personality disorder are significantly increased if it
with social anxiety disorder (see section 6.2) and many indi- is comorbid with social anxiety disorder (Ralevski, Sanislow,
viduals diagnosed with avoidant personality disorder also Grilo, Skodol et al., 2005),
social anxiety spectrum A spectrum o
receive a diagnosis of social anxiety disorder (Widiger, 2001; and (2) there is a genetic link
disorder proposed to include both avoi
Marques, Porter, Keshaviah, Pollack et al., 2012). However, between the two disorders, ant personality disorder and social anxie'
f x *
individuals with social anxiety disorder tend to be made as evidenced by the fact that disorder.

THOUGHTS ABOUT AVOIDANT PERSONALITY DISORDER
‘The way | see it, people like us [with avoidant personality

disorder] were born with brains that are very sensitive to Clinical Commentary
social situations. As a child | used to get so frightened and In this personal account of avoidant personal-
scared that | probably unconsciously decided to build up a ity disorder, the individual describes how her
defence system against terrible feelings in order to protect desire to avoid social encounters developed
myself. | just instinctively knew | had to do something, so during childhood from a fear of being criticized
my personality was formed in a way designed to avoid the (and possibly bullied) by her peers. When avoid-
harm. | hated the fact that other kids would be out to criti- ing social encounters (e.g. by staying off school),
cize me, so | adopted avoidance as a defence system. | had she would reward these avoidance responses by
very low self-esteem, so | didn’t think anyone liked me any- indulging in enjoyable activities, such as reading
way. So, | tried to stay away from potentially harmful situa- stories she liked. At adolescence she discovers
tions, and lived in a world of my own. When | was younger, she has become something of a social outcast
my classmates used to tell me that at parties they would and this maintains her low self-esteem and
turn the lights down and dance, but | would sit in the cor- feelings of not being liked, which further main-
ner playing with my bike lights. |would often stay off school tains social avoidance. She shows a number of
and read books all day — that would comfort me because | the symptoms of avoidant personality disorder,
liked the stories. My real life became less important to me including avoiding activities that involve sig-
and | didn’t participate in social events apart from just try- nificant interpersonal contact because of fears
ing to be pleasant when needed. As | grew older, | should of criticism, disapproval or rejection, a preoccu-
have developed a different defence system, but | couldn't pation with being criticized or rejected in social
because | had become pretty much a social outcast and the situations, and views herself as socially inept and
fear of being criticized and rejected had got stronger. It was personally unappealing to others.
like | was in a vicious circle that | couldn't get out of!
CHAPTER12 PERSONALITY DISORDERS ey
if an individual is diagnosed with one of the disorders, first- from a preset schedule causes them significant distress,
degree relatives of that individual are two to three times as does failing to achieve the highest of standards in the
more likely to be diagnosed with either of them (Tillfors, things they do, and their attention to detail and their inflex-
Furmark, Ekselius & Fredrikson, 2001). ibility will often annoy other people because of the delays
and inconvenience that this may cause (DSM-5 Summary
Dependent personality disorder Table 12.11). For example, they may hold up a work pro-
This disorder is characterized by a pervasive and excessive ject by insisting that their component of the project has
need to be taken care of that extends significantly beyond to be completed meticulously and in the way in which it
the caring relationships that most individuals would have was originally specified. Individuals with obsessive com-
with one another. Individuals with dependent personal- pulsive personality disorder nearly always plan ahead
ity disorder exhibit submissive and clinging behaviour and
have great difficulty making everyday decisions (e.g. what
clothes to wear) without receiving advice from significant DSM-5 SUMMARY TABLE 12.10 Criteria for dependent person-
others. They are usually passive and will allow others to ality disorder
make all important decisions for them, including where e Aninescapable and extreme need to be taken care of,
they should live, what job they should choose and how leading to submissive and clingy behaviour and fear
they should spend their free time. They have difficulty of separation, beginning in early adulthood and indicated
expressing disagreement with others and will often agree by at least five of the following:
with things that they know to be wrong or inappropriate ¢ Cannot make everyday decisions without an unneces-
rather than risk losing the support and help of those they sarily high level of advice and reassurance from others
look to for guidance. They will also go to excessive lengths
e Needs others to assume the majority of responsibility
to secure support and guidance from others — even to the for the major areas of his/her life
point of taking on jobs and tasks that they find unpleas-
e Struggles to express disagreement with someone for
ant — and they will make regular self-sacrifices and tolerate
fear of loss of support
continuous verbal, physical and even sexual abuse in order
to retain their relationship with those they are dependent e Has difficulty initiating/doing things on his/her own
on (e.g. the wife who will tolerate her husband’s infideli- e Feels uncomfortable or afraid when left alone due to a
ties, drunkenness and physical abuse because of fear of fear of not being able to care for oneself
losing the support she needs or of being left to care for e Urgently seeks to secure another caring and supportive
herself). Such individuals tend to be pessimistic and self- relationship when the previous one ends
doubting, and belittle their own achievements. They will
e Is unrealistically obsessed with fears of being left to take
regularly ‘tag along’ with significant others in order not to
care of oneself
be alone and will usually rebound from one relationship
to another in order to ensure the continual care and atten-
tion they need (DSM-5 Summary Table 12.10).
The characteristics of dependent personality disorder
appear to fall into two distinctive categories: (1) attach-
ment/abandonment, in which the individual fears aban-
donment and constantly seeks attachment with significant
others, and (2) dependency/incompetence, in which the
individual has constant feelings of incompetence which
drive them to rely on others (Gude, Hoffart, Hedley & Ro,
2004). Because of their selfdoubting and over-dependence,
individuals with dependent personality disorder often dis-
like themselves (Overholser, 1996), which may lead to
depression, anxiety, eating disorders and suicidal ideation
(e.g. Godt, 2002) (Photo 12.1).
Austria/Bridgeman
Musikfreunde,
Images.
der
Gesellschaft
Wien,
Obsessive compulsive personality disorder PHOTO 12.1 From letters and biographies of Wolfgang
Individuals with this disorder show exceptionally per- Mozart it was assumed he may have suffered from bipolar
fectionist tendencies, including a preoccupation with disorder because of periods of depression followed by bouts of
orderliness and control at the expense of flexibility, effh- mania. However, more recent analyses suggest he may have
ciency and productivity. They will stick to rules, work been suffering from dependent personality disorder because of
schedules and prearranged procedures to such a degree his mood lability, impulsiveness and his negative reactions to
that the overall purpose of the activity is lost. Diverging his wife's absences (Huguelet & Perroud, 2005).
ve Peed PSYCHOPATHOLOGY
DSM-5 SUMMARY TABLE 12.11 Criteria for obsessive a visit to a restaurant well in advance, the menu needs ‘to
compulsive personality disorder (OCPD) be checked to ensure that everyone will be happy with
* An ongoing pattern of concern with orderliness, perfection what is on offer, and the quality of the restaurant's ser-
and mental and interpersonal control, at the expense of vice must be checked with friends who have been there or
flexibility, openness and efficiency, beginning in early by consulting dining reviews. If this planning is disrupted
adulthood and indicated by at least four of the following: (e.g. if the restaurant is closed when the party arrives), this
e An obsession with details, rules, lists, organisation or will cause the individual considerable distress and a spon-
schedule to the exclusion of the main point of the activity taneous alternative will be difficult for them to consider.
e Perfectionism that hinders task completion
If things are not done ‘their way’, this also causes distress,
which may be taken to unnecessary extremes (such as ask-
e Excessive devotion to work to the prohibition of social
ing a child to ride his/her bike in a straight line or telling
and leisure activities
people that there is only one way to wash the dishes). They
e Inflexibility about matters of morals, ethics or values will then become upset or angry if people do not comply,
e Is unable to dispose of worn-out or worthless objects although the anger is rarely expressed directly. Because
despite them having no sentimental value of this they will rarely delegate tasks, but insist on doing
e Reluctant to delegate to others unless they submit to them themselves, and often become viewed as ‘workahol-
exactly his/her way of doing things ics’. Their perfectionist tendencies also mean that they
e Hoards money and is reluctant to spend on their self
often end up hoarding things rather than throwing them
or others away; they will also adopt a miserly attitude to spending,
believing that money should not be wasted. Because of
e ls rigid and stubborn
this, they often end up living at a standard well below what
they can afford. OCPD is.one of the most prevalent of the
meticulously and are unwilling to contemplate changes to personality disorders, with a recent large-scale epidemiol-
their plan. This means that even hobbies and recreational ogy study recording a lifetime prevalence rate of 7.8 per
activities are approached as serious tasks requiring organi- cent and rates being similar between males and females
sation and scheduling. For example, they will need to plan (Grant, Mooney & Kushner, 2012).
OBSESSIVE COMPULSIVE PERSONALITY DISORDER (OCPD)

Jane likes to describe herselfas a perfect mother. She takes pride in keeping an orderly household and attending
all of her daughters’ horse-riding events, while also being office manager in an insurance company. She knows
the schedules of each family member and follows rigid routines to make sure everyone gets to work or school
on time. Jane gets very upset when her teenage daughters want to go out with friends at weekends or in the
evenings. She says it takes away from their family time and all of her efforts and planning are wasted. She refuses
to go out for the evening if this interferes with her planned weekly activities in the house. Her husband doesn’t
mind Jane planning his schedule but he does complain when he helps out with the household chores because
HISTORY
CASE
12.2 she consistently complains that he hasn't followed her instructions properly. For example, if he does the shop-
ping but does not get the right discounted items, Jane gets upset and accuses him of being careless and extrava-
gant. Jane continually tells everyone that if she wants something doing properly, she has to do it herself, and she
will religiously clean the house in exactly the same way every week - whether things are dirty and untidy or not.
Clinical Commentary
Jane exhibits many of the symptoms of OCPD and probably has the minimum four symptoms required for
a DSM-5 diagnosis. These are a preoccupation with details, rules, lists, order, organisation or schedules to the
extent that the major point of the activity is lost (e.g. she will do the housework each week in exactly the same
way regardless of whether this is necessary), she is excessively devoted to work and productivity to the exclusion
of leisure activities, she is reluctant to delegate tasks or to work with others unless they submit to exactly her
way of doing things, she shows rigidity and stubbornness, and adopts a miserly spending style. From this brief
case description you can see that Jane frequently gets upset and anxious about family life because of her rigid
perfectionism (and this may well lead to a comorbid diagnosis of generalized anxiety disorder, see Chapter 6)
and her rigid and inflexible behaviour also puts severe strains on family relationships.
While these characteristics may seem very simi- patients diagnosed with OCD as ranging only between
lar to the symptoms of obsessive compulsive disorder 23 and 34 per cent (Albert, Maina, Forner & Bogetto,
(OCD) (see Chapter 6), the exact relationship between 2004; Lochner, Serebro, van der Merwe, Hemmings et
OCPD and OCD has been the subject of debate for al., 2011). However, regardless of whether OCPD is a
_ some time. Some clini- risk factor for OCD, individuals diagnosed with comor-
To complete Activity 12.1 go to \ cians have argued that bid OCPD and OCD do appear to exhibit more severe
www.wiley-psychopathology.com/ _ OCPD is a precursor for symptoms, are more functionally impaired and are
activities/ch12
the development of OCD _ likely to develop other problems such as alcohol depend-
(Krockmalik & Menzies, ence and depression (Garyfallos, Katsigiannopoulos,
2003). However, OCPD is not a necessary precursor of _Adamopoulou, Papazisis et al., 2010; Gordon, Salkovskis,
OCD and studies have found the prevalence of OCPD in Oldfield & Carter, 2013).
SELF-TEST QUESTIONS
® Personality disorders generally consist of a loosely bound cluster of subtypes. What are the four common features of all
personality disorders?
* What are the three clusters of personality disorders listed in DSM-5, what are the disorders listed in each cluster, and what
are their main defining features?
® Can you list the diagnostic criteria for (1) antisocial personality disorder, and (2) borderline personality disorder?
° Schizophrenia spectrum disorder, bipolar disorder spectrum and society anxiety spectrum are broader disorder categories
associated respectively with which individual personality disorders?
SECTION SUMMARY
12.2 PERSONALITY DISORDERS AND THEIR DIAGNOSIS
While the different personality disorders we have discussed may seem to take quite contrasting forms (e.g. some represent
withdrawn and avoidant forms of behaviour, some are characterized by behavioural and emotional lability and impulsivity,
and others are characterized by intense fears of criticism, rejection and abandonment), they are all assumed within DSM-5 to
represent enduring patterns of behaviour that we would consider to be close to the borderline of what is adaptive/maladap-
tive, normal/abnormal or culturally acceptable/unacceptable. Because the behavioural styles of individuals with personality
disorders can be conceptualized as being on normal personality dimensions — albeit at the extremes of these dimensions
(Costa & MacRae, 1990) - there is an issue about what it is that is ‘disordered’
or‘abnormal’ about personality disorders, and this
is likely to be addressed with dimensional measurements for personality traits in future editions of DSM (see section 12.1.3).
The key points are:
¢ DSM-5 lists 10 diagnostically independent personality disorders that are organized into three primary clusters: (1) odd/
eccentric — containing paranoid, schizoid and schizotypal personality disorders, (2) dramatic/emotional — containing anti-
social, borderline, narcissistic and histrionic personality disorders, and (3) anxious/fearful — containing avoidant, dependent
and obsessive compulsive personality disorders.
e Paranoid personality disorder is characterized by an enduring pattern of distrust and suspiciousness of others.
e |ndividuals with schizoid personality disorder are often described as ‘loners’
who fail to express a normal range of emotions
and appear to get little reward from any activities.
e Schizotypal personality disorderis characterized by‘eccentric’ behaviour marked by odd patterns of thinking and communication.
e The main features of antisocial personality disorder (APD) are an enduring disregard for, and violation of, the rights of others.
It is characterized by impulsive behaviour, lack of remorse and is closely linked with adult criminal behaviour.
© The defining characteristics of borderline personality disorder (BPD) are instability in personal relationships, a lack of well-
defined and stable self-image, regular and unpredictable changes in moods, and impulsive behaviour.
© The individual with narcissistic personality disorder overestimates their abilities, inflates their accomplishments, has a perva-
sive need for admiration, and also shows a lack of empathy with the feelings of others.
PSYCHOPATHOLOGY
© Individuals with histrionic personality disorder are attention-seeking and are uncomfortable or unhappy when they are not
the centre of attention.
Y
e The main features of avoidant personality disorder are avoidance of a wide range of social situations, feelings of inadequacy,
and hypersensitivity to negative evaluation and criticism.
° Dependent personality disorder is characterized by a pervasive and excessive need to be taken care of, submissive and cling-
ing behaviour, and difficulty making everyday decisions without advice from others.
* Individuals with obsessive compulsive personality disorder (OCPD) show exceptionally perfectionist tendencies, including a
preoccupation with orderliness and control at the expense of flexibility, efficiency and productivity.
e Many personality disorders are highly comorbid with other psychiatric disorders suchas anxiety and mood disorders
(including bipolar disorder, major depression, social anxiety disorder, panic disorder and PTSD).
epererrrerrrrrrrerrr rrr rrrrrrrrrr rrr rrr rtrrrrrtrrr ttt ite
temporal stability of personality disorder diagnoses over

12.3 THE PREVALENCE OF time (Zimmerman, 1994). This variability in estimated
PERSONALITY DISORDERS prevalence rates is reflected in the data presented in Table
12.3, showing a selection of sources providing preva-
lence rates from both American and European studies.
There has generally been some uncertainty about the These data suggest that the prevalence rate for person-
actual prevalence rates of personality disorders within ality disorders in the general population is between 10
the general population, and this uncertainty stems from and 14 per cent, which makes personality disorders one
issues to do with: (1) reliability in the diagnosis of per- of the most common of the psychopathologies (see also
sonality disorders (McGlashan, Grilo, Sanislow, Ralevski Sansone & Sansone, 2011). But the variability in these
et al., 2005; Paris, 2010); (2) potential gender bias in diag- figures across different studies makes it difficult to draw
nosis of some of the disorders — particularly histrionic, many conclusions about prevalence, except perhaps that
borderline and dependent personality disorders (Widiger obsessive compulsive personality disorder is probably the
& Trull, 1993; Hartung & Widiger, 1998); and (3) the poor most common.
TABLE 12.3 Personality disorders prevalence rates
Prevalence Prevalence Prevalence rate in

rate in general rate in general Prevalence rate in a community
population population general population sample
Personality (DSM-IV-TR (USA) (Norway) (UK)
Cluster disorder estimate) (Grant et al.,2004) (Torgersen et al., 2001) (Coid et al., 2006)
All personality 14.7% 13.4% 10.7%

disorders
Cluster A Paranoid 0.5-2.5% 44% 2.4% 0.7%

(odd/eccentric ae, ; ; ;
personality PEN Uncomnron 3.1% 1.7% io)
0.8%
disorders) Schizotypal 3% - 0.6% 0.06%
Cluster B Antisocial 3% in males 3.6% 0.7% 0.6%

(dramatic/ 1% in females
emotional :
personality seeleilin:
0
oe
a
0.7% 0.7%
disorders) Histrionic 2-3% 1.8% 2.0% 0%
Narcissistic <1% ~ 0.8% 0%
Cluster C Avoidant 0.5-1% 2.3% 5.0% 0.8%
fandeuss Dependent 0.4% 9
fearful person- P sae (pi: oN
ality disorders) Obsessive com- 1% 7.8% 2.0% 1.9%
pulsive personality
disorder
&
There are some significant gender differences in these and sexual abuse is also a significant risk factor for devel-
prevalence rates. Coid, Yang, Tyrer, Roberts & Ullrich oping a personality disorder (Johnson, Cohen, Brown,
(2006) report that all personality disorder categories Smailes & Bernstein, 1999) — especially borderline per-
were more prevalent in men, but Widiger & Trull (1993) sonality disorder (Hefferman & Cloitre, 2000) — and sig-
in their study found that 75 per cent of individuals diag- nificant levels of childhood verbal abuse increase the risk
nosed with borderline personality disorder were female. of a number of personality disorders, including paranoid,
Coid et al. (2006) also found that personality disorders borderline, narcissistic and obsessive compulsive (Johnson,
were highly comorbid, with the mean number of per- Cohen, Smailes, Skodol et al., 2001). However, although
sonality disorders per individual with a diagnosis being these findings suggest that childhood abuse may well be an
1.92 (see Table 12.4). The differences in prevalence rates important factor in the development of a personality dis-
recorded by different studies may be explained by dif- order in some individuals, it is unclear whether other types
ferences in sampling procedures, diagnostic procedures, of risk factors — such as low socio-economic status, living
number of disorder categories and cultural differences in in inner cities, being divorced, separated or never married —
the identification and diagnosis of personality disorders. are causal factors in developing personality disorders or are
Unfortunately, with the future changes proposed to the simply outcomes of having a personality disorder.
diagnosis of personality disorders, we are unlikely to get a Studies of those suffering from psychopathology
clear picture of prevalence rates for some time to come! suggest that individuals with personality disorders are
There are also numerous risk factors for personality amongst the most frequently treated by mental health
disorders and these include (1) low socio-economic class, professionals. In a study of psychiatric outpatients,
(2) living in inner cities, (3) being a young adult, and (4) Zimmerman, Rothschild & Chelminski (2005) found that
being divorced, separated, widowed or never married slightly less than one-third of all psychiatric outpatients in
(Torgersen, Kringlen & Cramer, 2001; Grant, Hasin, their sample were diagnosed with at least one personality
Stinson, Dawson et al., 2004). Childhood physical, verbal disorder. This is consistent with the fact that personality
TABLE 12.4 Comorbidity of borderline personality disorder and other personality disorders with psychological disorders
Borderline personality Other personality disorder

disorder patients with patients with other
Disorder category Disorder other diagnoses diagnoses
Mood disorders Major depression 83% 67%

Dysthymia 39% 25%
Bipolar II disorder 10% 1%
Substance abuse disorders Alcohol abuse/dependence 52% 45%

Drug abuse/dependence 46% 42%
Anxiety disorders Panic disorder 48% 20%

Agoraphobia 12% 3%
Social anxiety disorder 46% 19%

Specific phobia 32% 15%
OCD 15% 6%
PTSD 56% 21%
Generalized anxiety disorder 13% 3%
Somatisation disorders Somatisation disorder 4% 0%
Hypochondriasis 5% 2%
Somatoform pain disorder 4% 2%
Eating disorders Anorexia nervosa 21% 13%
Bulimia nervosa 26% 17%
Source: Data taken from Zanarini, Frankenburg, Dubo, Sickel et al. (1998). Diagnoses were determined using DSM-IILR criteria, which may give rise to
some inconsistencies in comorbidity rates when compared with current DSM-5 criteria.
426 PSYCHOPATHOLOGY
disorders are highly comorbid with other psychopatholo- behaviour patterns typical of antisocial or narcissistic per-
gies — particularly anxiety and mood disorders (Zanarini, sonality disorder to be less prevalent in men and histri-
Frankenburg, Dubo, Sickel, 1998) — and it is usually the onic, avoidant and dependent personality disorders less
comorbid and more specific disorder that has brought the prevalent in women because these behaviour patterns
individual into treatment. This reflects the view that the are considered to be relatively more acceptable. However,
individual with a personality disorder will often view their at present there is very little evidence to suggest that the
behaviour as quite normal (because they have ‘always’ prevalence rates of personality disorders do exhibit cul-
behaved like that), but what brings them to therapy are tural differences, as might be predicted if diagnostic cri-
the more specific and distressing consequences of their teria are strictly applied. More cross-cultural studies are
behaviour such as unstable or turbulent relationships, sex- required in this respect. «
ual dysfunction, substance abuse, eating disorders, anxiety Some studies have identified ethnicity as a factor affect-
disorders such as panic disorder or social phobia, mood ing rates of diagnosis of personality disorder. For example,
disorders, deliberate self-harm and suicide attempts. Chavira, Grilo, Shea, Yen et al. (2003) identified signifi-
Finally, because DSM-5 defines personality disorders cantly higher rates of borderline personality disorder in
in terms of behaviour that ‘deviates markedly from the Hispanic than in Caucasian and African Americans, and
expectations of the individual’s culture’, we might expect higher rates of schizotypal personality disorder in African
some cultural differences in the rates at which differ- Americans compared with Caucasians. McGilloway, Hall,
ent personality disorders are diagnosed. For example, in Lee & Bhui (2010) found a lower prevalence of personal-
some countries it is seen as more acceptable for men to be ity disorders among black compared with white patients
domineering, demanding and competitive while women in UK studies, but they conclude that this may indicate a
might adopt more submissive and dependent behaviours neglect of personality disorder diagnosis among minority
(see Alarcon, 1996). In such countries we might expect ethnic groups in the UK,
“SELF-TEST QUESTIONS
° What is the estimated prevalence rate for personality disorders in the general population?
* Do prevalence rates for personality disorders vary with culture and ethnicity?
SECTION SUMMARY
12.3. THE PREVALENCE OF PERSONALITY DISORDERS
¢ The prevalence rate for personality disorders in the general population is around 13-14 per cent, which makes them one of
the most common of the psychopathologies.
° Risk factors for developing a personality disorder include (1) low socio-economic status, (2) living in inner cities, (3) being a
young adult, (4) being divorced, separated, widowed or never married, and (5) childhood neglect and childhood physical,
verbal and sexual abuse.
behaviours, dramaticandimpulsive behaviours, dependent

12.4 THE AETIOLOGY OF and avoidant behaviours), so we might expect that different
PERSONALITY DISORDERS clusters and, indeed, different personality disorders may
be acquired in quite different ways. One characteristic that
was thought to be common to all personality disorders
Explaining the development of the extreme and enduring was that the respective behaviour patterns were rela-
behavioural styles characteristic of personality disorders tively enduring and can be traced back to childhood and
is still very much in its infancy. There will almost certainly early adolescence, suggesting that either inherited or
be no overarching or all-inclusive theory of the aetiology developmental factors may be quite important across
of personality disorders because the different clusters rep- all of the personality disorders. However, the belief that
resent quite different patterns of behaviour (e.g. eccentric personality disorders might be a lifetime affliction has
CHAPTER 12 PERSONALITY DISORDERS ar
been challenged, with research suggesting that person- a genetic link between Cluster A disorders and schizo-
ality disorder diagnoses have poor stability over time phrenia. Studies have indicated that risk for all three
(Zimmerman, 1994) and 75 per cent of individuals with types of Cluster A disorder is increased in relatives of
an early diagnosis of borderline personality disorder individuals diagnosed with schizophrenia (Bernstein,
no longer meet diagnostic criteria after 10 to 15 years Useda & Siever, 1993; Battaglia, Bernardeschi, Franchini,
(Zanarini, Frankenburg, Hennen, Reich & Silk, 2006). So Bellodi & Smeraldi, 1995; Nigg & Goldsmith, 1994).
there is evidence that at least some personality disorders Even in adopted children whose biological mothers
will either remit over time or will be responsive to effec- have been diagnosed with schizophrenia, there is a sig-
tive treatments. nificantly higher risk of developing schizotypal per-
We will continue by looking at aetiological factors in sonality disorder than if the biological mother was not
each of the three personality disorder clusters. diagnosed with schizophrenia (Tienari, Wynne, Laksy,
Moring et al., 2003). All of these studies suggest a genetic
link between Cluster A personality disorders and schizo-
12.4.1 Odd/Eccentric Personality phrenia. Secondly, individuals with Cluster A disorders
have been shown to possess brain abnormalities that
Disorders (Cluster A) closely resemble those found in schizophrenia (Fervaha
As we mentioned earlier, individuals diagnosed with & Remington, 2013). For example, individuals with schi-
Cluster A personality disorders have characteristics that zotypal personality disorder show abnormalities in frontal
resemble many of the symptoms of schizophrenia, such as lobe and temporal lobe activation that are very similar to
paranoid beliefs (paranoid personality disorder), they may those found in individuals with schizophrenia (Siever &
be socially withdrawn with flat affect (schizoid personality Davis, 2004). In addition, they also exhibit the enlarged
disorder), or exhibit rambling or disorganized thoughts and ventricles frequently found in the brains of schizophren-
speech (schizotypal personality disorder). As we shall see, ics (Buchsbaum, Yang, Hazlett, Siegel et al., 1997), sug-
these formalistic similarities between Cluster A disorders gesting similarities in abnormal brain development across
and schizophrenia have led researchers to argue that they schizophrenia and _ schizotypal personality disorder.
are part of a broader schizophrenia spectrum disorder and so Thirdly, individuals with Cluster A disorders (particularly
have causes that are closely linked to the aetiology of schiz- schizotypal personality disorder) also exhibit some of the
ophrenia itself (Siever & Davis, 2004; Bergman, Harvey,
physiological abnormalities possessed by individuals with
Mitropoulou, Aronson et al., 1996). Before we discuss the schizophrenia, and these include impairment of smooth
schizophrenia spectrum approach, let us briefly mention pursuit eye movements (see Chapter 8) and inability to
some other approaches to explaining Cluster A disorders. inhibit the startle response to weak stimuli (Siever, Haier,
Coursey, Sostek et al., 1982; Cadenhead, Swerdlow, Shafer,
Psychodynamic approaches Diaz & Braff, 2000). Fourthly, individuals with Cluster A
In the case of both paranoid and schizoid personality disor- disorders also show many of the deficits in cognitive and
ders, psychodynamic theorists have argued that the causes executive functioning exhibited by individuals with schiz-
of these disorders lie in the relationships that the sufferer ophrenia, and these include impaired working memory,
had with their parents. In the case of paranoid personal- episodic memory, spatial attention, and reduced verbal IQ
ity disorder, parents may have been demanding, distant, (Dickey, McCarley, Niznikiewicz, Voglmaier et al., 2005;
overly rigid and rejecting (Manschreck, 1996), and the lack Mitropoulou, Harvey, Zegarelli, New et al., 2005). Taking
of love provided by parents makes the individual suspi- all of these factors into account, there is strong evidence
cious and lacking in trust of others (Cameron, 1974). In linking schizotypal personality disorder to the aetiological
contrast, parents of individuals with schizoid personality factors implicated in schizophrenia generally, and schizo-
disorder may have rejected or even abused their children, typical personality disorder has been explicitly included in
resulting in the child being unable to give or receive love DSM-5 in its chapter on schizophrenia spectrum disorders.
(Carstairs, 1992). As we shall see later, there is certainly
some evidence that individuals with personality disorders
may have suffered childhood abuse and neglect (Johnson, 12.4.2. Dramatic/Emotional
Cohen, Brown, Smailes & Bernstein, 1999), so there is Personality Disorders (Cluster B)
some supportive evidence for this view.
Some of the Cluster B disorders share a number of char-
The schizophrenia spectrum disorder acteristics in common, such as impulsivity (antisocial
There are three lines of evidence suggesting that Cluster and borderline disorders), lack of empathy (antisocial and
A-type personality disorders are closely related to schiz- narcissistic disorders), emotional outbursts and agegres-
ophrenia and make up a schizophrenia spectrum dis- siveness (histrionic and borderline disorders). This sug-
order. Firstly, there is considerable evidence suggesting gests that there may be some common elements in the
428 PSYCHOPATHOLOGY
we IMPULSE-CONTROL DISORDERS
N
=
= in one study 42 per cent of those diagnosed with

2 kleptomania also met the criteria for a personality
fe) disorder (the most common were paranoid, schiz-
a. oid and borderline) (Grant, 2004). However, impulse
wv
=) disorders are classified separately from personality dis-
WU orders because they are also highly comorbid with a
fe)
Li number of other disorders. For instance, kleptomania
frequently co-occurs with substance use disorders and
sufferers often have first-degree relatives who are them-
selves suffering from a substance use disorder (Grant,
2006; Dannon, Lowengrub, Aizer & Kotler, 2006). High
rates of manic and depressive disorders have also been
recorded amongst those with impulse-control disorders
(Kim, Grant, Eckert, Faris & Hartman, 2006), but it isnot |
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clear whether these mood problems are causes or effects
Many of the personality disorders — especially Cluster B of the impulsive behaviour. For example, pathological
disorders — are characterized by impulsivity, including gamblers often begin to feel depressed as their financial
unpredictability in behaviour and aggressive outbursts. losses mount and their personal relationships are dis-
However, DSM-5 classifies a number of impulse-based rupted. Alternatively, some individuals who are initially
problems separately. These are known as disruptive, depressed may find compulsive gambling gives them an
impulse-control and conduct disorders, and are charac- exhilarating ‘buzz’ that distracts briefly from the pain of |
terized by the failure to resist an impulse, drive or temp- depression.
tation to perform an act that is harmful to the person Those diagnosed with kleptomania steal regularly, |
or to others. Examples of impulse-control disorders are: impulsively and will usually steal items that have no |
financial or personal worth. Sufferers experience an
Intermittent explosive disorder Discrete epi- often intense period of tension building up before the
sodes of failure to resist aggressive impulses that theft, but then experience relief and gratification after-
frequently result in criminal assaults or destruction wards. Thefts are usually undertaken alone, are not
of property. pre-planned and stolen goods may often be returned
after the event. Individuals with kleptomania are usu-
Kleptomania_ Recurrent failure to resist impulses
ally aware that the act of stealing is wrong and sense-
to steal objects that either have little or no mon-
less, and feel guilty and depressed about their actions.
etary or personal value (e.g. impulsive shoplifting).
Opportunistic shoplifting is one common form of klep-
Pyromania_ Recurrent patterns of fire setting for tomania, but studies suggest that only around 5 per
pleasure, gratification or relief of tension. cent of those convicted of shoplifting meet DSM crite-
ria for kleptomania (DSM-IV-TR, p.668). Kleptomaniacs
In most of these disorders, the individual feels an have been shown to rate their feelings of inner tension
increasing sense of tension or arousal before committing before stealing as significantly higher than undiag-
the impulsive act and then experiences pleasure, gratifi- nosed shoplifters, and they also exhibit significantly
cation or relief when the act is committed. Following the greater feelings of relief after the crime (Sarasalo,
act, the individual will often suffer regret or guilt, suggest- Bergman & Toth, 1997).
ing that the sufferer is aware that their behaviour is wrong A large-scale survey in the US estimated that the life-
but are unable to control it (known as ego dystonia). time prevalence rate for impulse-control disorders was
Many ofthe impulse-control disorders are frequen- 24.8 per cent, with a median age of onset as early as 11
tly comorbid with personality disorders. For example, years of age (Kessler, Berglund, Demler, Jin et al., 2005).
aetiology of these disorders, and, indeed, some theorists underlying disorder that manifests in men as APD and
argue that some of the different Cluster B disorders may women as BPD (Widiger & Corbitt, 1997), and narcis-
be different manifestations of a single underlying disorder sistic personality disorder shares antisocial behaviour,
with a common aetiology. For example, some research- deceitfulness and lack of empathy and remorse with
ers consider that antisocial personality disorder (APD) APD. However, as we shall see, most of the research on
and borderline personality disorder (BPD) are the same the aetiology of Cluster B disorders has been directed at
CHAPTER 12 PERSONALITY DISORDERS 429°
attempting to explain the development of the behaviour behaviour before the age of 11 is also a good predictor
patterns in individual disorders. of APD in adulthood (Robins, 1966), as is early fighting
and hyperactivity (Loeber, Green, Lahey & Kalb, 2000)
Antisocial personality disorder and low IQ and low self-esteem (Fergusson, Lynskey &
The main behavioural characteristics of antisocial per- Horwood, 1996). In particular, Loeber, Wung, Keenan,
sonality disorder are impulsivity, aggressiveness, deceitful- Giroux et al. (1993) have argued that there are three path-
ness, lying, irritability, repeated irresponsibility and lack of ways that predict APD in adulthood. These are:
remorse, and a history of criminal activity and childhood
1. an ‘overt’ aggressive pathway that progresses
conduct disorder. As with all personality disorders, the the-
from bullying to fighting to serious violence,
oretical challenge with APD is to explain why certain indi-
viduals develop these behavioural styles and why they can 2. a covert aggressive pathway that progresses
be so enduring and often resistant to change. Because APD from lying and stealing to more serious damage
is closely associated with criminal and antisocial behaviour, to property, and
considerable effort has been invested in attempting (1) to 3. an ‘authority conflict’ pathway that progresses
identify childhood and adolescent behaviours that may help through various degrees of oppositional and
to predict later adolescent and adult APD (e.g. patterns of defiant behaviour.
childhood antisocial behaviour or childhood abuse), (2)
Behaviours in the early stages of each of these path-
to identify the developmental factors that may give rise
ways predict more serious specific antisocial behaviours
to APD (e.g. factors associated with family and early envi- later in life.
ronment), (3) to ascertain whether there is an inherited or
Many studies have emphasized that adolescent problem
genetic component to APD, and (4) to identify any bio-
behaviours are strong predictors of adult APD. McGue &
logical or psychological processes that may be involved in Iacono (2005) found that adolescent smoking, alcohol use,
APD (e.g. brain abnormalities or dysfunctional cognitive illicit drug use, police trouble and sexual intercourse (all
processes such as faulty beliefs). We will look separately at before 15 years of age) each significantly predicted APD
these approaches to understanding APD. One caution we symptoms in later life. In fact, for those who exhibited
must post at this stage is that much of the research on APD four or more of these problem behaviours prior to age
has been conducted using a variety of different methods 15, there was a 90 per cent likelihood of subsequent APD
of defining APD: some studies have used DSM diagnos- diagnosis in males and a 35 per cent probability in females.
tic criteria while others have used earlier definitions of Furthermore, a possible link between childhood ADHD
antisocial behaviour such as the concept of ‘psychopathy’ and APD is discussed in Focus Point 12.2.
(Checkley, 1976) and only 20 per cent of people with a Perhaps disappointingly, most of these studies merely
DSM diagnosis of APD will score high on measures of psy- indicate that adult antisocial behaviour defined by APD
chopathy (Rutherford, Cacciola & Alterman, 1999). is predicted by adolescent and childhood antisocial
behaviour. However, such studies do demonstrate that
Childhood and adolescent behavioural precursors the behaviour patterns are often enduring and that these
of APD Because APD is closely associated with crimi- behaviours during childhood and early adolescence should
nal behaviour, and on many occasions with violent or be taken as indicators of the possible need for intervention.
homicidal criminal behaviour, there has been a keen inter- For factors involved in causing APD we need to explore
est in attempting to identify risk factors for it. Identifying developmental, psychological and biological factors.
potential risk factors might allow clinicians to predict the
development of APD from childhood behaviour patterns Developmental factors There is a range of views
or childhood experiences and might identify individuals about how familial factors might influence the develop-
who may respond to early clinical intervention. ment of APD and, because APD is an antisocial disorder,
One of the best predictors of APD in adulthood is a there has been much speculation about how maladap-
diagnosis of conduct disorder (CD) during childhood in tive socialisation might have contributed to this pattern
which the child exhibits a range of behavioural prob- of behaviour. One important fact is that there is a high
lems that include fighting, lying, running away from incidence of APD in the parents of individuals with APD
home, vandalism and truancy (Farrington, Loeber & van (Paris, 2001), suggesting that one important developmen-
Kammen, 1990). This, however, begs the question of how tal factor may be the learning of antisocial behaviours
such antisocial behaviours had developed in childhood through modelling and imitation (although this may also
and we may have to refer back to ineffective parenting indicate a genetic or inherited component — see below).
practices, discordant and unstable family life, poor peer For example, the children of parents with APD may
relationships and educational failure to trace the origins often see aggressive and deceitful behaviour rewarded —
of these behaviours (Hill, 2003). Persistent and aggressive especially if a parent has had a relatively successful
S IS ATTENTION DEFICIT HYPERACTIVITY DISORDER (ADHD)

N
A RISK FACTOR FOR ANTISOCIAL PERSONALITY DISORDER?
_
-
= Some researchers have suggested that conduct dis- 60
\e)
oa. order in childhood is not the only psychological diag-
Vv) nosis that predicts APD in later life. Lynam (1998) has 50
=) argued that children with hyperactivity/attention defi-
U 40
2) cits (such as attention deficit hyperactivity disorder) are
LL. ‘fledgling psychopaths’ who because of their impulsivity 30
and attentional problems are likely to develop into long-
20
term psychopaths - not least because their underlying
problems are of a neuropsychological nature that are (%)
years)
(18-19
APD
likely to be resistant to behavioural treatments. However,
more recent studies that have been based on structured
Neither ADHDonly CDonly ADHD+CD
diagnostic interviews do not necessarily support this view.
DSM-III-R diagnostic groups
Lahey, Loeber, Burke & Applegate (2005) investigated
whether a diagnosis of conduct disorder (CD) or ADHD in FIGURE 1 Laheyet al. (2005) investigated whether a
males between 7 and 12 years of age predicted a diagnosis
childhood diagnosis of conduct disorder (CD) or attention
of APD at 18-19 years. While conduct disorder predicted
deficit/hyperactivity disorder (ADHD) predicted a diagno-
subsequent APD in around 50 per cent of the participants,
sis of antisocial personality disorder (APD) at 18-19 years
ADHD predicted APD at rates no better than if the child had
of age. The results show that while around 50 per cent of
neither ADHD or CD at ages 7-12 (see Figure 1), suggesting
those diagnosed with either CD or CD and ADHD went on
that ADHD during childhood is not a significant differential
to develop APD, ADHD did not predict subsequent APD
predictor of APD in later life. More recent analyses suggest
any better than if a child had neither disorder.
only a weak link between ADHD and APD in prospective Source: Lahey, B.B., Loeber, R., Burke, J.D. & Applegate, B.
studies (Klein, Mannuzza, Olazagasti, Roizen et al., 2012), or (2005). Predicting future antisocial personality disorder in
that if youths with comorbid conduct disorder and ADHD males from a clinical assessment in childhood. Journal of
do develop APD it is due to the levels of conduct disorder, Consulting and Clinical Psychology, 73, 389-399. American
not the influence of ADHD (Smith & Hung, 2012). Psychological Association. Reproduced with permission.
Ls OY By Senet
ei etCA Nott Oe
PREDICTORS OF ANTISOCIAL BEHAVIOUR AND VIOLENT CRIME

A oe
iE Antisocial personality disorder (APD) is closely associ- e Fighting and hyperactivity
< ated with criminal and antisocial behaviour. Hence, ° Low !Q and low self-esteem
efforts have been focused on attempting to identify ° Persistent lying
|
7, childhood predictors of these behaviours. The hope e Running away from home
i here is that being able to identify such individuals at ° Vandalism
WU an early stage may prevent crime and enable either ® Truancy
Oo
Le
treatment or re-education programmes to be directed ° Discordant and unstable family life
at individuals at risk of developing APD. e Educational failure
Some childhood and early adolescent predictors of ° Adolescent smoking, alcohol use, illicit drug use,
APD that have been identified include: police trouble and sexual intercourse before the
age of 15 years
e Adiagnosis of conduct disorder in childhood ° Having at least one parent diagnosed with APD
° Persistent and aggressive behaviour before the * Coming from a background of family violence,
age of 11 years poverty and conflict.
criminal career. Alternatively, parents may have patterns toys or sweets — a reaction that is likely to increase the
of parenting which inadvertently reward their children frequency of such behaviours rather than suppress them.
for aggression, impulsivity and deceitfulness (Capaldi & Parents may play a more discrete role in developing
Patterson, 1994). For instance, parents may try to calm APD tendencies through the emotional relationship they
down an aggressive or impulsive child by giving him/her have with their children. Psychodynamic explanations of
CHAPTER 12 PERSONALITY DISORDERS 431-
APD argue that a lack of parental love and affection during any inherited antisocial characteristics exhibited by the
childhood is likely to lead to the child failing to learn trust adopted child in ways that may compound their prob-
(Gabbard, 1990). This lack of love and affection can take lems, for example, by responding to antisocial behaviour
a number of forms and there is evidence that individuals in the child with harsh discipline, hostility and lack of
with APD come from backgrounds of family violence, warmth (Ge, Conger, Cadoret, Neiderhiser et al., 1996).
poverty and conflict — including separation and divorce Heritability of APD and antisocial psychopathy traits
(Farrington, 1991; Paris, 2001). In such circumstances, the appear to be moderate, with estimates of heritability
child is likely to have had little experience of positive emo- between 40 and 69 per cent (Eley, Lichtenstein & Moffitt,
tional relationships and is more likely to have experienced 2003; Torgersen, Myers, Reichborn-Kjennerud, Roysamb
conflict and aggression as a normal way of life. Finally, et al., 2012), and with the highest estimates being related
some studies have identified both inconsistent parenting to aggressive aspects of APD (Burt & Donnellan, 2009).
and harsh parenting (e.g. corporal punishing, hitting, kick- In addition, studies suggest that the heritability of APD
ing, slapping and emotional coercion such as insulting, and substance use disorder may be related, and this may
threatening or belittling) as being important in developing account in part for the high comorbidity between these
antisocial behaviours (Burnette, Oshri, Lax, Richards & two disorders (Kendler, Prescott, Myers & Neale et al.,
Ragbeer, 2012). Parents of individuals with APD also fre- 2003; Gizer, Ehlers, Vieten, Feiler et al., 2012). Finally,
quently fail to be consistent in disciplining their children in molecular genetic studies are beginning to identify the
addition to failing to teach them empathy and responsibil- specific gene locations of some APD characteristics,
ity (Marshall & Cooke, 1999). At least one reason for this with the long allele of the serotonin transporter gene
lack of consistency in parenting is that many of the fathers 5-HTTLPR linked specifically with the emotional deficits
of individuals with APD also exhibit the disorder. found in APD (Sadeh, Javdani & Verona, 2013).
However, we must be cautious about how we inter-
pret these developmental factors. They may not represent Cognitive models Some recent models have argued
causal factors in the development of APD, but merely rep- that individuals with APD have developed dysfunctional
resent failures and inconsistencies in parenting that are a cognitive schemas that cause their responses to various situ-
consequence of having a child with severely disruptive and ations to be extreme, impulsive and changeable. For exam-
impulsive behaviour. We must also remember that because ple, Young, Klosko & Weishaar (2003) have suggested that
an individual with APD may have a parent with the disor- individuals with APD possess five important and relatively
der does not mean that they have learnt such behaviours independent dysfunctional schemas, and — when res-
from the parent — the disorder may involve psychological ponding to important events — they are assumed to switch
and biological dysfunctions that may be inherited rather quickly and unpredictably between schemas in a way
than learnt (such as maladaptive physiological reactions that makes their behaviour dysfunctional schemas In personality
that give rise to impulsivity and risk seeking — see below). 4PPeat impulsive — and disorders, a set of dysfunctional beliefs that
unpredictable. Young and are hypothesized to maintain problematic
Genetic factors There is clear evidence that APD his colleagues proposed five behaviour characteristic of a number of
personality disorders (e.g. antisocial per-
appears to run in families and, apart from the develop- important schema modes that sonality disorder and borderline personal-
mental factors that may contribute to this effect, there determine the responses ity disorder).
is also the possibility that there is a genetic or inherited and reactions of individuals
component to APD. Twin studies have demonstrated sig- with APD. As we will see from the nature of these schema
nificantly higher concordance rates for APD in MZ twins modes, it is claimed that they are developed as a result of
than in DZ twins (Lyons, True, Eisen, Goldberg et al., abuse and neglect experienced during childhood (Horowitz,
1995) and adoption studies have also shown that incidence Widom, McLaughlin & White, 2001; Marshall & Cooke,
of APD in the adopted child is better predicted by APD in 1999). The five dysfunctional schemas are:
the biological than in the adopted mother (Ge, Conger,
1. the ‘abandoned and abused child’ mode (genera-
Cadoret, Neiderhiser et al., 1996). However, twin and
ting feelings of pain, fear of abandonment, and
adoption studies have also indicated that there are impor- inferiority),
tant environmental factors also involved in the develop-
2. the ‘angry and impulsive child’ mode (where
ment of childhood antisocial behaviour and APD. The
bottled up aggression is discharged as anger),
home environment and parenting behaviour of adop-
tive parents have a significant role to play in the develop- 3. the ‘punitive parent’ mode (where the individual
ment of antisocial behaviours in the adopted child, with views themselves as having done something
conflict and violence in the adopted home contributing wrong or as evil and worthless),
significantly to the development of antisocial behav- 4. the ‘detached protector’ mode (a state where the
iours in the adopted child (Reiss, Heatherington, Plomin, individual endeavours not to feel the pain and
Howe et al., 1995). Adoptive parents may also react to emotion caused by the first three modes), and
By ee PSYCHOPATHOLOGY
; * %
5. the ‘bully and attack’ mode (where the individual behaviour such as their failure to learn from experience
hurts other people to overcompensate for, or to cope and their inability to empathize with the feelings of oth-
with, mistrust, abuse, deprivation and defectiveness) ers. Firstly, they exhibit significantly lower levels of anxi-
(Lobbestael, Arntz & Sieswerda, 2005). ety than normal control participants. This is exhibited
The development of instruments to measure these as a relative inability to learn to avoid physically aver-
various schema modes has shown that individuals diag- sive stimuli such as electric shock (Lykken, 1957), lower
nosed with APD do indeed score higher on measures reactivity and baseline levels of physiological indicators
of these five dysfunctional modes than non-clinical of anxiety such as skin conductance (Herperts, Werth,
participants (Lobbestael, Arntz & Sieswerda, 2005). Lukas, Qunaibi et al., 2001; Hare, 1978) and a failure to
Individuals with APD are assumed to switch rapidly exhibit increased startle. reactions when being shown
and unpredictably from a ‘healthy adult’ mode — where stimuli designed to elicit negative emotions (Levenston,
their behaviour appears normal — to pathological modes, Patrick, Bradley & Lang, 2000). Indeed, low skin con-
and this can occur rapidly when the individual expe- ductance responses to loud noises at 3 years of age have
riences negative emotions such as anger (Lobbestael & been found to predict psychopathology scores at age 28,
Arntz, 2012). Because schemas such as these form part of suggesting it is a potential risk factor for the develop-
the individual’s normal way of thinking, the person with ment of APD (Glenn, Raine, Venables & Mednick, 2007).
APD does not recognize them as faulty. If such dysfunc- Secondly, individuals with APD regularly respond to emo-
tional schemas do represent important causal factors in the tional or distressing stimuli with slow autonomic arousal
antisocial behaviour exhibited by individuals with APD, and appear to possess low levels of electroencephalo-
then challenging and replacing these dysfunctional sche- graphic (EEG) activity (Dinn & Harris, 2000; Lindberg,
mas may represent a useful starting point for treating the Tani, Virkkunen, Porkka-Heiskanen et al., 2005). This
disorder (Beck & Freeman, 1990). suggests that they may.have difficulty maintaining nor-
mal daytime arousal and may also be able to ignore
Physiological and neurological factors Individ- threatening or distressing stimuli more easily than most
uals with APD show some interesting physiological people. This in turn may explain why individuals with
characteristics which may help to explain aspects of their APD are unable to identify with the distress of others and
DEFICITS IN FEAR CONDITIONING IN ANTISOCIAL

PERSONALITY DISORDER (APD)
A seminal study by Lykken (1957) suggested that individuals with what ge @@=sessssscnececenmesmenemenomm
was then labelled as a sociopathic personality were unable to learn to j To read Lykken’s article on anxiety in
the sociopathic personality go to
avoid physically aversive stimuli, and this learning deficit may explain ; www.wiley-psychopathology.com/
why individuals with APD are able to ignore threatening signals and also ~ reading/ch12
appear to lack the ability to learn from experience about events that
have negative outcomes.
This learning deficit can be demonstrated in a simple laboratory-based conditioning experiment and labora-
tory studies such as this often serve as good analogues of real-life learning situations.
A study by Birbaumer, Viet, Lotze, Erb et al. (2005) replicated Lykken’s original study. They used a differential
aversive conditioning procedure in which male faces acted as the conditioned stimuli (CSs). For some partici-
pants, faces with a moustache (CS+) were followed by an aversive unconditioned stimulus (US) (in this case a
painful pressure applied to the hand or arm), while faces without a moustache (CS-) were followed by nothing.
For other participants the painful US followed the faces without moustaches and the moustached faces were
followed by nothing (a counterbalanced procedure so that conditioning could not be affected by the specific
features of the CS).
Normally, participants would show signs of anxiety during the CS+ (as recorded by physiological measures
such as skin conductance levels) and would also rate the CS+ face as less pleasant than the CS- face. Birbaumer
et al. compared the performance of 10 psychopaths (six of whom met DSM-IV criteria for APD) with 10 healthy
control participants. While the normal, healthy participants rated the CS+ as significantly less pleasant than the
CS-, the psychopaths showed no difference in pleasantness ratings even after 16 pairings of CS+ with the US,
suggesting that they had failed to learn the significance of the aversive-signalling CS+.
RESEARCH
METHODS
PSYCHOLOGY
CLINICAL
IN
12.1
may also be more risk-seeking than normal because of correlates of behaviour patterns that have been acquired
the need to experience higher levels of stimulation before in other ways (such as through childhood experiences).
they feel aroused (Hesselbrock & Hesselbrock, 1992).
Thirdly, individuals with APD frequently fail to show any Borderline personality disorder
signs of fear learning in aversive conditioning procedures Individuals with BPD exhibit a wide range of behavioural
(where, for example, a conditioned stimulus predicts the and psychological problems including fear of abandonment
presentation of an aversive unconditioned stimulus such and rejection, unpredictable mood swings, impulsivity, fre-
as an electric shock) (Lykken, 1995) and functional brain quent and prolonged bouts of depression often associated
imaging studies have shown that this failure to learn is with suicidal ideation, self-harm and suicide attempts. This
accompanied by inactivity in the brain circuits believed is a diverse range of characteristics for a single theory to
to mediate fear learning (e.g. the amygdala) (Birbaumer, encompass, and this is without considering the fact that
Viet, Lotze, Erb et al., 2005). These findings are consistent BPD is commonly comorbid with at least one other psy-
with the fact that individuals with APD will usually fail chological disorder (see section 12.2.2). As we shall see
to learn from experience about events that have negative below, theories developed to try to address the aetiology
outcomes and they will continue to persevere with their of BPD often attempt to explain the development of one
ingrained set of responses in such circumstances. aspect of the disorder (such as fear of abandonment, mood
A number of recent studies have also indicated that lability or impulsivity), but it is worth starting this section
individuals with APD have impaired performance on with an overview by reviewing some of the risk factors
neuropsychological tests of prefrontal cortex function- that predict the development of BPD and then moving on
ing (Dinn & Harris, 2000; Raine & Yang, 2007) and these to more specific biological and psychological theories.
areas of the brain play an important role in inhibiting
impulsivity. This may represent a brain abnormality that Risk factors for borderline personality disorder
contributes to the impulsive behaviour exhibited by such Many studies have reported that individuals with BPD
individuals and may help to explain some aspects of their report a history of difficulties in childhood — many asso-
antisocial behaviour by their apparent inability to inhibit ciated with problematic parenting. These include child-
inappropriate behaviours in social contexts. hood physical, verbal and sexual abuse (Herman, Perry &
van der Kolk, 1989; Zanarini, Williams, Lewis, Reich
Summary of theories of APD Predictive theories of et al., 1997), childhood neglect or rejection (Zanarini,
the aetiology of APD are still relatively underdeveloped, Frankenburg, Reich et al., 2000; Guttman, 2002), incon-
but we have already learnt some interesting facts about sistent or loveless parenting (Kernberg, 1985) and inap-
the kinds of factors that put an individual at risk for propriate parental behaviour such as persistent substance
developing APD. APD appears to run in families, with a and alcohol abuse or promiscuity (Graybar & Boutilier,
genetic element being involved and the family environ- 2002). Individuals with BPD report rates of childhood
ment also playing a significant role. Children raised in physical, sexual, verbal abuse and neglect ranging from
families low on parental love, with inconsistent or harsh 60-90 per cent (Gabbard, 1990), including 67-87 per cent
parenting, or with parental conflict are more likely to for sexual abuse (Bryer, Nelson, Miller & Krol, 1987).
develop APD, as are individuals who have suffered child- Herman, Perry & van der Kolk (1989) found rates of 71
hood abuse or neglect. Individuals with APD also appear per cent for physical abuse amongst people diagnosed
to have dysfunctional cognitive schemas that lead them to with BPD compared with only 38 per cent amongst psy-
behave either aggressively or impulsively, and we still chiatric patients who had not been diagnosed with BPD.
need to discover whether there is a link between the Other studies have identified a number of developmental
development of these dysfunctional schemas and their antecedents of BPD, including abuse, neglect, environ-
early experiences. Finally, individuals with APD show a mental instability, paternal psychopathology, academic
number of physiological and neurological characteris- underachievement, low intelligence and artistic skills
tics, such as physiological indicators of low anxiety, low (Helgeland & Torgersen, 2004). Prenatal adversity in the
levels of baseline arousal and reactivity, lack of learning in form of prenatal maternal distress, drug taking, tobacco
simple aversive conditioning procedures, and neurologi- smoking, or medical complications has also been shown
cal impairments indicative of impulsivity. These charac- to be a risk factor for the subsequent development of BPD
teristics all appear to be consistent with the behavioural (Schwarze, Mobascher, Pallasch, Hoppe et al., 2013).
characteristics of APD (such as aggressive and impulsive However, despite these developmental risk factors
behaviour, lack of empathy, and failure to learn accept- being significant predictors of BPD, we must remem-
able adaptive responses), but we are still unclear about ber that around 20 per cent of individuals who develop
whether these physiological and neurological indica- BPD have never reported experiencing childhood abuse
tors are true causes of APD or whether they are simply or neglect (Gabbard, 1996; Graybar & Boutilier, 2002),
so such experiences are not a necessary condition for features of BPD. In particular, activation of the ligubic
developing BPD. areas and the amygdala is often excessive, which may be
responsible for the extreme emotional reactions often dis-
Biological theories of BPD Biological theories cover played by individuals with BPD (Lis, Greenfield, Henry,
genetic factors, brain and neurological abnormalities, Guilé & Dougherty, 2007; Silbersweig, Clarkin, Goldstein,
and biological contributions to impulsivity. Tuescher et al., 2007). Nevertheless, while these abnor-
Firstly, there is some modest evidence for a genetic malities are important correlates of BPD symptoms, it is
component to BPD. The disorder does appear to run in still far from clear whether these abnormalities represent
families (Baron, Risch, Levitt & Gruen, 1985), and twin a consequence of the disorder or a genetically or develop-
studies have indicated concordance rates of 35 per cent mentally determined cause of the disorder (Lieb, Zanarini,
and 7 per cent for MZ and DZ twins respectively Schmahl, Linehan & Bohus, 2004).
(Torgersen, Lygren, Oien, Skre et al., 2000). Genetic analy-
ses have also indicated that traits common in BPD, such as Psychological theories of BPD We have seen that
neuroticism and emotional dysregulation (labile moods a majority of individuals with BPD report experiencing
and unpredictable rapid mood changes), have a strong relatively high levels of childhood abuse and difficult or
inherited component (Nigg & Goldsmith, 1994; Livesley, neglectful parenting, and a number of psychological the-
Jang & Vernon, 1998). More recent research has linked ories of BPD attempt to explain how these experiences
BPD with bipolar disorder, and the two are often comor- might cause the behavioural and emotional problems
bid (Smith, Muir & Blackwood, 2004). Deltito, Martin, characteristic of the disorder.
Riefkohl, Austria et al. (2001) have estimated that around Some forms of psychodynamic theory, such as object-
44 per cent of individuals with BPD belong to a broader relations theory, argue that people are motivated to
bipolar disorder spectrum, which may help to account respond to the world through the perspectives they have
for their regular and unpre- learnt from important
object-relations theory Argues that
bipolar disorder spectrum A proposed dictable mood changes. other people in their devel- individuals with borderline personality
spectrum of disorder encompassing both
Because we already know opmental past. However, if disorder (BPD) have received inadequati
bipolar disorder and borderline personality
disorder. that there is a significant these important others support and love from important other
genetic component to bipo- have offered only inade- (such as parents) and this results in an
insecure ego, which is likely to lead to la
lar disorder (see section 7.2.2), this provides circumstantial quate support and love, or of self-esteem and fear of rejection.
evidence for a genetic component to at least some of the in fact have been actively
symptoms characteristic of BPD. abusive, then this is likely to cause the child to develop an
Secondly, evidence suggests that individuals with insecure ego, which is likely to lead to lack of self-esteem,
BPD have a number of brain abnormalities that may give increased dependence and a fear of separation and rejec-
rise to impulsive behaviour. They tend to possess relation — all central features of BPD (Bartholomew, Kwong
tively low levels of the brain neurotransmitter serotonin & Hart, 2001; Kernberg, 1985). Object-relations theory
and this is associated with impulsivity (Norra, Mrazek, also argues that individuals with weak egos engage in a
Tuchtenhagen, Gobbele et al., 2003) and may account for defence mechanism called splitting, which means
their regular bouts of depression (see Chapter 7). There that they evaluate people, a
splitting An element of object relation
is also some evidence for dysfunction in brain dopamine events or things in a com- theory which argues thatindividuals
activity in BPD and such dopamine activity is known pletely black-or-white way, with weak egos engage ina defence
to play an important role in emotion information pro- often judging people as mechanism by which they evaluate peo
cessing, impulse control and cognition (Friedel, 2004). either good or bad with no events or things in a completely black
white way, often judging people as eithe!
However, much of this evidence is currently circumstan- shades of grey. This may good or bad with no shades of grey.
tial and derives mainly from the fact that administration give rise to their difficulties
of drugs that influence serotonin and dopamine activity with relationships, in which their all-or-none assessments
also appear to influence BPD symptoms. mean that someone they evaluate as ‘good’ can just as
Thirdly, neuroimaging techniques of individuals with quickly become ‘bad’ on the basis of a single act or state-
BPD have revealed abnormalities in a number of brain ment (e.g. if a partner does not return from a work social
areas, primarily in frontal lobe functioning and in the event at exactly the time they said they would, the indi-
limbic system, including the hippocampus and amygdala vidual with BPD is likely to respond with anger and
(Juengling, Schmahl, Hesslinger, Ebert et al., 2003; Soloff, threaten to withdraw from the relationship). People with
Meltzer, Becker, Greer et al., 2003). The frontal lobes are BPD also have a tendency to perceive others as quarrel-
thought to play an important role in impulsive behaviour some, which triggers negative affect and leads to more
and the amygdala is an important part of the brain system quarrelsome behaviour during their interactions with oth-
controlling and regulating emotion — these abnormali- ers (Sadikaj, Moskowitz, Russell, Zuroff & Paris, 2013).
ties may contribute to some of the defining behavioural Interestingly, Suvak, Litz, Sloan, Zanarini et al. (201 1)
CHAPTER 12 PERSONALITY DISORDERS — 435—
found that individuals with a diagnosis of BPD judged is a very frail self-esteem, which means they constantly
their own emotions primarily on dimensions of valency, need to seek reassurance.
and hardly at all on dimensions of arousal. This suggests Psychodynamic theories of narcissistic PD have argued
that they are likely to judge their emotions in an “all-or- that the traits associated with this disorder result from
nothing’ way with relatively little intensity control, lead- childhood experiences with cold, rejecting parents who
ing to extreme swings in emotions. rarely respond with praise at their children’s achievements
While object-relations theory is consistent with the fact or displays of competence (Kohut & Wolf, 1978). Indeed,
that a majority of individuals with BPD have experienced such parents may often dismiss their children’s successes
childhood abuse, conflict and neglect, one problem is that in order to talk about their own achievements. Because
such experiences are common features of many of the of these experiences, such children then try to find ways
personality disorders (including antisocial, paranoid, nar- of defending against feelings of worthlessness, dissatisfac-
cissistic and obsessive compulsive personality disorders) tion and rejection by convincing themselves that they are
(Klonsky, Oltmanns, Turkheimer & Fiedler, 2000). This worthy and talented (Wink, 1996; Kernberg, 1985). The
being the case, an account such as object-relations theory end product is someone with a vulnerable self-esteem
does not easily explain how such negative early experiences who seeks reassurance about their talents and achieve-
get translated into BPD rather than these other disorders ments from themselves and others, and who has devel-
which also have such experiences as part of their history. oped a lack of empathy with others because of the cold
We have already noted the high levels of comorbidity and uncaring parenting they have experienced. In support
between the different personality disorders (Marinangeli, of this view, there is some evidence that individuals with
Butti, Scinto, Di Cicco et al., 2000); in particular, between narcissistic PD are more likely to come from backgrounds
10 and 47 per cent of individuals with BPD also display involving child abuse, conflict and neglect (Kernberg,
antisocial behaviour and meet the diagnostic criteria for 1985). However, evidence of childhood abuse and neglect
antisocial personality disorder (Zanarini & Gunderson, is not a sufficient condition for a child to develop narcis-
1997). This suggests that there may be some common- sistic PD and some other theorists have argued that the
ality of aetiology between the two disorders and we disorder results from ‘doting’ parents who treat their chil-
have already noted that significant childhood abuse and dren too positively in a way that fosters unrealistic gran-
neglect is apparent in both groups. This has led Young, diose self-perceptions (Millon, 1996). Interestingly, there is
Klosko & Weishaar (2003) to suggest that individuals with some circumstantial evidence to support this view, in that
BPD may develop a similar set of dysfunctional schema measures of narcissism often show that scores are often
modes to those acquired by individuals with APD. We higher in first-borns or only children, where parents may
have already described these dysfunctional schemas in have been able to devote more time and attention to their
relation to APD and Young, Klosko & Weishaar have children (Curtis & Cowell, 1993).
argued that these dysfunctional schema also determine Narcissistic personality disorder is also closely asso-
reactions to events in individuals with BPD, such as dis- ciated with antisocial personality disorder. Narcissistic
sociation (Johnston, Dorahy, Courtney, Bayles et al., individuals will regularly act in self-motivated, deceitful
2009). Subsequent studies have confirmed that individu- and aggressive ways very reminiscent of APD and also
als with APD and BPD do score higher than non-patients exhibit lack of empathy (Ritter, Dziobek, Preissler, Ruter
on measures of these dysfunctional schemas and also et al., 2011) (see Case History 12.3). However, individuals
report levels of childhood abuse that were higher than with narcissistic PD can be reliably differentiated from
non-patients (Lobbestael, Arntz & Sieswerda, 2005). individuals with APD by their sense of grandiosity and
This suggests a significant amount of similarity in both self-importance (Gunderson & Ronningstam, 2001), so
the developmental history of BPD and APD and in the we need to look closely at factors that determine these
dysfunctional cognitive schemas that characterize these characteristics (Thomaes, Bushman, de Castro & Stegge,
disorders. This has led some researchers to argue that 2009). Narcissists appear to hold grandiose, but simulta-
APD and BPD may be different manifestations of one neously tentative, unstable self-views that require them
single underlying disorder which may express itself as to seek continuous self-validation and dominance over
BPD in women and APD in men (Paris, 1997; Widiger & others. As such they may be addicted to self-esteem and
Corbitt, 1997). continually create social situations in which they hope
they can receive boosts to their self-esteem (Baumeister &
Narcissistic personality disorder Vohs, 2001). But how does this tendency develop?
As we described earlier, the individual suffering narcis- Thomaes, Bushman, de Castro & Stegge (2009) argue that
sistic personality disorder is someone who overestimates it develops out of an interaction between an inherited sen-
their abilities and inflates their accomplishments but has sitivity to positive or desirable stimuli and an aversiveness
a complete lack of empathy with the desires and feelings to negative or undesirable stimuli combined with extreme
of others. However, underneath this grandiose exterior forms of parenting, such as parental overvaluation and
436 PSYCHOPATHOLOGY
NARCISSISTIC PERSONALITY DISORDER

In July 2005, Brian Blackwell - a 19-year-old public schoolboy from Liverpool — killed both his parents and then
used their credit cards to fund a £30,000 spending spree. After his arrest he was subsequently diagnosed as
suffering from narcissistic personality disorder, and was reported to have regularly fantasized about unlimited
success, power and brilliance. He had falsely claimed to be a professional tennis player and applied for numerous
credit cards to help fund his fantasies. After the killings, Blackwell went on holiday to the US with his girlfriend,
spending huge sums of money while staying at expensive hotels in New York.
12.3
HISTORY
CASE
Clinical Commentary
Many researchers believe that narcissistic personality disorder is closely associated with antisocial personality
disorder, and individuals with the disorder usually show clear signs of deceitfulness, lying, lack of empathy with
the feelings of others, acting impulsively and aggressively, showing no remorse for acts of harm or violence, and
going to any lengths to achieve their own personal goals. Narcissistic personality disorder is differentiated from
APD by the individuals’ grandiose view of themselves and their need to brag about fantasized achievements.
The parents of some individuals with narcissistic personality disorder undoubtedly dote on them and may treat
them too positively in a way that fosters unrealistic grandiose self-perceptions (Millon, 1996).
overindulgence (Twenge, 2006) or parental coldness, manifestations of underlying conflict — especially conflicts
extremely high expectations or lack of support (Kernberg, related to acceptance by and relationships with members
1985). This diathesis—stress model is consistent with the of the opposite sex. Psychodynamic theories often differ as
fact that narcissistic traits begin to develop at 8 years of to the causes of the conflicts that underlie attention-seeking
age — at just the time that children are beginning to form and dramatic behaviour. Some suggest that the disorder is
a conscious, global evaluation of themselves (Thomaes, fostered by inconsistencies in parental attitudes towards
Stegge, Bushman, Olthof & Denissen, 2008). sex, where parents convey the view that sex is both dirty
Case History 11.3 describes the story of Brian and exciting (Apt & Hurlburt, 1994). Others suggest that
Blackwell, a student from Liverpool diagnosed with nar- the disorder arises from a childhood experience of parent-
cissistic personality disorder who tragically murdered ing that is cold and controlling, and leaves the child search-
both his parents. His behaviour is suggestive of APD in ing desperately for love and assurance (Bender, Farber &
that he is deceitful, a pathological liar and apparently Geller, 2001). Finally, other psychodynamic views focus
remorseless in the killing of his parents. However, he had specifically on the relationship between father and daugh-
a grandiose view of himself as brilliant and untouchable, ter. Because of a lack of maternal attention, some daugh-
and regularly bragged about fantasy achievements and ters may actively seek the attention and approval of their
talents. Far from coming from a background of child- fathers and this leads to a flirtatious relationship between
hood abuse and neglect, he was an only child whose father and daughter that the daughter carries on to other
parents doted on him and told friends of their great aspi- relationships later in her life (Phillips & Gunderson, 1994).
rations for him. You might like to consider how these There is little objective evidence at present to differentiate
facts might fit in with the theoretical accounts of narcis- between any of these particular psychodynamic accounts
sistic PD that we have described in this section. and they do appear to be focused more on explaining the
disorder in females than in males. As such, they may all be
Histrionic personality disorder relatively inadequate accounts of histrionic PD — especially
There has been relatively little research into the aetiology since more recent surveys have indicated that it is a disorder
of histrionic personality disorder and its poor construct that is relatively equally distributed across men and women
validity suggests that it may well be excluded as a diagnos- (Mattia & Zimmerman, 2001).
tic category in future editions of the DSM (Bakkevig &
Karterud, 2010). Theories of histrionic personality disor-
der that are currently available tend to have developed from 12.4.3 Anxious/Fearful Personality
psychodynamic accounts originally designed to understand Disorders (Cluster C)
hysteria generally. These types of accounts argue that the
dramatic displays of emotion and attention-seeking behav- Personality disorders in Cluster C exhibit mainly anx-
iour characteristic of the person with histrionic PD are ious and fearful symptoms, and are frequently linked
ib
CHAPTER12 PERSONALITY DISORDERS 7
to comorbid anxiety disorders. Very little research has emotional abuse in the avoidant PD group than the
been carried out on the aetiology of disorders in this depressed group — but this factor did not differenti-
cluster, although there have been attempts to view them ate individuals with avoidant PD from individuals with
as part of larger anxiety-based spectra of disorders (such other forms of PD. What these studies do suggest is that
as avoidant personality disorder within a social anxiety (1) avoidant PD is closely associated with social anxiety
spectrum and obsessive compulsive personality-disorder disorder and both may be part of a broader social anxi-
within an obsessive compulsive spectrum) (e.g. Schneier, ety spectrum, and (2) there are some important child-
Blanco, Antia & Liebowitz, 2002). As such, it would be hood precursors that suggest underperformance across
assumed that the personality disorders would then share a variety of childhood social domains may be predictive
some of the aetiological features of their corresponding of later avoidant PD.
anxiety disorders — although this has yet to be confirmed Finally, avoidant PD is closely associated with low
empirically. self-esteem and feelings of shame and guilt, and psy-
chodynamic accounts suggest that negative childhood
Avoidant personality disorder experiences and childhood underachievement may con-
Avoidant personality disorder is characterized by feelings tribute to a negative self-image (Gabbard, 1990). We have
of inadequacy, fear of criticism, disapproval and rejection, seen that there is some evidence for childhood negative
and avoidance of most personal interactions with others. experiences and underachievement being precursors to
It is also associated with avoidance behaviour generally later avoidant PD, but it is still far from clear (1) whether
and may be part of a broader social anxiety spectrum these experiences are consequences of the developing
(Schneier, Blanco, Antia & Liebowitz, 2002). Like many disorder or (2) if they are causal factors, how such experi-
of the personality disorders, the aetiology of avoidant ences might lead to the development of low self-esteem,
personality disorder has not been extensively researched. shame and guilt.
However, there have been a few studies investigating the
correlates and risk factors associated with avoidant person- Dependent personality disorder
ality disorder. For example, avoidant PD has been shown Some clinicians have highlighted what appear to be many
to be closely associated with scores on a variety of per- formalistic similarities between dependent personality
sonality dimensions, including introversion, neuroticism, disorder and depression. These similarities include inde-
low self-esteem, pessimism, and to self-reports of elevated cisiveness and passiveness, ae
dependent personality disorder A
emotional responsiveness to threat and reduced emo- pessimism and self-doubt-
personality disorder characterized by a
tional responsiveness to incentives (Meyer, 2002). Family ing, and low self-esteem. pervasive and excessive need to be taken
studies have also found that having a family member diag- We have already seen in care of, submissive and clinging behaviour,
nosed with either social anxiety disorder or avoidant PD Chapter 7 that individuals and difficulty making everyday decisions
suffering depressed mood without advice from others.
increases the risk for both these disorders two- to three-
fold (Tillfors, Furmark, Ekselius & Frederickson, 2001), continually seek reassur-
suggesting a close relationship between the development ance from family and friends in a way that is similar to
of social anxiety disorder the manner in which individuals with dependent person-
» and avoidant PD. This may ality disorder continually seek support and guidance
To read an article on the assessment of
——
heritability of avoidant and dependent | also be linked to a genetic (Joiner, Metalsky, Katz et al., 1999). A possible link
personality disorder by Gjerde et al. go to predisposition for avoidant between dependent personality disorder and depression
reading/ch12
personality disorder, which is also supported by the fact that drugs used to treat
" is estimated to be around depression will also significantly decrease symptoms of
27-35 per cent, and over- dependent personality disorder (Ekselius & von
laps with genetic vulnerability to social anxiety disorder Knorring, 1998). This has led psychodynamic theorists to
(Reichborn-Kjennerud, Czajkowski, Torgersen, Neale develop models of the aetiology of dependent personal-
et al., 2007), although heritability levels have been found to ity disorder that closely resemble those for depression.
be as high as 64 per cent when different methods of assess- For example, object-relation theorists claim that depend-
ing avoidant PD have been used (Gjerde, Czajkowski, ence and fear of rejection is fostered by childhood neglect
Roysamb, Orstavik et al., 2012). or loss of a parent during childhood. Alternatively, some
When compared with individuals with either major other psychodynamic theorists claim that overprotective
depression or other personality disorders, individuals parenting may cause subsequent separation anxiety,
with avoidant PD report poorer child and adolescent depression and the development of dependent personal-
athletic performance, less involvement in hobbies dur- ity disorder (Bornstein, 1996). Clearly, these very differ-
ing adolescence and less adolescent popularity (Rettew, ent accounts require some further evidence to
Zanarini, Yen, Grilo et al., 2003), and this study also differentiate them, but unfortunately there are currently
demonstrated higher levels of childhood physical and no systematic data on the childhood experiences of
438 PSYCHOPATHOLOGY
Y ©
individuals who subsequently develop dependent per- of OCPD are very similar to those of OCD, the ceponted
sonality disorder that might help to shed light on these comorbidity of OCPD in individuals with OCD is
different accounts. relatively low at 22 per cent (Albert, Maina, Forner &
Apart from formalistic similarities with depression, Bogetto, 2004). In fact, this study found that comorbid-
dependent personality disorder has been found to be ity of OCPD in individuals with panic disorder was 17
regularly comorbid with a number of anxiety disorders, per cent, suggesting that OCPD is found at approxi-
particularly social anxiety disorder, obsessive compul- mately the same level in individuals with panic disor-
sive disorder and panic disorder (McLaughlin & Mennin, der as it is in individuals with OCD. In addition, family
2005). But once again, it is unclear whether dependent studies have indicated that individuals with OCPD are
personality disorder is associated with an increased no more likely than chance to have close relatives with
risk for developing an anxiety disorder (and what the OCD, which does not suggest a genetic link between
mechanism for this increased risk might be) or whether OCPD and OCD (Nestadt, Samuels, Riddle, Bienvenu
anxiety disorders increase the risk for dependent per- et al., 2000). At present there is very little evidence avail-
sonality disorder. Further research is needed to clarify able that enables us to identify important factors in the
these relationships and to help understand aetiological aetiology of OCPD, and significantly less that enables
factors important to the development of dependent us to predict those individuals who will develop OCPD
personality disorder. as opposed to OCD. Some studies of non-clinical popu-
lations indicate there may be a single underlying vul-
Obsessive compulsive personality disorder nerability factor for both OCPD and OCD, and this may
A first place to look for evidence relating to the aeti- be related to a parenting style that includes psychologi-
ology of obsessive compulsive personality disorder cal manipulation and guilt induction (Aycicegi, Harris
(OCPD) would be its apparently related disorder, obses- & Dinn, 2002) or family transmission of symptoms to
obsessive compulsive personality sive compulsive disorder children by parents who also have OCPD symptoms
disorder (OCPD) A personality disorder (OCD) — but a review of (Clavo, Lazaro, Castro-Fornieles, Font et al., 2009). But
in which individuals show exceptionally the facts does not indicate this still begs explanations of (1) why OCPD and OCD
perfectionist tendencies including a preoc- are not highly comorbid if they share similar vulner-
a particularly close link
cupation with orderliness and control at
the expense offlexibility, efficiency and between the two disor- ability factors and (2) why some people develop OCPD
productivity. ders. While the symptoms and not OCD.
SELF-TEST QUESTIONS
° Can you describe the evidence suggesting that Cluster A disorders are genetically linked with schizophrenia?
° What are the risk factors and childhood precursors predictive of adult antisocial personality disorder (APD)?
° What is the evidence for a genetic element to antisocial personality disorder (APD)?
* Some theories argue that dysfunctional cognitive schemas underlie antisocial personality disorder. Can you name the
important schema modes described by these theories?
* What are the physiological and neurological factors associated with antisocial personality disorder (APD) and how might
they contribute to typical APD behaviour patterns?
* Can you describe the evidence suggesting that negative childhood experiences might be important in the aetiology of
borderline personality disorder (BPD)?
° What is the evidence for a link between borderline personality disorder and bipolar disorder?
* How do psychodynamic theories attempt to explain the development of borderline personality disorder?
* What might be the role of abnormal parenting in the development of narcissistic and histrionic personality disorders?
* What is the evidence for a genetic link between avoidant personality disorder and social anxiety disorder?
° What is the evidence for a link between dependent personality disorder and mood disorders?
° Is there any evidence for a link between obsessive compulsive personality disorder (OCPD) and obsessive compulsive
disorder (OCD)?
CHAPTER12 PERSONALITY DISORDERS — 439_
SECTION SUMMARY
12.4 THE AETIOLOGY OF PERSONALITY DISORDERS
This section has illustrated that the aetiology of personality disorders — compared with many other psychopathologies - is
relatively underresearched. APD and BPD have received the most attention, while research on the aetiology of other personal-
ity disorders is still at a very early stage (e.g. the Cluster C disorders). Because personality disorders can be enduring features of
an individual’s behaviour from childhood into adulthood, researchers have tended to look for factors in childhood that might
either put an individual at risk for developing a personality disorder or a be a direct causal factor in determining the behav-
ioural styles characteristic of the different disorders. For example, a diagnosis of conduct disorder in childhood appears to bea
predictor of APD in later life, as do childhood neglect and abuse in BPD. Some studies have looked at whether there is a genetic
component to personality disorders but, apart from the Cluster A disorders (paranoid, schizoid and schizotypal personality
disorders), the evidence for an inherited factor in the other personality disorders is modest.
The key points are:
Cluster A Disorders
¢ Behavioural and genetic links between Cluster A disorders (paranoid, schizoid and schizotypal personality disorders) and
schizophrenia suggest that they may be part of a broader schizophrenia spectrum disorder.
e Psychodynamic approaches to paranoid personality disorder suggest that parents may have been demanding, distant,
overly rigid and rejecting, giving rise to a lack oftrust in others.
® The risk of all three types of Cluster A disorder is increased in relatives of individuals diagnosed with schizophrenia, suggest-
ing a genetic link between schizophrenia and the Cluster A personality disorders.
Cluster B Disorders
© One ofthe best predictors of antisocial personality disorder (APD) in adulthood is conduct disorder in childhood.
e Adolescent smoking, alcohol use, illicit drug use, police trouble and sexual intercourse before the age of 15 significantly
predict antisocial personality disorder in later life.
e Antisocial personality disorder appears to run in families, suggesting that APD may be acquired through social learning
and imitation.
® Psychodynamic approaches to antisocial personality disorder suggest that lack of parental love and affection during child-
hood and inconsistent parenting is likely to lead to the child failing to learn trust.
¢ Heritability of APD traits appears to be moderate, with estimates between 40 and 69 per cent, with highest estimates
related to aggressive traits.
¢ Individuals with both antisocial personality disorder and borderline personality disorder appear to possess a set of dysfunc-
tional cognitive schemas that give rise to their unpredictable mood swings and impulsive behaviour.
® |ndividuals with APD show a number of physiological and neurological characteristics, such as physiological indicators of
low anxiety, low levels of baseline arousal and reactivity, lack of learning in simple aversive conditioning procedures, and
neurological impairments indicative of impulsivity.
e Individuals with borderline personality disorder (BPD) report rates of childhood physical, sexual, verbal abuse and neglect
ranging from 60-90 per cent, suggesting that these experiences may be important in the development of BPD.
© Twin studies of borderline personality disorder have indicated concordance rates of 35 per cent and 7 per cent for MZ and
DZ twins respectively, suggesting a genetic element to BPD.
e Recent research has linked borderline personality disorder with mood disorders and around 44 per cent of individuals with
BPD belong to a broader bipolar disorder spectrum, which may account for the regular and unpredictable mood swings in BPD.
e Neuroimaging studies of BPD have identified brain abnormalities in the limbic system, including the hippocampus and
amygdala.
® Object-relations theory argues that individuals with BPD have received inadequate support and love from important others
(such as parents) and this results in an insecure ego, which is likely to lead to lack of self-esteem and fear of rejection.
¢ Between 10 and 47 per cent of individuals with borderline personality disorder also meet the diagnostic criteria for antiso-
cial personality disorder, suggesting a link between the two disorders.
PSYCHOPATHOLOGY
Psychodynamic theories of narcissistic personality disorder argue that the traits associated with this disorder result from
childhood experiences with cold, rejecting parents who rarely praised their children’s achievements.
Narcissistic personality disorder is also closely associated with antisocial personality disorder, and narcissistic individuals
will regularly act in self-motivated, deceitful and aggressive ways reminiscent of APD.
Narcissists appear to hold grandiose but simultaneously tentative, unstable self-views that require them to seek continuous
self-validation and dominance over others.
There is relatively little research on the aetiology of histrionic personality disorder and theories that are currently available
tend to have developed from psychodynamic accounts. .
Cluster C Disorders
® Having a family member diagnosed with either social anxiety disorder or avoidant personality disorder increases the risk for
both disorders two- to threefold, suggesting that both social anxiety disorder and avoidant personality disorder may be
part of a broader social anxiety spectrum that has a genetic element.
Dependent personality disorder has many features similar to depression, including indecisiveness, passiveness, pessimism,
self-doubting and low self-esteem, and drugs used to treat depression are also successful at alleviating the symptoms of
dependent personality disorder.
Dependent personality disorder is also regularly comorbid with a number of other | disorders, particularly social anxiety
disorder, panic disorder and obsessive compulsive disorder.
The reported comorbidity of obsessive compulsive personality disorder (OCPD) in individuals with obsessive compulsive dis-
order (OCD) is as low as 22 per cent, suggesting that the two disorders are not closely related.
12.5 TREATING PEOPLE add to these problems, disorders that are comorbid with
a personality disorder are difficult to treat successfully
WITH A DIAGNOSIS OF (Crits-Christoph & Barber, 2002) and there may be many
reasons for these difficulties. These include:
PERSONALITY DISORDER 1. such individuals are significantly more disturbed
and may require more intensive treatment
There are numerous important factors that make than individuals with other types of psychiatric
treating personality disorders problematic and means disorder alone;
that they require an approach rather different to those 2. many personality disorders consist of ingrained
employed for many other disorders. Firstly, as we have behavioural styles that are likely to continue
mentioned throughout this chapter, personality dis- to cause future life difficulties that may trigger
orders can be enduring patterns of behaviour that an symptoms of other disorders (e.g. the individual
individual has usually deployed from childhood into with borderline personality disorder is likely
adulthood. As a consequence, the individual usually to continue to have turbulent and unstable
cannot see that their behaviour is problematic and, as a
relationships that may cause future bouts of
result, they are unlikely to believe they need to change depression and suicidal ideation); and
their behaviour, let alone seek treatment for it. Secondly,
3. many of the personality disorders have features
individuals with personality disorders usually possess
which make such individuals manipulative
patterns of behaviour that are likely to make them sus-
and unable to form trusting relationships (e.g.
ceptible to a range of other psychiatric disorders (such as
antisocial personality disorder, borderline
anxiety disorders or depression) and we have discussed
personality disorder, narcissistic personality
the extent of this comorbidity earlier. It is often for treat-
disorder) and this makes the development of a
ment of the comorbid problems that an individual with
personality disorders is first referred for treatment (e.g. working, trusting relationship between therapist
and client very difficult — even when it comes to
depression and suicidal ideation in borderline personal-
just treating any comorbid disorder.
ity disorder; social anxiety disorder in avoidant person-
ality disorder; panic disorder or social anxiety disorder Thirdly, it is worth asking what it is about per-
in dependent personality disorder; see Table 12.4). To sonality disorders that is disordered and requires
treatment — especially if the behavioural styles typical with comorbid anxiety disorders such as social anxi-
of the personality disorders are really only extremes of ety disorder or panic disorder can be prescribed tran-
what otherwise might be considered to be normal per- quilizers such as benzodiazepine; those with comorbid
sonality dimensions (Costa & MacRae, 1990). Because major depression may receive antidepressants such as
individuals with personality disorders exhibit extremes the selective serotonin reuptake inhibitor fluoxetine
of behaviour on normal personality dimensions (such (Prozac) (Rinne, van den Brink, Wouters & van Dyck,
as extraversion/introversion, conscientiousness, agreea- 2002). Lithium chloride can also be administered to
bleness/antagonism), it may be more realistic to try to individuals who have comorbid bipolar disorder (some-
moderate the existing behaviours of such individuals times diagnosed with borderline personality disorder
rather than try to change them completely. For exam- and antisocial personality disorder) in order to sta-
ple, the behaviours of individuals with obsessive com- bilize their moods and reduce antisocial behaviour.
pulsive personality disorder may be quite adaptive in Antipsychotic drugs (such as risperidone) can also be
some circumstances and situations (e.g. when dealing effective in reducing the symptoms of Cluster A person-
with an important work project) but inappropriate and ality disorders, which are known to have some relation-
maladaptive in others (e.g. when obsessively trying to ship to the symptoms of schizophrenia (Koenigsberg,
organize family and friends on a holiday). Taking this Goodman, Reynolds, Mitropoulou et al., 2001), and,
into account, the therapist may be more successful in more recently, atypical antipsychotic drugs (such as
trying to ‘normalize’ the extreme behavioural styles of quetiapine) have been shown to reduce impulsivity, hos-
the individual with a personality disorder rather than tility, aggressiveness, irritability and rage outbursts in
trying to change their ingrained behaviour patterns individuals with antisocial personality disorder (Walker,
completely (Millon, 1996). Even given that these factors Thomas & Allen, 2003). In terms of drug treatment for
are taken into account when devising interventions for direct symptoms of the personality disorders them-
personality disorders, 37 per cent of people undergoing selves, antidepressants have been found to be effective
treatment for personality disorders still fail to complete with Cluster C symptoms (avoidant personality dis-
(McMurran, Huband & Overton, 2010), and factors asso- order and obsessive compulsive personality disorder)
ciated with non-completion include young age, lower (Pelissolo & Jost, 2011). Drugs for dealing with aggres-
education levels, unemployment, having juvenile convic- sion and impulsivity, including lithium, beta-blockers,
tions, and emotional neglect in childhood. These are all carbamazepine, antipsychotic drugs and SSRIs have also
factors to bear in mind when reviewing the treatments been found to reduce symptoms in Cluster B disorders
that have been applied to personality disorders. (Pelissolo & Jost, 2011). Having said this, there are very
Finally, the scope of the personality disorders and their few randomized controlled trials that have looked at the
varied behavioural characteristics mean that treatments effects of medication on personality disorder symptoms,
are very often geared towards the requirements of indi- and what little evidence is available is often equivocal,
vidual disorders. This being so, therapists have utilized poorly controlled or conducted on only small numbers
a broad range of differing therapeutic procedures with of participants (Olabi & Hall, 2010).
varying degrees of success and we will discuss these dif-
fering approaches in turn. However, in general, individu-
als with personality disorders will need to (1) acquire a
range of life skills, (2) learn emotional control strategies, 12.5.2 Psychodynamic
and
and (3) acquire the skill of mentalisation, which is the abil-
Insight Approaches
ity to reflect on their experiences, feelings and thoughts
and to assess their meaning and importance. These are As we saw in section 12.4.1, psychodynamic approaches
all goals of therapy that can be identified across a range have a long history of attempting to explain the develop-
of conceptually different treatments for the personality ment of personality disorders, so it is not surprising that
disorders. psychodynamic and insight therapies generally should
also be prominently involved in treatments for these dis-
orders. Problematic relationships with parents and child-
hood neglect and abuse are factors that are prominent in
12.5.1 Drug Treatments attempts to explain many of the personality disorders,
Drugs are frequently used in an attempt to treat individ- and exploring and resolving these developmental expe-
uals with personality disorders, but they tend to be used riences is seen as an important role for psychodynamic
to tackle symptoms of any comorbid disorder rather therapies. Such therapists view insight as the important
than the symptoms of the personality disorder itself mechanism of change in personality disorders — not least
(but see Newton-Howes & Tyrer, 2003). Individuals because most individuals with personality disorders do
442 PSYCHOPATHOLOGY
not initially view their behaviour as problematic. This 12.5.3 Dialectical Behaviour Therapy
approach is particularly important when treating individ-
uals with borderline personality disorder (BPD) because One particular form of therapy that has been success-
these individuals represent a serious challenge to thera- fully used to treat individuals with personality disorders
pists of any theoretical orientation. Individuals with BPD is dialectical behaviour
are manipulative and will frequently game-play with the therapy (Linehan, 1987). To watch a video on dialectical
behaviour therapy go to
therapist in order to ascertain how special they are to This approach takes the www.wiley-psychopathology.com/
the therapist (e.g. by phoning the therapist regularly at client-centred view of video/ch12
inconvenient times), or they will make dramatic gestures accepting the client for
to seek attention (e.g. by threatening suicide attempts). what they are but attempts dialectical behaviour therapy A clien
They also lack trust which will make it difficult to to provide them with centred therapy for personality disorde
develop a working therapist—client relationship whatever insight into their dysfunc- that attempts to provide clients with
the therapeutic approach being used. Finally, BPD is typi- tional ways of thinking ‘insight into their dysfunctional ways of
thinking about the world.
cal of most of the Cluster B personality disorders in that about and categorising the
the individual will view the causes of their problems as world, and it is designed to
external to them (i.e. they will be the fault of other peo- provide them with the necessary skills to overcome
ple) and this makes any form of insight therapy difficult. these problematic ways of thinking and behaving. This
However, psychodynamic therapists have tended to take is not an easy thing to do with a group of people who
a more active approach to treating personality disorders are usually very sensitive to criticism and emotionally
and have attempted (1) to identify and block manipulative unstable, and who will probably react to any challenge
behaviours at an early stage, and (2) to expose the ‘weak to their current ways of thinking in extreme ways (even
egos’ and fragile self-image that usually underlie many of threatening suicide). As a result, the dialectical behav-
the personality disorders. As a particular example of psy- iour therapist has to convey complete acceptance of
chodynamic treatment, object-relations psychotherapy what the client does to enable a successful dialogue to
attempts to strengthen the individual’s weak ego so that ensue about the client’s problems and difficulties.
they are able to address Dialectical behaviour therapy subsequently includes
object-relations psychotherapy A form
of psychodynamic treatment that attempts issues in their life with- skills training designed to teach individuals to be mind-
to strengthen the individual's weak ego so out constantly flipping ful of their maladaptive ways of thinking about the
that they are able to address issues in their
from one extreme view to world (e.g. that others are not always to blame for the
life without constantly flipping from one
extreme view to another. another (Kernberg, 1985). bad things that happen), to learn to solve problems
In the case of BPD, for effectively, to control their emotions (such as their anger
example, object-relations psychotherapy will (1) attempt outbursts), and to develop more socially acceptable ways
to show the client how their normal way of behaving of dealing with their life problems.
is defensive (e.g. when they blame others for problems Dialectical behaviour therapy can be split into four
in their life), (2) how their judgements are often simplis- distinct stages: (1) addressing dangerous and impul-
tic and fall into simple dichotomous categories (such as sive behaviours and helping the client to learn how
either ‘good’ or ‘bad’) that cause them to swing regularly to manage these behaviours, (2) helping the client to
from positive to negative ways of thinking, and (3) pro- moderate extremes of emotionality (e.g. learning
vide the client with more adaptive ways of dealing with to tolerate emotional distress), (3) improving the cli-
important life issues by, for example, teaching them that ent’s self-esteem and coaching them in dealing with
other people may possess both good and bad characteris- relationships, and (4) promoting positive emotions
tics rather than either being all ‘good’ or all ‘bad’. such as happiness.
While it is difficult to objectively assess the effective- This approach has been particularly successful
ness of psychodynamic approaches to treatment, there with individuals with BPD (Robins & Chapman, 2004;
is some evidence that psychodynamic psychotherapies Bloom, Woodward, Susmaras & Pantalone, 2012); it
do have a beneficial effect on the symptoms of person- has been shown to have long-lasting positive effects
ality disorders. Some studies have suggested that clients on suicidal and non-suicidal self-harm behaviours,
do show significant improvements in symptoms during depression, interpersonal functioning, anger control and
treatment (Svartberg, Stiles & Seltzer, 2004) and that re-hospitalization (McMain, Guimond, Streiner, Cardish &
short-term psychodynamic therapy is at least as effec- Links, 2012; Linehan, Heard & Armstrong, 1993);
tive as CBT (Leichsenring & Leibing, 2003) and a range and it is particularly effective as a treatment for
of other treatments-as-usual, including general com- BPD over the longer term when combined with appro-
munity-based psychiatric treatment (Fonagy, Roth & priate medication (Soler, Pascual, Campins, Barrachina
Higgitt, 2005). et al., 2005).
12.5.4 Cognitive Behaviour Therapy constructed depends very much on the individual person-
ality disorder diagnosed and on the cognitive factors rele-
Because of the resistance of many personality disorders to vant to that individual client (see Beck & Freeman, 1990).
‘insight’ therapies, it was originally felt inappropriate However, Treatment in Practice Box 12.1 provides a brief
to try to apply CBT to this category of psychopathologies. summary of the stages through which conventional CBT
However, over the past 10 years, there has been signifi- for personality disorders would proceed.
cant progress in developing CBT in ways that are directly As a specific example, the way in which dysfunctional
relevant to the behavioural, emotional and cognitive schemata may develop in borderline personality disor-
problems found in personality disorders. Applying CBT der (BPD) is outlined in Figure 12.2. Childhood abuse is
to the treatment of people with a diagnosis of personal- assumed to contribute to the development of a number
ity disorder was arguably first pioneered by Aaron Beck of schemata typical of BPD. This leads to the self being
and colleagues, who attempted to apply CBT methods viewed as bad, vulnerable and helpless; others as malevo-
first developed to treat depression (see Chapter 7) (Beck lent, abusing and rejecting. Experienced emotion is dan-
& Freeman, 1990). This meant exploring the range of gerous and ‘clinging’ becomes a strategy designed to get
logical errors and dysfunctional schemata that might support from others, but is alternated with ‘keeping dis-
underlie problematic behaviour within individual per- tance’ because of distrust. These negative, dysfunctional
sonality disorders. For instance, an example of a logical schemata give rise to hypervigilance and the constant
error would be the individual with obsessive compul- expectation of threat and danger (Arntz, 1999).
sive personality disorder (OCPD) believing that they are In addition, because childhood traumas have never
incompetent if they do just one thing wrong. They may been fully emotionally processed, this has resulted in
also have developed dysfunctional schemata that gener- stunted emotional—cognitive development, so that indi-
ate problematic behaviour and cause emotional distress. viduals with BPD show dichotomous thinking (‘black’—
In the case of OCPD, the individual may have developed ‘white’, ‘“good’—‘bad’ thinking with no shades of grey).
beliefs that everything has to be done correctly (perhaps CBT can be used in its traditional way to challenge the
because of parental pressure to be perfectionist) and when status of these dysfunctional schemata and to attempt to
one thing is not done properly this causes emotional dis- replace them with more functional schemata and views
tress and anxiety. In most cases the way in which CBT is of the world. However, when treating individuals with
CLINICAL PERSPECTIVE - TREATMENT IN PRACTICE 12.1

