A GUIDE TO 

ASSESSMENTS THAT WORK
A GUIDE TO ASSESSMENTS
THAT WORK

S e c o n d E di t i o n

EDITED BY

John Hunsley and Eric J. Mash

1
 1
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 Contents

Foreword to the First Edition Part II  Attention-​Deficit and Disruptive

by Peter E. Nathan  vii Behavior Disorders 

Preface  xi 4. Attention-​Deficit/​Hyperactivity Disorder  47

CHARLOTTE JOHNSTON
About the Editors  xv SARA COLALILLO

Contributors  xvii 5. Child and Adolescent Conduct Problems  71

PAUL J. FRICK
Part I  Introduction  ROBERT J. McMAHON

1. Developing Criteria for Evidence-​Based Part III  Mood Disorders and Self-​Injury 
Assessment: An Introduction to Assessments
That Work  3 6. Depression in Children and Adolescents  99
JOHN HUNSLEY LEA R. DOUGHERTY
ERIC J. MASH DANIEL N. KLEIN
THOMAS M. OLINO
2. Dissemination and Implementation of
Evidence-​Based Assessment  17 7. Adult Depression  131
AMANDA JENSEN-​DOSS JACQUELINE B. PERSONS
LUCIA M. WALSH DAVID M. FRESCO
VANESA MORA RINGLE JULIET SMALL ERNST

3. Advances in Evidence-​Based Assessment: 8. Depression in Late Life  152

AMY FISKE
Using Assessment to Improve Clinical ALISA O’RILEY HANNUM
Interventions and Outcomes  32
ERIC A. YOUNGSTROM
ANNA VAN METER 9. Bipolar Disorder  173
SHERI L. JOHNSON
CHRISTOPHER MILLER
LORI EISNER
vi Contents

10. Self-​Injurious Thoughts and Behaviors  193 Part VI Schizophrenia and Personality
ALEXANDER J. MILLNER Disorders 
MATTHEW K. NOCK
20. Schizophrenia  435
Part IV  Anxiety and Related Disorders  SHIRLEY M. GLYNN
KIM T. MUESER
11. Anxiety Disorders in Children and
Adolescents  217 21. Personality Disorders  464
SIMON P. BYRNE STEPHANIE L. ROJAS
ELI R. LEBOWITZ THOMAS A. WIDIGER
THOMAS H. OLLENDICK
WENDY K. SILVERMAN Part VII Couple Distress and Sexual
Disorders 
12. Specific Phobia and Social Anxiety
Disorder  242 22. Couple Distress  489
KAREN ROWA DOUGLAS K. SNYDER
RANDI E. MCCABE RICHARD E. HEYMAN
MARTIN M. ANTONY STEPHEN N. HAYNES
CHRISTINA BALDERRAMA-​DURBIN
13. Panic Disorder and Agoraphobia  266
AMY R. SEWART 23. Sexual Dysfunction  515
MICHELLE G. CRASKE NATALIE O. ROSEN
MARIA GLOWACKA
14. Generalized Anxiety Disorder  293 MARTA MEANA
MICHEL J. DUGAS YITZCHAK M. BINIK
CATHERINE A. CHARETTE
NICOLE J. GERVAIS Part VIII  Health-​Related Problems 

15. Obsessive–​Compulsive Disorder  311 24. Eating Disorders  541

SHANNON M. BLAKEY ROBYN SYSKO
JONATHAN S. ABRAMOWITZ SARA ALAVI

16. Post-​Traumatic Stress Disorder in Adults  329 25. Insomnia Disorder  563
SAMANTHA J. MOSHIER CHARLES M. MORIN
KELLY S. PARKER-​GUILBERT SIMON BEAULIEU-​BONNEAU
BRIAN P. MARX KRISTIN MAICH
TERENCE M. KEANE COLLEEN E. CARNEY

Part V Substance-​Related and Gambling 26. Child and Adolescent Pain  583
Disorders C. MEGHAN McMURTRY
PATRICK J. McGRATH
17. Substance Use Disorders  359
DAMARIS J. ROHSENOW 27. Chronic Pain in Adults  608
THOMAS HADJISTAVROPOULOS
18. Alcohol Use Disorder  381 NATASHA L. GALLANT
ANGELA M. HAENY MICHELLE M. GAGNON
CASSANDRA L. BONESS
YOANNA E. McDOWELL Assessment Instrument Index  629
KENNETH J. SHER
Author Index  639
19. Gambling Disorders  412 Subject Index  721
DAVID C. HODGINS
JENNIFER L. SWAN
RANDY STINCHFIELD
 Foreword to the First Edition
I believe A Guide to Assessments that Work is the right
book at the right time by the right editors and authors.
The mental health professions have been intensively
engaged for a decade and a half and more in establish-
ing empirically supported treatments. This effort has led
to the publication of evidence-​based treatment guidelines
by both the principal mental health professions, clinical
psychology (Chambless & Ollendick, 2001; Division 12
Task Force, 1995), and psychiatry (American Psychiatric
Association, 1993, 2006). A substantial number of books
and articles on evidence-​ based treatments have also
appeared. Notable among them is a series by Oxford
University Press, the publishers of A Guide to Assessments
that Work, which began with the first edition of A Guide
to Treatments that Work (Nathan & Gorman, 1998), now
in its third edition, and the series includes Psychotherapy
Relationships that Work (Norcross, 2002)  and Principles
of Therapeutic Change that Work (Castonguay &
Beutler, 2006).
Now we have an entire volume given over to evidence-​
based assessment. It doesn’t appear de novo. Over the
past several years, its editors and like-​minded colleagues
tested and evaluated an extensive series of guidelines for
evidence-​based assessments for both adults and children
(e.g., Hunsley & Mash, 2005; Mash & Hunsley, 2005).
Many of this book’s chapter authors participated in these
efforts. It might well be said, then, that John Hunsley, Eric
Mash, and the chapter authors in A Guide to Assessments
that Work are the right editors and authors for this, the first
book to detail the assessment evidence base.
There is also much to admire within the pages of the
volume. Each chapter follows a common format pre-
scribed by the editors and designed, as they point out,
“to enhance the accessibility of the material presented
throughout the book.” First, the chapters are syndrome-​
focused, making it easy for clinicians who want help in
assessing their patients to refer to the appropriate chapter
or chapters. When they do so, they will find reviews of the
assessment literature for three distinct purposes:  diagno-
sis, treatment planning, and treatment monitoring. Each
of these reviews is subjected to a rigorous rating system
that culminates in an overall evaluation of “the scientific
adequacy and clinical relevance of currently available
measures.” The chapters conclude with an overall assess-
ment of the limits of the assessments available for the syn-
drome in question, along with suggestions for future steps
to confront them. I believe it can well be said, then, that
this is the right book by the right editors and authors.
But is this the right time for this book? Evidence-​based
treatments have been a focus of intense professional atten-
tion for many years. Why wouldn’t the right time for this
book have been several years ago rather than now, to
coincide with the development of empirically supported
treatments? The answer, I think, reflects the surprisingly
brief history of the evidence-​based medical practice move-
ment. Despite lengthy concern for the efficacy of treat-
ments for mental disorders that dates back more than
50  years (e.g., Eysenck, 1952; Lambert & Bergin, 1994;
Luborsky, Singer, & Luborsky, 1976; Nathan, Stuart, &
Dolan, 2000), it took the appearance of a Journal of the
viii Foreword to the First Edition
American Mental Association article in the early 1990s
advocating evidence-​based medical practice over medi-
cine as an art to mobilize mental health professionals to
achieve the same goals for treatments for mental disor-
ders. The JAMA article “ignited a debate about power,
ethics, and responsibility in medicine that is now threat-
ening to radically change the experience of health care”
(Patterson, 2002). This effort resonated widely within the
mental health community, giving impetus to the efforts of
psychologists and psychiatrists to base treatment decisions
on valid empirical data.
Psychologists had long questioned the uncertain reli-
ability and utility of certain psychological tests, even
though psychological testing was what many psychologists
spent much of their time doing. At the same time, the
urgency of efforts to heighten the support base for valid
assessments was limited by continuing concerns over the
efficacy of psychotherapy, for which many assessments
were done. Not surprisingly, then, when empirical sup-
port for psychological treatments began to emerge in the
early and middle 1990s, professional and public support
for psychological intervention grew. In turn, as psycho-
therapy’s worth became more widely recognized, the
value of psychological assessments to help in the plan-
ning and evaluation of psychotherapy became increas-
ingly recognized. If my view of this history is on target, the
intense efforts that have culminated in this book could
not have begun until psychotherapy’s evidence base had
been established. That has happened only recently, after a
lengthy process, and that is why I claim that the right time
for this book is now.
Who will use this book? I hope it will become a favor-
ite text for graduate courses in assessment so that new
generations of graduate students and their teachers will
come to know which of the assessment procedures they
are learning and teaching have strong empirical support.
I also hope the book will become a resource for practitio-
ners, including those who may not be used to choosing
assessment instruments on the basis of evidence base. To
the extent that this book becomes as influential in clinical
psychology as I hope it does, it should help precipitate a
change in assessment test use patterns, with an increase in
the utilization of tests with strong empirical support and a
corresponding decrease in the use of tests without it. Even
now, there are clinicians who use assessment instruments
because they learned them in graduate school, rather than
because there is strong evidence that they work. Now, a
different and better standard is available.
I am pleased the editors of this book foresee it provid-
ing an impetus for research on assessment instruments
that currently lack empirical support. I  agree. As with
a number of psychotherapy approaches, there remain a
number of understudied assessment instruments whose
evidence base is currently too thin for them to be con-
sidered empirically supported. Like the editors, I believe
we can anticipate enhanced efforts to establish the limits
of usefulness of assessment instruments that haven’t yet
been thoroughly explored. I also anticipate a good deal
of fruitful discussion in the professional literature—​and
likely additional research—​on the positions this book’s
editors and authors have taken on the assessment instru-
ments they have evaluated. I  suspect their ratings for
“psychometric adequacy and clinical relevance” will be
extensively critiqued and scrutinized. While the resul-
tant dialogue might be energetic—​even indecorous on
occasion—​as has been the dialogue surrounding the evi-
dence base for some psychotherapies, I am hopeful it will
also lead to more helpful evaluations of test instruments.
Perhaps the most important empirical studies we might
ultimately anticipate would be research indicating which
assessment instruments lead both to valid diagnoses and
useful treatment planning for specific syndromes. A  dis-
tant goal of syndromal diagnosis for psychopathology has
always been diagnoses that bespeak effective treatments. If
the system proposed in this volume leads to that desirable
outcome, we could all celebrate.
I congratulate John Hunsley and Eric Mash and their
colleagues for letting us have this eagerly anticipated
volume.
Peter E. Nathan
(1935–2016)
References
American Psychiatric Association. (1993). Practice guidelines
for the treatment of major depressive disorder in adults.
American Journal of Psychiatry, 150 (4 Supplement),
1–​26.
American Psychiatric Association. (2006). Practice guidelines
for the treatment of psychiatric disorders: Compendium,
2006. Washington, DC: Author.
Castonguay, L. G., & Beutler, L. E. (2006). Principles of thera-
peutic change that work. New  York:  Oxford University
Press.
Chambless, D. L., & Ollendick, T. H. (2001). Empirically
supported psychological interventions:  Controversies
and evidence. In S. T. Fiske, D. L. Schacter, & C.
Zahn-​Waxler (Eds.), Annual review of psychology
(Vol. 52, pp. 685–​716). Palo Alto, CA: Annual Review.
Division 12 Task Force. (1995). Training in and dissemina-
tion of empirically-​validated psychological treatments:

Report and recommendations. The Clinical Psychologist,
48, 3–​23.
Eysenck, H. J. (1952). The effects of psychotherapy: An eval-
uation. Journal of Consulting Psychology, 16, 319–​324.
Hunsley, J., & Mash, E. J. (Eds.). (2005). Developing guide-
lines for the evidence-​based assessment (EBA) of adult dis-
orders (special section). Psychological Assessment, 17(3).
Lambert, M. J., & Bergin, A. E. (1994). The effectiveness
of psychotherapy. In S. L. Garfield & A. E. Bergin
(Eds.), Handbook of psychotherapy and behavior change
(4th ed., pp. 143–​189). New York: Wiley.
Luborsky, L., Singer, B., & Luborsky, L. (1976). Comparative
studies of psychotherapies: Is it true that “everybody has won
and all must have prizes?” In R. L. Spitzer & D. F. Klein
(Eds.), Evaluation of psychological therapies (pp. 3–​22).
Baltimore, MD: Johns Hopkins University Press.
Foreword to the First Edition ix
Mash, E. J., & Hunsley, J. (Eds.). (2005). Developing
guidelines for the evidence-​based assessment of child
and adolescent disorders (special section). Journal of
Clinical Child and Adolescent Psychology, 34(3).
Nathan, P. E., & Gorman, J. M. (1998, 2002, 2007). A guide
to treatments that work. New  York:  Oxford University
Press.
Nathan, P. E., Stuart, S. P., & Dolan, S. L. (2000). Research
on psychotherapy efficacy and effectiveness:  Between
Scylla and Charybdis? Psychological Bulletin, 126,
964–​981.
Norcross, J. C. (Ed.). (2002). Psychotherapy relationships
that work: Therapist contributions and responsiveness to
patients. New York: Oxford University Press.
Patterson, K. (2002). What doctors don’t know (almost every-
thing). New York Times Magazine, May 5, 74–​77.
 Preface
BACKGROUND
Evidence-​based practice principles in health care systems
emphasize the importance of integrating information
drawn from systematically collected data, clinical exper-
tise, and patient preferences when considering health
care service options for patients (Institute of Medicine,
2001; Sackett, Rosenberg, Gray, Haynes, & Richardson,
1996). These principles are a driving force in most health
care systems and have been endorsed as a necessary foun-
dation for the provision of professional psychological ser-
vices (American Psychological Association Presidential
Task Force on Evidence-​Based Practice, 2006; Dozois
et al., 2014). As psychologists, it is difficult for us to imag-
ine how any type of health care service, including psycho-
logical services, can be provided to children, adolescents,
adults, couples, or families without using some type of
informal or formal assessment methods. Nevertheless,
until relatively recently, there was an almost exclusive
focus on issues related to developing, disseminating, and
providing evidence-​based interventions, with only cursory
acknowledgment of the role that evidence-​based assess-
ment (EBA) activities play in the promotion of evidence-​
based services.
Fortunately, much has changed with respect to EBA
since the publication of the first edition of this volume in
2008. A growing number of publications are now available
in the scientific literature that address the importance of
solid assessment instruments and methods. Special sec-
tions on EBA have been published in recent issues of top
clinical psychology journals (e.g., Arbisi & Beck, 2016;
Jensen-​Doss, 2015). The evidence base for the value of
monitoring treatment progress has increased substantially,
as have calls for the assessment of treatment progress to
become standard practice (e.g., Lambert, 2017). There
is also mounting evidence for assessment as a key com-
ponent for engaging clients in effective mental health
services (Becker, Boustani, Gellatly, & Chorpita, 2017).
Unfortunately, some long-​ standing problems evident
in the realm of psychological assessment remain. Many
researchers continue to ignore the importance of evaluat-
ing the reliability of the assessment data obtained from
their study participants (e.g., Vacha-​Haase & Thompson,
2011). Despite the demonstrated impact of treatment
monitoring, relatively few clinicians systematically and
routinely assess the treatment progress of their clients
(Ionita & Fitzpatrick, 2014), although it appears that stu-
dents in professional psychology programs are receiving
more training in these assessment procedures than was the
case in the past (e.g., Overington, Fitzpatrick, Hunsley,
& Drapeau, 2015). All in all, though, when viewed from
the vantage point of the early years of the 21st century, it
does seem that steady progress is being made with respect
to EBA.
As was the case with the first edition, the present vol-
ume was designed to complement the books published
by Oxford University Press that focus on bringing the best
of psychological science to bear on questions of clini-
cal importance. These volumes, A Guide to Treatments
that Work (Nathan & Gorman, 2015) and Psychotherapy
xii Preface

Relationships that Work (Norcross, 2011), address inter- to (a)  understanding the patient’s or client’s needs and
vention issues; the present volume specifically addresses (b)  accessing the scientific literature on evidence-​based
the role of assessment in providing evidence-​based ser- treatment options. We also recognize that many patients
vices. Our primary goal for the book was to have it address or clients will present with multiple problems; to that end,
the needs of professionals providing psychological services the reader will find frequent references within a chapter
and those training to provide such services. A secondary to the assessment of common co-​occurring problems that
goal was to provide guidance to researchers on scientifi- are addressed in other chapters in the volume. To be opti-
cally supported assessment tools that could be used for mally useful to potential readers, we have included chap-
both psychopathology research and treatment research ters that deal with the assessment of the most commonly
purposes. Relatedly, we hope that the summary tables pro- encountered disorders or conditions among children,
vided in each chapter will provide some inspiration for adolescents, adults, older adults, and couples.
assessment researchers to try to (a)  develop instruments Ideally, we want readers to come away from each chap-
for specific assessment purposes and disorders for which, ter with a sense of the best scientific assessment options
currently, few good options exist and (b) expand our lim- that are clinically feasible and useful. To help accomplish
ited knowledge base on the clinical utility of our assess- this, we were extremely fortunate to be able to assemble a
ment instruments. stellar group of contributors for this volume. The authors
are all active contributors to the scientific literature on
assessment and share a commitment to the provision of
ORGANIZATION EBA and treatment services.
To enhance the accessibility of the material presented
All chapters and tables in the second edition have been throughout the book, we asked the authors, as much as pos-
revised and updated by our expert authors to reflect recent sible, to follow a common structure in writing their chap-
developments in the field, including the publication of ters. Without being a straitjacket, we expected the authors
the fifth edition of the Diagnostic and Statistical Manual to use these guidelines in a flexible manner that allowed for
of Mental Disorders (DSM-​ 5; American Psychiatric the best possible presentation of assessment work relevant
Association, 2013). For the most part, the general cover- to each disorder or clinical condition. The chapter format
age and organization of the first edition, which our read- generally used throughout the volume is as follows:
ers found useful, has been retained in the second edition. Introduction: A brief overview of the chapter content.
Consistent with a growing developmental psychopathol- Nature of the Disorder/​ Condition:  This section
ogy perspective in the field, the scope of some chapters includes information on (a)  general diagnostic consid-
has expanded in order to provide more coverage of assess- erations, such as prevalence, incidence, prognosis, and
ment issues across the lifespan (e.g., attention-​ deficit/​ common comorbid conditions; (b) evidence on etiology;
hyperactivity disorder in adults). The most important and (c)  contextual information such as relational and
changes in organization involve the addition of two new social functioning and other associated features.
chapters, one dealing with the dissemination and imple- Purposes of Assessment: To make the book as clinically
mentation of EBA (Chapter 2) and the other dealing with relevant as possible, authors were asked to focus their
new developments in EBA (Chapter 3). The contents of review of the assessment literature to three specific assess-
these chapters highlight both the important contributions ment purposes: (a) diagnosis, (b) case conceptualization
that assessment can make to the provision of psychological and treatment planning, and (c)  treatment monitoring
services and the challenges that mental health profession- and evaluation. We fully realize the clinical and research
als face in implementing cost-​effective and scientifically importance of other assessment purposes but, rather than
sound assessment strategies. attempting to provide a compendium of assessment mea-
Consistent with evidence-​ based psychology and sures and strategies, we wanted authors to target these
evidence-​based medicine, the majority of the chapters three key clinical assessment purposes. We also asked
in this volume are organized around specific disorders authors to consider ways in which age, gender, ethnicity,
or conditions. Although we recognize that some clients and other relevant characteristics may influence both the
do not have clearly defined or diagnosable problems, the assessment measures and the process of assessment for the
vast majority of people seeking psychological services disorder/​condition.
do have identifiable diagnoses or conditions. Accurately For each of the three main sections devoted to spe-
assessing these disorders and conditions is a prerequisite cific assessment purposes, authors were asked to focus on

assessment measures and strategies that either have demon-
strated their utility in clinical settings or have a substantial
likelihood of being clinically useful. Authors were encour-
aged to consider the full range of relevant assessment meth-
ods (interviews, self-​report, observation, performance tasks,
computer-​based methods, physiological, etc.), but both sci-
entific evidence and clinical feasibility were to be used to
guide decisions about methods to include.
Assessment for Diagnosis:  This section deals with
assessment measures and strategies used specifically for
formulating a diagnosis. Authors were asked to focus
on best practices and were encouraged to comment on
important conceptual and practical issues in diagnosis
and differential diagnosis.
Assessment for Case Conceptualization and Treatment
Planning:  This section presents assessment measures
and strategies used to augment diagnostic information
to yield a full psychological case conceptualization that
can be used to guide decisions on treatment planning.
Specifically, this section addresses the domains that the
research literature indicates should be covered in an EBA
to develop (a) a clinically meaningful and useful case con-
ceptualization and (b)  a clinically sensitive and feasible
service/​treatment plan (which may or may not include
the involvement of other professionals).
Assessment for Treatment Monitoring and Treatment
Outcome: In this third section, assessment measures and
strategies were reviewed that can be used to (a) track the
progress of treatment and (b) evaluate the overall effect of
treatment on symptoms, diagnosis, and general function-
ing. Consistent with the underlying thrust of the volume,
the emphasis is on assessment options that have support-
ing empirical evidence.
Within each of the three assessment sections, standard
tables are used to provide summary information about
the psychometric characteristics of relevant instruments.
Rather than provide extensive psychometric details in
the text, authors were asked to use these rating tables to
convey information on the psychometric adequacy of
instruments. To enhance the utility of these tables, rather
than presenting lists of specific psychometric values for
each assessment tool, authors were asked to make global
ratings of the quality of the various psychometric indices
(e.g., norms, internal reliability, and construct validity)
as indicated by extant research. Details on the rating sys-
tem used by the authors are presented in the introductory
chapter. Our goal is to have these tables serve as valuable
summaries for readers. In addition, by using the tables to
present psychometric information, the authors were able
to focus their chapters on both conceptual and practical
Preface xiii
issues without having to make frequent detours to discuss
psychometrics.
At the conclusion of each of these three main sec-
tions there is a subsection titled Overall Evaluation that
includes concise summary statements about the scientific
adequacy and clinical relevance of currently available
measures. This is where authors comment on the avail-
ability (if any) of demonstrated scientific value of follow-
ing the assessment guidance they have provided.
Conclusions and Future Directions: This final section
in each chapter provides an overall sense of the scope
and adequacy of the assessment options available for the
disorder/​condition, the limitations associated with these
options, and possible future steps that could be taken to
remedy these limitations. Some authors also used this sec-
tion to raise issues related to the challenges involved in
trying to ensure that clinical decision-​making processes
underlying the assessment process (and not just the assess-
ment measures themselves) are scientifically sound.
ACKNOWLEDGMENTS
To begin with, we express our gratitude to the authors. They
diligently reviewed and summarized often-​ voluminous
assessment literatures and then presented this informa-
tion in a clinically informed and accessible manner. The
authors also worked hard to implement the guidelines we
provided for both chapter structure and the ratings of vari-
ous psychometric characteristics. Their efforts in construct-
ing their chapters are admirable, and the resulting chapters
consistently provide invaluable clinical guidance.
We also thank Sarah Harrington, Senior Editor for clini-
cal psychology at Oxford University Press, for her continued
interest in the topic and her ongoing support for the book.
We greatly appreciate her enthusiasm and her efficiency
throughout the process of developing and producing this
second edition. We are also indebted to Andrea Zekus,
Editor at Oxford University Press, who helped us with the
process of assembling the book from start to finish. Her assis-
tance with the myriad issues associated with the publication
process and her rapid response to queries was invaluable.
Finally, we thank all the colleagues and contributors
to the psychological assessment and measurement litera-
tures who, over the years, have shaped our thinking about
assessment issues. We are especially appreciative of the
input from those colleagues who have discussed with us
the host of problems, concerns, challenges, and promises
associated with efforts to promote greater awareness of the
need for EBA within professional psychology.
xiv Preface

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generalization studies. Measurement and Evaluation in
clinical practice:  A Canadian survey of psychological
Counseling and Development, 44, 159–​168.
 About the Editors
John Hunsley, PhD, is Professor of Psychology in the
School of Psychology at the University of Ottawa and
is a Fellow of the Association of State and Provincial
Psychology Boards and the Canadian Psychological
Association. He has served as a journal editor, an edito-
rial board member for several journals, and an editorial
consultant for many journals in psychology. He has pub-
lished more than 130 articles, chapters, and books related
to evidence-​based psychological practice, psychological
assessment, and professional issues.
Eric J.  Mash, PhD, is Professor Emeritus in the
Department of Psychology at the University of Calgary. He
is a Fellow of the American Psychological Association, the
Canadian Psychological Association, and the American
Psychological Society. He has served as an editor, edito-
rial board member, and consultant for many scientific
and professional journals and has written and edited many
books and journal articles related to child and adolescent
mental health, assessment, and treatment.
 Contributors
Jonathan S. Abramowitz,  PhD: Department of
Psychology and Neuroscience, University of North
Carolina at Chapel Hill, Chapel Hill, North Carolina
Sara Alavi: Eating and Weight Disorders Program, Icahn
School of Medicine at Mt. Sinai, New York, New York
Martin M.  Antony, PhD: Department of Psychology,
Ryerson University, Toronto, Ontario, Canada
Christina Balderrama-​Durbin,  PhD: Department of
Psychology, Binghamton University—State University of
New York, Binghamton, New York
Simon Beaulieu-​Bonneau, PhD: École de psychologie,
Université Laval, Quebec City, Quebec, Canada
Yitzchak M. Binik,  PhD: Department of Psychology,
McGill University, Montreal, Quebec, Canada
Shannon M. Blakey, MS: Department of Psychology and
Neuroscience, University of North Carolina at Chapel
Hill, Chapel Hill, North Carolina
Cassandra L. Boness, MA: Department of Psychological
Sciences, University of Missouri, Columbia, Missouri
Simon P. Byrne,  PhD: Yale Child Study Center, Yale
School of Medicine, New Haven, Connecticut
Colleen E. Carney,  PhD: Department of Psychology,
Ryerson University, Toronto, Ontario, Canada
Catherine A. Charette: Département de psychoé-
ducation et de psychologie, Université du Québec en
Outaouais, Gatineau, Quebec, Canada
Sara Colalillo, MA: Department of Psychology,
University of British Columbia, Vancouver, British
Columbia, Canada
Michelle G. Craske,  PhD: Department of Psychology,
University of California at Los Angeles, Los Angeles,
California
Lea R. Dougherty,  PhD: Department of Psychology,
University of Maryland, College Park, Maryland
Michel J. Dugas, PhD: Département de psychoéducation
et de psychologie, Université du Québec en Outaouais,
Gatineau, Québec, Canada
Lori Eisner, PhD: Needham Psychotherapy Associates,
LLC
xviii Contributors
Juliet Small  Ernst: Cognitive Behavior Therapy and
Science Center, Oakland, California
Amy Fiske,  PhD: Department of Psychology, West
Virginia University, Morgantown, West Virginia
David M. Fresco,  PhD: Department of Psychological
Sciences, Kent State University, Kent, Ohio; Department
of Psychiatry, Case Western Reserve University School of
Medicine, Cleveland, Ohio
Paul J. Frick, PhD: Department of Psychology, Louisiana
State University, Baton Rouge, Louisiana; Learning
Sciences Institute of Australia; Australian Catholic
University; Brisbane, Australia
Michelle M. Gagnon,  PhD: Department of
Psychology, University of Saskatchewan, Saskatoon,
Saskatchewan, Canada
Natasha L.  Gallant,  MA: Department of Psychology,
University of Regina, Regina, Saskatchewan, Canada
Nicole J. Gervais,  PhD: Department of Psychology,
University of Toronto, Toronto, Ontario, Canada
Maria Glowacka: Department of Psychology and
Neuroscience, Dalhousie University, Halifax, Nova
Scotia, Canada
Shirley M. Glynn,  PhD: VA Greater Los Angeles
Healthcare System and UCLA Department of Psychiatry
and Biobehavioral Sciences, David Geffen School of
Medicine, Los Angeles, California
Thomas Hadjistavropoulos,  PhD: Department of
Psychology, University of Regina, Regina, Saskatchewan,
Canada
Angela M. Haeny,  MA: Department of Psychological
Sciences, University of Missouri, Columbia, Missouri
Alisa O’Riley Hannum, PhD, ABPP: VA Eastern
Colorado Healthcare System, Denver, Colorado
Stephen N. Haynes,  PhD: Department of Psychology,
University of Hawai’i at Mānoa, Honolulu, Hawaii
Richard E. Heyman, PhD: Family Translational Research
Group, New York University, New York, New York
David C. Hodgins,  PhD: Department of Psychology,
University of Calgary, Calgary, Alberta, Canada
John Hunsley, PhD: School of Psychology, University of
Ottawa, Ottawa, Ontario, Canada
Amanda Jensen-​Doss, PhD: Department of Psychology,
University of Miami, Coral Gables, Florida
Sheri L. Johnson,  PhD: Department of Psychology,
University of California Berkeley, Berkeley, California
Charlotte Johnston,  PhD: Department of Psychology,
University of British Columbia, Vancouver, British
Columbia, Canada
Terence M. Keane, PhD: VA Boston Healthcare System,
National Center for Posttraumatic Stress Disorder, and
Boston University School of Medicine, Boston, Massachusetts
Daniel N. Klein, PhD: Department of Psychology, Stony
Brook University, Stony Brook, New York
Eli R. Lebowitz,  PhD: Yale Child Study Center, Yale
School of Medicine, New Haven, Connecticut
Kristin Maich, MA: Department of Psychology, Ryerson
University, Toronto, Ontario, Canada
Brian P. Marx,  PhD: VA Boston Healthcare System,
National Center for Posttraumatic Stress Disorder,
and Boston University School of Medicine, Boston,
Massachusetts
Eric J. Mash, PhD: Department of Psychology, University
of Calgary, Calgary, Alberta, Canada
Randi E. McCabe,  PhD: Anxiety Treatment and
Research Clinic, St. Joseph’s Healthcare, Hamilton, and
Department of Psychiatry and Behavioral Neurosciences,
McMaster University, Hamilton, Ontario, Canada
Yoanna E. McDowell, MA: Department of Psychological
Sciences, University of Missouri, Columbia, Missouri

Patrick J. McGrath,  PhD: Centre for Pediatric
Pain Research, IWK Health Centre; Departments
of Psychiatry, Pediatrics and Community Health &
Epidemiology, Dalhousie University; Halifax, Nova
Scotia, Canada
Robert J. McMahon,  PhD: Department of
Psychology, Simon Fraser University, Burnaby, British
Columbia,  Canada; BC Children’s Hospital Research
Institute, Vancouver, British Columbia, Canada
C. Meghan McMurtry, PhD: Department of Psychology,
University of Guelph, Guelph; Pediatric Chronic Pain
Program, McMaster Children’s Hospital, Hamilton;
Department of Paediatrics, Schulich School of Medicine
& Dentistry, Western University, London; Ontario,
Canada
Marta Meana,  PhD: Department of Psychology,
University of Nevada Las Vegas, Las Vegas, Nevada
Christopher Miller, PhD: VA Boston Healthcare System,
Center for Healthcare Organization and Implementation
Research, and Harvard Medical School Department of
Psychiatry, Boston, Massachusetts
Alexander J. Millner, PhD: Department of Psychology,
Harvard University, Cambridge, Massachusetts
Charles M. Morin,  PhD: École de psychologie,
Université Laval, Quebec City, Quebec, Canada
Samantha J. Moshier, PhD: VA Boston Healthcare
System and Boston University School of Medicine,
Boston, Massachusetts
Kim T. Mueser,  PhD: Center for Psychiatric
Rehabilitation and Departments of Occupational
Therapy, Psychological and Brain Sciences, and
Psychiatry, Boston University, Boston, Massachusetts
Matthew K. Nock,  PhD: Department of Psychology,
Harvard University, Cambridge, Massachusetts
Thomas M. Olino,  PhD: Department of Psychology,
Temple University, Philadelphia, Pennsylvania
Contributors xix
Thomas H. Ollendick, PhD: Department of Psychology,
Virginia Polytechnic Institute and State University,
Blacksburg, Virginia
Kelly S. Parker-​Guilbert, PhD: Psychology Department,
Bowdoin College, Brunswick, ME and VA Boston
Healthcare System, Boston, Massachusetts
Jacqueline B. Persons,  PhD: Cognitive Behavior
Therapy and Science Center, Oakland, California and
Department of Psychology, University of California
at Berkeley, Berkeley, California
Vanesa Mora Ringle: Department of Psychology,
University of Miami, Coral Gables, Florida
Damaris J. Rohsenow,  PhD: Center for Alcohol and
Addiction Studies, Brown University, Providence, Rhode
Island
Stephanie L.  Rojas, MA: Department of Psychology,
University of Kentucky, Lexington, Kentucky
Natalie O. Rosen, PhD: Department of Psychology and
Neuroscience, Dalhousie University, Halifax, Nova Scotia,
Canada
Karen Rowa,  PhD: Anxiety Treatment and Research
Clinic, St. Joseph’s Healthcare, Hamilton, and
Department of Psychiatry and Behavioral Neurosciences,
McMaster University, Hamilton, Ontario, Canada
Amy R. Sewart, MA: Department of Psychology, University
of California Los Angeles, Los Angeles, California
Kenneth J. Sher,  PhD: Department of Psychological
Sciences, University of Missouri, Columbia, Missouri
Wendy K. Silverman,  PhD: Yale Child Study Center,
Yale School of Medicine, New Haven, Connecticut
Douglas K. Snyder,  PhD: Department of Psychology,
Texas A&M University, College Station, Texas
Randy Stinchfield,  PhD: Department of Psychiatry,
University of Minnesota, Minneapolis, Minnesota
xx Contributors
Jennifer L. Swan: Department of Psychology, University
of Calgary, Calgary, Alberta, Canada
Robyn Sysko,  PhD: Eating and Weight Disorders
Program, Icahn School of Medicine at Mt. Sinai,
New York, New York
Anna Van Meter,  PhD: Ferkauf Graduate School of
Psychology, Yeshiva University, New York, New York
Lucia M. Walsh: Department of Psychology, University
of Miami, Coral Gables, Florida
Thomas A. Widiger,  PhD: Department of Psychology,
University of Kentucky, Lexington, Kentucky
Eric A. Youngstrom,  PhD: Department of Psychology
and Neuroscience, University of North Carolina at
Chapel Hill, Chapel Hill, North Carolina
 Part I

Introduction
 1
Developing Criteria for
Evidence-​Based Assessment:
An Introduction to Assessments That Work
John Hunsley
Eric J. Mash
For many professional psychologists, assessment is
viewed as a unique and defining feature of their expertise
(Krishnamurthy et  al., 2004). Historically, careful atten-
tion to both conceptual and pragmatic issues related to
measurement has served as the cornerstone of psychologi-
cal science. Within the realm of professional psychology,
the ability to provide assessment and evaluation services
is typically seen as a required core competency. Indeed,
assessment services are such an integral component of
psychological practice that their value is rarely questioned
but, rather, is typically assumed. However, solid evidence
to support the usefulness of psychological assessment is
lacking, and many commonly used clinical assessment
methods and instruments are not supported by scientific
evidence (e.g., Hunsley, Lee, Wood, & Taylor, 2015;
Hunsley & Mash, 2007; Norcross, Koocher, & Garofalo,
2006). Indeed, Peterson’s (2004) conclusion from more
than a decade ago is, unfortunately, still frequently
true: “For many of the most important inferences profes-
sional psychologists have to make, practitioners appear
to be forever dependent on incorrigibly fallible inter-
views and unavoidably selective, reactive observations as
primary sources of data” (p.  202). Furthermore, despite
the current emphasis on evidence-​based practice, profes-
sional psychologists report that the least common purpose
for which they use assessment is to monitor treatment
progress (Wright et al., 2017).
In this era of evidence-​based health care practices,
the need for scientifically sound assessment methods
and instruments is greater than ever (Barlow, 2005).
Assessment is the key to the accurate identification of
3
clients’ problems and strengths. Whether construed as
individual client monitoring, ongoing quality assurance
efforts, or program evaluation, assessment is central to
efforts to gauge the impact of health care services pro-
vided to ameliorate these problems (Brown, Scholle, &
Azur, 2014; Hermann, Chan, Zazzali, & Lerner, 2006).
Furthermore, the increasing availability of research-​
derived treatment benchmarks holds out great promise
for providing clinicians with meaningful and attainable
targets for their intervention services (Lee, Horvath, &
Hunsley, 2013; Spilka & Dobson, 2015). Importantly,
statements about evidence-​ based practice and best-​
practice guidelines have begun to specifically incor-
porate the critical role of assessment in the provision
of evidence-​ based services (e.g., Dozois et  al., 2014).
Indeed, because the identification and implementation
of evidence-​based treatments rests entirely on the data
provided by assessment tools, ignoring the quality of
these tools places the whole evidence-​based enterprise in
jeopardy.
DEFINING EVIDENCE-​BASED ASSESSMENT
There are three critical aspects that should define
evidence-​
based assessment (EBA; Hunsley & Mash,
2007; Mash & Hunsley, 2005). First, research findings
and scientifically supported theories on both psycho-
pathology and normal human development should be
used to guide the selection of constructs to be assessed
and the assessment process. As Barlow (2005) suggested,
4 Introduction
EBA measures and strategies should also be designed to
be integrated into interventions that have been shown to
work with the disorders or conditions that are targeted
in the assessment. Therefore, while recognizing that
most disorders do not come in clearly delineated neat
packages, and that comorbidity is often the rule rather
than the exception, we view EBAs as being disorder-​or
problem-​specific. A problem-​specific approach is consis-
tent with how most assessment and treatment research is
conducted and would facilitate the integration of EBA
into evidence-​ based treatments (cf. Mash & Barkley,
2007; Mash & Hunsley, 2007; Weisz & Kazdin, 2017).
This approach is also congruent with the emerging
trend toward personalized assessment and treatment
(e.g., Fisher, 2015; Ng & Weisz, 2016; Sales & Alves,
2016; Seidman et al., 2010; Thompson-​Hollands, Sauer-​
Zavala, & Barlow, 2014). Although formal diagnostic sys-
tems provide a frequently used alternative for framing the
range of disorders and problems to be considered, com-
monly experienced emotional and relational problems,
such as excessive anger, loneliness, conflictual relation-
ships, and other specific impairments that may occur in
the absence of a diagnosable disorder, may also be the
focus of EBAs. Even when diagnostic systems are used
as the framework for the assessment, clinicians need to
consider both (a) the potential value of emerging trans-
diagnostic approaches to treatment (Newby, McKinnon,
Kuyken, Gilbody, & Dalgleish, 2015) and (b) that a nar-
row focus on assessing symptoms and symptom reduction
is insufficient for treatment planning and treatment eval-
uation purposes (cf. Kazdin, 2003). Many assessments are
conducted to identify the precise nature of the person’s
problem(s). It is, therefore, necessary to conceptualize
multiple, interdependent stages in the assessment pro-
cess, with each iteration of the process becoming less
general in nature and increasingly problem-​specific with
further assessment (Mash & Terdal, 1997). In addition,
for some generic assessment strategies, there may be
research to indicate that the strategy is evidence-​based
without being problem-​specific. Examples of this include
functional assessments (Hurl, Wightman, Haynes, &
Virues-​Ortega, 2016) and treatment progress monitoring
systems (e.g., Lambert, 2015).
A second requirement is that, whenever pos-
sible, psychometrically strong measures should be
used to assess the constructs targeted in the assess-
ment. The measures should have evidence of reli-
ability, validity, and clinical utility. They should also
possess appropriate norms for norm-​ referenced inter-
pretation and/​or replicated supporting evidence for the
accuracy (sensitivity, specificity, predictive power, etc.)
of cut-​scores for criterion-​referenced interpretation (cf.
Achenbach, 2005). Furthermore, there should be sup-
porting evidence to indicate that the EBAs are sensitive
to key characteristics of the individual(s) being assessed,
including characteristics such as age, gender, ethnic-
ity, and culture (e.g., Ivanova et  al., 2015). Given the
range of purposes for which assessment instruments
can be used (i.e., screening, diagnosis, prognosis, case
conceptualization, treatment formulation, treatment
monitoring, and treatment evaluation) and the fact that
psychometric evidence is always conditional (based on
sample characteristics and assessment purpose), support-
ing psychometric evidence must be considered for each
purpose for which an instrument or assessment strategy is
used. Thus, general discussions concerning the relative
merits of information obtained via different assessment
methods have little meaning outside of the assessment
purpose and context. Similarly, not all psychometric ele-
ments are relevant to all assessment purposes. The group
of validity statistics that includes specificity, sensitivity,
positive predictive power, and negative predictive power
is particularly relevant for diagnostic and prognostic
assessment purposes and contains essential information
for any measure that is intended to be used for screening
purposes (Hsu, 2002). Such validity statistics may have
little relevance, however, for many methods intended to
be used for treatment monitoring and/​or evaluation pur-
poses; for these purposes, sensitivity to change is a much
more salient psychometric feature (e.g., Vermeersch,
Lambert, & Burlingame, 2000).
Finally, even with data from psychometrically
strong measures, the assessment process is inherently
a decision-​ making task in which the clinician must
iteratively formulate and test hypotheses by integrating
data that are often incomplete or inconsistent. Thus,
a truly evidence-​based approach to assessment would
involve an evaluation of the accuracy and usefulness
of this complex decision-​making task in light of poten-
tial errors in data synthesis and interpretation, the costs
associated with the assessment process, and, ultimately,
the impact that the assessment had on clinical out-
comes. There are an increasing number of illustrations
of how assessments can be conducted in an evidence-​
based manner (e.g., Christon, McLeod, & Jensen-​Doss,
2015; Youngstrom, Choukas-​ Bradley, Calhoun, &
Jensen-​Doss, 2015). These provide invaluable guides
for clinicians and provide a preliminary framework that
could lead to the eventual empirical evaluation of EBA
processes.
 Developing Criteria for Evidence-Based Assessment
FROM RESEARCH TO PRACTICE: USING
A “GOOD-​E NOUGH” PRINCIPLE
Perhaps the greatest single challenge facing efforts to
develop and implement EBAs is determining how to
start the process of operationalizing the criteria we just
outlined. The assessment literature provides a veritable
wealth of information that is potentially relevant to EBA;
this very strength, however, is also a considerable liability,
for the size of the literature is beyond voluminous. Not
only is the literature vast in scope but also the scientific
evaluation of assessment methods and instruments can be
without end because there is no finite set of studies that
can establish, once and for all, the psychometric proper-
ties of an instrument (Kazdin, 2005; Sechrest, 2005). On
the other hand, every single day, clinicians must make
decisions about what assessment tools to use in their prac-
tices, how best to use and combine the various forms of
information they obtain in their assessment, and how to
integrate assessment activities into other necessary aspects
of clinical service. Moreover, the limited time available
for service provision in clinical settings places an onus
on using assessment options that are maximally accurate,
efficient, and cost-​effective. Thus, above and beyond the
scientific support that has been amassed for an instru-
ment, clinicians require tools that are brief, clear, clini-
cally feasible, and user-​friendly. In other words, they need
instruments that have clinical utility and that are good
enough to get the job done (Barlow, 2005; Lambert &
Hawkins, 2004; Weisz, Krumholz, Santucci, Thomassin,
& Ng, 2015; Youngstrom & Van Meter, 2016).
As has been noted in the assessment literature, there
are no clear, commonly accepted guidelines to aid clini-
cians or researchers in determining when an instrument
has sufficient scientific evidence to warrant its use (Kazdin,
2005; Sechrest, 2005). The Standards for Educational and
Psychological Testing (American Educational Research
Association, American Psychological Association, &
National Council on Measurement in Education,
2014) sets out generic standards to be followed in devel-
oping and using psychological instruments but is silent
on the question of specific psychometric values that an
instrument should have. The basic reason for this is that
psychometric characteristics are not properties of an
instrument per se but, rather, are properties of an instru-
ment when used for a specific purpose with a specific
sample. Quite understandably, therefore, assessment
scholars, psychometricians, and test developers have been
reluctant to explicitly indicate the minimum psycho-
metric values or evidence necessary to indicate that an
5
instrument is scientifically sound (cf. Streiner, Norman,
& Cairney, 2015). Unfortunately, this is of little aid to the
clinicians and researchers who are constantly faced with
the decision of whether an instrument is good enough,
scientifically speaking, for the assessment task at hand.
Prior to the psychometric criteria we set out in the
first edition of this volume, there had been attempts to
establish criteria for the selection and use of measures for
research purposes. Robinson, Shaver, and Wrightsman
(1991), for example, developed evaluative criteria for
the adequacy of attitude and personality measures, cov-
ering the domains of theoretical development, item
development, norms, inter-​ item correlations, internal
consistency, test–​retest reliability, factor analytic results,
known groups validity, convergent validity, discriminant
validity, and freedom from response sets. Robinson and
colleagues also used specific psychometric criteria for
many of these domains, such as describing a coefficient
α of .80 as exemplary. A different approach was taken by
the Measurement and Treatment Research to Improve
Cognition in Schizophrenia Group to develop a consen-
sus battery of cognitive tests to be used in clinical trials
in schizophrenia (Green et al., 2004). Rather than setting
precise psychometric criteria for use in rating potential
instruments, expert panelists were asked to rate, on a nine-​
point scale, each proposed tool’s characteristics, includ-
ing test–​retest reliability, utility as a repeated measure,
relation to functional outcome, responsiveness to treat-
ment change, and practicality/​tolerability. An American
Psychological Association Society of Pediatric Psychology
task force used a fairly similar strategy. The task force
efforts, published at approximately the same time as the
first edition of this volume, focused on evaluating psycho-
social assessment instruments that could be used in health
care settings (Cohen et al., 2008). Instrument character-
istics were reviewed by experts and, depending on the
available empirical support, were evaluated as promising,
approaching well-​established, or well-​established. These
descriptors closely resembled those that had been used to
identify empirically supported treatments.
Clearly, any attempt to develop a method for deter-
mining the scientific adequacy of assessment instruments
is fraught with the potential for error. The application
of criteria that are too stringent could result in a solid
set of assessment options, but one that is so limited in
number or scope as to render the whole effort clinically
worthless. Alternatively, using excessively lenient criteria
could undermine the whole notion of an instrument or
process being evidence based. So, with a clear awareness
of this assessment equivalent of Scylla and Charybdis, a
6 Introduction
decade ago we sought to construct a framework for the
chapters included in the first edition of this volume that
would employ good-​enough criteria for rating psycho-
logical instruments. In other words, rather than focus-
ing on standards that define ideal criteria for a measure,
our intent was to provide criteria that would indicate the
minimum evidence that would be sufficient to warrant
the use of a measure for specific clinical purposes. We
assumed, from the outset, that although our framework
is intended to be scientifically sound and defensible, it is
a first step rather than the definitive effort in designing a
rating system for evaluating psychometric adequacy. Our
framework, described later, is unchanged from the first
edition because there have been no developments in the
measurement and assessment literatures that have caused
us to reconsider our earlier position. Indeed, as we indi-
cate in the following sections of this chapter, several criti-
cal developments have served to reinforce our views on
the value of the framework.
In brief, to operationalize the good-​enough principle,
specific rating criteria are used across categories of psycho-
metric properties that have clear clinical relevance; each
category has rating options of adequate, good, and excel-
lent. In the following sections, we describe the assessment
purposes covered by our rating system, the psychometric
properties included in the system, and the rationales for
the rating options. The actual rating system, used in this
volume by all authors of disorder/​problem-​oriented chap-
ters to construct their summary tables of instruments, is
presented in two boxes later in this chapter.
ASSESSMENT PURPOSES
Although psychological assessments are conducted for
many reasons, it is possible to identify a small set of inter-
related purposes that form the basis for most assessments.
These include (a) diagnosis (i.e., determining the nature
and/​or cause[s]‌of the presenting problems, which may or
may not involve the use of a formal diagnostic or catego-
rization system), (b) screening (i.e., identifying those who
have or who are at risk for a particular problem and who
might be helped by further assessment or intervention),
(c) prognosis and other predictions (i.e., generating pre-
dictions about the course of the problems if left untreated,
recommendations for possible courses of action to be
considered, and their likely impact on the course of
the problems), (d)  case conceptualization/​ formulation
(i.e., developing a comprehensive and clinically rele-
vant understanding of the client, generating hypotheses
regarding critical aspects of the client’s biopsychosocial
functioning and context that are likely to influence the
client’s adjustment), (e)  treatment design/​planning (i.e.,
selecting/​developing and implementing interventions
designed to address the client’s problems by focusing on
elements identified in the diagnostic evaluation and the
case conceptualization), (f)  treatment monitoring (i.e.,
tracking changes in symptoms, functioning, psychologi-
cal characteristics, intermediate treatment goals, and/​or
variables determined to cause or maintain the problems),
and (g) treatment evaluation (i.e., determining the effec-
tiveness, social validity, consumer satisfaction, and/​or cost-​
effectiveness of the intervention).
The chapters in this volume provide summaries of
the best assessment methods and instruments available
for commonly encountered clinical assessment purposes.
While recognizing the importance of other possible
assessment purposes, chapters in this volume focus on
(a)  diagnosis, (b)  case conceptualization and treatment
planning, and (c)  treatment monitoring and treatment
evaluation. Although separable in principle, the purposes
of case conceptualization and treatment planning were
combined because they tend to rely on the same assess-
ment data. Similarly, the purposes of treatment monitor-
ing and evaluation were combined because they often,
but not exclusively, use the same assessment methods
and instruments. Clearly, there are some overlapping
elements, even in this set of purposes; for example, it is
relatively common for the question of diagnosis to be
revisited as part of evaluating the outcome of treatment.
In the instrument summary tables that accompany each
chapter, the psychometric strength of instruments used
for these three main purposes are presented and rated.
Within a chapter, the same instrument may be rated for
more than one assessment purpose and thus appear in
more than one table. Because an instrument may possess
more empirical support for some purposes than for others,
the ratings given for the instrument may not be the same
in each of the tables.
The chapters in this volume present information on
the best available instruments for diagnosis, case con-
ceptualization and treatment planning, and treatment
monitoring and evaluation. They also provide details on
clinically appropriate options for the range of data to col-
lect, suggestions on how to address some of the challenges
commonly encountered in conducting assessments, and
suggestions for the assessment process. Consistent with
the problem-​specific focus within EBA outlined previ-
ously, most chapters in this volume focus on one or more
specific disorders or conditions. However, many clients
 Developing Criteria for Evidence-Based Assessment
present with multiple problems and, therefore, there
are frequent references within a given chapter to the
assessment of common co-​occurring problems that are
addressed in other chapters in the volume. To be opti-
mally useful to potential readers, the chapters are focused
on the most commonly encountered disorders or condi-
tions among children, adolescents, adults, older adults,
and couples. With the specific focus on the three critical
assessment purposes of diagnosis, case conceptualization
and treatment planning, and treatment monitoring and
treatment, within each disorder or condition, the chapters
in this volume provide readers with essential information
for conducting the best EBAs currently possible.
PSYCHOMETRIC PROPERTIES
AND RATING CRITERIA
Clinical assessment typically entails the use of both idio-
graphic and nomothetic instruments. Idiographic mea-
sures are designed to assess unique aspects of a person’s
experience and, therefore, to be useful in evaluating
changes in these individually defined and constructed
variables. In contrast, nomothetic measures are designed
to assess constructs assumed to be relevant to all indi-
viduals and to facilitate comparisons, on these constructs,
across people. Most chapters include information on
idiographic measures such as self-​monitoring forms and
individualized scales for measuring treatment goals. For
such idiographic measures, psychometric characteristics
such as reliability and validity may, at times, not be easily
evaluated or even relevant (but see Weisz et al., 2011). It
is crucial, however, that the same items and instructions
are used across assessment occasions—​without this level
of standardization it is impossible to accurately determine
changes that may be due to treatment (Kazdin, 1993).
The nine psychometric categories rated for the instru-
ments in this volume are norms, internal consistency,
inter-​rater reliability, test–​retest reliability, content valid-
ity, construct validity, validity generalization, sensitivity
to treatment change, and clinical utility. Each of these
categories is applied in relation to a specific assessment
purpose (e.g., case conceptualization and treatment plan-
ning) in the context of a specific disorder or clinical con-
dition (e.g., eating disorders, self-​injurious behavior, and
relationship conflict). Consistent with our previous com-
ments, factors such as gender, ethnicity, and age must be
considered in making ratings within these categories. For
each category, a rating of less than adequate, adequate,
good, excellent, not reported, or not applicable was
7
possible. The precise nature of what constituted adequate,
good, and excellent varied, of course, from category to cat-
egory. In general, however, a rating of adequate indicated
that the instrument meets a minimal level of scientific
rigor; good indicated that the instrument would generally
be viewed as possessing solid scientific support; and excel-
lent indicated there was extensive, high-​quality support-
ing evidence. Accordingly, a rating of less than adequate
indicated that the instrument did not meet the minimum
level set out in the criteria. A rating of not reported indi-
cated that research on the psychometric property under
consideration had not yet been conducted or published.
A rating of not applicable indicated that the psychomet-
ric property under consideration was not relevant to the
instrument (e.g., inter-​ rater reliability for a self-​
report
symptom rating scale).
When considering the clinical use of a measure, it
would be desirable to only use those measures that would
meet, at a minimum, the criteria for good. However,
because measure development is an ongoing process, the
rating system provides the option of the adequate rating
in order to fairly evaluate (a) relatively newly developed
measures and (b) measures for which comparable levels
of research evidence are not available across all psycho-
metric categories in the rating system. In several chapters,
authors explicitly commented on the status of some newly
developed measures, but by and large, the only instru-
ments included in chapter summary tables were those
that had adequate or better ratings on the majority of the
psychometric dimensions. Thus, the instruments pre-
sented in these tables represent only a subset of available
assessment tools.
Despite the difficulty inherent in promulgating sci-
entific criteria for psychometric properties, we believe
that the potential benefits of fair and attainable criteria
far outweigh the potential drawbacks (cf. Sechrest, 2005).
Accordingly, reasoned arguments from respected psycho-
metricians and assessment scholars, along with summaries
of various assessment literatures, guided the selection of
criteria for rating the psychometric properties associated
with an instrument. Box 1.1 presents the criteria used in
rating norms and reliability indices; Box 1.2 presents the
criteria used in rating validity indices and clinical utility.
Norms
When using a standardized, nomothetically based
instrument, it is essential that norms, specific criterion-​
related cutoff scores, or both are available to aid in
the accurate interpretation of a client’s test score
8 Introduction
BOX 1.1  Criteria at a Glance: Norms and
Reliability
NORMS
Adequate = Measures of central tendency and distribu-
tion for the total score (and subscores if relevant) based
on a large, relevant, clinical sample are available.
Good = Measures of central tendency and distribution
for the total score (and subscores if relevant) based
on several large, relevant samples (must include
data from both clinical and nonclinical samples) are
available.
Excellent = Measures of central tendency and distribu-
tion for the total score (and subscores if relevant)
based on one or more large, representative samples
(must include data from both clinical and nonclini-
cal samples) are available.
I N T E R NA L C O N S I S T E N C Y
Adequate  =  Preponderance of evidence indicates
α values of .70–​.79.
Good = Preponderance of evidence indicates α values
of .80–​.89.
Excellent  =  Preponderance of evidence indicates
α values ≥ .90.
I N T E R -​R AT E R R E L I A B I L I T Y
Adequate  =  Preponderance of evidence indicates κ
values of .60–​.74; the preponderance of evidence
indicates Pearson correlation or intraclass correla-
tion values of .70–​.79.
Good = Preponderance of evidence indicates κ val-
ues of .75–​ .84; the preponderance of evidence
indicates Pearson correlation or intraclass correla-
tion values of .80–​.89.
Excellent  =  Preponderance of evidence indicates κ
values ≥ .85; the preponderance of evidence indi-
cates Pearson correlation or intraclass correlation
values ≥ .90.
T E S T –​R E T E S T R E L I A B I L I T Y
Adequate  =  Preponderance of evidence indicates
test–​retest correlations of at least .70 over a period
of several days to several weeks.
Good  =  Preponderance of evidence indicates test–​
retest correlations of at least .70 over a period of
several months.
Excellent  =  Preponderance of evidence indicates
test–​retest correlations of at least .70 over a period
of a year or longer.
BOX 1.2   Criteria at a Glance: Validity and Utility
C O N T E N T VA L I D I T Y
Adequate  =  The test developers clearly defined
the domain of the construct being assessed and
ensured that selected items were representative of
the entire set of facets included in the domain.
Good  =  In addition to the criteria used for an
adequate rating, all elements of the instrument
(e.g., instructions and items) were evaluated
by judges (e.g., by experts or by pilot research
participants).
Excellent  =  In addition to the criteria used for a
good rating, multiple groups of judges were
employed and quantitative ratings were used by
the judges.
C O N S T R U C T VA L I D I T Y
Adequate = Some independently replicated evidence
of construct validity (e.g., predictive validity, con-
current validity, and convergent and discriminant
validity).
Good  =  Preponderance of independently repli-
cated evidence, across multiple types of validity
(e.g., predictive validity, concurrent validity, and
convergent and discriminant validity), is indica-
tive of construct validity.
Excellent = In addition to the criteria used for a good
rating, there is evidence of incremental validity
with respect to other clinical data.
VA L I D I T Y G E N E R A L I Z AT I O N
Adequate = Some evidence supports the use of this
instrument with either (a) more than one specific
group (based on sociodemographic characteristics
such as age, gender, and ethnicity) or (b) in mul-
tiple contexts (e.g., home, school, primary care set-
ting, and inpatient setting).
Good  =  Preponderance of evidence supports the
use of this instrument with either (a) more than
one specific group (based on sociodemographic
characteristics such as age, gender, and eth-
nicity) or (b)  in multiple settings (e.g., home,
school, primary care setting, and inpatient
setting).
Excellent = Preponderance of evidence supports the
use of this instrument with more than one specific
group (based on sociodemographic characteristics
such as age, gender, and ethnicity) and across mul-
tiple contexts (e.g., home, school, primary care set-
ting, and inpatient setting).
 Developing Criteria for Evidence-Based Assessment
BOX 1.2  Continued
T R E AT M E N T S E N S I T I V I T Y
Adequate  =  Some evidence of sensitivity to change
over the course of treatment.
Good = Preponderance of independently replicated
evidence indicates sensitivity to change over the
course of treatment.
Excellent = In addition to the criteria used for a good
rating, evidence of sensitivity to change across dif-
ferent types of treatments.
CLINICAL UTILITY
Adequate  =  Taking into account practical consid-
erations (e.g., costs, ease of administration, avail-
ability of administration and scoring instructions,
duration of assessment, availability of relevant
cutoff scores, and acceptability to clients), the
resulting assessment data are likely to be clini-
cally useful.
Good  =  In addition to the criteria used for an
adequate rating, there is some published evi-
dence that the use of the resulting assessment
data confers a demonstrable clinical benefit
(e.g., better treatment outcome, lower treatment
attrition rates, and greater client satisfaction with
services).
Excellent  =  In addition to the criteria used for an
adequate rating, there is independently replicated
published evidence that the use of the resulting
assessment data confers a demonstrable clinical
benefit.
(American Educational Research Association, American
Psychological Association, & National Council on
Measurement in Education, 2014). For example,
norms can be used to determine the client’s pre-​and
post-​treatment levels of functioning and to evaluate
whether any change in functioning is clinically mean-
ingful (Achenbach, 2001; Kendall, Marrs-​Garcia, Nath,
& Sheldrick, 1999). Selecting the target population(s)
for the norms and then ensuring that the norms are
adequate can be difficult tasks, and several sets of norms
may be required for a measure. One set of norms may be
needed to determine the meaning of the obtained score
relative to the general population, whereas a different
set of norms could be used to compare the score to spe-
cific subgroups within the population (Cicchetti, 1994).
9
Regardless of the population to which comparisons are
to be made, a normative sample must be truly represen-
tative of the population with respect to demographics
and other important characteristics (Achenbach, 2001;
Wasserman & Bracken, 2013). Ideally, whether con-
ducted at the national level or the local level, this would
involve probability-​sampling efforts in which data are
obtained from the majority of contacted respondents. As
those familiar with psychological instruments are aware,
such a sampling strategy is rarely used for the devel-
opment of test norms. The reliance on data collected
from convenience samples with unknown response rates
reduces the accuracy of the resultant norms. Therefore,
at a minimum, clinicians need to be provided with
an indication of the quality and likely accuracy of the
norms for a measure. Accordingly, the ratings for norms
required, at a minimum for a rating of adequate, data
from a single, large clinical sample. For a rating of good,
normative data from multiple samples, including non-
clinical samples, were required; when normative data
from large, representative samples were available, a rat-
ing of excellent was applied.
Reliability
Reliability is a key psychometric element to be considered
in evaluating an instrument. It refers to the consistency of
a person’s score on a measure (Anastasi, 1988; Wasserman
& Bracken, 2013), including whether (a)  all elements
of a measure contribute in a consistent way to the data
obtained (internal consistency), (b) similar results would
be obtained if the measure was used or scored by another
clinician (inter-​ rater reliability),1 or (c)  similar results
would be obtained if the person completed the measure a
second time (test–​retest reliability or test stability). Not all
reliability indices are relevant to all assessment methods
and measures, and the size of the indices may vary on the
basis of the samples used.
Despite the long-​standing recognition of the central-
ity of reliability to all forms of psychological measure-
ment, there is a persistent tendency in psychological
research to make unwarranted assumptions about reli-
ability. For example, numerous reviews have found that
almost three-​fourths of research articles failed to provide
information on the reliability estimates of the measures
completed by participants in the studies (e.g., Barry,
Chaney, Piazza-​ Gardner, & Chavarria, 2014; Vacha-​
Haase & Thompson, 2011). Inattention to reliability, or
the use of an inappropriate statistic to estimate reliability,
has the potential to undermine the validity of conclu-
sions drawn from research studies. Concerns have been
10 Introduction
raised about the impact of these errors in a broad range of
research domains, including communication (Feng, 2015),
psychopathology (Rodebaugh et  al., 2016), and clinical
diagnosis (Chmielewski, Clark, Bagby, & Watson, 2015).
As emphasized throughout this volume, a careful consider-
ation of reliability values is essential when selecting assess-
ment instruments for clinical services or clinical research.
With respect to internal consistency, we focused on
coefficient alpha (α), which is the most widely used index
(Streiner, 2003). Although there have been repeated
calls to abandon the use of coefficient α in favor of more
robust and accurate alternatives (e.g., Dunn, Baguley,
& Brunsden, 2014; Kelley & Pornprasertmanit, 2016),
it is rare to find an internal consistency coefficient
other than α used in the clinical assessment literature.
Recommendations in the literature for what constitutes
adequate internal consistency vary, but most authorities
seem to view .70 as the minimum acceptable value for α
(e.g., Cicchetti, 1994), and Charter (2003) reported that
the mean internal consistency value among commonly
used clinical instruments was .81. Accordingly, a rating of
adequate was given to values of .70–​.79; a rating of good
required values of .80–​.89; and, finally, because of cogent
arguments that an α value of at least .90 is highly desirable
in clinical assessment contexts (Nunnally & Bernstein,
1994), we required values ≥ .90 for an instrument to be
rated as having excellent internal consistency. Note that it
is possible for α to be too (artificially) high, as a value close
to unity typically indicates substantial redundancy among
items (cf. Streiner, 2003).
These value ranges were also used in rating evidence
for inter-​rater reliability when assessed with Pearson corre-
lations or intraclass correlations. Appropriate adjustments
were made to the value ranges when κ statistics were used,
in line with the recommendations discussed by Cicchetti
(1994; see also Charter, 2003). Note that although a num-
ber of statistics are superior to κ, it continues to be the
most commonly used inter-​rater reliability statistic (Xu
& Lorber, 2014). Importantly, evidence for inter-​ rater
reliability could only come from data generated among
clinicians or clinical raters—​estimates of cross-​informant
agreement, such as between parent and teacher ratings,
are not indicators of reliability.
In establishing ratings for test–​retest reliability values,
our requirement for a minimum correlation of .70 was
influenced by summary data reported on typical test–​
retest reliability results found with clinical instruments
(Charter, 2003)  and trait-​ like psychological measures
(Watson, 2004). Of course, not all constructs or measures
are expected to show temporal stability (e.g., measures
of state-​like variables and life stress inventories), so test–​
retest reliability was only rated if it was relevant. A rating
of adequate required evidence of correlation values of .70
or greater, when reliability was assessed over a period of
several days to several weeks. We then faced a challenge
in determining appropriate criteria for good and excellent
ratings. In order to enhance its likely usefulness, the rating
system should be relatively simple. However, test–​retest
reliability is a complex phenomenon that is influenced by
(a) the nature of the construct being assessed (i.e., it can be
state-​like, trait-​like, or influenced by situational variables),
(b) the time frame covering the reporting period instruc-
tions (i.e., whether respondents are asked to report their
current functioning, functioning over the past few days,
or functioning over an extended period, such as general
functioning in the past year), and (c) the duration of the
retest period (i.e., whether the time between two admin-
istrations of the instrument involved days, weeks, months,
or years). In the end, rather than emphasize the value of
increasingly large test–​retest correlations, we decided to
maintain the requirement for .70 or greater correlation
values but require increasing retest period durations of
(a)  several months and (b)  at least 1  year for ratings of
good and excellent, respectively.
Validity
Validity is another central aspect to be considered when
evaluating psychometric properties. Recent editions of
the Standards for Educational and Psychological Testing
(American Educational Research Association, American
Psychological Association, & National Council on
Measurement in Education, 1999, 2014)  explicitly state
that validity is a unitary concept and that it is not appro-
priate to consider different types of validity. Despite these
admonitions, research on validity continues to use con-
cepts such as content validity, predictive validity, and
incremental validity. Setting aside the wide range of con-
ceptual and practical issues associated with the lack of
consensus on the framing of test validity (for a detailed
discussion, see Newton & Shaw, 2013), there is a very
simple reason for incorporating several types of validity
into the rating system used in this book: The vast majority
of the literature on clinical assessment, both historically
and currently, does not treat validity as a unitary concept
(cf. Strauss & Smith, 2009). To strike a balance between
the unitary approach advocated by the Standards and
the multiplicity of validity types used in the literature,
we focused on content validity, construct validity, validity
generalization, and treatment sensitivity. In the following
 Developing Criteria for Evidence-Based Assessment
paragraphs, we explain further the rationale for our use of
four types of validity. As is readily apparent by reviewing
the summary tables of instruments in the following chap-
ters, the extent and strength of research evidence across
these types of validity can vary substantially for a given
assessment instrument.
Foster and Cone (1995) drew an important distinc-
tion between “representational” validity (i.e., whether a
measure really assesses what it purports to measure) and
“elaborative” validity (i.e., whether the measure has any
utility for measuring the construct). Attending to the
content validity of a measure is a basic, but frequently
overlooked, step in evaluating representational valid-
ity (Haynes, Richard, & Kubany, 1995). As discussed by
Smith, Fischer, and Fister (2003), the overall reliability
and validity of scores on an instrument is directly affected
by the extent to which items in the instrument adequately
represent the various aspects or facets of the construct the
instrument is designed to measure. Assuming that repre-
sentational validity has been established for an assessment
purpose, it is elaborative validity that is central to clini-
cians’ use of a measure. Accordingly, replicated evidence
for a measure’s concurrent, predictive, discriminative,
and, ideally, incremental validity (Hunsley & Meyer,
2003)  should be available to qualify a measure for con-
sideration as evidence based. We have indicated already
that validation is a context-​sensitive concept—​inattention
to this fact can lead to inappropriate generalizations being
made about a measure’s validity. Thus, there should be
replicated elaborative validity evidence for each purpose
of the measure and for each population or group for which
the measure is intended to be used. This latter point is
especially relevant when considering an instrument for
clinical use, and thus it is essential to consider evidence
for validity generalization—​that is, the extent to which
there is evidence for validity across a range of samples and
settings (cf. Messick, 1995; Schmidt & Hunter, 1977).
In the rating system used in subsequent chapters, rat-
ings of content validity evidence required explicit consider-
ation of the construct facets to be included in the measure
and, as the ratings increased, involvement of content
validity judges to assess the measure (Haynes et al., 1995).
Unlike the situation for reliability, there are no commonly
accepted summary statistics to evaluate construct validity
(but see Markon [2013] and Westen & Rosenthal [2003]).
As a result, our ratings were based on the requirement of
increasing amounts of replicated evidence of elements of
construct validity such as predictive validity, concurrent
validity, convergent validity, and discriminant validity; in
addition, for a rating of excellent, evidence of incremental
11
validity was also required. As was the case when we intro-
duced the rating system in the first edition of this book, we
were unable to find any clearly applicable standards in the
literature to guide us in developing criteria for validity gen-
eralization or treatment sensitivity (a dimension rated only
for instruments used for the purposes of treatment moni-
toring and treatment evaluation). Therefore, adequate
ratings for these dimensions required some evidence of,
respectively, the use of the instrument with either more
than one specific group or in multiple contexts and evi-
dence of sensitivity to change over the course of treatment.
Consistent with ratings for other dimensions, good and
excellent ratings required increasingly demanding levels
of evidence in these areas.
Utility
It is also essential to know the utility of an instrument for
a specific clinical purpose. The concept of clinical util-
ity, applied to both diagnostic systems (e.g., Keeley et  al.,
2016; Kendell & Jablensky, 2003; Mullins-​Sweatt, Lengel,
& DeShong, 2016) and assessment tools (e.g., di Ruffano,
Hyde, McCaffery, & Bossuyt, 2012; Yates & Taub, 2003),
has received increasing attention in recent years. Although
definitions vary, they have in common an emphasis on gar-
nering evidence regarding actual improvements in both
decisions made by clinicians and service outcomes experi-
enced by clients. Unfortunately, despite thousands of studies
on the reliability and validity of psychological instruments,
there is only scant attention paid to matters of utility in most
assessment research studies (McGrath, 2001). This has
directly contributed to the current state of affairs in which
there is very little replicated evidence that psychological
assessment data have a direct impact on improved provision
and outcome of clinical services. Currently, therefore, for
the majority of psychological instruments, a determination
of clinical utility must often be made on the basis of likely
clinical value rather than on empirical evidence.
Compared to the criteria for the psychometric dimen-
sions presented thus far, our standards for evidence of
clinical utility were noticeably less demanding. This was
necessary because of the paucity of information on the
extent to which assessment instruments are acceptable
to clients, enhance the quality and outcome of clinical
services, and/​or are worth the costs associated with their
use. Therefore, we relied on authors’ expert opinions to
classify an instrument as having adequate clinical utility.
The availability of any supporting evidence of utility was
sufficient for a rating of good, and replicated evidence of
utility was necessary for a rating of excellent.
12 Introduction

The instrument summary tables also contain one final For information on important developments on rating
column, used to indicate instruments that are the best systems used in many areas of health care research, the
measures currently available to clinicians for specific pur- interested reader can consult the website of the Grading
poses and disorders and, thus, are highly recommended of Recommendations Assessment, Development and
for clinical use. Given the considerable differences in Evaluation (GRADE) working group (http://​www.grade-
the state of the assessment literature for different disor- workinggroup.org).
ders/​conditions, chapter authors had some flexibility in The second issue has to do with the responsible clini-
determining their own precise requirements for an instru- cal use of the guidance provided by the rating system.
ment to be rated, or not rated, as highly recommended. Consistent with evaluation and grading strategies used
However, to ensure a moderate level of consistency in through evidence-​ based medicine and evidence-​ based
these ratings, a highly recommended rating could only be psychology initiatives, many of our rating criteria relied
considered for those instruments having achieved ratings on the consideration of the preponderance of data rel-
of good or excellent in the majority of its rated psycho- evant to each dimension. Such a strategy recognizes both
metric categories. Although not required in our system, if the importance of replication in science and the fact
several instruments had comparable psychometric merits that variability across studies in research design elements
for a given assessment purpose, some chapter authors con- (including sample composition and research setting) will
sidered the cost and availability of an assessment instru- influence estimates of these psychometric dimensions.
ment when making this recommendation (see also Beidas However, we hasten to emphasize that reliance on the
et al., 2015). preponderance of evidence for these ratings does not
imply or guarantee that an instrument is applicable for all
clients or clinical settings. Our intention is to have these
SOME FINAL THOUGHTS ratings provide indications about scientifically strong mea-
sures that warrant consideration for clinical and research
We are hopeful that the rating system described in this use. As with all evidence-​based efforts, the responsibility
chapter, and applied in each of the chapters of this book, rests with the individual professional to determine the
will continue to aid in advancing the state of evidence-​ suitability of an instrument for the specific setting, pur-
based psychological assessment. We also hope that it will pose, and individuals to be assessed.
serve as a stimulus for others to refine and improve upon Third, as emphasized throughout this volume, focus-
our efforts (cf. Jensen-​Doss, 2011; Youngstrom et  al., in ing on the scientific evidence for specific assessment tools
press). Whatever the possible merits of the rating system, should not overshadow the fact that the process of clinical
we close this chapter by drawing attention to three critical assessment involves much more than simply selecting and
issues related to its use. administering the best available instruments. Choosing
First, although the rating system used for this volume the best, most relevant, instruments is unquestionably an
is relatively simple, the task of rating psychometric proper- important step. Subsequent steps must ensure that the
ties is not. Results from many studies must be considered instruments are administered in an appropriate manner,
in making such ratings, and precise quantitative standards accurately scored, and then individually interpreted in
were not set for how to weight the results from studies. accordance with the relevant body of scientific research.
Furthermore, in the spirit of evidence-​based practice, it However, to ensure a truly evidence-​based approach to
is also important to note that we do not know whether assessment, the major challenge is to then integrate all the
these ratings are, themselves, reliable. Reliance on indi- data within a process that is, itself, evidence-​based. This
vidual expert judgment, no matter how extensive and will likely require both (a) a reframing of the assessment
current the knowledge of the experts, is not as desirable process within the larger health and social system context
as basing evidence-​based conclusions and guidance on in which it occurs and (b)  the use of new technologies
systematic reviews of the literature conducted according to enable complex decision-​making and integration of
to a consensually agreed upon rating system. However, large amounts of assessment information in both tradi-
for all the potential limitations and biases inherent in our tional and nontraditional health service delivery settings
approach, reliance on expert review of the scientific lit- (Chorpita, Daleiden, & Bernstein, 2015). Much of our
erature is the current standard in psychology and, thus, focus in this chapter has been on evidence-​based meth-
was the only feasible option for the volume at this time. ods and instruments, in large part because (a)  methods
 Developing Criteria for Evidence-Based Assessment
and specific measures are more easily identified than are
processes and (b) the main emphasis in the assessment lit-
erature has been on psychometric properties of methods
and instruments. As we indicated early in the chapter, an
evidence-​based approach to assessment should be devel-
oped in light of evidence on the accuracy and usefulness
of this complex, iterative decision-​making task. Although
the chapters in this volume provide considerable assis-
tance for having the assessment process be informed by
scientific evidence, the future challenge will be to ensure
that the entire process of assessment is evidence based.
Note
1. Although we chose to use the term “inter-​rater reli-
ability,” there is some discussion in the assessment literature
about whether the term should be “inter-​rater agreement.”
Heyman et  al. (2001), for example, suggested that because
indices of inter-​rater reliability do not contain information
about individual differences among participants and only
contain information about one source of error (i.e., differ-
ences among raters), they should be considered to be indices
of agreement, not reliability.
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 17
Dissemination and Implementation
of Evidence-​Based Assessment
Amanda Jensen-​Doss
Lucia M. Walsh
Vanesa Mora Ringle
During the past two decades, there has been a major
push to increase the use of evidence-​based practices in
clinical settings. The American Psychological Association
Presidential Task Force on Evidence-​ Based Practice
(2006) defines evidence-​ based practice in psychology
(EBPP) as “the integration of the best available research
with clinical expertise in the context of patient character-
istics, culture, and preferences” (p.  271) and states that
the goal of EBPP is to improve public health through
the application of research-​ supported assessment, case
formulation, therapeutic relationship, and treatment
approaches. Although EBPP is defined broadly, many
efforts to improve practice have focused on treatment,
with less attention paid to other aspects of practice. There
is a particular need to focus on increasing use of evidence-​
based assessment (EBA), as assessment cuts across all of
these other areas of practice. For example, assessment
results should form the foundation of case conceptualiza-
tion; inform decisions about which treatments to use; and
provide data about whether treatment is working, whether
therapy alliance is strong, and when to end treatment.
There are several reasons why a focus on EBA will
increase the likelihood that EBPP will lead to improved
public health. First, EBA can improve the accuracy of
diagnoses, which is one important component of case
conceptualization and treatment selection (Christon,
McLeod, & Jensen-​Doss, 2015). Research linking diag-
nostic accuracy to improved treatment engagement and
outcomes (Jensen-​Doss & Weisz, 2008; Klein, Lavigne,
& Seshadri, 2010; Kramer, Robbins, Phillips, Miller, &
17
Burns, 2003; Pogge et  al., 2001)  suggests that improved
diagnostic assessment could have a positive effect across
the treatment process. As detailed throughout this book,
evidence-​based diagnostic assessment typically involves
the use of structured diagnostic interviews or rating scales.
Studies have demonstrated that when clinicians use
structured diagnostic interviews, they assign more accu-
rate diagnoses (Basco et al., 2000), better capture comor-
bidities (Matuschek et  al., 2016), assign more specific
diagnoses (Matuschek et  al., 2016), reduce psychiatrist
evaluation time (Hughes et al., 2005), and decrease the
likelihood that a psychiatrist will increase a patient’s medi-
cation dose (Kashner et al., 2003).
Using EBA for progress monitoring can support clinical
judgment by creating an ongoing feedback loop to support
ongoing case conceptualization (Christon et al., 2015) and,
if data suggest clients are at risk for treatment failure, revise
the treatment plan (Claiborn & Goodyear, 2005; Lambert,
Hansen, & Finch, 2001; Riemer, Rosof-​Williams, & Bickman,
2005). Gold standard progress monitoring of this nature typi-
cally involves administering rating scales every session or two
and then incorporating the feedback into clinical decisions.
This differs from what we refer to here as “outcome monitor-
ing,” or administering outcome measures before and after
treatment to determine treatment effectiveness. Although use-
ful for many purposes, this type of outcome monitoring does
not support clinical decision-​making during service provision.
Several monitoring and feedback systems (MFSs) have
been developed to support ongoing progress monitoring;
they typically include a battery of progress measures and
18
18 Introduction
generate feedback reports that often include warnings
if a client is not on track for positive outcomes (Lyon,
Lewis, Boyd, Hendrix, & Liu, 2016). Extensive research
with adult clients suggests that clinician use of MFSs can
improve outcomes, particularly for those “not on track”
for positive outcomes (Krägeloh, Czuba, Billington,
Kersten, & Siegert, 2015; Shimokawa, Lambert, & Smart,
2010); similar results have been found for youth clients
(Bickman, Kelley, Breda, De Andrade, & Riemer, 2011;
Stein, Kogan, Hutchison, Magee, & Sorbero, 2010),
although effects vary based on organizational support for
progress monitoring (Bickman et al., 2016).
The purpose of this chapter is to make the case that
significant work is needed to encourage the dissemina-
tion of information about EBA and its implementation in
clinical practice. First, we discuss “assessment as usual,”
how it differs from EBA, and reasons for these differences.
Then, we describe efforts to increase use of EBA through
dissemination and implementation efforts. Finally, we
present some ideas for future work needed to further
advance the use of EBA. Consistent with the other chap-
ters in this book, we focus on assessment of psychopathol-
ogy and its application to clinical diagnosis and progress
monitoring. Although similar issues likely exist for other
forms of assessment, such as psychoeducational assess-
ment, discussion of those is beyond the scope of this book.
Finally, although assessment tools to support case con-
ceptualization are described in the subsequent chapters
of this book, most of the literature studying clinician case
conceptualization practices and how to improve them has
focused on whether clinicians can apply specific theoreti-
cal models to client data and the validity of case concep-
tualizations (e.g., Abbas, Walton, Johnston, & Chikoore,
2012; Flinn, Braham, & das Nair, 2015; Persons &
Bertagnolli, 1999) rather than on how to collect and inte-
grate EBA data to generate a case conceptualization. As
mentioned previously, both diagnostic assessment and
progress monitoring can support case conceptualiza-
tion; therefore, much of the literature we discuss here
has implications for case conceptualization. However, in
the Future Directions section, we address steps needed to
advance assessment-​based case conceptualization.
IS THERE A RESEARCH–​P RACTICE
GAP IN ASSESSMENT?
Despite the proliferation of excellent assessment tools,
available data suggest there are significant training and
practice gaps in both diagnostic assessment and progress
monitoring. As discussed in the following sections, these
gaps have important implications for the accuracy of
clinician-​generated diagnoses and the accuracy of clini-
cian judgments about treatment progress.
Research–​Practice Gaps in Diagnostic Assessment
As detailed throughout the chapters in this book,
evidence-​based diagnostic assessment for most disorders
relies on standardized diagnostic interviews and/​or rat-
ing scales. Unfortunately, surveys of training programs
suggest that clinicians are not being prepared to conduct
these assessments during their graduate training. Several
surveys of psychology programs have been conducted in
the past three decades (e.g., Belter & Piotrowski, 2001;
Childs & Eyde, 2002), with the two most recent (Mihura,
Roy, & Graceffo, 2016; Ready & Veague, 2014)  finding
that training in assessment has generally remained con-
stant, but there has been an increase in training focused
on assessment of treatment outcomes, psychometrics,
and neuropsychology. However, these two studies found
inconsistent results regarding the use of clinical inter-
viewing. Ready and Veague reported only half to three-​
fourth of programs included clinical interviewing as a
focus of training. However, Mihura et al. found that 92%
of programs queried included clinical interviewing as a
required topic. These differences might reflect a change
during the 3  years that passed between the two studies.
However, it is also likely that the two studies also obtained
information from different programs, as Mihura and col-
leagues included more programs than Ready and Veague
and each study only obtained data from approximately
one-​third of all of the American Psychological Association
(APA)-​accredited programs.
Two studies have examined training in diagnostic
assessment specifically. Ponniah et  al. (2011) surveyed
clinical training directors from social work, clinical psy-
chology PhD and PsyD, and psychiatric residency pro-
grams regarding training in structured assessment based
on Diagnostic and Statistical Manual of Mental Disorders
(DSM) criteria. Only one-​ third of surveyed programs
reported providing both didactics and supervision in
diagnostic assessment, with clinical psychology PhD and
psychiatry residency programs being most likely to do so
and social work programs the least likely. These results are
concerning because master’s level clinicians represent the
majority of those providing services to those with mental
health disorders in the United States (Garland, Bickman,
& Chorpita, 2010). Focusing on clinical psychology PhD
and PsyD programs exclusively, Mihura et  al. (2016)
 19
Dissemination and Implementation of Evidence-Based Assessment
found that less than half of the programs required a course
and less than one-​fourth required an applied practicum
on any structured diagnostic interview. Differences in
required structured diagnostic interview courses were
found between training models:  73% of clinical science
and 63% of scientist-​ practitioner programs required a
course, whereas only 35% of practitioner-​ focused pro-
grams had a similar requirement.
Not surprisingly based on these training gaps, available
data suggest that clinicians are not engaged in EBA for
diagnostic assessment. Existing surveys across a range of
clinicians indicate that unstructured interviews are com-
monly relied on for diagnosis (e.g., Anderson & Paulosky,
2004), that evidence-​based tools are infrequently used
(e.g., Gilbody, House, & Sheldon, 2002; Whiteside,
Sattler, Hathaway, & Douglas, 2016), and diagnostic
practices often do not map on to best practice guidelines
(e.g., Demaray, Schaefer, & Delong, 2003; Lichtenstein,
Spirito, & Zimmermann, 2010).
Unfortunately, these gaps between “best practice”
and “as usual” assessment practices have implications for
the accuracy of diagnoses generated in routine practice.
Studies comparing clinician-​generated diagnoses to those
generated through comprehensive, research-​ supported
methods consistently find low rates of agreement between
the two (Rettew, Lynch, Achenbach, Dumenci, &
Ivanova, 2009; Samuel, 2015). Studies examining the
validity of clinician-​generated diagnoses also suggest that
these diagnoses are less valid than the evidence-​based diag-
noses (Basco et al., 2000; Jewell, Handwerk, Almquist, &
Lucas, 2004; Mojtabai, 2013; Samuel et al., 2013; Tenney,
Schotte, Denys, van Megen, & Westenberg, 2003).
Research–​Practice Gaps in Progress Monitoring
Most of what is known about graduate training in progress
monitoring focuses on trainee psychologists. As described
throughout this volume, most progress monitoring tools
are standardized rating scales, so many of the assessment
training gaps discussed previously also are relevant for
progress monitoring. However, other surveys have focused
on whether trainees are trained in utilizing these scales
for ongoing progress monitoring, rather than for diagnos-
tic assessment. With regard to APA accredited psychol-
ogy programs, Ready and Veague (2014) found that only
approximately half of programs offer courses focused on
progress monitoring, and Mihura et al. (2016) found only
10% of programs require their students to routinely use
outcome measures in their practical. Differing rates of
training in progress monitoring have been found between
19
different types of doctoral programs (e.g., counseling vs.
PsyD; Overington, Fitzpatrick, Hunsley, & Drapeau,
2015)  and training program models (e.g., practitioner-​
scholar models vs. clinical-​scientist models; Overington
et al., 2015), although little is known about progress moni-
toring training in master’s programs. Similar to training
programs, fewer than half of internship directors report
having their trainees use progress monitoring (Ionita,
Fitzpatrick, Tomaro, Chen, & Overington, 2016; Mours,
Campbell, Gathercoal, & Peterson, 2009), and nearly
one-​third of directors have never heard of progress moni-
toring measures (Ionita et al., 2016).
Similar to diagnostic assessment, there are low rates
of progress monitoring among practicing clinicians.
Much of the research in this area is focused on outcome
monitoring (Cashel, 2002; Hatfield & Ogles, 2004), with
relatively less focus given to ongoing progress monitor-
ing. Surveys suggest that many clinicians report track-
ing client progress (Anderson & Paulosky, 2004; Gans,
Falco, Schackman, & Winters, 2010). However, many
of them are not using validated measures, instead rely-
ing on tools developed within the clinic, unstructured
interviews, reports from clients, and clinical judgment
(Anderson & Paulosky, 2004; Gans et al., 2010; Johnston
& Gowers, 2005). This finding has been supported in
two recent large surveys of psychologists and master’s
level clinicians, in which fewer than 15% of clinicians
engaged in ongoing progress monitoring (Ionita &
Fitzpatrick, 2014; Jensen-​Doss et  al., 2016). Clinicians
who do use progress monitoring measures appear to be
using these measures to track progress internally and
for administrative purposes, but they rarely report using
them to plan treatment or monitor progress (Garland,
Kruse, & Aarons, 2003).
This lack of formal progress monitoring is concern-
ing in light of data showing that it is difficult for clini-
cians to accurately judge client progress based on clinical
judgment alone. For example, when Walfish, McAlister,
O’Donnell, and Lambert (2012) asked a multidisciplinary
sample of clinicians to rate their own level of skills, none of
them ranked themselves as below average, and one-​fourth
of them rated themselves at the 90th percentile of clinical
skill relative to their peers. These therapists estimated that
three-​fourths of their clients improved in therapy, with
less than 5% deteriorating; nearly half of them said that
none of their clients ever deteriorated. The study authors
point out that these estimates deviated wildly from pub-
lished estimates of improvement and deterioration rates.
Interestingly, available data suggest that even when clini-
cians are trained to engage in progress monitoring, this
20
20 Introduction
does not improve their ability to rate progress based on
clinical judgment alone. Hannan and colleagues (2005)
removed feedback reports from a setting that had been
using an MFS and asked clinicians to predict their clients’
outcomes. Those clinicians underestimated how many
clients would deteriorate or not improve, and they over-
estimated how many would improve.
WHY IS THERE A RESEARCH–​P RACTICE GAP
IN ASSESSMENT?
As detailed previously, lack of training is likely one factor
that contributes to clinicians’ not utilizing best assessment
practices. In addition, research has identified other clini-
cian and organizational variables that might be contribut-
ing to this research–​practice gap.
Several studies have focused on clinician attitudes
that might be driving assessment practices. Jensen-​Doss
and Hawley (2010, 2011)  conducted a national, multi-
disciplinary survey to assess clinicians’ attitudes toward
standardized assessment tools, with a particular focus on
diagnostic assessment. On average, clinicians reported
neutral to positive attitudes toward standardized assessment
tools, although this varied by discipline, with psychologists
reporting more positive attitudes compared to psychiatrists,
marriage and family therapists, social workers, and mental
health counselors (Jensen-​Doss & Hawley, 2010). Attitudes,
particularly beliefs about the practicality of standardized
assessment tools, predicted self-​reported use of these tools.
Other studies have found that clinicians have concerns that
structured diagnostic interviews would be unacceptable
to clients (Bruchmüller, Margraf, Suppiger, & Schneider,
2011), although data gathered directly from clients do not
support this view (Suppiger et al., 2009).
Studies have also examined clinician attitudes toward
progress monitoring. Across studies, attitudes toward these
measures have varied from neutral to positive, although
concerns regarding the validity of the measures (e.g.,
whether they accurately reflected client progress) are com-
mon (Cashel, 2002; Gilbody et al., 2002; Hatfield & Ogles,
2007; Ionita et  al., 2016; Johnston & Gowers, 2005). As
with diagnostic assessment, clinicians often report practi-
cal concerns about progress monitoring, including lim-
ited access to affordable measures, measures being too
long, difficulties reaching clients to fill out measures, and
little time to administer measures and keep track of when
to fill out measures (Gleacher et  al., 2016; Hatfield &
Ogles, 2004; Ionita et al., 2016; Johnston & Gowers, 2005;
Kotte et al., 2016; Meehan, McCombes, Hatzipetrou, &
Catchpoole, 2006; Overington et al., 2015). Clinicians also
report anxiety about progress monitoring data being used
for performance evaluation, use of these measures ruining
rapport, concern regarding how to present results correctly
to clients, and a general lack of knowledge about progress
monitoring (Ionita et al., 2016; Johnston & Gowers, 2005;
Meehan et al., 2006). In a study that separately asked about
attitudes toward the practice of progress monitoring and
attitudes toward standardized progress measures, clinicians
reported very positive attitudes toward the idea of monitor-
ing progress but more neutral attitudes toward the mea-
sures themselves (Jensen-​Doss et al., 2016), suggesting that
clinicians are open to engaging in the practice if their con-
cerns about the measures themselves can be addressed.
Consistent with research on diagnostic assessment, more
positive attitudes toward progress monitoring are associ-
ated with higher rates of self-​reported progress monitor-
ing practices (Hatfield & Ogles, 2004; Jensen-​Doss et al.,
2016; Overington et al., 2015).
A number of organizational barriers and facilitators of
EBA have also been identified in the literature. Lack of
organizational support is a barrier frequently mentioned by
clinicians, including both active discouragement from super-
visors and administration regarding the use of measures and
little guidance given by organizational leaders of when and
how often to use them (Connors, Arora, Curtis, & Stephan,
2015; Gilbody et al., 2002; Ionita et al., 2016; Overington
et al., 2015). Many of the practical concerns described previ-
ously also speak to organizational factors, such as the amount
of time clinicians are allowed to spend on assessment and the
budget available for purchasing assessment tools. Clinicians
also often report that administrators are more interested in
tracking administrative outcomes (e.g., length of wait list, cli-
ent turnover, and number of sessions) than outcomes such
as functioning and symptom reduction (Gilbody et al., 2002;
Johnston & Gowers, 2005). Conversely, clinicians who indi-
cate their organizations have policies or rules about assess-
ment are more likely to report using progress monitoring
(Jensen-​Doss et  al., 2016). Clinician assessment practices
also vary across organizational settings; providers working
in private practice settings are less likely to use standardized
diagnostic and progress monitoring tools than are those work-
ing in other settings (Jensen-​Doss et al., 2016; Jensen-​Doss &
Hawley, 2010).
EFFORTS TO IMPROVE ASSESSMENT PRACTICES
The studies reviewed previously indicate that although
effective assessment tools exist, they often are not making
 21
Dissemination and Implementation of Evidence-Based Assessment
their way into practice settings. As such, several efforts
have been made to bridge this research–​practice gap,
some focused on specific evidence-​based measures (e.g.,
rating scales for trauma; National Child Traumatic Stress
Network, 2016)  and others focused on EBA processes
(e.g., using an MFS to gather data and using feedback to
make decisions about treatment; Bickman et  al., 2016).
Efforts to improve clinician assessment practices can be
divided into dissemination efforts, or efforts to inform
clinicians about EBA tools, and implementation efforts
that seek to support clinicians in their use of such tools.
Implementation efforts can be subdivided into those
focused on training clinicians in EBA; those focused on
implementing EBA in individual organizations; and those
focused on integrating EBA into mental health systems,
such as state public mental health systems. Although a
comprehensive review of all of these efforts is beyond the
scope of this chapter, we highlight some illustrative exam-
ples of each approach.
Dissemination Efforts
Assessment-​focused dissemination efforts have typically
created sources for clinicians to identify evidence-​based
measures or guides for them to engage in EBA processes.
This volume is an example of an EBA dissemination
effort, as are publications in EBA special journal issues
(Hunsley & Mash, 2005; Jensen-​Doss, 2015; Mash &
Hunsley, 2005) and review papers, such as Leffler, Riebel,
and Hughes’ (2015) review of structured diagnostic inter-
views for clinicians. The DSM board has also embarked
on efforts to improve diagnostic practices and accuracy by
outlining steps for diagnosis and creating decision trees
to support differential diagnosis (First, 2013). Although
these dissemination efforts have typically focused on
what clinicians should do, Koocher and Norcross have
also published articles identifying discredited assessment
methods (Koocher, McMann, Stout, & Norcross, 2015;
Norcross, Koocher, & Garofalo, 2006).
There are also efforts to disseminate EBA informa-
tion online. For example, there is a website dedicated
to information about measures relevant to the assess-
ment of traumatized youth (http://​www.nctsn.org/​
resources/​online-​research/​measures-​review; National
Child Traumatic Stress Network, 2016), a repository of
information about assessment tools relevant to child wel-
fare populations (http://​www.cebc4cw.org/​assessment-​
tools/​measurement-​tools-​highlighted-​on-​the-​cebc; The
California Evidence-​ Based Clearinghouse for Child
Welfare, 2017), and the PROMIS website with measures
21
that assess outcomes for various health domains that pro-
mote and facilitate outcome and progress monitoring
(http://​www.healthmeasures.net/​explore-​measurement-​
systems/​promis; Cella et  al., 2010; HealthMeasures,
2017; Pilkonis et  al., 2011). In a novel approach to dis-
semination, the APA has recently funded a grant to update
assessment pages on Wikipedia, with a focus on assess-
ments that are freely available (Youngstrom, Jensen-​Doss,
Beidas, Forman, & Ong, 2015–​2016).
Training Efforts
Some groups are moving beyond dissemination to pro-
vide training in EBA to clinicians. Relative to the numer-
ous studies focused on training clinicians in treatments
(Herschell, Kolko, Baumann, & Davis, 2010), there are
fewer EBA training studies. Documented EBA training
efforts to date have consisted of workshops, workshops
plus ongoing consultation, and courses. Didactic training
workshops have helped improve clinician progress moni-
toring attitudes (Edbrooke-​Childs, Wolpert, & Deighton,
2014; Lyon, Dorsey, Pullmann, Silbaugh-​ Cowdin, &
Berliner, 2015), self-​ efficacy (Edbrooke-​Childs et  al.,
2014), and use (Persons, Koerner, Eidelman, Thomas, &
Liu, 2016).
Another training approach is to follow workshops with
ongoing consultation. For example, a training effort in
Washington state included 6 months of expert-​led phone
consultation and found that training impacted clini-
cian attitudes, skill, and implementation of standardized
assessment tools (Lyon et al., 2015).
Finally, online training has recently been applied to
EBA training. For example, Swanke and Zeman (2016)
created an online course in diagnostic assessment for mas-
ter’s level social work students. The course was based on a
problem-​based learning approach wherein students were
given diagnostic problems to solve by identifying symp-
toms and matching symptoms to DSM diagnoses. At the
end of the course, the average student grade on content
quizzes was 78.7% and the class was well-​received by the
students, although students’ levels of knowledge prior to
the course are not know, so it is difficult to determine
whether the course actually increased knowledge.
Organizational-​Level Implementation Efforts
Another approach to increasing use of EBA is for orga-
nizations to attempt to change assessment practices
organization-​wide. Several examples of such efforts have
been documented in the literature, including studies
2
22 Introduction
examining the impact of organizations incorporating
structured diagnostic interviews (e.g., Basco et al., 2000;
Lauth, Levy, Júlíusdóttir, Ferrari, & Pétursson, 2008;
Matuschek et al., 2016) and progress monitoring systems
(e.g., Bickman et al., 2011, 2016; Bohnenkamp, Glascoe,
Gracey, Epstein, & Benningfield, 2015; Strauss et  al.,
2015; Veerbeek, Voshaar, & Pot, 2012).
One illustrative example of organizational-​ level
implementation work focused on progress monitoring is
the work of Bickman and colleagues. Following an ini-
tial successful randomized effectiveness trial showing that
using an MFS called Contextualized Feedback System
(CFS) improved client outcomes (Bickman et al., 2011),
Bickman and colleagues (2016) conducted a second ran-
domized trial within two mental health organizations. All
clinicians within the agencies were required to administer
CFS, and cases were randomly assigned to receive feed-
back as soon as measures were entered into the system
(i.e., clinicians immediately received feedback reports
summarizing the CFS data) or to receiving feedback
every 6  months. Before the trial began, the investiga-
tors conducted a “pre-​implementation contextualization
phase,” during which they held workgroups to understand
existing clinic procedures and brainstorm about how CFS
would fit into those procedures. Training and ongoing
consultation in CFS was provided to clinicians and to
agency administrators to ensure both clinical (i.e., using it
with individual clients) and organizational (e.g., ongoing
review of aggregated data to identify problems with CFS
implementation) use of CFS. After finding that only one
clinic demonstrated enhanced outcomes with CFS, the
authors determined that the two agencies differed in their
rates of questionnaire completion and viewing of feed-
back reports. To better understand these findings, they
then conducted qualitative interviews with the participat-
ing clinicians (Gleacher et  al., 2016). Clinicians at the
clinic with better implementation and outcomes reported
more barriers to using CFS with their clients than did
clinicians at the other clinic, perhaps because they were
using it more often. However, they also reported fewer
barriers at the organizational level and more support from
their organizational leadership. The authors concluded
that organizational factors are strong drivers of implemen-
tation success.
System-​Level Efforts
Another approach to implementation is for mental health
systems, such as state public mental health agencies or
agencies like the Veteran’s Administration, to enact policies
requiring evidence-​based assessment. System-​level imple-
mentations documented in the literature have primarily
focused on progress monitoring. An early example was
the state of Michigan’s use of the Child and Adolescent
Functional Assessment Scale (CAFAS; Hodges & Wong,
1996). As described by Hodges and Wotring (2004), clini-
cians in the public mental health system were required
to use the CAFAS to track client outcomes. Data were
then used to provide clinicians and agencies feedback on
individual client and agency-​wide outcomes, including
comparison to agency and state averages.
Hawaii, which has been a pioneer in the advancement
of evidence-​based treatments (EBTs) in the public sec-
tor, has supported these efforts by developing and imple-
menting an MFS that is used statewide (Higa-​McMillan,
Powell, Daleiden, & Mueller, 2011; Kotte et  al., 2016;
Nakamura et al., 2014). To date, both clinicians and case-
workers across various agencies in the state have been
trained in and are implementing the MFS. In an effort to
encourage the use of EBA, Higa-​McMillan et al. reported
the use of “Provider Feedback Data Parties” during which
client progress and clinical utilization of the data are dis-
cussed. Other studies on Hawaii’s EBA efforts observed
that the fit between the MFS and case manager character-
istics facilitated MFS implementation, whereas provider
concerns about the clinical utility and scientific merit of
the MFS were reported as barriers (Kotte et al., 2016).
Internationally, system-​ level efforts to implement
progress monitoring have been reported in the United
Kingdom and Australia. Efforts to implement routine
monitoring throughout the United Kingdom have been
ongoing for well over a decade (Fleming, Jones, Bradley,
& Wolpert, 2016; Hall et al., 2014; Mellor-​Clark, Cross,
Macdonald, & Skjulsvik, 2016). The Child Outcomes
Research Consortium (CORC; http://​www.corc.uk.net),
a learning and planning collaboration of researchers, ther-
apists, managers, and funders, has spearheaded most of
this work. CORC has made valid, reliable, brief, and free
measures available to all clinicians working in the United
Kingdom, provided training in the measures, and created
an MFS to support their use. These measures are reported
to be widely implemented, but not at an optimal level
(Mellor-​Clark et al., 2016), so efforts are now focused on
adopting more theory-​driven approaches to implement-
ing the system (Mellor-​Clark et al., 2016; Meyers, Durlak,
& Wandersman, 2012). In Australia, efforts to implement
progress monitoring have been ongoing since the late
1990s and include training and development of computer
systems to support data collection and analysis (Meehan
et  al., 2006; Trauer, Gill, Pedwell, & Slattery, 2006).
 23
Dissemination and Implementation of Evidence-Based Assessment
Outcome data are collected at all public clinics and are
aggregated at a national level to be used for comparison
by local clinics.
Finally, note that policies focused on other aspects of
care can also have implications for assessment. For exam-
ple, the Precision Medicine Initiative (The White House
Office of the Press Secretary, 2015) focuses on increasing
personalized medical treatments that take individual dif-
ferences in genes and environment into account. Such
tailored approaches are likely going to require increased
use of psychosocial assessment in health care settings.
Similarly, the US Medicare and Medicaid system is mov-
ing increasingly toward value-​ based payment, where
reimbursement is based on quality, rather than quantity,
of care (Centers of Medicare & Medicaid Services, 2016).
As such, assessment of quality indicators within publicly
funded behavioral health settings is going to become
increasingly important. Finally, initiatives to implement
EBTs often lead to the development of assessment pro-
cesses to support those treatments, as evidenced by the
Hawaii initiative described previously.
FUTURE DIRECTIONS
As we hope this review has made clear, the literature
on EBA contains both good and bad news. On the one
hand, a number of excellent EBA tools exist and some
efforts are underway to encourage clinician use of those
tools. On the other hand, significant gaps continue to
exist between assessment best practices and what the
average clinician does in practice. To address these gaps,
we have several suggestions for future directions the field
should take.
1. Increase graduate-​level training in evidence-​based
diagnostic assessment and progress monitoring. Most of the
training and implementation efforts described previously
have primarily focused on retraining clinicians whose
graduate training likely did not include in-​depth training
in structured diagnostic assessment or progress monitor-
ing. Researchers focused on EBTs have called for an
increased focus on training at the graduate level because
training people well at the outset is likely easier and more
cost-​effective than trying to retrain them (e.g., Bearman,
Wadkins, Bailin, & Doctoroff, 2015).
One avenue for improving graduate training is increas-
ing the specificity of accreditation guidelines for training
programs (Dozois et al., 2014; Ponniah et al., 2011). For
both psychology and psychiatry training programs, past
accreditation standards stressed the need for students
23
to attain competence in diagnosis of clients via mea-
surement and interviews and to assess treatment effec-
tiveness, but they gave little guidance regarding what
constitutes appropriate assessment (APA, 2006; Canadian
Psychological Association, 2011; Ponniah et  al., 2011).
A  similar picture exists in accreditation guidelines for
mental health counseling (American Mental Health
Counselors Association, 2011), marriage and family
therapy (Commission on Accreditation for Marriage
and Family Therapy Education, 2014), and bachelor’s
and master’s level social work programs (Commission on
Accreditation & Policy, 2015), although these guidelines
do include training in progress monitoring as a way to per-
form program evaluation.
In January 2017, a new set of accreditation guide-
lines for the APA went into effect that include EBA as
a core competency (APA Commission on Accreditation,
2015). A recent Canadian task force focused on increas-
ing EBP use (Task Force on Evidence-​Based Practice of
Psychological Treatments; Dozois et  al., 2014)  empha-
sized monitoring progress and outcomes throughout treat-
ment. However, the Canadian Psychological Association
accreditation guidelines for doctoral programs have not
been updated to reflect this change as of this publication.
2. Increase “best practice” training strategies in EBA
dissemination and implementation efforts. Although
exceptions exist (Lyon et al., 2015), the primary approach
that has been taken to training clinicians in EBA is
what is sometimes referred to as a “train and pray”
approach:  Bring clinicians together for a workshop and
then hope they take what they have learned and apply it
in practice. The literature on training in EBTs suggests
that such an approach is unlikely to lead to sustained
practice changes (Herschell et  al., 2010). Rather, train-
ing needs to involve active learning strategies, ongoing
consultation in the practice, and attention to contextual
variables such as whether clinicians have adequate orga-
nizational support to continue using the practice (Beidas
& Kendall, 2010; Herschell et  al., 2010). Examples of
strategies that could be incorporated into EBA trainings
include engaging clinicians in behavioral rehearsal dur-
ing training (Beidas, Cross, & Dorsey, 2014); providing
ongoing consultation after initial training (e.g., Bickman
et al., 2016; Lyon et al., 2015); increasing sustainability of
assessment practices through “train the trainer” models
that train agency supervisors to provide ongoing supervi-
sion assessment (Connors et  al., 2015); and incorporat-
ing all levels of an agency into training through learning
collaborative models that address implementation at the
clinician, supervisor, and administrator levels (e.g., Ebert,
24
24 Introduction
Amaya-​Jackson, Markiewicz, Kisiel, & Fairbank, 2012;
Nadeem, Olin, Hill, Hoagwood, & Horwitz, 2014).
3. Increase our focus on pragmatic assessment. Studies
conducted with clinicians consistently suggest that
perceived lack of practicality is a major barrier to clini-
cian use of EBA (e.g., Ionita et al., 2016; Jensen-​Doss &
Hawley, 2010). In addition, the fact that many clinicians
who do gather assessment data do not actually incorpo-
rate that data into clinical decisions (Garland et al., 2003;
Johnston & Gowers, 2005)  suggests that they may not
find the data clinically useful. Glasgow and Riley (2013)
have called for the field to focus on pragmatic measures,
which they define as measures “that [have] relevance to
stakeholders and [are] feasible to use in most real-​world
settings to assess progress” (p. 237). They propose criteria
for determining whether a measure is pragmatic, includ-
ing that is it important to stakeholders, such as clients,
clinicians, or administrators; that it is low burden to com-
plete; that it generates actionable information that can be
used in decision-​making; and that it is sensitive to change
over time. Expanding our reviews of EBA tools to include
dimensions such as these might help identify measures
most likely to make their way into practice. One example
of such a review was conducted by Beidas and colleagues
(2015), who identified brief, free measures and rated their
psychometric support for a range of purposes, including
screening, diagnosis, and progress monitoring.
Another opportunity for increasing the practical-
ity of assessment is to take advantage of recent policies
emphasizing increased data collection and accountability
in health care settings (e.g., the “Patient Protection and
Affordable Care Act,” 2010). Lyon and Lewis (2016) point
out the opportunity that these policies provide for increas-
ing use of progress monitoring. As agencies increasingly
incorporate health information technologies, such as
electronic medical records, into their settings to meet
data reporting requirements, there is an opportunity to
integrate electronic MFSs into these systems (Lyon et al.,
2016). If progress monitoring can be built into the daily
workflow of clinicians, this greatly increases its practicality.
4. Leverage technology to increase the use of EBA.
Another avenue for increasing the practicality of assess-
ment is to incorporate technologies such as electronic
health care records platforms and smartphone applica-
tions into the assessment process. With the rise of policies
emphasizing increased data collection and accountabil-
ity in health care settings (e.g., “Patient Protection and
Affordable Care Act,” 2010), mental health settings are
increasingly relying on health information technolo-
gies, such as electronic health care records, to meet data
reporting requirements. Lyon and Lewis (2016) point out
these shifts provide an opportunity to increase the use
of progress monitoring. In a recent review, Lyon, Lewis,
Boyd, Hendrix, and Liu (2016) identified 49 digital MFSs
that could be used by clinicians with access to comput-
ers or tablets to administer progress measures and rap-
idly receive feedback. However, fewer than one-​third of
those were able to be directly incorporated into electronic
health care records, and Lyon and colleagues concluded
that additional work is needed to develop digital MFSs
that can be incorporated into the daily workflow of prac-
tice in a way that is sustainable.
Another technological advance with great potential
to enhance assessment is smartphone technologies that
support data collection. Researchers have developed
applications to support real-​time data collection (Trull
& Ebner-​Priemer, 2009) and have begun to examine the
clinical utility of such applications for gathering informa-
tion such as mood (e.g., Schwartz, Schultz, Reider, &
Saunders, 2016)  or pain ratings (Sánchez-​Rodríguez, de
la Vega, Castarlenas, Roset, & Miró, 2015). Such applica-
tions could facilitate self-​monitoring of symptoms between
sessions or efficient collection and scoring of progress
monitoring data in session. Many smartphone applications
to track psychological well-​being are already commercially
available (e.g., a November 15, 2016, search of the Google
Play store yielded more than 50 results for “mood track-
ing”), and an important next step is to determine how
these applications can be ethically developed and incorpo-
rated into clinical practice (Jones & Moffitt, 2016).
5. Develop theoretical models of organizational support
for EBA. Despite numerous studies suggesting that orga-
nizational context is critical to EBA (e.g., Gleacher et al.,
2016; Jensen-​Doss et al., 2016), there is a need for concep-
tual models that can guide organizational approaches to
improving assessment practices. Models of organizational
culture and climate have been developed to explain use
of EBTs (e.g., Williams & Glisson, 2014) and have been
translated into organizational interventions that improve
EBT uptake and client outcomes (e.g., Glisson, Williams,
Hemmelgarn, Proctor, & Green, 2016). Many aspects of
these models are likely applicable to the use of EBA, but
the constructs within them may need to be elaborated.
Although existing models might be helpful to guide
EBA implementation in agency settings such as clinics or
schools, these models are not as applicable to clinicians
working in private practice, who seem to be the clinicians
least likely to engage in EBA (Jensen-​Doss et al., 2016).
Additional work is needed to understand the needs of this
population.
 25
Dissemination and Implementation of Evidence-Based Assessment
6. Conduct more work focused on EBA processes.
Although EBA consists of both psychometrically sup-
ported assessment measures and the processes by which
those measures are applied, there has historically been a
dearth of research focused on EBA processes (Hunsley
& Mash, 2007). The rise in studies about MFSs, which
consist of measures, guidelines for how often to admin-
ister them, actionable feedback about clinical results,
and, increasingly, clinical guides suggesting next steps
to take in treatment (Krägeloh et  al., 2015), is a wel-
come advance on this front. However, additional work
is needed on diagnostic assessment processes and on
approaches to integrating assessment data to form a case
conceptualization.
In terms of diagnostic assessment, Youngstrom’s work
on grounding assessment decisions in probability nomo-
grams (e.g., Youngstrom, Choukas-​ Bradley, Calhoun,
& Jensen-​Doss, 2015)  is an interesting example of how
researchers can further develop and study the assessment
process. Drawing from approaches used in evidence-​
based medicine (Strauss et  al., 2015), Youngstrom and
colleagues have examined the diagnostic utility of various
risk factors and assessment tools (e.g., Van Meter et  al.,
2014; Youngstrom, 2014; Youngstrom et  al., 2004), gen-
erating data that can then be applied via a tool called a
nomogram, which helps clinicians translate assessment
information into estimated probabilities that a client meets
criteria for a disorder (for an illustration, see Youngstrom
et al., 2015). One benefit of this approach is that it can
be done sequentially, starting with lower burden assess-
ment strategies first, and only moving on to more inten-
sive assessment of diagnoses that are not ruled in or out at
earlier stages of assessment. Clinicians have been success-
fully trained to use the nomogram in two studies (Jenkins
& Youngstrom, 2016; Jenkins, Youngstrom, Washburn, &
Youngstrom, 2011), although research is needed to deter-
mine whether clinicians go on to apply the nomogram
in their work and whether use improves their diagnostic
accuracy with clients.
Another assessment process in need of additional
research is assessment-​ driven case conceptualization.
EBA case conceptualization models have been proposed
(Christon et al., 2015) and many theoretical conceptual-
ization models, such as the cognitive–​behavioral model,
indicate that assessment should support the conceptual-
ization process (Persons & Davidson, 2010). However,
most of the research on case conceptualization has
focused on whether clinicians who review the same clini-
cal vignettes or session recordings generate the same con-
ceptualizations (Flinn et al., 2015) or whether clinicians
25
can be trained to apply a particular conceptualization
approach to vignettes or recordings (Abbas et al., 2012).
To our knowledge, no studies have focused on whether
clinicians can be trained to gather assessment data and
use them to generate an accurate case conceptualization,
whether such training could lead to actual changes in
clinician conceptualization practices, and whether those
practice changes might improve client outcomes. This is
clearly an area in critical need of additional research.
Finally, some chapters in this volume highlight the
utility of functional assessment for case conceptualiza-
tion and ongoing progress monitoring. However, little
is known about whether clinicians are trained in this
practice, view it favorably, utilize it in practice, or find
it feasible. In education, the requirement to conduct
functional behavioral assessment in the Individuals with
Disabilities Act Amendments of 1997 led to the need for
widespread implementation of functional assessment in
schools (Scott, Nelson, & Zabala, 2003). Surveys sug-
gest that this practice is acceptable to school personnel
(Crone, Hawken, & Bergstrom, 2007; Nelson, Roberts,
Rutherford, Mathur, & Aaroe, 1999), although concerns
have been raised about its feasibility (Nelson et  al.,
1999). However, future research is needed to understand
how this practice is viewed and utilized in other settings.
CONCLUSIONS
As this volume illustrates, decades of excellent research
has generated a rich body of clinically useful EBA tools.
Unfortunately, many of these tools have not yet made it
into practice settings, limiting their public health impact.
Fortunately, researchers and policymakers are increasingly
attending to the dissemination of these tools, as well as their
implementation in mental health organizations and systems.
Through this work, the field will progress toward a more fully
realized application of EBPP that goes beyond treatment,
hopefully improving mental health outcomes for clients.
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the-​press-​office/​2015/​01/​30/​fact-​sheet-​president-​obama-​
s-​precision-​medicine-​initiative
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 31
Dissemination and Implementation of Evidence-Based Assessment
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Walfish, S., McAlister, B., O’Donnell, P., & Lambert, M. J.
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31
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32
Advances in Evidence-​Based Assessment: Using
Assessment to Improve Clinical Interventions
and Outcomes
Eric A. Youngstrom
Anna Van Meter
“Assessment” is the application of a measurement method
to support a particular goal. In the clinical enterprise,
measurement is not an end in itself. We are not trying
to simply describe our clients. They are seeking change,
and assessment should help identify problems, guide
the choice of solutions, and indicate whether things are
moving in the right direction (Hunsley & Mash, 2007).
Assessment plays a central role in psychoeducational
evaluation, custody evaluations, and forensic evaluations
as well as clinical evaluation. In each case, assessment
provides the data to guide recommendations and actions.
Our discussion focuses most on assessment in the clinical
context, recognizing that many of the principles and con-
cepts apply more generally as well.
Focusing on assessment as the application of measure-
ment to guide effective intervention distills evidence-​based
assessment (EBA) to a core principle. The potential value
added by assessment changes depending on the type of
intervention and the stage of treatment. Rather than being
separate clinical activities, assessment and treatment are
transactional and linked: Treatment provides the questions
and the context for EBA (Hunsley & Mash, 2007; Norcross,
Hogan, & Koocher, 2008). At the beginning of treatment,
assessment may most helpfully focus on screening, scop-
ing, and predicting diagnoses or key issues. Once refined
into a formulation, assessment shifts to prescribing an inter-
vention, with potential alternatives and moderating factors
defined. As treatment gets underway, then assessment shifts
to measuring progress, including shifts in severity, move-
ment toward goals, and sometimes measurement of process
variables that play a mechanism in the treatment.
32
Our goal is to lay out a practical model of EBA as a
transactional integration of assessment with treatment,
providing scaffolding for incorporating the different con-
tent and techniques presented in subsequent chapters. In
our model, perhaps best considered as EBA 2.0, we aug-
ment the “3 Ps” of EBA (Youngstrom, 2013)—​prediction,
prescription, and process—​with a preparation phase that
lays the groundwork for a successful installation of these
upgraded practices.
For concepts and principles to help anyone, they
need to be feasible. Evidence-​based medicine (EBM)
often uses the metaphor of a “leaky pipeline” that con-
nects the best research evidence with the person who
would benefit (Glasziou & Haynes, 2005). The research
only helps if the clinician is aware of it, accepts that
it is valid, views it as applicable to the client, has the
necessary resources to be able to implement, acts on it,
and secures the client’s agreement and adherence. The
chapters in this volume address the first half of the poten-
tial leaks: Anthologizing the information about measures
and their psychometrics and utility directly tackles the
problems of awareness and critical appraisal and also
guides choices about applicability. EBA 2.0 pushes the
information even further down the pipeline by building
a strategic approach to assessment that makes it easier
to evaluate common issues. It also combines research
and pragmatism to sequence the order of measurements,
minimizing redundancy or unnecessary testing that
will not inform key questions guiding care. As a result,
EBA 2.0 can often choreograph assessment sequences
that deliver better results in the same time or less than
 3
has been spent in traditional evaluations (cf. Camara,
Nathan, & Puente, 2000).
DIAGNOSIS AND TREATMENT FORMULATION
AS USUAL
A brief review of typical practices sets a counterpoint that
highlights contrasts with EBA. Surveys indicate that most
practicing clinicians have been doing minimal assessment
beyond an unstructured interview, with the exception of
those instances in which clinicians administer, score, and
interpret a battery of assessment and write a report (and
then rarely provide treatment; Garb, 1998; Jensen-​Doss
& Hawley, 2011). The multiplicity of factors involved in
each clinical scenario forces clinicians to rely on impres-
sionistic, pattern recognition approaches (Kahneman,
2011). Although our evolved cognitive strategies tended
to do well in our environment across evolutionary adapta-
tion, the complexity of modern life creates mismatches
where our fast, intuitive system often leaps to wrong clini-
cal conclusions, and we may not recover via our slower,
effortful processing strategies.
Clinical assessment appears to be a paragon of all that
can be problematic with our cognitive wiring. Our efforts
at empathy focus on emotionally salient material, process-
ing it swiftly to arrive at a hypothesis that we then seek
to confirm (and fail to systematically try to disconfirm;
Croskerry, 2003). We underestimate complexity, calling
off searches when we find a plausible suspect (Jenkins &
Youngstrom, 2016; Rettew, Lynch, Achenbach, Dumenci,
& Ivanova, 2009). Cultural differences in beliefs about
causes and framing of the problem lead to errors in
hypotheses that do not get corrected easily (Carpenter-​
Song, 2009; Yeh et al., 2005). As a result, studies of clini-
cal decision-​making accuracy are consistently humbling.
Vignette studies show tremendous variation across clini-
cians in formulations of the same presenting problem and
assessment data (Dubicka, Carlson, Vail, & Harrington,
2008; Jenkins, Youngstrom, Washburn, & Youngstrom,
2011). Even video-​recorded sessions intended as an inter-​
rater reliability exercise show massive differences in scor-
ing depending on culture and training (Mackin, Targum,
Kalali, Rom, & Young, 2006).
In contrast, IBM and other companies are betting
that machine learning may prove helpful in decision-​
making, feeding the multivariate data to artificial intel-
ligence robots to create decision support tools (Susskind
& Susskind, 2015). They are using machine learning to
mine complex relationships from staggering numbers of
Advances in Evidence-Based Assessment 33
variables and honing feedback to the provider and con-
sumer in formats that can lead care. These can result in
surprisingly large gains in predictive accuracy, although
they are still not a complete solution (James, Witten,
Hastie, & Tibshirani, 2013).
PREPARATION PHASE
EBA 2.0 need not wait for the robots to fix everything.
Techniques ranging from the simple to the sophisticated
are available that would upgrade our practice. The first
step is an easy one: Take stock of the most common pre-
senting issues at our practice and make sure that we are
well prepared for them. Depression, anxiety, and atten-
tion problems are all pervasive problems that will present
to any clinical practice. Other core issues may vary with
age range and practice setting. Externalizing behavior or
learning disabilities may be more common among school-​
aged referrals, whereas personality disorders or substance
misuse become more likely with advancing age. The ini-
tial step in EBA 2.0 is to identify the half-​dozen to dozen
most common issues. Given the sheer volume of cases
affected, even a small upgrade in assessment could pay
large dividends if it improves results for one of these fre-
quent referral issues.
A second step is to benchmark our local rates
against other clinics and settings. Benchmarking can
reveal gaps in our practice. If we see many clients with
anxiety but few with depression, that would be a sur-
prising pattern based on epidemiological studies and
clinic surveys (Rettew et  al., 2009). It is possible that
our practice has become so specialized that we mostly
get referrals for a narrow set of issues, but it is worth
considering whether we unknowingly have blind-
ers that eclipse our view of common comorbidities
or competing explanations for similar behaviors. We
can formally cross-​check our most common diagnoses
and case formulations against lists drawn from meta-​
analyses, epidemiological studies, or billing records.
The key point is to make sure that we are not overlook-
ing a common scenario. If we are, then that becomes
a priority for continuing education, additional reading,
professional supervision and consultation, and updates
in assessment practices.
Table 3.1 lists chapters in this volume that focus
on some of the most common conditions, along with
prevalence benchmarks based on different sources.
Epidemiological studies from the general population
probably provide a lower bound for rates that would be
34

34 Introduction

Table 3.1  Prevalence Benchmarks for Common Clinical Issues Discussed in This Volume

Clinical Rates (Rettew et al., 2009)

More Structured Diagnostic

Condition Chapter Diagnosis as Usual Interview General Populationa

ADHD 4 23% 38% 5% in children, 2.5% in adults

Externalizing problems 5 17% CD, 37% ODD 25% CD, 38% ODD 4% CD, 3% ODD
Mood disorders 6–​9 17% MDD, 26% MDD, 8% dysthymia 7% MDD,1.5% pervasive depressive
10% dysthymia disorder, 2.5% bipolar spectrum
Anxiety 11–​14
Child and adolescent 11 8% 18%
Social anxiety disorder/​phobia 12 6% 20% 7%
Panic 13 12% 11% 3%
Generalized anxiety disorder 14 5% 10% 3%
Post-​traumatic stress disorder 16 3% 9% 3.5%
Substance use disorders 17 14% 17% –​
Alcohol use disorder 18 10% 13% 5% in adolescents, 8.5% in adults

  The estimates are 12-​month prevalence rates as reported in DSM-​5 (American Psychiatric Association, 2013). Epidemiological rates refer to general
a

population, not treatment-​seeking samples, and so often represent a lower bound of what might be expected at a clinic.
ADHD, attention-​deficit/​hyperactivity disorder; CD, conduct disorder; MDD, major depressive disorder; ODD, oppositional defiant disorder.
Source: Adapted from Youngstrom and Van Meter (2016) and https://​en.wikiversity.org/​wiki/​Evidence_​based_​assessment

seen at a clinic. Rettew et al.’s (2009) meta-​analysis pro-
vides rates from an assortment of outpatient clinics. The
rates are a helpful starting point but are not etched in
stone. Prevalence estimates in each chapter may vary
as authors integrate different epidemiological studies or
clinical samples; for inpatient settings or specialty clinics,
it is likely that the rates of some conditions will be even
higher.
With our personal list of top referral questions in
hand, we can then organize our assessments by topic
and check whether there is a better method than the
incumbent measurement we are using for each. It need
not be a huge amount of work. This edited volume cre-
ates an easy opportunity to start at a high level: Cross-​
reference this list of common issues with Table 3.1.
Review each relevant chapter to determine if there are
measures that fill gaps in our current tool kit or offer
greater utility than what we already are using. That
strategy capitalizes on the expert review of the litera-
ture that informed each chapter to create a strong foun-
dation of assessment methods for the common issues.
The book can also be helpful in updating established
and thriving clinical practices. One could pick a “topic
of the month” and spend an hour checking if there are
better assessment options available for use in the prac-
tice. At a training clinic or large practice, the topic of
the month could be the focus of a brown bag lunch
seminar; in a private practice, it could be a good use of
a cancelled appointment slot. Over the course of a year,
cycling through the different topics will update the
whole practice while keeping the focus fresh and chal-
lenging each month. Avoid perfectionism—​the object
is not to find “the best” in any particular category but,
rather, to make sure that your practice is good enough
(Brighton, 2011; Hunsley, 2007) and that you ratchet it
steadily upwards.
The list of common issues also helps guide individual
assessments. At least screening or inquiring briefly about
each of the frequent topics, even if that is not what the
client first mentions, leverages the base rates. The simple
technique of asking about three to six common problems
instead of focusing on the first obvious topic avoids well-​
documented pitfalls of confirmation bias, failing to seek
disconfirming evidence, and search “satisficing” (calling
off the search as soon as one hypothesis seems confirmed
rather than continuing to explore other possibilities;
Jenkins & Youngstrom, 2016). Remember that comorbid-
ity is the rule, not the exception, and undetected comor-
bid problems can undermine treatment. More systematic
approaches to assessment also help broach awkward
topics—​such as substance misuse, sexual dysfunction, sui-
cidal ideation, or physical abuse—​that may be difficult for
clients to spontaneously volunteer (Lucas, Gratch, King,
& Morency, 2014).
 35
PREDICTION PHASE
Considering our common issues also informs our choice
of core measures. Start with broad measures that cover the
common issues, and augment with checklists about risk
factors. In the therapeutic context, the first wave of assess-
ment is a scouting exercise to discern the areas to explore in
more depth. For adults, there are a range of broad coverage
instruments available, including checklists (e.g., Derogatis
& Lynn, 1999) and personality inventories (e.g., Minnesota
Multiphasic Personality Inventory-​ 2 [MMPI-​ 2] interpre-
tive systems, in addition to self-​report options; Sellbom
& Ben-​Porath, 2005). If we are working with adolescents,
then it makes sense to start with a broad assessment instru-
ment such as the Achenbach System of Empirically Based
Assessment (ASEBA; Achenbach & Rescorla, 2003) or the
Adolescent Symptom Inventory (Gadow & Sprafkin, 1997).
Scores on these measures have shown good psychometric
properties across a variety of samples, and they provide
broad coverage of most of the common issues in childhood
and adolescence. Compared to the more comprehensive
personality tests and interviews, checklists are inexpensive
and fairly quick to score, and some provide good norma-
tive data to help tease apart what is developmentally typical
from the more extreme or problematic levels of behavior.
There also are free alternatives to many of these instru-
ments (e.g., Goodman, 1999; Ogles, Melendez, Davis, &
Lunnen, 2001), although the lower cost is often achieved
by reduced breadth of scales or sacrificing the quality of the
normative data (but for exceptions to this in the assessment
of adult depression, see Chapter 7, this volume).
Often, practitioners fall into the “rule of the tool,”
giving every client their favorite assessment instrument
without thinking much about how it matches up with
the presenting problem or the common issues. No mea-
sure is perfect. Considering strengths and shortcomings
of each measure compared to the common problems list
will help build assessment batteries that are much more
comprehensive and balanced without adding unneces-
sary components that burden the client. For example, the
ASEBA, MMPI-​2, and Symptom Checklist 90 (SCL-​90)
(Derogatis & Lynn, 1999)  all omit scales that directly
assess body image or disordered eating patterns, which
could be a prevalent and serious issue in teen or adult
women (Wade, Keski-​ Rahkonen, & Hudson, 2011).
Alternate scoring systems that rationally select items or
use analyses with distinct criterion groups may be needed
to cover other issues, such as post-​traumatic stress disor-
der (You, Youngstrom, Feeny, Youngstrom, & Findling,
2015) or substance misuse.
Advances in Evidence-Based Assessment 35
After the default or core assessment package is set, the
next step is to think through the interpretation of each
piece with regard to the common issues. If the goal were
an exhaustive review of the literature, then the project
would quickly become unmanageable (Youngstrom &
Van Meter, 2016). However, a comprehensive approach
is not necessary or particularly helpful; not all possible
permutations of assessment and construct are clinically
relevant:  We do not need to know how an attention-​
deficit/​hyperactivity disorder (ADHD) scale would do
at detecting depression, for example. We can match the
goal with the scale to focus our interpretive attention, and
we can use the “good enough” principle to keep moving
(Brighton, 2011).
At the prediction phase, a major source of value for an
assessment tool would be changing the probability of the
client having a diagnosis or problem. In a detective story,
successive clues raise or lower suspicion about each suspect.
The same is true with clinical assessment: Accumulating
risk factors raise the probability, as would high scores on
a valid measure of the same construct. Low scores on tests
might also reduce the probability, as would protective fac-
tors. It is possible to integrate such information in a much
more systematic way than just intuitive, impressionistic
interpretation. Bayes’ theorem offers an algorithm for
updating a probability estimate on the basis of new infor-
mation. Although it is centuries old, and authorities such
as Meehl (1954) have advocated for its use for decades, its
time is finally arriving. A combination of shifting winds—​
with EBM, politics, and sports all incorporating it (for
popular examples, see http://​fivethirtyeight.com)—​and
technology making it more accessible have made it fea-
sible to start using these methods in real time to integrate
information and guide decisions. The improvements are
profound, in terms of not just increased overall accuracy
but also improved consistency (i.e., a constructive reduc-
tion in the range of interpretations of the same data) and
reduced bias (protecting us from systematic misinterpre-
tations of the same data) (Jenkins & Youngstrom, 2016;
Jenkins et  al., 2011). Tools for synthesizing assessment
information now include websites and smartphone appli-
cations (search for “Evidence-​Based Medicine Calculator”
and choose from among the current best reviewed options)
as well as probability nomograms—​an analog to old slide
rules that used geometric spacing to accomplish various
computations. We include a probability nomogram as
Figure 3.1 because it helps illustrate the concepts and
represents a least common denominator in terms of tech-
nological requirements. For readers who are interested in
learning more about how to use this approach in clinical
36

36 Introduction

.1 99

.2

.5 95

1 1000
90
500

2 200 80
100
50 70
5
20 60

10 10 50
5
40
20 2 30
% 1 %
30 .50 20

40 .20
50 10
.10
60 .05
5
70 .02
.01
80 .005
2
.002
90 .001 1

95
.5

.2

99 .1
Pretest Probability Likelihood Ratio Posttest Probability

FIGURE 3.1   Probability nomogram used to combine prior probability with likelihood ratios to estimate revised, poste-
rior probability. Straus et al. (2011) provide the rationale and examples. Youngstrom (2014) and Van Meter et al. (2014,
2016) provide examples both of how to estimate diagnostic likelihood ratios from raw data and how to use a nomogram
to apply them to a case.

practice, we recommend the article by Van Meter et  al.
(2014), in which the authors provide extensive details on
how to integrate various types of clinical data in order to
inform the diagnostic decision-​making process.
Probabilistic interpretation involves the following
series of steps:  (a) Decide the starting, or prior, prob-
ability for a particular hypothesis; (b)  combine it with
the information added by a specific assessment finding;
and (c) review the updated probability and decide on the
next clinical action. The information about base rates and
common issues provides a starting estimate for step (a). In
a probability nomogram, the prior probability gets plot-
ted on the left-​hand column. The information from the
assessment finding gets plotted on the middle line, and
 37
then connecting the dots to cross the right-​hand line pro-
vides the graphical estimate of the revised probability.
For the probability nomogram to work, the information
from the assessment needs to be scaled using an effect size
called a diagnostic likelihood ratio (DLR). The DLR is a
ratio of how common a given finding would be in the pop-
ulation of interest divided by how common it would be in
the comparison group. For example, the DLR attached
to an implicit association task for risk of self-​injury would
be a ratio of how common the result (i.e., a “positive”
test result) was among those who self-​injured compared
to how common a similar result would be among those
who did not (Nock & Banaji, 2007). In older terminol-
ogy, the DLR for a high risk score would be the diagnostic
sensitivity of the result (the “true positive rate”; e.g., out of
100 cases with history of self-​injury, how many had a posi-
tive test result and were correctly classified as engaging
in self-​injurious behavior) compared to the false-​positive
rate (the complement of diagnostic specificity; e.g., out of
100 people who do not self-​injure, how many had a posi-
tive test result and were incorrectly classified). A DLR can
also be estimated for low risk, or “negative” test results; for
example, how many people with a history of self-​injury
had the low risk (negative) result (the false-​negative rate,
or 1-​sensitivity) divided by the number of people who
do not self-​injure and correctly got a low risk (negative)
test result (diagnostic specificity). The algebraic relation-
ship means that it is possible to take the sensitivity and
specificity for assessments reported in the chapters of this
volume and quickly calculate the DLRs for low risk (nega-
tive) and high risk (positive) scores. Although academic
standards are starting to require greater detail, including
the sensitivity and specificity, in articles reporting on diag-
nostic tools (e.g., Bossuyt et al., 2003), finding the neces-
sary information to calculate DLRs can be challenging.
However, this only needs to be done once if we write it
down, either as marginalia or on a cheat sheet of measures
that we routinely use in our practice. It also is not neces-
sary to do this for all measures—​only the ones that we are
going to use regularly.
The DLR approach is omnivorous, and it can be fed
any assessment result or data about risk or protective fac-
tors, as long as they are re-​expressed as DLRs. With a little
effort, almost any effect size can be converted (Hasselbad
& Hedges, 1995; Viechtbauer, 2010), along with inputs
such as percentiles from normative data (Frazier &
Youngstrom, 2006). Another advantage of the approach
is that it can add information sequentially, in a flexible
order, and as it becomes available. To add information
about second input, take the revised probability from
Advances in Evidence-Based Assessment 37
the first assessment, use it as the next prior probability
(i.e., put it on the leftmost line of the nomogram or in
the starting field of a calculator), connect it with the next
DLR, and get the updated probability. If several DLRs are
available at the same time, then they can be multiplied
to get a single combined DLR. The method trades the
assumption that the correlation between inputs is mod-
est for the flexibility of input sequence. Regression-​based
approaches work in the opposite way, optimally adjusting
for the degree of covariation among inputs, but at the cost
of greater complexity and an inability to work if any one of
the variables in the model is missing for a particular case
(Kraemer, 1992). More often, the ability to add new data
as they become available is a better match for the unfold-
ing process of the clinical encounter.
The third part of the EBA cycle is to consider the
updated probability of a given outcome or diagnosis and
then decide on the next clinical action. EBA 2.0 adapts
the EBM concept of two decision thresholds defining
three zones of clinical action. The low probability, inter-
mediate, and high probability zones signify watchful
waiting, assessment, and acute treatment in the EBM
formulation (Straus, Glasziou, Richardson, & Haynes,
2011). With EBA 2.0, there are distinct assessment strate-
gies and titrated interventions for each zone (Youngstrom,
2013). The low probability zone could still warrant a
surveillance or monitoring plan to detect worrisome
changes, and it could also be a place for primary pre-
ventions that are so low risk and low cost that they make
sense to deploy regardless of personal circumstances. The
intermediate zone is not just the place for more focused
assessment targeting the key hypotheses but also may be
the realm for using broad-​spectrum, low-​risk interventions
such as many forms of therapy. This is the arena in which
targeted prevention, peer counseling, bibliotherapy, and
generic supportive counseling all could be appropriate,
along with changes in sleep hygiene, diet, and other life-
style factors. The high probability zone may be the place
where treatment shifts to specialist interventions, acute
pharmacotherapy, and other tertiary interventions. At this
stage, assessment shifts to monitoring treatment response,
searching for cues of progress (and using failure to prog-
ress as a sign that the case formulation should be revisited;
Lambert, Harmon, Slade, Whipple, & Hawkins, 2005).
Neither threshold—​between low probability and inter-
mediate or between intermediate and high—​has a rigid
location on the probability scale. This is by design. The
threshold should shift depending on the relative risks and
benefits attached to the treatment, or the costs associated
with a false negative (i.e., missing a case that truly has the
38
38 Introduction
target problem) or false positive (i.e., overdiagnosis). With
very low-​risk, low-​cost interventions, the treatment threshold
could drop so low that everyone gets the intervention: This is
the primary prevention model, with inoculation and iodized
salt to prevent thyroid problems as widespread public health
examples. Although there are models to algebraically weight
costs and benefits and precisely shift the threshold (for four
different but conceptually related models, see Kraemer,
1992; Straus et al., 2011; Swets, Dawes, & Monahan, 2000;
Yates & Taub, 2003), these are complicated to implement
without computer support. They also probably are not suf-
ficient in themselves. Ultimately, the decisions about when
and how to treat are informed by clinical expertise and
patient values, and the decision-​making should be shared
with the client (Harter & Simon, 2011).
PRESCRIPTION PHASE
Returning to the flow through the EBA process, the com-
bination of risk factors and screening or initial assessments
will probably be enough to move hypotheses into the mid-​
range “assessment zone” or demote them from further
consideration, but they will not suffice to confirm hypoth-
eses on their own. Nor will they push revised probabili-
ties high enough to guide treatment in isolation. If the
EBA system is working, then the initial test results serve to
revise the list of hypotheses that are candidates for further
intensive evaluation.
Assess More Focused Constructs
and Add Collateral Informants
The next stages involve gathering more focused measures
and collateral perspectives, as well as perhaps selecting a
semi-​structured approach for confirming diagnoses. The
more focused measures include not just self-​report scales
and checklists, of which there are an abundance reviewed
in the following chapters, but also in many cases perfor-
mance measures such as neurocognitive tests. Collateral
informants are a routine part of evaluations for youths,
where parents or teachers may be initiating the referral.
Although less commonly used, they can play a valuable
role not just in couples counseling but also in assessing
behaviors when individuals may lack insight (e.g., mania,
psychosis, or adult autism; Dell’Osso et al., 2002) or when
they may not be motivated to provide accurate reports (as
might be the case with substance misuse, antisocial behav-
ior, or food intake with eating disorders). Treat each chap-
ter topic as a portfolio of options for a particular diagnostic
hypothesis, and then select an assessment instrument that
is “highly recommended” for evaluating each. If there
is information about collateral report options as well, it
is worth picking one of the top-​tier ones and having it
available, too. Although collaterals provide converging
perspectives, the correlations tend to be low to moderate
(r = .2 to .4 in adults, based on an extensive meta-​analysis;
Achenbach, Krukowski, Dumenci, & Ivanova, 2005).
Disagreements also are informative in terms of gauging
insight, motivation for treatment, and other valuable con-
textual information (for a detailed review and suggestions,
see De Los Reyes et al., 2015).
Semi-​Structured Diagnostic Interviews
If the goal is to establish a formal diagnosis, then a semi-​
structured diagnostic interview is the next step indicated
in the process. In contrast, the standard of practice for
decades has been an unstructured interview, where the
clinician listens to the presenting problem, generates a
hypothesis, and seeks confirming evidence. Clinicians
like this approach because it should employ our training
and expertise to be able to recognize complex patterns
of information and to sniff out key moderating variables.
Unfortunately, studies repeatedly show that rather than a
set of virtuoso diagnostic performances, what we accom-
plish with unstructured interviews are formulations with
near-​chance inter-​rater agreement. That state of affairs
guided the decision of the third and subsequent revi-
sions of the Diagnostic and Statistical Manual (DSM;
American Psychiatric Association, 2013)  to emphasize
improving reliability, and it also was the impetus for
developing structured diagnostic interviews. Fully struc-
tured interviews are highly scripted, to the point that they
could be delivered via computer. The scripting and auto-
mation push inter-​rater reliability to nigh perfection, at
the expense of sacrificing clinical judgment.
Semi-​structured interviews offer a middle way. They
are structured in the sense that they include the same set
of topics regardless of presenting problem or clinical intu-
ition, and they also embed the algorithms to satisfy spe-
cific diagnostic criteria. A semi-​structured interview about
depression, for instance, should ask about at least the nine
symptoms in the criteria for a major depressive episode,
as well as include questions checking that the symptoms
are part of an episodic change in functioning lasting at
least 2 weeks and causing impairment in at least one set-
ting. The “semi” aspect means that the interviewer need
not stick exactly to a script but instead can paraphrase,
or reword using the patient’s own terms. The clinician
 39
also can re-​inject clinical judgment to the process, but
now at the level of leaves and roots, rather than starting
with sweeping decisions about choice of branch in the
decision-​making tree. In practice, compared to fully struc-
tured interviews, semi-​structured approaches tend to take
longer to learn to administer reliably, and they may yield
lower reliability estimates. If that price affords better clini-
cal validity and more uptake, it is well worth paying.
Clinicians cling to unstructured interviews. We offer a
set of rationalizations: The more structured interviews will
take too long; they will damage rapport with our clients;
clients will not like the interview. Surveys decisively rebut
the issues of patient preference. Patients prefer the more
thorough approaches, believing that clinicians have a more
comprehensive and accurate understanding of the situation
afterwards (Bruchmuller, Margraf, Suppiger, & Schneider,
2011; Suppiger et  al., 2009). The issue of time could be
handled in any of at least three ways. First, use the previ-
ous information from the EBA 2.0 process to select specific
modules. Rather than grinding through an entire interview,
choose semi-​structured interview components focused on
the hypotheses still in contention. This method uses the
prior assessment data to accomplish what many interviews
implement with gating logic and skip out questions. The
selective approach also offers the possibility of choosing
modules from different interviews that are optimized for
particular conditions. The interviews reviewed in subse-
quent chapters provide the list of options, and a practitioner
could build an eclectic and modular follow-​up interview,
taking the best from each category. Second, spend longer
on the interview. Data show that clients do not mind, and
insurance companies are willing to reimburse for the more
focused follow-​up interview because the prior EBA steps
have documented medical necessity. Third, technology
is now making it possible to offload the structured inter-
view as an activity that the client does before meeting the
practitioner (Susskind & Susskind, 2015). Completely
computer-​administered interviews are decreasing in cost
and increasing in sophistication. The structured interview
could become another input in the assessment process,
leading to a set of most likely diagnoses, which the clinician
then probes before deciding on a final formulation.
Other More Intensive Testing
An EBA approach would deploy other assessments with
incremental or confirmatory value at this stage. These are
methods that are more burdensome or expensive, preclud-
ing use in a universal screening or core battery approach.
In the diagnostic arena, they may also put more of a
Advances in Evidence-Based Assessment 39
premium on specificity, even at the expense of lower sen-
sitivity, because now the goal is confirmation of a hypoth-
esis that has already passed through the earlier stages of
detection (a high-​sensitivity filter) and evaluation (Straus
et  al., 2011). This is the realm of systematic behavioral
observation with targeted hypotheses, of neurocognitive
testing, of drug testing kits, and of polysomnography to
evaluate the potential presence of a formal sleep disorder.
This could become the province of wearable consumer
devices and health-​related smartphone applications that
measure sleep, activity, heart rate, and other physiological
and behavioral parameters.
Treatment Planning and Goal Setting
The assessments should serve to identify treatment targets
by pushing the probability high enough to warrant cor-
responding intervention, by direct confirmation using a
sufficiently structured interview, or by a combination of
these. EBA should not only establish a treatment target
but also detect secondary targets, such as comorbidities
or areas of impaired functioning. It should also provide
alerts to factors that would change the choice of interven-
tion. Comorbid substance misuse, low verbal ability, or
a personality disorder all could significantly complicate
treatment and lead to poorer prognosis if not addressed.
Having arrived at a case formulation, the next step is
to negotiate a treatment plan and set measurable goals.
We view this as a negotiation because collaborative
approaches to care are desirable on ethical and utilitarian
grounds. When clients buy into the plan, they are more
invested in treatment and more likely to follow through on
recommendations and achieve better outcomes. Client
beliefs and preferences should be considered throughout
the assessment and treatment process, but they deserve
extra attention here. Many areas of medicine have devel-
oped decision aids to help the patient understand the risks
and benefits of different treatment options. This is an area
for growth in clinical psychology. At a minimum, a direct
and culturally sensitive discussion should occur, and the
provider should explicitly link elements of treatment to
the stated preferences and provide a meaningful rationale
for how treatment would promote attaining the goals. The
client may not be ready or motivated to work on every-
thing that the assessment process reveals. When it is pos-
sible to focus on shared goals, engagement and rapport
will be at a substantial advantage.
With targets agreed upon, assessments also establish
a baseline measure of severity, and many can add nomo-
thetic benchmarks against which to measure progress.
40
40 Introduction
Tools such as behavior checklists that have standardiza-
tion data offer normative comparisons in the form of per-
centiles, T scores, and the like. Interestingly, the scores
that are the most elevated are not always the most impair-
ing or distressing (Weisz et al., 2011), and so yet again it
is valuable to get the client’s input. Selecting one or more
scales as an operational definition of a treatment outcome
will provide a more quantifiable and perhaps objective
indication of progress.
PROCESS: TREATMENT MONITORING
AND TREATMENT OUTCOME
Therapy, like going on a diet, is a challenging form of
behavior change. The chances of success increase with
explicit goals and regular brief measures of progress—​like
weighing in on a bathroom scale—​and process. The psy-
chometric qualities and practical parameters are quite dif-
ferent for a progress or process measure compared to a
diagnostic assessment (Youngstrom et  al., 2017). Brevity
is a major consideration. Although loss of diagnosis may
be a goal of treatment, few practitioners or clients would
want to repeat a full structured interview several times
over the course of treatment. Sensitivity to treatment
effects is another key function; in part for this reason, per-
sonality or general cognitive ability tests are not used as
outcome measures. Treatment sensitivity requires a blend
of enough retest stability to indicate when problems per-
sist, yet also malleability that can indicate if the interven-
tion has the desired effect. Indices of retest reliability are
not adequate in isolation to judge suitability for measur-
ing outcome. Conceptually, generalizability coefficients
or intraclass correlations quantifying the amount of vari-
ance attributable to treatment would be ideal, although
they are rarely reported in the literature.
Nomothetic Goal Setting
Norm-​ referenced measures create an opportunity for
nomothetic definitions of treatment milestones. Jacobson
and colleagues developed an influential model for this,
framing clinically significant change as requiring psy-
chometrically reliable improvement along with transit-
ing an a priori benchmark (Jacobson, Roberts, Berns, &
McGlinchey, 1999). Jacobson and colleagues used a reli-
able change index (RCI) as a way of showing that individual
treatment response was unlikely to be due to measurement
error or instability. The RCI converts raw change scores
into a z-​score-​type metric, using the standard error of the
difference as the scale. Values greater than 1.65 would
connote 90% confidence that the change was reliable, and
1.96 would demarcate 95% confidence. In practice, retest
stabilities are rarely reported, and even less likely to match
the naturalistic length of treatment, so people often use the
internal consistency reliability as the basis for estimating
the standard error of the measure and then the standard
error of the difference (Ogles, 1996). Research reports
and reviews tend to focus on group statistics and not the
standard errors, so it may be necessary to calculate these
for the outcome measures we use regularly. For each com-
mon treatment target, select one assessment instrument
that will be feasible to use, and make a cheat sheet with
the standard error of the difference score; or, even more
conveniently, jot down the number of points required for
90% or 95% confidence in the change. A  more recent
alternative to the RCI is the minimally important differ-
ence (MID) method, which uses patient preferences to
define the smallest increment of change that they would
find meaningful (Thissen et  al., 2016). MID milestones
tend to be smaller than RCI ones, making them easier to
achieve and also indicating that more subtle changes can
still be important to the individual.
The second part of Jacobson and colleagues’ (1999)
definition involves passing a benchmark defined by nor-
mative data. There are three operational definitions: mov-
ing Away from the clinical range, moving Back into the
nonclinical range, and moving Closer to the nonclini-
cal than clinical average. The Back definition requires
normative data in a nonclinical sample, and the Away
definition needs a relevant clinical sample to generate
the benchmark; the Closer definition needs both the
nonclinical and the clinical samples for estimation. The
requirements create a practical barrier to implementa-
tion: Many assessments lack the requisite normative data
(Youngstrom et al., 2017). The thresholds are also rarely
reported, although they are relatively simple to calculate
if the data are accessible. Jacobson and colleagues recom-
mended using two standard deviations (SDs) as the rule
of thumb for defining the Away and Back thresholds (e.g.,
moving beyond 2 SDs from the clinical mean or back
within 2 SDs of the nonclinical mean), and the Closer
threshold is the weighted average of the clinical and non-
clinical means. Again, these are worth calculating for the
primary outcome measure we select for each common
treatment target. Writing them down leverages the few
minutes of work involved, providing a resource for treat-
ment across many cases.
From a psychometric perspective, measures best suited
for the nomothetic definitions of clinically significant
 41
change will have high reliability—​translating into precise
estimates of the client’s true score in classical test theory—​
coupled with large separation between the clinical and
nonclinical distributions, most often indexed as Cohen’s
d effect size. The high reliability is often achieved via
increasing scale length, as the number of items is part of
the internal consistency reliability formula. As a result,
the tools precise enough to measure change well may
be too long to repeat frequently. The nomothetic bench-
marks may work best as midterm and final exams—​panels
of evaluation that are used less often but that provide fairly
deep evaluation of progress (Youngstrom et al., 2017).
Idiographic Goal Setting
A complementary approach to goal setting and track-
ing is an idiographic approach, in which the client
defines targets of interest and uses a simple way of scal-
ing and recording them to provide frequent feedback.
Often, these are single-​item scales, with simple Likert-​
type scoring. The Youth Top Problems approach asks
the youth and the caregiver to each pick three things
that they want therapy to improve and then report on
them at every session using a 0–​10 scale (Weisz et  al.,
2011). The reliability of the approach derives from the
repeated measurement. One could think of the num-
ber of repetitions as the functional length of the scale.
The brevity and the salience of the content (because the
client chose it) make the approach feasible. It can be
remarkably sensitive to treatment effects. It also is likely
to enhance treatment effects, much as stepping regularly
on a bathroom scale increases the effectiveness of the
diet. Measurement-​ based care advocates using these
sorts of short, focused evaluations. These also can pro-
vide feedback in real time, allowing for course correc-
tions during treatment if there is failure to progress or if
there are iatrogenic effects.
Process Measurement
Many interventions are skill based, and it is possible to
track the behaviors that are components of the thera-
peutic process. The possibilities are broad and include
examples such as daily report cards when evaluating
interventions for impulsive or externalizing behaviors
(see Chapter  4, this volume), completion of three-​and
five-​column charts in cognitive–​behavioral therapy, use
of coping or diary cards in dialectical behavioral therapy,
or counting the number of core conflictual relational
themes surfaced during a session of psychodynamic
Advances in Evidence-Based Assessment 41
therapy (Luborsky, 1984). Tracking the number of cancel-
lations or no-​shows also provides a behavioral measure of
engagement, and other measures of adherence are pos-
sible. Process variables can include mediational variables
in treatment models, and some may be worth measuring
during the course of therapy to ensure that the interven-
tion is starting to produce the desired changes, even if the
more global outcomes may take some weeks to achieve.
The burgeoning number of mental health applications
for smartphones and other devices will create ways of trac-
ing utilization without requiring additional work on the
part of the client. These variables are more tied to the
particular intervention used, and so they are less likely to
be covered in a chapter devoted to assessment. They are
important, nonetheless, and will repay any investment in
planning and gathering them.
Maintenance Monitoring
When treatment goes well, termination planning should
celebrate the success, and also a plan should be devel-
oped for maintenance and for relapse prevention (Ward,
1984). The reality is that many conditions are recurrent
(e.g., mood disorders), chronic (e.g., ADHD and person-
ality disorders), or prone to relapse (e.g., substance mis-
use). There also may be predictable triggers and stressful
events, such as moving or separating from a partner,
that create opportunities to plan ahead and promote the
generalization of successful behaviors. As we conclude a
course of therapy, it makes sense to have an assessment
strategy that will monitor gains and provide early warning
of things worsening. Kazdin and Weisz (1998) discussed
a “dental model” of care, in which routine check-​ups
are scheduled without waiting for a crisis. These pro-
mote prevention as well as early intervention. For cli-
ents to use the monitoring strategies, the strategies need
to be low friction, convenient, and focused on things
that the clients care about (Youngstrom et  al., 2017).
Here, too, phone applications and wearable technology
are making innovations possible. Daily items tracking
substance use or stress, or wearables tracking exercise
and sleep, create new opportunities for monitoring
long-​term health.
UTILITY: HOW MUCH WILL IT COST?
Psychological assessment looks different viewed through
the lens of EBA 2.0, with different techniques woven
through the intervention process from before the
42
42 Introduction
start of treatment to after its conclusion. Although full
implementation of EBA adds several new techniques,
and moves assessment out of its traditional box at the
beginning of treatment (or even separated entirely from
treatment, as often happens with the assessment report
model), it does not usually demand extra time from the
client. Sequencing is key. If everyone were screened for
all conditions, regardless of prevalence, or if all com-
pleted comprehensive neurocognitive batteries along
with structured interviews, then time and cost would
balloon (Kraemer, 1992; Youngstrom & Van Meter,
2016). Using knowledge of base rates lets us configure
our assessment sequence to cover common scenarios
first. Then we selectively add an assessment only when
it has the potential to answer questions about prediction,
prescription, or process. Use of short forms, hybrid mod-
els that blend rating scales with modular semi-​structured
interviews, and brief idiographic items all promote feasi-
bility. Gathering the nuts and bolts in advance—​making
the cheat sheet with the diagnostic likelihood ratios, reli-
able change indices, and normative benchmarks—​is a
one-​time investment in enhancing the assessment and
treatment for all subsequent clients.
Fiscal costs are in flux, as test publishers are now
experimenting with subscription or fee-​for-​scoring mod-
els. There also are a plethora of public domain and free
options, many of which have accumulated evidence
of reliability and validity across a range of populations
and settings (Beidas et al., 2015; see also Chapter 7, this
volume). Professional societies are currently reviewing
and anthologizing many of these (e.g., the American
Academy of Child & Adolescent Psychiatry’s Practice
Toolbox [http://​www.aacap.org/​aaCaP/​Clinical_​Practice_​
Center/​Home.aspx] pages) and the Society of Clinical
Psychology’s assessment pages [http://​www.div12.org]),
making them more convenient to find, and a growing
number are now available on Wikipedia and Wikiversity
(Youngstrom et al., 2017). The proliferating mental health-​
related software applications also are low cost or free.
As a result, neither time nor cost is a serious obstacle
to implementing EBA 2.0. The gains in accuracy of
diagnosis are profound. Inasmuch as diagnosis and for-
mulation guide the effective choice of treatment, bet-
ter outcomes should follow. Measurement-​based care
also is showing that progress and process evaluation
enhance the implementation of treatment and provide
a small to medium-​sized boost in outcomes (e.g., Guo
et  al., 2015). Considering the evidence of utility, per-
haps the better question is whether we can afford not
to adopt EBA 2.0.
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 45

Part II

Attention-​Deficit and Disruptive

Behavior Disorders
46
 47
Attention-​Deficit/​Hyperactivity Disorder
Charlotte Johnston
Sara Colalillo
This chapter focuses on the assessment of attention-​
deficit/​hyperactivity disorder (ADHD) in clinical settings
and on measures appropriate for youth. Six-​to 12-​year-​old
children are the group most frequently referred for assess-
ment and treatment of ADHD, and therefore literatures
regarding assessment at other ages are not as well devel-
oped and not reviewed in this chapter. However, consis-
tent with the recent adoption of a lifespan perspective on
ADHD (American Psychiatric Association [APA], 2013),
in this chapter we do include brief information pertain-
ing to the assessment of ADHD in adulthood. Research
focused on the assessment of ADHD earlier in life, partic-
ularly in the preschool years, is mounting (e.g., Ghuman
& Ghuman, 2014; Harvey, Lugo-​Candeals, & Breaux,
2015; Rabinovitz, O’Neill, Rajendran, & Halperin, 2016).
There are a number of challenges to the identification of
ADHD in this younger age range, including less consis-
tency in the contexts in which children are assessed (e.g.,
preschool, day care, and home care) and less distinctive-
ness of ADHD symptoms and other problem behaviors.
However, the potential benefits to early identification of
the disorder make this area of work an important frontier.
Similarly, although most youth are diagnosed with ADHD
prior to adolescence, some symptom presentations (e.g.,
primary problems with inattention) or some circum-
stances may result in ADHD escaping earlier detec-
tion. In addition, the increased autonomy or academic
demands associated with adolescence often necessitate
a renewed focus on ADHD assessment as a precursor to
developing or modifying treatment plans. Readers are
referred to Barkley (2006) for an overview of issues related
to assessment of ADHD in adolescents.
The relatively high prevalence of ADHD, combined
with the pernicious nature of the problems associated with
it and the persistence of the disorder over time (APA, 2013),
47
make comprehensive and accurate clinical assessment an
imperative for guiding clinical care in this population. In
addition, perhaps more than many diagnoses, the ADHD
diagnosis has been the subject of considerable contro-
versy. Much of this controversy is fueled by frequent, and
at times sensationalistic, media reports. Many individuals,
including parents of children who undergo assessments
for ADHD, express fear that this is an overused diagnos-
tic label designed merely to control children’s naturally
rambunctious or extroverted nature and to justify the use
of psychotropic medications. Contrary to these concerns,
the scientific community has provided ample evidence
to support the validity of the disorder and its associated
treatments (Barkley, 2002; Kooij et  al., 2010; National
Institutes of Health, 2000). Furthermore, evidence sug-
gests that although the diagnosis may sometimes be over-
used, it is just as frequently missed (e.g., Angold, Erkanli,
Egger, & Costello, 2000; Levy, 2015; Sayal, Goodman,
& Ford, 2006). However, for each individual child there
is no substitute for careful, evidence-​based assessment to
provide the best possible clinical service and to assist par-
ents and children in understanding the meaning of the
diagnostic label, the link between assessment and treat-
ment recommendations, and the need to monitor impair-
ments and treatment effects over time.
We begin the chapter with an overview of ADHD, pro-
viding a sense of the core characteristics of the disorder
that need to be assessed. We then review assessment mea-
sures for children that serve three purposes, along with
the unique challenges that may accompany each purpose:
(a) measures used for diagnostic purposes, (b)  measures
useful for case formulation and treatment planning, and
(c) assessments for monitoring the course and outcome of
interventions. For each purpose, we have constructed a
table indicating measures that meet psychometric criteria
48
48 Attention-Deficit and Disruptive Behavior Disorders
set out by the editors in Chapter 1 of this volume. In the
text, we offer brief descriptions of these measures and
occasionally mention other promising assessment tools
that do not, as yet, meet the criteria used for including
measures in the tables. Following the review of assessment
tools appropriate for children, we consider the best tools
available for the assessment of ADHD in adults. Finally,
we conclude with an overview of the state-​of-​the-​art with
regard to the assessment of ADHD, with a focus on the
challenges that remain for research and clinical practice.
THE NATURE OF ADHD
The study of ADHD is one of the largest empirical lit-
eratures in child psychopathology and encompasses evi-
dence regarding the genetic, biological, neurological,
psychological, social, and cultural characteristics of the
disorder. Significant advances are being made in our
understanding of ADHD, including exciting theoretical
and empirical works probing the core causes and nature
of the disorder (e.g., Gallo & Posner, 2016; Karalunas
et al., 2014; Musser, Galloway-​Long, Frick, & Nigg, 2013;
Nigg, Willcutt, & Doyle, 2005; Sonuga-​Barke, Cortese,
Fairchild, & Stringaris, 2016). The vibrant nature of
research on ADHD bodes well for advancing our ability
to clinically assess, treat, and potentially even prevent this
disorder. However, the rapidly expanding and dynamic
nature of the research also means that evidence-​based
assessment of ADHD must continually change as it incor-
porates new evidence. Thus, one challenge to the assess-
ment of ADHD is the need for clinicians to constantly
update their knowledge about the disorder and to revise
assessment tools and methods accordingly. The first and
perhaps most critical recommendation we offer for the
assessment of ADHD is that the information in this chap-
ter has an expiry date, and only by keeping abreast of the
science of ADHD can clinical practice in this area remain
appropriate.
ADHD is defined in the most recent edition of the
Diagnostic and Statistical Manual of Mental Disorders
(DSM-​5; APA, 2013)  as a neurodevelopmental disorder
characterized by developmentally inappropriate and mal-
adaptive levels of inattention, impulsivity, and hyperactiv-
ity occurring in multiple settings with an onset prior to
age 12  years. So defined, ADHD has a prevalence rate
among school-​aged children of approximately 5%, with
more boys than girls affected. ADHD symptoms are per-
sistent over time, and at least two-​thirds of children who
meet diagnostic criteria will continue either to meet
diagnostic criteria or to suffer impairment due to symp-
toms into adolescence and adulthood (e.g., Kooij et  al.,
2010). Beyond the core symptoms of the disorder, indi-
viduals with ADHD frequently experience difficulties in
areas such as academic or job performance, interpersonal
relations, oppositional and conduct problems, and inter-
nalizing problems (anxiety and mood disorders).
Depending on the type of symptoms that an individual
displays at the time of assessment, ADHD diagnoses are
assigned as predominantly inattentive, predominantly
hyperactive–​ impulsive, or combined presentations.
Individuals with the predominantly inattentive presenta-
tion have problems such as difficulties in paying close
attention to details or sustaining attention. The predomi-
nantly hyperactive–​impulsive presentation is character-
ized by behaviors such as motor overactivity or restlessness
and also difficulties inhibiting behavior. The combined
presentation includes both types of problems. The two
symptom dimensions, inattention and hyperactivity–​
impulsivity, are highly related (e.g., Martel, von Eye, &
Nigg, 2012; Toplak et  al., 2009), and most individuals
with the diagnosis show elevations in both types of symp-
toms. The predominantly hyperactive–​impulsive presen-
tation appears most common in younger children and
may reflect a developmental stage of the disorder (e.g.,
Hart et  al., 1995). The overlap between the predomi-
nantly inattentive presentation and what has been called
sluggish cognitive tempo or concentration deficit disorder
remains somewhat unclear, although recent evidence
suggests these may be distinct disorders (e.g., Becker et al.,
2016). Although some research shows differential links
between the type of ADHD symptom presentation and
patterns of comorbidity or elements of treatment response
(e.g., MTA Cooperative Group, 1999; Pliszka, 2015),
other work suggests poor stability and specificity related to
which type of symptom is most prevalent in an individual
(e.g., Willcutt et al., 2012), and DSM-​5 has moved away
from subtyping ADHD to the more descriptive focus on
symptom presentation.
ASSESSMENT OF ADHD IN CHILDREN
The assessment of ADHD in childhood shares the conun-
drum assessors face with many childhood disorders, where
multiple sources of information must be considered. As
defined by DSM, ADHD is characterized by symptoms
and impairment that occur cross-​situationally. In the prac-
ticalities of assessment, this means that information from
both home and school contexts is considered essential
 49
to the assessment process. Given the limitations of child
self-​report (e.g., Loeber, Green, Lahey, & Stouthamer-​
Loeber, 1991), the assessment of childhood ADHD
places a heavy reliance on parent and teacher reports of
the child’s behavior. Although information from multiple
informants and contexts is viewed as critical to the assess-
ment of ADHD, there is abundant evidence that these
sources frequently show only minimal convergence (e.g.,
Achenbach, McConaughy, & Howell, 1987). In addition,
evidence is meager with respect to the best methods for
combining this information (for exceptions, see Gadow,
Drabick, et  al., 2004; Martel, Schimmack, Nikolas, &
Nigg, 2015)  or specifying which combinations of infor-
mation offer the best incremental validity in the assess-
ment process (Johnston & Murray, 2003). The influence
of rater (e.g., depressed mood or ADHD symptoms in
the parent) or situational (e.g., classroom structure and
home routines) characteristics must also be considered
in evaluating the information provided by the multiple
sources (e.g., De Los Reyes, 2013; Dirks, De Los Reyes,
Briggs-​Gowan, Cella, Wakschlag, 2012). Thus, the puzzle
of how to best combine multiple, often discrepant, pieces
of information remains a challenge for assessment.
PURPOSES OF ADHD ASSESSMENT
Clinical assessments of childhood ADHD serve a variety
of purposes, ranging from confirming an ADHD diag-
nosis to ruling out differential diagnoses such as anxiety
disorders or learning problems to assessing the response
of a child’s ADHD symptoms and functioning to a psy-
chosocial treatment or change in medication regimen.
Varied assessment approaches and tools may be needed
for addressing each of these different purposes. In this
chapter, we focus on assessments for the purpose of diag-
nosis, treatment planning, and treatment monitoring. In
selecting and evaluating assessment tools for each of these
purposes, we employed the rating system used throughout
the chapters of this volume, as described in Chapter 1.
At this point, we offer a caveat regarding our selection
and evaluation of the assessment measures included in
our tables. We searched broadly for measures and infor-
mation supporting their use. However, we used practical
criteria that limited this search. To meet the dual goals of
accessibility and independent research validation of the
measures, we prioritized measures that are currently com-
mercially or publicly available but that also have evidence
of reliability, validity, or both reported by independent
investigators in published studies. Given the breadth of
Attention-Deficit/Hyperactivity Disorder 49
the assessment literature, we acknowledge that we may
have missed a small number of measures or information
that would allow measures to meet the psychometric cri-
teria required for inclusion in the tables. Within the text
of the chapter, we occasionally describe other measures
that do not meet the psychometric criteria required for
table entry but that hold promise in the assessment of
ADHD. For such measures, although we continue in an
attempt to be comprehensive, the sheer number of mea-
sures with limited psychometric information requires a
selective approach to inclusion.
ASSESSMENT FOR DIAGNOSIS
Although most evidence supports a dimensional view of
ADHD symptoms (e.g., Marcus & Barry, 2011), assess-
ment for diagnosis requires a categorical decision. There
are no objective neurological, biological, or other diagnos-
tic markers for ADHD, and the diagnostic decision rests
on perceptions of the child, typically offered by parents
and teachers. These reports of whether or not the child
shows particular symptoms will be influenced by variables
such as the context in which the child is observed (e.g.,
home vs. school), characteristics of the rater (e.g., expecta-
tions and mood), and clarity of the assessment questions.
In making diagnostic decisions, the clinician must remain
aware of the assumptions underlying not only diagnostic
categories but also the use of informant perceptions and
the multiple possible explanations for discrepancies across
informants. Research remains sorely needed to guide and
improve the diagnostic validity of such decisions, and cli-
nicians are best advised to resist unwarranted adherence
to the use of arbitrary cut-​offs or algorithms for combining
information.
According to DSM-​5 (APA, 2013), an ADHD diag-
nosis in childhood requires not only that at least six of
the nine symptoms of either inattention or hyperactivity–​
impulsivity be present but also that these symptoms have
existed for at least 6 months, at a level that is maladaptive
and inconsistent with developmental level. The symp-
toms must have presented before the age of 12 years and
lead to clinically significant impairment in social and/​
or academic functioning evidenced in two or more set-
tings. In addition, the symptoms should not be better
explained by other conditions such as oppositional defi-
ant disorder or anxiety disorders. Thus, the assessment of
ADHD requires not only measuring symptoms but also
their onsets and their associated impairments in multiple
settings and gathering information regarding co-​occurring
50
50 Attention-Deficit and Disruptive Behavior Disorders
problems. Each of these requirements presents an assess-
ment challenge.
Defining symptoms as developmentally inappropri-
ate requires that assessment tools permit comparisons to
a same-​aged normative group. In addition, consideration
should be given to the gender and ethnic composition of
the normative sample. DSM-​5 criteria do not specify gen-
der or ethnic differences in how the disorder is displayed
and would suggest the use of norms combined across child
gender and based on samples with representative numbers
of ethnic-​minority children (as well as population charac-
teristics). However, studies have revealed differences in
the rates and severity of ADHD symptoms across genders
and ethnic groups (e.g., Arnett, Pennington, Willcutt,
Defries, & Olson, 2015; DuPaul et  al., 2016; Morgan,
Staff, Hillemeier, Farkas, & Maczuga, 2013). Although
such evidence would encourage the use of gender-​or
ethnicity-​specific norms, such use carries a strong caveat
given that the DSM diagnostic criteria are specified with-
out regard to such child characteristics. Where possible,
clinicians would be wise to consider comparisons to both
specific and general norms; where specific norms do not
exist, clinicians should at least acknowledge the possible
role of culture, gender, or other characteristics in inter-
preting assessment information regarding the relative
level of ADHD symptoms presented by the child.
Assessing the diagnostic criteria related to the age of
symptom onset and duration of symptoms also can be
challenging. Few established measures tap these aspects
of the diagnosis, and clinicians typically rely on more
informal parent interviews to provide this information.
This reliance on unstandardized retrospective recall
carries an obvious psychometric liability (e.g., Angold,
Erkanli, Costello, & Rutter, 1996; Russell, Miller, Ford,
& Golding, 2014).
Given that ADHD is defined by its presence in mul-
tiple situations, strategies are needed for combining
assessment information from parent and teacher reports
into a single diagnostic decision. The most common
methods employ either an “or” rule, counting symptoms
as present if they are reported by either the parent or the
teacher, or alternately an “and” rule, counting symptoms
as present only if endorsed by both parent and teacher.
Evidence suggests that of these two options, the “or” rule
for combining information may have the greatest valid-
ity, but either method of combination of informants
generally outperforms the reliance on a single reporter
(e.g., Shemmassian, & Lee, 2016). Other combinatorial
methods, including averaging across raters to reduce the
influence of any one informant, also show promise (e.g.,
Martel et  al., 2015). In addition, studies from our lab
(Johnston, Weiss, Murray, & Miller, 2011, 2014) demon-
strate that the convergence between parent and teacher
reports of child ADHD symptoms can be improved by
providing parents with instructional materials that clarify
the nature of ADHD behaviors and how to rate them
(e.g., distinguishing between behaviors that occur only
when the child is tired versus those that are more per-
vasive and distinguishing between age-​appropriate and
age-​inappropriate behaviors). Still, we know that rater
or source variance is substantial and often accounts for
more variance in rating scale scores than the inattentive
and hyperactive–​impulsive dimensions of behavior (e.g.,
Gadow, Drabick, et  al., 2004; Gomez, Burns, Walsh, &
De Moura, 2003). Until further evidence is available,
clinicians must rely on clinical judgment, grounded in a
solid knowledge of the empirical literature, in combining
information from multiple sources and methods to arrive
at a final diagnostic decision in childhood ADHD.
Finally, in assessments intended to offer a diagnosis of
ADHD, the clinician must have a working knowledge of
other childhood disorders in order to make informed dif-
ferential and comorbid diagnoses. The process of teasing
apart whether inattentive or impulsive behaviors are best
accounted for by ADHD or by problems such as fetal alco-
hol effects, autism, learning problems, or anxiety remains
a challenge. Given the space limitations of this chapter,
we do not cover measures useful for assessing these other
childhood disorders and instead refer the reader to other
child assessment resources (Frick, Barry, & Kamphaus,
2010; Mash & Barkley, 2007) and the relevant chapters in
this volume. However, we note that the limitations of our
current knowledge and diagnostic systems often contrib-
ute to the difficulties of discriminating among disorders,
and the clinician may need to assign an ADHD diagnosis
as a “working hypothesis” rather than as a confirmed deci-
sion. To the extent that the core nature of ADHD remains
under debate, best practices for discriminating this condi-
tion from other related conditions will remain somewhat
elusive.
A related problem of discriminating among disorders
arises in the use of assessment measures, especially older
measures, in which conceptualizations of ADHD are con-
founded with symptoms of other disorders. For example,
the hyperactivity scales of earlier versions of the Conners
Parent and Teacher Rating Scales (Goyette, Conners,
& Ulrich, 1978)  included items more characteristic of
oppositional problems. Similarly, the hyperactivity sub-
scale of the 1982 version of the Personality Inventory for
Children-​Revised (Lachar, 1982) assesses behaviors such
 51