CBT FOR PERSONALITY DISORDERS
The normal stages through which CBT would progress in that may have contributed to the dysfunctional
the treatment of a personality disorder are the following: behaviour patterns (such as problematic early
childhood and parenting experiences).
1. During the initial sessions the therapist will deal with 5. In collaboration with the patient, the therapist will
any coexisting psychiatric problems (usually specific prepare homework assignments tailored to the
anxiety disorders such as panic disorder or social patient's specific issues.
anxiety disorder or major depression — see Table 12.4). 6. Finally, the therapist will apply specific cognitive,
2. The therapist then teaches the patient to identify behavioural, and emotion-focused schema restruct-
and evaluate key negative automatic thoughts (e.g. uring techniques to dispute core beliefs and to
‘Nobody likes me’ or ‘I am worthless’ in avoidant or develop new and more adaptive beliefs and behaviour
dependent personality disorders). (see also section 12.5.5 on Schema-Focused Cognitive
3. The therapist will then structure the sessions Therapy).
) carefully to build a collaborative and trusting
relationship with the patient — especially in the case
of those disorders where the client is distrusting or Two main treatment objectives are, first, to help the
manipulative (e.g. borderline personality disorder). patient develop new and more adaptive core beliefs
4. The therapist may then employ guided imagery to and, second, to help the patient develop more adaptive
unravel the meaning of new and earlier experiences problem-solving and interpersonal behaviours.
444 PSYCHOPATHOLOGY
CHILD SCHEMATA
1. Sexual Abuse SELF = bad, vulnerable, helpless
2. Physical Abuse OTHERS = malevolent, abusing, rejecting
3. Emotional Abuse EMOTIONS = dangerous Vv

Hypervigilance
RELATIONS = needs help (clings) . (attentional bias)
|
Xx l
|
expects abuse/abandonment |
(repulses)
|
|
|
|
DICHOTOMOUS > BORDERLINE 4-2 5.
THINKING PD
FIGURE 12.2 A schematic representation of the way that dysfunctional schema are thought to develop in borderline personality
disorder (BPD) — see text for further elaboration.
Source: Arntz, A. (1999). Do personality disorders exist? On the validity of the concept and its cognitive-behavioral formulation and treatment.
Behaviour Research and Therapy, 37, S97-S134. Reproduced with permission.
CLINICAL PERSPECTIVE - TREATMENT IN PRACTICE 12.2

TREATING ANTISOCIAL PERSONALITY DISORDER: CAN PERSONALITY
DISORDERS BE TREATED IN PRISON POPULATIONS?
We noted earlier in this chapter that the diagnosis of individuals and recommended that people diagnosed
antisocial personality disorder (APD) is closely linked with DSPD might be required to be detained indefinitely.
with adult criminal behaviour. Surveys of prison popu- This raises the issue of whether the symptoms of indi-
lations have indicated that between 50 and 70 per cent viduals with APD who have committed serious criminal
of males in prisons meet the diagnostic criteria for APD acts can be successfully treated. We have discussed the
(Fazel & Danesh, 2002; Widiger, Cadoret, Hare, Robins etal., general difficulties of treating individuals with Cluster B
1996) and many of these have been imprisoned for vio- personality disorders. They are manipulative, suspicious,
lence, sexual offences and homicide. Between 56 and hostile to criticism, lack trust in others and are constantly
72 per cent of men convicted of serious sexual offences prone to lying in order to achieve their aims. This makes it
have been shown to be diagnosed with APD (Dunsieth, difficult to form any kind of meaningful therapist—client
Nelson, Brusman-Lovins, Holcomb et al., 2004; McElroy, relationship regardless of the theoretical orientation of
Soutullo, Taylor, Nelson et al., 1999) and, in a Finnish the therapy. Finally, individuals with APD do not usually
study, a diagnosis of APD increased the likelihood of an believe there is anything wrong with their behaviour - it
individual being convicted of homicide tenfold (Eronen, has often enabled them to achieve their goals, so why
Hakola & Tihonen, 1996). In addition, the UK Home Office should they change? This does not bode well for success-
recognized the important link between violent crimi- ful treatment of APD in criminal populations.
nal behaviour and APD and coined the term ‘dangerous If an individual with APD is incarcerated in prison,
people with severe personality disorders (DSPD)’ to then this makes treating the disorder even more difficult
describe individuals who have APD plus at least. one because of the unusual cultural requirements of pris-
other personality disorder. The Home Office report also ons. DSM-5 defines a personality disorder as ‘an endur-
recognized the difficulty in successfully treating such ing pattern of behaviour that deviates markedly from.
CHAPTER 12 PERSONALITY DISORDERS 445,
expectations within that culture’ but as Rotter, Way, communities that may help to reduce reoffending -
Steinbacher, Sawyer et al. (2002) point out, jails and pris- although it is important to note that these aims are
ons have their own cultural norms that require behaviours not the same as attempting to reduce symptoms
such as suspiciousness, hostility, social withdrawal and self- of APD. Such therapeutic communities have been
centredness. These are all behaviours that could be con- based on behavioural or cognitive behavioural prin-
strued as adaptive in institutions such as prisons, where ciples in an attempt to target cognitive deficits that
the individual has to look out for themselves and distrust relate to offending behaviour. This scheme is known
others in order to survive (Rotter & Steinbacher, 2001). For as Reasoning & Rehabilitation (R&R) (Robinson &
example, an ‘inmate code of conduct’ might include: Porporino, 2001) and the treatment targets are self-
control (thinking before acting), interpersonal prob-
¢ Do your own time (mind your own business, look
lem-solving skills, social perspective taking, critical
out for yourself, keep to yourself).
reasoning skills, cognitive style and understanding
¢ Don't snitch (don’t report other inmates, don’t trust
the values that govern behaviour; and it is worth
staff).
noting that many of these goals would address behav-
¢ Don't show weakness (look tough, appear danger-
iours typical of individuals with APD (e.g. impulsiveness,
ous, act violently if necessary).
lack of empathy). The programme has been used in
Such behaviours look exactly like the main symptoms prisons in the USA, Spain, UK, Canada and New Zealand
of APD! (Rotter et al., 2002). So, in effect, attempting to and outcome studies have suggested they result in a
treat APD in prisons is equivalent to trying to persuade modest but significant reduction in reoffending, nor-
incarcerated prisoners to behave maladaptively and per- mally of between 5 and 15
haps to leave themselves open to abuse and manipula- per cent (Robinson, 1995; To read an article on CBT for
tion by other prisoners. Friendship, Blud, Erikson, imprisoned offenders go to
Nevertheless, there have been many attempts both Travers & Thornton, 2003
reading/ch12
in Europe and the USA to develop prison therapeutic Raynor & Vanstone, 1996).
BPD in particular, the therapist (1) must avoid direct therapy (Leichsenring & Leibing, 2003). Preliminary
challenges with the client about their beliefs because of studies also indicate that, after being treated with CBT,
their intense sensitivity to criticism, and so must usually between 40 and 50 per cent of clients will have recov-
approach this stage of therapy empathetically (McGinn & ered after 1.3 to 2 years (Perry, Banon & Ianni, 1999;
Young, 1996), and (2) may attempt to approach the pro- Svartberg, Stiles & Seltzer, 2004).
cess of changing dysfunctional schemata by ‘reparent-
ing’ the client, which allows the therapist to form an
emotional attachment to the client in order to challenge 12.5.5 Schema-Focused
dysfunctional schemata (Young, Klosko & Weishaar
Cognitive Therapy
2003).
The development of specific CBT procedures for per- A more recent development of CBT for personality disor-
sonality disorders is still an active process. Procedures ders is known as schema-focused cognitive therapy or
have been developed that are specific to the cognitive and schemata therapy. Central to this approach is the concept
behavioural requirements of individual disorders (Beck & of early maladaptive schemas (EMSs) that are thought to
Freeman, 1990) and current attempts are being made to develop during childhood
schema-focused cognitive therapy In
identify maladaptive schemata that are important deter- and result in dysfunctional
the treatment of personality disorders,
minants of the behavioural styles typical of disorders beliefs and behaviours a specially developed cognitive therapy
such as BPD and APD (Young, Klosko & Weishaar, 2003). during adulthood (Young, which is used to address dysfunctional
Klosko & Weishaar, 2003). ways of thinking and maladaptive cogni-
It is still very early to be able to say with any confidence
tive schema.
that CBT offers an important and effective method of We touched on these mala-
treatment for personality disorders. However, a number daptive schemas and their
putative role in determining schemata therapy Central to this
of controlled studies have shown that CBT for personal-
approach is the concept of early maladap-
ity disorders are superior to non-therapy control condi- the unpredictable, antisocial tive schemas (EMSs) that are thought to
tions in reducing symptoms (Linehan, Tutek, Heard & and impulsive behaviours develop during childhood and result in
Armstrong, 1994; Linehan, Schmidt, Dimeff, Craft et al., typical of the more severe dysfunctional beliefs and behaviours dur-
personality disorders earlier ing adulthood.
1999) and are equally as effective as psychodynamic
446 PSYCHOPATHOLOGY
Ls ®%
in this chapter. For example, if a child is continually overly related to unfortunate childhood circumstances rather than
criticized by parents, then he/she may develop the schema representing truths about the way that person is. The sec-
‘Lam defective’. In order to deal with and cope with this ond stage is to attempt to identify and prevent schemata
schema, the child will develop strategies that in the longer avoidance responses, so that the client can experience,
term are maladaptive and act to reinforce the schema. For accept and tolerate the negative and painful emotional
example, they may develop a variety of strategies that ena- states that ensue when schemata avoidance is prevented.
ble them to avoid thinking about this schema, such as Thirdly, through the therapist’s questioning and comments,
storming off at the slightest hint of criticism, summarily the client is helped to examine the life experiences that have
breaking off relationships if there is an indication that their given rise to the maladaptive schemata. This final stage of
partner is not being affectionate, or self-harming as a means therapy is intended to reduce the belief in maladaptive sche-
of distracting from the schema. Schemata therapy outlines mata and to develop adaptive alternative perspectives on
three specific stages for therapy in these circumstances. their problematic life experiences. There is modest empiri-
First, the client needs to be convinced that their problems cal evidence for the existence of many of the elements in
and symptoms are not evidence for their maladaptive sche- schemata theory and there are a small number of effective-
mas, but in contrast their maladaptive schemas are actually ness studies available which suggest it may be a promising
a cause of their symptoms. Developing self-knowledge is and cost-effective treatment for personality disorders such
important in understanding that maladaptive schema are as BPD (Sempértegui, Karreman, Arntz & Bekker, 2013).
SELF-TEST QUESTIONS
* Can you name the factors that make personality disorders so difficult to treat?
° What is the evidence in favour of a role for drug treatment in the management of personality disorders?
* Whatare the difficulties involved in adapting cognitive behaviour therapies to the treatment of personality disorders such
as antisocial and borderline personality disorders?
° Whatare the main features of object-relations psychotherapy and dialectical behaviour therapy as applied to the treatment
of personality disorders?
SECTION SUMMARY
12.5 TREATING PEOPLE WITH A DIAGNOSIS OF PERSONALITY DISORDER
We have reviewed a range of difficulties that are involved in the treatment of individuals with personality disorders and these
difficulties often make successful treatment challenging to achieve. These difficulties include (1) denial of any psychopathology,
(2) personality characteristics that make forming a trusting relationship with a therapist difficult, (3) persistent behavioural
patterns that are likely to continue to cause future life difficulties, and (4) comorbid psychiatric disorders that usually need
to be addressed and treated before tackling any underlying personality disorder. Despite these difficulties, therapists have
been imaginative in attempting to develop a range of psychological treatments designed to tackle the important features of
personality disorders. First, drugs may be used to reduce the symptoms of any comorbid disorder, such as major depression,
bipolar disorder or anxious psychopathologies generally, and have recently been successfully deployed in the reduction of
direct symptoms of personality disorders themselves. Subsequently, a range of insight based therapies (such as dialectical
behaviour therapy) or specially developed cognitive therapies (such as schema-focused cognitive therapy) can be used to
address dysfunctional ways of thinking and maladaptive cognitive schema. In general, individuals with a personality disorder
need to (1) acquire a range of adaptive life skills (which allow them to interact and socialize successfully), (2) learn emotional
control strategies (that control anger outbursts and acute periods of depression), and (3) acquire skills which enable them to
reflect objectively on their experiences, feelings and thoughts, rather than reacting impulsively and emotionally to challeng-
ing events.
The key points are:
° Personality disorders are particularly difficult to treat successfully because individuals with personality disorders regularly
deny they have problems that require treatment and they are also highly comorbid with other psychiatric disorders, which
makes the individual significantly more disturbed.
¢ Drug treatments can be used to tackle symptoms of any comorbid anxiety or mood disorder, which in turn makes the per-
sonality disorder itself more accessible to treatment.
e Individuals with borderline personality disorder (BPD) represent a challenge to therapists of any theoretical persuasion
because they are manipulative, frequently game-play with the therapist and make dramatic gestures to seek attention
(such as threatening suicide).
*° Object-relations psychotherapy and dialectic behaviour therapy are both treatments that have been developed specifically
to deal with the difficulties posed by the treatment of individuals with personality disorders such as borderline personality
disorder.
° More recently, cognitive therapies have been developed which attempt to identify and change any logical errors, dysfunc-
tional beliefs and maladaptive schemas possessed by the individual with personality disorders (e.g. schema-focused cogni-
tive therapy or schemata therapy).
Lifetime prevalence rates for personality disorders are

12.6 PERSONALITY difficult to estimate because of differences in diagnostic
DISORDERS REVIEWED reliability and also the poor temporal stability of person-
ality disorders, but with estimates around 14-15 per cent
(see Table 12.3), they are likely to be one of the most
Personality disorders represent relatively long-standing, prevalent psychopathologies treated by mental health
pervasive and inflexible patterns of behaviour that devi- professionals (Zimmerman, Rothschild & Chelminski,
ate from acceptable norms within individual cultures. 2005).
They are regularly associated with unusual ways of Personality disorders are particularly difficult to treat
interpreting events (e.g. paranoid and schizotypal perfor a number of reasons. They are frequently comorbid
sonality disorders), unpredictable mood swings (e.g. with other psychiatric disorders such as depression and
borderline personality disorder), or impulsive behav- anxiety (which complicates treatment), individuals with
iour (e.g. antisocial personality disorder). These pat- personality disorders frequently deny their behaviour is
terns of behaviour can be traced back to childhood and problematic, and they can be distrusting and manipula-
early adolescence, and they represent ways of behaving tive in therapy. However, a number of recently devel-
that are likely to have consequences that put the individ- oped insight and cognitive therapies do appear to have
ual at risk for a range of other psychiatric disorders (such some success in treating some of the more problematic
as major depression or anxiety disorders). While DSM-5 personality disorders (such as borderline personality dis-
lists 10 diagnostically independent personality disorders order), and these include object-relations psychotherapy
that are organized into three primary clusters (odd/ (Kernberg, 1985), dialectical behaviour therapy (Linehan,
eccentric, dramatic/emotional and anxious/ fearful), 1987), cognitive therapy (Beck & Freeman, 1990) and
recent research has suggested that personality disorders schema-focused cognitive therapy (Young, Klosko &
are dimensional rather than categorical (i.e. they repre- Weishaar, 2003).
sent extremes of normal personality traits). This has led Explaining the aetiology and development of per-
DSM-5 to include an alternative approach to diagnosing sonality disorders is still largely in its infancy. However,
personality disorders that will be the subject of research because personality disorders can often be traced back
in the coming years. This alternative model requires that to childhood as persistent patterns of behaviour, many
clients be rated on various personality dimensions, and theories of personality disorders look to childhood expe-
how these dimensions combine will provide the basis for riences and developmental factors for the causes of these
diagnosis of a reduced number of specific personality extreme behaviour patterns, and it is certainly the case
disorders (see section 12.1.3). that childhood abuse, neglect and conflict can be found
Wades PSYCHOPATHOLOGY
; ; <a
in the history of many personality disorders such as to a broader bipolar disorder spectrum, which
borderline personality disorder and antisocial personal- may explain the regular mood swings in BPD
ity disorder (Gabbard, 1990; Paris, 2001). Nevertheless, (Deltito, Martin, Riefkohl, Austria et al.,
some other theorists note that individual personality 2001), and
disorders appear to have close links with other disorders 3. avoidant personality is closely associated with
and may form part of broader spectrums of disorder. For social anxiety disorder and may form part of
example: a broader social anxiety spectrum (Schneier,
Blanco, Antia & Liebowitz, 2002).
1. Cluster A disorders (paranoid, schizoid and
schizotypal personality disorders) have strong All of these factors indicate that personality disorders
behavioural and genetic links with schizophrenia are challenging to the researcher and therapist in many
and may form part of a broader schizophrenia respects: they are difficult to categorize as discrete dis-
spectrum disorder (Siever & Davis, 2004), orders, they are difficult to treat successfully, and theo- |
2. borderline personality disorder is frequently ries of their aetiology are still only at the speculative and
comorbid with bipolar disorder and may belong early stages of development.
ain To access the online resources for this chapter go to

Reading Activity
Journal article: A study of ¢ Dialectical behaviour Activity 12.1

anxiety in the sociopathic therapy Self-test questions
personality
Revision flashcards
Journal article: The herit-
Research questions
ability of avoidance and
dependent personality dis-
order assessed by personal
interview and questionnaire
Journal article: Cognitive-
behavioural treatment for
imprisoned offenders: An
evaluation of HM Prison
Service's cognitive skills
programmes
Clinical issues
References
Somatic Symptom
Disorders
ee: g cane
ORE 4o) _
satire) TO access the online resources for this chapter go to
ch13
ine _ www.wiley-psychopathology.com/
This chapter begins by describing some of the features of

those disorders collectively known in DSM-5 as somatic 13.1. THE DIAGNOSIS AND CHARACTERISTICS OF SOMATIC
symptom disorders. The diagnostic criteria, characteris- SYMPTOM DISORDERS. 451
tics and prevalence rates of the main disorders are then
described (these are somatic symptom disorder, illness 13.2 THE AETIOLOGY OF SOMATIC SYMPTOM
anxiety disorder, conversion disorder, and factitious dis- DISORDERS 456
order). We then discuss some of the factors important in:
the aetiology of somatic symptom disorders. Finally, the 13.3 THE TREATMENT OF SOMATIC SYMPTOM
chapter describes the range of treatments that have been DISORDERS 464
used with somatic symptom disorders, together with an:
assessment oftheir modes of operation and their efficacy. : 13,4 SOMATIC SYMPTOM DISORDERS REVIEWED 467
450 PSYCHOPATHOLOGY
LEARNING OUTCOMES
1. Describe the main diagnostic criteria and symptom disorders and be able to
symptom characteristics for the DSM-5 listed compare psychological and biological
somatic symptom disorders and evaluate some of explanations.
the issues concerning diagnosis and comorbidity. 3. Describe and evaluate three or four psychological
2. Describe and evaluate the main factors therapies that have been developed to treat
contributing to the aetiology of somatic somatic symptom disorders.
| have a core belief that |am dying. | know it’s silly but you can't reason with a core belief. On top of that, |have a huge distrust of
doctors after one diagnosed my father with anxiety instead of checking him for bowel cancer (which he actually had) and there-
fore delaying his treatment. It doesn’t get any better when you get one doctor diagnosing you with a UTI and the other saying
that all UTIs are in my imagination so |end up avoiding doctors because all !am told is that |am making it up, to then get a rather
nasty infection because it actually wasn't in my head after all. |would love to know how | am supposed to think rationally when |
can’t even trust doctors any more. | don’t spend my entire life worrying. | don’t sit around doing nothing, despite the assumption
that many GPs make; | am not stressed but | am busy. However, as soon as | get a worrying symptom, that is it - |can no longer
function.
Kirsty’s Story
symptoms that may either be trivial or not continu-

Introduction
ously present. Illness anxiety disorder is a preoccupa-
How often do we have physical symptoms such as aches tion with having or acquiring an illness to the extent
and pains that trigger worries about contracting cancer that there is a high level of anxiety about health that
or heart disease? How often do we worry about becom- both causes distress and interferes with normal daily liv-
ing ill or even dying — even when we have no physical ing. Conversion disorder is when the individual begins
symptoms of illness? For some people these everyday to experience symptoms of altered motor or sensory
experiences are enough to cause significant distress functioning (e.g. unable to voluntarily move a hand or
and to interfere with their normal day-to-day living. temporary blindness) — even when there is little or no
When such concerns and worries become obsessive evidence of relevant neurological impairment. As you
or a source of chronic anxiety or depression, they may can imagine there is often a good deal of overlap in
be diagnosed as a somatic symptom disorder. This cat- symptoms between these three disorders and that is one
egory of disorders includes somatic symptom disorder, reason why they have been grouped together in their
illness anxiety disorder (formerly known as hypochon- own chapter in DSM-5. In all cases, DSM-5 emphasizes
driasis or health anxiety) and conversion disorder. This that diagnosis should be made on the basis of positive
is a new category of disorders listed in DSM-5 and all symptoms such as distress related to somatic symptoms
of these disorders share a common feature — the promi- and dysfunctional thoughts about health, and not on
nence of somatic symptoms associated with significant excessive anxiety in the absence of somatic symptoms
distress and impairment. With somatic symptom disor- (as had previously been the case in DSM-IV-TR). This is
der individuals find somatic symptoms — real or imag- because it is rarely the case that somatic symptom disor-
ined — distressing and spend significant amounts of time ders occur in the absence of actual somatic symptoms
in medical settings attempting to seek a diagnosis for (even with conversion disorder), and so the exaggerated
CHAPTER 13 SOMATIC SYMPTOM DISORDERS A451
responses that develop to health and physical symp- on them — and individuals diagnosed with factitious dis-
toms in these disorders can frequently have their basis orders are often pathological liars who have developed
in actual somatic symptoms. This can be seen in Kirsty’s an extensive knowledge of medicine and medical termi-
story at the beginning of this chapter. She reports having nology. A related disorder is factitious disorder imposed
a number of experiences with GPs in relation to illness by another, in which parents or carers make up or induce
that she believes have given rise to her illness anxiety — physical illnesses in others (such as their children). The
an illness anxiety that has become significantly disabling reasons that drive individuals to deliberately make others
whenever she develops any symptoms of illness. Many ill is unclear, although such individuals often crave the
individuals with somatic symptom disorders believe that attention and praise they receive in caring for someone
their problems are genuinely medical and are often dis- who is ill (Abdulhamid, 2002) (see Focus Point 13.1).
believing when told there is no diagnosable evidence for We will continue by describing the DSM-5 diagnostic
a medical problem. In addition, those with symptoms criteria and the main characteristics of somatic symptom
that mimic neurological disorders, such as full or par- disorder, illness anxiety disorder, conversion disorder
tial blindness or loss of feeling (anaesthesia), genuinely and factitious disorder.
believe they have a disability, but their normal function-
ing can often be demonstrated in situations where drugs
or hypnosis is used to alter levels of consciousness or 13.1 THE DIAGNOSIS
where elegant experimental methods are used to infer
ability (e.g. Grosz & Zimmerman, 1970). It is also impor- AND CHARACTERISTICS
tant when diagnosing some somatoform disorders to
differentiate true disorders from malingering (Merten & OF SOMATIC SYMPTOM
Merckelbach, 2013). Claiming to have a physical illness
when a person does not
DISORDERS
| To read the article Is illness ever‘all in the
‘\, is not just a ploy to avoid
' work or other situations
mind’? go to
Solel Somatic Symptom Disorder
) that the individual may
http://tinyurl.com/q2d4dph
not enjoy, but can also be The cardinal feature of somatic symptom disorders is
an actively deployed coping strategy during times of multiple, current, somatic symptoms that are distressing or
stress. The difference is that malingerers are fully aware result in significant disrup-
that they are exaggerating or inventing their symptoms, tion to daily life. Symptoms somatic symptom disorders A group of
but individuals with somatoform disorders are not. can either be specific (e.g. loosely associated disorders all of which
can be characterized by psychological
This is not an easy distinction to make, but malinger- localisable pain) or nonspe- problems manifesting as physical symp-
ers will tend to be defensive when interviewed about cific (e.g. general fatigue). toms or as psychological distress caused by
their symptoms, whereas many with somatoform dis- While it may not always physical symptoms or physical features.
orders may often display a surprising indifference about be possible to explain the
their symptoms (e.g. those with conversion disorder) — somatic symptoms medi- For a video on somatization go to
especially when the symptoms to most people would be cally, in most cases the indi- www.wiley-psychopathology.com/
disturbing (e.g. blindness, paralysis). This is sometimes vidual’s suffering is authentic video/ch13
known as la belle indifference or ‘beautiful indifference’. and not feigned. Those with
One somatic symptom disorder that is thought to be a diagnosis of somatic symptom disorder tend to have
related to malingering is factitious disorder (previously very high levels of worry about illness and will often cata-
known as Munchausen’s syndrome). Rather than being strophize the most minor of physical symptoms. Sufferers
concerned with existing somatic symptoms, factitious often seek medical attention for their symptoms, but are
disorder is associated with the deliberate falsification of particularly unresponsive to medical interventions, and
physical or psychological symptoms and the induction will often seek care from many different doctors for the
of injury, illness or disease through deception, and this same symptoms, frequently claiming that their medical
may include reporting fictitious neurological symptoms care has been inadequate (Tezzi, Duckworth & Adams,
or deliberately manipulating laboratory tests (e.g. by 2001). The main diagnostic criteria for somatic symptom
adding blood to urine). In the case of malingering, the disorder are listed in DSM-5 Summary Table 13.1.
individual may intentionally produce symptoms for a Somatic symptom disorder differs from illness anxiety
specific reason (e.g. to avoid jury service, to avoid work- disorder because in the former it is the symptoms them-
ing in a stressful environment). In contrast, in factitious selves (e.g. the pain they cause) that trouble the sufferer,
disorder the individual’s motivation is to adopt the sick whereas in the latter it is the prospect of contracting a
role — perhaps for the attention that this role may bestow disease or illness from the symptoms that is distressing.
452 PSYCHOPATHOLOGY
DSM-5 SUMMARY TABLE 13.1 Criteria for somatic mild. The distress is largely generatedby beliefs about
symptom disorder the meaning, significance or cause of a symptom, or
alternatively a fear of contracting an illness that the
e Shows at least one somatic symptom (present for at
least 6 months) that causes distress or disruption in individual believes might be disabling or life threaten-
everyday life ing (DSM-5 Summary Table 13.2). This preoccupa-
tion with health status means that the individual will
¢ Unwarranted thoughts, feelings or behaviours related
to the somatic symptoms or associated health concerns,
regularly become alarmed by hearing of someone else
indicated by at least one of the following: becoming ill or by encountering health-related news
stories. Illness anxiety disorder commonly leads suf-
¢ Disproportionate and persistent thoughts about how
ferers to search for medical information and advice,
serious the symptoms are
either by seeking reas-
* Constantly high levels of anxiety about symptoms or surances from family or illness anxiety disorder A preoccupati
health in general with fears of having or contracting a se
friends or by attempts to
ous illness based on a misinterpretatio
e Unwarranted levels of time and energy devoted to find medically relevant bodily signs or symptoms. Formerly kn
symptoms or health concerns information on the inter- as hypochondriasis.
net. Seeking medical reas-
surance about health status is also very common, but
While the symptoms they report are not usually indica- this rarely reassures the sufferer and a doctor's attempts
tors of any underlying medical condition, they will often at reassurance may often exacerbate their anxiety. Fear
develop medical disorders as a result of exploratory sur- of ageing and death is also associated with illness anxi-
gery and medication use (Holder-Perkins & Wise, 2001). ety disorder and may be associated with strict health
Somatic symptom disorder may be under-diagnosed in regimes and use of alternative medicines (Fallon &
older adults, largely because pain and fatigue are consid- Feinstein, 2001). Sufferers are also prone to intrusive
ered a normal part of the ageing process, but if excessive thoughts about illness, death and dying and usually
thoughts and catastrophising of somatic symptoms are catastrophize their symptoms. For example, they are
present, then a diagnosis of somatic symptom disorder likely to believe that an ambiguous bodily sensation
might be considered. (e.g. an increase in heart rate) is attributable to an ill-
Somatic symptom disorder is also closely associated ness rather than a non-threatening consequence (e.g.
with other psychiatric diagnoses such as anxiety disor- having just walked up a flight of stairs) (MacLeod,
ders and major depression (Gureje, Simon, Ustun, & Haynes & Sensky, 1998) and that a blotch on the skin
Goldberg, 1997). In younger individuals it can be asso- may be the start of a cancer (Rief, Hiller & Margraf,
ciated with impulsive and antisocial behaviour, suicide 1998). Such individuals are not necessarily better able
threats and deliberate self-harm, making the lives of to detect bodily sensations than non-sufferers, but they
such individuals chaotic and complicated. It is difficult do possess a negatively-based reporting style which
to estimate the prevalence rates of somatic symptom means they interpret sensations significantly more
disorder because it is such a new diagnostic category. negatively than non-sufferers (Aronson, Barrett &
However, based on previous similar diagnostic categories Quigley, 2006).
it is expected that lifetime prevalence rates will be around
or just above 1 per cent (DSM-5, p.312). There may also
be cultural variations in the way in which somatic symp-
toms are either described or accepted and these may DSM-5 SUMMARY TABLE 13.2 Criteria for illness
affect the diagnosis of somatic symptom disorder. For anxiety disorder
example, some cultures give negative meaning to many
¢ Obsession with having or contracting a serious illness
bodily symptoms that in other cultures are not described
in those ways (e.g. too much heat in the body, burning in ° Somatic symptoms are very mild or not present at all
the head) and which serve as the basis for worry about ¢ High levels of anxiety about health and easily alarmed
somatic symptoms. about personal health
e Performs excessive health-checking behaviour or shows
maladaptive avoidance
13.1.2 IlIness Anxiety Disorder * Illness preoccupation has been present for at least
6 months
This disorder centres on a preoccupation with having
or acquiring a serious, undiagnosed illness — especially e The symptoms are not better explained by another mental
disorder
when somatic symptoms are either not present or only
CHAPTER 13 SOMATIC SYMPTOM DISORDERS 453.
Illness anxiety disorder differs from its diagnostic deficits and the symptoms are often preceded by con-
predecessor, hypochondriasis, significantly. Around 75 flicts or other life stressors (Roelofs, Spinhoven, Sandijck,
per cent of those diagnosed with hypochondriasis in Moene et al., 2005), suggesting a psychological rather
DSM-IV-TR would now be re-diagnosed in DSM-5 with than a medical cause. Sufferers do not appear to inten-
somatic symptom disorder if the somatic symptoms tionally produce these symptoms, but more educated
on which the anxiety and distress is based are genuine individuals may tend to display more subtle symptoms
somatic symptoms. Because illness anxiety disorder is a and deficits that closely resemble known neurological
new diagnostic category it is difficult to estimate preva- deficits. However, DSM-5 specifies that conversion disor-
lence rates or comorbidity. However, the prevalence rate der should be diagnosed only when the clinical findings
for DSM-IV-TR hypochondriasis in the general popula- show clear incompatibility with neurological disease
tion is estimated to be 1-5 per cent (DSM-IV-TR, p.505) (DSM-5, p.319) and conversion symptoms often fail to
but can be as high as 36 per cent in chronic pain patients behave in ways expected by the known neurology. For
(Rode, Salkovskis, Dowd & Hanna, 2006). Illness anxiety example, in the conver-
disorder can begin at any age but onset is most common sion symptom known as glove anaesthesia A conversion disorder
symptom in which numbness begins at the
during early adulthood. It is frequently comorbid with glove anaesthesia, numb-
wrist and is experienced evenly across the
other disorders, including mood disorders and obses- ness begins at the wrist hand and all fingers.
sive compulsive disorder (Noyes, 1999; Abramowitz & and is experienced evenly
Braddock, 2006). across the hand and all fingers (Figure 13.1). However,
if a specific nerve to the hand, such as the ulnar nerve, is
damaged, numbness should extend only to the ring fin-
13.1.3 Conversion Disorder ger and little finger. Similarly, damage to the radial nerve
should affect only the thumb, index finger, middle finger
The basic feature of conversion disorder is the presence and part of the ring finger. Conversion symptoms are
of symptoms or deficits affecting voluntary motor or sen- also frequently inconsistent, so a sufferer may often use a
sory function suggestive of ‘paralysed’ limb when dressing or may reflexively catch
rsion disorder The presence of an underlying medical or
logical symptoms or deficits affect-
a ball unexpectedly thrown to them with their ‘paralysed’
neurological condition. To
luntary motor or sensory function hand. Individuals with conversion disorder also tend to
be diagnosed with conver-
stive of an underlying medical or exhibit what is known as la
ogical condition. , sion disorder, these symp- belle indifference (‘beautiful la belle indifference An indifference
toms must cause the about real symptoms (especially when the
indifference’) about their
symptoms would be disturbing to most
individual significant distress or impair social, occupa- disability. Whereas most people) sometimes displayed by individu-
tional or other functioning (DSM-5 Summary Table 13.3). people who experience als with somatic symptom disorders.
Common motor symptoms are paralysis, impaired a sudden loss of physical
balance, localized motor function weaknesses, atonia ability would be frightened and distraught, individuals
(lack of normal muscle tone), difficulty swallowing and with conversion disorder tend to be largely philosophical
urinary retention. Common sensory symptoms include
loss of touch or pain sensation, double vision, blindness,
deafness, hallucinations and on some occasions seizures
or convulsions. However, in conversion disorder, thor-
ough medical and neurological examination may fail to
reveal any significant underlying medical cause for these
DSM-5 SUMMARY TABLE 13.3 Criteria for conversion disorder
e Atleast one symptom of altered voluntary or sensory

function
e Evidence of incompatibility between the symptoms and
known neurological or medical conditions
FIGURE 13.1 Glove anaesthesia.
e The symptoms are not better accounted for by another (a) Areas of the arm’s skin that send sensory information to
medical condition or mental disorder the brain by way of different nerves. (b) A typical region of anaes-
thesia in a patient with conversion disorder. If there were a nerve
e The symptoms cause significant distress or impairment in injury (in the spinal cord), the anaesthesia would extend over the
important areas of functioning length of the arm, following the nerve distribution shown in (a).
454 PSYCHOPATHOLOGY
“\
about their symptoms and willing to talk at length about 13.1.4 Factitious Disorder
them. At least some psychodynamic approaches to the
explanation of conversion disorder suggest that this This disorder is characterized by the individual falsifying
appears to reflect a form of ‘relief’ that their symptoms medical or psychological symptoms in themselves or oth-
may prevent them from having to deal with current con- ers. The defining feature of factitious disorder is that this
flicts and stress in their lives (Kuechenoff, 2002; Temple, falsification of evidence is intentionally deceptive. Ways
2002). Prior to its inclusion of falsifying symptoms
factitious disorder A set of physical o}
hysteria A common term used in psy- in the DSM, conversion can include exaggeration
psychological symptoms that are inten-
chodynamic circles to describe conversion of symptoms, fabrication, tionally produced in order to assume t
disorder (prior to the latter's inclusion in
disorder was popularly
the DSM). known as hysteria in psy- simulation and induction. sick role.
chodynamic circles. Examples include claiming
Some diligence must be applied to ensure that con- symptoms of depression For a video on factitious disorder go to
version symptoms are not the result of developing neu- following the death of a www.wiley-psychopathology.com/
rological problems and it is estimated that between 13 loved one when this event video/ch13
and 30 per cent of individuals diagnosed with conver- did not happen, decep-
sion disorder have later been found to develop some tively reporting neurological symptoms such as dizziness
relevant neurological deficit (Maldonado & Spiegel, or blacking out and manipulation of laboratory tests
2003; Kent, Tomasson & Coryell, 1995). Conversion (e.g. by adding blood to urine) or ingesting a substance
disorder symptoms can develop throughout the life (such as insulin).
course and are often seen to develop after some stress- An alternative diagno-
factitious disorder imposed on
ful life event. Severity of the symptoms can be linked to sis is factitious disorder another The intentional falsification o
the severity of the life stressor and important stressful imposed on another and physical or psychological signs or symp-
life events that can contribute to conversion disorder this is where the individual toms, or induction of injury or disease, —
include work experiences and relationship difficulties is a perpetrator who falsi- another person.
(Roelofs, Spinhoven, Sandijck, Moene et al., 2005). fies medical or psychologi-
However, symptoms can often spontaneously remit, cal symptoms in another (with the victims of this action
only to return at a later time, and there is some evi- often being children). Focus Point 13.1 provides a detailed
dence to suggest that a history of trauma and child- example of factitious disorder imposed on another, pre-
hood abuse may be a vulnerability factor (Bowman & viously known as Munchausen’s syndrome by proxy. It is
Markand, 1996). still unclear why individuals take these deceptive actions,
The lifetime prevalence rate of conversion disorder although it may well be to gain attention for themselves
is thought to be less than 1 per cent, and it is significantly or to gain praise for their actions in the case of factitious
more common in women than in men (Maldonado & disorder imposed on another.
Spiegel, 2003). There are also important cultural dif-
ferences in the way that conversion disorder manifests
itself. For example, Janca, Isaac, Bennett & Tacchini
(1995) found that sexual and menstrual symptoms were DSM-5 SUMMARY TABLE 13.4 Criteria for factitious disorder
prominent in Western cultures, complaints of body ¢ Fabrication of physical or physiological symptoms or sign
temperature irregularities are only found in Nigeria, of injury or disease .
kidney problems only in China, and body odour com-
e Presenting oneself as ill or injured to others
plaints only in Japan. In addition, the lower the economic
or educational standards in a culture or community, ¢ The deception is evident despite a lack of obvious reward
the higher the prevalence of conversion disorder ¢ The behaviour is not better explained by another mental
(Maldonado & Spiegel, 2003). Similarly, the higher the disorder, such as delusional disorder
educational standards in a community, the more likely Factitious disorder imposed on another
it is that the symptoms will resemble a known medical
or neurological disorder (Tezzi, Duckworth & Adams, e Fabrication of physical or physiological symptoms or sign
of injury or disease in another
2001). Conversion disorder is also highly comorbid with
other disorders, particularly anxiety disorders, such as e Presenting another as ill or injured to others
panic disorder, and depressive disorders. A study by ° The deception is evident despite a lack of obvious reward
Sar, Akyuz, Kundakci, Kiziltyan et al. (2004) found at
¢ The behaviour is not better explained by another mental
least one other psychiatric diagnosis in 89.5 per cent of
disorder, such as delusional disorder
a group of individuals with a diagnosis of conversion
disorder. NB: The perpetrator, not the victim, receives the diagnosis.
CHAPTER 13 SOMATIC SYMPTOM DISORDERS 455
FACTITIOUS DISORDER IMPOSED ON ANOTHER

Beverley Allitt was a nurse who was convicted in emotionally needy and require attention and praise,
1993 of killing four children and injuring nine others and they receive this when appearing caring and
at Grantham Hospital, Lincolnshire. While working on loving towards their ill child. They often have poor
a children’s ward in the hospital she was found to be relationships with their partners, receive little in the
secretly injecting infants with insulin —- a drug that way of support outside of the medical environment
induced cardiac arrest, causing death and brain dam- and regularly exhibit low self-esteem. Many have a
POINT
FOCUS During the time that she was involved in these
13.1 age. good knowledge of medicine and medical proce-
killings, she was also befriending the parents of her dures, which allows them to cause their child’s ill-
victims and displaying what appeared to be a caring ness with a minimum of suspicion (Bluglass, 2001;
and sympathetic manner. She received 13 life sen- Adshead & Brooke, 2001).
tences for these crimes, yet her motives for the killings The syndrome is notoriously difficult to diagnose.
have never been fully explained. One theory is that she This is because most of the victims are very young chil-
suffered from factitious disorder imposed on another dren, many of whom may have genuinely experienced
(previously known as Munchausen’s syndrome by acute life-threatening events, the causes of which are
proxy), a controversial diagnosis in which sufferers are difficult to detect, such as sudden infant death syn-
prompted to deliberately falsify illnesses in others in drome (SIDS) (Galvin, Newton & Vandeven, 2005). In
order to attract attention to themselves. such circumstances, carers who present the problems
What motivates some carers and parents to delib- oftheir children in unusual ways are often treated with
erately inflict illness, pain and even death know- suspicion — especially if their own emotional needs are
ingly on young children? Most mothers diagnosed consistent with those often found in factitious disorder
with factitious disorder imposed on another are imposed on another (Pankratz, 2006).
S
| SELF-TEST QUESTION
e What are the main diagnostic criteria for somatic symptom disorder?
e What are the main psychiatric disorders that tend to be comorbid with somatic symptom disorders?
® Can you describe the main diagnostic criteria for illness anxiety disorder, and by what other name was this disorder previ-
ously known?
® Can you describe the main diagnostic criteria for conversion disorder together with its main features?
© How do cultural factors affect the prevalence rate and manifestation of conversion disorder symptoms?
© What is factitious disorder and what are its main diagnostic criteria?
® How does factitious disorder imposed on another differ from basic factitious disorder?
SECTION SUMMARY
13.1 THE DIAGNOSIS AND CHARACTERISTICS OF SOMATIC SYMPTOM DISORDERS
* Somatic symptom disorder is a pattern of recurring multiple, clinically significant somatic symptoms that require medical
treatment.
e Individuals diagnosed with somatic symptom disorder are usually major users of health care services.
e Somatic symptom disorder is closely associated with other mental health problems such as anxiety disorders and major
depression.
e /lIness anxiety disorder (formerly known as hypochondriasis) is a preoccupation with fears of having or contracting a serious
illness based on a misinterpretation of bodily signs or symptoms.
MSG =. PSYCHOPATHOLOGY
® :
® Individuals with illness anxiety disorder will regularly read about medical conditions and consult medical opinion on a
regular basis. They will also be entirely unconvinced by reassurances that they do not have a medical illness.
e The basic feature of conversion disorder is the presence of symptoms or deficits affecting voluntary motor or sensory
function.
® tis estimated that between 13 and 30 per cent of individuals diagnosed with conversion disorder have later been found
to have some neurological deficit.
® Conversion symptoms usually develop in adolescence and severity of symptoms can be linked to the severity of life
stressors.
y ~
® The lifetime prevalence rate for conversion disorder isless than 1 per cent.
e There are significant cultural differences in the way that conversion disorder symptoms manifest themselves.
© Conversion disorder is frequently comorbid with anxiety disorders, major depression, dissociative disorders, substance
abuse and personality disorders.
© Factitious disorder is characterized by the individual falsifying medical or psychological symptoms in themselves or others.
© Factitious disorder imposed on another is where the individual is a perpetrator who falsifies symptoms in another.
rere rrr rrr rrr rrr rrr rrrrr rrr rrr rrr
13.2 THE AETIOLOGY life stress could be manifested in somatic symptoms. The
basic psychodynamic view of somatic symptom disorders
OF SOMATIC SYM PTOM is a conflict resolution one in which distressing memo-
ries, inner conflict, anxiety and unacceptable thoughts are
D IS O R D E R S repressed in consciousness : : —
conflict resolution Psychodynamic i
PVE VET. 2 REDEOIIS (SURE SIESTA Preece neta: saree but outwardly expressed sietationsiofseiigeticecmmneendsoral
as somatic symptoms. For which distressing memories, inner con
The most traditional explanations of somatic symptom
example, Freud believed anxiety and unacceptable thoughts ar
disorders have been couched in psychodynamic terms — that somatic symptoms repressed in consciousness but outw
primarily because some of Freud’s most influential writ- expressed as somatic symptoms.
such as those found in
ings concerned hysteria and the causes of unexplained
conversion disorder (then
physical symptoms. However, since that time a number
known as hysteria) were associated with distressing
of different approaches to explaining somatic symptom
memories of childhood seduction. These might be actual
disorders have developed, including learning accounts
experiences of childhood abuse or simply imagined as fan-
and cognitive accounts. Nevertheless, regardless of how
tasies during the Oedipal period of development. When
the theorist approaches the aetiology of somatic symp-
these memories are reawakened during puberty this
tom disorders, explanations of these disorders must
causes intense anxiety and conflict resulting in somatic
address certain important questions. These include:
symptoms and repression of these memories. The
1. Are physical symptoms a manifestation of somatic symptoms served the purpose of helping to sup-
underlying psychological conflict and stress? press these memories and to relieve anxiety, and this was
consistent with the fact that most individuals with conver-
2. Are physical symptoms generated in an
sion disorder exhibited a calm philosophical attitude to
involuntary fashion?
their disability (la belle indifference), suggesting that it was
3. What is the role of life stress and childhood abuse a state in which they experienced some relief from stress
in the development of somatic symptom disorders? and conflict. Underlying sexual conflict was also seen by
4. How do sufferers acquire the biased thinking and psychodynamic theorists as being an important contribu-
dysfunctional beliefs about health that help to tor to other disorders such as somatic symptom disorder
maintain many of the symptoms of these disorders? _ and illness anxiety disorder. Freud believed that repressed
sexual energy was often turned inward on the self, trans-
forming it into physical symptoms that created physical
13.2.1 Psychodynamic Interpretations pain or were interpreted as indictors of illness and disease.
Indeed, psychodynamic theorists often view those sufter-
Some of Freud’s most famous writings were on the subject _ ing from somatic symptom disorders as regressing to the
of hysteria and how inner conflict, repressed emotions and _ state of a sick child, unconsciously seeking attention and
&
CHAPTER 13 SOMATIC SYMPTOM DISORDERS 457°
relief from symptoms and responsibilities, and thus reduc- had no peripheral vision would have reported a visual
ing experienced anxiety (Kuechenoff, 2002; Kellner, 1990; stimulus at chance level —i.e. on 50 per cent of the trials.
Phillips 1996). The girl with a somatic symptom disorder in fact per-
These psychodynamic accounts appear to make intui- formed significantly worse than this — suggesting that at
tive sense in that those who develop somatic symptom some level of consciousness she was aware of the periph-
disorders often appear to have either a history of*conflict, eral visual stimulus but was suppressing reporting it. In
stress and abuse or have recently experienced an impor- a similar study, Zimmerman & Grosz (1966) also found
tant life stressor (Bowman & Markand, 1996; Roelofs, that an individual with hysterical blindness performed
Spinhoven, Sandijck, Moene et al., 2005). Nevertheless, a visual task at significantly below chance level when a
an important aspect of the psychodynamic conflict- truly blind individual should be performing at chance
resolution model is that the physical symptoms either level. They also found that when visual stimuli were
cause relief from anxiety or from having to deal with presented in a non-random predictable sequence, their
current conflicts and stress (Temple, 2002). In contrast, patient still performed a well below chance level — even a
disorders such as somatic symptom disorder and illness truly blind person would have performed above chance
anxiety disorder appear to involve high levels of anxiety on this task. These studies indicate that the person with,
(Noyes, Kathol, Fisher, Phillips et al., 1994), and a sizable for example, conversion disorder can discriminate the
minority of those with conversion disorder also fail to relevant incoming sensory information at some level —
exhibit the calming effects of la belle indifference (Gureje, even if they use that information in a way that results
Simon, Ustun & Goldberg, 1997). This suggests that the in them performing significantly below what would be
supposed psychologically beneficial effects of somatisa- expected of someone who was blind! At first sight, evi-
tion as proposed by psychodynamic theory are difficult dence such as this suggests that the sufferer may simply
to find. be faking the symptoms and trying to behave in ways
that are consistent with these symptoms. However, if it
is faking, then the individual has taken great pains to be
consistent in this behaviour often over long periods of
13.2.2. Consciousness and Behaviour
time and in difficult situations.
One important feature of some somatic symptom dis- A very early explanation of these types of symp-
orders, such a toms was proposed by Janet (1907) who suggested that
patients suffering from ‘hysteria’ experience a sponta-
To read the article about hysterical
sufferer appears able to neous narrowing of attention after being exposed to
blindness by Theodor & Mandelcorn go to
www.wiley-psychopathology.com/ generate physical symp- trauma. This attentional narrowing limits the number of
reading/ch13 toms or deficits (e.g. medi- sensory channels that can be attended to and leads to the
cal symptoms, blindness) loss of voluntary control over neglected channels. This
in an involuntary fashion. That is, there is a dissociation results in the patient being rendered anaesthetic for any
between the individual’s behaviour and their awareness information coming in to the unattended modality even
of that behaviour. For example, in conversion disorder though it is still processed outside of conscious aware-
the sufferer appears genuinely unable to experience ness. As a result the patient may be unable to consciously
certain sensory input (e.g. when exhibiting blindness access information from these channels and experience
or loss of feeling). However, studies suggest that these blindness or paralysis, depending on the sensory chan-
individuals can experience the sensory input at some nel that has been neglected. A similar explanation of
level of processing but are consciously unaware of it. For these anomalous findings is provided by Oakley (1999).
example, Theodor & Mandelcorn (1973) describe a study He draws attention to the many similarities between
undertaken with a 16-year-old girl who complained of a the behaviour of the individual with conversion disor-
loss of peripheral vision with no underlying neurologi- der or somatic symptom disorder and the effects of
cal explanation for this. In their study they presented a hypnosis. First, many of
hypnosis A therapeutic technique in
buzzer followed by a bright visual stimulus to either the symptoms of conver- which the patient is placed in a trance.
the girl’s central or peripheral visual field on a percent- sion disorder are similar to
age of the trials. The girl’s task was to report whether physical states that can be easily established by hypnosis
a visual stimulus had followed the buzzer or not. They (e.g. blindness, paralysis) and they also display a degree
found that the girl always correctly reported when the of involuntariness. That is, both the conversion disorder
buzzer was followed by a stimulus to the central visual patient and the person under hypnosis regularly report
field. However, she was only 30 per cent correct when that they have no voluntary control over a movement or
reporting a visual stimulus to the peripheral visual field. a sensation (e.g. they may be unable to raise their arm).
Theodor & Mendelcorn argued that a person who truly In drawing these two areas together, Oakley (1999) has
458 PSYCHOPATHOLOGY
: a
proposed that similar mechanisms could be responsible the aetiology of somatic symptom disorders. First, not
for both conversion/somatisation symptoms and behav- everyone who develops a somatic symptom disorder
iour under hypnosis. So an action or incoming sensory reports having had high levels of childhood abuse or
information may often be processed at a range of dif- neglect, nor having had a significant number of negative
ferent levels of mental functioning but for some reason life events generally (e.g. Sar, Akyuz, Kundakci, Kiziltyan
may not be selected for conscious processing (presum- et al., 2004), so such experiences are not a necessary
ably one of the last stages of this process). Under hyp- condition for developing a somatic symptom disorder.
nosis this last stage of processing can often be prevented Second, the actual levels of stress reported by individu-
by suggestions from an external source (such as the als with somatic symptom disorders are not necessarily
hypnotist) and it will appear to the individual that they significantly higher than those reported by individuals
have no control over their actions or their perceptions. with other psychopathologies, so stress levels per se do
Oakley proposes a similar effect in conversion disor- not differentially predict the development of a somatic
der in which some presumably internal processes have symptom disorder (Roelofs, Spinhoven, Sandijck, Moene
prevented sensory information from being analysed by et al., 2005). Third, high levels of childhood trauma and
conscious awareness. Because the sensory information is negative life events can be found in the histories of a wide
processed at lower mental levels, this explains why the range of psychopathologies (e.g. personality disorders,
individual with hysterical blindness can respond in ways eating disorders, anxiety disorders and so on), so why
that suggest visual information is being received (e.g. by should someone who has this kind of traumatic history
performing at significantly below chance on a visual rec- develop a somatic symptom disorder rather than any of
ognition task), but is not consciously aware that visual these others (although it must be admitted that somatic
stimuli are being perceived and responded to. As appeal- symptom disorders are regularly comorbid with many
ing as this explanation is, it still begs the question of other psychiatric disorders)? Some theories do specify a
how and why sensory information is blocked from con- central role for stress and early negative experiences in
scious awareness in individuals with conversion disorder. the development of somatic symptom disorders and the
This aspect of this view still needs to be fully explored conflict-resolution model adopted by many psychody-
and understood. namic theorists is one example (see section 13.2.1) and
the attentional-narrowing model of hysteria proposed
by Janet (1907) is another (see section 13.2.2). However,
13.2.3 Risk Factors for Somatic the role of stress and childhood trauma in other theo-
ries is often underdeveloped and this is an aspect of our
Symptom Disorders
understanding of the aetiology of somatic symptom dis-
A significant factor in the history of most somatic symp- orders that needs to be explored.
tom disorders is either a history of trauma or abuse, or There are also several familial risk factors that have
significant periods of stress and anxiety, and these appear been identified for somatic symptom disorders and these
to be important risk factors in developing a somatic include parents with somatisation characteristics, hav-
symptom disorder. For example, a history of childhood ing a significant other/relative with an organic disease,
trauma appears to increase vulnerability to conversion psychopathology of close family members, a dysfunc-
disorder (Bowman & Markland, 1996), and high levels tional family climate and insecure attachment (Schulte &
of negative life events in the year prior to onset have Petermann, 2011). However, these factors are also risk
been found in individuals with globus pharyngis (a form factors for the development of many other psychiatric
of conversion disorder in which the sufferer experiences disorders, and so are not specific to somatic symptom dis-
a sensation of a lump in the throat) (Harris, Deary & orders alone.
Wilson, 1996). Individuals with somatic symptom disor-
der tend to report histories of physical and sexual abuse
(Holder-Perkins & Wise, 2001), as do many of those with
13.2.4 Learning Approaches
illness anxiety disorder (Salmon & Calderbank, 1996).
In addition, many somatic symptom disorders develop Numerous theorists have suggested that somatic symp-
following exposure to acute stressors, such as recent tom disorders may develop because many of the aspects
loss (Van Ommeren, Sharma, Komproe, Poudyal et al., of these disorders are learnt through specific types of
2001), relationship difficulties (Craig, 2001) and expo- experiences. For example, Craig, Boardman, Mills,
sure to dead bodies following military combat (Labbate, Daley-Jones & Drake (1993) have argued that many
Cardena, Dimitreva, Roy & Engel, 1998). Nevertheless, individuals learn to interpret emotional symptoms as
we must be cautious about what these findings mean in indicative of physical illness. This learning could occur
in a number of ways. First, individuals suffering con- that the individual is unable to cope with the normal rig-
version disorder, somatic symptom disorder or illness ours and challenges of daily life. Convincing evidence that
anxiety disorder often report having had early child- this is indeed the case still needs to be collected.
hood experiences where close members of their family Nevertheless, there does seem to be some reasonable
have experienced physical illness or somatic symptoms evidence that children may learn somatising attitudes
(Tezzi, Duckworth & Adams, 2001), and so expressing from their parents in various ways and this may provide a
any negative feelings (emotional or physical) may occur basis for the possible development of somatic symptom
through somatisation because of exposure to modelling disorders in later life.
by important family members. In support of this view,
Craig, Cox & Klein (2002) compared the childhood his-
tories of three groups of women — those with somatic
symptom disorder, those with a long-term illness and
13.2.5 Cognitive Factors
healthy controls. They found that those with somatic One important feature of most of the somatic symptom
symptom disorder were three times more likely than disorders is that the sufferer believes they have physical
those in the other groups to have had a parent with a deficits or symptoms that are significant and threatening,
serious physical illness. but in most cases there is little or no medical justification
A related view is that expressing symptoms of physi- for these beliefs. This strongly suggests that sufferers
cal illness may be reinforced by parents. For example, may have developed thinking and information process-
some parents may view all underlying problems (including biases that lead them to believe they have medical
ing psychological ones) as being physical rather than symptoms when in fact they do not. Such cognitive biases
emotional, and subtly encourage their children to report can take a number of forms. They may involve inter-
psychological problems in physical terms (Latimer, pretation biases, in which
1981). In an insightful study, Craig, Bialas, Hodson the individual interprets interpretation biases Cognitive biases in
which an individual interprets ambiguous
et al. (2004) observed mothers playing with their 4- to ambiguous bodily sensa- events as threatening and evidence for
8-year-old children. Mothers who exhibited somatisa- tions as threatening and potential negative outcomes.
tion symptoms were less emotionally expressive than evidence for a potential
control mothers during most play tasks. However, they serious illness (Marcus et al., 2007). For example, when
were significantly more responsive to their children when an individual with illness anxiety disorder experiences a
they played with medicine-related toys (e.g. a medical stomach pain they may interpret this catastrophically
box). In this way, mothers who already display somatisa- as a possible symptom of stomach cancer, rather than,
tion symptoms may pass this predisposition on to their say, the result of eating something that was ‘off’. This
children through the differential display of attention in biased thinking then gives rise to a range of conse-
medicine-related contexts. quences which are likely to reinforce the biased belief,
Finally, early learning of the kind described above means including increased fear and anxiety, preoccupation
that many individuals may learn to describe emotional with similar symptoms, overestimating the probability
symptoms in physical terms and in extreme cases begin that a symptom is a sign of a disease and reassurance-
to adopt what is known as seeking (Warwick, 1995; Rief, Buhlmann, Wilhelm,
le Playing the role of being sick a sick role. Adopting a sick Borkenhagen & Brahler, 2006) (see Figure 13.2). In a
ned by the society to which the
lual belongs.
role has a number of disad- similar vein, Barsky (1992) argued that patients with
vantages — it means a loss somatic symptom disorder have a bias towards describ-
of power and influence as the individual relinquishes tasks ing minor automatic bodily sensations in a catastrophic
and duties to others; it also involves a loss of pleasure, manner, which leads to a significantly higher level of
especially if an individual becomes house-bound or even reported symptoms. In support of these views, Lim &
bed-ridden because of their symptoms. However, Ullman Kim (2005) usedan emotional Stroop procedure to demon-
& Krasner (1975) have argued that adopting a sick role can strate that individuals diagnosed with a somatic symptom
have significant advantages and rewards in terms of the disorder showed a significant Stroop interference effect
attention the sufferer is likely to receive from others, and for physical threat words (e.g. injury, seizure, inflamma-
the absolving of responsibility can be viewed as a way of tion), suggesting that these individuals consciously and
opting out of having to directly deal with life stressors and selectively attended to physical-symptom related cues.
conflicts. In this case, adopting the sick role becomes a In addition, when given ambiguous health-related
coping style for adult life. While this view is consistent vignettes about illness and death, Haenen, de Jong,
with the fact that somatising mothers may teach their Schmidt, Stevens & Visser (2000) found that individu-
children similar tendencies, adopting a sick role implies als with illness anxiety disorder were significantly more
PSYCHOPATHOLOGY
: x
Physical symptoms shopping’. They would actively seek out and accept infor-
e.g. stomach pains mation that agreed with their own view of their medi-
cal state, but would ignore or reject arguments against
their own beliefs. This process will inevitably maintain
Negative automatic thoughts
e.g. '| have stomach cancer’ hypochondriacal thinking and generalized anxiety about
health issues. In addition, individuals with somatic symp-
tom disorders show greater attention allocation to words
Emotion and phrases that support their own beliefs about their
e.g. anxiety/fear/panic health than those that do not (Witthdéft, Rist & Bailer,
Fah
Behaviour changes Thinking changes
aire
Mood changes Symptoms
2009) — a process that isJikely to reinforce existing dys-
functional beliefs.
The preceding evidence strongly suggests that many
Checking, Preoccupation Feelingdown Heart racing somatic symptom disorders are maintained by cogni-
-—proddingtummy — Focus of attention, Mouth dry
— weighing self — thinking about
tive factors that take the form of (1) attentional biases
stomach to physical threats, (2) biases towards interpreting body
Avoiding, Selective attention, sensations and symptoms as threatening, (3) reasoning
—acid foods — reading items biases that maintain beliefs about illness and being ill,
about health in
newspapers
(4) memory biases that facilitate the retrieval of illness-
Reassurance-seeking,
relevant material, and (5) catastrophising of symptoms.
— asking wife However, none of these accounts explains how the
— seeing doctor individual with a somatic symptom disorder acquires
— ringing cancer helplines
these thinking and information processing biases. Some
FIGURE 13.2 This cognitive model of illness anxiety disorder insight into how these biases might develop has been pro-
illustrates how physical symptoms or bodily sensations evoke nega- vided by Brown (2004). Brown argues that ‘rogue repre-
tive automatic thoughts about illness. These thoughts then trigger sentations’ are developed
rogue representations |n somatic
feelings of anxiety, which in turn trigger a range of behavioural, by a range of experiences symptom disorders, representations that
cognitive and mood reactions that reinforce biased beliefs and and these representations provide inappropriate templates by whic
illness anxiety symptoms. provide inappropriate tem- information about body shape and healt
Source: After Warwick, H.M.C (1995). Assessment of hypochondriasis. plates by which informa- are selected and interpreted. —
Behaviour Research and Therapy, 33, 845-853. Reproduced with permission. tion is selected and interpreted. Rogue representations
can be created by experiences that include:
likely than controls to interpret these vignettes as serious
and threatening. 1. a history of physical illness that causes a
Recent studies also suggest that individuals with somatic tendency to interpret any sensation as a symptom
symptom disorders may also have a memory bias towards of illness,
remembering and retrieving illness relevant material. 2. a history of experiencing emotional states that
memory bias Individuals with many This bias also appears to have strong physical manifestations (e.g. anxiety
psychopathologies may have a bias make it difficult for somatic is associated with shaking, palpitations, nausea,
towards remembering and retrieving symptom disorder sufferers muscle tension, chest pain, dizziness) (such
illness relevant material. to suppress illness-related experiences might arise from childhood trauma
material, which may be rapidly retrieved from memory and abuse and result in a tendency to interpret
when thinking about potential symptoms or illnesses such symptoms fearfully), and
(Wingenfeld, Terfehr, Meyer, Lowe & Spitzer, 2013). Zu exposure to physical illness in others (e.g.
One interesting feature of individuals with illness abnormal levels of illness in the family), which
anxiety disorder and somatic symptom disorder is their creates a memory template by which one’s own
tendency to reject diagnoses that disagree with their own physical sensations are interpreted.
beliefs about their health, and to seek further opinions —
presumably in the belief that someone will agree with In support of this account, there is good evidence
their own view. Smeets, de to suggest that individuals with somatic symptom
reasoning bias The tendency of individu- Jong & Mayer (2000) found disorders do experience these factors with signifi-
als with illness anxiety disorder to reject
that individuals with ill- cantly greater frequency than non-sufferers (Schrag,
diagnoses that disagree with their own
beliefs about their health and to seek ness anxiety disorder pos- Brown & Trimble, 2004; Tezzi, Duckworth & Adams,
further opinions — presumably in the belief sessed a reasoning bias 2001; Holder-Perkins & Wise, 2001; Hotopf, Mayou >
that someone will agree with their view. that supported this ‘doctor Wadsworth & Wessely, 1999).
For an integrated view of cognitive behavioural symptoms. A recent example of this was reported by
models of somatic symptom disorders, the review by Cassady, Kirschke, Jones, Craig et al. (2005) within an
Witthoft & Hiller (2010) is recommended. Amish community in the US. Four of them developed
motor deficits (inability to hold up their heads) and
weight loss symptoms following a period of acute stress
13.2.6 within the closely knit Amish community. Examples of
Sociocultural Approaches
‘contagious hysteria’ such as this continue to be reported,
There is some evidence that sociocultural factors can but as yet there is no convincing explanation for these
influence both the prevalence of somatic symptom multiple cases of somatic symptom disorders.
disorders and the nature of the symptoms exhibited in
specific disorders. Being ill involves playing a social role
that is often shaped by the society to which the indi-
vidual belongs (Fox, 1989). As described earlier, this role
is known as the sick role and even across societies it is Because somatic symptom disorders involve what are
defined in ways that may help individuals to cope with apparently physical symptoms, it is reasonable to ask
psychological distress and conflict. For example, the sick whether there are any underlying biological causes for
role in most societies means that (1) the sick person is these disorders. We know that (1) a certain percentage
exempt from the normal social roles that the person has of those with conversion disorder and somatic symptom
for the duration of the illness, and (2) the sick person disorder do have medical conditions that could contrib-
is often seen as not responsible for their illness (Parsons, ute to their psychopathology (Maldonado & Spiegel,
1951). Thus, playing the sick role can provide relief from 2003; Hilder-Perkins & Wise, 2001), and (2) that many
the stresses and strains of everyday living. However, the who develop somatic symptom disorders have a his-
likelihood of an individual adopting the sick role as a tory of physical illness in their family (Hotopf, Mayou,
way of coping with stress and conflict will depend on Wadsworth & Wessely, 1999), and both of these factors
attitudes towards unexplained somatic symptoms in give grounds for exploring the role of biological factors.
different cultures. In some cultures, expressing physical Torgersen (1986) investigated a possible genetic com-
pain is an accepted way of communicating psychological ponent to somatic symptom disorders by investigating
distress and rates of somatic symptom disorders tend to the presence of somatic symptom disorder in MZ and
be higher in such cultures — e.g. in Latin countries and DZ twins. He found that MZ twins had a higher con-
amongst American Hispanic women (Tomasson, Kent & cordance rate for somatic symptom disorders than DZ
Coryll, 1991; Escobar, Burnam, Karno, Forsythe & twins, which is consistent with there being a genetic
Golding, 1987). In such communities, individuals may component to these disorders, but the sample he used
be encouraged to somatize psychological distress in was particularly small. Some studies have investigated
a way that allows them to more readily adopt a sick inherited aspects of somatic symptom disorder using
role (Goldberg & Bridges, 1988). In addition to cultural adoption studies, but these have only served to further
factors that affect the somatisation of psychological confuse the role of inheritance in somatic symptom dis-
distress, socio-economic standards also influence prev- orders. Bohman, Cloninger, von Knorring & Sigvardsson
alence rates. Individuals who live in rural areas, who (1984) and Cloninger, Sigvardsson, von Knorring &
are less well educated and have a poorer standard of Bohman (1984) traced the histories of the biological and
living are more likely to exhibit somatic symptom dis- adoptive parents of 859 women with somatic symptom
orders (Maldonado & Spiegel, 2003) — possibly because disorder. However, they rather surprisingly found that
in such socio-economic groups the expression of psy- the biological fathers of these women had significantly
chological distress is less acceptable and so psychologi- higher levels of alcoholism or violent crime than would
cal symptoms are expressed as physical illness. be expected by chance, suggesting a biological or genetic
One final social factor can be identified in the aetiology link between antisocial behaviour and somatic symptom
of conversion disorder. Physical symptoms associated disorder! We await further, larger scale genetic studies
with conversion disorder can often be ‘contagious’ and of somatic symptom disorders that may clarify these
affect a number of people within a single social setting findings.
or social group. This is similar to the physical symptoms Because of the startling symptoms of conversion
of hysteria that were often reported in young women disorder, such as paralysis and blindness, there have
at pop concerts during the 1960s and 1970s. Examples been numerous studies that have investigated the role
of contagion appear to occur following an acute period of of the brain in this disorder. Studies that have moni-
stress within a closely knit social group, where all those tored the brainwaves of individuals with conversion dis-
involved display very similar unexplained somatisation order suggest that sensory information is reaching the
appropriate areas of the brain, but they are not being would normally instigate movement are being activated,
registered in consciousness. Marshall, Halligan, Fink, but other areas of the brain that would not be involved
Wade & Frackowiak (1997) carried out a positron emis- are being activated in order to inhibit the movement
sion tomography (PET scan) study of a conversion dis- (e.g. orbitofrontal and anterior cingulated cortices —
order patient who had a paralysed left leg. They found see Research Methods 13.1).
increased activation in the right orbitofrontal and ante- Finally, recent research has identified a relationship
rior cingulated cortices, but an absence of activity in between somatic symptom disorders and heightened
the right primary cortex when the patient attempted activity in areas of the brain that are associated with
to move the leg. This suggests that unexplained paraly- unpleasant body sensations. These include the anterior
sis involves some form of inhibition of primary motor insula and the anterior cingulate, and their associations
activity by brain areas such as the orbitofrontal and with the somatosensory cortex — the latter being an
anterior cingulated cortices. Interestingly, this same pat- area of the brain involved in processing bodily sensa-
tern of excitation and inhibition can be found in PET tions (Landgrebe, Barta, Rosengarth et al., 2008). This is
scans of individuals who have leg paralysis induced by consistent with heightened activity in these areas mak-
hypnosis (Halligan, Athwal, Oakley & Frackowiak, 2000), ing individuals more vulnerable to the development of
suggesting that paralysis caused by conversion disorder somatic symptom disorders through the heightened
and hypnosis may reflect very similar underlying brain unpleasantness of these symptoms and an increased ten-
processes. These findings suggest that brain areas that dency to be aware of somatic sensations.
BRAIN IMAGING USING POSITRON EMISSION TOMOGRAPHY (PET)

Many psychopathologies are either associated with brain abnormalities or are caused by unusual patterns of
activation in the brain, and so understanding a particular disorder can be helped significantly by procedures that
allow the researcher to look directly at the structure and functioning of the brain.
Positron emission tomography (commonly known as ‘PET scans’) involves injecting radioactive molecules
into the bloodstream. These molecules are then tracked by a scanner as they are metabolized in the brain.
Differences in metabolism rates in the brain are detected and show up on a screen as different colour contrasts.
Lighter and warmer colours denote areas when metabolism (and therefore brain activity) is high. This tech-
nique is useful for detecting which areas of the brain
are active when the individual engages in a particular
13.1 behaviour.
METHODS
RESEARCH
A study by Marshall, Halligan, Fink, Wade &
Frackowiak (1997) used PET scanning methods to try to
identify the areas of the brain that became active when
At anterior
an individual with conversion disorder attempted to hgulate
move their paralyzed left leg. They found that when
the patient tried to move their paralyzed leg, areas not
normally associated with movement became active
(the right cingulated cortex and the right orbitofrontal
cortex). They hypothesized that the activation of these
areas somehow actively inhibited or prevented leg
movement.|na similar study, Halligan, Athwal, Oakley &
Frackowiak (2000) used the same PET procedure with
a patient whose left leg had been paralyzed by hypno-
sis. The resulting scan (Figure 1) shows that exactly the FIGURE 1 Relative changes in cerebral blood flow
same areas of the brain are activated when the hyp- associated with attempted movement of the hypnoti-
notized individual tries to move their leg — suggesting cally paralyzed left leg.
that paralysis in both conversion disorder and under Source: Marshal, J.C., Halligan, P.W., Fink, G.R., Wade, D.T. &
hypnosis may be a result of movement being inhibited Frackowiak, R.S.J. (1997) The functional anatomy of a hysterical
by the activation of certain cortical brain areas. paralysis. Cognition 64, B1-B8. Reproduced with permission.
CHAPTER 13 SOMATIC SYMPTOM DISORDERS 463.
SELF-TEST QUESTIONS ~
What are the main features of psychodynamic explanations of somatic symptom disorders, and what is meant by a conflict-
resolution view of somatic symptoms?
Can you describe at least one experimental study showing that those suffering from conversion disorder are aware of sen-
sory stimuli at some level or processing?
* What was Janet’s (1907) explanation of the aetiology of conversion disorder?
* Why is it helpful in understanding conversion disorder symptoms to make comparisons between conversion disorder and
behaviour under hypnosis?
* What kinds of negative life events and stressors have been noted as risk factors in the development of somatic symptom
disorders?
* What is the evidence that those suffering from somatic symptom disorders may have ‘learnt’ to adopt a sick role during
childhood?
* What is the experimental evidence that individuals with somatic symptom disorders have information processing biases?
° What are rogue representations and how might they affect thinking about illness symptoms?
* What is the sick role and how might it help an individual cope with stress?
* How have brain scanning technologies been used to throw light on the mechanisms underlying conversion disorder
symptoms?
SECTION SUMMARY
13.2 THE AETIOLOGY OF SOMATIC SYMPTOM DISORDERS
Theories of the aetiology of somatic symptom disorders attempt to explain the development of these disorders at a number of
different levels. Common to many of these accounts are (1) the role of anxiety, depression and existing psychological conflict
in generating somatic symptoms, (2) the part that playing the ‘sick role’ might have in coping with psychological stress, and the
way that this role might be reinforced by family, associates and medical practitioners, and (3) the role of biased thinking and
dysfunctional beliefs in maintaining beliefs about illness in those with somatic symptom disorders. The startling and disabling
nature of the symptoms in conversion disorder has meant that some theoretical accounts have been addressed solely to the
unique features ofthis disorder. These include accounts that attempt to explain how sensory information is blocked from con-
sciousness and how an individual may lose voluntary control over their movements (e.g. brain scan studies, and comparisons
of conversion disorder with hypnosis).
_ To summarize the key points:
e Psychodynamic interpretation of somatic symptom disorders is mainly a conflict-resolution one in which distressing
memories, inner conflict, anxiety and unacceptable thoughts are repressed in consciousness but outwardly expressed as
somatic symptoms.
e |n disorders such as conversion disorder, there appears to be a dissociation between the individual's behaviour and their
awareness of that behaviour.
e Studies suggest that in conversion disorder, sensory input is processed at some level, but is unavailable at the level of con-
scious awareness.
e There are many similarities between the behaviour of individuals with conversion disorder and the effects of hypnosis, sug-
gesting that similar mechanisms may be responsible for both.
° Risk factors in the history of many somatic symptom disorders are a history of trauma or abuse, significant periods of stress
and anxiety, and a range of familial risk factors.
e Some learning accounts of somatic symptom disorders suggest that expressing symptoms of physical illness may be rein-
forced during childhood by parents or carers.
PSYCHOPATHOLOGY
> sy ;
® Many individuals with somatic symptom disorders may have learnt to adopt a‘sick role’ which may be a form of coping with:
life stressors.
© Most of the somatic symptom disorders are characterized by cognitive and information processing biases, including (1) inter-
pretation biases, (2) reasoning biases, (3) memory biases, (4) catastrophising of symptoms, and (5) the development of
inappropriate ‘rogue representations: These reinforce the dysfunctional thinking that maintains somatic symptoms.
© Sociocultural factors can influence both the prevalence of somatic symptom disorders and the nature of the symptoms
exhibited.
® and affect a number of people within a

Physical symptoms associated with conversion disorder can often be ‘contagious’
~
single social setting or social group. ~
® Both twin and adoption studies have provided only indirect evidence for a genetic component to somatic symptom
disorders.
* PET scans suggest that increased activation in some areas of the brain may inhibit the movement of ‘paralysed’ limbs in
individuals with conversion disorder. A similar effect can be found in individuals whose limbs are paralysed by hypnosis.
13.3 THE TREATMENT disorder (OCD) and, as we shall see later in this sec-
tion, treatments for OCD are also successful in treating
OF SOMATIC SYMPTOM the symptoms of these somatoform problems (Phillips,
1998; Rosen, 1996).
DISORDERS This section will now consider the types of treatments
that are often used with somatic symptom disorders.
One of the main problems in treating somatic symptom
disorders is that they manifest as physical or medical
symptoms, and thus a sufferer will initially undertake a
lengthy period of medical treatment in order to discover
whether there are any underlying physical causes for In the section on aetiology, we noted that psychody-
their symptoms. This not only allows symptoms to namic accounts of somatic symptom disorders take a
become entrenched before psychological therapy is ‘conflict-resolution’ view of these disorders, in which
attempted but may also contribute to the resistance inner conflict, anxiety and distressing memories are
of sufferers to psychological therapy. For example, many repressed in consciousness and outwardly expressed
sufferers of disorders such as somatic symptom disor- as somatic symptoms.
der, illness anxiety disorder and conversion disorder Psychodynamic therapy psychodynamic therapy Therapeutic
frequently deny they have a psychological problem and therefore focuses on pro- approach that focuses on procedures
designed to bring repressed thoughts an
continue to search for a medical ‘solution’ to their symp- cedures designed to bring memories into consciousness where they
toms. This denial of an underlying psychological cause these repressed thoughts can be effectively dealt with.
makes treatment problematic. and memories into con-
Secondly, we have already noted that somatic symp- sciousness where they can be effectively dealt with.
tom disorders are highly comorbid with other disorders This will in turn alleviate the somatic symptoms that
such as anxiety and depression. This raises a “chicken and are a consequence of repression. Nevertheless, somatic
egg’ question about which symptoms come first. For symptoms are often quite resistant to a psychodynamic
instance, many people who are anxious and depressed approach — not least because the client may continue to
come to have concerns about their physical health as a believe that they have a physical and not a psychological
result of their anxiety and depression (Noyes, Kathol, problem. In a study following up the progress of individ-
Fisher, Phillips et al., 1994) and it is often the case that uals with somatic symptom disorders, Kent, Tomasson &
treating the anxiety or depression will significantly Coryell (1995) found that 63 per cent of conversion
reduce illness symptoms and worries (Smith, 1992). In patients and 92 per cent of somatisation patients still met
addition, illness anxiety disorder and somatic symptom the diagnostic criteria for these disorders 4 years after
disorder are often comorbid with obsessive convulsive initial diagnosis. However, meta-analyses have indicated
that psychodynamic therapy for somatoform disorders 13.3.3 Cognitive Behavioural

is (1) more effective than no treatment or treatment as
usual, and (2) is likely to be more successful the greater Therapy
the competence of the therapist and his/her ability to As we saw in the previous section on aetiology, cog-
form a therapeutic alliance with the client (Leichsenring, nitive factors appear to play an important role in the
2001, 2005). acquisition and maintenance of somatic symptom dis-
orders. Sufferers appear to acquire interpretation biases
(causing them to view ambiguous stimuli as evidence
of illness or physical problems); they possess reasoning
biases (causing them to accept only information that is
Many somatic symptom disorders involve some learn- consistent with their illness beliefs); they possess nega-
ing and behavioural-based components that can be tive thought patterns that lead to the catastrophising of
treated by the use of the learning principles implicit in physical symptoms into beliefs about full-blown illness;
behaviour therapy. Two prominent examples of such and they possess a set of underlying beliefs about their
components include (1) the reinforcing function of disorder that help to support their symptoms (e.g. the
attention given to individuals (e.g. by family members illness anxiety disorder sufferer may hold dysfunctional
or medical professionals), which will maintain their ‘ill- beliefs that all physical sensations are indicators of
ness’ behaviours (such as staying away from work or impending illness). Such cognitive factors appear to play
complaining about pain), and (2) continuous checking an important role in most somatic symptom disorders.
for physical signs of illness or deformity, which is con- This being the case, CBT seems particularly well suited
spicuous in illness anxiety disorder and somatic symp- to treating these dysfunctional beliefs and thought
tom disorder. patterns.
In the case of the former, Liebson (1967) reports an CBT has proven to be particularly effective for those
intervention that attempted to change the reinforcement diagnosed with illness anxiety disorder (formerly hypo-
contingencies controlling the illness behaviour of a cli- chondriasis). Such sufferers tend to interpret anything
ent who had given up his job because of pain and weak- to do with bodily symptoms or health issues as threat-
ness in his legs. Liebson persuaded the client’s family to ening (Smeets, de Jong & Meyer, 2000) and CBT can be
stop giving him attention for illness-related behaviours used to challenge these dysfunctional beliefs and replace
such as being idle at home or complaining of pain. In them with more functional health beliefs. Case History
addition, the therapist arranged for him to get a pay rise 13.1 relates the symptoms of an illness anxiety disorder
if he went back to work. This approach makes the rein- patient who was convinced he had leukaemia after devel-
forcement contingencies more functional by providing oping a harmless rash (Salkovskis & Warwick, 1986). The
motivation to work and removing any incentive to feel treatment for this case involved the client being asked to
ill or incapacitated. Similar approaches can be used to test two competing hypotheses — either (1) that he was
extinguish reassurance-seeking behaviour in individuals suffering from a life-threatening illness, or (2) he had a
with illness anxiety disorder. This type of programme problem with anxiety which was maintained by repeated
attempts to minimize the anxiety relief that clients get medical consultation and checking of his symptoms.
from reassurance seeking from the therapist, friends He was also asked to stop indulging in behaviours that
and family. It can also be supplemented by coping skills might maintain his anxiety such as checking to see if his
training, in which the client receives training and advice rash had extended, continually seeking consultations
on how to cope with anxiety and by training in the with his doctor, and reading medical text books. After
skills required for use in social or work settings. Also around 30 days his symptoms had significantly reduced.
useful are relaxation training and behavioural tech- He was no longer regularly seeking medical reassurance
niques designed to reduce about his symptoms and his self-rated scores on meas-
avioural stress management worrying. This form of ures of health anxiety and illness beliefs had also signifi-
avioural techniques designed to reduce behavioural stress man- cantly decreased.
rying and increase relaxation. agement has been found Randomized controlled trials (RCTs) indicate that
to be significantly more CBT for somatic symptom disorders is significantly more
effective than no treatment control conditions (Clark, effective at treating symptoms than normal medical care,
Salkovskis, Hackmann et al., 1998) and follow-up stud- andis still effective at 6- and 12-month follow-up (Barsky &
ies suggest that clients treated by these procedures were Ahern, 2004), but recent RCTs suggest that it may not
still symptom-free 5 years after treatment (Warwick & necessarily be more effective than other treatments
Marks, 1988). such as progressive muscle relaxation (Schroder, Heider,
466 PSYCHOPATHOLOGY
ILLNESS ANXIETY DISORDER

‘Nis a 32-year-old married engineer. He developed an acute urticarial rash, consisting of typical eruptions of
intensely itchy weals surrounded by red areas. (Urticaria may occur as a sensitivity response to certain foods
or as a reaction to drugs such as penicillin. However, in 50 per cent of chronic cases, a cause is never found. It
is, though, not associated with any malignant condition.) His rash persisted for several months despite advice
and treatment from his family doctor and dermatologist. He had had a previous episode of urticaria, which was
salicylate induced, but apart from this had been completely healthy. Physical examination and investigations
CASE revealed no significant abnormality and a diagnosis of idiopathic urticaria was made. Despite this reassurance,
HISTORY
13.1
he became increasingly anxious that he had a serious underlying condition such as leukaemia and sought
repeated consultations. His belief in the idea that he had leukaemia had arisen in the first instance because a skin
specialist had attempted to reassure him by giving him some medical details. Specifically, this doctor had told
him that the rash arose because his white blood cells were attacking foreign matter in his blood cells. The patient
had interpreted this as meaning that there was something wrong with his white blood cells, signifying that
he had leukaemia. He inspected his rash frequently, read textbooks in an effort to discover ‘the real cause’ and
could talk of little else to his wife, family and friends. Eventually, he became suicidal, unable to work and was
admitted into psychiatric care.
Source: Salkovskis, PRM. & Warwick, H.M.C. (1986). Morbid preoccupations, health anxiety and reassurance: a cognitive-
behavioural approach to hypochondriasis. Behaviour Research and Therapy, 24, 597-602, p. 598.
Clinical Commentary
This patient exhibits many of the classic symptoms of an individual with illness anxiety disorder (formerly
known as hypochondriasis) or somatic symptom disorder. He is obsessed with his symptoms — continually
checking his rash to see if it has grown, and can talk of nothing else to friends and families. The continual
checking of symptoms and reassurance-seeking from friends and family merely act to maintain his anxiety.
He also displays anumber ofcognitive biases typical ofillness anxiety disorder. He interprets his rash and the
explanation given to him by a skin specialist in threatening terms — even though there are many other expla-
nations for them. He is also unmoved by reassurances from doctors that his condition is not life threatening.
He has a bias to dismiss evidence that is not consistent with his own view ofhis symptoms and to accept only
evidence that is consistent with his view. Treatment consisted of CBT (described more fully in the text) to deal
with these cognitive biases.
Zaby & Gollner, 2013). Other studies have begun to look 2006). This suggests that pharmacological interventions
at the feasibility of new third-wave CBT interventions effective with anxiety and depression may to some extent
such as mindfulness-based cognitive therapy (MBCT) help to alleviate the symptoms of somatic symptom dis-
(see Chapter 4) in the treatment of somatic symptom orders. A range of drug
disorders and initial results indicate the effects of mind- treatments has regularly drug treatments The use of pharmaco-
logical or drug treatments to alleviate so
fulness may be favourable comparable to those of CBT been applied to somatic of the symptoms of psychopathologies.
(Fjorback, Arendt, Ornbol, Walach et al., 2013). symptom disorders and
these include tricyclic antidepressants (TCAs), selec-
tive serotonin reuptake inhibitors (SSRIs), serotonin—
13.3.4 Drug Treatments norepinephrine reuptake inhibitors (SNRIs), atypical
antipsychotics and herbal medications (e.g. St John’s
Throughout this chapter we have continually emphasized wort) (Somashekar, Jainer & Wuntakal, 2013).
the important relationship between somatoform disor- Antidepressants (TCAs, SSRIs and SNRIs) seem to be
ders and anxiety and depression. Anxiety and depression the most effective with somatic symptom disorders
are regularly comorbid with conversion disorder (Sar, generally, but more research is required to understand
Akyuz, Kundakci, Kiziltyan et al., 2004), somatic symp- how these drugs have their therapeutic effects and there
tom disorders (Gureje, Simon, Ustun & Goldberg, 1997) is also a need to develop drugs that will alleviate symp-
and illness anxiety disorder (Abramowitz & Braddock, toms of specific somatic symptoms disorders.
CHAPTER 13 SOMATIC SYMPTOM DISORDERS 467°
SELF-TEST QUESTIONS
What are the two main difficulties encountered when attempting to treat somatic symptom disorders with psychological
therapies?
Can you describe the main features of behavioural stress management procedures for somatic symptom disorders?
° How are CBT interventions use to treat somatic symptom disorders?
° What kinds of drug treatments are most effective in treating the symptoms of somatic symptom disorders?
SECTION SUMMARY
13.3. THE TREATMENT OF SOMATIC SYMPTOM DISORDERS
A range of different treatments has been utilized with somatic symptom disorders. Traditionally, psychodynamic therapy has
been an important method of treating somatic symptom disorders such as conversion disorder, although the evidence for the
medium-term success of such interventions is meagre. Both behaviour therapy and CBT have become important interven-
tions over the past 10-15 years with CBT being successfully used across a range of somatic symptom disorders to challenge
dysfunctional beliefs and to correct interpretational biases. Third-wave CBT treatments, such as mindfulness-based cognitive
therapy, are being tested out as possible new effective interventions for somatic symptom disorders. Finally, drug treatments
: can also be effective in helping to alleviate some of the symptoms of somatic symptom disorders, with the most effective
> being antidepressants.
To sum up the key points:
® Somatic symptom disorders can be difficult to treat because the sufferer believes their problems have medical rather than
psychological origins and they are usually associated with other comorbid disorders that complicate treatment.
e Psychodynamic therapy attempts to bring repressed thoughts and memories that may cause somatic symptoms into con-
sciousness where they can be effectively dealt with.
e Behavioural stress management attempts to deal with somatic symptom disorders by eliminating reassurance-seeking
from clients and supplementing this with coping skills training, relaxation training and techniques designed to reduce
worrying.
© CBT can be used across a range of somatic symptom disorders to challenge and replace the dysfunctional beliefs that
maintain somatic symptoms.
e Antidepressant drugs such as SSRIs or tricyclic antidepressants have been used to reduce the symptoms of many somatic
symptom disorders, although evidence for the long-term effectiveness of this kind of treatment is still modest.
sufferer. The causes of the symptoms appear to lie in

13.4 SOMATIC SYMPTOM psychological factors such as life stress, anxiety and a his-
tory of conflict or abuse. In many cases individuals may
DISORDERS REVIEWED have learnt through experience to adopt a ‘sick role’,
which allows the person to opt out of stressful daily
Somatic symptom disorders are a group of loosely living; in others it is clear the sufferer has developed a
associated disorders, all of which can be character- range of cognitive biases and dysfunctional beliefs that
ized by psychological problems manifesting as physical maintain their illness symptoms (e.g. illness anxiety dis-
symptoms or as psychological distress caused by physi- order). Interventions effective in addressing symptoms
cal symptoms or physical features. In many cases, the of somatic symptom disorders include psychoanalysis,
physical symptoms may have no detectable medical behaviour therapy, CBT and antidepressant pharmaco-
cause, but neither are symptoms being faked by the logical treatments.
468 PSYCHOPATHOLOGY

www.wiley-psychopathology.com/ch13 —
Reading Activity
Is an illness ever ‘all in the ¢ Somatization e Self-test questions

mind’? e Factitious disorder e Revision flashcards
Journal article: Hysterical e Research questions
blindness
Clinical issues
References
14 Dissociative Experiences

This chapter describes the diagnosis and characteristics of

three dissociative disorders, namely dissociative amnesia, 14. 1 THE DIAGNOSIS AND CHARACTERISTICS OF
dissociative identity disorder (DID, formally multiple per- DISSOCIATIVE DISORDERS 471
sonality disorder) and depersonalization disorder. The
aetiology section then discusses a range of theories of THE AETIOLOGY OF DISSOCIATIVE DISORDERS 477
the development ofdissociative experiences including psy-
chodynamic theory, cognitive models and the possible role THE TREATMENT OF DISSOCIATIVE DISGRDERS 486
that therapy can play in constructing dissociative symp-
toms. Finally, we discuss treatments for dissociative experi- DISSOCIATIVE DISORDERS REVIEWED 489
ences. These are relatively underdeveloped but in particular
we discuss the use of psychoanalysis and hypnotherapy.
"47024 PSYCHOPATHOLOGY
LEARNING OUTCOMES
1. Describe the main diagnostic criteria and symptom 3. Evaluate the difficulties associated with treating
characteristics for the DSM-5 listed dissociative dissociative experiences and describe at least two
disorders and evaluate some of the issues types of therapies that have been used to treat
concerning diagnosis, comorbidity and prevalence. dissociative experiences.
2. Describe and evaluate the main theories of the
aetiology of dissociative disorders.
This is DID . . . dissociative identity disorder . . . multiple personality disorder. We are a freak. I've started writing this a million
times .. . |don’t know how to explain this. | know I hide. |don’t want you to know me. | feel shame about who lam. . . maybe
that word defines me . . . shame. | lived through childhood abuses that one only hears about . . . between the ages of 4 and
20... 1think. am not sure. | don’t even know if |remember everything yet. That's a part of the disorder . . . forgetting. The other
part of the disorder is having 11 other people living inside of me. Therapy is working. Most of the time | remember when they are
out now... in the past they used to come out and |wouldn't know about it unless they left a clue behind . . . lots of clues for me
to see. Sometimes they would hurt me . . . intentionally. Sometimes | would hear them screaming in my head or saying things
tome... sometimes derogatory, sometimes soothing . . . sometimes they would only cry. Sometimes | would find things that
{ couldn’t understand. Waking with a teddy bear beside me that | didn’t remember. Buying toys and items that | would never
buy... losing money . . . people saying hello to me in the street who | didn’t know. My spouse looks at me and asks me who! am
half the time. My spouse no longer knows me but still loves me and |reciprocate. Without the support | couldn't make it.
Michael’s Story
Introduction symptoms such as amnesia, flashbacks, numbing, and

depersonalization. We will discuss the relationship
Dissociative disorders generally are characterized by between PTSD and dissociative symptoms later in this
significant changes in an individual’s sense of identity, chapter (section 14.1.4).
memory, perception or consciousness, and these changes Michael’s story above describes one particular form
can either be gradual or sudden, transient or chronic. taken by dissociative symptoms, and this is the presence
Symptoms of these disorders include an inability to of many distinct identities that each periodically take con-
recall important personal or life events (e.g. dissociative trol of his behaviour. These are often known as multiple
amnesia), a temporary loss or disruption of identity (e.g. personalities and identities, and the sufferer may often be
dissociative identity disorder), or significant feelings of unaware that they present these different personalities
depersonalization in which the person feels that some- to the world. This is known as dissociative identity disor-
thing about themselves has been altered (depersonali- der and represents a failure to integrate various aspects
zation disorder). Dissociative symptoms such as these of identity, consciousness and memory. As we shall see,
are often found in the aftermath of severe or prolonged in many cases dissociative disorders develop because the
traumatic experiences, such as childhood abuse, natural individual is attempting to cope with psychological dis-
disasters or life-threatening accidents. Because of this tress and conflict that may be related to earlier traumatic
close association with trauma, dissociative symptoms life experiences. Being able to adopt different personalities
are often found in individuals with a diagnosis of post- and repress specific memories is viewed by many theo-
traumatic stress disorder (PTSD) and DSM-5 recognizes rists as a way of coping with the anxiety and stress derived
this relationship by placing dissociative disorders in the from these earlier life experiences (e.g. Gleaves, 1996).
chapter next to trauma and stressor-related disorders Toa certain degree we all have dissociative experiences
(see Chapter 6). The diagnostic criteria for both PTSD at some time during our lifetime; we will sometimes have
and acute stress disorder contain reference to dissociative brief periods of memory loss, become confused about
CHAPTER 14 DISSOCIATIVE EXPERIENCES ATT
TABLE 14.1 Prevalence and comorbidity of dissociative disorders
Prevalence of disorder in the past year (mean age 33)
Males Females Total sample

, (N = 309) (N = 349) (N = 658)
Dissociative disorder n (%) n (%) n(%)
Depersonalization disorder 2 (0.6%) 3 (0.9%) 5 (0.8%)

Dissociative amnesia 3 (1.0%) 9 (2.6%) 12 (1.8%)
Dissociative identity disorder (DID) 5 (1.6%) 5 (1.4%) 10 (1.5%)
Dissociative disorder not otherwise specified (DDNOS) 21 (6.8%) 15 (4.3%) 36 (5.5%)
Any dissociative disorder 30 (9.7%) 30 (8.6%) 60 (9.1%)
Prevalence of dissociative disorder in the past year among

individuals (mean age 33)
Without co-occurring With co-occurring

Psychopathology psychopathology (%) (n/N) psychopathology (%) (n/N)
Anxiety disorder 5.6% (30 of 533) 33.3% (25 of 75)

Eating disorder 7.0% (39 of 558) 32.0% (16 of 50)
Mood disorder 5.3% (28 of 527) 33.3% (27 of 81)
Personality disorder 3.9% (20 of 512) 36.5% (35 of 96)
Substance use disorder 7.6% (40 of 526) 18.3% (15 of 82)
Any anxiety, eating, mood, personality or 2.1% (8 of 373) 20.0% (47 of 235)
substance use disorder
Source: Johnson, J.G., Cohen, P., Kasen S. & Brooks, J.S. (2006). Dissociative disorders among adults in the community, impaired functioning and Axis |
and Il comorbidity, Journal of Psychiatric Research, 40, 131-140. Reproduced with permission.
our identity, and sometimes just feel ‘strange’ or deper- dissociative disorders taken in an American community
sonalized (Kihlstrom, 2001). A community sample study sample (Johnson, Cohen, Kasen & Brooks, 2006). These
by Seedat, Stein & Forde (2003) found that 6 per cent figures suggest a 12-month prevalence rate of 9.1 per cent
of respondents endorsed four to five lifetime dissociative for dissociative disorders generally in individuals with a
symptoms and approximately one in three endorsed at mean age of 33 years. Such disorders are also comorbid in
least one lifetime symptom — suggesting that dissociative around one in three cases with anxiety disorders, eating
symptoms are relatively common in the general popu- disorders, mood disorders or personality disorders.
lation. Very often, these experiences will coincide with
periods of stress or trauma, and it is common for indi-
viduals who have experienced severe trauma — such as
combat troops, survivors of natural disasters or terrorist 14.1 THE DIAGNOSIS AND
attacks — to experience these kinds of dissociative symp-
toms (Kozaric-Kovacic & Borovecki, 2005). However,
CHARACTERISTICS OF
for some individuals these symptoms either become so
severe that they significantly disrupt their day-to-day liv-
DISSOCIATIVE DISORDERS
ing, or become chronic conditions, rather than tempo-
rary responses to stress, and cause significant distress to 14.1.1 Dissociative Amnesia
the individual. In such circumstances, they may become
diagnosable as a dissociative disorder. The main feature of this disorder is an inability to recall
In this chapter we will discuss three dissociative dis- important personal information that is usually of a stress-
orders, namely (1) dissociative amnesia, (2) dissociative ful or traumatic nature (DSM-5 Summary Table 14.1).
identity disorder, and (3) depersonalization disorder. This memory loss cannot be explained by normal forget-
Table 14.1 shows the prevalence and comorbidity rates for fulness, nor is it the result of any demonstrable damage to
YY eee PSYCHOPATHOLOGY
DSM-5 SUMMARY TABLE 14.1 Criteria for dissociative amnesia the event itself (and meyaese > this i in their legal defence
against prosecution
e Unable to remember important personal information, To complete Activity 14.1 go to
for violent crimes
usually relating to traumatic or stressful occurrences, that www.wiley-psychopathology.com/
is not in line with natural forgetting, causing significant such as murder — see activities/ch14
distress or impairment in important areas of functioning Focus Point 14.1).

Dissociative amnesia is associated with several types
e The symptoms are not the result of the use of asubstance,
or due to another neurological or medical condition
of memory disturbances. Localized amnesia is when
the individual is unable to recall events that occurred
¢ The disorder is not better accounted for by another mental during a specific time period (e.g. memory loss for a
disorder, such as dissociative identity disorder, post-
period of 2 days following a serious car accident).
traumatic stress disorder or acute stress disorder
Selective amnesia is where localized amnesia When an individual g
an individual can recall is unable to recall events that occurred ot
some, but not all, of the ing a specific time period (e.g. memorylo
the brain. Dissociative amnesia normally manifests itself
for a period of 2 days following a oa
as a retrospectively reported gap or series of gaps in the events during a specific
car accident).
dissociative amnesia An inability to recall individual’s ability to ver- time period (e.g. a combat
important personal information that is usu- bally recall aspects of their veteran may be able to selective amnesia A memory disturbance
ally of a stressful or traumatic nature. life history, and these gaps recall some events during a where an individual can recall some, but
not all, of the events during a
specific tim
are often related to traumatic or stressful experiences such violent military encounter
period (e.g. a combat veteran may be able
as physical or sexual abuse, involvement in a natural or but not others). The final to recall some events during a violent
man-made disaster, being in an accident, experiencing mil- three types of dissociative military encounter, but not others).
itary combat or terrorist attacks. Periods of amnesia may amnesia are the least com-
also extend to aspects of the individual’s own behaviour, mon, but represent the generalized amnesia A failure ofrecall 3
that encompasses the Pere entire _
such as memory loss for violent outbursts, suicide attempts most severe types of symp-
Such individuals may suddenk y report to
or self-harm, and the perpetrators of some violent crimes toms. Generalized amne- police stations or to hospitals as a result 7
have often claimed that they cannot recall anything about sia is a failure of recall that this disorientation.
AMNESIA AND CRIME

In May 2002, the BBC News website reported how Nevertheless, there are good incentives for a crimi-
Jan Charlton was convicted of the manslaughter of nal to fake symptoms of amnesia for a criminal act
her boyfriend after hacking him to death with an axe. and it is estimated that about 20 per cent of criminals
She claimed in court at Leeds that she did not know who claim amnesia are feigning their memory loss
she had killed him and ‘was in a daze, a total and utter (Hopwood & Snell, 1933). So how can we identify true
daze’ Professor Michael Kopelman, the psychiatrist amnesiacs from those that are faking? One method is
POINT
FOCUS
14.1 who interviewed her, said she claimed she did not
remember the killing until the memory came back
to use what is called symptom validity testing (SVT).
SVT is a forced-choice questionnaire in which defend-
more than a month after the incident and he told the ants are asked a series of questions about their crime.
court that amnesia in homicides In each question, the defendant must choose between
To read the news story ‘Axe killer “could ‘was most common in ‘crimes of two equally plausible answers, one of which is correct
have forgotten” crime’ go to : passion. and the other incorrect. Examples include: ‘The maga-
http://tinyurl.com/nzjlvau
' Claims of — crime-related zine that was stolen was (1) Penthouse, or (2) Playboy’;
amnesia such as this are rela- ‘In the bar there is a huge mirror, (1) yes or (2) no! If
tively common and between 20 and 30 per cent of the individual is truly suffering amnesia they should
individuals who commit violent crimes report no rec- perform at around chance level (i.e. get around 50 per
ollections of the event (Cima, Merckelbach, Hollnack cent correct). However, studies suggest that individu-
& Knauer, 2003). Although post-crime amnesia is most als who are faking amnesia (and so do know the correct
common for violent crimes, it can also be found in answer) perform at levels significantly below chance
those charged with non-violent crimes such as fraud (e.g. get less than 40 per cent correct) (Merckelbach,
(Kopelman, Green, Guinan, Lewis & Stanhope, 1994). Hauer & Rassin, 2002; Jelicic, Merckelbach & van
Amnesia may occur when the individual is in a highly Bergen, 2004). This is because they attempt to over-
altered physiological state, either because of extreme compensate for their knowledge of the crime by tend-
rage or anger, or because they are under the influence ing to choose the wrong answer rather than choosing
of alcohol or other substances (Kopelman, 2002). answers at random.
ig
CHAPTER14 DISSOCIATIVE EXPERIENCES A473
encompasses the person’s entire life and such individuals DSM-5 SUMMARY TABLE 14.2 Criteria for dissociative
may suddenly report to police stations or to hospitals as a identity disorder
result of this disorientation. Continuous amnesia is the e Disturbance of identity marked by at least two distinct
\tinuous amnesia A memory distur- inability to recall events personality states, which in some cultures may be seen
vce where there is an inability to recall from a specific time up to as evidence of possession
nts from a specific time up to and and including the present,
luding the present. e Recurring breaks in remembering everyday events,
and is also associated with personal information or traumatic events that is not in
tematic amnesia A memory distur- the forgetting of new events line with natural forgetting
ice where there is a loss of memory that as they occur. Systematic
tes to specific categories of informa- e The symptoms cause significant distress or impairment
amnesia is a loss of mem- in important areas of functioning
:such as family history.
ory that relates to specific
categories of information, such as family history. e The disturbance is not a normal part of broadly accepted
cultural or religious practice, e.g. children having an imagi-
Dissociative amnesia can present in any age group,
nary friend
from young children to adults. However, it is difficult to
diagnose in young children because it can be confused e The symptoms are not the result of the use of asubstance,
with attentional and educational difficulties. An episode or due to another medical condition
may last for minutes or years, but symptoms can often be

alleviated simply by removing the individual from the cir-
cumstances or situation that may have caused trauma or
stress (e.g. dissociative amnesia may spontaneously remit amnesia may vary with the nature of the different identi-
when a soldier is removed from the locality of the bat- ties (hostile personalities tend to have more complete
tlefield). Interestingly, individuals with dissociative amne- memories whereas passive personalities have fewer). The
sia are much less disturbed by their symptoms than we different identities will often deny knowledge of each
might expect, and this may imply that the amnesia serves other, but may battle for control of behaviour, and an
some kind of coping function that enables the individual identity that is not in control may gain access to con-
to deal with stress and trauma (Kihlstrom, 2001). sciousness by producing auditory hallucinations (e.g. by
The prevalence rate for dissociative amnesia in a giving instructions).
community sample is around 1.8 per cent, with rates Michael’s story at the beginning of the chapter
being higher in females than in males (Johnson, Cohen, describes how the sufferer is often unaware that different
Kasen & Brooks, 2006; see Table 14.1). identities are taking control of his behaviour, and he only
becomes aware afterwards by finding certain items
around (such as waking up with a teddy bear in his bed).
He is also surprised when people he doesn’t know say
14.1.2 Dissociative Identity hello to him — people whom one of his other identities
has presumably met. The time required to switch from
Disorder (DID) one personality to another is usually very brief and may
Formerly known as multiple personality disorder, this is a be preceded by various physical signs, such as rapid blink-
disorder where the individ- ing, changes in voice or demeanour, an interruption of
To read N's story on DID go to ) ual displays two or more ongoing speech or thought, and changes in facial expres-
http://tinyurl.com/nekzbdy ) distinct identities or per- sion. A distinction can be made between the host iden-
sonality states that take tity (the one that existed before the onset of the disorder)
turns to control behaviour (DSM-5 Summary Table 14.2). and alter identities (those host identity The identity that existed
Dissociative identity disorder is also associated with an that develop after the before the onset of dissociative identity
inability to recall impor- onset). In the simplest disorder.
sociative identity disorder A distant autobiographical form of the disorder, two
iative disorder characterized by the
ividual displaying two or more distinct information. DID reflects alternating identities take alter identities The identities that
develop after the onset of dissociative
ntities or personality states that take an inability to integrate turns to control behaviour,
identity disorder.
ns to control behaviour (formerly known aspects of identity, mem- and in many cases the alter
nultiple personality disorder). ory and consciousness to identity may know about the host personality, but not
the extent that each personality state is experienced as if vice versa (Dorahy, 2001). The host may become slowly
it has its own life history, self-image and identity. Different aware of the existence of the alter identity, as did Michael,
identities usually have different names and will quite by encountering evidence that a different personality
often have very contrasting personalities (e.g. controlling, state has been controlling behaviour. However, many
destructive or passive). DID is associated with gaps in DID sufferers have significantly more than just one alter
memory for various life events and the extent of this identity and surveys suggest that the average is around
A74 PSYCHOPATHOLOGY
13 per sufferer (Putnam, 1997). Around 85 per cent of once (DSM-5, 2013). This seems to suggest that DID may
sufferers also report having at least one alter identity that be a coping strategy adopted by children and adolescents
is a child and over 50 per cent report having an alter iden- to distance themselves from experienced trauma (Atchison
tity that is of the opposite sex (Putnam, Guroff, & McFarlane, 1994). We will discuss this issue more fully in
Silberman, Barban & Post, 1986). In general, alter identi- the section on aetiology. Individuals with DID also exhibit
ties tend to take on a range of contrasting personalities a large number of comorbid conditions, including PTSD,
and may individually take charge only of certain areas in depressive disorders, trauma- and stressor-related disor-
the sufferer’s life (such as one dealing with sex life, one ders, personality disorders (especially avoidant and bor-
with work, one with anger and so on). DID can also man- derline personality disorders, conversion disorder, somatic
ifest in the form of possession by ‘spirits’, supernatural symptom disorder, eating, disorders, OCD and substance
beings, ‘ghosts’, demons or personalities from previous use disorders) (DSM-5, 2013; see also Table 14.1).
lives. In some cultures, these ‘possession’ states are The prevalence rate for DID is around 1.5 per cent in
viewed as relatively normal, and as manifestations that a community sample (Johnson, Cohen, Kasen & Brooks,
have an explanation in the religious beliefs of the locality. 2006), but the number of reported cases has risen signifi-
One such example is that described in Focus Point 1.1, cantly in recent years. For example, Elzinga, van Dyck &
where spirit possession is a common trauma-related phe- Spinhoven (1998) found that the number of reported cases
nomenon in child soldiers in war-affected areas of Africa. worldwide rose from 79 in 1980 to 6000 in 1986, and the
A significant factor in the history of DID sufferers vast majority of these have been reported in the US. What,
appears to be childhood trauma, and surveys suggest that then, has caused this significant increase in diagnosed cases
over 95 per cent of individuals diagnosed with DID report of DID? There may be numerous factors and these include:
childhood sexual and physical abuse, including incest
(Putnam, 1997; Putnam, Guroff, Silberman, Barban & 1. the inclusion of DID for the first time as a
Post, 1986). Many sufferers report their disorder beginning diagnostic category in DSM-III published in 1980,
in childhood, often before 12 years of age, and at times of 2. early cases of DID may simply have been
severe trauma (Putnam, 1997), and over 70 per cent of out- diagnosed as examples of schizophrenia rather
patients with DID report having attempted suicide at least than a dissociative disorder (Rosenbaum, 1980),
THE EMERGENCE OF‘EVELYN’

The psychiatrist Robert F. Jeans reported the case of a single, 31-year-old professional woman called Gina. Her
initial symptoms included sleepwalking and screaming in her sleep, and he noted that she was uncomfortable
about being a woman, and about the thought of having a sexual relationship with her married boyfriend known
as TC. During the course of therapy, he noticed a second personality emerging, which was called Mary Sunshine
by Gina and her therapist. Mary was more feminine, outgoing and more seductive than Gina. Over time Gina
found evidence that Mary had been controlling her behaviour across various aspects of her life: she found hot
chocolate drinks in the sink (Gina did not like hot chocolate), large sums of money withdrawn from her bank
HISTORY
CASE
14.1 account and a sewing machine was delivered - that was presumably ordered by Mary. Mary also seemed to take
over Gina's relationship with TC and acted as a seductive and warm partner, whereas Gina had often been cynical
and cold. Eventually a third personality emerged that appeared to be a synthesis of the features of Gina and Mary.
Gina described how this happened:
| was lying in bed trying to go to sleep. Someone started to cry about TC. | was sure that it was Mary. | started to
talk to her. The person told me that she didn’t have a name. Later she said that Mary called her Evelyn but that she
didn't like that name. | asked her what she preferred to be called. She replied that she will decide later.
| was suspicious at first that it was Mary pretending to be Evelyn. |changed my mind, however, because the
person | talked to had too much sense to be Mary. She said that she realized that TC was unreliable but she still
loved him and was very lonely. She agreed that it would be best to find a reliable man.
She told me that she comes out once a day for a very short time to get used to the world. She promised that
she will come out to see you sometime when she is stronger.
| asked her where Mary was. She said Mary was so exhausted from designing her home that she had fallen asleep.
Source: Jeans, R.F. (1976). An independently validated case of multiple personality. Journal of Abnormal Psychology, 85,
249-255. American Psychological Association. Reproduced by permission.
CHAPTER 14 DISSOCIATIVE EXPERIENCES
Over time Evelyn appeared more and more and appeared to be an adaptive alter identity that allowed Gina to cope
better with the range of issues in her life. Within months she was Evelyn all the time, had no recollection of Mary and
later became successfully married to a physician.
Clinical Commentary
Like many alter identities in DID, Mary evolved primarily to take charge of certain areas of Gina’s life - particularly con-
trolling her feminine role and her relationship with TC. Typically, Gina had no recollection of her behaviour when Mary
was in control, and only came to be aware of Mary by encountering evidence that a different personality had been
controlling behaviour. In this particular case, Evelyn eventually merged as a synthesis of both Gina and Mary’s per-
sonalities and this proved to be an adaptive change that enabled Gina to deal with a range of matters across her life.
3. during the 1970s, interest in multiple personality DSM-5 SUMMARY TABLE 14.3 Criteria for depersonalization/
disorder was fuelled by the publication of Sybil derealization disorder
(Schreiber, 1973), a case history describing an e Recurring occurrences of depersonalization, derealiza-
individual with 16 personalities which was later tion, or both, causing significant distress or impairment in
popularized in a Hollywood film, important areas of functioning:
4. therapists have increasingly used hypnosis in e Depersonalization - experiences of detachment or
an attempt to get victims of childhood abuse outside observation of one’s own thoughts, feelings,
to reveal details of this abuse or to reveal alter body or actions
identities and there is some evidence that the e Derealization —- Experiences of detachment with regard
power of suggestion under hypnosis may be to surroundings
enough to generate ‘multiple personalities’ that e During the occurrences the individual is still able to
were not there in the first place (Piper, 1997; distinguish what is real from what is not
Powell & Gee, 1999),
e The disturbance is not directly due to the use of a
5. dissociative disorders such as DID are closely substance
associated with trauma and PTSD and interest in
e The disorder is not better accounted for by another
these syndromes grew following the experience
mental disorder, such as schizophrenia, panic disorder or
of veterans of the Vietnam war, and major depressive disorder
6. many of the symptoms of DID can be relatively
easily faked and some experts estimate that as
many as 25 per cent of DID cases are either faked
Depersonalization symptoms also occur regularly in
other disorders, such as panic disorder, schizophrenia
or are induced by therapy (Ross, 1997).
and other dissociative disorders, so it is important to
determine whether symptoms of these other disorders
are present when an individual presents with deperson-
14.1.3 Depersonalization Disorder
alization experiences.
The central feature of this disorder is persistent or recur- As is the case in panic disorder, sufferers of deper-
rent episodes of depersonalization (DSM-5 Summary sonalization disorder often think they are ‘going crazy’ —
Table 14.3). These symptoms are characterized by feelings especially if this is also associated with a sense of
of detachment or estrangement from the self. The sufferer derealization (a feeling that the world is strange or
may feel that they are living in a dream or in a film, and unreal). Other common symptoms include disturbances
that they are not in control of their behaviour but merely in the sense of time, obsessive rumination and somatic
standing outside of themselves, watching themselves. As concerns. Depersonalization disorder is also highly
we mentioned earlier, symptoms of depersonalization are comorbid with anxiety symptoms and depression, and
commonly experienced, so depersonalization disorder a past history of anxiety and depression is regularly
should only be diagnosed if reported in those suffering depersonalization disorder
ersonalization disorder Feelings of
achment or estrangement from the the symptoms are recurrent, (Baker, Hunter, Lawrence, Medford et al., 2003).
(such as living in a dream or standing cause severe distress and In everyday life, depersonalization experiences can
side of oneself, watching oneself). disrupt day-to-day living. occur when the individual is in transitional physiological
476 PSYCHOPATHOLOGY
states such as on waking up, when feeling tired, practic- PTSD and these symptoms include amnesia, flashback’,
ing meditation, or following an acute stressor or scary numbing and depersonalization. PTSD is related to dis-
experience. Interestingly, depersonalization disorder has sociative disorders in at least three possible ways. First,
been associated with severe life trauma such as child- persistent dissociative symptoms immediately after a
hood physical and emotional abuse (Simeon, Guralnik, traumatic experience are a significant predictor of the
Schmeidler, Sirof & Knutelska, 2001), and research sug- subsequent acquisition of full-blown PTSD (Murray,
gests that depersonalization during periods of stress or Ehlers & Mayou, 2002), so a tendency to dissociative
trauma may be adaptive in reducing symptoms of anxi- symptoms may make individuals vulnerable to the devel-
ety or depression immediately after the event (Shilony & opment of other PTSD-relevant symptoms. Second, dis-
Grossman, 1993). In fact, depersonalization may account sociation is a feature of ‘complex’ or severe PTSD (van
for the periods of emotional ‘numbing’ that individuals der Hart, Nijenhuis & Steele, 2088) in which individuals
feel immediately after a severe traumatic experience and suffer from a range of per-
before developing symptoms of post-traumatic stress sistent symptoms, endur- To read the article on dissociation as
a feature of PTSD by van der Hart,
disorder (see section 6.6). ing personality changes, | Nijenhuis & Steele go to
Depersonalization disorder often develops in late ado- affect disruption, somati- | www.wiley-psychopathology.com/
lescence or early adulthood, with a mean onset age of sation, and changes in self- ‘ reading/ch14
16 years and less than 20 per cent of sufferers reporting perception (Herman,
onset after 20 years of age. The 12-month prevalence 1992). Complex PTSD is often associated with early-age
rate for depersonalization disorder is relatively low at 0.8 interpersonal trauma and with dissociative symptoms
per cent (Johnson, Cohen, Kasen & Brooks, 2006), but it from that early age (Ford complex PTSD A severe form of PTSD _
must be remembered that individual depersonalization & Kidd, 1998; McLean & often associated with early age inter- 4
experiences are significantly more prevalent than this. Gallop, 2003), and has led personal trauma and with dissociative
some clinicians to argue symptoms from that early age. 4g
that dissociation and other PTSD symptoms may share a

14.1.4 Dissociative Disorders common central psychobiological pathology (Brewin,
2003). Third, there may exist a specific dissociative sub-
and PTSD type of PTSD that is defined by the severity of both
As we have already mentioned, there is a close relation- PTSD and dissociative sive and which may
ship between symptoms of PTSD and dissociative disor- account for up to 30 per sume Sam
ders. Studies have suggested that one in three individuals cent of cases of PTSD [ To read the article about the dissociative
(Wolf, Lunney, Miller,
: su bt Mes of f PTSDPTSD by Wolf
et al.
f go to
with PTSD also experience high levels of dissociation in ; t www.wiley-psychopathology.com/
the form of dissociative amnesia and depersonalization Resick et al., 2012). We | readin /ehgs
(Lipschitz, Winegar, Hartnick, Foote & Southwick, must await further ra
1999). This has led clinical researchers to speculate about research on the psychological andTore pathways
the relationship between these two diagnostic catego- through which dissociative and PTSD symptoms are
ries, with at least some clinicians arguing for a dissocia- acquired before we will be able to fully understand the
tive subtype of PTSD (Lanius, Vermetten, Loewenstein, relationship between dissociative symptoms and PTSD,
Brand et al., 2010). We noted earlier that dissociative-type and one outcome of this research might be a dissociative
symptoms are already listed in the diagnostic features of subtype of PTSD in future editions of the DSM.
SELF-TEST QUESTIONS
* What are the main diagnostic features of dissociative amnesia?

* Can you name the five types of memory disturbance that occur in dissociative amnesia?
° What are the main features of dissociative identity disorder (DID) and what was it previously called?
* Can you describe the difference between host identities and alter identities in DID?
* What is the estimated prevalence rate of DID and what problems are involved in estimating its prevalence?
* What are the main features of depersonalization disorder?
e What is complex PTSD and how is it related to dissociative experiences?
CHAPTER 14 DISSOCIATIVE EXPERIENCES Uae
SECTION SUMMARY
14.1 THE DIAGNOSIS AND CHARACTERISTICS OF DISSOCIATIVE DISORDERS
° Dissociative amnesia is an inability to recall important personal information, which is usually stressful or traumatic in nature.
° The symptoms ofdissociative amnesia can often be alleviated by removing the individual from the situation that may have
caused trauma (e.g. removing a soldier from the locality of a battlefield).
° Dissociative identity disorder (DID) was formerly known as ‘multiple personality disorder’ and is characterized by the indi-
vidual displaying two or more distinct identities.
¢ DID is often associated with childhood abuse and most sufferers usually exhibit many more than just two distinct alter
identities.
¢ The number of reported cases of DID increased dramatically between 1980 and 1986, and the reasons for this increase are
unclear.
e Depersonalization disorder is characterized by persistent or recurrent episodes of depersonalization, including feelings of

detachment and individuals not being in direct control of their behaviour.
e Dissociative experiences are often associated with symptoms of PTSD and sometimes give rise to what is known as
complex PTSD.
McFarlane, 1994). As we go through the various theories

14.2 THE AETIOLOGY OF of dissociative disorders, it is important to bear these two
DISSOCIATIVE DISORDERS central issues in mind.
The questions of how and why people develop disso- 14.2.1. Risk Factors for
ciative disorders are interesting ones. The symptoms are
Dissociative Disorders
often striking and quite frequently found in individuals
who have undergone experiences of extreme trauma or Risk factors for dissociative disorders include a history of
stress. There are two important issues that need address- anxiety and depression that pre-dates the disorder (Putnam,
ing when we attempt to look at the causes of dissociative Guroff, Silberman, Barban & Post, 1986) and a history of
disorders. The first is that we need to be able to explain childhood abuse (physical and sexual) and childhood
how the components of consciousness (e.g. cognition, neglect: up to 95 per cent of individuals diagnosed with
emotion) become dissociated. Consciousness is normally DID report instances of
a fully integrated entity, but in individuals with dissocia- childhood sexual and physi- childhood abuse The physical or psycho-
logical maltreatment of a child.
tive disorders some memories can be completely lost or cal abuse (Putnam, 1997;
suppressed (as in dissociative amnesia), some aspects of Putnam, Guroff, Silberman, Barban & Post, 1986).
consciousness can be isolated from others (such as the Dissociative amnesia is associated with a history of trauma
different identities experienced in DID), and the indi- and is more common after major stressful life events such
vidual can feel that they are dissociated from both them- as war or natural disasters (Coons, 1999). What is not clear
selves and the outside world (e.g. in depersonalization is whether childhood abuse actively contributes to the
disorder). Any theory of dissociative disorders needs to development of dissociative disorders in a causal way.
explain why some individuals develop these symptoms However, the strength of dissociative symptoms appears to
and how the different components of consciousness be directly related to the age of onset of physical and sexual
become dissociated. The second issue associated with the abuse, with higher levels of symptoms reported in those
aetiology of dissociative disorders is whether the symp- whose abuse began early in life, or who suffered disorgan-
toms actually have a functional significance — that is, do ized or insecure attachment early in life (Chu, Frey, Ganzel
the symptoms serve a purpose? In the previous sections & Matthews, 1999; Pasquini, Liotti, Mazzotti, Fassone et al.,
of this chapter we have alluded to the possibility that 2.002) PDISSOCIATIVE 7SVT rere
dissociative symptoms may protect individuals from toms are also commonly f —‘toread the article by Pasquini etal
found in homeless and run- / about early-life risk factors go to
stressful memories and experiences and help them to i www.wiley-psychopathology.com/
cope with day-to-day living, anxiety and depression (e.g. away youths who have suf- |
% reading/ch14
Kihlstrom, 2001; Riether & Stoudemire, 1988; Atchison & fered various forms of abuse “=== SLE
478 PSYCHOPATHOLOGY
prior to leaving home (Tyler, Cauce & Whitbeck, 2004). the difficulties in objectively measuring the concepts and
This provides some indirect support for the view that mechanisms described in psychodynamic theory. This
childhood abuse does play a causal role in the develop- is just as much true of psychodynamic accounts of dis-
ment of dissociative disorders. The issue of whether sociative disorders as it is of any other psychopathology
being male or female is a risk factor for dissociative disor- (see Chapter 1).
ders is still unclear; some studies suggest a significantly
greater risk of dissociative disorders in women than in
men (Putnam & Loewenstein, 2000; Simeon, Gross, 14.2.3 The Role of Fantasy and
Guralnik, Stein et al., 1997), but more recent community-
based studies suggest that this may be true only for dis- Dissociative Experiences
sociative amnesia (Johnson, Cohen, Kasen & Brooks, There is some evidence that dissociative disorders may
2006; see Table 14.1). develop more readily in individuals who have early dis-
sociative or depersonalization experiences and such indi-
viduals may learn to utilize such experiences in order to
14.2.2 Psychodynamic Theories suppress anxiety and painful memories. For example,
in a selection of prison inmates diagnosed with DID,
The general view of most psychodynamic theorists is Lewis, Yeager, Swica, Pincus & Lewis (1997) found that
that dissociative symptoms are caused by repression, 12 out of 14 cases had long-standing dissociative experi-
which is the most basic of the ego defence mechanisms. ences that pre-dated the full-blown DID symptoms and
repression A basic psychodynamic In these cases, repression 10 of the 14 reported having imaginary companions dur-
defence mechanism that helps to suppress helps to unconsciously sup- ing childhood. Reporting imaginary companions during
painful memories and prevent stressful press painful memories
childhood is common in individuals with DID (Sanders,
Senos and to prevent stressful 1992), and some theorists have argued that such experi-
thoughts entering consciousness. As a result, repression ences will predispose an individual to develop DID. For
helps to control conflict, anxiety and depression. example, Kluft (1992) has argued that a child who con-
According to Freudian views, dissociative amnesia is a structs imaginary companions may find that they can
simple example of repression, where stressful or trau- occasionally use these imaginary personalities to amelio-
matic memories are simply suppressed until the individ- rate periods of stress and conflict, and the child may then
ual has the strength to cope with them. These tendencies learn to actively construct these personalities into adap-
to repress unwanted or painful memories may be tive alter identities to protect themselves from stress.
acquired in childhood when excessively strict parents However, currently the only evidence in support of this
may instil a strict moral code in their children. When the view is that individuals with dissociative disorders do
individual violates this code during adulthood (such as appear to have a history of dissociative experiences and
by having an extramarital affair), the expression of these they also appear to have strong imaginations and a rich
‘unacceptable’ id impulses are repressed by unconscious fantasy life, which will contribute to the development of
mechanisms that prevent the retrieval of such memories. symptoms suchasalteridentities (Lynn, 1988). Most recent
DID is viewed as a further form of repression, but one in studies have also demonstrated a significant but mod-
which repression persists for significantly longer (e.g. est relationship between measures of fantasy-proneness
throughout a lifetime) in order to repress the memories and dissociative symptoms (Giesbrecht, Merckelbach &
of very traumatic childhood events (Brenner, 1999; Reis, Geraerts, 2007) and more detailed analysis seems to indi-
1993). In psychodynamic terms, the DID sufferer devel- cate that particular aspects of fantasy-proneness, such
ops alter egos in order to avoid the distressing world they as vivid mental imagery and parapsychological beliefs,
were brought up in, and also to protect themselves from are the best predictors of dissociative psychopathology
the impulses that they believe may have been the reason (Klinger, Henning & Janssen, 2009).
for their excessive punishments during childhood. Thus,
a DID sufferer can disown any ‘bad’ thoughts or impulses
by attributing them to a ‘rogue’ alter ego.
There is certainly some evidence that individuals with
14.2.4 Cognitive Approaches
dissociative disorders do experience less conflict and anxi- A central issue in explaining dissociative disorders is an
ety than individuals with other forms of psychopathology understanding of how various components of conscious
(e.g. substance abuse) and this is evidence that supports experience come to be detached from each other (e.g.
the psychodynamic view (Alpher, 1996). However, we how memory for some events becomes suppressed while
must once again return to the difficulties inherent in test- for others remains intact). Such characteristics suggest
ing predictions from psychodynamic accounts because of that an answer may lie in how normal memory and recall
CHAPTER 14 DISSOCIATIVE EXPERIENCES 479°
processes are affected in individuals suffering dissociative 40

symptoms, and many cognitive theorists believe that dis-
sociative disorders represent a disruption of all or part of
the sufferer’s memory processes (Dorahy, 2001).
For example, do individuals displaying dissociative
symptoms show poorer recall for trauma-*or abuse-
related material in experimental studies? If so, then
they may have developed a tendency to avoid encoding
traumatic material in memory or they may have devel-
oped impaired retrieval processes for such information
(McNally, Clancy & Schachter, 2001). Unfortunately, recall
Correct
(%)
much of the experimental evidence does not support

such a simple explanation. In explicit memory tasks —
where participants are asked to either remember or for-
get words presented in a recall task — individuals with
a history of childhood abuse showed no difference in
Trauma Neutral
recall of trauma-related words than non-abused control
Word category
participants (McNally, Metzger, Lasko, Clancy & Pitman,
1998; Cloitre, Cancienne, Brodsky, Dulit & Perry, 1996). FIGURE 14.1 Percentage correct recall of to-be-remembered
Although these studies did not directly investigate indi- neutral and trauma-related words presented under conditions
viduals with dissociative symptoms, the findings do sug- of divided attention. Blue bars represent participants who
gest that individuals with a history of abuse do not have scored high on dissociative experiences; red bars represent
an automatic tendency to suppress or avoid encoding those who scored low on dissociative experiences.
Source: After DePrince, A.P. & Freyd, J.J. (2004). Forgetting trauma
or recalling traumatic material. However, subsequent
stimuli. Psychological Science, 15, 488-492. Reproduced with
studies have suggested that individuals high in dissocia- permission.
tive symptoms do have impaired recall for words associ-
ated with trauma under conditions of divided attention
(i.e. when they are asked to perform a concurrent task recalling them in less traumatic emotional states. State-
as well as the memory task) (DePrince & Freyd, 2004) dependent learning has also been used to explain the
(see Figure 14.1). This suggests that attentional context is between-identity amnesia that is often experienced in
important in helping high dissociators to forget trauma- DID (Szostak, Lister, Eckhardt & Weingartner, 1995) and
related material and dividing their attention across a it has been suggested that most between-identities amne-
range of sources may help individuals with dissociative sia will occur between those alter identities that differ
symptoms facilitate forgetting of emotional-relevant or most in their normal mood states (e.g. there will be less
traumatic information. cross-identity knowledge between identities that display
An alternative explanation of the memory failures negative emotions, such as sadness or anger, and those
experienced by dissociative disorder sufferers is in terms that exhibit mainly positive emotions such as joy and hap-
of how changes in their physiological and emotional state piness) (Bower, 1981). Nevertheless, while state-depend-
can influence recall of memories. State-dependent ent memory may seem like an appealing explanation of
memory is a well-established cognitive phenomenon in dissociative amnesia, there are some difficulties with this
which the individual is explanation. Firstly, dissociative amnesia is usually much
e-dependent memory A well-
blished cognitive phenomenon in which more likely to remember more severe than has been reported in basic studies of
ndividual is more likely to remember an an event if they are in the state-dependent memory. Secondly, individuals with DID
it if he or she is in the same physiologi- same physiological state as have problems with both free recall memory and recogni-
tate as when the event occurred.
when the event occurred tion memory, but state-dependent memory is usually
(Bower, 1981). We have already noted that individuals only found with the former (Peters, Uyterlinde,
with dissociative disorders often experience severely trau- Consemulder & van der Hart, 1998). Thirdly, studies have
matic life events that cause significant changes in mood effectively demonstrated that different identities in DID
and physiology when such events occur (e.g. being can recall autobiographical information from the other
involved in a natural disaster such as an earthquake may identities when a concealed recognition test is used, sug-
be experienced during states of hyperarousal and panic). gesting that dissociative amnesia in DID probably does
If the events relating to this experience are encoded in not entail inter-identity memory systems or is constrained
memory during these unusual emotional states, then it by state-dependent learning (Huntjens, Verschuere &
may be that the individual will have difficulty properly McNally, 2012).
%
In addition, one other cognitive theory of dissociative reality monitoring (a form reality monitoring A form of source"i
symptoms involves the concept of reconstructive mem- of source monitoring requi- monitoring required to distinguish me nt
ory. This view argues that an individual autobiographical red to distinguish mental contents arising from experience from
those arising from imagination.
memory is stored as a series of discrete elements associ- contents arising from expe-
ated with that experience rience from those arising from imagination) may also lead
reconstructive memory A concept of a
(e.g. context, emotional them to doubt that they have actually had a particular
cognitive theory of dissociative symptoms
which argues that an individual autobio- state, sensory and percep- experience (Johnson & Raye, 1981), and both of these pro-
graphical memory is stored as a series of tual features). These vari- cesses may contribute to dissociative amnesia. Consistent
discrete elements associated with that ous elements will then be with this view are findings that women who have experi-
experience (e.g. context, emotional state,
recognized as an autobio- enced childhood sexual abuse and score high on dissocia-
sensory and perceptual features).
graphical memory to the tive experiences have greater difficulty than non-abused
extent that the various elements can be retrieved and control participants in distinguishing between words they
associated together (the act of reconstruction). In some had seen in a memory test and words they imagined see-
cases, not all of the elements that go to make up an auto- ing (McNally, Clancy, Barrett & Parker, 2005; Clancy,
biographical memory may be activated and this may lead Schachter, McNally & Pitman, 2000) — a finding that sug-
the individual to doubt that the retrieved fragments of gests they may well have a deficit in reality monitoring.
memory refer to a memory from his or her own past. However, deficits in reality monitoring can work both
Being unable to recall the relevant elements of an auto- ways. They can prevent a person from identifying an auto-
biographical experience from memory is known as a defi- biographical memory as one they have actually experi-
cit in source-monitoring ability (Johnson, Hashtroudi & enced, but they may also lead to the individual identifying
Lindsay, 1993): an example of this is when an individual an imagined event as an actual experience. This may be the
cannot remember whether basis for what have now become known as false recovered
source-monitoring ability The ability tothey read something in a memories of trauma (Loftus, 1993), in which various
recall the relevant elements of an autobio-
graphical experience from memory.
newspaper or whether it therapeutic techniques are false recovered memories of trauma —
was just a rumour they used to try to recover The recovery of repressed childhood
heard from a friend. It has been suggested that dissocia- repressed childhood mem- memories of trauma that turn out to
tive amnesia may result from deficits in both reconstruc- ories of trauma but which be false.
tive memory and source-monitoring abilities. For some may actually generate false memories of events that did
reason, individuals with dissociative symptoms may not not occur. Such techniques may inadvertently lead the cli-
be able to recover from memory sufficient elements of an ent to falsely recognize imagined experiences as ones that
autobiographical event to convince themselves it was an actually happened, and this issue is discussed more fully in
experience that happened to them. In addition, a deficit in Focus Point 14.2.
i
REPRESSED MEMORIES, RECOVERED MEMORIES AND
vr
= FALSE MEMORY SYNDROME
=
= There has been a belief among many therapists and cli- perpetrators will be unwilling to substantiate. There are
2) nicians that individuals can forget traumatic or stress- therefore a number of issues to address when consider-
a
Vv) ful events in their life for relatively lengthy periods of ing repressed memories. In particular these are:
=) time, and this view stems back to the original works
U ° Can memories of early childhood trauma or
of Freud who believed that severe trauma was repressed
O abuse be repressed?
LL to the unconscious mind because it was too painful to
tolerate. Many of the symptoms of dissociative disor- ° If they can be repressed, can they subsequently
ders seem to support this belief - especially because be recovered?
many of these disorders are characterized by amnesia ° If so-called repressed memories are recovered,
and childhood abuse is a common factor in the history are they accurate?
of many with dissociative disorders. However, attempt-
ing to confirm that memories have been repressed is a CAN MEMORIES OF CHILDHOOD TRAUMA OR
difficult process. For example, it is often difficult to find ABUSE BE REPRESSED?
corroborative evidence, even when repressed memo-
ries of abuse have been recovered, because many Williams (1995) used hospital files to identify 206
of the recovered memories may be of abuse that the women who, as children, had received medical
CHAPTER 14 DISSOCIATIVE EXPERIENCES
treatment for sexual abuse in the 1970s. Twenty years abused, and (2) that a list of symptoms (e.g. being heldina
later, the researcher located these individuals and inter- way that made them feel uneasy) may well be indicative of
viewed them about a range of topics including childhood actual childhood abuse. Their overriding principle was ‘if
sexual abuse. Thirty-eight per cent of those interviewed you feel something abusive happened to you, it probably
did not report the incident of sexual abuse for, which they did’! Therapists who subsequently adopted this approach
were hospitalized, but did report other incidents, sug- to treating psychopathology were thus given free rein to
gesting that they were not simply holding back sensi- indulge in a directive approach attempting to uncover evi-
tive information. Of those who did report the incident of dence of suppressed memories of childhood abuse - even
sexual abuse, 16 per cent reported that there were times to the point where clients were told they were ‘in denial’ if
in their lives when they had effectively forgotten it. This they could not remember instances of abuse! Under such
study suggests that there may be occasions when indi- conditions it is almost inevitable that clients may begin to
viduals do fail to recall traumatic events such as child- ‘recall’instances of abuse that did not actually happen.
hood abuse. However, this may simply be due to normal
processes of forgetting rather than active repression of IF SO-CALLED REPRESSED MEMORIES ARE
painful memories. In contrast, Zola (1998) reports a study RECOVERED, ARE THEY ACCURATE?
investigating the memories of individuals whose child-
hood traumas were a matter of historical record (e.g. kid- There have been numerous high-profile court cases -
nap and Holocaust survivors). In all of these cases there especially in the US — where parents or carers have been
was no evidence of repressed memories for these events convicted of childhood abuse on the basis of memories
in the survivors and they remembered most of the trau- of this abuse recovered by their children while undergo-
matic events quite vividly. Freyd (1996), however, has ing therapy. In 1990, George Franklin was convicted of
argued that childhood sexual abuse is qualitatively differ- murdering a child 20 years earlier on the basis that his
ent from the traumas experienced by Zola’s participants. daughter suddenly remembered him committing the act
She suggests that childhood sexual abuse is often perpe- while she was undergoing therapy. This conviction was
trated by a trusted caretaker, such as a parent or close rel- subsequently quashed in 1995 as a result of substantial
ative, and this gives rise to what is called ‘betrayal trauma’, doubts about the validity of his daughter’s memories.
which is more likely to be repressed than other forms This case is an example of what has come to be known as
of trauma. So, studies such as these provide conflicting false memory syndrome, in which some individuals recall
evidence as to whether trauma memories are repressed
or not. If they are subject to periods of amnesia, then it
needs to be established whether this is due to normal
processes of forgetting or whether it is the result of an
active repression process.
IF MEMORIES OF TRAUMA OR ABUSE CAN BE

REPRESSED, CAN THEY SUBSEQUENTLY
BE RECOVERED?
During the 1980s and 1990s many therapists came to ca

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Association
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©
hood sexual abuse (Kaplan & Manicavasagar, 2001). Much George Franklin (right) spent six years in prison for the murder of an
of the impetus for this loose therapeutic movement came 8-year-old girl based on the memories ‘recovered’ by his daughter,
from a book called The Courage to Heal, written in 1988 by Eileen (left), under hypnosis 20 years after the event. It turned out that
two feminist counsellors, Ellen Bass and Laura Davis. They the details Eileen recalled could have come from newspaper reports,
argued that (1) a large number of people are the victims and subsequent DNA evidence cleared Franklin of a second murder
of childhood sexual abuse but do not realize they were that his daughter accused him of.
PSYCHOPATHOLOGY
memoriesthatsubsequentlyturnouttobefalse.Thisdoesnot never seen before (Clancy, Schachter, McNally &

mean that the individual is actively lying or faking the Pitman, 2000) and are less able than control partici-
memory, but a variety of psychological processes might pants to discriminate words they had seen before
contribute to the individual developing a false memory from words they imagined seeing (McNally, Clancy,
and believing that it is an accurate record of past events. Barrett & Parker, 2005) (see Research Methods 14.1).
Processes that might contribute to false memories are:
° Over-directive psychotherapy or hypnotherapy, where CONCLUSIONS

the client is encouraged to hold the belief that they
This debate is complex and still ongoing. There is no doubt
have been abused (e.g. Loftus, 1993). Many clients
that some people probably do repress memories of child-
may actively want to believe they have been abused
hood abuse; some probably recover these memories — either
because it would help them to reattribute responsi-
with or without therapy — and some probably recall memories
bility or blame for their behaviour or their moods.
of childhood abuse that never actually happened. In a review
° Poor source-monitoring ability is when the individual
of the available evidence at the time, Brewin & Andrews
lacks the skills to identify the source of amemory. This
(1998) suggested that we should not rule out the possibil-
may lead the individual to believe that an event that
ity that any recovered memories might be genuine and that
was only imagined actually happened. In support of
each case should be considered on its own merits. In particu-
this view, laboratory-based studies have indicated
lar, clinicians should be aware that clients are susceptible to
that women who claim to have recovered memo-
suggestion and should avoid discourse that may shape the
ries of childhood abuse are more likely than control
memories that are eventually reported by their clients. |
participants to recognize material they have actually
LABORATORY STUDIES OF FALSE RECOGNITION

AND RECOVERED MEMORIES
Individuals who have suffered amnesia for stressful life events may occasionally recall what have now come to
be known as false recovered memories of trauma. That is, they may actually recall events that they believed hap-
pened, but which objective evidence subsequently suggests did not happen (see Focus Point 14.2).
We have described in section 14.2 why we think some people might be prone to recalling memories that are
false, but how do we go about studying this phenomenon experimentally?
False recognition — the mistaken belief that one has previously encountered a novel item — has been studied
extensively in the laboratory and the methods used to investigate this have been applied to the study of false
recovered memories in individuals with dissociative disorder symptoms.
In the laboratory procedure, participants are presented with lists of words, and each list is composed of words
RESEARCH
METHODS
14.1
associated to a single non-presented ‘theme word’ For example, a list may consist of words associated with sweet
(such as sour, sugar, bitter, candy and so on). After hearing the lists, participants are then given a recognition test
where they are presented with words (1) that were presented in the previous lists, (2) words that have not been
presented before but are related to the theme words (known as false targets), and (3) a control set of words that
have never been presented before but which are not related to the theme words.
Using college students as participants, many studies have suggested that rates of false recognition to false tar-
gets is high — so even non-clinical populations often believe they have seen words in the original lists when in fact
they have not (i.e. exhibit false recognition) (Roediger & McDermott, 1995; Schachter, Norman & Koutstaal, 1998).
A number of studies have used this paradigm to test whether individuals with dissociative disorder symptoms
have particularly high levels of false recognition. Clancy, Schachter, McNally & Pitman (2000) indeed found that a
group of women who reported recovered memories of childhood sexual abuse was more prone to false recogni-
tion in this laboratory procedure than other groups (such as women who believed they were sexually abused as
children but could not remember it, and women with no history of childhood sexual abuse). Interestingly, people
who report having been abducted by space aliens also exhibit proneness to false recognition (Clancy, McNally,
Schachter, Lenzenweger & Pitman, 2002) and the recall of such ‘recovered memories’ holds as much emotional
potency and causes as much physiological arousal as genuine traumatic encounters recalled by war veterans
(McNally, Lasko, Clancy et al., 2004).
CHAPTER 14 DISSOCIATIVE EXPERIENCES 483
Experimental studies such as these suggest that false recognition of past experiences may not be uncommon. However,
_ we must be wary of assuming that this experimental procedure (that was originally designed to investigate memory illu-
sions) is one that can be automatically applied to the recovery of false memories in trauma victims or to explain the pro-
cess of repression (even Roediger and colleagues are doubtful that this procedure alone can provide a full understanding
of false recovered memories; Roediger & McDermott, 1995). As Axmacher, Do Lam, Kessler, Fell et al. (2010) point out, the
laboratory-based procedure described above differs from the study of repressed memories in at least two important ways.
First, such studies do not involve the learning or forgetting of traumatic memories and repression is a hypothetical process
that should only be relevant to traumatic memories or those holding intense negative emotion. Second, Axmacher et al.
argue that repression is not a voluntary process, so attempting to understand repression and recovered memories in para-
digms that require voluntary learning and forgetting of neutral stimulus material cannot be analogous to the repression
and recovery of traumatic memories. So, at this time we await the development of experimental procedures that might
more faithfully replicate the processes involved in repressed memories and the false recognition of recovered memories
of trauma.
14.2.5 Biological Explanations of stress may also cause long-term, semi-permanent

alterations in the release of these neurotransmitters, caus-
Dissociative disorders generate symptoms — such as ing long-term amnesic effects for experiences related to
amnesia — that prima facie look as though they might trauma. More recent fMRI research has suggested that the
have been generated by neurological defects or abnor- prefrontal cortex may play an important role in inhibit-
malities in brain processes. Even so, there is very little evi- ing the activity of the hippocampus in individuals with
dence that these amnesic symptoms are caused by dissociative amnesia, a process that will result in memory
underlying deficits in brain function. First, memory loss repression (Kikuchi, Fujii, Abe, Suzuki et al., 2010).
tends to be selective and in many cases it is transitory.
This suggests that if there are brain abnormalities caus-
ing these symptoms, these too must be selective and tran-
sitory. One such candidate that has been suggested is
14.2.6 Dissociative Symptoms as
undiagnosed epilepsy (Sivec & Lynn, 1995). Epileptic Role-Playing and Therapeutic
seizures are known to be associated with DID and with
Constructions
epsy A disorder of the nervous system
symptoms of depersonal-
racterized either by mild, episodic loss ization disorder such as A number of theorists have argued that the more elabo-
ention or sleepiness or by severe blackouts and déja vu. Even rate symptoms of dissociative disorders, such as alter
vulsions with loss of consciousness. so, the symptoms of some identities in DID, are a form of role-playing by the suf-
dissociative disorders — such as DID — are very complex ferer in order to evoke sympathy and to escape responsi-
and it is unlikely that undiagnosed bouts of epilepsy bility for their actions (Spanos, 1996). Such role-playing is
could explain the intricate way in which knowledge about usually reinforced by family, friends and therapists, as it
alter identities is suppressed or recovered by the sufferer. evokes the required attention and allows the individual
An alternative biological explanation alludes to the role to absolve themselves of day-to-day responsibilities for
of the hippocampus. Recent brain scan studies have sug- their behaviour. In addition, people simulating DID in
gested that the hippocampus is the area of the brain that the laboratory are mostly indistinguishable from indi-
brings together the various elements of an autobiographi- viduals with a diagnosis of DID, suggesting that it is not
cal memory and integrates them to provide the individual a difficult condition to feign (Boysen & VanBergen,
with a memory that they recognize as a past personal 2013). In particular, alter identities in DID may be devel-
experience. Given that individuals with dissociative disor- oped in response to particular types of therapeutic inter-
ders appear to have problems recalling and integrating vention. For instance, in the ‘Emergence of Evelyn’
memories of certain experiences (such as childhood abuse), example (Case History 14.1) the therapist's interactions
this may be caused by abnormalities in the hippocampus. with Gina lead to an alter identity emerging and this new
Bremner, Krystal, Charney & Southwick (1996) have identity was given the name Mary by both the client and
argued that neurotransmitters released during stress can the therapist. In fact, therapists dealing with DID often
modulate memory function — particularly at the level of ask their clients to give a name to an alter identity so they
the hippocampus — and this release may interfere with the can talk about this personality more easily. Spanos (1996)
laying down of memory traces for high-stress incidents suggests that this interactive therapeutic process actually
such as childhood abuse. In addition, extended periods creates the client’s alter identities — so alter identities may
484 PSYCHOPATHOLOGY
be therapeutic constructions born of the therapeutic Nevertheless, there is still debate about whether most
process itself rather than genuine, full-blown symptoms cases of DID are strategic enactments or not. Gleaves
therapeutic constructions The view
that precede treatment. (1996) has provided a vigorous defence of the psychi-
that the multiple personalities found in The client then finds that atric view that DID is a legitimate diagnostic category
dissociative identity disorders are merely these well-defined alter and not a construction of the therapeutic process. He
constructions of the therapeutic process. identities serve a useful argues that:
function in their life by allowing them to explain away
their behaviour and alleviating stress and anxiety. 1. it is not surprising that the rate of DID diagnosis
What evidence is there that alter identities in DID are has increased significantly in recent years because
a construction of the therapeutic process? Supportive this may be a result of less scepticism about
evidence includes the following: the diagnostic category and a reduction in the
misdiagnosis of DID as schizophrenia,
1. Alter identities are significantly less well 2. there is relatively little evidence that
defined in childhood and appear in adulthood hypnotherapy actively contributes to the
usually after treatment by a therapist has begun development of DID symptoms because the
(Spanos, 1994; Lilienfeld, Lynn, Kirsch, Chaves number of clients diagnosed with DID after
et al., 1999). hypnotherapy is as low as one in four,
2. Relatives of individuals with DID rarely report 3. core symptoms of DID, such as amnesia, are
having seen evidence of alter identities before frequently found in DID sufferers before their first
treatment (Piper & Mersky, 2004). treatment session (Coons, Bowman & Milstein,
3. Individuals who develop DID usually have strong 1988), so DID cannot be entirely constructed as a
imaginations and a rich fantasy life that enables result of therapy, and
them to play different roles with some ease 4. rather than being openly collusive with
(Lynn, 1988). the therapist about their symptoms, many
4. There is some evidence that many cases of DID individuals with DID are highly reluctant to talk
could have been diagnosed by a relatively small about their symptoms and have an avoidant style
number of clinicians who might have a thera- that is not conducive to revealing a history of
peutic style that allows alter egos to develop — abuse or the existence of multiple personalities
for example, in a Swiss survey, Modestin (1992) (Kluft, 1994).
found that 66 per cent of the DID diagnoses in
As an epilogue to this debate, it is worth discussing
the country were made by less than 10 per cent of
an interesting study conducted by Spanos, Weekes &
the clinicians in the survey.
Bertrand (1985). They designed an experiment based
5. Individuals diagnosed with dissociative disorders on the famous case of Kenneth Bianchi who was
are very susceptible to suggestion and hypnosis accused of a series of murders and rapes in Los Angeles
(Bliss, 1980; Butler, Duran, Jasiukaitis, Koopman
in the 1980s. During his psychiatric evaluation under
& Spiegel, 1996) and hypnotherapy is a hypnosis, Bianchi revealed evidence of DID symptoms
common form of treatment for DID; indeed,
and eventually of an alter identity called Steve whom
Spanos (1996) argues that such susceptible he claimed committed the rapes and murders. When
individuals may adopt the ‘hypnotic role’ and he came out of the hypnotic state, Bianchi claimed to
simply produce the kind of behaviour that the know nothing about Steve or the murders, or what he
therapist wants.
had said under hypnosis. Table 14.2 provides a transcript
6. Spanos (1994) noted that those who support DID of part of the discussion between the clinician and
as a diagnostic category have described a wide Bianchi while the latter was under hypnosis. Spanos,
range of symptoms that may be indicative of DID Weekes & Bertrand (1985) claim that this is an excel-
and this justifies constant probing in therapy to lent example of how Bianchi’s alter identity was con-
confirm a diagnosis, and this may occur to the structed via the therapeutic discussion. Constructing
point where therapists insist to doubting clients ‘Steve’ served a useful purpose for Bianchi, because it
that they do have multiple alter egos (Mersky, allowed him to plead not guilty to murder by reason
1995). Consistent with the desire of many of insanity (i.e. his supposed DID). In their experimen-
clinicians to diagnose DID is the finding that tal study, Spanos, Weekes & Bertrand (1985) asked
the prevalence of diagnosed DID has increased three groups of students to act out variations of the
dramatically since 1980 (Elzinga, van Dyck & hypnotherapy procedure undergone by Bianchi. All
Spinhoven, 1998). groups were instructed to play the role of individuals
CHAPTER14 DISSOCIATIVE EXPERIENCES — 485_
TABLE 14.2 accused of murder. Group 1 was then hypnotized and

underwent questioning taken almost verbatim from
The following is a transcript of the discussion that took place
between accused murderer Kenneth Bianchi and a clinician
the Bianchi transcript. Group 2 were also hypnotized
while Bianchi is under hypnosis (see text for further elaboration). and told that under hypnosis many individuals reveal
evidence of hidden multiple personalities, but this
Clinician: I've talked a bit to Ken, but | think that perhaps aspect was then not directly addressed in the interview.
there might be another part of Ken that | haven’t
Group 3 were a control condition that were not hyp-
talked to. And | would like to communicate with
notized and were given little or no information about
that other part. And | would like that other part to
come to talk tome... And when you're here, lift hidden multiple personalities. After the interviews,
the left hand off the chair to signal to me that you all participants were questioned about whether they
are here. Would you please come, Part, so! can had a hidden personality or second identity. In Group
talk to you... Part, would you come and lift Ken’s 1 — which underwent a procedure similar to Bianchi —
hand to indicate to me that you are here... would 81 per cent admitted a second personality. In Group 2 —
you talk to me, Part, by saying ‘I’m here’? whose interview did not allude to hidden personalities
Bianchi: Yes. — only 31 per cent revealed an alter identity. Only 13 per
cent of those in Group 3 admitted a hidden personality.
Clinician: Part, are you the same as Ken or are you different in
Spanos, Weekes & Bertrand (1985) argued that these
any way?
results provided evidence that alter identities can be
Bianchi: I’m not him. developed as a result of the demand characteristics of
Clinician: You're not him. Who are you? Do you have a name?
the interview style of the therapist and that such alter
identities are strategic enactments that serve the pur-
Bianchi: I’m not Ken. poses of the client (e.g. by diverting or avoiding blame
Clinician: You're not him? OK. Who are you? Tell me about for their behaviour). Nevertheless, while this study pro-
yourself. Do you have a name | can call you by? vides convincing evidence that some alter identities can
be developed by the therapist’s interviewing style, it is
Bianchi: Steve. You can call me Steve.
still not evidence that all alter identities are strategic
Source: After Schwarz, 1981, pp.139-143. enactments.
SELF-TEST QUESTIONS —
* Can you describe some ofthe main risk factors for dissociative disorders?
© What is the psychodynamic concept of repression and how does it account for the symptoms of dissociative disorders?
* What is the evidence that fantasy and early dissociative experiences may play a role in the development of dissociative
disorders?
® Can you describe the procedure for a laboratory-based experiment designed to investigate deficits in memory processes in
individuals with dissociative disorders?
° What is state-dependent memory and how does it attempt to account for dissociative amnesia?
© Can you explain how deficits in source-monitoring ability or reality monitoring might account for both dissociative amnesia
and false recovered memories of trauma?
© What is the evidence that alter identities in DID are a construction of the therapeutic process?
SECTION SUMMARY
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14.2. THE AETIOLOGY OF DISSOCIATIVE DISORDERS
We posed two questions at the outset of this section on aetiology: (1) how do the normally integrated components of con-
sciousness become dissociated in the dissociative disorders?; and (2) do the distinctive symptoms of dissociative disorders
(such as amnesia and multiple personalities) have a specific function? We have reviewed a range of theories about how the
PSYCHOPATHOLOGY
bh
elements of consciousness become dissociated in these disorders and how memories might become suppressed. Cognitive
theories try to explain these dissociative symptoms primarily by attempting to describe the mechanisms that might mediate
effects such as selective amnesia. We reviewed two specific accounts, state-dependent memory and reconstructive memory.
The latter additionally argued that individuals with dissociative disorders may suffer deficits in source-monitoring ability and
reality monitoring - both may prevent an individual from identifying an autobiographical memory as one they have actually
experienced. Some relatively undeveloped biological accounts also intimate that selective amnesia may result from abnor-
mal brain processes (such as epilepsy) or specific brain functions which inhibit the ability of the hippocampus to lay down
or recall specific memories. An alternative view of the striking symptoms of dissociative disorders is that many of them may
be a construction of the therapeutic process. In particular, directive therapeutic approaches (including hypnotherapy) may
encourage the client to create alter identities that did not exist prior to therapy, or to recall false memories of events that
had never happened. We concluded that while some symptoms of dissociative disorders may be developed by overly direc-
tive therapy techniques, this was unlikely to explain all dissociative symptoms. Finally, in relation to our second question, it
is quite likely that the symptoms of dissociative disorders (particularly selective amnesia and alter identities) do serve some
kind of palliative role, and in the psychodynamic view they may allow the sufferer to repress traumatic memories that are too
painful to tolerate.
To summarize the key points:
¢ Risk factors for dissociative disorders include physical and sexual childhood abuse and a history of trauma generally (e.g.
experiencing major stressful life events such as war or natural disasters).
e Psychodynamic theorists view Gitte disorders as being caused by repression, which is one of the most basic of the
ego defence mechanisms.
© Dissociative disorders may develop more readily in those who have experienced dissociative symptoms as a child or who
have strong imaginations and a rich fantasy life.
© Cognitive theorists believe that dissociative symptoms are caused by a disruption to the susan Ss memory processes.
e Individuals with dissociative symptoms only appear to have poor memory for trauma information under conditions of
divided attention.
¢ Some theorists argue that dissociative amnesia is caused either by a deficit in source-monitoring ability or reality monitoring.
e Deficits in some memory processes may be the reason why some sufferers are prone to recover false memories of trauma
that never happened.
® Biological accounts suggest that dissociative symptoms may be caused by undiagnosed epilepsy or that stress causes
permanent changes in the release of neurotransmitters that inhibit the laying down of memory traces.
¢ Alter identities in DID may be the construction of the therapeutic process itself rather than full-blown symptoms that
precede treatment.
14.3 THE TREATMENT OF worldwide, which means that therapeutic

techniques are relatively underdeveloped, and
D |S S O C IATIV E D IS O R D E R S outcome studies designed to assess effectiveness
of therapy methods are almost nonexistent.
The main issues to be addressed in the treatment of dis- 2. Some dissociative disorders such as dissociative
sociative disorders are (1) helping to alleviate selective amnesia often spontaneously remit, so it is
amnesia for life events and helping the client to adapt difficult in these cases to assess whether those
to recovered memories if they are painful or traumatic therapeutic methods that have been applied are
ones, and (2) helping individuals with DID to identify effective or not.
alter identities and to merge them fully into a single, 3. Dealing with recovered memories is often a
integrated identity. severely traumatic experience for the client
Clinicians attempting to treat dissociative disorders and may involve the intense re-experiencing of
face a number of problems: traumatic events (known as abreaction), and
; this may continually abreaction The intense re-experiencinc
1. Some of these disorders are rare (e.g. DID) and plunge the client into of traumatic events.
there have been relatively few cases identified emotional crisis.
CHAPTER 14 DISSOCIATIVE EXPERIENCES A87—
4. Some overly directive therapeutic styles may well initiate further emotional turmoil. In an attempt
lead to the recovery of false memories, with the to avoid full-blown abreaction, some therapists have
potential broad range of negative consequences proposed that repressed memories of abuse should be
that this might have for the client and their family retrieved only piece by piece, with the client learning
(see Focus Point 14.2). to adapt emotionally to each memory fragment before
5. In DID, integrating alter identities into asingle, moving on to retrieve the next (Kluft, 1999). Second,
functional identity is an extremely difficult in the case of clients with DID, this second stage will
process; many clients find that having a series often be characterized by the client’s resistance to inte-
of alter identities is a useful way of explaining grating multiple identities. For the individual with DID,
their behaviour to others and absolving the multiple personalities appear to serve a coping function
‘host’ identity from blame and responsibility, so in allowing the sufferer to abdicate responsibility for
breaking this down is not easy (Hale, 1983). Ina actions and emotions to individual identities, and suc-
survey of 153 clients undergoing therapy for DID, cessful therapy will need to deal with these ‘responsi-
Piper (1994) found that only 38 of 153 (25 per bilities’ before integration can be achieved. Indeed, in
cent) achieved a stable integration of their alter many cases, the sub-personalities will view ‘fusion’ of
identities, but more recent longer term studies their identities as a form of death that has to be avoided
have intimated more optimistic outcomes, with (Kluft, 2001; Spiegel, 1994). Finally, if these stages of
Kluft (2000) finding a successful integration rate treatment are progressed successfully, the client will
of 68 per cent over a period of 3 months after normally need to have training in a range of skills to
therapy. enable them to cope with day-to-day living with either
6. All dissociative disorders are usually comorbid their recovered memories or their newly integrated per-
sonality. In particular, training will be needed in how to
with a range of other psychiatric disorders
(particularly with anxiety disorders, depression avoid dissociation when encountering future stressors
(Kihlstrom, 2001).
and PTSD) and dealing with these comorbid
Almost any form of psychotherapy is a lengthy
problems will also usually be a requirement in
process where dissociative disorders are concerned.
therapy.
Issues have to be approached cautiously and there
As we mentioned at the beginning of this section, may be many occasions when the therapeutic process
therapies for dissociative disorders are relatively undertakes steps backwards as well as forwards. In the case
developed, but we will discuss the most commonly used of DID, the greater the number of multiple identities
ones. These are psychodynamic therapy, hypnotherapy that need to be integrated, the longer the therapeutic
and — to a lesser extent — drug therapy. process will take — an average treatment programme
of 500 hours per client over an average of 2 years has
been reported (Putnam, Guroff, Silberman, Barban &
Post, 1986).
One common form of treatment for dissociative dis-
orders is psychodynamic therapy — especially psychoa-
14.3.2 Hypnotherapy
nalysis. Freud viewed dissociative symptoms, especially
dissociative amnesia, was a form of repression in which This is a method that is used relatively regularly with
memories that were considered too painful to tolerate those who suffer dissociative disorders. This is because
were repressed to the unconscious mind. Like most sufferers are unusually susceptible to suggestion and
approaches to dissociative disorders, psychodynamic hypnosis (Bliss, 1980), and at least some clinicians believe
therapy requires a measured step-by-step approach to that dissociative symptoms such as amnesia or multiple
revealing repressed memories or integrating multiple identities may be the result of a form of ‘self- hypnosis’
personalities. The usual process is first to establish a trust- by which individuals are able to restrict certain thoughts
ing and workable relationship between therapist and cli- and memories entering consciousness (Frischholz,
ent, followed by attempts to deal directly with repressed Lipman, Braun & Sachs,
hypnotherapy A form of therapy under-
memories or alter identities. This second stage is clearly 1992). Using hypnother- taken while the client is hypnotized.
the most challenging. First, memory retrieval may be as apy, the clinician can help
traumatising as the original experience; as noted above, guide the client through the recall of repressed memories.
this is known as abreaction. Re-experiencing trauma in Hypnosis is also used to help people to regress to child-
this way will clearly be distressing to the client and may hood states in an attempt to help them recall significant
haga PSYCHOPATHOLOGY
sodium amobarbital A drug which can events that they may have Stein & Hollander, 1995). Because there is some eVi-
be used concurrently with hypnotherapy repressed. Drugs such as dence for abnormalities in the endogenous opioid sys-
to help clients recall past events. sodium amobarbital and tems in depersonalization disorder, opioid antagonists
sodium pentobarbital can such as naltrexone have been used and found to reduce
sodium pentobarbital A drug which can depersonalization symptoms by an average 30 per cent
also be used concurrently
be used concurrently with hypnotherapy
to help clients recall past events. with hypnotherapy to help (Simeon & Knutelska, 2005).
clients recall past events
(Ruedrich, Chu & Wadle, 1985). One assumption in the
hypnotherapy approach is that hypnosis will recreate
14.3.4 Developments in Treatments
the physical and mental state the client was in prior to
experiencing any trauma, and this will help the individ- for Dissociative Disorders
ual to recall events during earlier stages of their life. This
Treating dissociative disorders can often be a lengthy
is known as age regres-
age regression In hypnotherapy, the process, whether through conventional psychotherapy
sion, and while some cli-
recreation of the physical and mental state or hypnotherapy. This picture is additionally clouded
that a client was in prior to experiencing ents find this helpful in
by the fact that many health insurers are increasingly
any trauma in order to help the individual recalling and dealing with
recall events during earlier stages of his or requiring treatments that are empirically supported,
repressed memories, there
her life. and in some countries — such as the Netherlands —
is no objective evidence
psychoanalysis is no longer being reimbursed as a treat-
that hypnosis does recreate any of the physical or men-
ment for dissociative disorders (Brand, 2012). More
tal states experienced earlier in life. Hypnotherapy is also
recently, staged treatments have been developed that
used in the treatment of DID in order to help bring poten-
are assessed using empirically based methods and may
tial alter identities into consciousness and to facilitate the
provide a more evidence-based alternative to traditional
fusion of identities. However, although widely used in the
psychoanalysis and hypnotherapy (Baars, van der Hart,
treatment of dissociative disorders, there have been no
Nijenhuis, Chu et al., 2011; Brand, Lanius, Vermetten,
systematic group- or single-case studies of the effective-
Loewenstein & Spiegel, 2012). However, therapy for dis-
ness of this technique (Cardena, 2000).
sociative disorders requires time, especially in allowing
clients to adapt to and cope with traumatic memories.
As we mentioned earlier, therapies for dissociative dis-
14.3.3 Drug Treatments orders are relatively underdeveloped and this is in part
because there are relatively few diagnosed cases of some
Because anxiety and depression are common features of these disorders (e.g. DID). As a consequence there
of dissociative disorders, and may be diagnosable are few adequately controlled outcome studies. Apart
comorbid conditions, some antidepressant and anxio- from the therapies we have discussed in this section,
lytic drugs have been used successfully to treat some many individuals with dissociative disorders can often
of these supplementary symptoms. Antidepressants be treated with CBT for their depression and anxiety
and tranquilizers have been used to address the depres- symptoms. Because both dissociative and PTSD symp-
sion and anxiety associated with DID, but these drugs toms may be an outcome of extreme trauma, those
tend to have little effect on the main symptoms of therapies used to treat PTSD also have some success in
DID itself (Simon, 1998). There is, however, some evi- dealing with dissociative symptoms (e.g. therapies such
dence that SSRIs such as Prozac may help to alleviate as cognitive restructuring and eye movement desensiti-
the symptoms of depersonalization disorder (Simeon, sation and reprocessing, EMDR; see Chapter 6).
SELF-TEST QUESTIONS
* What are the main problems facing clinicians who attempt to treat dissociative disorders?
* Can you describe the main characteristics of psychodynamic therapies for dissociative disorders?
® What is the evidence that hypnotherapy is an effective treatment for dissociative disorders?
CHAPTER 14 DISSOCIATIVE EXPERIENCES 489°
Ss ECTION SUMMARY
aiabt
14.3. THE TREATMENT OF DISSOCIATIVE DISORDERS
To summarize the key points: s “
° Abreaction and the recovery of false memories are important issues to consider in the treatment of dissociative
disorders.
e Psychodynamic therapies attempt to bring repressed memories back to the conscious mind so that they can be effectively
dealt with.
¢ Hypnotherapy is a common form of treatment for dissociative disorders and sufferers are unusually susceptible to sugges-
tion and hypnosis.
° Some antidepressant and anxiolytic drugs have been successful in treating some of the depression and anxiety-related
symptoms of dissociative disorders.
14.4 DISSOCIATIVE memories to the unconscious mind. Cognitive accounts

are much more interested in the mechanisms by which
DISORDERS REVIEWED memories are selectively repressed in dissociative dis-
orders and laboratory studies have identified deficits in
source-monitoring ability and reality monitoring (e.g.
In this chapter we have described the main features not being able to effectively differentiate imagined events
of three dissociative disorders — dissociative amnesia, from experienced events). In contrast, some theorists
dissociative identity disorder (DID) and depersonaliza- believe that many of the symptoms of dissociative dis-
tion disorder. All represent a failure to integrate vari- orders (such as the multiple alter identities in DID) are
ous aspects of identity, consciousness and memory, merely constructions of the therapeutic process. That is,
and most involve some form of amnesia for past life therapy that is either too directive or attempts to probe
events or autobiographical memories. All of these dis- too deeply to confirm a diagnosis of DID actually plays a
orders are associated with severe psychological stress. causal role in the development of alter identities.
Symptoms may manifest immediately after severe trau- Treatments for dissociative disorders are relatively
matic experiences (such as war or a natural disaster) or underdeveloped and the most popular are psychody-
they may develop over a number of years. In the lat- namic approaches and hypnotherapy. For many disso-
ter case, DID is a particular example where selective ciative disorders, therapy can be a lengthy process as the
amnesia and multiple identities may develop many sufferer often has to deal with recovered memories of
years after severe childhood trauma such as sexual or trauma that may involve intense re-experiencing of these
physical abuse. events. The therapeutic process can also be problematic,
There are numerous theories of the aetiology of as we discussed in Focus Point 14.2, where overdirective
dissociative symptoms but most relate in some way to psychotherapy can often create false recovered memo-
early trauma. Psychodynamic theories claim that disso- ries of trauma and abuse and these false memories can
ciative symptoms such as amnesia are ways of coping often have catastrophic consequences for both the client
with severe traumatic experiences by repressing these and their family.
490 PSYCHOPATHOLOGY , a

Reading 2a¢ Activity
News story: Axe killer ¢ Novideo clips online for Activity 14.1
crime ade
Revision flashcards
N’s story on DID Research questions
Journal article:
Dissociation — An insuffi-
ciently recognized major
feature of complex PTSD
dissociative subtype of
PTSD - A replication and
extension
Journal article: Risk
factors in the early
family life of patients
suffering from dissocia-
tive disorders
Clinical issues
References
15 Neurocognitive Disorders
To access the online resources for this chapter goto —

The chapter begins by describing some of the cognitive

impairments that characterize neurocognitive disor- 15.1 THE DIAGNOSIS AND ASSESSMENT OF
ders and identifying some of the brain areas associated NEUROCOGNITIVE DISORDERS 493
with these deficits. We then discuss some of the various
methods used by clinical neuropsychologists to assess 15.2 TREATMENT AND REHABILITATION FOR
cognitive functioning, and some of the difficulties asso- NEUROCOGNTIVE DISORDERS 511
ciated with diagnosis. The second part of the chapter :
looks more closely at the various types of neurocognitive 15.3 NEUROCOGNITIVE DISCRDERS REVIEWED 522
disorder described in DSM-5 and their causes. These can
involve cerebral infection, traumatic brain injury, cerebro-
vascular accidents such as strokes, and degenerative dis-
orders such as Alzheimer’s disease. Finally, we cover some
of the treatment and rehabilitation programmes that
have been developed to tackle neurocognitive disorders,
including drug treatments, cognitive rehabilitation proce-
dures and the role of caregiver support programmes.
LEARNING OUTCOMES
1. Describe some of the cognitive impairments that 3. Describe a range of types of neurocognitive
characterize neurocognitive disorders. disorders and evaluate their causes.
2. Describe some of the main methods that 4. Describe, compare and contrast the various types
clinical neuropsychologists use to assess of treatment and rehabilitation programmes that
cognitive functioning in neurocognitive have been developed to deal with neurocognitive
disorders. disorders.
Within the last 8 months, I've been at war with the cooker. |put the oven on ata temperature | know is right only to find the meat
burnt or not cooked because what | thought was the right temperature was not. It gets me so annoyed. | also forget what time |
put things in the oven — even if | repeat it to myself a few times and keep looking at the clock. If |do something else — go upstairs,
for example - | cannot remember what time the food went in, no matter how | try.
0 I've had to give up driving. | kept losing concentration and my speed just got
To view a video on Alzheimer’s
| faster and faster. | could have caused an accident - especially when feeling disori-
disease go to
www.wiley-psychopathology.com/ __ ented. | still work part-time, but that is slipping something awful. | do things at work
video/ch15 ' alone as muchas possible so no one can see the mistakes I’m making. I've had all the
tests now, but the neurologist tells me all the findings so far are consistent with AD
[Alzheimer’s disease]. To be honest, trying to get through the day is like knitting with a knotted ball of wool. Every now and again
| come toa knot. | try to unravel it but can't, so | knit the knot in. As time goes by, there are more and more knots.
Paddy’s Story
Introduction suffering such disorders. For example, some of the first

signs of neurocognitive disorders (such as dementia,
The majority of the disorders we have discussed in this brain injury or stroke) are deficits in basic cognitive
book so far appear to have psychological origins. That functions such as perception, learning, memory, atten-
is, people have experiences that give rise to problem- tion, language and visuospatial skills, and also deficits in
atic ways of thinking and behaving, and these ways of what are known as execu-
thinking and behaving may cause distress and form the tive functions (i.e. those executive functions Cognitive skills tha
basis for diagnosable psychopathologies. In contrast, skills that involve prob- involve problem-solving, planning and —
neurocognitive disorders have their origins in damage lem solving, planning and engaging in goal-directed behaviour. 3
or abnormalities in the biological substrates that under- engaging in goal-directed

lie thinking and behaving. This damage or degenera- behaviour). Clinical psychologists are therefore actively
tion can be caused by disease, physical trauma (such as engaged in assessing these abilities and interpreting
brain injury) or genetic predispositions causing irrevers- whether any deficits are early signs of neurocognitive
ible changes in the brain and central nervous system: disorders. In addition, neurocognitive disorders do not
By definition, the causes of neurocognitive disorders only generate deficits in basic cognitive functioning,
are biological and can usually be identified as biochemi- they can also affect disposition and personality. An indi-
cal imbalances in the brain and central nervous system vidual diagnosed with a neurocognitive disorder may
or direct or indirect damage to brain tissue. Despite the become both depressed and anxious, and require suita-
fact that the causes of neurocognitive disorders are pri- ble treatment for these conditions. They may also display
marily physical, psychology is centrally important in the radical changes in personality and behaviour, such as
diagnosis, assessment and rehabilitation of individuals impulsivity or outbursts of aggressive behaviour. These
CHAPTER 15 NEUROCOGNITIVE DISORDERS 493
ibilitatio n programmes Treatment also need to be managed and a failure to recall past events, but, more commonly,
Jrammes that usually combineamix- and treated. Finally, clini- a failure to recall events in the most recent past. If the
of group work, psychological interven-
cal psychologists are also neurological condition is caused by a specific traumatic
s, social skills training and practical and
ational activities. centrally involved in the event (such as a head injury), the individual may be unable
development of rehabili- to recall anything from the moment of the injury or to
tation programmes that may have a variety of aims, retain memories of recent
including events. This is known as anterograde amnesia Memory loss
anterograde amnesia or for information acquired after the onset
1. restoring previously affected cognitive and anterograde memory dys- of amnesia. Also known as anterograde
memory dysfunction.
behavioural functions (although this is often a function. The effects of
difficult task); anterograde amnesia are
anterograde memory dysfunction
2. helping clients to develop new skills to replace dramatically displayed in the Memory loss for information acquired
those that have been lost as a result of tissue 2000 film Memento in which after the onset of amnesia. Also known as
damage (e.g. learning to use memory aids); the lead character, Leonard, anterograde amnesia.
3. providing therapy for concurrent depression, is unable to form new
anxiety or anger problems; and memories as a result of an earlier head injury caused by
an assailant. The film graphically describes how Leonard
4. providing clients and carers with skills and
has to develop a series of ad hoc ways of coping with
advice that will help them structure their living
his inability to recall recent events. More commonly, in
environment in a way that will help to accommo-
degenerative disorders such as dementia, memory defi-
date changes in cognitive and behavioural abilities.
cits slowly develop from what initially appears like nor-
At the beginning of this chapter we described Paddy’s mal forgetfulness to become a more full-blown inability
story, which recounts the experiences of someone who is to recall events. In the latter case, sufferers may often
in the early stages of Alzheimer’s disease. This describes seem ‘rambling’ as they attempt to make up events to fill
her awareness of her memory lapses, mistakes and peri- the gaps in their memory.
odic disorientation that give rise to frustration, anxiety
and depression. For many who are in the early stages of Deficits in attention and arousal
a degenerative neurocognitive condition, these experi- Some first indications of neurocognitive problems are
ences can be both frequent and frightening. when the individual shows signs of lack of attention,
We will continue this chapter by discussing some of being easily distracted and performing well-learnt activi-
the more general characteristics of neurocognitive dis- ties more slowly than before (such as having difficulty
orders and the diagnostic and assessment issues that are using the controls of a DVD or video machine). They
relevant to them. may also have difficulty focusing on or keeping up with
a conversation, and they need more time to make simple
decisions.
15.1 THE DIAGNOSIS Language deficits
AND ASSESSMENT The individual may appear to be rambling during
conversations and have difficulty conveying what they
OF NEUROCOGNITIVE have to say in a coherent manner. They may also have dif-
ficultly reading and understanding the speech of others.
DISORDERS Language deficits are one of the most common features
of neurocognitive disorders and are collectively known as
First, let’s look at some of the cognitive impairments aphasias. Language impairments can take many forms,
that are commonly found in neurocognitive disorders including (1) an inability to comprehend or understand
(see Table 15.1). We will then discuss some broader diag- speech or to repeat speech
nostic and assessment issues. accurately and correctly, aphasias Speech disorders resulting in
difficulties producing or comprehending
(2) the production of inco- speech.
herent, jumbled speech
15.1.1 Cognitive Impairments (known as fluent aphasia), fluent aphasia The production of incoher-
in Neurocognitive Disorders and (3) an inability to initi- ent, jumbled speech.
ate speech or respond to
Learning and memory deficits speech with anything other non-fluent aphasia An inability to initiate
Amnesia is a common feature of many neurocognitive than simple words (known speech or respond to speech with anything
disorders, including an inability to learn new information as non-fluent aphasia). other than simple words.
(494 PSYCHOPATHOLOGY |
TABLE 15.1 Terminology: Cognitive impairments in neurocognitive disorders
Term Definition Main brain areas affected
Aphasia Speech disorder resulting in difficulties producing or |Language centres of the left hemisphere — usually
comprehending speech Broca’s area or Wernicke’s area (see Figure 1)
Agnosia Loss of ability to recognize objects, persons, sounds, — Occipital or parietal lobes (see Figure 2)
shapes or smells while the specific sense is not
defective; nor is there any significant memory loss
Apraxia Loss of the ability to execute or carry out learnt Parietal lobes of the left hemisphere (see Figure 2)
(familiar) movements, despite having the desire and
the physical ability to perform the movements
Anterograde Memory loss for information acquired after the onset — Hippocampus; medial temporal lobes; basal
amnesia of amnesia forebrain (see Figure 2)
Retrograde amnesia Inability to recall events that occurred before the Hippocampus; temporal lobes (see Figure 2)
onset of amnesia
Deficits in executive The inability to effectively problem-solve, plan, initiate, Frontal lobes, especially the prefrontal cortex
functioning organize, monitor and inhibit complex behaviours (see Figure 2)
Limbic system
Frontal Cingulate gyrus
Fornix
Occipital
Temporal lobe
lobe (| ; Amygdala
Broca Medulla |
Cerebellum
oblongata Parahippocampal
gyrus
| Frontal lobe: planning and central executive functions;

initiating and inhibiting complex goal-directed behaviour
Parietal lobe: somatosensory perception and integration
of visual and somatospatial information
Temporal lobe: language function and auditory perception,
Front Left side view Back long-term memory and emotion
[] Occipital lobe: visual perception and processing
FIGURE 1 Language centres ofthe left hemisphere
(Broca’s area and Wernicke’s area). FIGURE 2 Anatomy ofthe brain.
Broca’s aphasia Disruption of the ability A distinction can be made mispronunciation rather than mis-selection of words.
to speak consisting ofdifficulties with between Broca’s aphasia In contrast, Wernicke’s aphasia is a deficit in the com-
word ordering, finding the right word and and Wernicke’s aphasia. prehension of speech, involving difficulties in recognis-
articulation.
Disruption of the ability ing spoken words and converting thoughts into words.
Wernicke’s aphasia A deficitinthecom- tO speak is known gener- Damage to different areas of the left hemisphere (which
prehension of speech involving difficulties ally as Broca’s aphasia and controls speech) are specific to each of these deficits.
in recognizing spoken words and convert-consists of difficulties with Wernicke’s aphasia is associated with damage to regions
ing thoughts into words.
word ordering (agramma- behind the frontal lobes while Broca’s aphasia is more
tism), finding the right word (anomia) and articulation. It likely to result from damage to the left frontal lobe itself
is characterized by laborious non-fluent speech involving (see Table 15.1).
Deficits in visual-perceptual functioning poor judgement (e.g. erratic or unsafe driving), inappro-
In some cases the individual may be unable to recognize priate behaviour (e.g. leaving the house in inappropriate
everyday objects and name them correctly. This is known clothing such as pyjamas) and erratic mood swings (e.g.
as agnosia and it can affect from laughter to hostility).
sia The loss of the ability to recog- a wide variety of func-
objects, persons, sounds, shapes or
Ils while the specific sense is not defec-
tional skills, such as face Deficits in higher order intellectual functioning
and there is no significant memory perception (prosopagnosia) Impairment in more abstract mental tasks is another
and musical discrimina- possible indication of a neurological disorder, and indi-
tion (amusia). A famous viduals may be unable to make simple mathematical cal-
example of agnosia is recounted in the book The Man culations, to reason deductively or to draw on general
Who Mistook His Wife for a Hat and Other Clinical Tales by knowledge when undertaking a task or activity.
Oliver Sacks. He describes the case of Dr P, a music pro-
fessor who had developed visual agnosia. He was able to
identify and describe complex shapes but could often not 15.1.2 Assessment in Clinical
recognize his own students’ faces and could only identify
them when they spoke. The title of the book comes from Neuropsychology
an occasion when Dr P was leaving a house and reached Identifying that someone has a neurocognitive disorder
for his wife’s head, mistaking it for a hat and trying to lift is a difficult and often lengthy process. Assessment is
it off. Interestingly his agnosia only affected his visual per- important (1) for determining the actual nature of any
ceptions and did not affect his music abilities in any way. deficits and the location of any related tissue damage in
the brain, (2) for providing information about onset, type,
Motor skills deficits severity and progression of symptoms, (3) for helping to
Some neurocognitive disorders are characterized by discriminate between neurological deficits that have an
impairments in motor performance and coordination. organic basis and psychiatric symptoms that do not, and
This may involve the inability to move a limb, a tendency (4) for helping identify the focus for rehabilitation pro-
to suddenly become paralysed or difficulty in coordinat- grammes and to assess progress on these programmes
ing movements effectively. (Veitch, 2008). In many cases, a diagnosis has to be made
axia Loss of the ability to execute This is known as apraxia on the basis of cognitive and behavioural impairments
arry out learnt (familiar) movements,
dite having the desire and the physical and in more complex poe that are detected by a range of neuropsychological tests,
ity to perform the movements. the individual with apraxia but in recent times the results of these tests can be supple-
may be able to emit a mented by findings from EEG analyses, brain scans such
behaviour when it is under routine conditions (e.g. clean- as PET scans and fMRI, blood tests and chemical analyses
ing their teeth as part of their washing routine first thing of cerebrospinal fluids. Assessment of cognitive abilities
in the morning) but are unable to do this on command. is also supplemented with behavioural observation and
information from clients and their families about onset,
Deficits in executive functions type, severity and progression of symptoms, together
This reflects the inability to effectively problem-solve, with a detailed history of educational, occupational, psy-
plan, initiate, organize, monitor and inhibit complex chosocial, demographic and previous and current medi-
behaviours. These functions are normally associated with cal factors. Neuropsychological tests themselves can be
the prefrontal cortex, so remarkably accurate in detecting quite specific deficits
frontal cortex An area of the brain damage to this area of the and also identifying the brain areas where tissue dam-
ch is important in maintaining rep-
brain is frequently involved age may have led to the deficit. Brain scans can then sup-
ntationsof goals and the means to
eve them. é when executive function plement and confirm the results of neuropsychological
deficits are found. A widely tests (D’Esposito, 2000). One of the most widely used
consin card sorting task A widely used test of executive func- tests worldwide is the WAIS-IV (the Wechsler Adult
1 test of executive functioning where tioning is the Wisconsin Intelligence Scale, 4th edn)
viduals must sort cards for a number card sorting task, where (Wechsler, 2008) (see sec- WAIS-IV Fourth edition of the Wechsler
ials using one rule (e.g. colour) and Adult Intelligence Scale.
individuals must sort cards tion 2.2.3). This contains
1 sort cards using a different rule (e.g.
e).
for a number of trials using scales that measure vocab-
one rule (e.g. colour) and ulary, arithmetic ability, digit span, information compre-
then sort cards using a different rule (e.g. shape). This hension, letter-number sequencing, picture completion
requires the ability to shift attention and to inhibit an ability, reasoning ability, symbol search and object assem-
established response pattern. Deficits in executive func- bly ability. These measures can be aggregated to pro-
tioning are revealed in everyday behaviour by examples of vide scores on broader indices of ability such as verbal
comprehension, perceptual organization (a measure of injury, alcohol abuse, Alzheimer's disease, stroke), whether
nonverbal reasoning), working memory and informa- the damage occurred during childhood development, and
tion processing speed. In the UK, the Adult Memory and whether any deficits are progressive. Focus Point 15.1 pro-
Information Processing Battery (AMIPB) (Coughlan & vides an example of one of the basic tests — the trail mak-
Hollows, 1985) is in wide use and this comprises two tests ing test — that provides a measure of information processing
of speed of information processing, verbal memory tests speed anda range of recognition and visuomotor integration
(list learning and story recall) and visual memory tests abilities. Many of these tests are so extensive that they may
(design learning and figure recall). One of the common take as long as 6 hours to administer, requiring substantial
neuropsychological tests used in the US is the Halstead— patience and stamina on the part of both the clinician and the
Reitan Neuropsychological Test Battery (Broshek & Barth, patient. In contrast, some ather tests have been developed to
2000), which has been compiled to evaluate brain and nerv- be quick and simple to implement, and to provide a reason-
ous system functioning across a fixed set of eight tests. The ably reliable indication of general level of impairment. One
tests evaluate function across visual, auditory and tactile such test is the Mini Mental State Examination (MMSE),
input, verbal communication, spatial and sequential per- which is a brief 30 item test
ception, the ability to analyse information, the ability to used to screen for dementia Mini Mental State Examination
form mental concepts, make judgements, control motor (e.g. in Alzheimer’s disease) (MMSE) A structured test that takes 10
minutes to administer and can provide
output, and to attend to and memorize stimuli. and takes about 10 minutes able information on a client's overall leve
Test batteries such as these also provide useful infor- to administer (see Focus of cognitive and mental functioning.
mation on the source of any deficits (such as closed head Point 15.2).
oF THE TRAIL MAKING TASK

wh
=.
~
=
e)
a
Vi
=)
U
Oo
ity
Begin
@)
Above is an example of the trail making test. This con- The trail making test helps to evaluate information
sists of a page with circles containing the letters A to processing speed, visual scanning ability, integration
L and 13 numbered circles intermixed and randomly of visual and motor functions, letter and number rec-
arranged. The patient is instructed to connect the circles ognition and sequencing, and the ability to maintain
by drawing lines alternating between numbers and two different trains of thought.
letters in sequential order until they reach the circle For adults, scores above 91 seconds have tradition-
labelled ‘End’ This test would normally take 5-10 min- ally indicated brain impairment, but completion times
utes to administer. may vary significantly with age, education and culture.
ee MINI MENTAL STATE EXAMINATION (MMSE)

uy
=
|
ee The MMSE is a good instrument for assessing cognitive function in dementia and takes about 10 minutes to
= administer.
2)
ao. Orientation
WV
=| What is the (year) (season) (date) (day) (month)?
6
LL.
i
Where are we: (country) (city) (part of city) (number of flat/house) (name of street)?
5
Registration
Name three objects: one second to say each.