Attention-Deficit/Hyperactivity Disorder 51

as cheating and peer relations, which are not core ADHD requirement for ADHD. For both parent and teacher
symptoms. Clinicians are reminded to not judge the ratings, age-​and gender-​specific norms are available for
appropriateness of measures on the basis of titles or scale large representative samples. Limited information on
names but, rather, to give careful consideration to actual norms combined across genders is available. The man-
item content and whether this content is congruent with ual outlines evidence of small, but potentially meaning-
current conceptualizations of ADHD. ful, differences in scores across ethnic groups, and these
demand attention when using the measure with minority
group children. The reliability and validity of scores on
Overview of Measures for Diagnosis
the measure, either in the current DSM-​5 or in earlier
DSM-​IV versions, are generally good (Table 4.1). The
Narrowband ADHD Checklists
ADHD Rating Scale-​5 is the only measure in Table 4.1
Among measures designed to assess ADHD symptoms, with evidence of test–​retest reliability over a period of
we include only those that map onto the symptoms as months, in contrast to the shorter test–​retest intervals for
described in DSM. A number of rating scales have been other measures. Scores on the ADHD Rating Scale-​5 cor-
produced that are tied, more or less directly, to DSM relate with other ADHD measures and discriminate chil-
symptoms of ADHD, either those contained in DSM-​ dren with ADHD from nonproblem controls and from
IV or the essentially unchanged symptom list in DSM-​ clinical controls. Sensitivity and specificity information is
5. One of the most widely used of these is the ADHD available, with some evidence that teacher ratings on the
Rating Scale-​5 (DuPaul, Power, Anastopoulos, & Reid, ADHD Rating Scale provide greater specificity and par-
2016; DuPaul, Reid, et al., 2016). This recently updated ent ratings provide greater sensitivity in making ADHD
brief rating scale, which can be completed by parents or diagnoses (e.g., DuPaul, Power, et al., 2016).
teachers, lists the 18 DSM-​5 symptoms of ADHD, along In addition to the ADHD Rating Scale-​5, a number
with a six-​item scale assessing the impairment associated of very similar questionnaires exist, all with items listing
with these symptoms. The ADHD Rating Scale-​5 pro- the DSM symptoms of ADHD, and in some cases associ-
vides a total score and has inattentive and hyperactivity–​ ated problems such as sluggish cognitive tempo (e.g., the
impulsivity subscales, supported by factor analysis, that Disruptive Behavior Scale [Gomez, 2012] and the Child
are useful in determining ADHD presentation type. The and Adolescent Disruptive Behavior Inventory [Lee,
impairment scale is an addition to this most recent ver- Burns, Snell, & McBurnett,  2014]). These measures
sion of the ADHD Rating Scale, and it is advantageous range in the extent of psychometric and normative infor-
given that impairment due to symptoms is a diagnostic mation available to support their use. Other measures

Table 4.1  Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliabilitya Reliability Validity Validity Generalization Utility Recommended

Narrowband ADHD Rating Scales

  ADHD Rating Scale-​5
  Parent E E NA G A G E A ✓
  Teacher E E NA G A G E A ✓
  Conners 3 DSM-​IV-​TR Symptom Scales
  Parent E E NA A G G E A ✓
  Teacher E E NA A G G E A ✓
 ADDES-​4
  Parent E E NA A G A E A
  Teacher E E NA A G A E A
Structured Interviews
  DISC-​IV NA NR A A G G G A

a
  This column reflects inter-​rater agreement between clinical judges, and this information is not available for most measures where, instead, parent and
teacher agreement is more commonly assessed.
Note: ADDES-​4 = Attention-​Deficit Disorder Evaluation Scales; DISC-​IV = Diagnostic Interview Schedule for Children-​IV; A = Adequate; G = Good;
E = Excellent; NR = Not Reported; NA = Not Applicable.
52
52 Attention-Deficit and Disruptive Behavior Disorders
that are described for assessing ADHD offer content that
is not entirely consistent with DSM criteria and are not
recommended for diagnostic purposes. For example, the
Brown Attention-​Deficit Disorder Scales for Children and
Adolescents (Brown, 2001) is a parent and teacher report
measure of the deficits in executive functioning that are
thought to be associated with ADHD.
The DSM-​ IV-​
TR Inattentive and Hyperactive/​
Impulsive Symptom Scales of the Conners 3rd Edition
(Conners 3; Conners, 2008) are derived from the longer
parent (110 items) and teacher (115 items) forms and map
onto the DSM symptoms of ADHD. Although not all of
these items are worded exactly as the DSM symptoms,
they appear synonymous. The third edition of this mea-
sure also includes validity scales to assess the accuracy and
integrity of responses, as well as brief yes/​no items assess-
ing impairment due to symptoms. The normative sample
is large and representative, and information regarding the
scores of a large clinical group of children with ADHD is
available. Normative percentiles for the symptom scales
are available for the genders separately and combined.
The scales have good psychometric properties (Conners,
2008; see Table 4.1) and are well validated. The long his-
tory of the Conners Rating Scales in the study of ADHD
provides an extensive research background for this
measure.
The Attention-​ Deficit Disorder Evaluation Scales
(ADDES-​4; McCarney & Arthaud, 2013a, 2013b) are
updated versions of parent (46 items) and teacher (60
items) forms that yield inattention and hyperactive–​
impulsive subscale scores reflecting DSM symptoms of
ADHD. Items were developed with input from diagnos-
tic and educational experts. The normative samples are
quite large and generally representative. Information
from a sample of children with ADHD (although method
of diagnosis is not clearly specified) also is available for
the parent and teacher versions. Separate age and gender
scores are calculated. The reliability and validity informa-
tion for the measure as reported in the manual is gener-
ally good (McCarney & Arthaud, 2013a, 2013b; see Table
4.1); however, a limited number of independent valida-
tion studies are available, particularly for the most recent
fourth edition of the measure.
We note that several briefer measures of ADHD symp-
toms also exist and are used primarily for screening pur-
poses (e.g., Conners 3 ADHD Index). One prominent
example is the Strengths and Difficulties Questionnaire
(SDQ) Hyperactivity/​ Inattention Subscale (Goodman,
1997). This five-​item scale has reasonable psychomet-
ric properties and normative data and appears useful
in detecting possible cases of ADHD (Algorta, Dodd,
Stringaris, & Youngstrom, 2016; Goodman, 2001). The
SDQ is available free of charge, is easy to score, and
includes subscales reflecting other problems—​ clear
advantages in a screening measure.
Structured Interviews
We included one structured interview, the Diagnostic
Interview Schedule for Children-​IV (DISC-​IV; Shaffer,
Fisher, Lucas, Dulcan, & Schwab-​ Stone, 2000), in
Table 4.1. It is recognized that structured interviews often
have limited psychometric information. In particular,
the categorical model underlying these measures means
that normative information is considered unnecessary.
However, given the heavy reliance on structured inter-
views in many research and medical settings, we opted
to include at least one such measure. We caution the cli-
nician to consider carefully the costs of such interviews
(e.g., heavy investment of clinician and family time) in
contrast to the relatively low incremental validity offered
by these measures compared to parent and teacher ratings
of ADHD symptoms (e.g., Pelham, Fabiano, & Massetti,
2005; Vaughn & Hoza, 2013).
The DISC-​ IV (Shaffer et  al., 2000)  maps directly
onto DSM-​IV diagnostic criteria for a range of child dis-
orders, including ADHD, and it includes both symptom
and impairment questions. Given that DSM-​5 criteria for
ADHD are essentially unchanged from DSM-​IV criteria,
the interview remains appropriate for assessment. The
DISC-​IV is available in multiple languages and in parent
and youth versions. The child version has limited psycho-
metric properties, although some studies support the use of
combined responses across parents and children (Shaffer
et al., 2000). The highly structured nature of the DISC-​IV
diminishes the importance of estimating inter-​rater reliabil-
ity or inter-​judge agreement for this measure. Psychometric
information for the fourth version of the DISC is somewhat
limited; however, combined with information on earlier
versions, support is generally adequate for the reliability of
the measure for making ADHD diagnoses (Shaffer et al.,
2000). Similarly, evidence supports the convergent valid-
ity of ADHD diagnoses made using the DISC-​IV (e.g., de
Nijs et  al., 2004; Derks, Hudziak, Dolan, Ferdinand, &
Boomsma, 2006; McGrath, Handwerk, Armstrong, Lucas,
& Friman, 2004; Sciberras et  al., 2013). It is noteworthy
that there is heavy reliance on this measure in many large
research studies.
Other structured and semi-​structured interviews used
in the assessment of ADHD include the Kiddie Schedule
 53
for Affective Disorders and Schizophrenia (K-​ SADS;
Kaufman et  al., 1997)  and the Child and Adolescent
Psychiatric Assessment (CAPA; Angold & Costello, 2000).
As with the DISC-​IV, these interviews typically have not
been subjected to extensive psychometric study.
Measures Not Useful in the Assessment
of ADHD Diagnoses
The current diagnostic criteria for ADHD remain rela-
tively subjective, and the drive to develop and access
more objective indicators of the disorder has been strong.
A number of cognitive performance measures have been
proposed as useful in this regard, many of which are ver-
sions of continuous performance tests. Some of these
measures have come considerable distances in providing
normative information, evidence of stability over time,
and sensitivity to the effects of medication treatments
(e.g., the Conners CPT II [Conners & MHS Staff, 2000]
and the Objective QbTest [Ramtvedt, Røinås, Aabech, &
Sundet, 2013]), yet they remain limited in their clinical
utility (Hall et al., 2016). Although these measures offer
the promise of objective measurement of ADHD symp-
toms (in contrast to the subjectivity inherent in parent
and teacher reports), their relations to other measures of
ADHD symptoms often are modest, and there is limited
evidence to support their predictive or discriminant valid-
ity. In particular, scores on these measures produce high
rates of false-​negative diagnoses such that normal range
scores are often found in children who meet diagnostic
criteria for ADHD according to other measures. Again,
none of these measures are, as yet, sufficiently developed
to meet the designated psychometric criteria for this vol-
ume or to be useful in making diagnostic decisions for
individual children (Duff & Sulla, 2015). Similarly, pat-
terns of subscale scores on intelligence tests, biological
markers such as blood tests or brain imaging have not
been of demonstrated use in the clinical assessment of
ADHD (e.g., Kasper, Alderson, & Hudec, 2012; Koocher,
McMann, Stout, & Norcross, 2015).
Overall Evaluation
Based on ease of use and predictive power, combining
information from teacher and parent versions of brief
DSM-​5-​based rating scales appears to offer the best avail-
able option in the diagnosis of ADHD. Although child
self-​
report versions exist for several of the measures
reviewed, the validity of child report is typically lower
than that of parent or teacher reports, and for this reason
Attention-Deficit/Hyperactivity Disorder 53
we have not included these versions. Structured and semi-​
structured diagnostic interviews are a mainstay in research
on ADHD; however, evidence suggests that they may not
add incrementally to the diagnostic information gath-
ered more efficiently with rating scales (e.g., Ostrander,
Weinfurt, Yarnold, & August, 1998; Pelham et al., 2005;
Vaughn & Hoza, 2013; Wolraich et al., 2003). We do note,
however, consistent with recommended pediatric and
psychiatric assessment guidelines (American Academy
of Child and Adolescent Psychiatry, 2007; American
Academy of Pediatrics, 2011), that there is a definite need
for additional information, perhaps gathered through par-
ent interviews or child self-​report, to supplement rating
scales in order to fully assess for possible comorbid or dif-
ferential diagnoses, age of onset and history of symptoms,
and other important clinical information relevant to the
diagnosis of ADHD.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
Three treatments have received empirical support
for childhood ADHD (Evans, Owens, & Bunford,
2014): pharmacotherapy, behavioral treatment, and their
combination. In assessments for treatment planning, the
clinician is seeking information to assist with (a) develop-
ing a conceptualization of the factors contributing to the
child’s difficulties and prioritizing treatment targets or
goals (e.g., Which ADHD symptoms are most impairing
or most likely to respond quickly to treatment?), (b) match-
ing difficulties to recommended treatments (e.g., Do this
child’s primary difficulties match the ADHD problems
that have been targeted with behavioral or medication
treatments?), or (c)  identifying environmental elements
that may be used in treatment (e.g., Does the teacher offer
rewards for academic work completed?). Information
regarding factors that may interfere with treatment suc-
cess (e.g., Does this child have a physical condition that
may limit the utility of medication?) or the child’s inter-
ests and strengths (e.g., sports interests or skills) also will
be useful.
In this section, we review measures that provide
information relevant to conceptualizing the nature of
the problems experienced by children with ADHD and
the planning of treatments specifically targeting ADHD
symptoms, symptom-​ related impairment, or possible
comorbid conditions. However, we caution the reader that
this focus is narrow and that much case conceptualiza-
tion and treatment planning for ADHD involves broader
54
54 Attention-Deficit and Disruptive Behavior Disorders
consideration of co-​occurring difficulties in child, family,
academic, or peer functioning. Pelham and colleagues
(2005), in their excellent review of evidence-​based assess-
ments for ADHD, offer a cogent and convincing argu-
ment that adaptations and impairments in functioning,
rather than ADHD symptoms per se, should form the
basis for treatment planning in ADHD. Thus, adequate
treatment planning for ADHD necessitates gathering and
integrating information far beyond symptom or diagnostic
status. Information from a variety of sources, regarding a
wide range of child and family functioning, is necessary
to inform treatments that match the needs and resources
of each child and family. For example, the clinician must
consider the child’s family, social and cultural context,
relevant medical and educational history and concerns,
the child’s and family’s goals for treatment, and available
treatment options. Although difficulties in domains such
as academics and social relationships are often closely
linked to ADHD (and may even be the result of ADHD
symptoms), assessment methodologies in these areas
are only briefly considered here. The parent–​child rela-
tionship or parenting style, the parent’s psychological or
marital functioning, and the child’s peer relationships or
self-​esteem are among the areas that might be considered
in a more comprehensive definition of treatment plan-
ning for ADHD.
We refer the reader to chapters within this volume
and to other excellent child assessment resources (Frick
et al., 2010; Mash & Barkley, 2007) for detailed informa-
tion regarding assessment of the problems and conditions
that are frequently associated with ADHD and that often
figure prominently in conceptualizing the problems and
planning treatment for children with this disorder. We
cannot state strongly enough how important these other
domains of assessment are in planning treatments for
children with ADHD that will be maximally sensitive
to the child’s and the family’s needs and concerns and
that will also hold the greatest potential for altering not
only the child’s current functioning but also long-​term
outcomes.
Overview of Measures for Case Conceptualization
and Treatment Planning
Broadband Checklists
Parent and teacher reports on broadband measures of
child psychopathology provide useful information in plan-
ning treatments for children with ADHD (see Table 4.2).
These measures provide insight into a range of difficulties,
in addition to ADHD, and may direct the clinician to
more in-​depth assessments of coexisting disorders or disor-
ders that may account for ADHD-​like symptoms. Scores
on these broadband measures also allow the clinician to
incorporate knowledge of potential comorbidities into
treatment planning as appropriate. For example, some
evidence suggests that behavioral treatments for ADHD
may have better outcomes among children with comor-
bid anxiety disorders (MTA Cooperative Group, 1999),
and behavioral treatments are empirically supported for
addressing the oppositional or conduct disorder problems
or both that are frequently comorbid with ADHD (e.g.,
Powell et al., 2014).
We include only broadband rating scales with sub-
scales specifically targeting ADHD symptoms or behav-
iors. These measures vary in the extent to which their
subscales map directly onto DSM ADHD criteria or
symptom dimensions. For example, both the Attention
Problems subscale of the Child Behavior Checklist and
the ADHD Index of the Conners 3 include a mixture
of inattention and impulsivity/​ hyperactivity items and
are not comprehensive in covering DSM symptoms.
Thus, these subscale measures typically cannot be sub-
stituted for the narrowband checklists described previ-
ously. However, the subscales relevant to attention or
hyperactivity–​ impulsivity found on many broadband
checklists will offer supplemental information that may
be useful in arriving at diagnostic decisions, particularly
in complex cases. Because the role of these broadband
measures in treatment planning is to provide a screening-​
level assessment of a range of behavior problems, we
require satisfactory psychometric properties at the level of
subscale scores (as well as total scores).
The parent (Children Behavior Checklist [CBCL])
and teacher (Teacher Report Form [TRF]) versions from
the Achenbach System of Empirically Based Assessment
(ASEBA; Achenbach & Rescorla, 2001) are well-​known and
widely used measures, available in several languages, that
have lengthy clinical and research traditions. A Youth Self-​
Report form is available for children aged 11 to 18 years,
but it is not described here. The parent and teacher check-
lists are used for children 6 to 18 years of age (a version for
younger children also is available), and norms are based
on large representative normative samples, as well as sam-
ples of clinic-​referred children (although norms specific
to different clinical diagnoses are not generally available).
There are 118 items, requiring 15  to 20 minutes to com-
plete, as well as subscales assessing competence (although
the psychometric properties of the competence subscales
are generally not as strong as the behavior problem scales).
 5

Attention-Deficit/Hyperactivity Disorder 55

Table 4.2  Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliabilitya Reliability Validity Validity Generalization Utility Recommended

Broadband Rating Scales

 ASEBA
  Parent: CBCL E G NA G G G E A ✓
  Teacher: TRF E E NA G G G E A ✓
  BASC-​3
  Parent E G NA A G G E A ✓
  Teacher E E NA A G G E A ✓
  Conners 3
  Parent E E NA G G G E A ✓
  Teacher E E NA G G G E A ✓
 Vanderbilt
  Parent G E NA A A G E A
  Teacher G E NA NR A G E A
Measures of Impairment
  VABS-​II
  Parent E E NA A G G G A ✓
  Teacher E E NA NR G G G A ✓
 CAFAS NR A E NR A G G A
 IRS
  Parent NR NR NA G A G A A
  Teacher G NR NA G A G G A ✓
 COSS
  Parent E E NA A G A G A ✓
  Teacher E E NA A G A G A ✓

a
  This column reflects inter-​rater agreement between clinical judges, and this information in not available for most measures where, instead, parent and
teacher agreement is more commonly assessed.
Note: ASEBA = Achenbach System of Empirically Based Assessment; CBCL = Child Behavior Checklist; TRF = Teacher Report Form; BASC-​3 = Behavior
Assessment System for Children-​3; Vanderbilt = Vanderbilt ADHD Diagnostic Parent and Teacher Rating Scales; VABS-​II = Vineland Adaptive Behavior
Scales, 2nd Edition; CAFAS = Child and Adolescent Functional Assessment Scale; IRS = Impairment Rating Scale; COSS = Children’s Organizational
Skills Scale; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.

The ASEBA provides empirically derived subscales that
are similar across the multiple informant versions of the
measure and assess a variety of emotional and behavior
problems, such as attention, rule breaking, and aggres-
sion. The measures also yield overall Internalizing and
Externalizing scores, as well as rationally derived subscales
that map onto DSM diagnostic categories. The similarity
in item content across informants allows for the calcula-
tion of inter-​rater agreements, and information is available
to compare levels of agreement to those in the normative
sample. Considerable validity evidence is presented in the
ASEBA manual, and numerous reviews provide additional
evidence of the convergent, discriminant, and content
validity of the measures (e.g., Frick et al., 2010; Gladman
& Lancaster, 2003; McConaughy, 2001; Pelham et  al.,
2005). As indicated in Table 4.2, both parent and teacher
versions have solid psychometric properties, and evidence
supports the incremental validity of gathering information
from both sources (e.g., Ang et al., 2012; Hanssen-​Bauer,
Langsrud, Kvernmo, & Heyerdahl, 2010). However, as
with many of the measures reviewed in this chapter, few
studies have examined the incremental validity or clinical
utility of ASEBA scores.
The Behavior Assessment System for Children, 3rd
Edition (BASC-​ 3; Reynolds & Kamphaus, 2015)  is a
multidimensional measure of adaptive and problem
behaviors that has teacher and parent versions for chil-
dren aged 6 to 11  years (as well as preschool and ado-
lescent versions not considered here). The measure takes
approximately 10 to 20 minutes to complete and has mul-
tiple language versions. The BASC-​3 provides rationally
derived clinical subscales including Hyperactivity and
Attention Problems, as well as a number of other problem
dimensions and composite scores for Adaptive Behavior,
Externalizing and Internalizing Problems, and a total
Behavioral Symptoms Index. The teacher version also has
scales related to School Problems. One advantage of the
BASC-​3 is that it offers validity checks to assist the clinician
56
56 Attention-Deficit and Disruptive Behavior Disorders
in detecting careless or untruthful responding, misunder-
standing, or other threats to validity. BASC-​3 norms are
based on a large representative sample and are available
both in aggregate form and differentiated according to
the age, gender, and clinical status of the child. As noted
previously, not only does this measure evaluate behavioral
and emotional problems but also it identifies the child’s
positive attributes, an aspect with obvious use in planning
treatment. Current psychometric information is available
in the measure’s manual (Reynolds & Kamphaus, 2015).
Given the relative recency of this measure, in some cases
in Table 4.2 we have relied on the psychometric infor-
mation available for earlier parent and teacher versions,
specifically the BASC-​ 2 (e.g., Kamphaus, Reynolds,
Hatcher, & Kim, 2004; Pelham et al., 2005; Sandoval &
Echandia, 1994).
The Conners 3 (Conners, 2008)  is the most recent
revision to a set of scales that have been closely allied with
research and clinical work in ADHD for many years. The
Conners 3 has multiple language versions and there are
parent and teacher versions (as well as a youth self-​report
not described here), each with both short (5 to 10 minutes)
and long (15 to 20 minutes) forms available. The short
forms focus on a range of behavior problems, whereas
the longer forms also include subscales assessing DSM
symptom criteria for ADHD and oppositional defiant and
conduct disorders, as well as screening and impairment
scales. Norms are based on a large representative sample
of 6-​to 18-​year-​old children and are also available for a
clinical sample. Norms are available for the genders com-
bined, with some scales also having gender-​specific infor-
mation. The Conners 3 manual and published reviews
of the measure outline the strong psychometric proper-
ties of both the current and earlier versions of the mea-
sure (e.g., Conners, 2008; Kao & Thomas, 2010; Pelham
et al., 2005).
Finally, the Vanderbilt ADHD Diagnostic Parent and
Teacher Rating Scales (Bard, Wolraich, Neas, Doffing, &
Beck, 2013; Wolraich et al., 1998, 2003; Wolraich, Bard,
Neas, Doffing, & Beck, 2013) are another DSM-​based set
of symptom rating scales that include ADHD symptoms,
oppositional and conduct problems, as well as anxiety and
depression items. Norms are based on a relatively large
sample, but of limited representativeness. Preliminary
psychometric evidence is available, although further vali-
dation is needed.
Other broadband questionnaires have been developed
that may prove useful in treatment planning for ADHD,
although these measures require further research. For
example, the Child Symptom Inventory-​4 (CSI-​4; Gadow
& Sprafkin, 2002) assesses a variety of DSM-​IV emotional
and behavioral disorders in children between ages 5 and
12 years. Although a DSM-​5 version of this scale is listed
on the authors’ webpage, this version has not been fully
evaluated.
Measures of Impairment
As noted previously, there is a growing and appropri-
ate focus on adaptive functioning as central to under-
standing and treating ADHD, with efforts underway to
develop a core set of ability and disability concepts rel-
evant to ADHD within the International Classification
of Functional Disability and Health (Schipper et  al.,
2015). Global and multidimensional measures of impair-
ment are valuable in a comprehensive assessment of the
functioning of children with ADHD. In particular, these
measures are likely to be useful in decisions regarding the
need for treatment and in identifying appropriate treat-
ment foci. We concur with arguments made by others
(e.g., Pelham et  al., 2005)  that impairments in adaptive
behavior must figure prominently in treatment planning
and monitoring for children with ADHD, more so than
absolute levels of ADHD symptoms. As noted in our
description of measures useful for diagnosis of ADHD,
several of these measures now include items tapping
impairment, although these are typically brief ratings.
Thus, currently, the clinician must choose between brief
or promising measures specific to ADHD (e.g., ADHD
Rating Scale-​5 impairment items) and well-​established
measures of adaptive behavior that are broad and may not
be particularly appropriate to ADHD-​related difficulties
(e.g., the Vineland Adaptive Behavior Scales; Sparrow,
Cicchetti, & Bala, 2005).
The Vineland Adaptive Behavior Scales, Second
Edition (VABS-​II; Sparrow et al., 2005) has been a lead-
ing measure of the personal and social skills needed for
everyday living. A 2016 revision of the measure (VABS-​3;
Sparrow, Cicchetti, & Saulnier, 2016) includes updated
items, forms, and norms. However, the revision is not yet
widely available nor used extensively in research; there-
fore, we focus our comments on the VABS-​II. Although
typically used to identify individuals with developmental
problems, some evidence supports the use the VABS in
groups of children with ADHD (e.g., Craig et al., 2015;
Ware et al., 2014). Consisting of a Survey Interview Form,
Parent/​Caregiver Rating Form, Expanded Interview
Form, and a Teacher Rating Form, the VABS-​II requires
20 to 60 minutes to complete. It is organized around four
behavior domains (communication, daily living skills,
 57

Attention-Deficit/Hyperactivity Disorder 57

socialization, and motor skills) and has demonstrated Observational Measures

strong psychometric properties. Norms for the parent and
Informal observations of children in clinical settings have
teacher rating scale forms are based on large representa-
little clinical utility in detecting ADHD or planning for
tive groups, including a variety of clinical groups, and the
its treatment (e.g., Edwards et al., 2005). However, more
reliability and validity of scores on the measure range from
structured observational measures do have potential
adequate to excellent, as reported in the manual (Sparrow
utility in treatment planning. Using such measures can
et al., 2005; see Table 4.2).
clearly identify a child’s ADHD symptoms and the impair-
The Child and Adolescent Functional Assessment
ments that ensue from these symptoms, which should be
Scale (CAFAS; Hodges & Wong, 1996)  is an additional
targeted in treatment plans. Unfortunately, despite vari-
multidimensional measure of impairment that may
ability in the psychometric information available, all the
serve as an aid in case conceptualization and treatment
measures located failed to demonstrate adequate levels of
planning for children with ADHD. The CAFAS uses
the criteria used for table inclusion. For example, these
interviewer ratings to assess a child’s (ages 7 to 17 years)
observational measures seldom have norms or report the
degree of impairment due to emotional, behavioral, or
temporal stability of scores. These limitations preclude
psychiatric problems. Consisting of 315 items and mea-
the inclusion of these measures in the tables; however, we
suring functioning in areas such as school, home, and
do offer some suggestions for available observational mea-
community and behaviors such as emotional regulation,
sures designed for classroom use or for assessing parent–​
self-​harm, and substance use, the CAFAS requires only
child interactions.
10 minutes to complete. Although normative data are not
The Direct Observation Form (DOF) is an observa-
available, reliability and validity information for this mea-
tional component of the ASEBA (Achenbach & Rescorla,
sure are generally satisfactory, as indicated in Table 4.2.
2001)  and uses a 10-​minute observation of the child’s
The Impairment Rating Scale (IRS; Fabiano et  al.,
behavior in a classroom context, recommended to be
2006)  was developed specifically to assess the areas of
repeated on three to six occasions. Although the measure
functioning that are frequently problematic for children
includes a narrative and ratings of the child’s behavior,
with ADHD. Parent and teacher versions are available in
psychometric information is reported primarily for the
the public domain, with questions pertaining to areas such
time sampling of 96 behaviors (the behaviors overlap with
as academic progress, self-​esteem, peer relations, problem
items on the CBCL and TRF). For normative compari-
behavior, impact on the family, and overall function-
sons, the DOF recommends that two nonproblem chil-
ing. Preliminary norms are available only for the teacher
dren be observed simultaneously with the target child in
version. Test–​retest reliability has been established over
order to provide individualized norms. Although the man-
periods up to 1 year. Within samples of ADHD and con-
ual also presents norms based on moderate-​size samples
trol children, convergent and discriminant validity have
of clinic-​referred and nonproblem children, the value of
been demonstrated, and evidence suggests that parent
these norms is likely to be limited by the variability across
and teacher IRS ratings accounted for unique variance
classroom contexts (e.g., variables such as classroom rules,
in predicting child outcomes beyond ADHD symptoms
physical structure, and ratio of problem to nonproblem
(Fabiano et al., 2006; see Table 4.2).
children will undoubtedly influence the rates of problem
A recent, useful addition to measures assessing dif-
behaviors displayed by children). The manual reports
ficulties related to ADHD, particularly in the academic
moderate to high levels of inter-​rater reliability using the
domain, is the Children’s Organizational Skills Scales
DOF, and DOF scores correlate in expected ways with
(COSS; Abikoff & Gallagher, 2009). With parent,
other measures and with clinical status (Achenbach &
teacher, and child (not reported here) versions, this
Rescorla, 2001). In combination with an ASEBA form
measure taps children’s difficulties with task planning,
used to facilitate observations of child behavior in psy-
organized actions, and memory and materials manage-
chological test situations (the Test Observation Form),
ment, and also includes questions specifically measuring
some evidence points to the ability of these observations
the impairment caused by these organizational difficul-
to assess unique variance in child behavior beyond parent
ties. The measure has good psychometric properties,
or teacher ratings (McConaughy et al., 2010).
and norm information is available based on a large,
Another potential measure useful in tapping the
representative sample. Thus, it will offer useful informa-
classroom difficulties of children with ADHD is the
tion, particularly for assessing and planning for school
Behavioral Observation of Students in Schools (BOSS;
interventions.
58
58 Attention-Deficit and Disruptive Behavior Disorders
Shapiro, 2011). This measure, with many computerized
and interactive features, taps task engagement and off-​
task behaviors (both inattentive and hyperactive) during
classroom activities. Evidence of inter-​rater reliability is
provided (although several hours of training are required),
and the observations have been shown to discriminate
between children with ADHD and typically developing
classmates (DuPaul et al., 2004).
To assess aspects of ADHD that are problematic
within parent–​child interactions, a number of observa-
tional systems developed in research contexts are avail-
able, although most are too complex to provide reliable
estimates in clinical practice. Perhaps one exception to
this is the Behavioral Coding System (BCS; McMahon
& Forehand, 2003). Using the BCS, the clinician codes
parent and child behaviors in two 5-​minute interactions: a
free-​play situation and a situation in which the parent
directs the interaction. The presence of six parent behav-
iors (rewards, commands, time out, etc.) and three child
behaviors (compliance, noncompliance, etc.) is recorded
every 30 seconds, and the sequence of behaviors speci-
fying parental antecedents, child responses, and paren-
tal consequences can be analyzed. Such information is
readily translated into treatment goals, particularly for
behavioral treatments. Interobserver agreement and test–​
retest reliability of the BCS are adequate, and the system
is sensitive to differences in compliance between clinic-​
referred and nonreferred children (evidence reviewed in
McMahon & Forehand, 2003).
Finally, we highlight that observations of individual-
ized behavioral targets, by parents or teachers, are likely to
be useful in conceptualizing and planning for treatment
of each child’s difficulties. For example, with clear and
simple behavioral definitions, frequency counts of prob-
lematic behaviors that are relevant for each particular
child (e.g., times out of seat in the classroom and failure
to complete assigned household chores) can be made and
may serve as an integral part of treatment planning.
Overall Evaluation
Broadband parent and teacher checklists provide essen-
tial information regarding behavior problems that may
accompany or result from ADHD and which may inform
treatment planning. These measures are typically well
developed, possess solid psychometric properties, and
the clinician can feel confident in the information they
provide. However, even more relevant information for
treatment planning is likely to be derived from assess-
ment of the child’s functioning and impairments in daily
home and classroom situations. Emerging measures
of impairment, particularly those designed to be sensi-
tive to the aspects of functioning most closely linked to
ADHD, have clear potential in identifying appropriate
treatment targets and assisting the clinician in prioritiz-
ing these targets. In a similar fashion, the context-​specific
and objective nature of observational assessments of the
child’s behavior, both in school and at home, have great
potential for treatment planning. These measures may
also assess environmental antecedents and consequences
of the child’s behaviors, yielding information of immedi-
ate relevance to the planning of behavioral interventions.
An important future direction in the development of any
of these assessment measures will be to work to estab-
lish their incremental validity and clinical utility within
the context of multiple sources and types of assessment
information.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT EVALUATION
In conducting assessments to monitor and evaluate
treatment implementation or progress in children with
ADHD, there is a need for measures that are reliable
over time, sensitive to relatively small changes in behav-
ior or symptoms, and practical to use on a frequent basis
(e.g., brief and inexpensive). In monitoring medication
treatments, measurement of side effects also is recom-
mended (e.g., Barkley Side Effects Rating Scale; Barkley
& Murphy, 2006), although standardized measures for
this purpose are not available. One prominent issue in
considering assessment measures to be used in treat-
ment monitoring is the stability of scores over time and
the vulnerability of measures to the effects of repeated
assessments (Solanto & Alvir, 2009). For example, does
a decrease in symptom severity on a measure over time
reflect the benefits of treatment, or could the change
be predicted solely on the basis of regression of scores
to the mean? If treatment effects are to be assessed over
a longer period, the availability of age norms also will
be important in order to place score changes within the
appropriate context of developmental changes in the
behavior. As with disagreements in diagnostic informa-
tion gathered from multiple sources, discrepancies in
reports of treatment-​related changes in child behaviors
are expected across informants and settings. Again, cli-
nicians must struggle with how to combine or prioritize
the multiple bits of information in reaching an overall
conclusion regarding the progress of treatment.
 59
In this section, we consider measures that have dem-
onstrated not only basic psychometric properties but also
sensitivity to change due to medication, psychosocial
interventions, or both. Although several measures meet
these criteria, almost all of the evidence of this sensitiv-
ity is derived from studies aggregating across groups of
children, and information regarding performance of
the measures in individual cases awaits investigation.
Furthermore, it is common in research studies to amal-
gamate multiple measures into composite scores to cre-
ate more reliable scores for use in treatment comparisons
(e.g., MTA Cooperative Group, 2004). Although advan-
tageous from a research perspective, this approach limits
the ability of such studies to inform us regarding the sensi-
tivity to treatment of any of the measures used in isolation
or with individual children.
Overview of Measures for Treatment Monitoring
and Treatment Evaluation
Narrowband ADHD Checklists
No evidence of treatment sensitivity has yet been pub-
lished based on either the ADHD Rating Scale-​5 or the
Conners 3 DSM-​IV-​TR Symptom Scales. However, for
the ADHD Rating Scale-​5, evidence from the ADHD-​
IV Rating Scale version (relatively unchanged) indicates
sensitivity to medication treatment, at a group level, in
numerous studies (e.g., Huss et  al., 2016; Kollins et  al.,
2011). Other symptom-​level measures, although lacking
in some psychometric characteristics, may bear consid-
eration for treatment monitoring depending on the spe-
cific clinical needs of each case. For example, the IOWA
(Loney & Milich, 1982)  is a 10-​item measure derived
from an older version of the Conners’ Teacher Rating
Scale that assesses inattentive–​overactive and aggressive
symptoms. Considerable evidence supports the construct
validity, internal consistency, and stability of scores on the
measure (Johnston & Pelham, 1986; Loney & Milich,
1982; Nolan & Gadow, 1994; Waschbusch & Willoughby,
2008). At a group level, the measure has been proven use-
ful in multiple studies assessing the effectiveness of medi-
cation treatments for ADHD (e.g., Maneeton, Maneeton,
Intaprasert, & Woottiluk, 2014).
The BASC-​3 Flex Monitor (Reynolds & Kamphaus,
2016), which includes items tapping behaviors associated
with ADHD (as well as other problems), was designed
to allow frequent and individually tailored assessment to
monitor effectiveness of treatments for ADHD. Teacher,
parent, and child forms are available, with digital versions
Attention-Deficit/Hyperactivity Disorder 59
and graphical depiction of change in a child’s scores over
time. Normative performance on the Monitor can be
estimated from the BASC norms. Unfortunately, despite
being developed with the explicit purpose of treatment
monitoring, there is little published evidence of the valid-
ity of the scale for this purpose. A  similar measure, the
SKAMP (Swanson, 1992), is a brief 10-​item scale assess-
ing academic impairment related to inattention and dis-
ruptive behavior. Murray and colleagues (2009) reported
means and standard deviations for the measure from a
large sample, divided by gender, ethnicity, and grade level,
and documented good internal consistency. Satisfactory
single-​
day stability also has been demonstrated (e.g.,
Wigal, Gupta, Guinta, & Swanson, 1998). The SKAMP
has repeatedly demonstrated sensitivity to the effects of
medication or combined medication and psychosocial
treatment (e.g., Greenhill et al., 2001; Manos et al., 2015;
Wigal et  al., 2014). Unfortunately, the SKAMP is not
widely or easily accessible.
Broadband Checklists
As indicated in Table 4.3, the parent and teacher versions
of the ASEBA have demonstrated sensitivity to behavioral,
medication, and combined interventions for children with
ADHD or disruptive behaviors (e.g., Ialongo et al., 1993;
Kazdin, 2003; Masi et al., 2016; Wang, Wu, Lee, & Tsai,
2014). Earlier versions of the Conners 3, both parent and
teacher forms, have consistently demonstrated sensitivity
to medication treatments for children with ADHD (e.g.,
Gadow, Sverd, Sprafkin, Nolan, & Grossman, 1999; Weiss
et al., 2005), and some evidence supports their sensitivity
to behavioral interventions as well (e.g., Horn, Ialongo,
Popovich, & Peradotto, 1987; Pisterman et al., 1989).
Measures of Impairment
Among the measures of impairment, the CAFAS has
demonstrated sensitivity to behavioral or mental health
interventions, in both general and ADHD samples, with
generally adequate psychometric properties as indicated
in Table 4.3 (e.g., Puddy, Roberts, Vernberg, & Hambrick,
2012; Timmons-​Mitchell, Bender, Kishna, & Mitchell,
2006). However, this sensitivity has not been examined
specifically within ADHD samples. Both the IRS (Fabiano
et al., 2006) and the Weiss Functional Impairment Rating
scale (Weiss et al., 2005; available online at http://​naceon-
line.com/​AdultADHDtoolkit/​assessmenttools/​wfirs.pdf)
have demonstrated evidence of treatment sensitivity, for
both behavioral and medication treatments, specifically
60

60 Attention-Deficit and Disruptive Behavior Disorders

Table 4.3  Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliabilitya Reliability Validity Validity Generalization Sensitivity Utility Recommended

Narrowband ADHD Rating Scales

  ADHD Rating Scale-​5
  Parent E E NA G A G E E A ✓
  Teacher E E NA G A G E E A ✓
 IOWA
  Parent A G NA A A G G G A
  Teacher A G NA A A G G G A
Broadband Rating Scales
 ASEBA
  Parent: CBCL E G NA E G G E E A ✓
  Teacher: TRF E E NA G G G E E A ✓
  Conners 3
  Parent E E NA G G G E E A ✓
  Teacher E E NA G G G E E A ✓
Measures of Impairment
 CAFAS NR A E NR A G G G A
 IRS
  Parent NR NR NA G A G A E A
  Teacher G NR NA G A G G E A ✓
 Weiss A G NA A NR A A E A ✓

a
  This column reflects inter-​rater agreement between clinical judges, and this information in not available for most measures where, instead, parent and
teacher agreement is more commonly assessed.
Note: ASEBA = Achenbach System of Empirically Based Assessment; CBCL = Child Behavior Checklist; TRF = Teacher Report Form; CAFAS = Child
and Adolescent Functional Assessment Scale; IRS  =  Impairment Rating Scale; Weiss  =  Weiss Functional Impairment Rating Scale; A  =  Adequate;
G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.

in samples of children with ADHD (Hantson et al., 2012;
Owens, Johannes, & Karpenko, 2009; Stein et al., 2015;
Waxmonsky et  al., 2010). Both measures have a parent
version, and the IRS also has a teacher version, which is
useful in assessing intervention effects within the class-
room. The COSS does appear to be sensitive to classroom
interventions (Abikoff et  al., 2013); however, as yet, no
independent replications of this sensitivity are available.
Observational Measures
As noted previously, observational measures may be use-
ful in treatment planning, and similar to the procedures
of a daily report card, such observations can yield ongo-
ing assessment of treatment progress and documentation
of treatment outcome. For example, frequency counts of
problematic behavior in either home or school contexts
that are individualized for each child have an obvious util-
ity in monitoring treatment and guiding decisions regard-
ing needed changes in regimens. Such observations have
proven sensitive to the effects of both medication and
behavior management strategies (Pelham et  al., 2005),
and evidence suggests that functional assessments with
observable targets improve treatment effectiveness (Miller
& Lee, 2013). Structured parent–​child interaction obser-
vational measures, such as the BCS, have demonstrated
sensitivity to the effects of behavioral parent training (evi-
dence reviewed in McMahon & Forehand, 2003). Despite
the clear relevance of these observational measures for
assessing treatment-​related change, the advantages of these
measures are combined with a lack of information regard-
ing expected normative changes in scores over time and a
lack of traditional validity evidence (Kollins, 2004).
Overall Evaluation
As with measures useful for treatment planning, the
measures with the strongest psychometric properties
(i.e., ADHD symptom scales and broadband checklists),
although potentially useful in monitoring treatment out-
comes, are more limited in their ability to assess details
of each child’s impairments or to be sensitive to the rela-
tively rapid changes in child behavior that are common
in medication and behavioral interventions. In addition,
 61
the length of the broadband checklists is often prohibitive
for repeated assessments. Clinicians are advised to give
careful consideration to supplementing these measures
with others that may more directly assess the child’s daily
functioning (e.g., impairment scales or observational
measures), with appropriate caution in the use of these
measures due to their psychometric limitations. Clinical
research is urgently needed to expand the evidence of the
reliability and validity of scores on these measures and,
most important, to provide empirical support for the clini-
cal utility they are assumed to possess.
ASSESSMENT OF ADHD IN ADULTHOOD
Evidence supporting the lifespan persistence of ADHD
symptoms is strong (e.g., Turgay et  al., 2012), and the
DSM-​ 5 made revisions explicitly designed to address
assessment issues within the adult population. Specifically,
symptom examples were provided that are more appro-
priate for adults (e.g., feelings of restlessness rather than
overt motor activity and forgetful in paying bills or keep-
ing appointments) and, reflecting the normative decrease
in symptoms across age, only five symptoms of either
inattention or hyperactivity–​impulsivity are required for a
diagnosis in adulthood.
Assessment of ADHD in adulthood presents some
challenges that overlap with those present in child assess-
ments, but also some that are unique to the adult stage.
As in childhood, it is important that multiple sources of
information be considered in the assessment of symp-
toms. In contrast to childhood, in adulthood there is a
reliance on self-​reports as one source of information, and
these are considered alongside the perceptions of others
who know the individual well (e.g., a spouse). However,
as in childhood, the reports from these different sources
seldom converge completely (e.g., Barkley, Knouse, &
Murphy, 2011). Moreover, not only are there few guide-
lines for how to reconcile these reports in adulthood com-
pared to childhood, but also there are greater obstacles
to obtaining useful perceptions from other informants
(e.g., there is no close other available or the client may be
reluctant to consent to the gathering of this information).
ADHD in adults, as in children, is highly comorbid with
a range of other disorders (Kooij et al., 2012), and form-
ing clear, differential diagnoses is often a challenge. More
so than in childhood, the possibility of adults overreport-
ing symptoms, perhaps in order to receive special services
or dispensations, also must be considered (e.g., Sollman,
Ranseen, & Berry, 2010). Finally, although emerging
Attention-Deficit/Hyperactivity Disorder 61
evidence suggests the possibility that ADHD can arise in
adults who were not so diagnosed in childhood (Moffitt
et  al., 2015), the prevailing view continues to be con-
sistent with that of DSM-​5, which requires evidence of
an onset of symptoms and impairment prior to the age
of 12 years to substantiate an ADHD diagnosis. Thus, in
assessing ADHD in adults, evidence must be gathered
regarding the childhood occurrence of symptoms/​impair-
ment, and again, multiple sources of information (e.g.,
self-​reports, reports from parents or siblings, and school
records) are expected to provide the best approximation
of this information.
Several measures are available to assess current and ret-
rospective reports of ADHD symptoms in adults, although
few are well developed or, as yet, widely used. We have
focused our comments on the most recent, most widely
studied, and most easily accessible of these. One set of
measures, useful for diagnosis, case conceptualization,
and treatment monitoring, has been developed by Russell
Barkley. The set includes both self-​and other-​reports, for
both symptoms and impairment, in both adulthood and
retrospectively for childhood. The Barkley Adult ADHD
Rating Scale-​IV (BAARS; Barkley, 2011a) contains both
self-​and other-​reports of adult and childhood symptoms
as well as single-​item measures of age of symptom onset
and yes/​no assessments of impairment in four domains.
The items were developed to map onto DSM criteria, and
an additional nine items were added to tap the newer con-
struct of sluggish cognitive tempo (concentration deficit
disorder). Norms, based on a large sample representative
of the US population, exist for the self-​report versions of
the scale (allowing calculation of age-​referenced percen-
tile scores). Norms for the other-​report versions are not
available. The BAARS-​IV yields scores for Inattention,
Hyperactivity, Impulsivity, as well as sluggish cognitive
tempo, and a screener version using the items that best
discriminate clinic-​referred adults with ADHD from com-
munity and psychiatric controls also is available. The sub-
scale and total scores demonstrate internal consistencies
in the .78 to .90 range and 2-​to 3-​week test–​retest reliabili-
ties in the .66 to .88 range. Across a number of studies,
scores on the BAARS-​IV have demonstrated convergent
validity with other measures of adult ADHD symptoms
(Kooij et al., 2008) and with a range of occupational and
relationship outcomes (Barkley, 2011a). Versions of the
BAARS-​IV for use in non-​US populations also have been
presented (e.g., Vélez-​Pastrana et  al., 2016). Finally, the
BAARS-​IV has been used successfully to monitor out-
comes of both psychosocial (Safren et al., 2010) and medi-
cation (Spencer et al., 2007) treatments for adult ADHD.
62
62 Attention-Deficit and Disruptive Behavior Disorders
The clinical utility of the measure is enhanced by a pub-
lisher policy that grants limited permission to make copies
of the measure from the manual.
Similar ADHD symptom checklists for adults include
the Adult ADHD Rating Scale, developed in conjunc-
tion with the World Health Organization (Kessler et al.,
2005)  and available online (https://​www.hcp.med.har-
vard.edu/​ncs/​asrs.php), and the Conners Adult ADHD
Rating Scale (Conners et al., 1999), which includes long,
short, and screener forms and is normed with satisfactory
psychometric information.
Beyond self-​and other-​reported rating scales, clinical
interviews specific to adult ADHD also have been devel-
oped and may be useful for diagnostic purposes. These
include the Conners Adult ADHD Diagnostic Interview
for DSM-​IV (CAADID-​IV; Epstein, Johnson, & Conners,
2001) and the Diagnostic Interview for ADHD in Adults
(DIVA 2.0; Kooij, 2013), which is available online (http://​
www.divacenter.eu/​DIVA.aspx?id=499). Both measures
assess DSM symptoms of ADHD and, as is typical of
diagnostic interviews, neither is normed. Preliminary
evidence of inter-​rater reliability and convergent/​predic-
tive validity is available for both measures (e.g., Kooij,
2013; Solanto, Wasserstein, Marks, & Mitchell, 2012).
The DIVA 2.0 is available in several languages, free of
charge, and includes a computer application to facilitate
ease of administration and scoring. The CAADID-​IV is
composed of two parts. The first portion covers develop-
mental and demographic history, including comorbidities
and psychosocial stressors, and can be completed as a self-​
report measure prior to review with the clinician. The sec-
ond part covers both adult and childhood symptoms, with
useful prompts and adult-​appropriate symptom examples
provided to guide the assessment. Impairment, pervasive-
ness, and age of onset are assessed.
Assessment of the impairments associated with ADHD
symptoms is critical, particularly for case conceptualiza-
tion, and sometimes for treatment monitoring. Several of
the rating scales and interview measures described pre-
viously incorporate the assessment of impairment, given
its role in diagnostic criteria, and, as for children, efforts
are underway to develop a core set of concepts relevant
to adult ADHD for the International Classification of
Functioning, Disability and Health (Schipper et al., 2015).
Currently, assessment of impairment associated with
ADHD can be undertaken with the Barkley Functional
Impairment Scale (BFIS; Barkley, 2011b). This mea-
sure, developed to reflect a clearly defined construct of
psychosocial impairment, has both self-​and other-​report
forms. The self-​report version has norms derived from
the same representative normative sample used for the
BAARS-​IV. The BFIS items cover 15 domains of func-
tioning (e.g., home, community, occupational, and daily
responsibilities), and ratings load on a single factor with
strong internal consistency (alpha  =  .97) and test–​retest
reliability (r = .72). Evidence for convergent and discrimi-
nant validity is presented (e.g., correlations with symptom
severity, disability status, and clinical group membership).
Of course, in addition to impairment, as with children,
assessment of a range of possible comorbid conditions
and other aspects of functioning is critical in forming a
comprehensive case formulation of ADHD in adults,
and these constructs also may be important in monitor-
ing treatment progress. Given the nascent nature of the
adult ADHD assessment literature, we do not review such
measures here, but we encourage clinicians to follow
sound clinical practice guidelines (e.g., those provided by
the European Consensus on Adult ADHD, the National
Institute for Health and Care Excellence [NICE] from
the United Kingdom, or the Canadian ADHD Resource
Alliance).
CONCLUSIONS AND FUTURE DIRECTIONS
A multitude of tools for assessing ADHD across the lifes-
pan are available, both commercially and in the public
domain, and new additions emerge regularly. In contrast
to this abundant quantity of measures, few measures are
available that possess substantial research on their psy-
chometric qualities or that have been validated for uses
beyond diagnostic questions. In this final section of the
chapter, we draw attention to prominent unanswered
questions regarding assessments for ADHD diagnoses
and for treatment planning and monitoring. We again
note that our focus on assessment measures should not
overshadow the fact that the process of assessing an indi-
vidual with ADHD involves much more than simple
administration of a standard set of measures. Clinicians
must make client-​specific decisions regarding which mea-
sures are best suited for each individual client and family
(e.g., Is this child represented in the measure’s normative
group?), at which point in the assessment process (e.g., Is
the measure needed primarily for assigning a diagnosis or
for monitoring the child’s response to a new medication?),
and how information from multiple sources and measures
is best combined to answer the assessment question (e.g.,
Is a sibling an adequate reporter of childhood symptoms
in an adult client?). In addition, information derived from
the measures presented here must be supplemented with
 63
clinical judgments regarding each individual’s situation
and context (e.g., cultural factors) and must be employed
within the context of a caring and supportive therapeutic
relationship between clinician and client.
In diagnosing ADHD, the use of unstructured inter-
views as a guide for identifying general areas of con-
cern (in terms of both ADHD and comorbid disorders),
developmental and treatment history, and information
specific to the client’s circumstances remains common,
despite the known limitations of this assessment method.
Further efforts to develop and evaluate more structured
and semi-​structured tools that could couple the gather-
ing of this information in a systematic manner with a
sensitivity to individual client differences and the need
to establish a strong working relationship between clini-
cian and client would be clinically valuable. Similarly,
although a few standardized measures with adequate
psychometric properties have proven their value in plan-
ning and monitoring treatment progress in children, the
most promising measures in this area originate from a
behavioral perspective but lack standardization, norm
development, and broad psychometric evaluation. We
believe that these measures have the greatest potential
for enhancing the selection of appropriate treatment tar-
gets for children with ADHD and for providing careful,
continuous, and objective feedback regarding treatment
progress. However, one cannot ignore the inadequacies
of these measures in terms of traditional psychomet-
ric properties. Continued research is much needed to
address these limitations and to develop and test clini-
cally useful measures appropriate to assessing and moni-
toring change in the functional impairments that form
the core of ADHD treatment planning. Technological
advances, such as online data collection platforms, com-
puterized scoring and reporting templates, and portable
recording options, offer exciting possibilities in moving
forward with the development of assessment tools, but
they are perhaps particularly applicable within the realm
of treatment monitoring.
Turning to the more common and psychometrically
tested assessment methods commonly used in diagnosis,
particularly rating scales, consensus appears to be that
for both children and adults, information from multiple
informants and contexts is necessary (e.g., Barkley, 2011a;
Pelham et al., 2005). What is now needed is greater con-
centration on evaluating methods for combining this
information and establishing the relative incremental
validity of different informants and contexts. Similarly,
much further research is needed to clarify the relative mer-
its of different assessment methods (e.g., symptom-​specific
Attention-Deficit/Hyperactivity Disorder 63
rating scales, structured interviews, and observations) for
arriving at diagnostic or treatment decisions. We know
exceptionally little about which types of information are
the most crucial in determining which types of assessment
and treatment to administer. To maximize the extent to
which our assessments can boast of being both evidence-​
based and cost-​effective, research with a clear focus on
the clinical utility or incremental validity of how each
piece of assessment information fits (or does not) within
the puzzle of an optimally designed assessment process
for ADHD is urgently needed.
Beyond the need to refine the measures and process
of assessing ADHD, we have been struck by two signifi-
cant gaps that exist in this area. First, there often appears
to be a disconnect between assessments of ADHD diag-
noses and assessments with greater relevance to the
treatment of the disorder. As we have repeatedly noted,
among individuals referred with ADHD, it is often the
case that the most pressing clinical problems are those
related to functional impairments (e.g., in interpersonal
relationships or academic/​vocational functioning) or to
comorbid conditions (e.g., learning problems or depres-
sion). Symptom severity, the target of diagnostic assess-
ment, is clearly related to these impairments but not
synonymous with them. Knowledge of an individual’s
level of ADHD symptoms offers little treatment guidance
because changes in these symptom levels may not mir-
ror changes in the functional problems that instigated
help-​seeking. Second, as in many areas, there remains a
significant gap between research on ADHD assessment
and treatment and the delivery of these services outside
of research settings. The dissemination and uptake of the
most evidence-​based assessment tools (and treatments)
lags woefully behind the advancing scientific knowledge.
Recent work in the development and evaluation of clini-
cal care pathways for ADHD offers an important bridge
over this gap (e.g., Carroll et al., 2013; Coghill & Seth,
2015; Vander Stoep et al., 2017) and holds promise as a
future direction in improving the assessment (and subse-
quent treatment) of ADHD.
In closing, we acknowledge a number of resources rel-
evant to the assessment of ADHD and refer clinicians to
these resources for additional guidelines and information
useful in this endeavor. Recent books by Barkley (2015)
and Anastopoulos and Shelton (2001) provide excel-
lent coverage of assessment issues in ADHD. Clinical
guidelines for assessing ADHD have been provided
by the American Academy of Pediatrics (2011) and the
American Academy of Child and Adolescent Psychiatry
(2007). Pelham and colleagues’ (2005) contribution on
64
64 Attention-Deficit and Disruptive Behavior Disorders
evidence-​based assessment for ADHD continues to be an
excellent resource. We trust that this chapter, along with
these additional resources, provides the clinician with
an overview of the issues prominent in the assessment of
ADHD and with a guide to currently available and useful
measures.
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 71
Child and Adolescent Conduct Problems
Paul J. Frick
Robert J. McMahon
Conduct problems (CP) in youth are one of the most com-
mon reasons that children and adolescents are referred
to mental health clinics (Kimonis, Frick, & McMahon,
2014). This is not surprising given that CP often causes
significant disruptions for the child at home and school,
and it is the form of psychopathology that has been most
strongly associated with delinquency and violence (Odgers
et al., 2007). An extensive body of research has led to an
increased understanding of the many processes that may
be involved in the development of severe CP (Frick &
Viding, 2009). This research has many important implica-
tions for designing more effective interventions to prevent
or treat these problems (Conduct Problems Prevention
Research Group, 2000; Frick, 2012)  and for improving
the methods for assessing children and adolescents with
severe CP (McMahon & Frick, 2005). The focus of this
chapter is on the implications for assessment.
In the next section, we provide a brief overview of sev-
eral key findings from research on CP in children and
adolescents and highlight several findings that we believe
have the most direct relevance to the assessment process.
Specifically, we focus on research illustrating the great
heterogeneity in the types, severity, and course of CP in
youth, as well as the frequent co-​occurring problems in
adjustment that often accompany CP. We also summarize
research showing important dispositional and contextual
risk factors that have been related to CP and that could play
an important role in the development or maintenance of
CP. We then review some recent causal models that have
been proposed to explain how these many risk factors could
affect the development of the child and lead to CP.
After the brief overview of these select but critical areas
of research, we then focus on the implications of this
research for three types of assessments that are often con-
ducted for children with CP. First, we focus on methods
71
for determining whether the level of CP is severe, impair-
ing, and developmentally inappropriate enough to be con-
sidered “disordered” and in need of treatment. Second, we
focus on assessments that can be used for developing case
conceptualizations, which can guide comprehensive and
individualized treatment plans for children with CP. Using
comprehensive interventions that rely on multiple compo-
nents tailored to the child’s individual needs has proven to
be most effective for treating children and adolescents with
CP (Conduct Problems Prevention Research Group, 2000;
Frick, 2012). Third, we focus on measures that can be used
to monitor and evaluate treatment progress and outcomes.
Unfortunately, the availability of measures for this crucial
assessment purpose is quite limited.
After summarizing research on CP and its implica-
tions for assessment, we conclude this chapter with a
section highlighting some overriding issues related to
assessing children with CP, such as the need to assess chil-
dren with multiple measures that provide information on
their adjustment in multiple contexts. We also provide a
summary of some of the major limitations in the existing
assessment technology and make recommendations for
future work to overcome these limitations.
THE NATURE OF CP
Types and Severity of CP and Common
Co-​Occurring Conditions
CP constitutes a broad spectrum of “acting-​out” behaviors,
ranging from relatively minor oppositional behaviors such
as yelling and temper tantrums to more serious forms of
antisocial behavior such as physical destructiveness, steal-
ing, and physical violence. There have been numerous
72
72 Attention-Deficit and Disruptive Behavior Disorders
methods used to divide CP into more discrete and homo-
geneous types of behaviors (for comprehensive reviews,
see Frick & Marsee, 2006; Kimonis, Frick, & McMahon,
2014). For example, the fifth edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-​5;
American Psychiatric Association [APA], 2013)  includes
CP in the category of disruptive, impulse control, and
conduct disorders. The DSM-​ 5 makes a distinction
between the categories of oppositional defiant disorder
(ODD) and conduct disorder (CD). ODD is a pattern of
angry/​irritable (e.g., often loses temper), argumentative/​
defiant (e.g., defying or not complying with grown-​ups’
rules or requests), and vindictive (e.g., has been spite-
ful or vindictive) behaviors. CD consists of more severe
antisocial and aggressive behavior that involves serious
violations of others’ rights or deviations from major age-​
appropriate norms. The behaviors are categorized into
four groups:  aggressiveness to people and animals (e.g.,
bullying and fighting), property destruction (e.g., fire-​set-
ting and other destruction of property), deceptiveness or
theft (e.g., breaking and entering, stealing without con-
fronting victim), and serious rule violations (e.g., running
away from home or being truant from school before age
13 years).
In addition to this division in the DSM-​5, factor analy-
ses have resulted in another method for differentiating
among types of CP. In a meta-​analysis of more than 60
published factor analyses, Frick et  al. (1993) found that
CP could be described by two bipolar dimensions. The
first dimension was an overt–​covert dimension. The overt
pole consisted of directly confrontational behaviors such
as oppositional defiant behaviors and aggression. In con-
trast, the covert pole consisted of behaviors that were
nonconfrontational in nature (e.g., stealing and lying; see
also Tiet, Wasserman, Loeber, Larken, & Miller, 2001;
Willoughby, Kupersmidt, & Bryant, 2001). The second
dimension divided the overt behaviors into those that were
overt-​destructive (aggression) and those that were overt-​
nondestructive (oppositional), and it divided the covert
behaviors into those that were covert-​destructive (property
violations) and those that were covert-​nondestructive (sta-
tus offenses; i.e., those behaviors that are illegal because
of the child’s or adolescent’s age). One way in which this
clustering of CP is useful is that the four symptom patterns
are fairly consistent with the distinctions made in many
legal systems for differentiating types of delinquent behav-
iors, which generally distinguish between violent offenses
(overt-​destructive), status offenses (covert-​nondestructive),
and property offenses (covert-​destructive; e.g., Office of
Juvenile Justice and Delinquency Prevention, 1995).
Two specific forms of CP—​ noncompliance and
aggression—​deserve additional attention. Noncompliance
(i.e., excessive disobedience to adults) appears to be
important as one of the earliest predictors of the devel-
opment of CP, and it seems to play an important role
in many of the subsequent academic and social prob-
lems exhibited by children with CP (Chamberlain &
Patterson, 1995; McMahon & Forehand, 2003). Most
important, however, research has shown that when child
noncompliance is improved as a result of intervention,
there is often concomitant improvement in other CP
behaviors and a subsequent reduction in later risk for CP
(e.g., Russo, Cataldo, & Cushing, 1981; Wells, Forehand,
& Griest, 1980).
There is also evidence that aggression is an impor-
tant dimension of CP (Burt, 2013). By its very nature,
aggression results in harm to another child (Crick &
Dodge, 1996). Furthermore, research has consistently
shown that aggressive behavior in children and ado-
lescents is often quite stable after the preschool years
(Broidy et  al., 2003). Importantly, research has found
that there appears to be several different forms of aggres-
sive behavior (Crick & Dodge, 1996; Poulin & Boivin,
2000). The first type of aggression is often referred to
as retaliatory aggression, hostile aggression, or reactive
aggression, in which aggression is viewed as a defensive
reaction to a perceived threat and is characterized by
anger and hostility (Little, Jones, Henrich, & Hawley,
2003). The second type of aggressive behavior is gener-
ally unprovoked and is used for personal gain (instru-
mental) or to influence and coerce others (bullying and
dominance). This type of aggressive behavior is referred
to as instrumental aggression, premeditated aggression,
or proactive aggression (Poulin & Boivin, 2000).
Importantly, although these different types of aggres-
sion are often correlated (e.g., correlations ranging from
r = .40 to .70 in school-​aged samples; Little et al., 2003),
studies have consistently documented different correlates
to the two forms of aggression (for reviews, see Dodge &
Pettit, 2003; Marsee & Frick, 2010). For example, reac-
tive but not proactive aggression has been consistently
linked to a tendency to misinterpret ambiguous behaviors
as hostile provocation (Crick & Dodge, 1996; Hubbard,
Dodge, Cillessen, Coie, & Schwartz, 2001) and to poorly
regulated responses to emotional stimuli (Marsee & Frick,
2007; Vitaro, Brengden, & Tremblay, 2002). In contrast,
proactive but not reactive aggression has been associated
with the tendency to view aggression as an effective means
to reach goals (Crick & Dodge, 1996) and with reduced
levels of emotional reactivity (i.e., skin conductance and
 73
heart rate acceleration; Hubbard et  al., 2002; Muñoz,
Frick, Kimonis, & Aucoin, 2008).
In addition to proactive and reactive forms of aggres-
sion, both of which are overt in nature, several research-
ers have identified a form of indirect aggression, called
relational aggression, that involves strategies that attempt
to harm another child through harming his or her social
relationships (Marsee & Frick, 2010). These behaviors
include excluding a child from groups, rumor spreading,
and friendship manipulation. Several studies have shown
that when girls behave aggressively, they are more likely
to use relational aggression than overt aggression (e.g.,
Crapanzano, Frick, & Terranova, 2010; Marsee et  al.,
2014). Furthermore, research has suggested that it may
be possible to divide relational aggression into instrumen-
tal and reactive forms, similar to overt aggression (Little
et  al., 2003; Marsee et  al., 2014). Importantly, children
who show relational aggression show many of the same
social (e.g., peer rejection) and dispositional (e.g., impul-
sivity and callousness) risk factors as physically aggressive
youth (Marsee et al., 2014).
Epidemiology of CP
A meta-​analysis of epidemiological studies estimated that
the worldwide prevalence of ODD among children and
adolescents ages 6 to 18 years is 3.3% and the prevalence
of CD is 3.2% (Canino, Polanczyk, Bauermeister, Rohde,
& Frick, 2010). These prevalence estimates did not vary
significantly across countries or continents, although the
vast majority of studies included in the meta-​analysis
were conducted in North America and Europe. There
is, however, evidence for differences in prevalence
rates of CP for children of different ages. The level of
CP tends to decrease from the preschool to school-​age
years (Maughan, Rowe, Messer, Goodman, & Meltzer,
2004) and increase again in adolescence (Loeber, Burke,
Lahey, Winters, & Zera, 2000). For example, Loeber
et  al. reported prevalence rates for CD of 5.6%, 5.4%,
and 8.3% for boys aged 7, 11, and 13 years, respectively,
and prevalence rates for ODD of 2.2%, 4.8%, and 5.0%
for boys of the same age in a sample of 1,517 youth in
a large urban area. However, the increase in the preva-
lence of CP from childhood to adolescence may not
be consistent for all types of CP. Specifically, there is
evidence that mild forms of physical aggression (e.g.,
fighting) show a decrease in prevalence rates across
development, whereas nonaggressive and covert forms of
antisocial behavior (e.g., lying and stealing) and serious
aggression (e.g., armed robbery and sexual assault) show
Child and Adolescent Conduct Problems 73
an increase in prevalence rates from childhood to adoles-
cence (Loeber & Hay, 1997).
There also appear to be sex differences in the preva-
lence of CP. Overall estimates of the sex ratio for boys
and girls with CP range from 2:1 to 4:1 (Loeber et  al.,
2000). However, this overall ratio hides several important
developmental differences. Specifically, there are few sex
differences between boys and girls in the prevalence rates
of most types of CP prior to age 5 years (Maughan et al.,
2004). However, after age 4  years the rate of girls’ CP
decreases, whereas the rate of CP for boys either increases
or stays at the same rate, leading to a male predominance
of CP throughout much of childhood (Loeber et  al.,
2000). Numerous studies have also noted that the sex
ratio between girls and boys with CP narrows dramatically
from approximately 4:1 in childhood to approximately
2:1 in adolescence due to an increase in the number of
girls engaging in CP in adolescence (for a review, see
Silverthorn & Frick, 1999).
CP and Co-​Occurring Problems in Adjustment
A consistent finding in research with children who
show CP is that they often have a number of problems
in adjustment, in addition to their CP, and these prob-
lems are critical to address in assessment and interven-
tion. Attention-​deficit/​hyperactivity disorder (ADHD) is
one of the most common comorbid conditions associated
with CP. In a meta-​analytic study, Waschbusch (2002)
reported that 36% of boys and 57% of girls with CP had
comorbid ADHD. Importantly, this review also suggested
that the presence of ADHD often signals the presence of
a more severe and more chronic form of CP in children.
Internalizing disorders, such as depression and anxiety,
also co-​occur with CP at rates higher than expected by
chance (Zoccolillo, 1992). In most cases, CP precedes
the onset of depressive and anxiety symptoms, and these
symptoms are often viewed as consequences of the many
adjustment problems experienced by a child with CP
(Frick, Lilienfeld, Ellis, Loney, & Silverthorn, 1999;
Loeber & Keenan, 1994). In addition, children who pres-
ent with the angry/​irritable mood symptoms of ODD are
more likely to develop internalizing types of difficulties
(e.g., Burke, Hipwell, & Loeber, 2010; Rowe, Costello,
Angold, Copeland, & Maughan, 2010; Stringaris &
Goodman, 2009). CP is also related to substance use (e.g.,
Hawkins, Catalano, & Miller, 1992). The comorbidity
between CP and substance abuse is important because
when youths with CP also abuse substances, they tend to
show an early onset of substance use and they are more
74
74 Attention-Deficit and Disruptive Behavior Disorders
likely to abuse multiple substances (Lynskey & Fergusson,
1995). With preschool-​aged children, language impair-
ment may be associated with CP (Wakschlag & Danis,
2004), and in older children, CP is often associated with
academic achievement below a level predicted by their
intellectual level (Hinshaw, 1992).
Multiple Risks Associated with CP
Most researchers agree that CP is the result of a complex
interaction of multiple causal factors (Kimonis, Frick, &
McMahon, 2014). These factors can be summarized in
five categories:  biological factors, cognitive correlates,
family context, peer context, and the broader social ecol-
ogy (e.g., neighborhood and community). Although a
number of biological correlates (e.g., neurochemical and
autonomic irregularities) of CP have been identified and
are likely important for causal theories (Frick & Viding,
2009), they are not reviewed here because the current
state of knowledge is not sufficiently developed to have
clear implications for assessment.
In contrast, there are several aspects of the youth’s
cognitive and learning styles that have been associated
with CP that may be important to the assessment process.
First, compared to others, youths with CP tend to score
lower on intelligence tests, especially in the area of verbal
intelligence (Loney, Frick, Ellis, & McCoy, 1998; Moffitt,
2006). Furthermore, these scores are predictive of the per-
sistence of CP and engagement in delinquent behaviors
during adolescence (Frick & Loney, 1999). Second, many
children and adolescents with CP tend to show a learning
style that is more sensitive to rewards than punishments.
This has been labeled as a reward-​dominant response
style, and it could explain why many of these youths persist
in their maladaptive behaviors, despite the threat of seri-
ous potential consequences (Frick et al., 2003; O’Brien &
Frick, 1996). Third, many youths with CP show a variety
of deficits in their social cognition—​that is, the way they
interpret social cues and use them to respond in social
situations (Crick & Dodge, 1994; Webster-​ Stratton &
Lindsay, 1999). For example, children and adolescents
with CP have been shown to have deficits in encoding
social cues (e.g., lack of attention to relevant social cues),
to make more hostile attributional biases and errors in the
interpretation of social cues, to have deficient quantity
and quality of generated solutions to social conflict, and
to evaluate aggressive solutions more positively (Dodge &
Pettit, 2003).
The critical role of parenting practices in the
development and maintenance of CP has been well
established (e.g., Chamberlain & Patterson, 1995; Loeber
& Stouthamer-​Loeber, 1986). Types of parenting practices
that have been closely associated with the development
of CP include inconsistent discipline, irritable explosive
discipline, poor supervision, lack of parental involvement,
and rigid discipline (Chamberlain, Reid, Ray, Capaldi, &
Fisher, 1997). In addition to parenting practices, various
other risk factors that may have an impact on the family
and may serve to precipitate or maintain CP have been
identified. These familial factors include parental social
cognitions (e.g., perceptions of the child), parental per-
sonal and marital adjustment (e.g., depression, ADHD,
antisocial behavior, substance abuse), and parental stress
(McMahon & Estes, 1997; McMahon & Frick, 2005).
Research suggests that the child’s relationship with
peers can also play a significant role in the develop-
ment, maintenance, and escalation of CP. Research
has documented a relationship between peer rejection
in elementary school and the later development of CP
(Chen, Drabick, & Burgers, 2015). In addition, peer
rejection in elementary school is predictive of an asso-
ciation with a deviant peer group (i.e., one that shows
a high rate of antisocial behavior and substance abuse)
in early adolescence (Chen et al., 2015). This relation-
ship is important because association with a deviant peer
group leads to an increase in the frequency and severity
of CP (Patterson & Dishion, 1985), and it has proven
to be a strong predictor of later delinquency (Monahan,
Steinberg, Cauffman, & Mulvey, 2009)  and substance
abuse (Dishion, Capaldi, Spracklen, & Li, 1995;
Fergusson, Swain, & Horwood, 2002).
Finally, there are factors within the youth’s larger social
ecology that have been associated with CP. One of the
most consistently documented of these correlates has been
low socioeconomic status (SES; Frick, Lahey, Hartdagen,
& Hynd, 1989). However, several other ecological fac-
tors, many of which are related to low SES, such as poor
housing, poor schools, and disadvantaged neighborhoods,
have also been linked to the development of CP (Ray,
Thornton, Frick, Steinberg, & Cauffman, 2016). In addi-
tion, the high rate of violence witnessed by youths who
live in impoverished inner-​city neighborhoods has also
been associated with CP (Howard, Kimonis, Munoz, &
Frick, 2012; Oberth, Zheng, & McMahon, 2017).
Causal Theories of CP
Although there is general agreement that CP in children
and adolescents is associated with multiple risk factors,
there is less agreement as to how these risk factors play
 75
a role in the development of CP. Also, in addition to
accounting for the large number of risk factors, causal the-
ories of CP need to consider research suggesting that there
may be many different causal pathways through which
youth develop these behaviors, each involving a different
constellation of risk factors and each involving somewhat
different causal processes (Frick & Viding, 2009).
The most widely accepted model for delineating dis-
tinct pathways in the development of CP distinguishes
between childhood-​onset and adolescent-​onset subtypes
of CP. That is, the DSM-​5 (APA, 2013) makes the distinc-
tion between youths who begin showing CP before age
10 years (i.e., childhood onset) and those who do not show
CP before age 10 years (i.e., adolescent onset). This dis-
tinction is supported by a substantial amount of research
documenting important differences between these two
groups of youths with CP (for reviews, see Fairchild, van
Goozen, Calder, & Goodyer, 2013; Frick & Viding, 2009;
Moffitt, 2006). Specifically, youths in the childhood-​
onset group show more serious aggression in childhood
and adolescence and are more likely to continue to show
antisocial and criminal behavior into adulthood (Odgers
et al., 2007). More relevant to causal theory, many of the
dispositional (e.g., temperamental risk and low intelli-
gence) and contextual (e.g., family dysfunction) correlates
that have been associated with CP are more strongly asso-
ciated with the childhood-​onset subtype. In contrast, the
youths in the adolescent-​onset subtype show lower rates of
these same risk factors. If they do differ from other youths,
it seems primarily to be in showing greater affiliation
with delinquent peers and scoring higher on measures of
rebelliousness and authority conflict (Dandreaux & Frick,
2009; Moffitt & Caspi, 2001; Moffitt, Caspi, Dickson,
Silva, & Stanton, 1996).
The different characteristics of youths in the two sub-
types of CP have led to theoretical models that propose
very different causal mechanisms operating across the two
groups. For example, Moffitt (2006) has proposed that
youths in the childhood-​onset group develop CP behav-
ior through a transactional process involving a difficult
and vulnerable child (e.g., impulsive, with verbal defi-
cits, and with a difficult temperament) who experiences
an inadequate rearing environment (e.g., poor parental
supervision and poor-​quality schools). This dysfunctional
transactional process disrupts the child’s socialization,
leading to poor social relations with persons both inside
(i.e., parents and siblings) and outside (i.e., peers and
teachers) the family, which further disrupts the child’s
socialization. These disruptions lead to enduring vulner-
abilities that can negatively affect the child’s psychosocial
Child and Adolescent Conduct Problems 75
adjustment across multiple developmental stages. In con-
trast, Moffitt views youths in the adolescent-​onset pathway
as showing an exaggeration of the normative developmen-
tal process of identity formation that takes place in ado-
lescence. Their engagement in antisocial and delinquent
behaviors is conceptualized as a misguided attempt to
obtain a subjective sense of maturity and adult status in
a way that is maladaptive (e.g., breaking societal norms)
but encouraged by an antisocial peer group. Given that
their behavior is viewed as an exaggeration of a process
specific to the adolescent developmental stage and not
due to enduring vulnerabilities, their CP is less likely to
persist beyond adolescence. However, they may still have
impairments that persist into adulthood due to the conse-
quences of their CP (e.g., a criminal record, dropping out
of school, and substance abuse; Moffitt & Caspi, 2001).
This distinction between childhood-​ onset and
adolescent-​onset trajectories to severe CP has been very
influential for delineating different pathways through
which youths may develop CP, although it is important
to note that the applicability of this model to girls requires
further testing (Fairchild et al., 2013; Silverthorn & Frick,
1999). Furthermore, several authors have argued that the
distinction should be considered more quantitative than
qualitative (Fairchild et al., 2013; Lahey et al., 2000). That
is, a review by Fairchild et al. (2013) supports the conten-
tion that dispositional factors play a greater role in CP
when the onset is earlier. However, their review suggested
that this effect continues into adolescence. Furthermore,
this review noted that although the childhood-​onset path-
way tended to show a more chronic course across the lifes-
pan, there was still substantial variability in the outcomes
within each pathway. The authors concluded that the tim-
ing and severity of exposure to environmental adversity in
vulnerable individuals seem to account for the differences
in age of onset and differences in outcome.
Researchers have also begun extending this concep-
tualization in a number of important ways. For example,
research has identified a subgroup of youths (approxi-
mately 25%–​30%) within the childhood-​onset pathway
who show high rates of callous and unemotional (CU)
traits (e.g., lacking empathy and guilt) (Kahn, Frick,
Youngstrom, Findling, & Youngstrom, 2012). Despite
designating only a minority of children in the childhood-​
onset pathway, the subgroup is important for a number of
reasons. First, youth with CP who also show significant
levels of CU show a more stable pattern of behavior prob-
lems and more severe aggression that results in greater
harm to their victims (Frick, Ray, Thornton, & Kahn,
2014a). In addition to showing more severe aggression,
76
76 Attention-Deficit and Disruptive Behavior Disorders
youth with elevated CU traits display more instrumental
(i.e., for personal gain or dominance) and premeditated
aggression compared to other children and adolescents
with severe CP (Frick, Cornell, Barry, Bodin, & Dane,
2003; Lawing, Frick, & Cruise, 2010). Second, research
suggests that CU traits define a group of youth with serious
CP who show very different genetic, cognitive, emotional,
and social characteristics from those of other children and
adolescents with serious CP (Frick et al., 2014a). Third,
treatment outcome studies suggest that children with
CP who are high on CU traits show a poorer response to
many types of treatment compared to other children with
CP (Frick et al., 2014a; Hawes, Price, & Dadds, 2014).
To briefly summarize some of the key findings from
this research, children and adolescents with CP and CU
traits (compared to other youth with CP) show an insen-
sitivity to punishment cues, which includes responding
more poorly to punishment cues after a reward-​dominant
response set is primed, responding more poorly to gradual
punishment schedules, underestimating the likelihood
that they will be punished for misbehavior, and being less
sensitive to potential punishment when peers are present
relative to other youth with serious CP (Blair, Colledge,
& Mitchell, 2001; Frick, Cornell, Bodin, et  al., 2003;
Muñoz-​Centifanti & Modecki, 2013; Pardini, Lochman,
& Frick, 2003). Children and adolescents with CP and
elevated CU traits also show reduced emotional respon-
siveness in a number of situations, including showing
weaker responses to cues of distress in others, less reac-
tivity to peer provocation, less fear to novel and danger-
ous situations, and less anxiety over the consequences
of their behavior relative to other youth with serious CP
(Fanti, Panayiotou, Lazarou, Michael, & Georgiou, 2016;
Kimonis et al., 2008; Munoz, Frick, Kimonis, & Aucoin,
2008; Viding et  al., 2012). Finally, CP tends to have a
different association with parenting practices depending
on whether or not the child or adolescent shows elevated
levels of CU traits. Specifically, harsh, inconsistent, and
coercive discipline is more strongly associated with CP
in youths with normative levels of CU traits relative to
youths with elevated CU traits, whereas low warmth in
parenting appears to be more highly associated with CP in
youths with elevated CU traits (Pasalich, Dadds, Hawes,
& Brennan, 2012; Pasalich et al., 2016; Wootton, Frick,
Shelton, & Silverthorn, 1997).
The research on the different characteristics of chil-
dren with CP depending on their level of CU traits has led
to a number of theories to account for these differences
by hypothesizing different causal processes underlying the
CP in children with and without elevated CU traits. For
example, Frick, Ray, Thornton, and Kahn (2014b) have
proposed that children with CP and elevated CU traits
have a temperament (i.e., fearless, insensitive to punish-
ment, and low responsiveness to cues of distress in others)
that can interfere with the normal development of con-
science and place these children at risk for a particularly
severe and aggressive pattern of antisocial behavior. In
contrast, children and adolescents with childhood-​onset
CP who have normative levels of CU traits display higher
levels of emotional reactivity to distress in others and to
provocation from others. Furthermore, the CP in this
group is strongly associated with hostile/​coercive parent-
ing. Based on these findings, it appears that children in
this group show a temperament characterized by strong
emotional reactivity combined with inadequate social-
ization experiences that lead to a failure to develop the
skills needed to adequately regulate their emotional reac-
tivity (Frick & Morris, 2004). The resulting problems in
emotional regulation can result in the child committing
impulsive and unplanned aggressive and antisocial acts,
for which he or she may feel remorseful afterwards but
which he or she may still have difficulty controlling in
the future.
Based on this research supporting both the clinical
and the etiological importance of the presence of elevated
CU traits, the DSM-​5 (APA, 2013)  included a specifier
to the diagnosis of CD to designate those youths with
CP who also show elevated rates of CU traits. The speci-
fier of “with limited prosocial emotions” (LPE) is given
if the individual (a) meets criteria for CD and (b) shows
two or more of the following CU traits persistently over
12 months in more than one relationship or setting: lack
of remorse or guilt; callous—​lack of empathy; unconcern
about performance at school, work, or in other important
activities; and shallow or deficient affect.
ASSESSMENT FOR DIAGNOSIS
When a child or adolescent with CP is referred for assess-
ment, there are four primary goals for the assessment. First,
it is important to determine whether or not the youth is,
in fact, demonstrating significant levels of CP to rule out
the possibility of the occasional inappropriate referral due
to unrealistic parental or teacher expectations. Second, it
is important to identify the type and severity of the youth’s
CP and to determine the degree and types of impairment
associated with them. Some level of CP is normative and,
as noted previously, there can be quite a range of CP that
varies greatly in terms of how severe and impairing the
 7

Child and Adolescent Conduct Problems 77

behaviors are for the child. Assessing the level and sever-
ity of CP displayed by the child is critical to determine
whether treatment is indicated and how intensive it needs
to be. Third, given the high degree of comorbidity asso-
ciated with CP, it is critical to at least screen for a wide
variety of emotional, behavioral, social, and academic
problems that can further influence the child’s adjust-
ment. Fourth, given the large number of risk factors that
can contribute to the development and maintenance of
CP, and that could be important targets of intervention, it
is critical to assess the many dispositional and contextual
risk factors that research has linked to CP in children and
adolescents.
There are three primary assessment methods that can
be used to accomplish these goals: behavior rating scales,
structured diagnostic interviews, and behavioral observa-
tions. All of these methods have specific strengths and
weaknesses that they bring to the assessment process, and
we summarize these in the following sections. Table 5.1
lists some of the most commonly used empirically sup-
ported instruments for each method of assessment and
provides summary evaluations of their adequacy in terms
of normative data, reliability, validity, generalizability, and
clinical utility.
Behavior Rating Scales
Behavior rating scales are a core part of an assessment
battery for assessing children and adolescents with CP. As
noted in Table 5.1, a number of rating scales are commer-
cially available, and they have a number of useful charac-
teristics for meeting the goals outlined previously.
First, most scales have subscales assessing different
types of CP, and they can be completed by adults who
observe the youth in important psychosocial contexts (i.e.,
parents and teachers) and by the youth himself or her-
self. By having multiple informants who see the child in
different settings, this can provide important information
on the pervasiveness of the child’s behavior problems and
can help detect potential biases in the report of any single
informant. Most of the scales listed in Table 5.1 provide
analogous content across the different raters. One notable

Table 5.1  Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Rating Scales
ASEBA E E A E G E E A ✓
BASC-​3a E E A E E G E A ✓
CRS-​3a E E A E G G E A
ECBI/​SESBI-​R G E A G E E G A ✓
ECI-​5/​CASI-​5a G A A A E G G A
Structured Interviews
DICA NA NA G G E E G A
DISC NA NA G G E E G A ✓
Behavioral Observations
BCS NR NA A NR A G G A ✓
DPICS L NA A L A G E A ✓
Compliance Test L E E A A G A A
BASC-​SOS NA NA A G E E A A
ASEBA-​DOF NA NA G G E E A A
REDSOCS L NA G NR A A A A
Impairment Indices
CAFAS G NA G G E E G G ✓
CGAS A NA G G E E G G

  Ratings for this instrument were made on the basis of research conducted with the previous version of the instrument.
a

Note: ASEBA  =  Achenbach System of Empirically Based Assessment; BASC-​3  =  Behavior Assessment System for Children, 3rd Edition; CRS-​
3 = Conners Rating Scales, 3rd Edition; ECBI = Eyberg Child Behavior Inventory; SESBI-​R = Sutter–​Eyberg Child Behavior Inventory-​Revised; ECI-​
5 = Early Childhood Inventory-​5; CASI-​5 = Child & Adolescent Symptom Inventory-​5; DICA = Diagnostic Interview for Children and Adolescents;
DISC = Diagnostic Interview Schedule for Children; BCS = Behavioral Coding System; DPICS = Dyadic Parent–​Child Interaction Coding System;
BASC-​SOS  =  BASC Student Observation System; ASEBA-​DOF  =  ASEBA Direct Observation Form; REDSOCS  =  Revised Edition of the School
Observation Coding System; CAFAS = Child and Adolescent Functional Assessment Scale; CGAS = Children’s Global Assessment Scale; L = Less than
Adequate; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.
78
78 Attention-Deficit and Disruptive Behavior Disorders
exception is the Behavior Assessment System for Children,
Third Edition (BASC-​3; Reynolds & Kamphaus, 2015).
In this scale, the teacher and parent versions are fairly
similar in content, with the main difference being that
teachers also rate behaviors indicative of learning prob-
lems and study skills. The content of the self-​report ver-
sion, however, is quite different. For example, the child
does not rate his or her own level of CP but, instead, the
self-​report version provides more extended coverage of the
child’s attitudes (e.g., attitudes toward parents and teach-
ers), his or her self-​concept (e.g., self-​esteem and sense of
inadequacy), and his or her social relationships.
Second, rating scales provide some of the best norm-​
referenced data on a child’s behavior. The most widely
used rating scales (see Table 5.1) have large standardiza-
tion samples that allow the child’s ratings to be compared
to the ratings of other children of the same age and sex.
This provides critical information to aid in determining
whether the child’s behavior is abnormal, given the child’s
age and sex. For example, the standardization sample for
the Achenbach System of Empirically Based Assessment
(ASEBA; Achenbach & Rescorla, 2000, 2001)  is repre-
sentative of the 48 contiguous United States for SES, sex,
ethnicity, region, and urban–​ suburban–​ rural residence
(Achenbach & Rescorla, 2000, 2001). In addition, the
factor structures of the various ASEBA instruments have
been found to be comparable across multiple societies
(e.g., Achenbach & Rescorla, 2007, 2010).
Third, most rating scales contain additional subscales,
over and above those assessing CP. These typically include
scales assessing anxiety, depression, social problems, and
family relationships. Thus, these rating scales can be
very helpful in providing a broad screening of many of
the most common co-​occurring problems that are often
found in children with CP and many of the risk factors
that can play a role in the development and maintenance
of CP. However, rating scales can vary on how well they
assess the various co-​occurring conditions. For example,
the ASEBA does not include separate depression and
anxiety scales, nor does it include a hyperactivity scale.
A related issue has been a lack of correspondence of
some of the scales to their DSM counterparts. However,
the ASEBA (Achenbach, 2013) and the Conners Rating
Scales (CRS-​ 3; Conners, 2008)  now include scoring
algorithms for DSM-​5-​oriented scales. Also, the rating
scales developed by Gadow and Sprafkin (2002), such as
the Child Symptom Inventory (CSI-​4), Early Childhood
Inventory-​ 5 (ECI-​ 5), and the Child and Adolescent
Symptom Inventory-​5 (CASI-​5), were specifically devel-
oped to correspond to DSM criteria. With the exception
of the CSI-​4, these DSM scales reflect the current DSM-​5
classification.
Although an advantage of these rating scales is the
breadth of their coverage of multiple areas of child func-
tioning, the cost is that they often have only minimal
coverage of CP. There are, however, several rating scales
that focus solely on CP and provide a more comprehen-
sive coverage of various types of CP. For example, the
Eyberg Child Behavior Inventory (ECBI) and Sutter–​
Eyberg Student Behavior Inventory-​Revised (SESBI-​R)
(Eyberg & Pincus, 1999) are completed by parents and
teachers, respectively. Both scales include 36 items
describing specific CP behaviors and are scored on both
a frequency-​of-​occurrence (Intensity) scale and a yes–​no
problem identification (Problem) scale. The inclusion
of both frequency and problem ratings is very helpful in
the diagnostic process to determine the level of impair-
ment associated with the child’s or adolescent’s CP.
Interviews
The second major method used for the diagnosis of CP is
interviews. Interviews can be divided into two general cat-
egories:  unstructured clinical interviews and structured
diagnostic interviews. The clinical interview with the par-
ent is important in the assessment of CP for a number
of reasons. In addition to providing a method for assess-
ing the type, severity, and impairment associated with
CP, the clinical interview with the parent helps assess
typical parent–​child interactions that may be contribut-
ing to the CP, the antecedent conditions that may make
CP behaviors more likely to occur, and the consequences
that accompany such behaviors and either increase or
decrease the likelihood that CP will reoccur. A number
of interview formats are available to aid the clinician in
obtaining information from the parents about their child’s
behavior and parent–​ child interactions (e.g., Barkley,
2013; McMahon & Forehand, 2003; Patterson, Reid,
Jones, & Conger, 1975; Wahler & Cormier, 1970). An
individual interview with the child or adolescent may also
be useful in providing the clinician with an opportunity
to assess the child’s perception of why he or she has been
brought to the clinic and the child’s subjective evaluation
of his or her cognitive, affective, and behavioral character-
istics (e.g., Bierman, 1983).
One criticism of the unstructured interview has been
the difficulty in obtaining reliable information in this for-
mat. Structured interviews were developed in an attempt
to improve the reliability of the information that is
obtained. As listed in Table 5.1, two structured diagnostic
 79
interviews that are frequently used in the assessment of
children with CP are the Diagnostic Interview Schedule
for Children (DISC-​IV; Shaffer, Fisher, Lucas, Dulcan,
& Schwab-​Stone, 2000) and the Diagnostic Interview for
Children and Adolescents (DICA; Reich, 2000). These
and other similar interviews (for a review, see Loney &
Frick, 2003) provide a structured format for obtaining par-
ent and youth reports on the symptoms that constitute the
criteria for ODD and CD according to DSM-​IV-​TR (APA,
2000). They are both currently being updated with the
changes in criteria made in the new DSM-​5 (APA, 2013).
Similar to behavior rating scales, these interviews pro-
vide very structured question-​ and-​
answer formats and,
thus, often lead to very reliable scores. The questions are
typically asked in a stem and follow-​up format. That is,
a stem question is asked (e.g., “Does your child get into
fights?”), and follow-​up questions are only asked if the
stem question is answered affirmatively (e.g., “Is this only
with his or her brothers and sisters?” and “Does he or she
usually start these fights?”). Also similar to behavior rating
scales, most structured interviews assess many other types
of problems in adjustment, in addition to CP. Thus, they
can be very helpful for providing an assessment of pos-
sible comorbid conditions that are often present in youth
with CP.
However, as noted in Table 5.1, unlike behavior rat-
ing scales, structured interviews often do not provide
strong normative information on the child’s behavior.
Instead, structured interviews typically focus on assessing
how much CP and other problems in adjustment impair
a child’s or adolescent’s social and academic function-
ing. Also, unlike behavior ratings scales, most interview
schedules provide standard questions that assess the age
at which a child’s behavioral difficulties began to emerge
and how long they have caused problems for the child.
Also, the assessment of age of onset of CP and other
problems in adjustment allows for some estimate of the
temporal ordering of a child’s problems, such as whether
the child’s CP predated his or her emotional difficulties.
Such information could help in determining whether the
emotional distress is best conceptualized as being a result
of the impairments caused by the CP.
However, there are a number of limitations in the
information provided by structured interviews (Frick,
Barry, & Kamphaus, 2010). If the child has a number
of problems, and many stem questions are answered
affirmatively requiring the administration of extensive
follow-​up questions, the interviews can be very lengthy.
That is, their administration time can range from 45 min-
utes for youths with few problems to more than 2 hours
Child and Adolescent Conduct Problems 79
for youths with many problems in adjustment (Frick
et  al., 2010). Furthermore, most structured interviews
do not have formats for obtaining teacher information,
and obtaining reliable information from young children
(younger than age 9  years) has been difficult with most
structured interviews (Frick et al., 2010). Perhaps one of
the most  important limitations in the use of structured
interviews, however, is evidence that the number of symp-
toms reported declines within an interview schedule.
That is, parents and youths tend to report more symptoms
for diagnoses assessed early in the interview, regardless of
which diagnoses are assessed first (Jensen, Watanabe, &
Richters, 1999; Piacentini et al., 1999). This finding calls
into question the validity of diagnoses assessed later in the
interview. Unfortunately, CP is often assessed last in most
of the available interview schedules and, as a result, could
be most influenced by this limitation.
Behavioral Observation
Behavioral observations provide a third common way
of assessing CP behaviors. Behavioral observations in a
child’s or adolescent’s natural setting (e.g., home, school,
playground) can make an important contribution to the
assessment process by providing an assessment of the
youth’s behavior that is not filtered through the percep-
tions of an informant and by providing an assessment
of the immediate environmental context of the youth’s
behavior. For example, behavioral observations can indi-
cate how others in the child’s environment (e.g., parents,
teachers, peers) respond to the child’s CP; this could be
very important for identifying factors that may be main-
taining these behaviors.
Two widely used, structured, microanalytic observa-
tion procedures available for assessing CP and parental
responses to these behaviors in younger (3 to 8  years)
children in the clinic and the home are the Behavioral
Coding System (BCS; Forehand & McMahon, 1981) and
the Dyadic Parent–​ Child Interaction Coding System
(DPICS; Eyberg, Nelson, Ginn, Bhuiyan, & Boggs,
2013). The BCS and the DPICS are modifications of the
assessment procedure developed by Hanf (1970) for the
observation of parent–​child interactions in the clinic. As
employed in clinic settings, both the BCS and the DPICS
place the parent–​child dyad in standard situations that
vary in the degree to which parental control is required,
ranging from a free-​play situation (i.e., Child’s Game and
Child-​Directed Interaction) to one in which the parent
directs the child’s activity, either in the context of parent-​
directed play (i.e., Parent’s Game and Parent-​Directed
80
80 Attention-Deficit and Disruptive Behavior Disorders
Interaction) or in cleaning up the toys (i.e., Clean Up).
Each task typically lasts 5 to 10 minutes. In the home
setting, observations usually occur in a less structured
manner (e.g., the parent and child are instructed to “do
whatever you would normally do together”). In each cod-
ing system, a variety of parent and child behaviors are
scored, many of which emphasize parental antecedents
(e.g., commands) or consequences (e.g., use of verbal
hostility) to the child’s behavior. Both the BCS and the
DPICS have been shown to differentiate clinic-​referred
from nonreferred children (Eyberg et  al., 2013; Griest,
Forehand, Wells, & McMahon, 1980). One of the main
limitations of these observational systems is the very inten-
sive training (e.g., 20 to 25 hours for the BCS) required of
observers so that they reliably code the parent and child
behaviors. This characteristic often limits the usefulness of
these systems in many clinical settings (Frick et al., 2010).
However, simplified versions of both the DPICS and the
BCS have been developed to reduce training demands
and may ultimately prove to be more useful to clinicians
(Eyberg, Bessmer, Newcomb, Edwards, & Robinson,
1994; McMahon & Estes, 1994). For example, parental
negative attention (coded from the simplified version
of the BCS) during a structured child-​directed play task
predicted higher levels of parent-​ reported CP concur-
rently and at a 6-​year follow-​up, supporting the predic-
tive validity of this abbreviated coding system (Fleming,
McMahon, & King, 2016).
As noted previously, an important type of CP, espe-
cially in young children, is noncompliance. A  direct
observational assessment of child noncompliance can
also be obtained in the clinic with the Compliance Test
(CT; Roberts & Powers, 1988). In the CT, the parent
is instructed to give a series of 30 standard commands
without helping or following up on the commands with
other verbalizations or nonverbal cues. In one version
of the CT, two-​part commands are given (e.g., “[Child’s
name], put the [toy] in the [container].”). In another
version, the commands are separated into two codeable
units (e.g. “[Child’s name], pick up the [toy]. Put it in
the [container].”). The CT takes between 5 and 15 min-
utes to complete. The CT has proven useful in identifying
noncompliant preschool children in research and clinical
settings (Roberts & Powers, 1990).
Many common CP behaviors are by nature covert (e.g.,
lying, stealing, and fire-​setting), which makes them more
difficult to capture through observational techniques.
However, Hinshaw and colleagues have developed and
evaluated an analogue observational procedure to assess
stealing, property destruction, and cheating in children
ages 6 to 12  years (Hinshaw, Heller, & McHale, 1992;
Hinshaw, Simmel, & Heller, 1995; Hinshaw, Zupan,
Simmel, Nigg, & Melnick, 1997). Samples of boys (ages
6 to 12 years) with ADHD (most of whom also had ODD
or CD) and a comparison group were asked to complete
an academic worksheet alone in a room that contained a
completed answer sheet, money, and toys. Stealing was
measured by conducting a count of objects in the room
immediately following the work session, whereas property
destruction and cheating were assessed by ratings derived
from observing the child’s behavior during the session.
Each of these observational measures of covert CP was
correlated with parental ratings of covert CP. Stealing and
property destruction were also associated with staff ratings.
There are also several behavioral observational sys-
tems that have been developed for use in school set-
tings (Nock & Kurtz, 2005). For example, both the BCS
(Forehand & McMahon, 1981) and the DPICS (Eyberg
et  al., 2013)  have been modified for use in the class-
room to assess child behavior (e.g., Breiner & Forehand,
1981; Jacobs et  al., 2000). Psychometric properties of
the Revised Edition of the School Observation Coding
System (REDSOCS; Jacobs et  al., 2000), which is the
adaptation of the DPICS, have been reported with both
clinic-​referred and nonreferred samples (Bagner, Boggs,
& Eyberg, 2010; Jacobs et  al., 2000). For example, the
REDSOCS discriminated between nonreferred chil-
dren and children referred for school behavior problems
(Jacobs et al., 2000).
The BASC-​ 3 Student Observation System (SOS;
Reynolds & Kamphaus, 2015)  provides a system for
observing children’s behavior in the classroom using a
momentary time-​sampling procedure. With the purchase
of an application for a smartphone, tablet, or laptop, the
observations can be entered directly into a digital data-
base that can be integrated with the results of the parent
and teacher ratings on the BASC-​3. The SOS specifies
65 behaviors that are common in classroom settings and
includes both adaptive (e.g., “follows directions” and
“returns material used in class”) and maladaptive (e.g.,
“fidgets in seat” and “teases others”) behaviors. The obser-
vation period in the classroom involves 15 minutes that is
divided into 30 intervals of 30 seconds each. The child’s
behavior is observed for 3 seconds at the end of each
interval, and the observer codes all behaviors that were
observed during this time window. Although the newest
version of the SOS has not been extensively tested, scores
from the earlier version of this observation system differ-
entiated students with CP from other children (Lett &
Kamphaus, 1997).
 81
Another classroom observational system, the ASEBA
Direct Observation Form (ASEBA-​DOF; McConaughy
& Achenbach, 2009), was designed to observe students,
ages 5 to 14  years, for 10-​minute periods in the class-
room. Three types of information are recorded. First, at
the end of each minute during the observational period,
the child’s behavior is coded as being on or off task for 5
seconds. Second, at the end of the observational period,
the observer writes a narrative of the child’s behavior
throughout the 10-​minute observational period, noting
the occurrence, duration, and intensity of specific prob-
lems. Third, and also at the end of the observational
period, the observer codes 96 behaviors on a 4-​point scale
(0  =  “behavior was not observed” through 3  =  “definite
occurrence of behavior with severe intensity or for greater
than 3 minutes duration”). These ratings can be summed
into Total Problem, Internalizing, and Externalizing
behavior composites. The ASEBA-​DOF has been shown
to discriminate between referred and nonreferred chil-
dren in the classroom (e.g., Reed & Edelbrock, 1983), as
well as between children with CP and children with other
behavior problems (e.g., McConaughy, Achenbach, &
Gent, 1988).
One limitation in observational systems is the poten-
tial for reactivity, whereby the child’s behavior can change
because the child knows that he or she is being observed
(Aspland & Gardner, 2003). An alternative to observa-
tions by independent observers that can reduce reactivity
is to train significant adults in the child’s or adolescent’s
environment to observe and record certain types of behav-
ior. The most widely used procedure of this type is the
Parent Daily Report (PDR; Chamberlain & Reid, 1987),
a parent observation measure that is typically adminis-
tered during brief (5 to 10 minutes) telephone interviews.
Parents are asked which of a number of overt and covert
behaviors have occurred in the past 24 hours. The PDR
has shown moderate convergent validity with other parent
report measures of child CP (Chamberlain & Reid, 1987;
Webster-​Stratton & Spitzer, 1991).
Functional Impairment
Most of the measures described previously focus on the
type, frequency, and severity of the child’s CP. However,
the child’s or adolescent’s level of functional impairment
can vary greatly, even with similar levels of CP (Bird, 1999;
Bloomquist & Schnell, 2002). Knowledge of impairment
is important for a number of reasons. First, it can deter-
mine how intensive an intervention may need to be for a
child and the most appropriate setting for this treatment,
Child and Adolescent Conduct Problems 81
it can provide useful information to the clinician concern-
ing possible intervention targets, and it may also serve as
an important indicator of intervention outcome (Frick
et  al., 2010; Hodges, Xue, & Wotring, 2004). As noted
previously, structured interviews based on the DSM-​IV-​
TR (APA, 2000) allow for the assessment of impairment.
Table 5.1 lists two measures designed specifically to assess
the youth’s level of impairment:  the Children’s Global
Assessment Scale (CGAS; Bird et  al., 1993; Shaffer
et  al., 1983)  and the Child and Adolescent Functional
Assessment Scale (CAFAS; Hodges, 2000). Also, several of
the broad rating scales summarized in Table 5.1 include
subscales that assess important areas of potential impair-
ment of children with CP. For example, the BASC-​3
(Reynolds & Kamphaus, 2015)  contains scales assessing
the child’s academic adjustment (e.g., learning problems,
attitude toward school and teacher, study skills), social
adjustment (e.g., social stress, interpersonal relations),
and self-​concept (e.g., sense of inadequacy).
Overall Evaluation
In summary, assessing the types and severity of CP dis-
played by the child, as well as assessing common co-​
occurring problems in adjustment, is critical to the
assessment of children and adolescents with CP. Behavior
rating scales, unstructured and structured interviews, and
behavioral observations all can help in this process, and
each has its unique strengths and weaknesses. Thus, typi-
cal assessments of children with CP would include mul-
tiple methods of assessment that utilize the strengths of
these different approaches.
Behavior rating scales, such as the BASC-​ 3 and
ASEBA, typically provide the best norm-​referenced infor-
mation that allows for the comparison of a child’s level
of CP to a normative comparison group. Rating scales
also typically have formats for obtaining information from
several different informants who see the child in different
settings (e.g., parents and teachers), and they provide a
time-​efficient method for assessing a number of possible
co-​occurring problems that may be present in youths with
CP. In contrast, structured interviews, such as the DICA
and DISC, tend to be more time-​consuming and are often
limited in the normative information that they provide.
However, they typically provide more information on the
level of impairment associated with the child’s CP and the
age at which the problem behavior began. Finally, behav-
ioral observation systems, such as the BCS and DPICS,
provide an assessment of the child’s behavior that is not
filtered through the perceptions of an informant, and
82

82 Attention-Deficit and Disruptive Behavior Disorders

they provide a method for assessing the environmental
contingencies that can be involved in the development or
maintenance of CP. However, many behavioral observa-
tion systems require extensive training to reliably code the
child’s behavior, and they are often limited in the norma-
tive information they provide.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
The research reviewed previously indicated that children
with CP often have multiple comorbid conditions that are
important to consider in treatment planning, and there
are often numerous risk factors that can be involved in
the development or maintenance of CP. As a result, many
of the rating scales and structured interviews described
in the previous section on diagnosis are also included
in Table 5.2 because they are also critical for case con-
ceptualization and treatment planning purposes. These
measures provide a broad assessment of the child’s func-
tioning and capture the many important co-​occurring
problems in adjustment and risk factors that can be used
in treatment planning.
A key area of research for guiding the assessment
process is the research documenting various potential
developmental pathways to CP. As reviewed previously,
children with CP can fall into childhood-​onset or ado-
lescent-​onset pathways, depending on when their level
of severe antisocial and aggressive behavior started. Also,
there seem to be important differences between those
children with CP who do and those who do not show
high levels of CU traits. Knowledge of the characteristics
of children in these different pathways, and the different
causal mechanisms involved, can serve as a guide for
structuring and conducting the assessment (Frick et  al.,
2010; McMahon & Frick, 2005). Furthermore, interven-
tions can be tailored to the unique needs of youth in these
different pathways (Frick, 2012).
These developmental pathways can aid case concep-
tualizations by providing a set of working hypotheses con-
cerning the nature of the CP behavior, the most likely
comorbid conditions, and the most likely risk factors
(McMahon & Frick, 2005). For example, for a youth

Table 5.2  Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Rating Scales
APSD A L A G E G A A
ASEBA E E A E G E E A ✓
BASC-​3a E E A E E G E A ✓
ECBI/​SESBI-​R G E A G E E G A
ECI-​5/​CASI-​5a G A A A E G G A
ICU L A G G E E E A ✓
Structured Interviews
DICA NA NA G G E E G A
DISC NA NA G G E E G A ✓
Behavioral Observations
BCS U NA A U A G G A ✓
DPICS L NA A L A G E A ✓
Compliance Test L E E A A G A A
PDR L NR E A A G E A ✓
BASC-​SOS L NA A G E E A A
ASEBA-​DOF L NA G G E E A A
REDSOCS L NA G NR A A A A

  Ratings for this instrument were made on the basis of research conducted with the previous version of the instrument.
a

Note: APSD = Antisocial Process Screening Device; ASEBA = Achenbach System of Empirically Based Assessment; BASC-​3 = Behavior Assessment
System for Children, 3rd Edition; ECBI = Eyberg Child Behavior Inventory; SESBI-​R = Sutter–​Eyberg Child Behavior Inventory-​Revised; ECI-​5 = Early
Childhood Inventory-​5; CASI-​5 = Child & Adolescent Symptom Inventory-​5; ICU = Inventory of Callous–​Unemotional Traits; DICA = Diagnostic
Interview for Children and Adolescents; DISC = Diagnostic Interview Schedule for Children; BCS = Behavioral Coding System; DPICS = Dyadic
Parent–​Child Interaction Coding System; PDR = Parent Daily Report; BASC-​SOS = BASC-​3 Student Observation System; ASEBA-​DOF = ASEBA
Direct Observation Form; REDSOCS = Revised Edition of the School Observation Coding System; L = Less than Adequate; A = Adequate; G = Good;
E = Excellent; NR = Not Reported; NA = Not Applicable.
 83
whose CP appears to onset in adolescence, one would
hypothesize based on the available literature that he or
she is less likely to be aggressive, to have intellectual defi-
cits, to have temperamental vulnerabilities, and to have
comorbid ADHD. However, the youth’s association with a
deviant peer group and factors that may contribute to this
deviant peer group affiliation (e.g., lack of parental moni-
toring and supervision) would be especially important to
assess for youths in this pathway. In contrast, for a youth
whose serious CP began prior to adolescence, one would
expect more cognitive and temperamental vulnerabilities,
comorbid ADHD, and more serious problems in family
functioning. For those youths in this childhood-​ onset
group who do not show CU traits, the cognitive deficits
would more likely be verbal deficits and the tempera-
mental vulnerabilities would more likely be problems
regulating emotions, leading to higher levels of anxiety,
depression, and aggression involving anger. In contrast,
for a youth with childhood-​onset CP who shows high
levels of CU traits, the cognitive deficits are more likely
to involve a lack of sensitivity to punishment, and the
temperamental vulnerabilities are more likely to involve
a preference for dangerous and novel activities and a fail-
ure to experience many types of emotion (e.g., guilt and
empathy). Furthermore, assessing the level and severity of
aggressive behavior, especially the presence of instrumen-
tal aggression, would be critical for youths in this group.
As most clinicians recognize, people do not often fall
neatly into the prototypes that are suggested by research
(see also Fairchild et al., 2013). Therefore, these descrip-
tions are meant to serve as hypotheses around which to
organize an evidence-​based assessment. They also high-
light several specific important pieces of information that
are needed when assessing children and adolescents with
CP. One of the most critical pieces of information in guid-
ing assessment, and perhaps ultimately intervention, is
determining the age at which various CP behaviors began.
This information provides some indication as to whether
or not the youth may be on the childhood-​onset pathway.
Unfortunately, there has been little consistency in the
literature concerning the most appropriate operational
definition of childhood onset versus adolescent onset or
even whether this distinction should be based on chrono-
logical age or on the pubertal status of the child (Moffitt,
2006). For example, the DSM-​5 (APA, 2013) makes the
distinction between children who begin showing severe
CP behaviors before age 10 years (i.e., childhood onset)
and those who do not show severe CP before age 10 years
(i.e., adolescent onset) in its definition of CD. However,
other research studies have used age 11  years (Robins,
Child and Adolescent Conduct Problems 83
1966) or age 14 years (Patterson & Yoerger, 1993; Tibbetts
& Piquero, 1999) to define the start of adolescent onset.
Thus, onset of severe CP before age 10  years seems to
be clearly considered childhood onset and onset after age
13 years clearly adolescent onset. However, how to clas-
sify children whose CP onset between the ages of 11 and
13 years is less clear and probably dependent on the level
of physical, cognitive, and social maturity of the child.
Based on this research, it is therefore important for
treatment planning to assess the age at which the child
began showing serious CP. An important advantage that
many structured interviews have over behavior rating
scales and behavioral observations is that they provide a
structured method for assessing when a youth first began
showing serious CP, thereby providing an important
source of information on the developmental trajectory of
the CP behavior. For example, in the DISC-​IV (Shaffer
et  al., 2000), any question related to the presence of a
CD symptom that is answered affirmatively is followed
by questions asking the parent or youth to estimate at
what age the first occurrence of the behavior took place.
Obviously, such questions can also be integrated into an
unstructured interview format as well.
In either case, however, there is always some concern
about how accurate the parent or youth is in reporting
the timing of specific behaviors. There are three findings
from research that can help in interpreting such reports.
First, the longer the time frame involved in the retrospec-
tive report (e.g., a parent of a 17-​year-​old reporting on pre-
school behavior vs. a parent of a 6-​year-​old reporting on
preschool behavior), the less accurate the report is likely
to be (Green, Loeber, & Lahey, 1991). Second, although
a parental report of the exact age of onset may not be very
reliable over time, typical variations in years are usually
small and the relative rankings within symptoms (e.g.,
which symptom began first) and within a sample (e.g.,
which children exhibited the earliest onset of behavior)
seem to be fairly stable (Green et al., 1991). As a result,
these reports should be viewed as rough estimates of the
timing of onset and not as exact dating procedures. Third,
there is evidence that combining informants (e.g., a par-
ent and youth) or combining sources of information (e.g.,
self-​report and record of police contact), and taking the
earliest reported age of onset from any source, provide an
estimate that shows somewhat greater validity than any
single source of information alone (Lahey et al., 1999).
Assessment to examine the extent to which CU traits
may also be present is important, especially if the youth’s
history of CP is consistent with the childhood-​onset path-
way (but also see Fairchild et  al. [2013] concerning the
84
84 Attention-Deficit and Disruptive Behavior Disorders
relevance of also assessing for CU traits in youth with
adolescent-​ onset CP). To illustrate the importance to
treatment planning, Hawes et al. (2014) reviewed 16 treat-
ment outcomes studies and reported that CU traits were a
strong predictor of poor treatment outcomes across studies
(see also Frick et al., 2014a). For example, children with
CP and elevated CU traits seem to be less responsive to
the discipline components (e.g., time out) of parent man-
agement training (Hawes & Dadds, 2005). Furthermore,
although many learning-​ based parenting interventions
lead to improvements in CU traits, children with these
traits often started treatment with the most severe levels of
CP and still ended treatment with the most severe levels
of CP (White, Frick, Lawing, & Bauer, 2013). Thus, it is
important to include a measure of CU traits as part of the
treatment planning process (Manders, Dekovic, Asscher,
van der Laan, & Prins, 2013).
The Antisocial Process Screening Device (APSD;
Frick & Hare, 2001), included in Table 5.2, is a behavior
rating scale completed by parents and teachers to identify
children with CP who also exhibit CU traits (Christian,
Frick, Hill, Tyler, & Frazer, 1997; Frick, Bodin, & Barry,
2000; Frick, O’Brien, Wootton, & McBurnett, 1994).
A self-​report version of this scale is also available for older
children and adolescents, and it has been validated in a
number of studies (Muñoz & Frick, 2007). Unfortunately,
the APSD only includes six items directly assessing CU
traits, and it only has three response options for rat-
ing the frequency of the behaviors. The few items, the
limited range in response options, and the fact that rat-
ings of CU traits are negatively skewed in most samples
resulted in the APSD scores showing poor internal consis-
tency in many formats (Poythress, Dembo, Wareham, &
Greenbaum, 2006).
To overcome these limitations in the assessment of
CU traits, the Inventory of Callous–​unemotional Traits
(ICU) was developed to provide a more extended assess-
ment of CU traits (Kimonis et al., 2008). The ICU was
developed from the four items on the APSD that most
consistently loaded on the CU traits factor across vari-
ous samples (Frick et  al., 2000). To form the items on
the ICU, six items (three positively and three negatively
worded items) were developed to assess a similar content
to each of the four core traits. These 24 items were then
placed on a 4-​point Likert scale that could be rated from
0 (Not at all true) to 3 (Definitely true). Versions for par-
ent, teacher, and self-​report were developed to encourage
multi-​informant assessments. The ICU has a number of
positive qualities for assessing CU traits. The larger num-
ber of items and its extended response format has resulted
in a 24-​item total score that is internally consistent in
many samples, with Cronbach’s alpha ranging between
.77 and .89 (Frick & Ray, 2015). Furthermore, there is
a preschool version for use with children as young as
age 3  years (Ezpeleta, de la Osa, Granero, Penelo, &
Domenech, 2013), and the ICU has been translated into
more than 20 languages with support for its validity across
these translations (e.g., Ciucci, Baroncelli, Franchi,
Golmaryami, & Frick, 2014; Fanti, Frick, & Georgiou,
2009; Kimonis et al., 2008). Also, the ICU is one of the
few measures that include items that directly assess the
content included in the new “with limited prosocial
emotions” specifier in the DSM-​5 (Kimonis et al., 2015).
However, these positive qualities need to be weighed
against the lack of a large and representative normative
sample being available for the ICU and with empirically
derived cut-​offs being available for only certain versions
of the scale (Kimonis, Fanti, & Singh, 2014).
The key implication from research on the devel-
opmental pathways to CP is that the most appropriate
treatment for a child or adolescent with CP may differ
depending on characteristics of the child and factors in
his or her environment that are operating to maintain
these behaviors. This approach is very consistent with
functional behavioral assessment (FBA) methods that
focus on conducting an individualized assessment of
each child’s needs and matching intervention strategies
to those needs (LaRue & Handelman, 2006; Walker,
Ramsey, & Gresham, 2004). The typical FBA involves a
specification of problem behaviors in operational terms
(e.g., what types of CP are being exhibited in the class-
room), as well as identification of events that reliably
predict and control behavior through an examination
of antecedents and consequences. For example, an FBA
at school would determine whether the child’s CP is
occurring only in certain classes or situations (e.g., dur-
ing class change and at lunch) and if there are certain
factors that reliably lead to the CP (e.g., teasing by peers
and disciplinary confrontations with teachers). It would
also determine the consequences that are associated with
the CP that may contribute to their likelihood of occur-
ring in the future (e.g., getting sent home from school
and preventing further teasing). Information relevant to
an FBA can be gathered through interviews with signifi-
cant others in the child’s environment or through direct
observations of the child in his or her natural environ-
ment. Thus, several of the behavioral observation sys-
tems described previously are also quite important for
case conceptualization and treatment planning for the
child with CP.
 85

Child and Adolescent Conduct Problems 85

Overall Evaluation ASSESSMENT FOR TREATMENT MONITORING

AND TREATMENT OUTCOME
In summary, this section highlighted several critical
issues for using assessment information for planning
Most of the applications of research for guiding the assess-
treatment for children with CP. First, because chil-
ment process have focused on making diagnostic decisions
dren with CP often have many co-​occurring problems
(e.g., determining whether CP should be the primary
in adjustment that are important to address in treat-
source of concern and whether it is severe and impair-
ment, it is critical that methods for assessing potential
ing enough to warrant treatment) and on treatment plan-
comorbid problems, such as behavior rating scales and
ning (e.g., determining what types of intervention may be
structured interviews, can be used in treatment plan-
needed by the child; McMahon & Frick, 2005). However,
ning. Second, because children who show different
an important third goal of the assessment process is moni-
developmental trajectories of their CP may require dif-
toring the progress of intervention and evaluating treatment
ferent approaches to treatment, it is critical to assess key
outcome. That is, evidence-​based assessments should pro-
characteristics that distinguish among children in these
vide a means for testing whether interventions have brought
trajectories. Specifically, assessing the age at which the
about meaningful changes in the child’s or adolescent’s
child began to exhibit CP, through either structured or
adjustment, either for better or for worse (i.e., an iatrogenic
unstructured interviews, and assessing the presence of
effect). This is particularly important in the treatment of
CU traits are both critical to the treatment planning
CP, given a number of documented cases in which treat-
process. Third, because environmental contingencies
ments have led to increases, rather than decreases, in prob-
have proven to be very important for understanding
lem behavior for some youth with CP (Dishion, McCord,
factors that can either lead to or maintain CP in chil-
& Poulin, 1999; Dodge, Dishion, & Lansford, 2006).
dren and adolescents, assessment of these contingencies
Several of the behavior rating scales and observational
through unstructured interviews or behavioral observa-
measures described previously have demonstrated sensitivity
tions is also critical for the treatment planning process.
to intervention outcomes. These are described in Table 5.3.

Table 5.3  Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Rating Scales
ASEBA E E A E G E E G A ✓
ECI-​5/​CASI-​5a G A A A E G G G A
ECBI/​SESBI-​R G E A G E E G G A ✓
Behavioral Observations
BCS NR NA A NR A G G G A ✓
DPICS L NA A L A G E G A ✓
Compliance Test L E E A A G A G A
PDR L NR E A A G E E A ✓
REDSOCS L NA G NR A A A L A
Impairment Indices
CAFAS G NA G G E E G G G ✓
CGAS A NA G G E E G G G
Treatment Satisfaction Surveys
PCSQ NR NR NA NR A A NR NA A
TAI NR E NA G A G A NA A ✓

  Ratings for this instrument were made on the basis of research conducted with the previous version of the instrument.
a

Note: ASEBA = Achenbach System of Empirically Based Assessment; ECI-​5 = Early Childhood Inventory-​5; CASI-​5 = Child & Adolescent Symptom
Inventory-​5; ECBI = Eyberg Child Behavior Inventory; SESBI-​R = Sutter–​Eyberg Child Behavior Inventory-​Revised; BCS = Behavioral Coding System;
DPICS  =  Dyadic Parent–​Child Interaction Coding System; PDR  =  Parent Daily Report; REDSOCS  =  Revised Edition of the School Observation
Coding System; CAFAS  =  Child and Adolescent Functional Assessment Scale; CGAS  =  Children’s Global Assessment Scale; PCSQ  =  Parent’s
Consumer Satisfaction Questionnaire; TAI = Therapy Attitude Inventory; L = Less than Adequate; A = Adequate; G = Good; E = Excellent; NR = Not
Reported; NA = Not Applicable.
86
86 Attention-Deficit and Disruptive Behavior Disorders
For example, scores from the ASEBA have proven to be sen-
sitive to changes brought about by the treatment of youth
with CP (e.g., DeGarmo, Patterson, & Forgatch, 2004;
Eisenstadt, Eyberg, McNeil, Newcomb, & Funderburk,
1993; McCabe & Yeh, 2009). Also, scores on the ECI-​4 and
CASI-​4R scales have shown changes in response to parent-
ing and psychopharmacological interventions (e.g., Brock,
Kochanska, O’Hara, & Grekin, 2015; Gadow et al., 2014).
Scores on the ECBI/​SESBI-​R scales have been proven to
change after parent management training interventions with
young children (e.g., Eisenstadt et al., 1993; Jones, Forehand,
Cuellar, Parent, & Honeycutt, 2014; McCabe & Yeh, 2009;
Nixon, Sweeney, Erickson, & Touyz, 2003; Scott et al., 2010;
Webster-​Stratton & Hammond, 1997). Importantly, because
these rating scales often provide norm-​referenced scores,
these scales can be critical for determining not only whether
or not the intervention has led to significant decreases in the
child’s level of CP but also whether the behavior has been
brought within a level that is normative for the child’s age.
However, behavior rating scales completed by par-
ents who are involved in treatment could be influenced
by expectancy effects on the part of the parents who
anticipate positive responses to an intervention. Thus,
it is important to include ratings of the child’s behavior
from others who may not have been involved in the treat-
ment or to include behavioral observations of treatment
effects whenever possible, especially if the observer is
unaware if the child and his or her parents were involved
in treatment or unaware if the observation is pre-​or post-​
treatment. Two observational systems described previ-
ously, the BCS and the DPICS, have been used in this
way as an outcome measure for parenting interventions
for CP (e.g., Eisenstadt et al., 1993; Herschell, Calzado,
Eyberg, & McNeil, 2002; McCabe & Yeh, 2009;
McMahon, Forehand, & Griest, 1981; Peed, Roberts, &
Forehand, 1977; Webster-​Stratton & Hammond, 1997).
The PDR, which uses the parent as an observer, has also
been used as a treatment outcome indicator but, similar to
behavior rating scales, the observations by parents who are
involved in treatment could be biased (Bank, Marlowe,
Reid, Patterson, & Weinrott, 1991; Chamberlain &
Reid, 1991; Webster-​Stratton & Hammond, 1997). The
REDSOCS (Jacobs et  al., 2000)  school observation sys-
tem has reported treatment sensitivity with respect to the
classroom generalization effects of parent management
training (Bagner et  al., 2010). However, to our knowl-
edge, it has not yet been employed to assess the effects of
classroom-​based interventions.
As noted previously in the discussion of measures
used to diagnosis severe levels of CP, children with the
same level of CP can vary greatly on the level of impair-
ment associated with their CP. Thus, assessing the child’s
level of functional impairment after treatment is also an
important assessment goal. The two measures of func-
tional impairment included in Table 5.3, the CAFAS and
the CGAS, have both proven to be sensitive to treatment
effects (Hodges et al., 2004; Shaffer et al., 1983). Also, a
number of the rating scales noted in Table 5.3, such as the
ASEBA and BASC-​3, assess important areas of potential
impairment for children with CP, such as the child’s aca-
demic and social adjustment.
Although many measures have been used to assess
treatment outcome, there has been very little research on
the use of assessment measures to monitor the effects of
ongoing intervention for CP. Exceptions to this are the
structured observational analogues employed in some
parent management training programs for young opposi-
tional children that are employed repeatedly throughout
the course of treatment, not only to monitor progress but
also to determine whether the parent has met specific
behavioral performance criteria necessary for progression
to the next step of the parenting intervention (Herschell
et al., 2002; McMahon & Forehand, 2003).
A final assessment domain related to treatment out-
come that has had only minimal research focus is in the
assessment of treatment satisfaction. This is a form of
social validity that may be assessed in terms of satisfaction
with the outcome of treatment, therapists, treatment pro-
cedures, and teaching format (McMahon & Forehand,
1983). Given the diversity of treatments that are needed
for youth with CP, no single consumer satisfaction mea-
sure is appropriate for use with all types of interven-
tions for youth with CP and their families. The Therapy
Attitude Inventory (TAI; Brestan, Jacobs, Rayfield, &
Eyberg, 1999; Eyberg, 1993) and the Parent’s Consumer
Satisfaction Questionnaire (PCSQ; McMahon &
Forehand, 2003; McMahon, Tiedemann, Forehand, &
Griest, 1984) are examples of measures designed to evalu-
ate parental satisfaction with parent management training
programs (e.g., Eyberg & Funderburk, 2011; McMahon
& Forehand, 2003). Importantly, these measures largely
focus on the parents’ satisfaction with treatment. Children
and adolescents themselves have rarely been asked about
their satisfaction with treatment, with the exception of
some evaluations of Multisystemic Therapy with adoles-
cents (e.g., Henggeler et al., 1999).
There are several important issues involved in select-
ing measures suitable for treatment monitoring and out-
come evaluation (McMahon & Frick, 2005; McMahon
& Metzler, 1998). First, the way questions on a rating
 87
scale are framed could affect its sensitivity to change.
For example, the response scale on a behavior rating
scale may be too general (e.g., “never” vs. “sometimes”
vs. “always”), or the time interval for reporting the fre-
quency of a behavior (e.g., the past 6 months) may not
be discrete enough to detect changes brought about
by treatment. Second, a consistent finding when using
structured interviews is that parents and children often
report fewer symptoms on the second administration of
the interview (Jensen et al., 1999; Piacentini et al., 1999).
Thus, structured interviews are typically not good mea-
sures of treatment outcome because it is unclear whether
any reductions in CP between pre-​and post-​treatment
measures are due to the treatment or due to this normal
decrease in symptoms over repeated administrations.
Third, assessment-​by-​intervention interactions may occur
when evaluating treatment outcomes. For example, as a
function of intervention, parents may learn to become
more effective monitors of their children’s behavior. As
a consequence, they may become more aware of their
children’s CP. Comparison of parental reports of their
children’s behavior prior to and after the intervention
may actually suggest that parents perceive deterioration
in their children’s behavior, when in reality the parents
have simply become more accurate reporters of such
behavior (Dishion & McMahon, 1998).
Overall Evaluation
Unfortunately, the development of measures to adequately
monitor treatment progress and treatment outcome for
children and adolescents with CP has not advanced as far
as the development of measures for diagnosis and treat-
ment planning. This is a particularly unfortunate state
of affairs in the treatment of CP given that several treat-
ments have proven to have potentially harmful effects on
youth by leading to increases in behavior problems after
treatment. However, several behavior rating scales, most
notably the ASEBA and ECBI, have proven to be sensi-
tive to the effects of treatment, and both the ASEBA and
the ECBI provide norm-​referenced scores to determine
whether the child’s level of CP was brought within a level
that is normative for his or her age. Several behavioral
observation systems, such as the BCS and DPICS, have
also been used to both monitor the progress of treatment,
as well as to evaluate treatment outcome. A few measures
have been developed to assess child or parental satisfac-
tion with treatment. However, development of better evi-
dence-​based measures for this purpose is a critical area for
future research.
Child and Adolescent Conduct Problems 87
CONCLUSIONS AND FUTURE DIRECTIONS
In this chapter, we have summarized several areas of
research that have important implications for guiding
assessments for youth with CP and summarized some
recommended methods for accomplishing three primary
assessment goals: diagnosis of non-​normative and impair-
ing forms of CP, case conceptualization and treatment
planning, and monitoring and evaluating treatment out-
come. In this concluding section, we seek to highlight
some overarching issues that influence methods for meet-
ing all of these assessment goals and to highlight some
important areas for future research.
The first overarching issue is the need for a compre-
hensive assessment in most cases when assessing youth
with CP. That is, an adequate assessment of a youth with
CP must assess multiple aspects of the child’s or adoles-
cent’s adjustment (e.g., CP, anxiety and learning prob-
lems) in multiple settings (e.g., home and school; Frick
et  al., 2010; McMahon & Estes, 1997; McMahon &
Frick, 2005). However, it is also important to note that all
of the individual assessment techniques summarized in
Tables 5.1 have limitations. Thus, it is critical to assess the
child using multiple methods whenever possible (Frick
et al., 2010). Because of issues of time, expense, and prac-
ticality, how best to acquire and interpret this large array
of information become important issues. One approach
is to use a multistage method, which starts with more
time-​efficient measures (e.g., broadband behavior rating
scales and unstructured clinical interviews) that are fol-
lowed by more time-​intensive measures (e.g., structured
interviews and behavioral observations) when indicated
(McMahon & Estes, 1997; McMahon & Frick, 2005;
Nock & Kurtz, 2005).
Whether or not a multistage method is used, there are
few guidelines available to guide clinicians as to how to
integrate and synthesize the multiple pieces of informa-
tion that are obtained in the assessment to make impor-
tant clinical decisions. This endeavor is made more
complicated by the fact that information from different
informants (Achenbach, McConaughy, & Howell, 1987;
De Los Reyes & Kazdin, 2005) and information from dif-
ferent methods (Barkley, 1991)  often show only modest
correlations with each other. As a result, after collecting
multiple sources of information on a youth’s adjustment,
the assessor then must make sense out of an array of often
conflicting information.
Several strategies for integrating and interpreting
information from comprehensive assessments have been
proposed (Frick et  al., 2010; McMahon & Forehand,
8
88 Attention-Deficit and Disruptive Behavior Disorders
2003; Wakschlag & Danis, 2004). For example, Frick
et al. (2010) outlined a multistage strategy for integrating
results from a comprehensive assessment into a clear case
conceptualization to guide treatment planning. At the
first step, the assessor documents all clinically significant
findings regarding the youth’s adjustment (e.g., elevations
on ratings scales, diagnoses from structured interviews,
and problem behaviors from observations). At the second
step, the assessor searches for convergent findings across
these methods. At the third step, the assessor attempts
to explain, using available research as much as possible,
any discrepancies in the assessment results. For example,
a finding that a child and a parent, but not the teacher,
are reporting high rates of anxiety may be explained by
research suggesting that teachers may not be aware of a
student’s level of anxiety in the classroom (Achenbach
et  al., 1987). At the fourth step, the assessor develops a
profile of the areas of most concern for the child and
also develops a coherent explanation for the child’s CP,
again using existing research as much as possible. This
process was illustrated previously in using research on the
developmental pathways to CP to guide a case conceptu-
alization. Although this approach to interpreting results
of a comprehensive assessment is promising, much more
research is needed to guide this process of integrating data
from comprehensive assessments.
Another issue that requires further attention is the great
need to enhance the clinical utility of evidence-​based
assessment tools (Frick, 2000; Hodges, 2004). Many of the
assessment measures that have been used in research have
not been developed in such a way that makes them useful
in clinical practice. For example, Frick and Loney (2000)
reviewed a number of performance-​based measures that
have been used in research with children with CP. They
concluded that few of these measures have been used in
the same format across multiple samples that would allow
for the development of meaningful cut-​off scores that
could be used in clinical assessments. Also, as noted pre-
viously, many of the observational systems used to assess
parent–​child interactions require such intensive training
of observers that their potential utility in many clinical
assessments is also limited. Although we did review a few
attempts to develop brief and clinically useful assessment
methods, there are still too few such methods available.
Perhaps the most important limitation to evidence-​
based assessments of CP is the remaining disconnect
between assessment concerning case conceptualiza-
tion and treatment planning, on the one hand, and the
availability of evidence-​ based interventions that map
onto those assessment findings, on the other hand. For
example, interventions for youth who are engaging pri-
marily in covert forms of CP (e.g., stealing, fire-​setting)
are much less developed than those for more overt types of
CP such as noncompliance and aggression (McMahon,
Wells, & Kotler, 2006). Similarly, subtype-​specific inter-
ventions for reactive, proactive aggression and relational
aggression (e.g., Leff, Angelucci, Grabowski, & Weil,
2004; Levene, Walsh, Augimeri, & Pepler, 2004), and for
youths with and without CU traits (Hawes et al., 2014),
are in relatively early stages of development. Of note,
however, is the clear evidence suggesting that high lev-
els of noncompliance in a preschool-​age child are best
treated using one of several well-​validated parent manage-
ment training interventions (McMahon et al., 2006).
A critical issue in advancing the link between evi-
dence-​based assessment and treatment planning involves
emerging research on the different developmental path-
ways to CP. As noted previously, this area of research may
be the most important for understanding youths with CP
because it may explain many of the variations in sever-
ity, the multiple co-​occurring conditions, and the many
different risk factors that have been associated with CP.
This research could also be very important for designing
more individualized treatments for youths with CP, espe-
cially older children and adolescents with more severe
antisocial behaviors (Frick, 2012). However, in order for
research on developmental pathways to be translated into
practice, it is critical that better assessment methods for
reliably and validly designating youths in these pathways
be developed. This is especially the case for girls and
for ethnically diverse youth (McMahon & Frick, 2005).
Furthermore, the different causal processes and develop-
mental mechanisms (e.g., lack of empathy and guilt, poor
emotion regulation) that may be involved in the different
pathways need to be assessed, and this typically involves
translating measures that have been used in research into
forms that are appropriate for clinical practice (Frick &
Ray, 2015).
In conclusion, it is difficult to make a summary evalu-
ation of the state of evidence-​based practice related to the
assessment of CP. In some areas, there have been major
improvements during the past several decades, such as in
the development of behavior rating scales with large and
representative normative samples. In other areas, such as
in the development of measures to assess satisfaction with
treatment, there have been fewer advances. Also, as the
research base for understanding CP grows and evolves, so
too must the guidelines for using this research in prac-
tice. Thus, evidence-​based assessment is a moving target.
However, the hallmark of an evidence-​based approach to
 89
assessment is the commitment to never quit attempting to
hit this moving target. The goal of this chapter is to high-
light what we believe are currently some critical ways in
which research on CP can inform the assessment process
and to provide a structure whereby future advances in this
research can be used to further enhance the process.
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 97

Part III

Mood Disorders and Self-​Injury

98
 9
Depression in Children and Adolescents
Lea R. Dougherty
Daniel N. Klein
Thomas M. Olino
This chapter provides a review of evidenced-​based assess-
ments of depression in children and adolescents. We focus
on three phases of assessment:  diagnosis, case conceptu-
alization and treatment planning, and treatment monitor-
ing/​evaluation. Our goal is to outline the parameters of a
general assessment strategy and evaluate the efficacy of
various assessment tools. Nevertheless, we acknowledge
that additional areas will have to be explored for particular
cases or contexts.
Several changes were made to the depressive dis-
orders section of the fifth edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-​5;
American Psychiatric Association [APA], 2013). First,
DSM-​ IV categories of chronic major depression and
dysthymic disorder were integrated into a new category,
persistent depressive disorder. Second, disruptive mood
dysregulation disorder (DMDD) and premenstrual dys-
phoric disorder were added. Third, depressive disorder
not otherwise specified (DD-​NOS) was removed from
DSM-​ 5 and replaced with “other specified depressive
disorder” (which includes recurrent brief depression,
short-​duration depressive episode, and depressive episode
with insufficient symptoms) and “unspecified depressive
disorder.” Last, DSM-​5 removed the bereavement exclu-
sion and added “with anxious distress” and “with mixed
features” specifiers for MDD. These changes are not
without controversy and require further investigation into
their validity and clinical utility. In this chapter, we focus
primarily on DSM-​ IV-​
TR (APA, 2000)  major depres-
sive disorder (MDD) and, to a lesser extent, dysthymic
disorder (DD), given the scant research on the DSM-​5
changes. Nevertheless, we highlight any literature evalu-
ating DSM-​5 depressive disorders.
99
We believe that the diagnoses of the depressive disor-
ders have a moderate degree of clinical utility and construct
validity in children and adolescents. However, as under-
standing of the etiology and development of depression
increases, the classification of depression in young people
will undoubtedly change in significant ways. For instance,
the National Institute of Mental Health (NIMH) initiated
the Research Domain Criteria (RDoC) project to provide
a new framework for studying mental disorders. RDoC
integrates many levels of information (from genomics to
self-​report) to better understand basic biobehavioral dimen-
sions underlying the full range of human behavior (Insel
et al., 2010). As the RDoC framework is investigated, it may
have a substantial impact on how we classify depressive and
other mental disorders across the lifespan.
An assessment strategy should be driven by the avail-
able data on the clinical features, associated characteris-
tics, course, and treatment of depression, as well as what is
known about the processes involved in the maintenance
and recurrence of episodes. Hence, we begin with a brief
overview of the literature on the psychopathology and
treatment of depressive disorders in children and adoles-
cents. This is followed by a review and evaluation of the
tools used in each phase of assessment.
THE NATURE OF DEPRESSION
Psychopathology
In the DSM-​IV-​TR and DSM-​5, MDD in children and ado-
lescents is defined by a period of at least 2 weeks character-
ized by the presence of depressed or irritable mood or loss
10

100 Mood Disorders and Self-Injury

of interest or pleasure, and at least five of nine symptoms. functioning. Depressed children and adolescents often
DSM-​IV-​TR DD and DSM-​5 persistent depressive disorder exhibit significant impairment in family, school, and peer
in children and adolescents are defined as a period of at least functioning, and some degree of impairment may persist
1 year characterized by depressed or irritable mood and at after recovery from the depressive episode (Garber &
least two of six symptoms. Although DSM-​IV-​TR MDD and Horowitz, 2002; Lewinsohn & Essau, 2002). Depression
DD are not mutually exclusive (i.e., they often co-​occur, a is the leading risk factor for youth suicide, and it may be
phenomenon referred to as “double depression”), DSM-​ a risk factor for the development of other disorders such
5 persistent depressive disorder is mutually exclusive from as substance abuse (Birmaher, Arbelaez, & Brent, 2002).
MDD because the latter diagnosis reflects episodic depres- The causal relationship between depression and func-
sive episodes only. Although evidence supporting devel- tional impairment is complex: Depression causes signifi-
opmental differences in the factor structure for depressive cant impairment, but poor functioning may also be a risk
symptoms has been mixed, there is evidence for age-​related factor for depression.
increases in cognitive symptoms, anhedonia, hypersomnia,
weight gain, decreased energy, and social withdrawal, which
Comorbidity
likely reflect the age-​related increases in the rates of depres-
sive disorders rather than their changing presentations across
Depressive disorders are comorbid with other disorders
development (Gibb, 2014). However, there is evidence that across the lifespan. In school-​aged children and adoles-
the duration criterion for MDD should be reduced for very cents, approximately two-​thirds of depressed youth have
young children (Luby et al., 2003). at least one comorbid disorder (Avenevoli, Swendsen,
He, Burstein, & Merikangas, 2015; Ford, Goodman, &
Meltzer, 2003). In a meta-​analysis of studies using com-
Prevalence
munity samples, Angold, Costello, and Erkanli (1999)
Depressive disorders are relatively uncommon in children reported that the median odds ratios for the associations
but are more frequent in adolescents. In community sam- of depression with anxiety, conduct, and attention deficit
ples, the point prevalence of depressive disorders is 0.5% disorder were 8.2, 6.6, and 5.5, respectively. Depression
to 2% in preschool-​aged children, 1% to 3% in school-​ is also often comorbid with eating, reading, and develop-
age children, and 5% to 6% in adolescents; the lifetime mental disorders, and general medical conditions. Even
prevalence in adolescents is 15% to 20% (Gibb, 2014; after adjusting for the presence of other diagnoses and their
Lewinsohn & Essau, 2002). Not surprisingly, the preva- comorbidity among each other, youth depression continues
lence of depression is much higher in clinical settings, to evidence significant comorbidity with generalized anxi-
with estimated rates of 8% to 15% in children and greater ety, social anxiety, oppositional defiant disorder (ODD),
than 50% in adolescents (Garber & Horowitz, 2002). conduct disorder (CD), and attention-​deficit/​hyperactivity
There is no consistent gender difference in the preva- disorder (ADHD) (adjusted median odds ratios were 37.9,
lence of depressive disorders in children; however, the 9.9, 10.9, 2.5, and 1.5, respectively) (Copeland, Shanahan,
rates diverge in early adolescence, and by age 15 years the Erkanli, Costello, & Angold, 2013). In depressed pre-
prevalence is approximately two times higher in females schoolers, rates of comorbidity may be higher, and the
than in males (Hankin et al., 1998). overlap with anxiety disorders and the behavioral disorders
is present even at this young age (Egger & Angold, 2006;
Maughan, Collshaw, & Stringaris, 2013).
Associated Features

Two associated features that are important to consider

in assessing depression are functional impairment and
comorbidity, as both may influence course and treatment
response, as well as constituting important treatment tar-
gets in their own right.
Functional Impairment
Depressive disorders in children and adolescents are
associated with significant problems with psychosocial
Course
Almost all children and adolescents with an episode of
MDD recover, although many continue to experience
subsyndromal (or residual) symptomatology. The length
of episodes varies. The mean duration of episodes of
MDD is approximately 7 or 8  months in clinical sam-
ples, and episodes of DD last an average of 48  months
(Birmaher et  al., 2002; Kovacs, 1996). Rates of relapse
and recurrence of MDD are high, with the majority of
 10
depressed juveniles experiencing another episode within
several years (Birmaher et al., 2002; Kovacs, 1996). With
respect to homotypic continuity, long-​ term follow-​ up
studies indicate that adolescents with MDD are at high
risk for experiencing depressive episodes (Copeland,
Shanahan, Costello, & Angold, 2009; Lewinsohn,
Rohde, Klein, & Seeley, 1999) and significant functional
impairment (Copeland, Wolke, Shanahan, & Costello,
2015) in adulthood. Preschool-​onset depression has been
found to predict school-​age and early adolescent depres-
sion (Luby, Gaffrey, Tillman, April, & Belden, 2014), but
long-​term follow-​up studies into adolescence and adult-
hood are unavailable. Evidence for childhood depres-
sion predicting adolescent and adult depression is less
consistent (Birmaher et  al., 2002). Depressive disorders
also evidence significant heterotypic continuity (i.e., one
disorder predicts another disorder) with anxiety, ODD/​
CD, ADHD, and substance use disorders. The tempo-
ral sequence between disorders appears to change across
development and is often bidirectional (Maughan et al.,
2013). For example, although the temporal sequenc-
ing of the association between anxiety and depression is
bidirectional by late adolescence, anxiety often precedes
depression in childhood and early adolescence. There is
also evidence of an increased risk for depression associ-
ated with the irritable subcomponent of ODD.
The mechanisms and processes that serve to main-
tain depressive episodes and cause recurrences are
poorly understood. However, longitudinal studies of the
course of depression in children and adolescents have
identified a number of factors that appear to predict the
duration of MDD episodes and the probability of recur-
rence. Variables that are associated with a longer time to
recovery include an early age of onset, greater severity of
depression, suicidality, double depression, the presence of
comorbid anxiety or disruptive behavior disorders, depres-
sotypic cognitions, and an adverse family environment.
Variables that have been associated with an increased
risk of recurrence include greater severity, psychotic
symptoms, suicidality, a prior history of recurrent MDD,
double depression, the presence of subthreshold symp-
toms after recovery, a depressotypic cognitive style, recent
stressful life events, an adverse family environment, and
a family history of MDD (particularly if it is recurrent)
(Birmaher et al., 2002).
Children and adolescents with MDD and DD are
also at risk for developing manic and hypomanic epi-
sodes. The probability of “switching” to bipolar disorder is
higher in patients with psychotic symptoms, psychomotor
retardation, a family history of bipolar disorder, and/​or a
Depression in Children and Adolescents 101
high familial loading for mood disorders (Birmaher et al.,
2002; Geller, Fox, & Clark, 1994).
The processes and mechanisms involved in increased
risk for the onset of depression are likely multifaceted and
include a number of inherited, biological, and psychoso-
cial risk factors, including (but not limited to) a family his-
tory of depression, stressful life events, family separation
and conflict, child maltreatment, peer difficulties, child
temperament, early mood and behavioral dysregulation,
neuroendocrine and neurocognitive processes, neural
circuitry involved in the processing of threat and reward,
and genetic pathways involving gene–​environment corre-
lations and interactions (Gibb, 2014; Klein, Goldstein, &
Finsaas, 2017; Maughan et al., 2013; Thapar, Collishaw,
Pine, & Thapar, 2012).
Treatment
There is relatively strong support for the efficacy of
cognitive–​ behavioral therapy (CBT) and interpersonal
therapy (IPT) for depressed adolescents, but effects are
modest (effect sizes of Cohen’s d = 0.37 and 0.26 for CBT
and IPT, respectively; for a review, see Maalouf & Brent,
2012). Fewer data are available on the efficacy of psycho-
social interventions in school-​aged children. Although the
findings have varied, the majority of studies have reported
evidence supporting the efficacy of CBT (Maalouf &
Brent, 2012). Data on the treatment of depression in
young children are very sparse. Luby and colleagues
(Lenze, Pautsch, & Luby, 2011; Luby, Lenze, & Tillman,
2012)  adapted parent–​child interaction therapy (PCIT),
originally developed for early childhood externalizing
problems, for preschool-​ onset depression by adding an
emotional development module (termed PCIT-​ED); pre-
liminary findings suggest PCIT-​ED may be a promising
treatment for preschool-​onset depression. Some evidence
also suggests that CBT may be effective in preventing the
onset of depression and reducing symptoms, particularly
in high-​risk youth, but treatment effects decrease substan-
tially over time (Maalouf & Brent, 2012; Stockings et al.,
2016). The effects of family therapy either alone or in con-
junction with treatment for adolescents have been mixed;
however, treatment of parents’ depression, alone or in con-
junction with youths’ treatment, shows benefit (Maalouf
& Brent, 2012). Despite the efficacy of psychosocial inter-
ventions for depressed children and adolescents in clinical
trials, there is evidence that the types of treatments rou-
tinely provided in community settings are less successful
than these evidence-​based treatments (Weersing & Weisz,
2002). Treatments that are adapted for or developed in
102
102 Mood Disorders and Self-Injury
community settings are needed (for a review, see Weisz,
Krumholz, Santucci, Thomassin, & Ng, 2015).
Controlled pharmacotherapy clinical trials in children
and adolescents are also limited. The available evidence
indicates that the cyclic antidepressants are not effica-
cious. Several double-​blind placebo-​controlled trials have
reported benefits for selective serotonin reuptake inhibi-
tors (SSRIs) in adolescents or mixed samples of children
and adolescents (average effect size, Cohen’s d  =  0.25;
Bridge et al., 2007), although effects are modest and some
published and unpublished studies have failed to find dif-
ferences (Maalouf & Brent, 2012; Vasa, Carlino, & Pine,
2006; Vitiello, 2011). Some evidence suggests that the com-
bination of medication and CBT is superior to medication
alone, particularly for moderate to severe depression and
treatment-​resistant depression, although there are negative
findings; nevertheless, combined treatment appears to pro-
vide greater improvement of functional status (Dubicka,
et  al., 2010; Vitiello, 2009). Questions have also been
raised about whether SSRIs are associated with increased
suicidal ideation and behavior in children and adolescents
(Bridge et  al., 2007; Maalouf & Brent, 2012). Currently,
fluoxetine and escitalopram are the only SSRIs approved
for the treatment of adolescent depression in the United
States, and only fluoxetine is cautiously recommended for
use with preadolescent children; thus, the effects of medi-
cation use in youth must be closely monitored.
Even following an acute phase of one of these effec-
tive treatments, approximately 30% to 50% of depressed
youth do not improve (Vitiello, 2009), and of those who do
improve, rates of relapse and recurrence are high when psy-
chosocial and pharmacological treatments are terminated.
Although continued treatment with an SSRI has been
shown to lower relapse rates compared to placebo (Emslie
et al., 2008), the combination of medication management
and CBT demonstrates lower relapse rates compared
to medication management alone (Emslie et  al., 2015;
Kennard et al., 2014). Moreover, in youth with treatment-​
resistant depression who received an acute SSRI treatment,
switching to a combination of CBT and another antide-
pressant resulted in greater clinical response compared to
switching to another medication without CBT (Brent et al.,
2008). Continued monitoring of treatment response and
pursuing other treatment avenues when patients are not
responding to treatment are critical.
Data on predictors of treatment response in depressed
children and adolescents are limited. Although findings
are mixed, data suggest that greater baseline symptom
severity, comorbid anxiety, anhedonia, hopelessness,
nonsuicidal self-​injurious behavior, subsyndromal manic
symptoms, and severe parent–​child conflict predict poorer
treatment response (Emslie, Kennard, & Mayes, 2011).
Moreover, combined treatment may be more effective
for certain adolescents, including those with comorbid
conditions and moderate to severe depression (Emslie
et al., 2011).
DSM-​5 DMDD
DMS-​5 DMDD is characterized by severe temper tan-
trums and persistently angry/​irritable mood that are pres-
ent for at least 12  months and across contexts. DMDD
cannot be diagnosed in children before age 6  years and
must be observed by age 10  years. Emerging research
shows that DMDD may be relatively common in clinical
settings (26.0%–​30.5%) (Axelson et al., 2012; Margulies,
Weintraub, Basile, Grover, & Carlson, 2012)  but fairly
uncommon in community samples (with 3-​ month
prevalence rates ranging from 0.8% to 8.2%; Copeland,
Angold, Costello, & Egger, 2013; Dougherty et al., 2014,
2016). DMDD frequently co-​occurs with another disor-
der (60.5% to 92.0% in the community-​based studies), and
the highest rates of co-​occurrence are with depression and
ODD (Copeland, Angold, et al., 2013; Dougherty et al.,
2014). The course and stability of DMDD across child-
hood are largely unknown. Findings suggest that rates of
DMDD decrease across childhood (Copeland, Angold,
et al., 2013; Dougherty et al., 2016), and the majority of
children with DMDD (Deveney et al., 2015; Dougherty
et al., 2016) no longer meets criteria for the diagnosis at
3-​or 4-​year follow-​up. However, these children are at high
risk for continued impairment and other forms of psycho-
pathology across childhood and into adulthood, includ-
ing adult depressive and anxiety disorders (Copeland,
Shanahan, Egger, Angold, & Costello, 2014; Dougherty
et  al., 2016). No randomized control clinical trials for
DMDD have been conducted to date.
PURPOSES OF ASSESSMENT
Clinical assessment can be thought of as a sequence
including at least three phases: diagnosis, case conceptu-
alization and treatment planning, and treatment moni-
toring and evaluation. The major goal of the first phase
is to develop a preliminary diagnosis and prognosis. For
depression, this includes determining whether criteria
are met for MDD or persistent depressive disorder and
ruling out exclusionary diagnoses such as bipolar disor-
der and depression due to a general medical condition
 103
or substance. As part of the assessment of depression, the
clinician must assess key symptoms (e.g., suicidal ideation
and psychotic symptoms) that might influence treatment
decisions. In addition, it is important to carefully assess
the previous course of the depression (e.g., prior episodes
and chronicity) due to its prognostic value and possible
implications for long-​term treatment. It is also important
to assess comorbid psychiatric, developmental, and gen-
eral medical disorders, and areas of significant functional
impairment (e.g., family, school, and peers), in order to
determine whether depression is the principal diagnosis
that should be the primary target of intervention and
because of their prognostic implications. Given the high
comorbidity between the mood and anxiety disorders,
we refer the reader to Chapter 11 in this volume on the
assessment of child and adolescent anxiety disorders.
The second phase of assessment involves develop-
ing a case conceptualization and treatment planning. In
addition to variables already described, a comprehensive
assessment of personal, interpersonal, or systemic dynam-
ics is crucial in order to provide clues to the development
and maintenance of symptoms and dysfunctional life
patterns and to provide the focus of treatment. First, it is
important to assess the child’s family environment, school
functioning, peer relationships, significant stressors and
traumas, and family history of psychopathology because
these factors have considerable prognostic value and may
be involved in the development and/​or maintenance of
the disorder.
Second, it is important to consider other social factors
such as race, culture, ethnicity, and socioeconomic status.
Poverty, race, social stressors, and ethnicity have all been
linked to greater depression symptomatology in youth
(Taylor & Turner, 2002; Wight, Aneshensel, Botticello,
& Sepulveda, 2005). Furthermore, because current views
of depression are primarily shaped by Western culture,
depression may manifest itself differently across cultures
and ethnicity. This is suggested by differences in the
phenomenology and prevalence of depression across cul-
tures and ethnic groups (Chentsova-​Dutton, Ryder, &
Tsai, 2014). Moreover, we need to examine the validity
of assessment tools across cultures because evidence sug-
gests that they may also vary (e.g., Dere et al., 2015).
Third, data on the severity and prior course of depres-
sion, key symptoms such as suicidal ideation/​behavior
and psychotic symptoms, comorbidity, and functional
impairment are important for determining the appropri-
ate treatment setting (e.g., inpatient vs. outpatient), the
intensity and duration of treatment, and perhaps the treat-
ment modality. As noted previously, however, few data
Depression in Children and Adolescents 103
are available to guide these decisions. Information on
comorbidity is also necessary to determine whether other
disorders should be monitored or targeted for treatment.
Finally, it is critical to take a detailed history of previous
treatment and assess the goals, attitudes, and motivation
of the child and parents with respect to the relevant treat-
ment options. This information is critical both for treat-
ment selection and for engaging the child and family in
treatment. Because children and parents often disagree
on the selection of treatment targets (Hawley & Weisz,
2003), it may take considerable negotiation in order to
develop a treatment plan that is acceptable to all parties.
The third phase of assessment involves treatment moni-
toring and evaluation. This entails systematically assessing
the degree of change in target symptoms and impairments
in order to determine whether treatment should be con-
tinued, intensified, augmented, changed, or terminated.
Although few guidelines are available to help clinicians
determine when treatment should be modified, recent
work has begun development and preliminary evaluation
of “adaptive interventions” for use in child and adolescent
mental health services, which provide a sequence of deci-
sion rules that determine whether, how, or when to alter
the type, dosage, or delivery of service over the course of
treatment (Almirall & Chronis-​Tuscano, 2016; Gunlicks-​
Stoessel, Mufson, Westervelt, Almirall, & Murphy, 2016).
Research in this area is critically needed.
Information Source
It is important to obtain data from multiple informants,
including the child, parents, and teachers. Child report is
critical because parents and teachers tend to report lower
levels of depressive and other internalizing symptoms in
children than youths report themselves (Jensen et  al.,
1999). However, it is useful to supplement youths’ reports
with information from collaterals to assess externalizing
disorders. Parent reports are particularly important for
preschool and school-​age children. Due to developmen-
tal limitations in cognitive processes and language abili-
ties, children are less reliable reporters of psychopathology
than adolescents (Edelbrock, Costello, Dulcan, Kalas, &
Conover, 1985). In addition, younger children have diffi-
culty reporting on information regarding temporal param-
eters; therefore, parents must be relied on for information
on course such as age of onset, previous episodes, and
duration of current episode (Kovacs, 1986). Finally, par-
ents are more involved in the day-​to-​day lives of children
than adolescents and therefore are more knowledgeable
about their behavior and activities.
104
104 Mood Disorders and Self-Injury
Although obtaining data from multiple informants is
optimal, agreement between informants is only fair to
moderate (Achenbach, McConaughy, & Howell, 1987).
Informants tend to agree more when they observe youths
in the same context, when the target behavior is easy to
observe (e.g., externalizing vs. internalizing), and when
a dimensional measure (vs. a categorical measure) is
used (Achenbach et al., 1987; De Los Reyes et al., 2015).
Nevertheless, evidence suggests that informant discrepan-
cies provide meaningful and valid information, such as the
situational specificity of the child’s emotional and behav-
ioral problems. Several studies have demonstrated that
child, parent, teacher, and clinician ratings all account for
significant unique variance in predicting subsequent out-
comes (Ferdinand et  al., 2003; Verhulst, Dekker, & van
der Ende, 1997). In addition, depressed parents appear
to have a lower threshold for detecting depression in their
children; hence, their reports tend to yield higher rates of
both true and false positives (i.e., increased sensitivity but
decreased specificity) (Richters, 1992; Youngstrom, Izard,
& Ackerman, 1999).
The low agreement between data sources presents
a significant challenge for clinicians who must decide
how to interpret and integrate conflicting information.
A variety of approaches to integrating data from multiple
informants have been discussed in the literature, includ-
ing assuming that the feature or diagnosis is present if any
informant reports it (the “or” rule), requiring several infor-
mants to confirm the feature or diagnosis (the “and” rule),
relying on the informant who is judged to be the most
valid source of information for the feature or diagnosis,
or developing various statistical procedures for optimiz-
ing prediction (for a review, see De Los Reyes, Thomas,
Goodman, & Kundey, 2013). The approach that most
closely mirrors clinical practice is the “best estimate” pro-
cedure, in which the clinician uses his or her best judg-
ment to evaluate the informant’s credibility and integrate
and resolve conflicting reports. This raises the possibil-
ity of introducing the unreliability and idiosyncrasy that
structured interviews and standardized ratings scales were
developed to prevent (discussed later). However, there
is evidence from the adult literature that, when applied
following appropriate guidelines (e.g., self-​ report takes
precedence for internalizing disorders; informant report
is given priority for externalizing disorders), the reliabil-
ity of best estimate diagnoses can be very high (Klein,
Ouimette, Kelly, Ferro, & Riso, 1994). Nevertheless,
clinical science has not established “best practices” for
using and interpreting multi-​informant assessments, and
work in this area is particularly scarce for the assessment
of youths’ internalizing problems (De Los Reyes et  al.,
2015). However, recent theoretical work on interpreting
multi-​informant assessment outcomes in research (e.g.,
operations triad model; De Los Reyes et  al., 2013)  may
assist in future efforts toward developing evidence-​based
assessment practices in clinical practice.
Attenuation Effect
Studies of interviews and rating scales for both juvenile
and adult psychopathology have often found that rates of
diagnoses and ratings of symptom severity tend to decrease
with repeated administrations, a phenomenon referred to
as the “attenuation effect” (Egger et  al., 2006). Because
this has been observed in nonclinical samples, it cannot
be attributed to treatment or regression to the mean. This
has important implications for treatment monitoring and
evaluation because it is difficult to distinguish the attenu-
ation effect from a positive response to treatment for the
individual patient. Although there is no solution to this
problem at present, it behooves the clinician to be aware
of this phenomenon and to consider alternative explana-
tions for what appears to be improvement on rating scales.
Psychometric Considerations
In reviewing available instruments for each of the assess-
ment phases described previously in this section, accom-
panying tables are used to present general information on
a measure’s psychometric properties and clinical utility.
Thus, the presentation of specific psychometric data is
kept to a minimum in the text and tables. As a general
rule, we chose to include more widely used assessment
tools that have been independently examined by at least
two research groups. We made exceptions to this rule
when a new measure appeared exceptionally promising
due to unique features of the instrument. However, these
newer measures are not included in the tables because
there are insufficient data to evaluate their efficacy at
this time.
Measures were evaluated according to the criteria
presented in Hunsley and Mash’s introductory chapter in
this volume. Nevertheless, we mention several factors that
influenced our ratings. First, inter-​rater reliability can be
examined by raters independently rating a case vignette,
a videotaped or audiotaped assessment, a live assessment
(paired-​rater design), or by two examiners administering
the same instrument at two different time points usually
spanning only a few days (test–​retest design). The first
three approaches hold information constant across raters;
 105
hence, reliability should be higher than that of test–​retest
designs, in which information presented to each examiner
can vary substantially. In making the ratings, we tried to
take the type of design into account. In addition, examin-
ing the test–​retest reliability of depression in youth over
several months or a year is relatively uncommon because
depression in youth is often intermittent/​ episodic.
Therefore, most ratings of test–​retest reliability cannot
receive more than an adequate rating due to the shorter
time frames assessed.
Second, evaluating convergent and divergent valid-
ity of an instrument can be difficult because depression
tends to co-​occur with many other forms of psychopa-
thology. Although depression measures should correlate
more highly with other depression measures than with
measures of other forms of psychopathology, there should
be substantial correlations between measures of depres-
sion and measures of anxiety and/​or behavior problems.
Similarly, depressed youth are likely to differ from nonde-
pressed youth not only on measures of depression but also
on other measures of psychological dysfunction. Thus,
modest discriminant validity may not be a limitation of
the instrument but instead might reflect the comorbidity
between depression and other disorders. Last, very little
work has examined the clinical utility of youth depression
measures. We are aware of only one such study (Hughes
et al., 2005) that used the Schedule for Affective Disorders
and Schizophrenia in School-​Age Children (K-​SADS);
therefore, all other measures did not receive above an
adequate rating on this criterion. Obviously, this is an area
of research that needs much attention.
ASSESSMENT FOR DIAGNOSIS
The two major approaches to diagnosing and assessing
depression in children and adolescents involve inter-
views and rating scales. Interviews can be unstructured,
semi-​structured, or fully structured. Unstructured clinical
interviews are variable across clinicians, who often fail to
inquire about key aspects of psychopathology, particularly
if it is inconsistent with their initial diagnostic impressions
(Angold & Fisher, 1999), and formulate fewer diagnoses
than clinicians using structured interviews (Zimmerman,
2003). With semi-​structured interviews, the interviewer
is responsible for rating the criteria as accurately as pos-
sible, using all available information, and improvising
additional questions or confronting the respondent with
inconsistencies when necessary. In contrast, the inter-
viewer’s role in fully structured interviews is limited to
Depression in Children and Adolescents 105
reading the questions as written and recording the respon-
dent’s answers. As a result, semi-​structured interviews were
designed for use by mental health professionals or well-​
trained and supervised technicians, and seek to capitalize
on their clinical training and experience, whereas fully
structured interviews were developed for lay interviewers
in large-​scale epidemiological studies in which the cost
of interviewers with clinical training is prohibitive. There
have been few direct comparisons of the validity of semi-​
versus fully structured interviews, but some data support
their concordance (e.g., Green et al., 2012). Nevertheless,
given the limited data, we generally assume that the semi-​
structured approach yields higher quality data compared
to the structured approach because the interviewer pre-
sumably has a better sense of the constructs being assessed
than does the respondent.
Rating scales include clinician-​ administered, self-​
report, and parent-​and teacher-​ report measures.
Clinician-​administered rating scales are semi-​structured
interviews that focus on a circumscribed area of symp-
tomatology (e.g., depression). Self-​report and parent and
teacher rating scales are rated by the designated infor-
mant, although they can be read to younger children.
Unlike diagnostic interviews, rating scales do not collect
sufficient information to make a diagnosis (e.g., duration
and exclusion criteria are generally not assessed).
Due to their economy, self and informant rating scales
can be especially valuable as screening instruments, with
elevated scores leading to a more intensive evaluation.
Self-​ rating scales are generally superior to parent and
teacher rating scales in screening for internalizing disor-
ders due to their greater sensitivity. However, even the best
self-​rating scales have only moderate sensitivity and speci-
ficity, producing a substantial number of false positives
and false negatives (Kendall, Cantwell, & Kazdin, 1989).
Because the prevalence of child and adolescent depres-
sion tends to be fairly low in most screening contexts, the
number of false positives greatly outnumbers true posi-
tives (Matthey & Petrovski, 2002; Roberts, Lewinsohn,
& Seeley, 1991). Thus, the potential economy and effi-
ciency of screening must be weighed against the costs of
unnecessary extended evaluations for false-​positive cases
and the risks associated with missing false-​negative cases.
In the next section, we briefly describe several of the
better researched and more widely used semi-​structured
diagnostic interviews, fully structured diagnostic inter-
views, and rating scales. We also chose to include a few
promising assessment tools that are worth noting due to
some unique features of the instrument. We have been
highly selective, and there are a number of equally good,
106