Then ask the patient to name all three after you have said them.
Give one point for each correct answer. 30
Attention and calculation
Serial 7s: Ask the patient to begin with 100 and count backwards by 7. Stop after five subtractions |
(93, 86, 79, 72, 65). One point for each correct.
=)
Recall
Ask for the three objects repeated above (under Registration). Give one point for each correct.
36)
Language
Name apencil and watch: Show the patient a wrist-watch and ask him or her what it is. Repeat for pencil. (Two points.)
Repeat the following: ‘No ifs, ands or buts’ (one point).
Followa three-stage command: ‘Take a paper in your right hand, fold it in half and put it on the floor’ (three points).
Read and obey the following: Close your eyes (one point).
Write a sentence (one point).
Copya design (one point). On a clean piece of paper, draw intersecting pentagons (as below), each side about one
inch and ask him or her to copy it exactly as it is. All ten angles must be present and two must intersect to score 1
point. Tremor and rotation are ignored.
90
Total score
A score of 20 or less generally suggests dementia but may also be found in acute confusion, schizophrenia or
severe depression. Mild Alzheimer’s is usually linked to an MMSE score of 21-26, moderate Alzheimer’s to scores
of 10-20 and severe Alzheimer’s to an MMSE score of less than 10.
fees = EES a ee Seale ESA EO WE NA ee) —
15.1.3 The Diagnosis of example, cognitive deficits typical of neurocognitive

oge ° disorders are a regular feature of dissociative disorders
Neurocognitive Disorders (e.g. amnesia) and schizophrenia (e.g. language deficits,
Difficulties of diagnosis information-processing deficits, and deficits in executive
Diagnosis is made difficult by the fact that the symptoms functions). Motor coordination deficits, paralysis and
and deficits found in neurocognitive disorders often impairments of sensory input are also found in somatic
closely resemble those of other psychopathologies. For Symptom disorders such as conversion disorder (e.g.
498 PSYCHOPATHOLOGY
. » &
hysterical blindness and paralysis — see section 13.2.2). period of time. The person may not understand simple
In addition, in the early stages of a degenerative questions and may be unable to shift attention from
neurological disorder people will start to experience answering one question to answering another. Delirium
cognitive impairments that affect their daily lives and often occurs in the context of other neurocognitive
this will often lead to the development of psychological disorders and may be accompanied by memory and
problems (e.g. depression and anxiety) that compound learning deficits, disorientation and perceptual distur-
the difficulties of diagnosis (see Paddy’s story at the bances such as hallucinations. There may be evidence
beginning of this chapter). Indeed, prior to the devel- that the delirium is a result of the physiological con-
opment of modern brain scanning technology, it was sequences of a general medical condition, substance
often the case that a neurological disorder could only intoxication or withdrawal, or use of a medication ora
be diagnosed by autopsy after the death of the sufferer toxin, and may be associated with disturbances in the
(Patton & Shepherd, 1956). Even so, with the range of sleep-wake cycle, such as a reversal of the day-night
tests available today psychological problems can still be cycle, restlessness and hyperactivity. The individual
misdiagnosed as neurological ones (e.g. Iverson, 2006) may also exhibit emotional disturbances such as anxi-
and vice versa (e.g. Sumpter & McMillan, 2005), and this ety, fear, depression, irritability, anger, euphoria and
has important implications for rehabilitation and subse- apathy, accompanied by rapid and unpredictable shifts
quent care. from one emotional state to another (DSM-5 Summary
To add to the difficulties of diagnosis, the symptoms Table 15.1).
of a range of neurological disorders overlap consider- The symptoms of delirium can develop rapidly over
ably. For example, dam- hours to days but may begin abruptly after specific traumatic
closed head injury A concussion or head age to specific areas of the events, such as head injury. Equally, delirium may resolve
trauma, the symptoms of which include brain as a result of a closed in just a few hours, but alternatively persist for weeks to
loss of consciousness after the trauma,
confusion, headache, nausea or vomiting,
head injury can give rise months, especially in the elderly. Delirium appears to result
blurred vision, loss of short-term memory to similar cognitive deficits from widespread disruption of brain metabolism and neu-
and perseverating. as those found in broader rotransmitter activity that can be triggered by a range of
degenerative disorders such events (e.g. traumatic head injury, substance intoxication
as Alzheimer’s disease. Similarly, a single causal factor or withdrawal, surgery, sleep loss, malnutrition and psycho-
(such as a brain tumour) can manifest as a range of dif- logical stress generally). Delirium is particularly common
ferent symptoms including speech disorder, deficits in in older people, and particularly hospitalized older people.
sensory perception or emotionality and aggressiveness. The community prevalence rate for delirium is 1-2 per cent
These are some of the reasons why neurological assess- but increases with age, rising to 14 per cent among those
ment is thorough, multifaceted and continues to be over 85 years of age (DSM-5, p.600).
administered throughout the period of diagnosis and
rehabilitation. Major or mild neurocognitive disorders (NCDs)
DSM-5 defines neurocognitive disorders as conditions
DSM-5 Neurocognitive disorder where there is evidence of a significant decline in per-
diagnostic categories formance across one or more cognitive domains, such as
DSM-5 identifies two broader diagnostic syndromes
into which many neurological disorders fall. They are
delirium, which is characterized by confused and dis-
organized behaviour, and major or mild neurocogni- DSM-5 SUMMARY TABLE 15.1 Criteria for delirium
tive disorders (NCDs) (formally known in DSM-IV as
¢ Areduced ability to focus, direct and sustain attention
dementias), which are characterized by the impairment
and awareness, developing over a short period of time
of basic cognitive func- (hours to a few days) and fluctuates in severity through-
dementias Disorders involving the devel-
tions. We will look at these out that time
opment of multiple cognitive deficits that
include memory impairment and at least two diagnostic categories
¢ Additional disturbances in cognitive functioning are also
one other specific deficit. more closely. observed
Delirium The main fea- ¢ Disturbances are not a result of a pre-existing

delirium A disturbance of consciousness
ture of a delirium is a dis- neurological condition and do not occur during the
that develops over a short period of time.
course of a coma or other reduced level of arousal state
turbance of attention and
awareness, and the disturbance in attention is reflected e There is no evidence that the disturbance is as a direct
in a reduced ability to direct, focus, sustain and shift physiological result of another medical condition, sub-
stance use or withdrawal
attention. Also, the disturbance develops over a short
CHAPTER 15 NEUROCOGNITIVE DISORDERS 499°
complex attention, executive functioning, learning and objects despite intact sensory functioning). Disturbances
memory, language, perceptual-motor, or social cognition. in executive functioning are also common and are evi-
This decline can be diagnosed as either major neurocog- denced by the individual having difficulty coping with
nitive disorder (reflecting new tasks, shifting mental sets, generating novel verbal
or neurocognitive disorder DSM-5 a substantial impairment) information and using or recalling basic general knowl-
nes neurocognitive disorders (NCDs)
or mild neurocognitive edge. Simple tests for executive functioning include ask-
|: where there is evidence of a
ificant decline in performance across disorder (reflecting a mod- ing the individual to count to 10, recite the alphabet, do
or more cognitive domains, such as est impairment in cogni- subtraction or state as many animals as possible in 1 min-
\plex attention, executive function- tive performance). Major ute. Poor judgement and poor insight are also common
learning and memory, language,
neurocognitive disorders features of major neurocognitive disorders. They may
-eptual-motor, or social cognition. Major
)s reflect a substantial impairment. correspond to the catego- underestimate the risks involved in certain activities (e.g.
ries labelled as dementias driving) and indulge in inappropriate behaviours, such as
d neurocognitive disorder DSM-5
in previous editions of the making inappropriate jokes, neglecting personal hygiene
introduced disorder categories that are DSM. Examples of cogni- or disregarding conventional rules of social conduct.
igned to identify populations that are tive deficits include diffi- DSM-5 lists a number of specific major neurocogni-
sk for future mental health problems, culty remembering a short tive disorders and we will look at these individually in
these include mild neurocognitive dis-
er, which diagnoses cognitive decline in
grocery list or keeping track more detail below. These are Alzheimer’s disease, vas-
elderly. of the plot of a TV pro- cular neurocognitive disorders, NCD due to Parkinson’s
gramme; executive func- disease, NCD due to traumatic brain injury, NCD due to
tioning problems include difficulty resuming a task when HIV infection, NCD due to Huntington’s disease, NCD
interrupted, organising finances or planning a meal out. due to prion disease and NCD with Lewy bodies.
At the mild NCD level, the individual will describe these
tasks as requiring extra time or additional compensatory Types of major neurocognitive disorder
strategies. However, at the major NCD level, the individual In this section, we will look in more detail at some of the
will normally require assistance to complete these kinds prevalent neurocognitive disorders that are categorized
of tasks. The key diagnostic criteria for major and mild by their causes. These causes can range across cerebral
neurocognitive disorders are provided in DSM-5 Summary infection, traumatic brain injury, cerebrovascular acci-
Tables 15.2 and 15.3. dents (such as strokes) and degenerative disorders (such
In the major neurocognitive disorders, language func- as Alzheimer’s disease).
tion may deteriorate to the point where the individual’s
conversation is vague or empty, and they may be unable to NCD due to HIV infection Among the viruses that
name individual everyday objects (such as tie, dress, desk, can infect the brain is the human immunodeficiency virus
lamp). The condition may also (but not necessarily) be type 1 (HIV-1). The HIV virus tends to enter the central
associated with apraxia (impaired ability to execute motor nervous system early in the illness and neurological dif-
activities) and agnosia (the failure to recognize or identify ficulties can develop in up to 60 per cent of those infected
DSM-5 SUMMARY TABLE 15.2 Criteria for major DSM-5 SUMMARY TABLE 15.3 Criteria for mild
neurocognitive disorder neurocognitive disorder
e Significant cognitive deterioration from previous level in e Limited cognitive deterioration from previous level in at
at least one of the cognitive domains based on: least one of the cognitive domains based on:
e Concern of the patient, informant or doctor that there ° Concern of the patient, informant or doctor that there
has been a substantial decline in cognitive function has been a limited decline in cognitive function
e Asubstantial impairment in cognitive performance, ¢ A limited impairment in cognitive performance, pref-

preferably as documented by standard testing erably as documented by standard testing
e The cognitive deterioration interferes with self-reliance ¢ The cognitive deterioration does not interfere with self-
in everyday activities reliance in everyday activities
e The deficit does not occur in the context of delirium e The deficit does not occur in the context of delirium
e The deficit is not better accounted for by another ° The deficit is not better accounted for by another
mental disorder such as major depressive disorder or mental disorder such as major depressive disorder or
schizophrenia schizophrenia
500 ~ PSYCHOPATHOLOGY
DSM-5 SUMMARY TABLE 15.4 Criteria for neurocognitive HIV infection appears to cause these cognitive impair-
disorder due to HIV infection ments in a variety of ways. MRI scans indicate that HIV
infection is associated with progressive cortical atrophy
e The criteria are met for major or mild neurocognitive
disorder in the grey and white matter in the brain, particularly in
the later stages of the disease (Dalpan, McArthur,
e The patient is infected with human immunodeficiency
Aylward, Selnes et al., 1992) (see Figure 15.1). However,
virus (HIV)
while the HIV virus can itself attack the central nerv-
¢ The disorder is not better explained by non-HIV condi- ous system, neurological deficits are often caused by the
tions including secondary brain diseases body’s weakened immune system allowing other infec-
e The disorder is not due to another medical condition and. tions to attack the brain (Ghafouri, Amini, Khalili &
is not better explained by another mental disorder Sawaya, 2006).
NCD due to prion disease Many readers may recall

with the virus (Ghafouri, Amini, Khalili & Sawaya, 2006). the high profile given to what was called ‘mad cow disease’
On many occasions, the impairments caused by infection in the UK in the 1980s, 1990s and 2000s. ‘Mad cow dis-
are usually minor, but over the many years that a sufferer ease’ is a fatal infectious disease known as spongiform
may be hosting the virus, it may induce multiple symp- encephalopathy that attacks
spongiform encephalopathy A fatal
toms of motor and cognitive dysfunction and create a the brain and central nerv- infectious disease that attacks the brair
syndrome of impairment that is known in DSM-5 as neu- ous system. Outbreaks of and central nervous ,system. Commonl
rocognitive disorder due to HIV infection (sometimes the disease hit epidemic known as ‘mad cow disease’ or variant
also known as AIDS dementia complex (ADC) or HIV-1 proportions among cattle Creutzfeldt-Jakob disease (vCJD).
associated dementia (HAD)). Individuals that develop in the UK during the 1980s
this NCD diagnosis show impaired executive function- and evidence suggests that the disease was transmitted
ing, slowed speed of processing information, problems to humans through contaminated beef. In humans, this
with attentional tasks and difficulty learning new infor- became known as variant
variant Creutzfeldt-.-Jakob disease 4
mation. Other symptoms include impaired short-term Creutzfeldt_Jakob disease (vCJD) A fatal infectious disease that
memory, lack of concentration, leg weakness, slow- (vCJD) and estimates sug- attacks the brain and central nervous q
ness of hand movement and depression (Reger, Welsh, gest that over 150 people in system. Commonly known as‘mad cow
Razani, Martin & Boone, 2002) (DSM-5 Summary Table the UK died from the dis- disease’. ‘ ' q
15.4). Depending on the stage of their infection, around ease between 1995 and 2006 :
one-third to a half of HIV-infected individuals will (National Creutzfeldt-Jakob To view a video on Creutzfeldt-Jakob
develop at least mild neurocognitive impairment, but Disease Surveillance Unit, | disease go to
fewer than 5 per cent would normally meet the criteria 2006). The disease may have | video/ch15
for major neuorocognitive disorder (DSM-5, p.633). an incubation period of up
FIGURE 15.1 Functional MRI (fMRI) scans showing activation during a motor task for HIV patients with normal cognitive function
(NL), minor cognitive motor disorder (MCMD), and HIV associated dementia (HAD). Darkened regions indicate areas of activation.
Compared with NL, patients with MCMD and HAD have significantly less activation.
Source: Tucker, K.A., Robertson, K.R., Lin, W., Smith, J.K. et a/. (2004). Neuroimaging in human immunodeficiency virus infection. Journal of
Neuroimmunology, 157(1-2), 153-162. Reproduced by permission of Elsevier.
to 10-15 years, but, once symptoms begin to appear, death a description of how the progressive cognitive impairments
may occur within 4 months. Early signs of vCJD include caused by vCJD become manifest once symptoms appear.
changes in mood, temperament and behaviour followed by
impairments in memory and concentration, and confused NCD due to traumatic brain injury One of the
thinking. Deficits in verbal fluency, numeracy ability, face most common causes of neurological impairment is trau-
recognition, memory ability and executive functioning matic brain injury. This can result from blunt or penetrat-
appear rapidly once symptoms have been identified (Kapur, ing trauma to the head as a result of direct injury at the
Abbott, Lowman & Will, 2003) (DSM-5 Summary Table impact site. Indirect injury can also be caused by sudden
15.5). Thankfully, the annual incidence of Creutzfeldt— impacts causing movement of the brain within the skull,
Jakob disease is very low at around one or two cases per leading to injury on the opposite side of the brain to the
million people (DSM-5, p.635). The infectious agent in
vCJD is thought to be the prion (a prion is an abnormal,
DSM-5 SUMMARY TABLE 15.5 Criteria for neurocognitive
transmissible agent that is able to induce abnormal folding
disorder due to prion disease
of normal cellular proteins in the brain, leading to brain
damage) and rapid dementia in vCJD appears to result from ° The criteria are met for major or mild neurocognitive
prions or protein deposits encrusting or replacing neurons disorder
in the brain and central nervous system, hence the terme The onset is slow, with rapid progression of the impairment
prion disease. This occurs at both the cortical and subcor-
e Motor features of prion disease are obvious, such as
tical level, causing deficits in involuntary muscle twitching or ataxia
on disease Prion disease represents a cognitive functioning and
e The disorder is not due to another medical condition and
up of conditions that affect the nervous basic motor coordination.
tem in humans and animals. is not better explained by another mental disorder
Case History 15.1 provides
VARIANT CREUTZFELDT-JAKOB DISEASE (vCJD)

The patient was a right-handed man in his early 20s who presented at the end of July 1998 with a short history
of memory difficulties, occasional problems in speech articulation, a change in personality and two episodes of
urinary incontinence. His parents thought that the first sign of his illness was evident in May 1998, when he had a
slight slurring in his speech during a telephone conversation with them. The first noticeable manifestation of his
memory difficulties occurred in early July 1998 when he started a summer work placement and had major limita-
tions in assimilating new information in a computer-based environment where he was taught simple data entry
procedures and where, during a previous placement, he had excelled. Although he appeared to have no difficulty
15.1
HISTORY
CASE using equipment around the home (e.g. the video), he performed such activities much more slowly than before.
His mother reported that he was very irritable and argumentative when he came home from university. He later
became indifferent and apathetic. She said that he was often stuck for words and that his speech was sometimes
incoherent. He had recently written two letters to his girlfriend that did not make any sense. His mother thought
that he was nervous about going out on his own. His condition showed a progressive decline and he died in
December 1998.
Source: From Kapur, Abbott, Lowman & Will, 2003.
Clinical Commentary
vCJD may have an incubation period of up to 10-15 years but the first signs of the illness are emotional
changes and confused behaviour. The disease eventually affects every aspect of thinking and behaviour,
causing impairments in cognitive functioning, motor coordination and control over bodily functions — each
of which is manifested in this case history. Once symptoms have begun to appear, the disease is fatal, and
death usually occurs within 4-6 months. DSM-5 has provided diagnostic criteria for this neurocognitive
disorder under the title ‘neurocognitive disorder due to prion disease‘
502 PSYCHOPATHOLOGY
impact. Between 2000 and 2010 in the UK the incidence DSM-5 SUMMARY TABLE 15.6 Criteria for neurocognitive
of traumatic brain injuries requiring consultant attention disorder due to traumatic brain injury
increased by around 95 per cent (The Health & Social Care e The criteria are met for major or mild neurocognitive
Information Centre, 2012). Road traffic accidents account disorder
for around 40-50 per cent of all head injuries, while
¢ Traumatic brain injury has occurred with at least one of
domestic and industrial accidents account for between 20 the following:
and 30 per cent. A majority of the rest are caused by sports
and recreational activities (10-15 per cent) and assaults (10 e Unconsciousness
per cent). Twice as many males as females are likely to be e Post-traumatic amnesia
treated in hospital for traumatic brain injury and around ¢ Disorientation and confusion
40-50 per cent are children. While the vast majority of
¢ Neurological signs such as neuroimaging demonstrat-
these cases will suffer only a minor head injury, more seri-
ing injury
ous cases will lapse into coma, develop epilepsy or suffer
other forms of long-term disability (both physical and ¢ The disorder occurs immediately after the traumatic
intellectual). Although many victims of head injury will brain injury occurs
show a slow but gradual improvement over time (e.g.
recovery of any memory loss, recovery of motor func-
tions such as balance, dissipation of feelings of confusion
and disorientation), severe head injury can be associated fed by that blood flow. In haemorrhage When a blood vessel in
with a range of semi-permanent cognitive and neuro- contrast, a haemorrhage the brain ruptures
and affects local brain”
logical deficits, including general deficits in speed of infor- is when a blood vessel in tissue.
mation processing, attention, memory, language skills the brain ruptures and
and executive functioning, and may meet the diagnostic affects local brain tissue. cerebral embolism A blood clot that q
criteria for neurocognitive disorder due to traumatic brain The most common forms somewhere in the body before
travelling through the blood vessels and
injury, with around 2 per cent of the population of the US causes of infarction are
lodging in the brain, causing the brain cell
living with a traumatic brain injury-associated disability an embolism or a throm- to become damaged as a result of e
(DSM-5, p.625) (DSM-5 Summary Table 15.6). If recovery bosis. A cerebral embo- starvation. | is)
from such deficits occurs, it is likely to happen in the first 6 lism is a blood clot that
months following the injury. However, perhaps more dra- forms somewhere in the body before travelling through
matic than some of the cognitive deficits resulting from the blood vessels and lodging in the brain, causing the
brain injury are the emotional sequelae, and these include brain cells to become dam-
cerebral thrombosis An injury caused —
depression, irritability, fatigue, aggressive behaviour, anxi- aged as a result of oxy- when a blood clot (thrombus) forms in an
ety, rapid mood shifts and difficulty concentrating (Satz, gen starvation. Cerebral artery (blood vessel) supplying blood to —
Forney, Zaucha, Asarnow et al., 1998). These factors can thrombosis occurs when the brain. The clot interrupts the blood
supply and brain cells are starved of
cause a significant decline in the overall quality of life for a blood clot (thrombus)
oxygen.
those with severe brain injury, giving rise to intense bouts forms in an artery (blood
of depression and suicidal ideation as well as posing sig- vessel) supplying blood to
nificant challenges for post-injury care and rehabilita- the brain. Furred-up blood vessels with fatty patches of
tion (e.g. Horneman, Folkesson, Sintonen, von Wendt & atheroma (an abnormal inflammatory accumulation of
Emanuelson, 2005; Baguley, Cooper & Felmingham, 2006; macrophage white blood cells within the walls of arter-
Levin, McCauley, Josic, Boake et al., 2005). ies) may make a thrombosis more likely. The clot inter-
rupts the blood supply and brain cells are starved of
Vascular neurocognitive disorder Damage to brain oxygen.
tissue can also occur as a result of a cardiovascular acci- Haemorrhaging in the brain is often the result of
cardiovascular accident (CVA) Otherwise
dent (CVA) — otherwise hypertension or high blood pressure and is often due to an
known as a stroke. Strokes result from known as a stroke. Strokes aneurysm or bulgingin the
either a blockage or breaking of the blood result from either a block- wall of the blood vessel — aneurysm A localized bulging in a blood
vessels in the brain. vessel caused by disease or weakening of
age or breaking of the usually an artery at the base the vessel wall.
stroke A sudden loss of consciousness
blood vessels in the brain of the brain.
resulting when the rupture or occlusion ofa and can be defined in two Strokes are remarkably common - especially in indi-
blood vessel leads to oxygen lack in the brain. broad ways. An infarction viduals over the age of 65 years. In the UK, an estimated
is when the blood flow 130,000 people a year suffer a stroke — including around
infarction The injury caused when the
blood flow to the brain is impeded in some to the brain is impeded 1000 who are under 30 years of age. Strokes are the
way, resulting in damage to the brain tis- in some way, resulting in third most common cause of death in the UK and the
sue fed by that blood flow. damage to the brain tissue single most common cause of disability — over 250,000
CHAPTER 15 NEUROCOGNITIVE DISORDERS 503,
people currently live in the UK with a disability caused DSM-5 SUMMARY TABLE 15.7 Criteria for vascular
by a stroke (The Stroke Association, 2006). Symptoms neurocognitive disorder
of a stroke often occur very suddenly and unexpectedly.
Symptoms include numbness, weakness or paralysis on disorder
one side of the body (signs of this may be a drooping
arm, leg, a lowered eyelid, ora dribbling mouth), slurred e The clinical features suggest vascular aetiology as
marked by one of the following:
speech or difficulty finding words or understanding
speech, sudden blurred vision or loss of sight, confusion e Arrival of the cognitive deficit is timely related to at
or unsteadiness, and a severe headache. The type and least one cardiovascular event
severity of symptoms will depend entirely on the brain e Decline is evident in complex attention and frontal-
area affected by the CVA. The most common longer term executive function
symptoms of stroke include aphasia, agnosia, apraxia e There is evidence of cerebrovascular disease to account
(see Table 15.1) and paralysis, and a DSM-5 diagnosis of for the neurocognitive deficits
vascular neurocognitive disorder is established if there is
e The symptoms are not better accounted for by another
good evidence for a cerebrovascular event as the cause of brain disease or disorder
the disability, and if the criteria are met for major or mild
neurocognitive disorder (see Tables 15.1, 15.3 and 15.7).
One of the most common forms of stroke is thrombosis
in the left-middle cerebral artery, affecting the left hemi-
sphere. This will cause disability to the right-hand side treating post-stroke depression with antidepressant
of the body (which is controlled by the left hemisphere) medication also has the effect of significantly decreas-
and also cause significant impairment in language abil- ing mortality rates over a period of 9 years (Robinson,
ity (e.g. aphasia) because the left hemisphere is critically Schultz, Castillo, Kopel et al., 2000). All of this suggests
involved in language generation and comprehension. that depression is an important feature of disability
As well as physical and cognitive deficits, individu- caused by strokes and is an area where clinical psycholo-
als who have suffered a stroke also exhibit emotional gists might be suitably employed to manage depression
disturbance, often manifested as depressed mood or in attempts to improve recovery rates and reduce mor-
as emotional lability. Depression in particular is a com- tality rates.
mon and significant consequence of strokes. A recent
meta-analysis indicated that 29 per cent of stroke vic- Degenerative disorders Degenerative disorders rep-
tims suffer depression up to 10 years after their stroke, resent those neurocognitive disorders that are character-
with cognitive impairment being one of the main pre- ized by a slow, general deterioration in cognitive, physical
dictors of post-stroke depression (Ayerbe, Ayis, Wolfe and emotional functioning as a result of progressive phys-
& Rudd, 2013). Levels of depression are also correlated ical changes in the brain. Deterioration occurs gradually
with the severity of both physical and cognitive deficits over a number of years and degenerative disorders are
(Kauhanen, Korpelainen, Hiltunen, Brusin et al., 1999), most frequently a feature of older age, when around 7
suggesting that there may be a link between degree of per cent of individuals over 65 years of age have diagnos-
disability and depression, and depression is associated able signs of degenerative dementia; this rises to around
with a significantly increased risk of early mortality (Pan, 30 per cent in those over 85 years of age (Johansson &
Sun, Okereke, Rexrode & Hu, 2011). Recovery from Zarit, 1995; Kokmen, Beard, Offord & Kurland, 1989).
physical and cognitive impairment is also significantly Degenerative disorders can affect both the cerebral cor-
retarded in those with depression (Robinson, Lipsey, tex and subcortical regions of the brain. Those that
Rao & Price, 1986; Morris, Robinson, Andrezejewski, affect cortical areas cause impairments in cognitive abili-
Samuels & Price, 1993). There is a tendency here to con- ties such as memory, language, attention and executive
clude that the disabilities resulting from a stroke may functioning (causing amnesia, aphasia, agnosia, slowed
cause depression that in turn inhibits recovery. However, thinking and confusion; see Table 15.1). Disorders affect-
the picture is rather more complex than this and there ing subcortical regions of the brain may in addition cause
seems to be a bidirectional link between stroke and emotional disturbances and motor coordination difficul-
depression. For example, some studies have indicated ties. There are currently an estimated 800,000 people in
that depression may even be a risk factor for strokes. the UK with dementia, and one in three people over 95
In a prospective study, May, McCarron, Stansfeld, Ben- years of age have dementia (Alzheimer’s Society, 2013),
Shlomo et al. (2002) found that men with significant with the most common cause of degenerative dementia
depressive symptoms were significantly more likely to in the UK being Alzheimer’s disease (contributing 55 per
suffer a stroke within the following 14 years than those cent). Degenerative disorders that in addition significantly
without significant depression symptoms. Similarly, affect subcortical areas, and so affect emotional behaviour
504 PSYCHOPATHOLOGY
* ~~
and motor coordination, disease manifests as progressive impairments in short-

To view a video on Parkinson’s
disease go to
are Parkinson’s disease and term memory, with symptoms of aphasia, apraxia and
Huntington’s disease.
www.wiley-psychopathology.com/ agnosia, together with evidence of impaired judgements,
video/ch15
Diagnosis of degenera- decision-making and orientation. Early signs of the dis-
tive disorders is difficult ease are irritability, lack of concentration and basic fail-
and complex. Firstly, a degenerative disorder has to ures of short-term memory, such as forgetting that food
be distinguished from the normal process of ageing. is cooking or forgetting names. Eventually, the individual
Normal ageing naturally results in a moderate deteriora- becomes more and more confused and disoriented, and
tion of cognitive abilities (such as forgetfulness or cog- may be unable to remember basic general knowledge (e.g.
nitive slowness) and a deterioration in physical abilities be unable to recite the alphabet), may confuse night and
(such as problems with balance and motor coordina- day, and get lost in relatively familiar environments. Many
tion). However, degenerative disorders compound this individuals also show personality changes, may exhibit
natural process because they represent an active patho- paranoid behaviour and become generally irritable and
logical organic deterioration of the brain. Secondly, it is difficult to control. Eventually sufferers usually become
often difficult to distinguish between the different degen- physically weak and bedridden. Their erratic and unpre-
erative disorders that may affect cognitive and physical dictable behaviour will often become problematic for their
functioning. Many manifest with very similar cognitive carers, many of whom are likely to be the elderly spouses
impairments, such as amnesia. Thirdly, degenerative of the sufferer themselves. The average duration of the
disorders are most frequently found in the elderly and disease from onset of symptoms to death is around 8-10
this particular population will often present with a wide years.
range of psychological and medical problems that com- Known risk factors for Alzheimer’s disease include
plicate diagnosis. For example, anxiety and depression the following (Barranco-Quintana, Allam, Del Castillo &
are common features of old age and may complicate Navajas, 2005):
neurological testing. Performance during assessment
may also be affected by other physical illnesses or the 1. age, which is the principal marker for risk of the
effects of medications for other ailments. Finally, how disease;
a degenerative disorder manifests on presentation may 2. sex — prevalence is higher in women than in men;
differ significantly between individuals depending on fac- 3. genetics — having a first-degree relative with the
tors such as their level of education, level of family and disease significantly increases risk;
social support, and their psychological history. In effect,
4. family history of dementia — nearly 40 per cent
two individuals with the same disorder may present
of those with Alzheimer’s disease have a family
themselves quite differently and perform quite differ-
history of dementia;
ently in assessments depending on a range of social and
psychological factors. Overall prevalence estimates for 5. a history of head injury (McDowell, 2001); and
diagnosed dementia disorders are around 1-2 per cent 6. low educational status.
at age 65 years and as high as 30 per cent by age 85 years
(DSM-5, p.608). Interestingly, some activities appear to have a direct
The following sections continue by describing in or indirect protective value by predicting lower rates of
detail some of the main degenerative disorders. These Alzheimer’s disease (even in those with a family history
cover neurocognitive disorder due to Alzheimer’s dis- of dementia) and these include physical activity, smok-
ease, frontotemporal neurocognitive disorder, neurocog- ing, drinking moderate levels of alcohol and diets high
nitive disorder due to Parkinson’s disease, neurocognitive in vitamins B6, B12 and folic acid (Barranco-Quintana,
disorder with Lewy bodies, and neurocognitive disorder Allam, Del Castillo & Navajas, 2005). However, we must
due to Huntington’s disease. be cautious about how we interpret these factors. For
example, smoking may protect against Alzheimer’s
NCD due to Alzheimer’s disease Characteristics of disease largely because it may prevent smokers from
Alzheimer’s disease Alzheimer’s disease is the most reaching old age, which is when the disease becomes
common form of dementia. It is a slowly progressive disor- prevalent. In addition, low educational status may be
der and neural damage may correlated with Alzheimer’s disease because it may
Alzheimer's disease A slowly progressive
form of dementia involving progressive
start 20-30 years before any adversely affect performance on the cognitive tasks used
impairments in short-term memory, with overt cognitive or behay- to diagnose the disease. Several recent studies also sug-
symptoms ofaphasia, apraxia and agnosia, ioural signs of impairment gest that factors such as diet (e.g. a Mediterranean diet),
together with evidence of impaired judge- (Davies, Wolska, Hilbich, regular exercise and engagement in intellectual activities
ments, decision-making and orientation.
Multhaup et al., 1988). The also appear to be useful in warding off cognitive decline
CHAPTER 15 NEUROCOGNITIVE DISORDERS 505.
(Williams, Plassman, Burke, Holsinger & Benjamin, DSM-5 SUMMARY TABLE 15.8 Criteria for neurocognitive
2010; Hamer & Chida, 2009). For example, high levels disorder due to Alzheimer’s disease
of cognitive activity appear to protect against cognitive
decline even in individuals who have a high genetic risk disorder
for Alzheimer’s disease and have already developed the
plaques and tangles in their brain that are associated e The onset is slow, with gradual progression of the
impairment
with Alzheimer’s (Wilson, Scherr, Schneider, Tang &
Bennett, 2007). e For major neurocognitive disorder:
The diagnostic criteria for neurocognitive disorder Probable Alzheimer’s disease is diagnosed if either of the
due to Alzheimer’s disease is given in DSM-5 Summary following are present:
Table 15.8. However, Alzheimer’s disease itself is difficult
e Evidence of the Alzheimer’s disease genetic mutation
to differentiate from other forms of degenerative demen- in the family history of the patient or via genetic testing
tia and it is often easier to identify Alzheimer’s disease
e All three of the following are present:
by successively eliminating other types of disorder that
cause dementia symptoms, such as Parkinson’s disease, e Decline in memory and learning and at least one
Huntington’s disease, hypothyroidism, HIV infection, other cognitive ability
substance abuse or head trauma. This can be achieved e Steady, gradual decline in cognition
using thyroid function tests, blood tests and a battery of e No evidence of other neurodegenerative or cer-
neuropsychological tests of cognitive function. However, ebrovascular disease
the recent identification of some of the genes that carry a
Otherwise, possible Alzheimer’s disease should be
high risk for the development of Alzheimer’s disease means
diagnosed.
that genetic testing can be used to identify Alzheimer’s as
the possible cause of the dementia or cognitive decline. e For mild neurocognitive disorder:
In addition, neuroimaging plays an important part in the Probable Alzheimer’s disease is diagnosed if there is
diagnosis of Alzheimer’s disease by helping to exclude alter- evidence of the Alzheimer’s disease genetic mutation in
native causes of dementia such as brain tumour, cerebral the family history of the patient or via genetic testing.
atrophy and cerebrovascular disease. Otherwise, possible Alzheimer’s disease should be diag-
nosed if all three of the following are present:
Aetiology of Alzheimer’s disease It is only in the past e Decline in memory and learning and at least one
20-25 years that we have come to understand some of the other cognitive ability
causes of Alzheimer’s disease, and, indeed, become able e Steady, gradual decline in cognition
to identify it as a specific form of degenerative dementia.
e No evidence of other neurodegenerative or cerebro-
The changes that occur to the brain during Alzheimer’s
vascular disease
disease appear to be structural and involve the develop-
ment of beta amyloid plaques and neurofibrillary tangles. e The disturbance is not better explained by cerebrovascular
disease, another neurodegenerative disease or disorder
Beta amyloid plaques appear to be caused by abnor-
a amyloid plaques Abnormal cell mal protein synthesis in
elopment, possibly caused by abnor- the brain and they clump
protein synthesis in the brain, which together with the conse- Another factor that is thought to be important in
np together with the consequence of
quence of killing healthy Alzheimer’s disease is the faulty production of the brain
ng healthy neurons.
neurons. Neurofibrillary neurotransmitter acetylcholine; Alzheimer’s disease
rofibrillary tangles Abnormal collec- tangles consist of abnor- appears to affect structures
s of twisted nerve cell threads which mal collections of twisted involved in the produc- acetylcholine A neurotransmitter that
It in errors in impulses between nerve appears to be involved in learning and
nerve cell threads which tion of acetylcholine. The memory.
; and eventual cell death.
result in errors in impulses enzyme _acetylcholinester-
between nerve cells and eventual cell death (Blennow, de ase normally breaks down acetylcholine after use so it
Leon & Zetterberg, 2006) (see Figure 15.2). The result can be recycled, but in Alzheimer’s disease acetylcholine
of these abnormal cell developments is that there is a levels fall too low and memory and other brain functions
gradual shrinkage of healthy brain tissue. The grooves or are impaired. A number of drug treatments can be uti-
furrows in the brain, called sulci, are noticeably widened lized to help facilitate acetylcholine production in the
and there is shrinkage of the gyri, the well-developed brain and we will discuss these in more detail in the fol-
folds of the brain’s outer layer. In addition, the ventricles, lowing section on treatment and rehabilitation.
or chambers within the brain that contain cerebrospinal There also appears to be a significant inherited com-
fluid, are noticeably enlarged. ponent to Alzheimer’s disease, with an estimate of up
506 PSYCHOPATHOLOGY
' , %
to 50 per cent of the first-degree relatives of sufferers
also developing the disorder (Korten, Jorm, Henderson,
Broe et al., 1993). In addition, twin studies suggest that
the heritability of the disease is high — between 58 and
79 per cent (Gatz, Reynolds, Fratiglioni, Johansson et dl.,
2006). Several genes have been identified that are associ-
ated with a high risk of developing Alzheimer’s disease
and these include APOE4 and GAB2 (Bookheimer &
Burggren, 2009; Bertram & Tanzi, 2008), and currently,
genetic testing to identify these genes is often used to
enable diagnosis. Some of these genes may increase sus-
ceptibility to Alzheimer’s disease while others may have
a more direct cause in generating proteins that cause the
beta amyloid plaques that result in damage to brain tissue
(e.g. causing overproduction of the beta amyloid plaques
that leads to loss of healthy neurones). In addition, some
genes may play a role in early-onset Alzheimer’s disease,
while others appear to be linked to late onset (Bertram
& Tanzi, 2004). All this suggests that, while there is no
doubt about the importance of an inherited component
to Alzheimer’s disease, it may have multiple causes and
Plaques a number of genetic mechanisms may contribute to the
Tangles factors that cause degenerative brain damage.
FIGURE 15.2 Beta amyloid plaques and neurofibrillary
tangles in the cerebral cortex in Alzheimer’s disease. Plaques Frontotemporal neurocognitive disorder Fron-
appear to be caused by abnormal protein synthesis in the totemporal NCD is associated with a loss of neurones
brain and they clump together killing healthy neurones. from the frontal and temporal regions of the brain that
Tangles consist of abnormal collections of twisted nerve cell leads to progressive development of behavioural and
threads causing errors in impulses between nerves. Certain personality changes and language impairment. Unlike
genes such as APOE-4 have also been identified that promote Alzheimer’s disease, frontotemporal NCD does not usu-
the formation of abnormal amyloid plaques (Bookheimer & ally affect memory processes but has its main impact on
Burggren, 2009). emotional processes such as apathy and the ability to
Source: Blennow, K., de Leon, MJ. & Zetterberg, H. (2006). empathize with others. It is also characterized by a lack
Alzheimer's disease. Lancet, 368, 387-403. Reproduced by permis-
of insight into social conventions (e.g. someone might
sion of Elsevier.
not realize that a particular behaviour was embarrassing
THE PROS AND CONS OF GENETIC TESTING FOR

DEGENERATIVE BRAIN DISORDERS
Some people might wish to use genetic testing to * allow people who are at a high risk of developing
assess their risk of developing dementia later in life. dementia to benefit from new treatments that
Genetic testing is not a straightforward issue and indi- may become available in the future; and
viduals need to think very carefully before deciding to e help people to plan for the future.
take such a test. The experience could be very difficult
15.3
POINT
FOCUS emotionally, may not provide conclusive results either However, genetic testing might create problems for
way, and may cause practical difficulties. the following reasons:
Possible advantages of genetic testing include that
it might: * a genetic defect cannot be repaired and effec-
tive treatment to slow the disease is not yet gen-
* help genetic researchers understand the disease erally available. A genetic test might therefore
better and so lead to improved treatment; raise anxiety without offering a clear course of
* encourage someone to adopta healthier lifestyle; action;
° there is a risk of reading too much into the test old age. However, there is a moratorium (delay
results. Testing positive for one or two gene vari- or suspension of an activity or law) on the use of
ants does not mean a person will definitely develop genetic information by UK insurance companies
Alzheimer’s and testing negative does not guarantee until 2017, and this means that companies cannot
that they will be free from Alzheimer’s; and use this information at the moment.
* people testing positive for any genetic test could
face discrimination affecting their ability to buy Source: Adapted from Alzheimer’s Society: Genetics of dementia
property, get insurance or plan financially for their —http://www.alzheimers.org.uk/factsheet/405
—— oe —
to themselves or to others) and an inability to regulate (Le Ber, 2013), but with a high probability of a number
emotions. Regular neurocognitive symptoms include of different genes and genetic pathways being involved
lack of planning and organization, distractability and (Cruts, Gijselinck, van der Zee, Engelborghs et al., 2006).
poor judgement, which may lead to a lack of self-care, This fact also suggests that the neurological degen-
changes in social style, hoarding and changes in eating eration in frontotemporal NCD probably results from
behaviour (DSM-5 Summary Table 15.9). many different gene-controlled molecular processes
Frontotemporal neurocognitive disorder is a that contribute to the death of healthy brain neurones
common cause of early onset dementia in individuals in the frontal and temporal regions (Seelaar, Rohrer,
under 65 years of age but Pijnenburg, Fox & van Swieten, 2011).
itotemporal neurocognitive accounts for only 5 per cent
pdeteh-sociared withialossot
ones from the frontal and tempo-
of all cases of dementia NCD due to Parkinson's disease and NCD with Lewy
é ; : f risk ; , $
the brain that leads to
egions of in autopsy studies (DSM-5, bodies Parkinson’s disease is a progressive neurologi-
gressive development of behavioural p.616). The disorder has a__ cal condition affecting movements, such as walking, talk-
personality changes and language strong genetic component ing and writing, and it causes psychological disturbance in
airment.
of around 50-60 per cent between 40 and 60 per cent of sufferers. The main symp-
toms of Parkinson’s disease are (1) tremor, including
DSM-5 SUMMARY TABLE 15.9 Criteria for frontotemporal jerky movements of the [paitaontedsessempemsene
neurocognitive disorder arms, hands and head that neurological condition affecting move-
are also present during rest- ments such as walking, talking and writing,
e The criteria are met for major or mild neurocognitive ing periods, (2) slowness and causing psychological disturbance in
disorder of Groner Re dykin- between 40 and 60 per cent of sufferers.
e The onset is slow, with gradual progression of the esia) — people with Parkinson’s may find that they have
impairment
difficulty initiating movements or find that performing
e Either abehavioural or alanguage variant is present: movements takes longer, and (3) stiffness or rigidity of
e Behavioural: muscles, including problems in standing up from a chair
or rolling over in bed. The disease is named after Dr James
e Atleast three of the following:
Parkinson (1755-1824), the London doctor who first
° Lack ofinhibition identified Parkinson’s as a specific condition. Parkinson’s
° Sluggishness or lethargy disease occurs as a result of damage in the basal ganglia —
particularly the region of the basal ganglia known as the
¢ Compulsive/ritualistic behaviour
substantia nigra. Cells in this area are responsible for pro-
e Inserting inappropriate things into the mouth ducing the neurotransmit- : r rie
: ; substantia nigra A regionof the basa
i
pict ee ter dopamine, which allows rod
¢ Obvious decline in social cognition messages to be sent to the
e L :
parts of the brain that coordinate movement. With the
a eee depletion of dopamine-producing cells, these parts of the
* Obvious decline in language ability brain are unable to function normally. It is estimated that
e Limited learning and memory functions and perceptual over 4 million people worldwide suffer from Parkinson's
motor function disease, including 127,000 in the UK (Parkinson’s Disease
e The disturbance is not better explained by cerebrovas- Society, 2013). Symptoms first appear when the individual
cular disease, another neurodegenerative disease or is over 50 years of age, with men being marginally more
disorder, or by the effects of a substance likely to develop the disorder than women.
508 PSYCHOPATHOLOGY
Those sufferers who develop psychological problems ‘Neurocognitive disorder with Lewy bodies’. A diagnosis
experience memory difficulties and exhibit deficits in of NCD due to Parkinson’s disease is given if Parkinson's
learning, judgement and concentration, as well as becom- disease clearly precedes the onset of the neurocognitive
ing socially withdrawn and apathetic. It is estimated that disorder (DSM-5 Summary Table 15.10), and a diagnosis
up to 75 per cent of individuals with Parkinson’s disease of NCD with Lewy bodies is given if there is no con-
may eventually develop dementia and these symptoms vincing evidence of Parkinson’s disease in the aetiol-
can occur as early as 1-2 years after onset of the disease ogy (DSM-5 Summary Table 15.11). The prevalence of
(Williams-Gray, Foltynie, Lewis & Barker, 2006; Ehrt &
Aarsland, 2005). As well as signs of cognitive impairment, DSM-5 SUMMARY TABLE 15.10 Criteria for neurocognitive
Parkinson’s sufferers also regularly exhibit symptoms of disorder due to Parkinson's disease
psychosis and depression. Hallucinations occur in between
16 and 40 per cent of sufferers and this has often been con- disorder
sidered as a medication-induced phenomenon. That is, the
¢ The disturbance occurs during diagnosed Parkinson's
drugs used to facilitate substantia nigra dopamine produc-
disease
tion in sufferers are also known to produce psychosis-like
¢ The onset is slow, with gradual progression of the
symptoms. However, there is reason to believe that psy-
impairment
chosis symptoms such as hallucinations may also be intrin-
sic to the disease and result from progressive dementia or ¢ The disturbance is not better explained by another medi-
cal condition or mental disorder
impairments in primary visual processing (Williams-Gray,
Foltynie, Lewis & Barker, 2006). Studies also suggest that e Major or mild neurocognitive disorder probably due to
depression is a significant feature of Parkinson’s disease in Parkinson's disease should be diagnosed if both of the
following are met. Major or mild neurocognitive disorder
between 25 and 40 per cent of sufferers (Leentjens, 2004)
possibly due to Parkinson's disease should be diagnosed if
and this is often considered to be an understandable reac- one of the following is met:
tion to having to cope with a chronic and debilitating
¢ No evidence of other neurodegenerative or cerebro-
disease. However, as in the case of Alzheimer’s disease,
vascular disease
depression is also a significant predictor of subsequent
e The Parkinson's disease diagnosis pre-dates the neu-
Parkinson’s diagnosis, with the incidence of depression
rological disorder
increasing significantly in the 3 years prior to diagnosis
of Parkinson’s (Leentjens, van den Akker, Metsemakers,
Lousberg & Verhey, 2003). The fact that depression appears DSM-5 SUMMARY TABLE 15.11 Criteria for neurocognitive
disorder with Lewy bodies
to be a biological risk factor for a number of degenerative
dementias has given rise to the view that depression may e The criteria are met for major or mild neurocognitive
be accompanied by an allostatic state (a biological state disorder
of stress) that can acceler- e The onset is slow, with gradual progression of the
allostatic state A biological state of stress.
ate disease processes and impairment
cause atrophy of nerve cells in the brain, in turn leading to ¢ Probable major or mild neurocognitive disorder with Lewy
dementia (McEwen, 2003). bodies is diagnosed if the patient has two of the core
Post-mortem studies of individuals with Parkinson’s features or at least one suggestive feature with other
disease suggest an association between dementia and features. Possible major or mild neurocognitive disorder
Lewy body deposition. Lewy bodies are abnormal pro- with Lewy bodies is diagnosed if the patient has one of
tein deposits that disrupt the brain’s normal functioning. the core features or at least one suggestive feature
These Lewy body pro- ° Core features:
Lewy bodies Abnormal protein deposits
that disrupt the brain’s normal functioning. teins are found in an area ¢ Varying cognition with obvious changeability in
of the brain stem where attention and alertness
they deplete the neurotransmitter dopamine, causing ¢ Reoccurring, detailed hallucinations
Parkinson’s symptoms. These abnormal proteins can
¢ Features of Parkinsonism prior to the development
also diffuse throughout other areas of the brain, includ- of cognitive decline
ing the cerebral cortex, causing disruption of perception,
° Suggestive features:
thinking and behaviour. Around 80 per cent of indi-
viduals with Parkinson’s disease will develop dementia e Rapid eye movement sleep behaviour disorder
with Lewy bodies, but others without Parkinson’s dis- e Adverse reactions to neuroleptics
ease can develop neurocognitive disorders purely as a ¢ The disturbance is not better explained by cerebrovas-
result of the development of Lewy bodies. This has led cular disease, another neurodegenerative disease or
DSM-5 to introduce a new diagnostic category known as disorder, or by the effects of asubstance
CHAPTER 15 NEUROCOGNITIVE DISORDERS
Parkinson's disease in the US begins at around 0.5 per DSM-5 SUMMARY TABLE 15.12 Criteria for neurocognitive
cent between 65 and 69 years of age and rises to 3 per disorder due to Huntington's disease
cent by 85 years of age. Estimates of NCD with Lewy
bodies range between 1.7 and 30.5 per cent (DSM-5,
disorder
p.619) and this form of neurocognitive disorder may
e The onset is slow, with gradual progression of the
account for up to 30 per cent of all dementias:
impairment
NCD due to Huntington's disease ~Huntington’s dis- e The disturbance occurs during diagnosed Huntington's
ease is an inherited, degenerative disorder of the central disease, or the risk of Huntington's disease based on fam-
ily history or genetic testing
nervous system caused by a dominant gene. This means
that everyone who inherits e The disturbance is not better explained by another medi-
\tington's disease An inherited, cal condition or mental disorder
enerative disorder of the central nerv- the gene from one of his/
system, caused by a dominant gene. her parents will develop
the disease with 50 per cent
likelihood (see Focus Point 1.4 for a fuller explanation of
the genetics of Huntington’s disease). Symptoms of the brain responsible for posture, muscle tone and motor
disorder do not normally occur until after the age of 35 coordination. Pre-symptom testing is possible by means
years and can have an even later onset (however, the ear- of a blood test which counts the number of mutant
lier the onset, the more severe the disease tends to be). It repetitions on the relevant gene. A negative blood test
is principally a movement disorder, with the first observ- means that the individual does not carry the gene, will
able behavioural symptoms manifesting themselves as never develop symptoms and cannot pass it on to chil-
clumsiness and an involuntary, spasmodic jerking of the dren. A positive blood test means that the individual
limbs. However, many early signs of the disease tend does carry the gene, will develop the disease and has a
to be radical changes in temperament. The individual 50 per cent chance of passing it on to children, assuming
may become rude, exhibit unpredictable mood changes he or she lives long enough to do so. Because a posi-
and switch dramatically from depression to euphoria. tive blood test will have such a dramatic psychological
Cognitive functioning is affected as the disease develops impact, potential sufferers are given intensive coun-
and this is manifested as impairments in memory, atten- selling and psychological support before undergoing
tion and decision making, leading to full dementia. In pre-symptom testing. A diagnosis of neurocognitive
addition, as the disease progresses, the sufferer may also disorder due to Huntington’s disease is given if the indi-
begin to exhibit psychotic symptoms, including halluci- vidual meets the criteria for major or mild neurocogni-
nations and delusions. The general psychological syn- tive disorder and there is good evidence based on family
drome associated with Huntington’s disease includes history or genetic testing that Huntington’s disease is
affective symptoms, cognitive deficits, personality disor- a relevant aetiology (DSM-5 Summary Table 15.12).
ganization, bloody-mindedness, early loss of common The worldwide prevalence of Huntington’s disease is
sense, hallucinations, delusional ideation, odd behav- estimated to be around 2.7 per 100,000 (DSM-5, p.639),
iours and obsessions (Wagle, Wagle, Markova & Berrios, and neurocognitive deficits are an inevitable outcome of
2000). Psychopathological symptoms associated with the disease.
the disease include depression, mania, schizophrenia,
paranoia, anxiety and obsessive compulsive behaviours Summary of types of neurocognitive disorder In
(Barquero-Jimenez & Gomez-Tortosa, 2001). About 8 in this section we have discussed a number of different
every 100,000 people in the UK have Huntington’s dis- types of neurocognitive disorder and their DSM-5 diag-
ease — approximately 4800 people. Because the disease nostic categories. The main aetiology categories we
is a genetically inherited one, its prevalence will vary covered were infection (e.g. HIV infection), traumatic
according to the geographical distribution of those with brain injury, vascular causes (e.g. strokes) and degenera-
the defective gene. The highest prevalence of this disor- tive disorders (e.g. Alzheimer’s disease and Parkinson’s
der in the world is near Lake Maracaibo in Venezuela disease). All of these can cause cognitive impairment to
where it affects around 700 per 100,000 of the population. differing degrees, and the nature of the impairment will
The genetic abnormality in Huntington’s disease is depend on the areas of the brain affected by each factor.
found on the fourth chromosome. This results in the pro- Neurocognitive deficits may be relatively specific and
duction of a protein, mutant result from damage to tissue in areas of the brain deal-
ant Huntingtin (mHtt) A protein
Huntingtin (mHtt), that ing with specific functions such as language, memory or
h causes cell death in the basal
lia and contributes to Huntington's causes cell death in the basal visuomotor coordination (see Table 15.1). Such specific
se. ganglia — an area of the disabilities are found most often with traumatic brain
510 PSYCHOPATHOLOGY
injury, cerebrovascular accidents and brain tumours. feature common to almost all of these types of neuro-
Other types of disorder are progressive and can develop cognitive disorder is that the cognitive, behavioural and
from being diagnosed as mild neurocognitive disorders emotional deficits that ensue are almost entirely the result
to major cognitive disorders. A common feature of most of damage to brain tissue caused through trauma, dis-
types of neurocognitive disorder is that they are often ease or biochemical abnormalities in the brain. In some
associated with other forms of psychopathology, includ- cases, the means by which brain tissue is damaged may
ing anxiety, depression and psychosis. Depression is very be common across a number of different types of dis-
closely associated with some of the degenerative disor- order. For example, there is gathering evidence that the
ders, such as Alzheimer’s and Parkinson’s diseases, and deposition of Lewy bodies in the brain may be one part
is not only a frequent consequence of these disorders of the mechanism causing dementia in both Alzheimer’s
but also a pre-symptom predictor of the disorder. One and Parkinson’s disease.
SELF-TEST QUESTIONS
* Can you define the terms amnesia, aphasia, agnosia and apraxia?
* What is the difference between Broca’s aphasia and Wernicke’s aphasia?
° What specific skills are impaired when neurological disorders cause deficits in executive functioning?
* Can you name some of the difficulties involved in diagnosing specific neurological disorders?
e What kinds of individual abilities are assessed using the Wechsler Adult Intelligence Scale or the Adult Memory and
Information Processing Battery (AMIPB)?
® Can you describe the DSM-5 diagnostic criteria for both delirium and major/mild NCDs?
* Can you name two or more types of cerebral infection that may cause cognitive deficits?
e What are the main causes of traumatic brain injury?
° What are some of the emotional and psychological consequences of suffering a stroke?
* Can you name the main degenerative disorders?
° What is frontotemporal neurocognitive disorder and how does it differ from other neurocognitive disorders?
* Can you describe the main characteristics of Alzheimer’s disease?
* What are the main risk factors for Alzheimer’s disease and what changes in the brain are thought to occur during the
disorder?
* What areas of the brain are affected by Parkinson's disease? And what are the cognitive and emotional symptoms associ-
ated with the disorder?
° What are Lewy bodies and how are they involved in neurocognitive deficits?
SECTION SUMMARY
15.1 THE DIAGNOSIS AND ASSESSMENT OF NEUROCOGNITIVE DISORDERS
15.1.1 Cognitive Impairments in Neurocognitive Disorders

° The main cognitive impairments in neurological disorders are deficits in learning and memory, attention and arousal, lan-
guage and communication, visual-perceptual functioning, motor skills and executive functioning.
e Language deficits are known as aphasias. They include Broca’s aphasia and Wernicke’s aphasia.
¢ Agnosia is a disorder of the ability to recognize and name everyday objects.
CHAPTER 15 NEUROCOGNITIVE DISORDERS
¢ Apraxia is an impairment in motor performance and coordination.

° Deficits in executive functioning reflect the inability to problem-solve, plan, initiate, organize, monitor and inhibit
complex behaviours.
Assessment in clinical neuropsychology is based on a range of cognitive tests and can be supplemented by blood tests,
chemical analyses of cerebrospinal fluids, and-brain scans such as PET and fMRI.
15.1.2 The Diagnosis of Neurocognitive Disorders

° Delirium is a disturbance of consciousness that develops over a short period of time.
° Major or mild neurocognitive disorders are the two overarching categories into which DSM-5 conceptualizes neurocognitive
disorders. ;
* Neurocognitive disorders caused by infections include neurocognitive disorder due to HIV infection and neurocognitive
disorder due to prion disease.
® Traumatic brain injury is one of the most common causes of neurological impairment.
¢ Damage to brain tissue can occur as a result of a cardiovascular accident (CVA) — otherwise known as a stroke — and these are
remarkably common in individuals over the age of 65 years.
e Degenerative disorders represent those dementias that are characterized by a slow, general deterioration in cognitive,
physical and emotional functioning, and these affect around 7 per cent of individuals over 65 years ofage.
e Alzheimer’s disease is the most common cause of dementia in the UK (contributing 55 per cent), followed by vascular NCD
(contributing 20 per cent).
e The changes that occur in the brain during Alzheimer's disease appear to be structural and involve the development of
beta amyloid plaques and neurofibrillary tangles. \t is also associated with the faulty production ofthe brain neurotransmit-
ter acetylcholine.
® Frontotemporal neurocognitive disorder is associated with a loss of neurones from the frontal and temporal regions of the
brain causing behavioural, personality and language impairments.
@ Parkinson's disease causes psychological and cognitive disturbance in between 40 and 60 per cent ofsufferers and appears
to be caused as a result of degenerative damage to the region of the basal ganglia known as the substantia nigra.
® Lewy bodies are abnormal protein deposits that disrupt the brain’s normal functioning and can occur in around 80 per cent
of individuals with Parkinson’s disease.
® Neurocognitive disorder with Lewy bodies is diagnosed when Lewy bodies are present in the brain without convincing evi-
dence for a diagnosis of Parkinson’s disease.
1 5.2 TREATMENT disease, recent developments in drug treatments have

indicated that progressive impairment can be slowed,
A N D R E H A B iL iTAT ’O N affording some respite from the degenerative nature of
F O R N E U ROCOG N TIV E the disease. However, in many cases, neurological dam-
age is relatively permanent and the sufferer must learn to
DISORDER S live with the behavioural and cognitive deficits that the
disorder brings (e.g. traumatic brain injury, strokes). This
has led to the development of a range of rehabilitation
Many of the neurocognitive disorders described in this procedures designed to provide the individual with
chapter represent irreversible changes in impairment
and central nervous system damage. As a consequence, 1. exercises that help to improve impaired cognitive
functions (e.g. impaired language or memory
attempts at treatment tend to be oriented towards reha-
bilitation rather than cure. Nevertheless, impairment in function);
some types of neurocognitive disorder can be reversible, 2. training in the use of cognitive and behavioural
and deficits caused by some kinds of cerebral infection aids (e.g. using memory aids or labelling
(erg: meningitis and encephalitis). In cupboards and drawers in order to remember
are one example
the case of degenerative disorders such as Alzheimer’s where things are);

512 PSYCHOPATHOLOGY
3. assistive technology (e.g. equipment that may aid (Seltzer, 2006). Although the emphasis has been on
hearing, speaking or moving about); and identifying early signs of Alzheimer’s so that drug treat-
4. basic drug treatment and psychotherapy to ment can begin as soon as possible, there is also some
help deal with related mood disorders (such as evidence that cholinesterase inhibitors such as done-
depression). pezil can improve cognition in individuals with severe
Alzheimer’s (Winblad, Kilander, Eriksson, Minthon et al.,
Finally, in some severe cases of neurological disorder, 2006). Accumulating evidence suggests that donepezil
very little in the way of ameliorative therapeutic help can also help to alleviate behavioural symptoms, mood
can be provided for the sufferer, but support can be pro- disturbances and delusions associated with Alzheimer’s
vided for caregivers and many national associations pro- (Cummings, McRae & Zhang, 2006). However, recent
vide structured support and advice for such caregivers systematic reviews of cholinesterase inhibitors found no
(e.g. the UK Alzheimer’s Society, www.alzheimers.org. evidence that they could prevent dementia (Cooper, Li,
uk). We will now discuss the various forms of treatment Lyketsos & Livingston, 2013). The UK National Institute
and rehabilitation in more detail. for Health and Care Excellence (NICE) has recom-
mended to the NHS that donepezil, rivastigmine and
galantamine be made available as part of the manage-
ment of mild and moderate Alzheimer’s disease, and
those to be targeted should score 10 points or higher
Biological treatments for neurocognitive disorders take on the Mini Mental State Examination (MMSE) (NICE,
a number of forms. The most common are drug treat- 2011) (see Focus Point 15.2). While some cholinesterase
ments that help to stabilize or slow degenerative disor- inhibitors might be effective in slowing cognitive decline
ders; others include drug treatments to combat cerebral in a number of neurocognitive disorder diagnoses, there
infections and electrical brain stimulation for some is as yet no reliable evidence for the efficacy of any drug
forms of dementia. treatments for frontotemporal neurocognitive disorder
(Schwarz, Froelich & Burns, 2012).
Drug treatments Parkinson’s disease is associated with degeneration in
There has been some success in recent years in develop- the substantia nigra area of the brain, where the impor-
ing drugs that can help to slow the progress of degenera- tant neurotransmitter dopamine is produced. The main
tive disorders such as Alzheimer’s disease and Parkinson’s drug that is used to counteract this decline in dopamine is
disease. In the case of Alzheimer’s, we have already noted levodopa, a natural amino levodopa A natural amino acid that is 4
that the disease is often associated with abnormalities in acid that the brain converts converted by the brain into dopamine
the production of the brain neurotransmitter acetylcho- into dopamine to replace and is used in thetreatment of Sreinsol
line. During the course of the disease, an enzyme called the depleted neurotrans- disease. |
acetylcholinesterase breaks down acetylcholine and leads mitter. Although the drug
to depletion of the neurotransmitter dopamine. In order has been relatively successful in helping suffers to control
to combat this effect, drugs have been developed that tremor and other motor symptoms, there is little evidence
prevent acetylcholine breakdown in the synaptic cleft by that levodopa alleviates any of the cognitive impairments
acetylcholinesterase and increase its uptake in the post- associated with Parkinson’s disease (Morrison, Borod,
synaptic receptor. The most common of these drugs are Brin, Halbig et al., 2004). Levadopa administration has
donepezil, rivastigmine and galantamine, collectively to be closely supervised because it also has a number of
known as cholinesterase inhibitors (Petersen, Thomas, potential side effects including hypertension and delu-
Grundman & Thal, 2005). sions, and hallucinations similar to those found in schizo-
cholinesterase inhibitors A group of Randomized, double-blind, phrenia and amphetamine psychosis.
drugs that prevent acetylcholine break-
placebo-controlled _ trials Medication can also be successful in reducing dis-
down in the synaptic cleft by acetylcho-
linesterase and increase its uptake in the suggest that treatment for ability following cerebrovascular accidents (strokes).
postsynaptic receptor. The most common 6 months with cholinest- Thrombolytic therapy is
of these drugs are donepezil, rivastigmine erase inhibitors produces the use of drugs to break thrombolytic therapy The use of drugs
and galantamine to break up or dissolve blood clots - one q
moderate improvements up or dissolve blood clots — the main causes of strokes.
in cognitive function in one of the main causes of
those with mild to moderate Alzheimer’s disease strokes. The most commonly used thrombolytic drug is
(Hitzeman, 2006). They may also help to slow mem- tissue plasminogen activator (t-PA) and if this is admin-
ory decline (Birks, 2006) and prospects are best when istered within the first 3 hours of a stroke then disability
treatment begins early in the course of the disease is significantly reduced (Albers, 1997; Hacke, Donnan,
Fieschi, Kaste et al., 2004). Nevertheless, the success of Deep brain stimulation (DBS)
this treatment is critically dependent on the individual A recently developed form of treatment for Parkinson’s
being able to identify the early signs of a stroke and disease involves deep brain stimulation (DBS). This uses
seek rapid treatment. Although early administration a surgically implanted, battery-operated device called a
of thrombolytic therapy can significantly aid survival neurostimulator to deliver
and physical recovery, there is little evidence that such electrical stimulation to deep brain stimulation (DBS) A form of
treatment for Parkinson's disease which
an intervention helps to alleviate the cognitive deficits the ventral intermediate uses a surgically implanted, battery-
that may accompany stroke (Nys, van Zandvoort, Algra, nucleus of the thalamus operated device called a neurostimulator
Kappelle & de Haan, 2006). or the subthalamic nucleus to deliver electrical stimulation to the
Medication is also used in the treatment of brain area in the basal ganglia. ventral intermediate nucleus ofthe thala-
mus or the subthalamic nucleus area in the
deficits caused by cerebral infections. Bacterial infec- These areas of the brain basal ganglia. i
tions, such as certain types of encephalitis and bacterial control movement and,
meningitis, are treatable through mechanisms that are as yet unclear, electri-
‘terial meningitis The inflammation with antibiotics. However, cal stimulation in this area appears to block the abnor-
ection) of the meninges, which are the many viral infections are mal nerve signals that cause tremor and Parkinson’s
mbranes that cover the brain and spine.
much more problematic. symptoms (Perlmutter & Mink, 2006; Ananthaswamy,
Steroids can be used to 2004). DBS has been shown to result in improvements
combat viral infections such as herpes encephalitis, and, in physical abilities (e.g. mobility) and global measures
in the case of HIV-1 associated dementia, newly devel- of quality of life (Hamani, Neimat & Lozano, 2006) but
oped antiretroviral drugs there is little evidence at present that DBS has any sig-
iretroviral drugs Chemicals that
ibit the replication of retroviruses, such
are proving to be effective nificant effect on cognitive abilities (Laxton, Lipsman &
IV. in reducing the severity of Lozano, 2013), and it may even be associated with a mild
HIV dementia and reduc- decline in communication skills and language abilities
ing the prevalence of diagnoses of neurocognitive dis- (Castelli, Perozzo, Zibetti, Crivelli et al., 2006; Drapier,
order (Nath & Sacktor, 2006; Crum-Cianflone, Moore, Raoul, Drapier, Leray et al., 2005).
Letendre, Roediger et al., 2013). Usually, up to three to
four antiretroviral drugs are used that act at different
stages of the virus life-cycle. This produces a dramatic 15.2.2 Cognitive Rehabilitation
reduction in viral load (the level of virus in the blood)
and prevents further immune damage. The nature and structure of cognitive rehabilitation pro-
Finally, mood disorders (such as depression) are a grammes will inevitably depend on the nature of the cog-
common feature of neurological disorders, including nitive deficits that the individual has suffered and there is
stroke, traumatic brain injury and degenerative disor- a range of relatively successful procedures available that
ders, and depression can often adversely affect the course afford some significant gains across various functions
of the disorder, prevent recovery and increase mortality (Cicerone, Dahlberg, Malec, Langenbahn et al., 2005).
rates (Robinson, Lipsey, Rao & Price, 1986; Leentjens, Many of these programmes are basic training proce-
2004; Ramasubbu & Patten, 2003). The use of drugs dures which give the client structured extensive training
such as SSRIs and tricyclic antidepressants to help alle- in the area of their deficit (e.g. attention, memory, execu-
viate depressed mood has proven to be successful in tive functioning and so on). This may be in the form of
improving recovery from strokes (Hackett, Anderson extended practice at a task (e.g. attention process train-
& House, 2005), alleviating symptoms of depression in ing), perhaps with the additional use of concurrent feed-
Parkinson’s disease and Alzheimer’s disease (Weintraub, back on performance so that the client can adjust their
Morales, Moberg, Bilker et al., 2005; Modegro, 2010) functioning, or with the use of assistive technology (e.g.
and improving mood and cognitive performance follow- memory aids). In particular, the use of computer-based
ing traumatic head injury (Horsfield, Rosse, Tomasino, technology to assist rehabilitation training is a thriving
Schwartz et al., 2002). In at least some of these disorders area of development and clinicians may use computers to
(e.g. Parkinson’s disease) there is a view that depression is present specific training programmes, such as memory
an integral symptom of the disorder — especially because training programmes (Tam & Man, 2004; Cha & Kim,
depression often precedes and predicts other symptoms 2013), or to create virtual environments in which the
of the disease as well as affecting outcome. So, tackling client can learn to coordinate the relevant sequence of
depression can be considered a direct treatment of the actions to successfully complete a task (Zhang, Beatriz,
disorder itself rather than dealing with a side effect of Abreu, Seale et al., 2003). While many rehabilitation pro-
disability (e.g. Leentjens, 2004). grammes target quite specific impairments, some others
514 PSYCHOPATHOLOGY
attempt to address multiple aspects of dysfunction and attend to a new word following identification of a pr&
are known as holistic rehabilitation methods. These ceding target word. APT has been shown to be superior
may address a combina- to basic therapeutic support in promoting attention and
holistic rehabilitation Treatment tion of cognitive, emo- memory functioning (Sohlberg, McLaughlin, Pavese,
methods for neurological disorders which
: tional, motivational and Heidrich & Posner, 2000), and has also been shown to
attempt to address multiple aspects of
dysfunction. interpersonal impairments provide gains in other everyday skills such as independ-
in the context of an inte- ent living and driving ability (Sohlberg & Mateer, 2001).
grated programme of treatment (e.g. see Braverman, An alternative approach to dealing with attention deficits
Spector, Warden, Wilson et al., 1999; Prigatano, 2013). is not to try to improve attention itself, but to provide the
This section continues by providing some examples client with some compen-
of cognitive rehabilitation procedures that have been satory skills that will allow time pressure management (TPM) An /
shown to be effective in the rehabilitation of specific them to effectively man- approach to dealing with attention defici
which aims not to try to improve attenti
impairments. We will then look at an example of the age their slowed informa-
itself, but to provide clients with some _
holistic rehabilitation method. tion processing (Fasotti, compensatory skills that will allow them
Kovacs, Eling & Brouwer, effectively manage their slowed informa-
Attention deficits 2000). This is known as tion processing. 4
One form of rehabilitation training for attention deficits time pressure manage-
is known as attention process training (APT) and this ment (TPM) and is an alternative to ‘concentration’
uses a number of differ- training of the kind taught by the APT procedure.
attention process training (APT) A form ent strategies to promote
of rehabilitation training for attention and encourage attentional Visuospatial deficits
deficits that uses a number of different
strategies to promote and encourage
abilities (Park, Proulx & A number of programmes have been developed for the
attentional abilities. Towers, 1999). Exercises rehabilitation of unilateral visual neglect and to com-
include listening to an pensate for partial deficits in visual perception caused by
auditory tape that contains target words that must be neurological disorders. One such example is the com-
responded to by pressing a buzzer. Learning to shift puter-assisted training programme designed to aid visual
attention appropriately is also encouraged by learning to scanning (Webster, McFarland, Rapport, Morrill et al.,

THE VIRTUAL REALITY KITCHEN :
This virtual reality computer programme provides a safe

and controlled environment for patients with brain injury
to learn to improve basic daily skills such as preparing a
meal of a can of soup and a sandwich. All necessary objects
are found on the computer screen and can be accessed by
using the computer mouse. Prompts appear on the screen
initiating actions, sequencing actions and providing rein-
forcing feedback for correct actions. For example, one of the
first steps for preparing a can of soup is to remove the can
from the cupboard. If this does not occur within a pre-deter-
mined time, the cupboard door is highlighted by a pulsat-
ing colour. If the action is still not initiated, a verbal cue tells
the patient to ‘open the cupboard’ Each action performed
by the patient is recorded and their performance can be
Source: Zhang, L., Beatriz, M.D., Abreu, C., Seale, G.S. et al. (2003)
quantitatively assessed over time. Training in virtual envi-
A virtual reality environment for evaluation of a daily living skill
ronments such as this results in improved performance on in brain injury rehabilitation: Reliability and validity. Archives of
the tasks over time and performance on the virtual task cor- Physical Medicine & Rehabilitation, 84, 1118-1124. Reproduced
relates well with performance on the tasks in a real kitchen. with permission of Elsevier.
CHAPTER 15 NEUROCOGNITIVE DISORDERS 515.
2001). This consists of a series of tasks in which the patient imitation. Sufferers are particularly impaired when asked
is asked (1) to read out coloured numbers projected on to demonstrate how to use an object or carry out actions.
to a wall (scanning the full frontal environment), (2) to They appear to be unable to plan a sequence of actions or
manually track a red ball projected onto a wall (helping they may exhibit inappropriate gestures (e.g. they may try
coordination of scanning and physical movement), (3) to pour water from a bottle into a glass without removing
to react to moving images as they are projected in front the lid, or to stir the bottle opener in the glass). This is
of them (facilitating detection of stimuli in space), and assumed to be an impairment of gesture learning which
(4) to move the projected image of a wheelchair down a is generally considered to be the consequence of a motor
simulated three-lane road while avoiding obstacles. This memory disorder (Heilman, Schwartz & Geshwind,
procedure has been shown to reduce unilateral visual 1975). One form of rehabilitation training for limb apraxia
neglect symptoms and to improve performance on a is gestural training in
real-life wheelchair obstacle course. which the client is taught gestural training A form of rehabilitation
training for limb apraxia in which the client
to recognize gestures and is taught to recognize gestures and pos-
Apraxia and deficits in coordinated postures that are appro- tures that are appropriate and in context.
self-help behaviours priate and in context. For
Apraxia involves an inability to undertake learnt and pur- example, the patient may be required to demonstrate the
poseful activities, such as dressing and cooking, and means use of a common object (such as a guitar) or be shown a
that sufferers must rely increasingly on caregivers to help picture of the gesture (e.g. someone playing a guitar) and
with these activities. For example, limb apraxia is a com- to replicate that action, or to be shown simply a picture
mon symptom of left-hemisphere damage and consists of the object and asked to mimic how it is used. Patients
of a deficit in performing gestures to verbal command or may also be shown pictures of people appropriately or

GESTURAL TRAINING
One form of rehabilitation training for limb apraxia is

gestural training, in which the client is taught to recog-
nize gestures and postures that are appropriate and in
context. This example shows three gestures used in the
gesture-recognition test, and the patient must identify
which is an appropriate use of the object. (A) is an appro-
priate gesture. (B) is a semantically related but inappro-
priate gesture, and (C) is a semantically unrelated and
inappropriate gesture.
Source: Smania, N., Girardi, F., Domenicali, C., Lora, E. & Aglioti, S.
(2000). The rehabilitation of limb apraxia: A study in left-brain-
damaged patients. Archives of Physical Medicine & Rehabilitation,
81(4), 379-388. Reproduced with permission of Elsevier.
516 PSYCHOPATHOLOGY
inappropriately using objects and asked to identify which Another specific form of treatment that has been
of these are correct. Gestural training has been shown to shown to provide significant gains in the production and
significantly reduce errors in performing everyday actions comprehension of speech is known as group communi-
and to improve recognition of gestures (Smania, Girardi, cation treatment. This focuses on increasing initiation of
Domenicali, Lora & Aglioti, 2000). conversation and exchang- group communication treatment A f
In contrast, computer-based virtual reality environ- ing information using what- of treatment used in the production an
ments have been developed to enable disabled individu- ever communication means comprehension of speech, focusing
on
als with brain injury to learn to improve basic daily living possible, being aware of increasing initiation of conversation an
skills in a safe and controlled environment. For example, personal goals in commu- exchanging information possible.
using whateve
wer Bs communication means
Zhang, Beatriz, Abreu, Seale et al. (2003) developed a vir- nication, and gaining confi-
tual kitchen in which the patient can learn the sequence dence in the ability to communicate in personally relevant
of behaviours required to make a bowl of soup or pre- situations. Elman & Bernstein-Ellis (1999) demonstrated
pare a sandwich (see Treatment in Practice Box 15.1). that those patients who received group communication
Zhang et al. (2003) found that training in virtual environ- treatment showed significantly more improvement in func-
ments such as this resulted in improved performance on tional communication compared with patients not receiv-
both tasks — and performance on the virtual task corre- ing structured treatment.
lated well with performance at the tasks in a real kitchen Finally, a number of specific techniques exist to help
—and learning in virtual environments may be equally as individuals with aphasia and traumatic brain injury to
effective as other cognitive retraining procedures (Jacoby, improve their ability to name objects, to improve writ-
Averbuch, Sacher, Katz et al., 2013). ing skills and improve sentence production, and these
may range from the use of cueing techniques to help the
Language and communication deficits patient name specific objects to semantic feature analy-
Impairments in language and communication may mani- sis (SEA) designed to improve lexical retrieval by increas-
festina variety of ways, including deficits in the production ing the level of activation within a semantic network
of speech (e.g. fluent aphasia), an inability to comprehend (Coelho, McHugh & Boyle, 2000).
or understand speech and an inability to initiate speech
(e.g. non-fluent aphasia) (see also section 15.1.1 and Table Memory deficits
15.1). Many patients undergo standard forms of speech Procedures for dealing with memory impairments
therapy to help promote the production and comprehen- mainly revolve around what are known as compensa-
sion of speech, and many of these approaches may com- tory strategies — that is, providing patients with specific
bine speech therapy with procedures that permit massed strategies for remembering material on a daily basis.
practice of production and comprehension skills, such as Compensatory strategies of this kind tend to be more
the combination of therapist-delivered speech-language efficient than simple remedial strategies and more easily
training and home-based computer-assisted massed prac- generalizable to daily activities (Nadar & McDowd, 2010).
tice (e.g. Wallesch & Johannsen-Horbach, 2004). There Compensatory strategies may involve assistive techniques
are also several specific techniques that are regularly such as using diaries to aid recall of daily events, labelling
used to treat specific disorders. One common exam- cupboards to remember where everyday items are stored
ple used with aphasic patients is known as constraint- or located, or using a pager to remind the individual of
induced movement therapy (CIMT). This involves the important daily events. Wilson, Emslie, Quirk & Evans
mass practice of verbal responses in which the patient (1999) report the case study of a young man called George
may be required to com- who had severe memory impairments after a head injury
constraint-induced movement therapy municate without gestur- sustained in a road traffic accident. Treatment in Practice
(CIMT) A technique used with aphasic ing or pointing to describe Box 15.3 shows how the pager could be used to remind
patients which involves the mass practice various objects of varying George about a range of tasks and activities during the
of verbal responses in which the patient
may be required to communicate without
complexity (Mark & Taub, day. Using a pager as a memory prompt has been shown
gesturing or pointing to describe various 2004; Bogey, Geis, Bryant, to be effective, easy to use and significantly reduce the
objects of varying complexity. Moroz & O'Neill, 2004). number of memory and planning problems experienced
This constrains patients to by people with traumatic brain injury (Wilson, Emslie,
the systematic practice of speech acts while avoiding Quirk, Evans & Watson, 2005). Pagers are also helpful
the use of behavioural aids. This form of treatment has in establishing daily behavioural patterns, and gains in
been shown to produce improvement on standard clini- memory and behaviour can be found even in the weeks
cal scales and self-rated and blind-observer scales of day- after a patient has ceased using the pager.
to-day communication (Pulvermuller, Neininger, Elbert Computer-based procedures can also be used in a
et al., 2001). variety of ways to aid impaired memory. Computers can
CHAPTER 15 NEUROCOGNITIVE DISORDERS Sik

USING A PAGER AS A MEMORY AID
Below are daily pager messages sent as prompts to George, an individual who had severe memory impairments
after a head injury sustained in a road traffic accident.
Time Message Time Message

Monday Tuesday
7.15a.m. Time to get up 7.00 a.m. Time to get up
7.25a.m. Up yet? Time to wash and shave 7.10a.m. Up yet? Time to wash and shave
7.40 a.m. Take tablets and fill in the time on the checklist 7.25a.m. Take tablets and fill in the time on the checklist
3.00 p.m. Fold washing and put it away 8.30a.m. Remember keys, wallet and diary
5.00 p.m. Prepare the evening meal 5.00 p.m. Prepare the evening meal
6.20 p.m. Swimming tonight?
8.30 p.m. Read through today’s notes
8.30 p.m. Read through today’s notes
9.00 p.m. Take tablets and fill in the time on the checklist
9.00 p.m. Take tablets and fill in the time on the checklist
Source: Wilson, B.A., Emslie, H., Quirk, K. & Evans, J. (1999). George:
Learning to live independently with Neuropage. Rehabilitation
Psychology, 44, 284-296. American Psychological Association.
Adapted with permission.
function as simple memory aids to enhance prospective useful for teaching new knowledge or training in specific
memory (e.g. by acting as an electronic diary), by pro- skills such as helping the patient to find and use the right
viding memory training exercises, or by instructing the word to name objects. There is still some debate over
patient in the use of memory strategies (Kapur, Glisky & whether memory aids (e.g. pagers, diaries and personal
Wilson, 2004). organizers) are superior to memory treatments (e.g.
Teaching remembering strategies is also benefi- attempts to train better memory functioning), but in
cial. One technique involves training the patient in the many cases a combination of both aids and ‘treatments’
use of visual imagery is most effective (e.g. see Ownsworth & McFarland,
al imagery mnemonics A technique
mnemonics in order to 1999; Middleton & Schwartz, 2012).
2aching remembering strategies in
r to help store and retrieve items and help store and _ retrieve
its to be remembered. items and events to be Deficits in executive functioning
remembered. Ten weeks As described earlier, executive functioning involves the
of training in visual imagery techniques has been shown integrated use of several cognitive processes by which
to result in significant improvement in memory func- people problem-solve, plan, initiate, organize and moni-
tioning 3 months after treatment (Kaschel, Della Sala; tor goal directed activities. Deficits in this collection
Cantagallo, Fahlbock et al., of integrated skills will obviously require some train-
rless learning A training procedure
2002). Errorless learning ing in a range of basic abilities, such as attention and
in training individuals with amnesia
e people are prevented — as far as is another technique that memory, and more specifically will require training in
ible — from making any errors while has proven to be helpful in problem-solving skills and planning and goal manage-
jing a new skill or new information. training individuals with ment skills. Many effective
amnesia. Errorless learn- interventions involve train- goal management training (GMT) A pro-
cedure that involves training in problem
ing is a training procedure where people are prevented — ing in problem solving and solving to help evaluate a current problem,
as far as possible — from making any errors while learning one particular procedure followed by specification of the relevant
a new skill or new information (Baddeley & Wilson, is known as goal manage- goals, and partitioning of the problem-
solving process into subgoals or steps.
1994) and in the context of memory impairments it is ment training (GMT). This
involves training to help evaluate a current problem skills. Such approaches are holistic in the sense that they
(What am I doing?’), followed by specification of the attempt to develop the individual’s awareness of their
relevant goals and partitioning of the problem-solving disabilities and to provide them with compensatory skills
process into subgoals or steps. Patients are then assisted that will enable them to negotiate daily living and regain
with the learning and retention of subgoals (‘Do I know occupational skills. To this extent, holistic methods dif-
the steps?’), followed by self-monitoring of the results of ferentiate between restorative procedures that attempt
their actions (Am I doing what I planned to do?’) (Levine, to provide training to improve cognitive impairments
Robertson, Clare, Carter et al., 2000). Goal manage- (e.g. intensive training of memory skills) and compensa-
ment training appears to have beneficial effects on sus- tory procedures that enable the patient to achieve daily
tained attention to tasks as well as transfer of training goals through different means (e.g. using assistive tech-
across problems (Levine, Schweizer, O’Connor, Turner nology such as a pager as a memory aid). Holistic rehabili-
et al., 2011). Other procedures for aiding problem solv- tation methods have been shown to promote significant
ing involve cognitive-behavioural training in problem- improvement in overall functioning in individuals with
solving skills, exercises for analysing real-life problems traumatic brain injury (Ben-Yishay & Daniels-Zide,
and role-playing of real examples of problem situations. 2000), develop awareness of disabilities and impairments
Such training results in significant beneficial effects on (which is important when attempting to engage patients
measures of executive cognitive functioning up to 6 in rehabilitation programmes) (Fleming & Ownsworth,
months after the intervention (e.g. see Rath, Simon, 2006), and to be superior to standard neurorehabilitation
Langenbahn, Sherr & Diller, 2003). programmes in improving community integration and
Many types of intervention for executive functioning raising the patient’s level of satisfaction with cognitive
deficits focus on both behavioural and emotional regu- functioning (Cicerone, Mott, Azulay & Friel, 2004).
lation, and aim at training the individual in self-regula-
tion when confronting a problem and managing their
way through the sequence of cognitive and behavioural 15.2.3 Caregiver Support
actions required to solve a problem. One such procedure
is known as self-instructional training (SIT) where
Programmes
the individual learns a set Many individuals with neurological disorders are not in
self-instructional training A procedure of instructions for. talk-
primary care but live with their families or with caregiv-
used in the intervention for executive so Gumtherice
ies hE nae
functioning deficits where individuals learn & : & ers such as their spouses or partners. This puts a con-
a set of instructions for talking themselves particular problems. Such siderable burden on caregivers generally and will usually
through particular problems. types of intervention have require them to cope with behavioural and cognitive
been shown to raise per- deficits, physical disability, challenging behaviour (such
sonal self-awareness of deficits and increase use of suc- as anger and aggression), and problematic behaviour
cessful problem-solving strategies. Importantly these generally (such as inappro-
methods have the additional beneficial effects of improv- priate social behaviour). To complete Activity 15.1 go to
ing emotional self-regulation and reducing outward In the case of degenera- | www.wiley-psychopathology.com/
expressions of anger and frustration (Medd & Tate, 2000; tive disorders that do not | activities/ch15
Ownsworth, McFarland & Young, 2000). usually begin to manifest

until later life, the carers of such individuals will often
Holistic rehabilitation methods be their elderly spouses or partners (e.g. in the case of
Most cognitive rehabilitation techniques have been Alzheimer’s disease). This being the case, the carers of
developed to address individual deficits in cognitive func- individuals with neurological disorders will need both
tioning (such as attentional, memory or language defi- support and training.
cits). However, there are substantial benefits to adopting Caregivers need to give both physical and emotional
a more comprehensive holistic approach to rehabilita- support to suffers, and they may also pay a substantial
tion that collectively addresses cognitive, emotional and economic cost in terms of loss of income as well as liv-
functional impairments, as well as physical disability. For ing a restricted social life. It goes without saying that
example, Malec & Basford (1996) advocated a compre- the overall burden on a caregiver will usually be propor-
hensive integrated treatment for individuals with trau- tional to the disabilities experienced by the sufferer, and
matic brain injury that addressed cognitive, interpersonal caregivers usually report that their physical and emo-
and emotional concerns, used group interventions that tional health suffers as a result of caregiving, with many
addressed disability awareness and social skills training, beginning to exhibit symptoms of depression. In a study
and included procedures to enhance vocational func- of caregiver-burden in Parkinson’s disease, perceived
tioning (occupational therapy) and independent living burden and quality of life was proportional to disability,
CHAPTER 15 NEUROCOGNITIVE DISORDERS +519
A WEEK INTHE LIFE OF A CLINICAL PSYCHOLOGIST