106 Mood Disorders and Self-Injury

but less widely used, measures that we have not included.
For more information on this broader range of instru-
ments, readers are referred to some excellent reviews
(Brooks & Kutcher, 2001; D’Angelo & Augenstein, 2012;
Leffler, Riebel, & Hughes, 2015; Myers & Winters, 2002;
Simmons, Wilkinson, & Dubicka, 2015). There are also a
number of measures of specific components of the depres-
sive syndrome, such as self-​esteem, hopelessness, depres-
sive cognitions, and suicidality (for a review, see Winters,
Myers, & Proud, 2002) that may be useful for particular
cases but are not reviewed here.
Semi-​Structured Diagnostic Interviews
In this section, we briefly review the four most widely
used semi-​structured diagnostic interviews for child and
adolescent psychopathology: the K-​SADS (Puig-​Antich &
Chambers, 1978), the Child and Adolescent Psychiatric
Assessment (CAPA; Angold, Prendergast, et al., 1995) and
its downward extension, the Preschool Age Psychiatric
Assessment (PAPA; Egger & Angold, 2004), and the
Diagnostic Interview for Children and Adolescents
(DICA; Herjanic & Reich, 1982). Information on these
instruments is provided in Table 6.1. Each interview
assesses the criteria for most of the major child and ado-
lescent psychiatric disorders and provides parallel ver-
sions for children and parents, with the exception of the
PAPA, which has a parent version only. Although some
of the instruments are used to interview 6-​and 7-​year-​old
children, it is questionable whether children younger
than 8 or 9 years can provide valid information in a diag-
nostic interview (Angold & Fisher, 1999).
Evaluating the validity of semi-​structured diagnostic
interviews is complex because they are usually used as
the “gold standard” that other measures are compared
against. Construct validity is probably the best standard,
but given the current state of the literature, it is impossi-
ble to distinguish the construct validity of semi-​structured
interviews from the diagnoses that they are designed to
assess. In order to try to disentangle the construct validity
of interviews from diagnostic constructs, it is necessary to
conduct head-​to-​head comparisons of several interviews
using the same sample and the same criteria for construct
validation (e.g., family history and course). Unfortunately,
such studies have not been conducted. Although the dis-
tinction between MDD and DD has important prognostic
implications (Kovacs, 1996), the majority of studies com-
bine them in a higher order depressive disorder category
or focus solely on MDD. Hence, for present purposes, we
focus on depressive disorders as broadly conceived.
The K-​SADS (Puig-​Antich & Chambers, 1978) is the
most widely used semi-​structured interview for children
and adolescents (6–​18 years), and promising preliminary
data suggest that it could possibly be extended to chil-
dren as young as preschool age (Birmaher et al., 2009).
It is the least structured of the semi-​structured interviews,
and therefore it requires the greatest amount of clini-
cal training and experience. The K-​SADS was modeled

Table 6.1  Ratings of Instruments Used for Diagnosis and Prognosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Diagnostic Instruments
K-​SADS NA NA G A G E E G ✓
CAPA NA NA G A G G G A ✓
PAPA NA NA G A G G G A ✓
DICA NA NA A A G A E A
DISC NA NA A A G A E A
Screening and Symptom Severity Instruments
CDRS-​R A G E A G G E A ✓
CDI E G NA A G G E A ✓
MFQ A E NA A A G E A ✓
RCDS G E NA A A G A A
RADS E E NA A G G E A ✓

Note: K-​SADS = Schedule for Affective Disorders and Schizophrenia in School-​Age Children; CAPA = Child and Adolescent Psychiatric Assessment;
PAPA = Preschool Age Psychiatric Assessment; DICA = Diagnostic Interview for Children and Adolescents; DISC = Diagnostic Interview Schedule
for Children; CDRS-​R  =  Children’s Depression Rating Scale-​Revised; CDI  =  Children’s Depression Inventory; MFQ  =  Mood and Feelings
Questionnaire; RCDS = Reynolds Child Depression Scale; RADS = Reynolds Adolescent Depression Scale; A = Adequate; G = Good; E = Excellent;
NA = Not Applicable.
 107
after the adult Schedule for Affective Disorders and
Schizophrenia (SADS). There are a number of versions
of the K-​SADS that assess DSM-​IV criteria. These ver-
sions vary in format, whether they assess lifetime as well
as current psychopathology, and whether they also pro-
vide dimensional measures of symptom severity. Ratings
are based on all sources of information and clinical
judgment. Administration time of the parent and child
interviews range from 35 minutes to 2.5 hours each,
depending on the severity and breadth of the child’s psy-
chopathology. Inter-​rater reliability has been reported to
be adequate to excellent for depressive disorders in sev-
eral studies, and it has been particularly impressive with
the more recent versions of the K-​SADS (Ambrosini,
2000; Kaufman et  al., 1997). Evidence for convergent
validity derives from numerous studies reporting corre-
lations between the K-​SADS and a variety of clinician,
self, and parent rating measures of depression and inter-
nalizing behavior problems (Ambrosini, 2000; Kaufman
et  al., 1997). In addition, youths diagnosed with MDD
using the K-​SADS differed from controls on psychoso-
cial impairment, familial aggregation of mood disorders,
and numerous neurobiological parameters, and K-​SADS
diagnoses of depression predicted continued risk for
recurrence of affective disorders (Ambrosini, 2000).
Nevertheless, it has been suggested that MDD K-​SADS
diagnoses may identify a more severe clinical group than
other assessment tools (Hamilton & Gillham, 1999). In
addition, when K-​SADS items are coded dichotomously
and summed, this K-​ SADS depression scale provides
information that is restricted to more severe symptom
levels (Olino et  al., 2012). Finally, recent data reveal
clear psychometric advantages for the K-​SADS depres-
sion scale, including better coverage of the construct
of depression, when assessment algorithms incorporate
item response theory-​based estimates of symptom sever-
ity, discriminability, and subclinical levels compared to a
raw symptom count score (Cole et al., 2011).
The CAPA (Angold, Prendergast, et al., 1995) assesses
the criteria for most major diagnoses in children aged 9
to 17 years. The time frame for symptom assessment is
the preceding 3 months, and administration time takes
1 or 2 hours (Angold & Costello, 2000). The interview
has several attractive features. First, it is unique in that
it includes an extensive glossary defining specific symp-
toms and distress and frequency ratings. As a result, the
CAPA can be used by interviewers with minimal clini-
cal experience, as long as they adhere closely to the
definitions and conventions in the glossary. Second, it
includes a section for assessing impairment in a number
Depression in Children and Adolescents 107
of areas, including family, peers, school, and leisure
activities, and it also includes sections assessing the fam-
ily environment, life events, and trauma. One test-​retest
reliability study of the CAPA by its developers (Angold
& Costello, 1995) reported kappas for MDD and DD of
.90 and .85, respectively, and an intraclass correlation for
the MDD symptom scale of .88. Studies, not conducted
by the CAPA developers, also reported good to excel-
lent inter-​rater reliability values using audiotaped inter-
views for diagnoses of MDD and DD (Jozefiak et  al.,
2016; Wamboldt, Wamboldt, Gavin, & McTaggart,
2001) and for parent-​and child-​rated depression symp-
toms (Hammerton, Thapar, & Thapar, 2014; Mars
et  al., 2012). Angold et  al. (2012) compared diagnoses
generated from the CAPA to those generated using
the Diagnostic Interview Schedule for Children-​ IV
(DISC-​IV), and the rates of MDD/​DD obtained using
the CAPA (9.5%) and the DISC-​IV (5.3%) did not sig-
nificantly differ (κ = .56), suggesting that these measures
are relatively comparable. Supporting its convergent
validity, depression as diagnosed by the CAPA is asso-
ciated with significant levels of functional impairment,
higher concordance among monozygotic than among
dizygotic twins, lower income, nonsupportive parenting,
maternal history of depression, and similar psychosocial
risk factors as those observed in adult-​onset depression
(Angold & Costello, 2000; Luby et al., 2014; Shanahan,
Copeland, Costello, & Angold, 2011).
The PAPA (Egger, Ascher, & Angold, 1999)  was
developed as a downward extension of the CAPA that
incorporates developmental modifications for children
2-​to 5-​years-​old. Thus, the time frame, assessment time,
and other unique features of the CAPA described previ-
ously also apply to the PAPA. Given the limited diagnos-
tic assessment measures for children younger than age
8  years, the PAPA has been used in children up to age
8 years (e.g., Luby et al., 2014). Adequate test–​retest reli-
ability values for a depressive disorder diagnosis (κ = .62
to .72) and for depressive symptoms (intraclass correla-
tion coefficient [ICC] = .71 to .88) have been reported
using independent interviews (Egger et  al., 2006; Luby
et al., 2014). In addition, in a sample of 14 children, simi-
lar diagnoses were generally derived from the PAPA and
the K-​SADS (Birmaher et al., 2009). Inter-​rater reliability
values using audiotaped interviews of the parent inter-
view of the PAPA ranged from .63 to 1.00 for a depressive
disorder diagnosis and from .85 to .98 for depressive symp-
toms scale (Danzig et al., 2013; Gaffrey, Barch, Singer,
Shenoy, & Luby, 2013; Luby et  al., 2014; Wichstrøm
et  al., 2012; Wichstrøm & Berg-​Nielsen, 2014). Much
108

108 Mood Disorders and Self-Injury

of the research establishing the construct and criterion Fully Structured Diagnostic Interviews
validity of the PAPA depressive disorder diagnosis was per-
In this section, we review the DISC (Costello, Edelbrock,
formed by Luby and colleagues, although other groups
Dulcan, Kalas, & Klaric, 1984), the most widely used fully
have recently provided similar support. Depression diag-
structured diagnostic interview for child and adolescent
nosed with the PAPA using developmentally modified
psychopathology. There are other fully structured inter-
diagnostic criteria for preschoolers is associated with sig-
views, such as the Children’s Interview for Psychiatric
nificant functional impairment across multiple domains
Syndromes (ChIPS; Weller, Weller, Fristad, Rooney,
(Bufferd, Dougherty, Carlson, & Klein, 2011; Danzig
& Schecter, 2000), the Dominic-​R (Valla, Bergeron, &
et  al., 2013; Luby, Belden, Pautsch, Si, & Spitznagel,
Smolla, 2000), and the Development and Well-​ Being
2009), demonstrates homotypic continuity over both 12-​
Assessment (DAWBA; Goodman, Richards, Ford,
and 24-​month follow-​up (Luby, Si, Belden, Tandon, &
Gatward, & Meltzer, 2000), although the DAWBA also
Spitznagel, 2009), and predicts depression in school-​age
allows respondents to enter open-​ended responses, which
children (Luby et al., 2014). In addition, characteristics
can be reviewed by a clinician to modify final diagnoses.
and patterns of risk similar to those reported in depressed
These instruments are not reviewed here given the lim-
older children and adults have been observed in pre-
ited data for depression.
school depression diagnosed with the PAPA, including
The DISC (Costello et  al., 1984)  assesses a broad
rates of comorbidity, patterns of heterotypic continu-
range of psychiatric disorders that, in the latest version
ity, early predictors, and associations with temperament
(DISC-​IV), reflect DSM-​IV and International Statistical
and neurobiological correlates (e.g., Bufferd et  al.,
Classification of Diseases, 10th revision (ICD-​10; World
2014; Dougherty et al., 2011; Gaffrey et al., 2013; Luby,
Health Organization, 1992), criteria (Shaffer, Fisher,
Belden, et  al., 2009; Wichstrøm et  al., 2012). Finally,
Lucas, Dulcan, & Schwab-​ Stone, 2000). The DISC
several studies examining the structure of preschool
includes separate interviews for youth (9–​17  years) and
psychopathology using the PAPA yield a relatively simi-
parents of 6-​to 17-​year-​olds. The time frame includes the
lar structure observed in older youth and adults (Olino,
past 12 months and the past 4 weeks, and the DISC takes
Dougherty, Bufferd, Carlson, & Klein, 2014; Sterba,
between 1 and 2 hours to complete. Inter-​rater reliabil-
Egger, & Angold, 2007; Wichstrøm et al., 2014).
ity of the DISC was adequate in the initial DISC study
The DICA (Herjanic & Reich, 1982) was originally
(Costello et al., 1984). Test–​retest reliability estimates for
designed as a fully structured interview, but recent ver-
MDD for the earlier versions range from poor to good
sions have been semi-​structured in nature. The most
(Hodges, 1994; Shaffer et  al., 2000). However, results
recent version of the DICA (Reich, 2000) assesses both
obtained with the DISC-​IV suggest that it has better test–​
DSM-​III-​R and DSM-​IV criteria, and it includes sepa-
retest reliability than its predecessors, especially in clini-
rate interviews for children (6–​12  years), adolescents
cal samples (Shaffer et al., 2000). Concordance between
(13–​17 years), and parents. The interview adopts a life-
DISC diagnoses and clinicians’ diagnoses (Hodges, 1994;
time time frame and takes approximately 1 to 2 hours
Lewczyk, Garland, Hurlbert, Gearity, & Hough, 2003;
to complete. Data on inter-​rater reliability has varied
Schwab-​Stone et  al., 1996)  and self-​rated measures of
across studies, ranging from poor to good (Boyle et al.,
depressive symptoms (Angold, Costello, Messer, & Pickles,
1993; Brooks & Kutcher, 2001; Reich, 2000). DICA
1995; Hodges, 1994) range from poor to good, providing
diagnoses are moderately correlated with clinicians’
only limited evidence of convergent validity. Moreover,
diagnoses and also clinician and self-​rated measures of
the DISC (original version) evidenced very low concor-
depressive symptoms (Brooks & Kutcher, 2001; Reich,
dance with the K-​SADS for MDD and poor discrimi-
2000), providing evidence of convergent validity. DICA
nant validity (Hodges, 1994). Prevalence studies have
MDD specificity rates are generally high, but its sensi-
also suggested that the DISC (original version) has good
tivity rates are low, which suggests that the DICA tends
sensitivity but poor specificity, leading to overdiagnosing
to underdiagnose MDD compared to other measures
(Hodges, 1994). However, a recent study (Angold et al.,
(Ezpeleta et  al., 1997; Olsson & von Knorring, 1997).
2012) comparing the DISC-​IV and the CAPA found that
A downward extension of the DICA has been developed
the instruments were relatively comparable overall (with
for parents of preschool-​aged children (Ezpeleta, de la
the exception of specific phobia) and in their diagnosis of
Osa, Granero, Domenech, & Reich, 2011); however,
depression. Finally, Lucas, Fisher, and Luby (1998) used
data are too limited to recommend its use for the assess-
a downward extension of the DISC-​IV for preschoolers
ment of depression.
 109

Depression in Children and Adolescents 109

(DISC-​IV Young Child), which demonstrated encourag- severity in children with general medical conditions due
ing results for the diagnosis of depression, as well as data to its emphasis on somatic symptoms (Brooks & Kutcher,
on the external validity of MDD DISC-​IV diagnoses in 2001; Myers & Winters, 2002).
this age group (Luby, Mrakotsky, Heffelfinger, Brown, & There are a number of widely used self-​rating scales
Spitznagel, 2004; Luby et al., 2006). for child and adolescent depression. We briefly review
four:  Children’s Depression Inventory (CDI; Kovacs,
1992), Mood and Feelings Questionnaire (MFQ; Angold,
Rating Scales
Costello, et al., 1995), Reynolds Child Depression Scale
In this section and in Table 6.1, we review some of (RCDS; Reynolds, 1989), and Reynolds Adolescent
the more widely used clinician, self-​report, and multi-​ Depression Scale (RADS; Reynolds, 1987). Some of these
informant rating scales for depression. Information on measures, such as the MFQ, are based on older versions
rating scales designed for adults that are often used with of the DSM. However, their use is still warranted because
older adolescents can be found in Chapter 7 in this vol- there have been few changes in symptoms and criteria for
ume. The Hamilton Rating Scale for Depression (HAM-​ depressive disorders from DSM-​III to DSM-​5.
D), Beck Depression Inventory (BDI), and Center for The CDI (Kovacs, 1992) is the most widely used depres-
Epidemiological Studies-​Depression Scale (CES-​D) have sion rating scale for children and adolescents. Developed
similar psychometric properties in adolescent and adult as a modified version of the BDI, it assesses severity of
samples (Olino et  al., 2013; Roberts et  al., 1991), have depression during the previous 2 weeks in children aged
comparable reliability and validity values compared to 7 to 17 years. The original CDI includes 27 items, and the
measures that were specifically designed for juveniles, and revised version (CDI-​2; Kovacs, 2011) includes 28 items.
have been sensitive to treatment effects (Weisz, McCarty, The CDI and CDI-​2 have shorter versions with 10 and 12
& Valeri, 2006). These measures appear to be acceptable items, respectively. Items cover a broad range of depres-
alternatives for older adolescents. sive symptoms and associated features, with a particular
The most widely used clinician scale for rating depres- emphasis on cognitive symptoms, and the CDI takes 10 to
sion in children is the Children’s Depression Rating Scale 20 minutes to complete. A number of studies have reported
(CDRS; Poznanski, Cook, & Carroll, 1979). Based on the that the CDI (original version) has good internal consis-
HAM-​D, the CDRS was developed to assess current sever- tency, and many, but not all, studies have also reported
ity of depression in children aged 6 to 12 years and is often good short-​term test–​retest reliability estimates (Brooks &
used for adolescents as well. The revised version (CDRS-​ Kutcher, 2001; Kovacs, 1992; Silverman & Rabian, 1999).
R; Poznanski & Mokros, 1999) contains 17 items assessing Studies of the factor structure of the CDI (original version)
cognitive, somatic, affective, and psychomotor symptoms have produced inconsistent findings, with some indication
and draws both on the respondent’s report and the inter- that the factor structure varies by age and non-​English ver-
viewer’s behavioral observations. It takes 20 to 30 minutes sions (Cole, Hoffman, Tram, & Maxwell, 2000; Huang &
to administer. It is designed to be administered separately Dong, 2014; Weiss & Garber, 2003). The CDI (original
to the child and an informant (typically the parent), with version) is moderately to highly correlated with the CDRS,
the clinician subsequently integrating the data using clini- a number of other self-​rated depression scales, and other
cal judgment. Cut-​off scores are provided to aid in inter- measures of related constructs supporting its convergent
preting levels of depression severity. Scores on the CDRS validity (Brooks & Kutcher, 2001; Myers & Winters, 2002;
have good internal consistency and good inter-​rater reli- Silverman & Rabian, 1999). However, the discriminant
ability (Brooks & Kutcher, 2001; Myers & Winters, 2002). validity of the CDI (original version) is questionable
Its convergent validity has been supported by moderate because it is almost as highly correlated with measures
to high correlations with the HAM-​D, several self-​rated of anxiety as it is with other measures of depression, and
depression scales, and K-​SADS MDD diagnosis (Brooks studies examining its ability to distinguish depressed from
& Kutcher, 2001; Mayes, Bernstein, Haley, Kennard, & nondepressed patients have yielded conflicting findings
Emslie, 2010; Myers & Winters, 2002). The CDRS-​R (Myers & Winters, 2002; Silverman & Rabian, 1999). The
achieved moderate to good discriminative validity in clas- CDI-​2 demonstrated good internal consistency, test–​retest
sifying depressive disorders compared to other disorders reliability, construct validity, and discriminant validity in
(Yee et  al., 2015). However, some data suggest that the differentiating the MDD from a control group and other
CDRS scores may not distinguish between depression and psychiatric groups, and it correlated with other self-​report
anxiety and that the CDRS may overestimate depression measures of depression (Kovacs, 2011).
10
110 Mood Disorders and Self-Injury
The MFQ (Angold, Costello, et al., 1995) was devel-
oped to assess depression during the past 2 weeks in
youths aged 8 to 18  years. It consists of 32 items cover-
ing the DSM-​III-​R criteria for depression and additional
symptoms, such as loneliness and feeling unloved or
ugly. Angold, Costello, et  al. also developed a shorter
13-​item version (SMFQ) by selecting items that yielded
optimal discriminating power and internal consistency.
The MFQ takes approximately 10 minutes to complete.
Scores on the measure have been found to have excel-
lent internal consistency and adequate to good test–​retest
reliability (Angold, Costello, et  al., 1995; Daviss et  al.,
2006; Wood, Kroll, Moore, & Harrington, 1995). In addi-
tion, it has demonstrated good convergent validity with
respect to the CDI, DISC, CAPA, and K-​SADS (Angold,
Costello, et al., 1995; Thapar & McGuffin, 1998; Wood
et al., 1995). The MFQ was also relatively successful in
discriminating youths with diagnoses of depression from
those with non-​mood disorders (Daviss et al., 2006; Kent,
Vostanis, & Feehan, 1997; Thapar & McGuffin, 1998).
The RCDS (Reynolds, 1989)  and RADS (Reynolds,
1987)  are 30-​item scales designed to assess depressive
symptomatology (as represented in DSM-​III) during the
previous 2 weeks in youths aged 8 to 12 years and 13 to
18  years, respectively. Each scale takes approximately
10 minutes to complete. The Reynolds scales have been
used primarily with school, rather than clinical, samples.
Scores on both scales have excellent internal consistency
and adequate test–​retest reliability (Brooks & Kutcher,
2001; Myers & Winters, 2002). In addition, both are cor-
related with interview diagnoses and other depression
rating scales, such as the CDRS, HAM-​D, CDI, BDI,
and CES-​D (Brooks & Kutcher, 2001; Myers & Winters,
2002). Discriminant validity has not been well-​studied,
although like most depression rating scales, the RADS is
moderately correlated with measures of anxiety (Myers &
Winters, 2002). Revised versions of the RCDS (RCDS-​
2; Reynolds, 2010)  and RADS (RADS-​ 2; Reynolds,
2004)  have been developed, and initial reports support
similar psychometric properties as their predecessors
(Osman, Gutierrez, Bagge, Fang, & Emmerich, 2010;
Reynolds, 2004; Reynolds, 2010). Both the RCDS-​2 and
the RADS-​2 also expanded the age range to include youth
aged 7 to 13 years and 11 to 20 years, respectively.
Two new instruments are worth mentioning. First, the
NIMH recently initiated a Patient Reported Outcomes
Measurement Information System (PROMIS) network
that used psychometric methods to develop instru-
ments to address multiple domains of psychological
and physical health. The PROMIS network developed
a unidimensional 28-​ item depression measure for use
with adults, which has also been used in adolescents
(PROMIS-​Depression; Pilkonis et  al., 2011), and a 14-​
item depression pediatric measure for youth aged 8 to
17 years (Irwin et al., 2010). Both the adult and the pedi-
atric versions have a short 8-​item depression measure.
Preliminary evidence supports their construct validity and
reliability and their ability to assess the full range (none/​
mild to severe) of depressive symptoms (Irwin et al., 2010;
Olino et al., 2013; Pilkonis et al., 2011). Second, the Beck
Depression Inventory for Youth (BDI-​Y; Beck, Beck, &
Jolly, 2001)  assesses DSM-​IV symptoms of depression,
with a focus on cognitive features of depression, in youth
aged 7 to 14  years. The BDI-​Y includes 20 items, and
preliminary evidence demonstrates good internal consis-
tency, high correlations with the CDI, and successful dif-
ferentiation between youth with depression and controls
(Beck et al., 2001; Stapleton, Sander, & Stark, 2007).
As noted previously, it is important to obtain informa-
tion about child and adolescent depression from infor-
mants other than the youths themselves. Several of the
self-​rating scales, such as the CDI, have been reworded for
use by parents and, in some cases, by teachers and peers.
Some psychometric data have been reported on these
adaptations. Kovacs (2003) reported data on the norms
and factor structure of the parent and teacher versions of
the CDI, as well as good internal consistency for these
measures. In addition, Cole et al. (2000) compared child-​
and parent-​report versions of the CDI. They reported that
the two versions had similar internal consistencies and
test–​retest reliabilities and that the factor structure of the
CDI was relatively similar, although not identical, across
informants.
There are also a number of multi-​informant rating
scales that were designed to assess a broad range of child
and adolescent psychopathology using instruments that
are comparable across informants (Hart & Lahey, 1999).
The most widely used is the parent-​report Child Behavior
Checklist for ages 6 to 18 years (CBCL/​6-​18; Achenbach
& Rescorla, 2001a) and the CBCL for ages 1½ to 5 years
(CBCL/​1½-​5; Achenbach & Rescorla, 2001b) and their
accompanying teacher report (Teacher Report Form
[TRF]) and youth report for ages 11 to 18  years (Youth
Self-​Report [YSR]) versions. The CBCL and YSR assess
the child’s behavior during the past 6 months, whereas the
TRF uses a 2-​month time frame. All three measures take
approximately 10 to 15 minutes to complete.
The CBCL includes 118 items assessing two broad-
band and eight narrowband scales identified using factor
analysis, as well as a social competence scale. Extensive
 1
norms for the CBCL, TRF, and YSR are available for
both clinical and community samples, and favorable psy-
chometric properties of the instruments have been docu-
mented in hundreds of studies. Unfortunately, the CBCL’s
utility in assessing depression, at least as conceptualized
in the DSM, is limited. The scale that is most relevant
to depression is the narrowband Anxious/​Depressed scale,
which combines symptoms of anxiety and depression. In
addition, some other depressive symptoms are included
on other narrowband scales. Indeed, a latent class analysis
of the Anxiety/​Depression scale was unable to distinguish
distinct classes for depression and anxiety (Wadsworth,
Hudziak, Heath, & Achenbach, 2001). A set of diagnos-
tic scales that are more closely geared to DSM diagnoses
has been added to the CBCL. Recent findings suggest the
Affective Problems DSM-​oriented scale, intended to cor-
respond to DSM depressive disorders, demonstrated good
internal consistency and convergent validity (Nakamura,
Ebesutani, Bernstein, & Chorpita, 2009), with signifi-
cant associations with measures of depression, anxiety,
and oppositionality; however, the scale was more strongly
associated with measures of depression than opposition-
ality (Nakamura et  al., 2009). In addition, although the
Affective Problems scale corresponded with a depressive
disorder diagnosis derived from a parent-​based structured
interview and differentiated depressed from nondepressed
youth, the Affective Problems scale did not add incremen-
tal clinical validity above the empirically derived CBCL
syndrome scale (i.e., Withdrawn/​ Depressed) in these
analyses (Ebesutani et al., 2010).
The Child Symptom Inventory (CSI-​ 4; Gadow &
Sprafkin, 2002) and the corresponding Early Childhood
Inventory-​4 (ECI-​4; Gadow & Sprafkin, 2000) are rating
scales that assess symptoms of the most relevant DSM-​IV-​
TR psychiatric disorders in children aged 5 to 12 years and
3 to 5  years, respectively. There are parent and teacher
versions and both categorical and dimensional scoring
procedures. Scores on both the CSI-​4 and the ECI-​4 have
been found to have acceptable internal consistency, test–​
retest reliability, and convergent validity; however, the
discriminant validity, especially for the internalizing disor-
ders, has not been well documented (Gadow & Sprafkin,
2000, 2002).
A group of investigators sponsored by the McArthur
Foundation have developed a broad-​ band battery of
assessment instruments for children in the early school-​
age period (ages 4–​8  years). It includes a parent and
teacher rating scale, the McArthur Health and Behavior
Questionnaire (HBQ; Essex et  al., 2002), and a child-​
reported semi-​structured interview, the Berkeley Puppet
Depression in Children and Adolescents 111
Interview (BPI; Ablow et  al., 1999)  that uses puppets
in order to provide a more developmentally sensitive
assessment. Both measures include scales tapping vari-
ous domains of symptomatology (including a subscale
for depressive symptoms), physical health, and peer and
school functioning. In the initial reports from this group,
the depression scale score from the HBQ parent and
teacher forms had adequate internal consistency and good
test–​retest reliability, and it discriminated clinic from com-
munity subjects (Ablow et al., 1999). Although a categori-
cal measure of depression from the HBQ parent form was
not correlated with diagnoses of MDD derived from the
parent version of the DISC, it was associated with a num-
ber of teacher-​rated indices of impairment (Luby et  al.,
2002). Similarly, a categorical measure of internalizing
symptoms from the HBQ parent form demonstrated low
to moderate agreement with a DISC internalizing diagno-
sis (κ = .30), but the parent HBQ internalizing composite
score was significantly associated with parent ratings of
child impairment and global physical health and child-​
reported BPI scores (Lemery-​Chalfant et al., 2007).
The child-​rated BPI depression scale scores demon-
strated adequate internal consistency (α = .75) in a clinic
sample but poor internal consistency (α = .36) in a com-
munity sample, adequate test–​ retest reliability in both
samples (r  =  .42 to .43), and discriminated clinic from
community youth (Ablow et  al., 1999). Other research
groups demonstrated a similarly low internal consistency
estimate for the depression scale (α = .44) in a Dutch com-
munity sample (Ringoot et  al., 2013), adequate internal
consistency for the composite internalizing scale (α = .72
to .86) (Ringoot et  al., 2013; Stone et  al., 2014), and
adequate 1-​year test–​retest reliability for the depression
scale (r = .29) (Stone et al., 2014). Inter-​rater reliability of
the depression scale based on independent coders review
of the videotaped BPI interviews has been found to be
good (ICC = .74 to .86) (Stone et al., 2014). In addition,
Luby, Belden, Sullivan, and Spitznagel (2007) identified
a three-​item child-​rated BPI “core” depression symptoms
scale and found that the MDD group based on the DISC
had more BPI core depression symptoms compared to
the no disorder group, and the scale was related to DISC
depression severity scores and parent-​ reported CBCL
internalizing symptoms.
Assessment of DMDD
There are currently no published clinical interviews
updated for DSM-​5. Although the current clinical inter-
views do not assess DMDD, researchers have applied post
12

112 Mood Disorders and Self-Injury

hoc algorithms to several interviews, including the CAPA, ASSESSMENT FOR CASE CONCEPTUALIZATION
PAPA, and K-​SADS, using items from the depression and AND TREATMENT PLANNING
ODD sections that correspond with DMDD criteria.
These post hoc DMDD diagnoses have provided some In this section, we briefly discuss the assessment of con-
of the first data on DMDD in community and clinical structs that are useful for prognosis, case conceptualiza-
samples. Several scales assessing the severity or frequency tion, and treatment planning. We emphasize constructs
of youth irritability have been developed, including that have shown some value in predicting treatment
the Affective Reactivity Index (ARI; Stringaris et  al., response, either in general or differentially for some
2012)  and empirically derived scales from the CBCL treatments and not others (i.e., moderators; for reviews
(e.g., Roberson-​Nay et al., 2015), with promising psycho- of predictors and moderators of treatment response, see
metric properties. Emslie, Kennard, & Mayes, 2011; Nilsen, Eisemann, &
Kvernmo, 2013; Weersing, Schwartz, & Bolano, 2015),
are important in determining the appropriate treatment
Overall Evaluation
setting, or provide additional critical treatment targets.
For the purpose of diagnosis, we recommend the use of These constructs include severity of depressive symptoms,
semi-​structured interviews because they provide greater comorbid psychopathology, selected depressive symptoms
flexibility and allow for the clarification of questions and clinical features, psychosocial functioning, stress and
and responses and also the clinical judgment of the trauma, and family history of psychopathology.
interviewer. In particular, we recommend the K-​SADS Greater initial severity of depressive symptoms predicts
because of its fairly strong psychometric properties. In a poorer course and poorer treatment response (Emslie
addition, the CAPA and the PAPA are both good options et al., 2011; Nilsen et al., 2013). There is also some, albeit
for the assessment of depression, particularly because they inconsistent, evidence that the benefits of targeted psy-
collect additional information (severity, frequency, and chosocial or pharmacological treatments are evident only
duration) and assess functional impairment and life stress at higher levels of severity (Weersing et al., 2015). Thus,
(discussed later). Fully structured interviews, such as the depression severity can inform choices of the appropriate
DISC-​IV, can also play an important role in large-​scale type, intensity, and setting (e.g., outpatient or inpatient) of
epidemiological studies and in screening. treatment. As discussed in the previous section and sum-
As with fully structured interviews, we advise that rat- marized in Table 6.1, there are a number of well-​studied
ing scales not be used alone when formulating diagnoses rating scales that can be used to assess the severity of
because many of the scales appear to measure general depression for the purposes of case conceptualization and
distress rather than depression specifically. In addition, treatment planning.
they do not provide the necessary information to make a The presence of comorbid psychopathology also has
diagnosis (e.g., onset, duration, and frequency of symp- substantial prognostic value and may moderate treatment
toms), and when they are used to approximate diagnoses, response (Emslie et al., 2011; Nilsen et al., 2013; Weersing
they tend to overidentify youths as depressed. However, et al., 2015); in addition, it may indicate the need to incor-
rating scales provide useful information on the level of porate additional intervention approaches and/​or a lon-
symptom severity and can be used for screening. Our ger duration of treatment. Concurrent anxiety disorders
recommendations for rating scales differ depending on have been consistently shown to predict poorer treatment
sample characteristics. The CDI, MFQ, RCDS, and response, although several studies have also reported that
RADS have been widely used in community and school anxiety is associated with a relatively better response to
samples. They exhibit generally good psychometric evidence-​ based psychotherapies than other treatment
properties and function well as screening tools in such approaches (Weersing et al., 2015). Coexisting substance
populations. In clinical samples, we recommend the use disorders and subthreshold manic symptoms also
use of the clinician-​rated CDRS-​R along with the self-​ appear to predict a poorer response to treatment (Maalouf
report CDI and MFQ. Although these instruments lack & Brent, 2012; Weersing et al., 2015). The semi-​and fully
good discriminant validity, they have functioned well in structured diagnostic interviews reviewed in the previous
numerous studies of depressed youth, and when used in section and summarized in Table 6.1 assess most relevant
conjunction, they tend to yield prevalence rates that are comorbidities.
consistent with studies using diagnostic interviews (Myers Most diagnostic interviews also assess important
& Winters, 2002). clinical characteristics, such as duration of the current
 13
depressive episode and history of prior episodes, which
predict a poorer treatment response and greater likeli-
hood of recurrence (Emslie et al., 2011). Thus, these data
can play an important role in planning the intensity and
duration of treatment, as well as determining the need for
continuation and maintenance treatment.
Finally, diagnostic interviews and rating scales can
provide information about key symptoms that are rel-
evant to decisions regarding treatment intensity and set-
ting (e.g., suicidal ideation and behavior), as well other
features that are associated with a poorer response to
treatment and might suggest incorporating treatment
components designed to target specific symptoms (e.g.,
insomnia and anhedonia/​ social withdrawal; Maalouf
& Brent, 2012). The assessment of hopelessness and
suicidality is of particular importance, both to prevent
self-​harm and because they predict poorer response to
treatment (Emslie et al., 2011). Almost all the diagnostic
interviews and depression rating scales discussed previ-
ously assess hopelessness and suicidality. In addition, the
Hopelessness Scale (Beck, Weissman, Lester, & Trexler,
1974) is a well-​validated self-​report measure that can be
used with adolescents. Moreover, there are several widely
used measures of suicidal ideation and behavior in ado-
lescents (see Chapter  10, this volume), including self-​
report scales such as the Suicidal Ideation Questionnaire
(Reynolds & Mazza, 1999)  and the Columbia Suicide
Screen (Shaffer et  al., 2004)  and also clinician rating
scales such as the Columbia–​ Suicide Severity Rating
Scale (Posner et al., 2011).
Psychosocial Functioning
Depression in children and adolescents is associated with
significant impairment in family and peer relationships
and academic performance. The families of depressed
youths are often characterized by a lack of cohesion and
high levels of disengagement and conflict. The parents of
depressed children and adolescents exhibit less warmth
and support and greater control, criticism, and rejection
compared to parents of controls. Depressed youths have
significant social skills deficits, difficulties with peers, and
may be involved in problematic romantic relationships. In
addition, they often exhibit academic underachievement,
school attendance problems, and school failure (Garber
& Horowitz, 2002; Hammen, Rudolph, Weisz, Rao, &
Burge, 1999; Lewinsohn & Essau, 2002). Moreover, there
is evidence that family and peer problems predict a poorer
response to treatment but may be associated with a pref-
erential response to interpersonal therapy (Emslie et al.,
Depression in Children and Adolescents 113
2011; Weersing et al., 2015). Hence, identifying areas of
impaired functioning may be useful in understanding the
factors contributing to the youth’s depression and select-
ing areas to be monitored or targeted in treatment.
There are a variety of approaches and instruments for
assessing impairments and competencies in psychosocial
functioning (for reviews, see Canino, 2016; John, 2001;
Winters, Collett, & Myers, 2005). Parents’ reports of chil-
dren’s impairment appear to have greater validity com-
pared to children’s reports (Kramer et  al., 2004). Some
of the instruments discussed previously include subscales
assessing functional impairments and competencies.
For example, the CAPA and PAPA include comprehen-
sive assessments of the major areas of child psychoso-
cial functioning (Angold & Costello, 2000), the CBCL
(Achenbach & Rescorla, 2001a) has a 16-​ item social
competence scale, and the HBQ (Essex et al., 2002) and
Berkeley Puppet Interview (Ablow et  al., 1999)  include
scales tapping social and school functioning. In this sec-
tion, we discuss measures specifically designed to assess
psychosocial functioning in children and adolescents
(Table 6.2). However, due to limitations or lack of data,
particularly on depressed samples, we have not recom-
mended any of the measures above the others.
One group of measures consists of global or unidimen-
sional scales. Global measures provide information on
the severity of, and extent of impairment from, the dis-
order, which may influence the choice of treatment set-
ting (e.g., inpatient vs. outpatient), intensity and duration
of treatment, and treatment modality. The Child Global
Assessment Scale (C-​GAS; Shaffer et  al., 1983)  and the
Columbia Impairment Scale (CIS; Bird et al., 1993) are
two widely used global measures of functional impair-
ment. The C-​GAS, adapted from the Global Assessment
Scale for adults, is a single 100-​point scale designed for
clinicians to rate the severity of symptomatology and func-
tional impairment. A cut-​off of 70 is often used to indicate
clinically significant problems. The rating is based on
information collected through other means (i.e., a diag-
nostic interview with parent and/​or child) because the
C-​GAS does not provide questions. The CIS is a ques-
tionnaire that can be completed by a lay interviewer or
parent (for children older than age 4 years) or by children
aged 7 to 17  years. It includes 13 items tapping a vari-
ety of domains of social functioning and symptomatology
that are aggregated into a single score. It was recently rec-
ommended for use as a common measure across studies
funded by NIMH (Barch et al., 2016).
Both the C-​GAS and the CIS are economical, have
demonstrated good convergent validity, and differentiate
14

114 Mood Disorders and Self-Injury

relevant populations (e.g., clinical vs. community sam-
ples). However, they each yield only one score; hence,
they do not provide information on the nature of impair-
ment in specific areas of functioning. In addition, both
measures combine symptoms and functioning so that
a child’s score could reflect problems in either or both
domains.
A number of multidomain instruments assessing youths’
functioning across several areas, such as school, family,
and peer functioning, are also available (see Table 6.2).
The Child and Adolescent Functional Assessment Scale
(CAFAS; Hodges, 1999) is an interview that takes approxi-
mately 30 to 45 minutes to complete, although administra-
tion time can be shorter if it is administered in conjunction
with a diagnostic interview. Three of its eight subscales
assess functional impairment (role performance at school/​
work, home, and community); the others assess emotional
and behavioral problems (for reviews, see Bates, 2001;
Canino, 2016; Winters et al., 2005). However, the impair-
ment scales include some symptom items. The CAFAS was
designed for youth aged 5 to 19 years, but a preschool and
early childhood version is also available (the Preschool and
Early Childhood Functional Assessment Scale; see Murphy
et al., 1999). The CAFAS has demonstrated good inter-​rater
reliability, adequate test–​
retest reliability, correlates with
other measures of impairment, distinguishes child inpa-
tients from outpatients, and predicts later functioning.
The Social Adjustment Inventory for Children and
Adolescents (SAICA; John, Gammon, Prusoff, & Warner,
1987)  assesses school functioning, peer relations, home
life, and spare time activities in youths aged 6 to 18 years.
It takes 30 minutes or longer to complete and is adminis-
tered separately to the parent and the child. The SAICA
has demonstrated acceptable levels of inter-​rater reliabil-
ity, good test–​retest reliability, good convergent validity,
and discriminates relevant clinical and nonclinical groups
(Winters et  al., 2005). One study has reported that the
SAICA performed better than a global functioning scale
(i.e., C-​GAS) in predicting the course of depression in
adolescents (Sanford et al., 1995).
The Behavioral and Emotional Rating Scale (BERS;
Epstein, 1999; Epstein, Mooney, Ryser, & Pierce, 2004) is
a 52-​item scale that focuses on children’s strengths rather
than impairments. It assesses five domains:  interper-
sonal strengths, involvement with family, intrapersonal
strengths, school functioning, and affective strengths. It
takes approximately 20 minutes to administer, and it has
both parent and youth self-​rating versions. The parent ver-
sion is appropriate for children aged 0 to 18  years. The
BERS has been normed on a national sample, and it has
shown good test–​retest reliability, convergent validity, and
distinguishes groups of children with and without psycho-
pathology (Canino, 2016).
The Brief Impairment Scale (BIS; Bird et al., 2005) is
a highly economical parent interview that takes only 3 to
5 minutes and assesses functioning in the areas of school/​
work, interpersonal relations, and self-​fulfillment in youth
aged 4 to 17 years. It has shown good internal consistency
and test–​retest reliability, is correlated with the C-​GAS,
and distinguishes clinical and community samples.
The Psychosocial Schedule for School Age Children-​
Revised (PSS-​R; Puig-​Antich, Lukens, & Brent, 1986) assesses

Table 6.2  Ratings of Instruments Used to Assess Psychosocial Functioning for Case Conceptualization and
Treatment Planninga
Internal Inter-​Rater Test–​Retest Content Construct Validity Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Clinical Utility Recommended

Global Scales of Functioning

C-​GAS E NA A G A G E A
CIS E A NA A A G E A
Multidimensional Scales of Functioning
CAFAS G A G A A G E A
SAICA A A A A A G A A
BERS E E G G A G E A
BIS E A NA A A G E A

a
  A number of measures presented in Table 6.2 are also relevant for the purposes of case conceptualization and treatment planning. See text for a discus-
sion of these measures.
Note: C-​GAS = Child Global Assessment Scale; CIS = Columbia Impairment Scale; CAFAS = Child and Adolescent Functional Assessment Scale;
SAICA = Social Adjustment Inventory for Children and Adolescents; BERS = Behavioral and Emotional Rating Scale; BIS—​Brief Impairment Scale;
A = Adequate; G = Good; E = Excellent; NA = Not Applicable.
 15

Depression in Children and Adolescents 115

school functioning, relationships with parents, siblings, and

continuing stressors may contribute to the maintenance
peers, and the parents’ marital relationship in children aged
of the disorder and should be addressed in the treatment
6 to 16 years. Like the SAICA, it is administered separatelyplan. It is important to assess whether stressors are epi-
to the parent and child. Although it has good psychometric sodic or chronic and whether the stressor is independent
properties (Lukens et al., 1983), it has not been used much or dependent of the child’s behavior. For example, if a
in recent years. stressor is chronic, such as marital conflict, the clini-
Finally, a new instrument, the Child World Health cian may recommend marital counseling for the par-
Organization Disability Assessment Scale (C-​ WHO-​ents, and the child’s treatment may incorporate ways to
DAS), is worth mentioning. The C-​ WHO-​ DAS was cope with the ongoing stress. If the youth is “generating”
adapted for children from the adult WHO-​DAS by the life stress through his or her actions, it would be impor-
DSM-​ 5 Impairment/​ Disability Work Group (Canino, tant to focus on changing these problematic behaviors
Fisher, Alegria, & Bird, 2013). It has clinician, parent (Hammen, 2006).
report (for children aged 0–​17 years), and youth self-​report Life stress can be assessed through self-​administered
(for adolescents aged 12  years or older) versions, and it questionnaires (Vanaelst, De Vriendt, Huybrechts,
assesses six domains: understanding and communicating, Rinaldi, & De Henauw, 2012), which have the advantage
getting around (mobility), self-​care, getting along with of economy. However, semi-​structured interviews have a
people, life activities (school and nonschool), and par- number of significant strengths, including the ability to
ticipating in society. To date, only one study, conducted assess the temporal relationship between the stressor and
in Rwanda, has examined the psychometric properties of the depressive episode; distinguish potentially important
the C-​WHO-​DAS. In this study, internal consistency was features of events such as long-​term threat and whether
good and test–​retest reliability was adequate, confirma- the event is independent of, versus dependent on, the
tory factor analysis supported the scale’s structure, and the
child’s behavior; and minimize idiosyncratic interpreta-
instrument distinguished children who did and did not tions of items (Harkness & Monroe, 2016). Two of the
meet criteria for a psychiatric disorder (Canino, 2016). most widely used semi-​ structured stress interviews for
In addition to the more comprehensive instruments life stress in children and adolescents are the UCLA Life
noted previously, there are many measures designed to Stress Interview (LSI; Hammen et  al., 1999)  and the
assess specific areas of functioning. For example, there Stressful Life Events Schedule (SLES; Williamson et al.,
are a number of widely used inventories assessing key 2003). Both interviews assess episodic life events across
dimensions of family functioning (e.g., Epstein, Baldwin, a variety of domains (e.g., family, peers, romantic rela-
& Bishop, 1983) and parenting behavior (e.g., Schaefer, tionships, school, health, and family finances). The LSI
1965), laboratory tasks that have been used to examine also provides an extensive assessment of chronic stress-
the interaction patterns of families of depressed children ors in each of these areas. There is considerable overlap
(Garber & Kaminski, 2000), and interview and labora- between the LSI’s conceptualization of chronic stress and
tory measures of expressed emotion (Sher-​Censor, 2015). social functioning, so this part of the interview can also be
Finally, there are a variety of peer nomination measures viewed as a measure of functional impairment (Harkness
and teacher ratings of peer functioning that can be used & Monroe, 2016).
to assess children’s social status and functioning in school Most life events inventories and interviews also assess
(e.g., Huesmann, Eron, Guerra, & Crawshaw, 1994; traumatic stressors. Similarly, some of the more compre-
Ladd, Herald-​Brown, & Andrews, 2009). hensive measures of functional impairment discussed
previously assess some traumas, such as child maltreat-
ment (e.g., the PSS-​R). Many of the diagnostic inter-
Stressful Life Events
views discussed previously also assess traumatic events
Prospective studies in children have shown that stress—​ in the context of evaluating post-​traumatic stress disorder
particularly events related to loss, rejection, disappoint- (PTSD) (e.g., the K-​ SADS). Among diagnostic inter-
ment, and conflict—​ and traumas, such as childhood views, the CAPA and PAPA are particularly noteworthy
maltreatment, predict the onset and persistence of depres- in providing a broad assessment of life events and traumas
sive symptoms, as well as poorer response to treatment (Costello, Angold, March, & Fairbank, 1998). Finally,
(Gibb, 2014; Emslie et  al., 2011; Rudolph & Flynn, there are a number of instruments that focus specifi-
2014). Life stressors and traumas prior to the depressive cally on traumatic stressors (e.g., the Childhood Trauma
episodes may be precipitating factors, and subsequent or Questionnaire and the UCLA PTSD index; for a review,
16
116 Mood Disorders and Self-Injury
see Strand, Sarmiento, & Pasquale, 2005)  and on child
maltreatment (e.g., the Child Abuse Potential Inventory
and the Conflict Tactics Scale—​Parent–​Child Version;
for a discussion of issues in assessing child maltreatment
and a review of screening instruments, see Slep, Heyman,
& Foran, 2015).
Family History of Psychopathology
A number of studies have reported elevated rates of
depression, and often other forms of psychopathology, in
the relatives of depressed children and adolescents (e.g.,
Klein, Lewinsohn, Seeley, & Rhode, 2001). Clinicians
should be particularly cautious when youth have a family
history of bipolar disorder or psychosis, and they should
be alert to emerging signs of mania and/​or psychosis. In
addition, parental depression has been related to pro-
longed depressive episodes in their children and poorer
treatment response (Brent et al., 1998). Moreover, there
is growing evidence that treating maternal depression can
reduce children’s symptoms (Cuijpers, Weitz, Karyotaki,
Garber, & Andersson, 2015). Therefore, if a parent is suf-
fering from a psychiatric disorder and is not in treatment,
a referral for mental health services can benefit both par-
ent and child.
Family history data can be elicited using diagnos-
tic interviews conducted directly with family members
(the family interview method) or by interviewing key
informants about the other relatives (the family history
method). Although direct interviews are more accu-
rate, in most instances clinicians and researchers must
rely on informants to obtain family histories. The most
widely used interviews for eliciting family history infor-
mation from informants are the Family History Research
Diagnostic Criteria (Andreasen, Endicott, Spitzer, &
Winokur, 1977), the Family Informant Schedule and
Criteria (Chapman, Mannuzza, Klein, & Fyer, 1994), the
Family Interview for Genetic Studies (Nurnberger et al.,
1994), and the Family History Screen (Milne et al., 2009;
Weissman et al., 2000). Family history data collected from
informants tend to have high specificity but only moder-
ate sensitivity. Hence, it is best to obtain information from
at least two informants when possible to increase the prob-
ability of detecting psychopathology in relatives.
Overall Evaluation
Assessment for the purpose of case conceptualization and
treatment planning requires a combination of measures
assessing factors related to the disorder (i.e., severity and
duration of the depressive episode, comorbid psychopa-
thology, and family history of psychopathology) and a
variety of social domains (e.g., relationships with family,
peers, and romantic partners; schoolwork; and life stress-
ors and trauma). In addition, it is necessary to obtain
information from multiple informants (the child and a
parent, as well as additional informants such as teachers
when possible). It is also important to consider the context
of the youth’s behavior and the cultural milieu because
what is considered maladaptive in one context or culture
may be adaptive in another.
First, we recommend the use of one of the rating
scales and diagnostic interviews discussed previously to
obtain information about the severity and clinical fea-
tures of the depressive episode and comorbid conditions.
Second, we recommend using a multidimensional mea-
sure of functional impairment. The SAICA has been
mostly used by clinicians to assess functioning rather
than by mental health planners to determine service
needs. The CAFAS and BERS are reasonable options
for a multidimensional scale to guide selection of the
level and types of services. The BIS is a good option
when time is limited. In addition, the CAPA and PAPA
assess impairment in key domains. However, none of the
measures of functional impairment were highly recom-
mended in Table 6.2 because their psychometric proper-
ties have not been examined as thoroughly as our rating
criteria require, and only the SAICA and PSS-​R have
been used specifically in studies of child and adolescent
depression.
Third, it is important to assess stressful life events
and traumas. If time permits, the best option for assess-
ing life events is with an interview such as the LSI or the
SLES that provides qualitative information regarding the
stressor (e.g., the severity and independence/​dependence
of stressor, whether it is episodic or chronic, and the tim-
ing of the stressor in relation to symptoms). Alternatively,
the CAPA and PAPA provide assessments of life events and
traumas. Finally, there are a number of good interviews
to assess family history of psychopathology. Although it
may be challenging, we recommend using multiple infor-
mants to increase sensitivity.
In summary, assessment for case conceptualization
and treatment planning should provide the clinician
with information to assess the prognosis of the disor-
der, areas of impairment and strength, and factors that
appear to contribute to the onset and/​or maintenance of
the disorder.
 17
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
To evaluate the assessment tools used in the treatment
literature, we examined the various measures’ sensitivity
to treatment effects (Table 6.3). This included significant
change on depression measures, such as MDD diagnoses
and rating scales, as well as change on measures of func-
tional impairment using both global and multidimen-
sional scales. Furthermore, we included only published
pharmacological and psychotherapy treatment research
that reported at least one significant treatment effect on at
least one outcome measure of depression. Otherwise, it is
not possible to distinguish the treatment’s lack of efficacy
from the measure’s insensitivity in detecting change.
All studies examined compared depression treat-
ment to a wait-​list control or another active treatment.
In larger clinical trials involving psychopharmacology,
psychotherapy, or combined treatments for older chil-
dren and adolescents with depression, the predominant
index of treatment response in adolescence is the CDRS-​
R (Brent et al., 2008; Brooks & Kutcher, 2001; Goodyer
et al., 2007; March et al., 2004; Myers & Winters, 2002).
In the initial intervention studies of young children
with depression, dimensional depression scores derived
from the PAPA have indexed treatment outcome. Initial
evidence (Lenze et  al., 2011; Luby, Lenze, & Tillman,
2012)  suggests that these scores demonstrate treatment
sensitivity. Relative to the first edition of this book, there
has been less reliance on reporting changes in MDD
diagnoses (i.e., no longer meeting criteria). Previously,
many studies used the K-​SADS, which was sensitive to
change in all studies (Clarke et  al., 1995, 2001; Clarke,
Rohde, Lewinsohn, Hops, & Seeley, 1999; Diamond,
Reis, Diamond, Siqueland, & Isaacs, 2002; Lewinsohn,
Clarke, Hops, & Andrews, 1990; McCauley et al., 2016;
Stark, 1990; Vostanis, Feehan, Grattan, & Bickerton,
1996; Wood, Harrington, & Moore, 1996). Fewer studies
rely on other diagnostic instruments (e.g., the DISC) for
indexing treatment response (Weisz et al., 2009). A num-
ber of self-​ administered depression rating scales have
also been shown to be sensitive to treatment effects. The
CDI has also been widely used and has been shown to be
sensitive to change in several treatment studies (Brook &
Kutcher, 2001; Myers & Winters, 2002; Rosselló, Bernal,
& Rivera-​Medina, 2012). One study reported that it was
more sensitive than the RCDS in detecting the effects
of group CBT in school-​aged children (Stark, Reynolds,
& Kaslow, 1987); however, another study found that it
Depression in Children and Adolescents 117
was less sensitive to the effects of medication compared
to the CDRS (Emslie et al., 1997). Both the RCDS and
the RADS have detected treatment effects in controlled
clinical trials (March et al., 2004; Rawson & Tabb, 1993).
Although the MFQ has been used less frequently than
the other measures, it has demonstrated sensitivity to
change in some (e.g., Goodyer et  al., 2007; McCauley
et al., 2016), but not all, clinical trials (Brooks & Kutcher,
2001). Last, many of the youth self-​report rating scales
reviewed here (i.e., CDI, RADS, and MFQ) have been
shown to be more sensitive to treatment effects compared
to the parent versions (Kahn, Kehle, Jenson, & Clark,
1990; Wood et al., 1996).
Some treatment studies included parent versions of
the CBCL-​Anxious/​Depressed scale, CBCL Internalizing
scale, and an adapted depression scale from the CBCL,
with few of these studies being published recently.
Overall, few of these studies reported post-​ treatment
effects using these measures (Weisz et al., 2009), despite
other youth-​reported depression measures demonstrating
treatment effects (Clarke et al., 1999, 2001; De Cuyper,
Timbremont, Braet, De Backer, & Wullaert, 2004;
Rosselló & Bernal, 1999; Stark et al., 1987). Interestingly,
however, some of these studies later found post-​treatment
follow-​ up effects using parent-​ report measures (Clarke
et  al., 1999; De Cuyper et  al., 2004). This suggests that
parents and youths may be focusing on different indica-
tors of improvement (i.e., parents may rely more heavily
on behavioral, rather than mood, changes). Nevertheless,
it appears that parents are less sensitive than youths to
the more immediate changes in the youths’ depressive
symptomatology.
Last, it is important to emphasize that treatment
monitoring and outcome should include psychosocial
functioning in addition to symptom reduction/​ remis-
sion. There has been an increased emphasis on examin-
ing improvement in functioning. The Clinical Global
Impression–​Improvement (CGI-​I) and Clinical Global
Impression–​ Severity (CGI-​ S) scores have been used
in larger adolescent depression trials (Atkinson et  al.,
2014; Brent et  al., 2008; Goodyer et  al., 2007; March
et  al., 2004), and each was sensitive to changes in lev-
els of function across treatment. However, much of the
work in demonstrating validity of these assessments has
come from studies of adults and other disorder popula-
tions. Thus, additional work is needed to demonstrate
construct validity and reliability in child and adolescent
depression. The C-​GAS has been widely used to assess
functional impairment in treatment studies, and it has
18

118 Mood Disorders and Self-Injury

Table 6.3  Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

K-​SADS NA NR G A G E E E G ✓
CDRS-​R G G G A G G G E A ✓
CDI E G NA A G G E A A ✓
MFQ E E NA A A G E A A
RCDS E E NA A G A A A A
RADS E E NA G G G E G A ✓
C-​GAS E NA G G A G E E A ✓
SAICA A A A E G G A A A

Note: K-​SADS = Schedule for Affective Disorders and Schizophrenia in School-​Age Children; CDRS-​R = Children’s Depression Rating Scale-​Revised;
CDI = Children’s Depression Inventory; MFQ = Mood and Feelings Questionnaire; RCDS = Reynolds Child Depression Scale; RADS = Reynolds
Adolescent Depression Scale; C-​GAS  =  Child Global Assessment Scale; SAICA  =  Social Adjustment Inventory for Children and Adolescents;
A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

been sensitive to treatment of depression in children and
adolescents (Goodman, Schwab-​Stone, Lahey, Shaffer,
& Jensen, 2000; Goodyer et al., 2007; Muratori, Picchi,
Bruni, Patarnello, & Ramagnoli, 2003). The SAICA
is one of the few multidimensional measures of social
functioning to be used in youth depression treatment
studies. It demonstrated sensitivity to post-​ treatment
effects and 9-​month follow-​up effects (Vostanis et  al.,
1996). The CAFAS has also been shown to be sensi-
tive to treatment gains (Winters et al., 2005); however,
these studies did not focus on depression. Finally, the
BIS failed to show treatment effects in one large clini-
cal trial (Chorpita et al., 2013). Future research should
focus on the effects of treatment on adaptive functioning
and determine whether youths’ functioning targeted in
treatment actually improves.
Overall Evaluation
Determining which measures to use for monitoring and
evaluating treatment will depend on a number of fac-
tors, including the nature of the patient’s condition and
the form of treatment. For patients with diagnoses of
MDD, the K-​SADS MDD section can be used to assess
remission. In addition to the K-​SADS, the clinician-​rated
CDRS-​R, which has been sensitive to both pharmaco-
logical and psychotherapy treatment studies, is highly
recommended. However, if a clinician-​rating scale is too
costly, the youth-​rated CDI, which is sensitive to change
and widely used with child and adolescent populations,
is highly recommended; the RCDS, RADS, and MFQ
are also acceptable options. These measures have all been
shown to be sensitive to psychotherapy, and they are all
self-​report measures, which appear to be more sensitive
than parent-​report measures of depression. It may be of
value to use a combination of measures that are intended
to assess both modest/​ normative and clinically signifi-
cant levels of symptoms (Olino et al., 2012, 2013) so that
higher levels of severity are accurately assessed early and
more modest levels of severity are assessed later in treat-
ment. For example, the CDI and MFQ may be jointly
administered such that higher severity symptoms are
assessed via the CDI earlier in treatment and lower sever-
ity symptoms are assessed via the MFQ later in treatment.
This may help provide additional sensitivity in seeing
severity to complete remission. In Table 6.3, of the self-​
report measures, only the CDI and RADS are considered
highly recommended because they have been most widely
used and consistently shown to be sensitive to treatment
effects. Additional studies of depression in early childhood
are needed in order to make recommendations about spe-
cific measures that are sensitive to treatment in this devel-
opmental period.
Parent-​report measures may be more useful in assess-
ing and monitoring the youth’s functional impairment
(Kramer et  al., 2004). In addition, youth and teacher
reports on multidimensional measures of functional
impairment would also be advisable because multiple
informants may be required to get a comprehensive
assessment of functioning across different contexts and
relationships. We recognize that it is often difficult to
obtain information from multiple sources; nevertheless,
we strongly recommend that information from multiple
informants be obtained during the initial assessment and
treatment planning phase and in evaluating treatment
outcome. However, it would be acceptable to monitor
the youth’s functioning over the course of treatment using
only parent and/​or youth reports because these are more
 19

Depression in Children and Adolescents 119

easily obtainable in clinical settings. We recommend that assessing progress and allows for comparison to published
the C-​GAS be used as the global measure of functional treatment benchmarks.
impairment because the CIS (discussed previously) has
not been evaluated for sensitivity to change. Reliance
Issues for Future Research
on the CGI-​I and CGI-​S is promising but is currently
only considered adequate. Finally, we suggest that future Evaluating empirically supported assessments of child and
research examine the clinical utility and sensitivity to adolescent depression is a challenging task, and a number
change of a variety of multidimensional scales because of issues must be resolved in order to provide firm grounds
recommending one over another for treatment monitor- for recommendations. Unfortunately, most of the gaps in
ing and outcome seems premature at this time. the development of empirically supported assessments for
youth depression identified in the previous edition of this
volume remain. However, these gaps continue to define
CONCLUSIONS AND FUTURE DIRECTIONS an agenda for future research.
First, there are fundamental questions about the valid-
In this chapter, we reviewed the major approaches and ity of depression as a diagnostic construct and its relation-
measures for diagnosing and assessing depression in chil- ship to other conditions, such as anxiety disorders. For
dren and adolescents. We also identified a number of example, structural models of psychopathology indicate
additional variables that should be considered for progno- that much of the liability to psychiatric disorders can be
sis, treatment planning, case conceptualization, and treat- explained by one or two higher order dimensions, with
ment monitoring and evaluation, and we briefly discussed depression loading on a general factor and an internal-
their assessment. izing factor (Lahey, Van Hulle, Singh, Waldman, &
In summary, a comprehensive assessment of child and Rathouz, 2011; Olino et  al., 2014). This literature also
adolescent depression should include (a)  determining suggests that depression is almost indistinguishable
whether criteria are met for a diagnosis of depressive dis- from generalized anxiety disorder, and the two condi-
order and assessing the severity of depressive symptoms; tions should be collapsed into a single “distress” disor-
(b) assessing key symptoms such as hopelessness, suicidal der (Lahey et al., 2008). Whereas these models focus on
ideation, and psychotic symptoms that might influence clinical phenotypes, the NIMH RDoC initiative takes
treatment decisions; (c)  carefully assessing the previous a different approach, seeking to identify transdiagnostic
course of the depression (e.g., prior episodes and chronic- biobehavioral dimensions that can be assessed at mul-
ity); (d) evaluating comorbid psychiatric, developmental, tiple units of analysis. It will be important to watch these
and general medical disorders; (e) assessing family, school, developments because they may fundamentally alter our
and peer functioning; (f)  exploring significant stressors, core diagnostic constructs, treatment targets, and possibly
traumas, and social factors, including ethnicity and cul- intervention approaches.
ture; and (g) assessing family history of psychopathology. Second, there is a need for longitudinal studies focus-
Our recommendations are as follows. First, the ing specifically on the processes associated with the
assessment of psychopathology should include a semi-​ maintenance, recovery, and recurrence of depression in
structured diagnostic interview because less systematic children and adolescents. In addition, there is a need to
approaches frequently overlook key areas of psychopa- expand the surprisingly limited literature on predictors of
thology and also because respondent-​ based interviews differential treatment response (Weersing et  al., 2015).
pose several limitations, including overdiagnosis, poor This should provide valuable information regarding
discriminant validity, and the inability to clarify questions potential targets for assessment and treatment and also for
or responses. Second, data should be obtained from mul- choosing between treatment options.
tiple informants, including the child (if he or she is older Third, we need to determine the best method for inte-
than age 8 years) and primary caregiver. Finally, regular grating data from multiple informants for diagnosis and
monitoring and evaluation of treatment using clinician, self-​ treatment evaluation (De Los Reyes et al., 2015). Fourth,
rating, and parent-​rating scales assessing depressive symp- there is a need for methodologically rigorous compari-
toms and functional impairment is critical. Although a sons between different diagnostic interviews or rating
reduction in test scores when monitoring treatment effects scales and also a need to determine the cost-​effectiveness,
should be viewed cautiously in light of the possibility of incremental validity (Hunsley & Meyer, 2003), and treat-
attenuation effects, this provides a means of objectively ment utility of these measures. Hayes, Nelson, and Jarrett
120
120 Mood Disorders and Self-Injury
(1987) and Nelson-​Gray (2003) have described a number
of research designs that can be used to test treatment util-
ity and that are easily implemented.
Fifth, assessing the reliability and validity of case for-
mulations and treatment planning is a critical area in
which little work has been done for child and adolescent
depression (Kuyken, Fothergill, Musa, & Chadwick,
2005). Sixth, during the treatment monitoring phase of
assessment, there are few guidelines regarding whether
or when treatment with depressed youth should be inten-
sified, changed, or discontinued. Fortunately, there is a
growing body of work on these issues that can be drawn
upon (e.g., Shimokawa, Lambert, & Smart, 2010). Finally,
disseminating and implementing evidence-​based assess-
ment for depressed youth in community settings remains
a significant challenge (Garland et al., 2013; Weisz et al.,
2015). These gaps in the literature present us with many
critical research tasks that will further the development of
evidence-​based assessment tools and procedures for child
and adolescent depression and facilitate the development
of evidence-​based treatments for depressed youth.
ACKNOWLEDGMENTS
Daley DiCorcia’s assistance in preparing the manuscript
is gratefully acknowledged. Writing of this chapter was
supported by NIMH grants RO1 MH 069942 (Klein) and
R01 MH107495 (Olino).
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 13
Adult Depression
Jacqueline B. Persons
David M. Fresco
Juliet Small Ernst
We begin this chapter with an overview of the current
diagnostic criteria for major depressive disorder (MDD),
the epidemiology of MDD, and current theories of and
therapies for MDD. We review assessment tools for obtain-
ing a diagnosis, developing a case conceptualization and
treatment plan, and monitoring change in therapy. We
conclude with a brief discussion of some future directions
of assessment of depression.
We focus this review on MDD because space is lim-
ited and because the empirical support for the tools and
theories and therapies we describe focuses most frequently
on MDD. However, many other disorders, including per-
sistent depressive disorder (dysthymia), premenstrual dys-
phoric disorder, substance/​medication-​induced depressive
disorder, adjustment disorders, schizoaffective disorder,
and bipolar and related disorders, as well as phenomena
that are not disorders (e. g., grief), share features with
MDD, and many of the assessment tools described here
will be helpful in those cases. Chapter 9 in this volume
addresses the assessment of bipolar disorder.
THE NATURE OF MAJOR DEPRESSIVE DISORDER
Diagnostic Criteria
MDD is an episodic mood disorder characterized by
depressed mood or anhedonia (loss of interest and plea-
sure in life) that has persisted for most of the day, nearly
every day, for at least 2 weeks and is accompanied by five
or more of the following symptoms: weight gain or weight
loss not associated with dieting, decrease or increase in
appetite, insomnia or hypersomnia, psychomotor agitation
131
or retardation, fatigue or loss of energy, feelings of worth-
lessness, excessive or inappropriate guilt, diminished abil-
ity to think or concentrate, indecisiveness, or suicidality
(American Psychiatric Association, 2013). The symptoms
cause clinically significant distress or impairment in func-
tioning, and they are not due to the direct physiological
effects of a substance or a general medical condition.
Epidemiology of Major Depressive Disorder
MDD is a prevalent and debilitating national health
problem. The National Comorbidity Survey Replication
(NCS-​R; Kessler, Chiu, Demier, Merikangas, & Walters,
2005)  reported the lifetime prevalence of MDD in the
United States at 16.2%, the highest rate of 14 major psychi-
atric disorders. The 2014 National Survey of Drug Use and
Health found that 6.6% of adults suffered at least one major
depressive episode in the past year, a figure that equates
to roughly 15.7 million Americans (Center for Behavioral
Health Studies and Quality, 2015). Many patients with
MDD experience multiple episodes, with rates of recur-
rence up to 85% within a 15-​ year period (Hardeveld,
Spijker, De Graaf, Nolen, & Beekman, 2010). The preva-
lence of depressive symptoms in the United States is wide-
spread; 20.1% of the adults sampled in the National Health
and Nutrition Examination Survey reported significant
depressive symptoms (Shim, Baltrus, Ye, & Rust, 2011).
Depression is a leading cause of disability. MDD
accounts for the third greatest burden of all diseases
worldwide and the first greatest burden for middle-​and
high-​income nations (World Health Organization, 2008).
In the United States, estimates of the monetary burden of
MDD, whether through direct (e.g., medical services) or
132
132 Mood Disorders and Self-Injury
indirect costs (e.g., workplace presenteeism, or the act of
working while sick), approached $210.5 billion in 2010
(Greenberg, Fournier, Sisitsky, Pike, & Kessler, 2015).
The lifetime prevalence of MDD is higher in women
than in men in every age group (Pratt & Brody, 2014).
MDD is more likely to occur in Whites compared to
Hispanics or non-​Hispanic Blacks (Kessler et  al., 2003),
although this pattern is reversed in dysthymia (called
persistent depressive disorder in the fifth edition of the
Diagnostic and Statistical Manual of Mental Disorders
[DSM-​5]; American Psychiatric Association, 2013; Riolo,
Nguyen, Greden, & King, 2005) and may become insig-
nificant when the factor of poverty is controlled for (Pratt
& Brody, 2014). MDD is associated with high rates of
comorbidity with other psychiatric disorders; the NCS-​R
reported rates of comorbidity as high as 59.2% with anxi-
ety disorders, 24% with substance use disorder, and 30%
with impulse control disorders. Other common comorbid
conditions include pain and other somatoform disorders,
eating disorders, dementias, and personality disorders.
Theories of Depression
A variety of systems of psychotherapy with ostensibly
different mechanisms of action have been shown to be
effective in treating major depression and/​or reducing
the likelihood of a relapse. Here, we briefly describe the
major behavioral, cognitive, affect science, and interper-
sonal theories of depression and the therapies based on
them. These theories and therapies identify mechanisms
that cause and maintain symptoms of depression and that
clinicians will want to assess to inform their case concep-
tualization and treatment plan and also to monitor the
patient’s progress during therapy. Comprehensive reviews
of this literature are provided by Craighead, Johnson,
Carey, and Dunlop (2015), DeRubeis, Siegle, and Hollon
(2008), and Hollon, Stewart, and Strunk (2006).
We describe theories and mechanisms of depression
using a “silo” approach that emphasizes distinctions among
the theories and therapies of depression. However, as
Mennin, Ellard, Fresco, and Gross (2013) note, these ther-
apies are “blunt instruments”—​that is, although they are
intended to target certain mechanisms, they likely produce
change in many others. Thus, for example, many change
principles in our treatments, such as cognitive change
(e.g., decentering and cognitive reframing) have a bidirec-
tional relationship with behavior change (e.g., exposure
and behavioral activation). Our motivation for emphasiz-
ing the distinctions among the models is to help clinicians
solve clinical problems. For instance, many patients do not
respond to treatment (response rates for evidence-​based
treatments range from 25% to 64%; Craighead et al., 2015).
When treatment fails, using an alternate conceptual model
can provide new intervention ideas (Persons, 1990, 2008;
Persons, Beckner, & Tompkins, 2013).
Behavioral Models
Behavioral models of depression focus primarily on posi-
tive and negative reinforcement. For instance, Ferster
(1973) conceptualized that depression arises and is main-
tained when individuals orient their lives in service of
escape or avoidance instead of in the pursuit of positive
reinforcement. Ferster proposed a functional analytic
approach to treating depression that focused on decreas-
ing the depressed individual’s reliance on escape or avoid-
ance behaviors and expanding the individual’s behavioral
repertoire to increase the availability of positive rein-
forcements. Similarly, Lewinsohn (Lewinsohn & Gotlib,
1995)  posited that depressed individuals lack positive
reinforcement or have experienced life events or stressors
that caused them to lose positive reinforcers and that until
they learn to obtain positive reinforcement, they will be
inactive, withdrawn, and dysphoric. Lewinsohn’s therapy
helps depressed individuals increase the positive reinforce-
ment they experience by learning to identify and carry out
pleasant activities, practice relaxation, and improve their
social skills. These early behavioral models gave rise to
evidence-​based treatments of depression, including behav-
ioral therapy (Lewinsohn & Gotlib, 1995), behavioral
activation (BA) (Dimidjian, Barrera, Martell, Muñoz, &
Lewinsohn, 2011; Martell, Addis, & Jacobson, 2001), and
the rumination-​focused cognitive–​behavior therapy devel-
oped by Watkins and colleagues (Watkins, 2016).
Cognitive Content Models
Beck and Bredemeier (2016) propose that depression
results when individuals with negative and distorted
schemas experience life events that activate those sche-
mas. Beck defines schemas as organized, enduring rep-
resentations of knowledge and experience, generally
formed in childhood, which guide the processing of
current information. Beck’s model posits that emotions,
automatic thoughts, and behaviors are connected and
influence one another. Cognitive therapy of depression
(Beck, Rush, Shaw, & Emery, 1979) helps the depressed
patient modify distorted automatic thoughts and maladap-
tive behaviors and to change or replace the problematic
schemas to reduce depressive symptoms and the person’s
 13
vulnerability to future episodes of depression. The therapy
may also help patients change their life circumstances so
as to reduce activation of problematic schemas.
McCullough (2000) proposed a cognitive theory
of chronic depression that states that the chronically
depressed person lacks “perceived functionality,” or the
ability to perceive a “contingency relationship between
one’s behavior and consequences” (p.  71). Without
perceived functionality, the person loses the motiva-
tion to take action, with the result that he or she suffers
a dearth of positive reinforcers and an excess of punish-
ers. To address this deficit, McCullough developed the
Cognitive–​Behavioral Analysis System of Psychotherapy
(CBASP). In CBASP, the therapist guides the patient
through detailed examinations (assessment) of specific
interpersonal interactions and helps the patient learn to
identify and remediate his or her passive and ineffectual
behaviors. The goal is to teach patients that they actually
do have the power to get what they want in interpersonal
transactions.
Cognitive Process Models
A signature characteristic of many forms of psychopa-
thology, including MDD, is repetitive or perseverative
thought or negative self-​ referential processing (NSRP)
(e.g., Mennin & Fresco, 2013; Olatunji, Naragon-​Gainey,
& Wolitzky-​Taylor, 2013; Watkins, 2008). The tendency to
engage in repetitive negative thinking may reflect a mal-
adaptive cognitive reactivity associated with the inability
to disengage from aversive and conflicting emotional and
somatic experiences (Borkovec, Alcaine, & Behar, 2004;
Mennin & Fresco, 2014; Newman & Llera, 2011; Nolen-​
Hoeksema, Wisco, & Lyubomirsky, 2008), which in turn
further reinforces the use of these self-​ evaluative pro-
cesses. NSRPs, in turn, can result in considerable deficits
in cognitive and behavioral responding (e.g., Lissek, 2012;
Whitmer & Gotlib, 2012), as well as an inferior treatment
response and more frequent relapse (e.g., Jones, Siegle, &
Thase, 2008). Here, the problem is not so much the con-
tent of the thought but, rather, the process of thinking and
the individual’s rigidity or difficulty regulating where to
place his or her attention. Essentially, these processes are
enacted to create control and predictability, but instead
these individuals can find themselves vacillating between
a worried or ruminative mind and chronically distressed
body and, subsequently, reinforcing the use of these self-​
evaluative processes when they are momentarily effective
at staving off the aversive experience of strong emotional
responses (Borkovec et al., 2004; Mennin & Fresco, 2013,
Adult Depression 133
2014; Newman & Llera, 2011; Nolen-​Hoeksema et  al.,
2008; Olatunji et al., 2013; Watkins, 2008).
Perfectionism and self-​criticism are additional forms
of NSRPs that confer vulnerability for depression, main-
tain depressive symptoms, and interfere with treatment.
Behavioral activation (Martell et  al., 2001), cognitive
therapy (Beck et  al., 1979), and rumination-​ focused
cognitive–​behavioral therapy (CBT; Watkins, 2016)  tar-
get NSRP in MDD.
One biobehavioral capacity associated with reductions
in destructive self-​referentiality and that can be enhanced
with treatment is decentering, defined as a metacogni-
tive capacity to observe items that arise in the mind (e.g.,
thoughts, feelings, and memories) with healthy psycho-
logical distance, greater self-​awareness, and perspective-​
taking (Bernstein et al., 2015; Fresco, Moore, et al., 2007;
Fresco, Segal, Buis, & Kennedy, 2007; Safran & Segal,
1990). Bernstein and colleagues (2015) proposed that
decentering is composed of three interrelated metacog-
nitive processes:  meta-​awareness, disidentification from
internal experience (i.e., experiencing sensations, emo-
tions, and thoughts from a third-​person perspective), and
reduced reactivity to thought content (i.e., less impact
on attention, emotion, cognitive elaboration, motivation,
etc.). Most of the evidence supporting the construct of
decentering is derived from a well-​validated self-​report
measure that we describe later in the chapter (Fresco,
Moore, et al., 2007). Decentering is associated with acute
and enduring treatment effects for patients suffering
from MDD (Fresco, Segal, et al., 2007) and generalized
anxiety disorder (GAD; with and without MDD) (Hoge
et  al., 2015; Mennin, Fresco, Heimberg, & O’Toole,
2017; Mennin, Fresco, Ritter, & Heimberg, 2015; Renna,
Quintero, Mennin, & Fresco, 2017).
Emotion Models
Emotion models of psychopathology draw from basic and
translational findings in affective neuroscience that iden-
tify two core systems that regulate thoughts and behav-
iors (e.g., Gray & McNaughton, 2000). The approach or
reward system motivates actions toward goals and rewards,
and produces positive emotions such as enthusiasm and
pride. By contrast, the security system motivates avoidance
of aversive outcomes or punishments and is linked with
negative emotions. Optimal reward learning requires us
to assign value to possible rewarding and punishing stim-
uli, make predictions about when and where we might
encounter these stimuli, and take behavioral actions that
are informed by these predictions (O’Doherty, 2004).
134
134 Mood Disorders and Self-Injury
Reward learning is further defined in terms of con-
summatory pleasure (i.e., “liking”), which refers to the
hedonic impact that a reward produces, and anticipatory
pleasure (i.e., “wanting”), which refers to the incentive
salience associated with a particular reward (Berridge,
Robinson, & Aldridge, 2009; Sherdell, Waugh, & Gotlib,
2012). Reward learning is impaired in individuals suf-
fering from MDD. For example, depressed individuals
fail to distinguish between options yielding large versus
small rewards (Forbes, Shaw, & Dahl, 2007). Similarly,
depressed individuals, especially when they are ruminat-
ing, are more prone to misconstrue the likelihood and
intensity of a potentially punishing situation (Whitmer,
Frank, & Gotlib, 2012). Finally, depressed patients, espe-
cially when their clinical presentation includes comorbid
anxiety disorders, may struggle with the valuation of stim-
uli in their lives given that most situations are marked with
cues for both threat and reward (Stein & Paulus, 2009).
Two additional neurobehavioral systems are com-
monly impaired in MDD. The default network (DN; e.g.,
Raichle et al., 2001), which serves autobiographical, self-​
monitoring, and social cognitive functions, is associated
with adaptive and maladaptive forms of self-​referential
mentation. Psychiatric disorders are often marked by
excessive activation of the DN, thereby reducing activa-
tion of neural regions associated with executive control
(e.g., Whitfield-​ Gabrieli & Ford, 2012)  and emotion
regulation (e.g., Brewer et  al., 2011; Whitfield-​Gabrieli
& Ford, 2012). In addition, the salience network (SN;
e.g., Craig, 2009; Menon, 2015)—​ which governs our
attention to the external and internal world (Menon &
Uddin, 2010), integrates sensory, emotional, and cogni-
tive information, and is associated with optimal com-
munication, social behavior, and self-​awareness (Menon,
2015)—​is disrupted in many forms of psychopathology,
especially when there is excessive activity in the neural
regions associated with the DN (e.g., Hamilton, Chen, &
Gotlib, 2013; Paulus & Stein, 2010; Yuen et  al., 2014).
Thus, depression is marked by abnormalities in the inter-
play of the reward, default, and salience networks, which
lead to the clinical features that are commonly the targets
of treatment.
This neurobehavioral model of depression opens
many doors for clinicians who use empirically-​supported
treatments to treat MDD. The behavioral and cogni-
tive approaches, described previously, all possess inter-
vention principles that target threat and reward deficits
(e.g., exposure and behavioral activation), salience net-
work deficits (e.g., cue detection and self-​monitoring),
and excessive default network activation (e.g., cognitive
interventions). In addition, building from a solid founda-
tion of traditional and contemporary CBT principles and
informed by basic and translational findings in affect sci-
ence, emotion regulation therapy (ERT; Fresco, Mennin,
Heimberg, & Ritter, 2013; Mennin & Fresco, 2013,
2014)  was developed to specifically target the hypothe-
sized neurobehavioral deficits of commonly co-​occurring
disorders such as GAD and MDD. ERT is a theoretically
derived, evidence-​ based treatment that teaches clients
skills of attention and metacognitive regulation so they
can develop optimal behavioral repertoires associated
with threat and reward learning. ERT has demonstrated
promising preliminary clinical efficacy in open-​label and
randomized clinical trials (Mennin, Fresco, Heimberg,
& O’Toole, 2017; Mennin, Fresco, Ritter, & Heimberg,
2015; Renna et al., 2017).
Interpersonal Models
Interpersonal psychotherapy (IPT) was developed by
Klerman, Weissman, and their colleagues as a treatment
for MDD (Klerman, Weissman, Rounsaville, & Chevron,
1984). The interpersonal model of depression emphasizes
the reciprocal relations between biological and interper-
sonal factors in causing and maintaining depression. The
IPT theory proposes that problems or deficits in one or
more of four areas of interpersonal functioning (unre-
solved grief, interpersonal disputes, role transitions, and
interpersonal deficits [e.g., social skills deficits or social
isolation]) contribute to the onset and/​or maintenance of
depression, and the IPT therapist intervenes to address
the patient’s deficits in that area. Lewinsohn’s behavioral
model and McCullough’s CBASP also included propos-
als that depressed individuals have interpersonal skills
deficits, and the therapies based on those models include
skills training elements.
Relapse Prevention Models
Depression is a recurrent disorder, and relapse rates are
high (Hollon et  al., 2006). Mindfulness-​based cognitive
therapy (MBCT; Segal, Williams, & Teasdale, 2013)  is
predicated on the premise that intervention principles
that are effective in eliminating symptoms of depression
may not be ideally suited to prevent future episodes.
MBCT posits that previously depressed individuals are
vulnerable for relapse or recurrence because dysphoria
can reactivate patterns of thinking that maintain and
intensify the dysphoric states through escalating and
self-​perpetuating cycles of ruminative cognitive–​affective
 135

Adult Depression 135

processing (Teasdale, 1997, 1988). MBCT combines in time, and this is particularly important because without
elements of traditional CBT for depression with compo- a longitudinal assessment, it can be difficult or impossible
nents of the mindfulness-​based stress reduction program to distinguish between a unipolar and bipolar mood dis-
(MBSR) developed by Kabat-​Zinn and colleagues (e.g., order. The DSM-​5 version of the SCID is still relatively
Kabat-​Zinn, 1990)  to provide individuals with ways to new, and studies evaluating its psychometric properties
ward off emotion-​cued spirals into rumination. In particu- are not yet available. In a study of the use of the SCID
lar, MBCT seeks to improve former depressed patients’ to diagnose MDD based on the DSM-​IV-​TR (American
focused and flexible attention and ability to decenter (van Psychiatric Association, 2000), Ventura (1998) reported
der Velden et al., 2015). high inter-​rater agreement for current diagnosis based on
the DSM-​IV-​TR SCID, with an overall weighted κ of .82.
Kappas for MDD have been found to be good to excellent
PURPOSES OF ASSESSMENT (range = .80 to .91; Ventura, 1998). A streamlined clini-
cian version of the SCID-​5 is available exclusively from
We discuss assessment for diagnosis, for case conceptual- American Psychiatric Publishing (https://​www.appi.org/​
ization and treatment planning, and for monitoring prog- products/​structured-​clinical-​interview-​for-​dsm-​5-​scid-​5).
ress in treatment. The clinician working with a depressed The Anxiety and Related Disorders Interview Schedule
patient is likely to choose one or more of the behavioral, for DSM-​ 5–​Lifetime Version (ADIS-​5L; Brown & Barlow,
cognitive, emotion-​ focused, interpersonal, or relapse-​ 2014)  is a semi-​structured interview for the diagnosis of
prevention models to guide the therapy, and the choice of current and past DSM-​ 5 anxiety, mood, obsessive–​
assessment tools for case conceptualization and treatment compulsive, trauma, and related disorders (e.g., somatic
planning and progress monitoring will likely depend on symptom and substance use). A 0 to 8 clinician severity
the model or models the clinician chooses. Assessment rating (CSR) is assigned for each diagnosis based on the
tools for diagnosis, in contrast, are independent of the severity of the patient’s distress about his or her symptoms
model guiding treatment. There is significant overlap in and the degree of interference in daily functioning due to
the tools we describe for assessing diagnosis, conceptual- the symptoms. A CSR of 4 or higher is considered clini-
ization and treatment planning, and treatment monitor- cally significant. A disorder is designated as the principal
ing. For example, measures of depressive symptoms are diagnosis if it is given a CSR that is at least one point
useful for diagnosis, conceptualization and treatment higher than any other clinically significant diagnosis. If
planning, and monitoring progress in treatment. the goal of the interview is simply to confirm the pres-
ence of current and lifetime diagnoses, the ADIS-​5L takes
roughly the same amount of time to administer as the
SCID-​5. However, the clinician may want to make use of
ASSESSMENT FOR DIAGNOSIS
the extensive probes for assessing the specific impairment
associated with a particular disorder, the client’s strengths,
Semi-​Structured Interviews
hypothesized etiological factors and situational anteced-
The most frequently used instrument for assigning a diag- ents, and a “Diagnostic Timeline” approach to track the
nosis is the Structured Clinical Interview (SCID), recently onset, remission, and temporal ordering of diagnoses that
updated for DSM-​5 (First, Williams, Karg, & Spitzer, are unique features of the ADIS-​5L. Studies evaluating
2015). The SCID-​5 requires between 60 and 90 minutes the psychometric properties of the ADIS-​5L are not yet
to administer and allows the clinician to identify current available, but as detailed in Table 7.1, the norms of the
and lifetime psychiatric disorders. The SCID-​5 was fash- ADIS-​IV are adequate; the inter-​rater reliability, content
ioned after the traditional interview in which clinicians validity, construct validity, and validity generalization are
consider and test several diagnostic hypotheses simultane- good; and clinical utility is excellent.
ously. Each section begins with a YES/​NO probe followed
by queries that ask for elaborations. This strategy has two
Self-​Report Measures
main advantages: (1) Diagnostic decisions are known to
the interviewer during the interview, and (2)  interviews Many self-​report scales of depressive symptoms are avail-
are shorter because irrelevant sections are not exhaustively able to support diagnostic assessment. We review two: the
probed. The SCID-​5 allows the clinician to assess the life- Quick Inventory of Depressive Symptomatology–​ Self-​
time course of the disorder, not just a snapshot at one point Rated (QIDS-​SR) and the Patient Health Questionnaire-​9
136

136 Mood Disorders and Self-Injury

Table 7.1  Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Diagnosis
SCID-​5/​ A NA G NA G G G E E ✓
SCID-​5-​PD
ADIS-​5L A NA G NA G G G E E ✓
Depression Severity
QIDS E E NA E E E E E E ✓
PHQ-​9 E E NA E E E E E E ✓

Note: SCID-​5 = Structured Clinical Interview for DSM-​5; ADIS-​5L = Anxiety and Related Disorders Interview Schedule for DSM-​5–​Lifetime Version;
QIDS  =  Quick Inventory for Depression Severity; PHQ-​9  =  Patient Health Questionnaire 9; A  =  Adequate; G  =  Good; E  =  Excellent; NA  =  Not
Applicable.

(PHQ-​ 9). We do not review the Beck Depression
Inventory Second Edition (BDI-​II; Beck, Steer, & Brown,
1996), despite its wide use in research, because the scales
we chose to review are largely free, easy to access, and suf-
ficient to meet clinicians’ needs.
The QIDS-​SR (Rush et  al., 2003)  is a 16-​item self-​
report measure that is designed to assess the severity of
depressive symptoms. The scale evaluates all the criterion
symptom domains in the DSM-​5 criteria for MDD. The
QIDS-​SR is a shortened version of the 30-​item Inventory
of Depressive Symptomatology (IDS-​SR); the IDS-​SR, in
addition to assessing depressive symptoms, also assesses
many symptoms of anxiety. The QIDS-​SR and IDS-​SR
are, in turn, adaptations of clinician-​rated versions of the
IDS and QIDS. As indicated in Table 7.1, the norming,
reliability, and validity of the QIDS-​ SR are excellent.
Lamoureux et  al. (2010) conducted receiver operating
characteristic analysis in a sample of 125 primary care
patients who completed the QIDS-​SR and the SCID and
concluded that a score of 13 on the QIDS-​SR provided
the best balance of sensitivity (Sn  =  .77) and specificity
(Sp = .82) and correctly classified 81% of the sample as to
MDD status. The clinician-​rated and self-​rated versions
of the IDS and QIDS, as well as copious psychometric
information about the scales, are available free for down-
load online (http://​www.ids-​qids.org). The measures are
available in 13 languages.
The PHQ-​9 (Kroenke, Spitzer, & Williams, 2001)  is
a 10-​item self-​
report measure designed for screening,
diagnosing, and/​or monitoring depressive symptoms over
a 2-​week period. The first 9 items assess specific depres-
sive symptoms using a 4-​point Likert scale of 0 (not at all)
to 3 (nearly every day), and these items are summed for
a total score. The PHQ-​9 items correspond closely with
the DSM-​5 diagnostic criteria for MDD. The 9th item
assesses suicidal ideation and intent, and it is useful for
risk assessment and intervention. A 10th item (nonscored)
assesses the degree of functional interference from depres-
sive symptoms. Clinical interpretation guidelines catego-
rize a score of 0 to 4 as normal, 5 to 9 as mild, 10 to 14
as moderate, 15 to 19 as moderately severe, and 20+ as
severe depressive symptoms. The psychometric prop-
erties of the PHQ-​9 have been evaluated in two studies
of 3,000 patients in eight primary care clinics (Spitzer
et  al., 1999)  and 3,000 patients in seven obstetric clin-
ics (Spitzer, Williams, Kroenke, Hornyak, & McMurray,
2000). Scores on the PHQ-​9 have demonstrated high
internal consistency, test–​retest reliability, and diagnostic
validity (Kroenke et  al., 2001), and the measure shows
good specificity and sensitivity in grading and diagnos-
ing depression severity (Pettersson, Boström, Gustavsson,
& Ekselius, 2015). It is available copyright-​free at http://​
www.phqscreeners.com.
In addition to the traditional paper-​and-​pencil method,
measures of depressive symptoms can be administered
electronically with software programs or through mobile
apps downloaded from the web. Electronic assessment
can offer advantages, such as automated scoring and
charting of the data and remote data collection. However,
limitations include risks of loss of privacy and confidenti-
ality. In addition, if patients complete depressive invento-
ries remotely, the clinician must have a plan for alerting
the patient of the need to contact the clinician directly if
immediate intervention is needed to address suicidality.
Overall Evaluation
Excellent measures with strong psychometric properties
are available for diagnostic assessment of the depressed
patient. Although it is tempting to minimize or omit
 137
diagnostic assessment altogether, we encourage the cli-
nician to take the time to do this because diagnosis has
treatment implications. In particular, it is important to
distinguish between MDD, a unipolar mood disorder for
which psychotherapy alone is often sufficient, and bipolar
mood disorder, which generally requires pharmacother-
apy plus psychotherapy (Craighead et al., 2015).
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
Assessment for case conceptualization and treatment
planning requires two types of translation. One is from
disorder-​level (and sometimes symptom-​level) conceptu-
alizations and treatments to the case-​level conceptualiza-
tion and treatment plan. Most of the models we reviewed
previously are conceptualizations and therapies for the
disorder of MDD. A few of the models also provide con-
ceptualizations and interventions for symptoms (e.g., the
BA formulation of rumination as avoidance behavior).
A  conceptualization (or formulation) at the level of the
case is a hypothesis about the causes of all of the patient’s
symptoms, disorders, and problems and how they are
related, and the treatment plan describes all of the thera-
pies the patient is receiving for those symptoms, disorders,
and problems.
The second translation is from nomothetic to idio-
graphic. A nomothetic formulation and treatment plan is
stated in general terms (e.g., that depression results from
a dearth of positive reinforcers and can be treated by
increasing the individual’s positive reinforcers). An idio-
graphic case formulation and treatment plan describes a
particular individual.
Case Conceptualization
A case conceptualization is a hypothesis about the mech-
anisms causing and maintaining a particular patient’s
symptoms, disorders, and problems; the precipitants of the
symptoms/​disorders/​problems; and the origins of the mech-
anisms. We focus here on psychological mechanisms, but
the formulation might also include biological mecha-
nisms. We describe tools and strategies for assessing all the
elements of the formulation.
Symptoms/​Disorders/​Problems
The case conceptualization accounts for all of the
patient’s symptoms, problems, and disorders. We
Adult Depression 137
recommend that the clinician conduct a broad-​based
assessment of the following domains: psychiatric symp-
toms and disorders and treatment difficulties (e.g.,
multiple providers or inadequate treatment); medical
symptoms and disorders and treatment difficulties; and
interpersonal, occupational/​school/​homemaking satis-
faction and functioning, financial difficulties, housing
difficulties, and legal problems.
To obtain a comprehensive diagnostic assessment,
the clinician can use the measures described in the
Assessment for Diagnosis section. Additional tools for
assessing many of the depressed patient’s comorbid psy-
chiatric disorders, and symptoms that may not meet full
criteria for a disorder, are described in other chapters of
this volume.
Many MDD patients have a medical problem
(Moussavi et  al., 2007). MDD and medical problems
can cause or exacerbate one another, and MDD often
impedes the patient’s ability to obtain and adhere to
treatment for the medical problems. Thus, we recom-
mend that clinicians ask their patients to obtain a physi-
cal examination if they have not had one in the past
year. MDD is also commonly comorbid with psychoso-
cial and environmental problems, such as marital prob-
lems, occupational dissatisfaction, and similar, which
can cause, exacerbate, and/​or result from MDD. Lack
of satisfaction and difficulties functioning in domains
such as work, relationships, and leisure can appear on
the problem list element of the case conceptualization
and/​or might be precipitants.
We recommend three tools that assess functioning
difficulties. The first is the Outcome Questionnaire-​45
(OQ-​45; Lambert et al., 1996), which is described in the
section titled Assessment for Treatment Monitoring and
Treatment Outcome.
The second is the World Health Organization
Disability Assessment Schedule 2.0 (WHODAS 2.0;
World Health Organization [WHO], 2001), a 36-​item
self-​report assessment of patient difficulties during the past
30 days in six domains: understanding and communicat-
ing, getting around, self-​care, getting along with people,
life activities (household/​school/​work), and participation
in society. The measure was designed for both initial
assessment and progress monitoring. The WHODAS 2.0
is designed to be simple and relatively quick to administer
(5–​20 minutes, depending on whether the 12-​or the 36-​
item form is used). The WHODAS 2.0 has been adminis-
tered to diverse global populations and has demonstrated
excellent test–​ retest reliability (intraclass correlation
coefficient  =  .98), internal consistency, and concurrent
138

138 Mood Disorders and Self-Injury

validity, both with similar measures and with clinician rat-
ings of functioning (Üstün et al., 2010). This measure is
free for clinicians to reproduce and use with their clients.
Scoring guidelines are provided both in the DSM-​5 and
on the WHO website (http://​www.who.int/​classifications/​
icf/​whodasii/​en).
Third, item 10 of the PHQ-​9 provides a quick assessment
of global functioning by inquiring about the degree of func-
tional interference of the individual’s depressive symptoms.
Ratings range from not difficult at all to extremely difficult.
Psychological Mechanisms
We describe here and summarize in Table 7.2 several
measures for assessing the mechanisms from many of the
theories of depression reviewed above.
Behavioral Mechanisms
The Activity Schedule (presented originally in Beck
et al., 1979; see also pp. 126–​127 of Persons, Davidson, &
Tompkins [2001] for a version that clinicians may repro-
duce) is essentially a week-​long hourly calendar in which
patients log or plan activities. It is ideal for assessing how
the patient spends time as well as for use tracking behav-
ioral homework assignments, such as recording pleasant
activities.
The Pleasant Events Schedule (PES; MacPhillany
& Lewinsohn, 1982), published in Lewinsohn, Munoz,
Youngren, and Zeiss (1986), is a self-​report inventory of
320 potentially reinforcing activities. Respondents assign
ratings for each event for the frequency of occurrence dur-
ing the past 30 days on a 3-​point scale ranging from 0 (not
happened) to 2 (happened often; seven or more times) and
a pleasantness rating on a 3-​point scale ranging from 0
(not pleasant) to 2 (very pleasant). The PES scores have
good reliability and adequate to good validity (Grosscup
& Lewinsohn, 1980; MacPhillamy & Lewinsohn, 1982;
Nezu, Ronan, Meadows, & McClure, 2000). The PES
and supporting materials can be downloaded free of
charge at http://​www.ori.org/​scientists/​peter_​lewinsohn.
The Snaith–​Hamilton Pleasure Scale (SHAPS; Snaith
et al., 1995) is a 14-​item, self-​report measure designed to
assess an individual’s hedonic capacity. It assesses “lik-
ing” as opposed to “wanting” (discussed previously). The
SHAPS asks the patient to rate his or her ability to expe-
rience pleasure in the past few days with items such as
“I would enjoy my favorite television or radio program”
or “I would enjoy being with my family or close friends.”
Ratings range from definitely agree to strongly disagree.
Nakonezny et al. (2015) found that in a large sample of
adults meeting criteria for MDD, SHAPS scores dem-
onstrated high internal consistency (α  =  .91). The mea-
sure showed good construct validity; it was significantly

Table 7.2  Ratings for Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Symptoms/​Disorders/​Problems
WHODAS 2.0 E G E A E G E G E ✓
Behavioral Mechanisms
PES G G NA G G G A NA G ✓
SHAPS G E NR NR G G G A A
PTQ NR E G G G G G NR A ✓
Cognitive Mechanisms
FMPS A E NR NR G G G G G
EQ A G NA NR G G A NR G ✓
ACS A G E A G G NR NR G
Emotion-​Focused Mechanisms
ERQ A G NA NR A G A NR A
AIM A G NR G G G NR NR G
Interpersonal Mechanisms
SAS-​SR A A NA A G A G NA G

Note: WHODAS 2.0 = World Health Organization Disability Assessment Schedule 2.0; PES = Pleasant Events Schedule; SHAPS = Snaith–​Hamilton
Pleasure Scale; PTQ = Perseverative Thinking Questionnaire; FMPS = Frost Multidimensional Perfectionism Scale; EQ = Experiences Questionnaire;
ACS = Attentional Control Scale; ERQ = Emotion Regulation Questionnaire; AIM = Affect Intensity Measure; SAS-​SR = Social Adjustment Scale–​Self-​
Report; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.
 139

Adult Depression 139

negatively correlated (r = –​.65) with ratings of quality of Cognitive Mechanisms

life. SHAPS totals were only modestly positively corre-
A self-​ monitoring diary, such as the Daily Record of
lated with four measures of depressive symptoms (r = .48
Dysfunctional Thoughts (Beck et al., 1979) or the forms
to .55), a finding that may indicate that hedonic capacity
provided by Greenberger and Padesky (1995) or Persons
reflects a “related but distinct construct from depression”
et al. (2001), can be used to assess the automatic thoughts
(Nakonezny et al., 2015, p. 6). The measure was sensitive
described by Beck’s theory. Emotions, behaviors, and
to change (Snaith et al., 1995). The SHAPS is published
automatic thoughts are typically obtained by simply ask-
in Snaith et al. (1995), and the publisher gives permission
ing the patient to report them while recalling the specific
to readers to reproduce the scale from the journal article
concrete event that triggered them. J.  S. Beck (1995)
for personal use or research.
offered strategies for eliciting this information when a
The Perseverative Thinking Questionnaire (PTQ;
direct and straightforward approach fails, including ask-
Ehring et  al., 2011)  is a 15-​item self-​report scale that
ing patients to report images and asking them to vividly
assesses content-​ neutral repetitive negative thinking,
imagine and re-​create the event that triggered negative
including rumination and worry. The PTQ assesses five
painful emotions.
characteristics of perseverative thinking: repetitive (“The
The Frost Multidimensional Perfectionism Scale
same thoughts keep going through my mind again and
(FMPS; Frost, Marten, Lahart, & Rosenblate, 1990)  is
again”), intrusive (“Thoughts come to my mind without
a 35-​item measure grouped into six subscales:  Concern
me wanting them to”), difficult to disengage from (“I can’t
Over Mistakes, Personal Standards, Parental
stop dwelling on them”), unproductive (“I keep asking
Expectations, Parental Criticism, Doubts About Actions,
myself questions without finding an answer”), and cap-
and Organization. Respondents rate on a scale ranging
turing mental capacity (“My thoughts prevent me from
from 1 (strongly disagree) to 5 (strongly agree) such items
focusing on other things”). Scores on the PTQ have dem-
as “If I fail at work/​school, I am a failure as a person” or
onstrated excellent internal consistency (α = .95 in both
“Even when I  do something very carefully, I  often feel
German and English language versions), satisfactory test–​
that it is not quite right.” The FMPS scores have dem-
retest reliability (r = .69 at 4-​week retest for the German
onstrated good internal consistency (α = .77 to .93; Frost
language version of the scale), good convergent validity
et  al., 1990)  and good convergent validity compared to
compared to similar measures of rumination or worry, and
other similar measures of perfectionism (Stober, 2000).
good predictive validity when correlated with measures of
The measure is reprinted in Appendix B of Antony,
anxiety and depression (Ehring et al., 2011). The PTQ is
Orsillo, and Roemer (2001).
reproduced in the appendix of Ehring et al. (2011), which
The Experiences Questionnaire (EQ; Fresco et  al.,
is available online at http://​www.sciencedirect.com/​sci-
2007)  is an 11-​item self-​report measure of decentering.
ence/​article/​pii/​S000579161000114X. Clicking the link
This measure asks the patient to rate the frequency with
within the text that reads “under a creative commons
which he or she is currently having certain experiences,
license” on that web page will provide access to the PTQ
such as “I remind myself that thoughts aren’t facts” or “I
through the creative commons.
can observe unpleasant feelings without being drawn into
To identify antecedents and consequences of a target
them.” Ratings range from 1 (never) to 5 (all the time).
behavior to help identify the function of the behavior,
Fresco et al. used both exploratory and confirmatory fac-
clinicians can devise a paper-​and-​pencil or a computer-​
tor analysis techniques to examine the EQ factor structure
based/​smartphone-​based log. The patient can track each
in two large samples of college students and a sample of
instance of the target behavior (e.g., exacerbation of
depressed patients. Scores on the measure showed good
depressed mood, rumination, or suicidality), antecedents
internal consistency, ranging from α  =  .81 to .90, and
of the behavior (events, thoughts, emotions, bodily sen-
good concurrent and discriminant validity. The EQ has
sations, and behaviors), and consequences of the behav-
consistently shown sensitivity to treatment change in tri-
ior (events, thoughts, emotions, bodily sensations, and
als for MDD and GAD (Fresco, Segal, et al., 2007; Hoge
behaviors) and then review with the therapist to develop
et al., 2015; Mennin, Fresco, Ritter, & Heimberg, 2015;
a hypothesis about the function the target behavior
Mennin, Fresco, et  al., 2017; Renna et  al., 2017). The
might serve. Guidance on collecting assessment data
EQ is also correlated with a recently developed objective
for a functional analysis is provided in multiple sources,
measure of distancing that complements the assessment
including Haynes, O’Brien, and Kaholokula (2011) and
of decentering (Shepherd, Coifman, Matt, & Fresco,
Kazdin (2013).
140
140 Mood Disorders and Self-Injury
2016). The EQ is available from Fresco upon request via
e-​mail (fresco@kent.edu).
The Attentional Control Scale (ACS; Derryberry &
Reed, 2002) is a 20-​item self-​report measure that assesses
an individual’s ability to focus and shift attention. The
items of the ACS are divided among the capacities to
(a)  focus attention (“When concentrating, I  can focus
my attention so that I  become unaware of what’s going
on in the room around me”), (b)  shift attention (“It is
easy for me to alternate between two different tasks”), and
(c) control thought flexibly (“I can become interested in a
new topic very quickly when I need to”). The client rates
these items on a scale of 1 (almost never) to 4 (always);
higher scores indicate greater overall attentional control.
ACS scores have been found to be negatively correlated
with trait anxiety and positively correlated with indices of
positive emotionality, such as extraversion (Derryberry &
Reed, 2001). Scores on the measure have demonstrated
good internal consistency (α  =  .88; Derryberry & Reed,
2001), good content validity, and adequate test–​retest reli-
ability (r = .61; Fajkowska & Derryberry, 2010). The ACS
is available in Derryberry and Reed (2002) and is free for
clinicians.
Emotion-​Focused Mechanisms
The Emotion Regulation Questionnaire (ERQ; Gross
& John, 2003) is a 10-​item rationally derived measure of
two aspects of emotion regulation:  reappraisal and sup-
pression. The reappraisal subscale, consisting of 6 items,
assesses the ability to modify or change the emotions one
experiences (e.g., “I control my emotions by changing the
way I think about the situation I’m in”). The suppression
subscale, consisting of 4 items, assesses the ability to avoid
or prevent the expression of emotions (e.g., “I control my
emotions by not expressing them”). Fresco et  al. (2007)
reported that internal consistency was good for scores on
both the reappraisal subscale (α = .84) and the suppression
subscale (α = .82). The reappraisal scale was significantly
and positive correlated with decentering (r = .25), but it
was uncorrelated with depression symptoms (r = .14) and
depressive rumination (r = .14). Conversely, the suppres-
sion subscale was significantly and negatively correlated
with decentering (r =  –​.31) and significantly and posi-
tively correlated with depression symptoms (r = .39) and
depressive rumination (r = .31). The ERQ is available free
on the Internet https://​www.ocf.berkeley.edu/​~johnlab/​
measures.htm.
The Affect Intensity Measure (AIM; Larsen, 1984) is a
self-​report measure designed to assess the intensity of an
individual’s characteristic emotional reactions to typical
life events. The items of the AIM describe such events
as “I get upset easily” or “When I’m happy, I feel like I’m
bursting with joy.” The individual rates how often he or
she experiences such reactions on a scale from 1 (never)
to 6 (always). Weinfurt, Bryant, and Yarnold (1994) con-
ducted factor analyses and described the four basic factors
of the AIM as positive affectivity, negative reactivity, nega-
tive intensity, and serenity (or positive intensity). Rubin,
Hoyle, and Leary (2012) found that scores for items
comprising the negative reactivity and negative intensity
factors were positively correlated with measures of neu-
roticism, negative affect, and depression and negatively
correlated with self-​compassion. The AIM scores have
good internal consistency, test–​retest reliability, and crite-
rion-​related validity (Larsen, Diener, & Emmons, 1986).
The scale is available to clinicians and researchers for free
at http://​internal.psychology.illinois.edu/​~ediener/​AIM.
html.
Interpersonal Mechanisms
Weissman and Bothwell (1976) developed the Social
Adjustment Scale–​Self-​Report (SAS-​SR), a 54-​item self-​
report measure that assesses six social role domains: work/​
homemaker/​student, social and leisure activities, relation-
ships with extended family, marital partner role, parental
role, and role within the family unit. Internal consistency
of scores on the measure has been found to be adequate
(α =.74). The measure has good known-​groups validity,
distinguishing samples from the community, patients with
depression, and patients with schizophrenia from one
another on the basis of total score. The SAS-​SR is avail-
able for purchase from Multi-​Health Systems, Inc. (https://​
www.mhs.com/​MHS-​Assessment?prodname=sas-​sr).
Precipitants
Precipitants of episodes of MDD can be internal, exter-
nal, biological, or psychological stressors or some com-
bination of these. The WHODAS 2.0 and the Social
Adjustment Scale, described previously, can be used to
assess precipitants. The clinician can also use the illness
history timeline as described in Frank (2005) to identify
events that precipitated episodes of illness.
Origins
The origins part of the formulation offers a hypoth-
esis about how the patient learned or acquired the
 14

Adult Depression 141

hypothesized mechanisms of the formulation. Origins Developing an Initial Case Conceptualization

can be one or more external environmental events (e.g.,
After assessing all the elements of the case conceptualiza-
the death of a parent or early abuse or neglect), cultural
tion using the methods described previously, the clinician
factors, or biological factors (e.g., an unusually short
works with the patient to build a model describing how
stature that might elicit teasing from peers), including
all the elements are related. The model is a hypothesis,
genetics. Information about origins can point to mecha-
and one that is revised frequently as treatment proceeds.
nism hypotheses (e.g., early abuse can lead to views of
Figure 7.1 provides an example for the case of Thea that
self as bad or worthless). To generate hypotheses about
was developed using this strategy, with notes about some of
how the patient acquired the conditioned maladaptive
the standardized assessment tools that were used to develop
responses, learned the faulty schemas, or developed an
the formulation of her case.
emotion regulation difficulty, the therapist can conduct
Alternate strategies for developing a case conceptu-
a clinical interview that asks the patient to identify key
alization have also been developed. Kuyken, Fothergill,
events and factors in his or her upbringing and develop-
Musa, and Chadwick (2005) showed that clinicians
ment, including early trauma, neglect, and abuse (e.g.,
who used the method described by J. S. Beck (1995) to
Wiersma et al., 2009) and early loss, that are known to
develop a case conceptualization agreed fairly well with
serve as vulnerability factors for depression. In addi-
one another and with a benchmark formulation cre-
tion, the clinician will want to obtain a family history
ated by Judith Beck when they were given the task of
of depression and other psychiatric disorders, which can
identifying the patient’s presenting problems, but agree-
shed light on both biological and psychosocial causes of
ment was worse when the clinicians were called on to
the patient’s symptoms.

Case Formulation for Thea

Self-criticism and repetitive

negative thinking1
“It’s my fault”
“I shouldn’t need nurturing.
I’m a grown woman.”

Precipitant No action to get

Loss of important needs met Depressive symptoms2
relationship

Origins
• 6th of 7 kids
Loss of reinforcers3
• Mother died at age 11
• Father self-involved and alcoholic

Key of Corresponding Measures:

1-Perseverative Thinking Questionnaire
2-Patient Health Questionnaire; Quick Inventory of Depressive Symptomatology
3-Activity Schedule; Pleasant Events Schedule

FIGURE 7.1   Conceptualization of the Case of Thea

142
142 Mood Disorders and Self-Injury
make inferences (e.g., about the patient’s schemas). In
an initial assessment of the psychometric properties of
the Collaborative Case Conceptualization Rating Scale
(CCC-​RS) developed by Christine Padesky, Kuyken et al.
(2016) reported that the scale had excellent internal con-
sistency, split-​half, and inter-​rater reliability and that the
scores were moderately correlated with other measures of
related phenomena.
The Treatment Plan
A treatment plan includes several elements:  the goals
of treatment; the frequency and modalities of treatment
provided by the clinician who is writing the treatment
plan; and adjunct therapies, if any, that are provided by
other clinicians. We describe tools for assessing treatment
goals and progress toward the goals in the section titled
Assessment for Treatment Monitoring and Treatment
Outcome.
Overall Evaluation
Many psychometrically sound standardized measures,
described previously, are available to assess patients’ symp-
toms and problems and the psychological mechanisms
described by the major current evidence-​based theories
of depression in order to develop an idiographic case
conceptualization. As discussed previously, the clinician
may also elect to use idiographic tools such as a log to
monitor antecedents and consequences of target behav-
iors in order to develop a functional analysis of a prob-
lem behavior or symptom. However, the psychometric
qualities of idiographic assessment tools are rarely studied
(Haynes & O’Brien, 2000), and it can also be challeng-
ing for the clinician to incorporate nomothetic data into
an idiographic formulation. Figure 7.1, which describes
the case of Thea, provides an illustration of the clinician’s
use of nomothetic measures to assist in developing the
formulation of the case. Additional details are provided in
Persons, Brown, and Diamond (in press).
Another challenge is that there is little information
about the reliability and validity of the case conceptual-
ization, although contributions in this area are increasing
(Bucci, French, & Berry, 2016; Persons & Hong, 2016).
To strengthen their idiographic assessment data and the
conclusions they draw from them, we recommend that
clinicians rely on basic principles of behavioral assess-
ment (Haynes et al., 2011) and collect data (as described
in the next section) to test their formulation hypotheses
and monitor treatment progress for each case they treat.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
As therapy proceeds, the therapist monitors the outcome of
therapy to evaluate the patient’s progress and identify the
need for a change in the treatment plan if the patient is
not responding. The therapist also monitors the process of
therapy to evaluate whether the therapy is being delivered
as planned and the targeted psychological mechanisms
are changing.
Monitoring Outcome
To monitor changes in depressive symptoms during treat-
ment, we recommend the QIDS-​SR (described previ-
ously) and the Depression Anxiety Stress Scales (DASS;
described later in this section) because they are brief,
free, and have been demonstrated to have treatment
sensitivity. Whatever tool the clinician uses to monitor
outcome, it is essential to use it starting in the very first
session because there is good evidence that a large propor-
tion of the change in depressive symptoms happens very
early in treatment (Ilardi & Craighead, 1994), and some
evidence that patients who do not show early change
(Crits-​
Christoph et  al., 2001)  or who remain severely
symptomatic at week 4 of treatment (Persons & Thomas,
2016)  are very unlikely to remit. Evidence that sudden
gains, a large shift in symptoms between one session and
the next, predict outcome (Aderka, Nickerson, Boe, &
Hoffman, 2012) also highlights the usefulness of monitor-
ing outcome at every session. The clinician likely will also
want to monitor symptoms of anxiety, substance use, and
other comorbid difficulties identified as goals to change
during treatment. Sources of measures for this purpose
include other chapters in this volume, Nezu et al. (2000),
and Beidas et al. (2014).
The DASS (Lovibond & Lovibond, 1995)  is a self-​
report scale that includes three subscales assessing symp-
toms of depression (low positive affect, hopelessness, and
anhedonia; e.g., “felt downhearted and blue” and “diffi-
cult to work up the initiative to do things”), anxiety (panic
and physiological arousal; e.g., “felt I was close to panic”
and “trembling”), and stress (high negative affect; e.g.,
“hard to wind down” and “rather touchy”). Respondents
rate each item to reflect how much it applies to their expe-
rience over the preceding week on a Likert scale ranging
from 0 (“did not apply to me at all”) to 3 (“applied to me
very much”).
The scale is available in two versions, one with 21 items
and one with 42 items. The DASS is quick to complete,
 143
suitable for most adult outpatients, and responsive to
changes due to treatment (Brown, Chorpita, Korotitsch,
& Barlow, 1997). The DASS scores have been reported
to have good test–​retest reliability, high internal consis-
tency, and adequate convergent and discriminant validity
with other measures of anxiety and depression (Antony,
Bieling, Cox, Enns, & Swinson, 1998; Brown et  al.,
1997). The three subscales measure largely independent
constructs, which is consistent with the tripartite model
(Clark & Watson, 1991)  on which the DASS is based
(Brown et al., 1997).
The measure is in the public domain. Detailed infor-
mation can be found in the DASS manual (Lovibond &
Lovibond, 1995) as well as at http://​www2.psy.unsw.edu.
au/​groups/​dass. The measure’s sensitivity to change and
coverage of the three domains of positive affect, negative
affect, and physiological arousal/​panic make it especially
useful for monitoring progress. Its main weakness as a
progress-​monitoring tool for the depressed patient is the
fact that it does not assess suicidality.
Combined measures of symptoms and functioning
have been developed to monitor change during psycho-
therapy for adult psychiatric patients receiving treatment
for any problem or disorder, including depression. The
most studied of these is the Outcome Questionnaire
(OQ-45;  Lambert et  al., 1996), a 45-​ item self-​report
scale that assesses subjective discomfort, interpersonal
relations, social role performance, and positive aspects
of satisfaction and functioning. The measure includes
an item that assesses suicidality, which is particularly
important when working with depressed patients.
Respondents answer each question in the context of their
experience during the past week using a 5-​point Likert
scale. The scoring manual or software package classifies
each client, at each assessment point, as an improver,
nonresponder, or deteriorator based on benchmarking
data from a very large sample of clients. The software
tool plots the score over time. Internal consistency for
a sample of 504 Employee Assistance Program clients
was .93 (Lambert et  al., 1996). The total score on the
measure has good test–​retest reliability (.84) over an
interval of 3 weeks for a sample of 157 undergraduates.
The measure is sensitive to change in clients and sta-
ble in untreated individuals (Vermeersch, Lambert, &
Burlingame, 2000). The measure has good treatment
utility, as Lambert and Shimokawa (2011) have shown
that psychotherapy patients have better treatment out-
come when clinicians use the information to adjust
treatment as necessary (i.e., when the patient is classified
as a nonresponder or deteriorator). Using the Clinical
Adult Depression 143
Support Tool that the measure provides to help the clini-
cian assess factors that are known to be tied to poor out-
come of psychotherapy (the therapeutic alliance, social
support, and the patient’s readiness for change) has been
shown to lead to improved outcomes of cases classified
as deteriorators (Whipple et al., 2003).
Measures that assess a broad spectrum of the adult
patient’s treatment goals and monitor progress toward
the goals, and have been shown to be psychometrically
sound, are rare. We located two measures:  one that was
designed for this purpose and one that was designed for
monitoring treatment progress in youths.
Goal Attainment Scaling (GAS; Kiresuk & Sherman,
1968) measures changes in idiographic goals due to men-
tal health treatment. GAS calls for patient and therapist to
identify, at the outset of treatment, three to five goals that
will be the focus of treatment, and the expected level of
progress on each goal, and to evaluate later in treatment
whether the expected progress has been made. GAS is
widely used in program evaluation, has both nomothetic
and idiographic features, and allows for assessment of
affirmatives (goals and objectives that are positively val-
ued by the patient). Limitations of the measure include
the fact that the GAS measures the amount of change
relative to what was expected or predicted, and its psycho-
metric properties are not consistently impressive (Kiresuk,
Smith, & Cardillo, 1994).
The Top Problems measure was created by Weisz et al.
(2011) to identify problems and monitor severity of those
problems over the course of treatment in a sample of mul-
tiply comorbid youths receiving psychotherapy for anxi-
ety, mood, and/​or conduct problems. Weisz et al. reported
that the measure had good psychometric properties in
their sample, and the measure appears easy to adapt to
adults.
Monitoring Process
Process has two parts: the elements of the therapy that are
viewed as important to producing changes in mechanisms
and symptoms and the psychological mechanisms that are
hypothesized to cause and maintain the symptoms of
depression (e.g., engagement in pleasant activities and
self-​distance).
Elements of the Therapy
The therapist can use his or her clinical record to docu-
ment and monitor the degree to which the treatment
plan is being delivered as planned (e.g., to monitor the
14

144 Mood Disorders and Self-Injury

frequency of sessions and the patient’s participation in
recommended adjunctive therapies). Homework compli-
ance has been shown to predict outcome of psychotherapy
(Kazantzis, Whittington, & Dattilio, 2010), indicating the
importance of monitoring that aspect of therapy. To moni-
tor homework, the therapist can work with the patient to
develop a paper-​and-​pencil or other tool, locate an app, or
develop his or her own tracking form.
The Therapeutic Relationship
A large body of evidence shows that the therapeutic rela-
tionship predicts outcome of psychotherapy (Norcross,
2011)  and thus points to the importance of monitoring
this aspect of treatment.
We review two measures of the therapeutic relation-
ship. The Revised Helping Alliance Questionnaire (HAq-​
II; Luborsky et  al., 1996)  is a 19-​item self-​report scale
assessing the alliance between patient and therapist.
Both patient and therapist versions of the scale have been
developed. Internal consistency for both patient and ther-
apist versions of the scale has been found to be excellent
(α  =  .90 to .93), and test–​retest reliability of the patient
version has been found to be r = .78 over three sessions
(Luborsky et al., 1996). Concurrent validity demonstrated
by correlations between the HAq-​II and the California
Psychotherapy Alliance Scale ranged between r = .59 and
.71. In a demonstration of the measure’s treatment utility,
Whipple et al. (2003) showed that outcome of psychother-
apy (on the OQ-​45) was positively related to the clinician’s
obtaining weekly feedback on the patient’s HAq-​II scores.
The HAq-​II is available for download on the Internet at
http://​www.med.upenn.edu/​cpr/​instruments.html.
The Session Alliance Inventory is a six-​item measure
developed by Falkenström, Hatcher, Skjulsvik, Larsson,
and Holmqvist (2015) and is designed for administration
at every psychotherapy session. The measure is a short-
ened version of Horvath and Greenberg’s (1989) Working
Alliance Inventory. Falkenström et  al. reported that the
measure has good psychometric properties (Table 7.3)
and Falkenström, Ekeblad, and Holmqvist (2016) showed
that improvements during one therapy session predicted
reductions in depressive symptoms in the subsequent
therapy session. The measure is published in Falkenström
et al. (2015).
Psychological Mechanisms
The measures described in the section titled Mechanisms
can be used to monitor changes in mechanisms, particu-
larly the measures that are rated in Table 7.3 as sensitive
to change. Simple counts and logs can also be used. For
example, when Thea was working in therapy on increas-
ing her positive thoughts about herself and her experi-
ences, she tallied them on a golf-​score counter each day
and wrote the daily tally on a log that she brought to her
therapy session.
Overall Evaluation
Many measures are available to monitor the outcome
and process of treatment. Monitoring both process and
outcome allows the therapist to test hypotheses about the
relationships between process and outcome that guide
clinical decision-​
making. For example, the therapist
can assess whether an increase in a depressed patient’s

Table 7.3  Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Outcome
QIDS E E NA E E E E E E ✓
OQ-​45 G E NA G A G G G E ✓
DASS E E NA G E E G E G ✓
GAS A NA A A NA A A G E ✓
Therapeutic Relationship
HAQ-​II E E NA G G G G G G ✓
SAI NR E NR NR E E G E E ✓

Note: QIDS = Quick Inventory for Depression Severity; OQ-​45 = Outcome Questionnaire-​45; DASS = Depression Anxiety Stress Scales; GAS = Goal
Attainment Scaling; HAQ-​II = Helping Alliance Questionnaire-​II; SAI = Session Alliance Inventory; A = Adequate; G = Good; E = Excellent; NA = Not
Applicable; NR = Not Reported.
 145
pleasurable activities is associated with a decrease in
severity of depressive symptoms.
Monitoring outcome and process during treatment is
demanding; however, it is particularly important when
treating depression because the nonresponse rate is high,
even for the evidence-​ based treatments, and patients
appear to have better outcomes when their therapists col-
lect and review symptom-​monitoring data during treat-
ment (Lambert, Harmon, Slade, Whipple, & Hawkins,
2005; Whipple et  al., 2003). Hence, we recommend
that therapists monitor depressive symptoms, including
suicidality, at every session and review a plot of the data.
A visual record of the data on a plot that clearly displays
the time course of symptom change is a key part of the
use of monitoring data. Without it, the therapist can easily
accumulate a stack of measures in the clinical record that
does not inform the treatment process. The therapist will
likely elect to assess mechanisms less frequently, depend-
ing on the sensitivity of the measure (see Table 7.3) and
the therapist’s hypothesis about how quickly the mecha-
nism is likely to change.
Measures with strong psychometric properties that
can be used to monitor changes in symptoms and the
psychological mechanisms that the therapist conceptual-
izes as causing and maintaining the patient’s symptoms
and problems are available, and we summarize them in
Table 7.3. However, almost no measures with strong psy-
chometric properties are available to monitor the patient’s
progress toward accomplishing his or her idiographic
treatment goals. In part, this lack reflects the challenges
of evaluating the psychometric properties of idiographic
tools. However, even the standardized measures that are
available do not quite measure progress toward therapeu-
tic goals; as described previously, GAS assesses the dis-
crepancy between expected and actual goal attainment,
and the Top Problems measure assesses the severity of the
problems for which the patient seeks treatment; neither
assesses the degree to which the patient has accomplished
his or her treatment goals.
CONCLUSIONS AND FUTURE DIRECTIONS
Many strong measures of symptoms, diagnosis, and
psychological mechanisms are available to aid the cli-
nician who is treating the depressed patient. Here, we
describe several key gaps in the field. One is the dearth
of measures available to assess idiographic phenomena,
including the case conceptualization and the patient’s
treatment goals. The field’s slowness to develop measures
Adult Depression 145
for these phenomena and to develop strategies for evalu-
ating idiographic assessment tools may have its origin in
the tradition of treatment development that has stressed
the creation of standardized therapies that target single
disorders. As a result, researchers have developed tools to
assess disorders and symptoms, but they have been slow
to develop measures to assess functioning and a broad
spectrum of patient goals. The field’s recent shift to focus
less on disorders and more on transdiagnostic mecha-
nisms (e.g., Cuthbert & Insel, 2013) and to highlight the
importance of personalizing treatment (Fisher & Bosley,
2015)  has already led to positive developments in this
arena, as shown by the Top Problems tool developed by
Weisz et  al. (2011) to identify and monitor progress in
problems identified in a sample of multiply-​comorbid
youths receiving psychotherapy.
Another important gap is that few clinicians use assess-
ment tools in psychotherapy to monitor their patients’
progress in treatment (Hatfield & Ogles, 2004). The
importance of clinicians’ monitoring of their patients’
progress is highlighted by a meta-​ analysis (Harkin
et al., 2016) showing that monitoring goal progress pro-
moted goal attainment, especially when outcomes were
reported to another person or made public and when
information was physically recorded in some way. This
gap likely results from a failure to train clinicians to do
progress monitoring. Research to learn more about why
clinicians do not monitor their patients’ progress and
how obstacles to monitoring progress can be overcome
is needed.
Finally, clinicians encounter many impediments to
gaining access to evidence-​based assessment tools. Many
tools are difficult to learn about and retrieve, and are copy-
right protected and expensive, and some ask the clinician
to submit evidence of expertise in testing that is purport-
edly needed to administer and interpret the measure. One
element of a solution to this problem might include the
requirement that researchers who develop an assessment
tool using federal funding be asked to post it on an easily
accessible website, in the same way that data and manu-
scripts produced by federally funded grants are dissemi-
nated. The future of assessment is likely the Internet. Free
and inexpensive web-​based measures with excellent psy-
chometric properties that are easy for clinicians to access
and use are urgently needed.
ACKNOWLEDGMENT
We thank Jenna Carl for her assistance.
146
146 Mood Disorders and Self-Injury
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152
Depression in Late Life
Amy Fiske
Alisa O’Riley Hannum
Assessing depression in older adults presents unique chal-
lenges to the clinician for several reasons. First, depression
may be underreported in older adults because clients and
their families (and, unfortunately, sometimes their physi-
cians) often assume depressive symptoms are normal in late
adulthood (Karel, Ogland-​Hand, & Gatz, 2002). Second,
depression can sometimes be difficult to differentially
diagnose in older adulthood because of the prevalence
of comorbid physical and cognitive problems. Finally, it
may be difficult to diagnose depression in older adulthood
because older adults often demonstrate presentations of the
disorder that differ from typical presentations in other age
groups (Hegeman, Kok, van der Mast, & Giltay, 2012).
Given these challenges, it may be unwise to assess
depression in older adults with the same methods and
instruments used for younger adults. Even instruments that
are well validated and empirically supported for the assess-
ment of depression in younger adults may lack measure-
ment equivalence across the lifespan (Karel et al., 2002).
In this chapter, we examine the utility of current measure-
ments of depression for adults older than age 60 years. We
begin by elaborating on the nature of depression in older
adulthood. We then examine depression instruments in
terms of their utility for purposes of diagnosis, case concep-
tualization and treatment planning, and treatment moni-
toring and outcome measurement for older adults.
THE NATURE OF DEPRESSION IN LATE LIFE
Depression in late life is commonly defined as meeting
diagnostic criteria for one of several depressive disorders.
Categories within the 5th edition of the Diagnostic and
Statistical Manual of Mental Disorders (DSM-​5; American
152
Psychiatric Association [APA], 2013) include major depres-
sive disorder, persistent depressive disorder (dysthymia),
and adjustment disorder with depressed mood. The 10th
edition of the International Classification of Diseases (ICD-​
10; World Health Organization [WHO], 1992)  specifies
categories of mild, moderate, and severe recurrent depres-
sive disorders as well as dysthymia. ICD-​10 moderate and
severe depressive disorders are largely equivalent to DSM-​5
major depressive disorder. Bipolar disorder, which is seen
infrequently in older adults and which differs in important
ways from unipolar depression (Depp & Jeste, 2004), is not
discussed in this chapter (see Chapter 9, this volume).
The diagnosis of major depressive disorder requires
either dysphoria (depressed mood) or anhedonia (dimin-
ished interest or pleasure in activities) most of the day,
nearly every day, for at least 2 weeks, with other symp-
toms (i.e., appetite disturbance, sleep disturbance, psy-
chomotor retardation or agitation, low energy, feelings of
worthlessness or inappropriate guilt, inability to concen-
trate, or thoughts of death or suicide) totaling at least five.
Additional diagnostic criteria require impairment in
social, occupational, or other important areas of func-
tioning and exclude symptoms that can be attributed
to another medical condition or a substance. Persistent
depressive disorder (dysthymia) is diagnosed when symp-
toms are present for at least 2  years, without a break of
2 months or more. To meet criteria for persistent depres-
sive disorder, symptoms must include pervasive dysphoria
plus two additional symptoms from among the follow-
ing: appetite disturbance, sleep disturbance, low energy,
low self-​esteem, inability to concentrate, and hopeless-
ness. The diagnosis of adjustment disorder with depressed
mood is assigned when symptoms occur in response to a
specific stressor if the symptoms cause significant distress
 153
or impairment but do not meet criteria for major depres-
sive disorder or persistent depressive disorder.
The 12-​month prevalence of major depressive disor-
der among adults age 65  years or older in the National
Comorbidity Study Replication was 2.3% compared to
7.7% for adults age 18–​ 64  years (Kessler, Petukhova,
Sampson, Zaslavsky & Wittchen, 2012). Similarly, the
prevalence of dysthymia among older adults is approxi-
mately 2% (Devenand, 2014). Depressive syndromes that
do not meet diagnostic criteria for major depressive dis-
order are at least two or three times more prevalent than
major depression (Meeks, Vahia, Lavretsky, Kulkarni,
& Jeste, 2011). Note that the meaning and accuracy of
these prevalence estimates are affected by issues that are
described next.
Existing diagnostic criteria may not be appropriate
for the classification of depression among older adults
because older adults frequently present a symptom pic-
ture that differs from the profiles most often reported by
younger and middle-​aged adults. Although reports vary
somewhat regarding specifics, an emerging consensus is
that older adults are less likely to report certain ideational
symptoms, such as dysphoria, guilt, and suicidal ide-
ation (Blazer, Bachar, & Hughes, 1987; Gallo, Anthony,
& Muthén, 1994; Gallo, Rabins, & Anthony, 1999;
Hegeman, Kok, et al., 2012). Exceptions include findings
that reports of hopelessness, helplessness, and nonsuicidal
thoughts about death may be more common in older than
in younger adults (Christensen et al., 1999; Gallo et al.,
1994). In contrast to their general tendency to report
fewer ideational symptoms, older adults are more likely to
report somatic symptoms, such as fatigue, insomnia, psy-
chomotor retardation, agitation, or diminished appetite
and weight loss (Blazer et al., 1987; Brodaty et al., 1991;
Christensen et  al., 1999; Gallo et  al., 1994; Hegeman,
Kok, et al., 2012). This symptom pattern has been referred
to variously as “masked depression” (Blumenthal, 1980),
“depression without sadness” (Gallo et  al., 1999), and
“non-​dysphoric depression” (Onwuameze & Paradiso,
2014). Yet evidence shows that these somatic symptoms
cannot be attributed entirely to increases in physical ill-
ness (Nguyen & Zonderman, 2006) and (with the excep-
tion of changes in appetite and libido) are indicative of
depression in older adults (Norris, Arnau, Bramson, &
Meagher, 2004). Some reports also indicate that anhedo-
nia is increasingly common with age (Mora et al., 2012).
Nonetheless, there is evidence of substantial heterogene-
ity in the presentation of depressive symptoms among
older adults (Mora et al., 2012).
Depression in Late Life 153
Furthermore, the very nature of late adult life may
affect diagnostic classification. For example, diagnostic
criteria require that impairment be evident in social,
occupational, or other important areas of functioning.
However, the definition of normal functioning in these
domains has not been well operationalized for older
adults, raising the possibility that older adults may be less
likely than younger and middle-​aged adults to be seen as
functionally impaired. In addition, exclusionary criteria
may lead to underdetection of depression in older adults.
Symptoms that can be attributed to physical illness or
medication use are not to be considered when diagnosing
depression, but distinguishing the cause of these symp-
toms may not be straightforward. Taken together, these
factors suggest that existing diagnostic categories may lack
sensitivity for detecting depression among older adults.
Numerous new categories have been proposed to classify
depressive symptoms that do not meet diagnostic crite-
ria (for a discussion, see Kumar, Lavretsky, & Elderkin-​
Thompson, 2004), but a single standard has not emerged.
A widely used alternative for identifying cases of depres-
sion in older adults is use of a cut-​off score on a depressive
symptom checklist to indicate the presence of clini-
cally significant depressive symptoms. This dimensional
approach identifies older adults who are experiencing an
elevated level of depressive symptoms without excluding
individuals whose symptoms do not include dysphoria or
anhedonia, those without evidence of impaired function-
ing, or those with comorbid physical illness. Thus, this
method overcomes limitations of diagnostic criteria that
do not map well onto depressive experience in old age.
Because this approach lacks syndromal criteria, however,
it lacks specificity for ruling out causes of symptoms that
may not represent depression, such as those that are the
direct effects of physical illness.
Cognitive deficits may also complicate the measure-
ment of depression in late life. Evaluating whether these
deficits are symptoms of depression or dementia can be
challenging and may require the use of informants as
well as longitudinal assessments (Wang & Blazer, 2015).
Alexopoulos et al. (1997) proposed that cognitive deficits,
primarily deficits in executive functioning, accompanied
by cerebrovascular risk factors and a late age of depres-
sion onset, may indicate an etiologically distinct form of
depression, which they term “vascular depression.” A sub-
stantial minority of cases meeting proposed criteria for
vascular depression go on to develop dementia (Potter
et  al., 2013). Furthermore, rates of depression are ele-
vated among individuals with dementia (Vilalta-​Franch
154
154 Mood Disorders and Self-Injury
et al., 2006). Thus, cognitive dysfunction may represent a
symptom of depression, or depression may be a prodromal
symptom of, or reaction to, dementia.
Other psychiatric and medical comorbidities should
also be taken into account. As at other ages, anxiety is
highly comorbid with depression in late life, although there
is no evidence that it is more common in depression with
late onset (Janssen, Beekman, Comijs, Deeg, & Heeren,
2006). Comorbid physical illness may also complicate the
assessment of depression in older adults. Physical illness
may represent a cause of depression (Alexopoulos et  al.,
1997; Zeiss, Lewinsohn, & Rohde, 1996), an effect of
depression (Frasure-​Smith, Lesperance, & Talajic, 1993),
or simply co-​occurrence. Furthermore, illness may lead to
depression as a result of organic mechanisms (Alexopoulos
et al., 1997) or as a psychological reaction. Zeiss and col-
leagues concluded that functional impairment largely
mediates the relationship between illness and depression,
suggesting that depression is a psychological response to
limitations imposed by the illness. Whatever the direction
of causation or mechanism, the comorbidity of depression
and physical illness makes assessment more challenging
because certain symptoms are shared by both.
There is heterogeneity in the prognosis of late life
depression. Psychotherapy for depression is as effica-
cious in older adults as it is in younger adults (Cuijpers,
Andersson, Donker, & Van Straten, 2011). Nonetheless,
older adults who have recovered from depression
appear to be at risk of earlier relapse (Mueller et  al.,
2004). Earlier relapse is predicted by residual symptoms
following treatment (Chopra et  al., 2005), which sug-
gests that incomplete resolution of a depressive episode
may predispose to another episode. Time to relapse is
also predicted by the presence of executive dysfunc-
tion (Alexopoulos et  al., 2000), consistent with a neu-
robiological explanation such as vascular depression
(Alexopoulos et al., 1997).
Finally, depression in late life has been linked to
many of the same risk and protective factors as at other
points in the lifespan, although the prevalence of these
factors, and the strength of their association with depres-
sion, may vary by age. Age of depression onset has been
examined as a potential marker for vascular depres-
sion, an etiologically distinct subtype of the disorder
(Alexopoulos et al., 1997). There is little epidemiologic
research on the proportion of older adults with depres-
sion who experienced the first episode after age 60 years.
Some research suggests that half of cases are late onset
(e.g., Steingart & Herrmann, 1991). The proportion of
older adults with a lifetime history of depression who
met criteria for vascular depression (with onset at age
50 years or older) has been estimated at 22% (Gonzalez,
Tarraf, Whitfield, & Gallo, 2012).
Genetic factors have been implicated in depressive
symptoms among older adults. Estimates of heritability in
one study were .14 for men and .29 for women (Jansson
et al., 2004). Family studies suggest that genetic influences
play a greater role in depression earlier in life (Baldwin
& Tomenson, 1995). In contrast, other biological factors,
such as cerebrovascular risk factors (Alexopoulos et  al.,
1997; Nemeth, Haroon, & Neigh, 2014), may be more
influential in late life depression.
Stressors also contribute to the risk of depression in
older adults, as at other ages (for a meta-​analysis, see
Kraaij, Arensman, & Spinhoven, 2002). Among the spe-
cific stressors most frequently examined in older popu-
lations are physical illness and disability (as discussed
previously), bereavement, and caregiving. Bereavement
may be a risk factor for depression in late life, particu-
larly among individuals with a history of depressive
episodes (Zisook & Shuchter, 1993). Prigerson and
colleagues (e.g., Latham & Prigerson, 2004)  have
argued that abnormal distress following bereavement
generally does not resemble depression, and it should
instead be considered a different syndrome, which they
term “complicated grief.” Consistent with this logic,
the bereavement exclusion for major depression was
removed in DSM-​5 (APA, 2013). Caregiving for some-
one with dementia or disability is a potentially stressful
experience that occurs with greater frequency in late
life. High rates of depression among caregivers have
been reported (for a review, see Schulz & Martire,
2004). Social factors may act as either protective or
risk factors for depression in late life. Perceived social
support buffers the effects of stressors in older adults,
but support that is too intensive, or perceived as unsup-
portive, may also contribute to risk (for a review, see
Hinrichsen & Emery, 2005).
Thus, depression in late life differs from depression
earlier in the lifespan in terms of presentation, comor-
bidities, course, and risk factors. These differences imply
a need for special care in assessing depression in an
older adult. Assessment should consider the possibility
of medical comorbidity or declines in cognitive func-
tioning. Furthermore, due to the unique presentation
of depression in late life, diagnostic classification may
underestimate pathology in this group, whereas symp-
tom checklists may overestimate problems, suggesting
that categorical and dimensional measurements may
both be important.
 15
PURPOSES OF ASSESSMENT
In the following sections, we review assessment instru-
ments with a focus on three specific clinical purposes:
diagnosis, case conceptualization and treatment plan-
ning, and treatment monitoring and the assessment of
treatment outcome. We do not evaluate instruments for
use in screening. Much empirical work has focused on
the evaluation of instruments to screen for depression in
older adults, particularly within primary care settings. For
a review of specific screening instruments, the interested
reader is referred to Watson and Pignone (2003). For a dis-
cussion of the benefits and harms of screening for depres-
sion in primary care, see O’Connor, Whitlock, Beil, and
Gaynes (2009).
A specialized literature exists with respect to the assess-
ment of depression within dementia. Some individuals
with dementia may be able to provide accurate informa-
tion about their own depressive symptoms, but the validity
of self-​report varies with the level of awareness of deficits
(Snow et al., 2005). As a result, instruments that have been
developed specifically for this task are largely observer
rated, to be completed by a clinician or lay interviewer,
and some incorporate information from a caregiver or
other proxy as well. Information on the use of these mea-
sures for the assessment purposes discussed previously is
included in the relevant sections. Because older adults,
specifically older men, are at the highest risk of death by
suicide of any demographic group (Curtain, Warner, &
Hedegaard, 2016), a clinician assessing depression in this
population must also be prepared to assess suicide risk.
ASSESSMENT FOR DIAGNOSIS
Structured Interviews
Structured clinical interviews address all informa-
tion needed for a diagnosis. Table 8.1 summarizes the
Table 8.1  Ratings of Instruments Used for Diagnosis
Internal Inter-​Rater Test–​Retest
Instrument Norms Consistency Reliability Reliability
Structured Clinical Interviews
SCID NA NA E NR
SADS NA NA E NR
GMS NA NA G G
Note: SCID = Structured Clinical Interview for DSM; SADS = Schedule for Affective Disorders and Schizophrenia; GMS = Geriatric Mental State
Schedule; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.
Depression in Late Life 155
properties of structured clinical interviews when used to
diagnose depression in older adults. The primary advan-
tage of structured compared to unstructured clinical
interviews is reliability, as seen in the table. As previously
mentioned, however, a consideration when assessing older
adults is whether diagnostic criteria themselves may lead
to underdetection of depression. Lengthy administration
represents a challenge with respect to use of these instru-
ments in clinical settings with older adults. However,
administration time depends on the person’s responses.
Furthermore, increasingly brief versions have been pub-
lished in recent years. A further challenge is the extensive
training required to reach proficiency in the administra-
tion of structured clinical interviews, ranging from days to
weeks. Although training requirements may be viewed as
a burden, training and experience using structured inter-
views can be especially helpful for new clinicians (Segal,
Kabacoff, Hersen, Van Hasselt, & Ryan, 1995). Note that
for some of these measures, a DSM-​5 version is not yet
published or widely used.
The most widely used structured clinical interview
in the United States is the Structured Clinical Interview
for DSM (SCID; First, Williams, Karg, & Spitzer, 2015).
The current revision yields diagnoses according to DSM-​
5 (APA, 2013)  criteria. The current revision is available
in either research or clinical versions, with the clinical
version (SCID-​5-​CV; First et  al., 2015)  abbreviated to
minimize administration time. The SCID-​5-​CV assesses
the most common DSM-​ 5 disorders, including mood
disorders, and requires 45 to 90 minutes to administer,
but individual modules can be administered separately.
Although the current revision of the SCID-​CV has not
yet been evaluated in older adult samples, a previous form
of the SCID, which was based on DSM-​III-​R diagnostic
criteria (APA, 1987), has been found to have good inter-​
rater reliability for the diagnosis of major depressive disor-
der in older adult samples (Segal et al., 1995). Notably,
inter-​rater reliability appears to be lower for diagnosis of
Content Construct Validity Clinical Highly
Validity Validity Generalization Utility Recommended
A NR G A
A NR G A
G G G A ✓
156
156 Mood Disorders and Self-Injury
dysthymia (Segal et  al., 1995). Extensive pilot and field
testing (First et al., 2015) suggests good content validity,
but the measure was not developed specifically for use
with older adults. There is ample evidence of construct
validity for the SCID in mixed age samples (First, Spitzer,
Gibbon, & Williams, 2015), and available evidence
suggests content validity in older adult samples as well
(Stukenberg, Dura, & Kiecolt-​Glazer, 1990), but data are
too sparse to permit conclusions to be drawn. Evidence
from a mixed-​age sample suggests that using the SCID
(DSM-​III-​R version) improves diagnostic accuracy com-
pared to routine diagnostic procedures, and it appears
to improve clinical management of cases (Basco et  al.,
2000). Thus, the SCID-​CV may be useful for diagnos-
ing major depressive disorder in older adults, but train-
ing and administration requirements are substantial and
more empirical work is needed in older adult samples,
specifically using the SCID-​5-​CV version, before it can be
highly recommended for use in this population.
The Schedule for Affective Disorders and
Schizophrenia (SADS; Endicott & Spitzer, 1978)  yields
diagnoses according to the Research Diagnostic Criteria
(Spitzer, Endicott, & Robins, 1978). The SADS requires
extensive training (“weeks,” according to Dozois &
Dobson, 2002)  and takes 90 to 120 minutes to admin-
ister (Dozois & Dobson, 2002). In mixed-​age samples,
the SADS demonstrates excellent inter-​ rater reliability
(Endicott & Spitzer, 1978). Although use of the SADS
with older adults has not often been evaluated, one study
reported excellent inter-​rater reliability (Rapp, Smith, &
Britt, 1990). As with the SCID, development of the SADS
involved thorough evaluation of the content (Endicott &
Spitzer, 1978), but the measure was not designed specifi-
cally for older adults. The SADS has demonstrated good
efficiency in detecting “cases” of depression in older
adults as defined by a cut-​off score on the Beck Depression
Inventory (Gallagher, Breckenridge, Steinmetz, &
Thompson, 1983), but it has been tested too infrequently
in this population to support any conclusions regarding
construct validity. Thus, the SADS may be a reliable and
valid method of diagnosing depression in older adults, but
training and administration costs are high, and further
evaluation of its validity in this age group is needed before
it can be highly recommended.
Whereas the SCID and SADS were designed for
administration by a trained clinician, the Composite
International Diagnostic Interview (CIDI; Robins et  al.,
1988)  was initially developed for administration by
trained laypersons for use in research and has since been
used in clinical settings. The CIDI is a composite of the
Diagnostic Interview Schedule (DIS; Robins, Helzer,
Croughan, & Ratcliff, 1981) and the Present State Exam
(PSE; Wing, Birley, Cooper, Graham, & Isaacs, 1967). It
was designed to produce current and lifetime diagnoses
according to both DSM-​III-​R (APA, 1987)  and ICD-​10
(WHO, 1992) criteria. Although a DSM-​5 version of the
CIDI has not yet been developed, the previous version
has been extensively validated in mixed-​ age samples.
There is some evidence of reliability of the CIDI in the
elderly (Heun, Müller, Freyberger, & Maier, 1998), but
concerns have been raised about validity in this age group.
Specifically, older adults are less likely than their younger
counterparts to endorse the gateway items of dysphoria
and anhedonia (Trainor, Mallett, & Rushe, 2013), pos-
sibly due to the additional complexity of these questions
(O’Connor & Parslow, 2009). To address these concerns,
a revised version of the interview, the CIDI65+, has been
developed (Wittchen et al., 2015). Questions were short-
ened and the format was simplified in order to be more
appropriate for older adults with cognitive difficulties.
The CIDI65+ has demonstrated good test–​ retest reli-
ability; validity has yet to be examined (Wittchen et  al.,
2015). An epidemiologic study that used the CIDI65+
found greater prevalence of depression and other men-
tal disorders in older adults compared to other studies
(Andreas et  al., 2017), suggesting that the use of age-​
appropriate measures may improve detection of depres-
sion and other disorders in this age group. Several short
forms of the CIDI have also been developed. One short
form (UM-​CIDI-​SF; Kessler & Mroczek, 1993) was eval-
uated in a large sample of older adults and found to be as
strongly related to physician diagnosis as was the Center
for Epidemiological Studies–​Depression Scale (Turvey,
Wallace, & Herzog, 1999). Nonetheless, properties of the
CIDI, the CIDI65+, and various short forms of the CIDI
in older adult samples have yet to be well examined and,
therefore, these measures cannot yet be recommended for
clinical use with this population.
In contrast to most structured interview protocols, the
Geriatric Mental State Schedule (GMS; Copeland et al.,
1976) was developed specifically with older adults in mind.
A classification system (known as AGECAT) was empiri-
cally derived for use with the GMS and is implemented
through a computer-​based algorithm. The GMS with the
AGECAT system assesses for eight psychiatric syndromes
in older adults, including neurotic and psychotic depres-
sion. Ratings indicate level of diagnostic confidence, from
0 to 5, with 3 or greater indicating the presence of a case.
The GMS has demonstrated good to excellent inter-​rater
and test–​retest reliability (Copeland et  al., 1988). The
 157
GMS was derived from previous scales, including the
PSE (Wing et al., 1967), in consultation with experts and
extensive field testing with older adult samples, suggesting
good content validity. Construct validity has been demon-
strated with good correspondence with DSM-​III diagno-
sis in community (Copeland, Dewey, & Griffiths-​Jones,
1990)  and medical samples (Ames Flynn, Tuckwell,
& Harrigan, 1994), although GMS/​AGECAT is more
inclusive than DSM-​IV major or minor depression (de la
Cámara et al., 2008). Although the GMS has shown valid-
ity in US and UK samples (Copeland et al., 1976), a study
involving 26 sites in India, China, Latin America, and
Africa showed that sensitivity to depression varied widely
by country (Prince et  al., 2004). Taken together, these
findings indicate that the GMS is a reliable and valid tool
for diagnosing depression in older adults. A possible limi-
tation is that it yields diagnoses based on the empirically
derived AGECAT diagnostic criteria and not the more
widely accepted DSM or ICD criteria.
Overall Evaluation
In summary, structured interviews require more time and
training to administer than do unstructured interviews,
but they can yield highly reliable diagnoses and may be
particularly useful in the training of new clinicians. The
SCID and the SADS require the most training and are
among the lengthiest to administer, but they can also yield
extremely reliable results. Neither has been evaluated
fully in older adult samples. The CIDI and GMS offer
flexibility because they can be administered by trained
interviewers who are not clinicians. Thus, no single struc-
tured interview is clearly superior:  The choice should
depend on who will administer it and how much time can
be invested.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
It is important to note that all the instruments described
next and in the sections on treatment monitoring and
evaluation focus on the nature and severity of depressive
symptoms.
Self-​Report Measures
Several self-​
report depressive symptom measures may
prove useful for the development of case conceptualiza-
tions and treatment plans for older adults (Table 8.2). One
Depression in Late Life 157
of the most well-​known depressive symptom measures in
use today is the Beck Depression Inventory-​II (BDI-​II;
Beck, Steer, & Brown, 1996). The BDI-​II is a 21-​item
measure, scored using a 4-​point Guttman scale asking
respondents to indicate how they felt during the course
of the past 2 weeks (including the day of administration).
The BDI-​II takes approximately 10 minutes to adminis-
ter and has been translated into 14 languages. In terms
of case conceptualization and treatment planning, the
BDI-​II provides information about somatic–​affective and
cognitive dimensions of depression (Steer, Ball, Ranieri,
& Beck, 1999). In mixed-​age samples (using participants
aged 19–​80 years), the BDI-​II scores have demonstrated
very good internal consistency and test–​retest reliability,
and they are highly correlated with other measures of dis-
tress and psychopathology. The BDI-​II scores have also
demonstrated very good internal consistency and very
good test–​retest reliability in samples of older adults hos-
pitalized in a geriatric psychiatry unit (Steer, Rissmiller,
& Beck, 2000)  and in samples of community-​dwelling
older adults (Segal, Coolidge, Cahill, & O’Riley, 2008),
although one study found that the BDI-​II did not perform
as well as the Geriatric Depression Scale in a sample of
older women (Jefferson, Powers, & Pope, 2001). In addi-
tion, in examining the use of the original BDI with older
adults, some researchers have posited that older women
may be more hesitant to complete the measure (especially
a question related to sexual interest) than other measures
of depression (Jefferson et al., 2001) and that the somatic
items may be confounded with physical illness in older
adults (Clark, Cavanaugh, & Gibbons, 1983). In addition,
some researchers have suggested that the complexity of
the Guttman-​type response options may limit the assess-
ment’s utility in older adults with any cognitive dysfunc-
tion (Clark et  al., 1983). Given these concerns and the
paucity of research examining the use of the BDI-​II in
older adults, the BDI-​II is not highly recommended at
this time.
Another self-​ report measure is the Center for
Epidemiological Studies–​ Depression Scale (CES-​ D;
Radloff, 1977). The CES-​D is a 20-​item measure in which
individuals are asked to respond to items on a 4-​point
Likert-​type scale based on how they felt during the past
week. In terms of case conceptualization and treatment
planning, factor analyses show that the CES-​D can pro-
vide clinicians information about depressed mood, psy-
chomotor retardation, the absence of well-​ being, and
interpersonal difficulties (Gatz, Johansson, Pederson,
Berg, & Reynolds, 1993). Scores on the CES-​D have dem-
onstrated good internal consistency, test–​retest reliability,
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158 Mood Disorders and Self-Injury

Table 8.2  Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Self-​Report Measures
BDI-​II A G NA G A A A A
CES-​D E G NA G A G G A
GDS G G NA G A A A L
PHQ-​9 E G G G A G G E ✓
SDS A A NA NR A A A A
Structured Clinical Interviews
SCID NA NA E NR A NR G A
SADS NA NA E NR A NR G A
GMS NA NA G G G G G A ✓
Clinician Rating Scales
GDRS A E G NR A NR A A
MADRS A A E NR A A A A
Measures to Assess Depression in Dementia
CSDD A E A A E E E A ✓
DMAS A A A NR NR A A A

Note: BDI-​II = Beck Depression Inventory-​II; CES-​D = Center for Epidemiological Studies–​Depression Scale; GDS = Geriatric Depression Scale; PHQ-​
9 = Patient Health Questionnaire-​9; SDS = Zung Self-​Rating Depression Scale; SCID = Structured Clinical Interview for DSM; SADS = Schedule for
Affective Disorders and Schizophrenia; GMS = Geriatric Mental State Schedule; GDRS = Geriatric Depression Rating Scale; MADRS = Montgomery–​
Åsberg Depression Rating Scale; CSDD = Cornell Scale for Depression in Dementia; DMAS = Dementia Mood Assessment Scale; L = Less Than
Acceptable; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.