WORKING AS A CONSULTANT CLINICAL NEUROPSYCHOLOGIST
MONDAY WEDNESDAY
‘How do you spell neuropsychologist?’ asked the detec- Appropriate psychometric tests are chosen for the man who
tive sergeant on the telephone. He requests a statement has come for an outpatient assessment this morning. He has
relating to whether a client could be a reliable witness in experienced a history of memory problems for 2 years. Sadly,
a sexual assault case. | explained to him that since suffer- the man struggles with most tests but particularly those we
ing from encephalitis, her attention and memory abili- know are associated with dementia of the Alzheimer’s type.
ties are so poor that it was unlikely she could provide a A sense of sadness stays with me for the afternoon at the
reasonable account for the police. The call has taken my thought of what my feedback has meant to that couple. |
administration time and once again | begin a new week resolve to reduce my administration pile by the end of today.
behind schedule as | rush off to the first meeting of the
week. THURSDAY
The community disability team meeting focuses on
the most complex cases. A man who has motor neurone Seven ladies have arrived for my Thursday morning relatives’
disease has now found out his wife has developed multi- group, a meeting for people living with someone who has a
ple sclerosis. Concerns are expressed about a lady with a neurological diagnosis. The usual issues are discussed: how
brain stem stroke. There are concerns her female partner to cope with the feelings of loss, what to do in response to
is emotionally abusing her. All agree a vulnerable adults a partner’s temper outbursts and how to minimize cogni-
strategy meeting is required. The afternoon is spent tive difficulties. Thursday afternoons are usually set aside for
supervising colleagues and a new trainee. outpatient intervention appointments. Today a lady in her
forties talks about her sense of isolation since her stroke and
requests help to explain the nature of her difficulties to her
TUESDAY children. The last appointment of the day brings a feeling of
optimism as a young woman who suffered a severe head
The day is spent completing four initial consultations injury 2 years ago is pleased to inform me that she is finally
to decide whether psychological intervention can be living independently and has started a part-time job.
appropriately offered: a lady with Parkinson's disease
who has started having panic attacks; a man who suf- FRIDAY
fered a head injury in a car accident (his parents are
struggling to cope with his bad language and temper The morning is spent making an assessment as to the
outbursts); a lady with multiple sclerosis who is sad- capacity of a lady with Huntington’s disease to man-
dened by having to give up work; and, finally, a man of age her finances. Two further outpatient appointments
80 who suffered a stroke last summer and whose wife leave just an hour to write up client files and complete an
feels desperately isolated because he can no longer assessment report before meeting the final challenge of
drive. the week, Friday evening rush hour!
and the range of symptoms and the mental health prob- correlated with levels of depression in elderly caregiv-
lems exhibited by the individual with Parkinson’s disease ers or spouses of those with dementia (Mausbach,
(e.g. depression, hallucinations and confusion) (Schrag, Aschbacher, Patterson, Ancoli-Israel et al., 2006). To
Hovris, Morley, Quinn & Jahanshahi, 2006). Poor quality address these problems associated with caregiving, inter-
of life and depression in caregivers can often be traced ventions have been designed to provide caregivers with a
in part to a lack of skills or strategies for managing the range of skills that will help their day-to-day living with
sufferer, and many become avoidant copers by avoiding sufferers. These may include advice on how to modify
new situations and wishing the problems would simply the home environment to support the sufferer (Gitlin,
go away. Avoidant coping such as this is significantly Hauck, Dennis & Winter, 2005) or training in skills to
q520% PSYCHOPATHOLOGY
develop self-care behaviours by the sufferer or to control 2005). The effects of such support groups can be benefi-
ageression and wandering (Pinkston, Linsk & Young, cial even if communication is by telephone or by internet
1988). Such programmes have been shown to maintain videoconferencing (Marziali, Donahue & Crossin, 2005).
caregiver positive affect for a period of at least 12 months Finally, caregiver interventions may not only address
after the intervention and work best when tailored to the skills and knowledge that will help the caregiver
the needs of individual carers (Lopez-Hartmann, Wens, physically and emotionally manage a sufferer, but may
Verhoeven & Remmen, 2012). Peer support groups are also help the caregiver understand and respect the person
also an important means of maintaining quality of life with a neurological or degenerative disorder. Once some-
and positive affect in caregivers. National societies such one’s cognitive and physical abilities begin to decline —
as the UK Alzheimer’s Society (www.alzheimers.org.uk) especially in old age — it is quite easy to forget that they
provide information and advice for caregivers, including are still individuals who should be valued and respected.
advice on how to understand and respect persons with Such advice for caregivers includes (1) take time to listen
neurological disabilities or degenerative disorders, and to the sufferer, (2) take account of the abilities they do
also how to cope with caring for a sufferer. For example, possess and try to foster these, (3) use respectful forms
the Alzheimer’s Society recommends that caregivers of address, (4) try not to talk down to them and respect
their privacy, and (5) always try to understand how the
1. need to ensure they have sufficient support (either person feels and make them feel good about themselves
from family or local support groups); (Alzheimers Society, 2005) (see Table 15.2).
2. should make time each day for themselves;
3. need to understand their right to local services
(such as assessment of needs); TABLE 15.2 Tips for making a person with Alzheimer’s disease
4. should try to involve other family members in fee! good about themselves .
caregiving; e Avoid situations in which the person is bound to fail, as this
5. should look after their health (by eating regularly can be humiliating. Look for tasks they can still manage and
and healthily); activities they enjoy
6. should check whether they are entitled to any © Give them plenty of encouragement. Let them do things at
financial benefits; their own pace and in their own way
7. should confront and deal with feelings of guilt; © Do things with them, rather than for them, to help them
and retain their independence
8. ought to take a regular break or holiday by © Break activities down into small steps so that they feel a
seeking short-term respite care for the sufferer. sense of achievement, even if they can only manage part
of a task
In addition, local groups comprised of similar car- ° Our self-respect is often bound up with the way we look.
egivers can provide significant support across a range Encourage the person to take a pride in their appearance,
of needs, including (1) information and education, (2) and compliment them on how they look
referral and/or assistance on engaging with local health Source: http://www.alzheimers.org.uk/site/scripts/documents_info
services, and (3) emotional support (Salfi, Ploeg & Black, .php?documentID=84.
* What is the difference between a restorative treatment and compensatory skills training?
* How have drugs been used in the treatment of neurological disorders? Do such drugs help in the treatment of the cognitive
deficits caused by the disorder?
* Can you describe at least one specific intervention designed to treat each of the following: attention deficits, visuospatial
deficits, apraxia, language and communication deficits, memory deficits, and deficits in executive functioning?
* What are holistic rehabilitation methods and how do they differ from specific restorative interventions?
* What are the main problems encountered by those giving care to people suffering from neurological disorders and what
interventions have been developed to help them?
CHAPTER 15 NEUROCOGNITIVE DISORDERS 52a.
SECTION SUMMARY
15.2. TREATMENT AND REHABILITATION FOR NEUROCOGNITIVE DISORDERS
The neurocognitive disorders we have covered in this chapter often represent chronic impairments that are caused by irrevers-
ible damage to brain tissue or are the result of progressive degenerative disorders. Because of this, rehabilitation may often be
a lengthy process and sufferers are likely to require long-term care of some kind. We have noted that there have been attempts
to develop drugs that can slow the progress of degenerative disorders such as Alzheimer’s disease and Parkinson’s disease,
and antiretroviral drugs have similar effects in reducing the severity of HIV symptoms, but the evidence on whether these drug
developments have beneficial effects on cognitive deficits is still modest at best. Medication is also an important treatment for
depression, which is a common and important symptom of neurological disorders. Antidepressants not only help to improve
mood, but can also indirectly improve cognitive performance.
Cognitive rehabilitation programmes have been developed to help the individual with a range ofspecific cognitive deficits,
including attention deficits, visuospatial deficits, apraxia, language and communication deficits, memory deficits and execu-
tive function impairments. These may take a variety of forms, such as (1) massed training to improve cognitive impairments
(e.g. memory training), (2) compensatory skills training, which accepts that the individual has particular impairments and
helps them to achieve daily goals by other means, (3) computer-assisted training can provide the means for remedial cogni-
tive training in both the therapeutic and home environment, or provide virtual environments in which the sufferer can learn
skills in relative safety, and (4) assistive technology is being increasingly utilized as a means of helping the disabled individual
to cope with and negotiate daily living (e.g. using a pager to provide reminders for daily activities in individuals with memory
deficits).
Finally, because of the nature of neurocognitive disorders and the frequent need for long-term care, programmes of sup-
port and training are increasingly becoming available for caregivers. These include programmes to provide emotional support
for caregivers, programmes to provide appropriate management and coping skills for living with individuals with disabilities,
and local or national support groups that provide advice and information.
© Treatment of neurological disorders tends to be based on restorative treatment for individual cognitive deficits (e.g. mem-
ory training) or compensatory skills training based on helping the sufferer to deal with the daily living difficulties posed by
the deficit.
e Drug treatments include the use of cholinesterase inhibitors (Alzheimer’s disease), levodopa (Parkinson's disease), thrombo-
lytic therapy (cardiovascular accidents and strokes) and antiretroviral drugs (NCD due to HIV infection).
e Depression is also a common feature of many neurological disorders and can be treated with antidepressants and appro-
priate psychological therapy.
© Deep brain stimulation (DBS) alleviates symptoms of Parkinson's disease by delivering electrical stimulation to the thalamus
and basal ganglia.
© Cognitive rehabilitation programmes are usually directed at improving function within specific cognitive deficits
(e.g. memory, language).
® Rehabilitation programmes for attention deficits include attention process training (APT) and time pressure management
(TPM).
© Gestural training and the use of virtual reality environments can be utilized to treat apraxia and deficits in coordinated
self-help behaviours.
¢ Treatment of language and communication deficits will depend on the specific nature of the problem but common exam-
ples of rehabilitation procedures include constraint-induced movement therapy (CIMT) and group communication treatment.
e Memory deficits can be addressed with the use of assistive technology (such as pagers) or specific memory training proce-
dures such as visual imagery mnemonics or errorless learning procedures.
© Deficits in executive functioning often utilize interventions that involve problem-solving training such as goal management
training or self-instructional training (SIT).
© Holistic rehabilitation methods collectively attempt to address cognitive, emotional and functional impairments, as well as
physical disability.
© Because those suffering neurological disorders live with their families or caregivers, caregiver interventions have been
developed that help to provide the caregiver with training and support for the task.
ay bo PSYCHOPATHOLOGY
result in immediate impairment (such as traumatic brain

15.3 NEUROCOGNITIVE injury or stroke), many others are progressive degenera-
DISORDERS REVIEWED tive disorders that develop from mild symptoms of cog-
nitive impairment to full-blown dementia and physical
disability (e.g. Alzheimer’s disease). While most degen-
Unlike many of the other disorders described in this erative disorders afflict older adults, some can affect
text, neurocognitive disorders have their origins almost younger individuals (e.g. neurocognitive disorder due to
solely in damage or abnormalities in the biological HIV infection or prion disease). Many of the neurocog-
substrates that underlie thinking and behaviour. These nitive disorders are closely associated with other forms
disorders give rise to a range of disabilities and impair- of psychopathology, especially depression and psychosis.
ments, both physical and cognitive, and many are irre- Depression appears to be both a predictor and a conse-
versible and permanent deficits. The main causes of quence of some neurocognitive disorders (such as stroke
neurocognitive disorders are cerebral infections, trau- or Parkinson’s disease) and is considered by some to be
matic brain injuries, cerebrovascular accidents such as an integral feature of those disorders.
strokes, and degenerative disorders such as Alzheimer’s Because most neurocognitive disorders are caused by
disease and Parkinson’s disease. Clinical psycholo- irreversible damage to brain tissue, treatment and reha-
gists have a major interest in neurocognitive disorders bilitation often take the form of compensatory skills
because many of the major symptoms are deficits in training, which accepts that the individual has a particular
critical cognitive functions such as learning and mem- impairment and helps them to achieve their daily goals
ory, attention, language and communication, visual per- by alternative means (e.g. by using compensatory strate-
ception, motor skills and executive functions. Because gies, such as memory aids, or assistive technology, such
of this, clinicians are involved in the assessment of neu- as equipment to aid hearing, speaking or moving about).
rocognitive disorders and the treatment and rehabilita- Nevertheless, there are many specific cognitive rehabilita-
tion of these disorders. tion procedures that can be used with reasonable success
Assessment of neurocognitive disorders is often dif- in attempts to restore basic cognitive functions such as
ficult and involves a combination of tests of cognitive memory, attention, language and motor skills. However,
functioning (such as the WAIS-IV or the Adult Memory because of the long-term nature of many neurocogni-
and Information Processing Battery), blood tests and tive disorders, there is a basic need for long-term care
analyses of cerebrospinal fluids (to determine the pres- for sufferers and this is often provided by close family,
ence of inherited degenerative diseases or infections), spouses and partners. This need has given rise to a range
genetic testing (to determine whether the individual of programmes to provide support to caregivers, includ-
possesses genes likely to put them at risk for neurocog- ing basic caregiver skills training (e.g. how to structure
nitive or degenerative brain disorders), and brain scans the environment for a disabled individual) and emotional
using EEG, PET or fMRI. While some of the disorders support programmes.
oReaC To access the online resources for this chapter go to

eamesF
meses www.wiley-psychopathology.com/ch15
Reading Activity
Glossary of key terms ° Alzheimer’s disease Activity 15.1

Clinical issues ° Creutzfeldt—Jakob disease Self-test questions
Links to journal articles | oe Parkinson’s disease Revision flashcards
References Research questions
16 Childhood and Adolescent
Psychological Problems
"a To access the online resources for this chapter go to


This chapter begins by discussing some of the difficulties
involved in identifying and diagnosing childhood and 16.1 THE DIAGNOSIS AND PREVALENCE OF CHILDHOOD
adolescent psychological problems. We then go on to AND ADOLESCENT PSYCHOLOGICAL PROBLEMS: SOME
discuss the characteristics, prevalence rates and aetiology GENERAL ISSUES 526
of disruptive behaviour problems (discussing ADHD and
conduct disorder in detail) and childhood and adolescent 16.2 DISRUPTIVE BEHAVIOUR PROBLEMS 530
anxiety and depression. Finally, the chapter ends by dis- :
cussing the main treatment methods used with children 16.3. CHILDHOOD AND ADOLESCENT ANXIETY AND
and adolescents and how coordinated provision of treat- : DEPRESSION 543
ment extends across a range of services, including educa-
tion, health and social services. 16.4 THE TREATMENT OF CHILDHOOD AND ADOLESCENT
PSYCHOLOGICAL PROBLEMS 552
16.5 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL

PROBLEMS REVIEWED 558
LEARNING OUTCOMES
1. Describe and evaluate some of the difficulties 4. Compare and contrast theories of the aetiology
involved in diagnosing and treating childhood and of disruptive behaviour disorders, childhood
adolescent psychological problems. anxiety and childhood depression.
2. Describe the characteristics of at least two 5. Describe the characteristics of some of the main
disruptive behaviour disorders. therapeutic methods used to treat childhood and
3. Describe the characteristics of childhood and adolescent psychological problems and evaluate
adolescent anxiety and depression. their efficacy.
My own troubles began when | was 3 years old and my father died abruptly of a brain tumor. A few years later my mother was
diagnosed with breast cancer and she died when | was 11 years old. Watching so many important people die was frightening and
confusing. Even so, the most traumatic event of my childhood was my placement into foster care. Although my aunts and uncles
hinted at the possibility, | never believed they would give me away. | threatened to jump off a high building if they went ahead
with the plan. | knew they were conspiring to banish me and | didn’t trust a single one of them. But they did it anyway. I'd had
enough of the cycle of attachment and desertion and decided | wasn't going to become attached to my new foster parents. To the
outside world | was withdrawn and detached. Yet towards myself |was overwhelmed by intense feelings of rage and hatred. My
foster mother repeatedly spoke of her disappointment in me and angrily talked about sending me away. | knew from my brother
that foster children often go from place to place and that being physically or sexually abused was common. During the following
2 years | continued to float through time and space in a state of numb, disorganized misery, going through the emotions but not
really alive. |was aware of my impairment — and ashamed of it. | believed | was peculiar. When | was about 16, | became absorbed
with the idea that my central problem was a bodily defect, and | focused on one aspect of my anatomy after another, determined
to find the specific flaw. At 17 | developed the sensation of a lump in my throat and became convinced | was about to choke to
death. | had no labels for any of my experiences, so | didn’t realize that this latest state was a form of anxiety. Every night | stayed
awake to the point of exhaustion.
Frank’s Story
Introduction problems after the age of 5 years. Similarly, shyness and

withdrawal from social contact is often normal during
The study of childhood and adolescent psychopathology periods of social development as the child attempts to
is fraught with a range of difficulties that are not expe- understand the rules of social interaction and learns
rienced in the study of adult psychopathology. First, how to communicate verbally with others. However,
any behavioural or psychological problems have to in early adolescence these tendencies may represent
be assessed in the context of the child as a developing the first signs of psychopathology. In addition, children
organism. For example, bed-wetting is quite normal in may often go through brief stages of development when
infancy, but might be a sign of anxiety or adjustment they exhibit behavioural problems or fears and anxieties,
CHAPTER 16 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS 525,
but these problems often disappear as rapidly as they and how this distress may be manifested in behaviour.
appeared. Most parents have experienced a child who This personal account describes the negative emotional
refuses to eat, or very suddenly becomes frightened impact of the death of his mother and father, his feel-
of noises, strangers, or certain types of animals, only ings of abandonment and impotency and how this
for this to disappear within a matter of days or weeks. affected his ability to form relationships. This in turn
Second, because of their immaturity, children will tend gave rise to feelings of guilt, shame and inadequacy, and
to have poor self-knowledge. They may feel that some- in adolescence finally manifested as specific psychologi-
thing is wrong, but be unable to label it as anxiety or cal problems such as body dysmorphic disorder and
depression, or convey clearly how they feel to others. somatic symptom disorder. He related this story as an
In such circumstances, the clinician has to infer psycho- adult and as such was able to look back on his child-
logical states from overt behaviour and decide whether hood and put his behaviour and emotions into a per-
that behaviour is unusual for the developmental stages spective that enabled him to understand them. But as a
through which the child is passing. With these issues in child, events often seem confusing and uncontrollable,
mind, clinicians have tended to organize childhood psy- and a clinician has to interpret what a child might be
chological problems into two broad domains based on feeling and experiencing from their behaviour alone —
the general behavioural characteristics of the child. The for example, much of Frank’s behaviour might be seen
first domain covers externalizing disorders, which are as internalizing and suggestive of anxiety and depres-
based on outward-directed behaviour problems such as sion. Nevertheless, even during an upbringing that is
aggressiveness, hyperac- relatively trauma-free, children will frequently experi-
rnalizing disorders Disorders based tivity, non-compliance or ence childhood as a threatening and frightening time.
utward-directed behaviour problems
impulsiveness. The second They will develop anxieties as they experience new peo-
| as aggressiveness, hyperactivity, non-
pliance or impulsiveness. domain covers internal- ple and new situations (Crijnen, Achenbach & Velhulst,
izing disorders, which 1999), will worry about many of their everyday activi-
rnalizing disorders Disorders are represented by more ties such as attending school (Vasey, 1993; Ollendick,
esented by more inward-looking inward-looking and with- King & Muris, 2002) and will develop behavioural prob-
withdrawn behaviours, and may drawn behaviours, and lems such as temper tantrums, eating irregularities,
esent the experience of depression, — may represent the experi- nightmares and phobias. As the child moves into ado-
ety and active attempts to
socially
draw. | “op ir peor
ence of depression, anxi- lescence even more challenges await as the individual
ety and active attempts to develops sexually, changes physically, encounters edu-
socially withdraw. The former are now more commonly cational and occupational challenges and moves into a
known as disruptive behaviour disorders and include new period where feelings of responsibility are expected
DSM-5 diagnosable disorders such as conduct disorder of them. It is perhaps not surprising at this stage that
and attention deficit hyperactivity disorder (ADHD). The many adolescents encounter feelings of confusion,
internalizing disorders are still difficult to diagnose reli- anxiety and depression while attempting to cope with
ably but DSM-5 does include guidelines for diagnosing these changes (Lerner, 2002) and it is also not surpris-
childhood separation anxiety, generalized anxiety disorder ing, therefore, that the initial symptoms of many of the
and major depressive disorder. The childhood and adoles- disorders we have covered in Chapters 6-15 relating to
cent disorders discussed in this chapter are covered in a adult mental health first begin to develop during ado-
number of different chapters in DSM-5, including the lescence (e.g. schizophrenia, paraphilic disorders and
chapters on Disruptive, Impulse-Control, and Conduct somatic symptom disorders).
Disorders (oppositional defiant disorder, conduct dis- In the following section of this chapter we will look
order), Neurodevelopmental Disorders (attention defi- briefly at the difficulties involved in addressing psycho-
cit hyperactivity disorder, ADHD), Anxiety Disorders logical problems of childhood and adolescence, and
(childhood separation anxiety, childhood generalized then look at the prevalence rates of specific disorders.
anxiety disorder), Depressive Disorder (childhood major The remainder of the chapter will look in detail at the
depression), and Obsessive Compulsive and Related diagnosis, aetiology and treatment of the following:
Disorders (childhood OCD). (1) attention deficit and disruptive behaviour disorders,
Frank’s story at the beginning of this chapter illus- and.(2) childhood anxiety and depression. Discussion of
trates the kinds of experiences that might give rise to some other childhood psychological problems can be
psychological distress in childhood and adolescence found on the book’s website.
(526 PSYCHOPATHOLOGY ;
Sleaigl : Wy
disrespect and aggression are rarely tolerated by
16.1 THE DIAGNOSIS AND parents and teachers, and are controlled at an
PREVALENCE OF CHILDHOOD early stage in the child’s life.
4. Finally, during childhood and early adolescence,
AND ADOLESCENT developmental changes occur rapidly, which
means that psychological problems can escalate
PSYCHOLOGICAL PROBLEMS: quickly and dramatically. For example, behaviour
SOME GENERAL ISSUES problems can be generated very rapidly if the
development of language skills, self-control skills,
social skills and emotional regulation does not
16.1.1 Difficulties Associated proceed normally. This requires that childhood
problems need to be identified early and quickly
With Identification and Diagnosis in order to minimize the psychological damage
of Childhood and Adolescent that prolonged abnormal development could
inflict.
Psychological Problems
We have already alluded to some of the difficulties
involved in identifying whether a child needs help and
treatment for a mental health problem and it is worth 16.1.2 Childhood Psychopathology
considering some of these difficulties before we discuss as the Precursor of Adult
individual diagnoses.
Psychopathology
1. When considering what might be clinically
In Chapters 6-15, it was frequently described how impor-
relevant behaviour in children, we first have to
tant childhood experiences appear to be in the aetiology
consider what is normal for a particular age. For
of many diagnosable psychological disorders found in
example, bed-wetting is considered relatively
adulthood, so childhood trauma and abuse, for example,
normal in children up to the age of 5 years, but
not only affect childhood behaviour but may serve as the
may be a symptom of psychological distress if it
basis for the development of long-term psychological
occurs after that age.
maladjustment, including major depression, personality
2. Diagnosing a psychological problem is often disorders such as borderline and antisocial personality dis-
dependent on the individual being able to orders, somatic symptom disorders, dissociative disorders,
communicate with the practitioner and to eating disorders, and sexual and gender disorders. Indeed,
articulate how they experience the distress that prospective studies have indicated that preschool behav-
their problems are causing them. However, many iour problems predict psychopathology in later life (Caspi,
children are unable to communicate clearly how Newman, Moffit & Silva, 1996). Table 16.1 lists some of
they feel (e.g. they may not be able to differentiate the childhood risk factors that have been identified in the
feelings of anxiety from feelings of depression). aetiology of adult psychopathology and these are all dis-
They may also lack self-knowledge and be unable cussed more fully in the relevant chapters of this book.
to understand precisely what they are feeling. Childhood risk factors such as these enable researchers
In extreme cases, some disorders are explicitly and clinicians to identify those groups of children and ado-
associated with an inability to communicate lescents that are most likely to be at risk for adult mental
with others (e.g. autistic syndrome disorders), so health problems. With this in mind, an emerging area of
identification of psychological problems has to research is developmental
take place almost solely on the basis of external psychopathology, which developmental psychopathology An
observation of the child’s behaviour and their rate area of research concerned with a
is concerned with mapping how early childhood experiences may
of development. how early childhood expe- act as risk factors for later diagnosable
3. Differences in cultural norms will also affect riences may act as risk fac- psychological disorders. Italso attempt
whether childhood behaviours are seen as tors for later diagnosable to describe the pathways by which early
experiences may generate adult psycho-.
problematic or not. Externalizing behaviour psychological disorders and logical problems. p :
problems are most prominent in many Western attempts to describe the
societies but some oriental cultures have pathways by which early
relatively low levels of this type of problem experiences may generate To read Drabick & Kendall's article on
(Weisz, Suwanlert, Chaiyasit & Walter, 1987). adult psychological prob- developmental psychopathology go to
www.wiley-psychopathology.com/ _
For example, in those countries that practice lems (Drabick & Kendall, reading/ch16
Buddhism, externalizing behaviours such as 2010).
CHAPTER 16 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS 527.
TABLE 16.1 Childhood risk factors for adult mental health problems
Childhood experience
(risk factor) Adult mental health problem Reference CHAPTER
Abnormal parent-child Social anxiety disorder Moore, Whaley & Sigman (2004) 6
pitemiction style Narcissistic and obsessive compul- Johnson, Cohen, Kasen, Smailes & Brook (2002) 12
sive personality disorder
Antisocial personality disorder Gabbard (1990) 12

Borderline personality disorder Graybar & Boutilier (2002) 12
Histrionic personality disorder Bender, Farber & Geller (2001) 12
Childhood abuse Depression (reduced Raes, Hermans, Williams & Eelen (2005) 7
(physical and sexual) autobiographical specificity)
Suicide and suicidal ideation Gould & Kramer (2001) 1
Eating disorders Steiger, Leonard, Kin et al. (2000); Brown, Russell, 10
Thornton & Dunn (1997)
Hypoactive sexual desire disorder Stuart & Greer (1984) 11
Sexual aversion disorder Berman, Berman, Werbin, Flaherty et al. (1999) 11
Vaginismus DSM-IV-TR 11
Sexual dysfunction generally Najman, Dunne, Purdie, Boyle & Coxeter (2005) 11
Dyspareunia Binik, Bergerson & Khalife (2000) 11
Paedophilic disorder Freund & Kuban (1994) 11
Paraphilias generally Mason (1997); Murphy (1997) 11
Gender dysphoria Bradley
& Zucker (1997) 11
Personality disorders generally Johnson, Cohen, Brown, Smailes & Bernstein (1999) 12
Borderline personality disorder Hefferman & Cloitre (2000) 12
Antisocial personality disorder Horowitz, Widom, McLaughlin & White (2001) 12
Narcissistic personality disorder Kernberg (1985) 12
Avoidant personality disorder Rettew, Zanarini, Yen, Grilo et al. (2003) 12
Conversion disorder Bowman & Markland (1996) is
Illness anxiety disorder Salmon & Calderbank (1996) 13
Somatic symptom disorder Tezzi, Duckworth & Adams (2001) 13
Dissociative disorders generally Tyler, Cauce & Whitbeck (2004) 14
Dissociative identity disorder (DID) Putnam (1997) 14
Depersonalization disorder Simeon, Guralnik, Schmeidler, Sirof& 14
Knutelska (2001)
Childhood neglect Post-traumatic stress disorder (PTSD) — King, King, Foy & Gudanowski (1996) 6
(e.g. separation, Major depression Lara & Klein (1999); Goodman (2002) 7
inadequate and
ineffectual Cannabis, nicotine and alcohol Cadoret, Yates, Troughton, Woodworth & g
parenting) abuse Stewart (1995)
Hypersexuality Langstrom & Hanson (2006) 11
Paraphilias generally Mason (1997); Murphy (1997) 11
Antisocial personality disorder Hill (2003) 12
Borderline personality disorder Guttman (2002) 12
Dependent personality disorder Bornstein (1996) 12
Body dysmorphic disorder Cororve & Gleaves (2001) 6

(Continued)
528 PSYCHOPATHOLOGY
%
TABLE 16.1 (Continued)
Childhood experience
(risk factor) Adult mental health problem Reference CHAPTER
Childhood trauma Schizophrenia Read, van Os, Morrison & Ross (2005) 8
generally Alcohol dependency Sher (1991); Wilsnack, Vogeltanz, Klassen & 9

Harris (1997)
Nicotine dependency Anda, Croft, Felitti, Nordenberg et al. (1999) 9
Conversion disorder Bowman & Markland (1996) 33
Dissociative identity disorder (DID) Putnam (1997) 14
Childhood conflictand Specific phobias Freud 6
SUEUR Cannabis dependency Meltzer, Gatwood, Goodman & Ford (2003) 9
Childhood poverty Schizophrenia Byrne, Agerbo, Eaton & Mortensen (2004) 8

Alcohol, nicotine and cannabis abuse _ Alverson, Alverson & Drake (2000) 9
Substance dependency generally Petronis & Anthony (2003) 9
Antisocial personality disorder Paris (2001) 2
There are numerous possible ways in which child- may make them vulnerable to depression when experi-
hood psychopathology may link to adult mental health encing similar types of losses later in life (e.g. following
problems. Firstly, the simplest relationship is where a the death of a spouse or close friend). Fifthly, a childhood
childhood disorder merely persists into adulthood in disorder may be quite specific to childhood and disap-
the same form (e.g. where childhood anxiety or depres- pear or change form dramatically once the individual has
sion develops into experienced anxiety and depression in reached adulthood.
adulthood). One striking example of this was described All of these examples demonstrate that childhood
in Chapter 12, where we noted that childhood conduct psychopathology will have an important influence on
disorder and antisocial behaviour often persists into adult mental health, but the nature of this influence is
adulthood in the form of antisocial personality disorder not always direct and not always in the same form as
(Farrington, Loeber & van Kammen, 1990). Secondly, a the childhood difficulties. You may want to refer back
childhood psychopathology may have an adverse affect to Table 16.1 and consider what possible developmental
on subsequent development and indirectly lead to differ- processes might link certain childhood experiences with
ent forms of maladjustment in later life. For example, adult psychopathology.
children who fail to form adaptive relationships with
their parents early in life exhibit disruptive behaviour in
late infancy, and such disruptiveness can result in more
general adjustment problems and the development of
16.1.3 The Prevalence of
learning difficulties later in life. Thirdly, a childhood Childhood and Adolescent
psychopathology may simply represent the less cognitive
Psychological Disorders
precursor of a related adult disorder. For example, ado-
lescent height phobia has been shown to be a risk factor Studies of the prevalence of diagnosable childhood psycho-
for full-blown panic disorder in adulthood (Starcevic & logical disorders estimate that as many as 10-20 per cent of
Bogojevic, 1997) and this may result from the fact that children and adolescents have a diagnosable psychological
the catastrophizing of bodily sensations is a central fea- disorder (e.g. Phares, 2003;
ture of both disorders, and may extend across an increas- McDermott & Weiss, 1995) For a video on young people and
anxiety go to
ing number of cognitive and behavioural domains as the and boys exhibit higher www.wiley-psychopathology.com/
individual develops from childhood into adolescence prevalence rates than girls video/ch16
(Davey, Menzies & Gallardo, 1997). Fourthly, a childhood even though the opposite
disorder may not necessarily extend into adulthood but is the case in adulthood. Table 16.2 shows the prevalence
may render the individual vulnerable to later life stress- of psychopathologies found in children and adolescents
ors. For example, if a child loses a parent early in life, this aged between 5 and 16 years in the UK (Office for National
CHAPTER 16 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS 529°
TABLE 16.2 Prevalence of mental health problems in children and adolescents in Great Britain (2004)
aS
=N
(oe)
disorder
mental
with
children
of
Percentage
a
5-10 1116 All
Age
5- to 10-year-olds 11- to 16-year-olds All children
Boys Girls All Boys Girls All Boys Girls All
Percentage of children with each disorder

Emotional disorders 2.2 2.5 2.4 4.0 6.1 5.0 3.1 4.3 3.7
Anxiety disorders 2.1 2.4 DP 3.6 52 44 2.9 3.8 3.3
Separation anxiety 0.4 0.7 0.6 0.3 0.4 0.3 0.3 0.5 0.4
Specific phobia 0.8 0.7 0.7 0.8 0.9 0.9 0.8 0.8 0.8
Social phobia 0.1 0.1 0.1 0.5 0.6 0.5 0.3 0.3 0.3
Panic = = = 0.2 0.5 0.4 0.1 0.3 0.2
Agoraphobia - = - 0.2 0.4 0.3 0.1 0.2 0.1

Post traumatic stress 2 0.1 0.0 0.1 0.5 0.3 0.0 0.3 0.2
Obsessive compulsive 0.1 0.2 0.2 0.3 0.2 0.2 0.2 0.2 0.2
Generalized anxiety 0.2 0.3 0.3 0.9 1.6 (2 0.6 1.0 0.8
Other anxiety 0.6 0.7 0.7 0.9 ile EZ 0.8 ile 0.9
Depression 0.2 0.3 0.2 1.0 1.9 1.4 0.6 Te 0.9

Depressive episode (full ICD criteria) 0.1 0.2 0.2 0.8 1.4 1.1 0.5 0.8 0.6
Other depressive episode 0.0 0.1 0.1 0.3 0.5 0.4 0.2 0.3 0.2
Conduct disorders 6.9 2.8 4.9 8.1 5.1 6.6 7.5 3.9 5.8
Oppositional defiant disorder 4.5 2.4 35) 3.5 1.7 2.6 4.0 2.0 3.0
Unsocialized conduct disorder 0.9 0.3 0.6 ez 0.8 1.0 it 0.5 0.8
Socialized conduct disorder 0.6 > 0.3 2.6 1.9 Dp 1.6 0.9 13}
Other conduct disorder 0.9 0.1 0.5 0.7 0.8 0.8 0.8 0.4 0.6
Hyperkinetic disorder 2.7 0.4 1.6 2.4 0.4 1.4 2.6 0.4 1.5
Less common disorders 2.2 0.4 1.3 1.6 1.1 1.4 1.9 0.8 1.3
Autistic Spectrum Disorder 1:9 0.1 1.0 1.0 0.5 0.8 1.4 0.3 0.9
Tic disorders 0.0 0.1 0.1 - = : 0.0 0.1 0.0
Eating disorders 0.5 0.2 0.3 0.6 0.1 0.4 0.5 0.1 0.3
Mutism = 0.1 0.0 0.1 0.4 0.3 0.0 0.2 0.1
Any disorder 10.2 5.1 7.7 12.6 10.3 11.5 11.4 7.8 9.6
Base (weighted) 2010 1916 3926 2101 1950 4051 4111 3866 = 7977
Source: Office for National Statistics, licensed under the Open Government Licence v.1.0
530 PSYCHOPATHOLOGY
Statistics, 2005). These show that boys are more likely Comorbidity between childhood ‘disorders is al8o
to have a mental health problem than girls but that the common and around 2 per cent of children have more
prevalent disorders in boys are conduct disorders and in than one mental health diagnosis. In addition, childhood
girls emotional disorders. Around 7 per cent of 3-year- psychopathology is also associated with physical health
olds can be expected to show moderate to severe behav- problems and poor educational performance (Office for
ioural problems and a further 15 per cent to exhibit more National Statistics, 2005). So we can see from these facts
mild difficulties (Richman, Stevenson & Graham, 1982). that childhood psychiatric disorders can have implica-
However, some early developmental problems and spe- tions across a range of developmental domains. Studies
cific fears (such as delays in toilet training and ‘comfort’ of risk factors suggest that children of lone parents are
habits such as rocking) usually resolve by middle child- twice as likely to have a mental health problem as those
hood, but others (such as disruptiveness or conduct dis- living with married or cohabiting couples (16 per cent
orders) seem more persistent. The type of disorder that compared with 8 per cent) and other known risk fac-
a child will exhibit also changes with age and is probably tors for childhood psychiatric disorders include parental
related to the nature of the experiences that children will psychopathology, repeated early separation from par-
encounter at specific ages. For example, some problems ents, harsh or inadequate parenting, exposure to abuse
(such as chronic worrying) are rarely found in pre-school or neglect, and adverse peer group influences (Maughan,
children but increase significantly after school entry. 2000) (see also Table 16.1).
SELF-TEST QUESTIONS
® Can you describe four difficulties involved in the detection and diagnosis of childhood psychological disorders?
© What kinds of childhood events act as precursors or risk factors for adult mental health problems?
° How prevalent are childhood psychological disorders?
SECTION SUMMARY
16.1 THE DIAGNOSIS AND PREVALENCE OF CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL

PROBLEMS: SOME GENERAL ISSUES
° There are numerous difficulties associated with recognizing and diagnosing childhood psychological problems, including
communication difficulties and the child’s underdeveloped self-awareness.
¢ Childhood psychopathology is often a significant precursor to adult psychopathology.
¢ Between 10 and 20 per cent of children and adolescents have a diagnosable psychological disorder.
¢ Comorbidity between disorders is common.
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tantrums or to disrupt ongoing activities by failing to

16.2 DISRUPTIVE show restraint. However, by the time most children enter
BEHAVIOUR PROBLEMS school, they are expected to be able to restrain their
behaviour, attend to tasks when asked, and to attend to
and follow appropriate commands. Nevertheless, some
In this section we will cover those behavioural prob- individuals find this hard to do — even in late childhood
lems that are characterized by impulsive, disruptive and or adolescence. Their inability to restrain themselves and
poorly controlled behaviour. We all expect children of follow instructions leads to the disruption of cooperative
certain ages to have poor self-control, to throw temper and group activities (such as group learning in school)
CHAPTER 16 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS ork
and in extreme cases may represent overtly aggressive ADHD will exhibit excessive running or climbing when
behaviour to peers and adults, including criminal vio- inappropriate, or will talk excessively. Infants with the
lence and damage to property. We will discuss two par- disorder will appear to be constantly ‘on the go’, jump-
ticular disruptive behaviour problems that can be found ing and climbing on furniture, as well as having difficulty
in DSM-5, namely attention deficit hyperactivity disorder in participating in sedentary activities such as listening
(ADHD) and conduct disorder. In this section we will dis- to a story. Impulsivity
cuss these two syndromes individually, covering their manifests as impatience, a impulsivity The act of reacting to
a situation without considering the
diagnosis and aetiology. difficulty in appropriately consequences.
delaying responses (e.g.
attempting to run out of the house before their coat is
16.2.1. Attention Deficit on) and constantly interrupting others before they have
finished what they have to say; it may also reflect a desire
Hyperactivity Disorder (ADHD)
for immediate rewards over delayed rewards. Impulsivity
The main feature of attention deficit hyperactivity can also result in accidents (such as knocking things over)
disorder (ADHD) is a persistent pattern of inattention or indulging in dangerous activities (such as riding a bicy-
and/or hyperactivity-impulsivity that is at a significantly cle fast over rough terrain).
ntion deficit hyperactivity disorder higher rate than would be
HD) A persistent pattern of inattention expected for the child at The diagnosis of ADHD
for hyperactivity—impulsivity that is at that developmental stage. The main issue in diagnosing ADHD is to ensure that
nificantly higher rate than would be ADHD can manifest itself hyperactivity or inattention is significantly greater
scted for a child at his or her develop-
tal stage. behaviourally in many than normal for the child’s developmental stage and to
ways, including lack of ensure that it is a generalized and persistent predisposi-
. attention in academic, tion rather than one that is confined to a single context.
) For a video on children with ADHD go to occupational or social situ- DSM-5 Summary Table 16.1 describes the diagnostic
www.wiley-psychopathology.com/ | ations; making careless criteria for ADHD and this emphasizes that impairment
video/ch16
) mistakes in school work is present before 12 years of age and is found in two or
or other tasks; difficulty more contexts. Most individuals with ADHD present
maintaining attention until task completion; appearing with symptoms of both inattention and hyperactivity
to have their attention elsewhere and failing to take in but in some one or the other pattern may be dominant.
or respond to instructions; and a tendency to shift from This has given rise to two diagnostic subtypes, namely
one task to another without completing any of them. attention deficit hyperactivity disorder, predominantly inatten-
The child with ADHD will typically have a strong dis- tive presentation and attention deficit hyperactivity disorder,
like for tasks that require sustained self-application and predominantly hyperactive/impulsive presentation. If both
mental effort, and will be easily distracted by irrelevant inattentive and hyperactive/impulsive elements are pre-
stimuli or events. Hyperactivity may be manifest as sent this is known as a combined presentation. Each subtype
excessive fidgetiness and should be used if six (or more) of the dominant symp-
eractivity A higher than normal level
tivity . by not remaining seated toms are present with fewer than six of the less dominant
when asked. The child with symptoms present.
* ATTENTION DEFICIT HYPERACTIVITY DISORDER (ADHD)

Ke)
=
> Mark, age 14, has more energy than most boys his age. But then, he’s always been overly active. Starting at
ce age 3, he was a human tornado, dashing around and disrupting everything in his path. At home, he darted
O
= from one activity to the next, leaving a trail of toys behind him. At meals, he upset dishes and chattered relent-
es lessly. He was reckless and impulsive, running into the street with oncoming cars, no matter how many times his
= mother explained the danger or scolded him. In the playground, he seemed no wilder than the other kids. But his
Ud
V—) tendency to overreact - like hitting playmates simply for bumping in to him — had already got him into trouble
§ several times. His parents didn’t know what to do. Mark’s doting grandparents reassured them, ‘Boys will be boys.
U Don't worry, he'll grow out of it’ But he didn't.
Source: http://www.nimh.nih.gov/health/publications/attention-deficit-hyperactivity-disorder/index.shtm|
DSM-5 SUMMARY TABLE 16.1 Criteria for attention deficit the two disorders (e.g. see Quay, 1979). Opinion on this
hyperactivity disorder (ADHD) is currently undecided but what is clear is that when a
child is diagnosed with both ADHD and an oppositional
e An ongoing pattern of inattention and/or hyperactivity
and impulsivity that interferes with normal functioning
defiant disorder/conduct disorder, the individual will
or development, as marked by the following: usually exhibit the worst of both disorders (Biederman,
Newcorn & Sprich, 1991). In other cases, children with
e Inattention. At least six of the following for at least
ADHD can be distinguished from those with opposi-
6 months:
tional defiant disorder/ conduct disorder by the fact that
¢ Not paying close attention to details or making the latter are likely to (1) be more aggressive, (2) live in
careless mistakes
families with a lower socioeconomic status, and (3) have
e Difficultly in maintaining attention in activities parents who also exhibit antisocial behaviour (Faraone,
¢ Does not listen when spoken to directly Biederman, Jetton & Tsuang, 1997; Hinshaw, 1987). In
addition, recent studies have suggested that children
e Ignores instructions
with a single diagnosis of ADHD are likely to have a bet-
e Has difficulty organizing ter long-term prognosis than those with oppositional
e Dislikes or avoids tasks which require sustained defiant disorder/ conduct disorder and childhood ADHD
mental effort alone is not a differential predictor of antisocial per-
e Loses things needed for tasks
sonality disorder in adulthood (Lahey, Loeber, Burke &
Applegate, 2005). However, there is evidence that in
e Easily distractible some cases ADHD can lead to earlier onset of conduct
e Forgetful in daily activities disorder and around a quarter of those children with a
e Hyperactivity and Impulsivity. At least six of the combined presentation, ADHD diagnosis will be diag-
following for at least 6 months: nosed with conduct disorder (DSM-5, p.65). This may
be because some children with ADHD become involved
e High level offidgeting
in an escalation of symptoms caused by a vicious cycle
e Not sitting still or leaving seat when expected to sit where their disruptive behaviour causes aggressive reac-
e Runs or climbs in situations where it is tions in others and this in turn evokes aggressive and
inappropriate increasingly antisocial reactions in the sufferer (Hinshaw,
e Unable to engage in activities quietly Lahey & Hart, 1993). Anxiety and depressive disorders
are comorbid in a minority of children with ADHD and
e Excessive talking
this is at a slightly higher rate than in the general popula-
e Blurts out an answer before the question is finished tion (DSM-5, p.65; Furman, 2005).
e Has difficulty awaiting their turn In terms of its course, ADHD is usually first recog-
nized by parents when the child is a toddler but not all
e Interrupts or intrudes on others frequently
hyperactive toddlers go on to develop ADHD. The dis-
e Symptoms were present before the age of 12 order is usually first recognized and diagnosed after the
e Symptoms are present in at least two settings child first begins schooling and this is because learning
and adjustment at school is significantly affected by the
e Symptoms reduce the quality of educational, social or
occupational ability
disorder. As the child develops into adolescence, symp-
toms usually attenuate and become less pronounced,
e¢ Symptoms do not occur during schizophrenia or another although about half will continue to show symptoms
psychotic disorder and are not better explained by
well into adulthood and this can detrimentally affect
another mental disorder
intellectual functioning and IQ (Bridgett & Walker,
2006).
There is much discussion in the literature about
Around half of those diagnosed with the combined whether ADHD is a culturally constructed disorder —
presentation of ADHD will also be diagnosed with oppo- that is, whether the rates of diagnosis differ in differ-
sitional defiant disorder or conduct disorder (see section ent cultures because of differing cultural perceptions
16.2.2) and these rates of comorbidity are significantly of children’s behaviour. The evidence on this is equivo-
higher than comorbidity with other psychopathologies cal. Some studies suggest very similar rates of diagnosis
(Hinshaw, 1987). This indicates that in many cases across different cultures and ethnic groups (Rohde,
ADHD is associated with the violation of social norms Szobot, Polanczyk, Schmitz et al., 2005; Bailey & Owens,
and the basic rights of others, and raises the question 2005), whereas others indicate differing rates of ADHD
of whether there might be an underlying link between in different countries (Dwivedi & Banhatti, 2005). Studies
CHAPTER 16 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS
indicating different rates of diagnosis may do so because injury. However, in general, children with ADHD have
different cultural environments may directly affect a great difficulty making friends and integrating success-
child’s behaviour (e.g. Buddhist cultures tend not to fully into social groups — usually because their behaviour
tolerate externalizing behaviours) or may affect the atti- is aggressive and disruptive (Hinshaw & Melnick, 1995).
tudes of parents and clinicians towards what is accept- Indeed, in new social settings children with ADHD are
able behaviour. For example, Zwirs, Burger, Buitelaar & often singled out and rejected relatively rapidly by their
Schulpen (2006) found that detection of externalizing peers (Erhardt & Hinshaw, 1994). In part, this is due to
disorders was significantly lower in a sample of non- their disruptive behavioural symptoms but, in addition,
Dutch parents (Moroccan, Turkish and Surinamese) children with ADHD frequently fail to understand the
than Dutch parents and that cultural contexts may have intentions of their peers
an important influence on whether ADHD symptoms and are unable to translate / To complete Activity 16.1 go to
are detected and reported. the correct social response www.wiley-psychopathology.com/
activities/ch16
into appropriate behaviour
The prevalence of ADHD (Whalen & Henker, 1998).
DSM-5 estimates that around 5 per cent of school-age In adulthood, ADHD also has a number of impair-
children worldwide are diagnosed with ADHD and ing consequences, including less success and safety at
2.5 per cent of adults. Similar rates of diagnosis are also work (Kessler, Lane, Stang & van Brunt, 2009), poorer
found in pre-school children (aged 2-5 years) (Egger, interpersonal relationships (Biederman, Monuteasu,
Kondo & Angold, 2006) and about half of those diag- Mick, Spender et al., 2006), poorer academic outcomes
nosed with ADHD in childhood will carry that diagno- (Lewandowski, Lovett, Codding & Gordon, 2008) and
sis into adulthood (Kessler, Adler, Barkley, Biederman et poorer general life satisfaction (Biederman et al., 2006).
al., 2006). There is considerable evidence to indicate that
ADHD is more common in boys than girls but reasons The aetiology of ADHD
for this may include the fact that boys are more likely The causes of ADHD can be clustered under two broad
to be referred for treatment than girls. Recent reviews headings — biological and psychological, but the current
suggest that although there is a sex difference in rates view is that biological factors are particularly important
of diagnosis between boys and girls, ADHD symptoms in the aetiology of ADHD, especially inherited factors
are not sex specific (e.g. just as is the case with boys, that may play a strong role in mediating susceptibility to
girls with combined attention deficit and hyperactivity ADHD (Faraone & Khan, 2006).
were more likely to be disruptive than those diagnosed
with the predominantly single diagnosis) but identifica- Biological factors Genetic factors There is now
tion of girls with ADHD has been hampered by parental considerable evidence pointing to the involvement of
and teacher bias (Staller & Faraone, 2006). In addition, an inherited susceptibility to ADHD. ADHD appears
any sex differences found with ADHD in childhood do to be one of the most heritable psychiatric disorders:
not appear to be found in late adolescence or adulthood pooled data from 20 twin studies report a mean herit-
where male and female prevalence rates are equivalent ability estimate of 76 per cent (Faraone & Mick, 2010).
(Bauermeister, Shrout, Chavez, Rubio-Stipec et al., 2007). Adoption studies also suggest that ADHD in the adopted
child is more likely to occur if a biological parent has
The consequences of ADHD ADHD than if an adopted parent has ADHD (Faraone,
Like most psychopathologies the symptoms of ADHD Perlis, Doyle, Smoller et al., 2005). However, what is
also have detrimental consequences for the sufferer inherited is significantly less easy to determine. A meta-
across a range of life domains. First, their attentional analysis of gene linkage studies has revealed a region
deficits and hyperactivity may make them prone to on chromosome 16 that has the most consistent link-
temper outbursts, frustration, bossiness, stubbornness, age evidence (Coghill & Banaschewski, 2009). However,
changeable moods and poor self-esteem. As a result, identifying individual genes is much more problematic
academic achievement is usually impaired leading to and recent reviews of genome-wide association stud-
conflict with teachers and family. Because the disrup- ies have suggested that any individual gene variant for
tive consequences of their behaviour are pervasive, fam- ADHD must have a very small individual effect (Neale,
ily members often view their behaviour as intentional, Medland, Ripke, Asherson et al., 2010). However, many
wilful and irresponsible, and this can cause resentment of those genes identified may underlie abnormalities in
within the family. Individuals with predominantly inat- neurotransmitter systems — particularly the dopamine,
tentive symptoms tend to suffer most in terms of aca- norepinephrine and serotonin systems (Waldman &
demic achievement, while hyperactivity and impulsivity Gizer, 2006). Specific genes that may be involved are
are associated most with peer rejection and accidental the dopamine transporter gene, the dopamine D4 and
534 PSYCHOPATHOLOGY
D5 receptors and SNAP-25, a gene that controls the way brain volume in specific brain areas is inversely corre-
dopamine is released in the brain. However, while sus- lated with a variety of ADHD symptoms. For example,
ceptibility to ADHD appears to have a significant genetic children with ADHD are known to have deficits in exec-
component, additional studies strongly indicate a genes— utive functioning (involving planning and problem solv-
environment interaction. That is, what is inherited is a ing), and specifically have difficulty inhibiting responses,
vulnerability to ADHD but ADHD becomes manifest and these functions are normally controlled by the
only when certain environmental influences are found. brain’s frontal lobes. Studies have found that decreased
For example, Kahn, Khoury, Nichols & Lanphear (2003) frontal lobe volume predicts poor performance on tests
found that children with two copies of the 10-repeat of attention and on tasks that require behaviour to be
allele of a DAT1 gene (a gene related to dopamine regula- inhibited, suggesting that abnormalities in these brain
tion in the brain) who were exposed to maternal prenatal regions may be responsible for some of the symptoms
smoking exhibited significantly higher levels of hyperac- of ADHD (Casey, Castellanos, Giedd, Marsh et al.,
tivity, impulsiveness and oppositional behaviours than a 1997; Hill, Yeo, Campbell, Hart et al., 2003). Another
control group of children who possessed these genes but area of the brain that regularly exhibits abnormalities
whose mothers did not smoke during pregnancy. In addi- in association with ADHD symptoms is the cerebellum
tion, children who possessed only one of the risk factors (Cherkasova & Hechtman, 2009). In ADHD, abnormali-
(the high-risk genotype or a mother that smoked during ties are usually found in the cerebellum’s influence on
pregnancy) did not show significantly higher levels of the cortico-striatal-thalamo-cortical circuits and these
ADHD symptoms than children who possessed neither circuits are involved in choosing, initiating and carrying
of the risk factors. Studies such as this indicate that, while out complex motor and cognitive responses (Alexander,
inherited factors are critically important in the aetiology DeLong & Strick, 1986; Graybiel, 1998). In this case it
of ADHD, they may constitute a vulnerability that con- is not hard to imagine how dysfunctions in these path-
verts into ADHD only if certain environmental factors ways may result in the disruption of the planning and
are present (Coghill & Banaschewski, 2009). Other envi- execution of behaviour.
ronmental risk factors that have been proposed include
pre- or perinatal complications and maternal drinking Prenatal factors As we have already noted, at least
during pregnancy (Mick, Biederman, Faraone, Sayer et al., some prenatal experiences appear to interact with a
2002; Milberger, Biederman, Faraone, Guite & Tsuang, genetic predisposition to cause ADHD: these include
1997; Milberger, Biederman, Faraone & Jones, 1998). maternal smoking and drinking during pregnancy (Mick,
Biederman, Faraone, Sayer et al., 2002) and general com-
Neuroscience Magnetic resonance imaging (MRI) plications associated with childbirth, such as low birth
studies of the brains of individuals with ADHD have weight, respiratory distress and birth asphyxia (Tannock,
revealed a number of significant differences between 1998; Getahun, Rhoads, Demissie, Lu et al., 2013). In
ADHD sufferers and non-sufferers (e.g. Krain & a recent study, Schmitz, Denardin, Silva, Pianca et al.
Castellanos, 2006; Seidman, Valera & Makris, 2005; (2006) found that pregnant mothers smoking greater
Cortese, 2012). First, there is consistent evidence that than 10 cigarettes per day were significantly more likely
the brains of children with ADHD are smaller than to give birth to children with ADHD than non-smoking
those of healthy comparison children, and they develop mothers —even when other potential confounding factors
more slowly. Overall brain volume has been shown such as maternal ADHD, oppositional defiant disorder,
to be smaller by an average of 3.2 per cent, with the birth weight and alcohol use during pregnancy were con-
main areas affected being the frontal, parietal, tempo- trolled for. In addition, a study by Milberger, Biederman,
ral and occipital lobes (Durston, Hulshoff Pol, Schnack, Faraone, Guite & Tsuang (1997) found that 22 per cent
Buitelaar et al., 2004), and ADHD is also associated with of mothers of children with ADHD reported smoking
a global reduction in grey matter (Nakao, Radua, Rubia a pack of cigarettes a day during pregnancy compared
& Mataix-Cols, 2011). Other brain areas exhibiting with only 8 per cent of mothers whose children did not
decreased volume in ADHD include the frontal cortex, develop ADHD. Milberger et al. (1997) hypothesized that
basal ganglia and cerebellum (Krain & Castellanos, 2006). prenatal exposure to nicotine caused abnormalities in the
Comparisons of the development of brain structures in dopaminergic neurotransmitter system, resulting in dif-
children with ADHD and typically developing controls ficulties inhibiting behaviour.
also suggest that the median age by which 50 per cent
of the cortex reaches peak thickness is 10.5 years in chil- Environmental toxins Some early accounts of
dren with ADHD but only 7.5 years in normally devel- ADHD did allude to the possibility that hyperactivity
oping controls (Shaw, Eckstrand, Sharp, Blumenthal resulted from various biochemical imbalances caused by
et al., 2007). A range of studies has also indicated that such factors as food additives (Feingold, 1973), refined
COGNITIVE TESTS OF ADHD

A variety of tests has been devised that are capable of differentiating between children with ADHD and control
participants. The aim of most of these tasks is to test attention or to determine whether the individual is able to
successfully inhibit responses when required to do so (see Seidman, 2006).
THE CONTINUOUS PERFORMANCE TEST (CPT)
The CPT is a computerized visual vigilance/attention task in which the child is seated before a computer monitor
and instructed to observe a string of letters presented randomly and at varying speeds. Children are instructed
to press the space bar as quickly as possible following all letters except the letter X. Children with ADHD are less
METHODS
RESEARCH
16.1 able to inhibit responses following the presentation of the target letter X and also have longer reaction times fol-
lowing letters that should be responded to (Epstein, Johnson, Varia & Conners, 2001).
THE STROOP TASK
This is generally considered a test of ability to inhibit responses. In the task, a word describing a colour (e.g. RED)
is presented in a different colour (e.g. green) and the participant has to respond as quickly as possible by naming
the colour ink that the word is written in. Children with ADHD take more time to respond and make more errors
than control participants (Shin, 2005).
THE TRAIL MAKING TEST
This is a measure involving connecting circles on a page (Reitan, 1958). The child is instructed to connect the
circles by drawing lines alternating between circles labelled with numbers and letters in sequential order until
they reach the circle labelled ‘End’ (see Focus Point 15.1). Most studies show that children and adults with ADHD
perform significantly worse than control participants (Rapport, Van Voorhis, Tzelepis & Friedman, 2001).
THE CONTROLLED WORD ASSOCIATION TEST (COWAT)
This test measures verbal fluency in response to single letters, which taps into phonological associations and
category fluency (‘name all the animals you can beginning with the letter. . .’) (Benton, Hamsher, & Sivan, 1983).
This test appears to measure speed ofaccess to words, persistence at a task and processing speed. The majority of
studies show impaired performance on this task in children with ADHD compared with controls (Dinn, Robbins &
Harris, 2001).
CONNERS’ PARENT RATING SCALE (CPRS)
The CPRS (Conners, Sitarenios, Parker & Epstein, 1998) is an 80-item scale completed by the child’s parent using
a four-point scale. This instrument has well-accepted reliability and validity and is considered to be standard in
ADHD diagnosis (Barkley, 1991). Norms by age are available for males and females in 3 year intervals.
sugar cane (Goyette & Conners, 1977) and lead poison- hyperactivity (e.g. Fung & Lau, 1989; Polanska, Jurewicz &
ing (Thompson, Raab, Hepburn, Hunter et al., 1989). Hanke, 2012).
However, while there is little evidence to suggest that rote
food additives generally influence ADHD (Wolraich, Psychological factors Parent-child interactions
Wilson & White, 1995), there is some support for ADHD appears to run in families and this may have
the fact that both the levels of lead in the blood and implications beyond the fact that there is a genetic com-
chronic exposure to nicotine or tobacco smoke increase ponent to the disorder. For instance, it also means that
536 PSYCHOPATHOLOGY
.'
children with ADHD are more likely to be brought up a TOM task than control participants. In contrast, in a
by parents who also have the disorder, which may exacer- later study, Perner, Kain & Barchfeld (2002) found that
bate any symptoms that are caused by the genetic com- children with ADHD showed no impairment at all on an
ponent alone. For example, fathers who are diagnosed advanced TOM task. However, studies have been fairly
with ADHD have been found to be less effective parents consistent in showing that children with ADHD do show
(in terms of exhibiting ineffective discipline and adopting impaired performance compared with controls on tasks
traditionally conservative father roles) than parents with- of executive functioning (Fahie & Symons, 2003; Perner,
out an ADHD diagnosis (Arnold, O’Leary & Edwards, Kain & Barchfeld, 2002). Executive functioning is that
1997), and this might exacerbate any disruptive charac- range of skills that require goal directed behaviour, plan-
teristics the ADHD child may exhibit. Psychodynamic ning, attentional control and inhibition of inappropriate
approaches to ADHD have also pointed to the possible responses. Such studies have tended to suggest that chil-
role of inconsistent and ineffective parenting of children dren with ADHD have specific deficits related to planning
with ADHD. Bettelheim (1967) proposed that hyperactiv- and inhibition of behaviour (Papadopoulos, Panayiotou,
ity results when a predisposition to ADHD is accompa- Spanoudis & Natsopoulos, 2005) and it is deficits in these
nied by authoritarian parenting methods. He argued that areas of functioning that give rise to their behavioural
such parents are likely to become impatient with a dis- problems. This has recently been reinforced by studies
ruptive and hyperactive child, resulting in a vicious cycle showing that individuals with ADHD do show execu-
whereby constant attempts to discipline the child cause tive functioning deficits, but do not necessarily exhibit
even more defiant reactions on the part of the child who TOM deficits, indicating that ADHD symptoms may be
reacts by defying rules across a range of life contexts (e.g. linked directly to executive functioning problems rather
school, social situations and suchlike). than deficits in social functioning (Gonzalez-Gadea,
Learning theorists have suggested that parents may Baez, Torralva, Castellanos et al., 2013). The fact that
exacerbate ADHD symptoms in a rather different way. tests of executive functioning have indicated that this
Individuals with ADHD exhibit impulsive and disruptive is where the cognitive deficits in ADHD lie is consist-
behaviour that in many cases will require the need for ent with the neurological evidence we reviewed earlier,
control by the parent. In such circumstances the atten- which strongly indicates that children with ADHD have
tion from the parent that these behaviours demand may abnormalities in the frontal lobes of the brain, and it is
be rewarding or reinforcing them, thus increasing their the frontal lobes that control executive functioning.
frequency and intensity. While there is no direct evidence
to support this view, indirect support comes from studies Summary of ADHD The evidence on the aetiology
showing that time-out from positive reinforcement can of ADHD strongly indicates that there is a significant
act as an effective procedure for reducing negative and genetic component to the disorder and it may be one
disruptive behaviour in children with ADHD (Fabiano, of the most heritable psychological disorders. However,
Pelham, Manos, Gnagy et al., 2004). it is not fully clear yet whether this genetic compo-
Nevertheless, while parent-child interactions of vari- nent merely bestows a vulnerability for the disorder or
ous kinds may exacerbate ADHD symptoms, there is no whether it may be a direct cause of abnormalities that
evidence to suggest that they are the sole cause of these underlie ADHD; it has also not yet been possible to
symptoms (Johnston & Marsh, 2001). clearly identify the genes through which this heritability
is transmitted. There are clearly some brain abnormali-
Theory of mind (TOM) deficits We have already ties that characterize ADHD, including reduced overall
described how children with ADHD frequently fail to brain volume and grey matter, and reduced brain vol-
understand the intentions of their peers in social situa- ume, particularly in areas such as the frontal cortex,
tions and this has led some theorists to argue that chil- basal ganglia and cerebellum, and abnormalities in the
dren with ADHD have theory of mind (TOM) deficits. frontal lobes may contribute to the deficits in executive
Theory of mind is the ability to understand one’s own functioning that are found in ADHD using cognitive
and other people’s mental states (Premack & Woodruff, tests. Some pre- and perinatal factors have been identi-
1978) and it is not difficult to see that if a child has defi- fied that may contribute to abnormal development and
cits in such abilities they will often react in inappropriate these include maternal smoking and drinking during
ways to peers and family. However, studies have tended pregnancy as well as complications at birth, including
to be inconsistent in showing a relationship between low birth weight, respiratory distress and birth asphyxia.
poor performance on TOM tasks (see Chapter 17) and There is also some evidence that dysfunctional parenting
ADHD. For example, Buitelaar, van der Wees, Swaab- may contribute to the behavioural symptoms of ADHD
Barneveld & van der Gaag (1999) found that children in children but there is no evidence that dysfunctional
with ADHD diagnoses showed poorer performance on parenting is a sole cause of ADHD.
is
16.2.2. Conduct Disorder DSM-5 SUMMARY TABLE 16.2 Criteria for conduct disorder
While ADHD is characterized by behaviour that tends to e An ongoing pattern of behaviour where the rights of
others or social norms are infringed, as shown by at least
be disruptive and inappropriate, many children and adoles-
three of the following over a 12 month period:
cents exhibit behaviour that appears almost intentionally
vicious, callous and aggressive, and it is when such charac- e Bullying or threatening others
teristics appear that a diagnosis of conduct disorder may ° Starting fights
duct disorder (CD) A pattern of be appropriate. Behaviours e Using a weapon to do serious physical harm
aviour during childhood in which the typical of conduct disorder
d exhibits a range of behavioural include violent or agegres- e Physical cruelty to others
blems, including fighting, lying, run- sive behaviour, deliberate e Physical cruelty to animals
J away from home, vandalism and
cruelty towards people or e Mugging or similar crimes
ncy.
animals, wanton vandalism
or damage to property, lying, stealing and cheating, crimi- e Forcing another into sexual activity
nal theft and violation of the rights of others (e. g. trespass, e Fire setting to destroy/seriously damage property
threatening behaviour and verbal abuse). The following e Deliberate destruction of another's property
sections discuss the diagnosis, prevalence and the known
causes of conduct disorder. e Breaking into buildings or cars
e Lies to get goods or favours
The diagnosis of conduct disorder e Shoplifting or similar
DSM-5 devotes a chapter to disruptive, impulse-control
e Stays out at night despite parental intervention,
and conduct disorders, and these disorders are linked to
starting from before the age of 13
a common externalizing spectrum characterized by a
lack of inhibition or inability to control impulses. This e Has run away from home at least twice or once for
along period oftime
common theme throughout these disorders is one rea-
son why conduct disorder is regularly comorbid with e Often misses school, starting from before the age of 13
impulse disorders, such as intermittent explosive disor- e The disturbances cause significant impairment in social,
der (DSM-5, p.466), and other impulse control disorders academic or occupational functioning
such as pyromania (deliberate and purposeful fire-
e Ifthe patient is 18 years or older, the condition is not
setting) (DSM-S5, p.476) and kleptomania (recurrent fail- better explained by antisocial personality disorder
ure to resist impulses to steal objects) (DSM-5, p.478). In
this chapter we will discuss two disorders, namely con-
duct disorder and oppositional defiant disorder.
The main feature of conduct disorder is a repetitive property and they will indulge in acts of vandalism and petty
and persistent pattern of behaviour involving the viola- theft from others. Their lying will also extend to breaking
tion of accepted social norms or the basic rights of oth- promises to obtain goods or benefits, or simply ‘conning’
ers. There are four main categories of such behaviour: (1) others into providing benefits or favours. Finally, children
ageression towards people and animals, (2) destruction with conduct disorder will usually have a history of break-
of property, (3) deceitfulness or theft, and (4) the seri- ing rules, including staying out late despite prohibitions,
ous violation of accepted rules (such as driving offences). running away from home or staying away from school.
These behaviours must also cause severe impairment in There are two main subtypes of conduct disorder
social, academic or occupational functioning and should based on the age of onset. Childhood-onset conduct
be found in a range of different contexts such as home, disorder is defined by the childhood-onset conduct disorder
school or the community. For a diagnosis of conduct dis- onset of at least one crite- A sub-type of conduct disorder defined
order, characteristic behaviours must have been present rion characteristic of con- by the onset of at least one criterion
for at least 12 months (DSM-5 Summary Table 16.2). duct disorder prior to 10 characteristic of conduct disorder prior to
10 years of age.
Children or adolescents with this disorder would nor- years of age. Adolescent-
mally initiate violence or aggressive behaviour and react onset conduct disorder is adolescent-onset conduct disorder A
violently to others. Their behaviour will often include bul- defined by the appearance subtype of conduct disorder defined by
the appearance of conduct disorder symp-
lying or threatening behaviour: they will often initiate physi- of conduct disorder symptoms only after the age of 10 years.
cal fights, carry weapons, be physically cruel to people or toms only after the age of
animals, and intimidate people into activities by threats 10 years. Such individuals are less likely to be physically
of physical force (e.g. force others into sexual activity). ageressive than those with childhood-onset type and will
Individuals with conduct disorder also have little respect for usually have better peer relationships.
: =
Like individuals with antisocial personality disorder disorders, antisocial personality disorder, ADHD or sub-
(see section 12.2.2), children and adolescents with con- stance abuse.
duct disorder display little empathy with the feelings
and intentions of others and will usually believe that The prevalence and course
their aggressive reactions to others are justified. They of conduct disorder
will frequently try to blame others for their misdeeds Epidemiological studies indicate that conduct disorder
and exhibit little or any genuine guilt for their antisocial may be relatively common, with prevalence rates rang-
actions. Risk-taking, frustration, irritability, impulsivity ing from 4-16 per cent in boys and 1.2-9 per cent in girls
and temper tantrums are regularly associated with con- (Loeber, Burke, Lahey, Winters & Zera, 2000). A more
duct disorder and result in higher accident rates for such recent US study estimated the lifetime prevalence rate
individuals. Conduct disorder is also associated with of conduct disorder at 9.5 per cent (12.0 per cent among
early onset of a range of behaviours, including sexual males and 7.1 per cent among females) and a median age
behaviour, drinking, smoking, substance abuse and gen- of onset of 11.6 years (Nock, Kazdin, Hiripi & Kessler,
eral risk-taking behaviour (e.g. dangerous and erratic 2006).
driving). Finally, the disorder is more common in males The most significant symptoms of conduct disorder
than in females: males with a diagnosis will outnum- begin to appear between middle childhood to middle
ber females by a ratio of at least 4:1 and often higher adolescence, although ODD is a common precursor to
(Zoccolillo, 1993). conduct disorder in the pre-school years. In a majority of
It is important to mention at least three issues related individuals the disorder remits by adulthood, but some
to diagnosis of conduct disorder. Firstly, individuals do go on to meet the criteria for antisocial personality
diagnosed with conduct disorder will usually be under disorder. Indeed, studies suggest that childhood conduct
18 years of age and are only diagnosed with the disor- disorder (but not childhood ADHD) predicts antisocial
der at a later age if the criteria for antisocial personal- personality disorder in adulthood, but only in lower
ity disorder are not met. Secondly, the clinician will need socioeconomic status families (Lahey, Loeber, Burke &
to take account of the social context in which behav- Applegate, 2005). Children with conduct disorder are
iours characteristic of conduct disorder are found. For also more likely to develop into adulthood with antiso-
example, in certain deprived inner-city areas, behaviours cial personality disorder if they have a parent with anti-
characteristic of conduct disorder may be seen as being social personality disorder or have low verbal IQ (Lahey,
protective. That is, they may represent the norm for that Loeber, Hart, Frick et al., 1995).
environment and may serve an adaptive function in deal- Finally, we have already indicated that conduct disor-
ing with poverty and the threatening behaviour of oth- der prevalence rates for boys are significantly higher than
ers. In addition, immigrants from war-ravaged countries for girls, and the disorder also manifests differently in
can have a reputation for violence because such behavy- boys and girls. In boys, the main behaviours are aggres-
iour has been necessary for survival in their home coun- sive and violent behaviour, fighting, stealing, damage to
tries. Clinicians must be sure that a diagnosis of conduct property and school problems. However, for girls, the
disorder is made only when the characteristic behaviours most common behaviours are petty theft (such as shop-
are symptomatic of dysfunction rather than a reaction lifting), lying, running away from home, avoiding school
to a specific social context. Thirdly, a related category and prostitution (Robins, 1991). Indeed, these differential
of disruptive behaviour disorders in DSM-5 is known as behaviours may have a direct impact on gender differ-
oppositional defiant disorder (ODD). ODD is a diag- ences in prevalence rates since the crimes indulged in by
nosis usually reserved for girls (e.g. shoplifting) are often considered less serious
oppositional defiant disorder (ODD) A those children who do
mild form of disruptive behaviour disorders
than the violent crimes committed by boys, and boys are
not meet the full criteria usually considered more likely to commit crimes than
reserved for children who do not meet the
full criteria for conduct disorder. for conduct disorder (e.g. girls (Zahn-Waxler, 1993).
extreme aggression and
violence) but who have regular temper tantrums, refuse The aetiology of conduct disorder
to comply with requests or instructions, or appear to
deliberately indulge in behaviours that annoy others. Biological factors Genetic factors There is now
ODD is common in pre-school children and may even be some evidence that conduct disorder and its associated
a precursor to later childhood conduct disorder (Lahey, behaviours of aggressiveness and criminality may have
McBurnett & Loeber, 2000). It is found more often in a genetic component. Twin studies specifically involv-
families where childcare has been disrupted (through the ing conduct disorders have found heritability estimates
child experiencing a number of different caregivers) or in between 45 and 67 per cent (Viding & McCrory, 2012),
families where at least one parent has a history of mood while twin studies also suggest that aggressive and
violent behaviour (e.g. fighting, cruelty to animals) has drinking of alcohol during the first trimester (Larkby,
a significant inherited component (Edelbrock, Rende, Goldschmidt, Hanusa & Day, 2011), but this may be
Plomin & Thompson, 1995). Adoption studies have also restricted to mothers and children of low socioeconomic
reported significant genetic and environmental influ- status (Monteaux, Blacker, Biederman, Fitzmaurice et al.,
ences on both conduct disorder and criminal behaviour 2006). Similarly, delinquent behaviour and poor moral
(Simonoff, 2001). Some recent studies have even identi- judgement have also been found to be higher in children
fied a specific gene, GABRA2, which is associated with prenatally exposed to alcohol (Schonfeld, Mattson &
childhood conduct disorder (Dick, Bierut, Hinrichs, Fox Riley, 2005). Recent studies also suggest that external-
et al., 2006) and, interestingly, this gene is also related izing behaviours are associated with prenatal malnutri-
to adult alcohol dependence and drug dependence in tion, especially deficits in proteins, iron and zinc (Liu &
adolescence. However, the results from more extensive Raine, 2006). However, we must be cautious about how
candidate gene association studies have been less encour- we interpret all of these findings because correlations
aging, with few if any candidate genes having been iden- between prenatal exposure and conduct disorder may
tified to date (Viding, Price, Jaffee, Trzaskowski et al., be significantly confounded with other risk factors, such
2013). What these studies suggest is that there is probably as parental depression, family disadvantage and genetic
an inherited component to conduct disorder — perhaps influences (Maughan, Taylor, Caspi & Moffitt, 2004). If
in the form of inherited temperamental characteristics — so, prenatal exposure may simply be a risk factor for the
but that environmental factors also probably play an development of conduct disorder rather than a direct
important role in determining behaviour patterns typi- cause of the problem.
cal of conduct disorder.
Psychological factors The family environment
Neuropsychological deficits Just as with ADHD, and parent-child relationships While studies of
conduct disorder is associated with neuropsychologi- the heritability of conduct disorder suggest a significant
cal deficits in cognitive functioning, including deficits in genetic component to the disorder, these studies also
executive functioning (planning and self-control), ver- indicate that important and significant environmental
bal IQ and memory (Lynam & Henry, 2001). Low IQ factors are also involved, and arguably one of the most
is also associated with conduct disorder and is particu- important of the latter is the family environment and the
larly associated with early-age onset conduct disorder nature of parent-child interactions during childhood. It
independently of related socioeconomic factors such as is already well documented that risk factors for conduct
poverty, race or poor educational attainment (Lynam, disorder and ODD include parental unemployment,
Moffitt & Stouthamer-Loeber, 1993). Nevertheless, there having a parent with antisocial personality disorder, dis-
is some doubt about whether executive functioning defi- rupted childcare and childhood abuse or maltreatment
cits occur in conduct disorder in the absence of ADHD (Frick, 1998; Lahey, Loeber, Hart, Frick et al., 1995). For
symptoms. For example, Oosterlaan, Scheres & Sergeant example, inconsistent and harsh parenting is associated
(2005) found that while executive functioning deficits with the development of aggressive behaviour and other
were found in children with comorbid conduct disorder symptoms of conduct disorder (Coie & Dodge, 1998).
and ADHD, no deficits were found in children diagnosed This may be because inconsistent discipline may permit
solely with either ODD or CD. Similarly, meta-analyses the child to get away with behaving antisocially on many
have found that antisocial behaviour generally is associ- occasions; but, when disciplining does occur, the child
ated with poor executive functioning but this association may learn aggressive or violent behaviour from parents
is predominantly driven by relationships between poor who behave aggressively when disciplining their children.
executive functioning and criminality and externalizing Indeed, there is evidence that children who are physically
behaviours generally rather than conduct disorder spe- abused by their parents are more likely to be aggressive
cifically (Ogilvie, Stewart, Chan & Shum, 2011). when they grow up (Crick & Dodge, 1994) and parents
who are physically abusive to their children also report
Prenatal factors A number of prenatal factors have more behaviour problems in their children than non-
been identified in the aetiology of conduct disorder. abusive parents (Lau, Valeri, McCarty & Weisz, 2006).
These include maternal smoking and drinking during However, longitudinal studies are generally consistent
pregnancy and prenatal and postnatal malnutrition. in indicating that childhood abuse is associated with
Maternal smoking has been found to predict the early criminal behaviour, violence and diagnosis of conduct
emergence of conduct problems in the offspring, espe- disorder in later childhood and adolescence (Fergusson,
cially socially resistant and impulsively aggressive behav- Horwood & Lynskey, 1996; Widom & Maxfield, 1996),
iour (Wakschlag, Pickett, Kasza & Loeber, 2006), and and there is some evidence that childhood abuse may
conduct disorder is specifically associated with maternal give rise to conduct disorder in children only with a
540 PSYCHOPATHOLOGY
: y x
specific genetic predisposition (Taylor & Kim-Cohen, increase pre-existing tendencies rather than create delin-
2007; Dodge, 2009). In addition to childhood abuse, con- quent behaviour from scratch. There is some evidence
duct disorder has also been shown to be associated with that deviant peer affiliation is associated with later anti-
family environments that are less cohesive, have few social behaviour and substance abuse only in children
intellectual /cultural pursuits, have greater levels of fam- who already display symptoms of ODD and conduct
ily conflict and higher levels of parental stress (Blader, disorder. Deviant peer affiliation only weakly predicts
2006; George, Herman & Ostrander, 2006). Interestingly, future antisocial behaviour in individuals without these
many of these familial characteristics that are associated initial symptoms (Marshall & Molina, 2006).
with conduct disorder are also very closely linked to pov- Another view is that peer factors may facilitate symp-
erty and social deprivation, and we will look at how this toms of conduct disorder in a more indirect way. For
socioeconomic factor may influence aetiology later. example, being rejected by peers has been shown to
cause increased aggressiveness — especially in children
Media and peer influences Many children may that have an existing disruptive behaviour disorder such
develop antisocial and aggressive behaviour because as ADHD (Hinshaw & Melnick, 1995) —and this may also
they simply mimic the violent activities that they see become a vicious cycle, as peers continue to reject ado-
around them in the media or displayed by their peers. lescents whose behaviour exhibits increasing levels of
Interestingly, statistics from the US suggest that between antisocial behaviour (Kelly, Jorm & Rodgers, 2006).
1980 and 1995 violent crime by juveniles increased by In summary, media and peer mimicry are risk factors
over 50 per cent (US Bureau of the Census, 1997) and for conduct disorder but may facilitate antisocial and
at least part of this increase may be due to the increas- aggressive behaviour more in those children and adoles-
ing levels of violence viewed by children on TV and in cents who are already displaying symptoms of conduct
video games. However, while there is some evidence disorder. As such, they. probably represent mediating
that television violence contributes to children’s levels variables rather than true causes of the disorder.
of aggressiveness and subsequent criminality (Hughes &
Hasbrouck, 1996), more recent studies tend to suggest Cognitive factors Conduct disorder is associated with
that media violence has its effect primarily on children the development of deviant moral awareness. For exam-
who are already emotionally and psychiatrically dis- ple, most children grow up learning that certain behav-
turbed. Recent longitudinal studies indicate that simply iours are morally acceptable and others are morally and
watching more than 3 hours of TV a day at the age of socially unacceptable. However, children with conduct
5 years predicts an increase in conduct problems by age disorder fail to acquire this moral awareness. They are
7 years, but this effect is only significant for TV watch- content to achieve their goals using violence and deceit,
ing and not playing electronic games (Parkes, Sweeting, they have little respect for the rights of others, and they
Wight & Henderson, 2013). Finally, studies have demon- show little or no remorse for their antisocial acts. Much
strated an effect of violent TV programmes on behav- of this lack of awareness of moral standards may come
ioural and physiological measures of aggression only in from the fact that they may have developed highly biased
children who already have a diagnosis of ADHD, ODD, ways of interpreting the world. For example, a child
conduct disorder or disruptive behavioural disorders with conduct disorder regularly interprets the behaviour
generally (Grimes, Vernberg & Cathers, 1997; Grimes, of others as hostile or challenging and this appears to
Bergen, Nichols, Vernberg & Fonagy, 2004). give rise to their aggressive reactions. Dodge (1991, 1993)
A more important source of mimicry may be peer has proposed a social-information processing model of
behaviour and there is already evidence suggesting that antisocial and aggressive behaviour in which a history of
associating with peers who indulge in violent or crimi- trauma, abuse, deprivation and insecure attachment may
nal behaviour is likely to increase one’s own delinquent give rise to specific information processing biases. These
behaviour (Burt & Klump, 2013). In fact, a vicious include hypervigilance for hostile cues and attributing
cycle may develop in which associating with aggressive minor provocations to hostile intent, and these biases
peers may expose the individual to increasing levels of give rise to unwarranted fear and to aggressive reactions.
community violence (e.g. gang fights, violent assaults If the child is brought up in a family environment where
and robbery). This in turn will facilitate mimicry of vio- they learn aggressive behaviour in child—parent inter-
lence and will increase the perception of violent behav- actions (Patterson, Reid & Dishion, 1992), and if they
iour being the norm (Lambert, lalongo, Boyd & Cooley, also have their own experiences with successful aggres-
2005). However, what is not clear from this research sive tactics, they will evaluate aggression as an adaptive
is whether children who already have antisocial and social strategy and use it proactively (see Figure 16.1).
ageressive tendencies choose to mix with similar peers In support of this hypothesis, Gouze (1987) found that
in the first place, so the peer association may merely aggressive children direct their attention selectively
CHAPTER 16 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS BAL
Environment Brain
Coercive training Biased and limited response repertoire;

aggressive biased response evaluations
environment
Hypervigilance to Cognition
Trauma, abuse,
hostile cues;
deprivation,
hostile attributions;
insecure attachment
unwarranted fear
relationships
Reactive Behaviour
Proactive
aggressive aggressive
behaviour behaviour
FIGURE 16.1 Dodge's (1991) social-information processing model of antisocial and aggressive behaviourin which a history of
trauma, abuse, deprivation and insecure attachment can give rise to information processing biases including a tendency to interpret
even benign cues as signalling hostility.
Source: Krol, N., Morton, J. & De Bruyn, E. (2004). Theories of conduct disorder: A causal modelling analysis. Journal of Child Psychology and
Psychiatry, 45, 727-742, Figure 3. Reproduced with permission.
towards hostile social cues and have difficulty diverting may be a cause of conduct disorder rather than a conse-
their attention away from these cues. Aggressive chil- quence of it (Lahey, Miller, Gordon & Riley, 1999). A lon-
dren also exhibit what is called a ‘hostile attributional gitudinal study of familial and socioeconomic predictors
tileattributional bias The tendency bias’ (Naseby, Hayden & of conduct disorder in a Scottish cohort indicated that
\dividuals to interpret not only ambigu- DePaulo, 1979) in which individuals with conduct problems were more likely to
they will interpret not only
cues as signalling hostility, but also have mothers that smoked during pregnancy, less likely
vy cues that are generated with benign
ambiguous cues as signal- to be living with both parents, have poor general health,
ntions.
ling hostility but also many and to have a parent who agrees with smacking as a form
cues that are generated by benign intentions (e.g. Dodge, of punishment (Wilson, Bradshaw, Tipping, Henderson
Bates & Pettit, 1990). Once a hostile attribution is made, etal., 2013). Poverty in turnis likely to give rise to disrupted
studies also suggest that there is a 70 per cent probability family life, parental stress, poor educational opportuni-
of an aggressive response compared with only a 25 per ties and parental neglect — all of which may be contribut-
cent probability following a benign attribution (Dodge, ing factors to the development of conduct disorder. An
1991). Because of such information processing and attri- instructive study by Costello, Compton, Keeler & Angold
butional biases, the individual with conduct disorder (2003) suggests that poverty per se does have a direct
may be locked into a cycle of hostile interpretations and causal effect on the level of conduct disorder in a local
aggressive responding that becomes difficult to break — population. They studied conduct disorder in American
especially as continued aggressive behaviour by the suf Indian children before and after a casino opened on their
ferer is likely to generate genuine hostile intentions from reservation, which provided income that moved many
others in the future. families out of poverty. This constituted an interesting
natural experiment on the role of poverty in childhood
Socioeconomic factors Delinquent, violent behav- disorders. Before the casino opened, children of poor
iour has been shown to be highly associated with poverty, families suffered more symptoms of psychopathology
low socioeconomic class, unemployment, urban living than those of non-poor families. However, after the
and poor educational achievement, and such factors casino had opened the children of those families who
542 — PSYCHOPATHOLOGY
moved from the poor to non-poor class showed a signifi- family environments with disrupted childcare, child-
cant drop in symptoms of conduct disorder and ODD. hood abuse and maltreatment, and inconsistent parent-
Levels of these symptoms in families who remained poor ing. Some theories suggest that early experience with
after the casino opened did not change. This study pro- maladaptive and abusive parenting may give rise to infor-
vides a striking example of how poverty may represent a mation processing biases that lead the child to attend to
genuine causal factor for conduct disorder. However, the and interpret most social cues as indicative of hostile
exact mechanisms that mediate the relationship between intent, which generates aggressive responding. There is
poverty and conduct disorder remain unclear. some modest evidence that media and peer influences
may also facilitate aggressive and antisocial behaviour.
Summary of conduct disorder This section. has However, most recent research suggests that these fac-
indicated that conduct disorder may have a number of tors may facilitate aggressive antisocial behaviour mainly
contributing causes. First, there is an important genetic in children who are already displaying symptoms of con-
element that may be related to the inheritance of tem- duct disorder and ODD. Finally, low socioeconomic sta-
perament factors. However, these studies also tend to tus and poverty is closely linked with the development
implicate significant environmental factors in the aetiol- of conduct disorder and at least one study suggests that
ogy of conduct disorder. Certain types of familial envi- the link may be causal. However, as yet, the mechanisms
ronments and parent-child relationships are risk factors by which poverty may cause antisocial and aggressive
for the development of conduct disorder, particularly behaviour in children are unclear.
SELF-TEST QUESTIONS
* Can you name the main symptoms of attention deficit hyperactivity disorder (ADHD)?
° What are the different subtypes of ADHD and what other disorders is ADHD likely to be comorbid with?
e What is the evidence that ADHD is genetically determined?
° How might deficits in executive functioning cause ADHD symptoms?
* What prenatal factors have been identified as risk factors for ADHD?
* How might parent-child interactional styles exacerbate the symptoms of ADHD?
® Do children diagnosed with ADHD have a theory of mind (TOM) deficit?
e What are the four main categories of symptoms found with conduct disorder?
e What is oppositional defiant disorder (ODD) and how does it differ from conduct disorder?
* Can you summarize the biological factors that may be involved in the aetiology of conduct disorder?
* What is the evidence that children develop symptoms typical of conduct disorder by mimicking the violent activities they
see around them in the media or displayed by peers?
° How can interpretation biases account for behaviours typical of conduct disorder?
e What socioeconomic variables act as risk factors for conduct disorder?
SECTION SUMMARY
16.2 DISRUPTIVE BEHAVIOUR PROBLEMS
¢ Disruptive behaviour disorders are characterized by impulsive, disruptive and poorly controlled behaviour.
° The two main disruptive behaviour disorders are attention deficit hyperactivity disorder (ADHD) and conduct disorder.
¢ ADHD can manifest itself as lack of attention, hyperactivity or impulsivity.
CHAPTER 16 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS 543
* Around 5 per cent of school-age children worldwide are estimated to be diagnosed with ADHD.
¢ ADHD significantly affects educational achievement and social integration.
° ADHD appears to have a mean heritability estimate as high as 76 per cent.
° ADHD is associated with smaller brain size, deficits in executive functioning and abnormalities in the cerebellum.
¢ Dysfunctional parent-child interactions may contribute to ADHD but there is no evidence to suggest these are a sole cause
of the disorder.
° Conduct disorder can be described as behaviour that is aggressive, causes vandalism, property loss or damage, deceitful-
ness and lying, and serious violation of accepted rules.
* Oppositional defiant disorder (ODD) is a milder form of disruptive behaviour disorder reserved for children who do not meet
the full criteria for conduct disorder.
* Prevalence rates for conduct disorder are estimated at 4-16 per cent for boys and 1.2-9 per cent in girls.
¢ Both genetic and environmental factors appear to be important in the aetiology of conduct disorder.
e Psychological factors influencing conduct disorder symptoms include the nature of the family environment, parent-child
relationships and media and peer influences.
° Individuals with conduct disorder appear to develop an information processing bias that leads them to interpret the benign
intentions of others as hostile.
16.3 CHILDHOOD AND separation anxiety disorder, early onset generalized anxi-
ety disorder (GAD) and obsessive compulsive disorder
ADOLESCENT ANXIETY (OCD). However, anxiety and depression are frequently
comorbid in childhood (Manassis & Monga, 2001) and
AND DEPRESSION treatment may need to target both conditions. We will
now continue by looking separately at the characteristics
and known causes of childhood anxiety and childhood
Frank’s story at the beginning of this chapter graphically
depression.
illustrates some of the distress experienced by children
who are exposed to uncertainty and stress early in their
lives. As a result of the loss of his parents and being
moved to a foster home, he experiences a range of emo-
16.3.1 Childhood Anxiety
tions, including rejection, fear, confusion, anger, hatred In childhood, anxiety is primarily manifested as with-
and misery. By their very nature children are emotion- drawn behaviour (internalizing). The child will avoid
ally naive, and will often be unable to label the feelings activities where they may have to socialize with others
they experience — they may only know that they feel bad (e.g. school), they will be clinging and demanding of
and confused. As was the case with Frank, these feel- parents and carers (to the point of following a parent
ings often lead the individual to become withdrawn and from room to room), they will express a desire to stay
inward-looking (behaviour that may be labelled by the at home, and they will communicate exaggerated fears
clinician as representing an internalizing disorder) and over such things as the death of carers or of being bul-
may serve as the basis for future disorders in adolescence lied by peers. Children tend to be less concerned than do
and early adulthood. All of these factors make it difficult adults about the specific symptoms of their anxiety, but
for the clinician to identify childhood anxiety and depres- they do tend to report significantly more somatic com-
sion. Children who are anxious and depressed tend to plaints than non-anxious children (Hofflich, Hughes &
be clinging and demanding of their parents and carers, Kendall, 2006). Many childhood anxiety disorders do
will go to great lengths to avoid some activities, such as tend to be recognizable as those also found in adulthood
school, and will express exaggerated fears — especially (e.g. GAD, OCD and social anxiety disorder). However,
of events such as separation from, or the death of, a at least some manifestations of childhood anxiety tend
parent or carer. There has been some success recently to be confined to childhood, and separation anxiety is
in identifying specific disorders in childhood such as one such example.
544 PSYCHOPATHOLOGY
The features and characteristics of childhood vomiting (DSM-5 Summary Table 16.3). Separation anxi-
and adolescent anxiety problems ety is often a normal feature of early development but it
can be triggered and exaggerated by specific life stressors
Separation anxiety As the name suggests, separa- (such as the death of a relative or pet, an illness, a change
tion anxiety is an intense fear of being separated from of schools or moving home).
separation anxiety A childhood anxiety parents or carers. It is com- The estimated prevalence rate of diagnosable sepa-
monly found in many chil-
problem involving an intense fear of being ration anxiety is approximately 4 per cent in children
separated from parents or carers. dren at the end of the first between 6 and 12 months old, and has a 12-month preva-
year of life but in most children this fear gradually sub- lence rate of 1.6 per cent in adolescents (DSM-5, p.192).
sides. However, in others it persists well into the school However, once they have reached the age for school
years and may also reappear in later childhood following a attendance, many children suffering separation disorder
period of stress or trauma. Older children with separation go on to exhibit school refusal problems, including social
disorder will become distressed at being away from home anxiety disorder (Egger, Costello & Angold, 2003).
and will often need to know the whereabouts of parents.
They may also develop exaggerated fears that their par- Obsessive compulsive disorder (OCD) Often begin-
ents will become ill, die or be unable to look after them. ning in childhood, OCD is now recognized as a relatively
Consequences of this anxiety include a reluctance to common disorder and its phenomenology in childhood is
attend school or to stay at friends’ homes overnight, and very similar to adult OCD, with the main features of the
many will require that a parent or carer stay with them at disorder in children manifesting as intrusive, repetitive
bedtime until they have fallen asleep. As with most child- thoughts, obsessions and compulsions. The most common
hood anxiety disorders, sufferers will also report physical obsession themes in children are contamination, aggression
complaints such as stomach aches, headaches, nausea and (harm or death), symmetry and exactness; in adolescence,
religious and sexual obsessions also become common
(Geller, Biederman, Faraone, Agranat et al., 2001).
DSM-5 SUMMARY TABLE 16.3 Criteria for separation anxiety Common compulsive ssssssssmssssmemsmmm
behaviours in children and i Fora video on OCD in children go to
. i www.wiley-psychopathology.com/
e Excessive anxiety surrounding separation from those to adolescents include wash- | Wineenie
whom the individual is attached, as shown by at least
ing, checking, ordering, ETO
three of the following:
touching, repeating and
e Disproportionate distress when anticipating or experi- reassurance seeking, as well as covert behaviours such as
encing separation from home or attachment figures reviewing or cancelling thoughts, silent prayers or count-
e Ongoing and unnecessary concern about losing ing (Franklin, Kozak, Cashman, Coles et al., 1998). In
attachment figures or potential harm to them adults, compulsions (e.g. behavioural rituals) are rarely
¢ Ongoing and unnecessary concern about an unex- found without accompanying obsessions (e.g. intrusive
pected event which causes separation from attach- thoughts) but in children compulsions without obses-
ment figures sions can be quite common and these are frequently tac-
e¢ Ongoing aversion to going out or away from home tile (e.g. touching, tapping or rubbing rituals) and may be
because of fear of separation accompanied by behavioural tics (Leckman, Grice, Barr,
de Vries et al., 1995). While the range of obsessions and
¢ Ongoing and unnecessary fear of being left alone or
without attachment figures compulsions in childhood and adolescence is very similar
to that seen in adults, there are some differences between
e¢ Ongoing aversion to going to sleep alone or sleeping
boys and girls, with boys having an earlier age of onset
away from home
than girls (Garcia, Freeman, Himle, Berman et al., 2009),
e Repeated nightmares around separation girls exhibiting more hoarding compulsions than boys,
¢ Complaints of physical symptoms such as headaches but boys being more likely to have sexual obsessions than
or nausea when separated or anticipating separation girls (Mataix-Cols, Nakatani, Micali & Heyman, 2008).
from attachment figures Case History 16.2 provides a typical example of the
e The anxiety lasts at least 4 weeks in children and development of OCD in a 13-year-old adolescent boy and
6 months in adults demonstrates how rapidly OCD symptoms can manifest
and establish themselves in childhood, which is in some
e The disturbance causes significant impairment in impor-
tant areas of functioning contrast to the gradual acquisition found in adulthood.
Age of onset for childhood OCD can be as early as
e The disturbance is not better explained by another men-
3-4 years of age but the mean age of onset is more
tal disorder
likely to be around 10 years (Swedo, Rapoport, Leonard,
CHILDHOOD AND ADOLESCENT OCD

Andy was a 13-year-old boy diagnosed with isolated testicular relapse of acute lymphoblastic leukaemia 40 days
before coming to psychiatric attention. He was first diagnosed with acute lymphoblastic leukaemia at age 10.
After his initial diagnosis, he experienced remission at the end of chemotherapy induction and finished his treat-
ment for the disease.
Three years later he began further drug treatment for his leukaemia and the psychiatric consultation liaison
service evaluated him after he expressed bothersome obsessive thoughts, compulsive behaviors and insomnia
beginning 24-36 hours after he had completed a 28-day course of steroid drug treatment. Andy had no history
HISTORY
CASE
16.2 of psychiatric illness or treatment.
At his initial interview, Andy described increasingly bothersome obsessions over the previous 2 days. He felt
that he was ‘going crazy’ and feared that he would forget how to talk and lose his cognitive abilities. He repeated
mantras, reassuring himself that if he remained calm, these bothersome thoughts would pass. He sought reas-
surance from his mother and the interviewers, and he repeated the ‘ABCs’ to reassure himself that he could think
clearly. His mood was dysphoric, which he attributed both to insomnia and worry surrounding his constant
bombardment of unwanted thoughts. He reported no depressive symptoms, perceptual disturbances or suicidal
thoughts. He displayed no manic symptoms.
Andy's symptoms rapidly worsened within 24 hours. His thoughts became dominated by fears that he would
be condemned to hell and that he deserved this fate. He noted images in his mind of self-harm and harming fam-
ily members. He struggled against these thoughts and images, as well as guilt from having them, by repeatedly
telling family members that he loved them. He continued to deteriorate and struck himself in the head with the
blunt end of an ax. He stated that he had no desire to die but had become convinced of the validity of the emerg-
ing thoughts that he should harm himself. Although he did not sustain serious injury, he was admitted to a child
and adolescent psychiatric inpatient unit for safety.
Clinical Commentary
Andy’s symptoms are typical of many adolescents suffering OCD. In his case, these are obsessive thoughts
about going mad and harming himself and others. In an attempt to try and prevent his obsessive
thoughts entering consciousness, he indulges in protective behaviours, such as repeating mantras, seeking
reassurances from adults and reciting the alphabet. The symptoms appear to be precipitated by a stress-
ful illness, and such stressors are common precursors of OCD symptoms in both children and adults. OCD
symptoms would normally appear very slowly and have a gradual onset, unlike Andy’s which appeared very
rapidly over a period ofa few weeks. Such rapid acquisition may have been facilitated by the abrupt cessa-
tion ofsteroid drugs that he was receiving as part ofhis treatment for leukaemia.
Source: Adapted from Morris, D.R., Meighen, K.G. & McDougle, C.J. (2005). Acute onset of obsessive-compulsive disorder in
an adolescent with acute lymphoblastic leukemia. Psychosomatics, 45(5), 458-460, with permission.
Lenane & Cheslow, 1989). Childhood OCD is regularly and 50 per cent of children with Tourette’s syndrome subse-
found to be comorbid with a range of other disorders, quently develop OCD (Leckman, 1993). This suggests that
including tic disorders, Tourette’s syndrome, other anxiety childhood OCD and tic disorder may be different manifes-
disorders and eating disorders (Geller, Biederman, Griffin, tations of the same underlying disorder (Swedo, 1994) (see
Jones & Lefkowitz, 1996). Specifically, over 60 per cent Focus Point 16.1).
jisorders Uncontrollable physical of children seeking treat-
yements such as facial twitches, rapid ment for OCD symptoms Generalized anxiety disorder (GAD) In children,
king or twitches of the mouth. also have a lifetime history as in adulthood, GAD usually takes the form of antici-
rette’s syndrome Adisorderinwhich of tics or Tourette’s syn- patory anxiety, in which the main feature is chronic
‘or and vocal tics occur frequently drome (Leonard, Lenane, worrying about potential problems and threats (see
ughout the day for at least 1year. Swedo, Rettew et al., 1992) section 6.4). Even in childhood, GAD is differentiated
546 PSYCHOPATHOLOGY
CHILDHOOD OCD, TIC DISORDER AND TOURETTE’S SYNDROME

Tourette’s syndrome (also known as Tourette's or TS) is Lowerison et al., 2012). Tic disorders are relatively com-
a disorder with onset in childhood, characterized by mon in children, with a point prevalence of transient
the presence of multiple physical (motor) tics and at tic disorder of 2.99 per cent. Tourette's disorder is less
least one vocal (phonic) tic. It is important to under- common, with a point prevalence of only 0.77 per cent
stand that these are chronic and involuntary. Someone (Knight, Steeves, Day, Lowerison et al., 2012).
with TS may be able to suppress them for a period but Tourette’s syndrome and behavioural tics are
eventually they have to let the tics out. often comorbid with a diagnosis of OCD in childhood.
POINT
FOCUS
16.1
Tics usually start in childhood around the age of Studies suggest that up to 60 per cent ofchildren seek-
7 and are likely to persist throughout life, though the ing treatment for OCD have a lifetime history of tics
symptoms often decrease towards the end of ado- (Leonard, Lenane, Swedo, Rettew et al., 1992) and some
lescence. The first symptoms theorists believe that OCD is a heterogeneous disorder
For a video on Tourette's are usually facial tics such as with an inherited component that can manifest either
syndrome go to | rapid blinking or twitches of as OCD obsessions or compulsions, or as behavioural
video/ch16
| the mouth. However, TS may or vocal tics (Pauls, Alsobrook, Goodman, Rasmussen &
start with sounds such as throat Leckman, 1995).
clearing and sniffing, or even OCD symptoms and behavioural and vocal tics can
with multiple tics of movements and sounds. Tics can cause obvious problems for a child, with them being
be either simple or complex. Simple tics are of short a source of anxiety and fear for the sufferer and pro-
duration and may include eye blinks, shoulder shrug- voking ridicule and victimization by peers (Storch,
ging, sniffing, grunting or extensions of the extremi- Ledley, Lewin, Murphy. et a/., 2006). The severity of
ties. Complex motor tics are of longer duration and can behavioural and vocal tics is usually directly related to
consist of combinations of simple tics (e.g. head turn- levels of stress, so learning how to control stress can
ing plus shoulder shrugging). They can often appear greatly reduce symptoms (e.g. by learning relaxation
purposeful when the tic consists of imitating another techniques). In some cases, a less socially acceptable
person’s movements, making tic-like obscene or sexual tic can be replaced with a more socially acceptable one
gestures, or uttering socially unacceptable words. For using behaviour therapy methods and medication can
Tourette's disorder, both motor and vocal tics must also be used to help control the condition. Treatments
be present. Tic disorders are more common in chil- normally used with OCD symptoms (such as exposure
dren than in adults, in special education populations with response prevention or CBT —- see section 6.5.2)
than in general populations of children, and among can also be effective with behavioural tics (Verdellen,
boys more than among girls (Knight, Steeves, Day, Keijsers, Cath & Hoogduin, 2004; Turner, 2006).
hs go Wa lal
from other forms of childhood anxiety by being asso- estimates of GAD in childhood populations, with a
ciated with significantly increased levels of pathologi- UK study estimating GAD in less than 1 per cent of
cal worrying (Tracey, Chorpita, Douban & Barlow, 5—10-year-olds, but an American study reporting 11 per
1997; Wilson, 2010) and cent of 6-11-year-olds meeting the criteria for ‘overanx-
pathological worrying Perseverative
worrying that an individual finds
what a child worries about ious disorder’.
uncontrollable. appears to be determined
by their age. For example, Specific phobias Specific fears and phobias are often
Muris, Merckelbach & Luijten (2002) found that 4~7- common in the normal development of children. For
year olds tended to worry about personal harm, sepa- example, fears of heights, water, spiders, strangers and
ration from parents and imaginary creatures, whereas separation often occur in the absence of individual learn-
11—13-year-olds worried more about social threats and ing experiences and appear to represent characteristics
being punished. The number of worries also increases of normal developmental stages through which the child
with age, with the number of worries reported by passes. A fear may appear suddenly and intensely, but
8-year-olds almost double that reported by 5-year-olds then disappear almost as quickly (Poulton & Menzies,
(Muris, Meesters, Merckelbach, Sermon & Zwakhalen, 2002). However, for some children, a fear may persist
1998). Epidemiological studies have differed in their and become problematic in that it prevents normal daily
functioning. One such example in childhood is social disorders (Trzaskowski, Zavos, Haworth, Plomin &
phobia (social anxiety disorder) and this often begins in Eley, 2012) that may be transmitted by many genetic
childhood as a fear of strangers (Hudson & Dodd, 2011). variants, each with only a modest or small effect in itself
Most children will grow out of this fear by around 2-3 (Trzaskowski, Eley, Davis, Doherty et al., 2013). Finally,
years of age but some still persist with their fear of social a study of 1058 pairs of twins aged 8-16 years by Lau,
situations and may find it very difficult to speak to stran- Eley & Stevenson (2006) further implies that levels of
gers or to be in the presence of strangers. If pushed into state anxiety (anxiety experienced at the moment) are
social situations, they will often become mute, blush, largely determined by environmental factors but trait
withdraw or show extreme emotional responses (e.g. anxiety (representing a more longer term sensitivity to
burst into tears) (Vasey, 1995). However, children and anxiety) showed moderate genetic effects.
adolescents with social anxiety disorder are usually well
adjusted in all other situations that do not involve signifi- Trauma and stress experiences ‘Table 16.1 pro-
cant social interaction (e.g. at home) and this differs from vides striking examples of how childhood trauma and
separation disorder in that the latter is characterized by stress represent significant risk factors for a range of
clinging and demanding behaviour at home. later diagnosable adult psychological disorders. It is also
The prevalence for specific phobias in 8-9-year-olds self-evident that these experiences will inevitably cause
is estimated to be around 7 per cent for boys and 10 per significant psychological stress during childhood (see
cent for girls (Lichtenstein & Annas, 2000) but up to Frank’s story at the beginning of this chapter). Many of
76 per cent of adolescents in some cultures report at least these experiences (such as childhood physical and sexual
one fear and up to 36 per cent meet the lifetime criteria abuse) represent extreme experiences for any individual
for specific phobia, indicating that specific phobias are a and there are clear links between such experiences and
common and enduring problem during childhood and childhood anxiety generally (e.g. Feerick & Snow, 2005;
adolescence (Benjet, Borges, Stein, Mendez & Medina- Whiffen & MacIntosh, 2005). However, during child-
Mora, 2012). hood, even many experiences that seem relatively unex-
ceptional may seem stressful to a child who is relatively
The aetiology of childhood and inexperienced in the world and these can provide signifi-
adolescent anxiety problems cant events that trigger bouts of anxiety and distress. For
Childhood anxiety and its associated disorders appear to example, living with illnesses such as asthma or eczema
result from a combination of inherited factors and child- has been shown to significantly increase childhood anxi-
hood experiences. Children inherit a temperament that ety and reduce quality of life (Lewis-Jones, 2006; Gillaspy,
may make them more or less vulnerable to life stress- Hoff, Mullins, van Pelt & Chaney, 2002), and the death
ors such as inadequate parenting or physical trauma. In of a pet — with whom a child may become significantly
addition, children seem to be particularly vulnerable to attached — can cause prolonged anxiety and depression
learning fear and anxiety through indirect routes, such (Kaufman & Kaufman, 2006). Even an event such as a
as information from adults, peers, TV and so on (Field, minor road traffic accident may be a new and frighten-
2006a). Finally, we also need to be aware that the kinds ing experience to a child, and a common consequence
of life events that might mean relatively little to an adult of such an experience in childhood is a mixture of PTSD
can be viewed as extremely stressful for a child — these symptoms, anxiety and depression (Schafer, Barkmann,
include such events as the death of a pet, an illness, start- Riedesser & Schulte-Markworth, 2006).
ing school or moving house.
Modelling and exposure toinformation Whether
Genetic factors Twin and familial studies of child- it is in school, at home or through the media, young chil-
hood anxiety disorders tend to indicate a significant and dren are regularly exposed to information about potential
stable inherited component. In a familial study of child- threats and dangers. Children are bombarded with vio-
hood OCD, Pauls, Alsobrook, Goodman, Rasmussen & lent and threatening images on television and are being
Leckman (1995) found that rates of OCD were signifi- constantly warned about the dangers of sexual molesta-
cantly greater in the first-degree relatives of children tion, abduction or drugs. Recent experimental evidence
with OCD than the relatives of control participants with- suggests that information of this kind may be an impor-
out OCD. However, the inherited component appeared tant source of childhood fears. Field and his colleagues
to be non-specific, since children with OCD were just as have developed a valuable experimental procedure for
likely to have first-degree relatives with behavioural tics studying how information about a stimulus or event
as with specific OCD symptoms. More recent twin stud- might cause subsequent fear and anxiety. Children are
ies of anxiety disorders in 7-9-year-olds have suggested shown pictures of animals they are unfamiliar with (e.g.
a stable heritability averaging 54 per cent across anxiety rare Australian marsupials; Photo 16.1) and then given
548 PSYCHOPATHOLOGY
some information about that animal. Some participants about a stimulus or event — especially if it is provided
may be told the animal is benign and friendly, while oth- by an authoritative source such as an adult — can cause
ers may be told it is scary and dangerous. In a study with changes in fear beliefs and behavioural avoidance that
79-year-old children, Field, Argyris & Knowles (2001) are relatively long lasting (up to at least 6 months).
found that fear beliefs about an animal increased signifi-
cantly if the children had been given negative informa- Parenting style Children are highly dependent on
tion about the animal — but only if that information had their parents or carers for guidance and emotional sup-
been provided by an adult and not by a peer. Subsequent port during their development, so it is not surprising that
studies have indicated that the fear generated by nega- dysfunctional forms of parenting may cause psychologi-
tive information can be detected using both explicit cal and adjustment problems during childhood. Parents
and implicit measures of fear, will result in behavioural may be detached, rejecting, overly controlling, overpro-
avoidance of the animal, and can still be detected up to tective or demanding, and each of these different parent-
6 months later (Field & Lawson, 2003; Field, Lawson & ing styles may cause anxiety and maladjustment in the
Banerjee, 2006). In addition, studies indicate that the child. Research into how parenting style may influence
child’s levels of trait anxiety will facilitate the learning childhood anxiety is relatively underdeveloped at pre-
of fear in such situations by increasing biases to attend to sent. However, some studies do suggest links between
stimuli associated with threat information (Field, 2006b). overprotective and overanxious parenting and a child
Studies such as these indicate that negative information who is overanxious or suffers separation anxiety (Rapee,
1997; Giotakos & Konstantopoulos, 2002). This appears
to result from the parents’ overprotectiveness generating
a lack of confidence and feelings of inadequacy in the
child (Dadds, Heard & Rapee, 1991; Woodruff-Borden,
Morrow, Bourland & Cambron, 2002). Specifically,
Rapee (2001) has argued that there may be a reciprocal
relationship between child temperament and parenting
whereby parents of children with an anxious tempera-
ment are more likely to become overly involved with
the child in an attempt to reduce the child’s distress.
However, this over-involvement is likely to increase the
child’s vulnerability to anxiety by increasing the child’s
perception of threat, reducing the child’s perceived con-
trol over threat, and increasing avoidance of threat (e.g.
Gallagher & Cartwright-Hatton, 2009). Hudson & Rapee
(2002) provided some experimental support for this view
by reporting that mothers of children with an anxiety
disorder were more likely to be intrusive while the child
was completing a puzzle task than were mothers of non-
anxious control children.
While overprotective parents appear to generate
anxiety in their children, so do parents who are reject-
ing and hostile. Children who experience rejecting or
detached parents also show increased levels of anxi-
ety and are often overly self-critical and have poor self-
iStock.com/CraigRJD
©
PHOTO 16.1 Are you frightened ofthis animal? Professor esteem (Chartier, Walker & Stein, 2001; Hudson &
Andy Field has developed a procedure for investigating how Rapee, 2002). For example, anxiety sensitivity (concern
exposure to information about potential threats affects over the physical symptoms of anxiety, such as trem-
fear acquisition in children. This photo shows an Australian bling or shaking) is known to be a factor that mediates
Quoll — an animal not well known to most children in the emotional distress in both adulthood and childhood, and
northern hemisphere. Some are then told they are potentially this has been linked to exposure to parental threatening,
dangerous and others told that they are harmless and benign. hostile and rejecting behaviours (Scher & Stein, 2003).
Children told they are dangerous subsequently fear them Most recently, studies have investigated the differential
more and avoid possible contact with them in experimental effects on childhood anxiety that might be made sepa-
approach tasks, and this fear can often last up to 6 months. rately by mothers and fathers. Moller, Majdandzic,
de Vente & Bogels (2013) have argued that the evolved movement) and hypersomnia (excessive sleeping) are
basis of sex differences in parenting means that moth- more common in adolescents.
ers and fathers will convey different aspects of anxiety Rates of depression in children are variable and
to their offspring. Mothers will tend to transmit cau- can depend on age. Studies suggest a prevalence rate
tion and information about threat (with overly anxious of less than 1 per cent in pre-schoolers (Kashani &
mothers transmitting more anxiety to their offspring), Carlson, 1987) and between 2 and 3 per cent for school-
whereas fathers may be more likely to teach their off- age children (Cohen, Cohen, Kasen, Valez et al., 1993;
spring how to explore the environment and compete Lewinsohn, Hops, Roberts, Seeley & Andrews, 1993).
with others (and in doing so, reduce anxiety). This rises to between 4 and 8 per cent for adolescents
Clearly, parenting style is likely to be an important fac- (Birmaher, Ryan, Williamson, Brent & Kaufman,
tor influencing the development of anxiety symptoms in 1996). As we mentioned earlier, lifetime prevalence
children. Both overprotective and overly rejecting styles rates for depression in adolescents is estimated to be
appear to have adverse effects and facilitate anxiety and as high as 25-28 per cent (Lewinsohn, Rohde & Seeley,
its cognitive and behavioural correlates (e.g. hypervigi- 1998; Kessler, Avenevoli & Merikangas, 2001). There
lance for threat, avoidance behaviour, and suchlike). are also some gender differences in adolescence, with
Further research is clearly required in this area to clarify depression occurring at around 6 per cent for girls and
the various mechanisms by which such parenting styles 4 per cent for boys (Costello, Erkanli & Angold, 2006).
have their effects. In addition, depressed girls more often report weight/
appetite disturbances and feelings of worthlessness/
guilt than depressed boys (Lewinsohn, Rohde & Seeley,
1998). Lewinsohn, Roberts, Seeley, Rohde et al. (1994)
16.3.2 Childhood and estimated that the mean duration of major depression in
Adolescent Depression adolescence was 26 weeks, with longer durations associ-
ated with earlier onset and suicidal ideation. Estimates
Depression in childhood is notoriously difficult to iden-
suggest that around 1-2 per cent of adolescents will have
tify and parents and teachers regularly fail to recognize its
made a suicide attempt between the ages of 14 and 18
symptoms — especially in very young children (Tarullo,
years (Lewinsohn, Rohde & Seeley, 1998) and many will
Richardson, Radke-Yarrow & Martinez, 1995). In early
also self-harm (see section 7.3).
childhood, depression will manifest as clingy behaviour,
Childhood depression is highly comorbid with other
school refusal and exaggerated fears, and is also associ-
psychopathologies and around half of adolescents diag-
ated with an increased frequency of somatic complaints
nosed with depression will experience at least one other
such as stomach aches and headaches. However, as they
disorder during their lifetime. Twenty per cent of ado-
reach puberty and early adolescence, as many as 28 per
lescents with depression will be diagnosed with another
cent of them, aged up to 19 years, will have experienced a
anxiety disorder and between 13 and 30 per cent will also
diagnosable episode of depression (Lewinsohn, Rohde &
exhibit a substance use disorder (e.g. alcohol or drug
Seeley, 1998). In adolescence, depression will manifest as
abuse) (Lewinsohn, Rohde & Seeley, 1998). In addition,
sulkiness, withdrawing from family activities, weight dis-
pre-adolescent depression has been found to be a risk fac-
turbance, loss of energy, feelings of worthlessness and
tor for earlier onset of alcohol use in adolescence (Wu,
guilt, and — in extreme cases — suicidal ideation (Roberts,
Bird, Liu, Fan et al., 2006). Comorbid depression has a
Lewinsohn & Seeley, 1995). The following sections
number of serious negative consequences for children
cover the diagnosis and prevalence of childhood depres- and adolescents. It has been shown to adversely affect
sion, and then we will cover some of the theories of its
academic performance; it impairs social functioning gen-
aetiology. erally, when sufferers may be rejected by their peers; it
is associated with increased conflict with parents; and
The diagnosis and prevalence of childhood it increases the risk of suicide attempts (Lewinsohn,
and adolescent depression Rohde & Seeley, 1995).
With some minor amendments, the diagnostic criteria
for depression in childhood are essentially the same as The aetiology of childhood and
those specified for adult major depression (see DSM-5 adolescent depression
Summary Table 7.1). However, some of the symptoms Childhood depression appears to have only a modest
may change with age. Somatic complaints, irritability genetic component, so early experience appears to be a
and social withdrawal are prominent in younger chil- more significant contributor to the disorder. As a result,
dren but psychomotor retardation (slowed thinking and interest in the aetiology of childhood depression has
550 PSYCHOPATHOLOGY
focused mainly on early experiences, parent-child inter- adolescent depression, and this includes factors such
‘as
actions and cognitive factors. We will begin by review- financial hardship and chronic illness (Hazel, Hamman,
ing the risk factors for childhood depression and then Brennan & Najman, 2008).
assess the evidence for biological and psychological
influences. TABLE 16.3 Risk factors for adolescent depression
Risk factors of childhood depression Table 16.3 Domain Specific risk factor
provides an overview of the risk factors known to be
Cognitive Depressive negative cognitions
associated with depression in adolescents and these range Depressive attributional style
across (1) dispositional factors and existing psychological
problems, (2) stress experiences, (3) poor coping skills, Dispositional Self-consciousness
factors and other Low self-esteem
(4) poor social support, (5) physical health problems, and
psychopathologies Emotional reliance
(5) poor academic performance — and the greater the Current depression
number of these risk factors experienced by an adoles- Internalizing problem behaviours
cent, the greater the probability that he/she will become Externalizing problem behaviours
depressed in the future (Lewinsohn, Rohde & Seeley, Past suicide attempts
1998). Taking the relevant risk factors into account, Past depression
Lewinsohn, Rohde & Seeley (1998) have drawn up a Past anxiety
profile of the ‘prototypical adolescent most at risk for Stress Daily hassles
depression’. This is described in Focus Point 16.2. Major life events
In younger children, childhood abuse or neglect is Social and Low self-rated social competence
closely related to the development of depression and coping skills Poor coping skills
appears to generate feelings of worthlessness, betrayal, Interpersonal conflict with parents
loneliness and guilt (Dykman, McPherson, Ackerman,
Social support Low social support from family
Newton et al., 1997; Wolfe & McEachran, 1997). In addi- Low social support from friends
tion, predictors of depression in children younger than
Physical Physical illness
5 years of age include parental marital partner changes,
Poor self-rated health
mother’s health problems in pregnancy, the child’s health Reduced level of activities
over the first 6 months of life, maternal anxiety and mari- Lifetime number of physical symptoms
tal satisfaction early in the child’s development and the Current rate of tobacco use
mother’s attitude towards caregiving (Najman, Hallam,
Academic School absenteeism
Bor, Callaghan et al., 2005). Many of these risk factors may Dissatisfaction with grades
affect the quality of mother-child interactions during
Source: Lewinsohn, P.M., Rohde, P. & Seeley, J.R. (1998). Major depres-
early development and these may be a significant factor
sive disorder in older adolescents: Prevalence, risk factors, and clinical
in the development of childhood depression. Childhood implications. Clinical Psychology Review, 18, 765-794. Reproduced with
adversity generally is also a risk factor for childhood and permission.
Be THE PROTOTYPICAL ADOLESCENT MOST AT RISK FOR DEPRESSION

Ke)
=~
- Lewinsohn, Rohde & Seeley (1998, p.778) have pro- overly dependent on others, although she feels
= vided the following description of the prototypical that she is receiving little support from her family.
.°) adolescent most at risk for adolescent depression: She is experiencing both major and minor stress-
oa. ors, such as conflict with parents, physical illness,
74) The prototypical adolescent most likely to become
~ poor school performance, and relationship break-
U depressed is a 16-year-old female who had an early ups; she is coping poorly with the ramifications of
\e) or late puberty. She is experiencing low self-esteem/ these events. Other psychopathologies, including
LL.
poor body image, feelings of worthlessness, pes- anxiety disorders, smoking and past suicidality, are
simism, and self-blame. She is self-conscious and ~ probably present.
Genetic factors Studies of the heritability of child- typical of childhood depression. Unfortunately, many
hood depression have been variable in their findings. parents exhibit symptoms of depression — especially
Family, twin and adoption studies all suggest that in the immediate post-partum period — and this factor
genetic influences on childhood depression may be may be significant in generating internalizing symp-
indirect and have their effects in combination with envi- toms in their infant offspring. For example, Paulson,
ronmental risks (Rice, 2009; Thapar & Rice, 2006) and, Dauber & Leiferman (2006) estimated that 14 per cent
in particular, prepubertal depression is strongly asso- of mothers and 10 per cent of fathers exhibited sig-
ciated with psychological adversity (such as negative nificant levels of depressive symptoms up to 9 months
childhood experiences) and has a significantly lower after the birth of a child. In addition, mothers who
heritability component than adult depression (Rice, were post-partum depressed were less likely to engage
2010). Familial studies have indicated a strong link in healthy feeding and sleeping practices with their
between parental depression and childhood depres- infant and depression in both mothers and fathers was
sion, and a child with a depressed parent is almost associated with fewer positive enrichment activities
four times more likely to suffer childhood depression with the child (e.g. reading, singing songs and telling
than one without a depressed parent (Hammen & stories). Finally, those youths (especially girls) who are
Brennan, 2001). While this is evidence that is consist- the offspring of depressed mothers also show increased
ent with an inherited view of childhood depression, it interpersonal impairment and risk of interpersonal dys-
could also imply that the behaviour of depressed par- function (Hammen, 2012). These romantic and inter-
ents may create adverse early experiences that precipi- personal dysfunctions may not only be a consequence
tate depression in the child (see later). Finally, the fact of depression, they may also intensify and maintain the
that childhood experiences may be significantly more depression (Hammen, 2009).
important than inherited factors in causing childhood As the child grows older, symptoms of depression
depression comes from adoption studies. Such stud- often come to be associated with dysfunctional cognitive
ies have provided little or no evidence for a genetic characteristics that may function to maintain depressed
influence on depressive symptoms in childhood (Rice, behaviour. For example, attributional models of adult
Harold & Thapar, 2002). depression suggest that the depressed individual may
have acquired (1) a pessimistic inferential style (attribut-
Psychological factors Two major areas of research ing negative events to stable, global causes), (2) a tendency
into the aetiology of childhood depression are (1) the to catastrophize the consequences of negative events,
role of parent-child interaction, and (2) the develop- and (3) a tendency to infer negative self-characteristics
ment of dysfunctional cognitions that shape and support (see Chapter 7) (Abramson, Metalsky & Alloy, 1989).
depressive thinking in childhood. Research on cognitive factors in childhood depression
We have already noted that children who have has tended to focus mainly
pessimistic inferential style The attribu-
depressed parents are themselves more prone to depres- on the role of pessimistic tion of negative events to stable, global
sion and this relationship could be mediated in a variety inferential style and how causes,
of ways. First, parents who are depressed may simply this style interacts with
transmit their negative and low mood to their children negative experiences. For example, children with a pessi-
through their interactions with them and children may mistic inferential style have been shown to be more likely
simply model the behavioural symptoms of depression to experience increases in self-reported depressive symp-
exhibited by their parents (Jackson & Huang, 2000). toms following negative events than children who do
Alternatively, depressed parents may not be able to prop- not possesses this inferential style (Hillsman & Garber,
erly respond to their children’s emotional experiences 1995), and a pessimistic inferential style interacts with
and in so doing may leave the child either feeling help- daily hassles (everyday annoyances, like being caught in
less or unable to learn the necessary emotional regula- a traffic jam) to predict increases in depressive symptoms
tion skills required to deal with provocative experiences. (Brozina & Abela, 2006). Such studies suggest that as the
In support of this view, a study of mother-child interac- depressed child develops cognitively, they may develop
tions by Shaw, Schonberg, Sherrill, Huffman et al. (2006) negative ways of construing events that, in conjunction
found that depressed mothers were significantly less with negative experiences, act to maintain depressed
responsive to their children’s expressions of distress than symptomatology. Longitudinal studies have pinpointed
non-depressed mothers. This suggests that depressed a time around 13-14 years of age when depressive attri-
mothers may be less sensitive or less knowledgeable butional styles begin to become stable attributes of the
about their offspring’s emotional distress and this lack individual and may be a risk factor for lifelong depression
of responsiveness may facilitate internalizing symptoms (Cole, Ciesla, Dallaire et al., 2008).
552 PSYCHOPATHOLOGY
%
SELF-TEST QUESTIONS
* Can you name four different types of diagnosable childhood anxiety disorder?
* How might negative information provide a basis for the learning of anxious responding?
* What is the evidence that ‘overprotective parents’ generate anxiety in their children?
* How prevalent is depression in childhood and adolescence?
* Can you name some risk factors that may make individuals vulnerable to adolescent depression?
° What is the pessimistic inferential style and how might it contribute to depression in children and adolescents?
SECTION SUMMARY
16.3 CHILDHOOD AND ADOLESCENT ANXIETY AND DEPRESSION
¢ Childhood anxiety and depression are known generally as internalizing disorders.

® Diagnosable forms of childhood anxiety include separation anxiety, obsessive compulsive disorder (OCD), generalized anxiety
disorder (GAD), specific phobias and social phobia.
® Genetic factors play a relatively nonspecific role in childhood anxiety by determining general levels of temperament
probably transmitted through many gene variants.
® Both trauma and stress experiences, as well as exposure to threat-relevant information, have been shown to cause increases
in anxious-responding.
e An overprotective parenting style may contribute to, or exacerbate, childhood anxiety.
e Asmany as 28 per cent of adolescents up to the age of 19 years may have experienced diagnosable episodes of depression.
e Childhood depression is highly comorbid with other psychological problems and can have detrimental effects on educa-
tional and social functioning.
e Studies suggest a modest genetic component to childhood depression and a substantial environmental component.
® Being reared by a depressed parent may contribute to childhood depression and as the child grows older he or she may
develop a pessimistic inferential style.
16.4 THE TREATMENT relationships (such as issues relating to effective parent-

ing, parent-child communication, or childhood neglect
OF CHILDHOOD and abuse). In addition, treatment will have to be pro-
vided while the child is still a psychologically and physi-
AND ADOLESCENT cally developing organism, and in the context of possible
PSYCHOLOGICAL PROBLEMS ongoing educational, social and familial difficulties. It
can be seen that this multicomponent approach is most
likely to require a coordinated provision of supervision
Many of the treatment methods used with adults have been and treatment which extends across a range of services,
successfully adapted to treat childhood psychological prob- including education, health and social services.
lems. Children and adolescents with psychological problems In the remainder of this section we will look at indi-
will often require a multifaceted approach to treatment, vidual treatment methods that have been applied to
requiring procedures that address one or more of the fol- childhood psychological problems. The emphasis here
lowing: specific symptoms (e.g. enuresis), general emo- is on specific methodologies and how they have been
tional states and cognitions (such as anxiety or suicidal applied. It is important to note that such procedures may
ideation), behavioural problems (such as behavioural often form part of a broader collection of interventions
tics, aggressive and disruptive behaviour), and intrafamily depending on the needs of the individual child.
CHAPTER 16 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS 553"
16.4.1 Drug Treatments when used to treat children have been raised in
both the US and UK, to the extent that official
Drug-based treatments of psychological problems in warnings have been released in relation to the use
childhood and adolescence are becoming more widely of such drugs (Fegert, Janhsen & Boge, 2006).
used as we come to understand the effects that vari-
ous drugs may have on children (Walkup, Labellarte & Despite the difficulties of using pharmacological
Ginsburg, 2002). But the increase in the use of drug treatments with childhood anxiety and depression,
treatments for children has alarmed many. For exam- much greater use has been made of drug treatments in
ple, the paediatric use of SSRIs had risen by over 50 per ADHD. US studies indicate that stimulant medication is
cent between 1994 and 2000 (Moynihan, 2003). Much the most adopted form of treatment for children diag-
of this increase in prescribing has been for childhood nosed with ADHD, with 42 per cent being treated in
and adolescent depression and has often occurred with- this way (Robison, Sclar, Skaer & Galin, 2004), and has
out regulatory approval — so much so that in 2003 the been shown to be superior to placebos in reducing symp-
British Medicines and Healthcare products Regulatory toms (Schulz, Fleischhaker, Hennighausen, Heiser et al.,
Agency (MHRA) banned the use of SSRIs in children 2010). The most common form of stimulant medication
under 18 years of age except for Prozac/ fluoxetine. This is Ritalin (methylphenidate) and this has been used to
was followed by a meta-analysis conducted by the US treat hyperactive children
Food and Drug Administration (FDA) suggesting that since the 1950s. Ritalin is Ritalin (methylphenidate) A stimulant
medication that is used to treat ADHD.
there is an increased risk of suicidal acts with the use an amphetamine that, par-
of both SSRIs and SSNIs in young people up to the age adoxically, has a quietening effect on overactive children,
of 25 years and that in the case of many individuals the decreases distractibility and increases alertness (Konrad,
risks outweighed the benefits of such drugs (FDA, 2007). Gunther, Hanisch & Herpertz-Dahlmann, 2004). We are
However, other recent inclusive meta-analyses seem to still unsure about how drugs such as Ritalin have their
challenge the FDA conclusion and suggest that the ben- beneficial effects but it may be that they act on the neuro-
efits may outweigh the risks of SSRIs when treating a transmitters norepinephrine and dopamine in areas of the
range of childhood problems such as depression and brain that play a part in controlling attention and behav-
non-OCD anxiety disorders (e.g. Bridge, Iyengar, Salary, iour. As we saw in section 16.2.1, children with ADHD
Barbe et al., 2007), so the debate is still open on this issue. appear to have some deficits in attention and executive
Fluoxetine has also been used in the treatment of functioning that may be redressed by the effects that
childhood anxiety disorders (excluding the treatment Ritalin has on neurotransmitter production. Studies have
of childhood OCD) and clinical trials have found it to suggested that amphetamines such as Ritalin are effec-
be effective in reducing anxiety symptoms and improv- tive in reducing the amount of aggressive behaviour in
ing functioning generally (Seidel & Walkup, 2006). children with ADHD (Fava, 1997) and it can significantly
Nevertheless, there are a number of reasons why we facilitate educational progress (Charach, Ickowicz &
should be cautious about recommending the use of drug Schachar, 2004). However, despite these positive effects,
treatments with childhood disorders: there are still some drawbacks to the use of Ritalin with
ADHD. Firstly, while it is effective in reducing symptoms
1. Complete remission of symptoms is rarely in the short term, its longer term effects have not been
found, especially in the treatment of childhood fully documented (Safer, 1997). Secondly, Ritalin also
depression using SSRIs (Treatment for has a number of side effects, including reduced appe-
Adolescents with Depression Study Team, 2004); tite, sleeping difficulties, disruption of growth hormone,
2. SSRIs (whether used for the treatment of memory loss and stomach pains. Thirdly, Ritalin is an
depression or anxiety) have a number of amphetamine and so can also be used as a drug of abuse,
undesirable side effects in children, including and there is evidence of adolescents using Ritalin as a
nausea, headaches and insomnia; recreational drug to obtain a ‘high’ (Kapner, 2003).
3. To date, outcome studies vary considerably in

their trial methodology to the extent that the
safety and so) of such drug treatments
mm, Cannot yet be assured Behaviour therapy is a useful means of changing quite
To read Cheung, Emslie & Maye’s }) (Cheung, Emslie & Mayes, specific behaviours and can provide learning-based inter-
review ofthe efficacy and safety of
antidepressant use, go to
| 2005); and ventions that allow the individual to change old behav-
www.wiley-psychopathology.com/ 4. Doubts about the iour patterns or learn new ones. Examples of how this
reading/ch16
safety of many has been used in the treatment of childhood psychologi-
antidepressant drugs cal problems include (1) the treatment of symptom-based
disorders (such as enuresis), (2) the adaptation of adult and conduct disorder, One view of children with disrup-
behaviour therapy methods (such as systematic desen- tive behaviour disorders is that their disruptive behaviour
sitization) to use with childhood anxiety disorders, and is positively reinforced by the attention it receives from
(3) the development of behaviour change programmes both peers and adults, and this may especially be the case
for children with disruptive behaviour disorders. in the classroom setting. The purpose of introducing a
A widely used classical conditioning method for treat- behavioural programme into such settings would be to
ing nocturnal enuresis is known as the ‘bell-and-battery regularize the reinforcement contingencies in the environ-
technique’ (Mikkelsen, 2001). A sensor is placed in the ment — specifically to ensure that positive behaviours (e.g.
child’s underwear when they go to bed and a single drop attention to the teacher, or thinking through tasks before
bell-and-battery technique A widely of urine will be detected responding) were rewarded
used classical conditioning method for by the sensor and set off and disruptive behaviours time-out (TO) A means of reduc-
treating nocturnal enuresis. an auditory alarm that will were not. Time-out (TO) ing disruptive behaviours, including
wake the child (see Figure 16.2). This method allows the from positive reinforce- aggressiveness, destruction of propert
and non-compliance in the classroom, |
child to associate the alarm (the unconditioned stimulus, ment has been found to be
by removing the child from the situatio
UCS) with the sensation of a full bladder (the conditioned an effective means of reduc- and directing him or her, for example,
stimulus, CS), so that the child eventually learns to wake up ing disruptive behaviours, to sit in a specific time-out chair
when he/she experiences a full bladder. including aggressiveness, for periods of between 5 and
15 minutes.
Specific behaviour therapy techniques such as system- destruction of property
atic desensitization (see section 4.1.1) can also be success- and non-compliance in the
fully adapted to treat anxiety-based problems in children classroom (Fabiano, Pelham, Manos, Gnagy et al., 2004). In
(King, Muris, Ollendick & Gullone, 2005), although in vivo this case, the time-out consisted of the child merely sitting
methods appear to be significantly more successful than in a specific time-out chair in the classroom for periods of
‘imaginal’ desensitization, where the child has to imag- between 5 and 15 minutes. Other studies have established
ine being in fearful situations. Sturges & Sturges (1998) the effectiveness of ignoring non-attention in the classroom
report the successful use of systematic desensitization to (called ‘off-task’ behaviour) and of rewarding all behaviours
treat an 11-year-old girl’s elevator phobia. Following an that may contribute to the learning task in hand by praising
injury to her hand in an elevator door, she refused to ride the child. Such behaviours that would be reinforced might
in elevators. The clinicians developed a behavioural hier- include pausing for thought rather than impulsively begin-
archy in which the sequential steps involved approaching ning a task or communicating appropriately with peers and
and entering an elevator while reciting self-calming state- teachers (Stahr, Cushing,
ments that she had agreed with the therapists. The child Lane & Fox, 2006). behaviour management techniques
Treatment methods that can be used 7
very quickly resumed elevator use with no reoccurrence Finally, behaviour man- a range of environments and can even
of anxiety up to 1 year later. agement techniques can be taught to parents as an aid to control:
Selective reinforcement techniques have been used to be used in a range of envi- ling and responding to their children in
facilitate academic achievement in children with ADHD ronments and can even be he home.
1 2 3 4
drops of urine signal to alarm unit DRI Sleeper® alarm sounds child wakes up
(by wire or radio signal) ~—sAlarm unit §
a % >
+4 AA :
)J A
ee See 3
Urosensor™ é Trainsthe =
brain to wake ©©)
FIGURE 16.2 Bell-and-battery technique.
Drops of urine on the sensor pad set off an alarm that wakes the child; this enables the child with nocturnal enuresis to learn to associ-
ate a full bladder with waking up.
CHAPTER 16 CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS 555 _
taught to parents as an aid to controlling and responding 1982). In this context, you may also want to have
to their children in the home. For example, teaching par- a look at Treatment in Practice Box 10.1, where
ents to identify and reward positive behaviour also helps to Sandy — suffering from anorexia — may be using her
prevent parents from focusing on the negative and disrup- eating problems as a means of distancing herself
tive behaviours exhibited by children with both ADHD and from her parents’ conflicts and marriage problems.
conduct disorder. This has the effect of facilitating adaptive
behaviour in the child and reducing the parent's negative These various forms of family therapy have been
feelings towards the child (Kazdin & Weisz, 2003). used with children with conduct disorder, ADHD, child-
hood depression, anxiety problems and eating disorders.
Meta-analyses of systemic and family therapies generally
16.4.3 Family Interventions conclude that family interventions have a positive effect
when compared with no treatment and some alternative
Family interventions are popular forms of treatment treatments (Hazelrigg, Cooper & Borduin, 1987) and a
for many childhood psychological problems, especially meta-content analysis of 47 randomized controlled out-
because many aetiological models of childhood psycho- come studies found that systemic family therapy was
logical problems focus on parent-child relationships as effective for treating children with eating disorders, con-
one possible cause of the symptoms. Family interven- duct problems and substance use disorders (von Sydow,
tions take a number of forms. Beher, Schweitzer-Rothers & Retzlaff, 2006). However,
few studies are yet of sufficient methodological rig-
1. Systemic family therapy is based on the
our to enable us to make definite statements about the
view that childhood problems result from
longer term efficacy of family therapies; sample sizes
inappropriate family structure and organization,
are small, the age ranges
and the therapist is
of participants are varied
2mic family therapy A family concerned with the To read Cottrell & Boston's review of
and there is often a lack of |
vention technique based on the view boundaries between the effectiveness of family therapy go to
childhood problems result from inap- proper randomization in www.wiley-psychopathology.com/

parents and children reading/ch16
riate family structure and organiza- these studies (Cottrell &
The therapist is concerned with the as well as the ways in
Boston, 2002).
idaries between parents and children, which they communicate
the ways in which they communicate. (Minuchin, Rosman &
Baker, 1978).
16.4.4 Cognitive Behaviour
2. Parent management training attempts to
teach parents to modify their responses to their Therapy (CBT)
children so that acceptable rather than antisocial CBT is becoming an increasingly useful treatment
behaviours are reinforced and this is used method for children and adolescents, and especially those
especially with the families of children diagnosed suffering from anxiety and depression. CBT is mainly
with conduct disorder used with adolescents and has been shown to signifi-
nt management training (Kazdin, 2006). This cantly reduce symptoms of depression (Brent, Holder,
apeutic intervention which attempts to
method has been shown Kolko, Birmaher et al., 1997) and anxiety (Manassis,
1 parents to modify their responses
eir children so that acceptable to effectively decrease Mendlowitz, Scapillato, Avery et al., 2002). When used
+r than antisocial behaviours are antisocial behaviour and to treat adolescent depression, the purpose of CBT is to
orced and this is used especially with _ has long-term beneficial help the depressed individual become aware of pessimis-
amilies of children diagnosed with effects (Dishion & tic and negative thoughts, depressive beliefs and causal
luct disorder.
Andrews, 1995; Brestan & attributions in which the adolescent blames themselves
Eyberg, 1998). for failures but does not take the credit for successes.
3. Functional family therapy (FFT) incorporates Once these thoughts have been identified, the client is
elements of systemic family therapy and CBT. This taught how to substitute more realistic and constructive
approach views childhood problems as serving cognitions for the dysfunctional ones. A further goal of
a function within the family: they may represent the therapy is to increase the client’s engagement with
maladaptive ways of regulating distance or behaviours that will elicit positive reinforcement (e.g.
intimacy between other family members and this Rohde, Feeny & Robins, 2005). Other important com-
type of therapy attempts ponents of CBT for adolescent depression that help the
tional family therapy (FFT) A family efficacy of such treatments include (1) increasing and
to change maladaptive
d intervention which focuses on
interactional patterns and improving social interactions, (2) improving problem-
gthening relationships in the family
ening up communication between improve communication solving skills, (3) improving goal-setting and attainment
its and children. (Alexander & Parsons, skills, and (4) involving parents closely in the therapy
556 PSYCHOPATHOLOGY
(parents are often the ones who refer their children for family-based interventions already show much promise
treatment and ensure treatment attendance, and they (Cartwright-Hatton, McNally, Field, Rust et al., 2011).
may contribute to the child’s depression through their
own problems and difficulties) (Curry & Wells, 2005). 16.4.5 Play Therapy
CBT for anxious children is also constructed to enable
the child to become aware of problematic thoughts and Play therapy covers a useful set of techniques that can be
feelings (Kendall, Kane, Howard & Siqueland, 1990). A used with younger children who are less able to communi-
typical treatment programme involves (1) recognition of cate and express their feelings verbally (Carmichael, 2006).
anxious feelings and somatic reactions, (2) understanding Play in itself can have curative properties and can enable
the role of cognitions and self-talk in exacerbating anx- children to feel less anxious or depressed. However, it can
ious situations, (3) learning the use of problem-solving also be used to help children express their concerns, to
and coping skills to manage anxiety, (4) using self- control their behaviour (e.g. by learning restraint when a
evaluation and self-reinforcement strategies to facilitate child is impulsive or aggressive) and to learn coping strate-
the maintenance of coping, and (5) implementing a plan gies and adaptive responses when experiencing stress (e.g.
of what to do in order to cope when in an anxious situa- Pedro-Carroll & Reddy, 2005; Gil, 1991). Through play
tion. CBT has been successfully used to treat a range of therapy, children develop a positive relationship with a
childhood anxiety disorders, including OCD, GAD, spe- therapist, learn to communicate with others, express feel-
cific phobias, social phobia and separation anxiety, and ings, modify behaviour, develop problem-solving skills,
has been used with children aged between 8 and 18 years and learn a variety of ways of relating to others. As such,
(Chu & Kendall, 2004; O’Kearney, Anstey & von Sanden, play therapy has been used play therapy A range of play-based the
2006). Long-term follow-up studies suggest that treat- in a range of mental health peutic and assessment techniques that
ment gains are maintained over 3 years after treatment contexts to control anger, be used with younger children who are —
less able to communicate and express t
(Kendall & Southam-Gerow, 1996). CBT for childhood deal with grief and loss,
feelings. —
anxiety appears to be equally as effective as medication divorce and family prob-
alone (O’Kearney, Anstey & von Sanden, 2006) and fam- lems, crisis and trauma, and
ily psychoeducation alone (Kendall, Hudson, Gosch has proven useful across a range of childhood psychologi-
et al., 2008) but is less effective for children under 4 years cal problems including anxiety, depression, ADHD, con-
of age (Rapee, Abbott & Lyneham, 2006). More recent duct disorder, autism and learning disorders (see Chapter
developments include computerized CBT for children 17) (Landreth, 2002; Bratton, Ray, Rhine & Jones, 2005).
and adolescents (Stallard, Richardson, Velleman & Teenagers and adults have also benefited from play ther-
Attwood, 2011), CBT for violent behaviour in chil- apy methods and the use of these techniques has increased
dren (Ozabaci, 2011) and childhood insomnia (Paine & with these client groups in recent years (Pedro-Carroll &
Gradisar, 2011). Finally, family interventions can also be Reddy, 2005). Treatment in Practice Box 16.1 provides a
used successfully to teach parents how to use basic CBT couple of detailed examples of play therapies and more
procedures to address their children’s anxiety and such can be found in Hall, Kaduson & Schaefer (2002).
CLINICAL PERSPECTIVE: TREATMENT IN PRACTICE 16.1 7

PLAY THERAPY
Play therapy is a term used to cover a range of therapies

that build on the normal communicative and learning
processes of children. Clinicians may use play therapy
to help a child articulate what is troubling them, to
control their behaviour (e.g. impulsive or aggressive
behaviour), and to learn adaptive responses when the
child is experiencing emotional problems or skills defi-
cits. Below are two examples of specific play therapies,
one designed to help children practice self control
Jennifer
Harrison
© (the ‘Slow Motion Game’) and the other to enable chil-
Therapist playing with a child using puppets. Child dren to communicate any distress they are feeling (the
posed by model. ‘Puppet Game’).
THE SLOW MOTION GAME USING A PUPPET TO CREATE A SYMBOLIC CLIENT
Therapeutic rationale Therapeutic rationale

It is well known that children learn best by doing. The Puppets serve a crucial role in play therapy. Frequently,
Slow Motion Game (by Heidi Kaduson; see Kaduson & children project their thoughts and feelings onto pup-
Schaefer, 2001, pp.199-202) was designed to have chil- pets. In this way, puppets allow children the distance
dren actively practise self-control over their movements needed to communicate their distress. Furthermore, the
in a playful group context. puppets serve as a medium for the therapist to reflect
understanding and provide corrective emotional experi-
Description ences in the context of the children’s play. Most children
Materials needed: stopwatches for each child, cards naturally project their experiences onto the puppets.
(see below), dice, poker chips, paper and colouring However, some children are too fearful and withdrawn to
materials. become involved in any aspect of therapy. By using the
To begin, the therapist introduces the concept of self- puppet as a symbolic client (a game created by Carolyn J.
control, discussing how it is very difficult to maintain Narcavage; see Kaduson & Schaefer, 1997, pp. 199-203),
self-control when we are moving too fast. Next, the chil- the therapist is able to engage these children and over-
dren are asked to illustrate what fast moving looks like. come resistance. The creation of the symbolic client
Once it is clear that the children understand the concept removes the focus from the child, thereby increasing the
of self-control, each child is given a stopwatch. In the child’s comfort level and allowing him or her to remain at
centre of the table are cards created by the therapist a safe emotional distance.
with various scenes that the children must act out in
slow motion. For example, playing soccer, doing jumping Description
jacks or taking a maths test. The children are instructed Materials needed: puppets.
to roll their dice to see who goes first. The highest num- Once the therapist recognizes that the child is fright-
ber goes first and that child picks a card and goes to the ened, the therapist might show the child a puppet, remark
front of the room with the therapist. The therapist tells the that it is frightened, and reassure it of its safety. Next, the
group what that child is going to do in‘very slow motion’. therapist should enlist the help of the child in comfort-
On the count of three, all of the children start their stop- ing the puppet. By completing these few simple steps, the
watches. Every 10 seconds, the group reports to the therapist has achieved three essential goals: the therapist
child performing the task how much time has passed. has (1) responded and empathized with the child's feelings
When the child has reached a full minute, the group in anon-threatening manner, (2) begun the child's participa-
yells ‘Stop. Having successfully completed the task, the tion in therapy, and (3) started fostering a positive therapeu-
child receives a poker chip. Then the next child (work- tic relationship with the child. The puppet often becomes a
ing in a clockwise direction) picks a card and the game safety object for the child throughout therapy.
starts again. Once each child has had a turn, the time is
increased to 2 minutes and the second round begins. At
Applications
the end of the second round, each player will have two
This technique is particularly effective for any child
chips each and a snack or treat is provided as a reward.
between 4 and 8 years of age who is anxious or with-
The therapist can also give each child a certificate for drawn in the beginning stages of therapy. A variation of
‘Achievement in Slow Motion’ this technique would be to have the puppet present with
the same problem as the child and to enlist the child’s help
Applications in brainstorming solutions to solve the puppet’s problem.
The Slow Motion Game is successful with any group of
children that has difficulty maintaining self-control. Also, Source: From, Hall, Kaduson & Schaefer (2002). Fifteen effec-
common board games can be effectively used to increase tive play therapy techniques. Professional Psychology: Research
children’s self-control. For example, Jenga, Operation, and Practice, 33, 515-522. American Psychological Association.
Perfection and Don’t Break the Ice. Reproduced with permission.
There has been some criticism of play therapy in better after therapy than those who have had no treat-
the past, with critics suggesting that it lacks an ade- ment (Bratton, Ray, Rhine & Jones, 2005). Play therapy
quate research base to justify its use (Reade, Hunter & also appears to be effective across modalities, settings,
McMillan, 1999; Campbell, 1992). However, more age and gender, and has positive effects on children’s
recent meta-analyses of outcome studies suggest that behaviour generally, their social adjustment and their
children treated with play therapy function significantly personality.
558 _ PSYCHOPATHOLOGY
ba
SELF-TEST QUESTIONS
* What drugs are used in the treatment of ADHD and childhood depression? What are the risks of using such drugs?
° What is the evidence that SSRIs and SSNIs are dangerous for children and adolescents below the age of 18 years?
* How have behaviour therapy techniques been adapted to treat childhood behavioural problems?
* What are the different types of family intervention that might be used in dealing with childhood mental health problems?
® How can CBT be used to treat childhood and adolescent anxiety and depression?
* What is play therapy and what aspects of childhood psychopathology can it be used to treat?
SECTION SUMMARY
16.4 THE TREATMENT OF CHILDHOOD AND ADOLESCENT PSYCHOLOGICAL PROBLEMS
This section has described a number of different interventions that are regularly used to treat childhood and adolescent psy-
chological problems. Although drug treatments are becoming more common for a number of disorders, there is still much
uncertainty about their effectiveness and their safety. Common treatment methods include behaviour therapy, family therapy,
CBT and play therapy, and these forms of treatment will be adapted to the specific therapeutic needs of the child and often
used in a multifaceted approach to ensure improvements across emotional, educational and social functioning.
¢ Treatment for childhood psychological problems requires a coordinated provision of services that extends across educa-
tional, health and social services.
¢ Drug treatments are used for childhood anxiety and depression, and ADHD, but there are still significant doubts about the
safety of many medications used with children.
e Ritalin is a stimulant medication that is used to treat ADHD in around half of those diagnosed with the disorder.
e Behaviour therapy techniques can be adapted to treat many childhood behaviour problems. Techniques used include the bell-and-
battery technique for enuresis, systematic desensitization for anxiety problems and time-out (TO) to reduce disruptive behaviours.
¢ Important family interventions include systemic family therapy, parent management training and functional family therapy (FFT).
* Cognitive behaviour therapy (CBT) has been successfully adapted to treat childhood and adolescent depression and anxiety,
as well as anumber of other childhood psychological problems.
e Play therapy covers a range of techniques that can be used with younger children who are less able to communicate and
express their feelings.
16.5 CHILDHOOD psychopathology, such as anxiety or depression. Second,

childhood psychopathology is a relatively neglected
AND ADOLESCENT area of clinical research and much of childhood psy-
chopathology has previously been rather simplistically
PSYCHOLOGICAL labelled as either internalizing (reminiscent of anxiety
PROBLEMS REVIEWED or depression) or externalizing (exhibiting signs of dis-
ruptive and aggressive behavioural problems). However,
research in this area has increased significantly in recent
There is a range of difficulties involved in the identifica- years and we are now able to identify specific childhood
tion, diagnosis and treatment of childhood psychological disorders such as childhood depression, OCD and gener-
problems that are not usually encountered in adult men- alized anxiety disorder, as well as two important disrup-
tal health problems. First, children are often unable to tive behaviour disorders - ADHD and conduct disorder.
communicate any distress they are feeling and may lack We are still some way from fully understanding the
the self-awareness to identify individual symptoms of aetiology of most childhood psychological problems,
although some do have significant genetic components services. While there are drug treatments for many child-
(e.g. ADHD) while others appear to be related to impor- hood psychological problems, there are still significant
tant developmental factors such as the nature of the doubts about the effectiveness and safety of many of
family environment, parent-child relationships and the these treatments. More widely adopted are adaptations
socioeconomic climate in which the child is being reared. of adult psychotherapies, including behaviour therapy,
Treatment for childhood disorders is usually multifac- family based interventions and CBT. Play therapy also
eted and takes place in the context of a coordinated pro- offers a useful eclectic intervention that can be used with
vision of supervision and treatment that extends across a younger children who are less able to communicate and
range of services, including education, health and social express their feelings verbally.
ytd To access the online resources for this

pe go to
Reading Activity
Journal article: Young people and anxiety Activity 16.1

Developmental psychopa- Children with ADHD Self-test questions
thology and the diagnosis
OCD in children Revision flashcards
of mental health problems
among youth Tourette's syndrome Research questions
Journal article: Review of

the efficacy and safety of
antidepressants in youth
depression
Journal article: Practitioner
review: The effectiveness of
systemic family therapy for
children and adolescents
Clinical issues
References
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Neurodevelopmental Disorders
ii a To access the online resources for this chapter go to

This chapter begins by describing the way in which

learning, intellectual and developmental disabilities are 17.1 THE CATEGORIZATION AND LABELLING OF
defined and the terminology that is associated with these NEURODEVELOPMENTAL DISORDERS 563
disabilities. The chapter then proceeds to discuss factors
associated with the diagnosis, aetiology and treatment : 17.2 SPECIFICLEARNING DISABILITIES 564
of three groups of disabilities, namely specific learn- ;
ing disabilities (e.g. specific disorders of reading, writing 17.3 INTELLECTUAL DISABILITIES 571
and communication), intellectual disabilities and, finally,
autistic spectrum disorder. 17.4 AUTISTIC SPECTRUM DISORDER(ASD) 584
17.5 NEURODEVELOPMENTAL DISORDERS

REVIEWED 597
562 PSYCHOPATHOLOGY
wy
LEARNING OUTCOMES
When you have completed this chapter you should be able to:
1. Discuss the different ways in which learning and 5. Describe and evaluate the main forms of
developmental disabilities are categorized and intervention, care and support for intellectual
labelled. disabilities.
2. Describe and compare the various types of 6. Describe the diagnostic criteria for autistic
specific learning disabilities, their aetiology and spectrum disorder.
pee ee 7. Compare and contrast theories of the aetiology
3. Describe the various forms of intellectual of autistic spectrum disorder.
disability. 8. Describe and evaluate the main forms of
4. Compare and contrast genetic, biological and intervention, care and support for individuals
environmental causes of intellectual disabilities. with autistic spectrum disorder.
During childhood, no one knew what | had. | was considered ‘crazy’ by a doctor at age 1 because | had constant tantrums, which
only ended, one day, when my mother took me to the beach during a holiday. My nerves suddenly were calmed down by the sight
and the soothing sounds of the sea. | was beginning to say my first words and started to make some progress.
Despite the progress, | still had strange behaviours, like spinning plastic lids, jars and coins. | rejected teddy bears that other
toddlers liked, but held on to other objects, like dice (which had a smooth surface and were pleasant to touch). | was terrorized by
everyday noises, like planes passing by, thunder, machinery, drills, balloons bursting and any sudden noise.
Being the firstborn, my mother didn’t take notice of behaviours like rocking back and forth, or spending time on a rocking
horse in the day care centre as a toddler instead of playing with other kids.
Despite socializing difficulties, my interest for reading and learning the alphabet pleased my mother. Instead of pointing out
pictures in a newspaper my mother was reading, | asked her what the letters were, and that prompted her to teach me to read
before starting school.
Socially, |had problems that worried people. |was not able to recognize people easily, and was not able to decode nonverbal
cues. My mother complained about always having to spell things out to me. While my younger (non-autistic) brother seemed
to know instinctively when to bring up a subject, or when to say a joke, | was a nuisance, because | couldn't tell if somebody was
angry, sad, tired, and so on, just by looking at him/her. | took things literally and was terrorized by my mother’s ‘threats; which my
younger brother did not take seriously. She uttered threats like ‘I will send you away’ when we behaved badly. My brother was able
to understand that she never meant it; however, | was terrorized by them.
One thing that discouraged socializing was that most others did not like to talk about insects, calculators, or space all the
time. Other people liked my subjects ‘once in a while’ but got angry if |went on and on. My mother constantly reminded me not to
talk about the same things over and over. Changing subjects was hard for me. | was fixated on certain subjects like entomology
and arachnology. Nobody cares to hear about the chelate pedipalps of pseudoscorpions.
George's Story
Introduction and may affect intellectual, social and motor develop-

ment, and as a consequence will have effects on academic
Neurodevelopmental disorders are a category of disor- achievement, the development of social behaviours and
ders that typically begin to manifest in early development subsequent occupational functioning. In this chapter,
CHAPTER17 NEURODEVELOPMENTAL DISORDERS 563
we will cover three categories of neurodevelopmental

disorder — specific learning disorders, intellectual dis- 17.1 THE CATEGORIZATION
abilities and autistic spectrum disorder. Each of these AND LABELLING OF
categories is characterized by a specific impairment in
learning or control (e.g. language or communication NEURODEVELOPMENTAL
disorders, such as dyslexia), or impairments that can
cover both intellectual and social domains (e.g. autistic DISORDERS
spectrum disorder), or global impairments to intellec-
tual, social and motor skills (e.g. intellectual disability). In this chapter learning disabilities are divided into three
A neurodevelopmental disorder can be considered as broad categories. These are (1) specific learning disabilities,
a significant, lifelong condition that is usually present such as language and communication disabilities, (2) intel-
from birth, but it may often not be recognized until the lectual disability, covering some of the more severe learn-
individual fails to reach important milestones in their ing difficulties, and (3) autistic spectrum disorder, which
development. Failing to sit up, to talk, to read, or attend covers a range of deficits in social communication, often
to what is going on in the world are all possible signs with accompanying intellectual impairment.
of a learning disability if these activities do not appear There is considerable diversity across different areas of
as expected at normal developmental intervals. Most the world about how various learning disabilities should
neurodevelopmental disorders are permanent condi- be labelled. In the UK, Europe and much of Australasia
tions, but with suitable support and encouragement the term learning disability has often been used as an
many people with these conditions can acquire practical umbrella term to cover
and social skills even if this may take them longer than learning disability An umbrella term
disorders across all three to cover specific learning disabilities,
normal. of the main categories intellectual disabilities and pervasive
George’s story describes the early life of someone diag- described above — and it is developmental disorders.
nosed with autistic spectrum disorder. This involves diffh- especially used in this way
culties in interpreting nonverbal behaviour, impairment by health and social care For a video on learning and intellectual ( M
in communicating with others and a repetitive preoccu- services. In DSM-IV-TR,

disabilities go to
pation with individual objects, activities or topics. This the term mental retardation video/ch17
personal account provides a striking insight into how referred to a specific diag-
these disabilities can affect normal day-to-day living dur- nostic category of disorder defined asoGeueehty below
ing childhood. George prefers indulging in stereotyped average intellectual functioning, characterized by an IQ of
behaviours, such as rocking, to playing with other kids. 70 or below (DSM-IV-TR, p.49). However, the term mental
He is unable to understand both normal verbal innuendo retardation is now commonly frowned upon as stigmatiz-
and the nonverbal body language that most of us learn ing and demeaning and was replaced in DSM-5 by the label
to understand implicitly. This causes him to be seen by ‘intellectual disability’ and in ICD-11 by ‘intellectual devel-
others as ‘difficult’, uncommunicative and ‘a nuisance’, opment disorder’ — a change that was required by federal
all of which in turn causes him to feel more anxious and statute in the United States and was known as Rosa's Law.
distressed. Most neurodevelopmental disorders, no mat- There is as yet no genuine international consensus on the
ter how specific, cause problems across the whole range use of these categories and
of life activities, including educational, social and occu- labels, and even within coun- To read about Rosa's Law go to
pational, but the degree to which sufferers have prob- tries these terms can change http://tinyurl.com/pgyqk5n
lems in these areas of functioning will depend on their quite frequently to reflect
background and family circumstances and the nature shifts in social attitudes towards individuals with learning
and degree of the disability. disabilities. Nevertheless, no matter how much we may
This chapter will look in detail at the various types believe that labels for such groups of people may be stig-
of neurodevelopmental disorder, their aetiology and the matizing, it would be difficult to understand the aetiology
various treatment and caring options that are available of these disorders and to organize services and support if
for these disabilities. there were no way of defining their specific problems.
SELF-TEST QUESTION _
© Howare the terms specific learning disability, intellectual disability and autistic spectrum disorder defined?
564 PSYCHOPATHOLOGY
~~
SECTION SUMMARY
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17.1 THE CATEGORIZATION AND LABELLING OF LEARNING DISABILITIES
® The three main categories of learning disabilities are (1) specific learning disabilities (e.g. specific learning disorder),
(2) intellectual disabilities, and (3) autistic spectrum disorder (ASD).
eee e eee ene e eee eee e nese sees seEssE EEE eSESESEESEEEESSEEEESESESESEESEDESEOSESESESESESESESESSSEOTEEEEEEEEOEEEEGEO HEED PPPTTTITETTTIITTTITTTTITTITTI TTT
understanding the meaning of what is read, difficulties

17.2 SPECIFIC LEARNING with spelling and written expression, difficulty mastering
DISABILITIES number sense, and difficulties with mathematical reason-
ing. DSM-5 Summary Table 17.1 provides the diagnostic
criteria for specific learning disorder. Table 17.1 describes
DSM-5 divides specific learning disabilities into two some of the specific disabilities covered under this diag-
broad categories: (1) specific learning disorder, which cov- nostic category and provides some examples.
ers difficulties in learning and using academic skills such Specific learning disabilities such as these are often
as reading and writing, and (2) communication disorders, commonly comorbid with other childhood psychological
which covers deficits in language, speech and communi- problems, and studies suggest that specific learning dis-
cation generally. abilities can be diagnosed in 79 per cent of children with
bipolar disorder, 71 per*cent with ADHD, 67 per cent
with autism, and slightly lower percentages with anxi-
17.2.1 Specific Learning Disorder ety and depression (18-19 per cent) (Mayes & Calhoun,
2006). Literacy problems generally are associated with
Specific learning disorder refers to a number of dis- increased risk for both externalizing and internalizing
abilities that each affect the individual’s performance disorders in childhood and this may be due either to the
on standardized tests of academic ability such as read- stressors associated with academic failure (causing anxi-
ing, mathematics or written expression. Individuals with ety and depression) or the fact that certain types of cogni-
these disabilities show levels of achievement well below tive deficit (such as attention deficits) may be common to
what would be expected for their age, schooling and level a number of different disorders, including specific learn-
of intelligence. As we shall see below, individuals with ing disorders and disruptive behaviour disorders such as
specific learning disorders can show deficits in perceptual ADHD (Maughan & Carroll, 2006).
organization (organizing information), auditory and vis-
ual perception, memory, and attention. Without special
remedial support, individuals with these disabilities will
normally perform badly at school, be viewed as failures DSM-5 SUMMARY TABLE 17.1 Criteria for specific learning
by friends and family, and as a consequence exhibit low disorder
self-esteem and motivation (Bjorkland & Green, 1992).
e Impediments in learning and using academic skills, marked
Similarly, school drop-out rates for children with specific
by at least one of the following over a 6 month period:
learning disabilities are high and they will also experi-
ence difficulties in occupational and social functioning. ¢ Inaccurate or slow and struggling reading
Specific learning disorder is diagnosed when there are e Difficulty understanding the meaning of read words
deficits or impairments in the individual’s ability to either e Spelling difficulties
perceive or process information accurately, which will
eventually manifest in academic circumstances as difficul- ¢ Difficulties in expression through writing
ties in reading, writing or in mathematical ability. DSM-5 ¢ Difficulties understanding numbers
has incorporated a number of previously different disa- ¢ Difficulties with mathematical reasoning
bilities (such as dyslexia and dyscalculia) into a single spe-
cific learning disorder diagnostic category, and defines ° The affected academic skills are substantially below what
would be expected for the patient’s age
disabilities in this category as difficulties in learning and
specific learning disorder Diagnosticcat- Using academic skills in ° The difficulties are not better accounted for by intel-
egory including disorders such as dyslexia one or more areas such lectual disabilities, vision or hearing difficulties or other
and communication disorders. mental or neurological disorders
as slow reading, difficulty
CHAPTER 17 NEURODEVELOPMENTAL DISORDERS 565,
TABLE 17.1 Specific learning disabilities
Disability Description Example symptoms
Problems with accurate or fluent word Reading achievement is substantially Omit, add or distort the sound of
recognition, poor decoding and poor below the norm for chronological age, words when reading
spelling abilities (formerly classified intelligence and educational level Read slowly and with poor
as dyslexia) comprehension
Problems with written expression Writing skills are substantially below Regular errors in spelling, grammar or
those expected for chronological punctuation
age, intelligence and educational
level
Difficulties mastering number sense, Mathematics ability is substantially below Difficulty remembering arithmetic
number facts or calculation (formerly norm for chronological age, intelligence facts (e.g. to ‘carry’a number)
classified as dyscalculia) and educational level Failure to understand arithmetic
concepts
Difficulties with verbal and written Scores on tests of expressive language Markedly limited vocabulary
expression development are substantially below Making errors in tense
those for chronological age, intelligence Difficulty recalling the right word
and educational level
Dyslexia even though children with impaired reading skills show

Dyslexia is a complex pattern of learning difficulties an improvement in reading ability with age, a gap in
associated with difficulties in word recognition while reading ability remains across time between children
reading, poor spelling and difficulties with written with reading impairments and those without. In indi-
expression. Reading may be characterized by word viduals suffering dyslexic problems, writing skills fall
distortions, substitutions or omissions and is generally significantly below those expected for the child’s chron-
slow, with the child having difficulty fully comprehend- ological age, IQ and educational history. The child will
ing what has been read. Between 3 and 17.5 per cent of have difficulty composing written text (Photo 17.1) and
school-age children have specific developmental reading will exhibit grammatical errors, punctuation errors,
problems (DeFries, Fulker & LaBuda, 1987; Shaywitz, poor paragraph organization, spelling errors and poor
Shaywitz, Pugh, Fulbright et al., 1998) and around handwriting.
60-80 per cent of those diagnosed are likely to be boys
(Shaywitz, Shaywitz, Fletcher & Escobar, 1990). This
Dyscalculia
gender difference may be due to a number of factors, The main feature of dyscalculia is that mathematical
including or arithmetical ability falls significantly short of that
expected for the child’s chronological age, IQ and edu-
1. higher referral rates in males because they cational history. Individual skills that may be impaired in
may be more disruptive than girls in learning
environments; dyscalculia are (1) under- dyscalculia A specific learning
standing or naming mathe- disability characterized by mathematical
2. girls may at least partially offset their reading matical terms, (2) decoding ability being substantially below norm
difficulties by enjoying reading more than boys problems into mathemati- for chronological age, intelligence and
educational level.
(Chiu & McBride-Chang, 2006); and cal terms, (3) recognizing
3. girls may have more effective coping strategies and reading numerical symbols or arithmetical signs,
than boys for dealing with reading difficulties (4) copying numbers or symbols correctly, (5) remem-
(Alexander-Passe, 2006). bering to conduct certain mathematical operations
(such as ‘carrying’ figures when making calculations),
Most longitudinal studies suggest that reading prob- and (6) following sequences of mathematical steps in
lems can often be persistent and chronic, which does the correct order. It is estimated that around 3-4 per
not simply represent a developmental lag in reading cent of school-age children may suffer from develop-
ability but is evidence for a specific learning disorder mental dyscalculia, with the male to female ratio as
(Bruck, 1992; Scarborough, 1990; Francis, Shaywitz, high as 4:1 (Reigosa-Crespo, Gonzalez-Alemany, Leon,
Stuebing, Shaywitz & Fletcher, 1996). For example, Torres & Mosquera, 2013).
PSYCHOPATHOLOGY
with speech sound disorder (see below), reflecting a gen”

eral impairment in the fluidity of language and erratic
speech rhythms. Language disorder can be identified as
early as age 2-3 years (Eisenwort, Marschik, Fladerer,
Motl et al., 2004), but milder forms may not become
apparent until early adolescence.
Speech sound disorder

This is a disorder characterized by persistent difficulty
with speech sound production and to be diagnosed with
speech sound disorder these impairments must be prob-
lems in effective communi-
speech sound disorder Persistent dif-
cation that interfere with ficulty with speech sound production that
Will and Deni Mcintyre/Science Source, National Audubon Society Collection/Photo Researchers, social, academic or occupa- interferes with speech intelligibility or pr
Inc. Reproduced with permission.
tional achievement (DSM-5 vents verbal communication of messag
PHOTO 17.1 Dyslexia includes deficits in spelling and Summary Table 17.3). The
writing as well as reading. Other symptoms of dyslexia can disorder includes errors of sound production (e.g. using
include poor comprehension, reversal of words or letters a t sound to represent the letter k) and the omissions of
while reading, and difficulty decoding syllables or single sounds — especially from the ends of words. Sufferers will
words and associating them with specific sounds (phonics). also be unable to categorize speech sounds and will be
Here, a child with dyslexia attempts to reproduce a teacher's unable to decipher which sounds in the language make a
sentence. difference in meaning. The most severely misarticulated
sounds are those learnt later in the developmental process,
such as l, 7, s, z, th and ch, and lisping is particularly com-
mon (e.g. saying wabbit instead of rabbit). Speech sound
17.2.2 Communication Disorders disorder may often be associated with physical causes,
such as a hearing impairment, cleft palate, neurological
Communication disorders include impairments in limitations such as cerebral palsy, and ear, nose and throat
language, speech and communication, and here we problems (Fox, Dodd & Howard, 2002), but at least 3 per
will cover the DSM-5 diagnostic categories of language cent of pre-school children are diagnosed with a speech
disorder, speech sound disorder and childhood-onset fluency sound disorder of unknown origin. Prevalence rate of
comnilinicauondiserders Problemenim sorder (otherwise known similar or related speech sound disorders is around 2 per
the articulation of sounds. as ‘stuttering’). cent in 6-7-year-olds falling to 0.5 per cent by age 17 years
(DSM-IV-TR, p.66).
Language disorder
Language disorder concerns problems with language
acquisition and use as a result of problems in vocabu- DSM-5 SUMMARY TABLE 17.2 Criteria for language
lary comprehension and disorder
language disorder A disability concerned production, and in the
: : ¢ Ongoing difficulties in the attainment and use of lan-
with problems in vocabulary comprehen construction-of sentences:
guage (including spoken and written), due to difficul-
ein a Se This usually results in a sig- ties in understanding and emitting that include the
nificantly smaller vocabulary size, with grammatical and following:
tense errors. These problems will appear during early e Reduced vocabulary
development and persist into adolescence and adulthood
(DSM-5 Summary Table 17.2). General features of the ¢ Limited sentence structure ability
disorder include a limited amount of speech, limited e Difficulties in dialogue
vocabulary, difficulty learning new words, difficulty find- ¢ Abilities are substantially below what would be expected
ing the right word (e.g. unable to come up with the word for the patient’s age
car when pointing to a car), shortened sentences, simple
¢ Symptoms start in early development
grammatical structures (e.g. use of relatively few verb
forms), omission of critical parts of sentences, unusual ° The difficulties are not better accounted for by vision or
word order and slow language development generally. hearing difficulties, motor dysfunction or other mental or
neurological disorders
Language disorder is often comorbid in younger children
CHAPTER 17 NEURODEVELOPMENTAL DISORDERS +567
DSM-5 SUMMARY TABLE 17.3 Criteria for speech sound DSM-5 SUMMARY TABLE 17.4 Criteria for childhood-onset
disorder fluency disorder (stuttering)
¢ Ongoing difficulty with speech sound production that e Ongoing disturbance of normal fluency and time
causes problems with speech understanding or prevents patterns in speech, inappropriate to the patient's age
verbal communication and language skills, as marked by at least one of the
following:
e The difficulty causes limitations in effective communica-
tion, interfering with social participation, academic or e Sound and syllable repetitions
occupational performance
e Sound prolongation of consonants and vowels
¢ Symptoms start in early development
e Broken words
e Difficulties are not better accounted for by congenital or
e Filled or unfilled pauses in speech
acquired conditions including cerebral palsy, deafness or
other medical conditions e Word substitution to avoid difficult words
e Word pronunciation with excessive physical tension
e Monosyllabic whole-word repetitions

e The disturbance causes anxiety about speaking or limita-
Childhood-onset fluency disorder (stuttering) tion in effective communication
This is a problem with the fluency and time-patterning
of speech which involves (1) frequent repetitions or pro- e Symptoms start in early development
longations of sounds, (2) pauses within words, (3) filled e Difficulties are not better accounted for by speech-motor
or unfilled pauses in speech, (4) word substitutions to or sensory deficit or other medical condition
avoid pronouncing problematic words, (5) words pro-
duced with an excess of physical tension, and (6) mon-
osyllabic word repetitions (e.g. ‘go-go-go-go out of the
room’) (DSM-5 Summary Table 17.4). Fearful anticipa- Stuttering is more common in males than females, with
tion of stuttering may develop in many sufferers and this a male-to-female ratio of 4:1 in adolescents and 2.3:1
may make stuttering worse in stressful situations, such in both younger children and adults. Of those children
as when giving a speech or diagnosed with stuttering, 12.7 per cent also have speech
ttering A disturbance in the normal
at an interview. Stuttering sound disorder, 15.2 per cent have another learning dis-
ncy and time patterning of speech that ability and 5.9 per cent have ADHD (Blood, Ridenour,
appropriate for the individual’s age. may be accompanied by
physical symptoms such Qualls & Hammer, 2003).
as eye blinks, tics, tremors, jerking of the head and
clenching fists. As can be envisaged, stuttering can also
have highly detrimental effects on social and occupa- 17.2.3 The Aetiology of
tional functioning. Onset of stuttering typically occurs
Specific Learning Disabilities
between 2 and 7 years of age, with a peak onset around
5 years. The onset is usually insidious and initially the In the following section we will discuss the aetiol-
child may be unaware of stuttering. However, as aware- ogy and causes of some of the more common of the
ness increases, the child will develop compensatory specific learning disabilities we have described in this
strategies for avoiding words and situations that cause section.
stuttering. Community studies estimate prevalence
rates of childhood-onset
{hood-onset fluency disorder
tering) A problem with the fluency fluency disorder (stutter- Dyslexia
time-patterning of speech which ing) for all individuals at As mentioned earlier, dyslexia is a condition that
ves frequent repetitions or prolon- 0.7 per cent, rising to 1.4 affects both reading and written expression, and is a
ns of sounds, pauses within words,
per cent in young children persistent, chronic con-
es in speech, word substitutions, dyslexia A persistent, chronic learning
1s produced with an excess of physical and dropping to 0.5 per dition in which reading
disability in which there are developmental
on, and monosyllabic word repetitions. cent in adolescents (Craig, ability lags behind that of deficits in spelling, reading and writing
Hancock, Tran, Craig & non-impaired individuals abilities.
Peters, 2002). However, the prognosis for stuttering is for the course of most of
good, with around 40 per cent of sufferers overcoming their lifetime. The development of dyslexia can be pre-
the problem before they start school and 80 per cent over- dicted by a number of risk factors, including difficulty
coming it before adolescence (Couture & Guitar, 1993). recognizing rhymes at age 4 years (Bradley & Bryant,
568 PSYCHOPATHOLOGY
1985), difficulty naming everyday objects at age 5 years deficit is quite independent of other abilities, such a8
(Wolf, Bally & Morris, 1986) and difficulty learning general intelligence, reasoning, vocabulary and use of
syntactic rules at age 2-3 years (Scarborough, 1990). syntax (Share & Stanovich, 1995; Shankweiler, Crain,
However, the main causes of dyslexia now appear to Katz, Fowler et al., 1995). Shaywitz & Shaywitz (2005,
be identified as abnormalities in specific areas of the p.1302) characterize the experience of the dyslexic in
brain such as the temporoparietal region (Shaywitz & the following way:
Shaywitz, 2005). These abnormalities may be the result
of genetic factors and they may give rise to the difficul- The problem is that the affected reader cannot use
ties that sufferers have in decoding and comprehend- his or her higher order linguistic skills to access
ing written material. We will review these theories of the meaning until the printed word has first been
the aetiology of dyslexia by looking in turn at evidence decoded and identified. Suppose, for example, an
related to genetic inheritance, cognitive impairments individual knows the precise meaning of the spoken
and brain abnormalities. word ‘apparition’; however, she will not be able to
use her knowledge of the meaning of the word until
Genetic factors As early as 1950, Hallgren reported she can decode and identify the printed word on the
that more than 80 per cent of children with dyslexia page and it will appear that she does not know
also had other family members with the disability, with the word’s meaning.
more recent studies suggesting that between 23 and 65
per cent of children with dyslexia have a parent with
the disorder (Scarborough, 1990). In addition, 40 per Brain abnormalities Associated with problems
cent of the siblings of sufferers will also exhibit symp- in relating written letters to corresponding sounds are
toms of dyslexia (Pennington & Gilger, 1996). This sug- deficits in brain functioning in dyslexia — especially in
gests that dyslexia runs in families and so may have an the temporoparietal areas of the brain. Post-mortem
important genetic component, and evidence for this studies of the brains of dyslexia sufferers suggest abnor-
genetic component is supported by studies suggest- malities in the temporoparietal brain region (Galaburda,
ing that dyslexia concordance rates are significantly Sherman, Rosen, Aboitiz et al., 1985) and the number
higher in MZ than in DZ twins (Stevenson, Graham, and organization of neurones in the posterior language
Fredman & McLoughlin, 1987). Using genetic mark- area of the cortex (Galaburda, 1993). Nevertheless, these
ers for dyslexia, linkage studies have implicated genes abnormalities found in post-mortem studies might sim-
on a number of chromosomes in the aetiology of dys- ply represent the consequences of a lifetime of poor
lexia, including loci on chromosomes 2, 3, 6, 15 and reading rather than a causal factor in dyslexia. However,
18 (Fisher & DeFries, 2002). There is evidence from functional magnetic resonance imaging (fMRI) stud-
molecular genetics to suggest that many of these genes ies of the brains of young children with dyslexia indi-
participate in brain development and cause the abnor- cate that they show significantly less activation in a
malities in brain development associated with dyslexia number of left hemisphere sites when reading than do
(Galaburda, LoTurco, Ramus, Fitch & Rosen, 2006; non-impaired children. These areas include the inferior
Scerri & Schulte-Koene, 2010). frontal, superior temporal, parietotemporal and middle-
temporal-middle-occipital gyri (Shaywitz, Shaywitz,
Cognitive factors Research on the aetiology of dys- Pugh, Mencl et al., 2002). This represents a common
lexia has recently converged on the view that reading finding from functional brain imaging studies suggest-
disabilities in dyslexia are caused primarily by difficulties ing that a failure of proper functioning in left hemi-
in differentiating the elements of speech (phonemes) sphere posterior brain systems is a cause of impaired
and associating these sounds with the letters in a reading in children with dyslexia. Studies of lesions of
written word (Shaywitz, 2003). This is known as the the temporoparietal areas of the brain also indicate that
phonological theory of dyslexia where, in order to learn this area may be critical for analysing the written word
to read, the child must and transforming the symbol into the sounds associated
phonological theory The view that learn to recognize that with the linguistic structure of the word (Damasio &
reading disabilities in dyslexia are caused letters and letter strings Damasio, 1983; McCandliss, Cohen & Dehaene, 2003).
primarily by difficulties in differentiating
the elements of speech (phonemes) and
represent the sounds of Interestingly, brain imaging studies also suggest that
associating these sounds with the letters in spoken language. The individuals with dyslexia may attempt to compensate for
a written word. deficits in dyslexia impair the lack of function in the temporoparietal areas of the
the child’s ability to break brain by using other brain areas to help them identify
up a spoken word into its basic phonological elements words and associate them with sounds. These compen-
and link each letter to its corresponding sound. This satory effects involve brain sites required for physically
CHAPTER 17 NEURODEVELOPMENTAL DISORDERS 569
articulating a word, enabling the individual with dys- sound production may not represent the whole picture.
lexia to develop an awareness of the sound structure For example, there is growing evidence of a familial and
of a word by forming the word with their lips, tongue genetic component to communication disorders such
and vocal apparatus (Brunswick, McCrory, Price, Frith as stuttering (Canhetti-Oliveira & Richieri-Costa, 2006;
& Frith, 1999). Compensatory effects such as this may Andrews, Morris-Yeates, Howie & Martin, 1991) that
explain why reading performance in children with dys- indicates that the heritability of stuttering may be as high
lexia improves with age but still fails to reach the stand- as 71 per cent. There is also evidence from brain scan
ard of non-impaired children. studies of abnormalities in certain brain circuits that are
related to stuttering. One such circuit is the basal ganglia—
Dyscalculia thalamo-cortical motor circuit, which, if impaired, may
Dyscalculia appears to be a specific but chronic condi- affect the ability of the basal ganglia to produce tim-
tion, in which sufferers may perform better than average ing cues for the initiation of the next motor segment
on measures of IQ, vocabulary and working memory, in speech (Alm, 2004). The fact that stuttering may be
but still perform significantly poorly on tests of math- a problem associated with the sequential production of
ematical ability (Landerl, Bevan & Butterworth, 2004). sounds and words is supported by evidence that suggests
The disorder appears to be the result of specific disabili- that stuttering rarely occurs in one-word utterances and
ties in basic number processing and can take three basic is affected by the length and grammatical complexity of
forms: (1) a deficit in the memorizing and retrieval of utterances (Bloodstein, 2006). Furthermore, stuttering is
arithmetic facts, (2) developmentally immature strate- often a consequence of brain injury in the basal ganglia,
gies for solving arithmetic problems, and (3) impaired suggesting that it is an important area in the production
visuospatial skills resulting in errors in aligning numbers of normal speech (Tani & Sakai, 2011).
or placing decimal points (Geary, 1993, 2004). Finally, there is some evidence that the production
Dyscalculia appears to have a familial component of sounds in communication disorders may be affected
(Monuteaux, Faraone, Herzig, Navsaria & Biederman, by emotional factors such as anticipatory anxiety or lack
2005) and abnormalities in brain function associated of control over emotional reactions (Karrass, Walden,
with dyscalculia may be partially transmitted genetically Conture, Graham et al., 2006). However, at least some
(von Aster, Kucian, Schweiter & Martin, 2005), and are researchers view this association between disorders such
also associated with the genes that mediate mathemati- as stuttering and anticipatory anxiety as secondary, and
cal ability generally (Plomin & Kovas, 2005). However, a as a conditioned consequence of previous stuttering
number of studies have also implicated prenatal factors experiences (Alm, 2004).
such as fetal alcohol spectrum disorder (FASD) and low
birth weight (O’Malley & Nanson, 2002; Shalev, 2004).
Brain functions specializing in number processing are 17.2.4 The Treatment of Specific
located in various areas of the brain: fMRI studies have
Learning Disabilities
implicated abnormalities in the left parietotemporal
and inferior prefrontal cortex areas of the brain and the The inclusion of specific learning and communication
intraparietal sulcus in mathematics disorder (Dehaene, difficulties in DSM over the years has been controversial.
Molko, Cohen & Wilson, 2004; Molko, Cachia, Riviere, Many view these problems as developmental ones that
Mangin et al., 2003). Thus, the current evidence suggests require attention in an educational rather than a clinical
a genetic or developmental cause that results in abnor- setting and, indeed, many learning disabilities are tackled
malities of function in those areas of the brain responsi- primarily in the context of the child’s educational devel-
ble for processing numbers and arithmetic calculations. opment (Mishna, 1996). However, specific learning dif-
ficulties are frequently associated with clinical problems
Communication disorders such as anxiety, depression and disruptive behaviour,
Many communication disorders may be caused by and they can create significant problems in social, educa-
organic problems relating to abnormal development of tional and familial functioning that may require referral
the physical apparatus required to make and articulate to clinical services. Many of the treatments required by
sounds. For example, speech sound disorder and stutter- individuals with specific learning disorders can be pro-
ing can be associated with physical causes such as hearing vided by educational psychologists or speech therapists
impairment, cleft palate, cerebral palsy and ear, nose and rather than clinical psychologists and it is not intended to
throat problems. In addition, some theories of stuttering cover these forms of treatment here.
argue that this disorder results from problems with the In many cases, such as reading impairments, appro-
physical articulation of sounds in the mouth and larynx priate reading instruction for at-risk younger children
(Agnello, 1975). However, organic difficulties related to can enable them to become accurate and fluent readers
570 PSYCHOPATHOLOGY
(Alexander & Slinger-Constant, 2004). However, with auditory feedback it gives the sufferer when speaking
older individuals suffering from reading disabilities such or through a change in frequency of the voice. Such
as dyslexia, acommon approach in educational settings is devices appear to have success in reducing the levels
to provide learning materials in a form that allows them of stuttering, but it is still not clear by what mecha-
to be most easily negotiated by the dyslexic student. In nism they have this effect or whether they work equally
addition, to compensate for the fact that the dyslexic stu- well for everyone with a stuttering problem (Lincoln,
dent’s reading is less automatic and more effortful, extra Packman & Onslow, 2006; Lincoln, Packman, Onslow
time is given during assessments such as examinations. & Jones, 2010). Another successful set of techniques
Treatment of communication disorders is normally used to address stuttering is known as prolonged speech.
the domain of speech therapists and related disci- This teaches the sufferer.a set of new speech patterns
plines, and there is a range of successful treatment pro- that result in changes in the phrasing and articulation of
grammes and equipment available for disabilities such speech and of the respiratory patterns produced by stut-
as phonological disorder and stuttering (Saltuklaroglu terers while speaking (Packman, Onslow & van Doorn,
& Kalinowski, 2005; Law, Garrett & Nye, 2004). For 1994). The success rates of treatments for stuttering
example, hand-held equip- are particularly high and estimated to be around 60-80
altered auditory feedback (AAF)
A form of treatment for stuttering in which
ment can provide altered per cent, but this may at least in part be confounded
delayed auditory feedback or a change in auditory feedback (AAF) by the fact that much childhood stuttering will usually
frequency of the voice is given to clients for the stutterer, either spontaneously remit after a few years (Saltuklaroglu &
when they are speaking. in terms of the delay of Kalinowski, 2005).
SELF-TEST QUESTIONS
e What are the defining characteristics of specific learning disorder as a diagnostic category?
© What are the individual skills that may be impaired in dyscalculia?
* What are the main characteristics of language disorder, speech sound disorder and childhood-onset fluency disorder?
* What is the evidence that dyslexia is an inherited disorder?
* Can you describe the phonological theory of dyslexia?
e What areas of the brain appear to be most affected in dyslexia?
° What is the evidence that communication disorders might be associated with physical rather than psychological causes?
* Can you describe treatments for stuttering such as altered auditory feedback (AAF) and prolonged speech?
SECTION SUMMARY
17.2. SPECIFIC LEARNING DISABILITIES
In this section we have reviewed the characteristics, aetiology and general treatment of anumber of specific learning disabili-
ties. These are largely disabilities associated with reading, writing and communication generally, and the most well-known of
these disorders is the reading disorder known as dyslexia. While many of these disabilities will require attention in educational
rather than clinical settings, they may come to the attention of clinical psychologists because they may often become associ-
ated with mental health problems and cause significant disruption to social, familial and educational functioning.
° Specific learning disorder refers to a range of disabilities that affect performance on tests of academic ability such as reading,
mathematics or written expression.
e Dyslexia is a learning disability associated with difficulty in recognizing words, poor spelling and difficulty with written
expression.
CHAPTER 17 NEURODEVELOPMENTAL DISORDERS Sa
¢ Dyscalculia is a disability that affects mathematical or arithmetic ability.