convergent validity, and criterion validity with respect to
diagnostic instruments (Head et al., 2013; Radloff, 1977).
Many researchers have demonstrated that it has measure-
ment equivalence across the lifespan (e.g., Gatz et  al.,
1993). A concern with this measure is that reverse-​scored
items have been shown to be problematic for older adults
(Carlson et al., 2011). The authors recommend imputing
reversed items based on responses to non-​reversed items.
Eaton, Muntaner, Smith, Tien, and Ybarra (2004) devel-
oped a revised version, the CESD-​R, that contains no
reverse-​scored items. The CESD-​R also includes several
symptoms of major depression that were not included in
the CES-​D (weight changes and thoughts of suicide) and
eliminates items in the CES-​D not related to the current
definition of major depression. Scores on the CESD-​R
have been found to have good reliability and some con-
vergent validity (it is highly correlated with the CES-​
D; Eaton et  al., 2004; Van Dam & Earleywine, 2011).
Although promising, this measure has not yet been thor-
oughly evaluated with older adults. Despite the strengths
of the CES-​D (and, possibly, the CESD-​R), researchers
have found problems with the use of this measure in
older adults. Some investigators have suggested that the
measure may contain items that are biased against being
older, female, widowed, or having a physical disorder
(Grayson, MacKinnon, Jorm, Creasey, & Broe, 2000).
Other researchers have demonstrated that the CES-​D is
only modestly related to symptoms reported in structured
interviews and that it often identifies individuals who
either do not meet criteria for depression or meet criteria
for other diagnoses (Myers & Weissman, 1980). This last
criticism may be reflecting the fact that older adults gen-
erally exhibit more subsyndromal rather than syndromal
symptoms of depression (Newman, 1989). When examin-
ing the criticisms made against this measure, it appears
that these issues are most likely problems related to the
use of the CES-​D as a diagnostic tool. The evidence sug-
gests that the CES-​D can be recommended as an instru-
ment for case conceptualization and treatment planning,
especially as part of a multimethod assessment that also
includes a thorough clinical interview.
A widely used self-​report measure designed to assess
depression in older adults is the Geriatric Depression
Scale (GDS; Yesavage et  al., 1983). The GDS is a 30-​
item measure with a yes/​ no answer format. There is
also a shortened version of the GDS consisting of 15
items (Sheikh & Yesavage, 1986). In response to con-
cerns that depression measures are often confounded
 159
by physical illness in older adults, the developers of the
GDS excluded somatic items from the scale. In terms of
its use for case conceptualization and treatment planning,
the measure provides information about unhappiness,
apathy, anxiety, loss of hope, and energy loss (Onishi,
Suzuki, & Umegaki, 2006). The GDS scores have shown
good internal consistency (Yesavage et  al., 1983), good
test–​retest reliability (Lesher, 1986), and good convergent
validity (Lesher, 1986; Yesavage et  al., 1983). Scores on
the measure have been shown to have good reliability and
validity in several settings, including primary care clinics
(Mitchell, Bird, Rizzo, & Meader, 2010), home care set-
tings (Marc, Raue, & Bruce, 2008), and long-​term care
facilities (Li et al., 2015). Interestingly, in a meta-​analysis
of primary care studies, the 15-​item version of the GDS
had better sensitivity and specificity than the full-​length
GDS (Mitchell et al., 2010). In terms of its use with older
adults, numerous researchers have questioned the strat-
egy of eliminating somatic items from a depression mea-
sure (Karel et al., 2002). As mentioned previously, older
adults tend to endorse cognitive items less frequently than
do younger adults. Thus, eliminating the somatic items
may reduce the sensitivity of the test. Furthermore, when
individual somatic symptoms are examined, only appetite
disturbance seems to be entirely confounded with age
(Norris et  al., 2004), which suggests there is no reason
to eliminate the valuable information the somatic items
on depression scales provide. In addition, there are both
strengths and limitations inherent in the yes/​no answer
format of this measure. On the positive side, the format
is not too cognitively demanding. As such, it may be use-
ful for older adults with cognitive dysfunction; however,
several studies have demonstrated that the Cornell Scale
for Depression in Dementia has better sensitivity and
specificity for older adults with cognitive impairment in
the United States and China (e.g., Kørner et  al., 2006),
and one study demonstrated that the GDS had very poor
sensitivity and specificity for detecting depression in older
adults with dementia (Li et al., 2015). In addition, in one
survey, older adults indicated they did not like the forced-​
choice aspect of this measure (Fischer, Rolnick, Jackson,
Garrard, & Luepke, 1996). Because this measure may not
be sensitive to somatic presentations of depression and
because there may be some issues with the format of the
measure, the GDS should be used with caution for case
conceptualization and treatment planning in older adults.
Another self-​report measure that may be useful in case
conceptualization and treatment planning for older adults
is the Patient Health Questionnaire-​9 (PHQ-​9; Kroenke
& Spitzer, 2002; Kroenke, Spitzer, & Williams, 2001).
Depression in Late Life 159
The PHQ-​9 is a 9-​item self-​report depression measure
that asks respondents to indicate how frequently during
the past 2 weeks they have experienced each of the nine
symptoms specified in the DSM-​5 criteria for a major
depressive disorder. The PHQ-​9 takes 5 to 10 minutes to
administer. It was originally developed for use in medi-
cal settings (outpatient primary care and obstetrics and
gynecology offices), and older adults were included in the
initial normative samples (Kroenke et al., 2001; Kroenke
& Spitzer, 2002). The PHQ-​9 scores have demonstrated
reliability and construct validity in a wide variety of set-
tings and populations (Kroenke et al., 2001; Kroenke &
Spitzer, 2002; Lamers et  al., 2008; Phelan et  al., 2010).
The PHQ-​9 scores have demonstrated very high sensitiv-
ity and specificity (compared to diagnostic interview—​
structured and unstructured) in samples of older adults
(Lamers et al., 2008; Phelan et al., 2010), with greater sen-
sitivity and specificity than GDS scores for older primary
care patients (Phelan et  al., 2010). Because the PHQ-​9
was found to be a more effective depression screener than
the Schedule for Affective Disorders and Schizophrenia
and the observational items of the Minimum Data Set 2.0
for long-​term care residents, the PHQ-​9 was incorporated
into the Minimum Data Set 3.0 (the data collected on
all long-​term care residents in the United States; Saliba
et al., 2012). Overall, the PHQ-​9 is highly recommended
for case conceptualization and treatment planning in
older adults.
A final self-​report measure that might be useful in case
conceptualization and treatment planning for older adults
is the Zung Self-​Rating Depression Scale (SDS; Zung,
1965). The SDS is a 20-​item measure scored on a 4-​point
Likert-​type scale. The SDS provides information about a
lack of well-​being and depressive affect (Schafer, 2006).
Scores on the SDS have been reported to have good reli-
ability and validity in mixed-​ age samples, including a
normative sample with adults up to age 69 years (Zung,
1965). Scores on the SDS have shown adequate inter-
nal consistency in older adult samples (Dunn & Sacco,
1989), and there is some evidence for their validity in this
population, especially as a screening measure (Dunn &
Sacco, 1989); however, more research is needed before
it can be recommended for case conceptualization and
treatment planning in older adults.
Structured Interviews
Because evidence suggests that structured interviews may
result in a more thorough and comprehensive picture of
a client’s presenting problem compared to unstructured
160
160 Mood Disorders and Self-Injury
interviews (Segal et  al., 1995), they may be useful for
case conceptualization and treatment planning, espe-
cially when used in conjunction with other assessment
methods. Structured interviews that could be utilized for
this purpose include the SCID-​CV (First et  al., 2015),
the SADS (Endicott & Spitzer, 1978), and the GMS
(Copeland et  al., 1976). All of these interviews were
described previously, and Table 8.2 summarizes the utility
of these measures for the purposes of case conceptualiza-
tion and treatment planning in older adults. In addition,
a version of the GMS developed specifically to assess
depression severity (GMS-​DS; Ravindran, Welburn, &
Copeland, 1994)  is particularly promising. It takes only
15 minutes to administer and has shown high internal
consistency and good convergent validity with respect to
self-​report and clinician ratings (Ravindran et al., 1994).
Replication is needed before the measure can be highly
recommended. Overall, all of these interviews have good
potential for the purposes of treatment planning and case
conceptualization with older adults; however, each needs
more empirical evaluation before it can be recommended
for these purposes.
Clinician Rating Scales
Clinician rating scales are generally developed to assess
severity of depression among individuals who have
been diagnosed with the disorder; however, the kinds of
questions asked in these scales may also provide useful
information for case conceptualization and treatment
planning. Table 8.2 summarizes properties of clinician
rating scales that may prove useful for the development
of case conceptualizations and treatment plans for older
adults.
Perhaps the most popular clinician rating scale is the
Hamilton Rating Scale for Depression (HRSD; Hamilton,
1960, 1967), which is often utilized in treatment outcome
studies. A  comprehensive review of the HRSD across a
wide range of samples concluded, however, that the mea-
sure’s weaknesses outweigh its strengths (Bagby, Ryder,
Schuller, & Marshall, 2004). In particular, the authors
noted that individual items are poorly designed, the
total score does not reflect a unidimensional structure,
and the measure has not been updated despite numer-
ous revisions in accepted diagnostic criteria for depres-
sion. There are multiple versions of the HRSD, which
vary in length (17–​27 items) and even what domains
of depression are addressed; all versions assess somatic
symptoms, whereas only some versions include items to
assess cognitive symptoms of helplessness, hopelessness,
and worthlessness. The HRSD requires a trained clini-
cian and takes 30 minutes to administer to depressed
older adults (Moberg et al., 2001). A meta-​analysis dem-
onstrated that scores on the HRSD have acceptable
internal consistency, inter-​rater reliability, and test–​retest
reliability (Trajkovic et  al., 2011). Nonetheless, scores
on the scales have questionable internal consistency in
older adults (e.g., Cronbach’s α = .46; Hammond, 1998).
In terms of validity, reports vary widely. Studies have
repeatedly failed to confirm the unidimensionality of
the HRSD (Bech, Paykel, Sireling, & Yiend, 2015; Cole
et al., 2004). Concurrent validity has been reported to be
equivalent to that of other clinician rating instruments in
a sample of depressed older adults (Mottram, Wilson, &
Copeland, 2000) but no better than that of the BDI in a
community sample (Stukenberg et al., 1990). Rapp and
colleagues (1990) used an extracted version of the HRSD
and reported moderate to high correlations with the BDI,
the SDS, and the GDS and better concurrent validity
than these measures in a sample of older male medical
inpatients; however, Baker and Miller (1991), also using
a medical sample, reported that concurrent validity was
lower than for the GDS. In a sample of older adults with
dementia, validity was particularly problematic (sensitiv-
ity was 8% for the HRSD compared to 82% for the GDS;
Lichtenberg, Marcopulos, Steiner, & Tabscott, 1992).
Indeed, some researchers have suggested that the HRSD
does not actually measure depression at all because fac-
tor analysis has shown that the scale may instead mea-
sure aspects of anxiety and insomnia (Cole et al., 2004;
Hammond, 1998; Stukenberg et al., 1990). Finally, the
disproportionate number of somatic items may make the
measure especially problematic for use with older adults
(Jamison & Scogin, 1992). Given all this, the HRSD is
not recommended as a measure for treatment planning
or case conceptualization with older adults.
The Geriatric Depression Rating Scale (GDRS;
Jamison & Scogin, 1992)  was developed in response to
problems with the HRSD. It may provide information
useful for treatment planning and case conceptualiza-
tion in older adults because it is based on the GDS,
with the addition of somatic items that are considered
only if responses are not attributable to physical illness.
The GDRS is a 35-​item measure that requires a trained
interviewer and takes 35 minutes to administer. Scores
have been found to be highly internally consistent, with
fairly high inter-​rater reliability. Finally, scores on the
measure have also been found by the developers to have
some validity for older adults based on correlations with
the HRSD, BDI, and GDS (Jamison & Scogin, 1992).
 16

Depression in Late Life 161

However, more research must be conducted before this Measures to Assess Depression in Dementia
measure can be recommended for case conceptualization
Several measures that assess depression in individuals
and treatment planning.
with dementia may be useful for case conceptualization
Another clinician rating scale that may be useful in
and treatment planning (see Table 8.2). The most fre-
case conceptualization and treatment planning is the
quently used measure of this type is the Cornell Scale for
Montgomery–​Åsberg Depression Rating Scale (MADRS;
Depression in Dementia (CSDD; Alexopoulos, Abrams,
Montgomery & Åsberg, 1979). The MADRS is a 10-​item
Young, & Shamoian, 1988a). The scale includes 19 items
clinician rating scale of depression severity. Scores on the
that are rated by a mental health professional on a 3-​point
MADRS have been shown to have good inter-​rater reli-
scale (absent, mild or intermittent, and severe). Ratings
ability (Zimmerman, Posternak, & Chelminski, 2004),
are based on observation of the client as well as interviews
adequate construct validity (e.g., correlated with HRSD),
with the client and a caregiver. Administration requires
and good sensitivity and specificity (Engedal et al., 2012;
30 minutes. The CSDD provides information about gen-
Hammond, 1998; Mottram et  al., 2000; Zimmerman
eral depression, rhythm disturbance (including insom-
et  al., 2004)  in older adult samples. Compared to the
nia), agitation/​psychosis, and negative symptoms (Ownby,
HRSD, the MADRS contains fewer somatic items and
Harwood, Acevedo, Barker, & Duara, 2001); however,
has a factor structure that more clearly measures aspects
factor analysis has demonstrated other factor structures in
of the depression construct (dysphoria and anhedonia;
various settings (Barca, Selbæk, Laks, & Engedal, 2008;
Hammond, 1998). Like the HRSD, however, scores on
Harwood, Ownby, Barker, & Duara, 1998; Kurlowicz,
the MADRS have only fair internal consistency in this
Evans, Strumpf, & Maislin, 2002). Scores on the scale
population (Bent-​Hansen et al., 2003; Hammond, 1998).
have good internal consistency and adequate inter-​rater
Thus, the MADRS may be a better alternative than the
reliability (Alexopoulos et  al., 1988a). Scores have been
HRSD as a clinician rating instrument, and with modi-
shown to distinguish individuals with dementia who
fication, it could be a useful measure in this population,
meet criteria for depression from those who do not meet
but it cannot be highly recommended at this time.
criteria (Alexopoulos et  al., 1998a), and they are signifi-
The Inventory of Depressive Symptomatology (IDS;
cantly correlated with other measures in the expected
Rush et  al., 1986)  initially contained 28 items, but it
directions (Mack & Patterson, 1994). When comparing
was revised to include 30 items (Rush, Gullion, Basco,
the CSDD to other depression measures, the CSDD has
Jarrett, & Trivedi, 1996). Items are rated on a scale of
been shown to have better specificity and sensitivity than
0 to 3.  Clinician-​rated (IDS-​C) and self-​report (IDS-​
the GDS when administered for older adults with and
SR) versions have equivalent item content. The IDS
without cognitive impairment (Kørner et al., 2006), and
provides useful information for case conceptualiza-
the CSDD was generally comparable to the MADRS in
tion and treatment planning in terms of information
terms of sensitivity and specificity (Leontjevas, Gerritsen,
about severity of symptoms. In younger and mixed-​age
Vernooij-​ Dassen, Smalbrugge, & Koopmans, 2012;
samples, the IDS scores have been found to be highly
Leontjevas, van Hooren, & Mulders, 2009). However,
internally consistent (Rush et al., 1986, 1996) and have
in one study, the MADRS was better at distinguishing
good inter-​rater reliability (Rush et  al., 1996). Finally,
depressed and nondepressed patients in a memory care
the measure demonstrates convergent validity (it is cor-
clinic (Knapskog, Barca, & Engedal, 2011). Similarly, in
related with the HRSD and the BDI; Rush et al., 1986,
one study, the CSDD had similar specificity and sensi-
1996). There has been little research examining the IDS
tivity as the observation version of the PHQ-​9 (Phillips,
in older adults. A factor analysis of the IDS-​SR in older
2012), and another study demonstrated that the sensitivity
adults identified three factors—​mood, motivation, and
and specificity of the CSDD were equivalent to those of
somatic—​differing from the factor structure found in
the Hamilton Depression Scale in older adults (Vida, Des
younger adults (Hegeman, Wardenaar, Comijs, de Waal,
Rosiers, Carrier, & Gauthier, 1994).
Kok, & van der Mast, 2012). Internal consistency was
The CSDD scores have been shown to reliably
good for scores on the mood and motivation factors, but
measure depression in individuals with Parkinson’s dis-
it was marginal for the somatic items. Although evidence
ease (with and without cognitive impairment; Williams
supports the reliability and validity of the IDS in younger
& Marsh, 2008)  and in older adults without cognitive
populations, there is not yet enough information about
impairment (Alexopoulos, Abrams, Young, & Shamoian,
the use of the IDS in older adults for this scale to be
1988b). The CSDD has also been shown to be a valid
highly recommended.
162
162 Mood Disorders and Self-Injury
depressive tool for a variety of settings, including memory
care clinics (Hancock & Larner, 2015), long-​term care
facilities (Jeon et al., 2015), and inpatient settings (Barca,
Engedal, & Selbæk, 2010). Furthermore, the CSDD is
not confounded by cognitive status (Maixner, Burke,
Roccaforte, Wengel, & Potter, 1995).
In examining the CSDD critically, experienced inter-
viewers who evaluated the instrument reported that instruc-
tions lack detail in places and that the focus on behaviors
occurring within the past week may limit the measure’s
sensitivity, but the option to indicate “unable to rate” was
particularly helpful (Mack & Patterson, 1994). One study
demonstrated low concordance between answers on the
CSDD completed by proxies and depressive symptoms
endorsed when the CSDD was administered as a self-​report
measure (Towsley, Neradilek, Snow, & Ersek, 2012), but
another study did not replicate this finding (Wongpakaran,
Wongpakaran, & van Reekum, 2013), especially when
the instrument was used with older adults with cognitive
impairment. Some public health researchers have found
that screening with the CSDD in large-​scale public health
initiatives aimed at long-​term care residents does not result
in improvements in depression care and creates undue
burden on nursing staff (Davison et al., 2012; Jeon et al.,
2015; Snowdon, Rosengren, Daniel, & Suyasa, 2010).
Despite these criticisms, the CSDD is considered a psy-
chometrically sound instrument to measure depression
severity in individuals with dementia for purposes of con-
ceptualization and treatment planning.
The Dementia Mood Assessment scale (DMAS;
Sunderland et  al., 1988)  includes 17 items that assess
depressive symptoms in the past week in individuals with
dementia on a 0 to 6 scale. Administered by a trained cli-
nician, the measure involves a semi-​structured interview
and observation of the patient, along with input from
collateral sources. Factor analyses vary slightly in summa-
rizing the domains assessed by the DMAS; in the largest
reported study, factors were depressed affect, environ-
mental interaction, diurnal patterns, agitation or suspi-
cion, and somatic indicators (Onega & Abraham, 1997).
Adequate internal consistency (Camus, cited in Perrault,
Oremus, Demers, Vida, & Wolfson, 2000), inter-​ rater
reliability (Sunderland et al., 1988), and construct validity
(Camus, cited in Perrault et al., 2000; Sunderland et al.,
1988) have been reported for scores on the measure, but
sample sizes have generally been small and little detail
has been provided in some of the reports (Sunderland &
Minichiello, 1996). Thus, this measure is promising, but
more evidence of reliability and validity is needed before
it could be highly recommended.
In addition to scales that measure depression specifi-
cally, several instruments have been developed to assess
for depressive symptoms among other disturbances in
persons with dementia. Although these instruments may
be useful in case conceptualization and treatment plan-
ning, in most cases, psychometric information is not given
specifically for the depression subscale. One exception is
the Neuropsychiatric Inventory (NPI; Cummings et  al.,
1994), a semi-​structured interview that is conducted with
a knowledgeable informant. The measure includes ques-
tions to screen for the presence of depressed mood, apa-
thy, and 10 other psychiatric symptoms. Each screening
question is followed by a series of questions to confirm the
presence or absence of the symptom, along with ratings of
symptom frequency and severity. Although psychometric
information specific to subscales is limited, scores on the
NPI as a whole demonstrate acceptable to good reliability
and good validity (Cummings et al., 1994). Employing a
version developed for use in nursing homes (NPI-​NH),
Wood and colleagues (2000) showed that the depression
and apathy subscales correlated moderately with research
observations. Thus, the NPI or NPI-​NH may be useful in
detecting depression among individuals with dementia,
but further work is needed to establish the validity of the
relevant subscales specifically for this purpose.
Overall Evaluation
Formalized assessment can provide clinicians with
invaluable information for case conceptualization and
treatment planning when working with older adults who
are demonstrating symptoms of depression; however, for
measurement devices to be useful for this purpose, they
must be chosen based on reliability, validity, and utility in
older adult populations. The preceding section examined
several different types of measures commonly used in the
assessment of depression in older adults, and in terms of
fulfilling the goal of case conceptualization and treatment
planning, several measures stand out as being particularly
useful for these purposes. When using a self-​report mea-
sure, it is recommended that the PHQ-​9 (Kroenke et al.,
2001; Kroenke & Spitzer, 2002) or the CES-​D (Radloff,
1977) be considered before any other measures because
they are well validated in older adults and provide infor-
mation across several domains of depressive symptoms.
Several structured clinical interviews may also provide
useful information for case conceptualization and treat-
ment planning for older adults with depression. The
GMS-​DS (Ravindran et  al., 1994)  is a promising struc-
tured interview because it was developed specifically for
 163
use with older adults, preliminary data show good reliabil-
ity and validity, and it requires the least time to administer,
but further evaluation is needed. Although there are some
promising clinician rating scales, at present it is difficult
to recommend a specific measure for treatment plan-
ning and case conceptualization. Finally, when assessing
depression in older adults with dementia, it would be
worth considering the CSDD because it has adequate to
good reliability and good validity in this population.
Whether self-​report, structured interview, or clinician
rating scales are used for treatment planning and case
conceptualization, it is important to keep in mind that
each type of measure is subject to biases and, therefore,
a multimethod approach may be the most effective way
to formulate case conceptualizations and treatment plans.
In particular, it is important to address other key aspects
of case conceptualization within an informal clinical
interview. For older adults, it is particularly important
to assess general social functioning, medical health and
medications, and the ability to perform activities of daily
living (e.g., walking, dressing, and eating) and instrumen-
tal activities of daily living (e.g., balancing a checkbook,
grocery shopping, and cooking; Karel et  al., 2002). In
addition, it may be useful to utilize a more formal mea-
sure of overall functioning. For example, the Short-​Form
Health Survey (SF-​36; Ware & Sherbourne, 1992)  is a
well-​validated measure of several components of func-
tioning, including physical function, role limitations,
bodily pain, general health, vitality, social functioning,
emotional functioning, and mental health. Finally, every
evaluation of an older adult client for the purposes of case
conceptualization should include some sort of evaluation
of cognitive functioning, such as the Mini-​Mental State
Examination (Folstein, Folstein, & McHugh, 1975)  or
the Neurobehavioral Cognitive Status Examination
(COGNISTAT; Kiernan, Mueller, Langston, & Van
Dyke, 1987).
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
Self-​Report Measures
Because of their efficiency and cost-​ effectiveness,
self-​
report measures can be very useful for treatment
monitoring and measuring treatment outcomes. Most
self-​report measures for depression can be administered
in less than 20 minutes, and several of the instruments
that are described here have shorter versions that can be
Depression in Late Life 163
administered in just a few minutes. Despite the useful-
ness of self-​report measures in terms of their inherent
efficiency, there are some limitations to the use of these
measures for treatment monitoring and outcome assess-
ment. Specifically, when used repeatedly, they may be
subject to internal validity problems because of carryover
effects (Whitley, 2002).
There are several self-​report measures that may prove
useful for treatment monitoring and measuring treat-
ment outcomes in older adults with depressive symp-
toms (Table 8.3). For a complete discussion of self-​report
measures, see the previous section on measures used for
case conceptualization and treatment planning. In this
section, we only discuss in detail the two measures most
recommended for treatment monitoring and measuring
treatment outcomes.
One self-​report measure that may prove particularly
useful for treatment monitoring and assessing outcomes
in older adults is the CES-​D (Radloff, 1977; discussed
previously). The CES-​D may be a particularly advanta-
geous self-​report measure because it explicitly instructs
respondents to reflect on symptoms during the past week,
which may lessen testing effects. In addition, the CES-​D
may be a useful measure of change because its scores have
demonstrated good test–​retest reliability (Radloff, 1977).
Researchers have also demonstrated that changes in
CES-​D scores are significantly related to changes in older
patients’ self-​report ratings of change in their depressive
symptoms (Datto, Thompson, Knott, & Katz, 2006). In
terms of efficiency, there are several CES-​D short forms
available. For example, 8-​and 10-​item versions, respec-
tively known as the Boston and the Iowa forms, yield
scores that have both demonstrated good reliability and
validity with older adults (Kohout, Berkman, Evans, &
Cornoni-​Huntley, 1993). All in all, the CES-​D is recom-
mended as a good assessment instrument to use to track
treatment progress and outcomes in older adults with
depressive symptoms.
In addition, the PHQ-​9 (Kroenke et al., 2001; Kroenke
& Spitzer, 2002; see previous section for information
about reliability and validity) is a very useful tool for
assessing treatment progress and outcomes in older adults.
As mentioned previously, scores on the PHQ-​9 have dem-
onstrated very good reliability and validity in a variety
of older adult populations (Lamers et  al., 2008; Phelan
et al., 2010). The PHQ-​9 has also been successfully used
for treatment monitoring in several large-​scale random-
ized controlled trials for depression treatment in older
adults (Bernd, Unützer, Callahan, Perkins, & Kroenke,
2004; Ciechanowski et al., 2004). There is also evidence
164

164 Mood Disorders and Self-Injury

Table 8.3  Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Self-​Report Measures
BDI-​II A G NA G A A A A A
CES-​D E G NA G A G G G A
GDS G G NA G A A A L L
PHQ-​9 E G G G A G E E E ✓
Clinician Rating Scales
GDRS A E G NR A NR A G A
MADRS A A E NR A A A G A
Measure to Assess Depression in Dementia
CSDD A E A A E E E A A ✓

Note: BDI-​II = Beck Depression Inventory-​II; CES-​D = Center for Epidemiological Studies–​Depression Scale; GDS = Geriatric Depression Scale;
PHQ-​9  =  Patient Health Questionnaire-​9; GDRS  =  Geriatric Depression Rating Scale; MADRS  =  Montgomery–​Åsberg Depression Rating Scale;
CSDD = Cornell Scale for Depression in Dementia; L = Less Than Acceptable; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not
Applicable.

that this measure has excellent treatment utility (i.e., staff
were able to use the PHQ-​9 results to appropriately and
successfully address depressive symptoms in long-​ term
care facilities) and is easy to use (Saliba et al., 2012). The
PHQ-​9 is highly recommended as a self-​report measure of
treatment response in older adults.
Structured Interviews
Unlike self-​report measures, structured interviews are
often time-​intensive and require extensive training for
administration; as such, they are generally not used for
treatment monitoring. However, as noted previously,
administration times vary and short forms are available. In
addition, structured interviews may provide useful infor-
mation about treatment outcomes.
The structured interview that appears to have the
most utility for the assessment of treatment outcomes is
the GMS-​DS (Ravindran et  al., 1994; discussed previ-
ously), which was specifically designed to assess changes
in depression levels in older adults, although further
evaluation is needed. It takes 15 minutes to administer
to depressed older adults and has demonstrated good
reliability and validity (Ravindran et  al., 1994). As a
measure of treatment outcomes, the GMS-​ DS per-
forms well, with pre-​to post-​treatment change scores
correlating .89 and .85, respectively, with clinician and
patient ratings of improvement (Ravindran et al., 1994).
Unfortunately, there is little research examining the util-
ity of the GMS-​DS, but available evidence suggests it is a
promising measure for assessing outcomes in depressed
older adults.
Clinician Rating Scales
Several clinician rating scales have been evaluated for
the purposes of treatment monitoring and assessment of
treatment outcomes in older adults (see Table 8.3). The
HRSD (Hamilton, 1960; discussed previously) is often
touted as a good measure for both treatment monitoring
and assessments of outcome, but many problems have
been noted (e.g., Bagby et al., 2004). The HRSD scores
do not have good reliability in older adults and may not
actually be measuring depression (Baker & Miller, 1991;
Hammond, 1998; Lichtenberg et al., 1992), which makes
this measure’s usefulness in tracking changes in depres-
sion in older adults questionable. Also, some researchers
have found that it can be time-​consuming and difficult to
administer to some populations of older adults (Baker &
Miller, 1991), which suggests that this measure may be
inconvenient to administer repeatedly. Given these con-
cerns, the HRSD is not recommended for treatment mon-
itoring and assessment of treatment outcome in depressed
older adults.
A measure that may prove useful for treatment moni-
toring and outcome assessments in depressed older adults
is the GDRS (Jamison & Scogin, 1992; discussed previ-
ously). The GDRS scores have fairly good inter-​ rater
reliability (Jamison & Scogin, 1992), but test–​retest reli-
ability has not been assessed. It is somewhat lengthy to
 165
administer (35 minutes), so it may be more appropriate
for outcome assessment than for monitoring treatment
progress. Although there is not enough empirical support
for the GDRS (particularly as a measure of change) to
recommend its use at this time, it appears to be promising
as an outcome measure.
The MADRS (Montgomery & Åsberg, 1979)  was
specifically designed to be sensitive to change with treat-
ment. However, MADRS scores have only fair internal
consistency in older adult samples (Bent-​Hansen et  al.,
2003) and thus may not be stable enough to assess change
reliably. On the positive side, scores on the measure
have shown very good inter-​rater reliability (Zimmerman
et  al., 2004)  and fairly good efficiency (Mottram et  al.,
2000) when used with older adults. Finally, the measure
has been shown to differentiate significantly between pla-
cebo and maintenance phase of treatment in older adults
(Bent-​Hansen et al., 2003). Despite these promising find-
ings, the problems with this measure’s score reliability and
the relative dearth of research examining this measure in
older adults suggest that it cannot be recommended for
the assessment of progress and outcomes in the treatment
of older adults with depression until more research evalu-
ating the MADRS is conducted.
The IDS (Rush, Gullion, Basco, Jarrett, & Trivedi,
1996; discussed previously) may prove useful for mea-
suring treatment progress and outcomes, although it has
not yet been empirically examined in older adults. In
particular, the measure’s fairly good internal consistency
(Rush et al., 1996) suggests that it is stable enough to be
used as a repeat measure. However, the IDS has not been
assessed for test–​retest reliability, which is problematic in
terms of its use as a measure for treatment monitoring.
Despite this promising evidence from research in mixed-​
age samples, the IDS cannot be recommended for use
with older adults until its properties are evaluated in this
population.
Measures to Assess Depression in Dementia
The CSDD (Alexopoulos et  al., 1988a; discussed pre-
viously) may be useful for monitoring the outcome of
depression treatment in individuals who have dementia.
Scores on this rating scale have demonstrated adequate
to good reliability and good validity, as described previ-
ously, and the ability to detect treatment effects has been
demonstrated (Mayer et  al., 2006). As Perrault and col-
leagues (2000) cautioned, however, most evidence for the
reliability and validity of scores on this measure derives
Depression in Late Life 165
from inpatient samples and may not be generalizable to
community-​dwelling individuals with dementia.
The DMAS (Sunderland et  al., 1988; discussed pre-
viously) scores have adequate reliability and validity, but
test–​retest reliability and sensitivity to change have not yet
been demonstrated. Consequently, the use of this scale
for outcome monitoring is not recommended until fur-
ther research is conducted.
Overall Evaluation
Given measurement considerations described previously in
this section, several measures stand out as potentially useful
for treatment monitoring and assessment of treatment out-
comes in older adults with depression. Among self-​report
measures, the CES-​ D (Radloff, 1977)  and the PHQ-​ 9
(Kroenke et al., 2001; Kroenke & Spitzer, 2002) may be the
most useful assessment tools for this purpose. For structured
interviews, the GMS-​DS (Ravindran, et  al., 1994)  is the
most promising assessment tool, but it is not yet supported
by sufficient research. In terms of clinician rating scales,
several scales appear promising for treatment monitoring
and evaluation, but more research is needed before any can
be recommended. The CSDD score can provide a reliable
and valid measure of change in depression severity among
individuals with dementia. In general, it is important to
keep in mind that each type of instrument is vulnerable to
testing effects and other threats to internal validity if admin-
istered repeatedly. Thus, it would be important to obtain
data from multiple measures when making decisions about
how effective treatment was for a particular client.
CONCLUSIONS AND FUTURE DIRECTIONS
Our examination of the assessment of depression in late
life leads to several conclusions. First, assessing depres-
sion in older adults poses unique challenges to clinicians.
Many older adults suffer from physical illnesses that result
in symptoms similar to somatic symptoms of depression.
Given this fact, differential diagnosis of depression in this
population can be difficult. Failure to account for this dif-
ficulty may result in overidentification of depression in
this age group. Eliminating somatic symptoms from mea-
sures of depression seems less than ideal because somatic
symptoms are often prominent in late life depression. It
appears that the best solution at this time is to incorpo-
rate information from different types of measures into the
assessment process.
16
166 Mood Disorders and Self-Injury
Another challenge posed when assessing late life
depression centers on differentially diagnosing depres-
sion and dementia. Cognitive symptoms of depression
are prominent in late life, and it can often be difficult to
determine if these symptoms are truly reflecting depres-
sion or if the patient is experiencing cognitive decline.
Again, measures often fail to take this difficulty into
account. In addition, due to the complexity of their for-
mat, some measures of depression can present real dif-
ficulties for older adults experiencing mild cognitive
decline. This difficulty may limit the validity of such
measures in older adults.
A further challenge is that older adults often display
symptoms of depression that differ from those presented
by younger and middle-​aged adults; thus, measures of
depression need to be validated and normed with older
adults specifically before they can be considered valid in
this population. Unfortunately, this research step has not
yet been taken for many measures.
Similarly, different subgroups should be considered
when measuring depression in older adults. Although
many instruments originally developed for younger adults
have demonstrated validity in healthy older adults, it may
be imprudent to utilize these same instruments with indi-
viduals with either physical illness or cognitive impair-
ment. Before using any measure of depression with an
older adult, it is essential to get information about medi-
cal illnesses and cognitive functioning and use measures
validated specifically with these populations.
More research is needed on the assessment of depres-
sion in older adults. Most depression instruments need to
be more thoroughly evaluated for their utility with older
adult clients. Some instruments that have been designed
specifically for this population appear promising, yet they,
too, require further validation. It may be useful to develop
measures specifically to assess depression in older adults
for the purposes of diagnosis, case conceptualization,
treatment planning, treatment monitoring, and the assess-
ment of treatment outcomes. An area that remains to be
addressed is the empirical examination of clinical utility.
Despite the challenges of assessing depression in older
adults, some instruments show evidence of good reliabil-
ity and validity—​it now remains to be established whether
their use improves clinical outcomes.
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 173
Bipolar Disorder
Sheri L. Johnson
Christopher Miller
Lori Eisner
The goal of this chapter is to review measures that are rel-
evant for the clinical evaluation and treatment of bipolar dis-
order. Specifically, we focus on assessment measures relevant
to diagnosis, treatment planning, and treatment monitoring.
In each area, we focus on those few assessment measures that
have gained at least moderate psychometric support.
Only a small number of measures meet established psy-
chometric criteria, perhaps as a consequence of the limited
amount of psychological research on bipolar disorder com-
pared to other psychopathologies. With the advent of lithium
treatment and the recognition of the genetic basis of disorder,
psychological researchers all but abandoned the study of this
disorder for several decades, and the development of new
assessment instruments languished. Psychological research
on the disorder entered a renewed phase of interest in the
1990s, with the volume of research increasing each year
since then. Nonetheless, research on bipolar disorder lags far
behind that available on other psychopathologies, and many
of the assessment needs for conducting research and clinical
work within this field remain relatively unaddressed.
Despite this relative dearth of exhaustively validated
measures of bipolar disorder, several existing measures
have been translated into different languages to serve the
needs of clinicians worldwide. Given the difficulties of
comparing validation studies across different languages,
however, we generally limit our consideration to English
versions of assessment tools throughout this chapter.
NATURE OF BIPOLAR DISORDER
The fifth edition of the Diagnostic and Statistical Manual
of Mental Disorders (DSM-​ 5; American Psychiatric
173
Association, 2013) defines several different forms of bipo-
lar disorders, differentiated by the severity and duration of
manic symptoms. Bipolar I  disorder is diagnosed on the
basis of a single lifetime episode of mania. A  manic epi-
sode is diagnosed on the basis of euphoric or irritable mood
with accompanying increases in energy or activity, the pres-
ence of at least three other symptoms (four if mood is only
irritable), and marked social or occupational impairment.
The inclusion of energy or activity as a required criterion is
new to DSM-​5. Criteria specify that symptoms must last at
least 1 week or require hospitalization. Bipolar II disorder is
diagnosed on the basis of hypomania and episodes of major
depression. Hypomania is less severe than mania: Criteria
specify a distinct change in functioning rather than severe
impairment. Hypomanic episodes can be diagnosed with
4 days of symptoms. A third form of bipolar disorder, cyclo-
thymia, is diagnosed based on recurrent mood swings, both
high and low, which do not meet the severity of bipolar
I or bipolar II disorder. Criteria for cyclothymia specify that
numerous mood swings must be present.
Manic symptoms may be secondary to drugs (e.g.,
cocaine and amphetamines) and medical conditions
(e.g., thyroid conditions). The use of antidepressants with-
out mood-​stabilizing medication can trigger episodes of
mania or hypomania, particularly among those with an
individual or family history of bipolar disorder (Ghaemi,
Lenox, & Baldessarini, 2001). Such episodes are not
considered in making a diagnosis of bipolar I or bipolar
II disorder but, rather, can contribute to a diagnosis of
medication-induced bipolar disorder.
Prevalence rates are approximately 1% for bipolar I dis-
order and 3.9% for bipolar I  and II disorders combined
(Kessler, Berglund, Demler, Jin, & Walter, 2005). Rates
174
174 Mood Disorders and Self-Injury
of comorbidity within bipolar disorder are quite high, and
treatment planning will require consideration of these
syndromes. Although not required for diagnosis of bipolar
I disorder, as many as 66% to 75% of people with bipolar
I  disorder in community surveys experience episodes of
major depression (Karkowski & Kendler, 1997; Kessler,
Rubinow, Holmes, Abelson, & Zhao, 1997). Similarly, as
many as 93% of people with bipolar disorder meet life-
time diagnostic criteria for at least one anxiety disorder
(Kessler et al., 1997), and as many as 61% do so for alco-
hol or substance abuse (Reigier et al., 1990). Indeed, in
a Veterans Administration sample, 78% met criteria for
comorbid conditions during their lifetime (Bauer et  al.,
2005). Hence, initial assessments should consider the pos-
sible presence of comorbid syndromes.
Estimates from twin studies suggest that heritability
accounts for as much as 93% of the variability in whether
or not this disorder develops (Kieseppa, Partonen,
Haukka, Kaprio, & Lonnqvis, 2004). For those affected
by the disorder, though, psychosocial variables predict the
course of symptoms. Depression within bipolar disorder
appears triggered by negative life events, deficits in social
support, and negative cognitive styles (Johnson & Kizer,
2002), whereas mania has been found to be predicted
by sleep dysregulation (Leibenluft, Albert, Rosenthal,
& Wehr, 1996)  and variables relevant to excessive goal
engagement (Johnson, Edge, Holmes, & Carver, 2012).
The evidence for genetic contributions to bipolar disorder
led to a focus on medication approaches, such as lithium
and other mood-​stabilizing medications (Prien & Potter,
1990). With increased evidence that psychosocial vari-
ables influence the course of disorder, adjunctive psycho-
social treatments have become more common (Johnson
& Leahy, 2004).
Table 9.1  Ratings of Instruments Used for Diagnosis
Internal Inter-​Rater Test–​Retest
Instrument Norms Consistency Reliability Reliability
Clinician Rated
SCID E NA G G
SADS A NA G G
Pediatric Clinician Rated
K-​SADS-​PL A NA E E
Self-​Report
GBI NA E NA A A
MDQ NA G NA A A
Note: SCID = Structured Clinical Interview for DSM-​IV; SADS = Schedule for Affective Disorders and Schizophrenia; K-​SADS-​PL = Kiddie Schedule
for Affective Disorders and Schizophrenia–​Present and Lifetime Version; GBI = General Behavior Inventory; MDQ = Mood Disorder Questionnaire;
L = Less Than Adequate; A = Adequate; G = Good; E = Excellent; NA = Not Applicable.
ASSESSMENT FOR DIAGNOSIS
There is no biological assay for bipolar disorder, so diag-
nosis is based entirely on review of symptoms and of
potential organic explanations. In practice, most clini-
cians review the DSM symptoms in an informal man-
ner, although clinicians using unstructured diagnostic
interviews tend to miss approximately half of all diagnoses
(Shear et al., 2000; Zimmerman & Mattia, 1999).
Even though many people with a history of major
depression will meet diagnostic criteria for bipolar disor-
der, most practitioners report that they do not routinely
screen for bipolar disorder among people with depression
(Brickman, LoPiccolo, & Johnson, 2002). Perhaps as a
consequence of poor screening, people with bipolar dis-
order may wait as long as 6 to 8  years on average to be
correctly diagnosed (Drancourt et al., 2013; Lish, Dime-​
Meenan, Whybrow, Price, & Hirschfeld, 1994). Failure
to detect this diagnosis can have serious repercussions, in
that antidepressant treatment without mood-​stabilizing
medication can trigger iatrogenic mania (Ghaemi et al.,
2001; Tondo, Vázquez, & Baldessarini, 2010).
In this section, we discuss diagnostic instruments for
bipolar disorder (for a summary of relevant measures, see
Table 9.1). This material should be considered in the con-
text of the aforementioned modification to the diagnosis
of bipolar disorder in DSM-​5. Unfortunately, very little
literature has validated diagnostic or screening instru-
ments against DSM-​5 criteria. We therefore focus on diag-
nostic and screening measures that have been validated
against DSM-​IV (American Psychiatric Association, 1994,
2000) or other older bipolar diagnoses.
For adults, two semi-​structured diagnostic instruments
have been most commonly used: the Structured Clinical
Content Construct Validity Clinical Highly
Validity Validity Generalization Utility Recommended
G G E A ✓
G G E A ✓
A G G A ✓
G NA NA
A L NA
 175
Interview for DSM-​ IV (SCID) and the Schedule for
Affective Disorders and Schizophrenia (SADS). Both pro-
vide interview probes, guidelines for symptom thresholds,
and information about potential exclusionary criteria (e.g.,
medical and pharmacological conditions that could pro-
voke manic symptoms). The SCID is designed to assess
DSM-​ IV diagnoses, whereas the SADS is designed to
assess the Research Diagnostic Criteria (RDC). Although
the two diagnostic systems are similar for mania, RDC
criteria are slightly stricter than the DSM criteria about
the nature of psychotic symptoms that can be manifested
within bipolar disorder, in that certain psychotic symptoms
are considered indicative of schizoaffective rather than
bipolar disorder. We begin by describing these measures as
tools for assessing bipolar disorder in adults, and then we
discuss some concerns regarding the diagnosis of bipolar II
disorder. Next, we discuss issues and tools for the diagnosis
of child and adolescent bipolar disorder. We conclude our
discussion of diagnostic assessment with a description of
self-​report measures designed to aid diagnostic screening.
Diagnostic Assessment of Bipolar I
Disorder in Adults
The Structured Clinical Interview for DSM-​IV-​TR
The SCID is recommended as a part of clinical intake pro-
cedures (Spitzer, Williams, Gibbon, & First, 1992), and a
clinician’s version is available through American Psychiatric
Publishing (First, Spitzer, Gibbon, & Williams, 1997). The
recent transition to DSM-​5 has been accompanied by a
new version of the SCID (First, Williams, Karg, & Spitzer,
2016), but validation data for the SCID-​5 are not yet widely
available. The clinician’s version includes less detail about
subtype and course distinctions than is provided within the
research version. The SCID is a semi-​structured interview
with recommended probes, but diagnosticians are expected
to rephrase probes and ask clarifying questions as needed to
determine whether a given criterion is met.
Inter-​
rater reliability for the SCID diagnoses has
been established in a large international multisite trial
(Williams et al., 1992) and at least 10 other major trials
(Rogers, Jackson, & Cashel, 2001). Initial attempts to
test the mania module within a community sample were
thwarted by the low base rates of the disorder (Williams
et al., 1992). Diagnoses of bipolar disorder based on the
SCID, however, were substantially more reliable than
those obtained by clinicians who were not using a diag-
nostic interview or by paraprofessionals using more struc-
tured interviews such as the Composite International
Bipolar Disorder 175
Diagnostic Interview (CIDI; World Health Organization,
1990). The SCID has achieved high concordance for
bipolar diagnoses between twins and has been validated
in a number of countries (Kieseppa et al., 2004).
The Schedule for Affective Disorders
and Schizophrenia
Considerable evidence has accrued for the reliability of
SADS (Endicott & Spitzer, 1978) diagnoses across 21 stud-
ies (for a review, see Rogers et al., 2001). SADS diagnoses
of bipolar disorder have been found to robustly correlate
with other measures of mania (Secunda et al., 1985), and
the SADS appears to accurately capture diagnoses across
different cultural and ethnic groups within the United
States (Vernon & Roberts, 1982). Lifetime mania diagno-
ses have achieved good test–​retest reliability over 5 years
among samples of adults (Rice et  al., 1986)  and adoles-
cents (Strober et al., 1995), as well as 10 years among a
sample of adults (Coryell et al., 1995).
Diagnostic Assessment of Bipolar II
Disorder in Adults
Bipolar II disorder was not recognized within the DSM
as a diagnostic category until the fourth edition. It is
worth noting that hypomania is the only major syndrome
within the DSM in which functional impairment is not
a criterion for diagnosis. That is, persons can qualify for
hypomanic episodes with a relatively mild shift in func-
tioning. Perhaps because of the minimal severity, bipolar
II disorder is not diagnosed unless the person also suffers
from episodes of major depression. Intriguingly, consid-
erable debate still exists about the criteria for hypoma-
nia; whereas the DSM-​5 criteria specify four symptoms
with duration of at least 4 days, the RDC criteria are less
stringent, specifying three symptoms with duration of at
least 2  days. Given ongoing debates about the diagnos-
tic threshold, it is not surprising that assessment tools for
bipolar II disorder are less well established.
Despite debate about diagnostic criteria and instru-
ments, though, there is evidence that the diagnosis itself
may be important to capture. Diagnoses of bipolar II dis-
order using the SADS show expected correlations with
trait measures of mood lability and energy/​activity (Akiskal
et al., 1995), as well as family history of bipolar II disorder
(Rice et al., 1986). Several studies have also suggested that
people with bipolar II disorder are at higher risk for suicide
than are persons with bipolar I disorder or unipolar depres-
sion (Dunner, 1996; Undurraga, Baldessarini, Valenti,
176
176 Mood Disorders and Self-Injury
Pacchiarotti, & Vieta, 2012). Hence, identification of
bipolar II disorder is important in planning treatment.
The lower threshold for this disorder appears to create
difficulty in reliably capturing symptoms, an issue that is
particularly well documented for the SADS. Even when
interviewers rate the same recordings, reliability estimates
for bipolar II disorder within the SADS are quite inade-
quate and much lower than the estimates for bipolar I dis-
order reflected in Table 9.1 (Keller et al., 1981), although
some teams achieved higher estimates (Simpson et  al.,
2002; Spitzer, Endicott, & Robins, 1978). In addition
to poor reliability for the diagnostic category, interview-
ers also have been found to have very poor agreement on
mild symptoms of mania (Andreasen et al., 1981). Test–​
retest reliability over a 6-​month period was quite poor
for bipolar II disorder, intraclass r = .06, and even poorer
for cyclothymia (Andreasen et  al., 1981). In a 5-​ year
test–​retest study, SADS diagnoses of bipolar II disorder
achieved kappa scores of only .09 (Rice et al., 1986), and
in a 10-​year study, only 40% of persons initially diagnosed
with bipolar II disorder on the SADS experienced further
episodes of hypomania or mania (Coryell et al., 1995).
Inter-​rater reliability can be limited by either a lack
of specificity or a lack of sensitivity. Both the SCID and
the SADS have been found to have inadequate sensitiv-
ity in detecting cases of bipolar II disorder. Despite some
evidence for high inter-​rater agreement of unstructured
expert clinical interviews in one study, approximately one-​
third of cases that were diagnosed through expert clinical
interview with bipolar II disorder were not identified as
such within SCID interviews (κ = .67) (Dunner & Tay,
1993; Simpson et al., 2002).
In summary, a set of issues mar the diagnostic assess-
ment of bipolar II disorder, including difficulties identify-
ing hypomanic symptoms that do not cause impairment
and broad questions about the duration of hypomanic epi-
sodes. Based on this, it is perhaps not surprising that avail-
able tools do not produce reliable diagnoses of bipolar II
disorder. Given that people who meet criteria for bipolar
II disorder may be at high risk for suicidality, improving
the detection of this disorder remains an important goal
for the field.
Diagnostic Assessment of Bipolar Disorder
in Children and Adolescents
The DSM-​5 diagnostic criteria for juvenile bipolar disor-
der are the same as those for adult bipolar disorder, with
the exception that cyclothymic disorder can be diagnosed
within 1  year, rather than 2  years, of symptoms. There
is considerable debate in the field about the diagnostic
criteria as some researchers have argued many diagnoses
of bipolar disorder among children and adolescents are
missed because the criteria are too stringent. Some have
argued that episodes of shorter duration or diminished
symptom severity should be diagnosable, particularly
given that children may not have the same opportuni-
ties to exhibit symptomatic behavior in domains such
as hypersexuality or overspending. On the other hand,
recent dramatic increases in the sheer number of bipo-
lar diagnoses among youth and adolescents (e.g., Blader
& Carlson, 2007; Moreno et  al., 2007)  have raised the
possibility that bipolar disorder is now overdiagnosed in
these populations. This has in turn been associated with
a rapid increase in the number of prescriptions of second-​
generation antipsychotics—​which can cause dangerous
cardiovascular side effects—​ in young people (Fraguas
et al., 2011). In one attempt to address this concern, DSM-​
5 introduced a separate diagnosis of disruptive mood dys-
regulation disorder, characterized by severe and recurrent
temper outbursts in children that do not coalesce into full
manic or hypomanic episodes (Axelson et al., 2012).
Taken together, these developments emphasize that
accurately diagnosing bipolar disorder in children and
adolescents is notoriously difficult. Here, we focus briefly
on the key issues involved in diagnosing bipolar disorder
in youth. Readers interested in more in-​depth coverage are
referred to more detailed works (e.g., Jenkins, Youngstrom,
Washburn, & Youngstrom, 2011; Youngstrom, Findling,
Youngstrom, & Calabrese, 2005).
In diagnosing juvenile bipolar disorder, there is value
in using multiple sources of data, including youths, par-
ents, and teachers (Youngstrom, Findling, & Calabrese,
2003). Youths can be poor reporters of hyperactivity, inat-
tention, and oppositional behaviors (Youngstrom, Loeber,
& Stouthamer-​Loeber, 2000). To the extent that mania
involves externalizing symptoms, youths may be poor
reporters of manic symptoms. For internalizing prob-
lems, youth and caregiver reports are preferable (Loeber,
Green, & Lahey, 1990). Teacher reports are often discrep-
ant with the reports of parents and youths (Youngstrom
et al., 2000) because children may show different behav-
iors across different settings. Given that impairment may
not be equal across all settings, averaging scores from dif-
ferent sources appears to enhance reliability (Youngstrom,
Gracious, Danielson, Findling, & Calabrese, 2003).
Parent report offers several advantages in mak-
ing accurate psychiatric diagnoses, especially among
 17
younger children. Parents are more psychologically
minded than youths (Anastasi & Urbina, 1997), and
they are aware of a child’s developmental history and
family functioning (Richters, 1992), as well as low base
rate phenomena (e.g., fire-​setting and suicide attempts;
Kazdin & Kagan, 1994). Not surprisingly, then, parent
report tends to be more accurate in predicting diagnostic
status than either youth or teacher reports (Youngstrom
et al., 2004).
Youth report should not be discounted in the diagnos-
tic process, however. Parent and youth reports have been
shown to be more discrepant for externalizing disorders
than internalizing disorders, for girls than boys, and for
older children than younger children (Verhulst & van der
Ende, 1992). Adolescents, especially as they grow older,
are important informants on their own problem behaviors
given that internalizing behaviors and concealed high-​
risk behaviors may go unnoticed by their parents (Loeber,
Green, & Lahey, 1990). One way to approach clinical
interviewing with parents and their children is by using
diagnostic interviews, described next.
Kiddie Schedule for Affective Disorders and
Schizophrenia for School-​Age Children—​Present
and Lifetime Version
Many different versions of the Kiddie Schedule for
Affective Disorders and Schizophrenia for School-​ Age
Children (K-​SADS) have been developed. The K-​SADS-​
PL, however, is the only instrument that provides global
and diagnosis-​specific impairment ratings (Kaufman et al.,
1997). Excellent estimates of inter-​rater reliability (98% to
100%) and test–​retest reliability (κ for current and lifetime
diagnosis both = 1.00) have been documented for bipolar
disorders with the K-​SADS-​PL (Frazier et al., 2007).
Several groups have attempted to refine the mania
section of the K-​SADS. Axelson et al. (2003) developed
a Child Mania Rating Scale module that, in their sam-
ple, demonstrated excellent inter-​rater reliability (intra-
class correlation  =  .97), excellent internal consistency
(α  =  .94), and, using a cut-​off score of 12 or higher,
demonstrated sensitivity of 87% and specificity of 81%
with clinical judgments of mania (Axelson et al., 2003).
These results suggest that the K-​SADS-​MRS holds prom-
ise as a rating scale for manic symptoms in children and
adolescents.
Geller and colleagues (2001) at Washington
University in St. Louis developed a more detailed version
of the K-​SADS (WASH-​U-​KSADS). Although scores on
Bipolar Disorder 177
the measure have achieved good to excellent inter-​rater
reliability for mania symptoms (κ range from .82 to 1.00;
Geller et al., 2001), the training and time burdens may be
too extensive for general clinical practice.
Self-​Report Measures
Detailed assessment by a trained clinician is considered
the most reliable and valid way to obtain a diagnosis
of bipolar disorder (Akiskal, 2002). Several self-​ report
screeners have been developed, however, to aid in detect-
ing potential diagnoses of bipolar disorder. At this point
in their development, information on psychometric ade-
quacy is limited (see Table 9.1).
Of these measures, the General Behavior Inventory
(GBI; Depue et  al., 1981)  has demonstrated promis-
ing psychometric properties (Ratheesh, Berk, Davey,
McGorry, & Cotton, 2015). GBI items were designed to
cover symptom intensity, duration, and frequency using a
response scale that ranges from 1 (“never or hardly ever”)
to 4 (“very often or almost constantly”). The original GBI
consisted of 69 items, chosen to cover the core symptoms
of bipolar disorder by the consensus of three item writers.
Modified versions have been developed, as well, that tap
both the depressed and the manic poles of bipolar disor-
der (e.g., Depue & Klein, 1988; Mallon, Klein, Bornstein,
& Slater, 1986). The variety of different versions, ranging
from 52 to 73 items, makes generalizations regarding psy-
chometric properties difficult.
Normative data have not been reported for the GBI
in any large clinical samples, but its scores have gener-
ally demonstrated excellent internal consistency and
adequate test–​retest reliability, with initial evidence of
structural invariance in Black and White young adults
(Pendergast et al., 2015). Several studies have assessed the
GBI’s ability to discriminate bipolar cases from noncases.
In general, the GBI scores have demonstrated sensitiv-
ity to bipolar disorder of approximately 75%, and speci-
ficity greater than 97% (Depue & Klein, 1988; Depue,
Krauss, Spoont, & Arbisi, 1989; Klein, Dickstein, Taylor,
& Harding, 1989; Mallon et  al., 1986), in both clinical
and nonclinical samples. Scores have also demonstrated
the ability to predict development of bipolar disorder in
young adults (e.g., Alloy et al., 2012). Unfortunately, gen-
eralizability is limited because cut-​off scores were not con-
sistent across studies but, rather, were determined within
each study to maximize predictive power.
The GBI has also been adapted for use with parents
to capture mood symptoms in children aged 5 to 17 years
178
178 Mood Disorders and Self-Injury
and has been shown to be diagnostically informative,
especially for young children (Findling et  al., 2002;
Youngstrom, Findling, Danielson, & Calabrese, 2001).
Parallel to the original GBI, the Parent GBI (P-​GBI)
consists of depressive and hypomanic/​biphasic subscales,
both of which demonstrate excellent internal consistency.
The scale also demonstrated strong validity in differenti-
ating children with mood disorders from those with dis-
ruptive behavior disorders (80.6% accuracy), as well as
distinguishing children with bipolar disorder from those
with other mood disorders (86.1% accuracy; Youngstrom
et al., 2001). Additional work has demonstrated promise
for a 10-​item version of the P-​GBI focused specifically on
mania (Youngstrom et al., 2008, 2012).
Several studies have examined the validity of youth
report on the GBI (e.g., Danielson, Youngstrom, Findling,
& Calabrese, 2003). The GBI depression scale demon-
strates good discriminative validity distinguishing between
those with Axis I mood disorders and those with disruptive
behavior disorders or no diagnosis, and the hypomanic/​
biphasic scale distinguishes between children with bipo-
lar spectrum diagnoses and those with other disorders
(depression, disruptive behavior disorder, and no diagno-
sis). Not surprisingly, the GBI is better at differentiating
children with bipolar disorder from healthy controls than
it is at differentiating children with bipolar disorder from
those with unipolar depression (Pendergast et al., 2014).
Overall, then, the GBI is a promising screening tool for
identifying bipolar disorder among adult and pediatric
populations. Nonetheless, more research is needed to
establish norms and to evaluate this scale using consistent
items and cut-​off scores.
One other measure that has been increasingly popular
is the Mood Disorder Questionnaire (MDQ; Hirschfeld
et  al., 2000). The first 13 items of the MDQ are yes–​no
questions covering the full range of manic symptoms; at
least 7 must be answered “yes” to achieve a positive screen.
Additional items query as to whether the symptoms identi-
fied co-​occurred and caused at least moderate problems.
The MDQ scores have attained good internal consistency
ranging from .79 (Isometsä et al., 2003) to .90 (Hirschfeld
et  al., 2000), adequate 1-​month test–​retest reliability in
clinical samples (Weber Rouget et al., 2005), and fair sensi-
tivity in differentiating bipolar disorder from unipolar disor-
der clinical samples (.73 to .90). Nonetheless, specificities
have been low in many studies, with considerable variabil-
ity across settings (.47 to .90; Hirschfeld et al., 2000, 2003;
Isometsä et al., 2003; Miller, Klugman, Berv, Rosenquist, &
Ghaemi, 2004; Weber Rouget et al., 2005). Poor psycho-
metric properties for the MDQ have emerged especially in
nonclinical samples (Dodd et al., 2009; Hirschfeld et al.,
2003; Miller, Johnson, Kwapil, & Carver, 2011) and clini-
cal settings that include disorders and comorbidities other
than bipolar disorder and unipolar depression (van Zaane,
van den Berg, Draisma, Nolen, & van den Brink, 2012;
Zimmerman, Galione, Chelminski, Young, & Dalrymple,
2011). In other cases, researchers have applied different
cut-​points and modified scoring algorithms, in several
cases concluding that no cut-​off adequately balances sensi-
tivity and specificity (Zimmerman, 2012; Zimmerman &
Galione, 2011). Despite these limitations, the MDQ has
been translated into numerous languages and has been
tested in many countries throughout the world (e.g., de
Sousa Gurgel, Rebouças, de Matos, Carneiro, & Souza,
2012; Gervasoni et al., 2009; Meyer et al., 2011; Sanchez-​
Moreno et al., 2008).
Other scales await more testing. Scores on the
Hypomanic Personality Scale (HPS; Eckblad &
Chapman, 1986)  have been found to predict the devel-
opment of manic episodes at multiyear follow-​up in two
samples of undergraduates (Kwapil et  al., 2000; Walsh,
DeGeorge, Barrantes-​ Vidal, & Kwapil, 2015), and a
Spanish language version is available (Ruggero, Johnson,
& Cuellar, 2004), but the scale has been subjected to min-
imal study in clinical populations (e.g., Parker, Fletcher,
McCraw, & Hong, 2014). The Bipolar Spectrum
Disorder Scale (BSDS; Ghaemi et  al., 2005)  and the
Mood Spectrum Self-​Reports (MOODS-​SR; Dell’Osso
et al., 2002) have only been tested in a handful of studies
each (e.g., Carvalho et al., 2015; Miniati et al., 2009). The
Hypomania Checklist (HCL-​32; Angst, Adolfsson, et al.,
2005), as its name implies, was designed to detect hypo-
mania specifically, but it has predominantly been tested
outside of the United States (Carta et al., 2006; Wu, Angst,
Ou, Chen, & Lu, 2008). The Temperament Evaluation
of Memphis, Pisa, Paris, and San Diego (TEMPS; Akiskal
& Akiskal, 2005)  is a measure to which an issue of the
Journal of Affective Disorders was dedicated, but to our
knowledge it has not been compared with a diagnostic
interview, and more than one version or cut-​offs have
appeared across studies. The cyclothymia subscale of a
TEMPS self-​report version (the autoquestionnaire) has
shown promising correlations with diagnostic interviews
(Mahon, Perez-​ Rodriguez, Gunawardane, & Burdick,
2013; Mendlowicz, Kelsoe, & Akiskal, 2005). The Child
Mania Rating Scale (Pavuluri, Henry, Devineni, Carbray,
& Birmaher, 2006) and the Parent-​Young Mania Rating
scale (P-​ YMRS; Gracious, Youngstrom, Findling, &
Calabrese, 2002)  are both designed to assess current
symptoms of mania among youths, but few studies have
 179
Table 9.2  Ratings of Instruments Used for Case Conceptualization and Treatment Planning
Internal Inter-​Rater Test–​Retest Content
Instrument Norm Consistency Reliability Reliability Validity
FAD A A NA A A
SAI-​E A A G NA A A
Note: FAD = Family Assessment Device; SAI-​E = Schedule for Assessment of Insight-​Expanded Version; G = Good; A = Adequate; NA = Not Available.
investigated their psychometric properties (e.g., Serrano,
Ezpeleta, Alda, Matalí, & San, 2011). The Inventory of
Depression and Anxiety Symptoms (IDAS) was recently
updated (now labeled the IDAS-​II) to incorporate assess-
ment of manic and euphoric symptoms, but it has not yet
been extensively studied (Watson et al., 2012).
Overall Evaluation
To date, two measures of diagnosis are dominant in diag-
nosing bipolar disorder among adults: the SCID and the
SADS. Both have excellent psychometric characteristics
for the assessment of bipolar I disorder but function poorly
in identifying bipolar II disorder. It is not currently clear
whether the limits in detection of bipolar II are strictly a
measurement issue or reflect underlying issues in the defi-
nitions of hypomanic episodes. These results should be
considered in the context of the recent DSM-​5 changes
to diagnostic criteria for bipolar disorder that promote
increased energy/​ activity to a cardinal symptom. We
know very little about how these changes to the diagnostic
code affect the psychometric performance of diagnostic
measures.
Although there is much debate regarding the diag-
nostic criteria for pediatric bipolar disorder, assessment
should include a detailed clinical interview that assesses
family history, as well as the intensity and duration of any
mood symptoms. The mania modules of the K-​SADS
have achieved psychometric support, and obtaining infor-
mation from multiple sources (e.g., parents or teachers)
may be useful as well.
The potential benefits of robustly validated screen-
ing tools for bipolar disorder are recognized by clinicians
and researchers alike but developing such tools has been
extremely challenging. When considering self-​ report
scales as screening tools, several issues must be kept in
mind. For instance, Phelps and Ghaemi (2006) dem-
onstrated that the usefulness of a screening tool varies
depending on clinicians’ previous estimates of the prob-
ability of the disorder in question. Thus, clinician knowl-
edge about a disorder’s prevalence in the population of
Bipolar Disorder 179
Construct Validity Clinical Treatment Highly
Validity Generalization Utility Sensitivity Recommended
G G A A ✓
A A NA ✓
interest may be more important than a screening tool’s
sensitivity or specificity. Second, different measures have
been used as reference standards. Third, several authors
have expanded the diagnostic interviews used as a refer-
ence standard to capture milder forms of bipolar spec-
trum disorder, yet provide only vague information about
the modifications. Fourth, suppressor effects—​by which
the inclusion of some items in a scale may boost the pre-
dictor power of other items—​may be especially relevant
for bipolar disorder given that many people with bipolar
disorder experience high levels of both positive and nega-
tive affect (Watson, Clark, Chmielewski, & Kotov, 2013).
Each of these issues complicates comparisons between
measures.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
A growing body of work suggests that psychological treat-
ments can be helpful when added to pharmacological
treatment for bipolar disorder. Well-​studied psychologi-
cal treatments include family-​focused therapy, cognitive
therapy, interpersonal psychotherapy, and psychoedu-
cation. Nonetheless, several trials have suggested com-
parable effects of these active psychological treatments
(Miklowitz et al., 2007). Given this, a key question is how
to determine which treatments would be most helpful.
Unfortunately, research on the predictors of treatment
outcome remains in its infancy within bipolar disorder
(Miklowitz & Johnson, 2014). Hence, there are few mea-
sures available to predict response to a given treatment
approach (for a review of key measures, see Table 9.2).
Certainly, there is evidence that severity of symptom
history, whether defined by multiple episodes per year,
earlier age of onset, severity of depressive symptoms dur-
ing manic periods, or comorbid medical and psychiatric
conditions, will predict poorer outcome. Hence, clini-
cians will do well to gather a good clinical history to
document the severity of the manic episodes, as well as
the presence of comorbid complications. Reviewing the
180
180 Mood Disorders and Self-Injury
history of episodes can be somewhat bewildering because
the median time to relapse, even on adequate medica-
tion levels, is approximately 1  year (Keller et  al., 1992).
Hence, most patients will have had many episodes, and
the episodes will have varied in their triggers, severity,
and consequences. One strategy that can be very helpful
in organizing the complex information is the Life Chart
(Denicoff et al., 1997), a graphing procedure developed
at the National Institute of Mental Health, which can
provide a collaborative tool for helping a patient describe
the pattern of episodes over time, potential triggers, and
effectiveness of different treatment approaches. Although
frequently used, little psychometric information on the
Life Chart is available.
Other measures are relevant for tracking specific
dimensions related to outcome. One of the best predic-
tors of poor outcome is treatment nonadherence, with
substantial evidence that treatment dropout increases
risk of relapse, suicide, and hospitalization (Keck et al.,
1998). It is also well established that treatment nonad-
herence is normative within bipolar disorder—​less than
25% of patients remain continuously adherent with
medication (Merikangas et al., 2011). Hence, predicting
treatment nonadherence would be a primary goal of any
baseline assessment. The Scale to Assess Unawareness of
Mental Disorder (SUMD; Amador et al., 1993), a semi-​
structured interview to assess awareness of symptoms of
mental disorder, symptoms, social consequences of dis-
order, and misattributions for symptoms, has been shown
to differentiate people with bipolar disorder from those
without bipolar disorder (Varga Magnusson, Flekkoy,
Ronneberg, & Opjordsmoen, 2006). However, baseline
scores have not been found to predict treatment success
over time (Ghaemi, Boiman, & Goodwin, 2000), particu-
larly when baseline function is considered (Novick et al.,
2015). On the other hand, the Schedule for Assessment
of Insight-​Expanded Version (SAI-​E; Kemp & David,
1996)  has been found to predict treatment adherence
at 1-​year follow-​up among people with bipolar disorder
(Yen et al., 2005), to differentiate people with and with-
out bipolar disorder (Sanz Constable, Lopez-​lbor, Kemp,
& David, 1998), and to achieve a cross-​sectional corre-
lation of .70 with other indices of treatment adherence
(Sanz et al., 1998). The self-​report Insight and Treatment
Attitudes Questionnaire has been used in several studies
of persons with bipolar disorder, but little psychometric
or predictive information is available. Inter-​ rater reli-
abilities of .92 and higher have been reported (Ghaemi,
Stoll, & Pope, 1995; Michalakeas et al., 1994; Sajatovic
et al., 2009).
Choices regarding which other risk factors to assess
will likely depend on the treatment being employed.
Hence, if offering cognitive therapy to address maladap-
tive negative cognitions about the self, clinicians may
want to draw from the measures of negative cognition
routinely used within the unipolar depression literature
(for a review, see Chapter  7, this volume), such as the
Dysfunctional Attitudes Scale (DAS; Weissman & Beck,
1978) or the Automatic Thoughts Questionnaire (Hollon
& Kendall, 1980). These measures have been extremely
well tested in both unipolar depression and general pop-
ulations. Scores on both measures are elevated during
depressive episodes of bipolar disorder compared to those
of healthy control groups (Cuellar, Johnson, & Winters,
2005; Pavlickova et al., 2013), and DAS scores have been
found to predict increased depressive symptoms over
time (Fletcher, Parker, & Manicavasagar, 2014; Johnson
& Fingerhut, 2004). Psychometric data within bipolar
disorder is available for a sample of more than 300 par-
ticipants (Reilly-​Harrington et  al., 2010). Nonetheless,
the factor structure of the DAS appears to differ among
people with bipolar disorder compared with the general
population, and studies have varied widely in which sub-
scales they used (Lam, Wright, & Smith, 2004).
For clinicians who offer interpersonal and social
rhythm psychotherapy (Frank, 2005), a substantial com-
ponent of treatment focuses on helping clients develop
a more regular schedule of daily activities. One measure,
the social rhythm metric, has been most widely used to
test the constancy of the daily schedule (Monk, Flaherty,
Frank, Hoskinson, & Kupfer, 1990). The scale has been
shown to correlate with indices of sleep (Monk, Reynolds,
Buysse, DeGrazia, & Kupfer, 2003) and to be lower among
persons with rapid cycling bipolar disorder compared to
healthy controls (Ashman et al., 1999). Nonetheless, the
scale correlates with, rather than predicts, mania symp-
tom fluctuations disorder over time (Frank et al., 2005),
so it is currently not recommended  for treatment out-
come prediction. Several researchers have shown that
the Pittsburgh Sleep Quality Index (PSQI) is predictive
of symptom changes over time within bipolar disorder
(Murray & Harvey, 2010; Saunders, Fernandez-​Mendoza,
Kamali, Assari, & McInnis, 2015). Because evidence is
more limited regarding how this instrument predicts
change for those in a given treatment, it is not recom-
mended at this time for treatment outcome prediction.
Drawing on expressed emotion (EE) theory, family
treatment programs in bipolar disorder aim to help fami-
lies become less critical of their ill relative (Miklowitz &
Goldstein, 1997). The most feasibly administered scale
 18

Bipolar Disorder 181

of family criticism is the Perceived Criticism scale (PCS; Overall Evaluation

Hooley & Teasdale, 1989). Patients rate on a scale of 1 to
10 how critical they think they are of their relative and
how critical they think their relative is of them. Scores on
this scale have demonstrated temporal stability as well as
concurrent validity with the other validated measures of
EE, such as the Camberwell Family Interview (r  =  .45,
p < .01; van Humbeeck et al., 2004). Unfortunately, the
scale has not been found to predict the outcome of fam-
ily therapy (Miklowitz, Wisniewski, Miyahara, Otto, &
Sachs, 2005).
In contrast, the Family Assessment Device (FAD;
Epstein, Baldwin, & Bishop, 1983) is a 60-​item self-​report
measure. FAD scores have been found to be elevated
among families of those with bipolar disorder compared to
controls (Du Rocher Schudlich, Youngstrom, Calabrese,
& Findling, 2008; Young et al., 2013) and to predict more
gain in family therapy compared to pharmacotherapy
(Miller et al., 2008), but FAD scores does not appear to
predict more general change in outcomes (Weinstock &
Miller, 2010). Six subscales have attained factor analytic
support, and a general function score aggregates those
subscales (Kabacoff, Miller, Bishop, Epstein, & Keitner,
1990). Adequate construct validity, compared to other
measures of family function, as well as indices of social
desirability, has been demonstrated (Miller, Epstein,
Bishop, & Keitner, 1985), and the scale has been used
in a wide range of samples, with large normative data sets
available for those with psychiatric diagnoses and controls
(Friedmann et al., 1997). A concern, however, is that 1-​
week test–​retest reliability scores are only modest (r = .66
to .75, Mn = .71; Miller et al., 1985).
Because clinical severity and comorbidity are important
predictors of poorer outcome, clinicians should assess
these parameters during intake interviews. The Life Chart
provides a way of organizing clinical history. Beyond clini-
cal severity, the SAI-​E has been found to predict poorer
medication adherence. Although the current state of
research does not offer clinicians much guidance on how
to choose treatment predictors, there are some promising
developments in measuring constructs relevant to case
conceptualization and treatment planning, particularly in
the domain of insight and family function.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
In this section, we consider measures that can be used
to track the progress of treatment (Table 9.3). Currently,
well-​validated measures for this purpose exist only for
the purpose of documenting changes in symptom levels.
The Young Mania Rating Scale and the Bech–​Rafaelsen
Mania Rating Scale are among the most widely used
scales for this purpose.
The Young Mania Rating Scale (YMRS) was designed
to be administered by a trained clinician in a 15-​to 30-​
minute patient interview that captures the patient’s report
of manic symptoms during the past 48 hours as well as
the clinician’s observations during the interview (Young,
Biggs, Ziegler, & Meyer, 1978). The 11 items, which
assess elevated mood, increased energy, sexual interest,

Table 9.3  Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

YMRS A E E NA A G A G A
MAS A E E NA A G A G G ✓
SADS-​C A NA G NA A G G E G ✓
ASRM A A NA A A* G A A G
SRMI A G NA A G A A A A
WASSUP A A NA NA A A A A A
SHPSS A G NA A A A A G A
Brief QoL.BD A G NA A G G NA NA A

*  But missing grandiosity.

Note:  YMRS  =  Young Mania Rating Scale; MAS  =  Bech–​Rafaelsen Mania Scale; SADS-​C  =  Schedule for Affective Disorders and Schizophrenia-​
Change Mania Scale; ASRM  =  Altman Self-​Rating Mania Scale; SRMI  =  Self-​Rating Mania Inventory; WASSUP  =  Willingly Approached Set of
Statistically Unlike Pursuits; SHPSS = Sense of Hyper-​Positive Self Scale; Brief QoL.BD = Brief Quality of Life in Bipolar Disorder; A = Adequate;
G = Good; E = Excellent; NA = Not Applicable.
182
182 Mood Disorders and Self-Injury
irritability, speech, thought disorder, content, aggressive
behavior, appearance, and insight, are rated on a sever-
ity scale of 0 to 4, and 4 items are given twice the weight
of other items. Total scores range from 0 to 60. In the
original study, the YMRS showed excellent inter-​rater reli-
ability for total scores (intraclass correlation = .93). The
YMRS is sensitive to changes in severity but may not be
suitable to assess hypomania, the milder form of mania
(Vieta, 2010). A  score on the YMRS greater than 25 is
suggestive of severe or marked illness (Lukascwiez, 2013).
The YMRS (as opposed to the parent-​ YMRS) has
also been used to measure manic symptoms in children.
When the YMRS was administered by a clinician com-
bining impressions from child and parent interviews, the
total YMRS score showed good validity in differentiating
bipolar disorder from attention-​deficit/​hyperactivity disor-
der (Fristad, Weller, & Weller, 1992, 1995; Serrano et al.,
2011)  and other diagnoses (Frazier et  al., 2007). The
YMRS still demonstrated good discriminative validity
when administered to children in a quicker and “unfil-
tered way” that did not differentiate chronic from episodic
symptoms nor account for symptom onset or duration
(Yee et al., 2015).
The Bech–​ Rafaelsen Mania Rating Scale (MAS;
Bech, Bolwig, Kramp, & Rafaelsen, 1979) is an 11-​item
rating scale. Each item is rated on a 5-​point scale (0–​4),
and the total score, ranging from 0 to 44, is obtained by
summing the items. Scores of 15 or higher are indicative
of mania. The MAS has been used in many different tri-
als of anti-​manic therapies due to its strong psychometric
characteristics (see Table 9.3). The scale has strong valid-
ity in detecting changes with treatment and discriminating
between active and placebo therapy groups (Bech, 2002).
The Schedule for Affective Disorders and
Schizophrenia-​Change Version (SADS-​C) for mania is
a 5-​item interview designed to assess current severity of
manic symptoms. Each item is rated on a 6-​point scale
based on behavioral anchors. Inter-​rater reliability esti-
mates have been reported in a range of settings, including
forensic settings (Rogers, Jackson, Salekin, & Neumann,
2003). One exception to a pattern of good inter-​reliability
results was found in a sample of patients referred for emer-
gency evaluation (intraclass correlation = .63 for mania;
Rogers et  al., 2003). The scale has been found to show
expected elevations within a bipolar sample compared
to patients with other psychiatric disorders, and it also
shows robust correlations with another interview to assess
manic severity, the MAS (r  =  .89; Johnson, Magaro, &
Stern, 1986). In factor analytic studies, all items load on a
single scale that is distinct from dysphoria, insomnia, and
psychosis (Rogers et  al., 2003). Nonetheless, less factor
analytic support was obtained in a study that considered
the item loadings for the SADS-​C and a nurse observation
scale for mania (Swann et al., 2001).
Self-​Report Measures
Several self-​report measures have been used to track
patients’ symptoms throughout the course of treatment.
Of these, only two have a broad range of supporting psy-
chometric evidence—​the Altman Self-​Rating Mania Scale
and the Self-​Rating Mania Inventory (see Table 9.3)—​with
others in development.
The Altman Self-​ Rating Mania Scale (ASRM;
Altman, Hedeker, Peterson, & Davis, 1997) consists of
five items. For each item, participants choose from a set
of five statements to best capture their feelings or behav-
ior during the past week. Each item is scored on a scale
of 0 (absent) to 4 (severe) so that total scores can range
from 0 to 20. Additional items assess psychosis and irri-
tability, but they are not included in the total score.
Grandiosity is not covered. Two studies have reported
comparable norms for the ASRM in patient samples
(Altman et  al., 1997; Altman, Hedeker, Peterson, &
Davis, 2001), but few data are available regarding scores
for nonpatients.
Scores on the ASRM have demonstrated adequate
internal consistency and concurrent validity compared
with several different reference standards, includ-
ing SADS-​based diagnoses, the YMRS (Young et  al.,
1978), and the Clinician-​Administered Rating Scale for
Mania (CARS-​M; Altman et  al., 1997, 2001; Altman,
Hedeker, Janicak, Peterson, & Davis, 1994). On the
basis of an area under the curve analysis (Hanley &
McNeil, 1982), Altman and colleagues concluded
that a cut-​off score of 5.5 resulted in an optimal com-
bination of sensitivity and specificity (85% and 86%,
respectively), although this cut-​off might result in lower
specificity (Altman et al., 2001). Finally, the ASRM has
demonstrated good sensitivity to treatment, with scores
dropping an average of 5 points after discharge from
the hospital in one study (Altman et al., 2001). Overall,
the ASRM has demonstrated good psychometric prop-
erties. However, the scale covers fewer symptoms com-
pared to other mania indices.
The Self-​ Report Manic Inventory (SRMI; Braünig,
Shugar & Kruger, 1996; Shugar, Schertzer, Toner, & Di
Gasbarro, 1992) is a 47-​item true/​false inventory covering
a range of manic symptoms, with one additional item cov-
ering insight. Expert clinicians reviewed each item during
 183
the development phase. In its original design, the time
frame for items was the past month; later editions assessed
symptoms during the previous week. Normative data have
been reported for the SRMI in three small studies of inpa-
tients, and it has demonstrated good internal consistency
(Altman et al., 2001; Braünig et al., 1996; Shugar et al.,
1992). Two studies have found that the scale differenti-
ates people with bipolar disorder from those with other
psychopathologies (Braünig et  al., 1996; Shugar et  al.,
1992), although one other study found the SRMI to have
low concurrent validity (Altman et  al., 2001). The scale
appears sensitive to change in symptoms, but eight of the
SRMI items capture behaviors that would not be possible
within a hospital setting (Altman et al., 2001). Hence, it
has been argued that the content of the scale may not be
well-​suited to inpatient assessment.
The Internal State Scale (ISS; Bauer et  al., 1991)  is
a 17-​item scale designed to assess the severity of manic
and depressive symptoms. Of its four subscales, only the
5-​item activation subscale has correlated significantly
with mania ratings. These items were designed to cover
behavioral activation (e.g., restlessness and impulsivity)
but not other mania symptoms (e.g., euphoria). The ISS
also does not assess some other behavioral symptoms that
are characteristic of mania, such as decreased sleep or
rapid speech (Altman et al., 2001). The ISS has demon-
strated correlations with other measures of mania ranging
from .21 to .60 and rates of correct classification ranging
from .55 to .78 (Altman et al., 2001; Bauer et al., 1991;
Bauer, Vojta, Kinosian, Altshuler, & Glick, 2000; Cooke,
Krüger, & Shugar, 1996). The ISS has demonstrated sen-
sitivity to treatment change, in that scores diminish appre-
ciably post-​treatment (Altman et  al., 2001; Bauer et  al.,
1991; Cooke et al., 1996). Despite these strengths, scor-
ing algorithms have varied substantially across studies, as
have means and standard deviations (Altman et al., 2001;
Bauer et al., 1991; Cooke et al., 1996). The scale has also
been found to have a low sensitivity to manic symptoms
at the time of hospitalization (Altman et al., 2001). Given
these concerns, the ISS is not currently recommended.
There is a growing literature that demonstrates that
people with bipolar disorder set high goals and focus on
achievement independent of mood state, and these may
be important to assess in the context of treatment plan-
ning and outcome. The Willingly Approached Set of
Statistically Unlike Pursuits scale (WASSUP; Johnson &
Carver, 2006) is a self-​report measure designed to assess
highly ambitious life goals. Thirty items assessing high
goals in the seven domains of popular fame, friendships,
world well-​ being, political influence, family, financial
Bipolar Disorder 183
success, and creativity are rated from 1 (no chance I will
set this goal for myself) to 5 (definitely will set this goal for
myself). Persons at risk for mania and people diagnosed
with bipolar spectrum disorder show consistent elevations
on the Popular fame and Financial success subscales,
and elevations on these two subscales predicted manic
symptoms over time (Carver & Johnson, 2009; Johnson &
Carver, 2006; Fulford, Johnson, & Carver, 2008; Gruber
& Johnson, 2009; Johnson & Jones, 2009). WASSUP
scores have been shown to decrease in a pilot trial of a
cognitive–​ behavioral treatment focused on preventing
mania in bipolar patients by directly addressing goal dys-
regulation, including overly ambitious goals (Johnson &
Fulford, 2009).
Individuals with bipolar disorder who are likely to set
unrealistically high goals may also view themselves in a
distinct way, and this may influence how they respond to
psychosocial treatment. The Sense of Hyper-​Positive Self
Scale (SHPSS; Lam, Wright, & Sham, 2005) assesses pos-
itive attributes that bipolar patients believe they possess
when their mood state is mildly “high.” These include
confident, dynamic, adorable, entertaining, outgoing,
optimistic, and creative and are rated on a 7-​point scale
from 1 (not at all) to 7 (extremely) as to (a) how well these
words describe the patient most of the time and (b) ideally
how the patient would like him-​or herself to be. High
scores on this scale identify positive mood, increased
arousal, and increased behavioral activation characteris-
tic of mild elation and distinct from clinical hypomania
or mania. Scores on the scale have demonstrated good
internal reliability and test–​ retest reliability. Patients
who value and perceive themselves as possessing these
attributes demonstrated a poorer response to cognitive
therapy in the absence of a relationship between SHPSS
scores and current manic symptom scores (Lam, Wright,
& Sham, 2005).
Although symptom measures are the primary outcomes
typically seen in studies of bipolar disorder, inclusion of
measures of quality of life may provide a richer picture of
the patient and be a useful tool for both treatment plan-
ning and assessment of treatment outcomes (Murray &
Michalak, 2012). Given the growing evidence that people
with bipolar disorder experience severe decline in qual-
ity of life and recognizing a need for a disorder-​specific
assessment, Michalak and Murray (2010) developed a
quality of life measure drawn from both qualitative inter-
views with bipolar patients, caregivers, and research and
treatment experts and literature review. The QoL.BD
assesses 14 domains during the prior 7 days using a 5-​point
Likert scale ranging from strongly disagree (1) to strongly
184
184 Mood Disorders and Self-Injury
agree (5). The domains assessed include physical, sleep,
mood, cognition, leisure, social, spirituality, finances,
household, self-​esteem, independence, identity, and the
optional domains of work and education. The brief form
of the scale draws one item from each domain and dem-
onstrated moderate to large correlations with the 12 basic
scales of the QoL.BD.
Finally, clinicians should bear in mind that naturalis-
tic studies suggest that people with bipolar disorder experi-
ence at least some depressive symptoms one-​third of the
weeks in a year (Judd et al., 2002). Higher risk of suicide
has been documented during depression within bipolar
disorder (Angst, Angst, Gerber-​Werder, & Gamma, 2005).
Given this, it is recommended that clinicians track not
only manic symptoms but also depression and suicidality.
Overall Evaluation
Ideally, outcome assessments should incorporate both
interview and self-​report measures. Clinicians have several
interview-​based measures available for tracking change in
symptoms over time:  the SADS-​C, the YMRS, and the
MAS. Although more data are available to support the
YMRS and the MAS, the SADS-​C has the advantage of
brevity. Self-​report measures such as the ASRM and the
SRMI can also be completed quickly. This brevity and
ease of use can come with the price, however, of reduced
precision. To track progress, many clients find it help-
ful to create their own self-​monitoring forms or to com-
plete brief checklists. Comparing results of the interview
with self-​reported symptoms can be helpful for clients in
building a greater awareness of symptoms. As treatment
progresses, clients often find it helpful to begin to attend
to smaller fluctuations in symptoms, such that they can
implement early intervention strategies to promote calm
and good medical care before symptoms intensify (Lam &
Wong, 2005). Given the common problems with insight
within this disorder, research is needed on how best to
integrate self and clinician ratings of manic symptoms.
Beyond traditional symptom measures, examining ten-
dencies toward highly ambitious goal setting, sense of
hyper-​positive self, and quality of life may provide for a
richer picture of patients and prove to be useful assess-
ments for treatment planning and outcome.
CONCLUSIONS AND FUTURE DIRECTIONS
In this chapter, we have considered assessment tools
that are effective or promising in diagnosis, treatment
planning, and treatment outcome monitoring of bipolar
disorder. In evaluating current measures, the need for
ongoing research is quite apparent. In regard to diagnos-
tic assessment, there is ongoing discussion about the req-
uisite severity and duration of symptoms for hypomania.
Similarly, substantial debate exists concerning the best
criteria for the diagnosis of bipolar disorder among chil-
dren and adolescents. Hence, diagnostic instruments are
likely to be modified over time to increase their applica-
bility for milder forms of the disorder and for younger age
groups. Beyond the need for better diagnostic measures,
there is a fundamental need for research on the pre-
dictors of outcome within psychological forms of treat-
ment. Measures that could help define the best choice
of therapy would be extremely helpful for clinicians.
Finally, there is a need for measures that are specifically
developed to capture the types of social dysfunctions that
are most prevalent in bipolar disorder. Although many
researchers apply social functioning measures developed
for depression and schizophrenia, it will be important to
consider ways in which manic symptoms can damage
relationships.
Currently, however, several excellent resources for
assessment of bipolar disorder are available. For diagno-
sis, the SCID and the SADS allow for reliable and valid
diagnosis of bipolar I disorder. For case conceptualization
and treatment planning, the SAI-​E predicts medication
nonadherence in bipolar disorder, and the Life Chart
can help assess the history of episodes and triggers. The
SHPSS, although relatively new, has predicted outcomes
of cognitive therapy in one study. Once treatment com-
mences, interview measures such as the YMRS and the
MAS, as well as self-​report measures such as the ASRM
and the SRMI, are available for monitoring symptom
severity. We hope that this review stimulates clinical use of
the available measures and encourages research focused
on addressing the gaps in the assessment literature.
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10
Self-​Injurious Thoughts and Behaviors
Alexander J. Millner
Matthew K. Nock
Self-​injurious thoughts and behaviors (SITB) are an enor-
mous global public health problem. Suicide is a leading
cause of death worldwide (Lozano et al., 2012), and cross-​
national studies estimate that the prevalence of nonlethal
SITBs ranges from 3% to 9% (Nock, Borges, et al., 2008).
Given the possibility of death associated with SITB and
that nearly all mental health clinicians will assess and
treat patients with suicidal thoughts and behaviors during
their career (Dexter-​Mazza & Freeman, 2003; Kleespies,
Penk, & Forsyth, 1993), it is crucial that SITB assessment
instruments have a strong evidence base.
In this chapter, we provide basic background informa-
tion on the assessment of SITB and summarize the evi-
dence supporting instruments that assess SITB. Note that
assessment of suicide risk—​determining the likelihood that
a person will actually try to kill him-​or herself in the near
future—​is an overlapping but distinct process. An impor-
tant part of determining suicide risk is the direct assessment
of SITB history, presence, and severity using measures with
empirical support. This chapter provides guidance in the
selection of an instrument for determining risk. However,
suicide risk assessment also includes the consideration of
other factors (e.g., hopelessness and impulsiveness) associ-
ated with suicidal behaviors that are beyond the scope of
this chapter. For readers interested in suicide risk assess-
ment, we provide several useful sources containing guide-
lines and practical recommendations in the context of
clinical care (Berman & Silverman, 2014; Fowler, 2012;
Jacobs et al., 2010; Silverman & Berman, 2014).
This chapter builds on the chapter with the same title
from the first edition of this volume (Nock, Wedig, Janis,
& Deliberto, 2008)  by updating the psychometric evi-
dence for the instruments included in the first edition and
introducing and evaluating several recently established
193
interviews to assess SITB. To provide context, the chap-
ter begins with a discussion of two fundamental issues in
the assessment of SITB: classification and measurement.
We also discuss prevalence and conditional probability of
the behaviors as well as the goals and challenges of SITB
assessment. We then review instruments appropriate for
determining the presence and frequency of SITB, case
conceptualization and treatment planning, and treat-
ment monitoring and outcome evaluation. In our review,
we (a)  separate measures suitable for assessing children
and adolescents from those for assessing adults, (b) state
precisely which thoughts and behaviors each measure
assesses (e.g., suicidal thoughts and nonsuicidal self-​injury
[NSSI]), and (c) make recommendations based on which
instruments have the strongest empirical support.
NATURE OF SITB
Classification and Measurement
SITB consists of a broad array of thoughts and behaviors
that involve imagined or actual intentional physical injury
to one’s body. During the past several decades, one of the
major obstacles facing research and clinical practice has
been the lack of a consistent classification of SITB. In
many instances, people failed to distinguish among distinct
behaviors—​for example, referring to suicidal and nonsui-
cidal behaviors collectively as “deliberate self-​harm” or com-
bining suicidal thoughts and behaviors under the umbrella
term “suicidality.” Fortunately, these practices have largely
been abandoned following the publication of consensus
articles (Silverman, Berman, Sanddal, O’Carroll, & Joiner,
2007)  and the introduction of new classification systems
194
194 Mood Disorders and Self-Injury
and measurement strategies. For example, beginning in
the early 2000s, pertinent classification systems were imple-
mented in U.S. government agencies, such as the U.S. Food
and Drug Administration (FDA), the Centers for Disease
Control and Prevention, and the Department of Defense
(Brenner et  al., 2011; Posner, Oquendo, Gould, Stanley,
& Davies, 2007; FDA, 2012). Although largely similar, the
classification systems across these agencies contain some
minor differences (Matarazzo, Clemans, Silverman, &
Brenner, 2013), and despite the clear advancement in this
area, they continue to receive criticism (Sheehan, Giddens,
& Sheehan, 2014b). The particular issues regarding classi-
fication and measurement systems are beyond the scope of
this chapter, but they generally hinge on the level of granu-
larity with which behaviors should be classified (Sheehan,
Giddens, et al., 2014b).
In general, consensus classification makes a distinc-
tion between suicidal self-​injury, in which people have
some intent (i.e., non-​zero) to die from their behavior,
and nonsuicidal self-​injury, in which people injure them-
selves with no intent to die. Within suicidal self-​injury,
there are three major categories:  suicidal ideation (i.e.,
thoughts), which refers to thinking about engaging in a
behavior to end one’s life; suicide plan, which includes
thinking about how (i.e., method) and where (i.e., place)
one intends to injure oneself; and suicide attempt, which
refers to engaging in a potentially harmful or lethal behav-
ior with some intention of dying from the behavior.
More recently, researchers and clinicians have defined
a spectrum of more subtle suicidal thoughts and behav-
iors as well, including passive suicidal ideation, which
includes thoughts such as wishing one were dead; pre-
paratory behaviors, which include actions either to pre-
pare for one’s suicide attempt (e.g., obtaining a gun) or
to prepare for the possibility that one might be dead soon
(e.g., preparing a will); aborted attempt, in which people
take steps to attempt suicide but stop themselves prior to
engaging in a potentially harmful or lethal behavior; and
interrupted attempt, in which someone or something pre-
vents a person from attempting suicide. Another behav-
ior that is related to suicidal behaviors but is considered
a nonsuicidal behavior is a suicide gesture, in which a
person carries out an action to give the appearance of a
suicide attempt for some purpose (e.g., to communicate
pain) but with zero intention of dying.
Currently, most suicidal behaviors have consensus
definitions with one important exception: a suicide plan
(Millner, Lee, & Nock, 2017). As stated previously,
a suicide plan consists of, at the very least, formulating
a method, but there is no settled definition (e.g., Does a
plan require thinking of a place and/​or a time to attempt
suicide?). Some have differentiated between a “plan” and
a “specific plan,” with the latter defined as “details of a
plan fully or partially worked out,” but there is no precise
operationalization (Posner et al., 2011).
One problem with poor operationalization is that it can
lead to inaccurate measurement. For example, one study
that examined the use of a single-​item question to assess
the presence of a suicide plan among people who had
thought about suicide but never made a suicide attempt
found that 40% of those who denied having a plan had
engaged in at least four out of five planning steps (e.g.,
settling on a method and settling on a place to attempt
suicide) compared with 52% among those who endorsed
having a plan (Millner, Lee, & Nock, 2015). These results
suggest respondents’ interpreted the term “suicide plan”
inconsistently, questioning the validity of suicide planning
items (similar problems exist for other aspects of SITB,
such as the presence of “suicidal intent”).
Similar measurement problems can occur for terms
with consensus definitions if respondents or questioners
(e.g., interviewers or clinicians) do not clearly under-
stand the criteria for the behavior in question or there is
no option for a behavior in which a respondent engaged
(e.g., no item for aborted attempts). Studies have reported
that when participants answer a single question regard-
ing the presence or absence of a past suicide attempt,
10% to 40% incorrectly endorse making a prior attempt
(Hom, Joiner, & Bernert, 2015; Millner et al., 2015; Nock
& Kessler, 2006; Plöderl, Kralovec, Yazdi, & Fartacek,
2011). In addition to inaccurate endorsement of past sui-
cide attempts, prior research has also found that among
people with suicide ideation, 10% deny having made a
suicide attempt even though their description of a prior
behavior fits the definition of a suicide attempt (Millner
et al., 2015). This problem extends to clinical settings, in
which researchers found that medical notes incorrectly
labeled a behavior as a suicide attempt 6% of the time
and failed to identify a suicide attempt 18% of the time
(Brown, Currier, Jager-​Hyman, & Stanley, 2015).
Millner et  al. (2015) found that classification can be
improved by (a) increasing the clarity of the question (e.g.,
asking “Have you ever engaged in a potentially harmful or
lethal behavior with some intention of dying?” rather than
asking “Have you ever tried to kill yourself?”) and (b) increas-
ing the coverage by providing several thoughts or behaviors
that people can choose from (e.g., asking about NSSI, sui-
cide gestures, aborted and interrupted attempts, as well as
attempts). For interview-​based assessments, it is important
that assessors are trained in the definitions of different terms
 195
to accurately classify behavior. The government agency clas-
sification systems discussed previously can aid with train-
ing, and some instruments, such as the Columbia-​Suicide
Severity Rating Scale (Posner et al., 2011), offer free web-​
based trainings (http://​cssrs.columbia.edu).
Note that these measurement problems are unlikely
to be resolved by the standard practice of testing valid-
ity because most studies validate instruments using other
measures with similar wording. For example, a measure
that inquires about prior “suicide attempts” is frequently
validated with another measure that assesses the same
outcome with the same terminology. Given these cir-
cumstances, it would be surprising if scales using similar
terms (“suicide attempt”) and measuring similar or identi-
cal outcomes were uncorrelated. However, strong valid-
ity metrics alone do not necessarily indicate an absence
of the types of measurement error discussed previously.
Research into misclassification and its reduction is very
recent, and continued work in this area will help improve
the validity and reliability of the assessment of SITB.
Prevalence and Conditional Probability
The prevalence of SITB is important to consider dur-
ing assessment. Studies with large-​scale, representative
samples suggest that the prevalence of suicidal ideation,
plans, and attempts within the United States is 16%, 5%,
and 5%, respectively (Nock, Borges, et  al., 2008). In a
cross-​national study of people from 17 different countries
throughout the world, these estimates are 9%, 3%, and 3%,
respectively (Nock, Borges, et al., 2008). Most people who
attempt suicide have thought about suicide prior to their
attempt, and many have made a plan as well. Therefore, it
is useful to understand the rates at which people transition
from one behavior to more severe SITB. Among people
who think about suicide, 34% will make a suicide plan,
and 29% will make a suicide attempt. Among those with a
plan, 56% will make a suicide attempt. Importantly, most
people who transition to a plan or an attempt do so within
the first year after the onset of suicide ideation (Nock,
Borges, et al., 2008).
The prevalence of NSSI is unknown because represen-
tative epidemiological studies have not included this behav-
ior. Furthermore, rates of NSSI vary depending on how it is
assessed; checklists of differing behaviors elicit higher rates
than does a single-​item question (Swannell, Martin, Page,
Hasking, & St. John, 2014). After taking into account assess-
ment approach and other methodological considerations, a
recent meta-​analysis examining cross-​national, fairly large-​
scale (although not truly representative) studies among
Self-Injurious Thoughts and Behaviors 195
nonclinical samples reported NSSI rates of 17.2% among
adolescents, 13.4% among young adults, and 5.5% among
adults (Swannell et al., 2014). Rates reported by studies con-
ducted in U.S. samples vary widely but are generally con-
sistent with cross-​national rates (Jacobson & Gould, 2007;
Klonsky, 2011; Whitlock, 2010; Whitlock, Eckenrode, &
Silverman, 2006).
Purposes of Assessment
Although there is no official diagnosis for SITB, the fifth
edition of the Diagnostic and Statistical Manual of Mental
Disorders (DSM-​ 5; American Psychiatric Association,
2013) provisionally established suicidal behaviors disorder
and NSSI disorder as conditions that require further study.
A  small number of studies have started to investigate the
clinical utility and validity of these disorders, but currently,
assessment is not intended to establish the presence of diag-
nosis. Instead, the primary purpose of assessment of SITB
is to determine (a) the presence or absence of SITB itself;
(b) characteristics of SITB, such as frequency and severity;
and (c) whether SITB change over time and, if so, how.
Compared with the first edition of this chapter, we have
altered the inclusion criterion to review measures in
which the majority of items assess SITB outcomes or
aspects of SITB (frequency, severity, functions, etc.). For
example, scales such as the Suicide Probability Scale,
which has 6 items that assess suicidal ideation and 30
items that assess potential SITB risk factors such as hope-
lessness and hostility, are excluded from this chapter. We
selected this inclusion criterion because of the large num-
ber of scales measuring the same outcomes and several
new scales focused on assessing multiple SITB exclu-
sively. We provide tables in which we rate each measure
on several psychometric categories based on the evidence
for each measure and guidelines provided by the editors
of this volume (see Chapter 1).
Assessing SITB
We recommend that the direct assessment of SITB be
included within any comprehensive clinical interview
(e.g., intake or discharge interview) to all patients, even
those who appear to be low risk. Often, people who
lack key risk factors still engage in SITB. We further
emphasize the need for direct expression of SITB or self-​
injurious intentions and recommend that clinicians not
judge SITB risk based on ancillary “warning signs,” such
as giving things away, which lack empirical support (Rudd
et al., 2006).
196

196 Mood Disorders and Self-Injury

Table 10.1a  Ratings of Instruments Used for Assessing SITB in Adults

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Adults
Structured and Semi-​Structured Interviews
SITBI G NA E A G A G A ✓
SASII A G E E A G A G ✓
C-​SSRS G G G NR G G E G ✓
S-​STS G G NR G G A G G ✓
SSI G G NR G E E E ✓
SSI-​W NR G G A G E G A ✓
MSSI NR G E L G E G E ✓
Self-​Report Measures
BSI A E NA A G E A G ✓
ASIQ NR E NA A NR E E A
SIS NR G NA NR A A A A
SBQ NR G NA A NR A A G ✓
SBQ (4-​items) NR G NA A NR G G G ✓
SBQ-​R NR E NA A NR G G G ✓
SHBQ NR G NA A A G L A
DSHI NR G NA G A A A A
SHI A A NA NR A G A A

Note: SITBI  =  Self-​Injurious Thoughts and Behaviors Interview; SASII  =  Suicide Attempt Self-​Injury Interview; C-​SSRS  =  Columbia-​Suicide
Severity Rating Scale; S-​STS  =  Sheehan-​Suicidality Tracking Scale; SSI  =  Scale for Suicide Ideation; SSI-​W  =  Scale for Suicide Ideation-​Worst;
MSSI = Modified Scale for Suicide Ideation; BSI = Beck Scale for Suicide Ideation; ASIQ = Adult Suicide Ideation Questionnaire; SIS = Suicide Ideation
Scale; SBQ  =  Suicidal Behaviors Questionnaire; SBQ-​R  =  Suicidal Behaviors Questionnaire-​Revised; SHBQ  =  Self-​Harm Behavior Questionnaire;
DSHI = Deliberate Self-​Harm Inventory; SHI = Self-​Harm Inventory; L = Less Than Adequate; A = Adequate; G = Good; E = Excellent; NR = Not
Reported; NA = Not Applicable.

There is a natural concern that the direct assessment
of SITB will increase the risk of the person actually engag-
ing in SITB. There is a robust literature, including three
randomized controlled trials, suggesting that there are
no harmful effects of assessing SITB, such as an increase
in suicidal ideation or suicide risk (Gould et  al., 2005;
Harris & Goh, 2017; Husky et al., 2014; Law et al., 2015).
Nevertheless, discussing SITB is a sensitive topic, and we
recommend that clinicians start with less sensitive (e.g., a
history of depression) and less severe constructs (e.g., his-
tory of suicidal ideation) before moving on the more severe
behaviors (e.g., attempts). Next, we review the wide array
of instruments available to assess the presence of SITB.
The psychometric ratings for these instruments are pre-
sented in Tables 10.1a for adults and 10.1b for children and
adolescents.
MEASURES FOR USE WITH ADULTS
Structured and Semi-​Structured Interviews
Although some instruments are referred to as structured
interviews (Linehan, Comtois, Brown, Heard, & Wagner,
2006; Nock, Holmberg, Photos, & Michel, 2007), instruc-
tions included with these scales generally require that
interviewers are knowledgeable about classification of
SITB and encourage interviewers to probe with unstruc-
tured follow-​up questions to clarify details of a behavior in
question in order to ensure accurate measurement. Given
these circumstances, we do not distinguish among struc-
tured and semi-​structured interviews in this section.
The Self-​Injurious Thoughts and Behaviors Interview
(SITBI; Nock et al., 2007) is a structured interview (long
form:  169 items; short form:  72 items) that assesses the
presence of several SITB, including suicidal ideation,
plans, and attempts as well as NSSI. In 2010, the interview
was modified to include interrupted and aborted attempts
as well as to assess knowledge of others with a suicide his-
tory; however, the reliability and validity of these items
have not been tested. If the respondent endorses the life-
time presence of an outcome, the interviewer enters a lon-
ger module to assess the age of onset, frequency, severity,
methods used, function of the behavior, degree to which
external stressors (e.g., “work/​school” or “relationships”)
or internal stressors (e.g., “mental state”) contributed to
the behavior, use of alcohol or drugs, experience of pain,
 197

Self-Injurious Thoughts and Behaviors 197

Table 10.1b  Ratings of Instruments Used for Assessing SITB in Children and Adolescents

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Child/​Adolescent
Structured and Semi-​Structured Interviews
SITBI G NA E A G A G A ✓
SSI NR G NR NR E G G G ✓
SBI NR E E NR G A G A
CSPS NR A E NR A G E A ✓
Self-​Report Measures
BSI A E NA NR E G A G ✓
SBQ-​R NR G NA A NR A NR A
SIQ E G NA A A G G G ✓
SIQ-​JR E G NA A A G G G ✓
HASS NR E NA NR A G A A

Note: SITBI = Self-​Injurious Thoughts and Behaviors Interview; SSI = Scale for Suicide Ideation; SBI= Suicide Behaviors Interview; CSPS = Child
Suicide Potential Scales; BSI  =  Beck Scale for Suicide Ideation; SBQ-​R  =  Suicidal Behaviors Questionnaire-Revised; SIQ  =  Suicidal Ideation
Questionnaire; SIQ-​JR  =  Suicidal Ideation Questionnaire Junior; HASS  =  Harkavy–​Asnis Suicide Scale; A  =  Adequate; G  =  Good; E  =  Excellent;
NR = Not Reported; NA = Not Applicable.

or impulsiveness of the SITB. Respondents are also asked
to predict the likelihood they will engage in the behavior
again in the future. The authors of the SITBI state that
the interview is to be administered exactly as worded but
that trained interviewers may use follow-​up questions to
clarify behaviors. Thus, to ensure accurate measurement,
interviewers require several hours of training and ongoing
supervision to be adequately knowledgeable about catego-
ries of SITB. Furthermore, note that the excellent inter-​
rater reliability metrics stated in the following discussion
occurred in the context of well-​trained and supervised
interviewers. Administration requires 3 to 75 minutes
depending on the number of modules administered.
The one study that tested the reliability and validity of
the English version of the SITBI among young adults and
adolescents (aged 12–​19  years) reported excellent inter-​
rater reliability and adequate test–​retest reliability for the
presence of each self-​injurious outcome assessed during a
6-​month period (Nock et al., 2007). In addition, foreign
language versions of the SITBI have also shown strong psy-
chometric properties (Fischer et al., 2014; García-​Nieto,
Blasco-​ Fontecilla, Paz Yepes, & Baca-​ García, 2013).
Multiple sections of the SITBI have been converted into
a self-​report form, but the psychometric properties have
not been assessed (Bryan & Bryan, 2014; Muehlenkamp,
Walsh, & McDade, 2010).
The Suicide Attempt Self-​ Injury Interview (SASII;
Linehan, Comtois, Brown, et  al., 2006)  is a structured
interview with 31 items that assesses in-​ depth charac-
teristics of and motivations for a self-​injurious event (or
“cluster” of events). For each episode, the following are
assessed:  intent and outcome expectation of the self-​
injury, method used, degree to which the action was
impulsive, lethality, medical consequences of the injury
and treatment, communication of self-​injurious intent,
context, function, and other mental characteristics (e.g.,
being “disconnected from feelings”). The SASII focuses
on the circumstances around an event in which self-​injury
actually occurred and does not assess suicidal thoughts or
plans unrelated to a self-​injurious event, interrupted or
aborted attempts, or suicide gestures.
The SASII is intended to assess detailed characteris-
tics for each self-​injurious event that a respondent can
remember and therefore is comprehensive but potentially
time-​intensive if the respondent has an extensive history of
self-​injury. Alternatively, one can choose to cover the self-​
injury history within a given time period. Scores on the
SASII show excellent inter-​rater reliability and adequate
validity metrics. Similar to the SITBI, interviewers should
state the questions as worded but are encouraged to ask
follow-​up questions to obtain specific details or clarify a
response (Bland & Murray-​Gregory, 2006). Given that
interviewers are instructed to use clinical judgment, they
should be trained to ensure that they collect valid data.
The Columbia-​ Suicide Severity Rating Scale (C-​
SSRS; Posner et al., 2011) is a semi-​structured interview
that assesses the presence of lifetime SITB. The first sec-
tion contains five suggested prompts to assess suicidal
mental states (i.e., ideation, plans, and intent), ordered
in increasing severity, starting with passive ideation (e.g.,
198
198 Mood Disorders and Self-Injury
“I wish I was dead”) and ending with active ideation with
a specific plan and intent to act. The second section
assesses the frequency, intensity, controllability, and deter-
rents of suicidal ideation as well as reasons for ideation.
In the final section, the interviewer assesses the pres-
ence and frequency of suicide attempts, interrupted and
aborted attempts, preparatory actions, and, finally, if there
was a suicide attempt, the actual and potential lethality.
Response options for most items are yes/​no, although ide-
ation is rated on a 1 to 5 scale, depending on the number
of items endorsed in the first section. Items assessing fre-
quency are free response, and each item in the second
section has a unique response scale.
The C-​SSRS scores have been found to have high
internal consistency and moderate to good convergent
validity for each section. In addition, a “since last visit”
version (which was used in studies assessing SITB out-
comes every 4–​6 weeks) shows strong convergent validity
and sensitivity to change. There is also an electronic ver-
sion of the C-​SSRS (eC-​SSRS; Mundt et al., 2010) that
yields scores with adequate reliability and good conver-
gent and predictive validity (Greist, Mundt, Gwaltney,
Jefferson, & Posner, 2014; Mundt et  al., 2013). In addi-
tion, there are other versions of the C-​SSRS, including
a pediatric form, and several screeners that contain con-
densed versions of the sections, although no psychometric
evidence is available for these alternative versions. The
authors of the C-​SSRS provide several options for training
on scale administration. In addition, the measure provides
definitions for each SITB in question. The scale provides
questions to be helpful guidelines, but emphasis is placed
on gathering enough information to correctly classify the
behavior rather than precisely reading specified questions.
Studies have found that the C-​SSRS takes between 5 and
11 minutes to administer (Sheehan, Alphs, et al., 2014).
Finally, it is worth noting that the FDA and other govern-
ment agencies endorse the C-​SSRS as a scale for clinical
trials.
The Sheehan-​ Suicide Tracking Scale (S-​ STS;
Sheehan, Giddens, & Sheehan, 2014a) is a structured
interview (although there is an identical self-​report ver-
sion as well) with 16 items that assess a wide range of
SITB, including “accidental” overdoses, several forms of
passive ideation (within a single question), active ideation,
suicidal command hallucinations, specific planning steps,
intention to act on suicidal thoughts, intention to die from
the act itself, feeling an impulse to kill oneself, preparatory
actions, NSSI, and suicide attempts. Each item is rated on
a scale from 0 (not at all) to 4 (extremely), and some items
collect frequency information. Although interrupted
and aborted attempts are not explicitly assessed, they are
inferred through a combination of selecting a time to
attempt suicide and taking active steps to prepare for an
attempt, although this has been found to result in impre-
cise measurement (Youngstrom et  al., 2015). In some
studies, the authors of the S-​STS used computerized self-​
report and clinician interview assessments in which, at the
conclusion of the interview, the clinician was alerted to
deviations between the interview and self-​reported rating.
The clinician and patient then returned to those items
and continued the interview until those items were rec-
onciled (Sheehan, Alphs, et al., 2014; Sheehan, Giddens,
et al., 2014a).
The main study evaluating the reliability and valid-
ity of the S-​STS was conducted with a sample of young
Italian adults on an 8-​item earlier version of the scale with
questions that were similar but not identical to those of
the 16-​item version (Preti et al., 2013; Sheehan, Giddens,
et al., 2014a). In the 8-​item version, scores on the section
assessing ideation and also the global score obtained by
adding all items showed acceptable internal consistency
and test–​rest reliability. Scores on the section assessing
just suicidal behaviors showed acceptable internal consis-
tency but moderate to poor test–​retest reliability. S-​STS
sections showed acceptable convergent and criterion
validity as well. The S-​STS has a patient-​rated version,
a clinician-​rated version, and a “clinically meaningful
change measure” version, and all versions have flexibility
regarding the time period assessed. The authors recom-
mend that interviewers are trained in the definitions of
suicidal behaviors similar to those used in the C-​CASA
classification system. Interviewers are encouraged to use
data from all available sources. The administration time
is 4 to 13 minutes for the S-​STS self-​report scale, 3 to 15
minutes for the S-​STS interview, and 1.5 to 3.5 minutes
for the reconciliation form (Sheehan, Alphs, et al., 2014).
The Scale for Suicide Ideation (SSI; Beck, Kovacs, &
Weissman, 1979)  is a 21-​item semi-​structured interview
that assesses past week thoughts of suicide. The SSI mea-
sures different aspects of suicidal ideation (e.g., presence,
frequency, and severity) as well as reasons for suicide,
planning, and the presence and intent of prior attempts.
All items are rated on unique 0 to 2 scales, and the first
19 items (excluding items regarding prior attempts) are
summed to determine a total score. Administration takes
approximately 10 minutes. The SSI has been validated
across a wide array of samples, including adolescents
(Holi et  al., 2005), adults (Beck et  al., 1979), older
adults (Witte et  al., 2006), and diverse racial and ethnic
groups (Beck et  al., 1979), as well as within clinical
 19
settings (Vuorilehto, Melartin, & Isometsä, 2006). Given
the widespread use and psychometric evidence, we rec-
ommend the SSI as a general measure to assess suicidal
ideation.
The Scale for Suicide Ideation-​Worst (SSI-​W; Beck,
Brown, & Steer, 1997) is identical to the SSI but partici-
pants should rate items within the context of their most
severe suicidal ideation (i.e., their “worst point”). Scores
on the SSI-​W have been reported to have good internal
consistency and inter-​rater reliability, and importantly,
the SSI-​W is predictive of suicide attempts and suicide
death (Beck et al., 1997; Beck, Brown, Steer, Dahlagaard,
& Grisham, 1999; Joiner et al., 2003).
The Modified Scale for Suicidal Ideation (MSSI), is
an altered version of the SSI that assesses different aspects
of suicidal ideation (13 of 18 items are from the original
SSI), has increased ratings range, provides standardized
prompts, and utilizes screening items (Miller, Norman,
Bishop, & Dow, 1986). Scores on the MSSI have good to
excellent reliability, and the measure has shown good con-
vergent and divergent validity (Clum & Yang, 1995; Joiner
et  al., 2005; Joiner, Rudd, & Rajab, 1997; Miller et  al.,
1986; Pettit et al., 2009; Rudd, Joiner, & Rajad, 1996).
Self-​Report Measures
Batterham and colleagues (2015) provide a comprehen-
sive review of easy-​to-​administer, self-​report measures that
assess suicidal SITB within adults for use in population-​
based research. The PhenX Toolkit also provides recom-
mended instruments to assess SITB and related risk factors
for epidemiological studies (Suicide Specialty Collection
at https://​www.phenxtoolkit.org; PhenX Toolkit Suicide
Workgroup, 2014).
The Beck Scale for Suicidal Ideation (BSI, BSS, or
BSSI; Beck & Steer, 1991)  is a self-​report version of the
SSI. Like the SSI, it contains 21 items, each of which is
rated on a 0 to 3 scale. It has been found to have excellent
internal consistency, good construct validity (Beck, Steer,
& Ranieri, 1988), and other beneficial psychometric fea-
tures (de Beurs, Fokkema, de Groot, de Keijser, & Kerkhof,
2015). The BSI has been used across clinical and research
settings (Healy, Barry, Blow, Welsh, & Milner, 2006).
The Adult Suicide Ideation Questionnaire (ASIQ;
Reynolds, 1991a) contains 25 items assessing passive and
active suicidal ideation, intent, social aspects of suicide,
and planning steps. Scores on the ASIQ have shown good
reliability across multiple populations, such as college
students (Reynolds, 1991b), adults in the general popu-
lation (Reynolds, 1991a), adult outpatients (Reynolds,
Self-Injurious Thoughts and Behaviors 199
1991a), and psychiatric patients (Horon, McManus,
Schmollinger, Barr, & Jimenez, 2013; Osman et  al.,
1999). In one study, the ASIQ predicted suicide attempts
over a 3-​month period (Osman et al., 1999).
The Suicide Ideation Scale (SIS; Rudd, 1989)  con-
tains 10 items and assesses the presence and intensity
of suicidal ideation as well as suicide attempt history.
Substantial evidence for the reliability and validity of the
SIS scores has been supported in a college sample (Rudd,
1989)  and in a military clinical sample (Luxton, Rudd,
Reger, & Gahm, 2011).
The Suicidal Behaviors Questionnaire (SBQ;
Linehan, 1981)  is a 34-​item measure to assess the pres-
ence and frequency of suicidal ideation, attempts, and
NSSI. Scores from the SBQ have good to excellent reli-
ability and supported validity (Linehan, Camper, Chiles,
Strosahl, & Shearin, 1987; Simon et al., 2007), although
some of the most cited evidence is unpublished (Addis &
Linehan, 1989; Linehan, 1990). In addition, scores from
an abbreviated 4-​item version of the SBQ (also referred
to as the SBQ) have demonstrated adequate to good
internal consistency, adequate test–​retest reliability, and
convergent validity (Cole, 1988; Cotton, Peters, & Range,
1995). Finally, another 4-​item derivation of the SBQ, the
SBQ-​Revised (SBQ-​R), also has demonstrated strong psy-
chometric properties and has been used widely (Osman
et  al., 2001; Pedrelli et  al., 2014; Rudd, Goulding, &
Bryan, 2011).
The Self-​ Harm Behavior Questionnaire (SHBQ;
Gutierrez, Osman, Barrios, & Kopper, 2001) is a 32-​item
scale that assesses the presence and characteristics (e.g.,
age of onset, frequency, lethality, method, and intent) of
nonsuicidal self-​harm, suicidal ideation, suicide attempts,
and suicide threats. The validity and reliability of the
SBHQ scores have been supported in multiple studies
(Fliege et al., 2006; Gutierrez et al., 2001; Muehlenkamp,
Cowles, & Gutierrez, 2009), and the SBHQ has been
used across ethnically and racially diverse samples, differ-
ent age groups, and Veteran samples (Andrews, Martin,
Hasking, & Page, 2013; Brausch & Gutierrez, 2010;
Kleespies et al., 2011; Muehlenkamp & Gutierrez, 2004;
Muehlenkamp et al., 2009).
The Deliberate Self-​Harm Inventory (DSHI; Gratz,
2001) is a 17-​item questionnaire that assesses the presence
and characteristics (e.g., frequency, severity, duration,
and method used) of NSSI. The reliability and validity of
scores on the DSHI were supported in a study among col-
lege students (Gratz, 2001) and a study among a German-​
speaking clinical sample using a German version of the
scale (Fliege et al., 2006).
20
200 Mood Disorders and Self-Injury
The Self-​Harm Inventory (SHI; Sansone, Wiederman,
& Sansone, 1998)  is a 22-​item self-​report measure that
assesses the presence and absence of 22 SITB, such
as overdosing, cutting, burning, and suicide attempts.
Studies support the reliability and validity of scores on
the instrument among psychiatric outpatients (Sansone,
Pole, Dakroub, & Butler, 2006), psychiatric inpatients
(Sansone, Songer, & Miller, 2005), and community sam-
ples (Sansone et al., 1998).
MEASURES FOR USE WITH CHILDREN
AND ADOLESCENTS
Structured and Semi-​Structured Interviews
Some of the measures discussed previously have been
validated in samples with children and adolescents, and
some have been specifically designed for this popula-
tion. The multiple studies supporting the validity and
reliability of the SITBI scores were among samples of
adolescents and young adults (12–​19 years; Fischer et al.,
2014; Nock et al., 2007). The SITBI has also shown good
concurrent validity among a sample of adolescents in a
psychiatric inpatient setting (Venta & Sharp, 2014) and
has been used to assess SITB in children as young as
age 7  years (Barrocas, Hankin, Young, & Abela, 2012).
For the SSI, scores have good to excellent internal con-
sistency, and their validity has been supported in studies
of psychiatric inpatient children and adolescents (Allan,
Kashani, Dahlmeier, Taghizadeh, & Reid, 1997; Nock
& Kazdin, 2002) as well as outpatient adolescents (Holi
et al., 2005).
The Suicide Behaviors Interview (SBI; Reynolds,
1990) is a semi-​structured interview with 22 items rated
on 0 to 2 or 0 to 4 scales to measure suicidal behaviors
among adolescents. The first section of the SBI assesses
risk factors of suicidal behaviors, such as general distress,
chronic stress, level of social support, and major negative
life events. The second section assesses suicidal SITB,
including multiple items to assess ideation and suicide
planning and suicide attempts as well as follow-​up ques-
tions to assess some details regarding the most recent
attempt (e.g., confidence of death). Scores on the SBI
have good internal consistency and excellent inter-​rater
reliability, as well as adequate content and good conver-
gent validity (Reynolds, 1990; Reynolds & Mazza, 1999).
The Child Suicide Potential Scales (CSPS; Pfeffer,
Conte, Plutchik, & Jerrett, 1979)  is a semi-​structured
interview with eight scales that measure suicidal behav-
ior (ranging from nonsuicidal to serious attempts on a
5-​point spectrum), precipitating events, affect and behav-
ior within 6 months and then in a separate scale, more
than 6 months prior, family background, one’s concept
of death, ego functioning, and ego defense. The psycho-
metric properties of the CSPS are relatively strong, with
evidence of adequate to excellent internal consistency
for all but one scale (precipitating events), excellent
inter-​rating reliability (Ofek, Weizman, & Apter, 1998;
Pfeffer et  al., 1979), and concurrent validity demon-
strated in numerous studies across both clinical and
typical populations (Pfeffer, Conte, Plutchik, & Jerrett,
1980; Pfeffer, Newcorn, Kaplan, Mizruchi, & Plutchik,
1988; Pfeffer, Solomon, Plutchik, Mizruchi, & Weiner,
1982; Pfeffer, Zuckerman, Plutchik, & Mizruchi, 1984).
Self-​Report Measures
Several self-​report measures that were reviewed in
the adult assessment section have also been evaluated
for their use with youth. The validity and reliability of
BSI scores (Beck & Steer, 1991)  have been supported
among adolescent psychiatric inpatients (Steer, Kumar,
& Beck, 1993)  and outpatients (Rathus & Miller,
2002). Multiple studies have supported the reliability
and validity of scores on the SBQ-​R among adolescents
(Glenn, Bagge, & Osman, 2013; Osman et  al., 2001).
The Suicidal Ideation Questionnaire (SIQ; Reynolds,
1988)  and Suicidal Ideation Questionnaire Junior
(SIQ-JR; Reynolds, 1987), which were created by the
same researcher who created the ASIQ, were devel-
oped specifically for use in grades 10 through 12 and
7 through 9, respectively, and both have well-​supported
psychometric characteristics (Gutierrez & Osman, 2009;
Huth-​Bocks, Kerr, Ivey, Kramer, & King, 2007; Pinto,
Whisman, & McCoy, 1997; Reynolds & Mazza, 1999).
The Harkavy–​ Asnis Suicide Scale (HASS; Harkavy
Friedman & Asnis, 1989)  is a three-​part questionnaire
that assesses the presence and frequency of active and
passive suicidal thoughts, plans and attempts, as well as
substance abuse history and exposure to suicidal behav-
ior. The reliability and validity of scores on the HASS
have been supported in studies with high school students
(Harkavy Friedman & Asnis, 1989) and adolescents drawn
from a psychiatric outpatient clinic (Wetzler et al., 1996),
a treatment study (Rathus & Miller, 2002), and a pediat-
ric emergency department (Asarnow, McArthur, Hughes,
Barbery, & Berk, 2012).
 201
OVERALL EVALUATION
There is a large assortment of instruments to assess
SITB. The selection of an instrument should be based
on the purpose and focus of the assessment, as well as
the psychometric support (summarized in Tables  10.1a
and 10.1b). There is large variation in the characteristics
assessed by the different instruments. Some instruments
collect in-​depth characteristics (e.g., presence and fre-
quency) of an array of SITB (e.g., SITBI, SASII, C-​SSRS,
and S-STS), whereas others focus exclusively on col-
lecting detailed information about a specific outcome,
such as NSSI (e.g., DSHI and SHBQ) or suicide ideation
(e.g., SSI and BSI). We encourage the reader to carefully
consider the goals of assessment and the outcomes that
need to be assessed to achieve those goals. For clinical
settings, given the co-​occurrence of many SITB, and that
less severe forms of SITB predict more severe outcomes,
we recommend that each form of SITB be comprehen-
sively assessed.
The few studies that have examined agreement
between self-​ report and interview assessment have
found poor agreement (Klimes-​ Dougan, 1998;
Prinstein, Nock, Spirito, & Grapentine, 2001), par-
ticularly among adolescents, with self-​report showing
higher rates of SITB compared to parent and clinician
reported measures. The causes of this poor agreement
are unknown but could be related to respondents being
more forthcoming in self-​ report format rather than
having to tell a face-​to-​face interviewer about their
SITB history and/​ or respondents erroneously alter-
ing their responses due to subtle wording differences
between instruments, although discrepancies have
been found even when the wording and format of the
question are similar (Prinstein et  al., 2001). Another
SITB measurement issue, discussed previously, is that
structured interviews and self-​ report questionnaires
require respondents to rely on their own interpreta-
tions of SITB terms, such as “suicide attempt,” that
may differ from researchers’ consensus definitions,
leading to misclassification. Although no research has
clarified reasons for discrepancies between self-​report
and interview-​based assessment, research on misclas-
sification suggests that questions that include a longer
stem with an embedded definition and provide mul-
tiple response options for more subtle suicidal behav-
iors can reduce, but not eliminate, misclassification
(Millner et  al., 2015). However, none of the instru-
ments reviewed here contain questions that have these
Self-Injurious Thoughts and Behaviors 201
characteristics, and little research has examined the
measurement and misclassification issues discussed
previously.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
In addition to measuring the presence or absence of each
SITB when conceptualizing a case or planning treatment,
it is also important to assess patient-​reported factors that
influence the occurrence of each SITB. The causes of
SITB are multidetermined, and there is a wide range of
risk factors, but there is also a lack of clarity about how
these factors work together to produce specific SITB
within an individual. We provide a brief list of some
risk factors in this section, but note that a recent meta-​
analysis suggests that most risk factors are relatively weak
prospective predictors of suicidal thoughts and behaviors
(Franklin et al., 2017). This finding could be due to SITB
risk factors varying greatly among individuals such that
there could be completely distinct risk factors for different
people. Therefore, clinicians should assess individuals’
specific reasons and circumstances that precede instances
of a SITB. We review measures to accomplish this goal
in this section and provide ratings for each instrument in
Table 10.2.
Although it is impossible to calculate precisely the
risk of SITB for an individual, there are a few factors
and issues worth considering. First, mental disorders are
associated with all forms of suicidal SITB (Nock, Borges,
et al., 2008). An important consideration is that the disor-
ders that are among the largest cross-​sectional predictors
of suicidal ideation, such as major depressive disorder, dif-
fer from disorders that are among the largest predictors
of which people with ideation transition to attempting
suicide (Nock et  al., 2009; Nock, Hwang, Sampson, &
Kessler, 2010). These results suggest that it is important
to identify patients’ severity of SITB and understand that
risk factors may change as behavior becomes more or less
severe.
Structured and Semi-​Structured Interviews
Two of the interviews reviewed previously, the SITBI and
the SASII, collect information pertaining to individuals’
self-​reported reasons for engaging in SITB and circum-
stances around occurrences of SITB, such as preceding
stressful events or triggers.
20

202 Mood Disorders and Self-Injury

Table 10.2  Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Interviews
SITBI G NA E A G A G A ✓
SASII A G E E A G A G ✓
FASM G A NR NR A A G A
Self-​Report Measures
RFL E E NA G A E E G ✓
B-​RFL G G NA NR A E G A ✓
RFL-​A G E NA NR A A G G ✓
CSRLI G G NA NR A A E A
RFL-​YA A E NA NR A A A A
RFL-​OA G E NA NR A A A A
RSAQ E A NA NR A A E A
MAST G G NA NR A G E A ✓
ISAS G G NA NR G G E A

Note: SITBI  =  Self-​Injurious Thoughts and Behaviors Interview; SASII  =  Suicide Attempts Self-​Injury Interview; FASM  =  Functional Assessment
of Self-​Mutilation; RFL  =  Reasons for Living Inventory; B-​RFL  =  Brief Reasons for Living Inventory; RFL-​A  =  Reasons for Living for Adolescents;
CSRLI = College Student Reasons for Living Inventory; RFL-​YA = Reasons for Living for Young Adult; RFL-​OA = Reasons for Living for Older Adults;
RSAQ = Reasons for Suicide Attempts Questionnaire; MAST = Multi-​Attitude Suicide Tendency Scale for Adolescents; ISAS: Inventory of Statements
about Self-​Injury; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.

The Functional Assessment of Self-​ Mutilation
(FASM; Lloyd, Kelley, & Hope, 1997) is an interview that
assesses characteristics and functions of NSSI exclusively.
The FASM requires a respondent to endorse or deny 12
NSSI methods and, for each endorsed item, to report the
frequency and whether medical treatment was necessary.
Other items include other characteristics of NSSI, includ-
ing the age of onset, the impulsiveness of the behaviors,
substance use, and the amount of pain. It also provides
22 different reasons for engaging in NSSI. Studies have
found excellent to adequate internal consistency for
scores on the FASM (Guertin, Lloyd-​Richardson, Spirito,
Donaldson, & Boergers, 2001; Klonsky, May, & Glenn,
2013)  and excellent convergent validity with the SITBI
(Nock et al., 2007).
Self-​Report
The Reasons for Living Inventory (RFL; Linehan,
Goodstein, Nielsen, & Chiles, 1983)  contains 48 items
that assess different reasons for living. There is an
expanded version that contains 72 items. The RFL is
made up of six subscales based on factor analyses: survival
and coping beliefs, responsibility to family, child con-
cerns, fear of suicide, fear of social disapproval, and moral
objections (to suicide). A recent review concluded that the
RFL is inversely associated with both suicide ideation and
attempts (Bakhiyi, Calati, Guillaume, & Courtet, 2016).
There are age and gender differences, as well as an age by
gender interaction, on the RFL, with older participants
and women reporting higher scores (Ellis & Lamis, 2007;
McLaren, 2011); however, the gender gap decreases as
people age (Bakhiyi et  al., 2016). There are also differ-
ences between racial and ethnic groups (Morrison &
Downey, 2000; Walker, Alabi, Roberts, & Obasi, 2010).
The RFL has adequate psychometric characteristics
(Osman et al., 1993). The RFL has inspired several RFL-​
related instruments specifically tailored for different cir-
cumstances (e.g., when a briefer scale is required) and
populations (e.g., adolescents, young adults, college stu-
dents, and older adults). These RFL variants are reviewed
briefly next.
The Brief Reasons for Living Inventory (BRFL;
Ivanoff, Jang, Smyth, & Linehan, 1994)  consists of 12
items all drawn from the original RFL. The BRFL sub-
scales show high correlations with the corresponding RFL
subscales, and the BRFL retains the same factor structure
(Ivanoff et  al., 1994). Scores on the BRFL have shown
adequate to good internal consistency and demonstrated
validity (Bryant & Range, 1997; Kovac & Range, 2002;
Marion & Range, 2003).
The Reasons for Living for Adolescents (RFL-​ A;
Osman et  al., 1998)  contains 32 items, none of which
overlap with the RFL, to assess five factors:  future
 203
optimism, suicide-​related concerns, family alliance, peer
acceptance and support, and self-​acceptance. The RFL-​A
scores show good reliability and predictive validity within
both high school students (Gutierrez, Osman, Kopper, &
Barrios, 2000; Osman et al., 1998) and psychiatric inpa-
tient adolescents (Osman et al., 1998).
The College Student Reasons for Living Inventory
(CSRLI; Westefeld, Cardin, & Deaton, 1992)  contains
46 items that differ from those in the original RFL. Five
of the six original RFL factors were retained, and a new
factor reflecting college and future-​ related concerns
replaced the original child concerns factor. Studies have
supported good psychometric properties for the CSRLI
(Rogers & Hanlon, 1996; Westefeld, Badura, Kiel, &
Scheel, 1996; Westefeld et  al., 1992; Westefeld, Scheel,
& Maples, 1998).
The Reasons for Living for Young Adults (RFL-​YA;
Gutierrez et  al., 2002)  contains 32 items, including 12
items from the RFL-​A, to assess reasons for living specifi-
cally among those aged 17 to 30  years. Factor analyses
suggest factors that largely overlap with those found for
the RFL-​A (Gutierrez et  al., 2002). Studies among col-
lege students support the reliability and validity of scores
on this measure (Bagge, Lamis, Nadorff, & Osman, 2014;
Gutierrez et  al., 2002; Wang, Nyutu, & Tran, 2012).
No study has directly compared the RFL-​ YA and the
CSRLI, which have overlapping objectives. Clinicians
and researchers seeking to assess reasons for living among
college students should review both scales to determine
which scale best fits their needs.
The Reasons for Living Scale–​Older Adult version
(RFL-​OA; Edelstein et  al., 2009)  contains 69 items, 28
of which come from the original RFL, and it contains
five of the six subscales of the RFL (child concerns is
omitted). Scores on the RFL-​OA show excellent internal
consistency and good convergent and divergent validity
(Edelstein et al., 2009; Heisel, Neufeld, & Flett, 2016).
Several other measures, rather than assessing reasons
for living, assess reasons for making a suicide attempt.
The Reasons for Suicide Attempt Questionnaire (RASQ;
Holden, Kerr, Mendonca, & Velamoor, 1998)  contains
14 items that assess motivations for attempting suicide.
The RASQ has two subscales: extrapunitive/​manipulative
reasons (8 items) and internal perturbation based motiva-
tions (6 items). The RASQ has shown good psychometric
properties within several populations, including adults in
psychiatric crisis care (Holden et al., 1998), adults with a
prior suicide attempt (Holden & Delisle, 2006), and male
prisoners (Holden & Kroner, 2003).
Self-Injurious Thoughts and Behaviors 203
The Multi-​ Attitude Suicide Tendency Scale for
Adolescents (MAST; Orbach et  al., 1991)  is a 30-​item
measure that examines attraction and repulsion to life
and death, respectively. Scores on the MAST have dem-
onstrated adequate to excellent reliability (Orbach et al.,
1991; Osman et al., 1994) and concurrent validity (Cotton
& Range, 1993; Gutierrez, Osman, Kopper, Barrios, &
Bagge, 2000; Muehlenkamp & Gutierrez, 2004).
The Inventory of Statements About Self-​ Injury
(ISAS; Klonsky & Glenn, 2009)  mirrors many of the
same items as the FASM, such as providing 12 NSSI
methods, age of onset, impulsiveness of the behaviors,
experience of physical pain, and reasons for engag-
ing in self-​injury (or behavioral functions served by
the behavior). Factor analyses of the FASM (Nock &
Prinstein, 2004)  and rationally derived subscales of
the SASII (Brown, Comtois, & Linehan, 2002)  con-
verge on a four-​function model of self-​injury engage-
ment, including whether the behavior is negatively
or positively reinforced (i.e., to terminate a nega-
tive experience or trigger a positive experience) and
either intrapersonal (i.e., carried out to affect one’s
own emotions) or interpersonal (i.e., to affect others).
This model has received empirical support in dozens
of studies of developmentally disabled and typically
developing samples (Bentley, Nock, & Barlow, 2014).
The authors of the ISAS stated that they believe there
are not 4 but, rather, 13 behavioral functions of NSSI,
and they created this new scale to assess them. Factor
analysis of the ISAS suggests that it captures only 2
functions:  the interpersonal and intrapersonal func-
tions of NSSI (Klonsky & Glenn, 2009; Klonsky et al.,
2013). Nevertheless, scores on the ISAS have good
internal consistency (Klonsky & Glenn, 2009; Klonsky
et al., 2013) and adequate to good test–​retest reliability
(Glenn & Klonsky, 2011).
Overall Evaluation
Overall, as with the general initial assessment of SITB,
the selection of an instrument for case conceptualization
and treatment planning should be based on the evidence
supporting it and the purpose of the assessment. There
are several instruments that measure reasons for living.
Although the strength of the evidence varies among these
measures, one should also consider the population being
assessed. For example, items referring to one’s children
on the original RFL are usually not applicable to college
students or adolescents. However, no studies have directly
204
204 Mood Disorders and Self-Injury
compared, for example, the RFL and the CSRLI in a col-
lege sample to determine the degree to which the two
scales correspond.
A number of interview and self-​report measures are
available for assessing why a person engages in suicidal
or NSSI, and such measures can help clinicians with
case conceptualization and point toward treatment tar-
gets. For example, if assessment reveals that a person
engages in a suicide attempt or NSSI to escape from
intolerable emotional suffering, then treatment focused
on emotion regulation or distress tolerance skills might
help serve a similar function to replace these behaviors.
If, on the other hand, self-​injury is intended to com-
municate psychological pain to family or friends, then
interpersonal effectiveness skills might provide an adap-
tive approach to achieving similar ends. Although this
approach seems sensible and is incorporated in some
empirically supported treatments, such as dialectical
behavior therapy, no studies have explicitly tested the
utility of these scales to improve case conceptualization
or guide treatment.
ASSESSMENT FOR TREATMENT MONITORING
AND OUTCOME EVALUATION
Several randomized controlled trials conducted dur-
ing the past two decades have provided some empirical
support for treatments that aim to reduce SITB directly
(Bateman & Fonagy, 2009; Brown et al., 2005; Linehan,
Comtois, Murray, & et al., 2006; Linehan et al., 2015). On
balance, meta-​analyses have indicated that there is mod-
est support for such treatments (Brent et al., 2009; Glenn,
Franklin, & Nock, 2015; Kliem, Kröger, & Kosfelder,
2010) and have suggested there appears to be some degree
of publication bias in the treatment literature (Tarrier,
Taylor, & Gooding, 2008). Moreover, prior representa-
tive studies in the United States suggest that even when
a large percentage of people receive treatment for SITB,
it does not change the overall rate of these outcomes
(Kessler, Berglund, Borges, Nock, & Wang, 2005). This
could be due, in part, to a lack of evidence-​based treat-
ments available to those in community settings (McHugh
& Barlow, 2010).
Treatment monitoring and outcome evaluation
approaches focus on assessing changes in the presence,
frequency, and severity of SITB. Therefore, many of the
measures listed in Tables 10.1a and 10.1b are appropri-
ate for treatment monitoring and outcome evaluation,
and several have been used in this role in prior studies.
However, there is little psychometric evidence supporting
instruments specifically designed for assessing changes
in SITB outcomes over time. Therefore, one of the first
steps in selecting a measure for this purpose is to make
sure that the time period assessed maps on to the time
between assessment sessions. Obviously, it is inappropri-
ate to use measures that assess cumulative outcomes,
such as lifetime presence of a behavior, or a set period of
time that does not correspond with the amount of time
between monitoring sessions because this could cause
single SITB occurrences either to be counted more than
once (e.g., if monitoring occurs weekly but an instrument
assesses monthly) or to be missed entirely (e.g., if monitor-
ing occurs monthly but an instrument assesses only the
past week). For these reasons, the C-​SSRS has a “since
last visit” version (Posner et al., 2011), and the C-​SSRS,
S-​STS, and SASII provide flexibility regarding the time
period being assessed (Bland & Murray-​Gregory, 2006;
Sheehan, Giddens, et  al., 2014a). The SASII has been
used in several studies to monitor treatment and evaluate
outcome (Bryan et al., 2014; Linehan, Comtois, Murray,
et al., 2006; Linehan et al., 2015; McMain et al., 2009).
The SITBI has a section that asks about past month and
therefore would be appropriate if monitoring sessions
occurred at that interval. In addition to the standard
versions, the C-​SSRS also has abbreviated screeners for
assessment of past month or “since last contact,” and
the S-​STS has a “clinically meaningful change” version
that assesses a broader array of factors potentially related
to SITB as well as the severity of self-​injurious thoughts
and capacity to not engage in SITB (Sheehan, Giddens,
et al., 2014a). Among these various instruments and ver-
sions, however, only the C-​SSRS “since last visit” scale
has been formally tested for sensitivity to change (i.e., it
was correlated with other measures assessing SITB over
time) and only in two studies (Greist, et al., 2014; Posner
et al., 2011). Given the sparse data in this area, we do not
present a table to review the measures but, rather, recom-
mend the C-​SSRS and the SASII based on their evidence
and use for the purposes of treatment evaluation and out-
come monitoring.
Overall Evaluation
There are many instruments with strong psychometric
properties that assess the presence, frequency, and other
characteristics of SITB and measure these outcomes
over varying periods of time. Given that the primary goal
of treatment monitoring and outcome evaluation is to
assess changes in SITB over time, one would assume
 205

Self-Injurious Thoughts and Behaviors 205

that these instruments would detect such fluctua-
tions of these outcomes, but there is a dearth of studies
examining whether this is the case. However, repeated
assessments of SITB may alter participants’ self-​report,
causing them to be more or less forthcoming. If this
occurred, then the psychometric properties of instru-
ments tested during one assessment session may not be
applicable to use with repeated assessments. Ecological
momentary assessment (EMA) studies (i.e., in which
participants report thoughts, behaviors, or feelings on a
mobile device soon after they occur) repeatedly assess
SITB but, generally, they have used single questions—​
not instruments—​to directly assess the presence of SITB
(Armey, Crowther, & Miller, 2011; Nock, Prinstein, &
Sterba, 2009). Regardless of which instrument is used,
it is recommended that clinicians conduct rigorous and
comprehensive clinical assessment of primary outcomes
of interest in order to best inform treatment planning.
It is further recommended that these primary outcomes
be assessed repeatedly throughout treatment and used to
inform treatment modifications when necessary. From a
utility perspective, it is crucial that researchers and cli-
nicians examine the clinical utility of the information
collected by these assessment instruments. Although
generally assumed to be the case, there is sparse evi-
dence confirming that these tools provide valuable infor-
mation and enhance clinical care and decision-​making.
In lieu of a list of instruments with the specific purpose
of treatment monitoring and outcome evaluation, Box
10.1 contains an overview of general recommendations
for SITB assessment.
CONCLUSIONS AND FUTURE DIRECTIONS
We have provided an overview of the evidence and recom-
mendations for the relatively large number of instruments
available for assessing SITB and related characteristics.
We have also reviewed recent work suggesting that some
forms of measurement of SITB outcomes result in mis-
classification, within both research and clinical settings
(Brown et  al., 2015; Hom et  al., 2015; Millner et  al.,
2015; Plöderl et al., 2011). Therefore, we emphasize the
importance of having interviewers well trained in the clas-
sification of SITB when using interviews and using self-​
report measures with increased clarity and coverage. We
also reiterate the importance of carefully considering the
purpose of assessment, target of assessment, and quality of
evidence when selecting among the measures described
in this chapter.
Several instruments were omitted from this chap-
ter due to insufficient replicated psychometric support.
Although we do not review the evidence supporting
these instruments, several are noteworthy as promising
measures that require additional testing. First, both the
C-​SSRS and the S-​STS have versions for administration
to children, although the psychometric properties of
these versions have not been investigated. The Alexian
Brothers Assessment of Self-​Injury (ABASI; Washburn,
Juzwin, Styer, & Aldridge, 2010)  and the Non-​Suicidal
Self-​
Injury Disorder Scale (NSSID; Victor, Davis, &
Klonsky, 2017) are two novel measures intended to assess
NSSI disorder, and both have initial psychometric sup-
port. The Inventory of Motivations for Suicide Attempts

BOX 10.1  Clinical Recommendations and Research Questions for Evidence-​Based Assessment of SITB

1. Identification of SITB
(a) Assess the presence of each type of SITB in all patients.
(b) Use multiple assessment methods (interview, questionnaire) and informants (patient, clinician, parent)
whenever possible.
(c) If SITB is identified on any measure, conduct a more thorough SITB evaluation and risk assessment.
2. Case conceptualization and treatment planning
(a) Assess risk and protective factors for future SITB.a
(b) Assess the function of SITB.
(c) Treatment should target SITB directly.
3. Treatment monitoring and outcome evaluation
(a) Assessment should begin before treatment and continue as frequently as feasible.
(b) Measure multiple forms of SITB vand select measures with evidence of treatment sensitivity.
(c) Examine clinical utility of information gained from SITB assessment.
See sources cited in text for detailed guidelines for conducting an SITB risk assessment.
a
206
206 Mood Disorders and Self-Injury
(IMSA; May & Klonsky, 2013)  is intended to assess a
wider array of reasons for attempting suicide than does the
RSAQ. Finally, the Non-​Suicidal Self-​Injury-​Assessment
Tool (NSSI-​AT; Whitlock, Exner-​Cortens, & Purington,
2014) is a 12-​module assessment to measure many char-
acteristics of NSSI and intended to be administered on
the Internet.
There are several needed directions for future work
in this area. First, many of the constructs of interest here
are non-​arbitrary metrics (e.g., not on a scale from 1 to 5;
Blanton & Jaccard, 2006; Embretson, 2006) in the form
of the actual presence of self-​harm thoughts or behav-
iors. This is important because reliability and validity are
predicated on assessing a single construct (Cronbach &
Meehl, 1955), whereas SITB, such as suicidal ideation
and suicide attempts, are independent constructs gener-
ally measured together on a single instrument. Therefore,
one future direction is for studies to focus evaluations of
reliability and validity on measures of each SITB con-
struct separately.
Second, and related, there are threats to reliability and
validity that can be addressed by research that examines
each SITB construct separately. For example, one threat
to reliable and valid measurement is that participants may
not understand the SITB term in question (e.g., suicide
plan or suicide attempt; Millner et al., 2015). Therefore,
future research could continue to focus on increasing the
clarity of assessment questions and testing how to further
reduce inaccurate responses among participants. A  sec-
ond threat to reliability and validity is that some partici-
pants may intentionally withhold reporting prior suicidal
behaviors because of stigma or embarrassment (Conner,
Langley, Tomaszewski, & Conwell, 2003; Kim, Thomas,
Wilk, Castro, & Hoge, 2010). Thus, future research could
focus on testing certain prompts that cause participants
to be more comfortable and forthcoming answering ques-
tions about SITB.
Finally, aside from issues of reliability and validity,
there are several future directions that would advance the
understanding of SITB. First, currently, we lack a basic
description of many important SITB processes. For exam-
ple, little is known about (a) the degree to which SITB such
as NSSI and suicidal ideation fluctuate throughout a day,
week, or month (Armey et al., 2011; Kleiman et al., 2017;
Nock, Prinstein, et al., 2009); (b) how suicidal thoughts or
NSSI or other problematic behaviors (e.g., alcohol use)
change in the hours or days prior to an attempt (Bagge,
Glenn, & Lee, 2013; Bagge, Lee, et  al., 2013; Bagge,
Littlefield, Conner, Schumacher, & Lee, 2014); and,
related, (c) the suicide planning steps people take as they
move from thinking about suicide to actually engaging in
a suicide attempt and how far in advance of the attempt
these steps are typically carried out (Bagge, Littlefield, &
Lee, 2013; Millner, Lee, & Nock, 2017). Initial work in
these areas using EMA, which allows for real-​time assess-
ment via smartphone apps, and recent retrospective report
(i.e., interviewing people within 1 or 2 weeks of a suicide
attempt) has started to describe these processes, but more
work is required to gain a basic description of these pro-
cesses in order to advance the understanding of when
and why people kill themselves. Second, there are several
exciting but unverified approaches to improve the predic-
tion of SITB. For example, wearable technology such as
smart wristbands can collect passive data, such as walk-
ing pace, amount of movement throughout the day, and
heartbeat (Onnela & Rauch, 2016), that may contribute
to improved prediction of suicidal behaviors. In addition,
some studies have found that computerized reaction time
behavioral tasks can improve the prospective prediction
of suicidal outcomes (Nock & Banaji, 2007; Nock, Park,
et  al., 2010; Randall, Rowe, Dong, Nock, & Colman,
2013), but more research is required to confirm these
findings. Future research may reveal methods to aug-
ment retrospective self-​report assessments by integrating
these various data sources (EMA, passive monitoring, and
computerized tasks) into predictive models that greatly
improve efforts to prevent SITB. For now, this chapter
provides current evidence on the most empirically sup-
ported instruments to be used by researchers and practi-
tioners working in psychiatric settings.
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 Part IV

Anxiety and Related Disorders

 11
Anxiety Disorders in Children and Adolescents
Simon P. Byrne
Eli R. Lebowitz
Thomas H. Ollendick
Wendy K. Silverman
In this chapter, we summarize the research evidence sup-
porting psychological assessment measures and strategies
for use with children and adolescents with anxiety disor-
ders. The focus is on assessment measures and strategies
that are evidence based as well as clinically relevant and
feasible for use by practitioners. The focus is also on broad
measures of anxiety and related processes, including sev-
eral that have been developed since the writing of the pre-
vious chapter for the first edition of this book. Our aim
is to inform readers about the scientific suitability of the
measures and associated strategies, as well as their utility
for specific clinical and research purposes.
We begin with a brief description of anxiety disor-
ders in children and adolescents. This is followed by
a discussion of the measures and strategies, as well as
issues involved in using them to accomplish three pri-
mary goals: (a) diagnosis, (b) case conceptualization and
treatment planning, and (c)  treatment monitoring and
evaluation. An “Overall Evaluation” concludes each
section. The chapter ends with summary comments and
recommendations.
Before proceeding, we note that measures aimed
directly at assessing the brain, such as electroencephalo-
gram (EEG) and functional magnetic resonance imaging
(fMRI), also show promise and are opening up areas of
inquiry and discovery that were not widely known about
at the time of the first edition of this volume. The readers
are referred to Pine (2011) for further discussion. If the
strides that have been made thus far continue at the same
rapid pace, we are likely to have a great deal more to say
about the utility of these “brain measures” for diagnosis,
217
treatment planning and evaluation. Also, as in our first
edition chapter, we do not cover projective measures and
strategies. Despite their use by some in clinical practice,
their utility lacks adequate empirical evidence (Lilienfeld,
Wood, & Garb, 2000).
NATURE OF THE DISORDERS
Anxiety problems are among the most common forms
of emotional disturbance in children and adolescents
(e.g., Ollendick & March, 2004; Rapee, Schniering, &
Hudson, 2009). Although mild anxiety is often transient
and short-​ lived, anxiety disorders can be chronic and
interfere substantially with adaptive functioning. Many
persist into adulthood, and many adult anxiety disor-
ders appear to have their onset in childhood or adoles-
cence (see Ollendick & Seligman, 2006; Saavedra &
Silverman, 2002).
As defined most recently in the Diagnostic and
Statistical Manual of Mental Disorders (DSM-​5; American
Psychiatric Association, 2013), the most common anxiety
disorder subtypes relevant to children are specific phobia
(SP), separation anxiety disorder (SAD), selective mutism,
social phobia (SOP), and generalized anxiety disorder
(GAD). The removal of obsessive–​compulsive disorder
(OCD) as an anxiety disorder and the reclassification of
post-​traumatic stress disorder (PTSD) and acute stress
disorder as trauma and stressor-​related disorders are new
features of DSM-​5. Selective mutism is now classified as
an anxiety disorder. Furthermore, the DSM-​5 separates
218 Anxiety and Related Disorders
panic disorder (PD) and agoraphobia (AG) into two dis-
tinct diagnoses.
Epidemiology
Anxiety disorders are relatively common in youths, with
Rapee et  al. (2009) reporting between 2.5–​5% of children
or adolescents experiencing an anxiety disorder at any one
time. Merikangas et al. (2010) reported a lifetime prevalence
of anxiety disorders in youths as high as 31.9%. Anxiety disor-
ders are associated with an impairment in areas that include
family relationships (Ezpeleta, Keeler, Alaatin, Costello,
& Angold, 2001), peer relationships, and academic perfor-
mance (Essau, Conradt, & Petermann, 2000, 2002). Anxiety
often starts early and can be chronic; anxiety symptoms can
start as early as preschool age and continue into adulthood
(e.g., Rapee, 2011; Rapee et  al., 2009). Merikangas et  al.
(2010) reported that adolescents who experienced an anxiety
disorder had a median age of onset of 6 years. Sometimes
anxiety symptoms spontaneously remit, yet more often symp-
toms persist unless treated (e.g., Rapee et al., 2009). Whether
impairment is considered when estimating prevalence can
influence the rates reported in research studies (i.e., rates
are lower if impairment is considered). Costello, Egger,
Copeland, Erkanli, and Angold (2011) described such
prevalence estimates by diagnosis for young people aged
2–​21  years based on a meta-​analysis of 55 studies. They
found a point estimate prevalence rate of 10.2% for all
anxiety disorders (standard error [SE] = 0.5%), 5.4% for SP
(SE  =  .08%), 3.6% for SOP (SE  =  .70%), 2.6% for SAD
(SE = .5%), and 0.8% for panic disorder (SE = .02%).
Anxiety disorders are more prevalent in girls than boys
(e.g., Costello, Mustillo, Erkanli, Keeler, & Angold, 2003;
Essau et  al., 2000). The general pattern across commu-
nity studies is that girls report higher and more intense
normative, subclinical, and clinical levels of fear, worry,
and anxiety than do boys. Clinic studies have found more
inconsistent patterns of prevalence rates by sex, with rates
varying by anxiety disorder subtypes (Silverman & Carter,
2006). Such inconsistencies could be related in part to
differences in families’ perceived need and willingness to
seek mental health services for their sons and daughters.
Just what these differences are with regard to variables
such as race and ethnicity, socioeconomic status, and
parents’ psychopathology requires further study. Anxiety
is often associated with comorbidity, including depres-
sion, other anxiety disorders, and externalizing disorders
(Bittner et al., 2007; Essau, 2003). Autism is another com-
mon comorbid disorder, and some of the research on this
topic is summarized later in the chapter.
Etiological Factors
In this section, we provide an overview of the major etio-
logical factors implicated in the development of anxiety
in childhood and adolescence. Although each factor is
discussed separately, there are likely multiple pathways
to a given anxiety disorder in youth, reflecting complex
transactions among multiple factors (Cicchetti & Cohen,
1995). Depending on the configuration of other factors
with which the disorder occurs, any given pathway may
lead to several different anxiety disorders, to other disor-
ders, or to no disorder at all. Such a position is consistent
with a developmental psychopathology perspective on
the development of anxiety disorders (see Silverman &
Ollendick, 1999; Weems & Silverman, 2006).
Genetic Factors
Anxiety, as a trait, is believed to be influenced by mul-
tiple genes combining with multiple environmental
factors. Researchers have worked toward identifying can-
didate genes associated with the development of child-
hood anxiety. The serotonin transporter polymorphism
(5-​HTTLPR) is considered a viable candidate because
serotonin is implicated in mood. However, the serotonin
transporter polymorphism has generally been shown
to have an inconsistent association with anxiety in chil-
dren and adults (Gregory & Eley, 2011). Other potential
candidate genes include catechol-​ O-​methyltransferase
(COMT), the dopamine (DRD4) receptor, and the
γ-​aminobutyric (GABA) system. However, for these too,
results have been inconsistent regarding their role in
the etiology of anxiety in children and adolescents (see
Gregory & Eley, 2011 for a review).
Temperamental Factors
Negative affectivity (Watson & Clark, 1984)  and simi-
lar temperamental dimensions, including neuroticism
(Eysenck & Eysenck, 1985)  and behavioral inhibition
(BI) to the unfamiliar (Reznick, Hegeman, Kaufman,
Woods, & Jacobs, 1992), have been shown to increase
risk for anxiety and to be moderately heritable (Lonigan,
Phillips, Wilson, & Allan, 2011). Of these overlapping
constructs, BI has received the most attention as a risk fac-
tor. BI is associated with heightened risk for anxiety disor-
ders in children, particularly in a subset of children who
show stable BI from infancy through middle childhood
and into adolescence (Turner, Beidel, & Wolff, 1996).
Because studies also show that many children with high BI
do not develop anxiety disorders and uninhibited children
 Anxiety Disorders in Children and Adolescents
sometimes do, BI is neither sufficient nor necessary to pro-
duce anxiety disorders. Paths to anxiety disorders involv-
ing BI or similar anxiety-​prone temperamental factors also
involve shared and unshared environmental factors (Eley,
2001). A  rather consistent finding is that BI more often
predicts social anxiety. For example, Hirshfeld-​ Becker
et al. (2007) found that BI assessed at 1.5–​6 years was pre-
dictive of social anxiety 5 years later. It remains unclear
whether BI is a general risk for anxiety or a specific risk
for social anxiety (Ollendick & Benoit, 2012), or psycho-
pathology more broadly construed (Muris & Ollendick,
2005). In a cross-​sectional study of the concurrent associa-
tion between attachment security, behavioral inhibition,
maternal anxiety, and child anxiety in an at-​risk sample
of infants, Shamir-​Essakow, Ungerer, and Rapee (2005)
found insecure attachment was associated with BI, even
after controlling for the effect of maternal anxiety.
Exposure to Stressful Events
and Uncontrollable Environments
Exposure to severe and chronic life stressors also contrib-
utes to the onset of anxiety disorders in childhood (e.g.,
Allen, Rapee, & Sandberg, 2008). The controllability of
environmental events, especially early in childhood, may
be particularly important (Weems & Silverman, 2006).
Early exposure to controllable environments appears to
reduce anxiety, whereas uncontrollable environments
may predispose individuals to anxiety. For example, infant
rhesus monkeys exposed to chronically uncontrollable
environments responded to novel stimuli with greater fear
and less exploration (Mineka, Gunnar, & Champoux,
1986), as well as higher cortisol levels (Insel, Scanlan,
& Champoux, 1988)  compared with monkeys that had
control over their environment. Studies with children and
adolescents also support the predisposing role of uncon-
trollability to anxiety (e.g., Weems, Silverman, Rapee, &
Pina, 2003) and the protective role of controllable experi-
ences (Weems & Silverman, 2006).
Learning Influences
Rachman (1977) influentially proposed a theoretical
model of fear acquisition, whereby new fearful learning is
acquired via direct conditioning experience with the feared
stimulus, through observation of others, and through nega-
tive information regarding the feared stimulus. The prin-
ciples of direct conditioning suggest several mechanisms
by which environmental experiences may predispose to,
precipitate, or protect against the development of anxiety
219
disorders (Bouton, Mineka, & Barlow, 2001). Consistent
with this view, evidence suggests that a substantial percent-
age of children and adolescents with fears and phobias
have a history of direct or indirect conditioning (Ollendick
& King, 1991). However, even severely traumatic experi-
ences are not always sufficient to produce phobic anxi-
ety (e.g., Vernberg, La Greca, Silverman, & Prinstein,
1996), and traumatic conditioning episodes are not neces-
sary causes because phobic anxiety can develop in their
absence (Menzies & Clarke, 1995). Traumatic condition-
ing episodes appear to interact with predisposing factors
such as temperament and prior learning history to pro-
duce heightened risk for phobic responses in vulnerable
individuals. Growing evidence further suggests that direct
conditioning experiences may account for only a small
percentage of childhood phobias, with observation-​based
learning and information-​processing modes of acquisition
being predominant (e.g., Field & Lawson, 2003).
Family Processes
Attachment theory provides a framework for understand-
ing the enduring bonds that human infants form with
their caregivers, for the classification of those bonds
based on the quality of the attachment, and for concep-
tualizing the long-​term impact of these attachments on
human behavioral and emotional patterns (e.g., Bowlby,
1977; Esbjørn, Bender, Reinholdt-​ Dunne, Munck, &
Ollendick, 2012). Warren, Huston, Egeland, and Sroufe
(1997) found that children classified as anxious/​resistant
in their attachment (assessed at 12 months of age) were
more likely to have anxiety disorders at 17 years age than
were children classified with other types of attachment,
even when controlling for temperament and maternal
anxiety. Insecure attachment also has been linked with
increased levels of anxiety sensitivity (Weems, Berman,
Silverman, & Rodriguez, 2002).
The risk associated with insecure attachment status,
however, is likely to depend on the co-​occurrence of other
predisposing factors, such as a BI temperament. For exam-
ple, Warren and Simmens (2005) followed 1,200 infants
who had sensitive mothers and found they showed fewer
anxiety and depressive symptoms at 2 to 3  years of age.
They also found that children with difficult temperaments
with sensitive mothers were less likely to have depression
and anxiety. Dallaire and Weinraub (2007) examined
attachment security at 15 months and anxiety at 4.5 years
and found that insecurely attached children who experi-
ence negative life events exhibited more anxiety than did
securely attached children.
220 Anxiety and Related Disorders

Parenting behavior, particularly parenting that is Cognitive Biases and Distortions

viewed as overcontrolling, overinvolved, dependent,
Childhood anxiety disorders are associated with a vari-
or intrusive, has also been linked to the development
ety of information-​ processing biases at various stages,
of childhood anxiety. Research, overall, suggests that
including encoding, interpretation, and recall (see Vasey,
parents who exhibit such parenting behavior may
Dalgleish, & Silverman, 2003). The attentional and inter-
(a)  prevent youth from facing fear-​provoking events, a
pretational biases present in adults are also present in chil-
developmentally important task that allows children to
dren (Field & Lester, 2010). Clinically anxious and highly
develop solutions to face fear; and/​or (b)  send a mes-
test-​anxious children, for example, show an attentional
sage that particular stimuli are threatening or dan-
bias in favor of threat-​relevant stimuli (Vasey, Daleiden,
gerous, which may reinforce avoidant behavior (see
Williams, & Brown, 1995). Compared with normal con-
Silverman & Nelles, 1988; Vasey & Ollendick, 2000).
trols, clinically anxious and highly test-​anxious children
Such parenting behavior, however, likely interacts in
also show a bias toward interpreting ambiguous infor-
important ways with characteristics of the child. For
mation as threatening (Dadds, Barrett, Rapee, & Ryan,
example, the presence of anxiety in either the child or
1996). Whether attention and interpretation biases pre-
the mother in mother–​child dyads elicited maternal
dispose individuals to or result from anxiety, once present,
overcontrol during their interactions (Whaley, Pinto, &
these biases seem to foster the maintenance and intensifi-
Sigman, 1999).
cation of anxiety (Vasey et al., 2003). By virtue of their ten-
Recently, there has been a surge of interest in the role
dency to show attentional biases toward threat cues and to
of family accommodation (FA) in childhood anxiety dis-
interpret ambiguous information as threatening, anxious
orders (e.g., Lebowitz et al., 2013; Norman, Silverman,
children and adolescents construct their own anxiogenic
& Lebowitz, 2015). Family accommodation describes
experiences. Anxiety sensitivity—​ the belief that anxi-
the changes that parents make to their own behavior to
ety sensations have negative social, psychological, and/​
help their child avoid or alleviate their distress and anxi-
or physical consequences—​ is another cognitive factor
ety. FA can reduce a child’s anxiety in the short term, but
implicated in the etiology of anxiety disorders, especially
it is likely to impede the child’s development of more
panic attacks and panic disorder (e.g., Ollendick, 1998;
independent coping and self-​regulation skills, to pro-
Silverman & Weems, 1998). The previously discussed
mote and facilitate ongoing avoidance, and to hinder the
emergent research has clinical translational implications.
child’s sense of self-​efficacy (e.g., Norman et al., 2015).
For example, attention training away from threat can be
Examples of accommodation include parents speaking
used to reduce anxiety symptoms in youths (e.g., Cowart
for a socially anxious child, providing excessive reassur-
& Ollendick, 2011; Rozenman, Weersing, & Amir, 2011).
ance to a child with generalized anxiety, or allowing a
Researchers have also more recently used a visual
child with separation anxiety to sleep in their bed (e.g.,
search paradigm, which requires participants to make
Norman et  al., 2015). FA was initially studied in fami-
decisions about the presence/​absence of a specific target
lies of children with OCD (Calvocoressi et  al., 1995;
among distractors. Findings have shown that children
Lebowitz, Panza, Su, & Bloch, 2012), however, there is
with high levels of anxiety symptoms display increased
now ample evidence that FA is highly prevalent across
efficiency to detect angry faces compared with either
the anxiety disorders, associated with greater symptom
neutral or happy faces (e.g., Perez-​Olivas, Stevenson, &
severity, and may predict poor treatment outcomes
Hadwin, 2008; Waters, Henry, Mogg, Bradley, & Pine,
(Jones, Lebowitz, Marin, & Stark, 2015; Lebowitz,
2010; Waters & Lipp, 2008).
Panza, & Bloch, 2016; Lebowitz, Scharfstein, & Jones,
2014, 2015). Of emergent interest is FA’s biological basis
vis-​à-​vis childhood anxiety. Recent research has indi-
Summary
cated that higher levels of FA are associated with low
levels of salivary oxytocin in anxious youth (Lebowitz, Anxiety disorders are among the most common mental
Leckman, Feldman, et al., 2016), an intriguing finding disorders in childhood and adolescence. Prevalence
given the role of the oxytocinergic system for both anxi- estimates vary, depending on whether the samples are
ety regulation and the modulation of close interpersonal clinic-​referred or community-​ based, whether impair-
and attachment behavior (Feldman, 2016; MacDonald ment is considered, as well as other sample charac-
& Feifel, 2014). Later in this chapter, we discuss recent teristics. The etiology of anxiety disorders is multiple,
developments in measuring FA. complex, and overdetermined, including both biological
 Anxiety Disorders in Children and Adolescents 221

and environmental determinants (Lebowitz, Leckman, Semi-​Structured and Structured Diagnostic

Silverman, & Feldman, 2016). There is likely more than
one pathway to any one disorder. Likewise, the pheno-
type and presentation of anxiety disorders is multifaceted,
including a wide variety of neurological, physiological,
cognitive, emotional, and behavioral manifestations.
The measure and strategy used to assess anxiety disorders
depend on the specific assessment purpose. We turn now
to a main assessment purpose: diagnosis.
ASSESSMENT FOR DIAGNOSIS
In this section, we consider assessment measures and
strategies most useful for deriving anxiety disorder diag-
noses in children and adolescents, namely diagnostic
interview schedules. Emphasis is placed on the Anxiety
Disorders Interview Schedule for Children:  Child and
Parent Versions, which has the most research support for
deriving reliable and valid diagnoses. The utility of rating
scales for the purpose of diagnosis is also covered. Next,
we discuss “best practices” with respect to conceptual and
practical issues in diagnosis, including differential diagno-
sis. We conclude this section with an overall evaluation of
available assessment instruments.
Interview Schedules
The use of semi-​structured and structured interview sched-
ules represents best practice for the purpose of deriving
an anxiety disorder diagnosis in children and adolescents.
A  number of diagnostic interview schedules have been
developed to cover the different types of anxiety disorders
specified in the DSM-​5. The most widely used interview
schedules for diagnosing clinical disorders of childhood
and adolescence, including the anxiety disorders, are
presented in Table 11.1. Compared with unstructured
clinical interviews, semi-​structured and structured inter-
views are more standardized in terms of the questions that
are asked of informants. The increased standardization
reduces error variance attributed to interviewers and also
variance in usage of diagnostic criteria (Silverman, 1994).
Anxiety Disorders Interview Schedule
for Children: Child and Parent Versions
The Anxiety Disorders Interview Schedule for
Children:  Child and Parent Versions (ADIS-​C/​P) is the
most widely used semi-​structured interview schedule in
the field, including in randomized clinical trials. A down-
ward extension of the adult interview (Brown, DiNardo,

TABLE 11.1   Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Diagnostic Interview Schedules

ADIS C/​P-​IV NA NA E E E E E E ✓
DISC-​IV NA NA A G G G G G
DICA NA NA A G G G G G
K-​SADS NA NA G A A A G A

Child Self-​Rating Scales

RCMAS E G NA G G E G G
STAIC G G NA G G G G A
FSSC-​R A E NA G E G G G ✓
MASC G G NA G G E E G ✓
SCARED G E NA G G G G G
SCAS A G NA A E E G G
SPAIC A G NA E E G G G ✓
SASC-​R A G NA G G G G G
CASI A G NA G G G G G

Note:  ADIS C/​ P-​

IV  =  Anxiety Disorders Interview Schedule; DISC-​ IV  =  Diagnostic Interview Schedule for Children, Version IV;
DICA = Diagnostic Interview Schedule for Children and Adolescents; K-​SADS = Schedule for Affective Disorders and Schizophrenia for School-​
Age Children; RCMAS = Revised Children’s Manifest Anxiety Scale; STAIC = State–​Trait Anxiety Inventory for Children; FSSC-​R = Fear
Survey Scale for Children-​Revised; MASC  =  Multidimensional Anxiety Scale for Children; SCARED  =  Screen for Child Anxiety-​Related
Emotional Disorders; SCAS = Spence Children’s Anxiety Scale; SPAIC = Social Phobia and Anxiety Inventory for Children; SASC-​R = Social
Anxiety Scale for Children-​Revised; CASI = Children’s Anxiety Sensitivity Index; A = Adequate; G = Good; E = Excellent; NA = Not Applicable.
222 Anxiety and Related Disorders
& Barlow, 1994), the ADIS-​C/​P was constructed initially
to allow for DSM-​III (APA, 1980) and DSM-​III-​R (APA,
1987) diagnoses (Silverman, 1991), and it was revised for
DSM-​IV (APA, 1994; ADIS for DSM-​IV: C/​P; Silverman
& Albano, 1996)  and for DSM-5 (Albano & Silverman,
2017). The DSM-​5 version contains additional modules
to reflect some of the other changes made to the system
not mentioned previously (e.g., inclusion of hoarding as
a psychiatric disorder). Additional questions are included
that allow interviewers to obtain information about the
history of the problem as well as factors that may maintain
the anxiety.
In addition to containing modules of almost all the dis-
orders included in the DSM-​5, with heaviest coverage of
the anxiety and related disorders, the interview contains cli-
nician severity rating scales that assess for degree of impair-
ment or interference in child functioning associated with
the specific anxiety disorder endorsed by the child and par-
ent, respectively. Based on the information obtained from
the child and parent versions of the interview, interviewers
assign the degree of distress and interference associated
with each disorder (0 = “none” to 8 = “very severely dis-
turbing/​impairing”) overall with respect to peers, school-
work, family life, and personal distress. Each module
also contains questions that allow interviewers to assign 0
to 8 ratings regarding fear and avoidance of diverse situ-
ations relevant to a specific disorder (e.g., SOP and SP).
Similar to the adult interview, clinician severity ratings of
4 (“definitely disturbing/​impairing”) or higher are viewed
as “clinical” diagnoses, and those less than 4 are viewed as
“subclinical” or subthreshold. The clinical severity ratings
are further discussed later in the chapter.
Reliability of Diagnoses
A number of studies conducted in university-​ based
research clinics have confirmed empirically the reliability
of diagnoses formulated using the ADIS for DSM-​IV: C/​P,
including inter-​rater reliability (e.g., Grills & Ollendick,
2003; Silverman et al., 1988), retest reliability of specific
diagnoses (Silverman & Eisen, 1992), and retest reliabil-
ity of symptom patterns (Silverman & Rabian, 1995).
Lyneham, Abbott, and Rapee (2007) also found that
when using both child and parent reports on the ADIS,
the level of agreement between independent raters for
anxiety diagnoses was excellent. In a sample of children
and adolescents with specific phobias, Reuterskiöld, Ost,
and Ollendick (2008) also found excellent parent–​child
agreement on specific phobia diagnosis and moderate lev-
els of agreement for comorbid diagnoses.
Research has confirmed empirically the validity of
diagnoses formulated using the ADIS-​IV:  C/​P by show-
ing that scores on child and parent rating scales converge
in expected ways with diagnoses (e.g., Weems, Silverman,
Saavedra, Pina, & Lumpkin, 1999; Wood, Piacentini,
Bergman, McCracken, & Barrios, 2002). Wood et  al.
(2002), for example, evaluated concurrent validity of
ADIS-​IV: C/​P diagnoses of SOP, SAD, GAD, and PD in
children and adolescents referred to an outpatient anxi-
ety disorders clinic. Specifically, high correspondence
was found between ADIS-​IV: C/​P diagnoses and empiri-
cally derived factor scores corresponding to each of these
diagnoses on the Multidimensional Anxiety Scale for
Children (MASC; March, Parker, Sullivan, Stallings, &
Conners, 1997), with the exception of GAD. A  DSM-​5
version of the ADIS Child and Parent interview schedules
has recently been developed (Albano & Silverman, 2017).
The psychometric data found for the DSM-​IV version
are likely to generalize to the DSM-​5 version given the
high overlap and similarity between the two. Selective
mutism, previously classified under “Disorders Usually
First Diagnosed in Infancy, Childhood, or Adolescence,”
now classified as an anxiety disorder, is similarly likely to
be assessed in a reliable and valid manner with the DSM-​
5 interview. This is because of the high concordance
between children and parents in their respective inter-
views that correspond with a diagnosis of selective mut-
ism. For example, parents have little difficulty responding
in the affirmative to the selective mutism question,
whereas children, although not usually responding ver-
bally, will shake their heads or point to the words “Yes” or
“No” printed on cards.
Additional Diagnostic Interview Schedules
Other diagnostic interview schedules available to assess
for anxiety disorders in children and adolescents are the
Diagnostic Interview Schedule for Children (DISC-​IV;
Shaffer, Fisher, Lucas, Dulcan, & Schwab-​Stone, 2000),
the Diagnostic Interview for Children and Adolescents
(DICA; Reich, 2000), and the Schedule for Affective
Disorders and Schizophrenia in School-​ Age Children
(K-​SADS; Ambrosini, 2000). Similar to the ADIS-​IV: C/​
P, these structured or semi-​structured interview schedules
have child and parent versions, assess most of the DSM-​
IV disorders of childhood and adolescence beyond anxi-
ety, and can be used across a wide age range of children.
Diagnoses are formulated upon completion of both child
and parent versions, and they are determined by rules
derived by the interview developers.
 Anxiety Disorders in Children and Adolescents
Rating Scales
A number of self-​rating scales are available to assess anxi-
ety in children and adolescents. The most widely used
scales are presented in Table 11.1. Also contained in the
table are scales that are not discussed in this narrative sec-
tion. Most are omnibus measures and were not designed
to identify specific anxiety disorders. Historically, the
Revised Children’s Manifest Anxiety Scale (RCMAS;
Reynolds & Richmond, 1985) and the State–​Trait Anxiety
Inventory for Children (STAIC; Spielberger, 1973) were
used to identify the presence of anxiety and to quan-
tify anxiety symptoms in youth (Silverman & Saavedra,
2004). The RCMAS is a 37-​item (28 Anxiety and 9 Lie
items) rating scale (yes/​ no) that contains three sub-
scales:  physiological, worry/​oversensitivity, and concen-
tration. The STAIC is a 20-​item rating scale that assesses
the chronic (trait) and acute (state) symptoms of anxiety
using a 3-​point scale (hardly ever, sometimes, and often).
The Fear Survey Schedule for Children-​Revised (FSSC-​
R; Ollendick, 1983) has been most widely used to assess
fear. Containing 80 items, which are rated along a 3-​point
scale (none, some, and a lot), the factor scales consist of
the following:  fear of failure and criticism, fear of the
unknown, fear of danger and death, medical fears, and
fear of small animals.
Discriminant Validity of Youth Anxiety
Self-​Rating Scales
The chapter in the first edition summarized studies that
examined the ability of the RCMAS and STAIC scores
to discriminate between youth with anxiety disorders and
youth with no disorders or youth with other disorders
(Lonigan, Carey, & Finch, 1994; Perrin & Last, 1992), as
well as the results of a meta-​analysis of 43 published stud-
ies (Seligman, Ollendick, Langley, & Baldacci, 2004).
The overall conclusion, which remains valid still, is that
although both measures can discriminate anxiety disorders
from no disorders, there is little support for the RCMAS’s
and the STAIC’s scores to discriminate between anxiety
disorders and other disorders, specifically oppositional
and conduct disorders and depressive disorder.
Recently, the following anxiety scales have become
more widely used by researchers:  the MASC, the
Screen for Child Anxiety-​Related Emotional Disorders
(SCARED; Birmaher et  al., 1997), and the Spence
Children’s Anxiety Scale (SCAS; Spence, 1998). The lat-
est revision of the MASC, the MASC-​2 (March, 2013),
is described later. The SCARED is a 38-​item rating scale
223
that assesses symptoms of SAD, GAD, SOP, and school
phobia using a 3-​point scale (not true or hardly ever true,
sometimes true, and often true). The SCAS is a 44-​item
rating scale that assesses symptoms of SAD, GAD, SOP,
OCD, PD/​AG, GAD, and fears of physical injury using a
4-​point scale (never, sometimes, often, and always).
Scores on the MASC, SCARED, and SCAS have
been found to have high internal consistency and to be
able to discriminate “anxiety disorders” from “no anxiety
disorders,” as well as among the anxiety disorder subtypes
to some extent (e.g., SAD vs. SOP; Muris, Merckelbach,
Ollendick, King, & Bogie, 2002). As with the RCMAS and
STAIC, their associations with depression are also positive
and significant. Specifically, respective total scores on the
SCARED, SCAS, and MASC correlate near or above .70
with the Children’s Depression Inventory (Kovacs, 1992),
similar to the correlations found with the RCMAS and
STAIC. Only the FSSC-​R showed clear divergent validity
with depression (Muris et al., 2002).
Using receiver operator characteristic (ROC) curves
to estimate diagnostic accuracy across the range of
scores on specific scales, Dierker et al. (2001) compared
the RCMAS and the MASC and also included a ROC
analysis of a depression self-​rating scale, the Center for
Epidemiologic Studies-​ Depression Scale (CES-​ D), in
a school-​ based sample survey of ninth-​ grade students.
Students scoring at or above the 80th percentile on any
one or more of the three rating scales and a random
sample scoring below this threshold participated in ADIS-​
C interviews within 2  months of the screening sessions.
Results indicated that MASC scores were only partially
successful in identifying GAD, and only among the girls.
More encouraging are findings by Villabø, Gere,
Torgensen, March, and Kendall (2012). Villabø and col-
leagues found the MASC had moderate to high internal
consistency across the subscales in a treatment-​seeking
sample. MASC scores also were able to successfully dis-
criminate those with and without anxiety disorders, espe-
cially SAD and SOP, but less so for GAD. Wei et al. (2014)
found the MASC had low agreement between parent and
child; however, it had good internal consistency across
subscales and informants. They found it could discrimi-
nate between youth with and without anxiety disorders. In
an inpatient sample, Skarphedinsson, Villabø, and Lauth
(2015) found the MASC could detect whether or not the
patient had any anxiety disorder moderately well, but it
had limited utility in detecting specific anxiety disorders,
apart from GAD. Overall, recent analyses of the MASC
reveal a generally similar picture as that presented by ear-
lier analyses: It is useful in differentiating anxiety disorders
224 Anxiety and Related Disorders
from no disorder but less so in differentiating among anxi-
ety disorders or between anxiety disorders and other dis-
orders, and its ability to do so decreases as comorbidity
increases. Further work is needed for its utility as a screen.
Compared with the MASC, less analysis has occurred
with the SCARED and SCAS. Brown-​Jacobsen, Wallace,
and Whiteside (2011) examined parent, child, and clini-
cian agreement across the SCAS rating subscales, as well
as their predictive value. Results indicated that parent and
child agreement on the SCAS was moderate to high for
most symptoms, consistent with clinician ratings, and both
child and parent provided unique diagnostic information.
Updated Versions of Youth Self-​Rating Scales
Since the original version of this chapter, modifications
or revisions of several of the rating scales have been
made. These include a short form (SF) of the Fear Survey
Schedule Children (FSSC-​ R-​
SF; Muris, Ollendick,
Roelofs, & Austin, 2014)  and the updated MASC-​ 2 olds). The RCMAS-​2 subscales are the same as those in
(March, 2013)  and RCMAS-​2 (Reynolds & Richmond,
2008). The FSSC-​R-​SF is a shortened 25-​item version of
the 80-​item FSSC-​R (Ollendick, 1983). The FSSC-​R-​SF
contains the 5 items from each factor of the FSSC-​R (i.e.,
“fear of failure,” “fear of death,” “fear of small animals,”
“medical fears,” and “fear of the unknown”) that have the
highest factor loadings. Fear of failure items, for example,
are “being teased” and “failing a test.” Muris et al. (2014)
reported that the FSSC-​R-​SF scores had good internal
consistency (Cronbach’s α = .87 to 91), and both conver-
gent validity and discriminant validity were demonstrated.
Although more research is needed, including the gather-
ing of normative data, Muris et al. (2014) highlighted that
this short form may have utility as a brief screen for child-
hood fears and phobias.
The MASC-2 was designed to improve upon the
MASC by assessing a broader range of anxiety symp-
toms using the following six scales:  Separation Anxiety/​
Phobias, GAD Index, Social Anxiety, Obsessions and
Compulsions, Physical Symptoms, and Harm Avoidance.
The MASC-​2 has 50 items, compared to 39 items in
the original. MASC-​2 norms were established using a
sample of 3,400 youths (aged 8–​19 years) and 1,600 par-
ent reports. The MASC-​2 includes two new scales that
measure GAD and OCD symptoms. The MASC-​2 also
contains a new “Inconsistency Index,” in which eight
pairs of items assess for identical content and thus can be
used to determine reliability of respondents’ ratings. Also
new is an “Anxiety Probability Score” for each subscale,
which estimates the probability that the respondent has a
clinically significant anxiety disorder. The MASC-​2 has a
self-​report version for the child (MASC-​2-​SR), as well as a
parallel version for the parent (MASC-​2-​P). The MASC-​
2-​SR has shown generally strong psychometric properties
(see Fraccaro, Stelniki, & Nordstokke, 2015). For internal
consistency, the MASC-​2-​SR has a coefficient α of .92, for
the total score and a median α value of .79 for the scales
and subscales. The MASC-​ 2-​SR also has shown high
test–​retest reliability estimates, with corrected correlation
values ranging from .80–​.94. It has also shown strong con-
vergent validity with other anxiety measures. For example,
the MASC-​2-​SR is moderately to highly correlated with
the Beck Youth Inventory-​Anxiety (r  =  .73; Beck, Beck,
& Jolly, 2001).
The Revised Children’s Manifest Anxiety Scale Second
Edition (RCMAS-​2; Reynolds & Richmond, 2008) has 49
yes/​no items, compared with 37 in the initial RCMAS
(Reynolds & Richmond, 1978). It is based on a more eth-
nically diverse norming sample (N = 3,086; 6-​to 19-​year-​
the RCMAS (i.e., physiological anxiety, worry, and social
anxiety). The previous “lie” scale, now referred to as the
“defensiveness” scale, contains 9 items. It measures the
extent to which respondents try to present themselves in
a positive light. Ang, Lowe, and Yusof (2011) examined
the psychometric properties of the RCMAS-​2 in a sample
of 1,618 Singaporean students. They found evidence of
the utility of the RCMAS-​2 in this sample, suggesting the
measure has cross-​cultural value in an Asian sample and
that the U.S. norms are still appropriate. The RCMAS-​2
also includes a short form, containing the first 10 items of
the measure. It can be completed in less than 10 minutes.
Rating Scales for Specific Anxiety Domains
Several other rating scales are available to assess more spe-
cific anxiety (see Table 11.1). Two relevant to social anxiety
and worth highlighting are the Social Phobia and Anxiety
Inventory for Children (SPAIC; Beidel, Turner, & Morris,
1999) and the Social Anxiety Scale for Children-​Revised
Version (SASC-​R; La Greca & Stone, 1993). The SPAIC
is a 26-​item rating scale that assesses children’s distress to
social situations along three factors—​assertiveness/​general
conversation, traditional social encounters, and public
performance—​using a 3-​point scale (never or rarely, some-
times, and most of the time or always). The SASC-​R is a
26-​item rating scale that assesses children’s experiences of
social anxiety along three factors—​fear of negative evalu-
ation, social avoidance and distress in new situations, and
general social avoidance and distress—​using a 5-​ point
 Anxiety Disorders in Children and Adolescents
scale (not at all, hardly ever, sometimes, most of the time,
and all of the time). There is also an adolescent version
consisting of 22 items (La Greca & Lopez, 1998).
Conceptual and Practical Issues in Diagnosis
Differential Diagnosis
Because of the overlap that exists among the anxiety disor-
der subtypes, differential diagnosis can prove challenging,
even when a diagnostic interview schedule is used. It is
beyond the scope of this chapter to analyze the myriad of
issues involved in the differential diagnosis of the anxiety
disorders. However, to illustrate how challenging differ-
ential diagnosis can be, issues involved in the differential
diagnosis of GAD, SOP, and PD are presented here.
In GAD, worry is a process in which all individuals with
the disorder actively engage (e.g., Silverman, La Greca, &
Wasserstein, 1995). However, worry is a pervasive clinical
feature of most of the anxiety disorder subtypes (Weems,
Silverman, & La Greca, 2000). The differential diagnosis
of GAD requires that the individual’s worry does not focus
solely on areas that pertain to the other anxiety subtypes,
such as social evaluative situations (i.e., SOP), specific
objects or situations (i.e., SP), and separation from attach-
ment figures (i.e., SAD). The worries also cannot have
emerged from exposure to a traumatic event (i.e., PTSD).
GAD must be further distinguished from excessive worry
about having panic attacks (i.e., PD) as well as worrying
in the form of obsessions (i.e., OCD).
The specific differential between GAD and SOP can
be especially challenging. In GAD, the worry about social
situations and academic tasks stems usually from a fear
of failure due to not reaching a self-​generated standard.
In SOP, the fear or worry stems from a fear of negative
evaluation by others relating to social evaluative situa-
tions such as academic-​or peer-​related events. The social
avoidance associated with SOP must be further distin-
guished from the social avoidance relating to having an
unexpected panic attack (PD) and not wanting this attack
to occur in public places (i.e., agoraphobia). Also impor-
tant is distinguishing SOP from autism spectrum disor-
der (ASD): Children with SOP have the capacity for and
interest in social relationships; children with ASD have a
general lack of interest in social relationships.
Panic is another common clinical feature that is
pervasive across the different anxiety disorder subtypes
(Ollendick, Mattis, & Birmaher, 2004). The differen-
tial diagnosis of PD requires, however, that the panic
attacks are not cued by social evaluative situations (i.e.,
225
SOP), specific objects or situations (i.e., SP), separation
from attachment figures (i.e., SAD), excessive worry (i.e.,
GAD), traumatic events (i.e., PTSD), and concerns about
exposure to objects or situations related to an obsession
(i.e., OCD).
Dealing with Comorbidity
Comorbidity, or the presence of multiple disorders, occurs
at high rates in children and adolescents with anxiety dis-
orders. It is the rule rather than the exception. Estimated
rates of comorbidity run as high as 91% in clinic samples
(e.g., Angold & Costello, 1999) and 71% in community
samples (e.g., Woodward & Fergusson, 2001). Although
some of these reported high rates of comorbidity reflect
methodological artifacts including referral bias, comor-
bidity cannot be explained simply as artifact. Research
further shows that anxious youth who are comorbid with
another disorder, a depressive disorder particularly, are
more severely impaired than are youth with one disorder
only (Franco, Saavedra, & Silverman, 2007; Seligman &
Ollendick, 1998).
These findings highlight the importance of carefully
considering the different types of comorbid patterns that
often accompany anxiety disorders. Use of the ADIS-​C/​P,
for example, which covers the full range of DSM disor-
ders, is a way to increase assurance that the diverse comor-
bid patterns that often co-​occur with anxiety disorders
have been carefully and thoroughly assessed.
Measuring Anxiety with Comorbid Autism
The comorbidity between autism and anxiety is well estab-
lished, with up to 40% of youth diagnosed with autism
spectrum disorder (ASD) meeting criteria for an anxiety
disorder (Davis, White, & Ollendick, 2014; Kaat, Gadow,
& Lecavalier, 2013). Yet the phenomenology of anxiety
in ASD is not well understood. There is debate about
whether anxiety in this population should be viewed as
a separate disorder, a symptom of ASD, or separate but
not independent of ASD (Lecavalier et al., 2014). There
is also overlap with DSM symptoms in individuals with
ASD and anxiety. For example, avoidance of social inter-
actions, or awkwardness during these interactions, could
reflect either ASD or social phobia (or both). Difficulties
due to cognitive and language delays also can make the
use of self-​reports difficult with some young people with
ASD (e.g., Lecavalier et al., 2014).
Researchers have examined the utility of anxiety mea-
sures in this comorbid population. Storch et  al. (2012)
226 Anxiety and Related Disorders

administered the ADIS-​C/​P to 85 children and adoles- most evaluation. Additional research is needed to deter-
cents (aged 7 to 17 years) with ASD. Diagnostic agreement mine reliability and validity of diagnoses when the inter-
between the youths and parents or clinical consensus was view is used in community settings, as well as in deriving
poor; however, agreement was good to excellent between diagnoses of disorders with varying base rates. Research
parents and clinician. The authors concluded that clini- on the utility of other assessment methods for the purpose
cians should primarily base their diagnostic decisions on of diagnosis and differential diagnosis is limited. Of the
parent reports. In a subsequent study, Ung et  al. (2014) currently available self-​rating scales, the MASC has the
examined the inter-​rater reliability of the ADIS-​C/​P in strongest evidence base as a screen for diagnosis. The
70 youths with high-​functioning autism. The researchers more recent MASC-​2 and RCMAS-​2 appear to be well
compared inter-​rater reliability between a live administra- designed and validated across large samples, yet at this
tion of the ADIS-​C/​P and a taped recording of the live stage they have not been as thoroughly researched as the
administration. Ung et  al. (2014) found good to excel- older versions. When measuring anxiety with comorbid
lent clinician-​to-​clinician reliability across different ASD autism, we defer to Lecavalier et al. (2014) in suggesting
diagnoses. Kaat and Lecavalier (2015) examined internal the parent-​rated 20-​item CASI, MASC, PARS, and ADIS
consistency, test–​retest reliability, and inter-​rater reliabil- as most suitable.
ity of the MASC-​2 and the Revised Children’s Anxiety
and Depression Scale (RCADS) in 46 children with
ASD. They found internal consistency was adequate, but ASSESSMENT FOR CASE CONCEPTUALIZATION
inter-​rater reliability was poor. Divergent and convergent AND TREATMENT PLANNING
validity were adequate and parent–​child agreement was
higher when the child had a higher IQ and lower symp- This section presents assessment measures and strate-
tom levels. gies for use in arriving at a fuller case conceptualization
Lecavalier et al. (2014) conducted a review of 38 pub- that can guide decisions about treatment planning. Case
lished studies and 10 assessment measures to determine conceptualization is similar to diagnosis, but they are not
the suitability of existing measures for assessing anxiety inone in the same. Case conceptualization focuses more on
young people with ASD. Four measures were viewed as psychological processes associated with the etiology and
suitable for use in clinical trials: the parent-​rated 20-​item
maintenance of a disorder. A definitive understanding of
version of the Child and Adolescent Symptom Inventory children’s psychological problems is difficult to achieve,
(CASI; Hallett et al., 2013), the parent-​rated MASC, the and initial conclusions about how to conceptualize the
Pediatric Anxiety Rating Scale (PARS; Research Units on “case” and plan treatment are best viewed as hypotheses
Pediatric Psycho-​pharmacology [RUPP], 2002), and the that await verification based on additional information
ADIS-​C/​P. That is, scores on these measures were deemed (Ollendick & Hersen, 1993; Silverman & Saavedra,
to have good clinical relevance and good to excellent reli- 2004). The assessment process ideally continues through-
ability and validity. out treatment, which can also serve as an opportunity
to obtain additional information based on treatment
response.
Overall Evaluation
Thus, evidence-​ based assessments de-​ emphasize
Assessment for diagnosis of anxiety in children and adoles- quick, definitive conclusions and focus more on obtain-
cents continues to face a number of challenges. Younger ing information that unfolds over time and is directly
children may have difficulties with language and self-​ relevant to treatment. “Relevance for treatment” refers to
report. They may also be susceptible to social desirability the clinical utility of information in planning the treat-
and demand characteristics. To determine diagnoses, it is ment and, in the final analysis, the evaluation of interven-
preferable to have multiple informants, multiple meth- tion outcomes (Mash & Terdal, 1988). A related concept
ods, and to assess across different contexts (e.g., Essau & is treatment utility, which refers to the degree to which
Barrett, 2001). There is also a trade-​off between time com- assessment strategies are shown to contribute to beneficial
mitment and validity. For diagnosis, interview schedules treatment outcomes (Hayes, Nelson, & Jarrett, 1987).
have the most empirical evidence for deriving reliable The most widely used measures for case conceptual-
and valid diagnoses. Among the interview schedules avail- ization and treatment planning are presented in Table
able, the ADIS C/​P has been used in most of the youth 11.2. The table also includes several measures that are
anxiety research studies, and it has been subjected to the not discussed in the narrative. The discussion focuses on
 Anxiety Disorders in Children and Adolescents 227

TABLE 11.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Diagnostic Interview Schedules

ADIS C/​P-​IV NA NA E E E E E E ✓
DISC-​IV NA NA A G G G G G
DICA NA NA A G G G G G
K-​SADS NA NA G A A A G A
Child Self-​Rating Scales
RCMAS E G NA G G E G G ✓
SRAS A E NA G G G G E
MASC G G NA G G E E E ✓
SCAS A G NA A E E G G
SPAIC A G NA E E G G G ✓
FASA/​FASA-​CR A E G E E G E E ✓
Behavioral Observations
BAT NA NA G G G G G G ✓
SET/​PYIT NA NA G G G G G G ✓
SM NA NA NA G G G G G

Note: ADIS C/​P-​IV = Anxiety Disorders Interview Schedule; DISC-​IV = Diagnostic Interview Schedule for Children, Version IV; DICA = Diagnostic
Interview Schedule for Children and Adolescents; K-​ SADS  =  Schedule for Affective Disorders and Schizophrenia for School-​ Age Children;
RCMAS = Revised Children’s Manifest Anxiety Scale; SRAS = School Refusal Assessment Scale; MASC = Multidimensional Anxiety Scale for Children;
SCAS = Spence Children’s Anxiety Scale; SPAIC = Social Phobia and Anxiety Inventory for Children; FASA/​FASA-​CR = Family Accommodation Scale-​
Anxiety/​Family Accommodation Scale-​Child Report; BAT = Behavioral Avoidance Task; SET/​PYIT = Social Evaluative Task/​Parent–​Youth Interaction
Task; SM = Self-​Monitoring; A = Adequate; G = Good; E = Excellent; NA = Not Applicable.

measures and strategies that have supportive evidence for Chorpita, 2016; Motoca & Silverman, 2011; Ollendick,
developing (a)  a clinically meaningful and useful case King, & Chorpita, 2006). Although several authors have
conceptualization and (b)  a clinically sensitive and fea- criticized the linkage between diagnosis and treatments in
sible treatment plan. A  discussion of best practices for the evidence-​based treatment movement (e.g., Goldfried
case conceptualization and treatment planning is also & Wolfe, 1998), this concern is dampened with regard
provided. The section concludes with an overall evalua- to treating phobic and anxiety disorders because of the
tion of instruments. strong evidence for exposure-​based CBT approaches.
The implications of the above are clear: if one wishes
to use the treatment approach that possesses the most
Semi-​Structured and Structured Diagnostic
research evidence, it is important to first have high confi-
Interview Schedules
dence that one has reliable and valid information that the
The initial set of decisions that need to be made when child is suffering primarily from clinical levels of anxiety
working with children and adolescents with anxiety disor- and not another clinical disorder. Second, it is important
ders is how to best conceptualize the case, to determine to have confidence about the specific type(s) of anxiety
whether an anxiety disorder exists, and to plan treatment disorder to ensure that the appropriate exposure tasks can
accordingly. Differences between the anxiety disorders be planned and implemented (e.g., exposure to social
and other disorders, as well as differences within the anxi- evaluative situations for SOP cases and exposure to sepa-
ety subtypes, constitute the primary reason why the use ration situations for SAD cases).
of structured and semi-​structured interview schedules are As discussed previously in the section titled Assessment
critical from an evidence-​based perspective. for Diagnosis, semi-​structured and structured diagnostic
Furthermore, cognitive–​behavioral treatment (CBT), interviews are useful in the initial stages of deriving diag-
which involves exposure-​ based exercises, both in ses- noses of anxiety disorders. See Table 11.2 for a listing of the
sion and out of session, remains the strongest evidence-​ schedules used most in the anxiety field. Specific aspects
based treatment for anxiety disorders in children and of anxiety diagnoses yield further clinically suggestive
adolescents (Higa-​McMillan, Francis, Rith-​Najarian, & information about treatment targets and treatment plans.
228 Anxiety and Related Disorders

Prescriptive Treatment Strategies contained 4 items devoted to each of the four functional
conditions. Child and parent versions of the scale were
The reader is referred to Table 11.2 for a listing of the
developed. Item means were averaged across functions to
main measures and strategies, with some additional ones
derive functional profiles that included the primary and
noted that are not discussed in the narrative. In an early
secondary reasons why a particular child refused school.
study, Eisen and Silverman (1993) showed CBTs were
The original SRAS and its recent revision (24 items with
most effective for children with overanxious disorder
parent and child versions) have been found to be reli-
(i.e., the DSM-​III-​R precursor to GAD) when they were
able across time and between parent raters (Kearney,
matched with specific symptoms. For example, children
2002, 2006; Kearney & Silverman, 1993; Silverman &
with primary symptoms of worry, defined by the worry/​
Ollendick, 2005).
oversensitivity subscale of the RCMAS, responded more
The scale is useful in the prescriptive treatment of
favorably to a cognitive therapy, whereas children with
school refusing children. Prescriptive treatment for nega-
primary symptoms of somatic complaints, defined by the
tively reinforced school refusal behavior (Functions 1
physiological arousal subscale of the RCMAS, responded
and 2) consists of psychoeducation, fear hierarchy devel-
more favorably to relaxation training aimed at dealing
opment, cognitive therapy, modeling, and behavioral
with physiological and somatic complaints.
exposures designed to gradually reintroduce the child to
This early study was replicated by Eisen and Silverman
school. Prescriptive treatment for positively reinforced
(1998) in that although both treatments were effective,
school refusal behaviors (Functions 3 and 4)  consists of
the prescriptive treatments produced greater improve-
developing daily routines, escorting the youth to school,
ments for the children to meet specific positive end-​state
contingency contracting, and communications skills
functioning criteria. Similar effects of matching were
training. Single-​ case experimental design treatment
shown by Ollendick, Hagopian, and Huntzinger (1991)
studies have shown that the SRAS and the SRAS-​R are
with separation anxious children and by Ollendick (1995)
useful in determining which prescriptive treatment best
with adolescents with PD with agoraphobia. Each of these
fits a particular case and which treatments may be less
studies used single case multiple baseline designs to illus-
effective (Chorpita, Albano, Heimberg, & Barlow, 1996;
trate the controlling effects of the matched interventions.
Kearney, Pursell, & Alvarez, 2001; Kearney & Silverman,
Overall, CBTs were shown to be maximally effective in
1993, 1999).
these studies when the assessment of diagnoses was sup-
plemented with the assessment of symptom profiles.
Behavioral Observations
A prescriptive approach is also illustrated in the treat-
ment of school refusal behavior in children and adoles- Systematic direct behavioral observations can play a
cents. Although not a specific psychiatric diagnosis, school particularly helpful role in case conceptualization and
refusal is a common mental, health, and educational treatment planning (see Table 11.2 for a summary). One
problem that refers to child-​motivated refusal to attend useful role of behavioral observations is for identifying
school and/​or difficulties remaining in school for an entire and quantifying specific fear and anxiety symptoms and
school day (Kearney, 2003). Children who refuse school behaviors, such as avoidance. Ost, Svensson, Hellstrom,
frequently meet criteria for one or more of the anxiety dis- and Lindwall (2001), for example, observed children
orders in childhood, and they may also meet criteria for engage in behavioral avoidance tasks, which consisted of
one of the disruptive behavior disorders (Heyne, Sauter, a series of graduated steps, and the percentage of steps the
Ollendick, van Widenfelt, & Westerberg, 2014). children accomplished was recorded.
Kearney and Silverman (1990) proposed a functional Perhaps because behavioral avoidance tasks have
model suggesting children refused school for one of four long been known to be affected by instructional set and
probable reasons: (a) to avoid stimuli that provoke nega- demand characteristics (e.g., “go as far as you can” vs. “stop
tive affectivity, (b) to escape aversive social and/​or evalua- whenever you feel too scared”), direct observations have
tive situations, (c) to seek attention from significant others, been used more often to assess subjective judgments of
and (d)  to pursue tangible reinforces outside of school. children’s levels of fear/​anxiety in fear/​anxiety-​provoking
To address these functions, they developed the School situations/​t asks or observers’ subjective judgments of chil-
Refusal Assessment Scale (SRAS; Kearney & Silverman, dren’s levels of fear/​anxiety. In some studies, observers’
1993)  and its recent revision (SRAS-​R; Kearney, 2002). subjective ratings are obtained by providing the observers
The original SRAS was a 16-​ item instrument that with global rating scales (e.g., a Likert rating scale from 1
 Anxiety Disorders in Children and Adolescents
to 5). In other studies, observers are provided with behav-
ioral dimensions to help assist the observers in making
their subjective ratings (Silverman & Ollendick, 2005).
Two other types of behavioral observation tasks are
social evaluative tasks and parent–​youth interaction tasks.
With regard to social evaluative tasks (Beidel, Turner, &
Morris, 2000), participants are informed of the evaluative
nature of the task and are given standard behavioral asser-
tiveness instructions. For example, Beidel et  al. (2000)
invited children and adolescents to read aloud a story
in front of a small group and were told to “Respond as if
the scene were really happening.” With regard to parent–​
youth interaction tasks (e.g., Hudson & Rapee, 2002),
parents and their children were observed while engaging
in problem-​solving situations. Specifically, Hudson and
Rapee conducted observations of “normal” and anxious
children and their siblings while completing a separate
set of tangram or puzzle tasks designed to be slightly too
difficult to complete during the allocated 5 minutes. Of
interest was the degree of parental involvement during
the task (e.g., degree of unsolicited help and degree to
which the parent physically touched the tangram piece).
From a best-​practices perspective, we believe system-
atic direct observational procedures have clinical util-
ity with regard to case conceptualization and treatment
planning. They can yield helpful conceptual information
about the nature of family interactions among anxious
children or just “how far children can go” when it comes
to interacting with a feared object or event. However, they
can be time-​consuming and difficult to arrange.
We are encouraged by a novel and promising behav-
ioral assessment approach that provides an objective index
of fear-​related avoidance and that is also presented to
children as a fun game. Relying on motion tracking soft-
ware, the Yale Interactive Kinetic Environment Software
(YIKES) is a flexible experimentation platform that facili-
tates examination of approach and avoidance during an
episode of immersive gameplay. In a series of experi-
ments focused on behavioral avoidance of spider images,
approach toward spider images was compared to approach
toward matched neutral images. Behavioral avoidance of
the spider images in both anxious youth and their moth-
ers was associated with subjective ratings of fear of spiders.
Behavioral avoidance in the mothers significantly moder-
ated the association between mother and child fear, and
anxiety sensitivity moderated the association between fear
and avoidance in the anxious children (Lebowitz, Shic,
Campbell, Basile, & Silverman, 2015; Lebowitz, Shic,
Campbell, MacLeod, & Silverman, 2015). These findings
229
highlight the ability of novel behavioral measurement
methodologies to contribute to assessment and allow for
the testing of otherwise difficult to examine hypotheses.
Self-​Monitoring
Self-​monitoring often has been viewed as a more effi-
cient and easier way to accomplish the same goals as
direct observation. Although relatively common in prac-
tice among behaviorally oriented clinicians, little has
been done in the child and adolescent anxiety research
area to evaluate feasibility and psychometric properties.
An exception is Beidel, Neal, and Lederer (1991), who
devised and evaluated the feasibility (i.e., child compli-
ance), reliability, and validity of a daily diary for assess-
ing the range and frequency of social evaluative anxious
events in elementary school children (N = 57; n = 32,
test anxious; n = 25, non-​test anxious) during a 2-​week
assessment phase. Structured in nature, the daily diary
listed events such as I had a test and The teacher called
on me to answer a question, as well as a list of poten-
tial responses to the occurrence of the events, including
positive (e.g., practiced extra hard and told myself not to
be nervous and it would be okay), negative (e.g., cried
and got a headache or stomachache), and neutral (e.g.,
did what I was told) behaviors. The children also rated
the degree of distress they experienced using a pictorial
5-​point rating scale that depicted increasing degrees of
anxious arousal.
With regard to feasibility or compliance, with no
incentives offered, the mean number of days the diary was
completed for the 2 weeks ranged from 7.9 to 11.5 days,
although only 31% to 39% of the children complied for
the full 2 weeks (Beidel et al., 1991). Retest reliability was
modest, but that is probably because the events listed on
the diary showed true fluctuations. Evidence for valid-
ity was demonstrated in that the test-​anxious children
reported significantly more emotional distress and more
negative behaviors such as crying or behavioral avoidance.
Thus, as with direct observation procedures, self-​
monitoring procedures have clinical utility in yielding
helpful conceptual information (e.g., the specific situ-
ations that elicit anxiety in a child and the child’s cog-
nitions when faced with a specific object or event).
Furthermore, the prevalent use of digital technology,
including smartphones, has led to the development of
self-​
monitoring applications for anxiety (Anxiety and
Depression Association of America, 2016). Although the
use of applications for treatment and monitoring seems
230 Anxiety and Related Disorders
a promising development, particularly for technologically
savvy young people, more research is needed to deter-
mine their value (e.g., Radovic et al., 2016).
Conceptual and Practical Issues in Assessing for Case
Conceptualization and Treatment Planning
Demonstrating Treatment Utility
The studies summarized in this section regarding pre-
scriptive treatment strategies represent important efforts
in demonstrating the treatment utility of assessment. For
example, in the studies by Eisen and Silverman (1993,
1998), which showed CBTs were most effective for spe-
cific aspects of the treatment (e.g., cognitive therapy and
relaxation therapy) when matched with the child’s spe-
cific symptoms (e.g., worry and physiological arousal), the
treatment utility of assessing for these specific symptoms
was empirically shown because the assessment produced
better treatment outcome. However, the treatment util-
ity of deriving DSM diagnoses using interview schedules
still has not been demonstrated in other treatment out-
come studies (Nelson-​Gray, 2003). For example, how do
children who had diagnoses assigned with a structured
or semi-​ structured diagnostic interview schedule fare
in anxiety reduction programs compared with children
who had diagnoses assigned using an unstructured clini-
cal interview? What about in comparison with children
whose anxiety was assessed using rating scales? Answers to
these questions can lead to more cost-​and time-​effective
practice, which is of high relevance in efforts to transfer
evidence-​based practices to community settings.
Considering Impaired But Not Diagnosed
Children and Adolescents
Diagnostic interview schedules emphasize DSM anxiety
disorders and symptoms and are in line with the treatment
targets of CBT. Research shows, however, that a substan-
tial proportion of children and adolescents who present
to community mental health clinics do not meet criteria
for a DSM disorder but, rather, evidence impaired func-
tioning (Angold, Costello, & Erkanli, 1999). Anxiety is a
specific problem area that has been found likely to lead
to youth impairment, but it is not necessarily a diagnosis
(Angold et al., 1999).
Because impairment may not be reported by the par-
ents and/​or children, it is important to probe carefully for
whether the child is mastering expected developmental
tasks (e.g., developing peer relationships). If not, then
anxiety may be deemed as potentially impairing. As noted
previously, contained on the ADIS-​C/​P is the clinician
rating scale, which allows for an assessment of interfer-
ence of each anxiety diagnosis along a 0-​to 8-​point scale,
where 4 is considered a clinical diagnosis; less than 4 is
subthreshold. Retest reliability estimates of the clinician
rating scale ratings have been found to be satisfactory
(e.g., Silverman & Eisen, 1992). The clinician rating
scale can also be adapted to assess for interference of anxi-
ety symptoms, even if DSM diagnostic criteria are not
met. For example, for a child who does not meet full cri-
teria for SAD but cannot sleep alone at night without her
mother, the child could be asked the following: “You just
told me that sometimes you have trouble sleeping alone
at night without your mother. How does not being able to
go to sleep by yourself mess things up in terms of how you
now are doing in school? How about in terms of things
with your family? And how much does it affect things with
friends? And how much does it make you feel very upset
[personal distress]?”
The PARS (RUPP Anxiety Study Group, 2002)  is
another measure designed to assess the frequency,
severity, and associated impairment across SAD, SOP,
and GAD symptoms in children and adolescents (aged
6–​17  years). The internal consistency of scores on the
PARS has been found to be satisfactory, but its retest reli-
ability needs further study (e.g., retest reliability  =  .55
for the total scale score using an average retest interval
of approximately 3 weeks). The PARS’s convergent and
divergent validity also needs further examination. For
example, although observed correlations have been found
to be in the expected directions (i.e., positive correlations
with ratings of internalizing symptoms and negative cor-
relations with externalizing symptoms), this was especially
true of the correlations between PARS ratings and clini-
cian ratings and also other sources’ ratings, including chil-
dren’s ratings on the MASC.
Because anxiety is clinically significant only when there
is an associated level of interference in functioning (APA,
2013), the Child Anxiety Impact Scale (CAIS; Langley,
Bergman, McCracken, & Piacentini, 2004; Langley et al.,
2014) is a scale that represents the growing understanding
of the critical role of impact or interference. The CAIS
is a 27-​item rating scale (i.e., 4-​point Likert scale, from
0 [not at all] to 3 [very much]) that measures functional
impairment of anxiety symptoms on psychosocial func-
tioning in school, social, and family domains. Children
are asked to rate the amount of difficulty they have in
completing the activity described by the item due to anxi-
ety. The CAIS has a parallel version for parents. Internal
 Anxiety Disorders in Children and Adolescents
consistency has been found to be adequate to good for the
total scores and subscale scores (Cronbach’s α  =  .70 to
.90). Scores on the CAIS also predict other anxiety scores,
including on the MASC, PARS, SCARED, and the Child
Behavior Checklist (CBCL) internalizing scales (Langley
et al., 2014).
Best practices suggest the consideration of impairment
when assessing children and adolescents who present
with anxiety difficulties. Impairment rating scales provide
reliable and valid estimates of the extent of the youth’s
impairment. For those children and adolescents who
show significant impairment in their functioning, even if
subthreshold in diagnosis, treatment services still could be
important to provide.
Considering Family Accommodation
Rather than viewing a child’s anxiety primarily as an indi-
vidual phenomenon impacting the child, an alternative
conceptualization is to view childhood anxiety as sys-
temic, emphasizing the importance of family interactions.
Researchers have begun to focus on parents’ involvement
in childhood anxiety disorders through the process of fam-
ily accommodation. Parents who regularly attempt to alle-
viate their child’s distress by changing their own behavior
may inadvertently maintain their child’s anxiety (e.g.,
Lebowitz, Scharfstein, et al., 2014). Assessing FA as part of
a case conceptualization provides clinicians with alterna-
tive or additional treatment targets, and treatments have
emerged that emphasize the reduction of FA through
parent-​based work (Lebowitz & Omer, 2013; Lebowitz,
Omer, Hermes, & Scahill, 2014). This approach may be
particularly useful if the child is not willing or is unable to
participate directly in treatment.
The Family Accommodation Scale-​ Anxiety (FASA;
Lebowitz et  al., 2013)  requires parents to rate the fre-
quency with which they engage in FA, and it includes two
subscales for specific domains of FA: (a) active participa-
tion in symptom-​driven behaviors and (b)  modifications
to parent or family routines and schedules. The FASA also
queries parental distress relating to the need to accommo-
date the child as well as negative child consequences of
refusing to accommodate. A child report version of FASA
(FASA-​CR; Lebowitz, Scharfstein, et  al., 2015)  parallels
the parent version and also queries child beliefs relating
to FA, such as whether the child believes it is helpful
and whether he or she believes the parents should cease
accommodating. Results from several independent stud-
ies indicate that FA is very prevalent across the anxiety
disorders (e.g., 97% of parents endorsing FA), is associated
231
with more severe symptoms, and reduction in FA is asso-
ciated with treatment response of childhood anxiety dis-
orders (Jones et  al., 2015; Kagan, Peterman, Carper, &
Kendall, 2016; Lebowitz, Panza, et  al., 2016; Lebowitz
et al., 2013).
Overall Evaluation
The field has available many promising assessment mea-
sures and strategies to augment information obtained
from diagnostic interviews to guide decisions about treat-
ment planning, but it has a long way to go in achieving an
evidence base to guide these efforts. Although the use of
these measures can help in arriving at a clinically mean-
ingful and useful case conceptualization and implement
a clinically sensitive and feasible treatment plan at the
individual level, these measures have not yet been shown
to be useful at the group or nomothetic level. Similarly,
despite the preliminary evidence for adopting an idio-
graphic, prescriptive approach to treat anxiety disorders
and/​or school refusal behavior, through the identification
of problematic symptoms and/​or functionally motivating
conditions, evidence is needed that the former is more effi-
cacious than a nomothetic, statistically based approach
(Silverman & Berman, 2001). Another important devel-
opment in the field is the assessment and targeting of
family accommodation, as a maintaining factor in the
development of anxiety. It is important for future research
to compare the relative efficacy of an idiographic, pre-
scriptive approach to a standard CBT package.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
This section deals with assessment measures and strate-
gies most useful for tracking the progress of treatment
and evaluating the overall effect of treatment on anxiety
symptoms, diagnosis, and general functioning. Diagnoses
derived from interview schedules have been used for treat-
ment evaluation purposes. In treatment studies, 100% of
participants meet diagnostic criteria for an anxiety dis-
order at pretreatment. An important outcome variable
is diagnostic recovery rate at post-​treatment and follow-​
up. Most studies report 60% to 80% of participants as
recovered or no longer meeting diagnostic criteria at
post-​treatment, with maintenance of recovery at 1-​year
follow-​up (Ollendick et al., 2006; Silverman et al., 1998).
Studies vary to the extent that the primary diagnosis is
reported versus “all” anxiety diagnoses.
232 Anxiety and Related Disorders

TABLE 11.3   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Diagnostic Interview Schedules

ADIS C/​P-​IV NA NA E E E E E E ✓
DISC-​IV NA NA A G G G G G
DICA NA NA A G G G G G
K-​SADS NA NA G A A A G A
Parent
CBCL-​I E G NA G E E G G ✓
Clinician
ADIS-​C/​P: CRS NA NA G E G NA NA E ✓
Child
CAIS G E NA NA G G G E ✓
RCMAS E G NA G G E G G ✓
STAIC G G NA G G G G A
FSSC-​R A E NA G E G G G ✓
MASC G G NA G G E E E ✓
SCAS A G NA A E E G G
SPAIC A G NA E E G G G
Behavioral Observations
BAT/​SET/​PYIT NA NA G G G G G G ✓

Note: ADIS C/​P-​IV = Anxiety Disorders Interview Schedule; DISC-​IV = Diagnostic Interview Schedule for Children, Version IV; DICA = Diagnostic
Interview Schedule for Children and Adolescents; K-​SADS = Schedule for Affective Disorders and Schizophrenia for School-​Age Children; CBCL-​
I = Child Behavior Checklist-​Internalizing Scale; ADIS-​C/​P: CRS = Anxiety Disorders Interview Schedule-​Child and Parent Versions: Clinician
Rating Scale; CAIS = Child Anxiety Impact Scale; RCMAS = Revised Children’s Manifest Anxiety Scale; STAIC = State–​Trait Anxiety Inventory for
Children; FSSC-​R = Fear Survey Scale for Children-​Revised; MASC = Multidimensional Anxiety Scale for Children; SCAS = Spence Children’s
Anxiety Scale; SPAIC = Social Phobia and Anxiety Inventory for Children; BAT/​SET/​PYIT = Behavioral Avoidance Task/​Social Evaluative Task/​
Parent–​Youth Interaction Task; A = Adequate; G = Good; E = Excellent; NA = Not Applicable.

Because interview schedules were discussed previously
and because data from self-​ monitoring procedures are
reported in many case studies or single case designs but
rarely in randomized trials, emphasis is placed in this sec-
tion on rating scales and observational methods (Table 11.3).
The section also includes a discussion of best practices with
respect to conceptual and practical issues and concludes
with an overall evaluation.
It is worth noting first that rating scales and obser-
vational methods were not often administered over the
course of a child or adolescent treatment program, but
just at pretreatment, post-​ treatment, and follow-​ up; in
some studies, they were administered at mid-​treatment
(Kendall et al., 1997). As interest has grown over the years
in identifying mediators of treatment, the importance in
administering measures of hypothesized mediators and
the primary outcome measures during the course of treat-
ment (e.g., every other session) has grown as well. This
allows for a more precise evaluation of temporal prece-
dence of the mediator(s) over the outcome(s) (Maric,
Prins, & Ollendick, 2015). If one is concerned about cli-
ent burden, one could administer an abridged version of
a rating scale. This can be accomplished by determining
the three or four items of the scale that correlate most
highly with the total score (or total subscale scores) and
administering only those items on a weekly or biweekly
basis. In addition, because there are fluctuations in rat-
ing scale scores irrespective of treatment, usually attenu-
ation, it can also be useful to administer scales at least
twice prior to the intervention—​first at the initial intake
and then immediately prior to treatment.
Rating Scales
The use of rating scales represents best practices for the
assessment of treatment progress and treatment outcome
because they are sensitive to treatment change. Rating
scales completed by youth, parents, teachers, or clinicians
are easy to administer, have relatively low cost, and have
objective scoring procedures (Silverman & Rabian, 1999;
Silverman & Serafini, 1998). See Table 11.3 for the most
widely used rating scales for this assessment purpose. The
most common rating scales used in clinical trials that
have been shown to be sensitive to treatment effects have
been the teacher and parent rating versions of the CBCL;
(Achenbach, 1991a, 1991b). The CBCL is a 118-​item
(parent version) and a 120-​item (teacher version) behav-
ior checklist that assesses the behavior problems and social
 Anxiety Disorders in Children and Adolescents
competencies of children and adolescents using a 3-​point
scale (not true, somewhat or sometimes true, and very true
or often true). The CBCL includes broadband subscales
(i.e., externalizing and internalizing) and narrowband sub-
scales (i.e., withdrawn, somatic complaints, and anxious/​
depressed). Van Meter et al. (2014) examined the proper-
ties of the CBCL and Youth Severity Rating (YSR) inter-
nalizing scales in two large samples (N = 1,084 and 651).
They found that both measures discriminated between
youth with any anxiety disorder or GAD from other diag-
noses, leading them to conclude that the CBCL and YSR
provide valuable information as to whether a youth is expe-
riencing an anxiety disorder. Evans, Thirlwall, Cooper,
and Cresswell (2016) examined whether the CAIS and
SCAS could be used to identify recovery from an anxiety
disorder in 337 children. They found that both measures,
particularly the CAIS parent version, were useful for this
purpose, except in cases of specific phobia. The Clinician
Rating Scale of the ADIS for DSM-​IV: C/​P (Silverman &
Albano, 1996) also has been used in a number of studies.
It, too, has been found to be sensitive to treatment effects
(Silverman & Ollendick, 2005).
Behavioral Observations
The use of direct behavioral observation represents another
approach for assessing treatment progress and treatment
outcome, although it has been far less used for this pur-
pose relative to interviews (i.e., diagnostic recovery rates)
and rating scales (i.e., statistically significant declines in
dimensional scores; see Table 11.3). In studies by Kendall
et  al. (1997) and Beidel et  al. (2000), participants were
asked to engage in an evaluative task and were given stan-
dard behavioral assertiveness instructions. Both Kendall
et  al. (1997) and Beidel et  al. (2000) reported treatment
improvements in participants’ performance on these tasks.
Using a family observation task, however, Barrett et  al.
(1996) did not find significant pre-​to post-​treatment dif-
ferences between an individual-​versus family-​based CBT.
The extent that newer developed behavioral assessment
measures, such as the YIKES, are sensitive to treatment
change is currently under investigation.
Conceptual and Practical Issues in the Assessment
of Treatment Progress and Treatment Outcome
Using Normative Data
There are concerns about using normative values to assess
clinical significance. Norming mainly indicates a child’s
relative standing; it still does not indicate a child’s absolute
233
standing on anxiety. When the CBCL (Achenbach,
1991a, 1991b), for example, is used to assess treatment
outcome, clinically significant improvement is defined as
meeting a minimum criterion T score on the CBCL inter-
nalizing scale of less than 70 (adjusted according to age
norms; Kendall et al., 1997; Silverman et al., 1999). Thus,
cases that shift from being above this cut-​off value to being
below the cut-​off value are viewed as clinically significant
improvement following the treatment (see Kazdin, 1999).
There is no clear evidence, however, that children who
score below 70 have fewer worries or display less avoidant
behaviors compared to children who score above 70. That
is, this shift on the CBCL from pre-​to post-​treatment does
not inform whether the treatment had meaningful impact
on the day-​to-​day functioning of the treated youth (see
Kazdin, 1999). Examples such as meeting role demands,
functioning in everyday life, and improvement in the
quality of one’s life would also be useful to assess.
Reporting Biases
It is reasonable to assume that some anxious children
are reluctant to self-​disclose their personal anxious reac-
tions on rating scales. The RCMAS Lie Scale and the
RCMAS-​2 Defensiveness Scale are useful in this regard.
The RCMAS Lie Scale, a downward extension of the Lie
Scale on the adult version of the Manifest Anxiety Scale,
was derived from the social desirability/​Lie Scale of the
Minnesota Multiphasic Personality Inventory. Containing
items such as “I never get angry,” “I like everyone I know,”
and “I am always kind,” the Lie Scale has been used as
an indicator of social desirability or defensiveness (Dadds,
Perrin, & Yule, 1998; Reynolds & Richmond, 1985),
reflecting a tendency to present oneself in a favorable
light and/​or to deny flaws and weaknesses that others are
usually willing to admit.
Research using the RCMAS Lie Scale in unselected
school samples (Dadds et  al., 1998)  and clinic-​referred
anxious samples (Pina, Silverman, Saavedra, & Weems,
2001) reveals younger children score significantly higher
on the Lie Scale compared to older children; no signifi-
cant sex differences have been found. These findings
underscore the need for clinicians and researchers to
recognize that younger anxious children are more likely
than older age groups to evidence social desirability when
using anxiety rating scales. The findings also underscore
the need to emphasize to anxious youth that there are “no
right or wrong answers” during the assessment process.
Similar pressure to please and to be viewed in a favorable
light may exist with other assessment strategies such as
behavioral observations, although the issue has not been
234 Anxiety and Related Disorders
studied. Research with the Defensiveness Scale of the lat-
est revision of the RCMAS is also needed.
Overall Evaluation
There has been little systematic assessment undertaken
over the course of child anxiety treatment studies to
monitor treatment progress. It is recommended that
such efforts be undertaken. Using abbreviated versions
of psychometrically sound measures may represent one
important way to move this work forward. Diagnostic
interviews and rating scales have been most widely used
for evaluating treatment outcome. Despite the wide
usage of rating scales and that the scales show sensitiv-
ity to change, more research is needed to determine
the clinical relevance or value of scores on these scales,
including changes in scores.
CONCLUSIONS AND RECOMMENDATIONS
We first provided an overview of anxiety disorders in
children and adolescents and then summarized the
research evidence for psychological assessment anxiety
measures and strategies. The focus was on measures
that are not only evidence based but also feasible and
useful for the needs of the practitioner. Based on the
information provided in this chapter, we make the fol-
lowing recommendations.
For the purpose of diagnosis, structured or semi-​
structured clinical interviews are recommended because
they lead to more reliable anxiety diagnoses compared to
unstructured clinical interviews. The interview schedule
used most frequently has been the ADIS-​C/​P. Although
reliability and validity of anxiety diagnoses have been
documented using this schedule, further evaluation of the
interview schedule is needed in community clinics and
with disorders of varying base rates.
To assist in screening for anxiety disorders for later
diagnostic workups, it is recommended that factor scale
scores of instruments be examined, not just total scores,
when trying to discriminate anxiety disorders from other
disorders. Also relating to screening, the MASC appears
to have the most research evidence, although the evi-
dence is limited. More research needs to be conducted
with the MASC-​2, including the new parent version.
The MASC-​ 2, as well as the RCMAS-​ 2, appears to
have valuable additional features, but more research is
required to scrutinize and better understand the utility
of these measures.
To assess for the purpose of case conceptualization and
treatment formulation, a prescriptive treatment approach
represents a potentially useful way to proceed and a fruit-
ful avenue for future research. Also clinically useful for
the purpose of case conceptualization and treatment for-
mulation are direct observations and self-​monitoring pro-
cedures, but questions exist about their feasibility, retest
reliability, and validity.
For the purpose of assessing for treatment outcome,
using the ADIS interviews, the RCMAS, and the CBCL
internalizing scales have been the most widely used
measures, and they all have been found to be sensitive
to change. The FASA and CAIS are both relatively new
measures to the field but hold much promise given the
growing interest in both family processes and impairment,
respectively. It is almost always important to consider
multiple sources of information, and not assume there is
one unique gold standard, because different perspectives
likely reflect biases and varying perceptions of what is in
the best interest of the child or adolescent.
ACKNOWLEDGMENTS
This work was supported in part by National Institute of
Mental Health grants R34 MH096915, R34 MH097931,
and K23MH103555 and by a NARSAD Young Investigator
Award (21470).
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 12
Specific Phobia and Social Anxiety Disorder
Karen Rowa
Randi E. McCabe
Martin M. Antony
Although it is widely accepted that assessment proce-
dures are an important part of understanding and treat-
ing anxiety-​based problems, relatively little attention has
been paid to developing and studying comprehensive,
evidence-​based assessment protocols for the anxiety dis-
orders. This is in contrast to the extensive attention that
has been paid to empirically supported treatment inter-
ventions for anxiety disorders during the past two decades
(e.g., Olatunji, Cisler, & Deacon, 2010) and to the large
number of studies regarding the psychometric proper-
ties of particular anxiety measures. The importance of
empirically supported assessment procedures for anxiety
disorders has been discussed (e.g., Antony & Rowa, 2005),
with the hope that research on these procedures and pro-
tocols will add to our growing knowledge regarding the
reliability and validity of particular instruments.
It is useful to summarize what we know about com-
monly used assessment tools and procedures because this
can provide guidance to clinicians and researchers regard-
ing the most appropriate tools for various assessment tasks.
This chapter reviews the scientific status and clinical
utility of the most commonly practiced assessment pro-
cedures for two of the anxiety disorders—​specific phobia
and social anxiety disorder.
NATURE OF SPECIFIC PHOBIA AND SOCIAL
ANXIETY DISORDER
Diagnostic Considerations
Specific phobia and social anxiety disorder (SAD) share
a number of features, including the presence of excessive
242
fear, anxious apprehension, and avoidance behavior.
However, it is the focus of fear that distinguishes between
the two anxiety disorders. In specific phobia, the exces-
sive fear is focused on a particular situation or object (e.g.,
animals or insects, heights, seeing blood or receiving a
needle, driving, and enclosed places, among others). In
SAD, the excessive fear is focused on one or more social
and performance situations in which the individual fears
acting in a way that will be embarrassing or lead to nega-
tive evaluation by others (e.g., public speaking, parties,
being assertive, making small talk, and dating) or reveal-
ing unbecoming personal attributes (Moscovitch, 2009).
Apart from the focus of the fear, the diagnostic cri-
teria as outlined in the fifth edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-​5;
American Psychiatric Association [APA], 2013) have sig-
nificant similarities for these two disorders. For both con-
ditions, exposure to the feared stimulus typically results
in an immediate anxiety response that may escalate into a
full-​blown panic attack, and feared situations are avoided
or endured with distress. Symptoms are persistent, lasting
6 months or longer. Moreover, the symptoms (i.e., fear,
anxious apprehension, and avoidance) cause the individ-
ual significant distress or impairment in functioning and
are not better explained by another mental disorder. In
addition, for SAD, the fear is not due to the physiological
effects of a substance or a general medical condition, and
if a general medical condition or another mental disorder
is present, the fear is unrelated to it (e.g., a fear of shak-
ing in the presence of Parkinson’s disease or a fear of eat-
ing in public in the presence of an eating disorder would
not be indicative of SAD). When assigning a diagnosis of
specific phobia, the category of fear is specified as one of

five types: animal (e.g., dogs, birds, and insects), natural
environment (e.g., heights and water), blood–​injection–​
injury (e.g., getting a needle and seeing blood), situ-
ational (e.g., driving, enclosed places, and flying), and
other (e.g., fear of choking or vomiting). When assigning
a diagnosis of SAD, the specifier performance only may be
used in cases in which the fear is limited to speaking or
performing in public.
Evidence suggests that avoidant personality disorder
and SAD may be alternative conceptualizations of the
same disorder, with avoidant personality disorder repre-
senting a more severe and more generalized form of the
condition (Ralevski et  al., 2005), although some have
argued against this assertion (e.g., Eikenaes, Egeland,
Hummelen, & Wilberg, 2015). Regardless, the assess-
ment measures reviewed in this chapter are likely insuf-
ficient to properly assess avoidant personality disorder.
Indeed, there is variability even within a group of people
diagnosed with SAD that needs to be considered for assess-
ment. Hoffmann, Heinrichs, and Moscovitch (2004)
noted that although individuals meeting symptom criteria
for a diagnosis of SAD share certain specific features, in
reality, they are a heterogeneous group that may be better
characterized along a dimensional continuum of emo-
tional response and behavioral tendencies encompassing
fearfulness, anxiousness, shyness, self-​consciousness, sub-
missiveness, and anger.
Epidemiology and Descriptive Psychopathology
Specific phobia is one of the most common anxiety dis-
orders, with a lifetime prevalence estimate of 12.5%
(e.g., Kessler et al., 2005). Studies in community samples
revealed a median lifetime prevalence rate of 6.65% for
SAD (Fehm, Pelissolo, Furmark, & Wittchen, 2005),
although the replication of the National Comorbidity
Survey suggested a lifetime prevalence of 12% (Kessler
et  al., 2005). Studies of college samples suggest a point
prevalence of 11.6% for SAD (Baptista et  al., 2012),
adding further evidence that SAD is a common disor-
der. There is no evidence that the prevalence rates of
anxiety disorders (including SAD and specific phobia)
have changed significantly during the past few decades
(Bandelow & Michaelis, 2015), lending support for ear-
lier prevalence estimates. Specific phobias are more com-
mon in women than in men (e.g., Curtis, Magee, Eaton,
Wittchen, & Kessler, 1998), although there is variability
across specific phobia types with respect to gender and
prevalence. Similarly, SAD is slightly more common in
women than in men (Fehm et al., 2005).
Specific Phobia and Social Anxiety Disorder 243
The majority of specific phobias (animal, blood–​
injection–​injury, and natural environment) typically have
an onset in childhood, typically before age 15  years (de
Lijster et  al., 2017). However, situational-​type phobias
(e.g., flying, driving, and elevators) have a later age of
onset, typically in late adolescence or early adulthood
(e.g., Antony, Brown, & Barlow, 1997b; Lipsitz, Barlow,
Mannuzza, Hofmann, & Fyer, 2002). Onset of SAD is
typically during childhood and adolescence, with a range
of 13 to 24 years in clinical studies and 10 to 16.6 years in
epidemiological studies (Wittchen & Fehm, 2003). Later
onset of SAD (after the age of 25 years) is rare and typi-
cally secondary to, or encompassed by, a separate men-
tal disorder (depression, eating disorder, etc.) (Koyuncu
et al., 2015; Wittchen & Fehm, 2003).
Specific phobias are often comorbid with other spe-
cific phobias and other anxiety disorders (Curtis et  al.,
1998; Sanderson, DiNardo, Rapee, & Barlow, 1990).
However, in the latter case, specific phobia tends to be
of lesser severity then the comorbid condition (Sanderson
et  al., 1990). SAD is associated with a high degree of
comorbidity. It is estimated that 50% to 80% of individ-
uals with SAD have at least one other mental disorder,
most commonly other anxiety disorders, major depressive
disorder, and substance use disorders (Fehm et al., 2005;
Wittchen & Fehm, 2003). Anxiety disorders, including
SAD and specific phobia, tend to precede the onset of
comorbid depression, with some evidence that interper-
sonal difficulties related to anxiety (e.g., interpersonal
sensitivity) may partially explain this association in SAD
(Starr, Hammen, Connolly, & Brennan, 2014).
Evidence suggests that specific phobia can be associ-
ated with high levels of psychosocial impairment in some
cases (Essau, Conradt, & Petermann, 2000), and type
of phobia may be important. For example, Ollendick,
Raishevich, Davis, Sirbu, and Öst (2010) found that, as
assessed by parent report, adolescents with natural envi-
ronment phobias had more social problems than those
with animal phobias. SAD is associated with a significant
degree of impairment and disability that increases over
the individual’s lifespan (e.g., Fehm et al., 2005; Wittchen
& Fehm, 2003). The disruption in quality of life in SAD
is similar to impairments found in other anxiety disorders
(e.g., Barrera & Norton, 2009). One study found that
21% of individuals with SAD had clinically severe impair-
ment (defined as being two or more standard deviations
below the community norm) in quality of life (Rapaport,
Clary, Fayyad, & Endicott, 2005). The presence of
SAD (at threshold or subthreshold levels) as a comor-
bid condition among individuals with panic disorder or
244 Anxiety and Related Disorders
generalized anxiety disorder is related to poor quality
of life (Camuri et  al., 2014). In addition, there is some
evidence that safety behaviors used by individuals with
SAD are related to significant impairment in social per-
formance (e.g., Rowa et al., 2015; Stangier, Heidenreich,
& Schermelleh-​Engel, 2006).
Etiology
Genetic factors appear to play a role in the development
of both specific phobia and SAD, though to different
degrees. First-​degree relatives of individuals with specific
phobia or SAD have an increased risk of having the disor-
der compared to first-​degree relatives of never mentally ill
controls (Fyer et al., 1990; Steinhausen, Jakobsen, Meyer,
Jørgensen, & Lieb, 2016), although family aggregation
appears to be stronger for SAD compared to specific pho-
bias (Steinhausen et al., 2016). Twin studies suggest that
genetic influences may be different depending on the
type of phobic stimulus in SAD and specific phobias. For
example, recent research does not support genetic fac-
tors in situational specific phobias, whereas genetic fac-
tors influence the development of other phobias (Loken,
Hettema, Aggen, & Kendler, 2014). Some studies have
failed to find a genetic role in the development of pho-
bias at all (Skre et al., 2000). Genetic influences in SAD
also seem to vary by age; in one study, younger individu-
als were significantly more affected by genetic influ-
ences than were adults (Scaini, Belotti, & Ogliari, 2014).
Further research is needed to more fully understand the
genetic contributions both across anxiety disorders and
within subtypes of particular disorders.
Rachman (1977) proposed three pathways to fear
development:  direct conditioning (being hurt or fright-
ened by the phobic object or situation), vicarious acqui-
sition (witnessing a traumatic event or seeing someone
behave fearfully in the phobic situation), and informa-
tional transmission (through messages received from
others). Numerous studies have found support for this
model (for a review, see McCabe, Hood, & Antony,
2015). In addition to these learning processes, a fourth
nonassociative pathway has been proposed to explain
findings that are not accounted for by an associative
model (e.g., some fears emerge without any prior asso-
ciative learning experience). According to Poulton and
Menzies (2002), a limited number of fears are innate
or biologically determined and are adaptive from an
evolutionary perspective. Other factors that may play
a role in phobia development include the tendency
to experience “disgust” in response to certain stimuli
(i.e., disgust sensitivity), cognitive variables (e.g., infor­
mation processing biases), and environmental factors
(e.g., the context of a traumatic event, stress, and pre-
vious and subsequent exposure to a phobic stimulus)
(McCabe et al., 2015).
In addition to genetics and learning pathways, research
has uncovered a number of specific risk factors associated
with increased vulnerability for onset of SAD, including
familial environment (overprotective or rejecting parent-
ing style, parental modeling, and degree of exposure to
social situations) and behavioral–​ temperamental style
(elevated behavioral inhibition as a child) (Wittchen &
Fehm, 2003). Rapee and Spence (Rapee and Spence,
2004; Spence & Rapee, 2016) have proposed an etiologi-
cal model of SAD that attempts to capture the complexity
of SAD based on available research evidence. According
to their model, individuals have a “set point” level of
social anxiety that is somewhat stable and consistent and
is directed by broad genetic factors (e.g., general emo-
tionality and sociability). The individual’s set point is
altered (up or down) largely due to environmental factors
(e.g., parents, peers, negative life events, culture, inter-
rupted social performance, and poor social skill), which
then have a reciprocal relationship on levels of social
anxiety. These environmental factors operate as powerful
influences due to timing (critical stage of vulnerability),
impact (intensity or meaning of the event), or chronic-
ity. Furthermore, the set point can be altered by protec-
tive factors (e.g., parenting style), decreasing the  risk of
developing SAD. For example, a significant number of
individuals with SAD report a history of being severely
teased or bullied (McCabe, Antony, Summerfeldt, Liss,
& Swinson, 2003), and peer exclusion predicts symptoms
of social anxiety in young adults (Levinson, Langer, &
Rodebaugh, 2013). On the other hand, recent research
illustrates the protective effects of social support for indi-
viduals who are genetically predisposed to SAD (Reinelt
et  al., 2014). In summary, this model underscores the
myriad interacting factors that can influence the devel-
opment of SAD.
PURPOSES OF ASSESSMENT
Antony and Rowa (2005) suggested the following 10 com-
mon purposes for which assessments are used:
1. To establish a diagnosis
2. To measure the presence, absence, or severity of
particular symptoms

3. To measure features that cannot be assessed
directly through an interview or self-​report scales
(e.g., physiological processes and nonconscious
processes)
4. To facilitate the selection of target problems for
treatment planning
5. To measure a phenomenon that is of interest for
research
6. To assess whether a particular treatment is “evi-
dence based”
7. To include or exclude participants from a research
study
8. To answer questions of interest for insurance
companies (e.g., the presence of malingering)
9. To predict future behavior (e.g., treatment
compliance)
10. To evaluate eligibility for employment, benefits,
legal status, school placement, and so on
In order to evaluate whether an assessment procedure is
evidence based, one must ask the question, For what pur-
pose? A particular assessment protocol or measure may be
empirically supported for some purposes but not others.
In this chapter, we review assessment procedures for spe-
cific phobia and SAD as they are used for three main clini-
cal purposes: (a) diagnosis, (b) case conceptualization and
treatment planning, and (c)  treatment monitoring and
evaluation. For precise psychometric information on the
measures we review (e.g., reliability values of scores with
various samples), we encourage interested readers to con-
sult the original sources cited in the following sections.
ASSESSMENT FOR DIAGNOSIS
Establishing a diagnosis for people suffering from specific
phobia and SAD is important for a number of reasons.
Diagnosis facilitates communication about the present-
ing problem and the accompanying symptoms, and it also
allows for the selection of the most appropriate evidence-​
based treatments, many of which have been developed
for particular disorders. Diagnostic clarification also
helps clinicians distinguish among different conditions
and make decisions about whether clinical issues are best
conceptualized as separate problems or as different fea-
tures of the same problem. For example, embarrassment
about losing bowel control may lead to avoidance of situ-
ations similar to that seen in SAD, but it would often be
better accounted for by a diagnosis of panic disorder or
agoraphobia. Furthermore, achieving a broad diagnostic
Specific Phobia and Social Anxiety Disorder 245
picture can also aid a clinician in understanding the
impact that comorbid conditions (e.g., substance use dis-
orders and personality disorders) may have on the course
and treatment outcome for specific phobia and SAD. The
presence of certain comorbid conditions may influence
a client’s readiness for treatment and decisions about the
order of treatment interventions (e.g., whether to treat
the anxiety disorder or the substance issue first) and the
treatment process (e.g., the necessity to develop alterna-
tive coping strategies for someone who is using substances
to manage symptoms of anxiety). Other chapters in this
volume provide more details about the assessment of rele-
vant comorbid conditions such as substance use disorders
(see Chapter 17) and depression (see Chapters 6–​8).
There is considerable debate about whether the focus
on a particular diagnostic category should be replaced by
assessment of continuous, transdiagnostic factors that cut
across anxiety disorders (e.g., Gros, McCabe, & Antony,
2013). However, there is still much emphasis on diagnosis
in clinical practice, and research supports a taxonic or cat-
egorical model of SAD compared to a dimensional model
(e.g., Weeks, Carleton, Asmundson, McCabe, & Antony,
2010). For these reasons, there seems to be an ongoing, rel-
evant place for diagnosis of SAD and specific phobia, sup-
porting the need to review common diagnostic methods.
Diagnoses can be established using unstructured
clinical interviews, fully structured interviews, or semi-​
structured interviews (for a review, see Summerfeldt,
Kloosterman, & Antony, 2010). The main way in which
these approaches differ is in the level of standardization.
Unstructured clinical interviews are the least standard-
ized, and they are the most commonly used clinical
interview format in routine practice. In unstructured
interviews, clinicians ask whatever questions they view
as appropriate for assessing the diagnostic features of par-
ticular disorders as well as other clinical characteristics of
interest. However, research suggests that rates of diagnos-
tic agreement using clinical interviews are often no better
than chance (Spitzer & Fleiss, 1974), rendering the reli-
ability and validity of diagnostic findings suspect.
In contrast, fully structured interviews (e.g., the World
Health Organization Composite International Diagnostic
Interview [WHO-​CIDI]; Kessler & Ustun, 2004) are the
most standardized format for diagnostic interviews. In
these interviews, questions are always asked in the same
way, and there is little flexibility to ask follow-​up questions
or to ask for clarification. These interviews are designed to
be used by trained lay interviewers, and they are primar-
ily used in large epidemiological studies rather than by
clinicians or clinical researchers. In addition, questions
246 Anxiety and Related Disorders
TABLE 12.1   Ratings of Instruments Used for Diagnosis
Internal Inter-​Rater Test–​Retest
Instrument Norms Consistency Reliability Reliability
ADIS-​IV NA NA G NR
SCID-​IV NA NA E NR
Note: ADIS-​IV = Anxiety Disorders Interview Schedule for DSM-​IV; SCID-​IV = Structured Clinical Interview for DSM-​IV; A = Adequate;
G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.
have been raised regarding the validity of anxiety disor-
der diagnoses as established by fully structured interviews
(see Antony, Downie, & Swinson, 1998; Summerfeldt
et al., 2010).
Semi-​structured interviews include many of the advan-
tages of both structured and unstructured interviews.
Standard questions are asked to assess each of the diagnos-
tic criteria necessary for making a diagnosis, but clinicians
are permitted to ask follow-​up questions for clarification
and to answer questions that respondents may have about
particular questions. Semi-​structured interviews are the
most common type of diagnostic interview used in clini-
cal research, and they are occasionally used in routine
clinical practice as well.
Two of the most extensively studied semi-​structured
interviews for diagnosing anxiety-​related problems includ-
ing specific phobia and SAD are the Anxiety Disorders
Interview Schedule for DSM-​ IV (ADIS-​ IV; Brown,
DiNardo, & Barlow, 1994; DiNardo, Brown, & Barlow,
1994)  and the Structured Clinical Interview for DSM-​
IV/​Axis I Disorders (SCID-​IV; First, Spitzer, Gibbon, &
Williams, 1996). With the publication of DSM-​5, updated
versions of both these interviews have been published,
although few data exist on the psychometric properties of
these revised measures. As a result, much of the following
discussion focuses on data from the SCID-​IV and ADIS-​
IV. Similar to the SCID-​IV and ADIS-​IV, both the SCID-​
5 and ADIS-​5 provide systematic questions to establish a
current diagnosis of specific phobia or SAD. Questions
and initial probes are outlined for interviewers, ensuring
that all clients receive the same questions, in the same
order, using the same terminology. Subsequent follow-​up
questions may deviate from the structured questions. For
example, additional questions may be necessary to differ-
entiate a specific phobia of driving from fears of driving
associated with panic disorder (e.g., “What is the focus
of your fear when driving? Having a panic attack? Being
in an accident?”). These interviews provide decision
trees to establish diagnoses once pertinent information is
Content Construct Validity Clinical Highly
Validity Validity Generalization Utility Recommended
E G G E ✓
E G G E ✓
collected. These instruments are described next in more
detail, and a summary of the psychometric properties of
the SCID-​IV and ADIS-​IV can be found in Table 12.1.
Anxiety Disorders Interview Schedule for DSM-​IV
and DSM-​5 (ADIS-​IV and ADIS-​5)
The ADIS-​ IV (DiNardo et  al., 1994)  and ADIS-​ 5
(Brown & Barlow, 2014) are clinician-​administered semi-​
structured interviews that provide both diagnostic and
dimensional information about a range of psychological
problems, including anxiety and related disorders, mood
disorders, somatoform disorders, and substance use disor-
ders. Screening questions are provided for other mental
disorders. Depending on the version of the ADIS-​IV or
ADIS-​5 used (adult and lifetime versions), current and
lifetime diagnoses can be ascertained. Clinicians require
extensive training in the administration of this interview,
and the interview duration can be lengthy (e.g., several
hours). Despite these drawbacks for everyday practice, the
ADIS has the benefit of providing clear criteria to help
determine the presence or absence of specific phobia and
SAD (as well as common comorbid disorders), as well as
assessing useful information such as the degree of fear
and avoidance in a variety of social settings. Indeed, the
ADIS goes well beyond the SCID-​IV or SCID-​5 in terms
of screening for a wide variety of social and performance
situations in which a person may experience fear, increas-
ing the chance that difficulties with social situations or
a specific phobia will be identified. If initial inquiries
reveal the possibility of symptoms of specific phobia or
SAD, a number of follow-​up questions are asked to assess
the intensity of the fear, the frequency and breadth of
avoidance, the level of distress and interference caused by
symptoms, and other relevant variables.
The ADIS-​ IV has demonstrated good reliabil-
ity:  Inter-​rater reliability was strong for specific pho-
bia and SAD, both when diagnosed as the principal
or additional diagnosis (Brown, DiNardo, Lehman, &

Campbell, 2001). In fact, agreement between clinicians
was good to excellent for most clinical diagnoses. The
main source of disagreement for both specific phobia
and SAD in this study involved rating the clinical sever-
ity of the disorder, with one clinician concluding that
the disorder was clinically significant and another clini-
cian concluding that the disorder severity did not exceed
clinical threshold for distress or impairment. This
study suggested that there were very few disagreements
between clinicians when deciding between SAD and
another disorder. In other words, clinicians appeared to
be successful in disentangling symptom presentations
to reliably diagnose SAD.
Structured Clinical Interview for DSM-​IV
(SCID-​IV) and DSM-​5 (SCID-​5)
The SCID-​ IV (First et  al., 1996)  and SCID-​ 5 (First,
Williams, Karg, & Spitzer, 2015)  are also clinician-​
administered semi-​ structured interviews that provide
diagnostic decisions about a wide range of psychiatric
disorders. The SCID-​IV is available in a clinician ver-
sion (SCID-​CV), a personality disorders version, and a
research version (SCID-​I). Four versions of the SCID-​5
are available—​a clinician version, a research version, a
clinical trials version, and a personality disorders version.
The clinician versions of this interview were designed for
use in clinical settings and have less extensive coverage
of disorders. The research versions have a broader focus.
Current and lifetime diagnoses are obtained for many dis-
orders. Extensive training is also required to administer
the SCID in all forms, and administration can be lengthy,
especially for the research version (i.e., 2 or 3 hours for
a typical outpatient administration of the SCID-​IV and
even longer for the SCID-​5).
Much of the evidence for the psychometric proper-
ties of the SCID-​IV is derived from research using an
earlier version based on DSM-​III-​R (APA, 1987)  cri-
teria, and no research thus far has examined the psy-
chometrics of the SCID-​5. Minimal changes affected
the revision of the SCID from DSM-​III-​R to DSM-​IV
(APA, 1994), but significant changes have affected the
revision to DSM-​5. Earlier studies suggested that the
SCID demonstrates adequate or better reliability (both
inter-​rater and test–​retest) for most diagnoses in patient
samples (Williams et  al., 1992)  but not in nonpatient
samples. Symptom agreement and diagnostic accuracy
using the SCID are also good (Ventura, Liberman,
Green, Shaner, & Mintz, 1998). The SCID-​IV has been
Specific Phobia and Social Anxiety Disorder 247
shown to reliably come to a diagnosis of SAD (Crippa
et al., 2008). However, for some populations, reliability
of diagnoses may be less robust. For example, a study
examining DSM-​III-​R lifetime diagnoses in a substance-​
abusing population found poorer test–​retest reliabilities
for lifetime diagnoses than has been found in other stud-
ies (Ross, Swinson, Doumani, & Larkin, 1995). Given
the comorbidity between SAD and substance use issues,
this issue is of relevance to consider. A summary of the
criterion-​related validity of the SCID suggests that there
is a high level of correspondence between SCID-​derived
diagnoses and other variables such as the clinical fea-
tures of disorders, the course of conditions, and treat-
ment outcome for certain conditions (Rogers, 1995).
Overall Evaluation
Because of their greater reliability, semi-​structured inter-
views such as the ADIS-​IV, ADIS-​5, SCID-​IV, or SCID-​5
are preferable to either unstructured clinical interviews
or fully structured clinical interviews, both in routine
clinical practice and in clinical research. However, given
the lack of research on the newly published ADIS-​5 and
SCID-​5, firm conclusions about the reliability of these
new versions cannot be made, and our recommendation
of these measures arises from research on their predeces-
sors. Although few studies have directly examined the
validity of these measures, there is a vast body of research
that indirectly supports their validity. For example, studies
often compare diagnostic results from the ADIS-​IV or the
SCID-​IV to scores on established questionnaire measures
for social or specific phobia, finding strong convergence
between the presence of the disorder (based on the inter-
view) and the presence of relevant symptoms (based on
self-​report scales). For example, the widely used Social
Interaction Anxiety Scale (Mattick & Clarke, 1998), a
self-​report measure of symptoms of social anxiety, demon-
strated a 97% correct classification rate when compared
to diagnoses of SAD made using the SCID-​IV or ADIS-​IV
(Rodebaugh, Heimberg, Woods, Liebowitz, & Schneier,
2006). Therefore, it is likely preferable to use a semi-​
structured interview such as the ADIS or SCID versus
unstructured or fully structured interviews when estab-
lishing a diagnosis of specific phobia or SAD. Given the
length and breadth of the SCID-​5 and ADIS-​5, clinicians
may want to consider using the clinician version of the
SCID-​5 or the most pertinent sections of either interview
to establish diagnoses while still constraining the length
of the interview.
248 Anxiety and Related Disorders

ASSESSMENT FOR CASE CONCEPTUALIZATION Self-​Report Measures of Severity

AND TREATMENT PLANNING and Phenomenology—​Specific Phobia

To plan an effective program of treatment for specific

An important function of assessment is to gather infor-
phobia, it is useful to understand the clinical presentation
mation for the purpose of case conceptualization and
of the person’s fear. Objectively, how severe is the indi-
planning treatment. Antony and Rowa (2005) reviewed
vidual’s fear compared to that of others with a similar diag-
the most important variables to assess when treating
nosis? What situations or objects does the person avoid
anxiety disorders, including the severity of the fear,
as a result of the fear? What kinds of anxious thoughts or
degree of avoidance, subtle avoidance and safety behav-
worries does the person have when confronting a feared
iors, use of maladaptive coping strategies, anxious cog-
situation?
nitions, motivation for treatment, treatment history,
Due to the heterogeneity of specific phobia, there
suitability for various forms of therapy, and the presence
are few assessment tools that provide information across
of skills deficits. In this section, we review a number
the broad range of phobic stimuli. Most measures are
of assessment measures designed to provide informa-
aimed at one particular type of specific phobia (e.g., a
tion on variables that are important to consider when
fear of spiders). An exception is the Fear Survey Schedule
developing an empirically supported treatment plan for
(FSS), versions II (Geer, 1965) and III (Wolpe & Lang,
an individual. Because empirically supported psycho-
1969). These two versions of the self-​ report measure
logical treatments for specific phobia and SAD include
are designed to assess a broad range of phobic stimuli
primarily cognitive and behavioral strategies, treatment
and objects. Individuals are presented with extensive
planning and conceptualization in this chapter will
lists of phobic stimuli and are asked to rate the severity
generally refer to preparing for a course of cognitive–​
of their fear based on Likert scales. Another exception
behavioral therapy (CBT). See Table 12.2 for summary
and a helpful screening tool for phobic stimuli is the
ratings of the instruments. Also, note that the diagnos-
Phobic Stimulus Response Scales (Cutshall & Watson,
tic instruments described previously may also be useful
2004). This tool screens individuals for a range of phobic
for gathering information relevant to treatment plan-
stimuli, including blood–​injection, animal, and physical
ning and conceptualization, and therefore such infor-
confinement fears. Preliminary analyses found adequate
mation (e.g., avoided situations and coping strategies)
psychometric properties for this screening tool (Cutshall
may already be known after completing a diagnostic
& Watson, 2004).
assessment. The measures described in this upcoming
Once a diagnosis of a particular specific phobia has
section provide additional as well as complementary
been made, it is likely to be more useful to use a measure
information to what is already known from a diagnostic
designed to assess the clinical features of that disorder.
assessment.

TABLE 12.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

FSQ A E NA A A G G G
SNAQ A G NA E NR G E G
DAI A E NA A A G E G
SPAI E E NA A E E E E ✓
SPIN E E NA A G G E E ✓
BFNE E E NA A G E E E ✓
DS G G NA NR E G A G
ASI-​3 E E NA G E E E E ✓
FMPS G G NA NR G G E G
SPRS G A G NR E G E A

Note:  FSQ  =  Fear of Spiders Questionnaire; SNAQ  =  Snake Questionnaire; DAI  =  Dental Anxiety Inventory; SPAI  =  Social Phobia and Anxiety
Inventory; SPIN = Social Phobia Inventory; BFNE = Brief Fear of Negative Evaluation Scale; DS = Disgust Scale; ASI-​3 = Anxiety Sensitivity Index,
third edition; FMPS = Frost Multidimensional Perfectionism Scale; SPRS = Social Performance Rating Scale; A = Adequate; G = Good; E = Excellent;
NA = Not Applicable; NR = Not Reported.

During the past three decades, researchers have devel-
oped a number of self-​report scales for measuring symp-
toms related to fears of snakes, spiders, dogs, heights,
blood, needles, dentists, enclosed places, storms, and
flying. We review several examples in the following para-
graphs and in Table 12.2; however, given the broad range
of specific phobia types, a comprehensive review of all
relevant measures is not possible. For a review of adult
measures, see Hood and Antony (2012). For a review of
child measures, see Ollendick, Davis, and Muris (2004)
or Southam-​Gerow and Chorpita (2007).
For a principal diagnosis of a specific phobia, ani-
mal type, psychometrically sound measures exist for
fear of spiders and snakes, two of the most commonly
feared animals. For example, the 18-​ item Fear of
Spiders Questionnaire (FSQ; Szymanski & O’Donohue,
1995) provides an objective measure of the severity of a
person’s fear of spiders, with scores clearly distinguishing
between phobic and nonphobic participants (Muris &
Merckelbach, 1996). This questionnaire seems best able
to predict conscious avoidance behaviors (i.e., behaviors
available to introspection and verbalization), whereas it
is less able to predict automatic fear responses, such as a
physiological startle response (Huijding & de Jong, 2006).
Therefore, the FSQ is useful for understanding the sever-
ity of a person’s fear of spiders and for understanding the
types of situations a client may avoid due to fears of spi-
ders, although it has less utility for helping understand
the role of implicit reactions to spiders when planning
treatment.
If a client reports a fear of snakes, the Snake
Questionnaire (SNAQ; Klorman, Hastings, Weerts,
Melamed, & Lang, 1974) provides a detailed understand-
ing of a person’s particular concerns about snakes and the
way this fear may affect his or her life. Individuals rate 30
fearful or nonfearful statements about snakes as true or
false. Total scores clearly distinguish patient populations
from nonclinical groups and from individuals with spi-
der phobias (Fredrikson, 1983). Psychometric properties
are robust in translation (e.g., Czech; Polák, Sedláčková,
Nácar, Landová, & Frynta, 2016). Scores are also sensitive
to treatment-​related changes (öst, 1978). However, scores
on this questionnaire do not correspond to actual behav-
ioral reactions to a caged snake, suggesting that this mea-
sure may have good, but not excellent, construct validity
(Klieger, 1987). Again, as a component of treatment plan-
ning, a questionnaire such as the SNAQ will provide the
clinician with an idea of the types of beliefs the individual
holds about snakes and the impact of these beliefs on the
person’s day-​to-​day functioning. Strongly held beliefs may
Specific Phobia and Social Anxiety Disorder 249
become the focus of cognitive restructuring efforts in ther-
apy, they may shape the provision of educational informa-
tion about snakes, or they may suggest ideas for in vivo
exposure exercises. For example, one item on the SNAQ
is “The way snakes move is repulsive.” If a person endorses
this item, it suggests that movement may form an impor-
tant part of his or her fear, and the person might benefit
from information about why snakes move the way they
do and from exposure exercises that incorporate a snake’s
movements.
Fear of dental and medical procedures is a common
type of specific phobia. There are numerous self-​report
measures of various dental and medical procedures that
can be useful in understanding the severity of a client’s
fear, the focus of the fear, and the types of situations
avoided due to the fear. Examples of these include the
Dental Cognitions Questionnaire (de Jongh, Muris,
Schoenmakers, & ter Horst, 1995), the Dental Fears
Survey (Kleinknecht, Klepac, & Alexander, 1973), the
Index of Dental Anxiety and Fear (Armfield, 2010), the
Medical Fear Survey (Kleinknecht, Thorndike, & Walls,
1996), and the Mutilation Questionnaire (Klorman et al.,
1974). One particular example of a useful self-​report mea-
sure for dental fears is the Dental Anxiety Inventory (DAI;
Stouthard, Mellenbergh, & Hoogstraten, 1993). This
36-​item measure provides information about the types of
dental-​related fears a client might have and the severity
of the fears. It was designed to provide information about
when a person experiences anxiety (e.g., in the dental
chair and in the waiting room); the situational aspects of
being at the dentist’s office that may bother people (e.g.,
dental treatments and the interaction between patient and
dentist); and the emotional, physical, and cognitive reac-
tions the person has to a dental situation. This measure
has been shown to have excellent internal consistency
and test–​retest reliability estimates (although only over a
short interval) and moderate correlations with a dentist’s
perception about a person’s anxiety (Stouthard et  al.,
1993). An independent test of the DAI’s convergent and
discriminant validity suggested that this measure is highly
related to other measures of dental fears, mildly related
to general fear and neuroticism, and not related to scales
hypothesized to be unrelated to dental fears (Stouthard,
Hoogstraten, & Mellenbergh, 1995). The questionnaire
has been translated into multiple languages, increasing its
clinical utility. We could find no treatment studies using
the DAI, and therefore its treatment sensitivity is currently
unknown.
In addition to the measures listed previously, there
are other self-​report measures for various phobias that are
250 Anxiety and Related Disorders
not reviewed in detail here, including the Emetophobia
Questionnaire (Boschen, Veale, Ellison, & Reddell,
2013); the abbreviated Spider Phobia Questionnaire
(Olatunji et  al., 2009); the Dog Phobia Questionnaire
(Vorstenbosch, Antony, Koerner, & Boivin, 2012); the
Storm Fear Questionnaire (Nelson, Vorstenbosch,
& Antony, 2014); and a questionnaire called the
Circumscribed Fear Measure, which measures antici-
pated reactions to a specified feared stimulus and can be
used for specific phobia (McCraw & Valentiner, 2015).
Self-​Report Measures of Severity
and Phenomenology—​Social Anxiety Disorder
As is the case for specific phobias, there are a number
of measures that provide useful information about the
severity and features of SAD that can guide treatment
planning. Again, there are too many existing measures to
provide comprehensive reviews of all of them, so inter-
ested readers are referred to Antony, Orsillo, and Roemer
(2001) or Fernandez, Piccirillo, and Rodebaugh (2014)
for a more detailed review. Features of interest found in
these measures include severity of symptoms, fearful cog-
nitions, and avoided situations.
A commonly used self-​report measure of SAD symp-
toms is the Social Phobia and Anxiety Inventory (SPAI;
Turner, Beidel, & Dancu, 1996; Turner, Beidel, Dancu,
& Stanley, 1989). This 45-​ item scale has two sub-
scales:  social anxiety disorder and agoraphobia. Short
forms with 18 and 23 items, respectively, appear to have
good psychometric properties for use as a screening mea-
sure (de Vente, Majdandžić, Voncken, Beidel, & Bögels,
2014; Schry, Roberson-​Nay, & White, 2012). A  version
of the SPAI is available for use with children (Scaini,
Battaglia, Beidel, & Ogliari, 2012). Norms for the original
SPAI are available for individuals with generalized SAD,
generalized SAD comorbid with avoidant personality
disorder, individuals with public speaking fears, socially
anxious college students, nonanxious college students,
adolescents, and community samples. Norms are also
available across ethnic groups (Gillis, Haaga, & Ford,
1995), and the SPAI has been translated into multiple
languages. The reliability of scores on the SPAI is strong,
especially for the social anxiety disorder subscale (Osman
et al., 1996). Evidence for the validity of the social anxiety
disorder scale of the SPAI is also strong (Orsillo, 2001). It
has demonstrated strong correlations with other measures
of SAD as well as with behavioral indicators of anxiety
(e.g., time spent speaking in a public-​speaking task before
escaping; Beidel, Borden, Turner, & Jacob, 1989), and
only minimal associations have been found with measures
thought to be unrelated to social anxiety. There is a strong
relationship between scores on this measure when com-
pleted by individuals with social anxiety and informant
completion of the measure (Beidel et  al., 1989). The
SPAI has shown measurement invariance across men and
women as well as in individuals with and without a diag-
nosis of SAD, supporting its broad use (Bunnell, Joseph,
& Beidel, 2013). The use of the SPAI has also been vali-
dated in adolescents (Clark et  al., 1994), increasing the
breadth with which this measure can be used.
Another widely used measure of SAD symptoms is
the Social Phobia Inventory (SPIN; Connor et al., 2000).
This is a 17-​item scale that assesses the severity of social
anxiety, fear of a number of social and performance
stimuli, degree of avoidance, and physiological discom-
fort. Norms are available for adults with SAD, adoles-
cents with SAD, adults with other anxiety disorders, and
community samples of adults and adolescents (Antony,
Coons, McCabe, Ashbaugh, & Swinson, 2006; Johnson,
Inderbitzen-​Nolan, & Anderson, 2006). The measure
has generally good to excellent psychometric proper-
ties, including internal consistency, test–​retest reliability,
and convergent and discriminant validity, both in adults
(Antony et al., 2006; Connor et al., 2000) and in adoles-
cents (Johnson et al., 2006), as well as in other cultures
(e.g., in a Brazilian sample; Osório, Crippa, & Loureiro,
2010). Studies of the factor structure of the SPIN are
equivocal; some studies have found a five-​factor model
(Connor et  al., 2000; Osório et  al., 2010), whereas oth-
ers support a three-​factor model (Campbell-​Sills, Espejo,
Ayers, Roy-​Byrne, & Stein, 2015). In Campbell-​Sills et al.,
the three factors loaded onto a higher order factor assess-
ing the broad construct of social anxiety, providing further
support for the validity of this instrument.
Research has consistently demonstrated that the core
construct in SAD is fear of negative evaluation, and the
diagnostic criteria for SAD in DSM-​5 reflects this body
of research by including fear of negative evaluation as a
core diagnostic feature. A widely used self-​report measure
of this construct is the Brief Fear of Negative Evaluation
Scale (BFNE; Leary, 1983). There are both 12-​item and
8-​item variants, adapted from the 30-​item Fear of Negative
Evaluation Scale (Watson & Friend, 1969), with research
suggesting that the 8 original straightforwardly worded
items form the strongest version of the BFNE (Carleton,
Collimore, McCabe, & Antony, 2011). Scores on the
BFNE have demonstrated high internal consistency and
test–​retest reliability (Leary, 1983), with indicators of
internal consistency tending to be strongest in clinical

samples (Weeks et al., 2005). The BFNE has shown con-
sistent psychometric properties in men, women, and Asian
populations (Harpole et al., 2015; Wei, Zhang, Li, Xue, &
Zhang, 2015). The BFNE has also shown good convergent
validity with measures of social anxiety (Collins, Westra,
Dozois, & Stewart, 2005; Leary, 1983). The BFNE has 4
reverse-​scored items that tend to cluster separately in fac-
tor analytic studies and have weaker psychometric prop-
erties than the other iterations of the scale (Rodebaugh
et al., 2004; Weeks et al., 2005). There are mixed findings
with regard to discriminant validity; studies have found
low correlations with measures of anxiety sensitivity and
depression but high correlations with measures of gener-
alized anxiety (Weeks et al., 2005). Scores on the BFNE
can discriminate between patients with SAD compared to
nonanxious controls (Weeks et al., 2005), individuals with
panic disorder (Collins et al., 2005), and individuals with
a variety of mood and anxiety disorders (Carleton et al.,
2011). The BFNE shows adequate sensitivity to change
after CBT (Collins et al., 2005; Taylor, Woody, McLean,
& Koch, 1997; Weeks et al., 2005).
In addition to the previously discussed measures,
there are a host of other measures of the severity of
SAD symptoms and related constructs that would also
be useful to consider incorporating into an assessment
protocol, although their psychometric properties are
not reviewed here due to space restrictions. Examples
include the Social Interaction Anxiety Scale (Mattick
& Clarke, 1998), the Social Phobia Scale (Mattick &
Clarke, 1998), and the recently developed Social Anxiety
Questionnaire for Adults (Caballo, Arias, Salazar, Irurtia,
& Hofmann, 2015).
Self-​Report Measures of Related Dimensions
in Specific Phobia and Social Anxiety Disorder
There are a number of additional dimensions that need
to be addressed in a thorough assessment of specific pho-
bia and SAD for the purpose of case conceptualization.
Examples include disgust sensitivity, anxiety sensitivity,
and perfectionism. This section discusses each of these
dimensions.
Disgust Sensitivity
Disgust sensitivity is a trait that has been implicated in the
etiology and phenomenology of certain specific phobias,
especially animal phobias and blood–​ injury–​
injection
(BII) phobias. For example, disgust sensitivity is elevated
in BII fears and phobias, in relation to both general (e.g.,
Specific Phobia and Social Anxiety Disorder 251
rotting food) and phobia-​specific (e.g., wounds) indicators
of disgust (Sawchuk, Lohr, Tolin, Lee, & Kleinknecht,
2000; Tolin, Lohr, Sawchuk, & Lee, 1997). Disgust sen-
sitivity has also been shown to be elevated in people with
spider phobias on both questionnaire measures of disgust
(e.g., Bianchi & Carter, 2012; Merckelbach, de Jong,
Arntz, & Schouten, 1993)  and physiological indicators
of disgust (e.g., de Jong, Peters, & Vanderhallen, 2002).
Studies suggest that disgust sensitivity significantly con-
tributes to multiple types of fear (McDonald, Hartman, &
Vrana, 2008). Given the elevation of disgust sensitivity in
many anxiety presentations, this is an important dimen-
sion to assess when planning treatment. One of the more
commonly used measures of this dimension is the Disgust
Scale (DS; Haidt, McCauley, & Rozin, 1994)  and the
Disgust Scale-​Revised (DS-​R; Olatunji et al., 2007). The
32-​item DS covers a broad range of disgust-​eliciting stim-
uli, including food, animals, body products, sex, bodily
violations (e.g., seeing a man with a fishhook in his eye),
death, hygiene, and magical pathways of disgust, making
it broadly applicable to many subtypes of specific phobia.
The DS-​R is a 25-​item measure whose items cluster into
three factors: core disgust, animal reminder disgust, and
contamination disgust. The DS-​R scores have shown good
reliability and validity (van Overveld, de Jong, Peters, &
Schouten, 2011), although a recent study found only a
modest correlation between scores on the DS-​ R and
reports of state disgust during exposure therapy (Duncko
& Veale, 2016). Recently, the Disgust Emotion Scale
(Olatunji, Ebesutani, & Reise, 2015) has shown promise
for measuring disgust proneness.
Anxiety Sensitivity
Anxiety sensitivity (i.e., one’s beliefs that the physical
sensations of fear and anxiety are dangerous) is another
relevant construct when assessing specific phobia and
SAD. Individuals with situational phobias or SAD may
be especially concerned with the physical sensations of
fear, focusing on the consequences of anxiety and panic
attacks when encountering the phobic stimulus or phobic
situation (Antony, Brown, & Barlow, 1997a). Research
generally supports this notion, demonstrating that individ-
uals with phobias from the situational type score higher
on the Anxiety Sensitivity Index (ASI; Peterson & Reiss,
1993)  than do individuals with animal phobias and BII
phobias (Antony et al., 1997a). Most people with SAD are
also fearful of physical signs of anxiety (sweating, blush-
ing, etc.), especially if these symptoms occur in front of
others. Indeed, both adults (Taylor, Koch, & McNally,
252 Anxiety and Related Disorders
1992)  and children (Alkozei, Cooper, & Creswell,
2014) with SAD show elevations on the ASI in compari-
son to healthy controls, and the presence of situation-
ally bound panic attacks in SAD is associated with more
severe presentations of SAD (Potter et al., 2014). Changes
in anxiety sensitivity contribute to post-​treatment social
anxiety symptoms above and beyond pretreatment symp-
toms (Nowakowski, Rowa, Antony, & McCabe, 2016).
Therefore, it is important to assess an individual’s fear of
physical sensations. The most commonly used measure
for this purpose is the ASI, and the most recent version
of the ASI is the ASI-​3, an 18-​item revision of the original
ASI (Taylor et  al., 2007). The ASI-​3 has strong psycho-
metric properties (Wheaton, Deacon, McGrath, Berman,
& Abramowitz, 2012). Elevated anxiety sensitivity scores
suggest that treatment should include a possible focus on
the meaning of physical sensations (i.e., through cognitive
restructuring) and the possible inclusion of interoceptive
exposure practices, where an individual engages in exer-
cises to purposely bring about feared physical sensations
in a safe environment.
Perfectionism
Research supports the idea that levels of maladaptive per-
fectionism are elevated in SAD. For example, people with
SAD appear to believe that other people have high expec-
tations for them (Bieling & Alden, 1997), and they show
elevated levels of concerns over mistakes, doubts about
their actions, and reports of parental criticism (Antony,
Purdon, Huta, & Swinson, 1998). Perfectionism predicts
aspects of SAD such as post-​event processing, the tendency
to ruminate about social events after the fact (Shikatani,
Antony, Cassin, & Kuo, 2016). Perfectionism is therefore
an important construct to investigate in the conceptual-
ization of an individual with SAD. A widely used measure
of perfectionism is the 35-​item Frost Multidimensional
Perfectionism Scale (FMPS; Frost, Marten, Lahart, &
Rosenblate, 1990). This self-​ report measure assesses a
number of dimensions of perfectionism (e.g., concern
over mistakes, personal standards, and parental expecta-
tions), allowing the clinician to determine which aspects
of perfectionism are elevated for a particular individual.
Scores on this measure have demonstrated strong psycho-
metric properties, including good internal consistency
and strong relations between the scores on this measure
and behavioral indications of perfectionism (e.g., reac-
tions to mistakes made in a task; Frost et al., 1997). There
is some question about the appropriate factor structure
of this measure, with different studies yielding different
factor solutions (e.g., Purdon, Antony, & Swinson, 1999;
Stober, 1998). Along with the FMPS, there are well over
20 measures that can be used to assess perfectionism. For
a review, see Egan, Wade, Shafran, and Antony (2014).
Behavioral Assessment
Behavioral assessment is an especially useful form of
assessment for planning cognitive or behavioral treat-
ments. The most common form of behavioral assessment
used with anxiety disorders is the behavioral approach test
(BAT). A  BAT for a specific phobia may involve seeing
how close the person can get to his or her feared stimulus
(e.g., an animal or high ledge), how long a person can
stay in a feared situation before escaping, or the degree
of fear a person experiences in the situation. A  BAT for
SAD may involve asking a person to engage in a feared
activity (e.g., giving a speech) and measuring the degree
of fear experienced during the activity. These tests provide
valuable information about the intensity of a person’s fear,
the cues that affect a person’s fear (e.g., size of spider and
sex of the conversation partner), the physical sensations a
person experiences, the person’s fearful thoughts, and the
use of avoidance or subtle avoidance strategies when in
the feared situation (e.g., avoiding eye contact and leaving
the situation).
Research suggests that responses to behavioral chal-
lenges such as a BAT are related to responses on self-​
report measures of social anxiety symptoms (e.g., Gore,
Carter, & Parker, 2002)  and subjective distress scores
for phobic stimuli (Ollendick, Allen, Benoit, & Cowart,
2011), supporting the convergent validity for behavioral
measures. Analogue behavioral assessment strategies have
demonstrated strong discriminative and convergent valid-
ity for the assessment of social functioning (Norton &
Hope, 2001).
Assessment of Skills Deficits
Individuals with specific phobia or SAD may have skills
deficits that impact upon treatment. For example, some
people with SAD appear to have impairment in social
skills (e.g., Beidel, Rao, Scharfstein, Wong, & Alfano,
2010; Fydrich, Chambless, Perry, Buergener, & Beazley,
1998), although other research has found no differences
from control participants (e.g., Voncken & Bögels, 2008).
Other research suggests that deficits may be accounted for
by other constructs, such as use of safety behaviors (Rowa

et al., 2015). Some people with specific phobias of driv-
ing may lack adequate driving skills, particularly if they
have avoided driving for many years. Although there are
no gold standard measures to assess skills deficits, these
deficits are important to address when planning for treat-
ment. For example, poor driving skills may necessitate
a course of remedial driving instruction either prior to
exposure therapy or concurrent with it. Driving skills are
likely best evaluated by a professional driving instruc-
tor. Social skills deficits in SAD may be readily apparent
during the course of initial meetings with an individual
(e.g., lack of eye contact may be noticeable during a
semi-​structured interview). To more formally assess these
deficits, the Social Performance Rating Scale (SPRS) can
be used. This behavioral assessment tool was originally
developed by Trower, Bryant, and Argyle (1978), modi-
fied by Turner, Beidel, Dancu, and Keys (1986), and then
further modified by Fydrich and colleagues (1998) to
provide a measure of social skill level during videotaped
role-​plays that yields reliable and valid scores. The modi-
fied SPRS provides information about the following skill
areas: gaze, vocal quality, speech length, discomfort, and
conversation flow. Although this measure provides broad
and useful ratings of behavioral skill deficits, it may not
be easily transferred to a clinical setting. For example, the
role-​plays require the presence of a confederate. Although
this may be easily accomplished in the context of a
clinic or hospital-​based program, it may be near impos-
sible in other clinical settings, such as private practice.
Furthermore, the training and time necessary for raters of
the role-​plays may be difficult to justify in many contexts.
Thus, although this measure appears to provide excellent
information on skills deficits, it may be more reasonable
for most clinicians to use some aspects of this measure. For
example, clinicians could use the behavioral anchors pro-
vided for this measure to rate the social skills that emerge
in the context of either an interview or other assessment
protocol or to conduct analogue role-​plays with their cli-
ents using themselves as the confederate.
Assessment of Treatment History,
Treatment Concerns, and Suitability
for Cognitive–​Behavioral Therapy
During the course of treatment planning, it is useful to
assess an individual’s treatment history, any treatment
concerns, and suitability for a therapeutic intervention
such as CBT. Previous treatment failures may provide
useful information about what not to try when treating a
Specific Phobia and Social Anxiety Disorder 253
particular patient. On the other hand, previous treatment
failures may have been the result of receiving inappropri-
ate interventions for a problem such as SAD or specific
phobia. Research suggests that individuals seen in a spe-
cialty anxiety clinic reported having received a number
of nonempirically supported treatments (especially psy-
chological treatments) prior to receiving cognitive or
behavioral interventions for their anxiety disorder (Rowa,
Antony, Brar, Summerfeldt, & Swinson, 2000). In cases
in which past treatment attempts were not successful, it
may be important to identify reasons for the negative out-
come. For example, treatment noncompliance and lack
of acceptance of the treatment rationale are predictors
of negative outcome following psychological treatment
(e.g., Addis & Jacobson, 2000; Woods, Chambless, &
Steketee, 2002). Furthermore, the presence of comor-
bid personality disorders is associated with lower likeli-
hood of individuals seeking treatment services for SAD
or specific phobia (Iza et al., 2013). Knowledge of these
kinds of issues suggests useful pathways the clinician
should consider when planning treatment and potential
obstacles that may arise. For example, the clinician may
consider investing more time at the beginning stages
of treatment to help the client fully understand and,
it is hoped, accept the rationale underlying treatment
interventions. Furthermore, a history of treatment non-
compliance may suggest the importance of contracting
about the completion of therapy assignments and session
attendance in order for therapy to proceed. One option
to better understand treatment history is to use multiple
informants, including both the client and previous thera-
pists (with permission from the client).
Individuals may have strong fears about treatment,
including fears that they will not get better. Measures
such as the Treatment Ambivalence Questionnaire
(TAQ; Rowa et  al., 2014)  may be helpful in evaluating
a host of treatment fears presented by individuals with
anxiety disorders. Finally, a clinician may want to con-
sider whether a particular client is a good match for
cognitive or behavioral interventions. Even though these
techniques are empirically supported for treating specific
phobia and SAD, this does not guarantee that a particular
individual is well-​suited for a CBT intervention. Clients
have to be willing to complete between-​session work, con-
front feared stimuli, and accept a CBT rationale for their
difficulties. Suitability interviews for CBT do exist, and
scores on one suitability instrument have shown moderate
correlations with both client and therapist ratings of suc-
cess in cognitive therapy for depression (Safran & Segal,
254 Anxiety and Related Disorders
1990). However, these interviews are detailed and time-​
consuming, focus more on suitability for cognitive inter-
ventions than behavioral interventions, have not been
validated for anxiety disorders, and may not be practical
for clinical practice. They may be best used when suit-
ability issues appear to be a potential obstacle in treatment
planning.
Assessment of Safety Behaviors
A final consideration when conducting assessment for
the purpose of treatment planning in specific phobia and
SAD is to ensure a thorough assessment of an individu-
al’s use of safety behaviors, subtle avoidance, and mal-
adaptive coping strategies (e.g., alcohol and drug use).
Elevated drug and alcohol use has been documented in
SAD (e.g., Van Ameringen, Mancini, Styan, & Donison,
1991), and it is often conceptualized as a means of cop-
ing with otherwise debilitating levels of anxiety. Other
examples of safety behaviors and coping strategies in
SAD include wearing high-​necked shirts to cover blush-
ing, over-​rehearsing or memorizing presentations, carry-
ing anti-​anxiety medication, and always bringing a “safe
other” when attending a social gathering. Safety behav-
iors or subtle avoidance in specific phobia may include
looking away when getting a needle, wearing long sleeves
or a hooded shirt to prevent spiders from falling directly
on one’s skin, holding a railing in a high place, and
playing the radio while driving to distract oneself from
fear. Although safety behaviors are prevalent and are a
crucial aspect of understanding a person’s social or spe-
cific phobia, the breadth and variety of strategies used
by individuals have been difficult to measure using a
particular instrument. One instrument that has been
developed to measure safety behaviors in social anxiety
is the Subtle Avoidance Frequency Examination (SAFE;
Cuming et al., 2009). This 32-​item measure assesses how
frequently an individual uses particular safety behaviors
in social situations. It has strong psychometric proper-
ties (Cuming et  al., 2009)  and is able to differentiate
adolescents with social anxiety from control participants
(Thomas, Daruwala, Goepel, & De Los Reyes, 2012).
The SAFE is sensitive to changes in safety behavior use
across treatment (e.g., Goldin et al., 2016).
Overall Evaluation
There are a number of topics to cover when using assess-
ment to aid conceptualization and treatment planning for
specific phobia and SAD. We have highlighted a series
of variables that we believe are valuable to cover, includ-
ing symptom severity, relevant cognitions and avoidance
behaviors, related constructs, coping strategies, skills
deficits, treatment history, and attitudes toward future
treatment. When reviewing these topics, it is encourag-
ing that a number of psychometrically sound, clinically
useful measures exist to assess these areas (for a summary,
see Table 12.2). Therefore, at minimum, this stage of
assessment should include a well-​studied and validated
measure such as the SPIN for SAD or the FSQ for spe-
cific phobia of spiders, for example, to complement the
diagnostic information already provided from a semi-​
structured interview. Even without a designation of
“highly recommended,” we still encourage practitioners
to use instruments such as these for the purpose of treat-
ment planning. Furthermore, it also seems reasonable
to include well-​validated measures of related constructs,
such as anxiety sensitivity, disgust, and perfectionism,
where relevant. The questionnaires highlighted to mea-
sure these constructs are all quick and straightforward
measures whose value clearly exceeds the time taken to
complete and score the instruments.
We also argue that the use of idiographic diaries,
questions, or monitoring forms to ascertain coping strat-
egies and safety behaviors, although not empirically
validated, is an essential aspect of treatment planning.
Similarly, behavioral assessment using a BAT is a use-
ful way to discover a great deal of valuable information
for treatment planning. Overlooking this information
could have serious implications for treatment outcome
(e.g., if the use of maladaptive coping strategies is never
targeted). The assessment picture becomes more com-
plicated when evaluating the utility of measuring con-
structs such as social skills and suitability for CBT in
a routine assessment for SAD. We argue that the lack
of quick and easily administered measures limits the
feasibility of systematically assessing these features in
routine practice, and we know of no data to suggest that
not measuring these constructs formally leads to com-
promised treatment outcome. Instead, therefore, we
recommend the use of measures specifically designed
to assess these topics only in scenarios when these topics
appear especially relevant (e.g., if an individual clearly
communicates a bad experience with previous CBT
and extreme skepticism about its effectiveness or for a
person who clearly has extreme social skills deficits).
Otherwise, the general theme of social skills, suitability
for CBT, and treatment fears can be assessed in a more
informal way during the course of a diagnostic interview
or assessment of these variables.
 Specific Phobia and Social Anxiety Disorder 255

TABLE 12.3   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Treatment Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Sensitivity Recommended

FSQ A E NA A A G G G E
SNAQ A G NA E NR G E G E
DAI A E NA A A G E G NR
SPAI E E NA A E E E E E ✓
SPIN E E NA A G G E E E ✓
LSAS G E NR NR G G E E E ✓
BSPS A A NR A A A A E G
BAT NR NR NA NR NA G E E E ✓
IIRS E E E G G E E E G ✓

Note: FSQ = Fear of Spiders Questionnaire; SNAQ = Snake Questionnaire; DAI = Dental Anxiety Inventory; SPAI = Social Phobia and Anxiety
Inventory; SPIN = Social Phobia Inventory; LSAS = Liebowitz Social Anxiety Scale; BSPS = Brief Social Phobia Scale; BAT = Behavioral Approach
Test; IIRS = Illness Intrusiveness Rating Scale; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

ASSESSMENT FOR TREATMENT MONITORING treatment sensitivity, in that scores meaningfully decline

AND TREATMENT OUTCOME
The final use of assessment procedures covered in this
chapter is assessment for the purpose of evaluating treat-
ment progress and outcome, both for medication and for
CBT. Clearly, a hallmark feature of CBT interventions
is the rigorous evaluation of their effectiveness. This is
also true when using these techniques with a particular
client. It is essential to understand whether treatment
strategies were helpful, in what way they were helpful,
and on what dimensions strategies had their impact. In
some instances, degree of improvement will have impor-
tant implications for course and duration of treatment. In
other cases, indicators of improvement will have implica-
tions for continued funding of treatment (e.g., by insur-
ance companies or third party payers). On a most basic
level, it is useful for a client to understand and be aware
of the degree of improvement made. Without explicitly
assessing these variables, important gains can be ignored
or missed. Table 12.3 provides a review of measures that
are useful for treatment evaluation.
Self-​Report Measures of Severity—​Specific Phobia
and Social Anxiety Disorder
One important way to assess treatment progress and
outcome is to compare self-​report questionnaire scores
obtained during and at the end of treatment with those
obtained at pretreatment. Possible assessment tools
include the self-​
report measures described previously
(e.g., FSQ, SNAQ, DAI, SPAI, and SPIN). Each of these
measures except for the DAI has shown at least adequate
after medication or psychological treatment (for a review,
see Antony, Orsillo, et al., 2001).
In addition to using empirically validated self-​report
measures for specific phobia and SAD, there is also
value to using more idiosyncratic self-​ report instru-
ments to monitor progress in therapy. For example, a
widely used tool of symptom progression is the exposure
hierarchy, used in exposure-​based treatments of spe-
cific phobia and SAD. An exposure hierarchy is a list
of feared situations ranked from most difficult at the top
to least difficult at the bottom. Each item on the hier-
archy is rated for fear, avoidance, or both. Hierarchies
are developed either before treatment or near the begin-
ning of treatment, and clients are encouraged to provide
updated fear and avoidance ratings on a regular basis
(i.e., each session; pre-​, mid-​, and post-​treatment; etc.).
Although no studies have examined the use of hierarchy
ratings in social or specific phobia, a study by our group
on patients with panic disorder provides support for
their utility. We found that fear and avoidance ratings
on hierarchies changed significantly across treatment of
panic disorder, with effect sizes even greater than those
obtained from standard outcome measures (Katerelos,
Hawley, Antony, & McCabe, 2008). Valuable infor-
mation can also be gleaned from monitoring forms
and exposure graphs completed by the client. For
example, notable shifts in the content of cognitions
can be an indicator that the client is benefiting from
CBT; hypothesized reductions in peak fear and the
time needed for fear to decrease can inform the thera-
pist of whether exposure exercises are producing the
desired effects.
256 Anxiety and Related Disorders

Interview Measures of Symptom Severity to these physical sensations is an important factor in

their experience of anxiety (e.g., Clark & Wells, 1995).
When evaluating progress and outcome as a result of
Elevated physiological reactivity may also be implicated
medication or CBT for SAD, there are two widely used
in specific phobias, with individuals often experiencing
clinician-​rated measures of symptom severity. Clinician-​
cued panic attacks in feared situations. Furthermore,
rated measures are a useful addition to self-​report mea-
individuals with BII phobias have an elevated risk of faint-
sures to broaden the breadth and source of data used to
ing when encountering their feared stimuli (Antony &
evaluate outcome. The first example is the Liebowitz
Barlow, 2002), a unique physiological response. Research
Social Anxiety Scale (LSAS; Liebowitz, 1987). This
also suggests that people with situational, as compared to
measure lists 24 situations that are commonly anxiety-​
nonsituational, phobias have a higher rate of unexpected
producing for people with social anxiety, and the inter-
panic attacks, and people with BII phobias have a greater
viewer rates each situation in terms of fear and avoidance.
focus on physical symptoms than on harm or catastrophe
It is relatively brief, taking approximately 20 minutes to
(Lipsitz et al., 2002). Thus, particular subtypes of specific
complete. The psychometric properties of the LSAS are
phobias may have unique physiological presentations. If
good to excellent, and it has demonstrated sensitivity
this is the case, it might be useful to measure physiologi-
to treatment outcome, having been a primary outcome
cal reactivity to behavioral tasks and exposure stimuli as
measure in many medication and cognitive–​behavioral
an indication of progress in therapy.
treatment trials for SAD. The LSAS is also available in a
Although it is clear that people with specific phobia
self-​report format with good psychometric properties (e.g.,
and SAD report greater than normal apprehension about
Baker, Heinrichs, Kim, & Hofmann, 2002). A  second
physiological sensations (e.g., Hugdahl & Öst, 1985),
widely used clinician-​rated measure of SAD symptoms
research is not clear regarding whether actual physiologi-
is the Brief Social Phobia Scale (BSPS; Davidson et al.,
cal differences exist between people with and without
1991). This 18-​item measure covers symptoms of fear,
these disorders. For example, Edelmann and Baker (2002)
avoidance, and physiological arousal and can be admin-
found no physiological differences between individuals
istered in 5 to 15 minutes.
with generalized SAD, anxious controls, and nonanxious
controls on measures of heart rate, skin conductance, and
Behavioral Indicators of Treatment Progress facial and neck temperatures on a series of behavioral,
Behavioral assessment (e.g., a BAT) is also a useful way of physical, and imagery tasks. Interestingly, participants
monitoring outcome of treatment for specific phobia and with SAD and other anxiety disorders provided higher
SAD. If an individual with a spider phobia is unable to subjective ratings of some sensations than did nonanxious
look at a spider during a pretreatment BAT but can hold controls even in the absence of physiological differences.
a spider comfortably during a post-​treatment BAT, the cli- This result is consistent across other anxiety conditions,
ent can be assumed to have improved. Hofmann (2000) including panic disorder and generalized anxiety disor-
used four behavioral tasks both before and after a treat- der (Hoehn-​ Saric, McLeod, Funderburk, & Kowalski,
ment trial of CBT for SAD and measured self-​statements 2004). Furthermore, changes in physiological response
made during these tasks. Results suggested that content can occur across a course of treatment but may occur
of self-​statements made while anticipating the behavioral separately from changes in fear and avoidance (Aderka,
tasks changed across successful treatment, with partici- McLean, Huppert, Davidson, & Foa, 2013). On the other
pants endorsing fewer negative self-​focused thoughts after hand, individuals with dental fears demonstrated changes
treatment. The use of behavioral tests in this example in physiology during exposure to scenes of dental treat-
allowed the evaluator to see related changes in cognition ment (Johnson et al., 2003), and individuals with spider
across treatment. phobia showed a reduction in heart rate during BATs
before, during, and after a session of exposure therapy
(Antony, McCabe, Leeuw, Sano, & Swinson, 2001). Also,
Physiological Indications of Treatment Progress
children with SAD may have impaired recovery from a
Models of the development and maintenance of SAD social stressor compared to healthy controls, but they have
place importance on the physiological manifestations similar changes in heart rate when the stressor is intro-
of anxiety, suggesting that people with SAD experience duced (Schmitz, Krämer, Tuschen-​Caffier, Heinrichs, &
elevated physical symptoms of anxiety (e.g., blushing and Blechert, 2011). Thus, currently, there is some empiri-
racing heart) and that the anticipation of and reaction cal support to conclude that physiology changes across

treatment but not enough to recommend using physiolog-
ical indicators to measure treatment progress. Given the
expense and burden of accurately measuring physiologi-
cal responses of anxiety, it appears more useful to measure
concern over physiological symptoms using validated self-​
report measures such as the ASI-​3, described previously.
Assessment of Functional Impairment
and Quality of Life
Traditionally, treatment outcome research in the area of
anxiety disorders has focused on measuring change in
symptom severity, paying less attention to whether treat-
ment improves associated distress, functional impairment,
and quality of life. There are no assessment tools designed
specifically to assess distress, functional impairment, and
quality of life in people with anxiety disorders, although a
number of more general scales (e.g., Sheehan Disability
Scale; Sheehan, 1983) have been used to measure these
constructs in this population (e.g., Antony, Roth, Swinson,
Huta, & Devins, 1998; Mendlowicz & Stein, 2000; Quilty,
van Ameringen, Mancini, Oakman, & Farvolden, 2003).
One such scale is the Illness Intrusiveness Ratings Scale
(IIRS; Devins et al., 1983). Originally developed for use
with medical populations, the IIRS has been adapted for
use with mental health populations. This brief self-​report
measure asks people to rate the degree to which their ill-
ness (i.e., anxiety disorder) interferes with 13 domains of
functioning (e.g., work, sex life, relationships, and reli-
gious expression). The IIRS has demonstrated strong psy-
chometric properties. Antony et al. found that individuals
with anxiety disorders (including SAD) reported higher
levels of functional impairment than did people with seri-
ous medical conditions, including end-​stage renal disease
and multiple sclerosis. Whether this finding reflects the
true level of functional impairment in anxiety disorders is
unknown because research has not examined the relation-
ship between scores on these scales and more objective
indices of impairment (e.g., missed days at work and rela-
tionship impairment) in people with anxiety disorders.
However, the IIRS appears sensitive to changes across
treatment (e.g., Rowa et al., 2007) and is a straightforward
way of measuring subjective changes in impairment as a
result of treatment efforts.
Overall Evaluation
Measuring treatment outcome is not only important in
the broad sense of validating the use of particular treat-
ment interventions but also useful on an individual basis
Specific Phobia and Social Anxiety Disorder 257
to quantify changes made by particular clients across
particular courses of therapy. Clinically, it is clear that
many clients make significant changes across the course
of therapy but do not recognize the magnitude or impor-
tance of these changes. Similarly, it is easy for clinicians to
“forget” the severity of a client’s original fears when they
have observed progress on a week-​to-​week basis. Efficacy
data from randomized controlled trials may not mirror
effectiveness of the treatment in a particular clinic or
with a particular client. For these reasons, it is valuable to
measure treatment outcome for individual clients as well
as in larger, well-​controlled treatment trials. We believe
that the measurement of treatment outcome should be
multifaceted, ideally including self-​ report, behavioral,
and clinician-​rated measures of improvement. In addi-
tion, treatment outcome should target not only improve-
ments in symptoms of social anxiety or specific phobia
but also improvements in a person’s general functioning
and quality of life. At minimum, assessment of treatment
outcome should involve examining changes on self-​report
measures with demonstrated treatment sensitivity, on idio-
graphic measures of progress (e.g., hierarchies and moni-
toring forms), on behavioral indicators of progress (e.g.,
ability to enter and remain in feared situations), and on
measures of everyday life functioning.
CONCLUSIONS AND FUTURE DIRECTIONS
It is clear that assessment plays a crucial role in under-
standing an individual’s presenting problems, making
informed decisions about treatment interventions, and
evaluating the effectiveness of any such interventions.
Within the anxiety disorders, there is a long tradition of
ensuring that assessment instruments possess strong psy-
chometric properties and that assessment tools that yield
reliable and valid scores are used to measure the efficacy
of treatment interventions. In addition, there is value in
developing and evaluating evidence-​ based assessment
protocols for the anxiety disorders. We have provided a
sample assessment strategy for SAD in Table 12.4. This
strategy involves using assessment measures for the purpose
of diagnosis, measures to assess clinical features of both
the disorder and related constructs (e.g., perfectionism)
for the purpose of treatment planning, and measures that
are sensitive to change across treatment. Unfortunately,
anxiety researchers often use assessment protocols that
are less multimodal, relying most often on self-​ report
scales only (Lawyer & Smitherman, 2004). Therefore,
despite our strong history of using well-​validated tools and
258 Anxiety and Related Disorders

TABLE 12.4  
Sample Assessment Protocol for Assessing about individual assessment instruments and techniques
Treatment Outcome in Social Anxiety Disorder to make informed judgments about what tools should be
considered when assessing SAD or specific phobias. In
Domain Assessment Tools Type of Tool
this vein, we have provided a review of some individual
Diagnostic features Structured Clinical Semi-​structured tools and techniques commonly used in the assessment
Interview for DSM-​5 interview
of specific phobia and SAD, with the idea that an empir-
(SCID-​5; First et al.,
2015)a ically supported assessment strategy must have its roots
Anxiety Disorders Semi-​structured in well-​validated, psychometrically sound instruments.
Interview Schedule interview Furthermore, we have reviewed these instruments
for DSM-​5 (ADIS-​5; and techniques from the perspective of clinical utility
Brown & Barlow,
as well, with the understanding that there has to exist
2014)a
Conceptualization a crossroads between empirically supported and clini-
Severity Social Phobia Inventory Self-​report cally feasible assessment strategies. For example, some
(Connor et al., 2000) semi-​structured interviews for DSM-​5 (e.g., the SCID-​5)
Situational cues Diaries to record Diary
are substantially longer than previous versions, making
situational fear,
avoidance, and safety them less practical to use in their entirety. One option
behaviors might be to move toward a more modular approach in
Avoidance Behavioral approach test Behavioral assessment which interviewers select the most relevant diagnostic
Related Anxiety Sensitivity Index-​3 Self-​report
constructs (ASI-​3; Taylor et al.,
modules to arrive at diagnostic decisions in a more effi-
2007) cient manner.
Disgust Scale (Haidt et al., Self-​report From these reviews, we have suggested some pos-
1994)
sible avenues for combining assessment techniques in
Frost Multidimensional Self-​report
Perfectionism Scale a way that may prove to be useful for assessment of spe-
(FMPS; Frost et al., cific phobia and SAD. From suggestions such as these,
1990) future research can focus on the optimal combination of
Treatment outcome
Severity, Social anxiety disorder Self-​report
assessment strategies for different purposes, how differ-
situational and Anxiety Inventory ent strategies affect the utility and efficacy of others used
cues,
cognitive (SPAI; Turner et al., concurrently, and how to balance clinical feasibility with
features, and 1989) maximal efficacy.
avoidance
behavior
Diaries to record Diary
situational fear,
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 13

Panic Disorder and Agoraphobia

Amy R. Sewart
Michelle G. Craske

In this chapter, we first describe the presenting features concern about their recurrence and their consequences
and prevailing theories regarding etiology and mainte- or a significant maladaptive change in behavior conse-
nance factors for both panic disorder and agoraphobia. quent to the attacks. Such behavioral changes include
Next, we describe the diagnostic, treatment conceptual- avoidance of particular situations that elicit panic-​like
ization and planning, and treatment outcome and moni- symptoms and are perceived to elevate the likelihood of
toring assessment methods and strategies specific to these a panic attack (e.g., exercise) and the use of safety behav-
diagnoses. iors (e.g., having a cell phone in case of a panic attack).
Frequency and symptom severity of panic attacks in indi-
viduals with panic disorder are highly variable (Craske &
NATURE OF PANIC DISORDER Barlow, 1988). Persons with panic disorder may experi-
AND AGORAPHOBIA ence daily episodes of panic or go months without an
unexpected attack.
Highly comorbid with panic disorder, agoraphobia
Presenting Features
refers to marked fear or avoidance of specific situations
Panic attacks are abrupt, discrete surges of intense fear from which escape is perceived to be difficult or in which
or discomfort, accompanied by physical and cognitive help may be unavailable in the event of panic-​like or
symptoms, as listed in the fifth edition of the Diagnostic other incapacitating or embarrassing symptoms (e.g.,
and Statistical Manual of Mental Disorders (DSM-​ incontinence and fainting; APA, 2013). Typical avoided
5:  American Psychiatric Association [APA], 2013). Such agoraphobic situations include open or enclosed spaces,
symptoms include accelerated heart rate, lightheaded- waiting in line, using public transportation, and being
ness, fear of losing control or dying, and shortness of outside of the home alone.
breath. Episodes of panic peak within minutes and may The diagnosis of agoraphobia and its relationship
be elicited by a cue or trigger (e.g., phobic object), or they to panic attacks have undergone redefinition from the
occur “out of the blue” with no obvious precipitant. Panic DSM-​IV-​TR (APA, 2000)  to the DSM-​5 (APA, 2013).
attacks occur across a variety of mood and anxiety-​related Although highly comorbid, agoraphobia again exists as a
disorders and are predictive of disorder onset, course, diagnosis independent of panic disorder and irrespective
and severity (Batelaan et  al., 2012; Kessler et  al., 2006; of panic attacks in the DSM-​5. This revision was driven
Kircanski, Craske, Epstein, & Wittchen, 2009). Thus, if by findings that agoraphobia does not invariably develop
an individual experiences four or more panic attack symp- as a secondary, conditional response to contexts in which
toms within the confinement of any disorder (e.g., an panic attacks occur and that a considerable number of
individual with social anxiety has panic symptoms prior individuals report clinical levels of agoraphobia without a
to giving a speech), a panic attack specifier is added to the history of panic attacks or panic-​like symptoms (Faravelli,
respective diagnosis (APA, 2013). Furukawa, & Truglia, 2009; Wittchen et al., 2008).
Panic disorder refers to recurrent, unexpected panic From the latest epidemiological study, the National
attacks, followed by at least 1  month of persistent Comorbidity Survey-​ Replication (NCS-​ R), lifetime

266

prevalence estimates in the adult American population
are 3.8% for panic disorder with or without agoraphobia
and 2.5% for agoraphobia with or without a history of
panic disorder (Kessler, Petukhova, Sampson, Zaslavsky,
& Wittchen, 2012). Although this study did not report
findings for agoraphobia without panic disorder or panic
attacks, a 10-​ year prospective longitudinal study con-
ducted by Wittchen and colleagues (2008) found that
approximately 1.5% of German individuals in adoles-
cence to mid-​adulthood experienced agoraphobia without
co-​occurring distressing spells of anxiety. Current preva-
lence estimates for agoraphobia without panic attacks are
limited given that agoraphobia was previously considered
secondary to panic disorder almost exclusively. Rarely do
the diagnoses of panic disorder or agoraphobia occur in
isolation of other psychiatric conditions. Commonly co-​
occurring disorders include major depressive disorder,
specific phobia, social phobia, post-​traumatic stress dis-
order, and substance use disorders (Brown, Campbell,
Lehman, Grisham, & Mancill, 2001; Kessler et al., 2006).
A striking 28% of adults in the United States will experi-
ence at least one panic attack within their lifetime (Kessler
et al., 2006). A substantial proportion of adolescents report
panic attacks (e.g., Hayward, Killen, Kraemer, & Taylor,
2000), with the modal age of onset for panic attacks and
panic disorder ranging from early adolescence to early
adulthood (Kessler et  al., 2005; Wittchen et  al., 2008).
In contrast, agoraphobia with and without panic disorder
has demonstrated onset as early as childhood (Wittchen
et al., 2008). Although 33.6% of adults with panic disorder
and 15.1% with agoraphobia initiate contact with a health
care provider for treatment within the first year of disor-
der onset, the median delay of treatment contact after this
period is estimated respectively at 10 and 12 years (Wang
et al., 2005). Furthermore, individuals with panic disorder
and agoraphobia are more likely to seek treatment dur-
ing the course of their lifetime for psychiatric problems
compared with panic disorder, agoraphobia with panic
attacks, and panic attack subgroups (Kessler et al., 2006).
Although no gender differences have been observed for
age of onset of panic disorder or agoraphobia, the hazard
ratio for women increases significantly over time for both
disorders (Wittchen et al., 2008).
Most people with panic disorder report identifi-
able stressors around the time of their first panic attack
commonly related to interpersonal issues or physical
well-​being, such as disease or negative drug experiences
(Craske, Miller, Rotunda, & Barlow, 1990; Pollard,
Pollard, & Corn, 1989). Approximately half of those
with panic disorder report having experienced panicky
Panic Disorder and Agoraphobia 267
feelings at some time before their first panic attack, sug-
gesting that onset may be either insidious or acute (Craske
et al., 1990).
Finally, both panic disorder and agoraphobia tend to
be chronic (Bruce et al., 2005), impairing conditions, with
severe financial and interpersonal costs. Yonkers, Bruce,
Dyck, and Keller (2003) demonstrated that although a
large percentage of individuals with panic disorder reach
full remission over the course of 8  years (76% women,
69% men), remission rates for panic disorder with agora-
phobia are more modest (39% women, 35% men), indi-
cating a higher chronicity associated with agoraphobia.
Furthermore, individuals with panic disorder overutilize
medical resources compared to the general public and
individuals with other psychiatric disorders (e.g., Roy-​
Byrne et  al., 1999). Given that panic attack symptoms
are largely somatic in nature, many individuals choose to
seek help in medical settings (e.g., general practitioner’s
office and the emergency room; Katerndahl & Realini,
1995). Panic attacks may be mistaken for a coronary
event, prompting individuals to seek costly emergency
hospitalization.
Etiological and Maintaining Factors
Several independent lines of research converged in the
1980s on the same basic conceptualization of panic dis-
order as an acquired fear of bodily sensations, particularly
sensations associated with autonomic arousal, which is
enhanced in the presence of certain psychological and
biological predispositions. The following descriptions
draw heavily from a more detailed description presented
in Craske and Barlow (2007).
Genetics
The occurrence of panic disorder and agoraphobia clus-
ters within families. According to a large meta-​analysis of
twin and family studies, heritability of panic disorder with
or without agoraphobia is estimated at a moderate .48 and
possesses a summary odds ratio predicting association of
illness in first-​degree relatives at 5.0 (Hettema, Neale, &
Kendler, 2001). More modest heritability estimates (95%
confidence interval  =  .30 to .34) have been found for
panic symptoms as measured by the Anxiety Sensitivity
Index (López-​Solà et  al., 2014). Such findings give evi-
dence to a strong familial component to panic disorder
and agoraphobia.
In a study of individuals who met diagnostic criteria for
panic disorder with or without agoraphobia, carriers of the
268 Anxiety and Related Disorders
polymorphic 5-​HTTLPR short allele variant experienced
more severe and frequent panic symptoms (Lonsdorf et al.,
2009). Furthermore, a strong association has been found
between bi-​and triallelic 5-​HTTLPR polymorphisms and
observer-​rated panic disorder symptoms (Lonsdorf et al.,
2009). Conversely, a meta-​analysis examining 10 previous
studies failed to find a significant association between 5-​
HTTLPR and panic disorder irrespective of agoraphobia
(Blaya, Salum, Lima, Leistner-​Segal, & Manfro, 2007).
In addition, the Val158Met (rs4680G/​A) polymorphism of
the catechol-​O-​methyltransferase (COMT) gene has been
implicated in panic disorder susceptibility in several inde-
pendent samples and has demonstrated female-​specific
effects (Domschke, Deckert, O’Donovan, & Glatt, 2007;
Domschke et al., 2008). The 5-​HTTLPR and Val158Met
polymorphisms have been implicated in other disorders,
such as major depressive disorder, and likely play a role
in broader affective dysfunction including panicogenesis
(e.g., Massat et al., 2005).
It is likely that many genetic variants collectively act
to produce the panic disorder phenotype, but each gene
itself may only account for minor influence. Recent
genome-​wide association studies (GWAS) have localized
specific single nucleotide polymorphisms (SNPs) that
may play a role in the pathogenesis of panic disorder (e.g.,
rs12579350; Otowa et al., 2009). However, most current
GWAS findings lack sufficient statistical power given the
large sample sizes necessary to detect small effects of cer-
tain susceptibility loci.
Neuroticism
Neuroticism, the predisposition toward experiencing
negative mood states (e.g., fear and disgust), is strongly
associated with anxiety disorders, including panic disorder
and agoraphobia (Eysenck, 1967/​2009; Watson & Clark,
1984). Neuroticism and its proxy (i.e., emotional reac-
tivity) predict the onset of panic attacks (e.g., Hayward
et  al., 2000)  and panic disorder (Craske, Poulton, Tsao,
& Plotkin, 2001). Numerous multivariate genetic analy-
ses of human twin samples consistently attribute approxi-
mately 30% to 50% of variance in neuroticism to additive
genetic factors (e.g., Eley, 2001). In addition, anxiety
and depression appear to be variable expressions of the
heritable tendency toward neuroticism (Kendler, Heath,
Martin, & Eaves, 1987). Furthermore, research also sug-
gests that neuroticism may be linked with specific genetic
polymorphisms also implicated in panic disorder patho-
genesis (e.g., 5-​HTTLPR; Gonda et al., 2009). Symptoms
of panic (i.e., breathlessness and heart pounding) may be
additionally explained by a unique source of genetic vari-
ance that is differentiated from the variance relevant to
neuroticism (Martin, Jardine, Andrews, & Heath, 1988).
Anxiety Sensitivity
Anxiety sensitivity is posited to play a critical role in the
pathogenesis of panic disorder and agoraphobia. The
nonspecific cognitive vulnerability factor of anxiety sensi-
tivity captures the extent to which an individual believes
that autonomic arousal-​related sensations result in harm-
ful physical, social, or cognitive consequences (Taylor,
2014; Zinbarg, Barlow, & Brown, 1997). Although such
concerns are observed across most anxiety and related
disorders, anxiety sensitivity is most elevated in panic
disorder (Wheaton, Deacon, McGrath, Berman, &
Abramowitz, 2012; Zinbarg & Barlow, 1996). Respiratory
abnormalities have been observed in healthy individuals
with high anxiety sensitivity, such as fast, shallow breath-
ing and avoidance of carbon dioxide stimulation during
laboratory breathing tasks (Blechert, Wilhelm, Meuret,
Wilhelm, & Roth, 2013). These abnormal psychophysi-
ological responses may predispose one to developing
panic disorder, wherein similar symptoms are exhibited
by individuals diagnosed with the disorder (Coryell, Fyer,
Pine, Martinez, & Arndt, 2001). Longitudinal studies
have demonstrated that anxiety sensitivity is predictive of
future panic attacks in adults irrespective of trait anxiety
and history of panic (e.g., Ehlers, 1995; Schmidt, Lerew,
& Jackson, 1997)  and over 1-​to 4-​year intervals in ado-
lescents (Hayward et al., 2000). In addition, high anxiety
sensitivity regarding physical concerns in conjunction
with high environmental stress was found to be predic-
tive of panic attacks and agoraphobic avoidance over and
above the influence of negative affect (Zvolensky, Kotov,
Antipova, & Schmidt, 2005).
History of Medical Illness and Abuse
Other studies highlight the role of medical illnesses in
the development of panic disorder and agoraphobia. For
example, experience with personal respiratory disturbance
as a youth predicted panic disorder and agoraphobia at the
ages of 18 or 21 years (Craske et al., 2001). Furthermore,
others report more respiratory disturbance in the history
of panic disorder patients compared to other anxiety disor-
dered patients (Verburg, Griez, Meijer, & Pols, 1995) and
also in first-​degree relatives of panic disorder patients com-
pared to first-​degree relatives of patients with other anxiety
disorders (van Beek, Schruers, & Griez, 2005). Childhood
 Panic Disorder and Agoraphobia 269

experiences of sexual and physical abuse may also prime (Bouton, Mineka, & Barlow, 2001). An extensive body of
panic disorder (Goodwin, Fergusson, & Horwood, 2005). experimental literature attests to the robustness of intero-
After controlling for related diagnoses, childhood sexual ceptive conditioning (e.g., Acheson, Forsyth, & Moses,
abuse history was found to be uniquely associated with 2012) and its independence from conscious awareness of
panic disorder with and without agoraphobia (Cougle, triggering cues (e.g., Block, Ghoneim, Fowles, Kumar, &
Timpano, Sachs-​Ericsson, Keough, & Riccardi, 2010). Pathak, 1987). Hence, slight changes in relevant bodily
Agoraphobia without panic disorder (DSM-​IV-​TR) was functions that are not consciously recognized may elicit
not found to be associated with childhood abuse in this conditioned anxiety or fear and panic due to previous
sample, which may be a consequence of the low base rate pairings with panic (Bouton et al., 2001). An alternative
of this condition. Retrospective reporting, however, limits model offered by Clark (1986) attributes fear of sensations
such findings. to catastrophic misappraisals (e.g., misinterpretation of
sensations as signs of imminent death). Others argue that
catastrophic misappraisals become conditioned stimuli
Maintenance Factors
that trigger panic (Bouton et al., 2001).
Following the first panic attack, individuals with panic Autonomic arousal generated by fear of sensations is
disorder develop an acute fear of bodily sensations associ- believed to contribute to ongoing panic by intensifying
ated with panic attacks (e.g., racing heart and dizziness; the sensations that are feared, thus creating a recipro-
Barlow, 2004). For example, they are more likely to inter- cating cycle of fear and sensations. In addition, because
pret bodily sensations in a catastrophic fashion (Clark, bodily sensations that trigger panic attacks are not always
1988)  and allocate more attentional resources to words immediately obvious, panic attacks appear to be unex-
that represent physical threat (e.g., Maidenberg, Chen, pected (Barlow, 2004), resulting in even further anxiety
Craske, Bohn, & Bystritsky, 1996)  and heartbeat stimuli (Craske, Glover, & DeCola, 1995). The unpredictability
(Kroeze & van den Hout, 2000). In addition, individuals of panic and perceived inability to escape from bodily
with panic disorder have been shown to exhibit greater sensations similarly increases anxiety (Bouton et al., 2001;
anxiety to panic word pairs relative to neutral word pairs Maier, Laudenslager, & Ryan, 1985). In turn, anxiety
(De Cort et al., 2013). In contrast, previous research failed increases the likelihood of panic by directly increasing the
to demonstrate a difference in reaction times to panic-​ availability of sensations that have become conditioned
threat words during an emotional Stroop task between cues for panic or by increasing attentional vigilance for
individuals with panic disorder, those with mixed anxi- these bodily cues. Thus, a maintaining cycle of panic and
ety disorders, and healthy controls (De Cort, Hermans, anxiety develops (Barlow, 2004). Indeed, the perceived
Spruyt, Griez, & Schruers, 2008). Given these conflict- probability of panicking in specific external contexts was
ing findings, further research on attentional biases toward found to be significantly related to agoraphobic avoidance
panic-​related threat in panic disorder is required. (Craske, Rapee, & Barlow, 1988). Furthermore, perceived
Individuals with panic disorder are more anxious in threat control was found to moderate the relationship
procedures that elicit bodily sensations similar to the ones between the belief that symptoms of anxiety are harm-
experienced during panic attacks, such as cardiovascu- ful (anxiety sensitivity) and agoraphobic avoidance in
lar, respiratory, audiovestibular exercises and inductions individuals with panic disorder (White, Brown, Somers,
(Jacob, Furman, Clark, & Durrant, 1992; Kaplan et al., & Barlow, 2006). Both agoraphobic avoidance and subtle
2012; Zarate, Rapee, Craske, & Barlow, 1988) and carbon avoidance behaviors (e.g., holding onto supports for fear
dioxide inhalations, compared to patients with other anxi- of fainting) are believed to maintain negative beliefs
ety disorders (e.g., Rapee, Brown, Antony, & Barlow, 1992; about feared bodily sensations and related contexts (Clark
Vickers, Jafarpour, Mofidi, Rafat, & Woznica, 2012) and & Ehlers, 1993; Craske & Barlow, 2014).
healthy controls (e.g., Gorman et al., 1994; Zvolensky & Agoraphobia may be acquired via exteroceptive
Eifert, 2001). Finally, individuals with panic disorder fear conditioning wherein panic-​ related sensations become
signals that ostensibly reflect heightened arousal and false paired with external stimuli (e.g., shopping malls) pres-
physiological feedback (Craske & Freed, 1995; Craske ent during an attack (Mineka & Zinbarg, 2006). Due to
et al., 2002). this associative process, individuals may begin to avoid
Fear of bodily sensations has been attributed to intero- situations and environments that are perceived to be pre-
ceptive conditioning, in which early somatic components dictive of a panic attack. As previously mentioned, agora-
of anxiety elicit conditioned bursts of anxiety or panic phobia may not always manifest as fear of interoceptive
270 Anxiety and Related Disorders
sensations (Pané-​Farré et al., 2014; Wittchen et al., 2008).
Agoraphobia without panic symptoms may develop
through the irrational belief that being in certain envi-
ronments or situations will increase the likelihood of a
negative event (unrelated to panic) occurring, such as
embarrassment due to incontinence, disorientation, or
injury due to falling (APA, 2013). Agoraphobic avoidance
is then reinforced by the non-​occurrence of the feared
event when environments are avoided. Research on spe-
cific phobias suggests that agoraphobia without panic
symptoms may be acquired through a traumatic condi-
tioning event (e.g., embarrassment due to incontinence),
vicariously, (e.g., witnessing someone be shamed for
incontinence), or informationally conditioned (e.g., hear-
ing that someone was shamed for incontinence) (Mineka
& Zinbarg, 2006).
PURPOSES OF ASSESSMENT
The focus of this chapter is on assessment for the purpose
of (a) diagnosis, (b) case conceptualization and treatment
planning, and (c)  treatment monitoring and evalua-
tion. Emphasis is given to multiple methodologies and
domains, including clinician-​ administered interviews,
self-​
report questionnaires, behavioral observations, and
measures of peripheral physiological functioning. In addi-
tion, we include measures of the constructs relevant to the
perpetuation of panic disorder and agoraphobia, includ-
ing anxiety sensitivity, fear, catastrophic misappraisals of
bodily sensations, and avoidance of not only agorapho-
bic situations but also bodily sensations. The methods of
cognitive–​behavioral therapy (CBT) uniquely designed,
and highly effective, for panic disorder and agoraphobia
(Craske & Barlow, 2007) are derived from models empha-
sizing these constructs. Hence, changes in measures of
these constructs are assumed to be critical indices of
therapeutic outcomes. These measures are also relevant
indices of the efficacy of pharmacological approaches to
treatment, which comprise the other effective treatment
option for panic disorder and agoraphobia (see Freire,
Machado, Arias-​Carrión, & Nardi, 2014).
ASSESSMENT FOR DIAGNOSIS
As a part of the diagnostic process, medical evaluation
is generally recommended to rule out several medical
conditions for the diagnosis of panic disorder, including
thyroid conditions, caffeine or amphetamine intoxication,
drug withdrawal, or pheochromocytoma (a rare adrenal
gland tumor). Furthermore, certain medical conditions,
such as mitral valve prolapse, asthma, allergies, and hypo-
glycemia, can exacerbate panic disorder because they pro-
duce sensations that overlap with panic attack symptoms
(e.g., shortness of breath); however, these are not rule-​
outs, and panic disorder is likely to continue even when
they are under medical control. In addition, for those
reporting nocturnal panic attacks, a polysomnographic
sleep assessment may be recommended to rule out other
sleep-​related disorders, such as sleep apnea, night terrors,
periodic movements, seizures, stage IV night terrors, non-
restorative sleep, sleep hallucinogenesis, and sleep paraly-
sis, all of which are distinct from nocturnal panic (Craske
& Tsao, 2005).
Informally generated clinical diagnoses are rarely as
reliable as diagnoses obtained from structured diagnos-
tic interviews (e.g., Basco et al., 2000). Given that panic
attacks are ubiquitous, differential diagnosis requires
carefully structured questioning regarding the degree to
which the panic attacks are a source of anxiety or a rea-
son for behavioral changes (as would be characteristic of
panic disorder and agoraphobia) or are part of another
anxiety disorder. Hence, diagnostic assessment of both
panic disorder and agoraphobia benefits from structured
interviews. However, fully structured diagnostic inter-
views provide almost no opportunity for probing and may
suffer from limited validity. Thus, preference is given to
semi-​structured interviews that involve flexibility in ques-
tioning and clinical judgment. The two semi-​structured
interviews used most often for the diagnosis of panic disor-
der and agoraphobia are the Anxiety Disorders Interview
Schedule (ADIS [ADIS-​5]; Brown & Barlow, 2014a) and
the Structured Clinical Interview for DSM Disorders
(SCID [SCID-​ 5]; First, Williams, Karg, & Spitzer,
2016c). Ratings of the available psychometric properties
for these two instruments are shown in Table 13.1. Given
the recent DSM-​5 updates to each instrument, psycho-
metric properties of previous versions are featured when
data are unavailable for the current versions.
Anxiety Disorders Interview Schedule
Recently updated to reflect new DSM-​5 diagnostic crite-
ria, the semi-​structured ADIS (ADIS-​5; Brown & Barlow,
2014a) is widely used for the assessment of anxiety,
trauma, obsessive–​compulsive, mood, and other associ-
ated disorders. The ADIS-​5 is advantageous for differ-
entiating among anxiety disorders as well as diagnosing
comorbid mood disorders, which may impact treatment

TABLE 13.1   Ratings of Instruments Used for Diagnosis
Internal Inter-​Rater Test–​Retest
Instrument Norms Consistency Reliability Reliability
ADIS NA NA G Aa
SCID NA NA G Aa
PDSS A G G Aa
  Different raters.
a
Note:  ADIS  =  Anxiety Disorders Interview Schedule; SCID  =  Structured Clinical Interview for the DSM; PDSS  =  Panic Disorder Severity Scale;
A = Adequate; G = Good; E = Excellent; NA = Not Applicable.
planning. Furthermore, the ADIS provides screening
questions for additional conditions, including psychotic
disorders, eating disorders, and impulse control disorders,
and it assesses chronic and episodic life stress. Some of
the interview questions require a “yes” or “no” response,
whereas others involve ratings of fear, avoidance, and
control on Likert scales. The panic disorder section of the
ADIS-​5 assesses full and limited symptom panic attacks.
The agoraphobia section includes a list of 25 situations
organized by situation type as featured in DSM-​5 (e.g.,
open spaces) that are each rated in terms of fear and avoid-
ance, as well as related questions such as probes for typical
safety signals. Although later versions of the ADIS include
a separate section to assess for nocturnal panic attacks, the
ADIS-​5 does not assess for such. In addition to determin-
ing diagnostic status, the interviewer rates each diagnosed
disorder on a 0-​to 8-​point rating to reflect overall levels of
clinical severity (symptom intensity, distress, and impair-
ment) associated with the disorder, with 4 representing the
cut-​off for clinical severity (Grisham, Brown, & Campbell,
2004). Thus, the ADIS encourages diagnostic categoriza-
tion as well as a dimensional approach to understanding
sets of symptoms and differentiation between clinical
and subclinical levels of anxiety. The ADIS is adminis-
tered by a trained clinician. Training typically involves at
least three observations of trained interviewers followed
by achievement of acceptable inter-​rater reliability while
being observed by a trained interviewer on at least three
consecutive occasions (e.g., Brown, Barlow, & DiNardo,
1994). The full ADIS may take several hours to complete,
although it can be shortened by excluding nondiagnostic
research-​based questions. Given the modular structure of
the ADIS, it is possible to limit its use to the panic disor-
der and agoraphobia sections, thereby reducing the time
investment considerably. However, given the ubiquitous
nature of panic attacks and the intricacies of differen-
tial diagnosis, completion of the entire ADIS interview
is advised. Although this will require more time for the
Panic Disorder and Agoraphobia 271
Content Construct Validity Clinical Highly
Validity Validity Generalization Utility Recommended
A A E A
A A E A
A A E A
clinician, we believe that an accurate diagnosis of panic
disorder and agoraphobia depends on differential diagno-
sis and that this should not be compromised.
Versions of the ADIS exist for DSM-​III, the DSM-​III-​
R, DSM-​IV, and currently the DSM-​5 (ADIS: DiNardo,
O’Brien, Barlow, Waddell, & Blanchard, 1983; ADIS-​
R:  DiNardo & Barlow, 1988; ADIS-​ IV:  Brown et  al.,
1994; ADIS-​ 5:  Brown & Barlow, 2014a, respectively).
Each ADIS version provides the assessment of both cur-
rent and lifetime psychopathology (e.g., ADIS-​5L; Brown
& Barlow, 2014b). Based on past DSM-​IV diagnostic cri-
teria, a child and parent version of the ADIS (ADIS-​C/​P;
Silverman & Albano, 2004) is available for the assessment
of anxiety and related disorders in children and adoles-
cents (see Chapter 11, this volume). The following discus-
sion includes references to various versions of the adult
version of this interview. As of mid-​2016, psychometric
data for the ADIS-​5 were not yet available.
In their college sample, Brown and Deagle (1993)
found good inter-​rater reliability for “panic classification”
when the ADIS-​R (DiNardo & Barlow, 1988) was rated by
two individuals (κ = .83). In Brown, DiNardo, Lehman,
and Campbell’s (2001) study, inter-​rater reliability was
good for both panic disorder (κ = .72) and panic disorder
with agoraphobia (κ = .77) diagnoses. On the whole, the
ADIS is judged to have good inter-​rater reliability.
The test–​retest reliability of panic disorder diagnoses
was generally good when lifetime diagnoses with and
without agoraphobia were combined (ADIS-​IV; κ  =  .75
to .79) and good to very good for diagnoses of panic
disorder (ADIS-​R; κ  =  .86) and agoraphobia (ADIS-​R;
κ = .90) (Brown, DiNardo, et al., 2001; DiNardo, Moras,
Barlow, Rapee, & Brown, 1993). However, reliability val-
ues were not consistent across levels of agoraphobia, and
most often, less than adequate values were obtained for
diagnoses of panic disorder without agoraphobia (ADIS-​
R and ADIS-​IV; κ = .39 to .72; Brown, DiNardo, et al.,
2001; DiNardo et al., 1993). Last, Brown, DiNardo, et al.
272 Anxiety and Related Disorders

obtained good ratings of Clinician Severity Rating (CSR) The structure of the SCID includes a general probe
test–​retest reliability (ADIS-​IV; r  =  .83). Given the vari-
question at the beginning of each disorder module, fol-
ability and short test–​retest time intervals (0–​44  days), lowed by other specific questions as deemed appropriate
the ADIS-​IV is judged to have only adequate test–​retest based on answers to the probe question. Although this
reliability. interview format is similar to the ADIS, the inclusion
The ADIS modules were developed to assess the of each diagnostic criterion next to relevant questions
diagnostic criteria as stated in the DSM-​5 (APA, 2013). makes the SCID more transparent. For each question,
However, given that the contents of the interview were the interviewer assesses how consistent the information is
not reviewed by outside judges (T. A.  Brown, personal with the diagnostic criterion of interest and gives a rat-
communication, August 17, 2016), the ADIS-​5 was rated ing of 1 (absent/​false), 2 (subthreshold), or 3 (threshold/​
as demonstrating only adequate content validity. Brown, true). According to Spitzer, Williams, Gibbon, and First
Chorpita, and Barlow (1998) reported convergent and dis- (1992), SCID training should include becoming familiar
criminant validity of the ADIS-​IV by showing that symp- with the related SCID User’s Guide (SCID-​5-​CV User’s
tom measures of anxiety and depression differentially Guide: First, Williams, Karg, & Spitzer, 2016a), watching
loaded on different higher order factors (e.g., autonomic videotaped interviews, and achieving acceptable inter-​
arousal), making panic disorder distinguishable from rater and test–​retest reliability.
other diagnoses. This led to the assignment of adequate As of October 2017, no psychometric data had been
construct validity. published for the SCID-​5. Evidence regarding the inter-​
The ADIS has been used with various demographic rater reliability of panic disorder using previous versions of
groups and in a variety of settings, including managed the SCID is mixed (SCID-​IV: First, Spitzer, Williams, &
care and pediatric primary care (Addis et al., 2004; Bowen, Gibbon, 1995; SCID-​I: Spitzer & Williams, 1984). Kappa
Chavira, Bailey, Stein, & Stein, 2008). Thus, it is rated values range from .65 to 1.0 (e.g., Dammen, Arnesen,
as having excellent validity generalization. Although the Ekeberg, Husebye, & Friis, 1999; Löwe et  al., 2003;
ADIS is frequently used as a treatment outcome measure, Zanarini & Frankenburg, 2001; Zanarini et  al., 2000).
it is rated as having demonstrated only adequate clinical There is some evidence for adequately reliable agorapho-
utility because there is no evidence that the use of data bia diagnoses (κ = .69; Zanarini & Frankenburg, 2001).
obtained with this particular interview results in a better Overall, the SCID is judged to have good inter-​rater reli-
treatment outcome than that which would have occurred ability because among the mixed data, there were several
by using a different instrument. excellent values.
Most test–​retest data for SCID diagnoses of panic dis-
order are slightly less than adequate to adequate. In a large
Structured Clinical Interview for DSM Disorders
study of patients and nonpatients (N  =  592), Williams,
The SCID (SCID-​5; First et  al., 2016c) is administered Gibbon, and colleagues (1992) obtained test–​ retest κ
by a clinician to assess common areas of psychopathol- values for panic disorder diagnoses, based on interviews
ogy, including anxiety and related disorders. Thus, it conducted 1 to 14  days apart, ranging from .54 to .65.
facilitates differential diagnoses and assessment of comor- However, studies with smaller sample sizes obtained κ
bid conditions (e.g., mood disorders). In addition to the values ranging from .61 to .82, dependent on whether
clinician version of the SCID (SCID-​5-​CV; First et  al., subtypes were examined (Williams, Spitzer, & Gibbon,
2016c), two research-​oriented versions exist—​the SCID-​ 1992; Zanarini & Frankenburg, 2001; Zanarini et  al.,
5-​RV (Research Version; First, Williams, Karg, & Spitzer, 2000). Data for agoraphobia diagnoses are mixed, with
2016d) and the SCID-​ 5-​
CT (Clinical Trials Version; κ values ranging from .43 to 1.0 (Williams, Gibbon,
First, Williams, Karg, & Spitzer, 2016b). A child version et  al., 1992; Williams, Spitzer, et  al., 1992; Zanarini &
of the SCID, the Structured Clinical Interview for DSM-​ Frankenburg, 2001). On the basis of the range of findings,
IV Childhood Diagnoses (KID-​SCID; Hein et al., 1998), a somewhat liberal rating of adequate test–​retest reliability
is available but has been rarely evaluated in research stud- was assigned.
ies. Versions of the SCID are available in many languages, As with the ADIS, although the SCID is worded to
including English, Mandarin, Spanish, German, Dutch, address each of the DSM-​5 diagnostic criteria, there is no
and Korean (http://​www.scid4.org/​trans.html; Skodol, evidence of its contents being evaluated by outside judges.
Bender, Rush, & Zarin, 2000). The focus of our discus- Hence, it too demonstrates only adequate content validity.
sion and ratings in Table 13.1 is on the SCID for adults. Kessler and colleagues (2005) found that anxiety disorder

diagnoses generated from the SCID-​I/​NP and the World
Mental Health Survey Initiative Version of the World
Health Organization Composite International Diagnostic
Interview (WMH-​CIDI; Kessler & Üstün, 2004) “gener-
ally were in good concordance” (p. 594). Thus, the overall
construct validity of the SCID is deemed adequate.
Evidence of the SCID’s excellent validity generaliza-
tion lies in the fact that it has been used in more than
1,000 studies (First & Gibbon, 2004)  and has been
administered to coronary heart patients (Bankier, Januzzi,
& Littman, 2004), individuals seeking community outpa-
tient treatment (Zimmerman & Mattia, 2000), and pri-
mary care patients (e.g., Rodriguez et al., 2004).
The SCID-​5 allows clinicians and assessors to follow
closely the DSM-​5 criteria when making diagnoses. It is
relatively inexpensive and does not require a scoring pro-
gram. In addition, it may result in more valid diagnoses
than those based on a standard clinical interview (Basco
et al., 2000). However, because further research is needed
on the usefulness of the SCID-​5 in assessing panic disor-
der and agoraphobia specifically, clinical utility is judged
to be adequate.
Panic Disorder Severity Scale
Following completion of a diagnostic assessment, a
dimensional assessment specifically designed for panic
disorder, such as the Panic Disorder Severity Scale
(PDSS; Shear et al., 1997), can be helpful. This clinician-​
completed scale rates seven areas using a 0 to 4 severity
rating scale:  panic attack frequency, distress, anticipa-
tory anxiety, agoraphobic and interoceptive-​related fears
and avoidant behavior, and work and social impairment.
Agoraphobic avoidance is assessed via one question and
within the context of “fear of panic”; thus, the PDSS
should not be used as a singular measure of agoraphobia.
Administration of this instrument requires less than 15
minutes (Antony, 2002).
Internal consistency is adequate to excellent
(Cronbach’s α ranging from .71 to .92; e.g., Houck,
Spiegel, Shear, & Rucci, 2002; Monkul et  al., 2004;
Yamamoto et  al., 2004), with “adequate” limited to one
study examining psychometrics of a Turkish translation
(Monkul et al., 2004). Overall, scores on this measure are
judged to possess good internal consistency.
Different translations of the PDSS have been found to
have adequate to excellent inter-​rater reliability (r = .79;
intraclass correlation coefficient [ICC]  =  .87 to .99;
Monkul et al., 2004; Shear et al., 1997; Yamamoto et al.,
2004), resulting in an averaged rating of good inter-​rater
Panic Disorder and Agoraphobia 273
reliability. Its test–​retest data range from less than ade-
quate to good (r = .63 to .71; ICC = .81 to .88) over short
periods of time (Houck et al., 2002; Monkul et al., 2004;
Shear et al., 1997, 2001), resulting in an overall rating of
adequate test–​retest reliability.
The PDSS has only adequate content validity because
there is no evidence to indicate that independent judges
reviewed this measure. Shear et al. (1997, 2001) found evi-
dence for construct validity in that ADIS-​R panic disorder
CSRs were strongly related to PDSS total scores (r = .55),
patients with panic disorder with agoraphobia scored
higher on the PDSS compared to patients with other anxi-
ety or mood diagnoses, and PDSS scores correlated with
various anxiety-​related questionnaires. However, overall,
the construct validity was judged to be adequate rather
than good, due to the lack of independently replicated
validity findings.
Validity generalization of the PDSS is judged to be
good. This measure has been used in diverse sociode-
mographic samples. Japanese (Yamamoto et  al.,
2004)  and Turkish versions of this measure (Monkul
et  al., 2004)  exist. In addition, a self-​report version of
this instrument (PDSS-​SR) possesses acceptable score
reliability and promising validity (Wuyek, Antony, &
McCabe, 2011). Although the PDSS and PDSS-​ SR
assess the same panic symptoms, correlations between
total score and panic attack frequency for these measures
were found to only fall into the moderate range (Wuyek
et al., 2011). Furthermore, although the PDSS may help
clinicians assess different aspects of panic disorder, it has
only adequate clinical utility because there is no research
to show that the use of its data results in additional ben-
efits beyond those seen when data are used from other
instruments.
Overall Evaluation
Although semi-​ structured diagnostic interviews may be
somewhat time-​consuming, the data they yield are help-
ful in making differential diagnoses, which is particularly
important given the ubiquitous nature of panic attacks. If
time does not permit to complete a full interview, the panic
disorder and agoraphobia modules may be complemented
by screener questions from the other anxiety disorder mod-
ules and/​or by self-​report questionnaires to gauge whether
the use of the term “panic” is related to other disorders.
Clinicians should also inquire about medical conditions
and stimulant drug use. Last, further research is needed
regarding the psychometric properties and comparative
clinical utility of the ADIS-​5 and the SCID-​5.
274 Anxiety and Related Disorders

TABLE 13.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

ASI G G NA A A E E A
ASI-​3 G G NA G G E E A ✓
BSQ G G NA G A G E A ✓
ACQ G G NA A A G E A ✓
FQ G A NA G A G E A ✓
MI G E NA A A A E A
APPQ G G NA A A A E A

Note: ASI = Anxiety Sensitivity Index; ASI-​3, Anxiety Sensitivity Index-​3; BSQ = Body Sensations Questionnaire; ACQ = Agoraphobic Cognitions
Questionnaire; FQ = Fear Questionnaire; MI = Mobility Inventory for Agoraphobia; APPQ = Albany Panic and Phobia Questionnaire; A = Adequate;
G = Good; E = Excellent; NA = Not Applicable.