Communication disorders include impairments in language, speech and communication.
Language disorder is a disability concerned with problems in vocabulary comprehension and production.
¢ Speech and sound disorder is a disability associated with difficulty in speech sound production.
* Childhood-onset fluency disorder is sometimes known as ‘stuttering’ and involves a problem with the fluency and time-
patterning of speech.
¢ Disorders of reading, such as dyslexia, are known to have an ge oe 4 genetic component and are associated with brain
abnormalities in the temporoparietal areas.
° Dyslexia appears to be associated with difficulties differentiating the elements of speech and associating these sounds with
the letters in a written word (the phonological theory).
° Treatment for specific learning disabilities often occurs in an educational rather than a clinical setting.
SAPS NOR eee eee en ener eee eee EEE eee ETOH Een ETeSETa Eee TET Ser SE SOEaNTEE EEE ESSE SA EEE SS HOE FREE O OHNE H DEH EEEEEE STS ESER ESR UEED SHES E EON OSES EER EHES USES HESESEOU SOE SSEESEEHUEEH ESSE HER STROHSOESEDEEESEEEHE SHOE EERE HOHE HEHE ESO HSeeeereneeneneet”
17.3. INTELLECTUAL DSM-5 SUMMARY TABLE 17.5 Criteria for intellectual disability
e Deficits in intellectual functions as confirmed by clinical

DISABILITIES assessment and standard intelligence tests
¢ Deficits in adaptive functioning resulting in an inability

to meet development and sociocultural standards for
17.3.1 DSM-5 Diagnostic Criteria personal independence and social responsibility
for Intellectual Disability e Symptoms start in developmental period
Intellectual disability is a disorder with onset during the

individual's developmental period (usually up to the age
of 18 years) that covers impairment in both intellectual
social responsibility, and IQ test scores should be inter-
and adaptive functioning.
lectual disability A modern term preted cautiously depending on whether the instrument
acing mental retardation to describe
DSM-5 defines intellectual
is culturally relevant, based on up-to-date norms, and
more severe and general learning disability according to three
takes into account any sensory or motor disabilities the
bilities. primary criteria:
individual may possess.
1. significantly below average intellectual functioning DSM-5 also allows intellectual disability to be specified
in areas such as reasoning, problem solving, according to its severity into mild, moderate, severe and
abstract thinking, planning and learning generally; profound, with mild being the least disabling, where suf-
and this below-normal intellectual functioning is ferers may only be mildly cognitively impaired, socially
defined by scores on IQ tests approximately two ‘immature’ rather than impaired, and may be able to deal
standard deviations below the population mean with the daily tasks of life given appropriate support. In
(i.e. an IQ below 70 on IQ tests with a mean of the case of profound severity the individual may have
100 and a standard deviation of 15); little understanding of symbolic communication and be
dependent on others for all aspects of daily care, their
2. impairments in adaptive functioning generally
health and their safety. Clinicians assessing individuals
(e.g. an inability to master social or educational
with intellectual disabilities would also gather informa-
skills that would be expected for the individual’s
tion about disabilities from other reliable independent
chronological age); and
sources, such as teachers and medical doctors.
3. these deficits should be manifest during the
individual’s developmental period (i.e. normally, up
to 18 years of age) (DSM-5 Summary Table 17.5).
17.3.2 Alternative Approaches
DSM-5 makes it clear that a good deal of clinical judge- to Defining Intellectual Disability
ment is required when diagnosing intellectual disability.
It should take into account whether the individual meets Rather than simply taking a negative approach to
community and cultural standards of independence and diagnosis and focusing on an individual’s limitations,
‘57202 PSYCHOPATHOLOGY
at a \
impairments and deficits, more recent views attempt to changes in attitude, support and legislation, more than
highlight those factors that might be required to facili- half of those people with intellectual disabilities in the
tate better intellectual and adaptive functioning in the UK now live with their parents or carers.
individual. People with intellectual disabilities differ sig-
nificantly in the severity of their disabilities, with some
able to function in everyday life almost without being 17.3.3 The Prevalence of
noticed while others may require constant supervision
and sheltered environments in which to live. Similarly, Intellectual Disabilities
individuals also differ significantly in their personalities. Estimates of the prevalence levels of intellectual dis-
Some will be passive, placid and dependent while others orders will depend very much on how intellectual
may be aggressive and impulsive. These kinds of issues disabilities are defined. DSM-5 estimates the prevalence
mean that each individual with an intellectual disability rate of a diagnosis of intellectual disability at around 1
is likely to differ in terms of both their level of function- per cent, and prevalence for severe intellectual disability
ing and what is required to achieve any form of adaptive at around 6 per 1000. However, a UK study looking spe-
functioning. In this sense, the notion of ‘intellectual dis- cifically at the prevalence rate of IQ scores less than 70
ability’ is more of a social construction than a diagnostic suggests that prevalence of such low IQ scores may be
category (a term that is a product of particular historical as high as between 5 and 10 per cent in school children
and cultural conditions rather than medical or psycho- aged 13-15 years. Further analysis suggested that only
logical science) (Webb & Whitaker, 2012). around 15 per cent of those with IQ scores below 70
The American Association on Intellectual and were already in receipt of a statement of special educa-
Developmental Disabilities (AAIDD) has promoted a tional needs (Simonoff, Pickles, Chadwick, Gringas et al.,
more individualized assessment of a person’s skills and 2006), implying that the majority of the group with low
needs rather than an approach based solely on categoriz- IQ either did not need educational support or were as
ing intellectual and adaptive impairments. This approach yet unrecognized as in need of support. Epidemiological
emphasizes that individuals have both strengths and studies indicate that there are around 580,000 people
limitations, and that an individual’s limitations need to
in the UK with mild intellectual disabilities (a preva-
be described in a way that enables suitable support to be lence rate of around 0.95 per cent) and 217,000 with
developed. So, rather than simply forcing the individual severe intellectual disabilities (a prevalence rate of
into a diagnostic category, this approach evaluates the 0.35 per cent) (Open Society Institute, 2005). However,
specific needs of the individual and then suggests strate- the Simonoff, Pickles, Chadwick, Gringas et al. study
gies, services and supports that will optimize individual implies there are likely to be many more people than this
functioning. Supports are defined as ‘the resources and suffering some form of intellectual disability and they
individual strategies necessary to promote the devel- are going unrecognized.
opment, education, interests, and personal well-being
of a person with intellectual disabilities’. Supports can
be provided wherever necessary by parents, friends,
teachers, psychologists, doctors and GPs or any other 17.3.4 The Aetiology of
appropriate person or agency. People with intellectual
Intellectual Disability
disabilities frequently face major stigma and prejudice,
and they are often confronted with significant barriers First and foremost, the causes of intellectual disabil-
to realizing their own potential. However, approaches ity in individual cases are often extremely difficult to
such as that advocated by the AAIDD are designed isolate and identify. Even when the cause of disability
to enable individuals with intellectual disabilities to can be identified (such as a chromosomal disorder) two
achieve their potential. In the UK, the Special Education individuals identified with the same cause may exhibit
Needs and Disability Act of 2001 extended the rights of quite different levels of disability. Differential diagno-
individuals with intellectual disabilities to be educated sis is also quite problematic: in many cases it is unclear
in mainstream schools and schools are required to draw whether an individual has a specific learning disability,
up accessibility strategies to facilitate the inclusion of has more general intellectual impairments, is suffering
pupils with intellectual from autistic spectrum disorder (see section 17.4), or
accessibility strategies Programmes
that extend the rights of individuals with
disabilities and to make has psychological or emotional problems. As we shall
intellectual disabilities to be educated reasonable adjustments so see in the following sections, the major causes of intel-
according to their needs in mainstream that they are not disadvan- lectual disability are biological in nature and over 1000
schools.
taged. As a result of such forms of impairment based on genetic, chromosomal or
CHAPTER17 NEURODEVELOPMENTAL DISORDERS ye
metabolic abnormalities have been identified (Dykens & disabilities categorized by the developmental period
Hodapp, 2001). However, many researchers believe when they have their effect.
that an individual’s resultant intellectual disability is
also influenced considerably by environmental fac- Biological causes
tors. For example, mild or moderate intellectual Biological factors represent the largest known group of
disability tends to occur more frequently in lower socio- causes of intellectual disabilities and we will divide these
economic groups, indicating that poverty and associ- into three main categories: (1) chromosomal disorders,
ated deprivation may retard intellectual development. (2) metabolic causes, and (3) perinatal causes.
One topical example of this is the case of teenage moth-
ers who choose to rear their children. They more often Chromosomal disorders For many years now, it
live in poor environments, are more likely to expose has been known that forms of intellectual disability are
their children to alcohol and poor nutrition, and are less genetically linked to abnormalities in the X chromo-
likely to provide sensitive parenting (Brooks-Gunn & some (the chromosome that also determines biologi-
Chase-Lansdale, 1995; Borkowoski, Whitman, Passino, cal sex) and these abnormalities will often manifest as
Rellinger et al., 1992). As a result, mild to moderate physical weaknesses in the chromosomes or abnor-
intellectual disability is found significantly more fre- malities resulting from irregular cell division during the
quently in children of teenage mothers than in the chil- mother’s pregnancy. Chromosomal abnormalities occur
dren of older mothers (Broman, Nichols, Shaughnessy, in around 5 per cent of all pregnancies and the major-
Kennedy et al., 1987). In the following section, we will ity usually end in spontaneous miscarriages. However,
look first at the known biological causes of intellec- it is estimated that 0.5 per cent of all newborn babies
tual disability, followed by some of the environmental have a chromosomal disorder, although many of these
factors thought to be involved. Table 17.2 provides a die soon after birth (Smith, Bierman & Robinson, 1978).
summary of some of the known causes of intellectual Chromosomal disorders account for around 25-30 per
cent of all diagnosed cases of intellectual disability and
the two most prominent forms are Down syndrome
TABLE 17.2 Causes of intellectual disability and fragile X syndrome.
Down syndrome was Down syndrome A disorder caused by '
Developmental first described by British the presence of an extra chromosomein —
period Cause or risk factor doctor Langdon Down pairigs byintellectual hee
Before/during Inherited recessive gene disorders (e.g. in 1866. However, it was oe gh peach ane ;
conception phenylketonuria, Tay-Sachs disease) not until 1959 that French -
Chromosome abnormalities (e.g. geneticist Jerome Lejeune first reported that individuals
Down syndrome, fragileXsyndrome) with Down syndrome almost always possess an extra
During Severe maternal malnutrition chromosome in pair 21, which is usually caused by errors
pregnancy Maternal iodine deficiency in cell division in the mother’s womb. Down syndrome
Maternal infections (e.g. rubella, syphilis, occurs in around 1.5 of every 1000 births (i.e. a prevalence
HIV, herpes simplex) rate of 0.15 per cent) (Simonoff, Bolton & Rutter, 1996)
ae eeepc: aconolisin and risk is related to the age of the mother. For women
tobacco abuse, illegal drug abuse) yea rae
Maternal medications (e.g. cancer aged 20-24 years the risk is 0.07 per cent. This rises to
chemotherapy) 1 per cent for women aged 40 years and up to 4 per cent
; ; ; ] ; in women aged over 45 years (Thompson, McInnes &
During birth Anoxia and hypoxia (oxygen starvation
Willard, 1991). Although this link between maternal age
or insufficient oxygen supply)
Low birth weight
and incidence of Down syndrome has been known for
some time, it is still unclear how maternal age contrib-
Early childhood Brain infections (e.g. encephalitis, utes to the chromosomal abnormalities. The majority
meningitis)
of individuals with Down syndrome have moderate to
Childhood malnutrition
Severe head injury (e.g. physical accidents, severe intellectual impairment with a measurable IQ usu-
physical abuse such as shaken baby ally. between 35 and 55. They also have a distinctive phys-
syndrome) ical appearance with eyes that slant upward and outward
Exposure to toxins (e.g. lead, mercury) with an extra fold of skin that appears to exaggerate the
Social deprivation and poverty (e.g. slant. They are usually shorter and stockier than aver-
poor parenting, unstimulating infant age, with broad hands and short fingers. They may also
environment)
have a larger than normal furrowed tongue that makes
574 PSYCHOPATHOLOGY
it difficult for them to pronounce words easily. They chemicals is impaired. There are many different types of
also suffer physical disability, such as heart problems, metabolic disorders and many can affect intellectual ability.
and appear to age rapidly, with mortality high after 40 Such disorders are often caused by genetic factors and
years of age. Ageing is also closely associated with signs may be carried by a recessive gene. When both parents
of dementia similar to Alzheimer’s disease (see Chapter possess the defective recessive gene, then their offspring
15) and this may be a result of the causes of both disor- are in danger of developing
ders being closely located on chromosome 21 (Zigman, the metabolic disturbances recessive gene A gene that must be
“ Pa 4
present on both chromosomes in a
.
Schupf, Sersen & Silverman, 1995; Selkoe, 1991). Down linked to that gene. We pair to show outward signs of a certain
syndrome can be identified prenatally in high-risk par- will provide examples of characteristic. 3
ents by using a procedure known as amniocentesis which two such genetically deter-
involves extracting and ana- mined metabolic disorders that affect intellectual ability.
amniocentesis A procedure which lysing the pregnant moth- These are phenylketonuria (PKU) and Tay-Sachs disease.
involves extracting and analysing the Phenylketonuria (PKU) is caused by a deficiency of
er’s amniotic fluid. This is
pregnant mother's amniotic fluid used
prenatally in identifying Down syndrome
now a routine procedure the liver enzyme phenylalanine 4-hydroxylase, which
in high-risk parents. for pregnant mothers that is necessary for the effective metabolism of the amino
is carried out after week 15 acid phenylalanine. As a result of this deficit, phenylala-
of pregnancy and is recommended in the UK and US for nine and its derivative phe- phenylketonuria (PKU) A metabolic
mothers over the age of 35 years. The results of this process nylpyruvic acid build up in disorder caused by a deficiency of the
can leave prospective parents with difficult decisions about the body and irreparably liver enzyme phenylalanine 4-hydroxyla Ss
whether to maintain a pregnancy or not but, even so, amni- damage the brain and cen- which is necessary for the effective metab
olism of the amino acid phenylalanine.
ocentesis will only identify between 15 and 30 per cent of tral nervous system by pre-
Down syndrome cases in pregnant mothers who are tested. venting effective myelination of neurons (myelination is
Another important chromosomal abnormality that the development of a protective sheath around the axons
causes intellectual disability is known as fragile X syndrome. of neurons that enables effective transmission between
This is where the X chromosome appears to show physi- nerve cells). This results in severe intellectual disability
cal weaknesses and may be and hyperactivity. In the UK, PKU has an incidence of
fragile X syndrome A chromosomal bent or broken, and frag- around 1 in 10,000 live births (NSPKU, 2004) and it is car-
abnormality that causes intellectual dis-
ile X syndrome occurs in ried on the phenylalanine hydroxylase gene (PAH) on
ability where the X chromosome appears
to show physical weaknesses and may be approximately 0.08-0.4 per chromosome 12 (Doss & Sethumadhavan, 2009). Several
bent or broken. cent of all births (Hagerman hundred mutations of this gene have been identified,
& Lampe, 1999). Individuals but just five account for approximately 60 per cent of
with fragile X syndrome possess mild to moderate levels of PKU cases in European populations. It is estimated that
intellectual disability and may also exhibit language impair- as many as 1 in 70 people may be carriers of the reces-
ment and behavioural problems such as mood irregulari- sive gene responsible for PKU. At-risk parents who may
ties (Eliez & Feinstein, 2001; Zigler & Hodapp, 1991). Like carry the gene are now routinely given blood tests to
individuals with Down syndrome, they also have specific determine the risk of having a child with PKU. Diet
physical characteristics, such as elongated faces and large, is also an important factor in controlling intellectual
prominent ears (see Photo 17.2). Studies suggest there may deficits in fetuses and offspring at risk of PKU. A special
be a syndrome of fragile X chromosome in which different diet low in phenylalanine is recommended for at-risk
individuals manifest rather different symptoms and degrees pregnant mothers and if children with PKU are given
of disability (Hagerman, 1995). For example, some may diets low in phenylalanine from birth to at least 6 years
have normal IQ levels but suffer specific learning disabili- of age, this can minimize neurological damage and
ties. Others may exhibit emotional lability and symptoms intellectual deficit (Mazzoco, Nord, van Doorninck,
characteristic of autism, such as hand-biting, limited speech Greene et al., 1994),
and poor eye contact (Dykens, Leckman, Paul & Watson, Tay-Sachs disease is also a metabolic disorder caused
1988), and around one in three will exhibit symptoms of by a recessive gene (often found in children of Eastern
autism spectrum disorder (Hagerman, 2006). Intellectual European Jewish ancestry). The defective gene results in
impairment will usually be greatest in males suffering frag- an absence of the enzyme hexosaminidase A in the brain
ile X syndrome because they only have one X chromosome. and central nervous system and this eventually causes
Because females possess two X chromosomes the risk of neurones to die. The dis-
intellectual disability is less (Sherman, 1996). order is degenerative, with Tay-Sachs disease A metabolic disorder
caused by a recessive gene which results i
infants of around 5 months an absence of the enzyme hexosominidas
Metabolic disorders Metabolic disorders occur showing an exaggerated Ain the brain and central nervous system
when the body’s ability to produce or break down startle response and poor eventually causing neurons to die.
Down syndrome
A
be
LAST
iStock.com/Denkuvaiev.
©
Willatt,
L.
Anglian
East
Regional
Library.
Genetics
Service/Science
Photo
Fragile X syndrome
Wellcome
Images. Medical
Custom
Stock
Photo/Science
Photo
Library.
PHOTO 17.2 The typical facial features of children born with Down syndrome or fragile X syndrome. Individuals with Down
syndrome almost always possess an extra chromosome in pair 21, while in fragile X syndrome the Xchromosome shows physical
weaknesses and may be bent or broken.
motor development. Only around 17 per cent of sufferers Perinatal causes From conception to the early post-
live beyond 4 years of age (Sloan, 1991) but those that do natal period is a dangerous time for an organism that is
show rapid decline in cognitive, motor and verbal skills. developing as rapidly as a human baby. Because of this,
The disorder is relatively rare, occurring in around 1 in there are considerable prenatal and immediately post-
360,000 live births worldwide, and this rate is being sig- natal factors that put normal development at risk and
nificantly reduced by effective screening. may cause lifelong intellectual disability. One type of risk
576 PSYCHOPATHOLOGY
involves those factors that can adversely affect the fetus’s or severe birth defects. Up to 20 percent of babies
interuterine environment and its food supply. These born live will have CRS causing heart disease, deafness
include factors such as maternal infections, substance and intellectual impairment. The incidence of CRS is
abuse or malnutrition. Disorders acquired during pre- between 70 and 170 per 100,000 live births and incidence
natal development are known as congenital disorders is still relatively high in developing countries (Cutts &
congenital disorders Disorders acquired because they are acquired Vynnycky, 1999). In contrast, maternal HIV infection
during prenatal development prior to birth prior to birth but are not has become an important maternal HIV infection The incidence o
but which are not genetically inherited. genetically inherited. cause of intellectual dis- a mother having HIV during pregnancy,
Maternal diet is one example. For instance, if there ability. If the mother is leading to a likelihood that the infection
will be passed on to the fetus.
is too little iodine in the mother’s diet during pregnancy not being treated for HIV.
this can give rise to the condition known as cretinism. during pregnancy there is a likelihood that the infection
The mother’s iodine deficiency may often be caused will be passed on to the fetus. The infection can also be
by a hormonal imbal- passed on through breastfeeding. There is then almost a
cretinism A congenital disorder resulting
ance called thyroxine defi- 50 per cent chance that the newborn child will develop
in slow development, intellectual disabili-
ties and small stature. ciency. Children suffering moderate to severe intellectual disabilities. However, in
from this disorder show utero transmission of HIV can be reduced from 25 per
slow development, intellectual disabilities and often cent to 8 per cent if the mother is given an antiretrovi-
have a small stature. Thankfully the condition is rela- ral drug such as zidovudine during pregnancy and if the
tively rare nowadays thanks to the availability of iodized newborn child then receives the drug for up to 6 weeks
table salt and the fact that most diets now contain suffi- postnatally (Belfer & Munir, 1997).
cient iodine. Similarly, mineral and vitamin deficiencies A further significant cause of intellectual disability
caused by maternal malnutrition during pregnancy can is maternal drug use during pregnancy. In many cases
also result in intellectual the drugs responsible for offspring intellectual disabil-
maternal malnutrition Mineral and ity may be ones taken for medicinal purposes (such as
disability and significantly
vitamin deficiencies during pregnancy that
can result in intellectual disabilities in the
affect the child’s physical drugs taken during cancer chemotherapy treatment)
child. and behavioural develop- but most other cases occur where the mother is a sub-
ment (Barrett & Frank, stance abuser. For instance, US studies indicate that
1987). However, the adverse effects of maternal mal- 18 per cent of pregnant women smoke tobacco, 9.8
nutrition can often be partially rectified by providing per cent drink alcohol and 4 per cent use illegal drugs
new-born infants with intellectually supportive environ- (Jones, 2006). Fetal alcohol syndrome (FAS) is one such
ments and appropriate food supplements (Zeskind & example of maternal drug abuse causing childhood
Ramsay, 1981; Super, Herrera & Mora, 1990). In most intellectual disabilities. Whenever a pregnant mother
Westernized societies maternal malnutrition is rela- drinks alcohol, it will enter the fetus’s bloodstream,
tively rare but when it does occur it probably occurs in slow down its metabolism and affect development. If
conjunction with other factors likely to harm the child’s this occurs on a regular basis, then development of
intellectual and physical development, such as mater- the fetus will be severely impaired. Children suffer-
nal drug or alcohol addiction, low socio-economic ing FAS will usually have lower birth weight, lower IQ
status and possibly maternal HIV or syphilis infection (between 40 and 80) and suffer motor impairments and
(see below). deficits in attention and working memory (Niccols,
Maternal infectious diseases during pregnancy are 1994; Burden, Jacobson, Sokol & Jacobson, 2005). They
another potential cause of intellectual disability in the will also frequently exhibit distinctive facial character-
offspring. Such diseases are most damaging during istics including slit eyes, short noses, drooping eyelids
the first trimester of pregnancy when the fetus has lit- and thin upper lips. In the UK around one in every
tle or no immunological protection. Common maternal six to seven thousand babies born have FAS (National
diseases that can cause intellectual impairment in the Organization on Fetal Alcohol Syndrome, 2012).
offspring include rubella (German measles), syphilis and Recently attention has also been focused on the intel-
HIV amongst others. If a mother contracts rubella dur- lectual and developmental effects on children of illegal
ing the first 10 weeks of drugs use by pregnant mothers. Use of both cocaine
congenital rubella syndrome (CRS) The pregnancy, there is almost and crack cocaine (see Chapter 9) by a pregnant
constellation of abnormalities caused a 90 per cent chance that mother can lead to babies being physically addicted to
by infection with the rubella (German
the baby will develop con- the drug before birth (known as ‘crack babies’). There
measles) virus before birth. The syndrome
is characterized by multiple congenital genital rubella syndrome is some evidence that this can adversely affect physi-
malformations (birth defects) and intel- (CRS) resulting in abor- cal development and brain development in particular
lectual disability. tion, miscarriage, stillbirth (Hadeed & Siegel, 1989) and result in slow language
CHAPTER 17 NEURODEVELOPMENTAL DISORDERS a
development (van Baar, 1990). However, it is clear that shaken baby syndrome. This refers to traumatic brain
maternal drug-taking while pregnant may often occur injury that occurs when a baby is violently shaken. In
in contexts that may also contribute to poor intel- comparison to babies who shaken baby syndrome A form of child
lectual development in the offspring, and these may receive accidental trau- abuse that is known to cause intellectual
include the abuse of other drugs, pregnancy depriva- matic brain injury, shaken disability. It refers to traumatic brain
tions (such as dietary imbalances) and economic and baby injuries have a much injury that occurs when a baby is violently
shaken.
social deprivation (Vidaeff & Mastrobattista, 2003). As worse prognosis, includ-
such, this makes it difficult to assess the specific affect ing retinal haemorrhaging that is likely to cause blindness
of maternal cocaine use on offspring intellectual devel- and an increased risk of mental disability such as cerebral
opment (Jones, 2006). palsy or intellectual impairment (Lind, Laurent-Vannier,
One final example of a perinatal cause of intellectual Toure, Brugel & Chevignard, 2013). Nevertheless, we
disability is anoxia, which must remain cautious about the degree to which shaken
xia A perinatal cause of intellectual is a significant period baby syndrome may contribute to intellectual disability
bility, being a significant period GED bbe tocctnn
jout oxygen that occurs during or é ye i j 8
because of current controversies over how the syndrome
ediately after delivery. during or immediately should be diagnosed (e.g. Kumar, 2005).
after delivery. Lack of oxy- During early development children may also be
gen to the brain during the birth process can damage exposed to toxins that can cause neurological damage
parts of the brain that are yet to develop and as a result resulting in intellectual impairment. One such toxin is
can cause both physical and intellectual impairment lead, which is still frequently found in the pollution from
(Erickson, 1992). The main neurological birth syndrome vehicles that burn leaded petrol. Lead-based paint is also
caused by anoxia is cerebral palsy which is character- found in older properties and so may well be a risk factor
‘bral palsy The main neurological ized by motor symptoms in children living in deprived, low socio-economic areas.
1 syndrome caused by anoxia which that affect the strength Lead causes neurological damage by accumulating in
aracterized by motor symptoms that and coordination of move- body tissue and interfering with brain and central nerv-
ct the strength and coordination of ment. While the primary ous system metabolism. Children exposed to high levels
fement.
disabilities are mainly of lead have been found to exhibit deficits in IQ scores of
physical, around one-third of those suffering from cer- up to 10 points (Dietrich, Berger, Succop, Hammond &
ebral palsy will also suffer some form of intellectual, cog- Bornschein, 1993). Even in Westernized societies aware
nitive or emotional disability as well. of the risks associated with exposure to lead the preva-
lence of lead poisoning in children aged 1-2 years is still
Childhood causes as high as 1 per cent (Ossiander, Mueller & van Enwyk,
Although a child may be born healthy, there are poten- 2005). Prevalence rates are significantly higher than this
tially numerous early childhood factors that might put is developing countries (Sun, Zhao, Li & Cheng, 2004).
the child at risk of intellectual disability. Very often these Finally, there is evidence to suggest that social depri-
factors may operate in conjunction with other causes vation and poverty can themselves contribute to intel-
such as perinatal problems. We will look briefly at four lectual disability. Although such factors may not directly
groups of potential childhood causes of intellectual dis- cause impairment to the biological substrates under-
ability, namely accidents and injury, exposure to toxins, lying intellectual ability, they may contribute a form
childhood infections, and poverty and deprivation. of intellectual impoverishment that can be measured
During their early developmental years, young children in terms of lowered IQ scores (Garber & McInerney,
will often be involved in accidents and these can often be 1982). Social deprivation and poverty are also inextrica-
severe enough to cause irreversible physical damage and bly linked to other risk factors for intellectual disability,
intellectual impairment (Ewing-Cobbs, Prasad, Kramer, including poor infant diet, exposure to toxins (such as
Cox et al., 2006). Common childhood accidents that may lead paint in old or run-down housing), maternal drug-
cause permanent intellectual disability include falls, car taking and alcoholism, and childhood physical abuse. A
accidents, near drownings, suffocation and poisoning. cycle of deprivation, poverty and intellectual disability is
However, at least some of the injuries that cause intellec- established when young adolescents in deprived environ-
tual disability in children may not be genuine accidents but ments themselves give birth teenage mothers In relation to intellectual
may be the result of physical abuse by others. A retrospec- to children while still teen- disabilities, young mothers who become
agers (Wildsmith, Manlove, pregnant before 18 years of age, and who
tive study of head injuries in children aged between 1 and
are likely to have lived in deprived areas
6 years of age estimated that 81 per cent of cases could Jekielek, Anderson Moore &
prior to giving birth, are often unmarried,
be defined as accidents and 19 per cent as definite cases Mincieli, 2012). Such teen- live in poverty as a result of their premature
of abuse (Reece & Sege, 2000). One form of child abuse age mothers are frequently motherhood, and are likely to have a signifi-
that is known to cause intellectual disability is known as found to live in deprived cantly lower than average |Q.
578 PSYCHOPATHOLOGY
areas, are often unmarried, live in poverty as a result Whitman, Passino, Rellinger et al., ‘1992; Bromaii>
of their premature motherhood, and have a signifi- Nichols, Shaughnessy, Kennedy et al., 1987). As we said
cantly lower than average IQ themselves (Carnegie earlier, it is difficult to estimate solely how much this is
Corporation, 1994; Borkowski, Whitman, Passino, due to the teenage mother’s age and her parenting prac-
Rellinger et al., 1992). Studies have shown that teenage tices, because the child of a teenage mother is signifi-
mothers are significantly more likely to punish their chil- cantly more likely to be raised in the kinds of deprived
dren than praise them and are significantly less sensitive environments that contain many other risk factors for
to their children’s needs than older mothers (Borkowski, intellectual disability.
Whitman, Passino, Rellinger et al., 1992; Brooks-Gunn & Finally, one important feature of deprived environ-
Chase-Lansdale, 1995). Asa result, children born to teen- ments is that they will usually provide significantly
age mothers are at increased risk of problematic parent— decreased levels of stimulation for young children,
child interactions, (Leadbeater, Bishop & Raver, 1996), including lower rates of sensory and educational stimu-
behavioural difficulties (Fergusson & Lynskey, 1993), and lation, lack of one-to-one child-parent experiences and
cognitive disadvantage and educational underachieve- poverty of verbal communication — all factors that are
ment (Fergusson & Woodward, 1999; Brooks-Gunn, thought to be associated with poor intellectual develop-
Guo & Fustenberg, 1993). Consequently, mild intellec- ment. There are some claims that lack of stimulation can
tual disability is reckoned to occur three times more fre- have a direct effect on the early physical development of
quently in the children of teenage mothers (Borkowski, the brain and so result in permanent impairments to
ae TEENAGE MOTHERS AND THE CYCLE OF UNDERACHIEVEMENT

N
=
= The UK has the highest teenage birth rate in Western * Teenage mothers are more likely to smoke dur-
2 Europe (Avery & Lazdane, 2008). In 2006, in England ing pregnancy and are less likely to breastfeed,
Oo 39,000 girls under 18 years of age became pregnant both of which have negative consequences for
a (Department for Education and Skills, 2006). Although the child.
mA)
ufe)
around half lead to an abortion, the remainder become ° Teenage mothers have three times the rate of
teenage mothers. They are mothers who are likely to postnatal depression of older mothers and a
(i
have lived in deprived areas priorto giving birth, they are higher risk of poor mental health for 3 years after
often unmarried, live in poverty as a result of their pre- the birth.
mature motherhood, and are likely to have a significantly e Children of teenage mothers are generally at
lower than average IQ (Borkowski, Whitman, Passino, increased risk of poverty, low educational attain-
Rellinger et al., 1992). When teenage girls become moth- ment, poor housing and poor health, and have
ers in deprived areas, this sets up a cycle of deprivation, lower rates of economic activity in adult life.
poverty and intellectual underachievement (Wildsmith, ° Rates of teenage pregnancy are highest among
Manlove, Jekielek, Anderson Moore & Mincieli, 2012). deprived communities, so the negative conse-
As a result of their relatively poor parenting skills and quences of teenage pregnancy are dispropor-
the stress that accrues from living in deprived areas, the tionately concentrated among those who are
children of teenage mothers are significantly more likely already disadvantaged.
than the children of older mothers to have behavioural
difficulties (Fergusson & Lynskey, 1993), and suffer cog- As we can see from reading section 17.3.4 many
nitive impairments and educational underachievement of these conditions represent risk factors for intellec-
(Fergusson & Woodward, 1999; Brooks-Gunn, Guo & tual disability and underachievement for the teen-
Fustenberg, 1993). The UK Department for Education age mother’s offspring. These include poor parenting
and Skills (2006) provided the following stark facts: skills, maternal mental health problems, being raised
in unstimulating environments abundant in potential
* Teenage mothers are less likely to finish their stressors, a high likelihood of maternal drug or alcohol
education and are more likely to bring up abuse during pregnancy, and increased risk of physical
their children alone in poverty. abuse or accidents (Moffitt & the E-Risk Team, 2002). At
* The infant mortality rate for babies born to teenage 5, the children of teenage mothers already have a
age mothers is 60 per cent higher than for babies significantly lower IQ than the children of older moth-
born to older mothers. ers (Lubinski, 2000).
CHAPTER 17 NEURODEVELOPMENTAL DISORDERS 579°
brain functioning. For instance, neural development of custodial care are now gone, and provision for such peo-
the brain occurs most extensively and rapidly in the first ple not only attempts to address their needs but also rec-
year after birth (Kolb, 1989) and a rich, stimulating envi- ognizes their fundamental rights as human beings and
ronment is necessary for full development of the brain’s citizens to an inclusive lifestyle. Thus, interventions for
structure (Nelson & Bosquet, 2000). Alternatively, an intellectual disabilities have a number of diverse aims. At
unstimulating, stressful environment can actually trigger the primary level there are those interventions aimed at
the secretion of hormones that prevent effective brain preventing intellectual disability in the first place by edu-
development (Gunnar, 1998). In a study comparing chil- cating potential parents about the risk factors for intel-
dren brought up in deprived inner city areas with a group lectual disability (e.g. educating parents about the effects
provided with good nutrition and a stimulating environ- of maternal alcohol and drug abuse during pregnancy).
ment, Campbell & Ramsey (1994) found that by 12 years A second broad aim of interventions is to make training
of age the deprivation experienced by the former group programmes available that will provide the sufferer with
had a significant negative effect on brain functioning. enough basic skills to cope with many of the challenges
of everyday life (e.g. self-help skills, communication
Summary of the aetiology of skills). Thirdly, approaches to helping those with intel-
intellectual disabilities lectual disabilities are based on the principle of inclusion
From the material covered in this section, you can see in an attempt to help such inclusion Strategies intended to teach
that the causes of intellectual disability are diverse. As we individuals achieve their high-functioning individuals self-help
mentioned earlier, very often it is impossible to pinpoint potential. For example, in strategies, social and fiving skills, and self-
the UK, schools are now management that are designed to help the
the specific cause of an individual’s intellectual disability, individual function more effectively
but intellectual disability caused by chromosomal disor- required to draw up acces- in society.
ders (such as Down syndrome and fragile X syndrome) sibility strategies to allow
pupils with intellectual disabilities to engage in the edu-
and inherited metabolic disorders are some of the more
easily identified. Individuals are most at risk of develop- cational process without being disadvantaged. Similarly,
ing permanent intellectual disabilities during early devel- social inclusion is also encouraged to provide those with
intellectual disabilities the opportunity for personal,
opment of their central nervous system, which is why
conditions in the uterus and in the immediate postnatal
social, emotional and sexual development. We will now
discuss each of these three types of approach to inter-
period are critical for normal development. Risk factors
vention in more detail.
that can disrupt normal prenatal development of the
brain and central nervous system include maternal infec-
tions, alcoholism, drug abuse and malnutrition. Early Prevention strategies
childhood factors that can affect normal neurological Table 17.2 lists many of the causes and risk factors for
development include accidents, physical abuse, expo- intellectual disability and you can probably glean from
sure to toxins, infectious illnesses and an early childhood this list that many of these causes are potentially prevent-
spent in deprivation and poverty. As we have mentioned able. This is particularly the case with many perinatal
many times in this section, many of these risk factors causes, and especially those involving maternal factors
may operate concurrently to determine levels of intel- during pregnancy. For example, fetal alcohol syndrome
(FAS) is a significant cause of intellectual disability and
lectual disability.
prevention programmes aim at identifying those women
at risk of alcohol abuse during pregnancy and provid-
ing interventions such as alcohol-reduction counselling
17.3.5 Interventions for (Floyd, O’Connor, Bertrand & Sokol, 2006). Recognizing
those at risk can be achieved by using established diag-
Intellectual Disabilities nostic and screening questionnaires (Ismail, Buckley,
Most forms of intellectual disability impose limitations Budacki, Jabbar & Gallicano, 2010) and interventions
on the sufferer’s ability to function fully and actively in include providing feedback on rates of drinking behav-
society. This means that — depending on the severity of iour during pregnancy, discussing strategies for avoiding
the disability — the individual will need support to cope alcohol cravings and binge drinking sessions and, more
with many of the rigours of everyday living. As a result recently, web-based interventions (Tenkku, Mengel,
of the disability, sufferers are at risk of underachieving in Nicholson, Hile et al., 2011). Controlled comparison stud-
many areas of their life, including educationally, occupa- ies suggest that such screening and intervention methods
tionally, economically and socially. In most societies, the significantly reduce the risk for alcohol-exposed pregnan-
days when people with intellectual disabilities were sim- cies compared with non-intervention control participants
ply institutionalized and provided with little more than (Ingersoll, Ceperich, Nettleman, Karanda et al., 2005).
580 PSYCHOPATHOLOGY
Prevention can also be achieved in a number of other Behavioural techniques that adopt basic principles of
ways. For example, genetic analysis and counselling ena- operant and classical conditioning are used extensively
bles those parents at risk of abnormal births to be identi- in these contexts, and the application of learning theory
fied, informed of the risk and counselled about how to to training in these areas
proceed. Blood tests and tests of amniotic fluid such as is also known as applied applied behaviour analysis Applying
the principles of learning theory (par-
amniocentesis enable parents to be informed of risks for behaviour analysis (Davey, ticularly operant conditioning) to the
a range of disorders, including Down syndrome, Tay-— 1998). Basic techniques that assessment and treatment of individual
Sachs disease, phenylketonuria and intellectual disability are used include operant suffering psychopathology.
caused by congenital rubella syndrome (CRS). In addi- reinforcement (rewarding
tion, those disabilities related to dietary irregularities can correct responses — for example, with attention or praise),
also be identified and treated, and these include provid- response shaping (breaking down complex behaviours
ing at-risk pregnant mothers with iodine supplements into small achievable steps and then rewarding each step
to prevent cretinism and providing diets low in pheny- successively), errorless learning (breaking down a behav-
lalanine for pregnant mothers and offspring at risk of iour to be learnt into simple components that can be learnt
phenyketonuria. without making errors — errorless learning is stronger and
Finally, as discussed earlier, conditions associated more durable than learning with errors), imitation learn-
with poverty and social deprivation also put children ing (where the trainer demonstrates a response for the
at risk of educational underachievement, lower than client to imitate), chaining (training the individual on
average IQ and mild intellectual disability, and support the final components of a task first and then working
programmes in the USA and Europe have been devel- backwards to learn the earlier steps) and self-instruc-
oped to try to counteract this risk factor. For example, tional training (teaching the client to guide themselves
family support programmes in the USA have indicated through a task by verbally instructing themselves what
that mothers of low socio-economic status participat- to do at each step). Very often, inappropriate, life-threat-
ing in such schemes are more affectionate and positive ening or challenging behaviours may inadvertently be
with their children and provide more stimulating envi- maintained by reinforcement from others in the environ-
ronments than mothers who are not in such schemes ment (e.g. self-mutilating behaviour may be maintained
(Johnson, Walker & Rodriguez, 1996). Being a teenage by the attention it attracts from family or care staff). In
mother is also a risk factor for children of lower IQ than these cases, a functional analysis can be carried out to help
average (see Focus Point 17.1) and this can be tackled identify the factors maintaining the behaviour, and this is
in a number of ways, including providing teenage girls done by keeping a record of the frequency of the behav-
with advice on and access to contraception, improving iours and noting the antecedents and consequences
teenage mothers’ access to education (Department for of the behaviour (see Treatment in Practice Box 17.1).
Children, Schools & Families, 2010), improving housing Once it is known what consequences might be maintain-
quality and encouraging the presence of a co-residential ing the behaviour, these can be addressed to prevent the
partner rather than raising a child alone (Berrington, behaviour being reinforced (Mazaleski, Iwata, Vollmer,
Diamond, Ingham, Stevenson et al., 2004). Zarcone & Smith, 1993; Wacker, Steege, Northrup,
Sasso et al., 1990).
Training procedures
The quality of life of people with intellectual disabili- Inclusion strategies
ties can be improved significantly with the help of basic Policy on the development and education of individu-
training procedures that will equip them with a range als with intellectual disabilities has changed significantly
of skills depending on their level of disability. Types of over the past 35 years. Prior to inclusion policies being
skills include self-help and adaptive skills (such as toilet- introduced, even individuals with mild intellectual dis-
ing, feeding and dressing), language and communication abilities were often deprived of any effective participa-
skills (including speech, comprehension, sign language), tion in the society in which they lived, and more often
leisure and recreational skills (such as playing games, than not they would be institutionalized or educated
cooking skills), basic daily living skills (using a telephone, separately. However, many countries have introduced
handling money) and controlling anger outbursts and accessibility strategies that extend the rights of individu-
aggressive and challenging behaviour (reducing the ten- als with intellectual disabilities to be educated accord-
dency to communicate through aggressive or challenging to their needs in mainstream schools. This approach
ing behaviours such as pushing or shouting). Training evaluates the individual’s specific needs and then sug-
methods can also be used in more severe cases to con- gests strategies, services and supports that will optimize
trol life-threatening behaviours such as self-mutilation or the functioning of these individuals within society. In the
head-banging. UK, the government’s strategy for individuals with
CHAPTER17 NEURODEVELOPMENTAL DISORDERS 581

A FUNCTIONAL ANALYSIS OF CHALLENGING BEHAVIOUR
Some individuals with intellectual disabilities typically is undertaken by keeping a record of the frequency of
display behaviour that may put themselves or others at the behaviours and noting the antecedents and conse-
risk, or which may prevent the use of community facili- quences ofthe behaviour. This will take the form of:
ties or prevent the individual having a normal home life.
Challenging behaviours may take the form of aggres- A. What happens before the challenging behaviour
sion, self-injury, stereotyped behaviour or disruptive and (the trigger);
destructive behaviour generally. In many cases, a func- B. What the individual does (the behaviour);
tional analysis may help to identify the factors maintain- C. What the person gets as a result of the behaviour
ing the challenging behaviour, and these factors may (the consequence).
range from social attention, tangible rewards such as a
hug, escape from stressful situations or they may sim- A typical ‘ABC’ chart on which family and carers will
ply provide sensory stimulation. A functional analysis keep a record of these behaviours will often look like this:
Antecedent (what Behaviour (describe Consequence (what

happened before the exactly what the happened immediately
Date behaviour occurred?) person did) after the behaviour?) Signature
A FUNCTIONAL ANALYSIS CASE HISTORY in the lounge when there were a number of people in
the room and the television was on. The consequence
Andy is a middle-aged man with severe intellectual of Andy starting to rock and slap himself was that staff
disability. He has recently moved into a group home would remove him from the room and take him into the
which he shares with seven other people. Since he kitchen where it was empty and quiet.
moved in, staff have observed several incidents of It was hypothesized that the function of the behaviour
self-injury. They report that Andy starts to rock back- for Andy was to escape from a noisy and crowded situa-
wards and forwards in his chair, and this then escalates tion. Staff decided to respond by watching Andy for early
into him slapping his face repeatedly. Staff have asked signs he may be feeling overstimulated and to ask him if
for help. he wanted to leave the room.
The staff team working with Andy were asked to com- This led to a reduction of self-injury and later it was
plete ABC charts for 4 weeks. These were then analysed noted that Andy would now try to attract staff attention
and it was found that the behaviour tended to occur when he wanted to leave.
special educational needs (SEN) involves improving with SEN, including the development of suitable educa-
the support system for these children and young people tional materials, and the training of specialist teachers
and their families, and providing an integrated educa- and support staff (Department for Education, 2013).
tion, health and care plan Social and educational inclusion also has indirect benefits
cial educational needs (SEN) A
1 used in the UK to identify those who for them (from birth to age for the individual. Kim, Larson & Lakin (2001) reviewed
lire instruction or education tailored 25 years), improving educa- those studies carried out between 1980 and 1999 that
reir specific needs. tional provision for pupils investigated the effects of the shift from institutionalized
582 PSYCHOPATHOLOGY
living to living in the community. Most studies reported have opportunities to pursue social, educational ands
an improvement in three areas: (1) overall improvements occupational goals and pursue their own personal devel-
in coping with day-to-day living and increases in self- opment. For example, individuals with intellectual dis-
esteem, (2) a decrease in the frequency of maladaptive abilities now have the right to pursue their own sexual
behaviours, such as aggression or anger outbursts, and and emotional development — usually with the support
(3) an improvement in self-care behaviours and social of their family. Whereas in the past involuntary sterili-
skills. Case History 17.1 recounts the story of Thomas, a zation was common for such individuals, appropriate
Down syndrome sufferer, who lives with his family and training and counselling now means that most of them
has benefited in a variety of ways from participating in a can be taught about sexual behaviour to a level appropri-
range of community activities. ate for their functioning. This often means that they can
Inclusion policies have resulted in significant improve- learn to use contraceptives, employ responsible family
ments to the quality of life experienced by individuals planning, get married and — in many cases — successfully
with intellectual disabilities, and such individuals now rear a family, either on their own or with the help of
THOMAS'’S STORY
Thomas is 23 and lives with his mum and dad. His brother now lives away but sees him quite regularly.
Thomas has Down’s syndrome and needs a great deal of support. He goes to college four days a week and, on
Fridays, attends a project where he is learning living skills and enjoying cooking. Thomas has a supported work
placement for two hours a week in a riding stable. He has a hectic social life with weekly activities including rid-
ing, sports, going to the gym, trampolining and football. He goes to monthly discos with a group of young people
with learning disabilities and is regularly to be found in the local pub playing pool with his friends.
We were transporting him to and from these activities and were concerned that he should be able to mix
HISTORY
CASE
17.1 more with his own age group. We arranged for 15% hours’ worth of direct payments for Thomas to choose some-
one in his peer group to help him access these activities. There was a great deal of interest in the advert we placed
at the local university for a student to help with this and we have had several different students helping over the
past year, who have become firm friends. Thomas's current helper, Laura, accompanies him on his outings and
Thomas has now become a part of a wider social circle, going to the pub, out for meals and watching videos at
Laura's house with her friends, which he greatly enjoys.
Thomas's moods, self-esteem and well-being are greatly improved by the stimulation and social nature ofall
that he does, as well as the routine and structure it brings to his life.
Thomas and his friends have gained enormous confidence from attending several drama courses and
the group has enjoyed the feeling of empowerment and also the opportunity to show their feelings. Last year,
a group of 11 young adolescents, including Thomas, attended a week-long outward bound course, run by the
Calvert Trust, without their families. Afterwards, the group made a presentation to about 80 people who had
been involved in organizing or fundraising their trip, with a very professional PowerPoint presentation and
question-and-answer session. They were all keen to contribute, wanted to find other groups to make their
presentation to and gained lots of confidence from this. It makes a change from the usual painting eggs and
bingo offered by local services, which are just not appropriate for a 22-year-old.
Source: From evidence from a family carer given to the Foundation for People with Learning Disabilities’ Inquiry into Meeting
the Mental Health Needs of Young People with Learning Disabilities - Count Us In.
Clinical Commentary
Thomas is an example of how individuals with intellectual disabilities can benefit significantly from acces-
sibility and inclusion strategies. He has work in a supported employment setting and has a full social life
in which he can mix with people of his own age. This approach has the benefit of building confidence and
self-esteem, as well as providing the individual with a real sense of empowerment.
CHAPTER 17 NEURODEVELOPMENTAL DISORDERS 583°
local services (Lumley & Scotti, 2001; Levesque, 1996). workshop have been shown to exhibit higher levels of
However, while inclusion in its broadest sense continues job satisfaction than those who work outside such a
to benefit individuals with intellectual disabilities, there is scheme, and those living in a semi-independent home
still much confusion over the way in which inclusion is and also working in a sheltered workshop showed the
defined and operationalized (Bigby, 2012) and this makes highest levels of self-esteem (Griffin, Rosenberg &
objectively measuring the success of such policies diffi- Cheyney, 1996).
cult (Martin & Cobigo, 2011).
People with intellectual disabilities are three to Summary of Interventions for
four times less likely to be employed than non-disa- Intellectual Disabilities
bled counterparts (Verdonschot, de Witte, Reichrath, This brief insight into some of the interventions
Buntinx & Curfs, 2009), but employment opportuni- deployed in helping people with intellectual disabili-
ties are being made increasingly available to individu- ties has included: (1) the use of prevention strategies
als with intellectual disabilities. Many are conscientious designed to identify those at risk of having offspring
and valued workers employed in normal work envi- with intellectual disabilities (e.g. those with recessive
ronments. Others with more specific needs may need gene disorders or mothers at risk during pregnancy),
to pursue employment within sheltered workshops providing them with skills to minimize risk and coun-
or supported employment settings, which provide selling them about the possible outcomes; (2) a range
tered workshops Settings that pro- employment tailored to of training programmes and techniques to provide indi-
> individuals with intellectual disabili- the individuals’ ownneeds. viduals with learning difficulties with a variety of eve-
with employment tailored to their own The UK government seeks
ds and abilities. : ryday skills; and (3) the adoption of inclusion strategies
to promote employment that provide the individual with educational and occu-
as another form of social inclusion for individuals with pational environments tailored to meeting their needs
intellectual disabilities. Those working in a sheltered within mainstream society.
| SELF-TEST QUESTIONS —
© Can you describe both the traditional and more recent alternative approaches to defining intellectual disability?
® Whatare the different levels of intellectual disability defined in DSM-5?
* What are the main chromosomal disorders that cause intellectual disability?
e Can you describe at least two metabolic disorders that give rise to intellectual disability?
® What is meant by the term ‘congenital disorder’ when used in relation to intellectual disability? Can you give some
examples of congenital causes of intellectual disability?
® What are the main childhood causes of intellectual disability?
© Can intellectual disability be prevented? If so, how?
® Can you describe the kinds of training procedures that are used to help individuals with intellectual disabilities acquire
self-help and communication skills?
® Can you describe some examples of inclusion strategies that have been used in relation to intellectual disability?
SECTION SUMMARY
17.3. INTELLECTUAL DISABILITIES
We began this section by describing the DSM-5 diagnostic criteria for intellectual disability and discussing some alternative
types of definition and terminology that focus on identifying needs and facilitating adaptive functioning. The aetiology of
intellectual disorders is a diverse topic, with no identifiable cause being found for a large proportion of those with intel-
lectual disabilities. Biological causes are primarily responsible for those aetiologies that can be identified, and these include
PSYCHOPATHOLOGY
CS DN
chromosomal disorders, recessive gene disorders and perinatal factors. Childhood problems can also contribute to intellec-
tual disability and we discussed the role of accidents, abuse, infectious diseases and the nonspecific detrimental effect that
social deprivation and poverty can have on intellectual development. In the final section we covered interventions for the
prevention of intellectual disability and programmes for the care, development and support of individuals with intellectual
disabilities.
¢ Intellectual disability is a term that covers impairments in both intellectual and adaptive functioning.
Intellectual disability involves significantly below average intellectual functioning, usually defined by a score on a standard-
ized IQ test of below 70.
¢ Modern approaches to defining intellectual disabilities attempt to highlight those factors that might be required to facili-
tate more adaptive functioning, and to draw up accessibility strategies to ensure that such individuals are not excluded or
disadvantaged in their education.
© Chromosomal disorders such as Down syndrome and fragile
X syndrome account for around 25-30 per cent ofall diagnosed
cases of intellectual disability.
¢ Metabolic disorders that cause intellectual disability are usually carried by a recessive gene and include phenylketonuria
(PKU) and Tay-Sachs disease.
* Congenital disorders are those that are acquired prior to birth but are not genetically inherited. Congenital causes of intel-
lectual disability include maternal malnutrition, congenital rubella syndrome (CRS), maternal HIVinfection and fetal alcohol
syndrome (FAS).
® Childhood environmental causes ofintellectual disability include childhood accidents (including intentional physical abuse
by others), exposure to toxins (such as lead), childhood infections and poverty and deprivation.
e Prevention strategies for intellectual disability include prevention campaigns and screening for such factors as maternal
alcohol abuse and genetic risk factors.
© Behavioural training procedures can equip sufferers with a range of self-help and adaptive skills, and the application of
learning theory in these areas is known as applied behaviour analysis.
e Inclusion strategies provide those with intellectual disabilities with access to mainstream educational and occupational
opportunities.
skills), and the development of stereotyped or self-injurious

17.4 AUTISTIC SPECTRUM behaviour patterns (e.g. hand biting and hair pulling). Prior
DISORDER (ASD) to DSM-5 there were several different ASD diagnostic cat-
egories and these included autistic disorder (autism), Rett’s
disorder, childhood disintegrative disorder and Asperger’s
Some disorders are characterized by serious abnormalities syndrome. However, DSM-5 has combined these into
in the developmental process and those that fall under the one single dimensional diagnostic category called autis-
heading of autistic spectrum disorder (ASD) are usually tic spectrum disorder. The reason for this change was that
associated with impair- there was little research evidence to support the independ-
autistic spectrum disorder (ASD) An ment in several areas of ence of all these different diagnostic categories and most
umbrella term that refers to all disorders
that display autistic-style symptoms across
development. From early shared several common features. DSM-5 field studies also
a wide range of severity and disability. infancy, some children will supported the validity of the new DSM-5 diagnostic cri-
exhibit a spectrum of devel- teria, although these new criteria are likely to reduce the
, opmental impairments and number of individuals who would receive a diagnosis of
For a video on autistic spectrum
disorder go to ; delays that include social autistic spectrum disorder (Frazier, Youngstrom, Speer,
www.wiley-psychopathology.com/ : and emotional disturbances Embacher et al., 2012; Wilson, Gillan, Spain, Robertson et
video/ch17
/ (e.g. poor social interaction al., 2013). We will discuss the DSM-5 diagnostic criteria in
with others), intellectual section 17.4.2 but first we will look more closely at some
disabilities (e.g. low IQ), language and communication of the defining characteristics of individuals with autistic
deficits (e.g. failure to learn to speak or develop language spectrum disorder.
17.4.1 The Characteristics of he appears unable to express his needs or has his very
detailed play routines disrupted. The two central features
Autistic Spectrum Disorder of autistic spectrum disorder are severe impairment in
The early development of some children is so profoundly social interaction and in communication but the sever-
disturbed that from as young as less than 1 year of age ity of these symptoms will depend on the developmental
it will become apparent to family and friends that the level and age of the individual.
infant’s development is not proceeding normally. The
child may seem withdrawn, have failed to develop nor- Impairments of reciprocal
mal means of communication, appear uninterested in social interaction
its surroundings and have difficulty learning new skills. The impairment in reciprocal social interaction is one of
Case History 17.2 relates some of the behavioural traits the most marked and sustained features of the disorder.
of Adam, a 1-year-old child who was later diagnosed Sufferers will exhibit impairment in the use of nonverbal
with autistic spectrum disorder. Typical of autistic spec- behaviours (e.g. eye contact, appropriate facial expres-
trum disorders, Adam shows no interest in his surround- sion) and are unable to regulate social interaction and
ings other than an obsessive interest in a small number communication. They will rarely approach others
of toys, he lacks normal communication skills for his and almost never offer a spontaneous greeting or make
age, and appears withdrawn and unable to learn new eye contact when meeting or leaving another individual
responses or skills. He also has temper tantrums when (Hobson & Lee, 1998). In young children, this is often
AUTISTIC SPECTRUM DISORDER

After Adam's first birthday party his mother began to pay attention to some characteristics of her son’s personal-
ity that didn’t seem to match those of the other children. Unlike other toddlers, Adam was not babbling or form-
ing any word sounds, while others his age were saying ‘mama’ and ‘cake’. Adam made no attempt to label people
or objects but would just pronounce a few noises, which he would utter randomly through the day.
At the birthday party and in other situations, Adam seemed uninterested in playing with other children or
even being around them socially. He seemed to enjoy everyone singing ‘Happy Birthday’ to him but made no
attempt to blow the candles out on the cake - even after others modelled the behaviour for him.
HISTORY
CASE
17.2 His parents also noted that Adam had very few interests. He would seek out two or three Disney toys and their
corresponding videotapes and that was it. All other games, activities and toy characters were rejected. If pushed
to play with something new, he would sometimes throw intense, inconsolable tantrums. Even the toys he did
enjoy were typically not played with in an appropriate manner. Often he would line them up in a row, in the same
order, and would not allow them to be removed until he decided he was finished with them. If someone else
tried to rearrange the toys he would have a tantrum.
As the months went by and he remained unable to express his wants and needs, Adam's tantrums
became more frequent. If his mother did not understand his noises and gestures, he would become angry
at not getting what he wanted. He would begin to hit his ears with his hands and cry for longer and longer
periods of time.
Source; Adapted from Gorenstein & Cromer, 2004.
Clinical Commentary
From avery early age, Adam exhibited symptoms ofthe triad of impairments typical of autistic spectrum dis-
order. He shows (1) no sign of engaging in or enjoying reciprocal social interactions (e.g. the lack ofinterest
in socializing with others at his birthday party), (2) a significant delay in the development of spoken speech
(illustrated by his failure to form word sounds, label objects or express his wants and needs), and (3) a lack of
imagination and flexibility of thought (as demonstrated by his inability to use toys in imaginative play and
his inflexibly stereotyped behaviour towards these toys).
(586 PSYCHOPATHOLOGY ’
manifested as a clear lack of interest in making friends, This can manifest in childhood as a specific and detailed
establishing relationships or any other form of peer com- interest in only a small number of toys. Like Adam in
munication. Particularly striking is the autistic child's Case History 17.2, they may line up the same set of toys
apparent inability to understand the intentions or emo- in exactly the same way time after time and become
tions of others and their universal indifference to what very distressed if their routine is disrupted or if they are
others are doing. This has led some theorists to suggest not allowed to complete the routine. There appears to
that children with autistic disorder fail to develop a ‘the- be a need to retain ‘sameness’ in all their experiences
ory of mind’ — that is, they fail to develop an ability to and an autistic child may become extremely distressed
understand the intentions, desires and beliefs of others — if the furniture in a room is changed around or they
and as a result this makes them unable to understand travel on a different route to school one day. Children
why other people behave in the way they do. While chil- with autistic disorder will often form strong attachments
dren with milder forms of the disorder may be able to to inanimate objects, such as keys, rocks, mechanical
learn what physical features of a person are associated objects, or objects with particular types of tactile char-
with the expression of an emotion (e.g. that a frown acteristics (such as the smooth-surfaced dice described in
is associated with anger or disapproval), they are often George’s story at the beginning of this chapter). However,
unable to explain why someone is expressing a particular when they do play with individual objects, such as a toy
emotion (Capps, Losh & Thurber, 2000). car, they rarely indulge in symbolic play (e.g. by moving
the car along the floor as if it were travelling somewhere)
Impairments in communication but instead will usually explore the tactile features of the
There is also a prominent delay in the development of toy in a stereotyped manner (e.g. by simply rotating
spoken language and in those who do learn to speak the car in their hands for long periods of time). A fur-
there is an inability to sustain a conversation. When ther common characteristic of autism is the appearance
speech does develop, it often fails to follow the normal of stereotyped body movements and these can include
rules of pitch, intonation or stress, and a child’s speech hand clapping, finger snapping, rocking, dipping and
may sound monotonous and uninterested. Grammatical swaying. These patterns of behaviour often appear to
structures are often immature and more than half of be self-stimulatory in nature and can often become so
those diagnosed with autistic disorder fail to speak at intense and severe that they may cause the individual
all, but may utter a range of noises and screams that physical injury, such as stereotyped hand and finger bit-
are often unrelated to attempts to communicate. Some ing, head banging, hair pulling and scratching.
individuals exhibit what is known as echolalia, which
is immediate imitation of Intellectual deficits
echolalia The immediate imitation of
words or sounds that have just been heard.
words or sounds they have In addition to these main symptoms, approximately
just heard (e.g. if asked 80 per cent of those diagnosed with autistic spectrum
‘Do you want a drink?’ the child will reply ‘Do you want symptoms exhibit signs of intellectual disability and will
a drink?’). Others that do develop language may only be have an IQ score of less than 70 (Gillberg, 1991; Bryson,
able to communicate in a limited way and may exhibit Clark & Smith, 1988). However, the nature of the intel-
oddities in grammar and articulation. For instance, lectual deficits in children with autistic disorder is often
some exhibit pronoun different to those with a primary diagnosis of intellectual
pronoun reversal An impairment in com-
reversal in which they disability (see section 17.3). Individuals suffering autistic
munication in which an individual refers to
himself or herself as ‘he’ ‘she’ or ‘you’. refer to themselves as spectrum disorder will usually perform much better on
‘he’, ‘she’ or ‘you’ and this tests of visuospatial ability than tests of social under-
is a feature of speech that is highly resistant to change standing or verbal ability. Thus, they are much better at
(Tramonta & Stimbert, 1970). An autistic child’s ability finding hidden figures in drawings, assembling disassem-
to learn language is a good indicator of prognosis. Those bled objects and matching designs in block-design tests
that have learnt meaningful speech by the age of 5 years (Rutter, 1983). However, in many cases individuals with
are the ones that are most likely to benefit from sub- autism may excel at one specific task (such as the abil-
sequent treatment (Werry, 1996; Kobayashi, Murata & ity to calculate dates) or in one particular area (such as
Yoshinaga, 1992). mathematics or music) (see section 17.4.4). In individu-
als with multiple cognitive
Impairments in imagination disabilities, extraordinary savant syndrome The phenomenon of
extraordinary proficiency in one isolated
and flexibility of thought proficiency in one isolated
skill in individuals with multiple cognitive
One common feature of individuals with autistic spec- skill is known as savant disabilities. It appears to be closely linkec
trum disorder is that they often display restricted, repeti- syndrome, and it is a to autistic spectrum disorder and is fre-
tive and stereotyped patterns of behaviour and interests. phenomenon that appears quently found in Asperger's syndrome.
CHAPTER17 NEURODEVELOPMENTAL DISORDERS -587_
rger’s syndrome Impairment in to be closely linked to DSM-5 SUMMARY TABLE 17.6 Criteria for autistic spectrum
linteraction, and the development of autistic spectrum disorder disorder
cted, repetitive patterns of behav-
interests and activities. A diagnostic
and is frequently found
¢ Ongoing deficits in social activities as marked by the
yory no longer used in DSM-5. in Asperger’s syndrome following:
(Heaton & Wallace, 2004).
e Social situation deficits — for example, abnormal social
approach or failure to initiate or respond to social
situations
17.4.2 The Diagnosis of Autistic e Nonverbal communication behaviour deficits — for

example, abnormalities in eye contact or poorly
Spectrum Disorder integrated verbal and nonverbal communication
The characteristics that we have just described form e Inability to develop, maintain or understand
the basis for the DSM-5 diagnosis of autistic spectrum relationships
disorder. These include persistent deficits in social e Restricted and repetitive patterns of behaviour, interest
communication and interaction such as deficits in or activity, as marked by at least two of the following:
social-emotional reciprocity (e.g. failure of normal e Repetitive motor movement, use of objects or speech
back-and-forth conversation), deficits in nonverbal com-
e Inflexibility and strong adherence to routine
munication (e.g. abnormal eye contact) and deficits in
making and maintaining relationships (e.g. difficulties e Abnormally intense fixated interests
in sharing imaginative play). In addition to these social e Hyper- or hyporeactivity to sensory input or unusual
communication deficits, individuals must also exhibit interest in sensory aspects of the environment
restricted, repetitive patterns of behaviour, interests
e Symptoms start in early development
or activities, such as stereotyped or repetitive motor
e Symptoms cause significant impairment in important
movements, or highly restricted, fixated interests. All of
areas of functioning
these criteria are exhibited in the example of Adam in
Case History 17.2. In addition to these criteria related e Symptoms are not better accounted for by intellectual
to social communication and restricted, repetitive pat- disability or global development delay
terns of behaviour, the symptoms must be present in
the early developmental period and must cause signifi-
cant impairment in social, occupational or other areas
of functioning. The diagnosis can also be individual-
and (3) autistic spectrum disorders are often comorbid
ized with the use of specifiers that indicate whether the
with other problems such as ADHD and epilepsy.
symptoms are accompanied by intellectual impairment
or language impairment (DSM-5 Summary Table 17.6).
The DSM-5 criteria also enable the clinician to specify
the severity level for the diagnosis from ‘requiring very 17.4.3 The Prevalence of Autistic
substantial support’ (e.g. rarely initiates interaction and Spectrum Disorder
becomes highly distressed when having to cope with
change), through ‘requiring substantial support’ (e.g. Epidemiological studies estimate the rate of autistic
limited initiation of social interactions and some distress disorder at between 5 and 13 cases per 10,000 (around
when having to cope with change) to ‘requiring support’ 0.05 per cent of births) (DSM-IV-TR, p.73; Fombonne,
(e.g. without support, deficits in social communication 2005). The latest studies of autistic spectrum disorder
cause noticeable impairments; and has difficulty switch- in the UK indicate a prevalence rate of around 1.1 per
ing between activities). cent, indicating that around 695,000 people in the UK
Finally, we must conclude by stressing that diagnos- may be diagnosable with autism (The National Autistic
ing an autistic spectrum disorder is complicated. For Society, 2013). Around 80 per cent of those diagnosed
example, autistic spectrum disorders can manifest over a are boys (Volkmar, Szatmari & Sparrow, 1993; Baron-
range of disabilities from severe to relatively mild high- Cohen, Scott, Allison, Williams et al., 2009) and autism
functioning autism, and at the high-functioning end of appears to occur equally in all socio-economic classes
the spectrum it is often hard to distinguish those symp- and racial groups (Fombonne, 2002). Epidemiological
toms that may be characteristic of autism. Similarly, surveys of autistic spectrum disorder suggest that the
diagnosis is complicated by the fact that (1) behaviour prevalence rate of the disorder has been increasing
patterns may change with age, (2) symptoms may be significantly over the past two decades, with some esti-
manifested with varying degrees of intellectual disability, mates as high as 1 or 2 per 1000 births (between 0.1 and
588 PSYCHOPATHOLOGY
0.2 per cent) (Chakrabarti & Fombonne, 2005). The rea- symptoms, as demonstrated in studies’ of sibling reoe
sons for this are unclear, although one possible cause may currence risk (i.e. studies investigating the probability
be the expansion of the criteria for diagnosis of autis- of developing autism given that an individual’s sibling
tic spectrum disorder in DSM-IV, which was published is autistic). These studies have estirnated that the rate
in 1994, while some others suspect this may be a real of autism in the sibling of someone with autism ranges
increase in incidence resulting from an increase in the between 2 and 14 per cent (Bailey, Phillips & Rutter, 1996;
prevalence of those factors that cause autistic spectrum Jorde, Mason-Brothers, Waldemann, Ritvo et al., 1990),
disorder (e.g. Blaxill, Baskin & Spitzer, 2003). However, which is significantly higher than the 0.05—0.2 per cent
it is clear that the changes to the diagnostic criteria intro- prevalence rate found in the general population. Autistic
duced in DSM-5 will almost certainly cause a reduction spectrum disorder also appears to co-occur with several
in future prevalence rates for autistic spectrum disorder. known genetic disorders such as phenylketonuria, fragile
Studies comparing DSM-5 and DSM-IV-TR diagnostic X syndrome and tuberous sclerosis (Smalley, 1998; Reiss
criteria indicate a reduction of up to 9 per cent in the & Freund, 1990), implying a genetic link in its aetiology.
number of individuals diagnosed with autistic spec- There are also familial links between autistic spectrum
trum disorder under DSM-5 compared with DSM-IV-TR disorder and other psychological problems. For instance,
(Huerta, Bishop, Duncan, Hus & Lord, 2012; Wilson, affective disorders are almost three times more common
Gillan, Spain, Robertson et al., 2013). in the parents of autism sufferers than in the parents of
children suffering from tuberous sclerosis or epilepsy.
While we might expect that having a child with a dis-
17.4.4 The Aetiology of Autistic ability might precipitate such psychological problems, a
majority of parents of autistic children developed their
Spectrum Disorder affective disorder before the birth of the child (Bailey,
In the 1960s, it was believed that autistic behaviour Phillips & Rutter, 1996). _
was caused by cold or rejecting parenting (e.g. see Numerous twin studies have confirmed this genetic
Bettelheim, 1967) — a view that simply added to the component to the disorder. In studies comparing con-
distress of parents already having to cope with a child cordance rates in MZ and DZ twins, Folstein & Rutter
with severe behavioural problems. However, subsequent (1977) found concordance in 4 out of 11 MZ twins but
studies have systematically failed to uphold this view none in DZ twins. Subsequent twin studies have found
and have confirmed that the parents of autistic children concordance rates of between 60 and 91 per cent for MZ
are no different in their parenting skills to those of non- twins and between 0 and 20 per cent for DZ twins (Rutter,
autistic children (Cox, Rutter, Newman & Bartak, 1975; MacDonald, Le Couteur, Harrington et al., 1990; Bailey,
Cantwell, Baker & Rutter, 1978). Nevertheless, the causes Le Couteur, Gottesman, Bolton et al., 1995; Steffenberg,
of autistic spectrum disorder are still relatively poorly Gillberg, Hellgren, Andersson et al., 1989; Lichtenstein,
understood, but it is becoming clear that there is a signifi- Carlstrom, Ramstam, Gillberg & Anckarsater, 2010).
cant genetic element. However, in individual cases there In addition, other recent twin studies have also demon-
is also likely to be a contribution from environmental strated that each of the symptom components of autistic
factors as well, such as perinatal risk factors (e.g. mater- spectrum disorder — social impairments, communication
nal infections during pregnancy), and the various combi- impairments and restricted repetitive behaviours — all
nations of genetics and environmental risk factors may be individually show high levels of heritability (Ronald,
the reason why autistic syndrome disorders vary so much Happe, Price, Baron-Cohen & Plomin, 2006).
in their symptomatology and their severity. As we shall Molecular genetics has identified abnormalities in
see below, it is now accepted that autistic syndrome dis- gene sequencing that is associated with autistic spectrum
order is caused primarily by aberrant brain development, symptoms, including a deletion on chromosome 16
which gives rise to the range of impairments in cognitive (Weiss, Shen, Korn Arking et al., 2008) and an abnor-
abilities and social understanding exhibited by sufferers. mality in gene sequencing on chromosome 5 (Wang,
Zhang, Ma, Bucan et al., 2009). This, along with other
Biological causes studies suggests that a single gene is not responsible for
the expression of autism, and as many as 15 different
Genetic factors There had been evidence available genes may be involved (Santangelo & Tsatsanis, 2005).
for some time that the social and language deficits and However, even when there is strong evidence to suggest
psychological problems reminiscent of autistic spec- the involvement of a single gene, the significance of the
trum disorder often had a family history (Folstein & gene in terms of brain development has been difficult
Rutter, 1988; Piven & Palmer, 1999). In particular, there to determine (Muhle, Trentacoste & Rapin, 2004). This
is evidence for a strong familial aggregation of autistic Suggests that autistic spectrum disorder is a complex
condition that may involve a range of different genetic (MMR) vaccine (Wakefield, Murch, Anthony, Linnell et
influences affecting symptom expression and severity, al., 1998). This claim caused some controversy in the
including several different gene copy number variations UK at the time because it led to many parents refusing
(Freitag, Staal, Klauck, Duketis & Waltes, 2010). to have their children immunized with the vaccine and
so put them at significant risk for these infections (see
Biochemical factors One source of the»cognitive Activity 17.1). However, subsequent studies have failed
and behavioural problems exhibited by individuals with to corroborate an association between administration of
autistic spectrum disorder may be abnormalities in the MMR and autism (e.g. Madsen, Hviid, Vastergaard et al.,
brain neurotransmitters that regulate and facilitate nor- 2002). In addition, recent studies have also failed to find
mal adaptive brain functioning, and this has led to a focus any association between infectious diseases in the first 2
of research on the role of specific neurotransmitters in years of life and autism. Rosen, Yoshida & Croen (2007)
autistic spectrum disorder. Unfortunately, much of the found that children with subsequent diagnoses of autism
research on the role of brain neurotransmitters in autism had no more overall infec-
has been inconclusive (Lam, Aman & Arnold, 2006). Early tions in the first 2 years of To complete Activity 17.1 go to
studies of children diagnosed with autistic disorder indi- life than children without | www.wiley-psychopathology.com/
cated low levels of the neurotransmitters serotonin and autism. activities/ch17
dopamine (Chugani, Muzik, Behen, Rothermel et al., In conclusion, while a

1999; Ernst, Zametkin, Matochik, Pascualvaca & Cohen, very small minority of cases of autism may be linked to
1997), both of which are essential for effective cognitive, perinatal factors such as those outlined above, congenital
behavioural and motor functioning and mood regulation. and perinatal factors are probably not the primary causes
Research in this area is currently plagued by methodologi- of the disorder.
cal difficulties, including small sample sizes, contradictory
findings using different research methodologies, and fail- Brain abnormalities There is now a good deal of
ure to use appropriate control conditions (Lam, Aman & converging evidence from autopsy studies, fMRI stud-
Arnold, 2006). However, provided that these issues can be ies and studies measuring EEG (electroencephalogram)
resolved, it appears to be a fruitful area for future research. and ERP (event-related potentials) that autism is associ-
ated with aberrant brain development. Autopsy studies
Perinatal factors We noted in our discussion of intel- of individuals diagnosed with autistic spectrum disorder
lectual disabilities that perinatal factors may play a signifi- have revealed abnormalities in a number of brain areas,
cant role in determining intellectual impairment and the including the limbic system and the cerebellum. For
same may be true in the case of autistic spectrum disor- example, neurons in the limbic system are smaller and
der. A range of birth complications and prenatal factors more dense than normal and the dendrites, which trans-
have been identified as risk factors in the development mit messages from one neurone to another, are shorter
of autistic spectrum disorder and these include mater- and less well developed (Bauman & Kemper, 1994).
nal infections such as maternal rubella during pregnancy Abnormalities in the cerebellum appear to correspond to
(Chess, Fernandez & Korn, 1978), intrauterine exposure deficits in motor skills such as impaired balance, manual
to drugs such as thalidomide and valproate (Stromland, dexterity and grip, which are often found in individuals
Nordin, Miller, Akerstrom & Gillberg, 1994; Williams, with autistic spectrum disorder (Gowen & Miall, 2005).
King, Cunningham, Stephan et al., 2001), maternal bleed- Finally, autopsy studies have also shown overly large
ing after the first trimester of pregnancy (Tsai, 1987) brain size and enlarged ventricles in the brain (Bailey,
and depressed maternal immune functioning during Luthert, Dean, Harding et al., 1998) and many of these
pregnancy (Tsai & Ghaziuddin, 1997). However, many abnormalities are typical of prenatal stages of brain
of these risk factors have been identified only in individ- development.
ual case reports, and they probably account for a very Anatomical and functional imaging studies have sup-
small percentage of cases of autistic spectrum disorder plemented the evidence from autopsy studies and given
(Fombonne, 2002; Muhle, Trentacoste & Rapin, 2004). us an insight into how brain abnormalities in autism pro-
For example, recent studies suggest that congential gress during different developmental stages. They have
rubella infection has been found to be present in less than confirmed that individuals with autism have abnormali-
0.75 per cent of autistic populations — largely because ties in a number of brain regions, including the fron-
of the near eradication of the disease in Western coun- tal lobes, limbic system, cerebellum and basal ganglia
tries (Fombonne, 1999). Some studies also claim to have (Sokol & Edwards-Brown, 2004), and they also confirm
linked autism to postnatal events such as a link between that autistic individuals have larger brain size and sig-
autistic spectrum disorder, inflammatory bowel disease nificantly poorer neural connectivity than non-sufferers
and administration of the measles, mumps and rubella (McAlonan, Cheung, Cheung, Suckling et al., 2005). We
590 PSYCHOPATHOLOGY '
; * \
have already alluded to the fact that individuals diag- exhibit difficulty in reciprocal social interaction, includ.
nosed with autism may lack a ‘theory of mind’ (the abil- ing deficits in communication and in understanding the
ity to attribute mental states to others or to understand intentions and emotions of others. Some theorists have
the intentions of others) (see section 17.4.1) and fMRI argued that these deficits in social skills are a result of
studies indicate that this is associated with decreased deficits in cognitive functioning (Rutter, Bailey, Bolton &
activation of the prefrontal cortex and amygdala, and Le Couteur, 1994). Firstly, individuals with autistic spec-
these are areas that are an important component of the trum disorder appear to exhibit deficits in executive func-
brain system underlying the understanding of the inten- tioning, resultingin poor problem-solving ability, difficulty
tions of others (Castelli, Frith, Happe & Frith, 2002). The planning actions, controlling impulses and attention, and
larger brain size of individuals with autistic spectrum inhibiting inappropriate behaviour, and these deficits all
disorder may provide some insight into the developmen- have an impact on the ability to act appropriately in social
tal factors that might impair normal brain development situations. Secondly, some theorists have argued that indi-
in childhood. It is only during 2-4 years of age that the viduals with autistic spectrum disorder lack a ‘theory of
brains of individuals with autistic symptoms begin to mind’ (TOM). That is, they fail to comprehend normal
become larger (Courchesne, 2004) but this then stops mental states and so are unable to understand or pre-
at around 4-5 years of age (Hazlett, Poe, Gerig, Styner dict the intentions of others. Thirdly, researchers such as
et al., 2011). Those areas of the brain that are particularly Simon Baron-Cohen have argued that individuals with
enlarged are the frontal, temporal regions and the cer- autistic spectrum disorder do not just exhibit cognitive
ebellum — areas that are associated with language, social impairments, they also have areas of strength, and one
and emotion-based abilities. such strength is their ability to systematize information.
In addition, one in four individuals with autistic spec- We will discuss these three cognitive accounts separately.
trum disorder also exhibit abnormal EEG patterns in the
frontal and temporal lobes, and many of these have actual Deficits in executive functioning Individuals with
clinical seizures (Dawson, Klinger, Panagiotides, Lewy autistic spectrum disorder generally perform poorly
& Castelloe, 1995; Rossi, Parmeggiani, Bach, Santucci & on tests of executive functioning, suggesting that they
Visconti, 1995). In contrast, ERP studies provide informa- may have difficulty problem solving, planning, initiating,
tion from brain activity about how individuals react to organizing, monitoring and inhibiting complex behav-
external stimuli in the environment, and individuals with iours (Ozonoff & McEvoy, 1994; Shu, Lung, Tien &
autism exhibit ERP patterns that indicate disrupted and Chen, 2001). Consistent evidence for executive function-
abnormal attention to a range of stimuli, including novel ing deficits has been found in adults, adolescents and older
stimuli and language stimuli (Courchesne, Townsend, children with autism (McEvoy, Rogers & Pennington,
Akshoomoff, Saitoh et al., 1994; Dunn, 1994). 1993). However, determining the significance of poor
Taken together, these sources of evidence indicate performance on tests of executive functioning is dif-
that individuals with autistic spectrum disorder exhibit ficult because executive functioning tasks require the
abnormalities in a number of different brain areas. These integration of a range of more basic cognitive abilities
brain areas exhibit both anatomical (i.e. structural) such as shifting attention, memory, sequencing events
abnormalities as well as functional abnormalities (i.e. and inhibiting responses. Nevertheless, even when the
they do not appear to be able to fulfil the cognitive func- basic cognitive processes required for successful execu-
tions they do in normally developed individuals). These tive functioning are analysed separately, individuals with
abnormalities appear to be determined by a period of autistic spectrum disorder exhibit deficits in a number
abnormal brain overgrowth in early childhood (hence of these skills, including categorization and concept for-
studies showing that autistic individuals develop oversize mation (Minshew, Meyer & Goldstein, 2002), shifting
brains) followed by abnormally slow or arrested growth, attention (Akshoomoff, Courchesne & Townsend, 1997;
and this deviant brain growth occurs at a time during Belmonte, 2000), planning and abstract problem solv-
development when the formation of brain circuitry is ing (Hill & Bird, 2006), and short-term and long-term
at its most vulnerable (Courchesne, 2004). memory (Bachevalier, 1994; Klinger & Dawson, 1996).
However, evidence suggests that they fail to exhibit
Cognitive factors deficits in cognitive inhibition (inhibiting inappropri-
Depending on the severity of their symptoms, individ- ate responses) (Kleinhans, Akshoomoff & Delis, 2005;
uals with autistic spectrum disorder clearly have prob- Ozonoff & Strayer, 1997) or on tests of semantic flu-
lems attending to and understanding the world around ency (Boucher, 1988; Manjiviona & Prior, 1999). Thus,
them. Most notably, they have difficulty with normal depending on the degree of severity of the disorder,
social functioning. In severe cases they may be with- individuals with autistic spectrum disorder may only be
drawn and unresponsive, while less severe cases may deficient in some of the basic cognitive skills required to.
CHAPTER17 NEURODEVELOPMENTAL DISORDERS 591,
successfully complete executive function tasks and not easily explain the non-social features of behaviour, such
in others. as narrow interests, need for sameness and attention to
detail. Baron-Cohen (2002, 2009) has argued that theory
Theory of mind (TOM) deficits One influential of mind deficits only address the difficulties that people
account of autistic spectrum disorder claims that the with autism experience and does not address their areas
fundamental problem for individuals with autism is that of strength. He suggests that individuals with autis-
they fail to develop a ‘theory of mind’ (Baron-Cohen, tic spectrum disorder may even have superior skills in
Leslie & Frith, 1985; Baron-Cohen, 2001; see Boucher, systematizing — that is, analysing or constructing systems
2012, for a recent review). That is, individuals with to understand the world — and they do this by noting reg-
autism fail to develop an awareness that the behaviour ularities, structures and rules within systems. This leads
of other people is based on mental states that include such individuals to focus on fully understanding indi-
beliefs and intentions about what they should do, and, vidual systems, such as collectible systems (e.g. distin-
as a result, individuals with autism fail to understand the guishing between types of stones), mechanical systems
intentions of others (refer back to George’s story at the (e.g. a video recorder), numerical systems (e.g. a train
beginning of this chapter to see how George was unable timetable), abstract systems (e.g. the syntax of a lan-
to comprehend that his mother’s threats to ‘send him guage), and motoric systems (e.g. bouncing on a tram-
away were not intentional). There are a number of ways poline) (Baron-Cohen, 2009). This is a helpful way of
to test whether a child has developed a ‘theory of mind’. explaining the narrow interests, repetitive behaviour and
One traditional method is known as the Sally-Anne resistance to change/need for sameness found in autis-
false belief task (Baron-Cohen, Leslie & Frith, 1985) and tic spectrum disorder, and it is this desire to systematize
this procedure is described that differentiates autism from other psychopathologies
-Anne false belief task An imagina-
more fully in Research that also exhibit theory of mind deficits (e.g. schizo-
srocedure that has been used many
Methods Box. 17.1.
s to assess theory of mind abilities in a phrenia, borderline personality disorder, conduct dis-
e of clinical populations. Even adults with high- order) (Corcoran & Frith, 1997; Fonagy, 1989; Dodge,
functioning autism (such 1993). The empathizing—-systematizing theory also
as Aspergers syndrome) also exhibit theory of mind helps to explain the inability
deficits on some measures. For example, many of the to ‘generalize’ in autistic empathizing-systematizing theory
A theory ofthe social and communication
traditional tests of theory of mind are rather static and spectrum disorders (Wing, difficulties experienced by individuals with
somewhat removed from the dynamic situations an indi- 1997). Baron-Cohen (2009, autistic spectrum disorder.
vidual with autism will experience in real life. To make pp.72-73) provides the fol-
such tests more akin to everyday experiences, Heavey, lowing example:
Phillips, Baron-Cohen & Rutter (2000) devised the ‘awk-
ward moments test’, in which participants view a series The typical clinical example is a teacher who teaches
of TV commercials and then are asked questions about a child with autism to perform a task in one setting
the events in each. Individuals with Asperger's syndrome (e.g. taking a shower at home) but has to re-teach
were significantly less able to answer questions about the it in a new setting (e.g. taking a shower at school).
mental state of the characters in the commercials than an Consider though that if the child is treating the situa-
age and gender matched control group without autism. tion as a system, the unique features of each (e.g. how
However, the two groups did not differ on scores on the shower at home differs to the shower at school
questions related to recall of events within the TV clips in the detail of their temperature control functions
(a memory test), suggesting that the poorer scores on or the angle and height of the shower-head) may be
mental state questions by Asperger’s syndrome partici- more salient than their shared features (e.g. that both
pants was not simply due to a memory deficit. Because require getting in, turning the shower on, turning it
of these difficulties in understanding the mental states of off, and getting out).
others, individuals with autistic spectrum disorder will
undoubtedly have difficulty indulging in symbolic play
with others, actively participating in human interactions, Summary of the aetiology of autistic
and forming lasting relationships. spectrum disorder
As we noted at the outset of this topic, autism is a com-
The empathizing-systematizing theory More plex disorder, which varies considerably in its symptom-
recently, some researchers have argued that theory of atology and severity across individuals. Recent research
mind deficits may help to explain many of the social and has indicated a significant genetic component to autistic
communication difficulties experienced by individuals spectrum disorder (up to 90 per cent heritability in some
with autistic spectrum disorder, but such deficits do not studies) and molecular genetic studies are beginning
592 PSYCHOPATHOLOGY
THE SALLY-ANNE FALSE BELIEF TASK

How can we measure whether someone can understand the intentions of others? Baron-Cohen, Leslie & Frith
(1985) designed an imaginative procedure that has been used many times to assess theory of mind abilities in
a range of clinical populations. This is known as the Sally-Anne false beliefs task. In this procedure two dolls are
used to act out the story shown above and at the end children are asked ‘Where will Sally look for her marble?’
Children who have developed a theory of mind will say that when Sally comes back from her walk she will look
in the basket for her marble because they will understand that she has not seen Anne move it. Children who are
unable to understand that others have different beliefs from themselves will say that Sally will look in the box
because that is where they themselves know it is. ;
Baron-Cohen, Leslie & Frith (1985) conducted this test with three groups ofchildren, all with a mental age of over
3 years. One group was diagnosed with autistic spectrum disorder, one with Down syndrome and the third group
METHODS
RESEARCH
17.1 consisted of normally developing children. Most of the children with autism answered incorrectly (saying Sally
would look in the box) while most of the children in the other two groups gave the right answer (saying
Sally would look in the basket). The inclusion in the study of a group of children with Down syndrome showed
that the failure on this task of children with autism could not be attributed to their learning difficulties more gen-
erally. In addition all children correctly answered two control questions ‘Where is the marble really?’ and ‘Where
was the marble in the beginning?’ demonstrating understanding of the change in the physical location of the
marble during the story.
Source: Baron-Cohen, S., Leslie, A. & Frith, U. (1985). Does the autistic child have a theory of mind? Cognition, 21, 37-46.
Reproduced by permission of Elsevier.
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Now Sally comes back.
Where will Sally look for her marble?

to identify some of the gene sequencing and structure programme has to begin at a very basic communica-
abnormalities that may mediate autistic syndrome symp- tion level by, for example, teaching the child to make eye
toms. Autopsies, fMRI, EEG and ERP studies suggest contact (Hwang & Hughes, 2000). Thirdly, children with
that individuals with autistic spectrum disorder exhibit autistic symptoms appear to show interest in only a very
deficits in a number of different brain areas, resulting in limited range of events and objects, which makes it
both structural and functional abnormalities. In cogni- very difficult to find effective reinforcers that can be used
tive terms, these abnormalities appear to significantly to reward them. Because of their apparent unresponsive-
affect executive functioning and prevent the autistic indi- ness to communications, praise is often ineffective as a
vidual from fully developing a ‘theory of mind’ that will reinforcer and attempts have to be made to find rewards
enable them to understand the intentions and emotions that are highly salient. In severe cases, this may mean hav-
of others. Nevertheless, at least some theories of autis- ing to pair praise with food (so that praise acquires sec-
tic spectrum disorder also claim that sufferers may well ondary reinforcing properties) (Davison, 1964) or using
have cognitive ‘strengths’ as well as impairments, and the tactile reinforcers such as a hug or a vibratory stimulus
ability to systematize information may be one of these applied to the skin (Johnson & Davey, 1978). Fourthly,
strengths. Autistic spectrum disorder is probably a multi- children with autistic symptoms have overly selective
faceted syndrome, with a range of different genetic, peri- attention that means if they do attend to the training
natal and environmental causes. task, it is likely that anything that is learnt may well be
situation specific and will not generalize to other envi-
ronments or to other similar tasks. Finally, even in high-
17.4.5 Interventions and Care functioning sufferers, their relatively idiosyncratic social
and communicative skills can mean that they are treated
for Individuals with Autistic with some suspicion and reserve by others in society —
Spectrum Disorder even though they are as capable as anyone else at success-
fully undertaking employment. As we shall see later, this
A range of attempts has been made to help individuals issue means that inclusion strategies will require support
with autistic spectrum disorder adapt to day-to-day living for both client and employer if the high-functioning indi-
and to increase their quality of life. As we have described vidual with autism is to integrate successfully into the
earlier, many individuals with autistic spectrum disorder working environment.
have severe communication difficulties and are unable to
live a normal life without continuous support and care. Drug treatments
Interventions have generally taken three broad forms: Several drugs are used in the treatment of autism
drug treatments to reduce problematic behaviour such symptoms, mainly to help control problem behaviours.
as withdrawal, aggression or self-injury; behavioural Antipsychotic medications are the type of drug most
training to promote basic communication and socializ- commonly used in the treatment of autism and these
ing skills; and inclusion strategies that will support the include haloperidol and,
client attempting to live a relatively normal life within haloperidol An antipsychotic medication
more recently, risperidone most commonly used in the treatment of
society. But first, because of the nature of the disorder, (see also Chapter 8). Anti- FaUitisiyiseesas :
there are difficulties associated with attempting to treat psychotic drugs such as
individuals with autistic spectrum disorder and we will these have been shown to risperidone A drug treatment for children
describe these first. reduce repetitive and stereo-
with autism.
typed behaviours, reduce levels of social withdrawal and

Difficulties in the treatment of individuals also reduce symptoms associated with aggression and chal-
with autistic spectrum disorder lenging behaviour such as hyperactivity, temper tantrums,
Many of the symptoms of autistic spectrum disor- mood changes and self-abusive behaviour (Malone, Gratz,
der cause problems for almost any form of interven- Delaney & Hyman, 2005). However, not all children with
tion designed to improve their skills or quality of life. autism respond well to this class of drugs and they can
Firstly, one of the main characteristics of the disorder is have potentially serious side effects such as sedation, diz-
that such individuals do not like changes from routine, ziness, increased appetite and weight gain, as well as result
and any intervention — by its very nature — is designed in jerky movement disturbances (dyskinesias) (Campbell,
to implement change. Secondly, autistic spectrum chil- Armenteros, Malone, Adams et al., 1997).
dren often appear to be oblivious to the outside world — The opioid receptor antagonist naltrexone has also
they respond very poorly to attempts at communication been found to be beneficial in the control of hyperactiv-
and even something as simple as trying to achieve eye- ity and self-injurious behaviour, and a study by Symons,
contact can be problematic. Because of this, any training Thompson & Rodriguez (2004) suggested that the drug
594 PSYCHOPATHOLOGY
decreased self-injurious behaviours by over 50 per cent these behavioural techniques at home (Erba, 2000). THis
in 47 per cent of the participants in their study. Some has a number of benefits. It enables the autistic child
studies have even indicated that naltrexone can produce to learn appropriate behaviours in the environment in
moderate increases in social interaction and communi- which he/she is most likely to be using them (the home).
cation (Aman & Langworthy, 2000; Kolmen, Feldman, It frees up professional therapists’ time and offers a tiered
Handen & Janosky, 1995). structure to treatment that provides a potentially larger
number of sufferers with day-to-day treatment. Some
Behavioural training methods studies even suggest that parents may be more effec-
Most training programmes for individuals with autism tive and efficient trainers than professionals: a study by
will attempt to develop basic self-help, social and com- Koegel, Schreibman, Britten, Burkey & O'Neill (1982)
munication skills in individuals who otherwise would suggested that 25-30 hours of parent training was as
be largely uncommunicative and require lifelong care. effective as 200 hours of similar treatment by profession-
Most training procedures adopt a conditioning-based als in a clinic setting. Parent-implemented early inter-
approach, in which the clinician will attempt to rein- vention has been shown to parent-implemented early Eby
force basic behavioural skills such as attention (eye con- improve child communica- intervention Using pa rents as tect
tact), toileting behaviour, self-help behaviours, initiating tion behaviour, increase trainers to teach children with intellectu
maternal knowledge of disabilities basic self-help and commu
interactions with peers and adults, and play behaviour
tion skills. =
autism, enhance maternal
Gg
with peers. These methods can also be used to reduce
the frequency of disruptive or inappropriate behav- communication style and parent-child interaction, and
iours such as temper tantrums, self-injurious behaviour, reduce maternal depression (McConachie & Diggle,
repetitive behaviours and aggressive responses (e.g. see 2007). Parents can not only learn to use behavioural tech-
the description of functional analysis in individuals with niques to train their own children, but can also effectively
intellectual disabilities in section 17.3.5) (Lovaas, 1987; train others who work with or care for their children to
Davison, 1964). To supplement basic conditioning prin- use these techniques (Symon, 2005). This approach effec-
ciples, therapists will also use a range of methods to try tively expands the group of individuals associated with
to promote the required behaviours in the first place, and an autistic child who are skilled in maintaining a consist-
these may include model- ent training regime for that child.
modelling The process of demonstrat-
ling (ie. demonstrating
ing a required behaviour to clients before
prompting them to imitate it. the required behaviour to Inclusion strategies
the client before prompt- Many home-based interventions for high-functioning
ing them to imitate it). This technique is especially individuals with autistic spectrum disorder teach self-help
helpful when attempting to teach autistic individuals to strategies, social and living skills, and self-management
communicate using sign language. Because many autis- practices that are designed to help the individual func-
tic children remain speechless, learning to communi- tion more effectively in society. However, even when an
cate through sign language has proved a useful way of individual has effectively acquired many of these skills,
facilitating interactions with others (Goldstein, 2002). they may still need to be supported through important
Despite the wide use of these methods to promote basic life transitions, such as finding and keeping a job. One
behaviours, there are very few properly controlled out- such support scheme is known as supported employment.
come studies that have assessed the relative efficacy of This provides support to both the employee with autism
these training procedures (Howlin, 2005). However, in and the employer, and includes
the absence of such studies the literature does suggest
that early intensive behavioural interventions may be the 1. providing training and support for the employer
most effective way of promoting the social functioning on how to manage the employee with autism;
of autistic individuals over the long term (Howlin, 2005) 2. provision of job preparation and interview skills
and a recent meta-analysis of behavioural interventions for the employee;
for individuals with autistic spectrum disorder indicated 3. support for the employee for as long as it is
significant gains in IQ, language skills, communication, needed; and
socialization and daily living skills when compared with
4. regular feedback sessions with both employee and
control interventions (Virués-Ortega, 2010). employer.
Most of these training procedures are time consum-
ing and repetitive, and require a significant investment of Supported employment schemes such as this have been
commitment and effort by those conducting the train- shown to increase the employee’s social integration,
ing. However, a way of supplementing treatment by pro- increase employee satisfaction and self-esteem (Kilsby &
fessionals is to train the parents so that they can apply Beyer, 1996; Stevens & Martin, 1999) and promote
higher rates of employment compared with a matched communicative skills in those most severely affected, and
control group (Mawhood & Howlin, 1999). Treatment this has been supplemented with the adoption of par-
in Practice Box 17.2 provides examples of the types of ent-implemented training programmes that extend the
employment found for individuals using this type of range of individuals with the skills necessary for success-
supported employment scheme. ful intervention. Drugs are commonly used primarily
to control negative behavioural symptoms such as self-
Summary of interventions for individuals injurious, challenging and hyperactive behaviours, and
with autistic spectrum disorder they may also have some positive impact on communica-
This section has given a flavour of the interventions that tion and social behaviour. High-functioning individuals
are available for individuals with autistic spectrum disor- with autistic spectrum disorder can also receive support
der. Basic behavioural training methods have proven to in the form of supported employment programmes that
be effective at promoting a range of self-help, social and help the individual to find and keep a suitable job.