ASSESSMENT FOR CASE CONCEPTUALIZATION Bright, & Gallagher, 1984), Agoraphobic Cognitions

AND TREATMENT PLANNING
Development of a thorough case conceptualization to
guide treatment planning for panic disorder and ago-
raphobia requires assessment of symptoms (includ-
ing severity and distress), as well as fear of and beliefs
about the symptoms, and avoidance of situations and
activities. Whenever possible, a variety of assessment
methodologies, including self-​report, in vivo, and physi-
ological measures, is preferred. This section provides
clinicians with a number of relevant instruments and
methodologies.
Self-​Report Instruments
Self-​report measures are relatively inexpensive, require
only a brief amount of time to complete, are often stan-
dardized, and allow for easy comparisons of effect sizes
across treatment studies. However, self-​report instruments
may result in an overestimation of panic attack frequency
(e.g., Margraf, Taylor, Ehlers, Roth, & Agras, 1987) and
physiological symptoms (e.g., Calvo & Eysenck, 1998).
Nonetheless, self-​report instruments yield useful informa-
tion and are likely to remain one of the primary methods
of assessing panic disorder and agoraphobia. The follow-
ing is not intended to be a comprehensive review of all
available self-​report measures for panic and agoraphobia
but, rather, covers the self-​report instruments that are most
helpful for assessing thoughts, feelings, and behaviors as
they relate to these disorders. The self-​report measures
to be discussed are the Anxiety Sensitivity Index (ASI;
Reiss, Peterson, Gursky, & McNally, 1986)  and Anxiety
Sensitivity Index-​ 3 (ASI-​ 3; Taylor et  al., 2007), Body
Sensations Questionnaire (BSQ; Chambless, Caputo,
Questionnaire (ACQ; Chambless et  al., 1984), Fear
Questionnaire (FQ; Marks & Mathews, 1979), Mobility
Inventory (MI; Chambless et al., 1984), and Albany Panic
and Phobia Questionnaire (APPQ; Rapee, Craske, &
Barlow, 1994). Ratings for the psychometric properties
of each instrument are shown in Table 13.2. Across mea-
sures, we were somewhat liberal in our ratings of the prop-
erty of norms, such that if there were at least two available
studies to cite and data from both clinical and nonclinical
samples, the norms were rated as good. In addition, none
of the reviewed measures received content validity or clin-
ical utility ratings that were better than adequate. This is
because there are no published data to indicate that any of
the measures in their entirety were evaluated by indepen-
dent judges and no published data to suggest that using
results from these self-​report measures leads to clinical
benefits above those gained by using data obtained from
other instruments.
Anxiety Sensitivity Index
The ASI (Reiss et al., 1986) is a 16-​item self-​report mea-
sure that assesses beliefs surrounding the consequences of
arousal-​related sensations. Zinbarg, Barlow, and Brown
(1997) evaluated the factor structure to find an overall
general factor representing level of sensitivity to anxiety,
as well as three factors that measure physical concerns
(e.g., “It scares me when my heart beats rapidly”), men-
tal incapacitation concerns (e.g., “When I  am nervous,
I worry that I might be mentally ill”), and social concerns
(e.g., “Other people notice when I  feel shaky”). Other
studies have found a taxonic latent class structure com-
posed of two dimensions of anxiety sensitivity (Bernstein
et al., 2007).

Norms for the ASI exist for nonclinical and clinically
anxious individuals (see Peterson & Reiss, 1992; Rapee
et  al., 1992). Scores on this measure have been found
to have good internal consistency (Cronbach’s α  =  .84
to .90) and adequate test–​retest reliability over a 2-​week
period (r  =  .75; see Shear et  al., 2000). On the basis of
the adjusted item-​to-​scale correlations and factor loadings,
Blais et al. (2001) reanalyzed ASI data from three earlier
studies with items 1, 5, 7, 8, and 13 removed. In compari-
son to the original ASI, the data produced by the 11-​item
version related more specifically to panic disorder than to
other psychiatric conditions and were highly correlated
with data from the 16-​item version (r > .95). The 11-​item
version’s two factors are “fears of somatic sensations of
anxiety and fears of loss of mental control” (Blais et al.,
2001, p. 273).
There is evidence for excellent construct validity
for the ASI, including convergent, criterion, construct,
predictive, and discriminative validity. For example, as
reviewed previously, longitudinal studies indicate that
high scores on the ASI predict the onset of panic attacks
and worry about panic. In addition, the ASI discriminates
panic disorder from other anxiety disorders (e.g., Zinbarg
& Barlow, 1996). Furthermore, treatment studies have
shown that the partial pressure of carbon dioxide (pCO2)
level partially mediated the effect of capnometry-​assisted
respiratory training (CART) on fear of bodily sensations
as measured by the ASI (Meuret, Rosenfield, Hofmann,
Suvak, & Roth, 2009). Thus, construct validity for the ASI
was judged to be excellent.
In terms of validity generalization, this measure is
available in a variety of languages (see Antony, 2002).
It has been administered to samples of various eth-
nic backgrounds (e.g., Native Americans and Alaskan
Natives:  Zvolensky, McNeil, Porter, & Stewart, 2001;
Russians:  Kotov, Schmidt, Zvolensky, Vinogradov, &
Antipova, 2005), although the ASI’s factor structure does
not hold true for all populations (e.g., African American
college students:  Carter, Miller, Sbrocco, Suchday, &
Lewis, 1999). In addition, the ASI has been used with
anxious patients in primary care settings (Craske et  al.,
2005). Hence, the overall rating for validity generalization
was excellent.
Anxiety Sensitivity Index-​3
Developed from the ASI, the ASI-​3 (Taylor et al., 2007) is
an 18-​item self-​report measure that also assesses anxiety
sensitivity. Unlike the ASI, the ASI-​3 was designed to be
a multidimensional measure to assess the three anxiety
Panic Disorder and Agoraphobia 275
sensitivity domains. Creators of the measure thoroughly
considered content validity during item selection (for
methods, see Taylor et al., 2007); thus, the ASI-​3 is rated
as possessing good content validity. Norms for the ASI-​
3 exist for both nonclinical and clinically anxious indi-
viduals, including average scores for individuals in partial
hospitalization with a variety of psychological disorders
(Rifkin, Beard, Hsu, Garner, & Björgvinsson, 2015;
Taylor et al., 2007).
Scores on this measure have demonstrated good inter-
nal consistency, outperforming the ASI social and cogni-
tive concerns subscales in both clinical and nonclinical
samples (Kemper, Lutz, Bähr, Rddel, & Hock, 2011;
Taylor et  al., 2007). In addition, test–​retest reliability of
the ASI-​3 scores has been found to range from accept-
able to good (1 month: r = .76 [Ghisi et al., 2016]; 15–​
30 days: r = .64 [Mantar, Yemez, & Alkin, 2010]). Based
on the findings, we rated the overall test–​retest as good.
The ASI-​3 is available in a variety of languages, including
English, Italian, and Turkish, and has been administered
in various populations (Mantar et  al., 2010; Petrocchi,
Tenore, Couyoumdjian, & Gragnani, 2014; Taylor et al.,
2007). Thus, validity generalization was judged as excel-
lent. Based on aforementioned findings for the ASI, the
ASI-​3 was also rated as possessing excellent construct
validity.
In terms of clinical utility, the ASI and ASI-​3 are inex-
pensive and take only 3 to 5 minutes to complete (Antony,
2002), and they can be used as a measure of treatment
outcome (e.g., Craske et al., 2007). The ASI and ASI-​3 are
rated as having adequate clinical utility. In summary, the
ASI and ASI-​3 measure a construct recognized to be cen-
tral to the onset and maintenance of panic disorder and
agoraphobia, described previously, and are critical to the
measurement of responsiveness to treatment. The ASI-​3
is recommended over the ASI given its superior psycho-
metric properties.
Body Sensations Questionnaire
The BSQ (Chambless et al., 1984) assesses level of fear
of somatic sensations (e.g., sweating, nausea, and dizzi-
ness) experienced during an anxious state. This measure,
which can be completed within 5 to 10 minutes, consists
of 18 items with ratings based on a Likert scale. The BSQ
is available in a variety of languages, including English,
Spanish, Portuguese, French, Greek, German, Swedish,
Mandarin, and Dutch (see Antony, 2002).
Norms for the BSQ exist for clinical as well as com-
munity samples (see Chambless et al., 1984; Chambless
276 Anxiety and Related Disorders
& Gracely, 1989). Scores on this measure have been
found to have good to excellent internal consistency
(Cronbach’s α ranging from .84 to .95; Carlbring et  al.,
2007; Chambless et  al., 1984; Novy, Stanley, Averill, &
Daza, 2001), with test–​retest reliability ranges from below
adequate to good (ranging from r  =  .67 over a median
of 31 days to a corrected r = .89 over a 3-​month period;
Arrindell, 1993b; Carlbring et al., 2007; Chambless et al.,
1984). Thus, an overall rating of good was assigned for
both test–​retest reliability and internal consistency.
The items for the BSQ were developed from discus-
sions and sessions with clients and therapists (Chambless
et  al., 1984), suggestive of adequate content validity.
Evidence for good construct validity derives from corre-
lated scores between the BSQ and the ACQ (see later)
and other self-​report measures of anxiety and also from the
finding that individuals with panic disorder, other anxiety
disorders, and no anxiety disorders score differently on the
BSQ (see Arrindell, 1993a; Chambless, Beck, Gracely,
& Grisham, 2000). In addition, Smits, Powers, Cho, and
Telch (2004) found that BSQ change scores were partial
mediators of the effects of group CBT on levels of anxiety,
agoraphobia, and frequency of panic attacks.
The BSQ has been used with people of different
sociodemographic backgrounds and in different settings
including primary care (van Boeijen et  al., 2005)  and
Internet-​based interventions (Carlbring et  al., 2006),
and thus it was rated as having excellent validity gener-
alization. According to Chambless et al. (1984), the BSQ
helps clinicians focus on the particular sensations that are
of most concern to clients. Furthermore, BSQ responses
may be useful in the development of individualized
behavioral approach tests (BATs; discussed later) and tar-
geted interoceptive exposures (e.g., Craske, Rowe, Lewin,
& Noriega-​Dimitri, 1997). Thus, the BSQ has adequate
clinical utility.
Agoraphobic Cognitions Questionnaire
The ACQ (Chambless et al., 1984) assesses the frequency
of particular thoughts while the respondent is in an anx-
ious state. This measure consists of 15 items with ratings
based on a Likert scale, and it can be completed within
5 to 10 minutes (Antony, 2002). The ACQ generates an
overall mean score of the first 14 items, a mean “physical
concerns” subscale score, and a mean “loss of control”
subscale score. The ACQ is available in a variety of lan-
guages, including English, Spanish, Portuguese, French,
Greek, German, Swedish, Mandarin, and Dutch (see
Antony, 2002).
Norms for this questionnaire exist for clinical as well
as community samples (see Chambless et  al., 1984). In
addition, scores on this measure have been found to have
good internal consistency (Cronbach’s α ranging from .80
to .87) and adequate test–​retest reliability (r = .86 to .92,
ranging from a nonspecified time period to a 3-​month
period; see Arrindell, 1993b; Carlbring et al., 2007).
Items on the ACQ were decided upon based on inputs
received from clients and therapists (Chambless et  al.,
1984), suggestive of adequate content validity. The con-
struct validity of the ACQ appears to be good given evi-
dence for correlations with the BSQ and other self-​report
measures of anxiety, as well as the finding that individuals
with panic disorder, other anxiety disorders, and no anxi-
ety disorders score differently on the ACQ (see Arrindell,
1993a; Chambless et al., 2000). Bouvard and colleagues
(1998) found evidence of internal consistency and validity
for the French version of the ACQ. The ACQ was rated as
exhibiting excellent validity generalization due to its use
with people of different language backgrounds and differ-
ent settings (e.g., van Boeijen et al., 2005).
The adequate clinical utility of the ACQ lies in its
identification of anxious thoughts to be targeted through
cognitive restructuring and exposures to feared situations
and bodily sensations.
Fear Questionnaire (Agoraphobia Subscale)
The FQ (Marks & Mathews, 1979) assesses phobic sever-
ity and distress, as well as related symptoms of anxiety and
depression. For current purposes, the discussion focuses
on the agoraphobia subscale. It consists of five situational
items for which level of avoidance is rated on a Likert
scale. Less than 10 minutes is required to complete the
entire 20-​item measure. It is available in a variety of lan-
guages, including English, Dutch, French, German,
Italian, Catalan, Chinese, and Spanish (Roemer, 2002).
Norms for this measure exist for a clinical sample
(Cox, Swinson, & Shaw, 1991), as well as for a normative
sample (Gillis, Haaga, & Ford, 1995). Although scores on
the agoraphobia subscale had less than adequate internal
consistency values in one study (Cronbach’s α ranging
from .59 to .69; Cox et al., 1991), other studies with clini-
cal and nonclinical samples, including a Spanish/​English
bilingual sample, indicate adequate to good internal con-
sistency (Cronbach’s α ranging from .76 to .84; e.g., Cox,
Swinson, Parker, Kuch, & Reichman, 1993; Novy et al.,
2001). Given the variable data, an overall internal consis-
tency rating of adequate, rather than good, was assigned.
Test–​retest reliability of the FQ agoraphobia subscale

scores has been assessed over different time delays rang-
ing from 1 to 16 weeks (Cronbach’s α = .85 to .89; Marks
& Mathews, 1979; Michelson & Mavissakalian, 1983),
although with small samples, resulting in an overall
assignment of good test–​retest reliability.
The items on the FQ were determined through mul-
tiple factor analyses (Marks & Mathews, 1979) and appear
to represent the constructs of interest, indicative of ade-
quate content validity. The construct validity of the FQ is
judged to be good based on correlations with other self-​
report measures of anxiety, as well as the finding that FQ
agoraphobia subscale scores are higher in individuals with
panic disorder with agoraphobia in comparison to other
individuals (see Cox et al., 1991; Oei, Moylan, & Evans,
1991). The FQ has been used with people of different
ethnicities, including Spanish-​speaking anxious individu-
als (Novy et al., 2001) and Chinese college students (Lee
& Oei, 1994), as well as with primary care and community
mental health patients (Craske et al., 2005; Wade, Treat,
& Stuart, 1998). Given the various populations and set-
tings in which the FQ has been studied, it is judged to
have excellent validity generalization. The FQ is rated as
having adequate clinical utility. The greatest utility of the
FQ is that it is a brief index of level of agoraphobic avoid-
ance, to be compared against established norms.
Mobility Inventory for Agoraphobia
The MI (Chambless, Caputo, Jasin, Gracely, & Williams,
1985) assesses degree of avoidance due to agoraphobia, as
well as the frequency and severity of panic attacks. The
MI has undergone some changes since its original devel-
opment (see Antony, 2002). The first part of the MI lists
27 agoraphobic-​ like situations (including one write-​ in
response). Using a Likert scale, two avoidance ratings are
given to each situation, one when accompanied and one
when alone. Separate mean values (for accompanied and
alone) are calculated for the first 26 items. The respon-
dent also circles the 5 situations that are most impairing.
Three questions, rated on a Likert scale, assess the fre-
quency and severity of panic attacks. Last, the respondent
is asked about his or her safety zone, including its size
and location. This questionnaire can be completed in
less than 20 minutes (Chambless et al., 1985) and is avail-
able in English, Spanish, Portuguese, French, Swedish,
Dutch, German, and Greek (Antony, 2002).
Norms exist for clinical as well as normal samples (see
Chambless et al., 1985), and the MI has been completed
by an elderly community sample (Hendriks et al., 2010).
Because item development was informed by exposure
Panic Disorder and Agoraphobia 277
session observations and information obtained through
client interviews, as well as by items on a measure of fear
(Chambless et  al., 2011), the MI has adequate content
validity. In addition, scores on this measure have been
found to have excellent internal consistency (for a review,
see Chambless et al., 2011) and adequate test–​retest reli-
ability (r  =  .75 to .90 over a 31-​day period; Chambless
et al., 1985). Furthermore, the MI demonstrates adequate
test–​retest reliability over longer intervals of time (e.g.,
5 years; Chambless et al., 2011). The MI has convergent
validity, as evidenced by correlations with other self-​report
measures of anxiety (e.g., Ehlers, 1995); however, more
research is required on discriminant validity of the MI.
Thus, the construct validity of the MI was rated as ade-
quate. The MI is available in different languages and has
been administered in various settings (e.g., Kenardy et al.,
2003). Thus, it possesses excellent validity generalization.
This measure has at least adequate clinical utility due to
its usefulness in generating a list of agoraphobic situa-
tions to be targeted during in vivo exposures (Chambless
et al., 1985).
Albany Panic and Phobia Questionnaire
The APPQ (Rapee et al., 1994) is a 27-​item questionnaire
that measures degree of fear imagined in a given situation
(e.g., “exercising vigorously alone”). Each item is rated
from 0 (no fear) to 8 (extreme fear). Scores are calculated
separately for agoraphobia, social phobia, and interocep-
tive subscales.
Descriptive statistics are available on the APPQ for
various anxiety disorders, as well as for a small nonclinical
sample (Rapee et al., 1994). In addition, norms are avail-
able for clinical populations (Brown, White, & Barlow,
2005). The APPQ items were tested in three pilot studies
(Rapee et al., 1994), but the measure was not judged inde-
pendently by others, and hence it was assigned adequate
content validity. The internal consistency of its subscale
scores ranges from good to excellent in English and
Spanish versions (Cronbach’s α ranges from .85 to .92;
Brown, White, & Barlow, 2005; Novy et al., 2001; Rapee
et al., 1994). Overall, its internal consistency appears to be
good. There is some evidence of scores on this measure
displaying adequate test–​retest reliability (r ranging from
.68 to .84, mean period of 10.9 weeks; Rapee et al., 1994).
Several studies have found evidence for this measure’s
construct validity (Brown, White, & Barlow, 2005; Novy
et  al., 2001; Rapee et  al., 1994), including correlations
with other self-​report measures of anxiety and evidence
that the subscale scores differ between groups. Examples
278 Anxiety and Related Disorders
include different interoceptive subscale scores for panic
disorder groups varying in levels of avoidance, as well
as differences in agoraphobia subscale scores between
a panic disorder group with varying levels of avoidance
and three comparison groups (social phobia, other anxi-
ety, and control; Rapee et al., 1994). Overall, a rating of
adequate construct validity was assigned.
There is evidence for the use of the APPQ with
various demographic groups and in different languages
(e.g., Kim et  al., 2004; Novy et  al., 2001). The APPQ
has been administered to a variety of groups across
different clinical settings (e.g., Gonzalez, Zvolensky,
Grover, & Parent, 2012); thus, validity generalization
was judged to be excellent. Notably, this scale assesses
fears of activities that produce bodily sensations (e.g.,
exercising vigorously or drinking coffee), a type of fear
that is central to panic disorder and is a target of treat-
ment. The instrument is useful for generating a list of
feared activities and is therefore beneficial to treatment
planning as well. At this time, the APPQ is judged to
have adequate clinical utility.
Behavioral Approach Tests
Behavioral approach tests (also referred to as “behavioral
avoidance tests”) assess the degree of behavioral approach
(or avoidance) of specific situations or internal stimuli
(i.e., bodily sensations). Although degree of avoidance can
be reported upon during diagnostic interviews or with self-​
report questionnaires, the BAT provides another modality
of assessment that is not constrained by the biases of retro-
spective judgment that limit verbal reporting.
The BAT can be standardized across patients or
individually tailored for a patient. The standardized
BAT for agoraphobia usually involves walking or driv-
ing a particular route, such as a 1-​mile loop around
the clinic setting (for examples, see Williams & Zane,
1989). Standardized interoceptive BATs involve exer-
cises that induce panic-​ like symptoms, such as spin-
ning in a circle, running in place, hyperventilating, and
breathing through a straw (Barlow & Craske, 2006).
The disadvantage of standardized BATs is that the spe-
cific task may not be relevant to everyone with panic
disorder and agoraphobia. Individually tailored BATs
usually assess approach/​avoidance of three to five indi-
vidualized situations or physical exercises designed to be
moderately to extremely anxiety-​provoking for a given
patient. Individually tailored BATs are more informative
for clinical practice, although they confound between-​
participant comparisons for research purposes.
With both individualized and standardized BATs, anx-
iety levels are rated at regular intervals throughout, and
actual distance or length of time is measured. Ongoing
anxiety typically is measured using the Subjective Units
of Distress Scale (SUDS; Wolpe, 1968), a verbal or writ-
ten rating of anxiety, ranging from 0 (no anxiety) to 100
(extreme anxiety). Some prefer to use a smaller range than
the original SUDS rating system (e.g., a 9-​point scale;
Mavissakalian & Michelson, 1982).
Standardized and individually tailored BATs are each
susceptible to demand biases, for distress before treatment
and improvement after treatment (Borkovec, Weerts, &
Bernstein, 1977). On the other hand, BATs are an impor-
tant supplement to self-​report of agoraphobic avoidance
because patients tend to underestimate what they can
actually achieve (Craske et al., 1988). In addition, BATs
often reveal information of which the individual is not
fully aware but that is important for treatment planning.
For example, safety signals and safety behaviors, which
alleviate distress in the short term but sustain anxiety in
the long term, may not be acknowledged until in the act
of attempting to approach a situation or a bodily sensa-
tion that had been previously avoided. Typical safety sig-
nals include other people and medication bottles. The
removal of safety signals and safety behaviors is critical to
effective exposure therapy (e.g., Salkovskis, 1991).
Physiological Measures
Advancements in technology have given rise to practi-
cal options for clinicians to assess ongoing physiological
responses. Most fitness watches and wearables feature
ongoing heart rate monitoring, with more recent models
allowing for blood pressure measurement. Ongoing mon-
itoring of heart rate and blood pressure during BATs, for
example, may illuminate discrepancies between reports of
symptoms and actual physiological arousal (i.e., report of
heart rate acceleration in the absence of actual heart rate
acceleration), which can serve as a therapeutic demon-
stration of the role of attention and cognition in symptom
production. Similarly, physiological data can disconfirm
misappraisals such as “my heart feels like its beating so fast
that it will explode.”
Another option is to record basal peripheral physiology
over protracted periods of time, such as 24-​hour ambu-
latory recordings as individuals engage in their normal
daily routine. However, the clinical value of such data is
not clear, especially because the results are inconsistent
(e.g., Bystritsky, Craske, Maidenberg, Vapnik, & Shapiro,
1995; Shear et  al., 1992). Nonetheless, the finding that

CBT effects are not limited to self-​reported symptoms but
extend to shifts in basal levels of physiology (Craske et al.,
2002) is useful information for the clinician.
Measures of In Vivo Cognition
In contrast to strong endorsements of perceived dangers
on self-​report questionnaires in anticipation of feared situ-
ations, Williams, Kinney, Harap, and Liebmann (1997)
reported a general absence of danger appraisals as patients
with panic disorder and other phobias confronted their
most feared driving and claustrophobic situations. That
is, patients reported very little anticipation of panic or the
situation itself while confronting those situations. Instead,
their verbal reports pertained mostly to perceived inability
to cope. This suggests that self-​report questionnaires tap
a different construct than in vivo measures of cognition.
Conceivably, endorsements on self-​report questionnaires,
when not faced with an agoraphobic situation, represent
anticipatory anxiety, whereas reports during in vivo expo-
sures represent fear responding. There is reason to believe
that cognitive functions differ between these two states.
That is, whereas anxiety is associated with improved atten-
tional selectivity for threat-​relevant stimuli, processing of
threatening information may be impeded at the height of
intense fear (e.g., Watts, Trezise, & Sharrock, 1986). In
addition, Goldsmith (1994) noted that cognitions associ-
ated with emotions (e.g., fear) are relatively elementary
or automatic, in contrast to the more complex cognitive
processing of mood states (e.g., anxiety).
Thus, a more comprehensive assessment of experi-
ence when faced with agoraphobic situations or feared
bodily sensations would entail behavioral observations,
anxiety ratings, physiological measurements, and cogni-
tions in the moment. There is no specific instrument to
recommend, however, other than instructing individuals
to verbalize their thoughts throughout the BAT.
Overall Evaluation
Several self-​report instruments are helpful in the assess-
ment of subjective state (i.e., ASI or ASI-​3, BSQ, ACQ,
and FQ). SUDS ratings and assessment of cognitions and
physiology during BATs can generate a more thorough
understanding of the individual’s subjective experience
and what to target during treatment. A  clear case con-
ceptualization necessary for individualizing treatment
for panic disorder and agoraphobia warrants gathering
information across all of these domains using multiple
methodologies.
Panic Disorder and Agoraphobia 279
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
Similar to case conceptualization and treatment plan-
ning, assessment for treatment monitoring and treatment
outcome should include measures of symptom-​related
misappraisals, fear, and avoidance, as well as cogni-
tions related to control and self-​efficacy. Although the
evidence to date remains sparse and inconsistent, there
is some evidence that measures of catastrophic think-
ing about panic attacks predict treatment outcome (e.g.,
Margraf & Schneider, 1991)  as well as follow-​up status
(Clark et al., 1994) for patients with panic disorder with
agoraphobia. In addition, there is other evidence to sug-
gest that measures of self-​efficacy and perceived control
may be more relevant and informative (Fentz et al., 2013;
Williams & Falbo, 1996). In multiple independent stud-
ies, greater agoraphobic avoidance has also been found
to be predictive of worse outcomes for CBT in individu-
als with panic disorder and agoraphobia (for a review, see
Porter & Chambless, 2015). In addition to assessing mul-
tiple constructs, it is also important that various method-
ologies be used in treatment monitoring and treatment
outcome assessment. Our discussion includes interview,
self-​
report, self-​
monitoring, and behavioral assessment
methodologies.
Interviews
ADIS
In addition to the diagnostic value of the ADIS (Brown
& Barlow, 2014a), there is ample evidence that CSRs
for the diagnoses of panic disorder and agoraphobia are
sensitive to change following CBT and acceptance and
commitment therapy (ACT) (ADIS-​IV; Arch et al., 2012;
Craske et al., 2007). Given that the ADIS is not restricted
to only one type of intervention modality, the ADIS is
rated as possessing overall excellent treatment sensitivity
(Table 13.3).
SCID
The SCID (First et  al., 2016c) is most often used as a
pretreatment diagnostic instrument rather than as an out-
come measure. Because we were able to locate only one
study in which pre-​to post-​treatment change was mea-
sured through the SCID (Carter, Sbrocco, Gore, Marin,
& Lewis, 2003), treatment sensitivity was judged to be
adequate.
280 Anxiety and Related Disorders

TABLE 13.3   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

ADIS NA NA G Aa A A E E A
SCID NA NA G Aa A A E A A
PDSS A G G Aa A A E E A
ACQ-​CON G G NA A A E E E A ✓
ASI G G NA A A E E E A
ASI-​3 G G NA G G E E E A ✓
BSQ G G NA G A G E E A ✓
ACQ G G NA A A G E E A ✓
FQ G A NA G A G E E A ✓
MI G E NA A A A E E A
APPQ G G NA A A A E E A

  Different raters.
a

Note:  ADIS  =  Anxiety Disorders Interview Schedule; SCID  =  Structured Clinical Interview for the DSM; PDSS  =  Panic Disorder Severity
Scale; ACQ-​ CON  =  Anxiety Control Questionnaire; ASI  =  Anxiety Sensitivity Index; ASI-​ 3  =  Anxiety Sensitivity Index-​
3; BSQ  =  Body
Sensations Questionnaire; ACQ = Agoraphobic Cognitions Questionnaire; FQ = Fear Questionnaire; MI = Mobility Inventory for Agoraphobia;
APPQ = Albany Panic and Phobia Questionnaire; A = Adequate; G = Good; E = Excellent; NA = Not Applicable.

PDSS Anxiety Control Questionnaire

The PDSS (Shear et al., 1997) has been found to be sen-
sitive to change following treatment (Kiropoulos et  al.,
2008). This instrument is judged to have excellent treat-
ment sensitivity due to its ability to detect change in panic
disorder and agoraphobia following various types of phar-
macological and psychotherapeutic interventions.
Self-​Report Instruments
Anxiety Sensitivity Index and Anxiety
Sensitivity Index-​3
Administration of the ASI (Reiss et  al., 1986)  before,
during, and after treatment maps the degree to which
beliefs about physical symptoms of anxiety change over
the course of treatment. The ASI is rated as having excel-
lent treatment sensitivity due to the empirical evidence
showing change on this instrument following group and
individual CBT (e.g., Arch & Ayers, 2013; Craske et al.,
2007), mindfulness-​based stress reduction (Arch & Ayers,
2013), ACT (Arch et  al., 2012), and pharmacological
treatments (e.g., Simon et  al., 2004). Furthermore, the
recently developed ASI-​3 has shown excellent treatment
sensitivity to brief mindfulness-​based (Tanay, Lotan, &
Bernstein, 2012) and computerized cognitive anxiety sen-
sitivity interventions (Schmidt, Capron, Raines, & Allan,
2014). Given that the ASI-​3 possesses stronger psychomet-
ric properties and is multidimensional, this version should
be given preference over the ASI.
The Anxiety Control Questionnaire (ACQ-​CON; Rapee,
Craske, Brown, & Barlow, 1996), not to be confused with
the Agoraphobic Cognitions Questionnaire, is a 30-​item
self-​report instrument that assesses perceived ability to
control external events and internal emotional responses.
Brown, White, Forsyth, and Barlow (2005) found evidence
of three factors (emotion control, stress control, and threat
control), and from their item analysis, they developed a
revised version (known as the ACQ-​R) composed of only
15 of the original 30 items. ACQ-​CON total score norms
and ACQ-​R subscale norms exist for anxious and non-
clinical samples (Brown, White, et al., 2005; Rapee et al.,
1996). The internal consistency of the ACQ-​CON scores
is generally good (ranging from .81 to .89), although some
data on the subscales were in the less than adequate to
adequate range (.65 to .74; see Ballash, Pemble, Usui,
Buckley, & Woodruff-​Borden, 2006; Brown, White, et al.,
2005; Craske et al., 2007; Lang & McNiel, 2006; Rapee
et al., 1996; Zebb & Moore, 1999). Adequate ACQ-​CON
test–​retest reliability data exist based on 1-​week to 1-​month
periods of time (r ranging from .82 to .88; Rapee et  al.,
1996). Although ACQ-​CON data from an anxious sample
were used in a factor analysis (Rapee et al., 1996), there
is no information to suggest that this sample evaluated
the items or the measure’s instructions, and thus content
validity is only adequate. There is evidence of the ACQ-​
CON’s construct validity (Lang & McNiel, 2006; Rapee
et  al., 1996), including data to support its incremental
validity in predicting interpretation biases associated with

ambiguous internal and external phenomena (Zvolensky
et  al., 2001), prediction of a latent factor of anxious
arousal (Brown, White, et al., 2005), and its relatedness to
trait anxiety (Kashdan, Barrios, Forsyth, & Steger, 2006).
Moreover, the threat control factor has been found to be
a moderator of the relationship between anxiety sensitiv-
ity and agoraphobia (White et al., 2006) and a mediator
of the relationship between some aspects of family func-
tioning and anxiety in a nonclinical sample (Ballash et al.,
2006). Thus, the construct validity of the ACQ-​CON was
judged to be excellent.
The ACQ-​CON (or ACQ-​R) has been used with vari-
ous samples, including outpatient clinical samples (e.g.,
White et  al., 2006), inpatient clinical samples (Lang &
McNiel, 2006), and nonclinical samples (e.g., Kashdan
et al., 2006). As a result of its use in more than one setting
and with different samples, this measure was given a rat-
ing of excellent validity generalization. The ACQ-​R has
recently been translated to Spanish, but data regarding its
clinical utility have yet to be published (Osma, Barrada,
García-​Palacios, Navarro-​Haro, & Aguilar, 2016). ACQ-​
CON scores (Rapee et  al., 1996)  have been sensitive to
change after CBT for panic disorder and agoraphobia, and
they are able to predict the severity of comorbid diagno-
ses at follow-​up assessment of CBT (Craske et al., 2007).
In addition, ACQ-​R scores have demonstrated sensitivity
to change in acceptance-​ based behavioral therapy for
individuals diagnosed with generalized anxiety disorder
(Treanor, Erisman, Salters-​Pedneault, Roemer, & Orsillo,
2011). As a result of these findings, treatment sensitivity
was judged to be excellent.
Body Sensations Questionnaire
BSQ scores are sensitive to change following short-​term,
intensive exposure treatment for agoraphobia (Chambless
et al., 1984), group CBT plus exercise treatment for panic
disorder with agoraphobia (Cromarty, Robinson, Callcott,
& Freeston, 2004), and individual CBT for panic disorder
with agoraphobia (Carlbring et al., 2007). Furthermore,
the BSQ has demonstrated change sensitivity following
ACT in individuals with primary panic disorder and/​or
agoraphobia previously deemed as treatment resistant
(Gloster et  al., 2015). Thus, the BSQ is judged to have
excellent treatment sensitivity.
Agoraphobic Cognitions Questionnaire
ACQ scores are sensitive to change following short-​term,
intensive exposure treatment for agoraphobia (Chambless
Panic Disorder and Agoraphobia 281
et al., 1984), group CBT plus exercise treatment for panic
disorder with agoraphobia (Cromarty et  al., 2004), and
individual CBT and ACT for panic disorder and agora-
phobia (Carlbring et al., 2005, 2007; Gloster et al., 2015).
Thus, the ACQ is rated as having excellent treatment
sensitivity.
Fear Questionnaire
The FQ has been used as a treatment outcome mea-
sure in more than 50 studies, and a meta-​analysis of 56
treatment groups revealed a mean effect size of d = 1.93
(Ogles, Lambert, Weight, & Payne, 1990). Thus, the FQ
is rated as exhibiting excellent treatment sensitivity.
Mobility Inventory
MI scores change following exposure therapy (Chambless
et al., 1985; Ehlers, 1995) and individual CBT and ACT
for panic disorder and agoraphobia (e.g., Carlbring et al.,
2005; Gloster et al., 2015). Thus, the MI is rated as having
excellent treatment sensitivity.
Albany Panic and Phobia Questionnaire
Rapee et al. (1994) provided some evidence of this mea-
sure’s treatment sensitivity following a course of CBT. The
APPQ has also demonstrated change following a cognitive–​
behavioral-​ based treatment for individuals with panic
disorder and moderate to severe agoraphobia (Sensation-​
Focused Intensive Treatment; Bitran, Morissette, Spiegel,
& Barlow, 2008). Furthermore, the APPQ has demon-
strated sensitivity to change following mindfulness-​based
cognitive therapy in adjunct to pharmacotherapy for
individuals with panic disorder (Kim et  al., 2010). As a
result, the APPQ is judged to have excellent treatment
sensitivity.
Self-​Efficacy to Control a Panic Attack Questionnaire
In anxiety-​ provoking situations, 15% of the reported
thoughts from a sample with agoraphobia were about
self-​efficacy (Williams et  al., 1997). Moreover, research
suggests that these judgments help predict behaviors
that are often the target of treatment (e.g., Kinney &
Williams, 1988) and mediate the effects of treatment for
panic disorder with agoraphobia upon approach behav-
iors (Williams, Kinney, & Falbo, 1989) and panic sever-
ity (Casey, Newcombe, & Oei, 2005). One self-​report
measure of self-​efficacy that is directly relevant to panic
282 Anxiety and Related Disorders
disorder is the Self-​Efficacy to Control a Panic Attack
Questionnaire (SE-​ CPAQ; Gauthier, Bouchard, Cote,
Laberge, & French, 1993). This measure is well suited to
be administered along with other measures discussed in
this chapter. It is a 25-​item measure, consisting of the Self-​
Efficacy–​Cognitions (6 items), Self-​Efficacy–​Mobility
(10 items), and Self-​Efficacy–​Symptoms (9 items) sub-
scales. Each item is assigned a rating indicative of the
respondent’s confidence in controlling panic attacks in
a given situation (i.e., when experiencing a particular
thought in a particular location or having a particular
physiological sensation). The thoughts, locations, and
sensations used in the SE-​CPAQ were adapted from the
ACQ (Chambless et al., 1984), the MI (Chambless et al.,
1985), and the BSQ (Chambless et  al., 1984). There is
some evidence of its validity (Gauthier et al., 1993) and
sensitivity to treatment-​related changes (Bouchard et al.,
1996). However, there is only limited research on its psy-
chometric properties.
Self-​Monitoring
Ongoing self-​monitoring is yet another modality of assess-
ment, albeit one that overlaps with other verbal report
measures (i.e., diagnostic instruments and self-​ report
questionnaires). To self-​monitor panic attacks, patients
typically are given portable paper forms, hand-​ held
devices, or mobile applications to record every occur-
rence of panic (i.e., frequency recording) in terms of
time of onset and offset, intensity, symptoms, and loca-
tion, among other things (e.g., Barlow, Craske, Cerny,
& Klosko, 1989). Most commonly, self-​monitoring con-
tinues over consecutive days for 1 or 2 weeks, especially
when used to evaluate pre-​to post-​ treatment changes
(e.g., Craske et al., 1997). Providing detailed instructions
to patients can enhance the consistency and accuracy of
data collection. This includes training in the use of rat-
ing scales and providing definitions of what constitutes a
panic attack (although patients’ self-​perceptions of panic
may be important in their own right; Basoglu, Marks, &
Sengun, 1992).
Self-​
monitoring of agoraphobic avoidance entails
monitoring excursions from home, recording the time of
beginning and end, whether alone or accompanied, max-
imum anxiety, destination or purpose, escape behavior,
distance traveled, and so on (e.g., Murphy, Michelson,
Marchione, Marchione, & Testa, 1998). This format of
self-​monitoring may be cumbersome for the mildly ago-
raphobic person who is relatively mobile. General anxi-
ety and accompanying moods also can be self-​monitored
(Barlow et  al., 1989). Mobile devices offer a particular
advantage that may preclude the delay in self-​monitoring
that likely occurs otherwise. For example, Stegemann,
Ebenfeld, Lehr, Berking, and Funk (2013) have devel-
oped a promising mobile application (GET.ON PAPP)
that functions as a self-​monitoring diary of panic attacks
and as an exposure guide.
Self-​monitoring strategies represent a quantification of
experience at the time of its occurrence (whether it be tied
to a specific event or to a moment in time), whereas self-​
reported estimates of frequency, duration, or content rep-
resent judgments of experience that is retrospective and
generalized in nature. Some investigators have attempted
to assess the level of agreement between self-​monitored
and self-​estimated data by having the same individuals
provide retrospective estimates of panic attacks and then
self-​monitor for an interval of time that is equivalent to the
interval that was estimated. Using this approach, patients
with panic disorder and agoraphobia were found to have
endorsed fewer panic symptoms during self-​monitoring
in comparison to previously collected estimates (Basoglu
et al., 1992; Margraf et al., 1987). Similarly, retrospective
estimates of the frequency of panic attacks and symptoms
collected during diagnostic interviewing have been found
to be substantially higher than the frequency obtained
with self-​monitored data (e.g., De Beurs, Lange, & Van
Dyck, 1992).
There is evidence that anxiety (Hiebert & Fox,
1981)  and panic (de Jong & Bouman, 1995)  decrease
with self-​monitoring. Nevertheless, reactivity effects are
generally short-​lived and subside when self-​monitoring
discontinues, perhaps because the self-​monitoring device
becomes a discriminative stimulus controlling the occur-
rence of the target behavior (Borkovec et  al., 1977).
Although there are potential problems associated with
the self-​monitoring methodology, it acts as a very effective
means of assessing panic disorder and agoraphobia and is
sensitive to change over the course of treatment.
Behavioral Approach Tests
Ogles, Lambert, Weight, and Payne (1990) calculated
effect sizes pertaining to BATs from their meta-​analysis of
21 treatment studies for agoraphobia. The behavioral score
(i.e., duration or amount completed) yielded a mean BAT
effect size of d = 1.15. The heart rate score during BATs
yielded an average effect size of d = 0.44, and the SUDS
score yielded a mean effect size of d = 1.36. Other individ-
ual studies similarly reported large treatment effect sizes
from individualized BATs (e.g., Steketee, Chambless, &

Tran, 2001). In addition, other studies have shown signifi-
cant reductions in subjective anxiety in response to brief
interoceptive exposure interventions (e.g., hyperventila-
tion; Keough & Schmidt, 2012).
Overall Evaluation
An accurate diagnosis and case conceptualization is only
the first step to conducting a thorough assessment as it
relates to the treatment of panic disorder and agorapho-
bia. The measures reviewed in this section gauge the level
of symptomatic improvement and shifts in variables con-
sidered critical to therapeutic success, such as cognition,
self-​efficacy, and perceived control. Because behaviors
and thoughts may arise during fear and anxiety that differ
from self-​reported estimates, observation and recording
of ongoing experience captures another aspect of panic
disorder and agoraphobia that is important for measuring
treatment change.
CONCLUSIONS AND FUTURE DIRECTIONS
From this review, it should be evident that there are a
variety of measures and assessment methodologies to help
guide clinicians or researchers in their work with indi-
viduals with panic disorder and agoraphobia. Throughout
this chapter, we have emphasized the importance of mea-
suring subjective, physiological, and behavioral aspects of
this disorder, preferably with multiple methodologies of
assessment, including diagnostic interviews, standardized
self-​
report questionnaires, self-​ monitoring, behavioral
observations, and physiological data.
Neither diagnostic interview reviewed in this chapter
met the criteria for being highly recommended for sev-
eral reasons. First, psychometric properties for the recent
DSM-​ 5 updated versions of the ADIS (ADIS-​ 5) and
SCID (SCID-​5) have yet to be published. As a result, the
diagnostic reliability of these versions has yet to be deter-
mined. Second, attempts to assess the validity of these
interviews cannot be separated from attempts at validating
the diagnostic system itself (Grisham et al., 2004), and “a
gold standard for psychiatric diagnoses remains elusive”
(First & Gibbon, 2004, p. 139). Clearly, more research of
this nature is needed. Third, because the SCID is rarely
used as an index of treatment outcome, data regarding its
sensitivity to change as a result of treatment continue to
be lacking.
Although semi-​ structured diagnostic interviews are
generally more time-​consuming than standard clinical
Panic Disorder and Agoraphobia 283
interviews, an assessment that allows for differential diag-
nosis (e.g., the ADIS or the SCID) is very important for
the diagnosis of panic disorder and agoraphobia. Time
and money wasted on an inaccurate diagnosis and inap-
propriate treatment will be significantly greater than the
additional time required to conduct a thorough diagnostic
assessment using a standardized instrument. Each inter-
view has its own strengths and weaknesses, and selection
can be based on purpose. For purposes of validity general-
ization, diagnoses being made in atypical settings or with
samples with varied ethnicities, the SCID instrument is
preferred. When the purpose is to obtain detailed infor-
mation for treatment planning, the ADIS is preferred.
Of the self-​report measures reviewed, five are highly
recommended for the assessment of panic disorder and
agoraphobia because they were assigned mostly good or
excellent ratings: the ACQ-​CON, ASI-​3, BSQ, ACQ, and
FQ. Although the remaining measures were not listed
as highly recommended, further research and refine-
ment could provide additional information and lead to
improvements in their psychometric properties.
Self-​monitoring and behavioral observational methods,
with accompanying measures of physiology and cognition
in the moment, cannot easily be reviewed in accordance
with the psychometric properties listed for the diagnos-
tic instruments and self-​report scales. Nevertheless, given
their value in treatment monitoring and treatment out-
come, we do judge these methods to be critical to the
assessment of panic disorder and agoraphobia.
Directions for future research include more research
on those measures that were not rated as highly recom-
mended, especially with respect to adding to or improv-
ing their test–​retest reliability and evidence of construct
validity. Second, although many measures are available
in multiple languages, continued research is needed on
the usefulness of these measures with different popula-
tions. Third, because measures may operate differently
in different settings (e.g., outpatient vs. inpatient vs. com-
munity centers), it is critical that researchers (especially
instrument developers) continue to expand the number
and variety of settings in which the measures are evalu-
ated. Fourth, many treatment studies (especially pharma-
cological studies) use diagnostic interviews only in the
pretreatment phase. In order to gather additional data on
treatment sensitivity, diagnostic assessments are needed
both prior to and following a course of treatment.
It is our hope that this chapter will help clinicians
choose measures and assessment methodologies that are
scientifically sound and that address the various compo-
nents of panic disorder and agoraphobia (i.e., cognitions,
284 Anxiety and Related Disorders
emotional reactions, physiological symptoms, and behav-
ioral avoidance) and how to use assessment data in
their treatment planning and monitoring of treatment
outcomes.
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 14
Generalized Anxiety Disorder
Michel J. Dugas
Catherine A. Charette
Nicole J. Gervais
The main goal of this chapter is to present a comprehensive
assessment option for clinicians working with clients with
generalized anxiety disorder (GAD). The chapter begins
with a discussion of the nature of GAD. Specifically, we
review the history of its diagnostic criteria and then sum-
marize the data on the disorder’s onset and course, etiol-
ogy, prevalence, sex and age differences, comorbidity, and
associated costs. We then provide a detailed description of
assessment strategies for identifying GAD, for treatment
planning, and for treatment monitoring and outcome.
Finally, we discuss the current status of assessment meth-
ods for GAD and suggest ways of enhancing our ability
to measure the symptoms and associated features of this
prevalent and costly anxiety disorder.
NATURE OF GENERALIZED ANXIETY DISORDER
History of the Diagnostic Criteria
The diagnostic category of GAD has undergone much
change since its debut in the third edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-​III;
American Psychiatric Association [APA], 1980). In DSM-​
III, GAD was considered a residual disorder characterized
by persistent anxiety occurring for at least 1  month and
accompanied by symptoms from three out of four catego-
ries (i.e., motor tension, autonomic hyperactivity, appre-
hensive expectation, and vigilance/​scanning). In contrast,
in the fifth edition of the DSM (DSM-​5; APA, 2013), GAD
is described as a chronic condition (minimum duration of
6  months) involving excessive and uncontrollable worry
and anxiety about a number of events or activities and
293
leading to significant distress or impairment in important
areas of functioning. In addition, the diagnosis of GAD
requires at least three of six somatic symptoms:  restless-
ness or feeling keyed up or on edge, being easily fatigued,
difficulty concentrating or mind going blank, irritabil-
ity, muscle tension, and sleep disturbance. This defini-
tion reflects attempts to identify features that are specific
to GAD, including muscle tension and excessive worry
about several events or activities. In general, worry is com-
mon among individuals with anxiety disorders; however,
for those with anxiety disorders other than GAD, the con-
tent of their worry tends to be confined to topics related
to their specific disorder. For example, individuals with
social anxiety disorder may worry about how others per-
ceive them, and those with obsessive–​compulsive disorder
with checking compulsions may worry about whether or
not they locked the front door.
It is worth noting that the diagnostic criteria for GAD
were essentially unchanged from DSM-​IV (APA, 1994) to
DSM-​5 (APA, 2013), even though the DSM-​5 Anxiety,
Obsessive–​ Compulsive Spectrum, Posttraumatic, and
Dissociative Disorders Work Group suggested a number
of major modifications (see Andrews et  al., 2010). For
example, the working group suggested that the terms
“generalized worry disorder,” “major worry disorder,” and
“pathological worry disorder” might better capture the
main clinical feature of individuals with GAD (i.e., exces-
sive worry). They also proposed that the minimal dura-
tion of GAD be reduced to 3 months from 6 months. The
reasoning behind this proposal was that it can sometimes
be difficult for a person to recall if his or her worry was
excessive 6 months ago, especially if that person is a child
(Starcevic, Portman, & Beck, 2012). The working group
294 Anxiety and Related Disorders
further suggested that retaining only two associated symp-
toms in the DSM-​5 (restlessness or feeling keyed up or on
edge, and muscle tension) could increase the discriminant
validity of GAD. Finally, and perhaps most important,
the working group noted that the addition of behavioral
symptoms to the DSM definition of GAD could markedly
improve the diagnostic reliability of the disorder. As such,
four behavioral symptoms were proposed:  avoidance,
overpreparation, procrastination, and reassurance seek-
ing. These behavioral symptoms, which can be thought
of as safety-​seeking behaviors, have been shown to be
associated with GAD (Starcevic et  al., 2012). In addi-
tion, given that individuals with GAD appear to engage in
these safety-​seeking behaviors in an effort to increase their
feelings of certainty (Andrews et al., 2010), the suggested
behaviors are consistent with current conceptualizations
of GAD as being rooted in intolerance of uncertainty
(Bennett-​Levy et  al., 2004; Clark & Beck, 2010; Dugas
& Robichaud, 2007). Unfortunately, although the sugges-
tions of the working group held the promise of increasing
the diagnostic validity and reliability of GAD, ultimately
none were retained for the DSM-​5.
Onset and Course
Some research suggests that there can be both an early
and a late onset of GAD, with the early onset occurring
between the ages of 11 years and the early 20s, and the late
onset typically occurring in middle adulthood (Blazer,
Hughes, & George, 1987; Brown, Barlow, & Liebowitz,
1994). According to these studies, although a significant
minority experience a late onset of GAD, an early onset is
more common, with approximately two-​thirds of individ-
uals with GAD developing the disorder by their early 20s.
Of note, Kessler and colleagues (2005) reported a slightly
different pattern of results. Specifically, the authors found
evidence for a steady increase in the onset of GAD dur-
ing the early 20s (which is consistent with the findings
reported previously); but rather than finding evidence of a
late onset, Kessler and colleagues found moderately lower
rates of onset between the ages of 31 and 47 years and dra-
matically lower rates after the age of 47 years. Therefore,
the data presented by Kessler and colleagues support a
peak onset age in the early 20s but find no evidence for
a later peak.
The symptoms of GAD rarely remit completely
without treatment (Stein, 2004). In the Harvard/​Brown
Anxiety Research Program (HARP), a prospective study
examining the course of anxiety disorders, GAD remis-
sion rates were examined in a large number of patients.
The results showed that 15% of patients with GAD remit-
ted after 1 year, 25% after 2 years, and 38% after 5 years
(Yonkers, Warshaw, Massion, & Keller, 1996). Overall, it
appears that GAD is characterized by the fluctuation of
symptoms over time in response to life stressors, with epi-
sodes of the disorder commonly persisting for more than
10 years (Kessler, Keller, & Wittchen, 2001; Stein, 2004).
Thus, the general consensus is that GAD is a chronic con-
dition that is unlikely to remit unless treated.
Etiology
Biological, environmental, and psychological factors all
play a role in the development and maintenance of GAD.
Biological factors include genetic predisposition and
alterations in neurotransmitter function. Genetic predis-
position plays a relatively modest role in the development
of GAD, with research suggesting that the disorder has a
heritability of 15% to 30% (Hettema, Prescott, & Kendler,
2001; Kendler, Neale, Kessler, Heath, & Eaves, 1992). In
addition, genetic predisposition appears to be nonspecific
in that individuals who are at higher risk of developing
GAD are also more likely to develop other anxiety and
mood disorders (Andrews, Stewart, Morris-​Yates, Holt, &
Henderson, 1990). It is likely that genetic predisposition
interacts with environmental and psychological factors to
determine if a given individual will in fact develop GAD
and/​or another disorder. Alterations in neurotransmitter
function also appear to be involved in GAD. However, the
exact mechanisms by which alterations in neurotransmit-
ter function affect the development and maintenance of
GAD have yet to be clearly understood (Gorman, 2002).
Research into environmental factors suggests that the
interactions between young children and their parents
(or caregivers) also play a role in the development of
GAD. Whereas a number of studies show that children
with insecure attachments to their parents are at risk of
developing GAD (for a review, see Hudson & Rapee,
2004), other studies show that high levels of enmeshment
characterize the childhood experiences of adults with
GAD (Lichtenstein & Cassidy, 1991; Peasley, Molina, &
Borkovec, 1994). In this context, enmeshed relationships
refer to the children attending to the needs of their par-
ents, without necessarily having their own needs met. In
other words, the parent–​child relationship is marked by
role reversal, with the child “taking care” of the parent.
Many psychological factors also appear to play a role
in the development and maintenance of GAD (Borkovec,
Alcaine, & Behar, 2004; Mennin, Heimberg, Turk, &
Fresco, 2002; Wells & Carter, 1999). Our research group
 Generalized Anxiety Disorder 295

has developed a cognitive model of GAD that has four Dugas and Robichaud (2007) suggest that such findings
main features: intolerance of uncertainty, positive beliefs can be explained by the many health complications older
about worry, negative problem orientation, and cogni- adults typically experience; as such, these complications
tive avoidance (Dugas, Gagnon, Ladouceur, & Freeston, can obscure the presence of GAD, especially when symp-
1998). According to this model, deep-​ seated negative toms of the health problem are similar to those seen in
beliefs about uncertainty (which manifest as intolerance GAD. Given that GAD is a chronic disorder that typically
of uncertainty) lead to biases in cognitive processing, con- commences in the early 20s and rarely remits on its own,
tribute to the other model components, and ultimately it seems obvious that middle-​aged adults would have a
lead to the development and maintenance of GAD higher likelihood of having GAD than would younger
(Dugas & Koerner, 2005). Research suggests that intoler- adults. However, more research examining the presence
ance of uncertainty is not only closely related to GAD but of GAD in adults aged 65  years or older is necessary
also plays a causal role in GAD (Ladouceur, Gosselin, & to clarify whether the rates of this disorder continue to
Dugas, 2000). Research also shows that although intoler- increase in this population.
ance of uncertainty is the central cognitive process of our
model, all model components nonetheless make signifi-
Comorbidity and Cost
cant and unique contributions to the prediction of GAD
symptoms (Dugas et al., 1998). Although GAD can present in individuals without other
disorders (Wittchen et  al., 1994), it is most commonly
accompanied by other mental health conditions. Carter
Prevalence, Sex Differences, and Age
and colleagues (2001) reported a 12-​month prevalence
GAD is highly prevalent in the general population and rate of 93% for other mental health disorders among
in clinical settings. In the Canadian Census Survey, 8.7% individuals from the general population meeting DSM-​
of a representative community sample reported symptoms IV criteria for GAD. This included 71% for any mood
consistent with lifetime GAD, and 2.6% met criteria for disorder and 56% for any anxiety disorder. In addition,
GAD in the past 12-​month period (Pearson, Janz, & Ali, individuals meeting GAD criteria were more likely to
2013). Similarly, the APA (2013) reported that the 12-​ have two or more comorbid conditions rather than just
month prevalence of GAD in the general population of one comorbid condition. Given its high comorbidity rate,
the United States is 2.9%. In clinical populations, the many have suggested that GAD is not a distinct disorder
prevalence rate is higher, with nearly 8% of all patients but, rather, a condition that promotes the development
seeking treatment meeting diagnostic criteria for GAD of anxiety or mood disorders (Akiskal, 1998; Maser, 1998;
(Maier et  al., 2000). Finally, Wittchen and colleagues Roy-​Byrne & Katon, 1997). However, this position has
(2002) argued that there is evidence that GAD is the most essentially been rejected because there is much evidence
frequent anxiety disorder and the second most frequent of supporting the notion that GAD is a distinct diagnostic
all mental disorders in clinical settings. category (e.g., Brown, Chorpita, & Barlow, 1998; Maier
In terms of sex differences, GAD is more common et al., 2000). For example, although the comorbidity rate
among women than men (Blazer, Hughes, George, for GAD is quite high, it is in fact comparable to those of
Swartz, & Boyer, 1991; Hunt, Issakidis, & Andrews, other anxiety and mood disorders (Holaway, Rodebaugh,
2002), which is consistent with the pattern found in most & Heimberg, 2006). In addition, with the exception of
other anxiety disorders (Kessler et al., 1994). For example, depression (Kessler, Walters, & Wittchen, 2004), GAD
Wittchen, Zhao, Kessler, and Eaton (1994) found that does not systematically precede or follow the onset of
women were approximately twice as likely as men to have other disorders (although GAD typically precedes depres-
had GAD at some point in their lives, with a reported life- sion, it follows depression in a significant minority of
time prevalence of 6.6% for women and 3.6% for men. cases). Other than anxiety and mood disorders, personal-
According to the APA (2013), the ratio of female to males ity disorders have also been found to occur frequently in
experiencing GAD is 2:1. individuals with GAD (Grant, Hasin, Stinson, Dawson,
Studies examining GAD in older adults suggest that it Chou, et al., 2005), with avoidant, obsessive–​compulsive,
is one of the most prevalent disorders in that population, and dependent personality disorders being the most com-
with some authors reporting a steady increase in the rate mon (Dyck et al., 2001).
of GAD that extends beyond the age of 65 years (Beekman Compared to non-​comorbid GAD (also referred to as
et al., 1998; Carter, Wittchen, Pfister, & Kessler, 2001). pure GAD), comorbid GAD is associated with a greater
296 Anxiety and Related Disorders
likelihood of impairment, help seeking, and medica-
tion use (Kessler DuPont, Berglund, & Wittchen, 1999;
Wittchen et  al., 1994). In a study conducted by Grant,
Hasin, Stinson, Dawson, Ruan, et al. (2005), individuals
with co-​occurring GAD and major depressive disorder
(MDD) diagnoses reported a lower health-​related quality
of life compared to those diagnosed with GAD or MDD
alone. However, pure GAD is also associated with signifi-
cant impairment, which is comparable to that found in
major depression (Kessler et al., 1999). GAD is costly not
only to the individual but also to society because it often
leads to decreases in work productivity and higher utiliza-
tion of health care services (Wittchen & Hoyer, 2001).
Despite the disproportionate use of primary care facilities,
many individuals with GAD avoid seeking proper treat-
ment for as long as 25 years (Rapee, 1991). Furthermore,
GAD is the anxiety disorder with the lowest diagnostic reli-
ability (Brown, DiNardo, Lehman, & Campbell, 2001),
making the disorder difficult to identify in help-​seeking
individuals. However, as discussed later, there have been
many recent advances in the diagnostic tools available for
the assessment of GAD, which have improved the diag-
nostic reliability of this disorder.
Summary
GAD is a prevalent, chronic, and disabling disorder that
has undergone numerous revisions in diagnostic criteria
since its introduction in the DSM. Considering the many
factors that can complicate the assessment of GAD, it is
imperative that clinicians use a sound assessment strategy
for diagnosing this disorder. In addition, it is important to
assess for the presence of comorbid conditions (including
mental health and physical conditions) because they can
influence diagnostic and treatment decisions that relate
to GAD. In the following sections, we provide a thorough
review of the diagnostic tools with the strongest empirical
support. We then present the measures that can be used
for case formulation and treatment planning. Finally, we
offer suggestions for the assessment of treatment progress
and outcome.
PURPOSES OF ASSESSMENT OF GAD
For the most part, the measures currently available for
the assessment of GAD consist of semi-​structured inter-
views and self-​report questionnaires. Given that different
research groups have developed self-​report questionnaires
that are specific to their conceptualization of GAD, not
all GAD measures are reviewed in this chapter. In the sec-
tions on assessment for case conceptualization/​treatment
planning and treatment monitoring/​treatment outcome,
we focus our presentation of instruments on (a)  con-
structs common to most models of GAD and (b) specific
components of our model of GAD, namely intolerance
of uncertainty, positive beliefs about worry, negative
problem orientation, and cognitive avoidance (Dugas &
Robichaud, 2007). Validated measures of GAD compo-
nents are available for other models of GAD, and the inter-
ested reader can refer to Borkovec et al. (2004), Mennin
et al. (2002), or Wells (2009) for more information.
ASSESSMENT FOR THE DIAGNOSIS OF GAD
Before conducting the psychological assessment of a cli-
ent, the clinician should ensure that a medical exami-
nation has been conducted by a physician to rule out
conditions that can produce symptoms that resemble
those of GAD (e.g., hyperthyroidism, hypoglycemia, and
anemia). Furthermore, either the physician or the clini-
cian should obtain information about family history of
both medical problems and mental health conditions.
Once a complete picture of the client’s physical state
is obtained, the clinician should then proceed with the
psychological assessment. In the following paragraphs,
we discuss both self-​report measures and semi-​structured
interviews that assess for the presence of mental health
conditions including GAD. The two self-​report measures
to be presented are screening tools for GAD that can be
used prior to conducting a semi-​ structured interview.
We recommend using semi-​structured interviews rather
than unstructured clinical interviews because the former
are likely to produce diagnoses that are more reliable.
Concerns have been raised regarding the precision and
rigor of unstructured interviews because they tend to pro-
duce lower comorbidity rates relative to semi-​structured
interviews (Miller, Dasher, Collins, Griffiths, & Brown,
2001; Zimmerman & Mattia, 1999). Because semi-​
structured interviews encourage clinicians to inquire
about a broad range of disorders, they reduce the risk
that clinicians will overlook comorbid disorders. This is
an especially important consideration for individuals with
GAD because many present for assessment without real-
izing that it is worthwhile to mention their excessive and
uncontrollable worry. Furthermore, individuals with GAD
may be seeking help for problems that are the result of
their worrying, such as painful muscle tension. However,
when they are specifically asked about the experience of

TABLE 14.1   Ratings of Instruments Used for Diagnosis
Internal Inter-​Rater Test–​Rest
Instrument Norms Consistency Reliability Reliability
WAQ G NR NA A G
GAD-​Q G E NA A G
ADIS-​IV NA NA A NA
SCID-​I/​P NA NA A NA
Note: WAQ = Worry and Anxiety Questionnaire; GAD-​Q = Generalized Anxiety Disorder Questionnaire; ADIS-​IV = Anxiety Disorders Interview
Schedule for DSM-​IV; SCID-​I/​P = Structured Clinical Interview for DSM-​IV-​TR for Axis I disorders, Patient Edition. A = Adequate; G = Good;
E = Excellent; NR = Not Reported; NA = Not Applicable.
worry, these individuals readily acknowledge its impor-
tance. There are, however, certain limitations to using
semi-​structured interviews, the most obvious being the
time required to conduct them. In addition, practice is
required before the clinician may feel fully comfortable
in the use of such interviews. Despite these limitations,
semi-​structured interviews are clearly superior to unstruc-
tured clinical interviews in terms of obtaining reliable
information about a broad array of symptom constella-
tions. A  summary of the psychometric properties of the
self-​report measures and the previous versions of the semi-​
structured interviews reviewed in this section is presented
in Table 14.1.
Self-​Report Measures
The following two self-​report measures can be used to
screen for GAD prior to administering a semi-​structured
interview. Given that the two provide similar information,
it is recommended that the clinician choose one. The
reader should keep in mind that although the symptoms
covered by self-​report measures are similar to those cov-
ered by semi-​structured interviews, self-​report can by no
means replace a diagnostic interview. Semi-​ structured
interviews provide the clinician with more comprehen-
sive, valid, and reliable information for the formal diagno-
sis of GAD. However, as mentioned previously, self-​report
questionnaires can be used to provide initial informa-
tion on the symptoms of GAD prior to administering an
interview.
Worry and Anxiety Questionnaire
The Worry and Anxiety Questionnaire (WAQ; Dugas
et al., 2001) is an 11-​item self-​report questionnaire assess-
ing DSM-​5 (and DSM-​IV) diagnostic criteria for GAD.
The WAQ assesses worry themes, the degree of excessive-
ness and uncontrollability of worry, the length of time that
Generalized Anxiety Disorder 297
Content Construct Validity Clinical Highly
Validity Validity Generalization Utility Recommended
A A A ✓
A NR A
A A G E ✓
A A G E
the person has experienced excessive worry, the severity
of GAD physical symptoms, and the degree of interfer-
ence and distress related to the worry and anxiety. With
the exception of the first item, which asks respondents to
list their worry themes, items are rated on a 9-​point Likert
scale. The WAQ can be scored categorically (Dugas et al.,
2001) or continuously (Deschênes & Dugas, 2013).
Overall, scores on the WAQ have demonstrated
adequate to good psychometric properties. For example,
Beaudoin and colleagues (1997) found the test–​retest reli-
ability of WAQ scores at 4 weeks to be adequate (r = .76).
There is evidence of good content validity and adequate
construct validity (Dugas et al., 2001). In addition, there is
good normative data available for the WAQ in nonclinical
and clinical samples (Buhr & Dugas, 2002; Dugas et al.,
2007). Both Buhr and Dugas (2002) and Dugas and col-
leagues (2007) report a gender difference, which is not
surprising given that women tend to report more worry
and anxiety symptoms than do men in the general popula-
tion (Robichaud, Dugas, & Conway, 2003).
Generalized Anxiety Disorder Questionnaire
The Generalized Anxiety Disorder Questionnaire
(GAD-​Q; Newman et al., 2002) is the most commonly
used self-​report measure assessing for the presence of
DSM-​ 5 (previously DSM-​ IV) diagnostic criteria for
GAD. The GAD-​Q consists of nine items, the majority
of which inquire about the presence or absence of spe-
cific symptoms of GAD (dichotomous response scale),
including whether the respondent experiences exces-
sive and uncontrollable worry as well as any of the six
GAD physical symptoms. There are, however, two items
on the GAD-​Q that are rated on a 9-​point Likert scale.
These items assess the severity of functional impairment
and subjective distress that result from the worry and
anxiety. In addition, the GAD-​Q contains one item ask-
ing respondents to list their most frequent worry topics.
298 Anxiety and Related Disorders

The GAD-​Q total score can be used to screen for GAD, diagnostic criteria for more than one condition, the disor-
and Newman and colleagues (2002) have suggested a der that has the highest rating on the CSR is considered
clinical cut-​off score. For a detailed description of the to be the primary diagnosis.
scoring system for the GAD-​Q, refer to the validation Although we highly recommend the ADIS-​5 for the
article (Newman et al., 2002). assessment of anxiety disorders, the interview is not with-
Scores on the GAD-​Q have demonstrated adequate out limitations. First, for reasons that are unclear to us,
to excellent psychometric properties, including excellent the ADIS-​5 does not assess all conditions that frequently
internal consistency (α = .93; Luterek, Turk, Heimberg, co-​occur with anxiety disorders. For example, the inter-
Fresco, & Mennin, 2002), adequate test–​retest reliability view does not allow for the assessment of eating disorders.
at 2 weeks (κ = .64), good content validity, and adequate Second, many of the sections of the ADIS-​5 are overly-​
construct validity (Newman et  al., 2002). Furthermore, detailed and include ancillary questions that provide little
there is good normative data on the GAD-​Q as provided diagnostic information. Finally, the ADIS-​5 requires a
in Newman and colleagues’ (2002) article. considerable amount of time to administer, sometimes as
much as 2 hours.
Due to the recent development of the ADIS-​5, its
Semi-​Structured Interviews
psychometric properties have yet to be adequately evalu-
ated. However, research suggests that the psychometric
Anxiety and Related Disorders Interview
properties of the previous version of the ADIS (ADIS-​IV;
Schedule for DSM-​5
Brown, DiNardo, & Barlow, 1994)  are good. In a large
The Anxiety and Related Disorders Interview Schedule reliability study conducted by Brown and colleagues
for DSM-​5 (ADIS-​5; Brown & Barlow, 2014)  is a semi-​ (2001), 362 patients received two independent ADIS-​IV
structured diagnostic interview designed to thoroughly interviews, and kappa values were calculated to obtain
assess all anxiety disorders. The interview screens for inter-​rater agreement. In this study, the diagnosis of GAD
many other conditions, including depressive, obsessive–​ demonstrated adequate inter-​rater agreement. Brown and
compulsive, trauma-​ related, somatic symptom, and colleagues also found that much of the diagnostic disagree-
substance-​ related disorders. The ADIS-​ 5 allows clini- ment frequently involved mood disorders, which have
cians to dimensionally and functionally assess patient considerable symptom overlap with GAD. Furthermore,
symptoms. The assessment is wide in its scope: It provides the ADIS-​IV has demonstrated adequate content and con-
screening questions for many conditions and explores struct validity, good validity generalization, and excellent
family psychiatric history and life stressors. The ADIS-​ clinical utility.
5 is available in two versions for adults:  (a) the current
version, which assesses the presence of pathology at the
Structured Clinical Interview for DSM-​5 Disorders
time of the interview, and (b) the lifetime version, which
assesses the presence of pathology at any point during the The Structured Clinical Interview for DSM-​5 Disorders,
respondent’s life. Although the lifetime version of the Clinician Version (SCID-​5-​CV; First, Williams, Karg, &
ADIS-​5 can be useful in that it provides clinicians with Spitzer, 2016) is an updated, current version of the SCID
information regarding the temporal development of each assessing various psychiatric conditions, including anxiety
condition, the ADIS-​5 current version generally suffices disorders, substance-​related disorders, somatic symptom
for clinical diagnostic use. disorders, psychotic disorders, adjustment disorders, eat-
The ADIS-​5 offers many advantages. For one, each ing disorders, and depressive disorders. The SCID-​5-​CV
section begins with a screening question for a particu- assesses patients’ symptoms within the past month and
lar disorder, followed by questions pertaining to specific over their lifetime, based on DSM-​5 criteria. The inter-
symptoms related to the disorder, which are rated on a 9-​ view takes 45 to 90 minutes to administer. Although the
point Likert scale (0–​8). Another advantage of the ADIS-​ SCID-​5-​CV covers more disorders than does the ADIS-​5,
5 over other semi-​structured interviews is that it contains the measure is limited by its categorical, rather than con-
a Clinician’s Severity Rating (CSR) scale, which also tinuous, rating scale. In other words, clinicians using the
consists of a 9-​point Likert scale (0–​8). The CSR allows SCID-​5-​CV can only determine if symptoms and disor-
the clinician to evaluate the severity of each diagnosed ders are present or absent. The interview is also limited by
condition. A  score of 4 or above indicates the presence the fact that it does not include items that directly address
of a clinically significant disorder. When a patient meets the differential diagnosis of anxiety disorders. In contrast

to the SCID-​5-​CV, the ADIS-​5 provides a continuous rat-
ing scale for symptoms and disorders, as well as detailed
questions that facilitate the differential diagnosis of anxi-
ety disorders.
Given the recent development of the SCID-​ 5-​CV,
the psychometric properties of the interview have yet to
be closely examined. However, research on the psycho-
metric properties of prior versions of the SCID (Williams
et al., 1992; Zanarini et al., 2000) suggests that the latest
version will likely be shown to have adequate psychomet-
ric properties. For example, the SCID-​I/​P (the previous
version of the SCID) has shown evidence of construct
validity, validity generalization, and clinical utility (First
& Gibbon, 2004). Thus, data from previous studies sug-
gest that the latest version of the SCID may well have con-
siderable clinical usefulness.
Overall Evaluation
As mentioned previously, two self-​report measures were
described in this section, but only one of the two is
required to screen for GAD. Therefore, the clinician must
decide which screening tool to use. Despite evidence of
similar psychometric properties, we suggest that the WAQ
may be superior as a screening measure for GAD because
it contains ratings for each item (with the exception of the
first item, which requires the respondent to list worry top-
ics), whereas the GAD-​Q possesses many (less sensitive)
dichotomous items.
Although other semi-​structured diagnostic interviews
can be used to identify individuals with GAD (includ-
ing briefer interviews), the ADIS-​5 and SCID-​5-​CV are
excellent choices because their previous versions have
considerable empirical support. Diagnosing GAD is quite
a challenge because many difficulties can be encoun-
tered, including overlapping symptoms with other anxi-
ety and mood disorders and also the high likelihood that
the condition will be comorbid. Semi-​structured inter-
views such as the two described previously are extremely
valuable because they require the clinician to go beyond
the client’s presenting complaints, thus facilitating the
identification of comorbid conditions. If the most psy-
chometrically sound semi-​structured interviews are uti-
lized, clinicians should find that many difficulties can be
reduced. Although the interviews require a considerable
amount of time to administer, they offer benefits that far
outweigh their costs. As was recommended previously for
the self-​report measures used to screen for the presence of
GAD, the clinician will need to choose which of the two
semi-​structured interviews to administer.
Generalized Anxiety Disorder 299
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
In this section, we discuss assessment tools for the pur-
poses of case conceptualization and treatment planning.
We first present measures designed to assess worry severity,
somatic anxiety, depression, and quality of life. Because
somatic anxiety symptoms, depression, and poor qual-
ity of life can negatively impact treatment progression,
clinicians should assess these factors prior to the start of
treatment to determine whether they should be addressed
during therapy. We then present measures of the cogni-
tive processes central to our model of GAD (intolerance
of uncertainty, positive beliefs about worry, negative
problem orientation, and cognitive avoidance; see Dugas
et al., 1998). Assessing these cognitive processes is essen-
tial for clinicians intending to use the treatment protocol
based on the model and described in detail in Dugas and
Robichaud (2007). Even for clinicians intending to use
another treatment for GAD, we suggest that it would be
useful to assess each of these cognitive processes because
they have been implicated in the maintenance of GAD.
Finally, although the WAQ was described in the previ-
ous section as a screening measure for GAD, it can also
be used to assess the severity of GAD symptoms (much
like the Beck Depression Inventory-​II for depressive symp-
toms). Given that the WAQ was presented in the previous
section, it is not presented again here. Ratings of the psy-
chometric properties of the instruments discussed in this
section are presented in Table 14.2.
Measure of Worry Severity
Penn State Worry Questionnaire
The Penn State Worry Questionnaire (PSWQ; Meyer,
Miller, Metzger, & Borkovec, 1990)  is the most com-
monly used measure of worry, the cardinal feature of
GAD. In fact, it is widely recognized as the gold standard
for the measurement of excessive worry. Given that there
is much normative data available for this questionnaire,
it is clearly the best choice for clinicians because clients’
scores can be interpreted with relative ease (for a review,
see Startup & Erickson, 2006). Although the available
data include cut-​off scores for different populations, we
recommend using this questionnaire simply as a mea-
sure of the severity of pathological worry. Interestingly,
although women report more worry than do men in the
general population, among GAD patients, there is no dif-
ference between the scores of women and men on the
300 Anxiety and Related Disorders

TABLE 14.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Rest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Measure of Worry Severity

PSWQ E E NA G G G E A ✓
Measures of Anxiety, Depression, and Quality of Life
BAI G E NA A A A G G ✓
BDI-​II G E NA A A A G G ✓
QLQ A G NA A NR NR NR A
QOLI NR G NA A NR A NR NR
Measures of GAD Cognitive Processes
IUS G E NA A G G G G ✓
WW-​II A E NA A A A G G ✓
NPOQ NR E NA A G G NR A ✓
CAQ A E NA A G G A G ✓

Note: PSWQ = Penn State Worry Questionnaire; BAI = Beck Anxiety Inventory; BDI-​II = Beck Depression Inventory, Second Edition; QLQ = Quality
of Life Questionnaire; QOLI = Quality of Life Inventory; IUS = Intolerance of Uncertainty Scale; WW-​II = Why Worry-​II; NPOQ = Negative Problem
Orientation Questionnaire; CAQ = Cognitive Avoidance Questionnaire; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not
Reported.

PSWQ. There also seems to be no major difference in
PSWQ scores across many ethnic and cultural groups.
However, age does appear to influence level of worry
on the PSWQ, as younger individuals have consistently
been found to report more worry relative to older adults
(Startup & Erickson, 2006).
The 16 items from the PSWQ are rated on a 5-​point
Likert scale. Examples of the items include “My worries
overwhelm me” and “I know I  shouldn’t worry about
things but I  just can’t help it.” Five items are reversed
scored (e.g., “I find it easy to dismiss worrisome thoughts”).
The psychometric properties of the PSWQ scores range
from adequate to excellent. The internal consistency is
excellent in both clinical and nonclinical samples. The
PSWQ scores have also shown good test–​retest reliabil-
ity over periods of 2 to 10 weeks. In addition, the PSWQ
shows evidence of content and construct validity (Molina
& Borkovec, 1994; Startup & Erickson, 2006). Finally,
given that there is considerable data supporting use of the
PSWQ in many different groups and across multiple con-
texts, it can be concluded that the measure shows excel-
lent validity generalization.
Anxiety, Depression, and Quality of Life
In addition to assessing the severity of GAD symptoms,
clinicians should also acquire information about somatic
anxiety, depression, and quality of life. Although somatic
anxiety is more characteristic of panic disorder, it is not
uncommon for individuals with GAD to experience
“panic-​like” symptoms. Therefore, it is important to
establish whether a particular client with GAD experi-
ences somatic anxiety, as it may need to be addressed
during treatment. Furthermore, given that GAD gener-
ally has a chronic and unremitting course, it should come
as no surprise that many individuals with GAD come to
experience symptoms of demoralization and depression.
Consequently, it is standard procedure to assess depres-
sive symptoms in a comprehensive assessment protocol
for GAD. Finally, individuals with GAD typically experi-
ence poor quality of life, which can often be attributed to
the distress and interference that result from worry and
associated symptoms. As discussed in the section on treat-
ment outcome, clinicians should also assess somatic anxi-
ety, depression, and quality of life at the end of treatment
because this can provide additional information on the
effects of treatment.
Beck Anxiety Inventory
Although a high level of somatic anxiety (i.e., autonomic
arousal) does not characterize GAD, its assessment is rec-
ommended for treatment planning. In fact, our clinical
experience suggests that somatic symptoms of anxiety are
more common in GAD than is generally acknowledged.
The Beck Anxiety Inventory (BAI; Beck, Epstein, Brown,
& Steer, 1988) is a 21-​item measure that assesses the sever-
ity of somatic anxiety symptoms. BAI items are rated on a

4-​point scale, with respondents indicating the degree to
which they have been bothered by each symptom during
the past week. Because the BAI was designed to discrimi-
nate anxiety from depressive symptoms, the majority of its
items describe symptoms of autonomic arousal and panic
(e.g., “heart pounding or racing” and “hands trembling”).
Overall, scores on the BAI have demonstrated adequate
to excellent psychometric properties. The BAI scores have
excellent internal consistency (Beck et al., 1988; de Beurs,
Wilson, Chambless, Goldstein, & Feske, 1997; Fydrich,
Dowdall, & Chambless, 1992)  and adequate test–​retest
reliability over a 5-​week period (r = .83; de Beurs et al.,
1997). The scores also show evidence of content and
construct validity, as well as good validity generalization
(Beck et  al., 1988; de Beurs et  al., 1997; Fydrich et  al.,
1992; Gillis, Haaga, & Ford, 1995). Finally, because the
BAI has been widely used, it has well-​established norms
in both clinical and nonclinical samples (Beck & Steer,
1990; Gillis et al., 1995).
Beck Depression Inventory, Second Edition
The Beck Depression Inventory, Second Edition (BDI-​II;
Beck, Steer, & Brown, 1996) is a 21-​item self-​report mea-
sure of the severity of depressive symptoms. Each item
contains four options referring to the degree to which
the symptom is experienced; respondents are asked to
indicate which of the options best describes them during
the past 2 weeks. For items assessing symptoms involv-
ing a change in either direction (e.g., sleep disturbance
includes either insomnia or hypersomnia), additional
options are included to account for both the increase
and the decrease in the symptom. The BDI-​II assesses all
DSM-​5 diagnostic criteria for depression. As is the case for
the BAI, there exist ample normative data for the BDI-​II
(see Beck et al., 1996; Steer & Clark, 1997). The BDI-​II
scores have demonstrated excellent internal consistency
and adequate test–​retest reliability at 1 week (Beck et al.,
1996). In addition, the BDI-​II shows evidence of content
and construct validity and also adequate validity general-
ization (Beck et al., 1996).
Quality of Life Questionnaire
The Quality of Life Questionnaire (QLQ; Léger, Freeston,
Dugas, & Ladouceur, 1998) is a 31-​item measure assess-
ing eight life domains:  health, family, activity, finance,
community, work, goals, and security. Each item is rated
initially on a 4-​point scale assessing level of satisfaction
Generalized Anxiety Disorder 301
and then rated on a second 4-​point scale assessing level of
importance of each domain. The psychometric properties
of scores on the QLQ include good internal consistency
(α  =  .86) and adequate test–​retest reliability at 6 weeks
(r  =  .86; Labrecque, Leblanc, Kirouac, Marchand, &
Stephenson, 2001). In addition, normative data are avail-
able for both clinical and nonclinical samples (Labrecque
et al., 2001).
Quality of Life Inventory
The Quality of Life Inventory (QOLI; Frisch, 1994) is a 17-​
item measure assessing quality of life. Each item refers to
a different life domain. Respondents are asked to indicate
the level of importance of each domain using a 3-​point
Likert scale and to rate their overall satisfaction with each
life domain using a 7-​point scale. The total score is calcu-
lated by averaging the weighted scores of the life domains
deemed to be relevant by the individual. The psychomet-
ric properties of the QOLI scores include good internal
consistency, adequate test–​ retest reliability over 2 or 3
weeks, and adequate construct validity (Frisch, Cornell,
Villanueva, & Retzlaff, 1992). Despite using the QLQ in
our clinical research, we equally recommend using the
QOLI. Currently, more research is needed to establish the
psychometric properties for each measure and so, for this
reason, we are unable to recommend one over the other.
GAD Cognitive Processes
As mentioned previously, this section focuses on the
measurement of the four cognitive processes germane to
our model of GAD (see Dugas et al., 1998). During the
past 20 years, we have developed and validated self-​report
questionnaires for each of the model’s four components
(intolerance of uncertainty, positive beliefs about worry,
negative problem orientation, and cognitive avoidance).
Overall, the measures have proven to be clinically useful,
not only in terms of identifying treatment mechanisms
but also in terms of predicting the maintenance of treat-
ment gains. The four measures described below are the
Intolerance of Uncertainty Scale, the Why Worry-​II, the
Negative Problem Orientation Questionnaire, and the
Cognitive Avoidance Questionnaire.
Intolerance of Uncertainty Scale.
Intolerance of uncertainty (IU) is a negative dispositional
characteristic that results from deep-​seated catastrophic
302 Anxiety and Related Disorders
beliefs about uncertainty (Dugas & Robichaud, 2007).
Within our cognitive model of GAD, IU is the central
component and is believed to contribute to the devel-
opment and maintenance of GAD both directly and
indirectly (via its impact on cognitive processing and
on the other model components). The Intolerance
of Uncertainty Scale (IUS; French version:  Freeston,
Rhéaume, Letarte, Dugas, & Ladouceur, 1994; English
translation: Buhr & Dugas, 2002) is a 27-​item self-​report
measure that assesses two beliefs about uncertainty:  (a)
Uncertainty has negative personal implications (“When
I am uncertain, I can’t go forward”), and (b) uncertainty
is unfair and spoils everything (“A small unforeseen event
can spoil everything, even with the best of planning”)
(Sexton & Dugas, 2009). Items on the IUS are rated on
a 5-​point Likert scale, and the measure takes between 5
and 10 minutes to complete.
Scores on the English version of the IUS have dem-
onstrated adequate to excellent psychometric properties.
The psychometric properties of the English translation
are consistent with those of the original French version
of the scale (Freeston et  al., 1994). For example, the
IUS scores have demonstrated excellent internal consis-
tency (α = .94), adequate test–​retest reliability at 5 weeks
(r  =  .74), good content and construct validity, and good
validity generalization (Buhr & Dugas, 2002, 2006).
Finally, normative data have been presented elsewhere
(Buhr & Dugas, 2002; Dugas et al., 2007).
Carleton, Norton, and Asmundson (2007) have vali-
dated a short form of the IUS. The IUS-​12 is made up of
12 items derived from the original IUS. Like the full-​scale
IUS, the IUS-​12 has a two-​factor structure:  (a) prospec-
tive IU (similar to Factor 2 from the original IUS) and
(b)  inhibitory IU (similar to Factor 1 from the original
IUS). The IUS-​12 has a strong correlation with the origi-
nal scale (r = .94 to .96) (Carleton et al., 2007; Khawaja
& Yu, 2010). The IUS-​ 12 scores have demonstrated
excellent internal consistency and have shown evidence
of convergent and discriminant validity (Carleton et  al.,
2007; McEvoy & Mahoney, 2011). Given that the psy-
chometric properties of the briefer IUS-​12 are similar to
those of the full-​scale IUS, it has been increasingly used
in applied and clinical research.
Why Worry-​II
Although other models of GAD include both positive and
negative beliefs about worry (Wells & Carter, 1999), our
treatment protocol (see Dugas & Robichaud, 2007) does
not directly address negative beliefs about worry (negative
beliefs are subsumed under the “cognitive avoidance”
component). For this reason, measures of negative beliefs
about worry are not presented this section. In terms of
positive beliefs about worry, previous research has shown
that these beliefs distinguish patients with GAD from
nonclinical individuals (Dugas et  al., 1998; Ladouceur
et  al., 1999). In nonclinical samples, positive beliefs
about worry have been found to predict level of worry
(Laugesen, Dugas, & Bukowski, 2003; Robichaud et al.,
2003). Finally, data from a treatment study show that
the re-​evaluation of positive beliefs about worry leads to
decreases in both positive beliefs and GAD symptoms
(Dugas et  al., 2004). Thus, positive beliefs about worry
appear to be important targets in the treatment of GAD.
Therefore, we suggest that clinicians assess positive beliefs
about worry prior to the start of treatment in order to
determine appropriate intervention strategies.
The Why Worry-​II (WW-​II; French version: Gosselin
et al., 2003; English translation: Hebert, Dugas, Tulloch,
& Holowka, 2014)  is a revised version of the original
Why Worry questionnaire (WW; Freeston et al., 1994).
The original version of the measure was revised to cover
five types of positive beliefs about worry that are related
to level of worry. The WW-​II is a 25-​item self-​report ques-
tionnaire that contains five subscales, with each subscale
measuring one type of positive belief about worry. The
subscales assess the following beliefs:  (a) Worry facili-
tates problem solving (e.g., “The fact that I worry helps
me plan my actions to solve a problem”); (b) worry helps
motivate (e.g., “The fact that I worry motivates me to do
the things I  must do”); (c)  worrying protects one from
difficult emotions in the event of a negative outcome
(e.g., “If I  worry, I  will be less unhappy when a nega-
tive event occurs”); (d) the act of worrying itself prevents
negative outcomes (e.g., “My worries can, by themselves,
reduce the risks of danger”); and (e)  worry is a posi-
tive personality trait (e.g., “The fact that I  worry shows
that I am a good person”). Items are rated on a 5-​point
Likert scale.
The WW-​ II scores have demonstrated adequate to
excellent psychometric properties, including excellent
internal consistency for the total score (α = .93) and good
to excellent internal consistency for all subscales (α = .71
to .93). The WW-​II total score also has shown adequate
test–​retest reliability at 6 weeks (r  =  .72) and adequate
content and construct validity (Gosselin et  al., 2003;
Hebert et  al., 2014). Furthermore, normative data are
available on the WW-​II for both clinical and nonclinical
samples (Dugas et al., 2007; Gosselin et al., 2003; Hebert
et al., 2014).

Negative Problem Orientation Questionnaire
The Negative Problem Orientation Questionnaire
(NPOQ; French version:  Gosselin, Ladouceur, &
Pelletier, 2005; English translation: Robichaud & Dugas,
2005a) is a 12-​item measure of a dysfunctional cogni-
tive set that interferes with the ability to solve everyday
problems effectively. Specifically, negative problem
orientation refers to the tendency to view problems as
threats, to doubt one’s own ability to problem solve, and
to be pessimistic about the outcome of problem-​solving
attempts. Using a 5-​point Likert scale, respondents rate
their reactions or thoughts when confronted with a prob-
lem. Examples include “I see problems as a threat to my
well-​being” and “I often see problems as bigger than they
really are.” In nonclinical samples, scores on the English
translation of the NPOQ have demonstrated adequate to
excellent psychometric properties, which include excel-
lent internal consistency (α  =  .92), adequate test–​retest
reliability at 5 weeks (r  =  .80), and good content and
construct validity (Robichaud & Dugas, 2005a, 2005b).
Note, however, that only normative data from nonclinical
samples are currently available (see Gosselin et al., 2005;
Robichaud & Dugas, 2005a).
Cognitive Avoidance Questionnaire
The Cognitive Avoidance Questionnaire (CAQ; French
version: Gosselin et al., 2002; English translation: Sexton
& Dugas, 2008) is a 25-​item measure of the tendency to
use avoidance strategies when dealing with threatening
intrusive thoughts. The process of cognitive avoidance,
although not specific to GAD, is a contributing process
in excessive and uncontrollable worry (Borkovec, Ray, &
Stöber, 1998). The CAQ contains five subscales, each
of which assesses a different avoidance strategy:  (a) sup-
pressing worrisome thoughts (e.g., “There are things I try
not to think about”); (b)  substituting neutral or positive
thoughts for worries (e.g., “I think about trivial details so
as not to think about important subjects that worry me”);
(c) using distraction as a way to interrupt worrying (e.g.,
“I often do things to distract myself from my thoughts”);
(d) avoiding actions/​situations that can lead to worrisome
thinking (e.g., “I avoid actions that remind me of things
I do not want to think about”); and (e) transforming men-
tal images into verbal–​linguistic thoughts (e.g., “When
I  have mental images that are upsetting, I  say things to
myself in my head to replace the images”). Items on the
CAQ are rated on a 5-​point Likert scale. Scores on this
measure have been shown to have adequate to excellent
Generalized Anxiety Disorder 303
psychometric properties. For example, the CAQ has dem-
onstrated excellent internal consistency for the total score
(α  =  .95), adequate test–​retest reliability over a 5-​week
period (r = .85), good content and construct validity, and
adequate validity generalization (Gosselin et  al., 2002;
Sexton & Dugas, 2008). Furthermore, adequate norma-
tive data for both clinical and nonclinical samples have
been described elsewhere (Dugas et  al., 2007; Gosselin
et al., 2002; Sexton & Dugas, 2008).
Overall Evaluation
Most of the questionnaires described in this section have
received at least adequate empirical support for their use
in clinical settings. The PSWQ, which has the most sup-
port, is a widely accepted measure of worry. The BAI and
BDI-​II also have strong support for use in clinical set-
tings. However, to our knowledge, no data have yet been
published on the clinical utility of either of the quality
of life measures described previously. Despite this lack of
information, assessing for quality of life, as well as both
somatic anxiety and depression, is important during the
initial assessment. As mentioned previously, the measures
of model-​specific components should be used by clini-
cians intending to use the treatment protocol described
in Dugas and Robichaud (2007) because these measures
offer the unique opportunity to assess each component
of the underlying cognitive model with a questionnaire
that was developed explicitly for that purpose. Even if the
clinician were to use an alternative treatment for GAD,
assessing for such cognitive processes, especially IU, is
important because beliefs about uncertainty play a cen-
tral role in the maintenance of worry/​GAD. However,
more research is necessary to further establish their use-
fulness as assessment tools for use in clinical settings.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
In this section, we present an overview of the measures
that can be used to monitor treatment progress and assess
treatment outcome. As a rule, the measures described
in the previous sections (semi-​structured interviews and
self-​report questionnaires) can be readministered at post-​
treatment and at follow-​up to assess treatment outcome
and maintenance. Therefore, the treatment outcome por-
tion of this section is brief and focuses on the evidence
supporting the sensitivity to change of the previously
described measures. This section also presents a simple
304 Anxiety and Related Disorders

TABLE 14.3   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Rest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Treatment Monitoring Measures

PSWQ-​PW A E NA L G G NR G A ✓
Self-​monitoring G NA NA NA NR A NR A A ✓
booklet
Treatment Outcome Measures
ADIS-​IV NA NA A NA A A G E E ✓
SCID-​I/​P NA NA A NA A A G E E
PSWQ E E NA G G G E G A ✓
WAQ G NR NA A G A A A A ✓
BAI G E NA A A A G A G ✓
BDI-​II G E NA A A A G A G ✓
QLQ A G NA A NR NR NR NR A
QOLI NR G NA A NR A NR NR NR
IUS G E NA A G G G G G ✓
WW-​II A E NA A A A G NR G ✓
NPOQ NR E NA A G G NR NR A ✓
CAQ A E NA A G G A NR G ✓

Note:  PSWQ-​ PW  =  Penn State Worry Questionnaire-​ Past Week; ADIS-​ IV  =  Anxiety Disorders Interview Schedule for DSM-​IV; SCID-​I/​
P = Structured Clinical Interview for DSM-​IV-​TR for Axis I disorders, Patient Edition; PSWQ = Penn State Worry Questionnaire; WAQ = Worry and
Anxiety Questionnaire; BAI = Beck Anxiety Inventory; BDI-​II = Beck Depression Inventory, Second Edition; QLQ = Quality of Life Questionnaire;
QOLI  =  Quality of Life Inventory; IUS  =  Intolerance of Uncertainty Scale; WW-​II  =  Why Worry-​II; NPOQ  =  Negative Problem Orientation
Questionnaire; CAQ = Cognitive Avoidance Questionnaire; L = Less than adequate; A = Adequate; G = Good; E = Excellent; NA = Not Applicable;
NR = Not Reported.

strategy that clinicians can use to determine clinically of one item, which was removed because it specifically
meaningful change in their clients. A  summary of the assessed trait worry (“I’ve been a worrier all my life”).
psychometric properties of the measures presented in Therefore, the PSWQ-​PW contains 15 items instead of
this section is provided in Table 14.3. As was the case for 16. A  further change was made to the response scale,
Table 14.1, ratings of the previous (i.e., DSM-​IV) versions which was changed from a 5-​point to a 7-​point scale. In
of the semi-​structured diagnostic interviews are presented general, the PSWQ-​ PW scores demonstrate excellent
in Table 14.3. internal consistency (α = .91) and a level of test–​retest reli-
ability (r = .59) that is appropriate for a measure designed
to assess weekly fluctuations in symptoms. The content
Treatment Monitoring
and construct validity of the PSWQ-​PW is good (Stöber
Given that excessive and uncontrollable worry is the cen- & Bittencourt, 1998), which is consistent with that of the
tral feature of GAD, the assessment of the severity of worry original PSWQ (Meyer et  al., 1990). Moreover, scores
on a weekly basis is essential to monitor the progress of on the revised questionnaire have shown good sensitivity
clients. For this purpose, we recommend that clinicians to treatment-​related changes in worry (more so than the
use an adapted version of the PSWQ, which was devel- original PSWQ).
oped to allow for the weekly assessment of excessive and In addition to the weekly assessment of excessive and
uncontrollable worry. Clinicians can simply ask clients uncontrollable worry, clinicians should also obtain daily
to complete this questionnaire prior to the start of every self-​ratings of worry, anxiety, depression, and medication
therapy session. The Penn State Worry Questionnaire-​ use (if applicable). Not only is daily self-​monitoring a use-
Past Week (PSWQ-​PW; Stöber & Bittencourt, 1998) is a ful tool for helping clients become more aware of their
reformulation of the original PSWQ (Meyer et al., 1990). affective states but also it provides valuable information
The instructions for the revised version emphasize worry about client progress. We typically use a self-​monitoring
during the past week (rather than trait worry). In addition, booklet that consists of four questions (proportion of the
each item was rephrased to past tense, with the exception day spent worrying, feeling anxious or tense, feeling sad
 Generalized Anxiety Disorder 305

or depressed, and name and quantity of any medication The clinician can use the information obtained fol-
consumed). There is evidence supporting the validity of lowing treatment to determine if the client has achieved
this type of self-​monitoring, which includes good norma- clinically significant change. According to Jacobson and
tive data, adequate construct validity, and adequate sen- Truax (1991), the clinician can assess the clinical sig-
sitivity to treatment (for a summary, refer to Table 14.3).nificance of change by determining whether a client’s
For example, one study using daily self-​monitoring book- post-​treatment score falls within the range of the general
lets found that patients with GAD reported significantly population rather than the range of the clinical popu-
more time spent worrying than did a nonclinical con- lation (in this case, GAD). Given that normative data
trol group (Dupuy, Beaudoin, Rhéaume, Ladouceur, & are available for most of the measures presented in this
Dugas, 2001). However, self-​monitoring booklets are not chapter, clinicians will be in a position to assess the clini-
without their limitations. In particular, they would ben- cal significance of change on these measures. Jacobson
efit from greater standardization because different GAD and Truax also argued that clinicians should determine
treatment protocols tend to use different self-​monitoring the degree of change on each measure for each client,
booklets. Despite this limitation, self-​monitoring book- which can be accomplished by calculating the index of
lets remain a useful means of monitoring treatment prog- reliable change (for the formulas for calculating the clini-
ress and assessing treatment outcome (e.g., Campbell & cal significance of change and the reliable change index,
Brown, 2002). see Jacobson & Truax, 1991). In addition to the meth-
ods described by Jacobson and Truax, some GAD studies
have defined treatment response as a 20% reduction from
Treatment Outcome
pre-​to post-​treatment on measures of GAD and associ-
As mentioned previously, the assessment of treatment out- ated symptoms (see, e.g., Borkovec & Costello, 1993;
come (and treatment maintenance) involves the readmin- Dugas et al., 2003; Ladouceur et al., 2000). Other meth-
istration of measures described in the previous sections. ods also exist for calculating clinically significant change,
Following treatment, either the ADIS-​5 or the SCID-​5-​ many of which are more complex than the one described
CV should be used to assess for the presence of GAD and by Jacobson and Truax. However, a study examining
any comorbid conditions. The same interview used at pre- the efficacy of different techniques for assessing clini-
treatment should be used at post-​treatment to allow for a cally significant change (Atkins, Bedics, McGlinchey, &
direct comparison of diagnostic impressions. The PSWQ Beauchaine, 2005) found that the method described by
and WAQ should also be readministered at post-​treatment Jacobson and Truax was comparable to other more com-
and follow-​up assessments, as well as the measures of plex methods.
somatic anxiety (BAI), depression (BDI-​II), and quality
of life (QLQ or QOLI). Likewise, clinicians should read- Overall Evaluation
minister the measures of the cognitive processes involved
in GAD (IUS, WW-​II, NPOQ, and CAQ) immediately There is considerable support for the use of the mea-
following treatment and at all follow-​up assessments. In sures described in this section (PSWQ-​ PW and self-​
fact, having clients complete the IUS at post-​treatment monitoring booklets) to assess progress during treatment.
may be particularly important. Data show that changes in Furthermore, the measures that can be used to assess
IUS scores from pre-​to post-​treatment predict GAD symp- for the presence/​ a bsence of GAD (and other disorders),
toms up to 2  years after treatment completion (Dugas the severity of worry/​ GAD symptoms, somatic anxi-
et al., 2003). We recognize that readministering each of ety, depression, quality of life, and cognitive processes
these measures at post-​treatment is time-​consuming and implicated in GAD also have empirical support for their
would probably take approximately two sessions to com- use following treatment. What is less clear is how much
plete. Although this is highly recommended, if it is not change is sufficient to terminate the therapy. Weighing
feasible for the clinician, then the BAI, WW-​II, NPOQ, the advantages and disadvantages for terminating treat-
and CAQ may be removed from the assessment protocol. ment while evaluating the level of clinically significant
Generally, all measures described previously have been change will aid the clinician in his or her decision.
shown to be sensitive to treatment changes (see, e.g., Relatedly, the assessment of clinically significant change
Borkovec & Costello, 1993; Dugas et  al., 2003, 2010; can also be of great use to determine if an adjustment in
Ladouceur et al., 2000). treatment is needed.
306 Anxiety and Related Disorders
CONCLUSIONS AND FUTURE DIRECTIONS
GAD is a diagnostic category that has undergone much
change since its introduction in the DSM-​III; thus, the
development of adequate assessment options has been
an arduous task. However, due to developments in our
understanding of GAD, there has been considerable
improvement in our ability to comprehensively assess
GAD for the purposes of treatment. The reader should
keep in mind, nonetheless, that some measures described
in this chapter do not yet have sufficient normative data.
As such, more research is needed.
There is currently much reliance on self-​report mea-
sures for the assessment of GAD, which is problematic
because this type of assessment method does not always
produce valid and clinically meaningful information.
Clearly, more attention needs to be directed at producing
more “objective” methods of assessing GAD to comple-
ment interview and self-​report methods. For example,
psychophysiological measures are used more frequently
for other anxiety disorders than for GAD. However, before
these measures can be incorporated into an assessment
battery for GAD, we need to learn more about the dis-
order’s psychophysiological features. For example, future
research should examine whether heart rate variability can
provide useful information for the differential diagnosis of
GAD. In addition, clarifying the neural circuitry of GAD
is another area in need of more attention. Identifying neu-
roanatomical structures and neural pathways implicated
in GAD (and discovering how these structures and path-
ways influence the development of specific symptoms of
GAD) can aid in the identification of GAD-​like patterns
of brain activity in at-​risk or symptomatic individuals.
Despite the challenges that are encountered when
assessing individuals with GAD, assessment options have
come a long way since GAD was first introduced as a diag-
nostic category. By presenting the assessment strategies
described in this chapter, we hope to help clinicians work-
ing with this population to better identify GAD, monitor
treatment progress, and assess short-​and long-​term treat-
ment outcomes. Although the comprehensive assessment
of GAD is a work in progress, it can be said that we now
possess a variety of measurement instruments that have
considerable clinical utility.
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 15
Obsessive–​Compulsive Disorder
Shannon M. Blakey
Jonathan S. Abramowitz
This chapter addresses the conceptualization and assess-
ment of obsessive–​compulsive disorder (OCD) in order to
aid the clinician in the treatment of this condition. After
identifying, defining, and describing the nature of OCD,
we provide a brief review of empirically based theories
and psychological treatments. Next, three sections address
assessment for the purposes of (a) establishing a clinical
diagnosis of OCD, (b) formulating a treatment plan, and
(c) measuring severity and treatment response. Not all of
the available measures of OCD are reviewed in this chap-
ter because some older measures have fallen out of favor
as our understanding of this disorder has advanced; other
measures have poor psychometric properties or confound
important variables. The chapter concludes with a discus-
sion of the strengths and limitations of existing assessment
options, as well as future directions in the assessment
of OCD.
THE NATURE OF OCD
Definition
OCD is classified in the fifth edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-​5;
American Psychiatric Association [APA], 2013)  as an
obsessive–​compulsive and related disorder characterized
by obsessions or compulsions. Obsessions are persistent
intrusive thoughts, ideas, images, or doubts that are expe-
rienced as unacceptable, senseless, or bizarre. The intru-
sions also evoke subjective distress (e.g., anxiety, fear, and
doubt) and are not simply everyday worries about work,
relationships, or finances. Common obsessions include
ideas of contamination by the Ebola virus, unwanted
impulses to harm others, doubts about one’s sexual
311
preference, the idea one might have emotionally harmed
someone, and intrusive sacrilegious images. Although
highly individualistic, obsessions typically concern the fol-
lowing general themes: aggression and violence, responsi-
bility for causing harm, contamination, sex, religion, the
need for exactness or completeness, and concerns about
serious illnesses. Most individuals with OCD evidence
multiple types of obsessions.
To control their anxiety, individuals with OCD
attempt to avoid stimuli that trigger obsessions (e.g., pub-
lic restrooms in the case of contamination obsessions).
If such stimuli cannot be avoided, however, the person
performs compulsive rituals—​behavioral or mental acts
that are completed according to self-​generated “rules.”
The rituals are deliberate yet clearly senseless or exces-
sive in relation to the obsessional fear they are designed
to neutralize (e.g., washing one’s hands for 30 minutes
after using the restroom). As with obsessions, rituals are
highly individualized. Common overt rituals include
excessive decontamination (e.g., washing), checking
(e.g., locks and the stove), counting, and repeating rou-
tine actions (e.g., going through doorways). Examples of
covert or mental rituals include excessive prayer and using
special “safe” phrases or numbers to neutralize “unsafe”
thoughts or stimuli (e.g., thinking the number 2 to “undo”
the number 666). Obsessions and compulsions are func-
tionally related in that obsessions (e.g., images of germs)
increase subjective distress, whereas rituals (e.g., washing)
reduce distress.
Individuals with OCD display a range of insight into
the senselessness of their symptoms in that some acknowl-
edge the irrationality of their obsessions and compulsions
and others are firmly convinced that these symptoms are
rational. Often, the degree of insight varies across time
and obsessional themes. For example, one person might
312 Anxiety and Related Disorders

recognize her obsessional thoughts of harm as senseless cognitive–​behavioral approach. Early conditioning mod-
but have poor insight into the irrationality of her contami- els proposed that obsessional anxiety is acquired when
nation obsessions. a previously neutral stimulus (e.g., the floor) becomes
associated with fear through classical conditioning. This
fear is then maintained by avoidance and the perfor-
Etiological Models and Treatment
mance of rituals, which prevent the natural extinction
of the fear. Avoidance and rituals are also negatively
Biological Models
reinforced by the reduction in fear they engender; thus,
Prevailing neurotransmitter theories posit that abnormali- they develop into compulsive-​like habits. Contemporary
ties in the serotonin system underlie OCD (Okuda & learning models focus on other sources of learning,
Simpson, 2015). Results from studies that have directly such as vicarious conditioning and social learning, to
examined the relationship between serotonin and OCD, account for the development of obsessions (e.g., Mineka
however, have been inconsistent. Whereas the preferential & Zinbarg, 2006).
response of patients with OCD to serotonergic medication Conditioning models form the basis for the most
is often championed as supporting the serotonin hypoth- effective treatment for OCD, which includes the
esis, this argument is of little value because the serotonin behavioral therapy techniques of exposure and response
hypothesis was initially derived from this treatment outcome prevention (ERP; Abramowitz & Jacoby, 2014).
result (i.e., it is therefore a circular argument). Moreover, to Therapeutic exposure aims to extinguish obsessional
reason backward with respect to specific neurotransmitter-​ fear by helping the individual systematically confront
related etiology from the apparent success of a medication situations and stimuli that evoke obsessions (e.g.,
represents a logical error called post hoc ergo propter hoc touching floors and thinking upsetting thoughts) and
(“after this, therefore because of this”). Indeed, there might remain in the feared situation until he or she learns
be numerous reasons for the observed efficacy of serotoner- that feared outcomes are less likely or less catastrophic
gic medications. Finally, there is no coherent explanation than anticipated (i.e., extinction). Response preven-
for how serotonin abnormalities might translate to obses- tion entails refraining from compulsive rituals, with
sions and compulsions and, given the efficacy of seroto- the aim of weakening the association between rituals
nergic medications for numerous psychiatric conditions, and anxiety reduction. Exposure exercises are repeated
no explanation for why one might develop OCD instead frequently and in multiple contexts, perhaps (although
of another disorder. Accordingly, the notion that serotonin not necessarily) using a hierarchy-​driven (i.e., gradu-
functioning mediates OCD symptoms is tenuous. ated) approach in which less distressing stimuli are
Predominant neuroanatomical models of OCD pro- confronted and mastered before more difficult stimuli
pose that symptoms arise from structural and functional are faced. The details regarding implementation of
abnormalities in orbitofrontal–​subcortical circuits within ERP are beyond the scope of this chapter but are well
the brain (Lapidus, Stern, Berlin, & Goodman, 2014). described elsewhere (e.g., Abramowitz & Jacoby, 2014).
These circuits are thought to connect regions of the brain Numerous studies conducted throughout the world
involved in information processing with those involved in indicate that ERP is highly effective, with the average
the initiation of certain behavioral responses. Although patient receiving a 60% to 70% reduction in symptoms
highly interesting, these models are derived from cross-​ (e.g., Olatunji, Davis, Powers, & Smits, 2013).
sectional data merely indicating differences in brain struc- Cognitive–​ behavioral models of OCD (e.g.,
ture and function between people with and without OCD. Salkovskis, 1999) are derived from Beck’s (1976) cogni-
Because of their correlational nature, however, such data tive specificity hypothesis, which proposes that different
cannot reveal whether OCD is a cause or a consequence types of psychopathology arise from disorder-​specific dys-
of the observed brain differences. It is indeed possible (and functional beliefs and appraisals. As applied to OCD,
even likely) that such observations represent the effects of such models consider unwanted intrusive thoughts
chronic anxiety on normally functioning brain systems. as normal stimuli that occur from time to time in just
about everyone but that develop into clinical obsessions
when the intrusions are appraised as highly significant
Psychological Models
and threatening.
Two psychological models are relevant to the effec- To illustrate, consider an unwanted intrusive thought
tive treatment of OCD: a conditioning approach and a of harming an infant. Whereas most people would regard

this experience as meaningless (“mental noise”), such an
intrusion could develop into a clinical obsession if the per-
son mistakenly appraised it as having serious implications
(e.g., “Only bad people think these kinds of thoughts”).
Such appraisals evoke distress and motivate the person to
try to suppress or remove the intrusion (e.g., via rituals).
The tendency to misappraise intrusive thoughts as having
serious consequences is thought to arise from dysfunc-
tional beliefs concerning responsibility, the importance
of thoughts, need for perfectionism, overestimation of
threat, and need for certainty. Rituals are conceptualized
as efforts to remove obsessional intrusions and to prevent
any perceived harmful consequences.
Treatment based on the cognitive–​behavioral model
incorporates ERP but emphasizes cognitive changes
that occur with this treatment. For example, exposure
is thought to modify erroneous expectations about the
likelihood and severity of feared outcomes. Therapy also
includes verbal techniques such as psychoeducation
and cognitive restructuring that help the patient to rec-
ognize and correct faulty beliefs and appraisals of intru-
sive thoughts and other feared stimuli (e.g., Clark, 2004;
Wilhelm & Steketee, 2006).
Epidemiology, Course, and Prognosis
The lifetime prevalence of OCD in the general adult
population is as high as 2.3% (e.g., Kessler et al., 2005).
Symptoms typically develop gradually, often beginning in
the teenage years. An exception is the abrupt onset some-
times observed following pregnancy (Speisman, Storch,
& Abramowitz, 2011). Left untreated, the disorder typi-
cally runs a chronic course, although symptoms may wax
and wane in severity over time, and in some cases improve
(often dependent on levels of psychosocial stress; e.g.,
Skoog & Skoog, 1999).
Most individuals with OCD suffer for several years
before they receive adequate diagnosis and treatment.
Factors contributing to the underrecognition of OCD
include the failure of patients to disclose symptoms, the
failure to assess for obsessions and compulsions during
mental status examinations, and difficulties with differ-
ential diagnoses. Because OCD represents a seemingly
complex set of thinking and behavioral symptoms, its
assessment has traditionally been considered highly chal-
lenging. This is likely because many clinicians undertake
assessment without a theoretical framework to guide the
process. The aim of this chapter is to facilitate a theo-
retically and empirically grounded approach to assess-
ing OCD that is also consistent with the empirically
Obsessive–Compulsive Disorder 313
supported cognitive and behavioral interventions for this
condition.
Associated Features
Most individuals with OCD also suffer from depressive
symptoms, which can exacerbate obsessional problems
and attenuate response to ERP (e.g., Abramowitz, Franklin,
Kozak, Street, & Foa, 2000). Therefore, it is necessary to
assess mood state and, in particular, to inquire about the
chronological history of mood complaints in order to
establish whether such symptoms should be considered as
a primary diagnosis (e.g., major depressive disorder) or as
secondary to OCD symptoms.
Relatives’ emotional and behavioral responses to the
patient’s OCD symptoms should also be considered. In
some instances, family members who wish not to see their
loved one suffer unwittingly contribute to the persistence
of OCD symptoms by performing rituals, providing fre-
quent reassurance, and engaging in avoidance to “help
the affected relative cope with anxiety.” Thus, family
accommodation is an important factor to assess (Boeding
et al., 2013). In other families, relatives are highly critical
and express hostility toward their loved one with OCD.
When relatives meddle or chronically intrude into the
patient’s daily activities, it can affect course and treat-
ment response. Relatives can be invited to take part in
the assessment process, thus providing an opportunity to
assess how they interact with the patient. Relatives can
be asked about (a)  the extent to which they participate
in the patient’s rituals and avoidance habits, (b) how they
respond when repeatedly asked questions for reassurance,
(c) what consequences they fear might occur if symptoms
are not accommodated, and (d) the extent to which the
family’s daily activities are influenced by the patient’s
OCD symptoms.
PURPOSES OF ASSESSMENT
Proper assessment of OCD is guided by conceptual models
of phenomenology, etiology, and treatment. Because the
cognitive–​behavioral model has strong empirical support,
this framework is used in this chapter to determine what
parameters are necessary to assess. The next sections include
a review and discussion of the use of particular instruments
and methodologies that clinicians and clinical researchers
will find helpful for the purposes of (a) making a diagnosis of
OCD, (b) case conceptualization and treatment planning,
and (c) evaluating the effects of treatment.
314 Anxiety and Related Disorders
ASSESSMENT FOR DIAGNOSIS
General Description of the Problem
It is useful to begin the diagnostic assessment in an
unstructured way by asking the patient to provide a gen-
eral description of his or her difficulties with obsessions
and compulsions. Reviewing a typical day can highlight,
for example, the frequency and duration of OCD symp-
toms, how these symptoms are managed, and the ways in
which the person is functionally impaired. Examples of
open-​ended questions to ask regarding the presence of
obsessions, compulsions, and related signs and symptoms
include the following:
• What kinds of activities or situations trigger anxiety
or fear?
• What kinds of upsetting or scary thoughts have you
been experiencing?
• What places or situations have you have been
avoiding?
• Tell me about any behaviors that you feel compelled
to perform over and over.
• What do you think might happen if you could not
perform these behaviors?
Information about the onset, historical course of the
problem, comorbid conditions, social and developmental
history, and personal/​family history of mental health treat-
ment should also be obtained. The most common comor-
bid conditions among individuals with OCD are unipolar
mood disorders (see Chapter  7, this volume) and other
anxiety disorders (e.g., generalized anxiety disorder; see
Chapter 14, this volume).
Yale–​Brown Obsessive Compulsive Scale
Symptom Checklist
Because OCD is highly heterogeneous in its presenta-
tion, a semi-​structured approach to assessing the topogra-
phy of a given patient’s symptoms is recommended as an
initial step. The Yale–​Brown Obsessive Compulsive Scale
Symptom Checklist (Y-​BOCS-​ SC; Goodman, Price,
Rasmussen, Mazure, Delgado, et  al., 1989; Goodman,
Price, Rasmussen, Mazure, Fleischmann, et  al., 1989;
reprinted in the Journal of Clinical Psychiatry, Vol. 60
[1999], Suppl. 18, pp. 67–​77) is the best available instru-
ment for such purposes. The first section of the Y-​BOCS-​
SC provides definitions of obsessions and compulsions
that are read to the patient. Next, the clinician reviews
a list of more than 50 common obsessions and compul-
sions and asks whether each symptom is currently present
or has occurred in the past. Finally, the most prominent
obsessions, compulsions, and OCD-​ related avoidance
behaviors are identified from those endorsed by the
patient.
Although it is comprehensive in scope, there are no
psychometric studies of the Y-​BOCS-​SC. Moreover, the
checklist merely assesses the form of the patient’s obses-
sions and rituals without regard for the function of these
symptoms. That is, there are no questions relating to how
rituals are used to reduce obsessional fears (later, we
describe a functional approach to assessing OCD symp-
toms that has incremental validity over the Y-​BOCS-​SC
for the purpose of developing a treatment plan). Another
limitation of the Y-​BOCS-​SC is that it contains only
one item assessing mental rituals. Thus, the clinician
must probe in a less structured way for the presence of
these covert symptoms (the assessment of mental ritu-
als is also discussed further in the section on case con-
ceptualization and treatment planning). Furthermore,
the checklist contains some items that do not pertain to
OCD per se, such as hoarding obsessions (hoarding is
defined as a separate disorder in DSM-​5) and hair pull-
ing and self-​injurious compulsions. Finally, because of
its emphasis on the overt characteristics of obsessions and
compulsions—​such as their repetitiveness and thematic
content (e.g., fears of illness and repetitive counting)—​
the Y-​BOCS-​SC offers little help in differentiating OCD
symptoms from other clinical phenomena that might
also be repetitive or thematically similar. For example,
worries might be repetitive and can focus on matters of
health and illness, depressive ruminations are repetitive
and involve negative thinking, and hair pulling disorder
(i.e., trichotillomania) can involve repetitive behaviors.
It is therefore necessary to distinguish OCD symptoms
from these other entities.
Distinguishing OCD Symptoms
from Other Phenomena
Whereas obsessions and worries can both involve themes
of illness and harm, obsessions focus on doubts about
unrealistic disastrous consequences (e.g., “What if I had
a hit-​and-​
run automobile accident and didn’t realize
it?”). Worries, in contrast, concern real-​ life (everyday)
situations such as relationships, health and safety, work or
school, and finances. In addition, compared with worries,
obsessions are experienced as more unacceptable, and
they evoke greater subjective resistance. Obsessions can
 Obsessive–Compulsive Disorder 315

TABLE 15.1   Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

ADIS-​IV NA NA E G E E E G ✓
SCID-​IV NA NA A A E E E A
Y-​BOCSC-​SC NA NA NA NA G E NA A ✓
BABS A G G A G G G G ✓

Note: ADIS-​IV = Anxiety Disorders Interview Schedule for DSM-​IV; SCID-​IV = Structured Clinical Interview for DSM-​IV; Y-​BOCS-​SC = Yale–​Brown
Obsessive Compulsive Scale Symptom Checklist; BABS = Brown Assessment of Beliefs Scale; A = Adequate; G = Good; E = Excellent; NA = Not
Applicable.

be differentiated from depressive ruminations based on Standardized Diagnostic Assessment

content as well as subjective experience. Depressive rumi-
When initial questioning reveals the apparent presence
nations typically involve overly negative thoughts about
of obsessions and/​ or compulsions, assessment should
oneself, the world, and the future (e.g., “No one will ever
include a standardized diagnostic interview to confirm
love me”). Moreover, depressive ruminations do not elicit
the diagnosis of OCD (as well as other common comor-
subjective resistance or ritualistic behavior.
bid anxiety and mood disorders). Two incrementally valid
Whereas obsessions are experienced as distressing,
instruments exist for this purpose and are described next.
unwanted, and unacceptable, fantasies are experienced
Table 15.1 shows ratings of various psychometric and
as pleasurable and therefore should not be confused
practical characteristics of these diagnostic interviews.
with obsessions. For example, the erotic thoughts of indi-
The reader should note that this chapter discusses assess-
viduals with paraphilia lead to sexual arousal (even if the
ment tools based on the DSM-​IV criteria for OCD (APA,
sufferer wishes not to have such thoughts or feels guilty
1994)  given that (a)  the diagnostic criteria have under-
about them). Sexual obsessions in OCD, however, do not
gone only very minor changes from DSM-​IV to DSM-​5
lead to sexual arousal (Schwartz & Abramowitz, 2003).
and (b)  diagnostic instruments consistent with DSM-​5
Similarly, repetitive “obsessive” thoughts about acquiring
have not yet been psychometrically evaluated (although
psychoactive substances (e.g., drugs and alcohol) are not,
updated versions have been published to allow for the
in and of themselves, experienced as distressing (although
diagnosis of OCD according to DSM-​5 criteria [APA,
the person might feel guilty about the consequences of his
2016; Brown & Barlow,  2014]). The most important
or her alcohol consumption). Finally, whereas obsessions
change from DSM-​IV to DSM-​5 regarding OCD is that it
and delusions might both have a bizarre quality, delusions
has been removed from the anxiety disorders and incorpo-
do not evoke anxiety or rituals.
rated as the flagship diagnosis of the obsessive–​compulsive
Tics (as in Tourette’s syndrome) and compulsive ritu-
related disorders (OCRDs)—​a completely novel diagnos-
als differ primarily in that rituals are usually purposeful,
tic class in DSM-​5. Other OCRDs include hair pulling
meaningful behaviors that are performed in response
disorder (trichotillomania), skin picking (excoriation) dis-
to obsessional distress and intended to reduce an obses-
order, hoarding disorder, and body dysmorphic disorder.
sional fear. Tics, in contrast, are often performed in
response to physical urges and sensations (i.e., premoni-
tory urges) and are not triggered by obsessional thinking
Anxiety Disorders Interview Schedule for DSM-​IV
or performed to reduce fear. Other repetitive behaviors,
such as “compulsive” hair pulling, gambling, skin pick- The Anxiety Disorders Interview Schedule for DSM-​IV
ing, overeating, stealing, and excessive shopping, are (ADIS-​ IV) is a clinician-​
administered, semi-​ structured,
problems with impulse control yet are often mistaken diagnostic interview developed to establish the differential
for OCD rituals. These impulsive behaviors, however, diagnosis among the anxiety disorders based on DSM-​IV
are not associated with obsessions and do not serve to criteria (DiNardo, Brown, & Barlow, 1994). Compared
reduce anxiety or the probability of feared outcomes. In with other diagnostic interviews, it provides greater detail
fact, these acts are experienced as pleasurable even if the about anxiety-​ related problems. The ADIS-​ IV begins
person wishes he or she did not feel compelled to do with demographic questions and items about general
these behaviors. functioning and life stress. Sections for assessing each
316 Anxiety and Related Disorders
anxiety, mood, and somatoform disorder appear next. The
OCD section begins with a screening question, a positive
answer to which triggers more detailed questions about
obsessions and compulsions based on DSM-​IV criteria.
In a large reliability study (Brown, DiNardo, Lehman,
& Campbell, 2001), scores on the ADIS-​IV OCD module
evidenced very good inter-​rater reliability, with the main
sources of unreliability coming from the occasional assign-
ment of a subclinical OCD diagnosis (as opposed to a dif-
ferent anxiety disorder). Although no studies have directly
examined the validity of the scores on the ADIS-​IV OCD
section, the many studies showing that OCD samples diag-
nosed with this instrument have higher scores on measures
of OCD severity, compared to non-​OCD samples, provide
evidence for its validity. Other advantages of the ADIS-​IV
include the fact that it contains a semi-​structured format,
which allows the clinician to collect detailed information.
It also includes a dimensional rating of symptom severity.
One limitation of the ADIS-​IV is that administration of the
entire instrument can be time-​consuming, although the
OCD module itself is not very long.
Structured Clinical Interview for DSM-​IV
Axis I Disorders
The Structured Clinical Interview for DSM-​ IV Axis
I  Disorders (SCID) is a clinician-​ administered, semi-​
structured interview developed for the purpose of diag-
nosing a range of DSM-​IV Axis I disorders (First, Spitzer,
Gibbon, & Williams, 2002). Accordingly, it contains a
module to assess the presence of OCD. The SCID begins
with an open-​ended assessment of demographic informa-
tion and various domains of functioning. The OCD section
includes probe questions about the presence of obsessions
and compulsions. Next to each probe appear the corre-
sponding DSM-​IV diagnostic criteria, which are rated as
absent (false), subthreshold, or present (true). Thus, ratings
are of diagnostic criteria, not of interviewees’ responses.
Research on the reliability of the SCID scores for assessing
the presence of OCD has provided mixed results. Whereas
some studies report low kappas, others report more accept-
able inter-​rater reliability (e.g., Williams et al., 1992).
Assessing Insight into the Senselessness
of OCD Symptoms
The Brown Assessment of Beliefs Scale
The Brown Assessment of Beliefs Scale (BABS) is a
brief (seven items) interview that provides a continuous
measure of insight into the senselessness of OCD symp-
toms (Eisen et  al., 1998). Administration begins with
the interviewer and patient identifying one or two of the
patient’s specific obsessional fears that have been of sig-
nificant concern during the past week. Next, individual
items assess the patient’s (a) conviction in the validity of
this fear, (b) perceptions of how others view the validity
of the fear, (c) explanation for why others hold a different
view, (d) willingness to challenge the fear, (e) attempts to
disprove the fear, (f) insight into whether the fear is part of
a psychological/​psychiatric problem, and (g)  ideas/​delu-
sions of reference. Only the first six items are summed to
produce a total score.
Norms for OCD samples have been established in
several studies (e.g., Eisen, Phillips, Coles, & Rasmussen,
2004). The BABS appears to yield scores that have
good internal consistency, and it discriminates OCD
patients with good insight from those with poor insight
(Eisen et  al., 1998). Whereas the BABS is sensitive to
treatment-​related changes in OCD symptoms, there is
mixed evidence regarding whether higher scores are
predictive of poorer response to treatment (e.g., Ravie
Kishore, Samar, Janardhan Reddy, Chandrasekhar, &
Thennarasu, 2004).
Practical Considerations
People with OCD often have difficulty discussing their
obsessions and compulsions. Embarrassment over the
theme (e.g., sexual) and senselessness of such symptoms
is a primary factor. The interviewer must be sensitive to
such concerns and demonstrate appropriate empathy
regarding the difficulties inherent in discussing these
problems with others. Clearly, the clinician should avoid
appearing shocked or disturbed by descriptions of obses-
sions and compulsions. Semi-​structured instruments such
as the Y-​BOCS-​SC and BABS help the interviewer nor-
malize such symptoms. Patients may also have difficulty
describing their symptoms if they are unaware that such
thoughts and behaviors represent obsessions and compul-
sions. Thus, including significant others in the interview
can help identify such symptoms.
Occasionally, features of OCD itself—​such as fear,
indecisiveness, rigidity, and the need for reassurance—​
attenuate the assessment process. Patients might be
afraid to verbalize their obsessional thoughts for fear that
doing so will cause harm to befall themselves or others
(e.g., thoughts of loved ones dying). They might also be
highly circumstantial in their responses because of fears
that if they do not provide “all the details,” they will not

benefit from therapy. Such obstacles require the clini-
cian’s patience but can often be managed with persistent
gentle, yet firm, reminders of the importance of accurate
reporting, as well as time constraints and the need for
short, concise responses.
Overall Evaluation
OCD is a highly heterogeneous condition in which each
individual presents with idiosyncratic and personalized
symptom content. Thus, the clinician must be flexible and
comprehensive, and he or she must also be able to distin-
guish bona fide OCD symptoms from symptoms of other
disorders with topographically similar presentations—​
especially other OCRDs such as hair pulling and skin
picking disorders (Abramowitz & Jacoby, 2015). Family
members living with patients may be able to serve as reli-
able sources of information regarding the validity of this
diagnosis. Keeping these points in mind and using careful
open-​ended questioning often leads to correctly identify-
ing whether or not an individual has OCD.
The ADIS-​IV and SCID are empirically established
and widely used semi-​structured interviews for confirming
the diagnosis of OCD. Some authors favor the ADIS-​IV
for the excellent reliability of its scores and wider scope
of information yielded compared with the SCID. Both of
these instruments, however, require that interviewers be
well trained in their administration, although BA-​or MA-​
level training in psychology is often sufficient to achieve
good reliability as long as the interviewers are supervised
by experienced doctoral-​level psychologists. How well the
individual recognizes his or her obsessions and compul-
sions as senseless and excessive is best assessed using the
BABS, a continuous measure of insight, as opposed to
using the categorical DSM-​5 insight specifiers (i.e., “good
or fair insight,” “poor insight,” and “absent insight/​delu-
sional beliefs”).
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
The cognitive–​behavioral model, from which effective
psychological treatment is derived, provides a framework
for collecting patient-​specific information and generating
an individualized case conceptualization and treatment
plan. This framework, referred to as functional assessment
(Abramowitz, Deacon, & Whiteside, 2011; Abramowitz
& Jacoby, 2014), is important because identifying the
particular stimuli to be confronted during exposure
Obsessive–Compulsive Disorder 317
therapy requires detailed knowledge of the patient’s idio-
syncratic fear triggers and cognitions. Similarly, assisting
patients to resist compulsive urges (i.e., response preven-
tion) requires knowing about all ritualistic maneuvers
performed in response to obsessive fear. This section
describes the procedures for conducting this type of
assessment.
Assessing Obsessional Stimuli
Guided by information already collected, a thorough
inventory of external triggers and intrusive thoughts that
evoke the patient’s obsessional fear is obtained. Some of
these stimuli will later be chosen for inclusion as exposure
therapy tasks. Because of the idiosyncratic nature of obses-
sional triggers, there are no psychometrically validated
instruments for this purpose. Therefore, the assessor must
rely on his or her clinical experience and knowledge of
the OCD research literature.
External Triggers
External triggers include specific objects, situations, places,
and so on that evoke obsessional fears and urges to ritualize.
Examples include toilets, knives, completing paperwork,
religious icons, feared numbers (e.g., 13 or 666), and leav-
ing the house. Examples of questions to help the patient
describe such triggers include “In what situations do you
feel anxious?” “What do you avoid?” and “What triggers
your urge to do compulsive rituals?”
Intrusive Thoughts
Intrusive thoughts include unwanted mental stimuli (e.g.,
upsetting images) that are experienced as unacceptable,
immoral, or repulsive and that evoke obsessional anxiety.
Examples include images of germs, impulses to harm loved
ones, doubts about one’s sexual preference, and thoughts of
loved ones being injured. Examples of questions to elicit
this information include “What intrusive thoughts do you
have that trigger anxiety?” and “What thoughts do you try
to avoid, resist, or dismiss?” Some patients are unwilling to
describe their intrusions, fearing that the therapist will not
understand that these are unwanted thoughts. To overcome
such reluctance, the assessor can educate the patient about
the universality of such intrusions and even self-​disclose his
or her own senseless intrusions. A list of intrusive thoughts
from nonclinical individuals that can be given to patients
to demonstrate the universality of such phenomena is pub-
lished elsewhere (e.g., Abramowitz, 2006a).
318 Anxiety and Related Disorders
Assessing Cognitive Features
Feared Consequences
Information should be obtained about the cognitive basis
of obsessional fear—​ that is, the feared consequences
associated with obsessional stimuli (e.g., “If I use a pub-
lic restroom I will get AIDS” and “If my receipt has the
number 13, I  will have bad luck”). Knowing this infor-
mation helps the therapist arrange exposure tasks that
will disconfirm such exaggerated expectations. Although
most patients readily articulate such fears, some do not.
When feared disasters cannot be explicitly articulated,
the patient might fear that anxiety itself will persist indefi-
nitely (or escalate to “out-​of-​control” levels) unless a ritual
is performed. Other patients might be afraid merely of not
knowing “for sure” whether a feared outcome (usually in
the more distant future) will occur. The following open-​
ended questions are appropriate for assessing feared con-
sequences: “What is the worst thing that could happen if
you are exposed to (obsessional trigger)?” “What do you
think might happen if you didn’t complete the ritual?”
“What would happen if you didn’t do anything to reduce
your high levels of anxiety?” and “What if you don’t know
for certain whether _​_​_​_​_​ will happen?”
Dysfunctional Beliefs
Cognitive therapy techniques (e.g., Wilhelm & Steketee,
2006), which can be used to supplement exposure
therapy, require assessment of the patient’s dysfunc-
tional thinking patterns that underlie obsessional fear.
An international group of researchers, the Obsessive
Compulsive Cognitions Working Group (OCCWG),
has developed and tested two instruments that provide a
comprehensive assessment of the cognitive landscape of
OCD:  the Obsessive Beliefs Questionnaire (OBQ) and
the Interpretation of Intrusions Inventory (III; OCCWG,
2005). The reader should note that additional measures
for assessing specific OCD-​related dysfunctional beliefs
are available (e.g., the Thought–​ Action Fusion Scale;
Shafran, Thordarson, & Rachman, 1996). However,
because the OBQ and III are comprehensive in their cov-
erage of the various domains of dysfunctional beliefs, this
chapter focuses on these measures. Information on many
of the other measures can be found in Antony, Orsillo,
and Roemer (2001).
An initial 87-​item version of the OBQ (OCCWG,
2001, 2003)  contained six rationally derived and highly
correlated subscales. Subsequent research, however, has
led to a 44-​item version with three empirically derived
TABLE 15.2   Domains of Dysfunctional Beliefs Associated
with OCD
Belief Domain Description
Overestimation Beliefs that negative events are especially likely
of threat and would be especially awful. Beliefs that one
and inflated has the special power to cause and/​or the duty
responsibility to prevent negative outcomes.
Overimportance Beliefs that the mere presence of a thought
of, and need to indicates that the thought is significant. For
control, intrusive
example, the belief that the thought has
thoughts
ethical or moral ramifications or that thinking
the thought increases the probability of the
occurrence of the corresponding behavior or
event. Also, beliefs that complete control over
one’s thoughts is both necessary and possible.
Perfectionism and Beliefs that mistakes and imperfection are
intolerance for intolerable. Beliefs that it is necessary and
uncertainty possible to be completely certain that negative
outcomes will not occur.
subscales (OCCWG, 2005), which assess domains of
dysfunctional beliefs (termed “obsessive beliefs”) thought
to increase risk for the development of OCD (e.g., Frost
& Steketee, 2002; see Table 15.2). Specifically, obsessive
beliefs are considered enduring trait-​like cognitive biases
that give rise to the misinterpretation of normally occur-
ring intrusive thoughts as highly significant and threaten-
ing, leading to obsessional anxiety and compulsive urges
(e.g., Taylor, Abramowitz, & McKay, 2007). When com-
pleting the measure, respondents rate their agreement
with each of the 44 items using a scale from 1 (disagree
very much) to 7 (agree very much).
A summary of the psychometric viability of the OBQ
appears in Table 15.3. The measure has been studied
extensively with clinical and nonclinical samples, and
its scores demonstrate very good internal consistency
and test–​retest reliability. Items were carefully designed
by the OCCWG and, as such, demonstrate excellent
content and construct validity. Prospective research also
indicates that, to some extent, scores on the OBQ are
predictive of the development of obsessive–​compulsive
symptoms (Abramowitz, Khandker, Nelson, Deacon, &
Rygwall, 2006). The OBQ is quite useful in clinical set-
tings because it identifies patterns of dysfunctional think-
ing that can be targeted by cognitive therapy techniques
(e.g., Wilhelm & Steketee, 2006).
The III is a semi-​idiographic measure designed to assess
negative appraisals of intrusive thoughts. The respondent
first reads a set of instructions that includes examples of
cognitive intrusions (e.g., “an impulse to do something
shameful or terrible”) and then is asked to identify one or

TABLE 15.3   Ratings of Instruments Used for Case Conceptualization and Treatment Planning
Internal Inter-​Rater Test–​Retest
Instrument Norms Consistency Reliability Reliability
OBQ E E NA G E
III E E NA G E
Note: OBQ = Obsessive Beliefs Questionnaire; III = Interpretation of Intrusions Inventory; G = Good; E = Excellent; NA = Not Applicable.
two examples of his or her specific intrusions. The respon-
dent next indicates the extent of agreement with the scale’s
31 items that concern various erroneous appraisals of intru-
sions (e.g., “I would be a better person if I didn’t have this
thought”). Although three theoretically derived subscales
were initially proposed, further psychometric analyses indi-
cate that only a single III factor exists (OCCWG, 2005).
As with the OBQ, the III has been studied in clinical
and nonclinical samples, and its scores show good to excel-
lent reliability (see Table 15.3). The scores also show excel-
lent construct validity and predict, in a prospective fashion,
the persistence of obsessional symptoms (Abramowitz,
Nelson, Rygwall, & Khandker, 2007). The III is well suited
for clinical practice because it is fairly brief and provides
valuable information regarding how the patient negatively
appraises the presence and meaning of his or her own
intrusive thoughts. The clinician can use this information
to illustrate how such faulty appraisals lead to obsessional
anxiety and also how such interpretations can be modified
(e.g., “It’s no wonder you spend so much time trying to
fight your unwanted thoughts about accidents. It looks like
you’re convinced that just by thinking these thoughts you
will cause innocent people to have accidents. I wonder if
that’s how our thoughts really work?”).
Assessing Responses to Obsessional Distress
As discussed previously, avoidance and compulsive ritu-
als performed in response to obsessional stimuli serve to
reduce anxiety in the short term, but they paradoxically
maintain OCD symptoms by preventing the natural
extinction of fear and by interfering with the disconfirma-
tion of fears of disastrous consequences. Accordingly, one
must ascertain the specifics of such behaviors so that they
can be treatment targets.
Passive Avoidance
Most individuals with OCD avoid situations and stimuli
associated with their obsessions in order to prevent obses-
sional thoughts, anxiety, or feared disastrous outcomes.
Obsessive–Compulsive Disorder 319
Content Construct Validity Clinical Highly
Validity Validity Generalization Utility Recommended
E G G ✓
E G G ✓
Avoidance might be overt, such as the evasion of certain
people (e.g., cancer patients), places (e.g., public wash-
rooms and places of worship), situations (e.g., using
pesticides), and certain words (e.g., “murder”). It might
also be subtle, such as staying away from the most often
touched part of the door handle and refraining from lis-
tening to loud music while driving. The assessor should
also ascertain the cognitive basis for avoidance (e.g., “If
I  listen to music, I  might not realize it if I  hit a pedes-
trian”). Examples of questions to elicit this information
about avoidance include “What situations do you avoid
because of obsessional fear and why?” and “What would
happen if you couldn’t avoid this situation?”
Behavioral Rituals
Because the external stimuli and intrusive thoughts that
evoke obsessional fear are often ubiquitous (e.g., using the
bathroom and intrusive thoughts), they might be difficult
to avoid successfully. Patients use rituals, therefore, as
“active avoidance” strategies that serve as an escape from
obsessional fear, which could not be avoided in the first
place. Some rituals could be called “compulsive” in that
they are performed repetitively and in accordance with
certain self-​prescribed rules (e.g., checking an even num-
ber of times, and washing for 40 seconds). Other rituals,
however, would not be classified as compulsive because
they might be subtle, brief, or performed only once at a
time (e.g., holding the steering wheel tightly, and using a
shirtsleeve to open a door).
Topographically similar rituals can serve very different
functions. For example, many patients engage in hand-​
washing rituals to decontaminate themselves. Such wash-
ing rituals are typically evoked by thoughts and images of
germs or by doubts of whether one has had contact with
a feared contaminant. Some individuals with OCD, how-
ever, engage in washing rituals in response to feelings of
“mental pollution” evoked by unwanted disturbing intru-
sive thoughts of a sexual or otherwise immoral nature (e.g.,
Fairbrother, Newth, & Rachman, 2005). A  functional
assessment, therefore, is necessary to elucidate how rituals
320 Anxiety and Related Disorders
are linked to obsessions and feared consequences—​for
example, checking the stove to prevent fires or using a
certain type of soap because it specifically targets certain
sorts of germs. Examples of probes to elicit this informa-
tion include “What do you do when you can’t avoid the
word ‘cancer’?” “What do you do to reduce your fears of
being responsible for accidents?” “Why does this ritual
reduce your discomfort?” and “What could happen if you
didn’t engage in this ritual?”
Mental Rituals
The function of mental rituals is the same as that of
behavioral rituals (de Silva, Menzies, & Shafran, 2003)—​
to reduce anxiety and prevent feared outcomes. Mental
rituals typically take the form of silently repeating special
“safe” words (e.g., “life”), images (e.g., of Jesus Christ),
or phrases (e.g., prayers) in a set manner to neutralize
or “deal with” unwanted obsessional thoughts. Other
common presentations include thought suppression,
privately reviewing one’s actions repeatedly (e.g., to reas-
sure oneself that one did not do something terrible), and
mental counting. Many clinicians fail to assess mental
rituals, or they confuse them for obsessions. Although
mental rituals and obsessions are both cognitive events,
they can be differentiated by careful questioning and by
keeping in mind that the former are unwanted, intrusive,
and anxiety-​ evoking, whereas the latter are deliberate
attempts to neutralize obsessional intrusions and, as such,
they function to reduce anxiety. Examples of questions to
elicit information about mental rituals include the follow-
ing:  “Sometimes people with OCD have mental strate-
gies that they use to manage obsessional thoughts. What
kinds of mental strategies do you use to dismiss unwanted
thoughts?” and “What might happen if you didn’t use the
strategy?”
Self-​Monitoring
Self-​monitoring, in which the patient records the occur-
rence of obsessive–​compulsive symptoms in “real time,”
provides data to complement the functional assessment.
Patients can be instructed to log the following parameters
of each symptomatic episode (i.e., using a form with cor-
responding column headers):  (a) date and time of the
episode, (b)  situation or thought that triggered obses-
sional fear, and (c)  rituals and the length of time spent
engaged. The task of self-​monitoring should be intro-
duced as a vehicle by which the assessor and patient can
gain a highly accurate picture of the time spent engaged
in, and situations that lead to, rituals. It also helps to
identify symptoms that might have gone unreported in
the assessment sessions. The patient should be instructed
that rather than guessing, he or she should use a watch
to determine the exact amount of time spent ritualizing.
Moreover, to maximize accuracy, each entry should be
recorded immediately after it occurs (as opposed to wait-
ing until the end of the day).
Case Conceptualization
The functional assessment described previously yields
the information necessary to construct an individualized
conceptualization of the patient’s idiosyncratic OCD
symptoms. This formulation serves as a “road map” for
cognitive–​ behavioral therapy and is synthesized by list-
ing the obsessional stimuli (external cues and intrusive
thoughts), cognitive appraisals of these stimuli (e.g., “I will
get sick” and “I will be responsible for”), and the avoid-
ance and ritualistic strategies used to reduce obsessional
anxiety. Arrows are then drawn to show the links between
stimuli, cognitions, emotions, and behavior as specified by
the cognitive–​behavioral model. An example of a patient’s
individualized model is shown in Figure 15.1. The model
suggests that the modification of faulty beliefs and interpre-
tations is required to reduce obsessional anxiety, and that the
cessation of avoidance and ritualistic behavior is necessary
for being able to modify the faulty cognitions. As discussed
previously, this leads to the use of exposure therapy, cogni-
tive techniques, and response prevention in the treatment
of OCD (e.g., Abramowitz 2006a, 2006b; Salkovskis, 1996).
Practical Considerations
As with the diagnostic assessment, patients may seem
hesitant to self-​disclose some of the details of their OCD
symptoms. Explaining the purpose and importance of
such an in-​depth analysis of obsessions and compulsions
might be helpful in this regard. One tactic that often
works well in building rapport and camaraderie (and
thus, more self-​disclosure) is to describe the functional
assessment phase as an exchange of information between
two “experts.” The patient, who is an expert on his or her
particular OCD symptoms, must help the therapist to
understand these symptoms so that an effective treatment
plan can be drawn up. Simultaneously, the therapist, an
expert on conceptualizing OCD in general, must help the
patient learn to think about his or her symptoms from a
cognitive–​behavioral perspective so that the patient can
get the most out of treatment.
 Obsessive–Compulsive Disorder 321

Fear Cues
– Driving by pedestrians
– Driving by schools
– Thoughts/doubts: “did I hit a pedestrian without knowing it?”

Beliefs/Interpretations
– “Because I’ve had this thought, I must be at high risk
for hitting a pedestrian”
– “I can not take the chance that it has happened”
– “I am a dangerous person/driver”

OBSESSIONAL ANXIETY

Rituals Avoidance
– C hecking the car for Driving through:
blood/marks – Neighborhoods
– Checking the road for – Parking lots
injured people – School zones
– Compulsively checking – After dark
the rear-view mirrors

FIGURE 15.1   Example of a cognitive–​behavioral case formulation for a patient with OCD.

As alluded to previously, patients are sometimes
afraid to mention certain symptoms due to dysfunctional
beliefs about the consequences of saying certain things.
For example, one individual was reluctant to describe
his unwanted blasphemous images of Jesus having sex-
ual intercourse with Mary because he feared that dis-
cussing these ideas (i.e., thinking about them) would
invite divine punishment. In such instances, gentle, but
firm, encouragement to openly discuss the obsession in
the spirit of reducing old avoidance habits is the rec-
ommended course of action. As mentioned previously,
to avoid reinforcing the patients’ fears, the interviewer
should be sure to react in a calm and understanding
manner when even the most unpleasant obsessions are
self-​disclosed.
Overall Evaluation
Because of the idiographic nature of functional assess-
ment, evaluation of the psychometric properties of
this approach is difficult. The goals of functional
assessment, however, include (a)  the identification of
target behaviors and the processes that maintain these
behaviors and (b) the selection of appropriate interven-
tions (Follette, Naugle, & Linnerroth, 2000). Therefore,
given consistent evidence that ERP—​which can only
be implemented with data derived from a functional
assessment—​ is often highly successful in reducing
OCD symptoms when assessed in this manner, it can
be indirectly concluded that functional assessment is
a valid and highly clinically useful tool. Incorporation
of the psychometrically sound OBQ and III can add to
the functional assessment by providing additional data
regarding the cognitive basis of obsessional fears and
compulsive urges. Advances in cognitive therapy for
OCD (e.g., Wilhelm & Steketee, 2006)  include the
development of specific cognitive techniques to target
the types of cognitive distortions measured by these
instruments. Despite these advances, the patient-​specific
nature and vast heterogeneity of OCD symptoms (and
associated cognitive distortions) can present challenges
for even the most skilled clinicians.
322 Anxiety and Related Disorders

TABLE 15.4   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Y-​BOCS E G G A G E E E A ✓
interview
PI-​R E E NA G G E G NA A
OCI-​R E G NA A G G A A A ✓
VOCI G E NA A G A A NA G ✓
SCOPI G G NA G G A A NA A
DOCS E E NA G G E E G A ✓

Note: Y-​BOCS = Yale–​Brown Obsessive Compulsive Scale; PI-​R = Padua Inventory-​Revised Version; OCI-​R = Obsessive–​Compulsive Inventory-​

Revised; VOCI  =  Vancouver Obsessional Compulsive Inventory; SCOPI  =  Schedule of Compulsions, Obsessions, and Pathological Impulses;
DOCS = Dimensional Obsessive Compulsive Scale; A = Adequate; G = Good; E = Excellent; NA = Not Applicable.

ASSESSMENT FOR TREATMENT MONITORING parameters of obsessions (items 1–​ 5) and compulsions

AND TREATMENT OUTCOME (items 6–​10) identified using the Y-​BOCS-​ SC. These
parameters are (a) time/​frequency, (b) related interference
Continually assessing the nature and severity of OCD in functioning, (c) associated distress, (d) attempts to resist,
and related symptoms throughout the course of treatment and (e)  degree of control. Each item is rated from 0 (no
assists the therapist in evaluating whether, and in what symptoms) to 4 (extreme), and the 10 items are summed
ways, the patient is responding. This is consistent with the to produce a total score ranging from 0 to 40. In most
empirical demonstration of treatment effectiveness. It is instances, Y-​BOCS scores of 0 to 7 represent subclinical
not sufficient for the clinician simply to conclude that the OCD symptoms, those from 8 to 15 represent mild symp-
patient “seems to be less obsessed” or even for the patient toms, scores of 16 to 23 relate to moderate symptoms, scores
(or an informant) to report that he or she “feels better.” of 24 to 31 suggest severe symptoms, and scores of 32 to 40
Instead, progress should be measured systematically by imply extreme symptoms. A strength of the Y-​BOCS is that
comparing current functioning against a baseline. Thus, it measures symptom severity independent of the number
periodic assessment using the instruments described in this or types of different obsessions and compulsions. In fact, it
section should be conducted to objectively clarify in what is the only measure of OCD that assesses symptoms in this
ways treatment has been helpful and what work remains way. A limitation is that it can take 30 minutes or longer to
to be done. A multimethod approach is suggested, involv- administer, especially if used together with the Y-​BOCS-​SC.
ing the use of clinician-​administered interview and self-​ Numerous studies have established clinical and
report instruments that tap into various facets of OCD and nonclinical norms and psychometric properties of the
related symptoms (i.e., depression, general anxiety, and Y-​BOCS. The scale scores have adequate internal con-
functional disability). Table 15.4 shows ratings of various sistency, and they have good inter-​rater reliability and
psychometric and practical characteristics of instruments test–​retest reliability over a period of several weeks (e.g.,
developed to measure the severity of OCD symptoms. The Goodman, Price, Rasmussen, Mazure, Delgado, et  al.,
individual measures are described next. As indicated previ- 1989). The Y-​BOCS differentiates people with OCD
ously, additional chapters in this volume provide guidance from nondisordered individuals and those with other anxi-
in selecting appropriate tools for evaluating and monitor- ety disorders (e.g., Rosenfeld, Dar, Anderson, Kobak, &
ing the symptoms of comorbid conditions. Griest, 1992). Finally, scores are also sensitive to changes
that occur as a result of treatment (for a review, see Taylor,
Interview Measures Thordarson, & Sochting, 2002).

Y-​BOCS Severity Scale Self-​Report Measures

The Y-​BOCS severity scale (Goodman, Price, Rasmussen, Some researchers and clinicians use the Y-​BOCS sever-
Mazure, Delgado, et al., 1989; Goodman, Price, Rasmussen, ity scale as a self-​report measure; however, relatively few
Mazure, Fleischmann, et al., 1989) was designed as a semi-​ studies have evaluated the psychometric properties of
structured interview consisting of 10 items that assess five the instrument when used in this way. Steketee, Frost,

and Bogart (1996) found that the self-​ report version
tends to yield higher scores compared to the interview
version. This might occur if respondents confuse other
phenomena (e.g., worries, depressive ruminations, and
impulsive behaviors) for obsessions and compulsions.
An advantage to using the Y-​BOCS as a self-​ report
measure, however, is that it can be administered more
quickly and, therefore, more regularly during a course of
treatment. Many additional self-​report inventories, how-
ever, have been developed to assess the main symptoms
of OCD. The most promising of these instruments are
discussed next.
Revised Padua Inventory
There are several available versions of the Padua Inventory.
Because the most recent revision (the Revised Padua
Inventory [PI-​R]; Burns, Keortge, Formea, & Sternberger,
1996)  is also the most widely used, it is described here.
The PI-​R is a 39-​item measure that contains five sub-
scales:  (a) contamination and washing, (b)  dressing and
grooming compulsions, (c)  checking, (d)  obsessional
thoughts of harm, and (e) obsessional impulses to harm.
Agreement with each item is rated from 0 (not at all) to
4 (very much); thus, the total score ranges from 0 to 156.
The scale requires approximately 10 minutes to complete,
and its scores demonstrate at least adequate reliability and
validity. It also differentiates between OCD symptoms
and worry, although PI-​ R scores are significantly cor-
related with scores on measures of worry. Although the
van Oppen, Hoekstra, and Emmelkamp (1995) revision
has been shown to have good sensitivity to treatment, this
characteristic has not been formally investigated for the
Burns et al. (1996) version.
Revised Obsessive Compulsive Inventory
There are two versions of the Obsessive Compulsive
Inventory (OCI). The original (Foa, Kozak, Salkovskis,
Coles, & Amir, 1998) contains 42 items that assess the fre-
quency and distress associated with a wide range of obses-
sional and compulsive symptoms. Items, each of which is
rated on two scales (frequency and distress) from 0 (not
at all) to 4 (extremely), are organized into the following
seven subscales:  washing, checking, obsessing, hoard-
ing, mental neutralizing, ordering, and doubting. The
original OCI, however, has a number of psychometric
and practical liabilities (e.g., the doubting and checking
subscales appear to measure the same construct; Wu &
Watson, 2003).
Obsessive–Compulsive Disorder 323
A revision of the measure (the OCI-​R; Foa et  al.,
2002) has addressed some of the limitations of the origi-
nal scale. The OCI-​R consists of only 18 items (Foa et al.,
2002)  and six subscales (although one of the subscales
pertains to hoarding symptoms, which are no longer
considered symptoms of OCD). Each subscale contains
3 items that are rated on a single 5-​point scale (0–​4) of
distress associated with that particular symptom. The
OCI-​R subscales include washing, checking, ordering,
obsessing, hoarding, and neutralizing. A total score may
be calculated by summing all 18 items, and subscale
scores can be calculated from the 3 items within each
subscale. Research suggests that scores on the OCI-​R and
its subscales have adequate convergent validity, although
divergent validity of some of the subscales is suspect
(e.g., Abramowitz & Deacon, 2006). The neutralizing
subscale has been specifically criticized because the 3
items on this subscale all pertain to counting symptoms
(e.g., Abramowitz & Deacon, 2006). Abramowitz, Tolin,
and Diefenbach (2005) found that the OCI-​R is useful
for measuring response to treatment. Moreover, a cut-​off
score of 21 can differentiate OCD patients from nonpa-
tients (Foa et al., 2002).
Vancouver Obsessive Compulsive Inventory
The Vancouver Obsessive Compulsive Inventory (VOCI;
Thordarson et  al., 2004)  is a 55-​item measure that rep-
resents an update of the 30-​item Maudsley Obsessional
Compulsive Inventory (MOCI; Hodgson & Rachman,
1977). Although the MOCI has sound psychometric
properties and was once widely used, it has largely fallen
out of favor due to two factors. First, it has poor sensitiv-
ity to treatment due to its true–​false response format and
inclusion of items assessing past and permanent events (as
opposed to current behaviors). Second, the MOCI mainly
measures the severity of washing and checking concerns
but not other symptoms of OCD, such as obsessions and
mental rituals. Although the VOCI is a lengthier instru-
ment than its predecessor, items assess a broader range
of OCD symptoms and are rated on a Likert-​type scale
from 0 (not at all true of me) to 4 (very much true of me).
The VOCI’s six empirically derived subscales include
contamination, checking, obsessions, hoarding, just right,
and indecisiveness. Thordarson et  al. examined the fac-
tor structure and psychometric properties of the scale and
found evidence of internal consistency, test–​retest reli-
ability, construct validity, and known groups validity of the
subscale scores. The sensitivity to treatment of the VOCI
has yet to be examined.
324 Anxiety and Related Disorders

Schedule of Compulsions, Obsessions, responsibility for harm and mistakes, symmetry/​ordering,

and Pathological Impulses and unacceptable thoughts (e.g., McKay et  al., 2004).
The DOCS is unique in that it affords an assessment of
The Schedule of Compulsions, Obsessions, and Pathological
OCD symptoms based on function rather than form. The
Impulses (SCOPI) is a 47-​ item self-​
report scale that is
DOCS also assesses multiple empirically based param-
designed to measure the presence of OCD symptoms while
eters of severity (frequency, avoidance, distress, and func-
also assessing a number of impulse-​control phenomena (e.g.,
tional interference; Deacon & Abramowitz, 2005)  for
“I sometimes feel a sudden urge to play with fire”; Watson
each of the four symptom dimensions.
& Wu, 2005). The impulse-​control focus was included on
A 20-​ item self-​report measure, the DOCS contains
the basis of evidence that there are links between impulse
four subscales that correspond to the symptom dimensions
control and OCD symptoms. Respondents rate their degree
mentioned previously. To accommodate the heterogeneity
of agreement with each item from 1 (disagree strongly) to 6
of OCD symptoms, and the presence of obsessions and
(agree strongly), and the scale contains five factors that cor-
rituals within each symptom dimension, each subscale
respond with empirically identified OCD symptom dimen-
begins with a description of the symptom dimension along
sions:  obsessive checking (14 items), obsessive cleanliness
with examples of representative obsessions and rituals. The
(12 items), compulsive rituals (8 items), hoarding (5 items),
examples clarify the form and function of each dimen-
and pathological impulses (8 items). The SCOPI was devel-
sion’s fundamental obsessional fears, compulsive rituals,
oped empirically from a large item pool that sampled a
and avoidance behaviors. Within each symptom dimen-
broad range of OCD and impulsive symptoms, which was
sion, five items (rated 0–​4) assess the following parameters
subjected to a series of factor analyses.
of severity (over the past month):  (a) time occupied by
In the only study evaluating the SCOPI, Watson and
obsessions and rituals, (b) avoidance behavior, (c) associ-
Wu (2005) found evidence that scores on the various sub-
ated distress, (d) functional interference, and (e) difficulty
scales are internally consistent, are stable over a 2-​month
disregarding the obsessions and refraining from the com-
interval, and show adequate convergent and discriminant
pulsions. The DOCS subscale scores have excellent reli-
validity. In particular, the SCOPI converges well with the
ability in clinical samples (α = .94 to .96), and the measure
OCI-​R. Although the measure is fairly easy to adminis-
converges well with other measures of OC symptoms.
ter, the impulse-​control items do not assess whether these
impulses (e.g., to steal and to act violently) are unwanted
intrusive urges (i.e., obsessions) or actual impulses that the Practical Considerations
person acts upon (i.e., premonitory urges). Indeed, such
In addition to some of the practical issues raised in the
impulses might occur among individuals with OCD and
previous sections, a few considerations regarding ongoing
those with impulse-​control disorders. Yet they are experi-
assessment deserve comment. First, patients sometimes
enced in very different ways depending on the disorder
attempt to either minimize their OCD symptoms or make
that affects the individual. This could lead to difficulties
themselves look worse off than they truly are. Self-​report
when interpreting responses to such items.
measures provide an easy vehicle for doing so. Such
behavior might be motivated by either resistance to begin-
ning treatment or the fear of ending treatment and termi-
Dimensional Obsessive–​Compulsive Scale
nating the therapeutic relationship. If this is suspected, it
One limitation of the measures described previously is might be helpful to gain observations from significant oth-
that they assess obsessions separately from compulsions. ers to provide additional data regarding symptom severity
Yet this is inconsistent with the most up-​to-​date structural and current functioning. A separate issue is that patients
analyses of OCD symptoms indicating broader symptom may feel tempted to minimize their symptoms in order to
dimensions composed of certain obsessions and rituals please their therapist. Gentle, yet firm, encouragement to
(e.g., McKay et  al., 2004). A  related limitation is that complete these forms for the purpose of providing impor-
because these instruments emphasize the form of obses- tant clinical information often helps.
sions and rituals, the function of these symptoms is over-
looked. To this end, Abramowitz and colleagues (2010)
Overall Evaluation
developed the Dimensional Obsessive–​Compulsive Scale
(DOCS) to assess the severity of the four most empirically There exists a wide array of interview and self-​report mea-
supported OCD symptom dimensions:  contamination, sures of OCD. In most instances, scale items have been

carefully written, submitted to appropriate statistical pro-
cedures, and examined for psychometric viability using
clinical or nonclinical samples. Some of these measures
are “global” in that they aim to assess the broad range of
OCD symptoms, whereas others focus on individual symp-
tom dimensions such as scrupulosity (e.g., Abramowitz,
Huppert, Cohen, Tolin, & Cahill, 2002) and symmetry/​
ordering concerns (e.g., Abramowitz et al., 2010; Coles,
Frost, Heimberg, & Rhéaume, 2003). The Y-​BOCS sever-
ity scale is unique in that it measures the severity of OCD
symptoms independent of symptom theme or the num-
ber of symptoms. Due to space limitations, the previous
review of self-​report instruments was restricted to global
measures of OCD that have the greatest potential (from
a practical and scientific standpoint) for use in clinical
and research settings. The heterogeneity of obsessions and
rituals presents a major challenge to developing a con-
cise global OCD self-​report symptom measure. Authors
of such scales must strike a balance between (a) including
enough items to comprehensively assess the various sorts
of OCD phenomena and (b) constructing a scale that is
manageable in length and therefore practical for wide-
spread use. Whereas each of the measures discussed in
this section provides an adequate self-​reported assessment
of OCD, the DOCS appears to most optimally achieve
this balance.
CONCLUSIONS AND FUTURE DIRECTIONS
This chapter provides the reader with a practical guide
for the comprehensive clinical evaluation of patients
with obsessions, compulsions, and related phenomena.
Advances in how we conceptualize OCD have been par-
alleled by improvements in the methods for assessment
and treatment of this disorder. Although there are numer-
ous valid and reliable instruments for assessing the signs
and symptoms of OCD,1 we underscore that the proper
assessment and treatment of this condition requires
more than simply administering empirically supported
tools. The assessment should be guided by a cognitive–​ References
behavioral theoretical framework in which obsessions and
Abramowitz, J. S. (2006a). Understanding and treating obsessive–​
compulsions are conceptualized in terms of their function
(i.e., antecedents and consequences) as opposed to their
topography (form or frequency). Whereas the clinician Abramowitz, J. S. (2006b). Obsessive–​compulsive disor-
1.  We remind the reader that our discussion of struc-
tured diagnostic interviews is based on DSM-​IV’s definition
of OCD, which was changed very little in the transition
to DSM-​5.
Obsessive–Compulsive Disorder 325
might be intrigued by descriptions of the often remark-
ably senseless and bizarre symptom presentations of OCD
(and legitimately so), he or she should avoid the temp-
tation to become sidetracked by form or topography and
instead keep in mind the essential features of OCD, which
are that (a) obsessional thoughts and images evoke anxiety
and distress and (b) avoidance and rituals serve to reduce
or neutralize this distress. The successful implementation
of empirically supported treatment (i.e., ERP) hinges on
an assessment strategy grounded within this model.
A multitrait–​multimethod approach to assessment will
yield the most comprehensive data regarding an indi-
vidual’s symptom presentation and related difficulties.
Although we have reviewed both self-​report and interview
measures of OCD, this chapter has not focused on the
measurement of traits or domains related to OCD, such
as depression, general anxiety, quality of life, and global
functional impairment. Nevertheless, such parameters
are important to assess during the initial interview and
functional assessment and also when measuring treat-
ment outcome. Several sources detail the assessment of
OCD-​related phenomena (e.g., Abramowitz [2006a] and
other chapters in the current volume on mood and anxi-
ety disorders) and can be consulted for suggestions regard-
ing specific measures to use.
Certainly there is room for the development of addi-
tional measures of OCD. In particular, the development
of standardized functional assessment techniques would
be advantageous as long as these could remain flexible
enough to accommodate the heterogeneity of the prob-
lem. Also, the assessment of children continues to lag
behind advances in the assessment of adults. Although the
age-​downward extensions of several measures discussed
here (e.g., OBQ and OCI-​R) have been developed, little
empirical work has appeared in the literature. Finally, it
will be advantageous to empirically examine the psycho-
metric properties of those newer diagnostic instruments
developed for assessing OCD in the context of DSM-​5.
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 16
Post-​Traumatic Stress Disorder in Adults
Samantha J. Moshier
Kelly S. Parker-​Guilbert
Brian P. Marx
Terence M. Keane
Post-​
traumatic stress disorder (PTSD) was first intro-
duced as a diagnosis in the third edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-​III;
American Psychiatric Association [APA], 1980)  and was
conceptualized as a relatively rare response to extraordinary
and severe stressors, such as war, violent acts, vehicular or
industrial accidents, sexual assault, and other disasters or
events that are outside the range of usual human experi-
ence. Today, traumatic events and PTSD are viewed as
worldwide phenomena that are prevalent and cross all
subgroups of the population. Epidemiological studies
have documented the prevalence of PTSD, providing
information on rates of exposure to trauma, the distribu-
tion of PTSD within different segments of the population
(adults and children, males and females, etc.), and those
factors that affect the onset and course of PTSD.
Recent events, including the mass shooting in Orlando,
Florida, in 2016, the terrorist attacks on September 11,
2001, and the 2010 Haiti earthquake, emphasize the
importance of arriving at best practices for the manage-
ment of disasters and violence on humanity. It is essential
for clinicians to utilize gold standard methods to diagnose
PTSD and related psychiatric conditions, monitor prog-
ress made throughout treatment, and measure treatment
outcomes. A multitude of PTSD measures are available; a
clinician seeking a tool to assess PTSD may find this array
of measures overwhelming. Therefore, the purpose of this
chapter is to discuss available methods for assessing PTSD
and make recommendations regarding their suitability in
a clinical context with a variety of populations. Our hope
is that clinicians will adopt the use of state-​of-​the-​science
329
methods of diagnosing and monitoring PTSD and trauma
symptoms in their work with traumatized adults. To pro-
vide a context for this discussion, we begin with a brief
review of diagnostic considerations related to PTSD, the
epidemiology of trauma, comorbid conditions, etiology,
and prognosis.
NATURE OF PTSD
Diagnostic Considerations and Associated Features
The diagnostic criteria for PTSD were revised sub-
stantially for the fifth edition of the DSM (DSM-​ 5;
APA, 2013). Among the more significant changes is the
removal of PTSD from the anxiety disorders category
and subsequent recategorization of it in a newly devel-
oped diagnostic category for conditions characterized as
a trauma-​and stressor-​related disorder. Other changes to
the diagnostic criteria include a modification to the defi-
nition of a potentially traumatic event (Criterion A); a
shift from three symptom clusters to four; and the addition
of three symptoms to the previously included 17 PTSD
symptoms to reflect “reckless or self-​destructive behavior,”
“distorted blame of self or others,” and “persistent negative
emotional states (e.g., fear, anger, guilt, shame, sadness).”
Furthermore, the wording of some other symptoms was
substantially modified to better define them.
The first PTSD symptom cluster (Criterion B) in
DSM-​5 is characterized by re-​experiencing, or reliving,
some or all of the traumatic event through recurring
330 Anxiety and Related Disorders
unwanted memories, vivid and intrusive nightmares,
flashbacks, and physiological reactions and psychological
distress when confronted with reminders of the trauma.
The second symptom cluster (Criterion C) involves avoid-
ance of stimuli (including people, places, cognitions, etc.)
that are associated with and remind the individual of the
traumatic event. Consequently, the lives of those with
PTSD can become increasingly constricted as they with-
draw from relationships, routine activities, or contexts that
serve as reminders. The third symptom cluster (Criterion
D) includes symptoms that are characterized by negative
alterations in cognitions and mood. Examples of such
symptoms are an inability to remember important aspects
of the traumatic event; persistent and exaggerated nega-
tive beliefs about oneself, others, or the world; distorted
cognitions about the cause or consequences of a traumatic
event; a persistent negative emotional state; loss of interest
or participation in significant activities; a sense of detach-
ment or estrangement from others; or an inability to feel
positive emotions such as love or happiness. The fourth
symptom cluster (Criterion E) is characterized by marked
alterations in arousal and reactivity and includes irritable
or angry behavior, reckless or self-​destructive behavior,
impaired concentration and memory, difficulty sleeping,
an exaggerated startle response, and hypervigilance.
Symptoms of PTSD must be present for more than
1 month and cause clinically significant distress or impair-
ment in functioning. In cases in which the full diagnos-
tic criteria for PTSD are not met until at least 6 months
following the traumatic event, a diagnosis of PTSD with
delayed expression is conferred. DSM-​5 criteria for PTSD
also include a diagnostic specifier indicating the presence
or absence of dissociative symptoms (defined as persistent
or recurrent symptoms of depersonalization or derealiza-
tion). In order to be diagnosed with PTSD, an individual
must experience an event that meets the definition of a
Criterion A stressor; endorse at least one symptom from
Criterion B, at least one symptom from Criterion C, at
least two symptoms from Criterion D, and at least two
symptoms from Criterion E; experience the symptoms for
1  month or longer; and experience either clinically sig-
nificant distress or functional impairment resulting from
the symptoms.
In contrast to the DSM-​5 criteria, a substantially nar-
rowed definition of PTSD has been proposed for the 11th
edition of the International Classification of Diseases
(ICD-​11). The PTSD Working Group for ICD-​11 has
selected diagnostic criteria that are assumed to be specific
to PTSD in an effort to improve diagnostic accuracy and
reduce comorbidity (Maercker et  al., 2013). The newly
proposed criteria include six symptoms and require the
presence of at least one re-​experiencing symptom (distress-
ing dreams or dissociative reactions), at least one symp-
tom of avoidance (of internal or external reminders of the
event), and at least one symptom of hyperarousal (exag-
gerated startle response or hypervigilance). Preliminary
research indicates that this narrower definition of PTSD
does not reduce the rates of common comorbidities and
may lead to a substantial reduction in the prevalence of
PTSD compared with both ICD-​10 and DSM-​5, suggest-
ing that the criteria may fail to capture some individu-
als with clinically significant PTSD symptoms (Wisco
et al., 2016).
The physical, emotional, societal, and interpersonal
costs of PTSD are substantial, making PTSD a major
public health issue. Individuals diagnosed with PTSD are
at an increased risk of developing chronic medical con-
ditions (Edmondson, Kronish, Shaffer, Falzon, & Burg,
2013; Wolf et al., 2016) and are more likely to be physi-
cally inactive, smoke, and be nonadherent with medica-
tions (Zen, Whooley, Zhao, & Cohen, 2012). Compared
to individuals in the general population, people with
PTSD are less likely to be married and are more likely to
divorce (Breslau et al., 2011), and they have greater levels
of discord and physical aggression perpetration in their
intimate relationships (Taft, Watkins, Stafford, Street,
& Monson, 2011). PTSD is also associated with unem-
ployment and disability (Desai, Spencer, Gray, & Pilver,
2010; Kimerling et al., 2009), homelessness, and money
mismanagement (Elbogen, Sullivan, Wolfe, Wagner, &
Beckham, 2013).
Epidemiological Evidence
When PTSD was initially conceptualized, both exposure
to traumatic events and the disorder were considered
relatively rare. However, researchers have reported that
exposure to a traumatic event is not uncommon. A recent
study of a nationally representative sample found that
when using the DSM-​5 Criterion A  definition, 68.6%
of adults reported exposure to at least one potentially
traumatic event (Goldstein et  al., 2016). Findings from
prior studies suggest that a trauma can activate PTSD in
individuals who are psychologically vulnerable but that,
fortunately, the majority of people who survive a trau-
matic event will not develop PTSD or any other form of
psychopathology (e.g., depression, anxiety, and substance
abuse disorder). Nonetheless, the likelihood of develop-
ing PTSD increases with repeated exposure to potentially
traumatic events and with exposure to traumatic events

characterized by assaultive violence (Goldstein et  al.,
2016; Kessler et al., 2014), regardless of personal resources
or emotional stability.
The lifetime prevalence of PTSD in the general
population has been estimated to be between 6.8% and
9.5% in epidemiological surveys based on DSM-​IV (APA,
1994)  and DSM-​ IV-​
TR (APA, 2000; Breslau, Davis,
Andreski, & Peterson, 1991; Kessler, Berglund, Demler,
Jin, & Walters, 2005). Women consistently demonstrate
higher lifetime prevalence of PTSD compared to men;
for instance, an analysis of 70,000 adults across 15 coun-
tries revealed the lifetime odds of PTSD to be 2.6 times
higher in women than in men (Seedat et al., 2009). With
the changes made to the diagnostic criteria in DSM-​
5, there has been concern regarding the impact these
changes may have on prevalence (Hoge, 2015). Studies
thus far do show some discordance between the two defi-
nitions (Hoge, Riviere, Wilk, Herrell, & Weathers, 2014);
however, the majority of individuals who meet criteria for
PTSD do so when using both DSM-​IV and DSM-​5 defi-
nitions (e.g., Kilpatrick et al., 2013). Furthermore, most
studies have found very similar prevalence between the
two sets of diagnostic criteria (Elhai & Palmieri, 2011;
Hoge et al., 2014; Kilpatrick et al., 2013).
In the first large-​scale nationally representative survey to
assess DSM-​5-​defined PTSD, the National Epidemiologic
Survey on Alcohol and Related Conditions-​III found a life-
time prevalence of 6.1% (Goldstein et al., 2016), which is
only slightly lower than the 6.8% found using DSM-​IV-​TR
in the National Comorbidity Replication Survey (Kessler
et al., 2005). Head-​to-​head comparisons of the two crite-
ria sets indicate that the slightly lower rates in prevalence
found with DSM-​5 are due to the more restrictive defini-
tion of a traumatic event as well as the requirement of at
least one avoidance symptom (Kilpatrick et al., 2013).
Certain subgroups within the population, including
combatants, are at increased risk for exposure to trauma.
Researchers have examined the impact of war on the psy-
chological functioning of soldiers because deployment,
combat, physical injury, and readjustment to civilian life
can be intensely stressful. The National Vietnam Veterans
Readjustment Study (NVVRS; Kulka et al., 1990) was the
first systematic study of combat-​related PTSD, and its
findings were striking. The authors reported that 64% of
Vietnam veterans were exposed to one or more traumatic
events in their lives. More than 15% of males and 9% of
females serving in Vietnam met the criteria for current
PTSD. More important, these rates were 5 to 10 times
higher than found for Vietnam-​era veteran and civilian
comparison subjects, highlighting the psychological toll
Post-Traumatic Stress Disorder 331
of war. Skeptics, however, have argued that these results
are inflated. In response, Dohrenwend et al. (2006) reana-
lyzed a sample of the NVVRS data and found little evi-
dence of malingering; according to their results, 9.1% of
the veterans met criteria for current PTSD and 18.7% met
criteria for lifetime PTSD when using the most stringent
criteria for confirming traumatic war experiences.
The United States’ involvement in the wars in Iraq and
Afghanistan has placed PTSD in the national spotlight
as reports of soldiers returning from deployment reveal
significant mental health problems, including PTSD.
Studies vary widely in reported prevalence rates. A recent
meta-​analysis involving more than 4.9 million Operation
Iraqi Freedom (OIF) and Operation Enduring Freedom
(OEF) veterans found a prevalence of 23% (Fulton et al.,
2015). This estimate was based largely on studies of OIF/​
OEF veterans enrolled in the Veterans Affairs health
care system; however, prevalence appears to be lower in
population-​based, non-​treatment-​seeking samples, which
include a high proportion of military support person-
nel. A meta-​analysis by Kok, Herrell, Thomas, and Hoge
(2012) of population-​based studies found a lifetime preva-
lence of 5.5% among the larger population of OIF/​OEF
veterans and 13.2% in combat infantry personnel.
When studied as a whole, U.S. veteran samples have
been found to have a slightly higher prevalence of PTSD
relative to community samples. For instance, data from
the National Health and Resilience in Veterans Study
(NHRVS), a nationally representative survey of U.S. vet-
erans, showed lifetime and current prevalence of DSM-​
5-​based probable PTSD of 8.0% and 4.8%, respectively
(Wisco et al., 2014).
Civilians exposed to war or mass violence are also at
risk for developing PTSD. The United Nations reported
that in 2015, 65.3 million people were forcibly displaced
due to violence, persecution, and human rights violations
(United Nations High Commissioner for Refugees, 2016).
A meta-​analysis of studies involving conflict-​affected per-
sons throughout the world found an average prevalence
of PTSD of 31% (Steel et al., 2009). Results also showed
that experiencing torture is strongly related to being diag-
nosed with PTSD. The cumulative nature of potentially
traumatic events was also associated with greater preva-
lence of PTSD, but it was even more strongly related to
major depressive disorder (MDD). Notably, prevalence of
PTSD was significantly lower among those who had per-
manently resettled compared with those living in refugee
camps or other temporary settings (Steel et al., 2009).
Researchers have also examined the psychological
impact of the terrorist attacks that occurred on September
332 Anxiety and Related Disorders
11, 2001. A  recent review of the literature found a high
prevalence of PTSD in the immediate aftermath of the
attacks, particularly among those living in the New York
City area (ranging from 11% to 20%; Neria, DiGrande, &
Adams, 2011). Studies show that the prevalence of PTSD
declined with time in the majority of longitudinal studies
available (Neria et al., 2011) but actually increased over the
course of two studies of highly exposed populations such as
rescue and recovery workers or World Trade Center evacu-
ees (Berninger et al., 2010; Brackbill et al., 2009).
Increases in PTSD prevalence can also be found
in the wake of natural disasters. For example, in 2005,
Hurricane Katrina struck the Gulf Coast, leaving hun-
dreds of thousands of individuals homeless and displaced.
The psychological impact of this disaster was also great,
with prevalence of serious psychological problems essen-
tially doubling from the predisaster levels (Kessler, Galea,
Jones, & Parker, 2006). Similarly, prevalence of PTSD
surpassed 20% among samples of survivors of the 2004 tsu-
nami affecting Sri Lanka, Thailand, India, and Indonesia
(Hollifield et  al., 2008)  and the 2008 earthquake in the
Sichuan province of China (Kun et al., 2009).
Comorbidity
Exposure to a traumatic event is a risk factor not only for
PTSD but also for a number of other mental disorders
and conditions. Goldstein and colleagues (2016) found
that when adjusting for sociodemographic factors, a
DSM-​5 diagnosis of PTSD was associated with increased
likelihood for every mood, anxiety, personality, and sub-
stance use disorder assessed (however, notably, PTSD was
not associated with alcohol use disorder in this study).
Similarly, in a nationally representative epidemiological
survey of U.S. adults using DSM-​IV-​TR criteria, individu-
als with a lifetime diagnosis of PTSD had elevated lifetime
prevalences of mood disorders (62%), anxiety disorders
(59%), and substance or alcohol use disorders (47%;
Pietrzak, Goldstein, Southwick, & Grant, 2011)  com-
pared with individuals in the general population. This
pattern of comorbidity has also been found in veteran
samples; for instance, Wisco and colleagues (2014) found
that lifetime probable PTSD diagnosed using DSM-​5 cri-
teria was associated with increased risk of every psychiatric
disorder assessed (and was most strongly associated with
mood and anxiety disorders). Personality disorders are also
highly comorbid with PTSD; for example, in one DSM-​
IV-​based epidemiological study of U.S.  adults, 24% of
those individuals with PTSD also met diagnostic criteria
for borderline personality disorder (Pagura et al., 2010).
Studies also commonly demonstrate a significant and
robust association between PTSD and suicidal behaviors.
A nationally representative study of U.S. adults found that
individuals with a lifetime diagnosis had an increased like-
lihood of a past suicide attempt (Odds Ratio [OR] = 5.1)
compared to those without PTSD (Pietrzak et al., 2011).
Similarly, the NHRVS survey of U.S. veterans found ele-
vated risk of past suicide attempts (OR = 11.8) and current
suicidal ideation (OR = 9.7) in those with probable life-
time PTSD (Wisco et al., 2014). In addition, the presence
of comorbid conditions amplifies suicide risk in individu-
als with PTSD (Gradus et al., 2010; Jakupcak et al., 2009;
Oquendo et  al., 2003). PTSD and its associated psychi-
atric comorbidities (e.g., MDD) are characterized by or
found to be associated with key aspects of the established
psychological theories of suicidal behavior (O’Connor &
Nock, 2014), including difficulties problem solving and
coping (Guerreiro et al., 2013), memory and attentional
biases (Cha, Najmi, Park, Finn, & Nock, 2010), and
social isolation (Haw & Hawton, 2011). Empirical studies
also suggest that PTSD may be one of a group of disorders
that provides the necessary activation and energy to move
from a state of contemplating suicide to one of acting on
suicidal thoughts, putting together a suicide plan, and
making preparations to die by suicide (Nock et al., 2009).
Traumatic brain injury (TBI) is also highly comorbid
with PTSD in veterans returning from recent conflicts in
Iraq and Afghanistan. TBI and PTSD are considered to be
the “signature injuries” of these conflicts, and more than
340,000 veterans have been diagnosed with some form of
TBI, most often mild TBI (mTBI), since 2000 (Defense
and Veteran Brain Injury Center, 2016). Studies show that
veterans experiencing mTBI are more likely to suffer from
PTSD (Hoge et al., 2008; Schneiderman, Braver, & Kang,
2008), and one recent prospective study found that TBI
during the most recent deployment was the strongest pre-
dictor of the development of PTSD, even when account-
ing for combat intensity, pre-​deployment symptoms, and
previous TBI (Yurgil et al., 2014). Furthermore, the asso-
ciation between the two disorders remains even when
accounting for overlapping symptoms (e.g., insomnia,
anger, and difficulty concentrating; Schneiderman et al.,
2008). Veterans comorbid for mTBI and PTSD also often
experience more severe PTSD symptoms (Spira, Lathan,
Bleiberg, & Tsao, 2014), and one prospective study of
U.S. Army soldiers found that PTSD, but not TBI, was
significantly associated with decrements in neuropsycho-
logical performance (Vasterling et al., 2012). Due to the
overlapping symptom profiles between these conditions,
they require careful assessment. Even with thorough

clinical interviewing and the use of standardized diagnos-
tic measures for assessment of PTSD, it may be difficult
to arrive at a clear conclusion regarding the etiological
source of post-​ concussive symptoms (Hoge, Goldberg,
& Castro, 2009). For a comprehensive discussion of the
interaction of PTSD and mTBI, see Vasterling, Bryant,
and Keane (2012).
The presence of one or multiple comorbid condi-
tions with PTSD can complicate the assessment process.
The overlap among symptoms of PTSD with conditions
such as MDD, mTBI, substance use disorders, and anxi-
ety disorders requires thorough assessment in order to
accurately attribute an individual’s symptoms to a spe-
cific disorder. A comprehensive discussion of assessment
measures of comorbid conditions is beyond the scope
of this chapter, although we note the importance of
screening for the most common co-​occurring disorders,
at a minimum, during the diagnostic assessment process,
because treatment of PTSD often is more effective when
the comorbid conditions are also addressed (e.g., Shalev,
Friedman, Foa, & Keane, 2000). Comprehensive diag-
nostic assessment measures, such as a structured or semi-​
structured diagnostic interview, facilitate identification
and diagnosis of comorbid conditions that can be incor-
porated into the therapeutic plan. We note that rigorous
assessment and ongoing monitoring of substance use
disorders is extremely important in planning for trauma-​
focused treatment; if an individual is using substances
to self-​medicate for PTSD symptoms, that individual
might be at greater risk for increased substance misuse in
response to distress related to therapy content or process.
See the chapters on substance abuse (Chapter  17) and
depression (Chapter  7) in this volume for a more thor-
ough discussion on how to efficiently assess these condi-
tions when they occur.
In addition, the strong salience of PTSD symptoms,
such as nightmares or flashbacks, may also lead clinicians
to overlook the presence of additional disorders that may
be important for case conceptualization and targeting in
treatment. Furthermore, the lack of comprehensive assess-
ment of comorbidities may also lead to misspecification of
treatment targets. Although current guidelines for PTSD
generally recommend treating PTSD and psychiatric
comorbidities concurrently, first-​ line PTSD treatments
may need to be delayed or referral to specialty care may
be necessary for individuals with high levels of suicidal-
ity or severe co-​occurring disorders (e.g., severe substance
use disorders and psychotic disorders; U.S. Department of
Veterans Affairs/​U.S. Department of Defense [VA/​DOD]
Management of Post-​Traumatic Stress Working Group,
Post-Traumatic Stress Disorder 333
2010). Thus, a sound understanding of these co-​occurring
psychiatric conditions and their manifestation in the pres-
ence of PTSD is essential when working with members of
this patient population.
Etiology
PTSD emerges from a complex chain of events that
begins with psychological and biological predispositions
and follows a precipitating traumatic event that leaves an
individual with intense and distressing emotions (Keane
& Barlow, 2002; Keane, Marshall, & Taft, 2006). Early
theories of the development and maintenance of PTSD
focused on the application of classical conditioning prin-
ciples (Keane, Fairbank, Caddell, Zimering, & Bender,
1985). In this model, the individual develops a learned
emotional response in the wake of a traumatic event. This
learned response is activated during exposure to situations
that symbolize or resemble the traumatic event, including
cognitions, feelings, and memories of the actual traumatic
event. More recent theories of PTSD have incorporated
individuals’ cognitive interpretations of the trauma, as
well as preexisting beliefs about one’s own competence
and safety (Foa & Rothbaum, 1998). For example, Ehlers
and Clark (2000) discussed the role of negative appraisals
related to the trauma and posited that PTSD results from
the lack of integration of trauma memories with autobio-
graphical information. Brewin and colleagues (Brewin,
Dalgleish, & Joseph, 1996; Brewin, Gregory, Lipton, &
Burgess, 2010) added to this by incorporating neurocog-
nitive aspects of memory into Ehlers and Clark’s theory.
They proposed two types of memory: situationally acces-
sible memories (SAM), which are not verbally accessible
and cannot be consciously remembered, and verbally
accessible memories (VAM), which resemble declarative
memories and can be consciously remembered. Brewin
and colleagues have suggested that traumatic memories
are largely stored in SAM and are therefore difficult to
integrate. In addition to the difficulty integrating the
trauma memory with one’s autobiographical memory out-
lined by Ehlers and Clark and also Brewin and colleagues
(1996, 2010), other factors can contribute to the develop-
ment of PTSD. For example, psychological and biologi-
cal vulnerabilities (e.g., family history of psychopathology,
previous trauma history, and genetic factors), poor coping
skills, and/​or inadequate social supports can all contribute
to the development of the disorder. For a more compre-
hensive review of the theories of PTSD, see Green, Marx,
and Keane (2017) or Bovin, Wells, Rasmusson, Hayes,
and Resick (2014).
334 Anxiety and Related Disorders
Treatment and Prognosis
Treatment programs to address symptoms of PTSD were
developed in response to the influx of returning Vietnam
veterans and rape survivors with psychological difficulties.
Early strategies were based on the conceptualization of
PTSD as a disorder arising from classical conditioning,
and therefore targeted avoidance and involved direct
therapeutic exposure to the traumatic memory (Fairbank
& Keane, 1982; Keane & Kaloupek, 1982; Keane et al.,
1985, 1989). As treatment strategies have evolved with
time, exposure to the trauma memory remains a com-
mon element across several psychotherapies for PTSD.
Currently, the most widely studied and recommended
treatments for PTSD are two cognitive–​ behavioral
approaches:  cognitive processing therapy (CPT) and
prolonged exposure therapy (PE). These treatments are
recommended as first-​line therapies in practice guide-
lines issued by the Institute of Medicine (2008), the
International Society for Traumatic Stress Studies (Foa,
Keane, Friedman, & Cohen, 2008), and the VA/​DOD
(2010). Research suggests that CPT and PE yield large
effects relative to control conditions (Chard, 2005; Forbes
et  al., 2012; Powers, Halpern, Ferenschak, Gillihan, &
Foa, 2010). Furthermore, these treatments have been
shown to be efficacious across a range of populations
with comorbid conditions including mTBI, MDD, and
substance use disorders (Kaysen et al., 2014; van Minnen,
Zoellner, Harned, & Mills, 2015). Yet despite their prom-
ise, a substantial proportion of individuals who complete
PE and CPT continue to experience clinically significant
symptoms, particularly veterans and active duty service
members (Steenkamp, Litz, Hoge, & Marmar, 2015).
Furthermore, high rates of attrition prevent many from
receiving a full course of treatment for PTSD across ther-
apeutic modalities (Imel, Laska, Jakupcak, & Simpson,
2013). These limitations speak to the importance of
developing and evaluating alternative treatment options
to CPT and PE, such as Seeking Safety (Najavits, 2002),
which addresses symptoms of PTSD and substance use
simultaneously, or Written Exposure Therapy (Sloan,
Marx, Bovin, Feinstein, & Gallagher, 2012), which uses
an abbreviated written disclosure protocol.
In terms of prognosis, the clinical course of PTSD is
highly variable, but for many, the disorder is a chronic
condition. In a large meta-​analysis of more than 80,000
patients with PTSD, spontaneous remission occurred
within 40 months of the index trauma in less than half of
cases (Morina, Whicherts, Lobbrecht, & Priebe, 2014).
Similarly, a review of longitudinal studies of PTSD found
that approximately 40% of individuals experienced a
chronic course (Santiago et al., 2013). Research examin-
ing the trajectories of PTSD symptoms over time suggests
that a number of risk factors, patient characteristics, and
treatment-​related variables may contribute to the varia-
tion in course and chronicity (Dickstein, Suvak, Litz, &
Adler, 2010; Orcutt, Bonanno, Hannan, & Miron, 2014).
Factors that may contribute to the chronic course of
PTSD include low rates of treatment seeking and a delay
in obtaining treatment; in one recent epidemiologi-
cal survey, 60% of participants with a lifetime diagnosis
had received treatment, and the average length of time
between the traumatic event and treatment was 4.5 years
(Goldstein et al., 2016).
ASSESSMENT OF PTSD
Since the first mention of PTSD in the DSM, there has
been excellent progress in developing sound measures to
assess trauma symptoms and PTSD in adults (Keane &
Barlow, 2002; Keane, Weathers, & Foa, 2000; Weathers,
Keane, & Davidson, 2001). Given the limitations of any
single assessment measure, a comprehensive assessment
of PTSD should use a multimethod approach (Bovin,
Marx, & Schnurr, 2015; Weathers, Keane, & Foa, 2009),
which may include use of a structured or semi-​structured
diagnostic interview to assess PTSD and other psychi-
atric comorbidities, self-​report measures of symptom
severity and psychosocial functioning, examination of
medical records and collateral source information, and
assessment of psychophysiological reactivity. Practice
guidelines issued by both the VA/​DOD (2010) and the
International Society for Traumatic Stress Studies (Foa
et al., 2008) present recommendations for assessment of
PTSD in detail, with both encouraging the use of multi-
method assessment that includes psychometrically sound
structured or semi-​structured interviews and self-​report
measures.
Multimethod approaches to PTSD assessment may
not be feasible for many clinicians. Therefore, when
selecting PTSD assessment instruments, it is especially
important that clinicians consider the specific assessment
questions and goals. The objective of many clinicians is
to diagnose a patient by conducting an evaluation that
includes a differential diagnosis, a functional assessment,
and the collection of other related data that can be helpful
in case conceptualization, as well as treatment planning.
Other practitioners may be involved in forensic assess-
ments or compensation evaluations in which diagnostic

accuracy is paramount. Researchers involved in epide-
miological or prevalence studies may be interested in the
extent to which PTSD is diagnosed among study partici-
pants, the risk factors associated with the condition, and
the occurrence of comorbid psychiatric conditions. These
different assessment contexts require different assessment
approaches.
In this chapter, we provide an overview of some of
the most commonly used diagnostic interviews and self-​
report measures for the assessment of PTSD, and we
review their utility for diagnostic purposes, case conceptu-
alization, treatment planning, and treatment monitoring
and outcome. Structured and semi-​structured diagnos-
tic interviews are considered to be the gold standard for
diagnosing PTSD and should be used whenever possible,
particularly when assessing diagnostic status. The struc-
tured nature of the interview ensures a higher degree of
clinical accuracy and reliability, whereas flexibility allows
for the use of clarifying and follow-​up questions, which
will lessen misinterpretation of questions by respondents
or minimization or exaggeration in reporting. Self-​report
measures provide information on the presence or absence
of PTSD and the severity of PTSD symptoms. Several
measures provide specific cut-​offs that are indicative of a
diagnosis of PTSD, whereas the majority incorporate con-
tinuous indicators of symptom severity. In general, self-​
report measures are more time-​and cost-​efficient than
diagnostic interviews and are of particular utility in clini-
cal settings in which a structured interview is not feasible
or practical. However, the validity of the data captured
by these measures depends on the extent to which the
patient understands and answers the questions accurately
(Bovin, Marx, & Schnurr, 2015).
Assessment instruments reflecting the updated PTSD
diagnostic criteria are in varying stages of development and
psychometric testing. The evidence base for DSM-​5 com-
mensurate measures is still relatively limited compared
with the wealth of data available for many DSM-​IV-​based
assessment tools. This may pose a challenge for clinicians
seeking to select measures that are grounded in current
definitions of PTSD and also have a strong evidence base.
Throughout the remainder of this chapter, we describe
the state of the research on DSM-​5-​based assessment tools
for PTSD; however, we expect that psychometric support
for many of the DSM-​5 measures presented here will
expand rapidly in the next few years.
As scientific advances have strengthened the biologi-
cal understanding of PTSD, an increasing focus has been
placed on using this knowledge to inform assessment.
Post-Traumatic Stress Disorder 335
Before discussing more traditional methods used to assess
and diagnose PTSD, we briefly consider the role of bio-
logically based assessment techniques.
Biologically Based Assessment of PTSD
During the past 20 years, research on biologically based
measures of PTSD has established a foundation for a
psychobiological description of PTSD. A  substantial
literature on the psychophysiology of PTSD has devel-
oped, utilizing measures of heart rate, skin conductance,
event-​ related potentials, electromyography reactivity,
and other biological indicators (for a review, see Pitman
et al., 2012). Results of a meta-​analysis of more than 1,000
adults with PTSD suggest the disorder is characterized by
a heightened resting physiological state, strong physiologi-
cal and emotional reactivity to general and idiographic
trauma cues, and exaggerated startle response (Pole,
2007). Although psychophysiological assessment can pro-
vide unique information, widespread use of this approach
in a clinical environment is not anticipated because it is
expensive and requires equipment and specialized train-
ing. In the majority of cases, more time-​and cost-​efficient
methods of assessment, such as diagnostic interviews or
self-​report measures, are more than adequate. Research
also indicates that individuals with PTSD report their
physiological arousal response to trauma-​ related cues
with relative accuracy, as evidenced by a significant asso-
ciation between subjective distress ratings and physiologi-
cal measures of skin conductance and heart rate (Marx
et  al., 2012). Because psychophysiological methods are
not accessible to the majority of clinicians, we do not dis-
cuss these methods in detail in this chapter. We refer the
interested reader to Orr, Metzger, Miller, and Kaloupek
(2004) for an excellent review.
Efforts are also underway to understand the neural
correlates of PTSD. Researchers have found PTSD to be
associated with alterations in both structure and function
in areas of the brain associated with emotional reactivity,
fear conditioning, emotion regulation, and episodic mem-
ory (for a detailed review, see Pitman et al., 2012). PTSD
is also characterized by changes in a range of other physi-
ological functions, such as hypothalamic–​pituitary axis
functioning and pro-​inflammatory immune response (also
reviewed by Pitman et al., 2012). As understanding of the
neurobiology of PTSD increases, efforts are being made
to identify biomarkers that might aid in more objective
assessment of PTSD. Promising results include the recent
use of resting-​state functional neuroimaging to distinguish
336 Anxiety and Related Disorders

TABLE 16.1   Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

CAPS-​IV E E E E E E E E ✓
CAPS-​5 A G E A E E A A ✓a
SCID-​IV E E A A G G E G ✓
SCID-​5 NR NR G NR G NR NR A ✓a
PSS-​I-​IV G G E G G G G G
PSSI-​5 G G G A G G G A
ADIS-​IV G G G A G G G G
ADIS-​5 NR NR NR NR G NR NR A
CIDI E NR E A G G E NA
IES-​R G G NA A G G G G
Mississippi E E NA G E E G G
PDS-​IV E E NA G G E E G ✓b
PDS-​5 G E NA A G G G A ✓a
PCL-​IV G E NA G G E E G ✓b
PCL-​5 A E NA A G G A A ✓a

a
 Limited data available for these measures; recommendations have been made tentatively based on available data and the strong psychometric support
for previous versions of these measures.
  Self-​report measures used as diagnostic instruments should include explicit assessment of the Criterion A event in addition to assessment of current
b

DSM-​5 symptoms.
Note: CAPS-​IV = Clinician-​Administered PTSD Scale for DSM-​IV; CAPS-​5 = Clinician-​Administered PTSD Scale for DSM-​5; SCID-​IV = Structured
Clinical Interview for DSM-​IV; SCID-​5 = Structured Clinical Interview for DSM-​5; PSS-​I-​IV = PTSD Symptom Scale Interview for DSM-​IV; PSSI-​
5 = PTSD Symptom Scale Interview for DSM-​5; ADIS-​IV = Anxiety Disorders Interview Schedule for DSM-​IV; ADIS-​5 = Anxiety Disorders Interview
Schedule for DSM-​5; CIDI = Composite International Diagnostic Interview; IES-​R = Impact of Event Scale-​Revised; Mississippi = Mississippi Scale for
Combat-​Related PTSD; PDS-​IV = Posttraumatic Diagnostic Scale for DSM-​IV; PDS-​5 = Posttraumatic Diagnostic Scale for DSM-​5; PCL-​IV = PTSD
Checklist for DSM-​IV; PCL-​5 = PTSD Checklist for DSM-​5; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

between PTSD and trauma-​exposed control cases with
more than 90% specificity and sensitivity (Christova,
James, Engdahl, Lewis, & Georgopoulos, 2015). Yet given
the complex and heterogeneous nature of the disorder, it
may be unlikely that a single biomarker of PTSD exists,
and current methods do not demonstrate the necessary
levels of accuracy to function as stand-​alone diagnostic
tests. For a comprehensive review of these issues, see
Michopoulos, Norrholm, and Jovanovic (2015).
diagnostic purposes, commenting on their comprehen-
siveness, their utility within a clinical context, and their
psychometric properties in the subsequent text. We do
not provide a comprehensive review of all available instru-
ments; rather, we highlight a select few based on the rela-
tive frequency with which they are used in the field. Table
16.1 contains ratings of those instruments currently avail-
able for making diagnoses of PTSD.
Structured Diagnostic Interviews

ASSESSMENT FOR DIAGNOSIS
Clinician-​Administered PTSD Scale

It is fundamental to case conceptualization and treat-
ment planning for clinicians to determine the appropri-
ate psychological diagnosis or diagnoses for their patients.
Paramount to a diagnosis of PTSD is the clear identifica-
tion of a Criterion A  event, to which subsequent symp-
toms are linked. Therefore, when selecting diagnostic
measures, clinicians should consider whether or not the
measure assesses the presence of a traumatic event, in
addition to ensuring that the measure is psychometri-
cally sound. We review methods of assessing PTSD for
Developed by the National Center for PTSD (Blake et al.,
1990; Weathers et al., 2013), the Clinician-​Administered
PTSD Scale (CAPS) is one of the most widely used struc-
tured interviews for diagnosing and measuring the severity
of PTSD (Weathers et al., 2001). The CAPS was initially
developed for DSM-​ IV, and an updated version (i.e.,
CAPS-​5) was developed for DSM-​5 in 2013. The CAPS
for DSM-​IV assesses all 17 DSM-​IV diagnostic criteria for
PTSD, as well as the associated symptoms of guilt and dis-
sociation. The CAPS-​5 assesses all 20 DSM-​5 diagnostic

criteria, as well as the associated dissociative symptoms of
derealization and depersonalization. The CAPS for DSM-​
IV contains separate ratings for the frequency and inten-
sity of each symptom. On the CAPS-​5, frequency and
intensity are still assessed, although they are combined
for one overall severity score for each item. Both older
and newer versions of the CAPS also promote uniform
administration and scoring through carefully phrased
prompt questions and explicit rating scale anchors with
clear behavioral referents. There is also flexibility built
into the administration of the CAPS. Interviewers can
administer all DSM criteria and/​or the associated symp-
toms. Administration time is approximately 30 minutes
to 1 hour, depending on those sections the interviewer
chooses to use, as well as the extent to which symptoms are
reported by the respondent. The CAPS-​5 has past week,
past month, and worst month (i.e., lifetime) versions.
The CAPS for DSM-​IV has excellent psychometric
properties (for a review, see Weathers et  al., 2001)  and
has been used successfully to assess PTSD with a wide
variety of trauma-​exposed samples (e.g., combat veterans,
Cambodian and Bosnian refugees, and victims of rape,
crime, motor vehicle accidents, incest, the Holocaust,
torture, and cancer). It has served as the primary diagnos-
tic or outcome measure in hundreds of empirical studies
on PTSD, and it has been translated into at least 12 lan-
guages (Hinton et al., 2006; Weathers et al., 2001). Thus,
the existing data strongly support its use across clinical
and research settings.
The CAPS-​5 has also demonstrated strong psycho-
metric properties in an initial study. Weathers and col-
leagues (2017) examined the psychometric properties of
the CAPS-​5 in two samples of military veterans and found
that diagnosis of PTSD on the CAPS-​5 demonstrated
excellent inter-​ rater reliability, test–​
retest reliability, as
well as strong agreement with PTSD diagnosis using
the CAPS for DSM-​IV. Furthermore, CAPS-​5 severity
scores demonstrated strong inter-​ rater reliability, inter-
nal consistency, and test–​retest reliability. In addition,
the CAPS-​5 showed good convergent validity with the
CAPS-​IV and the PTSD Checklist for DSM-​5 (PCL-​
5; Weathers et  al., 2013), as well as discriminant valid-
ity with measures of functional impairment (Inventory
of Psychosocial Functioning:  Marx et  al., 2009; World
Health Organization Disability Assessment Schedule
2.0:  Ustün, Kostanjsek, Chatterji, & Rehm, 2010), psy-
chopathy (Psychopathic Personality Inventory-​ Short
Version:  Lilienfeld & Andrews, 1996), and depression
(Patient Health Questionnaire:  Spitzer et  al., 1999).
Although these data support the use of the CAPS-​5 as a
Post-Traumatic Stress Disorder 337
psychometrically sound measure of PTSD symptomatol-
ogy, more work with other trauma-​exposed samples is
needed to further validate it.
Structured Clinical Interview for DSM-​5
The Structured Clinical Interview for DSM-​5 (SCID-​5;
First, Williams, Karg, & Spitzer, 2015)  assesses a broad
range of current and lifetime psychiatric conditions. It is
divided into separate modules corresponding to DSM-​5
diagnostic criteria, with each module providing the inter-
viewer with prompts and follow-​up inquiries intended
to be read verbatim to respondents. The SCID-​5 can be
administered by clinicians and highly trained interview-
ers. Although the administration of the full SCID-​5 can
be time-​consuming, the modular structure allows clini-
cians to tailor their assessment appropriately. Within the
context of a trauma clinic, it is recommended that the
anxiety disorders, affective disorders, and substance use
disorder modules be administered to rule out any comor-
bid diagnoses. Administration of the psychotic symptom
screen will also help rule out psychiatric conditions that
require a different set of treatment interventions (Keane
& Barlow, 2002).
Previous versions of SCID-​PTSD module (e.g., First,
Spitzer, Williams, & Gibbon, 2000), based on earlier ver-
sions of the DSM, are considered psychometrically sound.
Keane et al. (1998) reported that the SCID-​PTSD mod-
ule had adequate reliability, and McFall, Smith, Roszell,
Tarver, and Malas (1990) reported evidence of conver-
gent validity, finding significant correlations between the
SCID-​PTSD and other measures of PTSD, including the
Mississippi Scale (Keane et al., 1988) and the Minnesota
Multiphasic Personality Inventory (MMPI)-​PTSD Scale
(Keane, Malloy, & Fairbank, 1984). Earlier versions of the
SCID-​PTSD module also show strong convergent valid-
ity with the CAPS; for instance, the number of positive
symptoms assessed by the SCID-​IV PTSD module cor-
related with CAPS for DSM-​IV scores at r = .89 in one
study (Weathers et al., 2001). The SCID-​PTSD module
also had good diagnostic utility (Kulka et al., 1988).
Due to its recent publication, little has been pub-
lished on the psychometric properties of the SCID-​
5 PTSD module. Preliminary results indicate a high
degree of inter-​rater reliability (κ = .82; Wolf et al., 2016).
Although the SCID is a good diagnostic tool, it has some
important limitations. For example, the SCID does not
provide specific questions to the assessor to ask the respon-
dent about symptom frequency or intensity. In addition,
the SCID symptom ratings of “absent,” “present,” and
338 Anxiety and Related Disorders

“subthreshold” provide relatively limited information Schedule-​ Revised (ADIS) was designed to permit dif-
about symptom severity in comparison to interviews such ferential diagnoses among the DSM-​III anxiety disorder
as the CAPS-​5 or the PTSD Symptom Scale Interview. categories. The interview was revised to correspond to
DSM-​IV criteria (ADIS-​IV; DiNardo, Brown, & Barlow,
1994) and, recently, to DSM-​5 criteria (ADIS-​5; Brown &
PTSD Symptom Scale Interview
Barlow, 2014). The ADIS also includes an assessment of
Developed by Foa, Riggs, Dancu, and Rothbaum (1993), affective disorders, substance use disorders, and selected
the PTSD Symptom Scale Interview (PSS-​I) is a struc- somatoform disorders; a diagnostic timeline; and a dimen-
tured interview designed to assess symptoms of PTSD. Foa sional assessment of the key and associated features of
and colleagues (2016) then developed an updated version the disorders. The provision of a dimensional as well as
corresponding to DSM-​5 (i.e., PSSI-​5). Using a Likert a categorical assessment allows the clinician to describe
scale, interviewers rate the severity of 17 symptoms corre- subthreshold manifestations of each disorder, thus allow-
sponding to the DSM-​III-​R (APA, 1987) criteria for PTSD ing for better case conceptualization. In addition to being
for the PSS-​I and the 20 symptoms corresponding to the updated to DSM-​5 criteria, the PTSD module of the
DSM-​5 criteria for PTSD for the PSSI-​5. One limitation ADIS-​5 allows for the nature of the traumatic event to
of the PSS-​I is that it measures symptoms during the past 2 be assessed and coded more extensively than in previous
weeks rather than 1 month, which the DSM criteria spec- versions.
ify as necessary for a diagnosis of PTSD (Cusack, Falsetti, Results from psychometric studies of the ADIS-​PTSD
& de Arellano, 2002); however, the PSSI-​5 assesses the module are mixed. Originally tested in a small sample
past month. The PSS-​I is brief (administration time is of Vietnam combat veterans, the ADIS-​PTSD module
approximately 20 minutes) and may be administered by lay yielded strong agreement with interview-​ determined
interviewers who are trained to work with trauma patients. diagnoses (Blanchard, Gerardi, Kolb, & Barlow, 1986).
The PSS-​I was originally tested in a sample of women with However, DiNardo, Moras, Barlow, Rapee, and Brown
a history of rape and nonsexual assault, and the resulting (1993) tested the reliability of the ADIS in a commu-
scores were found to have good internal consistency, test–​ nity sample recruited from an anxiety disorders clinic
retest reliability during a 1-​month period, and inter-​rater and found only adequate agreement between two inde-
agreement for a PTSD diagnosis (Foa et  al., 1993). The pendent raters when PTSD was the principal diagnosis
PSS-​I scores are significantly correlated with other mea- or an additional diagnosis. In a test of the ADIS-​IV, the
sures of traumatic stress, such as the Impact of Events inter-​rater reliability across two interviews given 10  days
Intrusion score (Horowitz, Wilner, & Alvarez, 1979) and apart was also fair for current diagnoses (Brown, DiNardo,
the Rape Aftermath Symptom Test total score (Kilpatrick, Lehman, & Campbell, 2001)  but slightly improved for
1988). In addition, the scores have demonstrated good lifetime diagnoses. Psychometric analyses of the ADIS-​5
diagnostic utility compared to a SCID-​PTSD diagnosis. (including the PTSD module) are underway, but results
The PSSI-​5 was tested in samples of urban community are not yet available. Provision of additional reliability and
residents, undergraduates, and veterans, and its scores validity data on the ADIS-​5 is needed to ensure its contin-
were also found to have good internal consistency, test–​ ued use in clinical settings.
retest reliability, and excellent inter-​rater reliability (Foa
et  al., 2016). PSSI-​5 scores correlated significantly with
Composite International Diagnostic Interview
the CAPS-​5, the Posttraumatic Diagnostic Scale for DSM-​
5 (Foa et  al., 2016), and the PTSD Checklist–​Specific The World Health Organization (WHO) Composite
Version (Weathers, Litz, Herman, Huska, & Keane, 1993), International Diagnostic Interview (CIDI, version 3.0;
and they demonstrated discriminant validity with the Beck Kessler & Üstün, 2004) was developed for epidemiological
Depression Inventory-​II (Beck, Brown, & Steer, 1996) and purposes. Specifically, the CIDI has been used to assess a
the Trait subscale of the State–​Trait Anxiety Inventory​ variety of mental health disorders in the WHO World
(Spielberger, Gorsuch, Lushene, Vagg, & Jacobs, 1983). Mental Health Survey Initiative (Kessler et  al., 2007).
When originally developed, it was a semi-​ structured
interview that mapped on to DSM-​IV PTSD criteria. It
Anxiety Disorders Interview Schedule for DSM-​5
assesses whether diagnostic criteria are satisfied (yes/​no),
Developed by DiNardo, O’Brien, Barlow, Waddell, and it has been translated into many languages. The CIDI
and Blanchard (1983), the Anxiety Disorders Interview has demonstrated excellent inter-​rater reliability and good

test–​retest reliability (Andrews & Peters, 1998), although
there has been moderate support for its use as a PTSD
diagnostic instrument (Breslau, Kessler, & Peterson, 1998;
Haro et al., 2006). Kimerling and colleagues (2014) com-
pared the CIDI with the CAPS on both past year and life-
time PTSD diagnoses in a sample of female veterans and
found that the CIDI has good diagnostic utility. However,
the high specificity and low sensitivity of the measure indi-
cated that the CIDI tends to be very conservative when
identifying lifetime PTSD.
Self-​Report Measures
Impact of Event Scale-​Revised
Developed by Horowitz et al. (1979), the Impact of Event
Scale (IES) was one of the first self-​report measures devel-
oped to assess symptoms of PTSD. The initial 15-​item
questionnaire, which focused only on intrusion and avoid-
ance symptoms, was derived from a model of traumatic
stress developed by Horowitz (1976). A  revised 22-​item
version was developed to include all the DSM-​IV criteria
(IES-​R; Weiss & Marmar, 1997). Respondents complete
the measure by rating on a Likert scale “how distressed
or bothered” they were by each symptom during the past
week. The IES has been translated into several languages,
has been used with many different trauma populations,
and takes 5 to 10 minute to complete.
Support for the internal consistency and convergent
validity of the IES-​R scores is strong across diverse sam-
ples, including emergency response personnel, earth-
quake and motor vehicle accident survivors, and Vietnam
combat veterans (Beck et  al., 2008; Creamer, Bell, &
Failla, 2003; Weiss & Marmar, 1997). IES-​R scores have
correlated significantly with other well-​established mea-
sures, such as the CAPS and the PTSD Symptom Scale
Self-​Report (Beck et al., 2008, Rash, Coffey, Baschnagel,
Drobes, & Saladin, 2008). Notably, test–​retest reliability
data are available for only two samples (Adkins, Weathers,
McDevitt-​Murphy, & Daniels, 2008; Weiss & Marmar,
1997). Results from these studies show discrepant reliabil-
ity coefficients.
Although the IES-​R was not originally intended for
use as a diagnostic tool, a number of studies employed it
in this capacity. Results from these studies suggested good
sensitivity and specificity, but data suggest a potential for
overdiagnosis of PTSD using common cut-​off scores. For
instance, Morina, Ehring, and Priebe (2013) found that
although a cut-​off score of 34 led to identification of 89%
of PTSD cases in the sample, 45% of individuals who
Post-Traumatic Stress Disorder 339
scored above this cut-​point did not actually meet diagnos-
tic criteria for PTSD according to a semi-​structured inter-
view. Although the items on the scale parallel the DSM-​IV
symptom criteria, it does not fully map on to the DSM-​IV
PTSD criteria because, like other PTSD self-​report mea-
sures, it does not assess traumatic stress exposure, symptom
duration, and clinical significance (i.e., symptom-​related
distress and/​or impairment). Undoubtedly, these diagnos-
tic criteria omissions are, at least in part, responsible for
the higher than expected PTSD prevalence when using
this scale. As such, this and other similar self-​report PTSD
symptom scales should not be used to determine a diag-
nosis of PTSD. The IES-​R has not been updated to reflect
the DSM-​5 PTSD criteria.
Mississippi Scale for Combat-​Related PTSD
Developed by Keane et al. (1988), the 35-​item Mississippi
Scale is widely used to assess combat-​related PTSD symp-
toms. The scale items were selected from an initial pool
of 200 items generated by experts to match the DSM-​III
criteria for the disorder. Respondents are asked to rate,
on a Likert scale, the severity of symptoms over the time
period occurring “since the event.” The Mississippi Scale
yields a continuous score of symptom severity as well as
diagnostic information. It is available in several languages
and takes 10 to 15 minutes to administer. Although 4 addi-
tional items were later added to the scale to reflect addi-
tional DSM-​III-​R symptoms, the original 35-​item version
is frequently used because the two scales have performed
comparably (Lauterbach, Vrana, King, & King, 1997).
The Mississippi Scale has excellent psychometric
properties. In Vietnam-​ era veterans seeking treatment,
Keane et al. (1988) reported high internal consistency and
test–​retest reliability during a 1-​week time interval. In a
subsequent validation study, the authors found an overall
hit rate of 90% when the scale was used to differentiate
between a PTSD group and two non-​PTSD comparison
groups. McFall, Smith, Mackay, and Tarver (1990) repli-
cated these findings and further demonstrated that PTSD
patients with and without substance use disorders did not
differ on the Mississippi Scale. Given the high comor-
bidity between PTSD and substance use disorders, the
authors believed it was important to demonstrate that the
test assesses PTSD symptoms rather than effects associ-
ated with alcohol and drug use. McFall, Smith, Mackay,
et  al. also obtained information on convergent validity,
finding significant correlations between the Mississippi
Scale and other measures of PTSD, including the total
number of SCID-​PTSD symptoms, total IES score, and
340 Anxiety and Related Disorders
degree of traumatic combat exposure on the Vietnam Era
Stress Inventory (Wilson & Krauss, 1984). These findings
suggest that the Mississippi Scale is a valuable self-​report
tool in settings in which assessment of combat-​related
PTSD is needed.
Relatively recently, Orazem, Charney, and Keane
(2006) examined the psychometric properties of the
Mississippi Scale in more than 1,200 cases of Vietnam
War veterans participating in a multisite study of the
psychophysiology of PTSD (Keane et al., 1998). Results
indicated that scores on the Mississippi Scale possessed
excellent internal consistency and were highly correlated
with the Keane PTSD Scale of the MMPI-​2. Using the
SCID-​ PTSD module as the diagnostic gold standard,
the Mississippi Scale possessed excellent diagnostic util-
ity, suggesting strong support for the use of this test when
assessing combat-​related PTSD.
Notably, several variations of the Mississippi Scale are
available, including a brief 10-​item version (Hyer, Davis,
Boudewyns, & Woods, 1991), a modified scale for civil-
ians (the Revised Civilian Mississippi Scale; Lauterbach
et al.,1997), and an informant-​report version for partners
(Taft, King, King, Leskin, & Riggs, 1999).
Posttraumatic Diagnostic Scale
Developed by Foa et  al. (1997), the Posttraumatic
Diagnostic Scale (PDS) is a 49-​item scale designed to
measure DSM-​IV PTSD criteria and symptom severity.
Foa and colleagues (2016) then developed an updated
version of the PDS to correspond to DSM-​5 PTSD cri-
teria (i.e., PDS-​5). The PDS reviews trauma exposure
and identifies the most distressing trauma. It also assesses
all DSM-​5 criteria for PTSD distress and interference of
PTSD symptoms, and onset and duration of symptoms.
This measure has been used with numerous samples,
including combat veterans, accident victims, and sexual
and nonsexual assault survivors, and it has been validated
in other languages (e.g., German: Griesel, Wessa, & Flor,
2006). The PDS can be completed in 10 to 15 minutes.
The psychometric properties of the PDS for DSM-​
IV were evaluated among 264 volunteers recruited from
several PTSD treatment centers as well as from non-​
treatment-​ seeking populations at high risk for trauma
(Foa et  al., 1997). Investigators reported high internal
consistency for the PTSD total score and subscales and
adequate test–​retest reliability coefficients for the total
PDS score and for the symptom cluster scores. With
regard to validity, the PDS total score correlated highly
with other scales that measure PTSD symptoms, such
as the IES. In addition, the measure yielded high levels
of diagnostic agreement with a SCID diagnosis. Griffin,
Uhlmansiek, Resick, and Mechanic (2004) compared the
PDS for DSM-​IV with the CAPS for DSM-​IV in a sam-
ple of female survivors of domestic violence. They found
strong correlations between the two measures, although
the PDS tended to overdiagnose PTSD.
The psychometric properties of the PDS-​5 were evalu-
ated in a sample of urban community residents, under-
graduates, and veterans (Foa et  al., 2016). The PDS-​5
scores demonstrated excellent internal consistency and
test–​retest reliability. They also demonstrated convergent
validity with the PSSI-​5 (Foa et  al., 2016; r  =  .85), the
PTSD Checklist–​ Specific Version (PCL-​ S; Weathers
et  al., 1993; r  =  .90), and demonstrated discriminant
validity with the Beck Depression Inventory-​II (BDI-​II;
Beck et  al., 1996; r  =  .77) and the State–​Trait Anxiety
Inventory–​Trait Scale (STAI-​T; Spielberger et  al., 1983;
r = .64). Convergent and discriminant validity were com-
pared using the method created by Steiger (1980) and
Hoerger (2013), which demonstrated that the associations
between the PDS-​5 and the BDI-​II and STAI-​T were sig-
nificantly lower than the associations between the PDS-​5
and the PSSI-​5 and the PCL-​S (all ZH > 3.05, ps < .01).
Diagnostic agreement between the PDS-​5 and the PSSI-​
5 was 78% (sensitivity  =  .84, specificity  =  .73), where
scores were significantly higher on the PDS-​5 than on the
PSSI-​5. These findings suggest that the PDS-​5 can be
used to assess PTSD symptom severity as well as serve as a
screening instrument for probable PTSD but that, similar
to the IES-​R, clinicians should not use it as the sole means
of determining PTSD diagnostic status.
PTSD Checklist
Developed by researchers at the National Center for
PTSD (Weathers et al., 1993), the PTSD Checklist (PCL)
is a self-​report measure of DSM PTSD symptoms. The
original scale was based on the 17 symptoms included in
DSM-​III-​R criteria for PTSD, was subsequently updated
to reflect the DSM-​IV diagnostic criteria, and was most
recently updated to reflect the 20 DSM-​5 symptom cri-
teria (i.e., PCL-​5; Weathers et al., 2013). Different scor-
ing procedures may be used to yield either a continuous
measure of symptom severity or a dichotomous indica-
tor of diagnostic status. Dichotomous scoring methods
include an overall cut-​off score, a symptom cluster scoring
approach, or a combination of the two. Respondents are

asked to rate, on a Likert scale, “how much each prob-
lem has bothered them” during the past month. The time
frame can be adjusted as needed to suit the goals of the
assessment. The PCL for DSM-​IV has three versions:  a
civilian version (PCL-​C), a military version (PCL-​M),
and a specific version (PCL-​S). On the PCL-​C, respon-
dents are asked to report on symptoms related to any trau-
matic stressor, whereas on the PCL-​M, respondents are
asked to report on symptoms related to military stressor
exposures only. On the PCL-​S, symptoms are tied to one
specific traumatic event that the respondent indicates in
writing. Although the PCL-​5 has one version, there are
three separate formats of the measure:  one without the
Criterion A identification, one with a Criterion A identi-
fication, and one with the Life Events Checklist (LEC-​5)
and extended Criterion A  identification. Prior and cur-
rent versions of the PCL have been used extensively in
both research and clinical settings; all versions take 5 to
10 minutes to complete.
The PCL was originally validated with a sample of
Vietnam and Persian Gulf War veterans and found to
have strong psychometric properties (Weathers et  al.,
1993). Many studies provide evidence for the reliability
and validity of scores on the PCL for DSM-​IV in both
veteran and nonveteran samples (e.g., primary care
patients and severely mentally ill adults), although the
optimal cut-​off score varies across samples (Cook, Elhai,
& Arean, 2005; Dobie et  al., 2002; Grubaugh, Elhai,
Cusack, Wells, & Frueh, 2006; Keen, Kutter, Niles, &
Krinsley, 2004; Ruggiero, Del Ben, Scotti, & Rabalais,
2003; Walker, Newman, Dobie, Ciechanowski, & Katon,
2002). The many possible reasons for these discrepan-
cies (e.g., gender, recency of trauma, severity of trauma,
PTSD prevalence in the sample, and treatment-​seeking
status; Manne, DuHamel, Gallelli, Sorgen, & Redd,
1998)  warrant further investigation (for a comprehen-
sive review of the PCL for DSM-​IV, see McDonald &
Calhoun, 2010). In addition, there is evidence that dif-
ferent scoring options for the PCL (e.g., an absolute cut-​
off score vs. symptom cluster scoring vs. a combination
of the two) yield differences in sensitivity, specificity, and
diagnostic efficiency. The selection of a scoring routine
should therefore depend on the goal of the assessment
(Keen et al., 2004). However, it is important to note that
similar to the PDS and IES-​R, the PCL is not meant to
establish diagnostic status.
Although the PCL-​5 is relatively new, the psychomet-
ric properties of the measure already have been exam-
ined in several studies. Bovin and colleagues (2016)
Post-Traumatic Stress Disorder 341
tested the PCL-​5 in a sample of veterans and found its
scores to have excellent internal consistency, good test–​
retest reliability, as well as convergent and discriminant
validity. Armour and colleagues (2015) found excellent
internal consistency in samples of both veterans and stu-
dents. Furthermore, Keane and colleagues (2015) found
that the PCL-​5 scores correlated significantly with the
PCL for DSM-​IV and also that PCL-​5 scores demon-
strated excellent internal consistency, as well as conver-
gent validity, with the CAPS-​5 in two studies of returning
veterans and veterans from all eras. In addition, Hoge
and colleagues (2014) compared the PCL-​S with the
PCL-​5 and found them to be equivalent. However, they
did find that 67 (30%) of those who met DSM-​IV-​TR
criteria for PTSD did not meet criteria for DSM-​5 PTSD
and that an additional 59 participants met only DSM-​
5 criteria, indicating that there are prevalence differ-
ences between the two instruments. To date, only one
study has examined the performance of the PCL-​5 in a
non-​Western sample. Liu and colleagues (2014) exam-
ined the measure in a sample of Chinese earthquake
survivors, and the internal consistency of the PCL-​5
scores was found to be excellent. Although more data
are needed to further establish reliability and validity of
the PCL-​5, the data thus far support its use in assessing
PTSD symptom severity.
Overall Evaluation
Efforts to diagnose and assess patients for the presence
of PTSD symptoms should include a range of assess-
ment methods in addition to reviewing medical records,
accessing collateral sources, and taking a thorough his-
tory. Previously, we reviewed the use of semi-​structured
or structured diagnostic interviews and self-​ report
measures as primary methods for assessing PTSD in a
clinical context. In making choices about measures, it
is important to consider utility within a clinical context
(e.g., Are the measures time-​and cost-​effective?), as
well as psychometric properties. Using these guidelines,
the gold standard in PTSD assessment is the CAPS,
given that it is a sound measure with excellent psy-
chometric properties. Although only a single CAPS-​5
validation study have been published, it is still the most
comprehensive measure of PTSD and is thus still rec-
ommended as the gold standard for PTSD assessment.
As an adjunct, or in cases in which administering a
structured interview is not feasible or practical, we rec-
ommend the use of self-​report measures that explicitly
342 Anxiety and Related Disorders

TABLE 16.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planninga

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

BTQ A NA NA A A NR G A
LEC G NA NA G G NR G A
LSC-​R A NA NA A A NR G A
SLESQ A NA NA A A NR G A
TEQ A NA NA A A NR G A
TLEQ E NA NA E E NR E A ✓
TSS G NA NA A A NR G A

a
  Due to limited availability of psychometric data, DSM-​5-​related measures of trauma exposure are not included here. See text for description of these
instruments.
Note: BTQ = Brief Trauma Questionnaire; LEC = Life Events Checklist; LSC-​R = Life Stressor Checklist-​Revised; SLESQ = Stressful Life Events
Screening Questionnaire; TEQ = Traumatic Events Questionnaire; TLEQ = Traumatic Life Events Questionnaire; TSS = Traumatic Stress Schedule;
A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

assess the Criterion A  event or that are administered
with the instruction to anchor all symptom endorsement
to the index Criterion A event. Many of the self-​report
measures described previously can be used interchange-
ably; however, we recommend that clinicians consider
the available psychometric data for the instrument for
the population on which it is to be used. In doing this,
clinicians are maximizing the accuracy and efficiency
of the selected measure.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
On completion of a comprehensive diagnostic assessment
of PTSD that includes identification of the Criterion
A event and related symptoms, the clinician will have a
considerable amount of information regarding the index
trauma and the severity of its psychological sequelae.
This obviously is a necessary first step to case conceptu-
alization and treatment planning; however, selection of
a particular treatment and specific initial targets of treat-
ment require additional information. The augmentation
of diagnostic measures with more idiographic assessment
of trauma-​related symptoms, as well as the assessment of
comorbid conditions (e.g., Keane, Solomon, Maser, &
Gerrity, 1995), provides an excellent foundation for treat-
ment planning. We confine our discussion here primarily
to case conceptualization and treatment planning specific
to PTSD symptoms. Assessment for case conceptualiza-
tion and treatment planning incorporates the influence of
contextual factors that may or may not be revealed during
the diagnostic procedure. In this section, we focus on how
to address these contextual factors, and we refer the reader
to Table 16.2 for a review of instruments available for this
purpose.
Type of Trauma
There is a considerable range of traumatic events that
occur, and there are multiple ways in which to catego-
rize these events. For example, involvement in a combat
situation, a sexual assault, or a motor vehicle accident all
qualify as potential Criterion A events, given the exposure
to actual or threatened death, serious injury, or sexual
violation. However, these traumatic events may vary on
dimensions that are of particular salience in case concep-
tualization and treatment planning. For example, emo-
tions and beliefs secondary to the trauma might differ in
ways related to the trauma type. Guilt may be prominent
for a combat veteran, dissociation might be more likely
for a sexual assault victim, and conditioned fear of driv-
ing might be the most serious problem for an individual
involved in a motor vehicle accident. Previously, we dis-
cussed diagnostic measures that assess associated dissocia-
tive features, such as derealization and depersonalization,
in addition to the core 20 DSM-​5 symptoms. These ele-
ments of the diagnostic assessment are particularly valu-
able in the initial identification of idiographic factors
that aid in case conceptualization. In addition, although
many of the available diagnostic measures provide
only assessment of the presence or absence of the core
symptoms, continuous measures of symptom frequency
and severity also provide valuable information for case

conceptualization and treatment planning in the areas of
greatest distress and impairment.
Single Versus Multiple Trauma
Although the determination of a PTSD diagnosis includes
an assessment of an index trauma (Criterion A) to which
all other symptoms are presumed to be secondary, a strik-
ing percentage of individuals with PTSD have experi-
enced multiple traumas during their lifetimes (e.g., Kessler
et  al., 2005). Indeed, past trauma has been shown to be
a risk factor for the development of PTSD in response
to a subsequent traumatic event (e.g., Breslau, Chilcoat,
Kessler, & Davis, 1999). Generally, the index trauma
(i.e., the identified Criterion A  event) is the event that
prompted the patient to seek treatment, and sequelae of
that event often are the primary targets of treatment. It fol-
lows that the identification of additional events that may
have contributed to maladaptive functioning in response
to the Criterion A  event can aid in treatment planning.
Numerous checklists are available to assess exposure to
various traumatic events. These measures can be used as
part of an initial PTSD screen, but they also can be used
to identify additional traumatic experiences following a
comprehensive diagnostic assessment of the index trauma.
Five brief self-​report measures assess exposure to a vari-
ety of different potential DSM-​5 Criterion A events. The
Life Events Checklist (LEC; Gray, Litz, Hsu, & Lombardo,
2004)  was developed using DSM-​IV criteria, is typically
used in tandem with the CAPS, and also has been used
as an initial screen for potentially traumatic events. The
LEC lists 17 types of traumatic events that the respondent
may have experienced, as well as levels of exposure (i.e.,
happened to me, witnessed event, or learned about event).
The LEC scores demonstrated adequate test–​retest reli-
ability over 1 week for endorsement of direct exposure to
five of the listed events in a nonclinical sample, although
reliability was lower for the remaining items, perhaps
due to low base rates of those events (Gray et al., 2004).
The LEC was updated for DSM-​5 (i.e., LEC-​5; Weathers
et al., 2013), although the revisions are quite minor (i.e.,
Item 15, “Sudden, accidental death of someone close to
you,” was changed to “Sudden accidental death,” and
the response category “Part of my job” was added to each
item). Psychometrics are not yet available for the LEC-​5.
The Traumatic Stress Schedule (TSS; Norris, 1990)  is
a 10-​item measure with scores that have demonstrated
good reliability (r  =  .88) with multicultural samples.
The Traumatic Events Questionnaire (TEQ; Vrana &
Lauterbach, 1994) similarly assesses the experience of 11
Post-Traumatic Stress Disorder 343
potential Criterion A events; scores on this measure also
demonstrate excellent reliability. The Stressful Life Events
Screening Questionnaire (SLESQ; Goodman, Corcoran,
Turner, Yuan, & Green, 1998)  scores demonstrate good
reliability in the assessment of 13 potentially traumatic
events, and the questionnaire also incorporates age at
the time of trauma. The last Criterion A checklist is the
Brief Trauma Questionnaire (BTQ; Schnurr, Vielhauer,
Weathers, & Findler, 1999), which assesses the experience
of 10 potentially traumatic events. This measure is explicit
in its requirement that individuals respond to each item
as Criterion A; respondents are asked if they thought their
lives were in danger or if they thought they were injured or
could be injured during the event.
In addition to the five measures designed to identify a
range of potential Criterion A events, two checklist-​type
measures are slightly more in-​ depth. These measures
include a greater number of items that may be helpful
in case conceptualization and treatment planning. The
Traumatic Life Events Questionnaire (TLEQ; Kubany,
Haynes, et al., 2000) assesses exposure to 23 events; this
measure expands on the lists employed by the aforemen-
tioned Criterion A measures by breaking down a generally
traumatic experience (e.g., unwanted sexual experience)
into more specific items that include contextual factors
(e.g., childhood sexual touching and adolescent sexual
touching). Test–​retest reliability was shown to be good.
Note that some items on the checklist may not qualify
as Criterion A  events (e.g., sexual harassment). In addi-
tion, the Life Stressor Checklist-​Revised (LSC-​R; Wolfe,
Kimerling, Brown, Chrestman, & Levin, 1996)  assesses
exposure to 30 potential Criterion A events. The checklist
also includes follow-​up questions, including age at trauma
and degree of event-​related distress during the past year.
Item reliability ranges from good to excellent in a large
sample of women (McHugo et al., 2005). Also of note is
the inclusion of stressful events that may be of particular
relevance for women, such as abortion and miscarriage.
In general, checklists that identify exposure to various
potential traumatic events allow the clinician a more
comprehensive picture of client experiences for case con-
ceptualization and treatment planning.
In addition to broad Criterion A screening instruments,
it may be helpful to consider measures of exposure to com-
bat and other military-​related stressors when working with
veteran and active duty samples. A comprehensive review
of combat experience assessment is beyond the scope of
this chapter; however, the following measures may be use-
ful when determining the extent of an individual’s military
experiences. The 7-​item Combat Exposure Scale (Keane
344 Anxiety and Related Disorders

et al., 1989) was validated on Vietnam veterans, and scores the Posttraumatic Stress Related Functioning Inventory
have demonstrated good internal consistency and test–​retest (McCaslin et al., 2016). Instruments are also available to
reliability. The Deployment Risk and Resilience Inventory measure dimensions relevant to marital difficulty (e.g.,
(DRRI; King, King, Vogt, Knight, & Sampler, 2006)  and Conflict Tactics Scale-​Revised:  Straus, Hamby, Boney-​
the Deployment Risk and Resilience Inventory-​2 (DRRI-​2; McCoy, & Sugarman, 1996)  and quality of life (e.g.,
Vogt et  al., 2013)  are instruments used to assess a variety Quality of Life Inventory: Frisch, Cornell, Villañueva, &
of deployment-​related risk and resilience factors among Retzlaff, 1992). A  comprehensive listing and discussion
veterans. These 30-​item measures of warzone experiences of these measures is beyond the scope of this chapter,
were designed to assess the broader context of deployment although we note the importance of such adjunct assess-
(as well as pre-​deployment and post-​deployment) and fac- ment in case conceptualization and treatment planning,
tors that may impact an individual’s mental health. The and we suggest that, at a minimum, the patient history
DRRI was developed using samples of Gulf War veterans, incorporates multiple functional domains.
and the DRRI-​2 was validated on Iraq and Afghanistan
veterans. The measures include multiple subscales (e.g.,
Developmental Factors Related to Age at Trauma
Sexual Harassment, Postdeployment Stressors, and Family
Stressors) and are widely used. Although many/​all sub- Patient age at which the trauma occurred does not
scales may be appropriate to use, the particular subscalesappear to predict treatment outcome (e.g., Foa, Keane,
of Combat Experiences and Aftermath of Battle may Friedman, & Cohen, 2008). Despite the absence of evi-
be particularly relevant. Recently, the Critical Warzone dence for treatment effects specific to age, age variables
are important for case conceptualization and treatment
Experiences Scale (Kimbrel et al., 2014), a 7-​item measure
planning. A  30-​year-​old adult seeking treatment related
assessing combat experiences, was developed as a short ver-
sion of the 41-​item Marine Corps Mental Health Advisory to childhood sexual trauma that occurred at age 10 years
Team’s Combat Experiences Scale. Scores were validated is likely to present very differently from a 40-​ year-​
old
across independent samples of Iraq and Afghanistan veter- who seeks treatment for a sexual assault that occurred at
age 20  years. In both cases, 20  years have passed since
ans, and they demonstrated good internal consistency, test–​
retest reliability, and convergent validity. the trauma; however, the 10-​year-​old victim presumably
coped using strategies that were developmentally appro-
priate for a child, whereas the 20-​year-​old victim presum-
Assessment of Functioning
ably coped using strategies that were developmentally
Although many individuals who experience trauma-​ appropriate for a young adult. Such developmental factors
related symptoms present themselves for treatment have significant potential impact on the manner in which
relatively soon after the traumatic event, many others each individual initially processed the difficulty related to
experience symptoms for years before seeking treatment. the event and how he or she continues to experience it.
In its chronic form, PTSD often pervades an individual’s Patient age (or approximate age) at the time of the
life and has a deleterious impact in multiple domains, index trauma should be included in the patient history
including occupational functioning, social functioning, and, as noted, specifically is requested by several of the
and intimate relationships. Assessment of maladaptive Criterion A  assessment measures. In addition, an idio-
functioning in the relevant areas begins with a thorough graphic approach to the identification of beliefs resulting
patient history. In addition, the impact of the traumatic from the traumatic event(s) can incorporate developmen-
event on particular areas of functioning can be assessed tal factors and can be valuable in planning targets for
using a number of measures available to monitor a wider treatment. One such idiographic approach is employed
range of functional difficulty. For example, some par- within the Cognitive Processing Therapy manualized
ticularly useful measures of functioning across multiple treatment for PTSD (Resick, Monson, & Chard, 2014;
domains, including physical and psychiatric functioning, Resick & Schnicke, 1993). Patients are instructed to write
are the SF-​36 Health Survey (Ware & Kosinski, 2001), an “impact statement,” which is their own account of how
the BASIS-​32 (Eisen, Wilcox, Leff, Schaefer, & Culhane, their beliefs about themselves, others, and the world have
1999), the Inventory of Psychosocial Functioning (Marx changed due to the traumatic event. This procedure often
et  al., 2009), the World Health Organization Disability provides detailed information about potentially maladap-
Assessment Schedule (WHODAS 2.0; Üstün, et  al., tive beliefs related to safety, trust, intimacy, control, and so
2010), the Sheehan Disability Scale (Sheehan, 1983), and forth, and it provides the initial foundation for cognitive
 Post-Traumatic Stress Disorder 345

restructuring, should such techniques be utilized in the refugees from war-​torn countries may have been exposed,
treatment. We note that this is completely idiographic including exposure to torture, brainwashing, and depriva-
because the format is open-​ended and qualitative; we sug- tion of food or water. Originally developed in English, the
gest that such an addition to a comprehensive quantitative HTQ has been translated and validated in Vietnamese,
assessment offers important adjunct data that are useful in Laotian, Cambodian, Japanese, Bosnian, and Croatian.
treatment planning. The HTQ possesses linguistic equivalence across the
many cultures and languages with which it has been used
thus far. In addition, each version includes assessment of
Cultural Considerations
trauma-​related symptoms based on DSM-​IV criteria for
The generalizability of methods used to assess PTSD is a PTSD as well as additional items specific to the refugee
function of several features of the assessment setting and experience or to a particular culture. Mollica et al. have
patient characteristics. Culture, language, race, age, and reported good reliability for the HTQ scores.
gender are factors that might influence the use and the In addition, the  CAPS has been studied among cul-
interpretation of psychological instruments, whether they turally different groups with excellent success. As one
are structured diagnostic interviews or self-​report mea- example, Charney and Keane (2007) examined the psy-
sures. Attention to these variables is essential to discerning chometric properties of the CAPS after it was adapted for
the presence or absence of PTSD. use among Bosnian refugees. They applied contemporary
When selecting a measure, we recommend that cli- methods for translation, back translation, and then quali-
nicians consider the samples on which an assessment tative approaches for reconciling any differences in mean-
instrument for PTSD was validated. The need to develop ing that might have arisen as a function of this process.
instruments that are culturally sensitive has been of great The researchers found that the CAPS-​Bosnian translation
interest for many years as a result of documentation of was comparable in its psychometric properties to earlier
ethnocultural-​ specific responses to traumatic events. versions of the instrument. This indicates that the CAPS,
For example, researchers have provided evidence of dif- when properly adapted, can be successfully used to mea-
ferences in the reported risk for and severity of PTSD sure PTSD symptoms in culturally diverse populations
symptoms in Caucasians and ethnic minorities following and that PTSD secondary to war in civilians appears to be
a traumatic event (e.g., Alcántara, Casement, & Lewis-​ comparable in nature to other forms of PTSD.
Fernández, 2013; Roberts, Gilman, Breslau, Breslau, &
Koenen, 2011). Furthermore, there is substantial varia-
Overall Evaluation
tion in the prevalence of PTSD throughout the world.
Even across similarly low-​income and developing nations In conjunction with a comprehensive diagnostic strat-
recovering from conflict (which have high rates of trauma egy, assessment for case conceptualization and treatment
exposure and vulnerability factors), rates of PTSD vary planning broadens the scope of relevant data available
widely (de Jong et al., 2001), suggesting the importance to the clinician. Measures that take into account contex-
of considering unique contextual factors in the develop- tual factors that are relevant to PTSD, such as exposure
ment and use of PTSD assessment instruments. to multiple traumatic events or the presence of comor-
To date, evidence-​ based psychological assessment bid conditions, provide detailed information that can be
of PTSD has evolved primarily within the context of helpful in deciding on the therapeutic approach and the
Western, developed, and industrialized countries. Thus, specific targets of treatment. A variety of psychometrically
PTSD assessment may be limited by a lack of cultur- sound measures are available for these purposes, and we
ally sensitive measures and by the tremendous diversity have focused on those with the greatest clinical relevance.
among cultural groups of interest (Marques, Robinaugh, Table 16.2 presents our general recommendations for
LeBlanc, & Hinton, 2011). However, there has been prog- tools that should be considered for use.
ress in developing culturally sensitive measures. A  good
example of a measure that possesses culturally relevant
features is the Harvard Trauma Questionnaire (HTQ; ASSESSMENT FOR TREATMENT MONITORING
Mollica et al., 1992), which is widely used in refugee and AND TREATMENT OUTCOME
internally displaced samples. The HTQ assesses a range
of potentially traumatic events and trauma-​related symp- Monitoring the outcome of psychological treatment is
toms. The assessment of trauma includes events to which essential to help providers demonstrate the effectiveness
346 Anxiety and Related Disorders

of their treatments to patients and service payers. In an
early example of such monitoring, Keane and Kaloupek
(1982) presented the first empirical evidence that
cognitive–​behavioral treatments for PTSD had promise.
Within a single-​subject design, they assessed clients’ sub-
jective units of distress (SUD) ratings from 0 to 10 within
treatment sessions to monitor changes in the response to
traumatic memories in a prolonged exposure treatment
paradigm. In addition, they utilized the Spielberger State
Anxiety Inventory (STAI; Spielberger et al., 1983) to mon-
itor between-​session levels of anxiety and distress through-
out the course of the 19 treatment sessions.
Currently, the use of sound psychometric instruments
has become an important part of monitoring outcomes of
PTSD treatment, regardless of whether the intervention
is psychopharmacological, psychological, or both (e.g.,
Keane & Kaloupek, 2002). In addition to the provision
of a measurement of change within and between sessions
for a given individual, such measurements ideally pres-
ent normative information against which the individual’s
presentation and progress can be compared either with
the general population or with target populations of inter-
est (cf. Kraemer, 1992). It follows that clinicians would
do well to utilize tests or questionnaires with sound psy-
chometric properties when deciding how best to monitor
the outcomes of their interventions (Keane & Kaloupek,
1997). Table 16.3 provides an analysis of our perspective
on a variety of treatment monitoring and outcome mea-
sures for use in PTSD work.
When monitoring outcomes, clinicians are also encour-
aged to consider outcomes at several levels, including the
symptom level, the individual level, the system level,
and the social and contextual level. All are important
and can provide valuable information for both clinician
and client (Keane & Kaloupek, 1997, 2002). Numerous
measures are available to measure psychopathology, and
clinicians are encouraged to search for the measures that
are most appropriate for their circumstances and settings.
Use of these measures at regular intervals (daily, weekly,
monthly, quarterly, etc.) during the course of treatment
will provide knowledge of the client’s status and commu-
nicate to the clinician the extent to which the patient is
demonstrating change in the desired directions.
At the symptom level, regular assessment of PTSD
symptom frequency and severity can provide the clinician
with useful information regarding within-​and between-​
session change over the course of treatment. For exam-
ple, it may be that some clients experience clinically
significant symptom reduction in some symptoms early
in treatment, whereas other symptoms persist; frequent
assessment can help the clinician target particular prob-
lem areas while continually monitoring less problematic
symptoms that may not be addressed specifically in session
due to time constraints. In general, regular administration
of symptom checklists can provide ongoing feedback to
the clinician and the client. The brief PTSD symptom
checklists discussed previously in this chapter can be
quite useful for this purpose. In particular, the PCL-​5 can
be completed quickly, is anchored to the index trauma,
and assesses symptoms during a specific time frame rel-
evant to treatment monitoring. Also at the symptom level,
comorbid conditions such as major depression similarly

TABLE 16.3   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

CAPS-​IV E E E E E E E E E ✓
CAPS-​5 A G E A E E A NR A ✓a
IES-​R G G NA A G G G G G
PCL-​IV G E NA G G E E E G ✓
PCL-​5 A E NA A G G A NR A ✓a
PDS-​IV E E NA G G E E E G ✓
PDS-​5 G E NA A G G G NR A ✓a
SCID-​IV E E A A G G E G G
SCID-​5 NR NR G NR G NR NR NR A

a
 Limited data available for these measures; recommendations have been made tentatively based on available data and the strong psychometric support
for previous versions of these measures.
Note: CAPS-​IV = Clinician-​Administered PTSD Scale for DSM-​IV; CAPS-​5 = Clinician-​Administered PTSD Scale for DSM-​5; IES-​R = Impact of
Events Scale; PCL-​IV = PTSD Checklist for DSM-​IV; PCL-​5 = PTSD Checklist for DSM-​5; PDS-​IV = Posttraumatic Diagnostic Scale for DSM-​IV;
PDS-​5 = Posttraumatic Diagnostic Scale for DSM-​5; SCID-​IV = Structured Clinical Interview for DSM-​IV; SCID-​5 = Structured Clinical Interview for
DSM-​5; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

can be assessed easily using brief symptom measures (e.g.,
BDI-​II; Beck et  al., 1996). There are also a number of
measures available for the purpose of monitoring a wider
range of outcomes on the systems, social, and contextual
levels of clients’ lives. Selection of the most appropriate
measures of outcome is fundamentally a clinical decision
that should be determined by the provider in consultation
with the client. In the context of PTSD, we recommend
the use of the WHODAS in an effort to arrive at a system-
atic understanding of the impact of any single disorder or
the presence of concurrent disorders.
Assessment of outcomes at termination of treatment
should bring the clinician and the client full circle, by
again assessing diagnostic and functional status to exam-
ine change from pre-​to post-​treatment and identifying
remaining problem areas. Ideally, the clinician and the
client will repeat the initial diagnostic interview (e.g.,
CAPS and PSS-​I) to determine change in symptom fre-
quency and severity, as well as collateral change in other
areas of functioning. Due to clinicians’ time constraints,
it may not be feasible to repeat an entire structured inter-
view; in such cases, the self-​report symptom measures
outlined in section titled “Assessment for Diagnosis” may
provide an adequate substitute.
Screening for PTSD
A number of the self-​report measures described through-
out this chapter also have empirical support for use as
screening tools for PTSD. For instance, the PCL-​5 and
the PDS map directly onto the DSM-​5 criteria, and both
scales have validated cut scores or algorithms that are sug-
gestive of a PTSD diagnosis. However, briefer screening
instruments are also available and may be useful for effi-
cient screening of PTSD in settings in which more com-
prehensive assessment is not feasible (e.g., primary care).
Some of the more commonly used brief screening mea-
sures include the four-​item Primary Care-​PTSD screen
(PC-​PTSD; Prins et  al., 2004), the seven-​ item Short
Screening Scale for PTSD (Breslau, Peterson, Kessler,
& Schultz, 1999), and the four-​item SPAN (Davidson,
2002). Scores on these three screening tools have dem-
onstrated good sensitivity and specificity in the detection
of PTSD and have often been used and evaluated for use
in primary care clinics. However, the literature suggests
that of these three, the PC-​PTSD has optimal psychomet-
ric properties for the detection of PTSD (for a review, see
Spoont et al., 2015). The PC-​PTSD is a four-​item screen
consisting of yes/​no questions that assess the presence of
re-​
experiencing, avoidance, numbing/​ detachment, and
Post-Traumatic Stress Disorder 347
arousal symptoms within the past month (Prins et  al.,
2004). A score of 3 or more “yes” answers is indicative of
a positive screen for PTSD. The PC-​PTSD scores have
been shown to have very good sensitivity and specificity
in a range of settings, including VA primary care clinics
(Prins et  al., 2004; Ouimette, Wade, Prins, & Schohn,
2008), post-​deployment health assessments (Bliese et al.,
2008), civilian primary care settings (Freedy et al., 2010),
and civilian substance use treatment programs (Van
Dam, Ehring, Vedel, & Emmelkamp, 2010). An updated
version (the PC-​PTSD-​5) based on DSM-​5 criteria has
been developed and includes a new item assessing trauma-​
distorted blame and guilt as well as a revised stem ques-
tion that assesses for a Criterion A traumatic stressor (Prins
et al., 2016). Preliminary validation of the PC-​PTSD-​5 in
a veteran primary care sample has yielded strong support
for the revised version of the scale; however, further study
is needed to confirm its diagnostic utility across a range
of patient populations and settings and compare it with
diagnostic outcomes from the CAPS-​5.
Overall Evaluation
The most thorough assessment for PTSD treatment moni-
toring incorporates regular measurement of PTSD symp-
toms, symptoms of comorbid conditions, and indices of
functional domains such as marital relationships. In the
clinical setting, this task is best accomplished using brief
instruments that are relatively easy to administer and score.
Treatment outcome measurement should, at a minimum,
include brief assessment of symptoms, although the
readministration of diagnostic measures (e.g., structured
interview) allows the most comprehensive assessment of
change following treatment. We suggest that each of the
measures recommended in Table 16.3 has psychometric
properties appropriate for these purposes.
CONCLUSIONS AND FUTURE DIRECTIONS
We have discussed the assessment of PTSD for the pur-
poses of diagnosis, case conceptualization, treatment
planning, and treatment monitoring and outcome, with
emphasis on the most psychometrically sound measures
available. We also have attempted to consider clinical
feasibility in the use of these measures. We are confident
that the available assessment options can be easily incor-
porated into clinical practice.
With respect to assessment for diagnosis, we emphasize
the importance of the clear identification of a Criterion
348 Anxiety and Related Disorders
A event, to which subsequent symptom endorsements are
linked. We also recommend structured or semi-​structured
diagnostic interviews when possible, particularly those
that assess frequency and intensity of symptoms. For the
purposes of case conceptualization and treatment plan-
ning, a broader assessment of contextual factors, including
psychiatric comorbidity and exposure to other potentially
traumatic events, provides valuable adjunct informa-
tion. We further recommend regular brief assessments of
symptoms for the purposes of treatment monitoring and
a repeated diagnostic assessment to determine diagnos-
tic status and functional change at treatment or protocol
termination.
Clearly, the current review is not intended to be com-
prehensive in its evaluation of all instruments available
for the assessment of PTSD. The intent of the review
has been to provide a heuristic structure that clinicians
might employ when selecting a particular instrument
for their clinical purposes. By carefully examining the
psychometric properties of a measure, the clinician can
make an informed decision about the appropriateness of a
particular instrument for the task at hand (e.g., diagnosis,
case conceptualization, treatment planning, and moni-
toring outcomes). In addition to the psychometric prop-
erties of a measure, instruments that are developed and
evaluated on multiple trauma populations and culturally
diverse populations are highly desirable. Future efforts are
needed to establish the reliability and validity of scores on
new instruments, such as those developed using DSM-​
5 criteria, on a wider range of populations for clinicians’
use with diverse patients. The quality of our measures will
ultimately determine our understanding of PTSD and
will yield improved treatment of patients suffering from
this disorder.
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(2016). The impact of proposed changes to ICD-​11
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 Part V

Substance-​Related and Gambling Disorders

 17
Substance Use Disorders
Damaris J. Rohsenow
Clinicians working with substance use disorders (SUDs)
need good tools to help them evaluate patient needs, plan
treatment strategies tailored to these individual needs, and
monitor progress in treatment. This chapter provides an
overview of the most widely used, psychometrically sound
instruments that are potentially useful for clinicians work-
ing with clients with SUDs. Instruments that would prob-
ably only be used by researchers and commonly used,
but psychometrically weak, instruments are not included.
Accordingly, this chapter is not intended to provide an
exhaustive list of available instruments, and someone’s
preferred instrument may well be omitted. Nevertheless,
most of the best instruments that are likely to be clinically
useful are reviewed in the chapter. The focus is on alco-
hol and illicit drugs, not tobacco or other licit substances.
However, because assessments for alcohol use disorders
are covered in Chapter 18, measures specific to alcohol
are not discussed here. Additional instruments used in
research are described by Donovan and Marlatt (2005).
THE NATURE OF SUBSTANCE ABUSE
AND DEPENDENCE
Whether called addiction, abuse, or dependence, patients
with SUDs generally show a combination of physical
indicators (generally an abstinence syndrome), a vari-
ety of serious or ongoing negative consequences of drug
use that affect significant areas of their lives (including
financial, employment, health, family, social relation-
ships, and psychological function), and an apparent com-
pulsion to seek and use drugs despite ongoing negative
consequences. Many of the behaviors involved in getting
the drugs also lead to victimization of others in terms of
crime (usually committed to obtain funds to buy drugs)
or physical victimization (e.g., gunshot wounds). As such,
359
addiction has individual effects (physical, psychological,
and family), community effects (social, employment, and
financial burdens), and societal effects (crime, legal sys-
tem, politics, and societal costs). However, for the practi-
tioner, the primary focus is the individual with substance
misuse (using the term in a broad sense), along with the
consequences to that person and the effects of his or her
drug use on his or her own network. The diagnostic cri-
teria for SUDs are described later, but it should be noted
that the terms “abuse,” “misuse,” or “addiction” are often
used in the literature in a looser manner to refer to the
person who continues to have ongoing use despite serious
problems, regardless of whether formal diagnostic criteria
for SUDs are met.
Comorbidity
Because this text is oriented toward the clinical assess-
ment of SUDs, information on comorbidity derived from
clinical samples will be emphasized as more relevant
than community samples, to the extent that they differ.
Abuse of one substance is often comorbid with abuse of
a second substance of abuse. Approximately one-​third of
admissions to substance treatment programs are for both
alcohol and illicit drug use (Substance Abuse and Mental
Health Services Administration [SAMSHA], 2014). The
most common additional substances of abuse for patients
with opiate use disorders are marijuana, alcohol, and/​or
cocaine; for injecting drug abusers these are alcohol, ben-
zodiazepines, cannabis, and/​or amphetamines; and for
patients with cocaine use disorders, they are marijuana
or alcohol (SAMSHA, 2003). Patients with more than
one drug of abuse are less likely to achieve remission and
have more relapse after intensive treatment compared to
patients abusing a single drug (Ritsher, Moos, & Finney,
2002; Walton, Blow, & Booth, 2000).
360 Substance-Related and Gambling Disorders
An estimated 37% of adults older than age 18  years
with SUDs also have any mental illness, and 11% have a
serious mental illness (SAMHSA, 2015). Comorbid dis-
orders are most commonly affective disorders and anxi-
ety disorders (Acosta, Haller, & Schnoll, 2005). Among
people with cocaine use disorders, comorbidity rates
for depressive disorders range from 11% to 55% (with
depression usually preceding the SUD by approximately
7 years) and for bipolar disorder are approximately 42%;
panic disorder is a common result of cocaine abuse; and
the prevalence of post-​traumatic stress disorder among
those with SUDs is 10 times higher than among those
who do not have a SUD (Acosta et al., 2005). Psychiatric
comorbidities (other than personality disorders) for indi-
viduals with opioid use disorders are most commonly
bipolar or anxiety disorders (Dilts & Dilts, 2005). The
prevalence of current mood and/​ or anxiety disorder
among heroin injectors with multiple substances of
abuse is approximately 55%, with 25% having both a
mood and an anxiety disorder (Darke & Ross, 1997). An
excellent clinical guide to treatment issues involved with
psychiatric comorbidity in those with SUDs is provided
by Busch, Weiss, and Najavits (2005).
Personality disorders occur in approximately 27% of
people with past-​year alcohol dependence and 54% of
people with past-​ year drug dependence (corrected re-​
analysis of National Epidemiological Survey on Alcohol
and Related Conditions [NESARC] data of 2001–​2005
presented in Trull et  al., 2016). The most common
comorbid personality disorders for drug dependence
are antisocial (40.2%), borderline (27.88%), avoidant
(14.2%), schizoid or schizotypal (14.2%), obsessive–​
compulsive (10.6%), histrionic (10.3%), and paranoid
(7.8%) (Trull et al., 2016). The rates are lower for alcohol
dependence, ranging from the most prevalent, antisocial
personality (18.8%), to the least prevalent, histrionic per-
sonality (1.8%).
Prevalence, Gender, Race, Ethnicity, and Geography
The prevalence of current substance dependence or
abuse in the United States in 2013 (SAMHSA, 2014) was
approximately 8.2% of people aged 12 years or older. Of
these, approximately 12% had both alcohol and illicit
drug use disorders, 20% had an illicit drug use disorder
but not alcohol use disorder, and 68% had alcohol use
disorder without a disorder of illicit drugs. Although
from age 12 to 17  years the same number of males and
females have SUDs (5.3% vs. 5.2%, respectively), from
age 18  years on almost twice as many men as women
have SUDs in the past year (11.4% vs. 5.8%, respectively;
SAMSHA, 2014). The geographic distribution of people
in the United States with illicit drug use in the population
is fairly even, but with somewhat higher rates in the West
(11.8%) and Northeast (9.2%) than in the Midwest (8.7%)
or South (8.3%) (SAMHSA, 2014). Only approximately
1.6% of people aged 12 years or older with lifetime SUD
ever received any substance use treatment, and only 1.0%
received it in substance abuse treatment facilities in 2014
(SAMSHA, 2015).
The National Survey on Drug Use and Health study
(2013 survey; SAMHSA, 2014) showed the highest rates of
SUDs for American Indians or Alaskan Natives (14.9%),
then Native Hawaiians or Pacific Islanders (11.3%), mul-
tiracial people (10.9%), Hispanics (8.6%), non-​Hispanic
Whites (8.4%), and non-​ Hispanic Blacks (7.4%), with
the lowest rates for Asians (4.6%). Gender differences
in alcohol use disorders within each race/​ethnicity were
reported in the NESARC survey of 2001 and 2002
(National Institute on Alcohol Abuse and Alcoholism,
2006). In this survey, the highest rates were for American
Indians (17.3% of males and 16.8% of females), then
non-​ Hispanic Whites (17.3% of males and 8.1% of
females), non-​Hispanic Blacks (17.2% of males and 8.3%
of females), and Hispanics (17.3% of males and 7.2% of
females), with the lowest rates for Asians (11.0% of males
and 6.8% of females). However, Whites have the highest
rates of admission to publicly funded substance treatment
facilities (2008 survey by SAMHSA; National Institute on
Drug Abuse, 2011): Admissions were 59.8% White, 20.9%
Black, 13.7% Hispanic, 2.3% American Indian or Alaskan
Native, and 1.0% Asian or Pacific Islander.
The Addiction Career
There is little agreement on the etiology of SUDs—​a
topic difficult to study given that substances of abuse
are not all similar in mechanism, effects, or likely deter-
minants (Anthenelli & Schuckit, 1992). It is difficult to
study the etiology of drug abuse or dependence for each
drug of abuse completely separately, given the fact that
people may use various substances at different times or
the same time. Because different drugs of abuse involve
different mechanisms, it has been difficult to investigate
possible genetic factors specific to illicit drug abuse as
opposed to alcohol abuse, so such research has focused
on genetic factors in the neurotransmitters believed
to confer greater susceptibility to drug dependence
(e.g., mu or kappa opioid receptors or dopamine trans-
mission) along with genes influencing externalizing

psychopathology (Dick & Agrawal, 2008). Studies of
sociocultural factors do little to explain who specifically
will develop drug dependence given that such a small
number of people affected by these influences develop
drug dependence (Johnson & Muffler, 1992). There is
no one psychological or sociopsychological theory that
is generally accepted as explanatory (e.g., Schulenberg,
Maggs, Steinman, & Zucker, 2001). However, there may
be a general genetically influenced liability of negative
emotionality that is expressed as personality character-
istics and behavioral tendencies (inadequate emotional
regulations and maladaptive responses to stress) com-
mon to abuse of various substances as well as to other
comorbid disorders (Tully & Iacono, 2016). Adolescent
substance abuse is highest for those who have high nov-
elty seeking combined with low harm avoidance and low
reward dependence personality traits (Wills, Vaccaro,
& McNamara, 1994). These personality trait measures
were correlated with other measures of behavioral under-
control such as risk-​taking, impulsivity, anger, indepen-
dence, tolerance for deviance, and sensation seeking
(Wills et  al., 1994). A  childhood pattern of behavioral
undercontrol often leads to early onset of cigarette use,
which in turn increases the probability of the onset of
drug use (e.g., Brown, Gleghorn, Schuckit, Myers, &
Mott, 1996; Farrell, Danish, & Howard, 1992; U.S.
Department of Health and Human Services, 1989). The
etiology of this pattern of behavioral undercontrol itself
is unknown. However, this may not be the only pathway
to substance dependence. For a review of the concept
and evidence for and against behavioral undercontrol
and negative emotionality as mechanisms, see Smith and
Anderson (2001) and Tully and Iacono (2016).
A large study of the natural history of 581 people with
narcotic addictions tracked the course of events during
the 30-​year period from 1956 to 1986 (Anglin et  al.,
1988). There were several notable findings. First, 5 years
after starting narcotics use (approximately age 17 years),
most were daily users, with few remaining as occasional
users. Second, daily use peaked at approximately age
30 years, decreased slightly as people entered into metha-
done maintenance, and then remained stable. Third,
incarceration rates were highest between ages 20 and
30 years (approximately 60% of group) and then dropped
off to 11% for the last decade. Fourth, deaths started
occurring within 10  years, with a mortality rate of 27%
of the group at the end of 30  years (comparable to the
10% to 50% mortality rate within 8 years reported across
studies by Finney, Moos, & Timko, 2013). Fifth, for the
last 10 to 15  years of the study period, approximately
Substance Use Disorders 361
22% of the people were abstinent. Although these data
are rather old, to the extent to which they reflect com-
mon developmental factors, the progression may hold up
over time. Others have summarized the course of opiate
addiction more simply:  First use is usually in the teens
or 20s, most active opiate users are 20 to 50  years old,
the addiction abates slowly and spontaneously in middle
age, with 9  years being the estimated average duration
of active addiction (Dilts & Dilts, 2005; Jaffe, 1989).
Anglin et al. concluded that substance abuse treatment
is needed much earlier in the addiction careers because
treatment interrupts the typical progression of addiction.
The National Drug Abuse Treatment Outcome Study
showed that, overall, treatment does work, with the great-
est reductions in drug use occurring with treatments that
last 3 or more months for 1-​year results and 6 or more
months for 5-​ year recovery (Hubbard, Craddock, &
Anderson, 2003). Across 15 studies with 8 or more years
of follow-​up, the annualized “remission” rates averaged
4.0% (Finney et al., 2013).
PURPOSES OF ASSESSMENT
Three specific assessment purposes of most relevance for
clinical use are emphasized in this chapter: (a) diagnosis,
(b)  case conceptualization and treatment planning, and
(c)  treatment monitoring and outcome evaluation. The
emphasis in the case conceptualization and treatment
planning section is on problem severity. This section also
includes assessment of expectancies, high-​risk situations,
self-​efficacy in handling risk, and coping skills because
these can be useful in planning motivational interven-
tions, relapse prevention, and coping skills training spe-
cific to individual needs. Measures of overall functioning/​
impairment or functioning in interpersonal, family,
psychiatric, medical, and employment domains can be
useful in evaluating need for family or couples therapy,
employment assistance, legal or medical services, social
services, and so on. The focus in this chapter is on the
assessment of SUDs regardless of substance, with less
focus on measures that were developed for use with only
one substance. The assessment of other behaviors that are
sometimes seen as addictive, such as gambling or sexual
offending, is not discussed here (the assessment of gam-
bling is covered in Chapter  19). An excellent text that
covers an array of substance-​specific assessment measures,
addictive behaviors not involving chemical substance,
and measures designed for use in research studies is the
one by Donovan and Marlatt (2005).
362 Substance-Related and Gambling Disorders

ASSESSMENT FOR DIAGNOSIS unsuccessful attempts to cut down or control substance

The diagnostic criteria of the fifth edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-​5;
American Psychiatric Association [APA], 2013)  have
replaced those of DSM-​IV-​TR (APA, 2000)  as the stan-
dard for clinical practice in the United States. Measures
focused on World Health Organization (WHO) criteria
are not addressed because they are less likely to be rel-
evant to practice in the United States. DSM-​5 revisions
replaced the abuse and dependence categories with a
single continuum, but people can be categorized based
on number of criteria met into mild, moderate, and
severe levels of SUD. Substance-​related legal problems
were eliminated due to low occurrence, cultural vari-
ability, and poor fit with the other diagnostic information
(Goldstein et  al., 2015; Schuckit, 2012), and craving or
urge to use was added (to increase consistency with WHO
criteria), but otherwise the list of criteria is the same. The
SUD can be specified as “in a controlled environment,”
“in early remission,” “in sustained remission,” and, for cer-
tain substances, “on maintenance therapy” (craving is the
only criterion that can occur during remission).
SUDs are a maladaptive pattern of substance use lead-
ing to clinically significant impairment or distress as indi-
cated by two or more of the following occurring within
the same 12-​month period:  tolerance (increased amount
needed for same effect or markedly less effect with same
amount of use); withdrawal (either the characteristic with-
drawal syndrome or using the substance or a closely related
substance to prevent/​relieve withdrawal); amount or dura-
tion of substance use that is greater than intended; repeated
use; much time spent in activities needed to obtain, use,
or recover from the substance; important activities stopped
or reduced due to substance use; substance use continues
despite knowledge of a persistent or recurrent physical or
psychological problem caused or exacerbated by the sub-
stance; recurrent substance use resulting in failure to fulfill
major obligations at work, home, or school; recurrent sub-
stance use in situations in which it is physically hazardous;
continued substance use despite the use causing or exac-
erbating social or interpersonal problems; and craving or
strong desire or urge to use a specific substance. (For full,
exact wordings of these criteria and any substance-​specific
differences, see DSM-​5 or del Boca, Darkes, and McRee
[2016].) Two or three symptoms indicate a mild SUD,
four or five symptoms indicate a moderate SUD, and six or
more symptoms indicate a severe SUD.
Screening Measures
Screening measures are typically used in settings such as
general medical settings or employee assistance programs
to identify or rule out probable SUD without providing a
diagnosis. These are brief measures that can be quickly
administered to identify people who may be in need of
further evaluation or assistance. Cut-​off points for screen-
ing measures can be set to err on the side of false posi-
tives or false negatives, depending on the purpose of the
assessment. However, any positives should be followed
up with further evaluation rather than being considered
indicative of an SUD per se. The best known screening
measures are rated in Table 17.1 and described in the

TABLE 17.1   Ratings of Instruments Used for Screening or Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Screening for Substance Use Disorders

DAST NA E NA NR A A E A
DUSI-​R NA G NA NR A A E A ✓
Diagnostic Instruments
SCID-​5 NA NA G G G A E L
MINI NA NA G E G G E E ✓
CIDI NA NA G G G A E L
SDSS NA G NA G G Ga G A
GAIN-​I A G NA G G G E A ✓
MWC NA NR NA G G G G E

  Good except for ICD-​10 harmful use and cocaine dependence diagnoses, which were less than adequate.
a

Note:  DAST  =  Drug Abuse Screening Test; DUSI-​R  =  Drug Use Screening Inventory-​Revised; SCID-​5  =  Structured Clinical Interview for DSM-​
5 Axis I  Disorders-​Patient Version; MINI  =  Mini-​International Neuropsychiatric Interview 6.0; CIDI  =  Composite International Diagnostic Interview;
SDSS = Substance Dependence Severity Scale, section on diagnoses; GAIN-​I = Global Appraisal of Individual Needs-​Initial Interview, substance use scales;
MWC = Marijuana Withdrawal Checklist; L = Less Than Adequate; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.

following paragraphs. It was not necessary for test devel-
opers to update these measures to address DSM-​5 criteria
because they were never intended to assess those exact cri-
teria. In addition, because reasonably similar prevalences
of moderate to severe DSM-​5 SUD and DSM-​IV (APA,
1994)  substance dependence occur (Goldstein et  al.,
2015), the screening measures are likely to work as well
with the current DSM system. For a further discussion of
alcohol-​specific and adolescent-​specific measures, see the
review of assessments by del Boca et al. (2016).
Drug Abuse Screening Test
The Drug Abuse Screening Test (DAST; Skinner, 1982),
a 28-​item self-​report test, and the 10-​ item short form
(DAST-​10) provide an indicator of who might have an
SUD and need further evaluation, with evidence of excel-
lent internal reliability and good validity (Gavin, Ross, &
Skinner, 1989). Data on test–​retest reliability are unavail-
able. Both ask about drug abuse in the past year, rather
than over the lifetime, and an adolescent version is avail-
able. The DAST is composed of five factors (early psycho-
social complications with problem recognition, late-​onset
serious social consequences, treatment/​ help-​seeking,
illegal activities, and inability to control drug use), but
because psychometric properties of the separate factors
were not investigated (Staley & El-​Guebaly, 1990), only
the total score should be used. Both the DAST and the
DAST-​10 focus on negative consequences of use rather
than quantity or frequency of use.
Drug Use Screening Inventory
The Drug Use Screening Inventory (DUSI; Tarter, 1990),
which is a longer self-​report measure (140 yes/​no items)
with both adult and teen versions, assesses problem sever-
ity in the following 10 domains:  substance use prefer-
ences and consequences, behavioral maladjustment,
health, psychiatric disorder (depression, anxiety, antiso-
cial, and psychotic), school adjustment, work adjustment,
social competence, peer relationships (e.g., antisocial or
substance involvement), family dysfunction/​conflict, and
recreation. It takes approximately 20 minutes to complete
via paper or computer and is easy to manually score.
Efforts were made to ensure items are free of cultural
bias and at a fifth-​grade reading level. The revised version
(DUSI-​R) has a validity check and Lie scale, has been
found to have adequate or better psychometric qualities,
and includes cut-​off scores to indicate a probable diagno-
sis (Tarter & Kirisci, 1997). This measure is more highly
recommended than the DAST and DAST-​ 10, despite
Substance Use Disorders 363
the extra administration time, because it provides more
information.
Diagnostic Instruments
In clinical settings, diagnosis is often determined with-
out a formal structured set of specific questions. When a
formal system is needed to ensure accuracy of diagnosis
(e.g., for research or clinical statistics), the instruments
rated in Table 17.1 and described next are the best vali-
dated structured systems available. Because it can take up
to 10 years to develop and test the reliability and validity
of a structured interview, it may take a while before there
is psychometric evidence for instruments that have been
fully updated to DSM-​5 criteria.
The Structured Clinical Interview for the DSM
(SCID-​ 5; First, Williams, Karg, & Spitzer, 2015)  is
validated directly against both the DSM-​5 and the 10th
edition of the International Classification of Diseases
(ICD-​ 10; WHO, 1992; https://​www.cdc.gov/​nchs/​icd/​
icd10cm.htm) diagnostic criteria. This interview is con-
sidered the most valid method for determining DSM-​5
psychiatric diagnoses and is the most widely used struc-
tured diagnostic interview. The SCID-​5 should be admin-
istered by clinicians, not other trained interviewers, with
the version for clinicians called SCID-​5-​CV. This struc-
tured interview is very lengthy (1 hour or more for the full
interview) and requires formal training in administration
and scoring; as such, it may not be cost-​effective for treat-
ment agencies because the resulting data provide diag-
nostic information but no other information necessary for
treatment planning.
A much briefer alternative is the Mini-​International
Neuropsychiatric Interview (M.I.N.I. 6.0;https://​www.
psychcongress.com/ ​ s aundras- ​ c orner/ ​ s cales- ​ s creeners/​
structured-​ diagnostic-​ i nterview-​ i nstruments/​ m ini-​
international-​ n europsychiatric-​ i nterview-​ 6 0-​mini-​ 6 0;
Sheehan et  al., 1998), which evaluates all current diag-
noses in approximately 15 to 17 minutes, so determin-
ing alcohol or SUDs takes only a fraction of that time.
Although it was designed for researchers, a computer-
ized version makes it easy for any clinician to use; it is
used by health and mental health professionals in more
than 100 countries. Because each section starts with one
or more screening questions (questions about drinking a
certain amount or using street drugs for the alcohol and
substance use sections, respectively), the whole interview
does not need to be administered for people who do not
meet some minimal criteria for a section. Patients had
positive opinions about the interview and the interview
format (Pinninti, Madison, Musser, & Pissmiller, 2003).
364 Substance-Related and Gambling Disorders
The M.I.N.I.  was validated against the SCID for DSM-​
IV and the Composite International Diagnostic Interview
(CIDI; Robins et al., 1988) for ICD-​10 as well as against
expert opinion (Sheehan et  al., 1998), and it produces
separate diagnoses for current (past 12  months) alcohol
abuse, alcohol dependence, substance abuse, and sub-
stance dependence. So far, the mania/​hypomania sections
have been updated and validated for DSM-​5 (Hergueta
& Weiller, 2013) and a version for 17 DSM-​5 diagnoses
has been developed but was not available at the time this
chapter was written http://​harmresearch.org/​index.php/​
product/​mini-​international-​neuropsychiatric-​interview-​
mini-​7-​0-​2/​.
The Diagnostic Interview Schedule (DIS; Robins,
Helzer, Cottler, & Golding, 1989; Robins et  al.,
2000)  was designed to provide reliable and valid SUD
diagnoses based on DSM-​III (APA, 1980)  and DSM-​IV
criteria using a format involving fewer clinical judgments
so it could be administered by a trained technician. It was
replaced by the CIDI when WHO expanded and updated
the DIS to meet international criteria (ICD-​10). (A ver-
sion for DSM-​5 is due in 2018 https://​www.hcp.med.har-
vard.edu/​wmhcidi/​trc_​americas/​.) However, it is designed
for research, not clinical practice; takes 2 hours to admin-
ister; and requires extensive training, and is available only
as a computerized version. Therefore, these instruments
are usually not clinically useful.
For assessing withdrawal aspects specific to canna-
bis abuse, it is preferable to use a measure based on the
empirical work that established the cannabis withdrawal
syndrome. Budney, Moore, Vandrey, and Hughes (2003)
demonstrated a unique pattern of withdrawal symptoms,
including aggression, anger, anxiety, decreased appetite,
decreased body weight, irritability, restlessness, shakiness,
sleep problems, and stomach pain. A measure designed to
assess this pattern, the Marijuana Withdrawal Checklist
(MWC; Budney, Hughes, Moore, & Novy, 2001; Budney
et al., 2003), is a self-​report measure that includes the 15
items most frequently endorsed. Studies with the 15-​item
version found evidence of good test–​retest reliability and
validity and also the expected gradual change over days
along the predicted time course of withdrawal (Budney
et al., 2003).
Two instruments for assessing opiate withdrawal
with some supporting reliability and validity evidence
are the Subjective Opiate Withdrawal Scale (16 items,
self-​administered) and the Objective Opiate Withdrawal
Scale (13 items, interviewer-​administered), both devel-
oped by Handelsman et  al. (1987). For cocaine depen-
dence, withdrawal is an infrequently endorsed symptom.
These measures are not rated in Table 17.1 because there
is only limited evidence concerning their reliability and
validity.
The Substance Dependence Severity Scale (SDSS;
Miele et al., 2000a) is a semi-​structured clinical interview
that takes approximately 30 to 45 minutes and requires
extensive training. Part of it results in current diagno-
ses for DSM-​IV and ICD-​10 (WHO, 1997)  substance
abuse/​dependence/​harmful use disorders by operation-
alizing every criterion used in diagnosis. Each diagnostic
criterion is rated for both severity (usual and worst) and
frequency (number of days and number of days at the
worst). Scores on the SDSS scales have demonstrated
good to excellent test–​retest reliability (except for can-
nabis, for which it was fair to poor), internal consistency,
and validity for the DSM-​IV items (Miele et al., 2000a,
2000b). Percent agreement with DSM-​IV diagnoses was
83% to 92% for alcohol, cocaine, heroin, sedatives, and
cannabis (the only diagnoses investigated). The test–​
retest reliability and internal consistencies for the ICD-​
10 dependence scales of alcohol, heroin, and cocaine
were excellent, but the ICD-​ 10 harmful use scales
mostly had unacceptably poor test–​retest and/​or internal
consistency reliabilities. Percent agreement with ICD-​
10 dependence diagnoses was good to excellent for alco-
hol, heroin, and cannabis but only fair for cocaine, and
for harmful use diagnoses were only fair (unacceptable)
for heroin, cocaine, and cannabis. Therefore, as long
as ICD-​10 harmful use or cocaine dependence diag-
nostic information is not needed, this instrument will
produce valid DSM-​IV diagnoses for alcohol, cocaine,
heroin, sedatives, and cannabis use disorders. It is not
clear whether there are plans for an update to DSM-​5.
However, the SDSS severity scores, indicating degree
of severity similar to the DSM-​5 degree of severity, has
been validated against clinical severity ratings for alco-
hol, cocaine, and heroin (Miele et al., 2000b).
The Global Appraisal of Individual Needs (GAIN-​
I; Dennis, 1999; Dennis, Scott, & Funk, 2003; Dennis,
Titus, White, Unsicker, & Hodgkins, 2003)  is a semi-​
structured interview designed to obtain comprehensive
information about the functioning of adult or adolescent
patients (see further description later). The latest version,
GAIN 5.7, has been updated to DSM-​5 criteria. It takes
1½ to 2½ hours to administer, and it requires consider-
able training. There is a Web-​based Assessment Building
System format (GAIN-​ABS) that also provides DSM-​5
diagnoses. The Initial Interview version includes a diag-
nostic section, and the diagnoses of SUDs as well as other
disorders have evidence of good test–​ retest reliability

estimates and concordance with independently obtained
diagnoses (Dennis, 1999; Shane, Jasiukaitis, & Green,
2003). A  2-​to 5-​minute Short Screener (GAIN-​SS) is
available for rapidly identifying those who are likely to
have an SUD.
Overall Evaluation
The previously discussed screening and diagnostic
measures have all demonstrated scientific adequacy as
screening or diagnostic measures. Screening measures
such as the DAST are not relevant for SUD treatment
programs, but they are useful in other settings to iden-
tify people probably in need of further assessment or
treatment. The GAIN-​SS (screening version) is use-
ful for identifying people who need full diagnostic
assessment for certain diagnoses (SUD or other), but
psychometric information about this screener was not
available. The DUSI, although intended to screen for
SUDs, is also useful for screening for a number of areas
of life function in a way comparable to the Addiction
Severity Index (discussed later) but with easier admin-
istration and scoring; for this reason, it is highly recom-
mended. The diagnostic measures are relevant only if
accurate formal diagnoses are needed. Because many
SUD treatment programs treat anyone who presents
with substance-​ related problems or concerns, hav-
ing access to accurate diagnoses is unlikely to affect
treatment admission or planning, but diagnoses can
affect reimbursement. The M.I.N.I., when updated
to DSM-​5, is recommended as a method that is fast,
accurate, and shows patient acceptance. Otherwise,
the diagnostic section of the GAIN 5.7 is most highly
recommended as the next least time-​intensive way to
obtain the most diagnoses with good psychometric
support. The others were not recommended due to
the lengthy time and training needed (SCID-​5, CIDI,
and SDSS) or the cumbersome amount of information
produced (SDSS).
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
Rationale for Instrument Selection
A number of assessment instruments are commonly used
to provide clinicians with guidance for case conceptual-
ization and treatment planning. Some measures include
severity of drug use and problems specific to the drugs
Substance Use Disorders 365
per se; others address the severity of problems in related
aspects of life functioning (e.g., employment, legal, fam-
ily), whether or not drugs are perceived as the cause of
the problems, thus allowing for the determination of areas
of life functioning in need of improvement and for addi-
tional specialized services such as social services, employ-
ment assistance, or marital or family therapy. Assessment
of the patient’s anticipated positive and negative conse-
quences of drug use is sometimes used in developing
motivational interviewing treatment plans by investigating
sources of and barriers to motivation. Relapse prevention
training involves assessing high risk situations for relapse
so as to prepare patients to cope with their own “Achilles
heel” situations. Assessment of coping skills can provide
information about skills and resources that can already
be drawn on, maladaptive skills that need to be replaced,
and skills and resources that are lacking. Skills training for
substance abusers has focused either on making general
lifestyle changes consistent with sobriety or on developing
skills for coping with immediate urges to use in the pres-
ence of situations that pose a high risk for relapse (Monti,
Kadden, Rohsenow, Cooney, & Abrams, 2002). In most
cases, both types of skills need to be assessed.
Some potential assessment domains are not addressed
in the chapter, based on either clinical or scientific rea-
sons. First, measures of craving are not included because
it is not clear that degree of craving per se can be useful
in treatment planning, as opposed to identifying situations
or events that trigger craving, which can be quite impor-
tant. Second, although numerous studies have shown that
having social networks that include substance users (par-
ticularly one’s partner) poses a serious risk for continued
drug use (see review by Westphal, Wasserman, Masson, &
Sorenson, 2005), this risk is easy to assess without any for-
mal assessment tool. Although the Important People Drug
and Alcohol interview predicted outcome for patients with
cocaine use disorders, it was just the number of people in
the daily network that predicted less drinking, drug use,
and problem severity over 6  months, not the measures
of the supportiveness or drinking status of the network
(Zywiak et  al., 2009), and that is easy to assess without
using a measure. Therefore, this section focuses on tools
that have adequate psychometric information and that
could be useful in treatment planning. Detailed ratings of
their psychometric properties can be found in Table 17.2.
Increasing Honest Reporting
Structured interviews with individuals with SUDs about
their drinking or substance use have been found to
366 Substance-Related and Gambling Disorders

TABLE 17.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliabilitya Validity Validity Generalization Utility Recommended

Severity of Drug Use and Psychosocial Functioning

SDS NA E NA E E E NR A
SDSS NA E NA E E E E A
ASI-​6 NA G G G A A G A
GAIN-​I NA G NA NA G G A A ✓
Negative Consequences of Ongoing Use
IDUC NA E NA G G A A A ✓
SIP-​AD NA E NA G G A A A ✓
MPS NA E NA NR NR A NR A
CNCC-​87 NA G NA NR G G A A
Expected Acute Effects of Use
SUBQ NA E NA NR G G NR A
CEQ NA G NA NR G G A A
Assessment for Relapse Prevention Treatment Planning
IDTS A G NA NR G G G A ✓
DTCQ NA G NA NA A A G A ✓
AASE NA E NA NR A G NR A
CRACS-​SE NA E NA NR A G G A
POC-​10 items NA A NA NA A A NR A
USS/​GSC NA E NA NR G G A A ✓

Test–​retest reliability is generally not applicable because clients in treatment are unstable in these areas and are expected to have variability over short
a

periods of time.
Note:  SDS  =  Severity of Dependence Scale; SDSS  =  Substance Dependence Severity Scale; ASI-​6  =  Addiction Severity Index-​Version 6; GAIN-​
I = Global Appraisal of Individual Needs-​Initial Interview, substance use scales; IDUC = Inventory of Drug Use Consequences, four scales (exclud-
ing intrapersonal); SIP-​AD  =  Short Inventory of Problems–​Alcohol and Drugs; MPS  =  Marijuana Problems Scale; CNCC-​87  =  Cocaine Negative
Consequences Checklist; SUBQ = Substance Use Beliefs Questionnaire; CEQ = Cocaine Effects Questionnaire; IDTS = Inventory of Drug Taking
Situations; DTCQ = Drug-​Taking Confidence Questionnaire; AASE = Alcohol Abstinence Self-​Efficacy; CRACS-​SE = Self-​Efficacy ratings from the
Cocaine Related Assessment of Coping Skills: POC-​10 = 10 items extracted from the Processes of Change Questionnaire for a study with opiate-​using
patients; USS/​GSC = Urge-​Specific Strategies Questionnaire and General Change Strategies Questionnaire; L = Less Than Adequate; A = Adequate;
G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.

provide sensitive and reliable information when there is
(a)  an interviewer and clinical set that encourages hon-
est reporting (i.e., no unpleasant consequences, including
interviewer disapproval), (b) assurances of confidentiality,
(c)  breath alcohol testing at the interview to ensure the
person is alcohol-​free during the interview, and (d) inter-
viewee awareness that his or her reports will be corrobo-
rated by urine screens and/​or reports of family members
or close friends (Ehrman & Robbins, 1994; Sobell
et  al., 1996; Sobell & Sobell, 1986). Patients are likely
to become dishonest in their reporting when expecting
scolding, lectures, disappointing the therapist, changes in
treatment, or reporting to others who may impose conse-
quences as a result of disclosing use. Thus, the interviewer
set is particularly important both with interviews and with
self-​report measures: Knowing that there will be no nega-
tive consequences or disapproval for reporting substance
use removes the primary disincentive to honesty.
Severity of Substance Use
and Psychosocial Functioning
Number of DSM-​5 Symptoms
With DSM-​5 indicating severity on a continuum, the
number of criteria met is designed to be used as a mea-
sure of SUD severity.
The Severity of Dependence Scale
If the clinician is not assessing in order to obtain a for-
mal diagnosis, the simplest assessment alternative is the
Severity of Dependence Scale (SDS; Ferri, Marsden,
de Araujo, Laranjeira, & Gossop, 2000; Gossop, Best,
Marsden, & Strang, 1997; Gossop et  al., 1995), which
uses just five face-​valid items (about worry/​anxiety, feeling
out of control, and desire to stop or difficulty with stop-
ping) to assess a pattern of dependence severity across the

patient’s preferred substance. It has demonstrated excel-
lent psychometric properties, and although there is no
information about any racial diversity in any of the vali-
dation samples, it has been validated in three countries
(England, Australia, and Brazil).
Substance Dependence Severity Scale
The SDSS (Miele et al., 2000a), a semi-​structured clini-
cal interview, assesses the severity of every symptom of
both DSM-​ IV and ICD-​ 10 (WHO, 1997)  substance
abuse/​dependence/​harmful use disorders among people
aged 16  years or older. Substance-​ specific questions
assess frequency, recency, and amount of use in the past
30  days only, as well as asking usual and worst severity
of each diagnostic criterion and also number of days of
any use and number of days at the worst severity for each.
These questions cover a wide range of abused substances,
including alcohol, cocaine, heroin, stimulants, licit opi-
ates, sedatives, methadone, cannabis, hallucinogens, and
two “other” categories covering drugs such as inhalants.
However, the cannabis items omit withdrawal, which was
only found to be a valid symptom after this measure was
developed. The SDSS takes specialized training and can
require as much as 45 minutes to administer.
The SDSS scale scores have been found to demon-
strate good to excellent test–​ retest reliability, internal
consistency, and validity for the use (quantity/​frequency)
items, DSM-​IV severity items (except for cannabis), and
ICD-​10 dependence but not harmful use scales (Miele
et  al., 2000a, 2000b). The best validity was shown for
the alcohol, heroin, and cocaine severity scales. Patients
reporting more days that symptoms were present returned
to drug use more quickly, suggesting that this frequency
scale predicts need for more intensive care (Miele et al.,
2001). On the other hand, greater usual severity of depen-
dence symptoms predicted slower return to drug use
(Miele et  al., 2001), consistent with more serious prob-
lems or concern about consequences of drug use making
people more motivated for change. Therefore, this instru-
ment has generally excellent psychometric properties
(except for cannabis scales for either DSM-​IV or ICD-​10
harmful use) and can be a useful way to assess recent use
and severity of specific DSM-​IV SUD symptoms.
Addiction Severity Index
The Addiction Severity Index (ASI; Cacciola, Alterman,
Habing, & McLellan, 2011; McLellan, Luborsky, Woody,
& O’Brien, 1980; McLellan et  al., 1992). This structured
Substance Use Disorders 367
interview has become the most widely used instrument for
assessing both SUD severity and severity of other life prob-
lems in SUD treatment settings. It was recently updated to
the sixth edition so as to correct some psychometric prob-
lems with the widely used fifth edition, including adding a
6-​month time frame to the lifetime and 30-​day questions,
thus improving the structure and clarity of the questions,
and reducing the time burden of the many additional ques-
tions by adding screening questions with skip-​outs. The ASI
provides severity scores that have been found to be reliable
and valid for recent (past 30  days) drug use (not specific
to any one drug), alcohol use, and problems in five life
areas: medical, employment/​finances, legal, psychiatric, and
social/​family functioning (three scales for this aspect: adult
relationships (problems and support), use of free time,
and problems and needs regarding minor children). The
drug and alcohol use sections ask about past 30 days, past
6 months, and lifetime frequency of use of each of a num-
ber of drugs and also of a number of consequences of drug
or alcohol use. Each section of the interview previously
included an overall clinical rating of severity, but because
these ratings and the previous composite scores were not
acceptably reliable, they were replaced by newly developed
summary indices that were developed empirically (Cacciola
et al., 2011; Denis, Cacciola, & Alterman, 2013). However,
whether or not a summary score is desired, the specific
information derived from the interview provides the clini-
cian with a wealth of useful information. The ASI requires
specialized training offered by the authors in Philadelphia,
requires computerized scoring of the summary indices,
and requires approximately 45 to 90 minutes to administer.
A  computer-​administered version eases some of the bur-
den. The new version shows acceptable support for each of
the indices in terms of separation and stability, with strong
evidence of reliability and validity for the 30-​day indices
(Cacciola et al., 2011). (Psychometrics for the 6-​month and
lifetime indices were not reported.) Like the original ver-
sion, this edition was developed using patients in a variety of
community settings in an urban area, with the primary sub-
stance of abuse being cocaine, heroin, or alcohol, but it was
limited to mostly unemployed patients. Generalizability was
assessed between genders and between Whites and African
Americans and was found to be acceptable. It has been vali-
dated in Spanish (Díaz Mesa et al., 2010) and in Portuguese
in Brazil (Kessler et al., 2012).
Global Appraisal of Individual Needs
The GAIN’s (Dennis, 1999; Dennis, Scott, et  al., 2003;
Dennis, Titus, et  al., 2003; http://​www.chestnut.org/​li/​
368 Substance-Related and Gambling Disorders
gain) semi-​structured interview has sections on family/​
living arrangement, substance use, physical health, risk
behaviors, mental health, environment, legal, and voca-
tion. As such, it can provide comprehensive background
information on patients similar to that obtained by the
ASI. It can be used for American Society of Addiction
Medicine-​based level of care placement, Joint Committee
on Accreditation of Hospital Organization-​ based treat-
ment planning, and Drug Outcome Monitoring
Study-​based outcome monitoring. The GAIN can be
administered by paper or computer and takes 60 to 120
minutes for the initial evaluation. The substance use sec-
tion, in addition to providing diagnostic information (as
previously described), asks for self-​reported frequency of
use in the past month for categories of drugs or any sub-
stance, recency of use of each of these categories, peak
quantity of use of each category, frequency (days) of use of
each, number of days with problems from substance use,
number of past-​month SUD diagnostic symptoms, and a
current withdrawal scale, all with excellent reliability and
validity (Dennis, Titus, et al., 2003). In a comparison of
biometric data (hair and urine) and three self-​report mea-
sures (recency, quantity, and frequency) of use of mari-
juana, cocaine, opioids, and other substance, the GAIN’s
Substance Frequency Scale performed as well or better
than other measures or methods of combining measures
(Lennox, Dennis, Scott, & Funk, 2006). Other scales in
the GAIN, all with evidence of at least adequate reliabil-
ity and validity, include number of days of past treatment,
environmental risks for relapse, illegal activities, emo-
tional problems, and employment activities.
Negative Consequences of Use
Although the assessment of negative consequences of sub-
stance abuse overlaps with material addressed in the pre-
ceding section, the measures described previously either
focused on severity of diagnostic symptoms alone or on life
functioning (whether or not problems in life functioning
could be directly attributed to substance use). Assessment
of a range of consequences perceived by patients to be
specifically due to substance use can be useful for treat-
ment planning in two ways. First, it provides an overview
of areas of functioning that should improve as a result of
abstinence and treatment. Second, the information can
be used to increase the patient’s awareness of areas of life
that could be improved via abstinence.
The Inventory of Drug Use Consequences (IDUC;
Tonigan & Miller, 2002) is a 50-​item self-​report measure
of the consequences of drug or alcohol use (not differ-
entiated from each other). There are separate versions
for lifetime and the past 3  months of use, and each of
these has a version worded in the third person that can
be completed by a family member or friend. The IDTC
was developed to provide clinicians with a relatively brief
(approximately 10–​15 minutes) and easy tool that is in
the public domain. Scores on four of the five scales have
demonstrated excellent internal consistency reliability
(physical problems, social relationships, interpersonal
problems, and impulse control), and a confirmatory fac-
tor analysis showed that these same four scales adequately
represent a larger domain of negative consequences
and correlate with other measures of negative conse-
quences (Tonigan & Miller, 2002). Further work pro-
duced the 15-​item Short Inventory of Problems–​Alcohol
and Drugs (SIP-​AD; Blanchard, Morgenstern, Morgan,
Labouvie, & Bux, 2003). The items all load on one scale
(indicating the degree of adverse consequences) that has
been found to yield excellent reliability estimates and
that significantly correlates with other measures of alco-
hol and drug severity, dependence symptoms, substance
use frequency, and psychiatric severity. Although both
versions have demonstrated good to excellent reliability
and at least adequate validity (see Table 17.2), the long
version (excluding the intrapersonal section) would be
more useful in treatment planning because it provides
reliable indices of problems in four different life areas
that can be targeted for coping skills training or motiva-
tional approaches.
The Marijuana Problems Scale (MPS; Stephens,
Roffman, & Curtin, 2000) assesses 19 recent and lifetime
problems that patients with SUDs attribute to marijuana
use, each rated as no problem, minor problem, and seri-
ous problem, and that are summed to provide an index
of problem severity. This self-​report measure was derived
in part by rewording many DAST items for marijuana,
deleting the treatment items, and adding some other con-
sequences (Stephens, Wertz, & Roffman, 1993). (In one
publication, it was called the Marijuana Consequences
Questionnaire [Budney, Higgins, Radonovich, &
Novy, 2000], which can result in confusion with the other
measure by that name.) Domains include psychological,
social, legal, and occupational consequences (examples
include memory problems, family problems, and pro-
crastination). A  26-​item version is a checklist, but the
19-​item version asks patients to rate each item as a mild
or major problem versus no problem. There is limited
psychometric information available on either version of

this measure. For the 19-​item version, one study reported
very high internal consistency reliability (Stephens et al.,
2000) and showed change in problems during a 4-​month
period among marijuana-​ dependent patients in active
treatment versus delayed-​treatment condition that paral-
leled changes reported for frequency of marijuana use
and number of dependence symptoms (Stephens et  al.,
2000). However, no other forms of validity analyses have
been conducted. Although the 26-​ item checklist has
been used in more studies, there is virtually no support-
ing psychometric information for this version, with one
report of high internal consistency reliability at follow-​up
(Stephens et al., 1993) but no reported reliability pretreat-
ment, no concurrent correlations reported to support its
validity, and no differences between pretreatment abstain-
ers and users of marijuana in scores (Moore & Budney,
2002). Therefore, the 19-​item MPS is a brief and valid
measure of degree of initial problems, but further psycho-
metric information is needed and psychometric properties
of the 26-​item checklist version are unknown. A separate
50-​item measure called the Marijuana Consequences
Questionnaire (Simons, Dvorak, Merrill, & Read,
2012)  was developed and validated only on college stu-
dents and so is not recommended for clinical use.
The Cocaine Negative Consequences Checklist
(CNCC; Michalec et al., 1996) assesses long-​term nega-
tive life events that cocaine abusers perceive to result
from their own cocaine use. The items all fall on a single
scale that has demonstrated evidence of high reliability,
but they can also be scored for four reliable content area
scales:  physical health, emotional/​psychological, social/​
relationship, and legal problems. The scales correlated
significantly with other measures of use and severity
in two samples, and they were found to predict which
cocaine users would seek help (Varney et al., 1995). An
expanded second edition, with 75 items (CNCC-​75) that
added financial and vocational items (Rohsenow, Monti,
et al., 2004), has been reported to yield equally high reli-
ability estimates and predicts cocaine use outcomes after
treatment.
Expected Effects of Use
In addition to assessing past consequences, often due to
longer term use, the assessment of positive and negative
effects expected fairly immediately from an episode of
substance use can be used as feedback in motivational
interviewing (Miller & Rollnick, 1991, 2002) or in func-
tional analysis-​
based coping skills training (Rohsenow,
Substance Use Disorders 369
Monti, et al., 2004). These measures are inherently spe-
cific to specific substances. Measures developed on and
for college students are not covered because they are not
known to be relevant to clinical populations and often
involve a high reading level and large number of items.
Expectancies Across Four Substances
A brief Substance Use Beliefs Questionnaire (SUBQ) was
designed to assess expected effects of alcohol, nicotine,
opiates, and stimulants among users seeking treatment
or willing to seek treatment (Kouimtsidis, Stahl, West, &
Drummond, 2014). The two resulting factors are positive
versus negative expectancies, with good criterion and pre-
dictive validity. The 98-​item original version was reduced
to 28 items, with evidence of excellent internal reliability
estimates and substantial correlations with the long ver-
sion. The negative expectancies scales predicted change
in dependence level 3 months after treatment. No other
measures of opiate or stimulant expectancies were found
that had evidence of at least adequate reliability and valid-
ity. Most other measures of alcohol expectancies were
developed on and for university students, most of whom
did not have alcohol diagnoses.
Expectancies for Cocaine
The Cocaine Effects Questionnaire for Patient
Populations (CEQ; Rohsenow, Sirota, Martin, & Monti,
2004)  is a 33-​item self-​report instrument with seventh-​
grade reading level that assesses seven factors of fairly
immediate positive and negative effects that patients said
they expected from cocaine use. Reliability and validity
estimates have been found to be good, with several sub-
scales correlated with amount of cocaine use and with
urge to use cocaine. This information was used in cop-
ing skills treatment planning by helping patients iden-
tify alternative nondrug ways to obtain desired positive
effects and to remind patients of negative experiences
they wish to avoid (Rohsenow, Monti, Martin, Michalec,
& Abrams, 2000), and it was used in motivational inter-
viewing as a way to augment discussion of advantages and
disadvantages of cocaine use (Rohsenow, Monti, et  al.,
2004). Other cocaine expectancy measures and a paral-
lel measure for marijuana expectancies have been devel-
oped on college populations, most of whom did not use
cocaine/​marijuana, much less meet criteria for SUDs,
so these measures are not considered useful for patient
populations.
370 Substance-Related and Gambling Disorders

Assessment for Relapse Prevention 2002; Rohsenow et al., 2001), a structured interview devel-
oped to identify highly personal relapse risk situations for
According to social learning models of relapse preven-
use in cue exposure therapy, is easily adapted for use with
tion (e.g., Monti et al., 2002), some of the most impor-
any drug of abuse, as was done in identifying personal
tant areas to assess for treatment intervention include
high-​risk situations of cocaine-​dependent patients as the
(a)  situations (interpersonal, emotional/​ cognitive, and
basis of functional analysis-​based cocaine-​specific coping
environmental) that increase risk of relapse, (b)  self-​
skills training (Monti, Rohsenow, Michalec, Martin, &
efficacy about staying abstinent (both in general and in
Abrams, 1997; Rohsenow et al., 2000). However, there is
specific high-​risk situations), and (c) types of coping skills
insufficient psychometric information to allow this instru-
available to use and/​or actually used when in high-​risk
ment to be rated in the table.
situations or in general to prevent relapse. If initiation
of abstinence in treatment seekers who are not abstinent
is the goal, these same domains are important to target. Assessing Self-​Efficacy
The use of other substances is another source of relapse
Self-​efficacy for ability to resist using in high-​risk situations
risk, but methods of monitoring these are covered in
can be useful at any stage of treatment for identifying situ-
other sections of this chapter.
ations in which a patient expects to have the most trouble.
These can be assessed with several measures. First, the
Drug-​Taking Confidence Questionnaire (DTCQ; Sklar,
Assessing High-​Risk Situations
Annis, & Turner, 1997)  is a 50-​item measure that uses
The Inventory of Drug Taking Situations (IDTS; Annis & the same list of situations as in the IDTS to assess self-​
Martin, 1985; Turner, Annis, & Sklar, 1997) assesses high-​ efficacy. It requires respondents to rate how confident
risk situations for relapse based on common domains of they are that they would be able to resist the urge to use
relapse risk situations. The categories were derived from drugs in that situation. Thus, the IDTS is behavioral but
analyses of alcohol-​dependent patients’ relapse risk situa- past-​oriented, whereas the DTCQ is more subjective but
tions and therefore omit some triggers relevant to people future-​ oriented. This measure also was developed on
with drug dependence (e.g., the presence of money or people with a range of types of SUDs. The confirmatory
ATM cards [Rohsenow et  al., 2000; Rohsenow, Monti, factor analysis supported essentially the same three high-​
et al., 2004]), but the measure was normed on 364 drug-​ order factors as the IDTS: positive situations, negative sit-
dependent patients with primary cocaine (n = 159), can- uations, and temptation situations. An 8-​item short form
nabis (n = 98), or alcohol use disorders (n = 76). Factor also has been found to have generally good psychometric
structure and reliability estimates have been shown to properties (Sklar & Turner, 1999).
be good, but there is no simple way to validate items on Second, the Alcohol Abstinence Self-​Efficacy Scale
actual risk situations. The 50 self-​report items fall into fac- (AASE; DiClemente, Carbonari, Rosario, Montgomery,
tors of unpleasant emotions, pleasant emotions, physical & Hughes, 1994) has patients rate 20 situations on 5-​point
discomfort, testing personal control, urges/​temptations to scales for how confident they are that they would not drink
use, conflict with others, social pressure to use, and pleas- in each situation and again for how tempted they are to
ant times with others. These factors can be grouped into drink. The categories of high-​risk situations included are
three second-​order factors (with good psychometric model (a)  negative affect, (b)  social interactions and positive
fit): negative situations, positive situations, and urges and states, (c) physical and other concerns, and (d) withdrawal
testing personal control. Although the reliability (internal and urges. The total score had high internal reliability and
consistency) estimate was poor for the physical discom- good validity. A brief 12-​item version (McKiernan et al.,
fort scale, all other scales have demonstrated acceptable 2011)  has two factors (temptation and confidence) with
to good reliability. For each situation described, patients high internal consistency and concurrent validity. This
report how often they have used drugs in that situation in would be less useful for treatment planning because only
the past. The information can be used to design person- 6 situations are involved. It also has been adapted for use
alized relapse prevention training by emphasizing skills with drug abusers as the Drug Abstinence Self-​Efficacy
needed for handling the situations a person has actually Scale (DASE; Hiller, Broome, Knight, & Simpson, 2000),
most often associated with drug use. resulting in the same four subscales. However, because
For identifying highly idiosyncratic relapse risk situa- information on reliability and validity was not found, this
tions, the Drinking Triggers Inventory (DTI; Monti et al., measure was not rated in the table.
 Substance Use Disorders 371

Third, in the Cocaine Related Assessment of Coping designed to maintain abstinence (the General Change
Skills (Rohsenow, Monti, et al., 2004), cocaine-​dependent Strategies Questionnaire [GSC]). The measures were
patients rated how confident they would be to refrain developed, found to each consist of a single factor with
from substance use in each of 11 high-​risk situations. The excellent internal consistency, and validated first with
score demonstrated high internal consistency and con- alcohol-​dependent patients in treatment, with the sum-
current validity, and it predicted quantity and frequency mary scores for each differentiating between coping skills
of drug use 3 months after treatment (Dolan, Martin, & treatment versus control treatment and correlating with
Rohsenow, 2008). treatment outcome 3 to 6  months later (Monti et  al.,
Fourth, a simple 4-​point rating of confidence that the 2001). In analysis of the value of individual strategies,
person would not use drugs again during a specific period 13 of the urge-​specific strategies and 18 general lifestyle
of time predicts treatment outcome for opiate addicts change strategies correlated with successful treatment
(Gossop, Green, Phillips, & Bradley, 1990). However, outcome 3 to 6  months after treatment, whereas other
there is insufficient information on this measure to rate it common strategies did not (Dolan, Rohsenow, Martin,
in the table, and the broader situation-​specific measures & Monti, 2013), thus indicating the most important
are preferable because they can be used to individualize coping skills to focus treatment on. The measure was
relapse prevention and/​or coping skills training by focus- then adapted for use with cocaine-​dependent patients in
ing on the types of situations in which the patient would treatment with 21 strategies in each measure, with each
be most tempted to use or least confident about abstaining forming scales that demonstrated substantial reliability
from use. and validity estimates (Rohsenow et  al., 2005). These
were used to determine the specific skills that were cor-
related with less cocaine use at 3 and 6  months post-​
Assessing Coping Skills
treatment, with results indicating that 13 of the USS
Only a few studies investigating coping to predict out- strategies and 12 of the GSC strategies were effective in
come for opiate abusers used measures with substantial this regard (Rohsenow et al., 2005). Thus, the measures
evidence of reliability and validity. In one such study, were found to be heuristic across two types of substance
10 items were selected from the psychometrically sound use disorders. The open-​ended section can be used to
Processes of Change Questionnaire (POC; Prochaska, elicit patients’ free recall of all the strategies they plan
Velicer, DiClemente, & Fava, 1988). Among opiate-​ to use, and the frequency ratings are used to assess how
dependent individuals, abstinence was related to an often they say they have used each strategy. By identify-
increase in the 10 processes of change assessed (POC-​ ing the skills the patients already know or use, gaps in
10; Gossop, Stewart, Browne, & Marsden, 2002). These knowledge or use of effective skills can be targeted for
items were categorized into Avoidance (“remove things treatment.
from my home that remind me of drugs,” “stay away from
people who remind me of drugs,” and “stay with people
Overall Evaluation
who remind me not to use”), Cognitive (“I tell myself
I  can choose not to use drugs,” “I can keep from using There are a variety of clinically useful instruments that
if I try hard enough,” “I am able to avoid using if I want can be used in treatment planning. There is a choice of
to,” and “I must not use to be content with myself”), and scientifically sound measures that provide an evaluation
Distraction (“physical activity,” “do something to help me of the patient’s ability to function across major life areas.
relax,” and “think about something else when tempted to Whether or not problems in some of these areas result
use”). Scores for these three categories had adequate to from drug use, these areas may need to be addressed in
good internal consistency reliability in this study, and all treatment so as to maximize the individual’s structural
three types of coping were significantly greater in abstain- and functional support for abstinence, motivation to
ers, suggesting that only these 10 items are needed for use stay clean and sober, and quality of life. Drug-​specific
with opiate-​dependent patients. consequences an individual experienced can be par-
Because existing measures tapped only a limited ticularly useful in sustaining or increasing the person’s
number of the specific skills taught in many treatment motivation to become or stay abstinent from drugs by
programs, we developed measures of coping skills to be highlighting what he or she has to gain from abstinence,
used in high-​risk situations (the Urge-​Specific Strategies whereas expected acute effects can be used in functional
Questionnaire [USS]) and of lifestyle change skills analyses to focus on alternative ways to achieve many of
372 Substance-Related and Gambling Disorders

the desired outcomes (e.g., negative affect reduction or
social facilitation). The measures of situations in which
the patient would be more tempted to use or have less
confidence about staying abstinent can be used to target
relapse-​prevention treatment toward helping the patient
learn to better avoid or cope with unavoidable high-​risk
situations without using. Measures of both urge-​specific
and general lifestyle coping have been developed to assess
a range of coping skills that have been shown to be related
to reduced alcohol or cocaine use after treatment and can
be used to identify gaps in individual patients’ needed
skills. Good measures of social support for abstinence
may not be needed because such support is easy to evalu-
ate informally in a way that predicts outcome (e.g., better
treatment outcome for cocaine-​dependent patients was
predicted by number of people in one’s network regardless
of their support for treatment and by replacing substance-​
involved with substance-​free daily contacts in one’s net-
work [Zywiak et al., 2009]).
The measures selected for inclusion in this section are
all ones that could be good clinical tools, although some
require considerably more training and time than oth-
ers, and time is often of short supply in many treatment
contexts. Some of the measures in Table 17.2 with good
psychometric properties are not highly recommended
simply due to the amount of time and training required
for administration and the complexity of the scoring (i.e.,
SDSS and ASI-​6). Other measures were not highly recom-
mended because they were specific to only one substance
(e.g., CNCC-​87 and CEQ). The ones rated as highly rec-
ommended are the ones with good psychometric qualities
and seeming utility for treatment planning that are also
relatively easy to administer.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
There are several assessment measures and strategies that
can be used to track the effects of treatment on substance
use and problem severity. In addition to the IDUC, SIP-​
AD, and MPS described previously, the main options
are indices of symptom severity and toxicology analyses.
Details of the psychometric properties of these measures
are presented in Table 17.3.
Assessing Areas of Life Function
A briefer (118-​ item) form of the ASI-​ 6 (ASI-​ 30  day;
described previously) that includes only the questions
with a 30-​day time frame is commonly used for tracking
progress. However, there are few psychometric data on
the value of using the ASI to predict outcome or track
progress. Although this measure can be used to track
changes in functioning on a monthly basis, it is unclear
the extent to which changes in ASI-​6 scores correlate
with changes in drug use during the same time period.
Changes in life functioning could be somewhat inde-
pendent from changes in substance use, depending on
the extent to which these are direct targets of treatment.
However, increase in future crime at 2 years was predicted
by change in alcohol use from 0 to 6 months and not by

TABLE 17.3   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

ASI-​6 30-​day NA G G G A A G NR NR
TLFB NA NA G G NA E E E A
IDUC NA E NA G G A A A A ✓
SIP-​AD NA E NA G G A A A A
MPS NA NR NA NR NR A NR A NR
GAIN 90 Day M NA G NA NA G G A A A
Urine screens NR NA NA NA NA A E L Aa ✓
Urinalysis G NA NA NA NA G E E Ea ✓

Utility is excellent during the time a program requires 3 to 7 days/​week of attendance, but with high cost.
a

Note: ASI = Addiction Severity Index 30-​day form; TLFB = Timeline Followback Interview; IDUC = Inventory of Drug Use Consequences, four scales;
SIP-​AD  =  Short Inventory of Problems–​Alcohol and Drugs; MPS  =  Marijuana Problems Scale; GAIN 90 Day M  =  Global Appraisal of Individual
Needs–​90-​Day Monitoring version; urine screens  =  drug screening with on-​site test kits; urinalyses  =  urine drug toxicology analyses using standard
commercial laboratory methods such as EMIT or gas chromatography; L = Less Than Adequate; A = Adequate; G = Good; E = Excellent; NR = Not
Reported; NA = Not Applicable.
 Substance Use Disorders 373

the legal, drug, or other ASI Version 5 scores (Alterman control). These scales were sensitive to changes in drug
et al., 1998), contrary to what one would expect. use behavior over 3  months so that a 40% decrease in
The GAIN Monitoring 90-​ Day version (Dennis, drug use was paralleled by a 33% decrease in drug-​related
Scott, Godley, & Funk, 1999; (http://​www.chestnut. consequences (Tonigan & Miller, 2002). The short form
org/​li/​gain) is designed to evaluate change over time reviewed previously, the SIP-​AD (Blanchard et al., 2003),
in living arrangements, substance use (frequency, situ- is sensitive to treatment change, decreasing from pre-​to
ational antecedents, withdrawal, and problematic conse- post-​treatment, and with post-​treatment SIP-​AD scores
quences), treatment (use, satisfaction, and medications), correlating as expected with post-​treatment number of
physical health, risk behaviors, emotional health, legal substance use days (Blanchard et  al., 2003). Both mea-
system events, vocation, and finances. The full measure sures are rated in Table 17.3. Because of the demonstrated
takes 60 minutes and core questions take 25 minutes, sensitivity of these measures to change combined with
with a 10-​minute Quick Monitoring version available. ease of administration, they are highly recommended.
The measure has excellent statistics on change over time The MPS (Stephens et al., 2000), in the 19-​item 90-​day
in the most relevant areas across a variety of types of sub- version, may be used to track change in marijuana-​related
stance treatment settings. problems. The MPS was sensitive to change in problems
during a 4-​month period among marijuana-​dependent
patients in active treatment versus delayed-​ treatment
Assessing Drug and Alcohol Use Frequency
condition that paralleled changes reported for frequency
Although Timeline Followback (TLFB; Ehrman & of marijuana use and number of dependence symptoms
Robbins, 1994; Sobell & Sobell, 1980), a method of ask- (Stephens et  al., 2000). The 26-​item checklist version
ing about daily drug or alcohol use, is used primarily in showed no effects of treatment in one study (Budney
research, when retrospective self-​report of days of use is et al., 2000) but showed a significant decrease from before
desired, this method has been found to be the least sub- to after treatment independent of type of treatment in
ject to memory problems. The TLFB is a calendar-​assisted two other studies (Budney, Moore, Rocha & Higgins,
structured interview that provides a way to cue memory 2006; Stephens, Roffman, & Simpson, 1994). Although
so that recall is more accurate. For the period of time of change over time paralleled change in frequency of use,
interest, the person is asked to fill in all days with spe- no attempt was made to validate the measure in terms of
cial events such as holidays, birthdays, and days in jail or change in other measures of problems from cannabis use.
hospital. The person is then asked about alcohol/​drug use Therefore, the 19-​item measure may provide a basis for
on those days and the days immediately before and after seeing reduction over time in problems as a function of
those days, with other days gradually filled in from there. treatment, but replication in a second study and informa-
Although social drinkers cannot easily do this, people with tion on correlations of change in this measure to change
alcohol or drug use disorders are better at remembering in other indicators of problems are needed before the
this information. The TLFB has been found to yield good actual value of this measure is known. The limited avail-
to excellent reliability and validity estimates (Ehrman & able psychometric information prevents a high recom-
Robbins, 1994; Sobell et  al., 1996)  when the previous mendation from being made for this measure.
caveats about self-​report measures of substance use (see
the section titled Increasing Honest Reporting) are taken
Urine and Hair Toxicology Analyses
into account. This method has been found to be sensitive
to SUD treatment effects across a great many studies (e.g.,Urine toxicology drug analyses for substances of abuse
McKay et al., 1997; Rohsenow, Monti, et al., 2004). other than alcohol are the gold standard for monitoring
patients, but they require that patients still be enrolled
in a program that provides them with some reason to
Assessing Consequences of Drug or Alcohol Use
come in for such testing 3 to 7  days per week. Urine
The IDUC (Tonigan & Miller, 2002), a 50-​item self-​ screens and toxicology analyses test for the presence of
report measure of the consequences of drug or alcohol the drugs themselves and/​or of the metabolites of the
use, has a version asking about the past 3 months that can drugs (metabolites permit longer detection). The drugs
be used for tracking progress using the four scales with most commonly screened for include benzodiazepines,
evidence of substantial reliability (physical problems, cocaine, opiates, amphetamines, phencyclidine, and
social relationships, interpersonal problems, and impulse cannabinoids. Commercial laboratories usually provide
374 Substance-Related and Gambling Disorders
a standard panel of substances to be analyzed and the
option of testing for other drugs upon request. The assay
methodologies used in most laboratory testing meth-
ods (e.g., enzyme-​ multiplied immunoassay technique
[EMIT] or gas chromatography–​mass spectrometry [GC-​
MS]) yield data that are highly reliable and valid. On-​
site screening tests (strips or cups with detection strips
built in) are far less expensive and agree 97% of the time
with GC-​MS results. They do, however, have increased
false positives because they are designed to be highly
sensitive, so positive readings generally need to be con-
firmed with a laboratory test. A comparison of laboratory-​
analyzed urine toxicology data and self-​reports of days
of use 12 months after treatment entry for 337 patients
with SUDs found that neither urine tests nor self-​reports
were without their problems as a method of detection
(Lennox et al., 2006). Higher validity was seen, in gen-
eral, for self-​reported recency of use of cocaine, opioid,
and marijuana use (Lennox et al., 2006), indicating that
it is of value also simply to ask patients how recently they
used drugs when monitoring their use (when using the
guidelines described under the section titled Increasing
Honest Reporting).
There are problems that can be encountered with
urine drug testing. One such problem pertains to the win-
dow of detection. For example, although methadone pro-
grams routinely require daily testing, most drugs of abuse
can be detected with certainty over a 2-​or 3-​day window
even with qualitative methods of detection (just a positive
or negative answer, as opposed to quantitative methods
that give the amount detected). However, because most
drugs can stay in the tissues for approximately 7 days after
abstinence begins, and marijuana can be detectable (50
ng/​L) for 2 weeks after heavy use (Hawks & Chiang, 1986),
readings may be positive for some time after abstinence
begins. Therefore, programs often allow an initial wash-
out period for the urine to become clean before imposing
any consequences or before contingency management
programs start voucher reinforcement based on abstinent
readings (e.g., Budney et al., 2006). A second problem is
the potential for false-​positive test results. The method-
ologies involved in most laboratory tests greatly decrease
the chance of false positives, yet a person can still have
reason to claim that a test showed a false positive for opi-
ates if, for example, he or she had eaten a large amount of
poppy seeds. When not used for legal purposes, it may be
enough to require that patients avoid all non-​illicit sources
of positive readings. A third problem is related to the intro-
duction of contaminants by patients. Patients who expect
unpleasant consequences from positive readings may go
to great lengths to “beat” the test. This can include bring-
ing a hidden sample of urine from a clean person, adding
contaminants (e.g., soap, vinegar, lemon juice, salt, and
bleach) to invalidate the test, or drinking large quantities
of water before giving a sample to make the sample too
dilute for a valid test. Other evasion methods have been
developed, including an artificial penis or hidden plastic
tubing and an IV bag with heating strips. Some of these
can be overcome by requiring carefully monitored test-
ing and requiring some hours at the site without drinking
before obtaining the sample.
Testing hair for the presence of drugs of abuse has
raised some interest because hair will contain residue
of drugs over the length of the hair, thus providing a
detection window of months or years, depending on the
length of the hair. Drugs enter the hair at the follicle level
via blood, sebum (from glands in the scalp), and sweat
(Huestis, 2001). However, several problems limit the
adoption of this method more widely to date, including
two serious ones: hair color bias and environmental fac-
tors. First, drugs are more strongly detectable in darker
hair than in lighter hair (Joseph, Tsai, Tsao, Su, & Cone,
1997), leading to more false negatives among blond or
white-​haired people than among people with brown or
black hair. In addition, because the higher lipid content
in curlier hair (Cruz et  al., 2013)  may affect absorption
of lipid-​soluble drugs, there is a serious concern that this
would lead to racial or ethnic differences in accuracy of
detection. Second, drugs also can be absorbed into the
hair via environmental exposure, especially smoke, and
repeated shampoo treatments or solvent washes do not
completely remove environmental cocaine from the hair
(e.g., Wang, Darwin, & Cone, 1994). Therefore, some-
one can test positive despite remaining abstinent. A third
problem is that there are few places where hair testing for
drugs is available. A fourth is that hair testing is less sensi-
tive to detecting marijuana than is urine toxicology analy-
sis, and there is great individual variability in the sweat
that affects hair testing (Baron, Baron, & Baron, 2005).
Therefore, hair analysis has more pitfalls than advantages
at the present time. Given that urine detection is highly
reliable and fully adequate for within-​treatment monitor-
ing, it remains the preferred biological method.
Overall Evaluation
For monitoring of progress in terms of drug use, urine
drug analyses at least three times per week remain the
gold standard. Although urine drug screens are poor
at detecting alcohol use, due to the rapid metabolism

of alcohol, these are excellent for monitoring all other
drugs of abuse when the precautions described previ-
ously are handled. For monitoring of monthly change in
problems resulting from drug or alcohol use or function
in terms of family, legal, and psychological problems,
the GAIN-​90 Day M is developed for this purpose and
is scientifically sound. Both methods can identify when
the person might be using substances and, therefore,
be in need of some additional booster counseling. The
IDUC is effective in showing change in problems that
result from drug use over time and so is recommended
for this purpose.
CONCLUSIONS AND FUTURE DIRECTIONS
The clinician treating patients with SUDs has a number
of tools available for screening, diagnosis, assessment of
problem severity, assessment of risk factors for relapse to American Psychiatric Association. (2013). Diagnostic and sta-
address in treatment, and monitoring of treatment prog-
ress and outcomes. Some of the tools (particularly the
diagnostic and some problem severity tools) are time-​
consuming and require extensive training: These may be
more difficult to adopt into clinic practices that are short
on time. Other tools are quicker and/​or easier to adminis-
ter and score for rapid use in treatment planning or moni-
toring of progress. It is hoped that future work will focus Annis, H. M., & Martin, G. (1985). Inventory of Drug-​Taking
more on developing instruments that clinicians can use
easily and with minimal time to provide useful guidance
for treatment planning and evaluation.
Future development work with assessment instru-
ments needs to include more of a focus on determin-
ing validity and treatment sensitivity, in particular. For
example, although the ASI is widely used for monitor-
ing treatment progress, there is very little information to
demonstrate that it validly tracks changes in other indi-
cators of progress. Given such a widely used face-​valid
instrument, such information would be valuable. Future Blanchard, K. A., Morgenstern, J., Morgan, T. J., Labouvie,
work should also focus on making instruments that do
not require extensive training, long administration time,
and complex scoring procedures. Not only do these fac-
tors drive up costs, and often prevent use due to busy
schedules, but also when extensive training is needed, it Brown, S., Gleghorn, A., Schuckit, M., Myers, M., & Mott,
is too easy for assessors’ abilities to drift over time unless
regular retraining or testing of their abilities is conducted.
A number of instruments in the future will probably be Budney, A. J., Higgins, S. T., Radonovich, K. J., & Novy, P. L.
available not only via computer but also via Web-​based
applications, allowing interactive responses with patients,
computerized scoring, and access to expert help at the
touch of a mouse.
Substance Use Disorders 375
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 18
Alcohol Use Disorder
Angela M. Haeny
Cassandra L. Boness
Yoanna E. McDowell
Kenneth J. Sher
In this chapter, we consider various measures for assess-
ing alcohol use disorder (AUD) for the purposes of diag-
nosis, case conceptualization and treatment planning,
and treatment monitoring and evaluation. It is impor-
tant to preface this chapter with information about the
changes made to the AUD criteria in the fifth edition
of the Diagnostic and Statistical Manual of Mental
Disorders (DSM-​ 5; American Psychiatric Association
[APA], 2013). Unlike the DSM-​ IV-​
TR (APA, 2000),
which defined two diagnoses under the rubric of AUDs
(i.e., alcohol abuse and alcohol dependence), the DSM-​
5 defines a single AUD diagnosis. Key reasons for this
change are that there was scant psychometric evidence
that abuse and dependence were distinct constructs and
that some criteria of abuse appeared to be more severe than
some criteria for dependence (which contradicted the
assumption that abuse was a less severe form of AUD)
(Hasin et al., 2013). In addition, one could receive a diag-
nosis of abuse based on a single symptom, resulting in a
high prevalence of false-​positive diagnoses (i.e., “diag-
nostic impostors”; Martin, Chung, & Langenbucher,
2008). The AUD criteria were largely unchanged from
DSM-​IV-​TR to DSM-​5, retaining 10 of the 11 criteria
previously used to diagnose abuse or dependence; the
criterion legal problems was removed and craving was
added (for more details, see Hasin et al., 2013). To meet
DSM-​5 criteria for an AUD diagnosis, an individual
must endorse at least 2 of the 11 items within the same
12-​month period, and the symptoms must cause impair-
ment and/​or distress. The DSM-​5 also includes a sever-
ity continuum such that individuals who endorse 2 or 3
381
criteria meet the requirement for mild AUD, individuals
who endorse 4 or 5 criteria meet the requirement for
moderate AUD, and individuals who endorse 6 or more
criteria meet the requirement for severe AUD. Although
these changes influence measures used to diagnose and
conceptualize AUD as a syndrome, they have had little
influence on measures used for treatment planning,
treatment monitoring, or treatment evaluation.
GENERAL DIAGNOSTIC CONSIDERATIONS
Prevalence/​Incidence
The National Epidemiologic Survey on Alcohol Related
Conditions (NESARC-​III; Grant et al., 2014) is the most
recent U.S.  nationally representative survey that provides
information on the prevalence and incidence of AUD in
the past year (i.e., 12-​month prevalence) and over the course
of a person’s lifetime (i.e., lifetime prevalence). According
to published NESARC-​III data, the 12-​month and lifetime
prevalence rates of AUD are 14% and 29%, respectively
(Grant et al., 2015). Consistent with prior national epide-
miologic surveys, Grant et al. (2015) found that individuals
with the highest 12-​month and lifetime rates of AUD tended
to be male (18% and 36%, respectively), Native American
(19% and 43%, respectively), White (14% and 33%, respec-
tively), aged 18 to 29  years (27% and 37%, respectively),
and never married (25% and 36%, respectively). In terms
of socioeconomic status, individuals with a high school
degree and some college or higher had the highest rates
382 Substance-Related and Gambling Disorders
of 12-​month and lifetime AUD compared to those with
less than a high school degree. Those with an income of
less than $20,000 had the highest rate of 12-​month AUD
(16%) and those with an income greater than $70,000 had
the highest rate of lifetime AUD (30%). Generally, a posi-
tive relationship has been found between severity of AUD
and disability; endorsing a single AUD criterion is associ-
ated with greater disability compared to those who do not
endorse any AUD criteria. Notably, only 8% and 20% of
those with a 12-​month and lifetime AUD, respectively,
sought treatment or help for their alcohol problems, and
the mean age of first treatment episode was 29 years. The
most commonly used treatment resources included 12-​step
groups, health care practitioners, outpatient facilities, and
rehabilitation programs.
Course/​Prognosis
The general course of AUD begins with increasing alcohol
involvement during adolescence, peak involvement dur-
ing late adolescence and early adulthood, and a gradual
decrease during adulthood (Grant et al., 2004; Schuckit,
2009; Sher, Grekin, & Williams, 2005). Although this is
recognized as the general course of AUD, the course is
extremely heterogeneous across individuals. Four proto-
typical courses of alcohol involvement have been iden-
tified:  a non-​user/​
stable low-​
user course, a chronic or
high-​user course, a “developmentally limited” course that
declines over the lifespan (see Zucker, 1987), and a later-​
onset course that gradually increases over the lifespan
(Sher, Jackson, & Steinley, 2011).
Individuals who begin drinking alcohol at an earlier
age are at an increased risk for developing AUD and
alcohol-​ related problems in adulthood (Nelson, Van
Ryzin, & Dishion, 2015). For example, those who begin
drinking prior to age 15  years are 1.4 times more likely
to develop AUD compared to those who begin drinking
later (Dawson, Goldstein, Chou, Ruan, & Grant, 2008).
Although the majority of those with early onset AUD
“mature out” over time in large part due to the assump-
tion of adult roles that are incompatible with drinking
(e.g., increased work responsibilities and marriage) and
general psychosocial maturity, others persist in risky drink-
ing (Chassin, Sher, Hussong, & Curran, 2013; Lee &
Sher, in press). The relative risk ratio (RR) of mortality
among those with AUD is nearly one and a half times
higher for women than for men (RR = 4.64 vs. RR = 2.98,
respectively). Furthermore, those in younger age groups
and those in treatment have a substantially higher risk of
mortality than do those with AUD who are not in these
groups (Roerecke & Rehm, 2013).
Comorbidity
AUD is highly comorbid with other psychiatric disorders.
For example, individuals with lifetime AUD are at greater
odds of also having co-​occurring lifetime major depres-
sive disorder (odds ratio [OR]  =  2.0), bipolar I  disorder
(OR  =  5.0), post-​traumatic stress disorder (OR  =  3.0),
generalized anxiety disorder (OR  =  2.5), and border-
line personality disorder (OR  =  4.1) after controlling for
sociodemographic characteristics (Grant et al., 2015). After
adjusting for other co-​occurring disorders, relative odds for
most major disorders still remain quite high: major depres-
sive disorder (OR  =  1.3), bipolar I  disorder (OR  =  2.0),
post-​traumatic stress disorder (OR = 1.3), generalized anxi-
ety disorder (OR = 1.2), and borderline personality disor-
der (OR  =  2.0). Furthermore, AUD is highly comorbid
with other substance use disorders (SUDs). Odds ratios are
estimated to be approximately 7.8 between lifetime AUD
and any other drug use disorder and 4.6 between AUD
and nicotine use disorder after controlling for sociodemo-
graphic characteristics (Grant et  al., 2015). After adjust-
ing for co-​occurring disorders, these odds are 4.1 and 3.2,
respectively. Consequently, individuals presenting with
AUD should be evaluated for a range of frequently comor-
bid conditions, and AUD should always be considered
when assessing individuals with emotional, psychotic, and
personality disorders, as well as with other forms of SUDs.
Etiology
There exists a rich history of etiologic models of AUD,
which implicate various genetic, biological, psychosocial,
and environmental influences (e.g., Chassin, Colder,
Hussong, & Sher, 2016; Sher, Martinez, & Littlefield,
2011). Having a family history of alcohol problems is one
of the strongest risk factors for developing problems with
alcohol. Data from NESARC (Grant, Moore, Shepard,
& Kaplan, 2003; Grant et al., 2004) indicated that 22% of
adults in the United States have at least one parent with
alcohol problems, and this risk nearly doubles with two
(OR  =  4.44; 95% confidence interval [CI], 3.93–​5.02])
versus one parent (OR = 2.51; 95% CI, 2.38–​2.66) (Yoon,
Westermeyer, Kuskowski, & Nesheim, 2013). A  meta-​
analysis of twin and adoption studies indicated that the
heritability (i.e., the proportion of variance explained by
genetic factors) of AUD was 49% (95% CI, 43%–​53%), the

proportion of variation explained by shared environment
was 10% (95% CI, 3%–​16%), and the proportion of vari-
ance due to unique effects was 39% (95% CI, 38%–​42%)
(Verhulst, Neale, & Kendler, 2015). Although various
genetic variants have been implicated in the biological risk
for AUD (e.g., ALDH2, OPRM1, and GABRA2) (Jones,
Comer, & Kranzler, 2015; Stallings, Gizer, & Young-​
Wolff, 2016), the field is still in the early stages of char-
acterizing how genetic variation impacts susceptibility to
AUD. Some research has suggested that biological risk is
mediated by factors such as alcohol metabolism, subjec-
tive response to alcohol, and a general tendency toward
externalizing behavior. In terms of subjective response to
alcohol, some evidence suggests those with a family his-
tory of AUD, compared to those with no family history of
AUD, are more sensitive to the rewarding effects of alco-
hol (e.g., Morzorati, Ramchandani, Flury, & O’Connor,
2002; Schuckit, 1994; Söderpalm Gordh & Söderpalm,
2011). Furthermore, having a general tendency toward
externalizing behavior makes one more likely to engage
in a range of deviant behaviors such as excessive alcohol
use (Chassin et al., 2013). In fact, research demonstrates
that externalizing disorders are robust predictors of AUD
onset from ages 13 to 30 years (Farmer et al., 2016), and
much of the genetic influence on AUD is shared with
other externalizing disorders (Kendler, Prescott, Myers, &
Neale, 2003).
Many etiologic models, including positive and nega-
tive affect regulation models, propose AUD develops
through processes related to both positive and negative
reinforcement. These include expectancy models that
posit that drinking is related to the expectancy that alco-
hol use will enhance positive emotions or relieve nega-
tive emotions (e.g., Maisto, Carey, & Bradizza, 1999).
Similarly, motivational models of alcohol consumption
highlight the importance of consuming alcohol for both
positive reinforcement (“enhancement motives”) and
negative reinforcement (“coping motives” and “self-​
medication”), with the latter being more directly related
to alcohol problems (and presumably syndromal AUD)
(Cooper, Kuntsche, Levitt, Barber, & Wolf, 2016). As
such, drinking expectancies and motives can represent
a critical domain for assessment in those with AUD. For
instance, some individuals may drink to increase positive
affect, whereas others may drink to escape or avoid pain-
ful emotions. In fact, individuals are versatile in their
motivations and expectancies, as most heavily alcohol-​
involved individuals report drinking for both positive
and negative reasons. Both positive and negative affect
Alcohol Use Disorder 383
dysregulation are related to early onset, risky alcohol use
and AUD (Cheetham, Allen, Yucel, & Lubman, 2010).
Environmental factors such as experiences within the
family and peer relations have also been implicated in
etiologic models for AUD. Familial factors that increase
risk for offspring AUD include parenting practices, fam-
ily structure, prenatal exposure to alcohol and drugs,
poor parent–​ child relationships (characterized by dis-
harmony, low cohesion, and disorganization), family
environment effects, exposure to socialization messages
about substances, and increased opportunities to use.
Research has demonstrated, for example, that decreased
parental monitoring, low responsiveness (e.g., neglect),
excessive use of harsh discipline (e.g., abuse), and defi-
cits in parental warmth and control predict adolescent
substance use (Chassin, Colder, et  al., 2016; Chassin,
Haller, et al., 2016).
AUD must also be considered within the context of
interpersonal relationships outside the family of origin.
Individuals with AUD experience problems in their
relationships with others, particularly their relationships
with intimate partners. Marriage is generally related to a
reduced risk for AUD. Specifically, married individuals
tend to drink less and have fewer AUD symptoms com-
pared to their unmarried peers (Rodriguez, Neighbors,
& Knee, 2013). However, some married couples still
experience AUD. Spouses of individuals with AUD have
lower marital satisfaction and higher rates of depression,
anxiety, and psychological distress, in addition to more
frequent reports of physical and emotional abuse, com-
pared to spouses of individuals without AUD. In fact,
alcohol problems predict subsequent marital distress.
Interdependently, marital distress also predicts increased
alcohol use and alcohol-​related problems, demonstrating
the complex nature of the reciprocal relationship between
marriage and alcohol use (Rodriguez et al., 2013).
It is also important to understand the social context in
which the drinking occurs (e.g., while out with friends or
alone) as well as the drinking patterns of the individual’s
peers. For example, there is considerable evidence demon-
strating that affiliation with deviant peers in adolescence
is associated with substance use and related problems
(Chassin, Colder, et  al., 2016). There also exists a well-​
documented relationship between treatment outcomes
and both level of social support and social network char-
acteristics (including size, composition, and density;
Mavandadi, Helstrom, Sayers, & Oslin, 2015). Therefore,
given the importance of contextual factors such as peer
affiliations, the marital relationship, and social support,
384 Substance-Related and Gambling Disorders
the consideration of interpersonal and social consequences
of drinking and abstinence can provide valuable clinical
information.
PURPOSES OF ASSESSMENT
The purpose of this chapter is to review measures relevant
to assessing individuals with AUD. Specifically, this chap-
ter provides an overview of assessments intended for AUD
(a)  diagnosis, (b)  case conceptualization and treatment
planning, and (c)  treatment monitoring and evaluation.
Although this chapter primarily focuses on clinical assess-
ment, measures of alcohol-​ related constructs are also
important in research and forensic settings. Diagnostic
and outcome assessments may be especially useful in
treatment development and implementation research.
In addition, medical settings, such as hospitals, urgent
care facilities, and emergency rooms, use alcohol screen-
ing to evaluate patients and determine suitable care or to
provide treatment referrals for alcohol-​related conditions
such as alcohol withdrawal syndrome. Likewise, alcohol-​
related assessments are useful in legal settings for iden-
tifying intoxicated drivers and conducting psychological
evaluations (e.g., custody hearings). Thus, assessments
included in this chapter may be applicable in a variety of
both clinical and nonclinical settings.
A systematic approach was used to identify relevant
assessments within each of the three purposes mentioned
previously. First, we searched major books (Binge Drinking
and Alcohol Misuse: Among College Students and Young
Adults, Winograd & Sher, 2015; Center for Substance Abuse
Treatment, 1998; National Institute on Alcohol Abuse and
Alcoholism [NIAAA], 2003; ) and book chapter reviews (e.g.,
Del Boca, Darkes, & McRee, 2016; Martens, Arterberry,
Cadigan, & Smith, 2012; Martino, Poling, & Rounsaville,
2008)  of alcohol assessment measures for clinical practice
and research. In addition, all alcohol-​related journals were
reviewed from 2013 to 2016 for alcohol assessments. The 27
alcohol-​related journals reviewed included Alcohol; Alcohol
and Alcoholism; Alcohol Research; ISRN Addiction Journal
of Addiction; Journal of Alcoholism and Drug Dependence;
Drug and Alcohol Review; Journal of Studies on Alcohol and
Drugs (and supplemental journal); Addiction and Health;
Addiction Biology; Addiction Science & Clinical Practice;
Canadian Journal of Addiction; International Journal of
Mental Health and Addiction; Journal of Substance Abuse
Treatment; Substance Abuse and Rehabilitation; Substance
Abuse: Research and Treatment; Substance Abuse, Treatment,
Prevention and Policy; Addictive Behaviors; Alcoholism & Drug
Abuse Weekly; American Journal on Addictions; International
Journal of High Risk Behaviors & Addiction; Journal of
Addictions & Offender Counseling; Journal of Addictive
Diseases; Psychology of Addictive Behavior; Alcoholism,
Clinical and Experimental Research; Substance Abuse; and
Alcohol Research:  Current Reviews. Furthermore, major
websites providing a catalog of assessment measures were
reviewed, specifically those of The Center on Alcoholism,
Substance Abuse, and Addiction (CASAA) at the University
of New Mexico (https://​casaa.unm.edu/​Instruments); the
Alcohol and Drug Abuse Institute (ADAI) at the University
of Washington (http://​lib.adai.uw.edu/​instruments); and
the PhenX Toolkit sponsored by the National Institutes of
Health (NIH; https://​www.phenxtoolkit.org).
Google Scholar and Scopus search engines were used
to find relevant psychometric articles to rate each instru-
ment. Articles that provide the psychometric properties of
the instruments included in this chapter were identified
using the following search terms: “psychometrics,” “reli-
ability,” “validity,” and “internal consistency.” A  combi-
nation of data from the books, chapters, psychometric
articles, and manuals was used to rate each instrument
recommended in this chapter.
ASSESSMENT FOR CASE IDENTIFICATION
AND DIAGNOSIS
Case Identification
Although nearly 14% of the U.S.  population meets
criteria for a past-​year diagnosis of AUD (Grant et  al.,
2015), many individuals with alcohol use problems will
go undetected (NIAAA, 2003). Given that continued
risky drinking is associated with further alcohol-​related
negative consequences, screening is a prevention pri-
ority. In fact, the National Commission on Prevention
Priorities includes alcohol misuse screening among
the top prevention services (Maciosek et  al., 2006).
Research demonstrates that regular AUD screening is
cost-​effective from a health system perspective as well as
a societal perspective (Solberg, Maciosek, & Edwards,
2008). Interestingly, research has also indicated that
patients support being screened for at-​risk drinking by
their physicians whether in the form of biomarker labo-
ratory tests or self-​report measures (Miller, Thomas, &
Mallin, 2006).
The purpose of screening is to identify individuals
with alcohol-​related problems or consequences as well
as those who are at risk for experiencing such problems.