TYPES OF JOBS FOUND BY INDIVIDUALS WITH AUTISM OR
ASPERGER’S SYNDROME USING A SUPPORTED EMPLOYMENT SCHEME
Type of work Per cent of jobs Examples of jobs found
Administration/technical 8 Statistician, chemist, research officer, photography
Administration/accounts assistant 22 Archiving, bookkeeping

Technical assistant 13 Library, finance, technical, BT operator
Data entry 6 Keyboarding, data input
Data management 3:5 IT analyst, web design
Office work/clerical assistant 19 Offices, banks

Secretarial he) Hospital and university posts
Shop work 8 Customer service, travel agents, transport, check-out clerk
Stockroom 6 Loading/unloading, shelf stocking
Postal work 4 Mail delivery/sorting
Other 7 Support worker, nursery, messenger, joiner, gardening, seamstress
Catering es) Chef, kitchen porter
Cleaning 0.5
Source: Howlin, P., Alcock, J. & Burkin, C. (2005). An 8-year follow-up of a specialist supported employment service for high-ability adults with
autism or Asperger syndrome. Autism, 9, 533-549. Reproduced by permission of SAGE.
SELF-TEST QUESTIONS
© What is the triad of impairments that are important in the diagnosis ofautistic spectrum disorder?
© What are the current prevalence rates for autistic spectrum disorder and what factors might have caused recent increases
in those prevalence rates?
® What is the evidence for autistic spectrum disorder being an inherited disorder?
“
e What perinatal factors might contribute to autistic symptoms?

* What kinds of studies have contributed to our understanding of brain abnormalities in autistic spectrum disorder?
* What cognitive deficits have individuals with autistic spectrum disorder been shown to have?
® What are the main difficulties associated with the treatment of individuals with autistic spectrum disorder?
e What drugs are used to treat autistic spectrum disorder and what symptoms do they attempt to treat?
° What is parent-implemented early intervention and is it effective?
° What is supported employment when used with higher functioning individuals with autism? How successful is it?
*
SECTION SUMMARY
17.4 AUTISTIC SPECTRUM DISORDER (ASD)
Autistic spectrum disorder represents a dimension of deficit covering arrested development across a range of skills. The main
characteristics are impairment in reciprocal social interactions, impairments in communication skills and the presence of ste-
reotyped or repetitive behaviour patterns. Genetic factors have been identified in the aetiology of autistic spectrum disorder
and we are currently beginning to identify some of the gene sequencing and structure abnormalities that may mediate autistic
syndrome symptoms. Individuals with autistic spectrum disorder also exhibit both functional and structural deficits in a num-
ber of brain areas, and cognitive symptoms of autistic spectrum disorder include deficits in some of the skills that contribute
to executive functioning and ‘theory of mind’ deficits that mean autistic individuals are frequently unable to understand the
emotions and intentions of others. More recently, the narrow interests, repetitive behaviour and resistance to change/need for
sameness found in high-functioning autistic spectrum disorder has been interpreted as a strong desire to systematize, and it
may be this analytical feature that differentiates autism from other psychopathologies that also exhibit theory of mind deficits.
Psychological and behavioural interventions are arguably the most successful ways of treating and supporting individu-
als with autistic spectrum disorder, although drugs can be used to help control the more disruptive behavioural elements of
autistic spectrum disorder (such as self-injurious behaviour and aggressive behaviour), and early intensive behavioural inter-
ventions appear to be the best way of promoting social functioning over the long term. Finally, high-functioning individuals
with autistic spectrum disorder can be helped to establish a successful working career with the help of community inclusion
strategies and supported employment schemes.
e The triad of impairments in autistic spectrum disorder are impairments in (1) reciprocal social interaction, (2) communica-
tion, and (3) imagination and flexibility of thought.
e The prevalence rate of diagnosed autistic spectrum disorders has been increasing over recent years to estimates as high as
1 to 2 per 1000 births.
e There is an important genetic element to autistic spectrum disorder and we are beginning to identify some of the gene
sequencing and structure abnormalities that may mediate autistic symptoms.
° Perinatal factors may account for a small percentage ofautistic spectrum disorder cases and such factors may include mater-
nal rubella during pregnancy, interuterine exposure to drugs, maternal bleeding after the first trimester and depressed
maternal immune functioning during pregnancy.
° There is good evidence from autopsy, fMRI, EEG and ERP studies that autism is associated with aberrant brain development.
* Cognitive factors contributing to autistic symptoms include impaired executive functioning and ‘theory of mind’ (TOM) deficits.
¢ The narrow interests, repetitive behaviour and resistance to change/need for sameness found in high-functioning autistic
spectrum disorder has been interpreted as a strong desire to systematically analyse information.
° Drug treatments for children with autism include haloperidol, risperidone and naltrexone, all of which attempt to treat the
negative symptoms ofthe disorder.
° Behavioural training methods used to teach basic self-help and communication skills include operant conditioning
techniques, modelling and parent-implemented early interventions.
* Supported employment has proven successful at helping higher functioning individuals with autism to find and maintain
employment.
17.5 NEURODEVE LOP- The range of disability covered by these three areas is
broad, with some individuals being so severely affected
MENTAL DI SORDERS by the disability as to require lifelong specialized support.
However, many others with these disabilities can function
R EVI EW E D sufficiently well to enjoy relatively normal daily living and,
RR re Oe aL selcater nS c cudaielsd sa foamed Mpa ehowas OPS with structured support schemes, can succeed in both edu-
cational and occupational environments. Recent years have
In this chapter we have covered three distinctive types
seen rapid development in inclusion policies designed to
of developmental disorder, namely specific learning
extend the rights of individuals with learning and develop-
disorders (such as language disorder and speech sound
mental disabilities to be educated and employed in main-
disorder), intellectual disabilities and autistic spectrum
stream settings, and this has
disorder. All of these disabilities represent lifelong condi- developmental disabilities A broad |
tions that are usually present from birth, and are char- led to a significant te as umbrella term used, in the USA, to refer
ment in the quality of life intellectualdisabilities and pervasive —
acterized by the individual failing to meet important
and self-esteem experienced developmental disorders such as autism
developmental milestones in social behaviour, commu- by sufferers. and Asperger's syndrome.
nication and learning skills.
me To access the online resources for this chapter go to

eave www.wiley-psychopathology.com/ch17
Reading i Activity
Rosa's Law e Learning and intellectual Activity 17.1

Glossary of key terms disabilities Self-test questions
Clinical issues * Autistic spectrum disorder Revision flashcards
Links to journal articles Research questions
References
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Index
AAF (altered auditory childhood depression 551 as therapeutic constructions 483 link to childhood sexual abuse 350
feedback) 570 conduct disorder and criminal altered auditory feedback and negative affect 350
AAIDD (American Association behaviour 539 (AAF) 570 neurobiological factors 345-346
on Intellectual and schizophrenia 250 alternative delivery systems 356 and perfectionism 352
Developmental somatic symptom disorder 461 alternative hypothesis 82 treatment 355
Disabilities) 572 substance use disorders 318 ** Alzheimer’s disease 504-506 enhanced CBT 358
ABA design 87 suicidality 232 caregiver support 520 family therapy 356-357
ABAB design 87 Adult Memory and Information drug treatment 512, 513 anoxia 577
ABC approach, observational Processing Battery amenorrhoea 335 Antabuse (disulfiram) 326-327
method 57, 65 (AMIPB) 54, 496 American Association on Intellectual antagonism, facets of 412
chart examples 58, 59 adult mental health problems, and Developmental anterior cingulate cortex (ACC)
ABM (attention bias childhood risk Disabilities (AAIDD) 572 heightened activity, conversion
modification) 172 factors 526-528 American Psychiatric Association disorder 462
abnormal attributional aetiology, defined 75 (APA) 38 role in depression and mood
processes 280 affectionless control, parenting Diagnostic and Statistical Manual disorders 203
abnormal motor behaviour, style 205 (DSM) 38-43 anterograde amnesia 493, 494
psychosis 240-242 affective flattening 242 AMIPB (Adult Memory and anterograde memory
abnormal psychology 14 age and sexual dysfunction 368, Information Processing dysfunction 493
abreaction 486 31-372, 37> Battery) 54 anti-androgen drugs 396-597,
absorption, mental state 262 age regression 488 amnesia antidepressant drugs 11 203
abstinence violation 325 agnosia 494, 495, 503, 504 anterograde 493, 494 bupropion 297
abuse see childhood abuse; substance agoraphobia 162, 164 dissociative 471-473 childhood anxiety disorders 553
abuse aetiology 165 biological explanations 483 dissociative disorders 489
acamprosate 294, 326 diagnosis and cognitive for eating disorders 354, 355, 356
acceptance and commitment prevalence 164-165 explanations 478-480 effectiveness study 123
therapy (ACT) 109-110 AIDS dementia complex (ADC) 500 psychoanalytic views 478 fluoxetine 218, 356, 553
accessibility strategies 572, 580-581 alcohol 290 treatment 486-489 linked to sexual
acetylcholine 505, 512 alcohol myopia 316 retrograde 494 dysfunction 370, 374, 375
acetylcholinesterase 512 alcohol use disorder 290-292 amniocentesis 574, 580 monoamine oxidase inhibitors
ACT (acceptance and commitment costs of 294-295 amotivational syndrome, cannabis (MAOIs) 112, 162, 202, 221
therapy) 109-110 course of 294 users 301 for mood improvement in
active stage, psychotic dependence 292-293 amphetamine intoxication 305 degenerative disorders 513
symptoms 248 treatment of 293-294 amphetamine psychosis 252-253 for panic disorder 168
acupuncture 298 diagnostic criteria 293 amphetamine-type stimulants personality disorders 441
acute stress disorder (ASD) during pregnancy (ATS) 285 for post-stroke depression 503
diagnostic criteria 186 and fetal alcohol ‘bath salts’ 305 selective serotonin reuptake
symptoms 188 syndrome 80, 292, 576, 579 MDMA/Ecstasy 308, 309 inhibitors (SSRIs) 112, 174,
addiction 287 link to conduct disorder in methylphenidate (Ritalin) 553 185, 203, 221, 379, 397, 466,
reward pathways in offspring 539 amphetamine use disorder 305 488, 553
brain 315-316 prevalence 291, 294 amphetamines 302, 304 for somatic symptom
see also substance use disorders Alcoholics Anonymous (AA) 322 amygdala 21, 494 disorders 466
(SUDs) ALDH2 gene and alcohol and mood disorders 203 for symptoms of OCD 185
ADHD see attention deficit dependency 318-319 and phobic fear 153-154 tolerance to 113
hyperactivity disorder alien abduction beliefs 262-263 AN see anorexia nervosa (AN) treatment for early
(ADHD) all-or-none thinking 208 analogue observations 59 ejaculation 379
adolescent psychological problems allostatic state 508 analogue populations 83 for treatment of GAD 173-175
see childhood and adolescent alogia 242 analogue research 75 tricyclic antidepressants (TCAs)
psychological problems alter identities 473-474 androgens 393 112, 202, 221, 466, 513
adolescents of Bianchi, Kenneth 484 aneurysm 502 antipsychotic drugs 112, 270-272
adolescent-onset conduct emergence of 474-475 anhedonia 242 autism treatment 593
disorder 537 and fantasy-proneness 478 animal models/studies 83-84 and dopamine activity 252,
risk factors for antisocial personality integration of during anorexia nervosa (AN) 333-335 253-254
disorder 429, 430 therapy 486, 488 comorbidities 335, 354 olanzapine for bipolar 218, 221
adoption studies 250 and role-playing 483-485 cultural factors 341 for personality disorders 441
antisocial personality and state-dependent memory 479 diagnostic criteria 335 phenothiazines 252
disorder 431 as strategic enactments 484 genetic influences 343-345 for psychosis symptoms 112-113,
attention deficit hyperactivity therapeutic construction incidence 337 252, 270

disorder 533 of 483-485 known risk factors 344 side effects D2, 20
NEGO woex
antiretroviral drugs 513 dependent personality attentional factors in treatment, (ADHD); conduct disorder
antisocial behaviour 278 disorder 421 controlling for 120 (CD)
learningof 429, 431 obsessive compulsive personality attenuated psychosis behaviour therapy 26, 105-107
parent management disorder (OCPD) 421-422 syndrome 42-43 for autistic spectrum
training 555 prevalence rates 424 attenuated psychotic symptoms disorder 593
peerinfluences 540 aphasias 493-494 syndrome 247-248 for childhood psychological
predictorsof 430 appetite, brain areas attribution theories of problems 53D.
antisocial personality disorder regulating 345 depression 210-213 for depression 223, 224
(APD) 409, 412 applied behaviour analysis 580 attributional biases 261 dialectical, personality
aetiology 429 applied family management 276 Attributional Style Questionnaire disorders 442
childhood/adolescent applied scientist 70 (ASQ) 211 intellectual disabilities 580, 581
precursors 429 approved mental health auditory hallucinations 263-264 paraphilic disorders 395
cognitive models 431—432 workers 132 autistic disorder (autism) 585 for sexual dysfunctions 376-378
familial factors 429-43] apraxia 494, 495 autistic spectrum disorder somatic symptom disorders 465
genetic factors 431 rehabilitation for 515-516 (ASD) 584 for substance use
physiological & neurological APT (attention process aetiology 588-593 disorders 323-324
factors 432-433 training) 514 characteristics 585-587 see also cognitive behaviour
diagnosis and features arbitrary inference 208 diagnosis 587 therapy (CBT)
of 416-417 arousal and desire, disorders interventions and care 593-595 behavioural activation
and narcissistic personality of 367-369 prevalence 529, 587-588 therapy 223, 224
disorder 418 arousal deficits 493 autobiographical memory 480 behavioural inhibition (BI) 158,
prevalence 424 ASD see acute stress disorder; aversion therapy 106, 323 160
treatment in prison autistic spectrum disorder for quitting smoking 297-298 behavioural model 25-26
populations 444-445 ASI (Anxiety Sensitivity Index) 166 avoidance strategies, PTSD behavioural rehearsal 175
anxiety and stressor-related asociality 242 sufferers 189 behavioural selfcontrol 107
problems 146-147, Asperger's syndrome 587 avoidant personality disorder behavioural self-control therapy
193-194 ASQ (Attributional Style correlates and risk (SCInne 23
comorbidity of anxiety 147-148 Questionnaire) 211 factors 437 behavioural stress
generalized anxiety disorder assertive community treatment diagnosis and features 419-421 management 465
(GAD) 170-176 13, 2/76 prevalence 424 behavioural theories
obsessive compulsive disorder assertive outreach 11-13, avoidant/ restrictive food intake depression 206-207, 223
(OCD) 176-186 276-277 disorder 340 psychotic symptoms 257-259
panic disorder 162-170 assessment methods 44 avolition 242 beliefs and meta-beliefs, general
post-traumatic stress disorder biologically based axons 22 anxiety disorder 173
(PTSD) 185-193 methods 54-57 beliefs, dysfunctional SHUG, SDI)
prevalence rates 147, 148 clinical interviews 45-47 bacterial meningitis 513 beliefs, dysfunctional see
social anxiety disorder 157-162 clinical observation 57-60 barbiturates 306 dysfunctional schema
specific phobias 149-157 cultural bias 60-63 basal ganglia 255 beliefs, negative 224-226
anxiety disorders psychological tests 47-54 celldeath 509 bell-and-battery technique 554
children and adolescents 543 reliability and validity 44-45 and communication benzodiazepines 112, 162, 168,
aetiology 547-549 assessment stage in clinical disorders 569 174, 441
cognitive behaviour work 136,137, deep brain stimulation beta amyloid plaques 505, 506
therapy 555-556 asylums 9-10 treatment 513 Bethlem Hospital, London 9
drug treatment 112, 553 Ataque de Nervios 15, 16 roleinOCD 180 ‘betrayal trauma’ 481
generalized anxiety disorder attention bias modification substantial nigra 507 Bianchi, Kenneth, multiple
(GAD) 546-547 (ABM) 172 ‘bath salts’ 285, 305 personalities 484
obsessive compulsive disorder attention deficit hyperactivity battered woman syndrome 210 biases
(OCD) 544-545 disorder (ADHD) 531 BD see body dissatisfaction attentional 172-173, 207, 259;
prevalence 529 aetiology 533-536 Beating the Blues®, computerized 261, 460
separation anxiety 544 and antisocial personality CBT 114-115, 219-220 attributional 261
specific phobias 546-547 disorder 430 Beck’s cognitive therapy 108-109 hostile attributional bias 541
comorbidity with personality behaviour therapy 553-555 Beck's cognitive theory of cultural, in assessment and
disorders 418, 425, 437 comorbidities 532 depression 207-209, diagnosis 60-63
438, 441 diagnosis Dal oS 223-224 interpretational 263-264
definition 147 drug treatment 553 BED see binge-eating disorder (BED) reasoning 261
and sexual dysfunction 374 prevalence 2295533 bed nucleus of the stria terminalis binge drinking 291
anxiety sensitivity 166 attention deficits 493 (BSTc) 401 binge-eating disorder
Anxiety Sensitivity Index cognitive rehabilitation 514 bed-wetting, behaviour (BED) 337-338
(ASI) 166 attention process training therapy 554 case history 339
anxiolytic drugs LIM 112, 326, (APT) 514 befriending 120 comorbidities 338
375, 488 attentional biases 259, 261 behaviour analysis 105 diagnostic criteria 339
anxious/ fearful personality to negative information, behaviour management incidence of 338-339
disorders (Cluster C) 410, depressed people 207 techniques 554 treatment 355-356
413, 419 somatic symptom disorders, behaviour modification 26, 105 cognitive behaviour therapy
aetiology 436-438, 440 maintenance of 460 behaviour problems see antisocial (CBT) 358-359
avoidant personality to threat, anxious people behaviour; attention deficit binge-eating/ purging type anorexia
disorder 419-421 172, 261 hyperactivity disorder nervosa 335
woex [GOT
biological challenge tests 165 bizarre behaviour 258 comorbidities 337, 354 CD (communication
biological models 18-23 BMI (body mass index) 333, 335, diagnostic criteria 336 deviance) 266-267, 275
biological preparedness 152-153 346 incidence 333-337 cerebellum 255
biological theories BN see bulimia nervosa (BN) known risk factors 344 cerebral cortex 21, 22
attention deficit hyperactivity bodily sensations, misinterpretation treatment 355 cerebral embolism 502
disorder 533-536 of 166-167 antidepressants 356 cerebral infections 499-501
autistic spectrum body dissatisfaction (BD) cognitive behaviour therapy treatment of 513
disorder 588-590 cultural similarities “341, 342 (CBT) 358-359 cerebral palsy 577
bipolar disorder 217-218 definition 347 buprenorfine 327 cerebral thrombosis 502
borderline personality female body shape bupropion 297 CES (chronic fatigue
disorder 433-434 dissatisfaction 348 syndrome) 199, 201
conduct disorder 538-539 and media influence 346-347 caffeine 306 challenging behaviour, functional
dissociative disorders 483 tripartite model 347 CAMHS (Child and Adolescent analysis 581
eating disorders 343, 345 body dysmorphic Mental Health Child and Adolescent Mental Health
gender dysphoria 401-402 disorder 178-179 Services) 131 Services (CAMHS) 131
generalized anxiety body mass index (BMI) 333, 335, cannabis 298 child rapists 387
disorder 171-172 346 medical applications 299 childhood and adolescent
intellectual disabilities 573-577 bogus pipeline procedure 392-393 cannabis intoxication 300 psychological
major depression 201-204 borderline personality disorder cannabis use and psychotic problems 524-525,
obsessive-compulsive (BPD) 408, 409 symptoms 260 558-559
disorder 180 aetiology 427-428, 433-435 cannabis use disorder 298-299 anxiety and depression 543
panic disorder 165-166 comorbidity 418, 425 costs of 301-302 anxiety disorders 543-549
paraphilia 393-394 with bulimia nervosa 337, dependence 300 depression 549-551
post-traumatic stress S355) diagnostic criteria 300 diagnostic difficulties 526
disorder 188-189 diagnostic criteria and prevalence 299-300 disruptive behaviour
psychotic symptoms 249-257 features 417-418 risk factor for other psychiatric problems 530-531
sexual dysfunctions 374-375 prevalence 424 diagnoses 300-301 attention deficit hyperactivity
somatic symptom treatments capabilities and competencies disorder (ADHD) 531-536
disorders 461-462 cognitive behaviour therapy of clinical conduct disorder 537-542
specific phobias 152-156 (CBT) 443-444 psychologists 135-138 precursor to adult mental health
see also genetic factors dialectic behaviour cardiovascular accident problems 526-528
biological treatments therapy 442 (CVA) 502-503 prevalence 528-530
neurocognitive object-relations caregiver support treatment 553
disorders 512-513 psychotherapy 442 programmes 518-520 behaviour therapy 553-555
for psychotic brain abnormalities case formulation 64-66, 137 cognitive behaviour
symptoms 270-272 antisocial personality disorder case manager 280 therapy 555-556
sexual dysfunction 378-380 (APD) 433 case studies 86-87 drug treatments 553
substance use disorders 326-327 autism spectrum castration anxiety 390 family interventions 555
biologically based assessment 54 disorder 589-590 CAT (computerized axial play therapy 556-557
neuroimaging techniques 56-57 borderline personality disorder tomography) 56 childhood abuse
psychophysiological tests 54-55 (BPD) 434 catastophising 170 and development of paraphilic
biphasic 292 children with ADHD 534, 536 in childhood depression 551 disorders 391
Bipolar disorder I, diagnostic and depression 203-204 example of magnification 208 false memories 481, 482
criteria 217 dissociative disorders 483 of minor physical link to conduct
Bipolar disorder II, diagnostic dyslexia 567-569 symptoms 452, 459, 465 disorder 539-540
criteria 217 and gender dysphoria 401-402 misinterpretation of bodily memories of, repression and
bipolar disorders 40, 215 paraphilias 394 sensations, panic recovery 478, 480-482
aetiology schizophrenia 254-257, 427 disorder 166-167 psychoanalytic treatment
genetic factors 217-218 schizotypal personality in worriers and of dissociative identity
neurochemical factors 218 disorder 427 non-worriers 171 disorder 488-489
and borderline PD 434, 441 brain anatomy 494 catatonic motor and reality monitoring
client perspective 215 brain imaging studies behaviours 241-242 deficits 480
and creativity 216 see neuroimaging studies categorical approach to risk factor of adult mental health
definition 198 brain imaging techniques 56-57 diagnosing personality problems 527
diagnostic criteria 216-217 brain neurotransmitters 21-22 disorders 409-410 risk factor for dissociative
prevalence 217 see also neurotransmitter problems with 410 disorders 474, 477-478
and suicide risk 231 abnormalities causation 75 risk factor for personality
treatments brain structure and function 21 and correlation 77, 79 disorders 424-426, 427,
cognitive therapy 225 brain surgery 270, 280 CBT see cognitive behaviour therapy 433, 434, 435, 443,
drug therapy 218, 221 brief interventions, alcohol-related (CBT) 447-448

triggers for depression and problems 294 CBTp (cognitive behaviour therapy childhood causes of intellectual
mania 218 brief psychotic disorder 244 for psychosis) disabilities 577-579
birth complications British Psychological Society 273-274 childhood neglect, risk factor
and autistic spectrum (BPS) 139 CCBT (computerized of adult mental health
disorder 589 Broca’s aphasia 494 CBT) 114-115 problems 527
and intellectual disability bulimia nervosa (BN) 336 CD (conduct disorder) see conduct childhood-onset conduct
BY, PIL case history 338 disorder disorder 537
TEO2Y woex
childhood-onset fluency disorder key capabilities and cognitive distortions, sexual conduct disorder (CD) 537: om
(stuttering) 567, 569, 570 competencies 135-138 offenders 391-393 aetiology of 538-542
childhood poverty, risk factor reflective practitioner cognitive enhancement therapy behaviour therapy 553-555
for adult mental health model 138 (CET) 274, 275 comorbid with ADHD 532
problems 528 regulation of |138-139 cognitive impairments in diagnosis of |537-538
childhood predictors of antisocial training 139-141 neurocognitive predictive of antisocial PD 428,
PD 429, 430 typical working week 136 disorders 493-495 429, 430
childhood risk factors for clinical psychology, definition 5 cognitive model 26-27 prevalence 529, 538
adult mental health clinical significance 121-123 cognitive rehabilitation 493, confidentiality 98-99
problems 526-528 clinical training 139-141 513-518 confirmatory bias 62
childhood sexual abuse, and eating clinical trials 84 cognitive remediation training conflict avoidance/lack of
disorders 350 closed head injury 498 (CRT) 274-275 resolution, dysfunctional
childhood trauma Cluster A personality disorders see cognitive restructuring 156, 161, families 349
and aetiology of anxiety odd/eccentric personality 175, 192-193;
224; 225—226 conflict resolution 456
disorders 547 disorders cognitive retraining 224 congenital disorders 576
risk factor for adult mental health Cluster B personality disorders see cognitive theories congenital rubella syndrome
problems 528 dramatic/emotional antisocial personality disorder (CRS) 576, 580
cholinesterase inhibitors 512 personality disorders (APD) 431-432 Connors’ parent rating scale
CHPCCP (Clearing House for Cluster C personality disorders see autism spectrum (EPRS) 535
Postgraduate Courses in anxious/ fearful personality disorder 590-591 consciousness and
Clinical Psychology) 139 disorders conduct disorder 540-541 behaviour 457-458
chromosomal disorders 573-574 CMHNs (community mental health of dissociative constraint-induced movement
chronic fatigue syndrome nurses) 130 disorders 478-482 therapy (CIMT) 516
(CFS) 199, 201 cocaine 302 dyslexia 568 construct validity 45
Cialis (tadafil) 378 cocaine dependence 303 of psychosis 260-264 contagious hysteria 461
cingulotomy 184-185 cognitive behaviour therapy social anxiety disorder 160-161 continuing professional
clanging, schizophrenic speech (CBT) 27,109 somatic symptom development (CPD) 139
pattern 240, 241 for bulimia nervosa 358-359 disorders 459-461 continuous amnesia 473
classical conditioning 25, 26 combined with drug cognitive therapies 107-110 continuous performance test
bell-and-battery technique 554 therapy 356 for depression 223-226 (CPT) 535
explanation for paraphilic for children and communication deficits, treatments control of events, research 74-75
disorders 390 adolescents 555-556 for 516 control group 81
and panic disorder 166 computerized (CCBT) 114-115, communication deviance controlled drinking 323
and PTSD 189 220 (CD) 266-267, 275 controlled drug user 307
and specific phobias 151-152 effectiveness, systematic communication difficulties, controlled word association test
therapies based on 105-106 reviews 88 children 526 (COWAT) 535
classification of for generalized anxiety play therapy 556-557 conversation of
psychopathology 37 disorder 174-175 communication disorders 566-567 schizophrenics 240
development of classification improving access to 116-117 aetiology 569 conversion disorder 453
systems 37-38 for obsessive-compulsive treatment 570 diagnosis 453
DSM-5 38-43 disorder 183-185 communication impairment in dissociation between behaviour
Clearing House for for panic disorder 168, 169 ASD 586 and awareness 457-458
Postgraduate Courses paraphilic disorders 395-396 community-based programmes, prevalence 454
in Clinical Psychology for personality substance use risk factors 458
(CHPCCP) 139 disorders 443-445 disorder 322-323 corpus callosum 21
client-centred therapy 27, 111 for psychosis (CBTp) 273-274 community care 10-11, 13 correlation between
clinical audit 76 for quitting smoking 298 schizophrenia 276-279 measures, prospective
clinical constructsand OCD 181 sex offenders 396 community mental health nurses studies 212-213
inflated responsibility 181 social anxiety disorder 161-162 (CMHNs) 130 correlational research
mental contamination 182 for somatic symptom comorbid psychiatric disorders and designs 77-78
thought-action fusion disorders 465-466 regular substance use 319 cortisol levels and depression 204
(TAF) 181 substance use disorders 324-326 comorbidity 39 cost of substances and early
clinical interviews 45-47, 137 telephone-based 115-116 complementary therapies, for use 314
clinical neuropsychologist, week in ‘third wave’ 109-110 quitting smoking 298 counselling 114
the life of 519 cognitive-behavioural model of complex PTSD 476 counsellors 130-131
clinical observation 57-60 eating disorders 352 compulsions 176 counterconditioning 105
clinical practice 128-129, 142 cognitive biases 259 computer-based virtual reality couple therapy, drug abusers 326
clinical psychologist attentional 259, 261 environments 514, 516 couples therapy 378
role 135-141 attributional 261 computerized axial tomography covert conditioning 395
economic cost of mental health interpretational 263-264 (CAT) 56 COWAT (controlled word
problems 129 reasoning 261-262 computerized CBT (CCBT) 114— association test) 535
mental health cognitive deficits 115, 220 CPA (cyproterone acetate) 397
professionals 130-132 from long-term substance concordance studies 19, 249-250 CPD (continuing professional
mental health services 133-135 use 319 concurrent validity 45 development) 139
clinical psychologists 130 from regular use of conditioning 105 crack cocaine 302
continuing professional cannabis 301 see also classical conditioning; craving 287, 317
development 139 schizophrenia 259 operant conditioning creativity, and mood disorders 216
cretinism 576 demographic factors, eating social anxiety disorder 158-160 psychiatric defence of 484
crime-related amnesia 472 disorders 341-342 developmental model of substance psychodynamic perspective 478
criminality and antisocial personality demonic possession 6-7 abuse and dependence 313 risk factors 477
disorder (APD) 416, 417, demonology 6 developmental psychopathology treatment of 486-489
428, 429, 430, 444-445 dendrites 22 526 see also alter identities
Cronbach’s a 44 dendritic spines 254 developmental stages 24 distress
cross-sectional design 79 denial defence mechanism 24 diagnosis 136-137 caused by symptoms 17
CRS (congenital rubella dental phobia, qualitative cultural bias 60-63 causing during research 97-98
syndrome) 576, 580 study 91-92 Diagnostic and Statistical Manual distress disorders 40
CRT (cognitive remediation dependence on substances, risk (DSM) 38 Dodo Bird Verdict 123, 124
training) 274-275 factors 318 DSM-5 38-43 dopamine 22
cultural bias in assessment and concurrent psychiatric dialectic behaviour therapy 442 and cannabis use 260
diagnosis 60-61 diagnoses 319 diathesis-stress model 20, 248 and depression 202
addressing 62-63 genetic predisposition 318-319 dichotomous thinking 442, 443, dopamine hypothesis, schizophrenia
causes of 61-62 long-term cognitive deficits 319 444 symptoms 252-254
examples 61 and poverty 319-320 and splitting 434 dopamine pathways in the
cultural differences 15, 16, 29 dependent personality dieting 333, 346, 347-349 brain 253
common phobias 149-151 disorder 421 dimensionality of symptoms 39, 43 dopamine transporter gene
conversion disorder 454 aetiology 437-438 diminished emotional DAT 346
in eating disorders 29, 341-342, prevalence 424 expression 242 double bind hypothesis 266, 267
346 dependent variable (DV) 81 direct treatment of double-blind procedure 82
EE-schizophrenia relapse depersonalization symptoms 376-377 ‘doubting’, central feature of
link 268 disorder 475-476 directed masturbation training 377 OCD 180
fear/phobic reactions 150-151 drug treatment 488 directive psychotherapy 481 Down syndrome 573-574
manifestation of OCD 176-177 prevalence and comorbidity 471 disease-avoidance model 155 downward drift 266
personality disorder depression 196-197 disease model 8-9 dramatic/ emotional personality
diagnosis 426 Beck’s cognitive disgust, link with specific disorders (Cluster B) 409-
post-traumatic stress disorder therapy 108-109 phobias 154 410, 413, 415-416
(PTSD) 188 in children and adolescents 549 disinhibition, facets of 412 aetiology 427-436, 439-440
regular druguse 318 aetiology 549-550 disorder spectrum 40 antisocial personality disorder
schizophrenia cognitive behaviour disorganized thinking (APD) 416-417
prevalence 245-246 therapy 555-556 (speech) 240, 241 borderline personality disorder
somatic symptom disorders 461 comorbidity 549 displacement 24 (BPD) 417-418
cultural factors diagnosis 549 dispositional factors and eating histrionic personality
ADHD diagnosis 5325539 drug treatment 553 disorders 350-352 disorder 418-419
custodial care 270 prevalence 529, 549 disruptive behaviour narcissistic personality
CVA (cardiovascular cognitive symptoms 197-198 disorders 530-531 disorder 418
accident) 502-503 and dependent PD 437 attention deficit hyperactivity prevalence rates 424
cyclothymic disorder 217 drug treatments for 112 disorder (ADHD) 531-536 dream analysis 104
cyproterone acetate (CPA) 397 embodiment component 197 conduct disorder (CD) 537-542 dream interpretation 222
cytokines 205 and sexual dysfunction 374 dissociation and PTSD 189 drug abuse see substance abuse
see also major depression dissociative amnesia 471-473 drug addiction, brain reward
‘dangerous people with severe depression and mood prevalence and comorbidity 471 pathways 315-316
personality disorders disorders 196-198, 234 dissociative experiences 470-471 drug, definition 284
(DSPD)’ 444 bipolar disorder 215-216 aetiology 477-485 drug maintenance therapies 327
deception 97 aetiology 217-219 comorbidities 474 drug-prevention schemes 322
deep brain stimulation (DBS) 513 diagnosis & depersonalization drug replacement treatment 327
defence mechanisms 24 prevalence 216-217 disorder 475—476 drug therapy 111-113
definitions 14-17 deliberate selfharm 227-229 dissociative amnesia 471-473 alcohol dependence 294
of psychopathology 14-18 major depression 198 dissociative identity disorder autism symptoms 593-594
degenerative disorders 503-504 aetiology 201-213 (DID) 473-475 cerebral infections 513
Alzheimer’s disease 504-506 diagnosis& prevalence 471, 474-475 childhood and adolescent
frontotemporal NCD 506-507 prevalence 198-201 andPTSD 476 psychological
genetic testing 506-507 suicide PupRS INE) risk factors 477-478 problems 553
Huntington’s disease 509 treatments 219-226 role of fantasy 478 degenerative disorders 512
Parkinson’s disease 507-509 derailment, speech disorder 240 treatment 486-489 for depression and mood
delayed ejaculation 370 derealization 475 dissociative identity disorder disorders 220-221
deliberate selfharm 227-229 description of events, research (DID) 473 dissociative disorders 489
delirium 498 goal 74 between-identity amnesia 479 for eating disorders 356
delirium tremens (DTs) 292 desire and arousal, disorders comorbidity 471 generalized anxiety disorder 174
delusional disorder 243 of 367-369 diagnostic criteria 473 obsessive compulsive
delusions 238-239 detachment, facets of 412 and epileptic seizures 483 disorder 185
delusions of control 238 detoxification 326 faking of 483 panic disorder 168-169
delusions of reference 238-239 developmental disabilities 597 imaginary childhood paraphilic disorders 396-397
demand characteristics 82 developmental factors companions 478 for personality disorders 441
dementia praecox 237 antisocial PD 429-431 prevalence rates 471 for psychotic
dementias 498 borderline PD 433 increase in 474-475, 484 symptoms 270-272
1604) woex
drug therapy (continued) cultural differences 341 encounter groups, group and alcohol” 292 9
sexual dysfunction 378-379 demographic factors 341-342 therapy 114 substance users 317-318
for social phobia 162 diagnosis 335, 336 endogenous opioids 345-346 experiential factors, and eating
for somatic symptom historical examples 334 endorphins 307 disorders 350
disorders 466 prevalence 335, 336, 337, ‘enhanced’ form of CBT, eating experiment, definition 80-81
strokes 512-513 338-339, 529 disorders 358 experimental designs 80-81
DSM-5 38-39 treatment 354-356 enmeshment 349 basic features 81-83
alternative diagnostic cognitive behaviour enuresis 554 use in clinical psychology
model for personality therapy 358-359 environmental toxins and research 83-84
disorders 410-412 drug therapy 356 ADHD = 534-535 experimental group 81
categorical approach family therapy 356-357 epidemiological studies 80 experimental hypothesis/
to personality prevention epigenetics 20-21 prediction 81
disorders 409-410 programmes 359 epilepsy 483 . experimental psychopathology 209
changesin 41-42 ECG (electrocardiogram) 55 erectile disorder 368, 380 experimentation with substances,
criticism of development echolalia 586 erotomanic delusions 239 factors influencing 314
process 41 ecological momentary assessment ERP (exposure and ritual explanatory approaches 18
criticisms of changes in 42-43 (EMA) 60 prevention) treatment 183 biological models 18-23
DSM-IV-TR ecological validity 59 errorless learning 517 psychological models 23-29
categorical approach economic cost of mental health ethical issues in research 95 exposure and ritual prevention
to personality problems 129 causing distress or withholding (ERP) treatment 183
disorders 409-410 economic recession and benefits 97-98 exposure therapies 105
definition of a personality suicide 231 informed consent 95-97 for panic disorder 168-169
disorder 444-445 Ecstasy (MDMA) 309 privacy and forPTSD 192
dual representation ECT (electroconvulsive confidentiality 98-99 social anxiety disorder 161
theory 190-191 therapy) 2NON2225 270 ethnic differences 29 specific phobias 155-156
dyscalculia 565 educational underachievement alcohol dependence 294 expressed emotion (EE)
aetiology 569 and avoidant PD 437 body shape ideals 341 267-268, 275
Dysfunctional Attitude Scale children of teenage diagnosis 61 external validity 87
(DAS) 208 mothers 578 1Q test results 53-54 externalizing disorders 525
dysfunctional schemas due to poverty and social nicotine dependence 296-297 extinction, behaviour therapy 105
antisocial personality deprivation 580 personality disorder 426 eye movement desensitisation and
disorder 431—432, 433 due to regular substance psychotic symptoms 245-246 reprocessing (EMDR) 192
and borderline personality use 301, 319 PTSD prevalence 188
disorder 435, 443, 444, 445 EE (expressed emotion) 267-268, see also cultural differences face validity 45
obsessive compulsive personality 275 ethnic stereotypes 61, 62 factitious disorder 454
disorder 443 EEG (electroencephalogram) 55 ethyl alcohol 291 imposed on another 454, 455
and schema-focused cognitive effect size 82, 89 evaluation of treatment 118-119 false memory syndrome 262, 481
therapy 445-446 effectiveness of therapies factors affecting 119-120 false recovered memories of
dyslexia 43, 565 assessment methods 120-123 methods of assessing trauma 480-482, 486
aetiology 567-569 Dodo Bird Verdict 123-124 effectiveness 120-123 fames canina 334
definition 567 ego 23 treatment vs. no familial factors
treatment 569-570 ego defence mechanisms 23 treatment 123-124 antisocial personality disorder
dyspareunia 375 electrocardiogram (ECG) 55 evaluation research (clinical (APD) 429, 431
dysthymic disorder 199 electroconvulsive therapy audit) 76 childhood depression 551
(BCT) 219, 222, 270 evaluation, stage of treatment 138 conduct disorder 539-540
e-therapy 115 electrodermal responding 55 evidence-based treatments 72 and early substance use 314
early ejaculation 370-371 electroencephalogram (EEG) 55 evolutionary approach to eating disorders 345, 349
early experiences and eating electromyogram (EMG) 55 phobias 1522153 schizophrenia 266-268
disorders 350 EMA (ecological momentary executive functioning deficits 427, social anxiety disorder 158-160
early intervention services, for assessment) 60 494, 495 somatic symptom disorders 458
psychotic symptoms 274 embodiment component to autistic spectrum family interventions/therapies 111
early maladaptive schemas depression 197 disorder 590-591 childhood psychological
(EMSs) 445 EMG (electromyogram) 55 children with ADHD 534, 536 problems 555
eating disorders 332-333, 360 emotional ‘numbing’ 476 conduct disorder and drug abusers 326
aetiology 343-345 emotional processing ADHD 539 eating disorders 356-357
biological factors 343-345 theory 189-190 interventions for 378, 517-518 schizophrenia 275-276
experiential factors 349-350 empathizing-systematizing neurocognitive disorders 499, family psychoeducation 275
psychological factors 350-352 theory 591 500, 501, 502 family systems theory 111, 349, 356
sociocultural empathy 111 obsessive compulsive fantasy and dissociative
influences 346-349 and befriending 120 disorder 180 experiences 478
transdiagnostic models 352 client-centred therapy 27, 111 schizophrenia 252, 254, 263 FAS (fetal alcohol syndrome) 292,
anorexia nervosa (AN) 333-335 lack of, antisocial PD executive functions 492 576, 579
binge-eating disorder 417, 432 exercise, and depression 197 faulty learning 105
(BED) 337-340 lack of, children with conduct exhibitionistic disorder 385-386 fear
bulimia nervosa (BN) 336-337, disorder 538 existential-humanist learning of in childhood 547-548
338 lack of, narcissistic PD 418, approaches 27-28 non-associative fear acquisition
comorbidities 335, 337, 425 435, 436 expectations model 153
specific phobias in conduct disorder 538 genome-wide association studies histrionic personality
childhood 546-547 eating disorders 342, 344 (GWAS) 252, 533 disorder 418-419, 436
see also anxiety and stressor- PTSD prevalence 188 German measles (rubella) prevalence 424
related problems specific phobias 149 infection 576, 580, 589 HIV infection
fear disorders 40 gender dysphoria 399-400 Gestalt therapy 110 antiretroviral drugs 513
Fear Fighter (computer-based CBT aetiology 400-402 gestural training 515-516 HIV-1 associated dementia
programme) 115 client perspective 401 glove anaesthesia 453 (HAD) 500, 513
fear learning deficit, diagnosis and description 400 goal management training maternal 576
antisocial personality treatment 402-404 (GMT) 517-518 neurocognitive disorder due
disorder 432-433 gender identity 399 grandiose delusions 238 to 499-500
female orgasmic disorder 370 influenced by hormones taken grooming by online predators 387, risk for opiate users 307
female sexual dysfunction 369-370 during pregnancy 401 388 hoarding disorder 178, 179
female sexual interest /arousal psychological treatments to grossly disorganized motor holistic rehabilitation 514, 518
disorder 368-369 modify 403-404 behaviour 240-242 holistic therapies 110
fetal alcohol syndrome (FAS) 292, gender reassignment grounded theory 93 effectiveness, evaluation of 119
DUS, BD surgery 402-403 group communication holy anorexia 334
fetishistic disorder 384 gene-environment interaction treatment 516 hopelessness theory of
injuries resulting from 385 and ADHD 534 group therapy 113-114 depression 211-212
first-generation antipsychotic andPTSD 188 GWAS (genome-wide association hormonal treatments
drugs 271 general paresis 8 studies) 252 paraphilic disorders 396-397
flooding, exposure therapy 105 generalized amnesia 472 for sexual dysfunction 379
fluent aphasia 494 generalized anxiety disorder HAD (HIV-1 associated hormones 375, 393
fluoxetine (Prozac) 218 (GAD) 170-176 dementia) 500 cortisol and depression 204
paediatric use 553 aetiology 171-173 haemorrhage 502 use of during pregnancy, and
fMRI (functional magnetic children and hair-pulling disorder 178 gender dysphoria 401
resonance imaging) 57 adolescents 546-547 hair sample analysis 325 hospitalization 9-10, 270
food preload tests 351 diagnosis and hallucinations 239-240, 262 experience of 12-13
fragile X syndrome 574, 575 prevalence 170-171 hallucinogen-related token economies 10-11
free association, treatment 173-175 disorders 308 hostidentity 473, 487
psychoanalysis 104 genetic factors Ecstasy 309 hostile attributional bias 541
free-basing 302 ADHD, inherited susceptibility lysergic acid diethylamide Human Genome Project 18-19
Freud, Sigmund, psychoanalytical to 533-534 (LSD) 308-309 human immunodeficiency virus see
model 23-25 Alzheimer’s disease 505-506 hallucinogens 290 HIV infection
frontal lobe 21, 22, 494 antisocial personality disorder haloperidol (Haldol) 593 humanist-existential
abnormalities (APD) 431 Halstead-Reitan Neuropsychological approach 27-28
and ADHD symptoms 534, anxiety disorders 171-172, 547 Test Battery 54 humanistic therapies 110-111
536 autistic spectrum disorder harmful dysfunction 17 Huntington’s disease 19, 509
borderline PD 434 (ASD) 588-589 hashish 298 hybrid disorders 39-40
and Broca’s aphasia 494 bipolar disorder 217-218 see also cannabis use disorder hyperactivity 5315532
schizotypal PD 427 borderline personality hazardous drinkers 290-291 hypersexuality 389
decreased activity, disorder 433-434 HCPC (Health and Care Professions hypertension 292, 502
schizophrenia 254-255 childhood depression 551 Council 138-139 hyperventilation and panic
roleinOCD 180 chromosomal disorders 573-574 head injury/trauma 498 attacks 165
see also executive functioning Cluster A personality disorders Health and Care Professions Council hypervigilance 172, 187, 414, 443,
deficits and schizophrenia 415, 427 (HCPC) 138-139 444, 540, 541
frontotemporal NCD 506-507 conduct disorder 538-539 hearing voices 263-264 hypnosis 475
frotteuristic disorder 386 depression 201-202 heritability 20 and conversion disorder 457—
functional analysis 106 dyslexia 568 see also genetic factors 458, 461-462
for people with intellectual eating disorders 345 heroin use 5, 306, 307 hypnotherapy 119, 298
disabilities 580, 581 frontotemporal neurocognitive association with crime 307 for dissociative disorders 489
functional family therapy disorder 507 controversial treatment 324 producing DID
(FET) 555 gender dysphoria 402 drug replacement symptoms 483-484
functional magnetic resonance metabolic disorders 574-575 treatment 327 hypochondriasis (illness anxiety
imaging (f(MRI) 57 post-tramatic stress disorder methadone maintenance disorder) 452-453, 466
(PTSD) 188-189 programmes 326 hypomania 215, 216, 217, 218
GABA meurotransmitter 22, 112, schizophrenia 249-252 transition from soft drugs 313 hypotheses 72
166, 254, 257, 292, 315 social anxiety disorder 158 unobtrusive users 307 significance testing 82
GAD see generalized anxiety somatic symptom disorders 461 higher order intellectual functioning hypothetical constructs 49-50
disorder substance use disorders 318-319 deficits 495 hypoxyphilia 389
galvanic skin response (GSR) 55 suicide 232 hippocampus 21, 22, 253, 494 hysteria 454, 461
gamma-aminobutyric acid genetic linkage analysis 20, 251 abnormalities
(GABA) 22, 112, 166, 254, genetic testing for degenerative borderline PD 434 IAPT (Improving Access
257292,
BV5: brain disorders 505 dissociative disorder 483 to Psychological
gender 29 pros and cons of 506-507 risk factor for PTSD 188 Therapies) 116-117
gender differences genetics 18-21, 251-252 in schizophrenia 255 ICD (International List of Causes of
adolescent depression 549 genito-pelvic pain/penetration role in depression 203, 204 Death) 37-38
anxiety disorders 148 disorder 371 history of psychopathology 6-13 id 23
06) woex
illness anxiety disorder 452-453, 466 internal consistency 44 and cortisol levels 204 media contagion and suicide among
cognitive model 459-460 internal validity 119 and eating disorders 350 the young 230
imaginal flooding 192 internalizing disorders 525 lifetime prevalence 80 media influences
imaginary companions during International List of Causes of Death limbic system 21, 22, 494 antisocial behaviour in
childhood 478 (ICD) 37-38 excessive activation in borderline children 540
imagination impairment in internet PD 434 eating disorders 346-348
ASD 586 alternative access to line of best fit 77 and substance use 314
implicit cognitive theories 393 treatment 356 lithium carbonate 221 medical applications of
Improving Access to Psychological caregiver support groups 520 lobotomy 270 cannabis 299
Therapies (IAPT) 116-117 computerized CBT 114 localized amnesia 472 medical model 6, 8-9
impulse-control disorders 428 drug prevention schemes 322 longitudinal studies 78-79 medicalisation of everyday living
impulsivity 531, 532 e-therapy 115 loose associations, schizophrenics’ problems 31
personality disorders 409, 416, paedophile ‘grooming’ 387, 388 conversations 240 medroxyprogesterone acetate
417, 418, 432, 434 interpersonal problems, low selfesteem 351-352 (MPA) 397
inattention, ADHD diagnosis 532 causal factor in sexual LSD (lysergic acid melatonin 201
incest 387 dysfunction 373 diethylamide) 308-309 memory
inclusion 579 interpretation, in lysergic acid diethylamide of childhood trauma,
inclusion strategies psychoanalysis 104 (LSD) 308-309 recovery 480-482, 487-488
autistic spectrum interpretation biases 83, 160, dissociative amnesia 471-473

disorder 594-595 263-264 magnetic resonance imaging false memories 481, 482
intellectual disabilities 579, definition 459 (MRI) 57 reconstructive 480
580-582 hostile attributional bias, conduct magnification and repression/suppression of 478
independent variable (IV) 81 disorder 541 minimization 208 biological explanations 483
infarction 502 somatic symptom major depression 198 cognitive
infectious diseases disorders 459, 465 aetiology explanations 478-479
during pregnancy and intellectual threat-interpretation biases, biological theories 201-204 state-dependent 479
disability in offspring 576 GAD 173 psychological memory bias 460
spongiform intervention, stage of theories 204-213 memory deficits
encephalopathy 500-501 treatment 137 comorbid with somatic symptom Ecstasy use 309
see also HIV infection interviews, clinical 45-47 disorders 452, 464, 466 neurocognitive disorders 493
inflammation and depression intoxication, alcohol’s comorbidity 199-200 compensatory
symptoms 205 effects 291-292 diagnosis 198-200 strategies 516-517
inflated responsibility, OCD 181 introjection 204-205 and eating disorders 335, 337, obsessive compulsive disorder
influenza virus and psychotic IQ (intelligence quotient) 351, 354, 356, 360 (OCD) 180
symptoms 256 tests 53-54 prevalence 200-201 see also amnesia
information exposure, source of treatments 219-221 memory training
childhood fear 547-548 jumping to conclusions 261 biological 220-222, programmes 516-517
information processing biases 263 psychological 222-226 menopause and sexual
generalized anxiety kleptomania 428 major depressive episode 198 dysfunction 369, 372, 375
disorder 172-173 Korsakoff’s syndrome 292 major neurocognitive disorder 499 mental contamination, OCD 182
sexual offenders 39392 maladaptive behaviour SESW. mental defeat 190
somatic symptom disorders 459 la belle indifference 453 male hypoactive sexual desire mental health and stigma 30-33
thinking biases in language, brain areas for 494 disorder 368 mental health counsellors 114
depression 207-208 language deficits 493-494 mania 1975215, mental health problems, economic
informed consent Dy interventions for 516 diagnostic criteria 216 cost 129
inherited factors see genetic factors language disorder 566 MAOIs (monoamine oxidase mental health
inpatient hospital care 133 lateral hypothalamus 345 inhibitors) 112, 121, 162, professionals 130-132
insight therapies 441-442 lead exposure and brain 202 mental health services
integrated cognitive schemata, damage 577 marijuana 298-299 facilities available 133
sexual offenders 393 lead poisoning and see also cannabis use disorder recovery model 134-135
intellectual disabilities hyperactivity 535 marriage counsellors 114 structure of 133-134
aetiology DI2—579 learned helplessness 209-210 masturbatory satiation 395 mesocortical pathway 253
alternative approaches to learning deficits 493 maternal drug use during mesolimbic pathway 253
defining 571-572 antisocial personality pregnancy 576-577 MET (motivational-enhancement
in autistic spectrum disorder disorder 432-433 maternal HIV infection 576 intervention) 325
(ASD) 586-587 learning disabilities see specific maternal malnutrition 576 meta-analyses 88-90
defined 571 learning disabilities Maudsley approach, eating and treatment effectiveness 123
DSM-5 diagnostic criteria 571 learning theories disorders 357 meta-beliefs, in GAD 173
interventions 579-583 of somatic symptom MBCT (mindfulness-based cognitive metabolic disorders 574-575
prevalence 572 disorders 458-459 therapy) 109, 110, 226 methadone 306
intelligence learning theory 25 MCMD (minor cognitive motor methadone maintenance
low IQ and conduct left hemisphere language disorder) 500 programmes 326, 327
disorder 539 centres 494 MDMA (3,4-methylenedioxymethamphetamine 304, 305, 306,
low IQ prevalence 572 levodopa 512 methamphetamine), 319
intelligence tests 53-54 Lewy bodies 508 Ecstasy 308, 309 methylphenidate (Ritalin) 553
inter-rater reliability 44 lie detectors 55 MDTs (multidisciplinary mild neurocognitive disorder 499
intermittent explosive disorder 428 life stressors teams) 132 milieu therapies 10
mimicry of violence/criminal narcissistic personality disorder cognitive impairments 493-495 dysfunction in borderline
behaviour 540 diagnosis and features 418 delirium 498 PD 434
mindfulness-based cognitive therapy link with antisocial personality diagnosis eating disorders 346
(MBCT) 109, 110 disorder 435, 436 difficulties 497-498 psychotic symptoms 252-254
for somatic symptom and parenting styles 435-436 DSM-5 categories 498-499 neurotransmitters 21-22
disorders 466 prevalence 424 major or mild NCDs 498-499 new age beliefs 262-263
treatment of depression 226 psychodynamic theories 435 treatment and NICE see National Institute for
Mini Mental State Examination National Health Servivce rehabilitation 511-512 Clinical Excellence; National
(MMSE) 496, 497 (NHS) 133-134 biological Institute for Health and Care
Minnesota Multiphasic Personality National Institute for Clinical treatments 512-513 Excellence
Inventory (MMPI) 47-48 Excellence (NICE) cognitive nicotine 290, 295
minor cognitive motor disorder guidelines for treatment of eating rehabilitation 513-518 costs of use 297-298
(MCMD) 500 disorders 35551358 types of major prenatal exposure 534, 535
mixed anxiety-depressive National Institute for Health degenerative prevalence of use 295-296
disorder 40, 199-200 and Care Excellence disorders 503-509 tobacco use disorder 296-297
mixed designs 84-85 (NICE) 72, 103, 220 NCD due to HIV nicotine replacement therapy 297
MMPI (Minnesota Multiphasic Alzheimer drug treatment infection 499-500 nihilistic delusions 239
Personality recommendations 512 NCD due to prion no treatment control condition 98
Inventory) 47-48 guidelines for treatments disease 500-501 nocturnal enuresis 554
MMR (mumps and rubella) vaccine, for substance use NCD due to traumatic brain non-adherence to medication
and autism 589 disorder 325-326 injury 501-502 248, 270
mnemonics, visual imagery 517 natural experiments 85-86 vascular neurocognitive non-associative fear acquisition
model, definition 75 naxolone 327 disorder 502-503 model 153
modelling of behaviour 594 negative affectivity neurodevelopmental non-fluent aphasia 493
molecular genetics 20 and eating disorders 351 disorders 562-563,
597 non-suicidal self-injury 227
and schizophrenia 251-252 facets of 412 autistic spectrum disorder diagnostic criteria 228
monoamine oxidase inhibitors and sexual dysfunction 374 (ASD) 584-595 noradrenergic overactivity, panic
(MAOIs) 112, 162, 202, 221 negative attributional style and categorization and labelling disorder 165-166
mood-as-input hypothesis 182 depression 212-213 of 563 norepinephrine 22
mood alteration effects of drug negative automatic thoughts 224, intellectual disabilities 571-583 amphetamines 304
use 315-316 225 specific learning antidepressant effect on 112,
mood disorders negative cognitions and disabilities 564-571 220-221
comorbidity with borderline selfschema 207-209 neuroendocrine factors in bipolar disorder 218
personality disorder 425 negative correlation 77 depression 204 and depression 202, 203
feature of neurological negative life experiences and eating neurofibrillary tangles 505, 506 panic disorder symptoms 166
disorders 513 disorders 350 neuroimaging studies yohimbine 379
see also depression and mood negative schema 207, 224 ADHD 534 normal distribution 15
disorders negative self-evaluations dyslexia 568 norms, deviation from 14-15
moral treatments 10 eating disorders 344, 358 generalized anxiety nucleus accumbens (NAc) 315, 316
motivational deficits, social anxiety disorder 160 disorder 172 null hypothesis significance
depression 197 negative symptoms of obsessions and compulsions 180 testing 82
motivational-enhancement schizophrenia 242 schizophrenia 253, 255 number processing difficulty,
intervention (MET) 325 negative triad of beliefs 207 schizotypal personality dyscalculia 565, 569
motivational-enhancement neglect in childhood, risk factor disorder 415
therapy 293 adult mental health specific phobias 153-154 obesity 333, 344, 347
motor skills deficits problems 527 see also neuroscience object-relations psychotherapy 442
autistic spectrum disorder 589 borderline personality neuroimaging techniques 56-57 object-relations theory 434-435
neurocognitive disorders 495 disorder 433 neuroleptics 271 observation, clinical 57-60
MPA (medroxyprogesterone childhood depression 550 see also antipsychotic drugs observational coding forms 58-59
acetate) 397 dependent personality neurological impairment tests 54 obsessions 176
MRI (magnetic resonance disorder 437 neuroscience 21-22 obsessive compulsive disorder
imaging) 57 eating disorders 350 antisocial personality disorder (OCD) 176
multidisciplinary teams paraphillic disorder 391 (APD) 432-433 aetiology 180-183
(MDTs) 132 substance use bipolar disorder 218 case history 177
multiple-baseline design 87-88 disorder 314 eating disorders 345-346 in children and
multiple personalities see alter see also childhood abuse major depression 202-203 adolescents 544-545
identities neologisms 241 schizophrenia 254-257 comorbid with somatic symptom
multiple personality disorder see neurobiological factors see biological see also brain abnormalities; disorders 464
dissociative identity disorder theories neuroimaging studies; diagnosis 176-178
(DID) neurochemical factors see neurotransmitter prevalence 176-178
Munchausen’s syndrome by neurotransmitter abnormalities related disorders 178-179

proxy 454 abnormalities neurosurgery for OCD 184-185 treatment 183-186
mutant Huntington (mHtt) 510 neurocognitive disorder with Lewy neurotransmitter abnormalities obsessive compulsive personality
mutations, genetic 252 bodies 508-509 ADHD 533-534 disorder (OCPD)
neurocognitive disorders autistic spectrum disorder 589 aetiology 438
naltrexone 327, 593-594 (NCDs) 492-493, 522 bipolar disorder 218 CBT treatment 443
narcissism, primary 257 assessment 495-497 depression 202-203 diagnosis and features 422-423
GOST) woex
and eating disorders 335 diagnosis 164 with eating disorders 335, client perspective 186
prevalence 424 prevalence 164-165 337, 350, 354 comorbidity with borderline
occipital lobe 21, 494 treatment 168-169 contemporary issues in personality disorder
occupational therapists 131 paradoxical communication 267 diagnosis 409-412 418, 425
OCD see obsessive compulsive paralysis, conversion disorder 453 cultural and ethnic factors 426 diagnosis 185-188
disorder and hypnosis 461-462 diagnosis 413 and dissociative disorders 470,
ODD see oppositional defiant paranoid personality Cluster A disorders 413-415 474, 476
disorder (ODD) disorder 413-414 Cluster B disorders 415-419 prevalence 188
odd/eccentric personality disorders comorbid with schizotypical Cluster C disorders 419-423 treatment 191-192
(Cluster A) 409, 413 PD 415 contemporary issues 409-412 poverty 29
aetiology 427, 439 prevalence 424 prevalence 424 in childhood, and adult mental
paranoid personality paranoid schizophrenia 259 risk factors 425 health problems 528
disorder 413-414 paraphilic disorders 383-384 treatment 440-447 and intellectual disability 577,
prevalence rates 424 aetiology 389-394 personality functioning levels 410, 580
schizoid personality diagnosis and 411 link to conduct
disorder 414 description 384-389 personality inventories 47-48 disorders 541-542
schizotypal personality risk factors 389-390 specific trait inventories 48-50 and substance use 319-320
disorder 414-415,
416 treatment 394-397 personality trait domains and poverty of content, conversation of
oestrogen 375 parasuicide 227 facets 410, 411, 412 schizophrenics 240
olanzapine (Zyprexa) 218 parent-child interactions personality traits and eating prediction of events, research
one-month prevalence 80 exacerbating ADHD 535-536 disorders 350—352, goal 74
online predators, paedophile leading to conduct disorder 539 pessimistic inferential style 551 preference molesters 387
‘grooming’ 388 risk factor for adult mental health pessimistic thinking 198, 208, prefrontal cortex 203, 495
operant conditioning 25, 26 problems 527 209, 210 abnormalities,
reinforcement of bizarre parent-implemented early PET (positron emission schizophrenia 253,
behaviour 258 intervention 594 tomography) 56-57, 462 254-255, 256-257
therapies based on 106-107 parent management pharmacological treatment see drug prefrontal lobotomy 270
use in ADHD and conduct training 555 therapy A pregnancy
disorder 554 parenting style phencyclidines 308 alcohol consumption 80, 292,
opiates 306-307 and antisocial personality phenothiazines 252 536, 539, 576
opioid levels and eating disorder 429, 431 phenylketonuria (PKU) 574 amniocentesis 574
disorders 345-346 and anxiety symptoms in phobias, specific see specific phobias chromosomal abnormalities 573
opioid use disorder 307 children 548-549 phobic beliefs 149 cocaine use 304, 576-577
opportunistic shoplifting 428 and conduct disorder 539 phonological theory of dyslexia 568 congenital disorders 576
oppositional defiant disorder parietal lobe 21, 494 physical illness, link to diet/malnutrition 574, 576
(ODD) 538 Parkinson’s disease 507-509 depression 205 factors causing intellectual
comorbid with ADHD 532 and low dopamine levels 252 physiological activity, measurement disability in offspring 573
prevalence 529 partialism 384 of 54-55 hormone use and identity
oral stage of development, passive smoking 298 physiological factors, dysphoria 401
Freud 24 pathological personality APD 432-433 infectious diseases 576
orgasm, disorders of 367, 369-371 traits 411-412 pica 340 rubella infection 576, 580, 589
orgasmic reorientation 395 pathological worrying 546 placebo control condition 84 smoking, effects of 534, 541
orienting response 259 PCP, phencyclidine 308, 315, 316 placebo effects 84, 120 premature ejaculation 370-371
outpatient treatment 133 peer influences play therapy 556-557 premenstrual dysphoric disorder
over-directive hypnotherapy/ and antisocial behaviour 540 PMDD (premenstrual dysphoric (PMDD) 199, 201
psychotherapy 482, 487 and dieting behaviour 348-349 disorder) 199, 201 prenatal factors
overgeneralization 208 anddruguse 314 point prevalence 80 and ADHD 534
overprotection 349 peerleadership 322 political norms, deviation from 15 brain abnormalities,
overprotective parenting peer pressure resistance polygraphs 55 schizophrenia 255
style 548-549 training 322 positive correlation 77 conduct disorder 539
and dependent PD 437 penile prosthesis 379-380 positive symptoms of schizophrenia intellectual disabilities SST
oxygen deficiency at birth perceived stigma/self-stigma 30 spectrum disorder 238 viral inflection and
(anoxia) 577 perfectionism 352 delusions 238-239 schizophrenia 256
performance anxiety 373 disorganized thinking prevalence 80
paedophile ‘grooming’ over the perinatal factors (speech) 240 prevalence rates 80
internet 388 autistic spectrum disorder 589 grossly disorganized or abnormal prevention programmes/ strategies
paedophilic disorder 386-388 intellectual disabilities 575-577 motor behaviour 240-242 for eating disorders 359
risk factors 390 persecutory delusions 238 hallucinations 239-240 intellectual disabilities 579-580
palliative effect 103 perseveration, OCD 182-183 positron emission tomography primary narcissism 257
panic, defined 155 personal therapy 274 (PET) 56-57 prion disease, neurocognitive
panic disorder 162-164 personalisation 208 conversion disorder study 462 deficits resulting
aetiology 165-168 personality disorder types 410, possession states, dissociative from 500-501
Ataque de Nervios 5% 1s) 411, 413 identity disorder 474 PRISMA flow diagram, systematic
comorbid with personality personality disorders (PDs) 408— post-partum depression 551 reviews 89
disorders 418, 419, 425, 438 409, 447-448 post-traumatic stress disorder prison inmates ‘code of
comorbid with specific aetiology 426-440 (PTSD) 185 conduct’ 445
phobias 154-155 comorbidity 425, 435 aetiology 188-191 privacy 98
woex [GOST
prodromal stage, psychotic aetiology of childhood rational emotive therapy prospective designs 78-79
symptoms 246-248 depression 551 (RET) 107-108 qualitative methods 90-93
progressive muscular aetiology of psychosis 257-264 rationalization 24 single-case studies 86-88
relaxation 175 attention-deficit hyperactivity RCTs see randomized controlled systematic reviews 88-90
projection, defence mechanism 24 disorder(ADHD) 535-536 trials (RCTs) residential rehabilitation
projective tests 50-53 of borderline personality disorder reaction formation 24 centres 322-323
prolactin 375 (BPD) 434-435 reading disabilities 565, 568, residual stage, psychotic
pronoun reversal 586 conduct disorder 539-542 569-570 symptoms 248
prospective designs 78-79 generalized anxiety disorder reading disabilities 565, 568, response shaping 107, 108
prospective studies, (GAD) mize i73 569-570 restricted type anorexia
depression 212-213 major depression 204-213 reality-monitoring deficit 240, 480 nervosa 335
protected title 138-139 for obsessive-compulsive disorder reasoning bias 261-262, 460 RET (rational emotive
Prozac 379 (OCD) 180-183 Reasoning & Rehabilitation therapy) 107-108
psychedelic drugs 308 of panic disorder 166 (R&R) cognitive skills retrograde amnesia 494
psychiatric comorbidity PTSD 189-190 programme 445 reward pathways in the brain and
paedophilic disorder 390 psychological well-being reattribution training 224 drug addiction 315-316
and regular substance use 319 practitioners (PWPs) 116 recall of traumatic material 479 rigidity 349
psychiatrists 130 psychometric approach 47 recessive gene 574 risk factors 74
psychiatry 8 psychopathology 5 reciprocal inhibition 105-106 risk management, anorexia
psychoanalysis 23 criteria for defining 14-18 reciprocal social interaction, nervosa 355
accounts of phobias 151 psychopathy 416-417, 429, 431 impairment in risky use 286, 287
effectiveness 104-105 psychophysiological tests 54-55 ASD 585-586 risperidone (Risperdal) 593
Freud's conception of 104 psychosis see psychotic symptoms recognition, false 482 Ritalin (methylphenidate) 553
as treatment for ‘psychosis risk syndrome’ 247-248 reconstructive memory 480 rogue representations 460
depression 222 psychosurgery 270, 280 recovery rates 123 role-playing, dissociative symptoms
psychodynamic psychotherapists 131 reflective practitioner model 138 as 483-484
approaches 103-105 psychotic symptoms 237, 280-281 regional secure units 133 Rorschach Inkblot Test 50, 51
psychodynamic models 23-25 aetiology regression 24 rubella (German measles) 576,
psychodynamic theories biological theories 249-257 regular use of substances, factors 580, 589
aetiology of psychosis 257-258 psychological influencing rumination 213
borderline personality theories 257-264 cultural variables 318 rumination theory 213
disorder 434-435 sociocultural long-term expectations and
of depression 204-206 theories 264-268 beliefs 317-318 SAD see seasonal affective disorder;
of dissociative disorders 478 course of 246-248 mood alteration effects of drug social anxiety disorder
narcissistic personality nature of 238-243 use 315-316 safety behaviours, employed
disorder 435 treatments 270 selfmedication 316-317 by panic attack
paranoid and schizoid personality antipsychotics 112-113 regulation of clinical psychology sufferers 167-168
disorders 427 biological 270-272, profession 138-139 Sally—Anne false belief task 591,
of paraphilias 390 community care 276-279 rehabilitation programmes 493, 592
of sexual dysfunction 372 family interventions 513-518 satiety, role of serotonin 346
of somatic symptom ZID=276 rejecting parents 257, 427, 435, savant syndrome 586-587
disorders 456-457 psychological 272-275 548, 549, 588 SBNT (social behaviour and
psychodynamic therapy PTSD see post-traumatic stress relapse-prevention training 396 network therapy) 294
psychoanalysis for dissociative disorder (PTSD) relapse, schizophrenia 248, 270, scattergrams 77,78
disorders 487 puppets, play therapy 556-557 274, 275, 276, 281 schema-focused cognitive
for somatic symptom PWPs (psychological well-being high expressed emotion (EE) therapy 445-446
disorders 464-465 practitioners) 116 predicting 267-268 schemata therapy 445, 446
psychoeducation 275-276 pyromania 428 relaxation training 175 schizoaftective disorder 245
psychological debriefing 191 reliability 44 diagnostic criteria 244
psychological dependence 287 qualifications, pre-requisite remission rates, schizophrenia 270 schizoid personality disorder
psychological interventions/ for clinical psychology remote causes of sexual diagnosis and features 414
therapies training 139 dysfunction 374, 378 prevalence 424
for gender dysphoria 403-404 qualitative research repressed memories, recovery psychodynamic
psychotic symptoms/ methods 90-92 of 480-482 perspective 427
schizophrenia 2I2Z=275 conducting and analysing repression 24, 478 schizophrenia spectrum
sexual dysfunction 376-378 qualitative studies 92-93 research 70 disorders 237
psychological models 25-22) quantitative methods 90 goals of 74-76 brief psychotic disorder 244
psychological paralysis, questionnaire studies 2ZU2-=Z213 and science THe) and Cluster A personality
Seizisman 15, 16 quitting smoking 297-298 research designs in clinical disorders 427
psychological tests 47 * psychology 76-77, 94 delusional disorder 243
intelligence tests 53-54 racism 62 correlational designs 77-78 historical perspective 237-238
neurological impairment random assignment 81-82 epidemiological studies 80 prevalence 245-246
tests 54 randomized controlled trials experimental designs 80-84 schizoaffective disorder 245
personality inventories 47-48 (RCTs) 121 longitudinal studies 78-79 schizophrenia 244
projective tests 50-53 problems with 121-123 meta-analyses 88-90 see also psychotic symptoms
specific trait inventories 48-50 rape memories, mixed designs 84-85 schizophrenogenic mother 257
psychological theories recovering 487—488 natural experiments 85-86 schizotypal personality disorder
GION) woex
, *
case history 416 and depression 202-203, 204 social behaviour and network treatment 464-467
close relation to serotonin metabolites 346 therapy (SBNT) 294 somatisation disorders
schizophrenia 415 serotonin-norepinephrine reuptake social constructionism 73 comorbidity with PDs 425
diagnostic criteria 415 inhibitors (SNRIs) 112, social deprivation and intellectual somatogenic hypothesis 8
features 414-415 174, 466 disability 577, 580 source-monitoring ability, deficits
prevalence 424 service user groups 14 social impairment 286, 287 in 480, 481
SCID (Structured Clinical Interview sex change surgery 402-403 social-information processing model special educational needs
for DSM-IV-TR) 46 Sex Offender Treatment Programme of antisocial/aggressive (SEN) 581
scientific method 71-72 (SOTP) 396 behaviour 540-541 specific learning disabilities 43,
pros and cons 72-73 sex therapy 377 social labelling 266 564-571
scientist-practitioner 70 sexual behaviour, social norms, deviation from 15 aetiology 567-569
screening during pregnancy 574, pathological 364-365 social phobia treatment 569-570
579-580 sexual dysfunction 366-367 and avoidant PD 420, 437 specific learning disorder 564
seasonal affective disorder aetiology 372-376 and borderline PD 418 specific phobias 149
(SAD) 199, 201 diagnosis and in childhood 547 aetiology 151-155
and bulimia 337 description 367-372 familial /developmental in children and
second-generation antipsychotic risk factors for 372 factors 158-160 adolescents 546-547
drugs 271, 272 treatment 376-381 self-focused attention 373 diagnostic criteria 149
second-hand smoke 298 sexual fetishes, conditioning treatment of, RCT study 121, prevalence 149
sedative use disorders 306 of 390 122 treatment 155-156
opiates 306-307 sexual masochism disorder 388 versus Japanese syndrome speech patterns,
sedatives 290 sexual offences 384 Taijin-kyofusho 150 schizophrenia 240, 241
Seizisman 15, 16 sexual offenders, cognitive social-selection theory 266 speech sound disorder 566
selective abstraction 208 distortions of 391-393 social skills training spider phobia 149
selective amnesia 472 sexual pain disorders 371 depression 222-223 one-session treatment 156
selective reinforcement sexual sadism disorder 388-389 schizophrenia 272-273 spirit possession 474
techniques 554 sexual skills and communication social anxiety disorder 161 Ugandan child soldiers 7
selective serotonin reuptake training 378 social skills training, depression splitting 434
inhibitors (SSRIs) 112, shaken baby syndrome 577 treatment 222-223 spongiform encephalopathy 500
205221 sheltered workshops 583 social stigma 30 spontaneous remission 119-120
action of 202 sick role 459, 461 social support, therapeutic effect SPSS (Statistical Package
depersonalization disorder 488, 489 significance testing 82 of 120 for the Social
generalized anxiety disorder 174 single-case experiment 86 social withdrawal 197, 252, 254, Sciences) 77
OCD treatment 185 single-case studies 86-88 257, 549 squeeze technique 376
paediatric use 553 situationally accessible memory people with psychotic symptoms/ SSRIs see selective serotonin
paraphilia 397 (SAM) system 190 schizophrenia 237, 264, reuptake inhibitors (SSRIs)
sexual dysfunction 379 skin conductance 266 stages of development 24
side effects 221 response 55 social workers 131 stages of sexual cycle 367
somatoform disorders 466 skin-picking disorder 178 socio-economic status (SES) stalking and erotomania 239
self-esteem issues, eating sleep paralysis 262 and diagnosis of standardization 47
disorders 347, slow motion game, play schizophrenia 264-266 state-dependent memory 479
351-352,
358 therapy SEX a/ sociocultural factors 29 statistical norms, deviation
self-focused attention 161 smartphone apps for causes of sexual from 14-15
selfharm 227-229 self-monitoring 60 dysfunction 375-376 Statistical Package for the Social
selfhelp groups 114 smoking eating disorders 346-349 Sciences (SPSS) 77
alcohol dependence 293 cessation 119 schizophrenia 264-268 statistical significance 77, 82
bulimia nervosa B55, 356 in pregnancy somatic symptom disorders 461 and clinical
self-instructional training link to ADHD in socioeconomic factors and conduct significance 121-123
(SIT) 378, 518 children 534 disorder 541-542 stepped-care models 219
self-medication, substance predictive of conduct sociogenic hypothesis 264 stereotype biases 61, 62
use "3116-317. disorder 539 sociopaths 409, 416 stigma
self-monitoring 60, 174, 175 see also tobacco use disorder sodium amobarbital 489 associated with drug
apps for 60 smooth-pursuit eye-tracking, sodium pentobarbital 489 addicts 324
of smoking behaviour 61 genetic marker for ‘soft’ drugs, transition to ‘hard’ and mental health 30-33
self-monitoring deficit 240 schizophrenia 251 drugs 313 stimulant use disorders 302
selfobservation 60 SNRIs (serotonin-norepinephrine somatic symptom amphetamines 304-305
self-starvation reuptake inhibitors) 112, disorders 450-451 caffeine 306
brain mechanisms 345-346 174, 466 aetiology 456-464 cocaine 302-304
physical effects 335 social anxiety disorder conversion disorder 453-454 stimulants 290
self-stigma 30 (SAD) 157 diagnostic criteria 451-452 stimulation, low levels of,
SEN (special educational aetiology 158-161 factitious disorder 454-455 and intellectual
needs) 581 client perspective 159 illness anxiety disorder 452-453 disability 578-579
Sentence Completion Test diagnosis and prevalence 452 stimulus control treatment, for
50=5 15:52 prevalence 157-158 risk factors 458 generalized anxiety disorder
separation anxiety 544 treatment 161-162 somatic symptom (GAD) 174
serotonin 22 social anxiety spectrum 420 disorder 451 stop-start technique 376
stress risk factors 231-232 therapeutic constructions neurocognitive disorders due
acute stress disorder (ASD) 188 superego 23-24 of dissociative ton) 5015502
cortisol levels 204 supported employment 272-273 symptoms 483-485 shaken baby syndrome 577
experiences in childhood and autistic spectrum thinking biases, treatments for psychopathology 102,
anxiety disorders 547 disorder 594-595 depression 207-208 125-126
see also post-traumatic stress supportive family third wave CBT treatments evaluation of 118-124
disorder (PTSD) management 276 109-110, 226, 466 mode of delivery WIG SNA,
stroke 502-503 symbolic loss 205 thought-action fusion (TAF), theoretical approaches 103-113
stroop task 535 symptom validity testing OCD 181 triad of impairments, autistic
Structured Clinical Interview for (SVT) 472 thought flexibility, impairment in spectrum disorder 585
DSM-IV-TR (SCID) 46 synapses 22 ASD 586 communication delay 586
structured interviews 46 synaptic transmission 21-22 thought suppression 182 imagination and flexibility of
student counsellors 114 syndrome, definition 37 thoughts, negative 224-226 thought 586
stuttering 567 systematic amnesia 472 thrombolytic therapy 512-513 reciprocal social
aetiology 569 systematic desensitisation 105 thrombosis 502, 503 interaction 585-586
treatment 570 anxiety-based problems in tic disorders 545, 546 trichotillomania 178
sublimation, defence mechanism 24 children 554 prevalence 529 tricyclic antidepressants (TCAs)
substance abuse therapy for specific Time to Change campaign, 112, 202, 221, 466, 513
cannabis-psychotic symptoms phobias 155 UK, mental health twin studies 19-20
link 260 systematic reviews 88-90 stigma 32-33 autistic disorder 588
comorbidity with personality of treatment effectiveness 123 time-out (TO) 554 bipolar disorder 218
disorders 425 systemic family therapy 555 time pressure management schizophrenia 250
definition 286 systemic theory 111 (TPM) 514 two-factor model of sexual
and eating disorders 337 tobacco use disorder 295 dysfunction, Masters and
individuals with psychotic Taijin-kyofusho (TKS) 150 costs of nicotine use 297-298 Johnson 372-373
symptoms 279 tangentiality, speech disorder, diagnostic criteria 296-297
in pregnancy 576 schizophrenics 240 prevalence 295-296 unconditional positive regard 111
substance dependence 286 tardive dyskinesia 271 token economy 10-11, 106-107 understanding , research aim 75
substance use disorders TAT (Thematic Apperception tolerance 287 unipolar depression (major
(SUDs) 285-286, 329 Test) 50551 TOM see theory of mind (TOM) depression) 198
aetiology 312-314 Tay-Sachs disease 574-575 deficits aetiology 201-213
abuse and tease technique 376 Tourette’s syndrome 545, 546 diagnosis & prevalence 198-201
dependence 318-320 teenage mothers 577-578, 580 toxins and neurological treatments 219-226
experimentation 314 telephone therapy 115-116 damage 577 unobtrusive heroin user 307
regular use 315-318 telepsychiatry 115-116 trail making test 496, 535
comorbidity 289 television violence and aggression in training 139-141 vacuum erection device (VED) 380
definition 286 children 540 clinical training 139-141 vaginismus 372
diagnosis 286-288 temporal cortex pre-training qualifications and validity 44, 45
features of specific 290 abnormalities 255 experiences 139 variant Creutzfeldt-Jakob disease
alcohol use temporal lobe 21, 494 training programmes (vCJD) 500-501
disorder 290-295 temporoparietal areas of the brain for individuals with autism 594 vascular neurocognitive
cannabis use and dyslexia 568-569 for people with intellectual disorder 502-503
disorder 298-302 test batteries 495-496 disabilities 580 ventral tegmental area(VTA) 315,
hallucinogen-related test-retest reliability 44 transdiagnostic models of eating 316
disorders 308-309 testosterone 375 disorders 352 ventricles, enlarged in
sedative use anti-androgen drugs reducing in transference, psychoanalysis 104 schizophrenia 254
disorders 306-307 paraphiliacs 393-394 transvestic disorder 384-385 verbally accessible memory (VAM)
stimulant use decrease in during trauma system 190
disorders 302-306 menopause 375 in childhood Viagra (sildenafil citrate) 378-379
tobacco use disorder 295-298 and hormone replacement aetiology of anxiety videoconferencing
prevalence 288-289 therapy 379 disorders 547 therapy 115-116
treatment 321-322 reduction in regular cannabis predictor of adult mental violence
behavioural therapies 323-324 users 301-302 health problems 528 media and peer influences 540
biological tests see psychological tests experiences/ events in schizophrenia 278-279
treatments 326-327 THC (tetrahydrocannabinol) 299 and dissociative violent crime, and antisocial
cognitive behaviour Thematic Apperception Test disorders 470, 474, 476 personality disorder 430
therapies 324-326 (TAT) 50,51 re-experiencing of viral infections during pregnancy,
community-based theory of mind (TOM) deficits (abreaction) 486 psychosis aetiology 256
programmes 322-323 attention deficit recall of, state-dependent virtual reality programmes, for
family and couple hyperactivity disorder memory 479 brain injury patients
therapy 326 (ADHD) 536 memories 514, 516
substantia nigra 507 autism spectrum false recovery of 481-482 visual imagery mnemonics 517
suffocation alarm theories 165 disorder 586, 590, 591, repression of 478, 481 visual-perceptual functioning
suicide 229-230 592; 593 see also post-traumatic stress deficits 495
identifying and schizophrenia 264, 265 disorder (PTSD) visuospatial deficits, rehabilitation
preventing 232-233 theory, definition 71-72 traumatic brain injury programmes 514-515
IZ woex
voices, hearing, psychotic WAIS-IV (Wechsler Adult weight gain management, anorexia word salad, schizophrenic
symptom 263-264 Intelligence Scale, 4th nervosa 355 language 240, 241
voluntary, defined 97 edn) 53, 495-496 Wernicke’s aphasia 494 worrying, in generalized
voyeuristic disorder 386 waiting list control 121 Wisconsin card sorting task 495 anxiety disorder
VTA (ventral tegmental area) 315, Wechsler Adult Intelligence withdrawal from drugs 287-288 (GAD) 170, 173
316 Scale (WAIS-IV) 53, withholding of benefits, ethical issue
vulnerability factors for PTSD 189 495-496 inresearch 98 yohimbine 379
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fascinating historical context is complemented by in-depth descriptions ofpsychological and biological bases of
psychopathology, with new material on neuroscience and genetics. As with the first edition, the intertwining of
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Graham C. L. Davey, Ph.D. is Professor of Psychology at the University of Sussex, UK. Professor Davey
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Psychological Disorders; and Phobias: A Handbook of Theory, Research & Treatment. He has served
as President of the British Psychological Society, and is currently Editor-in-Chief of the Journal of
Experimental Psychopathology and Psychopathology Review. |
ISBN 978-1-118-65933-5
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he only seri

BPS Wiley presents a comprehensive and authoritative series covering everything

GEORGE GREEN LIBRARY OF

BRA the British WI LEY

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Set in 11/12.5pt Dante MT by MPS Limited, Chennai, India

Senior Commissioning Editor: Andrew McAleer

Accompanying Online Resources for Instructors and Students

PART! INTRODUCING PSYCHOPATHOLOGY: CONCEPTS, PROCEDURES AND PRACTICES

Chapter 1 An Introduction to Psychopathology: Concepts, Paradigms and Stigma

Chapter 2 Classification and Assessment in Clinical Psychology

Chapter 3 Research Methods in Clinical Psychology

Chapter 4 Treating Psychopathology 101

Chapter 5 Clinical Practice 127

PART Il PSYCHOPATHOLOGY AND PSYCHOLOGICAL DISORDERS 143

Chapter 6 Anxiety and Stressor-Related Problems 145

Chapter 7 Depression and Mood Disorders 195

Chapter 8 Experiencing Psychosis: Schizophrenia Spectrum Problems 235

Chapter 9 Substance Use Disorders 283

Chapter 10 Eating Disorders 331

Chapter 11 Sexual and Gender Problems 363

Chapter 12 Personality Disorders 407

Chapter 13 Somatic Symptom Disorders 449

Chapter 14 Dissociative Experiences 469

Chapter 15 Neurocognitive Disorders 491

Chapter 16 Childhood and Adolescent Psychological Problems 523

Chapter 17 Neurodevelopmental Disorders 561

PART! INTRODUCING PSYCHOPATHOLOGY: CONCEPTS, PROCEDURES AND PRACTICES 1

Chapter 1 An Introduction to Psychopathology: Concepts, Paradigms and Stigma 3

Chapter 2 Classification and Assessment in Clinical Psychology 35

22, Methods of Assessment 44

Chapter 3 Research Methods in Clinical Psychology 69

Chapter 4 Treating Psychopathology 101

Chapter 5 Clinical Practice 127

PART Ii PSYCHOPATHOLOGY AND PSYCHOLOGICAL DISORDERS 143

Chapter 7 Depression and Mood Disorders 195

Chapter 8 Experiencing Psychosis: Schizophrenia Spectrum Problems 255

Chapter 9 Substance Use Disorders 283

Chapter 10 Eating Disorders

Chapter 11 Sexual and Gender Problems

Chapter 12 Personality Disorders

Chapter 13 Somatic Symptom Disorders 449

13m The Diagnosis and Characteristics of Somatic Symptom Disorders 451

Chapter 14 Dissociative Experiences

Chapter 16 Childhood and Adolescent Psychological Problems 523

Chapter 5 — Clinical Practice The OCD-related disorder body dysmorphic

RESOURCES FOR STUDENTS

Sample Student Lecturer Further

|Click to view all student resources

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RESOURCES FOR LECTURERS

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1. Anlntroduction to Psychopathology: 3 Research Methods in Clinical Psychology

ROUTE MAP OF THE CHAPTER CHAPTER OUTLINE