An important goal of utilizing alcohol screeners is the
early detection of individuals with alcohol-​related prob-
lems, with the intention of initiating further assessment
and treatment when indicated. Screening tests are evalu-
ated among a range of dimensions, including sensitivity,
specificity, positive predictive value (PPV), and negative
predictive value (NPV). Sensitivity, also known as the true
positive rate, quantifies the extent to which test scores
correctly identify people with the problem of interest.
Specificity, or true negative rate, quantifies the extent to
which test scores can identify people without the prob-
lem of interest. PPV is the proportion of individuals who
screen positive that actually have the disorder, whereas
NPV is the proportion of individuals who screen negative
that do not have the disorder. Cut-​off values for screening
tests are chosen such that they maximize sensitivity, speci-
ficity, PPV, and NPV.
An important characteristic when considering screen-
ing measures is ease of administration. Providers often
have limited financial and time resources, which means
screening tests for AUDs and related problems should be
brief, easily administered with minimal time needed for
training and scoring, and straightforwardly incorporated
with other assessments or procedures. Our recommenda-
tions for screening measures favor these characteristics.
Finally, it is important to consider the populations
for which various instruments have been normed. Each
of the measures described in this section has been vali-
dated across a range of populations (e.g., college students
and adolescents) and settings (e.g., hospitals and mental
health centers). In cases in which this is not the case or
the instruments are strongly supported in a particular
population (e.g., the Fast Alcohol Screening Test for use
in hospital settings), this is noted in the text. Table 18.1
summarizes the ratings of various screening and diagnos-
tic measures. Specific values for reliability and validity
estimates are not reported in the text. Interested readers
should consult the citations reported for each instrument
in order to augment the general information provided in
the Table 18.1.
Three major approaches to screening and case iden-
tification exist: laboratory tests, screening interviews, and
self-​
report questionnaires. Laboratory tests are used to
assess biomarkers, which are reflections of physiological
reactions to heavy drinking. Biomarkers are useful because
they do not rely on self-​report and, as a result, are not vul-
nerable to subjective recall and various self-​report biases.
Phosphatidylethanol (PEth; e.g., Walther et al., 2015) is a
specific metabolite of ethanol and, unlike other biomark-
ers, is not influenced by liver diseases (Litten, Bradley, &
Alcohol Use Disorder 385
Moss, 2010). Numerous studies have demonstrated that
PEth has a low rate of false positives and has the highest
sensitivity compared to carbohydrate-​ deficient transfer-
rin (CDT), mean corpuscular volume (MCV), and γ-​
glutamyl transferase (GGT) (e.g., Bajunirwe, Haberer, Ii,
& Hunt, 2014). GGT (e.g., Reynaud et al., 2000) is a gly-
coenzyme and is included in most standard blood panels.
GGT is elevated when an individual has engaged in heavy
alcohol use over the course of a few weeks, which makes
it appropriate for the detection of severe AUDs. Although
the evidence on the sensitivity of CDT is mixed, for some
purposes it has adequate psychometric properties as an
AUD screening laboratory test. CDT (e.g., Walther et al.,
2015)  is often very sensitive to changes in drinking and
therefore useful for both screening and relapse identifi-
cation. CDT has been widely studied across a variety of
samples and settings; however, the fact that it is not rou-
tinely included in blood panels makes it somewhat more
expensive and time-​consuming as a screener than GGT.
Although GGT is useful as a screening biomarker, stud-
ies suggest CDT is superior to GGT in terms of specific-
ity. Some work has demonstrated the utility of combining
CDT and GGT in the screening of AUD because this
results in increased sensitivity and specificity relative to
either metabolite on its own (e.g., Bertholet, Winter,
Cheng, Samet, & Saitz, 2014). MCV (e.g., Mundle,
Munkes, Ackermann, & Mann, 2000) is a measure of the
size of red blood vessels and is affected by many other con-
ditions, such as liver disease and anemia, which reduces
its specificity as a screening tool. MCV responds slowly
to abstinence and may remain at high levels in an indi-
vidual’s system as long as 3  months after the individual
has stopped using alcohol. There is also evidence that
MCV performs differently in males and females, so dif-
ferent cut-​ offs are recommended. Furthermore, MCV
has been shown to increase linearly with age. Overall, if
a biomarker is desired, PEth appears to be the laboratory
test with the best psychometric properties for the screen-
ing of hazardous/​harmful drinking persisting for at least a
few weeks. If the aim is to screen for hazardous/​harmful
drinking that has lasted less than a few weeks, CDT is
recommended (Snell, Bhave, Takacs, & Tabakoff, 2016).
Four screening interviews are psychometrically sound
for screening across various populations and settings: the
CAGE (Ewing, 1984), the Fast Alcohol Screening Test
(FAST; Hodgson, Alwyn, John, Thom, & Smith, 2002),
the Alcohol, Smoking and Substance Involvement
Screening Test (ASSIST; WHO ASSIST Working
Group, 2002), and the Global Appraisal of Individual
Needs Short Screener (GAIN-​ GSS; Dennis, Feeney,
386 Substance-Related and Gambling Disorders

TABLE 18.1   Ratings of Instruments Used for Case Identification and Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity validity Generalization Utility Recommended

Screening and Case Identification Laboratory Tests

PEth E NA NA NR NA E G A ✓
GGT E NA NA NR NA A E A
MCV E NA NA NR NA A A A
CDT E NA NA A NA G A A
Screening Interviews and Self-​Report Questionnaires
AUDITa E G NA G A G E A ✓
ASSIST G G E A G G E G ✓
GAIN-​GSSa G G NR NR A G G G ✓
CAGE G G G A A G G A ✓
MASTa A G NA G A G A A ✓
FAST G A NR A NR A A A
RAPS-​4 G NR NA NR A A G A
DUSI-​R G A NA NR A G E A
SAAST-​R A E NA NR NR G A G
PAWSS A NR E NR A NR NR A
PDSQ A G NA A NR G A A
SSI-​AOD (SSI-​SA)a A G NA A G A E E
ADS A G NA A A G G A
Diagnostic Assessments
AUDADISa G NR NR G A A G A ✓
SCID A NR G A A A A A ✓
PRISM A NR G A A NR A A
SDDS A G NR A A NR A A
SSAGAa A NR G G A A G A

  Measure available at https://​www.phenxtoolkit.org.

a

Note:  PEth  =  phosphatidyl ethanol; GGT  =  γ-​glutamyl transpeptidase; MCV  =  Mean Corpuscular Volume; CDT  =  Carbohydrate-​ Deficient
Transferrin; AUDIT  =  Alcohol Use Disorders Identification Test; ASSIST  =  Alcohol, Smoking, and Substance Involvement Screening Test; GAIN-​
GSS = Global Appraisal of Individual Needs–​Gain Short Screener; CAGE = not an acronym—​the letters cue the questions that compose the instrument;
MAST = Michigan Alcoholism Screening Test; FAST = Fast Alcohol Screening Test; RAPS-​4 = Rapid Alcohol Problems Screen-​4; DUSI-​R = Drug
Use Screening Inventory-​Revised; SAAST-​R = Self-​Administered Alcohol Screening Test-​Revised; PAWSS = Prediction of Alcohol Withdrawal Severity
Scale; PDSQ = Psychiatric Diagnostic Screening Questionnaire; SSI-​AOD (SSI-​SA) = Simple Screening Instrument for Alcohol and Other Drugs (also
called the Simple Screening Instrument for Substance Abuse); ADS = Alcohol Dependence Scale; AUDADIS = Alcohol Use Disorder and Associated
Disabilities Interview Schedule; SCID = Structured Clinical Interview for DSM; PRISM = Psychiatric Research Interview for Substance and Mental
Disorders; SDDS  =  Substance Dependence Severity Scale; SSAGA  =  Semi-​Structured Assessment for the Genetics of Alcoholism; A  =  Adequate;
G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

Stevens, & Bedoya, 2006). The CAGE takes less than
1 minute to administer and requires minimal training.
Each letter in CAGE represents a single question, mak-
ing the instrument easy to administer and replicate. It
assesses the following: ever felt the need to cut down on
drinking, ever felt annoyed by others criticizing your
drinking, ever felt bad or guilty about your drinking, and
ever have a drink first thing in the morning (i.e., eye-​
opener). The original instrument uses a cut-​off score of
2, but a cut-​off score of 1 has been recognized as clini-
cally significant and indicative of the need for further
assessment (Bradley, Bush, McDonell, Malone, & Fihn,
1998). The FAST is also a 4-​item, brief interview (as
described later, it can also be administered as a self-​report
measure). The first item is a screener assessing how often
the individual has one drink or more on a single occa-
sion. If the subject does not respond “never,” then he or
she is asked about blackout or memory loss, failure to
do what was expected because of drinking, and concern
from others about drinking behavior or being advised by
others to cut down. This procedure, in both interview
and questionnaire formats, is effective for mass screen-
ing in epidemiologic work or in hospital settings, for
example. The ASSIST is more extensive than the other
interviews because it assesses both alcohol and other
drug use. The skip logic employed by the instrument
aims to keep administration time relatively brief, with
estimates ranging from 5 to 15 minutes. ASSIST requires
 Alcohol Use Disorder 387

more training in administration and scoring compared Diagnosis

to the other interviews. The GAIN-​GSS is one of the
DSM-​5 defines AUD as a problematic pattern of alcohol
few available screeners addressing both mental health
use leading to clinically significant impairment or distress.
and drug and alcohol problems. It includes 20 items and
To receive a “current” diagnosis of AUD, an individual
takes 3 to 5 minutes to administer. GAIN-​GSS is highly
must have experienced at least two of the following symp-
recommended by the NIH Data Harmonization Project
toms within the past 12 months: drinking more alcohol or
(i.e., https://​www.PhenX.org). The CAGE, ASSIST, and
over a longer time period than initially intended; a recur-
GAIN-​GSS have been normed in both adolescent and
rent desire to cut down on alcohol use or failed attempts
adult populations, whereas the FAST has been normed
to control use; spending a significant amount of time
mainly among adults.
finding, consuming, or recuperating from the effects of
Among self-​report questionnaire measures, the
alcohol; craving (i.e., a powerful desire or urge to con-
Alcohol Use Disorder Identification Task (AUDIT;
sume alcohol); failure to meet important responsibilities
Babor, Biddle-​Higgins, Saunders, & Monteiro, 2001) and
at work, school, or home due to alcohol use; continued
Michigan Alcoholism Screening Test (MAST; Selzer,
alcohol use regardless of social or relational conflicts;
1971) are the most highly recommended. Developed by
important activities given up or reduced due to alcohol
the World Health Organization (WHO), the AUDIT is
use; repeated use in situations in which there is potential
a brief, 10-​item instrument with excellent psychometric
for physical harm to self or others; continued use despite
properties across gender, ages, and culture as well as a
awareness of a physical or psychological ailment caused or
range of settings. There are various short versions of the
made worse by alcohol; tolerance (i.e., a need for larger
AUDIT, including the AUDIT-​3 and AUDIT-​4, which
amounts of alcohol to attain the anticipated effect); and
are respectively 3-​and 4-​item versions of the full scale
withdrawal. To receive a lifetime diagnosis of AUD, an
(Gual, 2002). The AUDIT-​Primary Care (AUDIT-​PC;
individual must endorse two of the aforementioned cri-
Piccinelli et  al., 1997)  is a 5-​item abbreviated version,
teria within the same 12-​month period. Lifetime diag-
and the AUDIT-​Consumption (AUDIT-​C; Bush et  al.,
nosis of AUD serves many important purposes, such as
1998)  is a 10-​ item abbreviated version that includes
estimating prevalence of AUD. However, clinicians and
items on alcohol consumption. These short versions
researchers conducting lifetime assessments of AUD
have promising psychometric properties, but more
should be aware of the limitations of these assessments,
research is needed before they can be recommended
such as underreporting of problems at a single assess-
for widespread use. The MAST is a 25-​item instrument
ment and the limited validity of late-​onset cases (Haeny,
that has performed well in a variety of settings (e.g., inpa-
Littlefield, & Sher, 2014a, 2014b, 2016).
tient and outpatient) across a wide range of populations.
Accurate diagnosis is fundamental to AUD treatment
The MAST has various short forms, including the 10-​
and research. Formal diagnosis has many benefits. For
item Brief MAST (BMAST; Pokorny, Miller, & Kaplan,
example, it provides a shared nomenclature for clinicians
1972)  and the 13-​item Short MAST (SMAST; Selzer,
to discuss treatment planning and outcome, serves as a
Vinokur, & van Rooijen, 1975).
basis for organizing and retrieving information, provides
Notably, some of the measures in Table 18.1 can be
a basis for predictions, and serves a sociopolitical function
administered as either interviews or questionnaires. These
(e.g., allows reimbursement from insurance companies)
include the MAST (Selzer, 1971), FAST (Hodgson et al.,
(Blashfield, Keeley, Flanagan, & Miles, 2014). Although
2002), AUDIT (Babor et  al., 2001), Simple Screening
many clinicians and researchers may gather information to
Instrument for Alcohol and Other Drugs (SSI-​ AOD;
inform diagnosis during initial sessions, formal and struc-
Winters & Zenilman, 1994), GAIN-​GSS (Dennis et al.,
tured (and semi-​structured) assessment tools can improve
2006), Alcohol Dependence Scale (ADS; Horn, 1984;
the validity and reliability of diagnoses. Furthermore, the
Skinner & Horn, 1984), and CAGE (Ewing, 1984). All
use of structured interviews as a basis for diagnosing AUD
screening measures listed in Table 18.1 have adequate
also allows clinicians and researchers to collect relevant
psychometric properties, but compared to those described
information within an acceptable time frame. Although
in the text, the other measures require more time to
diagnostic interviews tend to require more time and train-
administer (e.g., the Drug Use Screening Inventory-​
ing compared to screening instruments, research demon-
Revised [DUSI-​R]; Tarter & Kirisci, 2001)  or have less
strates that structured diagnostic interviews are accepted
research supporting their generalizability across settings
by patients in a variety of settings (Suppiger et al., 2009).
and populations.
388 Substance-Related and Gambling Disorders
Table 18.1 summarizes the psychometric properties
of instruments used for the diagnosis of DSM-​5 AUD.
Specific values for reliability and validity estimates are
not reported in the text. Interested readers should consult
the citations reported for each instrument in order to aug-
ment the general information provided in the table. Only
instruments that have been adapted for DSM-​5 AUD (i.e.,
they must include the recently added craving criterion)
are included in this review. However, because the DSM-​5
is relatively new, few studies examining the psychometric
properties of these newer instruments exist. Therefore,
psychometric information from the corresponding DSM-​
IV-​TR version was examined when necessary because it
is reasonable to suspect a certain level of concordance
between the two versions given the minor changes to the
AUD criteria and the fact that some measures assessing
DSM-​IV-​TR included craving even though that symptom
was not included in DSM-​IV-​TR.
The most highly recommended diagnostic interviews
are the Structured Clinical Interview for DSM-​5 (SCID-​
5; First, Williams, Karg, & Spitzer, 2016) and the Alcohol
Use Disorder and Associated Disabilities Interview
Schedule-​5 (AUDADIS-​5; Grant et al., 2011). The SCID-​
5 is a semi-​structured interview with available clinical and
research versions. The research version is slightly more
comprehensive than the clinical version. The entire
SCID-​5 takes between 60 and 90 minutes to adminis-
ter, but the section assessing AUD takes 5 to 10 minutes.
Previous versions of the SCID have been adapted for
multiple languages (e.g., Spanish, Chinese, French, and
German) and validated across a range of populations (e.g.,
inpatient and outpatient). The entire AUDADIS-​5 takes
approximately 60 minutes to administer, shows adequate
psychometric properties, and has been validated across
a range of clinical and general population samples. The
section specifically assessing AUD should typically take
less than 10 minutes. Despite these desirable properties,
the AUDADIS may overestimate the prevalence of with-
drawal by failing to adequately disambiguate withdrawal
from hangover symptomatology (Boness, Lane, & Sher,
2016). As a result, researchers and clinicians should take
care to address this shortcoming by further assessing with-
drawal symptoms if that is a key concern. The remain-
ing diagnostic assessment instruments in Table 18.1 have
versions for assessing DSM-​5 AUD but have less psycho-
metric research available. However, those instruments
that do have psychometric information available appear
to be adequate for both clinical and research use. Of note
is the Semi-​Structured Assessment for the Genetics of
Alcoholism (SSAGA; Bucholz et al., 1994), which has not
been updated for DSM-​5 but includes an item on craving,
thus making it possible to derive a DSM-​5 AUD diagnosis.
In addition, it is important to distinguish between
diagnostic instruments that must be administered by
clinical interviewers and those that can be administered
by lay interviewers, as all these instruments require dif-
ferent levels of training. Clinician interviewers are
trained mental health professionals (e.g., psychologist or
psychiatrist) familiar with diagnostic classification and
diagnostic criteria, whereas lay interviewers are nonclini-
cians. Although clinicians must go through training for
administration of these instruments, lay interviewers are
often trained much more extensively via a combination
of directed self-​study, intensive classroom training, and
supervised practice administrations. The level of train-
ing required for administration varies by instrument. The
SCID, the Psychiatric Research Interview for Substance
and Mental Disorders (PRISM; Hasin et al., 1996), and
the Substance Dependence Severity Scale (SDSS; Miele
et  al., 2000)  each must be administered by clinicians,
whereas the AUDADIS and SSAGA are designed to be
administered by trained lay interviewers.
Overall Evaluation
As a whole, there exists a wide range of instruments for
AUD screening and diagnosis. The most highly rec-
ommended laboratory test is PEth. For the purposes of
screening, the most highly recommended interviews and
self-​report questionnaires include the AUDIT, ASSIST,
GAIN-​ GSS, CAGE, and MAST. The SCID-​ 5 and
AUDADIS are the recommended measures for syndromal
diagnosis of DSM-​5 AUD. Overall, screening laboratory
tests are useful for identifying those at risk for alcohol-​
related problems and are therefore in need of further
diagnostic assessment. Given that screening instruments
may be impacted by recall bias or social desirability, the
possibility of false negatives should be considered when
using them. Although AUD diagnostic instruments are
more thorough and time-​ consuming than screening
instruments, they can provide detailed clinical informa-
tion useful for treatment planning and coordination.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
For individuals with AUD, case conceptualization and
treatment planning requires the consideration of many
different issues and client characteristics. This includes

aspects such as the need for detoxification, screening for
medical/​health problems, comorbid conditions, level of
care determination, client treatment preference, con-
sumption patterns, consequences of drinking, family his-
tory of alcoholism, readiness to change, drinking goals,
treatment history, craving, possible high-​ risk/​
relapse
situations, alcohol outcome expectancies, drinking self-​
efficacy, and social network characteristics. Table 18.2
provides a summary of measures that can be used to assess
this range of constructs.
Need for Detoxification
When conceptualizing a case and planning treatment,
it is important to assess for symptoms of alcohol with-
drawal syndrome (AWS) in individuals who recently quit
or reduced their alcohol use. This is because those with
moderate to severe AWS may require supervised detoxi-
fication in either an inpatient or an outpatient setting.
AWS involves experiencing two or more of the follow-
ing symptoms causing significant distress or impairment
within a few hours to several days after a reduction in
heavy or prolonged alcohol use: (a) autonomic hyperac-
tivity; (b) increased hand tremor; (c) insomnia; (d) nau-
sea; (e) transient visual, tactile, or auditory hallucinations;
(f) anxiety; and/​or (g) seizures (APA, 2013). Despite that
fact that several measures have been developed to assess
AWS, the most widely used measure continues to be
the revised Clinical Institute Withdrawal Assessment for
Alcohol (CIWA-​ Ar; Sullivan, Sykora, Schneiderman,
Naranjo, & Sellers, 1989). This is a 10-​item clinician-​
report questionnaire that can be completed in less than
2 minutes. However, the CIWA-​Ar is not without limita-
tions. Investigations of the psychometrics of this measure
indicate that is has been found to have poor internal
consistency in some studies (Holzman & Rastegar, 2016;
Pittman et al., 2007) and may underestimate the severity of
AWS in Native Americans, which limits its generalizabil-
ity (Rappaport et  al., 2013). Newly developed measures
are often compared to the CIWA because it is regarded as
the “gold standard” measure for assessing AWS. A briefer
measure than the CIWA that has acceptable psycho-
metric properties is the Short Alcohol Withdrawal Scale
(SAWS; Gossop, Keaney, Stewart, Marshall, & Strang,
2002), which is a 10-​item self-​report questionnaire.
Medical/​Health Screening
Excessive alcohol consumption and AUD are associ-
ated with a range of health conditions. The presence of
Alcohol Use Disorder 389
medical or health conditions can complicate the clinical
picture; thus, it is important to take this into account dur-
ing treatment conceptualization and planning. A review
of the chronic diseases and conditions related to alcohol
use (Shield, Parry, & Rehm, 2013)  indicated that alco-
hol consumption is often the primary or the sole cause
of 25 chronic diseases (e.g., liver cirrhosis, gastritis, and
pancreatitis) listed in the 10th edition of the International
Classification of Disease (ICD-​10; WHO, 2004). In addi-
tion, alcohol use increases risk for certain cancers, tumors,
neuropsychiatric conditions, and many cardiovascular
and digestive diseases, and it can have both beneficial and
detrimental effects on diabetes, stroke, and heart disease
(Shield et al., 2013).
Multiple measures are available for assessing general
health status. The highly recommended measures are
those with evidence of strong psychometric characteristics
and include the Addiction Severity Index (ASI-​5; Denis,
Cacciola, & Alterman, 2013)  and the 12-​and 36-​Item
Short Form Health Surveys (SF-​12 [Ware, Kosinski, &
Keller, 1996] and SF-​36 [Medical Outcomes Trust, 1991;
Ware & Sherbourne,  1992], respectively). These mea-
sures do not assess specific physical diseases but, rather,
overall current health and whether health problems are
interfering in important areas of life.
Comorbid Psychopathology
As mentioned previously, AUD is highly comorbid with
other mental disorders, including mood disorders, anxiety
disorders, personality disorders, and other drug use dis-
orders (Grant et al., 2015). Thus, it is essential that case
conceptualization and treatment planning involve the
assessment of co-​occurring psychiatric disorders. Several
measures have been widely used to assess mental disor-
ders co-​occurring with AUD; however, there is currently
a limited number of published measures for diagnosing
AUD and other mental disorders that have been updated
for the DSM-​5. Given that the most relevant instruments
for assessing AUD and co-​occurring mental disorders are
the semi-​ structured interviews listed in Table 18.1, to
avoid redundancy, these measures are not included in
Table 18.2 but are discussed in the text.
The most widely used measures for assessing AUD
and commonly co-​occurring mental disorders include the
SCID, the Mini-​International Neuropsychiatric Interview
(M.I.N.I.; Sheehan, 2014; Sheehan et  al., 1994), the
SSAGA, and the AUDADIS. The SCID has been updated
to reflect DSM-​ 5 diagnoses (First, Williams, Karg, &
Spitzer, 2014 [research version]; First, Williams, Karg, &
390 Substance-Related and Gambling Disorders

TABLE 18.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Need for Detoxification

CIWA-​Ar A Ab G NR NR G Ab A ✓
SAWS A G NR NR NR A A A
Medical/​Health Screening
ASIa E G A A E A G G ✓
SF-​36a E G G A G G E G ✓
SF-​12 E G G A G G E G ✓
LISRES A A NR NR A NR A A
Form 90 A NR NR A NR A G A
Level of Care Determination
RAATE A A A NR NR A G A ✓
ASAM PPC A NR A A NR A G A
Drinking Patterns
TLFB A NR NR A A A A A ✓
Form 90 A NR NR A A A A A ✓
DMSL A NR NR NA A A A A ✓
LDH A NR NR A A A A A ✓
Q-​F Measures A NR NR A A A A A ✓
AUI A A NR A NR A G A
Consequences of Drinking
RAPI G G NR NR A A A A ✓
B-​YAACQ A G NR A A A G A ✓
MAST A G NA G A G A A ✓
AUI A A NR A NR A G A
SIP A A NR A A A A A
DrInC A A NR A A A A A
YAACQ A A NR A A A G A
Readiness to Change
URICA G G NA A NR G E A ✓
SOCRATES E G NA G E A E A ✓
RCQ G G A NR NR NR E A
Treatment History
Form 90 A NR NR A A A A A ✓
TLFB A NR NR A A A A A
Craving
PACS A G NR NR A A E A ✓
OCDS A G NR A A A E A ✓
AUQa A G NR A A A E A ✓
TRI A A NR NR A A A A
PACS A A NR NR A A A A
ACQ-​R A E NR G A A A A
ACQ-​Now A G NR NR A G A A
JACQ A E NR G A A A A
High-​Risk Drinking Situations/​Relapse Situations
DMQ-​Ra G G NR A A G G G ✓
IDS A G NR NR A G G A ✓
IDS-​42 A G NR NR A G G A ✓
DCS A G NR NR NR A G A
DPQ A A NR NR NR A A A
Alcohol Outcome Expectancies
CEOA E G NR A A G G A ✓
B-​CEOA E A NR NR A G A A ✓
Drinking Self-​Efficacy
DRSEQ A G NR NR E A A A ✓
 Alcohol Use Disorder 391

TABLE 18.2  Continued

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly

Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

DRSEQ-​R E A NR NR E A A A ✓
SCQ A A NR NR A A A A
AASE A G NR NR A A A A
Social Network
IPA A NR NR A NA A A A ✓

  Measure recommend by the PhenX Toolkit (https://​www.phenxtoolkit.org).

a

b
  The internal consistency and validity of the CIWA-​Ar have been inconsistent; however, this measure was included because it is considered the gold
standard and is currently the best measure available despite these limitations.
Note: CIWA-​Ar = Clinical Institute Withdrawal Assessment for Alcohol Scale; SAWS = Short Alcohol Withdrawal Scale; ASI = Addiction Severity Index;
SF-​36  =  36-​Item Short Form Health Survey; SF-​12  =  12-​Item Short Form Health Survey; LISRES  =  Life Stressors and Social Resources Inventory;
RAATE = Recovery Attitude and Treatment Evaluator; ASAM PPC = American Society of Addiction Medicine Patient Placement Criteria; TLFB = Timeline
Followback; DSML = Drinking Self-​Monitoring Log; LDH = Lifetime Drinking History; Q-​F Measures = Quantity–​Frequency Measures; AUI = Alcohol Use
Inventory; RAPI = Rutgers Alcohol Problem Index; B-​YAACQ = Brief Young Adult Alcohol Consequences Questionnaire; MAST = Michigan Alcoholism
Screening Test; SIP = Short Index of Problems; DrInC = Drinker Inventory of Consequences; YAACQ = Young Adult Alcohol Consequences Questionnaire;
URICA = University of Rhode Island Change Assessment; SOCRATES = Stages of Change Readiness and Treatment Eagerness Scale; RCQ = Readiness
to Change Questionnaire; PACS = Penn Alcohol Craving Scale; OCDS = Obsessive Compulsive Drinking Scale; AUQ = Alcohol Urge Questionnaire;
TRI = Temptation and Restraint Inventory; PACS = Penn Alcohol Craving Scale; ACQ-​R = Alcohol Craving Questionnaire-​Revised; ACQ-​Now = Alcohol
Craving Questionnaire—​Now (assessing craving in the present moment); JACQ = Jellinek Alcohol Craving Questionnaire; DMQ-​R = Drinking Motives
Questionnaire-​Revised; IDS = Indices of Problems; IDS-​42 = Indices of Problems; DCS = Drinking Context Scale; DPQ = Drinking Patterns Questionnaire;
CEOA = Comprehensive Effects of Alcohol; B-​CEOA = Brief Comprehensive Effects of Alcohol; DRSEQ = Drinking Refusal Self-​Efficacy Questionnaire;
DRSEQ-​R  =  Drinking Refusal Self-​Efficacy Questionnaire-​Revised; SCQ  =  Situational Confidence Questionnaire; AASE  =  Alcohol Abstinence Self-​
Efficacy; IPA = Important People and Activities; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

Spitzer, 2016 [clinician version]). The SCID was devel-
oped to assess the most frequently diagnosed disorders
in adults, including psychotic disorders, mood disorders,
drug and alcohol use disorders, anxiety disorders, somato-
form disorders, eating disorders, adjustment disorder, and
personality disorders. There are patient and nonpatient
versions of the SCID for those conducting assessments
in clinical or nonclinical settings. The SCID can take,
on average, 60 to 90 minutes to administer. A briefer ver-
sion of the SCID is the M.I.N.I., which has also been
updated to reflect DSM-​5 criteria and assesses mood dis-
orders, anxiety disorders, drug and alcohol use disorders,
psychotic disorders, and antisocial personality disorder.
The M.I.N.I.  can be administered in roughly 10 min-
utes, which increases its clinical utility. The SSAGA was
specifically developed to distinguish between symptoms
of AUD, depression, and antisocial behaviors to ensure
accuracy of diagnosis for genetics research. The disorders
assessed in the SSAGA include drug and alcohol use dis-
orders, major depression, dysthymia, mania, somatization,
antisocial personality disorder, anorexia, bulimia, panic,
agoraphobia, social phobia, and obsessive–​ compulsive
disorders. The SSAGA was developed specifically to dis-
entangle disorders that commonly co-​occur with AUD,
which may increase its clinical utility. However, the
administration time is much longer than other measures
(approximately 120 minutes), which may limit the clinical
utility of the SSAGA. The AUDADIS was developed to
assess AUD and other related conditions in both clinical
samples and the general population. Diagnoses assessed
by the AUDADIS include drug and alcohol use disorders,
mood disorders, anxiety disorders, eating disorders, and
personality disorders. The AUDADIS takes approximately
60 minutes to administer.
Level of Care Determination
Level of care needed is an important factor to consider
when treatment planning. It is widely known that there is
no single treatment model that effectively treats all indi-
viduals with alcohol problems (e.g., Institute of Medicine,
1990; National Institute on Drug Abuse, 2009). Despite
this knowledge, many programs emphasize one main
treatment model whether it is abstinence only, 12-​step
based, harm reduction, behavior therapy, or therapeutic
communities (Mee-​Lee & Gastfriend, 2014). Often, the
image of drug and alcohol treatment is a 28-​day program
in a residential setting. Given the heterogeneity of prob-
lems associated with alcoholism, it is understandable that
a variety of treatment options are needed. Some treatment
programs may have a single standard of care regardless of
the case presentation; however, data suggest that match-
ing clients to services based on their identified problem
needs improves treatment outcomes (e.g., Camilleri,
392 Substance-Related and Gambling Disorders
Cacciola, & Jenson, 2012; Gastfriend & McLellan, 1997;
McLellan et al., 1997). There are measures designed to
determine the level of care needed when planning treat-
ment. These methods were developed with the goal of
providing a rationale for the treatment approach recom-
mended. The Patient Placement Criteria (PPC; Hoffman,
Halikas, Mee-​Lee, & Weedman, 1993) published by the
American Society of Addiction Medicine (ASAM) is one
method available to assess patients for (a) acute intoxica-
tion or withdrawal potential, (b)  biomedical conditions
or complications, (c) treatment acceptance or resistance,
(d)  relapse potential, and (e)  recovery environment.
These criteria are then used to assign clients to one of four
levels of care:  I, outpatient; II, intensive outpatient; III,
medically monitored inpatient; and IV, medically man-
aged inpatient (Camilleri et al., 2012). There is extensive
evidence suggesting that using the PPC to match patients
to levels of care is associated with lower rates of morbidity,
improved functioning, and lower rates of service utiliza-
tion compared to mismatching patients to lower levels of
care (Gastfriend & Mee-​Lee, 2004).
Treatment Preference
There exists an abundance of research on shared decision-​
making (e.g., Crawford et  al., 2003; Härter et  al., 2011;
Härter, van der Weijden, & Elwyn, 2011; Joosten, De
Jong, De Weert-​van Oene, Sensky, & Van Der Staak, 2009;
Neuner et al., 2007), in which clients participate in selecting
the treatment (e.g., motivational enhancement, cognitive
behavioral, and 12-​step facilitation) they prefer. Evidence
suggests that matching clients to their preferred treatment
can result in higher treatment adherence, improved symp-
tom related-​outcomes, and higher treatment retention rates
(Graff et al., 2009; Swift & Callahan, 2009). For example,
clients matched to their preferred treatment tended to
drink less than their unmatched counterparts (Adamson,
Sellman, & Dore, 2005). Notably, other researchers found
no differences in number of drinking days, days intoxicated,
and a reduction in drinking among clients matched to their
preferred treatment (McKay, Alterman, McLellan, Snider,
& O’Brien, 1995). Friedrichs, Spies, Härter, and Buchholz
(2016) suggested that shared decision-​ making interven-
tions might be a useful approach for assessing and utilizing
treatment preferences in treatment planning given prelimi-
nary data on their effectiveness (Brener, Resnick, Ellard,
Treloar, & Bryant, 2009; Joosten, De Weert-​van Oene,
Sensky, Van Der Staak, & De Jong, 2010; Joosten et  al.,
2009); however, the data have been mixed, and additional
research is needed to further investigate the effectiveness
of these approaches in improving drug and alcohol treat-
ment outcomes. Given there are currently limited data on
evidence-​based measures for identifying treatment prefer-
ence, there are no measures to assess treatment preference
listed in Table 18.2.
Consumption Patterns
Assessing consumption patterns is important for under-
standing the extent of a client’s use prior to treatment.
Identifying how much and when a client typically drinks
can be valuable information for developing treatment tar-
gets. In addition, quantitative variables such as percent-
age of days drinking, percentage of abstinent days, mean
drinks per drinking day, typical blood alcohol content,
peak blood alcohol content, and percentage of low, mod-
erate, and heavy drinking days can be used as important
feedback to clients regarding their drinking patterns and
associated consequences.
Several measures are available for assessing consump-
tion patterns, including the Timeline Followback (TLFB;
Agrawal, Sobell, & Sobell, 2008; Sobell & Sobell, 1995;
Sobell, Sobell, Bogardis, Leo, & Skinner, 1993) and the
Form 90 (Miller, 1996; Tonigan, Miller, & Brown, 1997),
which are the mostly highly recommended interviews.
Although both methods utilize calendars as memory
aids to allow for estimating daily drinking patterns and
the information needed to estimate the aforementioned
quantitative variables, there are several important distinc-
tions. The TLFB assesses the number of standard drinks
consumed each day during the assessment period, which
can range from 30 days to 1 year. The Form 90 assesses
common drinking patterns while isolating drinking epi-
sodes, which is used to estimate the amount of drinking
each day during the period of assessment. In addition to
assessing drinking patterns, the Form 90 assesses general
functioning with regard to work, school, religious prac-
tice, medical concerns, legal issues, and psychiatric care.
Despite the many benefits of the TLFB and the Form 90,
both are time-​consuming and require extensive training
to achieve an adequate level of reliability. Specifically, the
TLFB can take 10 to 15 minutes to assess the past 90 days
and up to 30 minutes to assess the past 12 months, and the
Form 90 takes on average 45 minutes to administer. The
use of these measures for the purposes of case conceptu-
alization and treatment planning is important for under-
standing contextual factors that contribute to drinking
episodes, which aid in identifying targets for treatment.
There are also several self-​report questionnaires that are
highly recommended, including drinking self-​monitoring

logs, lifetime drinking measures, and quantity–​frequency
measures. Drinking self-​monitoring logs (e.g., Sobell &
Sobell, 1995; Vuchinich, Tucker, & Harllee, 1988) provide
concurrent data on alcohol consumption that can be used
to identify high-​risk situations, monitor urges, and track
treatment progress. Lifetime drinking measures include
the Lifetime Drinking History (LDH; Skinner & Sheu
1982), the Concordia Lifetime Drinking Questionnaire
(CLDQ; Chaikelson, Arbuckle, Lapidus, & Gold, 1994),
and the Cognitive Lifetime Drinking History (CLDH;
Russell et  al., 1997, 1998). The LDH is the most widely
used and only takes 20 to 30 minutes to complete, the
CLDQ uses visual aids and takes 20 minutes to complete,
and the CLDH is a computer-​administered interview that
also includes cognitive techniques similar to those used
in the TLFB. There are several quantity–​frequency mea-
sures, including the Volume–​Variability Index (VV Index;
Cahalan & Cisin, 1968), the Khavari Alcohol Test (Khavari
& Farber, 1978), the Graduated–​ Frequency Measure
(Clark & Midanik, 1982; Midanik, 1994), the NIAAA
Quantity Frequency (Armor, Polich, & Stambul, 1978),
and the CLDH (Russell et  al., 1997). These measures
provide a quick and easy assessment of total consumption
and number of drinking days. Notably, there are many
limitations of quantity–​ frequency measures, including
that they are subject to underreporting alcoholic beverages
consumed; often fail to assess the type of drink consumed
in a day (and when type of drink consumed is assessed, it
increases the administration time); and often do not have
the ability to detect fluctuations in drinking, including days
of sporadic heavy drinking (Sobell & Sobell, 2004).
There are advantages and disadvantages to using either
interview formats or self-​report questionnaires (including
computerized methods) for assessing alcohol consump-
tion. Clinicians and researchers must weigh the impor-
tance of the accuracy of information provided, the type of
information desired, and the time of administration when
selecting a measure of drinking patterns. The TLFB and
Form 90 are most beneficial in settings in which the accu-
racy and type of information are most important. When
time is of the essence, as in most clinical situations, life-
time drinking measures and quantity–​frequency measures
may be most useful. Drinking self-​monitoring logs should
be used throughout treatment to monitor urges and treat-
ment progress.
Consequences of Drinking
Another important factor to consider during the case
conceptualization and treatment-​ planning phase is
Alcohol Use Disorder 393
consequences of drinking. Because individuals who
drink the same amount of alcohol may have vast dif-
ferences in the consequences they experience as a
result of their drinking, it is important to assess conse-
quences of drinking in addition to alcohol consump-
tion patterns. Although the diagnostic and screening
instruments noted previously assess various conse-
quences of drinking, they are typically limited in scope
of consequences surveyed. In addition, if there exists
a discrepancy in the client’s perception of negative
consequences as a result of drinking compared to the
actual consequences, using a standardized measure of
alcohol consequences can highlight this discrepancy.
Identifying consequences of drinking may also help
increase motivation for change.
One measure used to assess consequences of drink-
ing is the Drinker Inventory of Consequences (DrInC;
Miller, Tonigan, & Longabaugh, 1995), which is a 50-​
item measure that comprehensively assesses lifetime
and recent adverse events as a result of drinking in
five domains:  physical, intrapersonal, social responsi-
bility, interpersonal, and impulse control. The Short
Inventory of Problems (SIP; Miller et  al., 1995)  is a
condensed version of the DrInC. This measure con-
tains only 15 items and can be administered in 5 min-
utes or less.
The Alcohol Use Inventory (AUI; Horn, Wanberg,
& Foster, 1974; Wanberg, Horn, & Foster, 1977)  is a
228-​item measure assessing many dimensions of an
individual’s drinking, including alcohol consequences
(e.g., loss of control, hangover, and role maladapta-
tion). Briefer measures than the AUI include the
MAST and the Rutgers Alcohol Problem Index (RAPI;
White & Labouvie, 1989). The RAPI is a 23-​item self-​
report questionnaire assessing the frequency of nega-
tive alcohol-​related consequences, whereas the MAST
consists of 25 items assessing alcohol-​ related prob-
lems. The AUI, RAPI, and MAST all have evidence
of strong psychometric properties. The Young Adult
Alcohol Consequences Questionnaire (YAACQ; Read,
Kahler, Strong, & Colder, 2006) is a 48-​item measure
that assesses eight domains of alcohol problems: social-​
interpersonal, impaired control, diminished self-​
perception, poor self-​care, risky behavior, academic/​
occupational, physiological dependence, and blackout
drinking. In addition to the broader range of alcohol
problems assessed, an advantage of the YAACQ is
that the subscales provide a way of aggregating alco-
hol consequences that may be used in motivational-​
enhancement, skill-​based, and personalized-​feedback
394 Substance-Related and Gambling Disorders
interventions. A  briefer version of the YAACQ, the B-​
YAACQ (Kahler, Strong, & Read, 2005), consists of 24
items and may be preferred over the YAACQ given its
shorter administration time and adequate psychometric
properties.
Family History of Alcoholism
Research indicates that assessing family members directly
is the optimal method for obtaining a family history of
alcohol problems (Andreasen, Endicott, Spitzer, &
Winokur, 1977; Andreasen, Rice, Endicott, Reich, &
Coryell, 1986), although this method is not without limi-
tations. However, assessing family members directly is
not always realistic or feasible. Family history methods
may be a more realistic approach and have been shown
to have good sensitivity but poor specificity (Andreasen
et  al., 1977). Although family history methods tend to
have lower reliability and sensitivity (Andreasen et  al.,
1986) than direct assessments of relatives, optimal family
history methods are those that are structured, such as the
Family History Research Diagnostic Criteria (FHRDC;
Andreasen et  al., 1977; Endicott, 1978). Unfortunately,
this specific method is outdated because it does not
include the most recent iteration of the AUD diagnostic
criteria. In addition, there is evidence that simply asking
a single question about whether anyone in one’s family
had problems with alcohol is an equally effective method
(Crews & Sher, 1992; Cuijpers & Smit, 2001; Slutske
et al., 1996). Thus, risk for alcohol problems can simply
be assessed by asking this single question, whereas more
detailed information about family history is best gath-
ered using the Family Tree Questionnaire (FTQ; Mann,
Sobell, Sobell, & Sobell, 1985). The FTQ is a brief and
easy way to identify first-​and second-​degree biological
relatives who range from lifelong abstainers to definite
problematic drinkers.
Although the Children of Alcoholics Screening Test
(CAST; Jones, 1983) has been widely used, there is ques-
tionable evidence of its reliability and validity; thus, it is
not a recommended measure for assessing family history
of alcoholism (Schinke, 1989). A self-​report technique that
has initial evidence of strong psychometric properties for
assessing family history of alcoholism is the Short Michigan
Alcoholism Screening Test (SMAST; Selzer, Vinokur, &
van Rooijen, 1975) adapted to assess mother’s alcoholism
(M-​SMAST) and father’s alcoholism (F-​SMAST) (Crews
& Sher, 1992). However, additional research is needed
testing the psychometric properties of the M-​SMAST and
F-​SMAST by independent investigators.
Readiness for Change
It has been suggested that assessing motivation to change
drinking behavior is important for tailoring treatment
goals to match the individual’s motivation level (Bergly,
Stallvik, Nordahl, & Hagen, 2014; Norcross, Krebs, &
Prochaska, 2011; Prochaska, DiClemente, & Norcross,
1992). Prochaska and DiClemente (1983) theorized that
change occurs in five stages, a process that they describe
using the transtheoretical model of change. Assignment
to these stages is achieved using various algorithms (e.g.,
Prochaska, 1994; Prochaska et al., 1994). Throughout the
years, the stages of change have been modified, but they
can be described in general as follows: (a) Individuals with
evidence of a problem but no intention to quit may be
classified into the precontemplation stage, (b) individuals
intending to quit within the next 6 months are assigned
to the contemplation stage, (c) individuals who may have
taken steps toward change and are interested in changing
within 1 month may be assigned to the preparation stage,
(d) individuals in the process of making a change are in the
action stage, and (e) individuals who have made a change
may be assigned to the maintenance stage until they have
maintained their changes for 6 months or longer (Carey,
Purnine, Maisto, & Carey, 1999). There are many mea-
sures that purport to assess readiness to change problem-
atic alcohol use behavior. The measures with evidence
of adequate or better psychometric properties include
the University of Rhode Island Change Assessment
(URICA; McConnaughy, Prochaska, & Velicer, 1983),
the Stage of Change Readiness and Treatment Eagerness
Scale (SOCRATES; Miller & Tonigan, 1996), and the
Readiness to Change Questionnaire (RCQ; Rollnick,
Heather, Gold, & Hall, 1992). There have been mixed
findings on the validity of these measures despite their
wide use (e.g., lack of predictive validity for the URICA
[Bergly et  al.,  2014], limited predictive validity for the
RCQ [Carey et al., 1999], and limited convergent valid-
ity between the URICA and the SOCRATES [Napper
et  al.,  2008]). It has also been proposed that examining
commitment to change in addition to examining motiva-
tion to change is important. Specifically, some argue that
expressing commitment may represent a stronger desire
for change and may be less susceptible to factors that pro-
mote ambivalence about change (Kaminer, McCauley
Ohannessian, McKay, & Burke, 2016; Kelly & Greene,
2013). Currently, there exists a single-​item commitment
to abstinence measure (Havassy, Hall, & Wasserman,
1991)  that has been validated by others (Mensinger,
Lynch, TenHave, & McKay, 2007; Morgenstern, Frey,

McCrady, Labouvie, & Neighbors, 1996)  and a 5-​item
commitment to sobriety scale (Kelly & Greene, 2013).
The Adolescent Substance Abuse Goal Commitment
(ASAGC) questionnaire is a recently developed 16-​item
measure used to assess commitment to treatment goals in
adolescents and has promising psychometric properties.
Unlike the other commitment measures, the ASAGC
offers the option to rate commitment to abstinence versus
harm reduction. Future research should investigate the
psychometric properties of the ASAGC as well as mea-
sures assessing both commitment and readiness to change
more broadly.
Drinking Goals
As discussed previously, an important part of treatment
planning is assessing the client’s drinking goals. Although
there are many abstinence-​only programs, these programs
may not be effective for all clients. Individuals who partici-
pate in an abstinence-​only treatment program when their
drinking goal is not to abstain from alcohol use will miss out
on opportunities to learn how to moderate use by drinking
in a way that minimizes problems caused by alcohol use.
Despite the importance of taking into account
drinking goals when treatment planning, no psycho-
metrically validated measures are currently available. It
is recommended that drinking goals be assessed infor-
mally and considered when treatment planning. Future
research is needed to fill the gap in the area of assessing
drinking goals.
Treatment History
Given the chronic nature of AUD, relapse is not an
uncommon phenomenon among those addicted to alco-
hol. Thus, another pertinent part of case conceptualiza-
tion and treatment planning is to obtain the client’s history
of drug and alcohol treatment. Learning about the client’s
treatment history can provide a sense of which methods
were helpful and which were not helpful. Obtaining indi-
vidual treatment history may happen informally during
the intake or the initial session with the client. When ask-
ing about treatment history, it may be helpful to discuss
the client’s motivation for change at the time of the pre-
vious treatment episodes. If the client reports a different
level of motivation to change, this may lend the client
to being open to repeating similar treatment approaches
from their client’s past because they may be more recep-
tive to the treatment material compared to their prior
treatment attempt.
Alcohol Use Disorder 395
The TLFB and the Form 90 are psychometrically
sound instruments that provide mechanisms for obtaining
a history of drug and alcohol treatment. However, these
are time-​limited measures. CASAA provides the Lifetime
Treatment History Interview (Center on Alcoholism,
Substance Abuse, and Addictions Research Division,
1994)  that parallels the Form 90. This measure assesses
lifetime and the date of the most recent medical hospi-
talization, detoxification, residential treatment, incarcera-
tion, outpatient treatment, and participation in Alcoholics
Anonymous or 12-​step meetings. Although this measure
provides a briefer method of assessing lifetime treatment,
there is little evidence of its psychometric properties. It is
recommended that treatment history be obtained, along
with questions regarding which aspects of prior treatments
were helpful and not helpful.
Craving
Craving is perhaps the most subjective DSM-​5 AUD diag-
nostic criterion. It plays an important role in relapse, and
various medications are viewed as targeting this symptom
directly. Thus, craving is an important factor to consider
in treatment planning. However, when Sayette and col-
leagues (2000) reviewed the literature on psychometri-
cally sound measures assessing craving, they concluded
that there was a need for a clear theoretical framework of
craving to drive measurement development and adoption.
Thirteen years later, Kavanagh and colleagues (2013)
indicated that this still remains true. The ICD-​10 has
described craving as “a strong desire or sense of compul-
sion to take the substance” (WHO, 1993, p. 70), and the
DSM criteria for AUD define it as “craving, or a strong
desire or urge to use alcohol” (APA, 2013, p. 491), which
both represent the severe end of the craving spectrum.
Other definitions of craving have included cognitions
such as expectancies, intentions, or perceived behavioral
control (Kavanagh et al., 2013).
When assessing craving, it is important to consider the
time frame. Tonic craving can be defined as retrospec-
tive reports of craving during a specific period of time,
whereas phasic craving refers to experiences of craving in
the moment (Ray, Courtney, Bacio, & MacKillop, 2013).
Tonic craving measures can be useful for understanding
a client’s pattern and triggers of craving. The most psy-
chometrically sound tonic craving measures include the
Obsessive Compulsive Drinking Scale (OCDS; Anton,
Moak, & Latham, 1995), the Temptation and Restraint
Inventory (TRI; Collins & Lapp, 1992), the Penn Alcohol
Craving Scale (PACS; Flannery, Volpicelli, & Pettinati,
396 Substance-Related and Gambling Disorders

1999), the Preoccupation with Alcohol Scale (PACS;
Leonar, Harwood, & Blane, 1988), the Jellinik Alcohol
Craving Questionnaire (JACQ; Ooteman, 2006), the
Alcohol Craving Questionnaire Revised (ACQ-​R; Raabe
et al., 2005), and the Alcohol Craving Questionnaire Now
(ACQ; Singleton, Tiffany, & Henningfield, 1995). Phasic
craving measures are useful for tracking cravings through-
out treatment. The only psychometrically sound pha-
sic craving measure is the Alcohol Urge Questionnaire
(AUQ; Bohn, Krahn, & Staehler, 1995).
negative emotions outside of drinking. In the event that a
client experiences a relapse during or after treatment, the
Reasons for Drinking Questionnaire (RFDQ; Westerberg,
Miller, & Heather, 1996)  could be used as a learning
opportunity to identify additional relapse factors to be
considered and addressed in treatment. Results of initial
research suggest adequate psychometric properties of the
RFDQ, but further evidence for the measure is needed.
Alcohol Outcome Expectancies

Expectancy theory describes alcohol outcome expectan-

High-​Risk Drinking Situations/​Relapse Situations
cies as our beliefs about the effects of consuming alcohol
In developing the treatment plan with the client, it is (Brown, Goldman, Inn, & Anderson, 1980), which influ-
important to identify situations that put the client at risk ence drinking behavior. Elucidating alcohol outcome
for relapse (or, for treatments that are not abstinence expectancies is important for case conceptualization and
based, at risk for excessive consumption). Encountering treatment planning, especially when using expectancy
cues (e.g., people, places, events, or feelings) associated challenge interventions (Darkes & Goldman, 1993; Scott-​
with drinking may evoke a variety of cognitive, behav- Sheldon, Terry, Carey, Garey, & Carey, 2012). Among the
ioral, and affective responses that increase risk of relapse alcohol outcome expectancy measures, the most widely
for abstainers or returning to excessive alcohol consump- used is the Alcohol Expectancy Questionnaire (AEQ;
tion among those desiring to maintain a moderate level of Brown et al., 1980), which assesses six domains of positive
drinking. Ascertaining antecedents to drinking behavior expectancies. A  major limitation of this measure is that
is helpful for identifying potential strategies to discuss in it neglects to assess negative alcohol outcome expectan-
treatment. For example, if anger is a common anteced- cies and the subjective valuation of the effects of alcohol.
ent to drinking behavior, then the therapist may consider The Comprehensive Effects of Alcohol Questionnaire
including techniques for identifying and managing anger (CEOA; Fromme, Stroot, & Kaplan, 1993)  addresses
as one treatment strategy for reducing the risk of relapse. both of these concerns. Specifically, the CEOA consists of
The most widely used and empirically validated self-​ 38 items assessing four positive expectancies (sociability,
report measure for assessing high-​ risk drinking condi- tension reduction, enhanced sexuality, and liquid cour-
tions is the Inventory of Drinking Situations (IDS; Annis, age) as well as three negative expectancies (cognitive and
Graham, & Davis, 1987). The IDS is a 100-​item measure behavioral impairment, risk and aggression, and nega-
assessing frequency of past-​year drinking in the follow- tive self-​perception). The CEOA also includes perceived
ing eight areas:  unpleasant emotions, physical discom- desirability of each of the expected effects. The adminis-
fort, pleasant emotions, testing personal control, urges or tration time for the CEOA can be as long as 10 minutes.
temptations to drink, conflict with others, social pressure A briefer version, the B-​CEOA (Ham, Stewart, Notron, &
to drink, and pleasant times with others. A  briefer ver- Hope, 2005), consists of 15 items that tap into the same
sion, the IDS-​42 (Isenhart, 1991), is also available and has domains and is psychometrically sound.
strong psychometric properties. The Drinking Motives
Questionnaire-​Revised (DMQ-​R; Cooper, 1994; Cooper,
Drinking Self-​Efficacy
Russell, Skinner, & Windle, 1992)  provides important
information for conceptualizing the client’s motivations In addition to assessing readiness and importance of mak-
for drinking and identifying treatment targets. The DMQ-​ ing a change, it is important to assess the client’s per-
R assesses four drinking motives:  enhancement (e.g., to ceived ability to make the change. Some clients may feel
enhance positive mood), social (e.g., to augment social ready and willing to change but do not believe they have
situations), coping (e.g., to relieve negative emotions), the skills needed to take the first step. Identifying the cli-
and conformity (to external social pressures). If a client’s ent’s self-​efficacy to make a change is an important part of
motivation for drinking is primarily to cope with negative treatment planning. Measures used to assess self-​efficacy
emotions, for example, the treatment plan may include include the Situational Confidence Questionnaire
identifying alternative ways to effectively cope with (SCQ; Annis, 1987), the Alcohol Abstinence Self-​Efficacy

Scale (AASE; DiClemente, Carbonari, Montgomery, &
Hughes, 1994), and the Drinking Refusal Self-​Efficacy
Questionnaire (DRSEQ; Young, Oei, & Crook, 1991).
Although the SCQ has been widely used, it is limited
because it assesses ability to resist heavy drinking without
clearly defining heavy drinking (Oei, Hasking, & Young,
2005). The DRSEQ addresses this limitation by assessing
the ability to resist drinking, which provides an opportu-
nity for high-​risk situations to be revealed for both social
drinkers and problematic drinkers. A briefer version of the
DRESQ is available. The Alcohol Reduction Strategies–​
Current Confidence (ARS-​CC; Bonar et  al., 2011)  is a
promising newer measure of self-​efficacy. The ARS-​CC
consists of 31 items assessing perceived ability to utilize
each of the drinking-​reduction self-​control skills, and pre-
liminary data support its psychometric properties.
Social Network
Social network drinking is another important factor to
assess as part of the case conceptualization and treatment
planning processes. Assessing a client’s social network
drinking patterns can identify people who may provide
support for the client throughout treatment and others
who may serve as stressors to be discussed in treatment.
Often, alcohol interventions will include modifications to
the social network in order to increase support for changes
with problematic drinking. The Important People and
Activities (IPA) interview (Longabaugh & Zywiak, 1999) is
an instrument that has been tested extensively in a vari-
ety of multisite randomized alcohol-​related clinical trials
(Project MATCH: Allen et al., 1997; Kadden, Carbonari,
Litt, Tonigan, & Zweben, 1998; COMBINE: COMBINE
Study Research Group, 2003). This 19-​item interview
involves asking clients to name important people in
their social network and to specify the drinking behav-
iors of each person identified, which can take roughly 20
minutes to administer. Similarly, the Important People
instrument (IP; Clifford & Longabaugh, 1991) is another
commonly used measure of social network drinking. The
IP was originally developed as an interview but is also
available as a questionnaire in both paper-​ and-​pencil
and computer-​based formats. Notably, the computerized
format requires less training to administer and includes
a scoring algorithm that allows for immediate feedback
after completion (Hallgren, Ladd, & Greenfield, 2013).
The IP requires respondents to identify up to 10 important
people in their social network with whom they have had
recent contact. Despite extensive evidence of its reliabil-
ity and validity (e.g., Hallgren et al., 2013; Longabaugh,
Alcohol Use Disorder 397
Wirtz, Zweben, & Stout, 1998), the IP may contain up to
80 items (8 items per person in the social network) and
takes, on average, 12 minutes to administer. There is also
preliminary psychometric support for the five-​person ver-
sion of the Important People measure (IP-​5; Hallgren &
Barnett, 2016)  derived from the original IP (Clifford &
Longabaugh, 1991). A major advantage of the IP-​5 is its
reduced administration time, which may be especially
important in clinical or research settings in which time
is of the essence.
Overall Evaluation
There are several psychometrically sound measures that
can be used in the process of case conceptualization and
treatment planning. The CIWA-​ Ar remains the most
psychometrically sound measure of alcohol withdrawal
despite its limitations in internal consistency and gener-
alized validity. The ASI, SF-​36, and SF-​12 are the best
measures for assessing medical health concerns. The
RAATE can be used to determine the most appropriate
level of care for the client. Several measures are available
to identify drinking patterns, such as the TLFB and the
Form 90. The RAPI and the B-​YAACQ are good measures
to assess alcohol consequences. Family history of alcohol-
ism may be best assessed using a single question followed
up by the FTQ for more detailed information. When
assessing readiness to change, the URICA is highly rec-
ommended. Treatment history may be assessed using the
Form 90. Several psychometrically sound measures are
available for assessing craving, including the AUQ, which
assesses craving at the time of the assessment. High-​risk
drinking or relapse situations may be identified using one
of the IDS measures. Alcohol outcome expectancies can
be assessed using one of the CEOA measures. Either of
the DRSEQ measures may be used to assess drinking self-​
efficacy. Finally, use of the IPA is the best way to identify
the drinking patterns of important people in a client’s
social network.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
In order to monitor progress and treatment outcome,
clinicians often assess alcohol use, alcohol-​related conse-
quences, motivation to discontinue alcohol use, treatment
adherence, and general functioning. This section out-
lines alcohol instruments assessing consumption patterns,
drinking consequences, motivation to change, quality of
398 Substance-Related and Gambling Disorders
life, Alcoholics Anonymous (AA)/​12-​step affiliation, and
coping skills. Generally, the goal of alcohol treatment
is to reduce alcohol consumption and its related nega-
tive consequences. Thus, measures of consumption and
drinking consequences provide clinicians and researchers
with objective measures of progress and post-​treatment
changes related to harmful alcohol use. In addition, the
individual’s commitment and motivation for change are
also indicators of progress. Understanding commitment
and motivation levels can be especially helpful during
treatment monitoring to guide treatment approaches.
Moreover, measures that assess overall quality of life
are reviewed. These measures are useful in treatment
monitoring and treatment evaluation because they are
indicators of improved functioning. Last, we discuss AA
involvement/​ 12-​
step affiliation and coping skill assess-
ments. AA involvement and acquisition of coping skills
tend to be positively associated with treatment effective-
ness. Therefore, assessments of AA/​12-​step commitment
and acquisition of coping skills can be critical measures
of treatment gains. This section concludes with an overall
evaluation of the measures recommended for treatment
monitoring and evaluation. Instruments that are “highly
recommended” have strong psychometric properties
across all domains. A full list of measures and their psy-
chometric characteristics are presented in Table 18.3.
Consumption Patterns
Consumption pattern is a widely used indicator of treat-
ment progress and outcome. Monitoring rate of consump-
tion during and following treatment can be an objective
method to assess an individual’s risk, change in drink-
ing, and effectiveness of the treatment method. Thus, it
is important to assess drinking patterns in both clinical
and research settings when monitoring treatment and out-
come. As noted previously, the TLFB and Form 90 are
highly recommended consumption measures due to their
“good” to “excellent” psychometric properties across clin-
ical and nonclinical samples. The TLFB and Form 90 are
good measures of treatment outcome and are commonly
used to gather baseline and follow-​up data. One advan-
tage of the Form 90 compared to the TLFB is its inclusion
of collateral reports, specifically the Form 90-​Collateral
(Form 90-​AC; Miller & Del Boca, 1994). For treatment
outcome evaluation, collateral reports can provide infor-
mation on relevant alcohol-​related consequences that are
not captured in the TLFB and can corroborate self-​report
data. Examples of consequences include hospitaliza-
tion, treatment utilization, and incarceration following
treatment. The level of detail in the Form 90-​AC can
limit its usefulness in some settings; therefore, the Form
90-​ACS, a shortened form focusing on drinking behav-
iors, can be used for more general applications.
As described previously, the utility of both TLFB and
Form 90 instruments is limited by the need for training
and the length of administration. For settings necessitat-
ing brief measures of alcohol consumption that do not
require training, screening measures such as the AUDIT
or Daily Drinking Log may be appropriate. Furthermore,
the Brief Addiction Monitor (BAM; Center for Excellence
in Substance Abuse Treatment and Education, 2010), a
brief monitoring and outcome measure, may also be an
alternative. Despite its limited number of psychometric
investigations, the BAM appears to be a promising self-​
report measure with strong content validity and good con-
struct validity and reliability (e.g., Cacciola et  al., 2013;
Nelson, Young, & Chapman, 2014).
Similarly, the Patient-​Reported Outcomes
Measurement Information System alcohol item bank
(PROMIS; Pilkonis et  al., 2013)  assesses alcohol use,
consequences, and expectancies. The PROMIS alcohol
use items assess past 30-​day typical quantity, maximum
number of drinks, number of days intoxicated, and subjec-
tive ratings of drinking behavior (e.g., “I spent too much
time drinking” or “I drank too much”). These measures
of alcohol use can be used to determine an individual’s
change in drinking patterns and beliefs about his or her
drinking. Moreover, the PROMIS assesses negative and
positive alcohol-​related consequences and expectancies.
These items describe an individual’s maladaptive drink-
ing patterns (i.e., consequences) and further elucidate
beliefs, or expectancies, about drinking. We did not rate
the PROMIS alcohol item bank as highly recommended
because of the limited number of independent psycho-
metric investigations of the measure. Initial develop-
ment and early psychometric investigations indicate the
PROMIS scores have excellent psychometric properties,
specifically excellent normed data, internal consistency,
and content validity (Pilkonis et al., 2016). Future investi-
gations are needed to further validate the PROMIS alco-
hol use items.
Biological Measures
In addition to screening, biological measures of alco-
hol consumption can be used in conjunction with self-​
report measures for treatment monitoring and outcome
evaluation. Due to the varying levels of specialized train-
ing and testing needed for biological measures, clinical
TABLE 18.3   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Consumption Patterns
TLFB G NA NA A NR G E E A ✓
PROMIS E E NA NR E A G G A
BAM A A NA A G A A A NR
MAP G A A A NR NR G NR A
Form 90 G NA NA G NR A E G A ✓
5-​HTOL G NA NA NR NA NA G G A ✓
GGT E NA NA NR NA G E E A ✓
CDT G NA NA NR NA G E E A ✓
PEth E NA NA NR NA NA G E A
EtG A NA NA NR NA NA G A A
EtS A NA NA NR NA NA G E A
AST A NA NA NR NA NA E G A
ALT A NA NA NR NA NA E G A
FAEE A NA NA NR NA NA G A A
MCV G NA NA NR NA NA E G A
Transdermal A NA NA NR NA NA A A A
monitoring via
sweat/​SCRAM/​
Giner TAS
Drinking Consequences
DrInC G G NA A A G E E A ✓
SIP G G NA A A G E A A
RAPI G G NA G A A G G A
YAACQ G G NA A A A G A A
B-​YAACQ G G NA A A A G G A
ATOM A G NA A G A A A A
Readiness to Change
SOCRATES E G NA G E A E G A ✓
URICA G G NA A NR G E A A ✓
Change E E NA A A A E NR A
Questionnaire
AA Involvement/​12-​Step Affiliation
AAS G G NA NR G A G NR A
AAI G G NA A NR NR G A A
B-​PRI A G NA NR E A A A A
GAATOR A G NA NR A A G NR A
Quality of Life
LSS G G NA A G A G G A
SF-​36 E G NA A G G E E A ✓
SF-​12 E G NA A G G E E A ✓
WHOQOL-​BREF E G NA A G G E NR A
Coping Skills
Alcohol-​Specific A G G A G A A NR A
Role-​Play Test
Impaired Control G G NA A G G G A A
Scale
PBSS G A NA NR G G A NR A

Note:  TLFB  =  Timeline Followback; PROMIS  =  Patient-​Reported Outcomes Measurement Information System Alcohol Use Bank; BAM  =  Brief
Addiction Monitor; MAP = Maudsley Addiction Profile; 5-​HTOL = 5-​hydroxytryptophol; GGT = serum γ-​glutamyl transferase; CDT = carbohydrate-​
deficient transferrin; PEth  =  phosphatidyl ethanol; EtG  =  ethyl glucuronic; EtS  =  ethyl sulfate; AST  =  aspartate aminotransferase; ALT  =  alanine
aminotransferase; FAEE = fatty acid ethyl esters; MCV = mean corpuscular volume; SCRAM = secure continuous remote alcohol monitor; TAS = trans-
dermal alcohol sensor; DrInC  =  Drinker Inventory of Consequences; SIP  =  Short Index of Problems; LDQ  =  Leeds Dependence Questionnaire;
RAPI  =  Rutgers Alcohol Problem Index; YAACQ  =  Young Adult Alcohol Consequences Questionnaire; B-​YAACQ  =  Brief Young Adult Alcohol
Consequences Questionnaire; ATOM = Alcohol Treatment Outcome Measure; SOCRATES = Stages of Change Readiness and Treatment Eagerness
Scale; URICA  =  University of Rhode Island Change Assessment; AA  =  Alcoholics Anonymous; AAS  =  Alcoholics Anonymous Affiliation Scale;
AAI = Alcoholics Anonymous Involvement Scale; B-​PRI = Brown–​Peterson Recovery Progress Inventory; GAATOR = General Alcoholics Anonymous
Tools of Recovery Scale; LSS = Life Situation Survey; SF-​36 = Medical Outcome Study Health-​Related Survey Short Form; SF-​12 = Medical Outcome
Study Health-​Related Survey Short Form; WHOQOL-​BREF = World Health Organization Quality of Life Survey–​BREF; PBSS = Protective Behavioral
Strategies Survey; A = Acceptable; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.
400 Substance-Related and Gambling Disorders

utility is often limited. However, the high precision, Consequences of Drinking

sensitivity, and specificity of biological markers and lim-
ited reporting bias increase their utility as objective mea-
sures for treatment monitoring and evaluation. The two
most commonly studied biological measures are GGT
and CDT levels. As mentioned previously, GGT has
been shown to have moderate levels of specificity and
sensitivity to ethanol and is most accurate for chronic,
heavy consumption, whereas CDT has been shown to
have high specificity and moderate sensitivity for heavy
consumption (Djukic, 2012; Snell et al., 2016). Despite
their treatment sensitivity, GGT and CDT are limited
to heavy alcohol consumers and remain in the body for
long periods (up to 8 weeks for GGT and up to 3 weeks
for CDT). Researchers have suggested assessing GGT
and CDT levels in combination to increase accuracy,
specificity, and sensitivity for heavy drinking populations
(Djukic, 2012; Snell et al., 2016).
Tests for biological markers, such as 5-​hydroxytryp-
tophol (5-​ HTOL) and ethyl glucuronide (EtG)/​ ethyl
sulfate (EtS), can be used to measure acute alcohol
intoxication spanning one to several days, respectively.
These biological measures have been shown to have high
specificity and sensitivity in identifying ethanol levels
following recent alcohol consumption; however, they are
limited by their susceptibility to individual differences
(sex, size, etc.).
In addition, biomarkers such as PEth, fatty acid ethyl
esters (FAEE), MCV, aminotransferase (ALT), aspartate
aminotransferase (AST), and transdermal alcohol moni-
tors are potentially useful in treat monitoring. These
measures were not highly recommended due to their
limited utility in treatment monitoring. For example,
FAEE is best used to distinguish heavy alcohol drinkers
from light alcohol drinkers and can be detected up to
24 hours after drinking and remain in hair for several
months after drinking (Djukic, 2012). Heavy alcohol
drinkers who cut down on drinking may not have low
enough FAEE levels after the first few weeks of cutting
down. Thus, this biomarker may be useful in determin-
ing pre-​and post-​treatment drinking status rather than
monitoring alcohol use throughout treatment. Similarly,
ALT and AST better assess liver damage rather than
alcohol consumption (Djukic, 2012), limiting their
use in monitoring alcohol consumption during treat-
ment. However, they may be useful in assessing alcohol
relapse following treatment. Although not highly recom-
mended, these biomarkers may play an important role
in assessing some aspects of treatment monitoring and
evaluation.
As noted previously, drinking consequences can be used
as biopsychosocial measures of impairment from alcohol
use. Researchers and clinicians can use measures of pre-​
and post-​drinking consequences as indicators of alcohol-​
related dysfunction to monitor treatment and evaluate
outcome. The DrInC assesses lifetime and past 3-​month
alcohol consequences. The DrInC was originally normed
for adults, which may limit its applicability to adoles-
cent or young adult populations. The RAPI (White &
Labouvie, 1989) and the YAACQ (Read et al. 2006) are
two alcohol consequences measures that have “accept-
able” to “good” treatment sensitivity and validity general-
ization, and they are designed specifically for adolescents
and college students. In addition, the Alcohol Treatment
Outcome Questionnaire (ATOM [also known as the
Australian Alcohol Treatment Outcome Questionnaire];
Simpson, Lawrinson, Copeland, & Gates, 2007) is a brief
measure designed for alcohol treatment outcome with
potential for good clinical utility. The ATOM has differ-
ent versions for research (ATOM-​R) and clinical practice
(ATOM-​C; Simpson et al. 2007). Reliability and validity
investigations of the ATOM-​C suggest evidence of strong
internal consistency and content validity, with recent work
illustrating satisfactory treatment sensitivity and construct
validity (Simpson, Lawrinson, Copeland, & Gates, 2009).
Readiness for Change
Similar to case conceptualization and treatment planning,
readiness for change is also an important part of treatment
monitoring and evaluation. Understanding which stage
of change an individual is in is helpful to monitor prog-
ress throughout treatment and can be used to prepare for
potential relapse. The URICA and the SOCRATES are
highly recommended measures that can be used for treat-
ment conceptualization as well as treatment monitoring
and outcome evaluation. The URICA is normed for clini-
cal and nonclinical samples and exhibits high generaliz-
ability to a broad range of groups. Moreover, pretreatment
measures of readiness to change using the URICA and
SOCRATES instruments have been related to treatment
outcome (Edens & Willoughby, 2000; Isenhart, 1997),
making it a potentially useful tool in assessing treatment
outcome.
Quality of Life
Assessing quality of life is also a useful method of moni-
toring treatment progress and outcomes. Evidence
 Alcohol Use Disorder 401

suggests that maladaptive drinking patterns are nega-
tively associated with quality of life (Donovan, Mattson,
Cisler, Longabaugh, & Zweben, 2005). Thus, monitor-
ing an individual’s functioning via quality of life (QoL)
instruments can provide insight into the effectiveness
of alcohol treatment and the impact of treatment on an
individual’s health. The SF-​12 and SF-​36 are two highly
recommended measures for assessing QoL given they are
commonly used in alcohol research due the availability of
norms specific to psychological treatment. Although these
instruments do not assess all domains of life functioning,
their relevance to alcohol treatment, good psychometric
properties, and treatment sensitivity make them highly
recommended for assessing QoL outcomes.
(PBSS; Martens et al., 2005) has promising psychometric
properties. The PBSS is a 25-​item questionnaire assess-
ing the use of protective behavioral strategies related to
alcohol consumption and alcohol-​related problems. This
measure was initially developed for college student popu-
lations, and it has strong content validity and normative
data. The PBSS is negatively correlated with alcohol-​
related consequences (e.g., Pearson, Kite, & Henson,
2012). Reduction in negative alcohol-​ related conse-
quences can be an indicator of treatment effectiveness.
Despite limited data on the validity of measures assessing
coping skills, these measures may be useful in clinical and
research settings in which coping skills are a component
of AUD treatment.

AA Involvement/​12-​Step Affiliation Overall Evaluation

In AA-​focused treatments, adherence to the values and Many of the measures mentioned in this chapter may
beliefs of the AA/​12-​step model is viewed as a marker of be applicable to treatment monitoring and evaluation.
progress among those desiring to remain abstinent from Instruments administered at the beginning of treatment
alcohol. Thus, for settings using AA-​focused treatments, (e.g., screening or diagnostic measures) can be readmin-
regular assessments of AA involvement/​12-​step affiliation istered during and following treatment to assess change.
can be used to monitor treatment progress and evaluate However, the measures included in this section are
outcomes. As noted in Table 18.3, several AA/​ 12-​stepspecifically designed to be primary and secondary mea-
measures have satisfactory psychometric properties. sures for treatment monitoring and evaluation, or they
These instruments were not highly recommended due to are most relevant for assessing treatment effectiveness.
The TLFB and Form 90 are commonly used measures
limited evidence of their validity (e.g., construct validity).
However, readers should note the listed instruments have of consumption that are easy to administer. Their ease
been described elsewhere as valid measures of AA involve- of use and high treatment sensitivity make these instru-
ment/​12-​step affiliation (Allen, 2000). ments useful for treatment monitoring and evaluation.
In addition, biological measures such as GGT and
CDT can be used in conjunction with other consump-
Coping Skills
tion assessments to improve detection of ethanol during
Coping skills are a major component of cognitive–​ and following treatment. Not only should consumption
behavioral therapy (CBT) AUD treatments. Examples of patterns be monitored throughout treatment but also a
coping skills include monitoring mood, managing crav- reduction in alcohol-​related problems is an important
ing, or managing difficult situations involving alcohol indicator of change. The DrInC has strong psychomet-
(e.g., saying “no” to an offer to drink). CBT-​focused alco- ric properties and sensitivity to changes in the number of
hol treatments provide individuals with coping skills to adverse consequences during and following treatment.
help maintain treatment gains and prevent future relapse. Moreover, understanding an individual’s motivation for
Understanding an individual’s coping skills can be help- change can help determine appropriate treatment goals.
ful in identifying progress, areas for improvement, and Measures such as the SOCRATES and the URICA can
treatment effectiveness. Moreover, assessing coping skills aid in determining an individual’s motivation to better
can be useful in non-​CBT-​focused treatments. Measures monitor potential gains or losses during or following treat-
of an individual’s competency in managing cravings or ment. In addition, QoL indexes the overall functioning of
high-​risk situations can be used to determine treatment an individual. The inverse relationship between maladap-
progress or likelihood of relapse. The coping skill mea- tive QoL and alcohol consumption makes QoL a useful
sures reviewed in this chapter could not be highly rec- metric of progress for treatment monitoring and evalua-
ommended because of limited evidence of their validity. tion. Last, AA involvement/​12-​step affiliation and coping
However, the Protective Behavioral Strategies Scale skills can be useful measures of an individual’s adherence
402 Substance-Related and Gambling Disorders

to common alcohol treatments. Treatments such as AA psychometric properties to record “accurate data in order
and CBT focus on adherence to the treatment model to study alcohol-​related health outcomes, disease progres-
and acquisition of coping skills. Relevant AA/​12-​step or sion, treatment efficacy, and recovery. A wearable alcohol
CBT-​centered treatments may benefit from monitoring monitoring device could have consumer appeal as well;
AA/​12-​step commitment and coping skills as proxies for much like counting one’s steps, this information could
improvement during and following treatment. Readers help individuals make better health choices” (https://​
should be aware that the measures provided in this section www.niaaa.nih.gov/​challenge-​prize). Although it is not
are not exhaustive. In addition, measures not identified as yet clear when such devices will be “ready for prime time”
“highly recommended” may still have good clinical util- for clinicians and the general public, achievement of this
ity. Other measures that are relatively new have promising goal could revolutionize the assessment of consumption,
psychometric properties, such as the PROMIS and the especially when coupled with information about “when
BAM for assessing consumption and the ATOM-​C for and where” such consumption takes place.
assessing consequences of drinking. Similarly, electronic diaries in various forms have been
used in alcohol (and other types of substance use) research
for many years, but they have not yet achieved widespread
CONCLUSIONS AND FUTURE DIRECTIONS acceptance in clinical practice. Real-​time measurement
of consumption, drinking situations, motivation, affective
Assessment of AUD and related variables continues to states, and drinking consequences figures prominently in
evolve in multiple ways that reflect refinement of basic basic research (e.g., Shiffman, 2016) and is used in some
constructs on the basis of both theory and the ever-​ clinical trials, but no single standard instrumentation has
increasing evidence base. Researchers and clinicians have been widely adopted. It is possible that part of the issue
a range of tools available to them to assess risk factors for is that most researchers develop their own programs or
problematic alcohol involvement, to evaluate the nature “apps” for individual studies without making them gener-
and extent of drinking patterns and associated problems ally available to the public. However, it seems likely that
(including AUD), to characterize a patient’s profile on a as more health-​ related apps are disseminated through
range of key variables that help guide the clinician with commercial vendors, a standard will emerge that will help
respect to gauging motivation for change, to identify clinicians (and users) use common approaches to assess
appropriate treatment targets, and to monitor treatment alcohol use and related constructs in real time and pro-
progress and outcomes. In each of these areas, high-​ vide useful summaries of these data.
quality measures have been developed with an eye toward Although we believe that the next version of this
both psychometric adequacy and patient and provider handbook is more likely than not to discuss real-​time
acceptability. assessment of drinking and related intra-​individual and
Although not highlighted in the current chapter contextual variables, the armamentarium available to
because of our emphasis on existing measures that have the clinician is vast and even passing familiarity with the
been established as “tried and true” in the field, a number range of constructs assessable now can only help clini-
of evolving measurement approaches have proven useful cians choose what constructs are likely to be most useful
in basic research and are finding their way into clinical in their work and how to best assess them. To this end, we
practice. For example, basic research on the metabolic encourage readers to not only become familiar with the
pathways and physiological consequences of alcohol constructs and their measures described in this chapter
intake on the individual is providing a scientific basis for but also use these as a basis for monitoring further devel-
novel biomarkers that are likely to be better at characteriz- opments in the field.
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et  al., 2016). Notably, “wearable” ethanol sensors have
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 19
Gambling Disorders
David C. Hodgins
Jennifer L. Swan
Randy Stinchfield
Gambling is defined as wagering money or something
else of value on an outcome that is partially or primarily
determined by chance. This broad definition comprises a
wide range of activities, including the purchase of raffle
tickets for a local charity, playing the animal lottery in Sao
Paulo, betting on the outcome of a weekly golf game in
Los Angeles, dog track betting in Miami, or playing casino
games at the Grand Casino in Ashgabat, Turkmenistan, or
Pachinko in a parlor in Tokyo. People can become over-
involved in any of these activities, although certain types
of gambling appear to be more likely to lead to problems.
Types of gambling such as slot machines and other elec-
tronic formats that provide relatively quick feedback are
considered most risky for the development of problematic
gambling. These formats are typically relatively inexpen-
sive, easy to learn and play, and often widely available
both inside and outside casinos, which also contributes to
the risk associated with them. Although the financial cost
of limited social play is small, uncontrolled involvement
leads to overwhelmingly large expenditures. Although
gambling problems have been recognized for centuries,
and have been described in the Diagnostic and Statistical
Manual of Mental Disorders since 1980, their prevalence
and visibility have increased significantly since gam-
bling has become broadly available during the past three
decades (Hodgins, Stea, & Grant, 2011). Currently,
online gambling is mushrooming in popularity, which
may lead to even further growth in the prevalence of gam-
bling problems.
Clinicians from both the mental health and addic-
tion communities have begun to respond to the need for
treatment for gambling disorders. This chapter briefly
describes the nature of gambling disorders and then
412
reviews the various assessment instruments that are avail-
able to help clinicians with diagnosis, case conceptualiza-
tion and treatment planning, and treatment monitoring
and evaluation. The psychometric research for each type
of assessment instrument is summarized, and instruments
are rated in terms of their clinical utility.
THE NATURE OF GAMBLING DISORDERS
The fifth edition of the Diagnostic and Statistical Manual
of Mental Disorders (DSM-​ 5; American Psychiatric
Association [APA], 2013)  provides diagnostic criteria for
gambling disorder, a disorder characterized by impaired
control over gambling activities. Most general popula-
tion prevalence surveys, in contrast, describe two levels
of problems—​disordered gambling, which roughly cor-
responds to the DSM-​5 category, and problem gambling,
which is a significant but less severe type of problem.
National and state prevalence surveys have been con-
ducted worldwide, mostly using random digit telephone
dialing methodologies. Combined rates of problem and
disordered gambling range from 0.2% to 5.3% of adults,
depending on methodological differences and on local
availability and accessibility of gambling opportunities
(Hodgins et al., 2011).
Although gambling disorders can affect anyone,
younger people, males, and individuals with lower socio-
economic status have higher rates (Petry, 2005). Gambling
disorders are associated with significant distress and social
and family impairment. Huge financial debts contribute
to high levels of stress and pressure to be less than honest
with family members, friends, colleagues, and even with
 Gambling Disorders 413

themselves. Nongambling leisure activities are curtailed,
and increasing time and energy go into gambling or
obtaining the money for gambling. Sometimes checks are
knowingly cashed without sufficient money in the bank
to cover them, and not infrequently funds are embezzled
from employers. Rates of suicidal ideation, attempts, and
completed attempts are high among individuals with gam-
bling disorders (Hodgins, Mansley, & Thygesen, 2006).
Other mental health diagnoses are highly comorbid
with gambling disorders, especially substance use, mood,
and anxiety disorders (Crockford & el-​Guebaly, 1998).
For example, a community survey of more than 43,000
Americans revealed that almost three-​fourths of pathologi-
cal gamblers had a lifetime alcohol use disorder, 38% had
a lifetime drug use disorder, 50% had a mood disorder,
and 41% had an anxiety disorder (Petry, Stinson, & Grant,
2005). Our understanding of the temporal onset and pat-
terning of pathological gambling and other mental health
disorders is limited, but the relationship appears to vary
by disorder. Substance abuse tends to precede patho-
logical gambling (e.g., Cunningham-​Williams, Cottler,
Compton, Spitznagel, & Ben-​Abdallah, 2000). On the
other hand, the onset of major depression was found to be
equally likely to precede or to follow the development of
pathological gambling in one study (Hodgins, Peden, &
Cassidy, 2005) and more often followed the onset of path-
ological gambling in others (Taber, McCormick, Russo,
Adkins, & Ramirez, 1987).
A variety of psychological treatment approaches have
been offered, including mutual support groups such as
Gamblers Anonymous, psychodynamic therapies, behav-
ioral and cognitive–​ behavioral treatments, and brief
motivational treatments. Cognitive–​behavioral and brief
motivational treatments have the most empirical support
to date (Yakovenko & Hodgins, 2016). Natural or non-​
treatment-​assisted recovery rates are also sizeable. Surveys
that report past-​year prevalence as well as lifetime preva-
lence consistently indicate recovery rates of approximately
40%, with the vast majority of these recovered individu-
als reporting never having accessed treatment (Hodgins,
Wynne, & Makarchuk, 1999; Slutske, 2006).
ASSESSMENT FOR DIAGNOSIS
There has been a proliferation of disordered gambling
assessment instruments during the past decade, and the
majority of them fall into the area of interview or self-​
report diagnostic instruments (Stinchfield, 2014). The
preponderance of measures have been developed for use
in prevalence surveys, and their design reflects the need
to balance maximal reliability and validity with the brev-
ity that is required in such research. Some of these diag-
nostic instruments have only had psychometric properties
assessed in community samples. However, as discussed
later and shown in Table 19.1, a number have also been
validated in clinical populations and are becoming widely
used by clinicians.
The majority of the available diagnostic instruments
are based on the DSM-​ IV (APA, 1994)  criteria for

TABLE 19.1   Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommendeda

SOGS E G G A A E E G
SOGS-​R E G NR A A E A G
NODS NR G NR A A G A G
GAMTOMS–​DSM A A NR G A G A A
DIGS-​DSM NR E NR NR A A NR G
SCI-​PG NR NR E A A G NR G
GBI A E NR NR A G NR A
CPGI–​PGSI A G NA A L A A A
PPGM L G NA A G A A L

  See page 418 for the reasons that no measure is currently highly recommended for this assessment purpose.
a

Note:  SOGS  =  South Oaks Gambling Screen; SOGS-​R  =  SOGS past-​year version; NODS  =  National Opinion Research Center (NORC) DSM-​
IV Screen for Gambling Problems; GAMTOMS = Gambling Treatment Outcome Monitoring System; DIGS = Diagnostic Interview for Gambling
Schedule; SCI-​PG = Structured Clinical Interview for Pathological Gambling; GBI = Gambling Behavior Inventory; CPGI–​PGSI = Canadian Problem
Gambling Index–​Problem Gambling Severity Index; PPGM = Problem and Pathological Gambling Measure; L = Less Than Adequate; A = Adequate;
G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.
414 Substance-Related and Gambling Disorders
pathological gambling or criteria from previous versions
of the DSM. A small number have been updated to assess
the DSM-​5 diagnosis of gambling disorder. The DSM-​IV
and DSM-​5 criteria are nearly identical, except for the
following:  (a) The DSM-​IV illegal activity criterion was
omitted from the DSM-​5; (b)  the number of required
criteria for diagnosis of gambling disorder was reduced
by one; (c)  DSM-​5 now specifies that symptoms occur
within a 12-​month time period; and (d) some minor word-
ing revisions were made to three of the criteria, such as
inserting the word “often” in the preoccupation criterion
(Stinchfield et al., 2016). As a result, instruments can be
easily modified; however, any modified measures would
require psychometric evaluation. The current criteria
include items such as tolerance (escalating gambling
activities over time), withdrawal-​like symptoms (restless-
ness and irritability), attempts to control one’s gambling,
impaired control (“chasing losses”), and continuing to
gamble despite negative consequences. Generally, the cri-
teria are behavioral and objective in nature. An individual
receives a diagnosis if four or more of the nine criteria are
met (Criterion A) and the gambling behavior is not better
accounted for by a manic episode (Criterion B).
The problem gambling category that is often reported
in prevalence surveys, but not included in the DSM, is
typically conceptualized as subthreshold pathological
gambling. Many of the diagnostic instruments reviewed
here and summarized in Table 19.1 provide a lower cut-​
off for determining problem gambling, and some instru-
ments provide one or two additional “at risk” categories
that reflect even lower levels of problem severity.
The medically based conceptualization of disordered
gambling in the DSM has been criticized as ignoring the
role of the social and environmental context of gambling
disorders. In response, broader “harm-​based” models of
gambling problems have been proposed in which prob-
lems are defined as gambling that creates negative conse-
quences for the gambler, others in the social network, or
the community (Ferris & Wynne, 2001; Ferris, Wynne, &
Single, 1998). The Problem Gambling Severity Index of
the Canadian Problem Gambling Index (Ferris & Wynne,
2001), reviewed later, was developed from this alternative
conceptualization and has been popular in Canada as
well as in numerous other countries (e.g., Australia and
New Zealand).
South Oaks Gambling Screen
The most well-​
known instrument is the South Oaks
Gambling Screen (SOGS; Lesieur & Blume, 1987). The
SOGS, developed in the 1980s to screen clinical popula-
tions, was based on the DSM-​III (APA, 1980) and DSM-​
III-​R (APA, 1987)  criteria. It subsequently became the
most widely used instrument in general population preva-
lence surveys (Shaffer, Hall, & Vander Bilt, 1999)  and
has been translated into French, Spanish, Italian,
Swedish, Lao, Chinese, Vietnamese, Portuguese, and
Cambodian. The original SOGS consisted of 20 true–​
false self-​completion items that reflect lifetime gambling
involvement, although parallel past-​ year and 3-​month
versions were subsequently developed (SOGS-​R; Lesieur
& Blume, 1993; SOGS-​ 3; Wulfert et  al., 2005). The
SOGS-​3 is useful in evaluating outcome, and is discussed
in the treatment monitoring section. The SOGS can be
administered either in self-​report format or via face-​to-​face
or telephone interview. Although the original scale was
designed to identify pathological gambling, a lower cut-​
off score for problem gambling has been established, and
the SOGS total score is also used as an indicator of gam-
bling problem severity.
The content of the SOGS includes items that inquire
about hiding evidence of gambling, spending more time
or money gambling than intended, arguing with family
members about gambling, and borrowing money from
a variety of sources to gamble or to pay gambling debts.
Each of these sources of money is scored as a separate
item, which weights this criterion very heavily. Because
the SOGS items were developed from DSM-​III crite-
ria, there is some concern regarding its content validity
for DSM-​ 5 assessments because a number of criteria
have been changed significantly in the DSM revisions.
Nonetheless, an investigation of the psychometric prop-
erties of the past-​year self-​report version of the SOGS in
three large clinical samples found good internal reliability
and concurrent validity compared with DSM-​IV assess-
ments (Stinchfield, 2002). Classification accuracy overall
was good (.96), with better sensitivity (.99) than specific-
ity (.75). Regarding specificity, the SOGS appears to be
a liberal measure of DSM-​ IV pathological gambling.
In general population samples, the SOGS identifies a
greater number of pathological gamblers than do DSM-​
IV-​oriented measures (Cox, Yu, Afifi, & Ladouceur, 2005;
Stinchfield, 2002). Fewer comparative data are available
for clinical samples, although the same concern about
false positives exists (Grant, Steinberg, Kim, Rounsaville,
& Potenza, 2004; Hodgins, 2004). With a reduction in the
number of symptoms required for diagnosis of gambling
disorder in the DSM-​5 (thereby raising the population
prevalence of disordered gambling), problems with false
positives on the SOGS could be expected to decrease.

However, limitations with the classification accuracy
of the SOGS remain unchanged when evaluated with
DSM-​5 criteria (Goodie et al., 2013).
Test–​retest reliability was acceptable with the original
interview version (Lesieur & Blume, 1987) and the past-​
year self-​report version in a clinical sample (Stinchfield,
Winters, Botzet, Jerstad, & Breyer, 2007). The self-​report
SOGS often acts as the comparison standard in the assess-
ment of other measures, so evidence of concurrent validity
of both past-​year and lifetime versions across a variety of
clinical and nonclinical samples is available and is gener-
ally positive (see Table 19.1; Grant et al., 2003; Hodgins,
2004; Lesieur & Blume, 1987; Stinchfield, Govoni, &
Frisch, 2005; Wulfert et  al., 2005). Ladouceur and col-
leagues (2000) investigated validity at the item level and
reported that most respondents in a community sample
misinterpreted one or more items. Because all the true–​
false items are keyed in the true direction (true reflecting
a problem), community respondents were more likely to
overreport than underreport symptoms—​clarification of
item meaning reduced the number of individuals classi-
fied as pathological gamblers. Similar research has not
been conducted with clinical samples, but clearly inter-
pretation at the item level is likely to be unreliable for
any scale.
National Opinion Research Center DSM-​IV Screen
for Gambling Problems
The National Opinion Research Center DSM-​IV Screen
for Gambling Problems (NODS) was originally devel-
oped for a U.S. national gambling telephone survey as a
past-​year and lifetime diagnostic measure based on DSM-​
IV diagnostic criteria (Gerstein et  al., 1999). As well as
being designed for use in an interview format, it is also
used as a self-​report instrument, although no psychomet-
ric information is available for the self-​ report version.
Seventeen true–​false items measure the 10 DSM-​IV diag-
nostic criteria (and therefore the 9 DSM-​5 criteria), and
the past-​year items are asked only if the lifetime item is
answered with a positive response. The NODS total score
is used to identify pathological gambling, and lower cut-​
offs indicate problem and low-​risk gamblers. A  number
of the DSM criteria are operationalized with the use of
time periods (e.g., past 2 weeks) and frequency parameters
(e.g., three or more times) in order to increase the item
reliability. Because these changes represent a tightening
of these criteria relative to their description in the DSM-​
IV and DSM-​5, the NODS may underidentify patho-
logical gamblers. Consistent with this concern, in the
Gambling Disorders 415
U.S. national sample, the estimated prevalence was lower
than that found in other surveys (Gerstein et  al., 1999).
However, without a gold standard for comparison, it is
unclear that this lower estimate is less valid. When using
clinician rating (based on DSM-​IV criteria) as the thresh-
old for comparison in a sample of gamblers, the NODS
identified only 68.5% of problem gamblers identified by
clinicians, but it provided a reasonably accurate overall
prevalence rate (Williams & Volberg, 2014). However,
clinician ratings do not necessarily reflect a gold standard,
and there have not been similar published comparisons
of the NODS with other DSM-​IV or DSM-​5 measures in
clinical populations.
The NODS has less supporting psychometric research
than the SOGS. In terms of additional indicators of valid-
ity, during the scale development phase the NODS was
administered to a small sample of individuals in outpatient
problem gambling treatment programs. Of the 40 indi-
viduals, 38 scored 5 or more on the lifetime NODS, and
2 obtained scores of 4. Retest reliability over 2 to 4 weeks
in an overlapping sample of 44 gamblers in treatment
was high (r = .99 and r = .98 for lifetime and past year,
respectively). The authors did not report internal consis-
tency coefficients, although alpha coefficients in clinical
samples were reported to be adequate in the past-​year
version administered via telephone (Hodgins, 2004) and
good in the past-​year and lifetime versions administered
face-​to-​face (Wickwire, Burke, Brown, Parker, & May,
2008; Wulfert et al., 2005).
The validity of the lifetime and past-​year total scores
was also assessed in these clinical samples. Using a vari-
ety of discriminant and convergent measures, good
validity results were generally obtained (Hodgins, 2004;
Wickwire et  al., 2008; Wulfert et  al., 2005). Hodgins
also reported the validity of the categorical cut-​ points
compared with the SOGS pathological and problem cat-
egories. Agreement was poor, with most NODS problem
gamblers categorized as pathological on the SOGS (i.e.,
more severe). Because it is unclear which categorization
is more valid in the absence of a gold standard indicator,
clinicians should be cautious about relying too much on
cut-​off scores to indicate the presence or absence of a diag-
nosable condition.
Following the development of the NODS, a subset of
three items were found to identify nearly all pathologi-
cal gamblers and more than 90% of problem gamblers.
These three items—​ evaluating loss of control, lying,
and preoccupation—​comprise the NODS-​CLiP (Toce-​
Gerstein, Gerstein, & Volberg, 2009). This brief screen
has demonstrated excellent sensitivity (.96) and adequate
416 Substance-Related and Gambling Disorders
specificity (.90) in the general population, but it did not
perform as well in a clinical sample. Although it cap-
tured nearly all pathological and problem gamblers, the
NODS-​CLiP also captured a high proportion of low-​risk
and at-​risk gamblers (Volberg, Munck, & Petry, 2011).
Volberg and colleagues identified a different subset of four
items evaluating preoccupation, escape, risked relation-
ships, and chasing (NODS-​PERC). This alternative set
of items demonstrated better psychometric properties in
a clinical sample than the NODS-​CLiP (Volberg et  al.,
2011). The authors recommend use of the NODS-​PERC
over the CLiP in settings with a higher base prevalence
rate of disordered gambling (e.g., substance abuse treat-
ment programs).
In summary, the NODS appears to identify fewer
individuals as pathological gamblers in both general
population and treatment samples. It provides a DSM-​
IV diagnosis plus a subclinical problem gambling cat-
egory. To date, positive, but limited, psychometric
research is available for the interview version. Subsets
of NODS items also appear to form promising brief
screeners for gambling problems in the general popula-
tion (i.e., NODS-​CLiP) and in clinical populations (i.e.,
NODS-​PERC).
GAMTOMS–​DSM-​IV Measure
The Gambling Treatment Outcome Monitoring
System (GAMTOMS; Stinchfield, Winters, et  al.,
2007) is a multidimensional questionnaire or interview
assessment tool designed for outcome assessment. It is
described in detail in the sections on other assessment
purposes. However, it also contains a 10-​item true–​false
DSM-​ IV measure relevant for diagnostic purposes.
Both the questionnaire and interview versions of the
GAMTOMS have been subjected to a number of psy-
chometric evaluations in clinical samples (Stinchfield,
Govoni, & Frisch, 2007). The DSM-​ IV total score
showed good internal reliability in one treatment
sample but less than adequate reliability in two other
samples. Retest reliability over 1 week was good in the
three samples but slightly lower than the SOGS retest
estimate in the same samples. The total scores showed
good convergent and discriminant validity with a variety
of criteria, including the SOGS. The categorical diag-
nosis of pathological gambling showed good sensitivity
(.96) and specificity (.95) identifying clinical from non-
clinical individuals and good sensitivity (.97) and speci-
ficity (1.0) using SOGS classification as the criterion
(Stinchfield, 2003; Stinchfield et al., 2005).
Other DSM-​IV Measures
A number of additional DSM-​IV-​based measures have
been developed but, to date, have had limited psy-
chometric evaluation. For example, a brief gambling
module of the Diagnostic Interview Schedule (DIS;
Robins, Cottler, Bucholz, & Compton, 1996) has been
used in a number of investigations (e.g., Cunningham-​
Williams, Cottler, Compton, & Spitznagel, 1998;
Welte, Barnes, Wieczorek, Tidwell, & Parker, 2001),
although no psychometric data have been reported.
A revised and more extensive Composite International
Diagnostic Interview includes assessment of DSM-​IV
pathological gambling and has demonstrated good psy-
chometric properties in a U.S.  household population
(Kessler et al., 2008).
Two other diagnostic assessment measures are appeal-
ing because they allow the clinician to probe responses
to determine whether each diagnostic criterion is passed.
The Diagnostic Interview for Gambling Schedule–​DSM-​
IV Diagnosis (DIGS-​ DSM-​ IV; Winters, Specker, &
Stinchfield, 2002)  is a structured clinical interview for
assessment and treatment planning that contains a 20-​
item assessment of the DSM-​IV criteria for the past-​year
and lifetime time frames. Psychometric data were assessed
in only one treatment sample but were positive (Winters
et  al., 2002). Grant and colleagues (2004) describe
a similar measure, the Structured Clinical Interview
for Pathological Gambling (SCI-​ PG) that is modeled
after the Structured Clinical Interview for the DSM-​IV
(SCID; Spitzer, Williams, Gibbon, & First, 1990), which
is widely used for assessment of DSM disorders but does
not include a pathological gambling module. A  DSM-​
5 updated version of the instrument (SCID-​ 5; First,
Williams, Karg, & Spitzer, 2015a) includes an optional
module to assess current (past-​year) gambling disorder in
the research version of the instrument (SCID-​5-​RV); how-
ever, this module is unavailable for the clinician version
(SCID-​5-​CV; First, Williams, Karg, & Spitzer, 2015b). In
a SCID assessment, trained clinicians use a series of probe
questions to determine whether each of the 10 criteria has
been met over the lifetime and currently. If the gambling
module of the SCI-​PG (or the SCID-​5-​RV) is used in
conjunction with the full SCID, then the clinician can
assess the DSM exclusion criterion for pathological gam-
bling: The gambling behaviors are not better accounted
for by a manic episode (Criterion B). In a small clinical
sample, inter-​rater reliability and retest reliability over a
1-​week period were excellent and sensitivity was .88 and
specificity was 1.00 assessed against clinical ratings.

A final DSM-​ based alternative is the Gambling
Behavior Inventory (GBI; Stinchfield, 2003; Stinchfield
et al., 2005), which is a 76-​item structured interview that
includes a 10-​item past-​year DSM scale. The DSM scale
has shown excellent internal reliability in two treatment
samples as well as convergent and discriminant validity
with a variety of measures (Stinchfield, 2003; Stinchfield
et al., 2005; Stinchfield, Winters, et al., 2007). The cat-
egorical diagnosis of pathological gambling showed good
sensitivity (.91), but lower specificity (.83), in identifying
clinical from nonclinical individuals (Stinchfield et  al.,
2005). Sensitivity and specificity improved using a cut-​off
of four versus five criteria. The GBI and the GAMTOMS
have been evaluated with current DSM-​ 5 criteria by
removing the illegal acts criterion and lowering the cut-​
score, and they demonstrated satisfactory reliability, valid-
ity, and classification accuracy (Stinchfield et al., 2015).
A number of brief screens, including the NODS-​CLiP
and NODS-​PERC discussed previously, have been devel-
oped to quickly assess disordered gambling. An additional
brief screen, the Brief Biosocial Gambling Screen (BBGS;
Gebauer, LaBrie, & Shaffer, 2010), consists of three yes/​
no items. The screen assesses for disordered gambling
over a 12-​month time frame and has been shown to have
high sensitivity (.96) and high specificity (.99) using a
cut-​off of 1 (Gebauer et  al., 2010). The BBGS appears
to demonstrate satisfactory classification accuracy, with
reported hit rates, sensitivity, and specificity values of
.88, .91, and .87, respectively (Himelhoch et  al., 2015).
Furthermore, although the BBGS was developed using
DSM-​ IV diagnostic criteria, the psychometric proper-
ties appear to remain strong with current DSM-​5 criteria
(Brett et al., 2014).
Canadian Problem Gambling Index–​Problem
Gambling Severity Index
The Canadian Problem Gambling Index (CPGI; Ferris
& Wynne, 2001) is an interview tool assessing gambling
involvement and social context designed for prevalence
surveys. It has been used in surveys in most Canadian
provinces and nationally, which provides a large norma-
tive database (Cox et  al., 2005). The CPGI contains a
nine-​item Problem Gambling Severity Index (PGSI) that
has a past-​year time frame. The PGSI total score indicates
non-​problem, low-​risk, moderate-​risk, and problem gam-
bling. The total score has demonstrated good internal reli-
ability and adequate test–​retest reliability over a 4-​week
period in the general population. It also shows good con-
vergent validity with the SOGS, DSM-​IV, and clinical
Gambling Disorders 417
ratings in a treatment sample. Classification accuracy of
the problem gambling category showed adequate sensitiv-
ity (.83) and excellent specificity (1.0) using DSM-​IV clas-
sification as the criterion (Ferris & Wynne, 2001).
However, several weaknesses of the classification
categories of the PGSI have been noted. Given that
researchers often merge moderate-​risk and problem gam-
bling categories to increase statistical power due to low
prevalence (Afifi, Cox, Martens, Sareen, & Enns, 2010;
Crockford et al., 2008), more attention needs to be paid
to the validity of the instrument’s cut-​ off scores. The
scale developers proposed a cut-​off score of 3 to identify
moderate-​risk gamblers. When using a cut-​off score of 3,
the PGSI has shown poor correspondence with clinical
ratings, producing a problem gambling rate 1.85 times
higher than clinical ratings (Williams & Volberg, 2014).
Using the proposed cut-​off score of 8 for problem gam-
bling, the PGSI has demonstrated excellent specificity
(.99) but only identified 49% of problem gamblers iden-
tified using clinical ratings (Williams & Volberg, 2014).
Some research teams have proposed that using a cut-​off
score of 5 on the PGSI provides a more distinctive classifi-
cation between low-​and moderate-​risk gamblers (Currie,
Hodgins, & Casey, 2013)  and provides significantly
higher specificity, positive predictive power, and diagnos-
tic efficiency compared to a cut-​off score of 3 (Williams
& Volberg, 2014).
Problem and Pathological Gambling Measure
The Problem and Pathological Gambling Measure
(PPGM; Williams & Volberg, 2010)  is a relatively new
instrument developed for use in population prevalence
surveys. The development of the PPGM aimed to
address identified weaknesses in previous instruments,
including limited assessment of gambling-​related harms
and inability to capture problem gamblers in denial or
who lack insight. The PPGM assesses a past-​year time
frame and consists of 14 items divided into three sec-
tions:  Problems, Impaired Control, and Other Issues.
Respondents are classified as a nongambler, recreational
gambler, at-​risk gambler, problem gambler, or pathologi-
cal gambler based on section scores, frequency of gam-
bling, and reported gambling loss. The PPGM scores
have demonstrated good internal consistency and ade-
quate 1-​month test–​retest reliability, and they have shown
higher agreement with clinical ratings compared to other
instruments, such as the SOGS, PGSI, and NODS. The
PPGM has demonstrated good convergent validity with
the SOGS, PGSI, and NODS and clinical ratings in the
418 Substance-Related and Gambling Disorders
general population (Williams & Volberg, 2010). The
scale has demonstrated good psychometric properties in
two large samples (Williams & Volberg, 2014); however,
independent replication of the psychometric properties
of the PPGM is needed for it to be highly recommended.
Overall Evaluation
Because gambling disorder is a relatively new area of
investigation, there is a lack of consensus about the gold
standard diagnostic instruments. The SOGS was almost
unanimously used until it was eclipsed by the desire for
a DSM-​IV-​based instrument. Subsequently, a number of
DSM-​IV alternatives have been developed, but none has
the extensive psychometric database of the SOGS and
none has become universally used in either research or
clinical contexts. These instruments can easily be modi-
fied to provide a DSM-​5 diagnosis by eliminating one
of the diagnostic criteria and making minor revisions to
wording, but few psychometric evaluations have been
reported of DSM-​5 revised instruments. Although the
SOGS and DSM-​IV measures generally appear to assess
the same construct, it also appears that the SOGS patho-
logical and problem gambling categories represent a
lower threshold for the disorders compared to the DSM-​
IV measures. The SOGS also lacks content validity with
respect to the DSM-​IV criteria.
All of the proposed DSM-​IV measures have positive
preliminary psychometric support and, not surprisingly,
the items on the various scales are quite similar. In fact,
even the CPGI–​PGSI, which was not derived from a
DSM conceptualization, has eight of nine items that over-
lap with either the SOGS or DSM-​IV items. The mea-
sures vary in other ways. The NODS and GAMTOMS
DSM are the only self-​completion options, although all
of the psychometric evaluation of the NODS has been
on the interview format. The interview options include
the GAMTOMS, NODS, GBI, DIGS, and SCI-​PG. The
NODS and GBI can be administered via telephone as
well as face to face. The GAMTOMS, NODS, and GBI
can be administered by lay persons, and the DIGS and
SCI-​PG require clinical training and experience. These
latter two measures are, arguably, true diagnostic mea-
sures because interviewers probe to ensure that each cri-
terion is reached, whereas the others can be better viewed
as screening measures. Nonetheless, further psychometric
evaluation is required before any of these instruments can
be highly recommended for routine use (see Table 19.1).
In the meantime, the information available for each
instrument is generally supportive, and clinicians are
advised to use the instrument that best fits their purpose
from a practical perspective.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
Table 19.2 outlines important domains in case conceptu-
alization and treatment planning for gambling disorders.
Together, the domains provide a comprehensive descrip-
tion of the severity and consequences of the problem.
These factors point to potential treatment targets. It is also
recommended that some type of functional analysis of the
precipitants of gambling be performed. This type of infor-
mation is particularly relevant for cognitive–​behavioral
therapy but can also inform the therapeutic direction in
other treatment models. Assessment of comorbidity serves
a similar purpose and also may provide information about
etiology (as does family history). A  clear understanding
of the client’s treatment goal, previous treatment experi-
ence, and motivation is also essential.
Limited instrumentation exists for many of these areas
and, in fact, research regarding the specifics of the con-
struct is also limited in some instances. A good example is
the first domain in Table 19.2, Severity/​Impaired Control.
An issue exists in the field that parallels a long-​standing
debate in the alcohol field—​the advisability of gambling
moderation goals versus complete abstinence from gam-
bling (Ladouceur, 2005). The issue in gambling is com-
plicated by the possibility that gambling abstinence can
be narrowly defined as quitting the types of gambling
that have caused problems for the individual or broadly
defined as all types of gambling even if they have never
caused problems (Stea, Hodgins, & Fung, 2015).
In the alcohol field, the most robust clinical indica-
tor of the likelihood of the success of moderation ver-
sus abstinence from alcohol is the degree of alcohol
dependence (Rosenberg, 1993). Efforts are underway
to delineate a similar construct in the gambling field,
impairment of control over gambling, although efforts to
develop a reliable measurement tool have yielded mixed
results (Dickerson & O’Connor, 2006). Kyngdon (2004)
described a 12-​item unifactorial scale that in preliminary
studies correlated highly with measures of severity, such
as the SOGS, which suggests that until measurement of
impaired control further develops, severity of problem
can be used as a proxy. Problem severity has been shown
to be related to natural versus treatment assisted recovery
(Hodgins & el-​Guebaly, 2000) and response to brief inter-
ventions (Stea et  al., 2015), and it is used by clinicians
 Gambling Disorders 419

to help determine the optimal treatment goal (Robson, TABLE 19.2  

Important Domains in Case
Edwards, Smith, & Colman, 2002). Table 19.2 provides Conceptualization and Treatment Planning
a number of suggestions for standardized tools to assess for Gambling Disorders
severity of problem, and these tools are described in detail
General Dimension Specific Construct Standardized Tools
in the preceding diagnostic section. As outlined previ-
ously, psychometric research has focused on the validity Severity/​Impaired Impaired control SOGS, NODS,
Control CPGI–​PGSI
of these scales as indicators of pathological gambling, and
Gambling Quantity Lifetime history
little work has assessed the validity of these scales as indi-
Recent (past month) Timeline Followback
cators of lower degree of problem severity. DSM-​based method
measures are designed to have items that measure severe Consequences Health (e.g., ASI–​GSI,
pathology. For example, an examination of the SOGS gastrointestinal, GAMTOMS,
insomnia) DIGS
with a Rasch model of measurement (Strong, Breen,
Family
Lesieur, & Lejuez, 2003) found that SOGS items could Social relationships
be ordered in terms of their level of gambling problem Employment
severity, similar to a Guttman scale, but that the scale Financial
Emotional (self-​esteem)
is composed of mostly items reflecting severe gambling Legal
problems and that more low-​and moderate-​ severity Association/​ Functional analysis IGS, TGS, GMQ,
Circumstances of
items would be necessary to obtain an optimal measure Gambling
GFA
of the entire continuum of problem severity. In contrast Comorbid Psychiatric DSM-​5 SCID-​5, DIS, CIDI
Disorders
to DSM-​based scales, the CPGI–​PGSI was specifically
Other Drug Use Prescription and illicit AUDIT, DAST
designed to assess the full range of severity, although the drugs
low-​and moderate-​risk interpretation categories also have Nicotine, caffeine
not been validated for the CPGI–​PGSI. Family History Biological and family
exposure to gambling
There are several omnibus instruments that cover a Treatment History Programs started and GAMTOMS
number of the remaining relevant assessment domains completed
outlined in Table 19.2. The first is an adapted version of Twelve-​step involvement
Periods of abstinence
the Addiction Severity Index (ASI; McLellan, Kushner,
or nonproblematic
Metzger, & Peters, 1992). The ASI is among the most gambling
widely used and validated tools for assessing and moni- Treatment Goal Goal (abstinence or GASS, SCQG
toring patients with substance abuse problems. It pro- moderation)
Self-​efficacy
vides assessment of the severity and need for treatment Motivation Readiness to change GAMTOMS
in the medical, employment, family–​ social, psychiat- Reasons to change
ric, legal and substance abuse domains, which are all Family and social support
relevant for individuals with gambling disorders. The
Note: SOGS = South Oaks Gambling Screen; NODS = National Opinion
ASI was developed as an interview, although comput- Research Center DSM-​ IV Screen for Gambling Problems; CPGI–​
erized and self-​ completion versions are also available. PGSI = Canadian Problem Gambling Index–​Problem Gambling Severity
The ASI–​Gambling Severity Index (Lesieur & Blume, Index; ASI–​GSI  =  Addiction Severity Index–​Gambling Severity Index;
GAMTOMS  =  Gambling Treatment Outcome Monitoring System;
1991)  is a supplemental module that uses five items to DIGS = Diagnostic Interview for Gambling Schedule; IGS = Inventory
assess gambling severity and need for treatment. It was of Gambling Situations; TGS  =  Temptation to Gamble Scale;
initially validated in the interview format with inpatients GMQ = Gambling Motives Questionnaire; GFA = Gambling Functional
Assessment; SCID-​ 5  =  Structured Clinical Interview for the DSM-​
5;
in a substance abuse and gambling program (Lesieur & DIS = Diagnostic Interview Schedule; CIDI = Composite International
Blume, 1991) and later with a large sample drawn from Diagnostic Interview; AUDIT  =  Alcohol Use Disorders Identification
four different populations—​ pathological gamblers in Test; DAST = Drug Abuse Screening Test; GASS = Gambling Abstinence
Self-​efficacy Scale; SCQG  =  Situational Confidence Questionnaire for
outpatient treatment, pathological gamblers participat- Gambling.
ing in a treatment study, community problem gamblers,
and substance abusers (Petry, 2003). In the first study,
internal reliability was adequate, and some evidence of as well as convergent and discriminant validity across a
convergent validity was presented. The second study was range of external variables, including collateral and clini-
more comprehensive, revealing strong internal reliabil- cal ratings. The ASI, together with the ASI gambling
ity and good test–​retest reliability over a 1-​month period module, can provide a profile of the treatment needs of
420 Substance-Related and Gambling Disorders

an individual, although the composite severity scores for
each of the domains are difficult to compute by hand. As
indicated later, each index is responsive to change, which
makes it a useful tool for monitoring outcome, but its
value for treatment planning is limited by lack of interpre-
tation guidelines and norms (see Table 19.3).
A second omnibus instrument is the GAMTOMS
(Stinchfield, Winters, et al., 2007), which is a self-​report
or interview instrument that takes approximately 30 to
45 minutes to complete. As shown in Table  19.3, the
GAMTOMS receives generally good psychometric rat-
ings, although information is unavailable in three areas.
The latest version of the GAMTOMS includes, in addi-
tion to the DSM-​IV measure described previously, scales
assessing gambling frequency, mental health, financial
problems, legal problems, and stage of change. The
GAMTOMS also incorporates the SOGS scale. Content
validity for assessing outcome was confirmed by an expert
panel of gambling treatment professionals. Gambling
quantity is measured by items enquiring about the fre-
quency of gambling for 14 specific types of gambling.
Scores on these items in both the interview and self-​
administered versions generally show good test–​ retest
reliability over a 1-​week period as well as convergent
validity with a time line interview of gambling behav-
ior described later (Stinchfield, Winters, et  al., 2007).
Mental health is measured with the ASI Psychiatric
composite severity score described previously. The ASI
psychiatric score had inadequate internal reliability but
good retest reliability over 1 week (intraclass correlation
coefficient [ICC]  =  .83) and good convergent validity
with the BASIS-​32 (Eisen, Dill, & Grob, 1994), a self-​
report instrument validated with psychiatric outpatients.
Scores on the 23-​item financial consequences scale and
the 7-​item legal consequences scale had good internal
reliability and retest reliability as well as convergent and
discriminant validity with other GAMTOMS scales and
with federal bankruptcy and court records and collat-
eral reports (Stinchfield, Winters, et  al., 2007). Finally,
the GAMTOMS includes a single item assessing stage
or readiness to change according to the Prochaska
and DiClemente model (Prochaska, DiClemente, &
Norcross, 1992). The item showed poor retest reliability
over a 1-​week period, although it was sensitive to change
and showed good convergent validity with gambling
items (Stinchfield, Winters, et al., 2007).
In summary, the GAMTOMS covers a number of
important content domains for treatment planning and
for monitoring treatment outcome. Psychometric evi-
dence for both the self-​report and interview versions is
accumulating and is generally positive. To date, as with
the ASI, interpretation norms for the various scales have

TABLE 19.3   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

SOGS E E G E A E E G ✓
NODS NR A NR A A G A G
CPGI–​PGSI A G NR A L A A A
GAMTOMS NR G NR G G G NR G ✓
ASI–​GSI NR A NR A A G G G ✓
DIGS NR A NR NR A A NR G
TLFB NR NA A A A A E G
IGS A E NA NR G G A A ✓
TGS NR E NA A G A NR A
GFA-​R NR E NA A A G A A
GMQ NR G NA NR A G G L
GMQ-​F NR A NA NR G G A L
GASS A E NA A G G NR A ✓
SCQG NR E NA A G A NR A

Note:  SOGS  =  South Oaks Gambling Screen; NODS  =  National Opinion Research Center DSM-​IV Screen for Gambling Problems; CPGI–​
PGSI = Canadian Problem Gambling Index–​Problem Gambling Severity Index; GAMTOMS = Gambling Treatment Outcome Monitoring System;
ASI–​GSI = Addiction Severity Index–​Gambling Severity Index; DIGS = Diagnostic Interview for Gambling Schedule; TLFB = Timeline Followback;;
IGS = Inventory of Gambling Situations; TGS = Temptations to Gamble Scale; GFA-​R = Gambling Functional Assessment-​Revised; GMQ = Gambling
Motives Questionnaire; GMQ-​F = Gambling Motives Questionnaire–​Financial; GASS = Gambling Abstinences Self-​efficacy Scale; SCQG = Situational
Confidence Questionnaire for Gambling; L = Less than Adequate; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.

not been published, which limits its value for clinicians
assessing individual clients.
The DIGS (Winters et  al., 2002)  is a third omnibus
instrument, previously described, designed to assess
numerous dimensions relevant to case conceptualization
and treatment planning. The DIGS assesses demograph-
ics, gambling involvement and history, legal problems,
other impulse disorders, medical status, and family and
social functioning, and it also includes a mental health
screen. These domains represent the majority of the rel-
evant assessment areas but, as mentioned previously, the
DIGS has had limited psychometric evaluation, although
the available data are positive.
These three omnibus instruments collect basic gam-
bling frequency information. More detailed descriptions of
gambling frequency, expenditures, time spent gambling,
and monthly patterns can be assessed using the Timeline
Followback (TLFB) methodology, adapted from the alco-
hol field. The TLFB has been shown to provide reliable
and valid gambling reports, at least in the research context
(Hodgins & Makarchuk, 2003; Weinstock, Whelan, &
Meyers, 2004). The method involves providing the indi-
viduals with a calendar, reviewing with them personal and
public events to cue memories, and having them recon-
struct their daily gambling over a period of 1 to 6 months.
Frequency and expenditure information can be summa-
rized into reliable indices for weekly or monthly time
periods, but clinically rich information about patterns of
gambling can also emerge.
Table 19.2 lists the assessment of the associations and
circumstances associated with gambling behavior as a
third important domain. Prospective research examining
the process of relapse in pathological gamblers seeking
abstinence (Hodgins & el-​Guebaly, 2004)  has revealed
that individuals are most likely to be alone and thinking
about finances, but that a positive mood state is as likely
as a negative mood state to precede the initiation of gam-
bling. A relapse associated with social pressure to partici-
pate or a desire to fit in socially typically led to a relatively
minor relapse, whereas gambling associated with a false
optimism about winning or a feeling of financial pressure
was more serious. Women were more likely to relapse in
response to feelings of depression, whereas men described
gambling in response to being bored or having unstruc-
tured time or in response to the need to make money
(Hodgins & el-​Guebaly, 2004). A detailed assessment of
these potential high-​risk situations at the individual level
is important for treatment planning and can be accom-
plished by conducting an informal functional analysis of
recent heavy gambling situations.
Gambling Disorders 421
The Inventory of Gambling Situations (IGS) has been
developed to assess these factors (Turner, Littman-​Sharp,
Toneatto, Liu, & Ferentzy, 2013). The self-​ report scale
contains 63 items that comprise 10 subscales:  Negative
Emotions, Conflict with Others, Urges and Temptations,
Testing Personal Control, Pleasant Emotions, Social
Pressure, Need for Excitement, Worried About Debts,
Winning and Chasing, and Confidence in Skill. The IGS
scale scores showed excellent internal reliability and the
factor structure was confirmed in two clinical samples.
Preliminary evidence of discriminant and convergent valid-
ity was also reported. The subscales all correlated highly with
the SOGS and DSM-​IV criteria, and the pattern of correla-
tions with a group of external measures such as depression,
impulsivity, and cognitive errors conformed to expectation.
The scale has good potential for clinical use, although it is
lengthy and a computer scoring program is recommended
because it is difficult to score by hand. A 10-​item short form
of the IGS (IGS-​10; Smith, Stewart, O’Connor, Collins,
& Katz, 2011) demonstrated good convergent validity and
internal consistency in a sample of undergraduate gamblers,
although additional psychometric evaluation is required.
An alternative option is the Temptations to Gamble
Scale (TGS; Holub, Hodgins, & Peden, 2005), which has
21 items that comprise four subscales:  Negative Affect,
Positive Mood/​ Impulsivity, Seeking Wins, and Social
Factors. The TGS has good content validity and demon-
strated strong internal and test–​retest reliability over a 3-​
week period in a sample of pathological gamblers.
To examine gambling motives more broadly, the
Gambling Motives Questionnaire (GMQ; Stewart &
Zack, 2008)  draws from the alcohol literature and mea-
sures the frequency of gambling for a variety of reasons.
The 15-​ item GMQ was adapted from the Drinking
Motives Questionnaire (DMQ; Cooper, Russell, Skinner,
& Windle, 1992) and consists of three subscales: Coping,
Enhancement, and Social motives. The GMQ scores
demonstrated good internal consistency and concurrently
validity (Lambe, Mackinnon, & Stewart, 2015; Stewart
& Zack, 2008). Adapted from the drinking literature, the
GMQ is limited in its scope of motives specific to gam-
blers, particularly around financial and charitable motives
(Dechant & Ellery, 2011; Hodgins, 2008). An extended
version of the GMQ that includes financial motives
(GMQ-​F; Dechant, 2014) consists of 16 items across four
subscales: Coping, Enhancement, Social, and Financial
motives. The GMQ-​F scores have demonstrated fair to
good internal consistency, good criterion validity, and
factor structure in nonclinical samples (Dechant, 2014;
Schellenberg, McGrath, & Dechant, 2016).
422 Substance-Related and Gambling Disorders
The Gambling Functional Assessment (GFA; Dixon &
Johnson, 2007) is another self-​report instrument designed
to identify potential mechanisms maintaining an indi-
vidual’s gambling behavior. The original GFA includes
20 items that can be scored into four subscales: Sensory,
Attention, Escape, and Tangible. Although the proposed
structure of the GFA was theoretically strong, subsequent
factor analysis yielded a two-​factor solution instead of the
proposed four factors (Miller, Meier, Muehlenkamp, &
Weatherly, 2009). A revised version of the GFA (GFA-​R;
Weatherly, Miller, & Terrell, 2011)  consists of 16 items
comprising two subscales:  Positive Reinforcement and
Escape. The GFA-​ R scores have demonstrated good
to excellent internal consistency for the overall score
and both subscales (Weatherly, Miller, Montes, & Rost,
2012; Weatherly & Terrell, 2014), good construct valid-
ity (Weatherly, Dymond, Samuels, Austin, & Terrell,
2014), and good 4-​week test–​retest reliability (Weatherly
et  al., 2012). Test–​retest findings over a 12-​week period
were more mixed; overall GFA-​ R scores and Positive
Reinforcement subscale scores were much more reliable
than Escape subscale scores. Although intended for use
with clinical populations, much of the available psycho-
metric data derive from nonclinical, university samples.
To date, one study has examined the GFA-​R in a sample
of probable problem and disordered gamblers (Weatherly
& Terrell, 2014). The GFA-​R demonstrated good to excel-
lent internal consistency and good construct validity in
this sample. However, the authors propose scoring only
15 of the 16 scale items when using the GFA-​R with prob-
able problem or disordered gamblers because this scale
structure appeared to be a better fit (Weatherly & Terrell,
2014). Replication in independent clinical samples is
required to determine if this modified structure holds.
Table 19.2 also lists routinely assessing comorbid psy-
chiatric disorders and substance use and abuse. A number
of well-​validated structured assessment instruments are
available for psychiatric disorders (e.g., SCID-​5; First et al.,
2015b). The Alcohol Use Disorders Inventory (AUDIT;
Babor, de la Fuente, Saunders, & Grant, 1992) provides
a brief, 10-​item, self-​report assessment of alcohol prob-
lems. The AUDIT is most easily administered in a self-​
report version, but it can also be administered orally or via
computer. The AUDIT covers three domains—​alcohol
consumption, alcohol dependence, and alcohol-​related
problems—​and was designed to be appropriate for use in
a number of cultures and languages. The psychometric
properties of this scale, including the validation of cut-​
points for identifying high-​ risk and abusive drinking,
have been assessed in a broad range of populations (e.g.,
primary care, students, and emergency room patients; for
a review, see Reinert & Allen, 2002), although not specifi-
cally with pathological gamblers. Less well validated but
also widely used is a similar self-​completion measure for
other drug use, the Drug Abuse Screening Test (DAST;
Skinner, 1982). There are 28-​, 20-​, and 10-​item versions
of the DAST with interpretation guidelines, although the
majority of the psychometric data were derived from the
longest version (Cocco & Carey, 1998). Studies with gam-
bling samples have not been reported.
Treatment history and experience, treatment goals, and
motivation are also important assessment domains that
are identified in Table 19.2. Because standardized tools to
assess these domains are not available, they are typically
assessed through clinical interview. It is recommended
that treatment goals be assessed in clear behavioral terms
in which the person identifies a goal of abstinence or
moderation for each type of gambling and that modera-
tion goals be specified in terms of frequency and expendi-
ture limits (Hodgins & Makarchuk, 2002). The setting of
specific goals also facilitates the task of monitoring treat-
ment progress.
Two self-​completion measures are available to assess
self-​efficacy: the Gambling Abstinence Self-​efficacy Scale
(GASS; Hodgins, Peden, & Makarchuk, 2004)  and the
Situational Confidence Questionnaire for Gambling
(SCQG; May, Whelan, Steenbergh, & Meyers, 2003).
The GASS has 21 items that parallel the temptation items
of the TGS (described previously) and that are scored into
the same four subscales. Scores from a sample of patholog-
ical gamblers revealed strong internal and test–​retest reli-
ability over a 3-​week period (ICC = .86) and also showed
evidence of predictive validity over 12  months. Higher
GASS scores predicted less gambling, which is consistent
with self-​efficacy theory. The SCQG has 16 items, similar
to the GASS items, and yields a single score. Psychometric
properties of the SCQG have not been assessed in clini-
cal samples, although internal reliability in a community
sample of gamblers (α  =  .96) and test–​retest reliability
over 2 weeks with a college sample (r = .86) were good,
yielding adequate ratings in Table 19.3.
Overall Evaluation
Substantial progress has been made in the develop-
ment of gambling treatment planning assessment tools
over a short period of time, although many gaps remain,
as shown in Tables 19.2 and 19.3. Table 19.3 identifies
recommended instruments that have mostly good or
excellent psychometric support for these purposes, albeit

based on limited research. These include the SOGS,
GAMTOMS, ASI–​GSI, IGS, and GASS. The omnibus
instruments, the ASI–​ GSI and GAMTOMS, provide
much potentially useful clinical information for individ-
ual clients, although the initial phases of measurement
development have focused on their utility in outcome
monitoring where scores are aggregated over groups of
individuals. Interpretation guidelines and norms for indi-
vidual scores are necessary for these scales to be optimally
useful to clinicians.
The gambling field has benefited from a long his-
tory of measurement in alcohol, other drug, and mental
health disorders, although we need to exert caution when
adopting tools from these areas, such as the AUDIT and
DAST. It is also important that we establish psychometric
properties and collect norms from gambling samples.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
There is considerable variability in the focus of outcome
measurement in the small, but growing, body of disor-
dered gambling treatment efficacy trials, which makes
comparison of trials challenging. In response, an expert
panel of outcome researchers has provided a set of rec-
ommendations on outcome measurement (Walker et al.,
2006). The panel identified three important elements
in determining the effectiveness of treatment interven-
tions: reduction in the frequency or intensity of gambling
behavior, reduction in gambling-​related consequences,
and evidence that the reduction in gambling behavior
results from the hypothesized therapeutic mechanism.
This framework for reporting outcomes in gambling
treatment research (known as the “Banff framework”) is
also instructive for clinicians because it clearly identifies
two readily measured domains:  gambling behavior and
gambling-​related consequences. The third element, mea-
surement of process variables, will vary in focus depend-
ing on the type of intervention.
Measurement of Gambling Behavior
The Banff framework noted that the wide individual varia-
tion in types, frequency, and intensity of gambling means
that any single measurement of gambling involvement
is unable to capture all relevant aspects. At minimum,
two specific indicators of gambling behavior are recom-
mended for evaluation:  financial losses and gambling
frequency. Financial losses should be reported as net
Gambling Disorders 423
expenditure (i.e., the amount of money that the individ-
ual brought to or accessed during the gambling session
minus the amount left at the end of the session). Asking
how much an individual “spent gambling” leads to incon-
sistent responses depending on the pattern of wins and
losses during the gambling session, which is typically quite
lengthy. Disordered slot machine gamblers, for example,
report gambling sessions that are typically 5 to 8 hours
in length. Net expenditure, in contrast, ignores any wins
that are subsequently lost during the session. It is further
recommended in the Banff framework that money lost
not be normed against total personal or family income or
expendable income. It is true that the same monetary loss
will have different consequences for individuals of differ-
ent financial means, but it is also true that individuals do
not easily provide reliable reports of their financial means
(Walker et  al., 2006). The attempt to normalize loss
reports with financial means is apt to lead to an overall less
reliable expenditure index. Because the focus in outcome
monitoring is individual change over the course of time or
treatment, the expenditure information does not require
this adjustment in order to monitor change. Per session
expenditures need to be averaged over a monthly or lon-
ger time period to reduce the variability in gambling that
results from variability in access to money and gambling
opportunities. Gambling behavior often varies according
to employment pay schedules, for example, which can be
weekly, biweekly, or monthly. The optimal time frame for
summarizing expenditures has not yet been identified,
although a 3-​month period is often reported in efficacy
studies (e.g., Petry et al., 2006). Future research will help
establish the benefits of this time frame versus a shorter
(e.g., 1 month) or longer period (e.g., 6 months). Finally,
the framework recommended that the expenditure mea-
sure include only forms of gambling that are causing the
individual problems in order to minimize error variance.
Monitoring involvement in nonproblematic types of gam-
bling is also advisable, but it should be reported as a sepa-
rate factor.
The second critical indicator of gambling behavior
is gambling frequency. Frequency can be measured in a
variety of metrics, such as hours, number of sessions, time
spent thinking about gambling, and so forth, although
days of gambling appears to be the easiest for individu-
als to recall reliably (Hodgins & Makarchuk, 2003). As
with expenditures, days are typically averaged over a
time period of 1 to 3  months. The TLFB interview is
one procedure for eliciting reliable expenditure and fre-
quent reports, and it is rated as highly recommended in
Table 19.4. The use of other methodologies, such as daily
424 Substance-Related and Gambling Disorders

TABLE 19.4   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

GAMTOMS-​D NR G NR NR G G NR A G ✓
GAMTOMS-​F NR G NR NR G G NR A G ✓
TLFB NA NA G A G G E E G ✓
ASI–​GSI NR A NR G A A G G A
GASS NR G NA A E G A A G ✓
SOGS-​3 NR G NR NR A A NR G G ✓
NODS-​3 NR G NR NR A A NR A G
GBQ NR G NR A NR A NR NR G
GCI NR E NR A A G NR NR G
PG-​YBOCS NR NR G NR L A NR G G

Note: GAMTOMS = Gambling Treatment Outcome Monitoring System, D = discharge questionnaire, F = follow-​up questionnaire; TLFB = Timeline
Followback; ASI–​GSI = Addiction Severity Index–​Gambling Severity Index; GASS = Gambling Abstinence Self-​efficacy Scale; SOGS-​3 = 3-​Month
Version South Oaks Gambling Screen; NODS-​3 = 3-​Month Version–​National Opinion Research Center DSM-​IV Screen for Gambling Problems;
GBQ  =  Gamblers’ Beliefs Questionnaire; GCI  =  Gambling Cognitions Inventory; PG-​YBOCS  =  Yale–​Brown Obsessive–​Compulsive Scale
Pathological Gambling Modification; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.

diaries or quantity–​frequency summary measures, has not
yet been evaluated.
Measurement of Gambling-​Related Consequences
Table 19.2 outlined specific gambling-​ related conse-
quences that are relevant for outcome monitoring as
well as treatment planning. We have already reviewed
two omnibus instruments, the ASI and the GAMTOMS,
which cover some of these consequences. Table 19.4
provides ratings of psychometric research for purposes of
outcome monitoring. The ASI provides composite scores
in each of the eight assessment areas that are responsive
to change and are often used in substance abuse efficacy
research (McLellan et  al., 1992). The composite scales,
including the ASI-​ GSI, assess frequency of behavior,
related problems, and perceived need for treatment in a
30-​day window using a 0-​to-​1 range. Ideal outcome would
involve a score of zero on the scale indicating no prob-
lems (McLellan et  al., 1992), although more typically
statistically significant pre-​and post-​treatment differences
are used to demonstrate improvement. Because the scores
are not pure measures of behavior, related problems, or a
therapeutic mechanism, interpretation of specific scores
is problematic. A score of 0.5, for example, could indicate
a number of different problems. There are no interpreta-
tion guidelines for specific non-​zero values, which limits
the usefulness of these scores for clinicians.
The GAMTOMS includes a treatment discharge
and a treatment follow-​up questionnaire or interview to
complement the intake assessment. The questionnaire
version has been used to evaluate outcome in Minnesota
state treatment programs, and its content validity for
this purpose has been assessed positively by an expert
panel. Psychometric evaluation of these scales is promis-
ing, albeit limited to date. The discharge questionnaire
(88 items, 30 minutes) provides outcome indices in six
areas:  gambling frequency, stage of change, efforts at
recovery, psychiatric symptoms, treatment component
helpfulness, and client satisfaction. In support of con-
struct validity, principal component analyses of the latter
four of these scales, which are designed to be summed
total scores, confirmed that they are unifactorial in a treat-
ment sample that completed the self-​report version and
one that completed the interview version (Stinchfield,
Winters, et  al., 2007). Internal reliability in these same
samples varied from unacceptable to excellent, but over-
all it is rated good (see Table 19.4).
The follow-​up assessment is designed to be admin-
istered after 6 to 12  months (95 items, 30–​45 minutes)
and provides a broader range of indicators: gambling fre-
quency; gambling debt; stage of change; alcohol, tobacco,
and other drug use frequency; post-​treatment service uti-
lization; gambling-​related illegal activities; occupational
problems; problem gambling severity (DSM and SOGS);
financial problems; psychiatric symptoms; and general
treatment outcome. Principal component analyses of five
of these scales, which are designed to be summed total
scores, confirmed that they are unifactorial in a treat-
ment sample completing the interview version. Overall,
the internal reliability for scores on these scales was good
(Stinchfield, Winters, et al., 2007).

As with the ASI, norms are not provided to facilitate
interpretation of these scores, although scores of zero indi-
cate optimal functioning. The GAMTOMS incorporates
both the SOGS and the DSM-​IV measure as outcome
indicators. Continuously scored data from these diagnostic
scales are often reported in efficacy trials and could serve
as benchmarks against which to compare the progress of
individual patients. The Banff framework cautions against
the use of these severity measures as primary outcome mea-
sures because of the ambiguity in meaning of low, but non-​
zero, scores. Nonetheless, these measures can act as useful
secondary indicators of outcome. Most of these measures
were developed to assess lifetime and past-​year function-
ing (Hodgins, 2004)  and, therefore, cannot be used for
treatment monitoring with follow-​up time periods shorter
than 1 year. However, Wulfert et al. (2005) examined the
reliability and validity of 3-​month versions of the SOGS
and NODS and concluded that they are potentially use-
ful for outcome evaluation. Scores on the 3-​month versions
showed good internal reliability and convergent validity
with gambling frequency and expenditure in a treatment
sample (Wulfert et al., 2005), as well as sensitivity to change
in an efficacy study (Wulfert, Blanchard, Freidenberg, &
Martell, 2006). The SOGS-​3 has been shown to be sensi-
tive to change in other treatment studies, so it currently is
recommended over the NODS-​3 (see Table 19.4).
Measurement of Therapeutic Mechanisms
Relative to measurement of outcome, the measurement of
therapeutic variables, the third element recommended in
the Banff framework, is underdeveloped. Our ability to mea-
sure accurately what occurs during treatment in terms of the
client, the therapist, and the therapeutic approach is limited,
but it is crucial for improving treatment outcomes. Based
on the growing empirical support of cognitive–​behavioral
treatments (Cowlishaw et al., 2012) and the interest in phar-
macological efficacy, measurement in four process domains
is reviewed in this chapter. Reduction of gambling in
cognitive–​behavioral therapy is hypothesized to be mediated
by reductions in cognitive errors, increases in coping skills,
and increases in self-​efficacy. Reduction of gambling related
to pharmacological agents (e.g., naltrexone) is thought to be
related to reductions in urges to gamble.
Measurement of Cognitive Distortions,
Coping Skills, and Self-​Efficacy
Cognitive–​behavioral therapy targets, in part, changes
in cognitive distortions, coping skills, and self-​efficacy.
Gambling Disorders 425
Assessment of self-​efficacy was addressed previously in rela-
tion to general treatment planning; in addition, the GASS
has been shown to be sensitive to change and to mediate
improvement in gambling (Peden, 2004; see Table 19.4
for relevant ratings for this purpose). To date, we are not
aware of any established measures of coping skills that
have been validated for gambling, although a number of
similar behavioral role-​play and self-​completion measures
are available in the alcohol field (Finney, 1995). Content
validity may be an issue if these measures are adapted to
gambling, given that they assess methods for coping with
typical drinking situations. The coping skills targeted in
cognitive–​behavioral therapy for gambling disorders are
overlapping, but not identical to, those targeted in alcohol
use disorders.
Assessment of cognitive distortions is relevant for both
treatment planning for this type of therapy and outcome
monitoring, but it is a challenge because these distortions
are thought to operate outside of conscious awareness
(Toneatto, 1999). Theoretically, a number of assessment
options exist. It is possible to observe gambling behavior
to assess underlying cognitions. For example, throwing
dice vigorously when a high number is desired and lightly
when a lower number is desired is indicative of an illu-
sion of control over the outcome. However, this assess-
ment depends on an inference concerning the cognition
underlying the behavior, which may limit the reliability
and validity of this technique. The think-​aloud method
(Ericsson & Simon, 1980) provides a more direct assess-
ment of cognitions. It requires that, after a brief training,
gamblers verbalize their thoughts while they are engaged
in a gambling activity. These verbalizations are typically
recorded, transcribed, and then examined for the pres-
ence of irrational statements. This method has been effec-
tively used in research paradigms, and trained raters can
provide reliable categorizations of cognitive distortions
(Ladouceur, Gaboury, Bujold, Lachance, & Tremblay,
1991). However, reactivity is an issue that compromises
validity: Once voiced, a certain statement may sound dubi-
ous or surprising to the participant and therefore influ-
ence his or her subsequent thoughts and actions (Stewart
& Jefferson, 2007). The verbalization requirement has
also been criticized as “unnatural,” not reflecting cogni-
tions but rather self-​descriptions of behavior (Delfabbro &
Winefield, 1999). More research is required concerning
validity, and practicality of the paradigm is necessary prior
to clinical use.
Finally, cognitions can be assessed directly with self-​
report scales, which is a practical method but one that
also requires individuals to report on a process that is
426 Substance-Related and Gambling Disorders
assumed to be unconscious. Steenbergh, Meyers, May,
and Whelan (2001) developed a 21-​item self-​report scale
measuring two factors: luck/​perseverance and illusion of
control. Scores on the Gamblers’ Beliefs Questionnaire
showed evidence of factorial validity, good internal and
test–​retest reliability, and some evidence of discrimina-
tive and convergent validity within student and com-
munity samples. The scale has not been validated in
clinical samples and has not been shown to be sensitive to
change. Holub (Holub, 2003; Holub, Hodgins, & Rose,
2007)  described the Gambling Cognitions Inventory, a
40-​item self-​report scale that measures four categories of
cognitive distortions: probability errors, magical thinking/​
luck, information processing biases, and illusion of con-
trol. The scale consists of two subscales: the Skill/​Attitude
subscale and the Luck and Chance subscale (McInnes,
Hodgins, & Holub, 2014). The scores have shown excel-
lent internal consistency in student and pathological
gambling samples, as well as evidence of convergent and
discriminant validity. The total score was not, however,
related to the number of cognitive errors during a think-​
aloud task, which supports the need for more research on
the validity of different assessment approaches. This scale
also has not been shown to be sensitive to change related
to improvement in cognitive–​behavioral treatment.
Measurement of Urges
Pharmacological trials often target urges to gamble
(Hollander, Begaz, & DeCaria, 1998), and these stud-
ies often include measures of overall outcome that mix
urge items with behavior items (e.g., Gambling Symptom
Assessment Scale; Kim et  al., 2001). The Pathological
Gambling Modification of the Yale–​ Brown Obsessive
Compulsive Scale (PG-​ YBOCS; Hollander, DeCaria,
et  al., 1998), however, is a widely used scale that pro-
vides separate behavior and urge scores, as well as a total
score. The PG-​YBOCS interview includes five urge and
five behavior items that are clinician-​rated. To date, psy-
chometric study has been very limited, but scores on the
two subscales show good inter-​rater reliability and the
total score shows convergent validity with the SOGS and
another clinical rating scale in a small clinical sample.
The PG-​YBOCS is also sensitive to change, as shown in a
number of efficacy trials (Grant et al., 2003).
Overall Evaluation
The outcome monitoring area is more advanced than the
treatment planning area because of the strong interest in
the field of developing evidence-​based treatments. The
Banff framework is designed to encourage increased con-
sistency among studies by recommending basic measures
of gambling behavior, related problems, and therapeutic
mechanisms. These same dimensions are important for
clinicians. Measurement of gambling behavior (frequency
and expenditure) can be done easily, reliably, and validly
using the timeline interview method. Alternative meth-
ods, such as diaries and retrospective quantity–​frequency
reports, may also be feasible, although they have not been
assessed. Measurement of gambling-​related problems is
less advanced, although the ASI and GAMTOMS are
promising omnibus measures. On the basis of the avail-
able psychometric research, the GAMTOMS is recom-
mended for use in Table 19.4. Omnibus measures have
appeal to clinicians because they are comprehensive and
do not require compiling a battery of individual measures
to cover the important domains to be assessed.
Two additional instruments are highly recommended
in Table 19.4. The SOGS-​3 provides a brief measure
of severity of problems using a 3-​month window. The
GASS is the only instrument that measures a thera-
peutic mechanism that currently meets the criteria for
recommendation.
CONCLUSIONS AND FUTURE DIRECTIONS
It is exciting to work in a nascent and expanding clini-
cal area in which policy makers and treatment providers
are thirsty for new information and novel ideas about
organizing and delivering effective treatment. The clear
advances, made in assessment and treatment of gambling
problems over the past few years, reflect this attention.
The DSM-​ IV conceptualization underpins much
of the clinical research that is conducted. The criteria
were developed based on expert opinion and have not
been subjected to extensive psychometric study to evalu-
ate the validity of the criteria. For example, the cut-​off of
four or more criteria in the DSM-​III-​R was raised to five
for the DSM-​IV based on expert opinion, not empirical
data. However, the elimination of the illegal acts criteria
and the reduction of the cut-​off to four for DSM-​5 was
based on empirical analyses of existing data that showed
improved diagnostic accuracy. The DSM criteria are indi-
cators of extreme pathology, and items that are ideal for
a diagnostic classification measure may be different than
those that are ideal for a continuous severity measure, so
it may be helpful to develop content and construct valid
measures of severity that are independent from the DSM

criteria. Item selection would be based on the ability to
discriminate different levels of severity versus using a
DSM diagnosis or DSM-​based continuous measure as the
gold standard.
One of the issues that has not been addressed in this
area is the heavy reliance on information obtained from
the individual with the gambling problem. All of the mea-
sures identified as promising are self-​report or interview
measures. There is evidence that pathological gamblers
provide accurate self-​reports in the research context, in
which confidentiality is emphasized and the information
provided does not have personal consequences for the
individual (Hodgins & Makarchuk, 2003). However, little
is known about accuracy in clinical settings, in which the
implications of honesty are more variable. Lying to “fam-
ily members, therapist or others to conceal the extent of
involvement with gambling” is one of the DSM-​5 criteria
(APA, 2013) and should be expected to be the norm among
individuals in treatment. Certainly such individuals are
likely to withhold sensitive information until trust is estab-
lished with the treatment provider (Stinchfield, Govoni,
et al., 2007). Multimethod assessment, which is advisable
with all clinical assessment, seems even more important
with gambling disorders, although this has received little
attention in the assessment literature. In the research con-
text, family members and friends are sometimes used as
collateral reporters (e.g., Hodgins, Currie, & el-​Guebaly,
2001), but family members, even if more honest, typically
have less complete information than the identified gam-
bler about his or her behavior (Hodgins & Makarchuk,
2003). Other sources of collateral information, such as
bank or court records, are impractical for routine clinical
use. Assessment techniques such as the “think-​aloud” pro-
cedure for cognitive distortions have potential, but they are
not yet sufficiently developed for clinical use.
We have noted that measurement in the field is
advancing rapidly. It is imperative that we take the steps to
“do it right” and set a solid empirical measurement foun-
dation on which to conduct meaningful research and pro-
vide effective intervention. Although rapid progress has
been made and a number of assessment tools are promis-
ing in terms of their diagnostic, treatment planning, and
monitoring ability, very few were rated as highly recom-
mended. In many instances, the only psychometric infor-
mation that is available for other promising instruments
is based on the development sample—​that is, the sample
used to derive the instrument. Accuracy in measurement
in this field will require not only the development of new
instruments but also further psychometric research on
existing instruments.
Gambling Disorders 427
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 Part VI

Schizophrenia and Personality Disorders

433
 20
Schizophrenia
Shirley M. Glynn
Kim T. Mueser
Schizophrenia is a major mental illness characterized
by psychosis, apathy and social withdrawal, and cogni-
tive impairment, which often results in impaired func-
tioning in the areas of work, school, parenting, self-​care,
independent living, interpersonal relationships, and
leisure time. Among psychiatric disorders, schizophre-
nia is the most disabling, and its treatment requires a
disproportionate share of mental health services. For
example, people with schizophrenia and other nonaf-
fective psychotic disorders accounted for approximately
33.7% of all U.S. Medicare-​paid psychiatric hospitaliza-
tions in 2012 and 2013 (Winterstein et al., 2016). The
combined economic and social costs of schizophrenia
place it among the world’s top 10 causes of disability-​
adjusted life-​years (Murray & Lopez, 1996), account-
ing for an estimated 2.3% of all burdens in developed
countries and 0.8% in developing economies (Institute
of Medicine, 2001).
Because of the sometimes pervasive impact of schizo-
phrenia across the full range of life domains, assessment is
necessarily broad, ranging from basic psychopathology to
cognitive functioning to social and community function-
ing. In this chapter, we describe standardized assessment
instruments for diagnosis, treatment planning, and moni-
toring outcomes of persons with schizophrenia spectrum
disorders, including schizoaffective disorder and schizo-
phreniform disorder. We begin with a brief description of
schizophrenia, including diagnosis, clinical presentation
and associated features, epidemiology, and etiology. This
is followed by discussion of the purposes of assessment
and then consideration of specific instruments for assess-
ing diagnosis and specific domains of functioning com-
monly impaired in schizophrenia.
435
THE NATURE OF SCHIZOPHRENIA
Modern conceptualizations of schizophrenia are based
on the work of Kraepelin (1919/​1971), who focused on
the long-​ term deteriorating course of the illness, and
Bleuler (1911/​ 1950), who defined the core symptoms
of the disorder as difficulties thinking clearly (loosening
of associations), incongruous or flattened affect, loss of
goal-​directed behavior or ambivalence due to conflict-
ing impulses, and retreat into an inner world (autism).
Although the prognosis in these early conceptualizations
of schizophrenia was often posited to be bleak, more
recent research highlights the potential for remission in
schizophrenia (Ciompi & Muller, 1976; Harding, Brooks,
Ashikaga, Strauss, & Breier, 1987), as well as the benefits
of early treatment (Kane et al., 2016) and the possibility
of having occupational success even when living with the
disorder (Cohen et al., 2017). The availability of newer,
more effective treatments makes attention to assessments
that yield accurate diagnoses and lead to well-​developed
treatment plans particularly timely.
The two major diagnostic systems for schizophrenia
in common use are the 10th revision of the International
Classification of Diseases (ICD-​ 10; World Health
Organization, 1992) and the 5th edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-​5;
American Psychiatric Association [APA], 2013). Both
systems objectively define symptoms and characteristic
impairments of schizophrenia in a similar fashion, and
both have improved the reliability of diagnostic assess-
ments compared to more subjectively based approaches.
The major differences between the systems are the DSM-​
5 requirements of social or occupational dysfunction (not
436 Schizophrenia and Personality Disorders
included in ICD-​10); the 6-​month duration of illness (vs.
1 month for ICD-​10), resulting in a somewhat narrower
definition of the disorder in DSM-​5; and the retention of
subtypes of the disorder in ICD-​10 but not DSM-​5. The
stability of diagnosis over time is moderate, with most vari-
ability immediately following onset of the disorder; 21%
to 30% of people treated for a first episode have no symp-
tom relapses during the next 5  years (Häfner & an der
Heiden, 2003).
Symptoms and Associated Impairments
Schizophrenia is characterized by three broad types of
symptoms: psychotic symptoms, negative symptoms, and
cognitive impairment (Liddle, 1987; Tandon, Nasrallah,
& Keshavan, 2009). Psychotic (or positive) symptoms
involve the loss of contact with reality, including false
beliefs (delusions), perceptual experiences not shared by
others (hallucinations), or bizarre behaviors. A variety of
different types of hallucinations occur in schizophrenia,
including auditory, visual, olfactory, gustatory, or tactile
hallucinations, with auditory hallucinations most com-
mon. Common delusions in schizophrenia include per-
secutory delusions, delusions of control (e.g., the belief
that others can interfere with one’s thoughts or behav-
iors), grandiose delusions (e.g., the belief that one is Jesus
Christ), and somatic delusions (e.g., the belief that one’s
brain is rotting away). The presence and severity of psy-
chotic symptoms tend to be episodic over time but are
persistent in a subgroup of persons following onset of the
disorder (Friis et al., 2016).
Negative symptoms are characterized by the relative
absence or paucity of cognitive, emotional, and behavioral
processes. Common negative symptoms include blunted
affect (e.g., immobile facial expression and monotonous
voice tone), anhedonia (lack of pleasure), avolition or apa-
thy (diminished ability to initiate and follow through on
plans), and alogia (reduced quantity or content of speech).
Although negative symptoms may have a variable trajec-
tory in the early course of schizophrenia (Gee et al., 2016),
over the long term they tend to be more persistent than
psychotic symptoms (Fenton & McGlashan, 1991)  and
are strongly associated with poor psychosocial functioning
(Rabinowitz et al., 2012). Because it is less readily appar-
ent to others that negative symptoms are manifestations
of a psychiatric illness, people with high levels of nega-
tive symptoms are often perceived by relatives and others
to be lazy and willfully unengaged in bettering their lives
(Weisman, Nuechterlein, Goldstein, & Snyder, 1998).
The defining symptoms of schizophrenia are fre-
quently accompanied by negative emotions, including
depression (Bosanac & Castle, 2012), anxiety (Achim
et  al., 2011), and anger or hostility (Witt, Hawton, &
Fazel, 2014). The lifetime risk of completed suicide
in schizophrenia is estimated to be approximately 5%
(Inskip, Harris, & Barraclough, 1998). There is also a
modest increase in violence in schizophrenia relative to
the general population, with different phenotypes corre-
sponding to whether the aggression appears before the
onset of the disorder, coinciding with the onset of symp-
toms, or following many years of symptoms (Hodgins,
Piatosa, & Schiffer, 2014).
Cognitive impairment is a common feature associ-
ated with schizophrenia that encompasses problems in
attention and concentration, psychomotor speed, learn-
ing and memory, and executive functions such as abstract
thinking, planning, and problem solving (Harvey, 2013).
Lower levels of premorbid intelligence compared to those
of other family members increase the risk of developing
schizophrenia (Kendler, Ohlsson, Mezuk, Sundquist,
& Sundquist, 2016), and a decline in cognitive abilities
frequently precedes the onset of schizophrenia by several
years (MacCabe et al., 2013; Meier et al., 2014). Despite
this decline, some clients’ cognitive functioning is in
the normal range. Similar to negative symptoms, cogni-
tive impairment tends to be relatively stable over time
(Dickerson et  al., 2014)  and is strongly associated with
functional impairment, including community living
and work (Green, Llerena, & Kern, 2015; McGurk &
Mueser, 2004).
Impaired role functioning or significant change
in self-​care are also included as diagnostic criteria for
schizophrenia. Problems in these areas include reduced
ability to work, attend school, parent, have close rela-
tionships, attend to one’s grooming and hygiene, and
enjoy one’s leisure time, with difficulties often emerging
several years before frank psychotic symptoms (Häfner
& an der Heiden, 2008). Impairment in functioning is
sometimes pronounced, resulting in the need for dis-
ability entitlements (when available) and extensive assis-
tance with meeting daily living needs such as housing,
medical care, food, and clothing. Improving function-
ing remains the most important challenge for the man-
agement of schizophrenia. Impairment in functioning
tends to be relatively stable over time in schizophrenia,
with some improvements over the long term, including
some partial or complete symptom remissions (Harding
& Keller, 1998).

In addition to symptoms and impaired role function-
ing, schizophrenia affects many other areas of living.
People are at increased risk for alcohol and drug prob-
lems (Thoma & Daum, 2013), infectious diseases such
as hepatitis C (Rosenberg et  al., 2001), violent victim-
ization (Khalifeh et  al., 2015; Roy, Crocker, Nicholls,
Latimer, & Reyes Ayllon, 2014)  and post-​ traumatic
stress disorder (PTSD; Grubaugh, Zinzow, Paul, Egede,
& Frueh, 2011; Mueser, Rosenberg, Goodman, &
Trumbetta, 2002), housing instability and homelessness
(Aubry et al., 2016), and tobacco use and related illnesses
(Correll et al., 2014). The net result of exposure to these
risks is a sharply increased rate of premature mortality
(Gale et al., 2012).
Epidemiology
The annual incidence of schizophrenia is 0.2 to 0.4 per
1,000, with lifetime prevalence (risk) of approximately
1% (Jablensky, 1997). The incidence of schizophrenia is
the same across genders, although women tend to have a
later age of onset compared to men (Murray & Van Os,
1998)  and also a more benign course of illness, includ-
ing fewer hospitalizations and better social functioning
(Angermeyer, Kuhn, & Goldstein, 1990). The later age
of onset in women is associated with higher attainment of
pre-​illness social role functioning, which confers a better
outcome (Häfner, 2000).
The incidence of schizophrenia is approximately
15.2 per 100,000 people per year (McGrath et  al.,
2004), with variations reported across different locations
that are reduced when standardized diagnostic criteria
are used (Jablensky, 1997). The lifetime prevalence of
schizophrenia has been estimated to be 0.7%, with again
some variation across studies (Saha, Chant, Welham,
& McGrath, 2005). Overall, research indicates that the
often cited 1% prevalence of schizophrenia is approxi-
mately accurate, but it may be somewhat of an overes-
timate of the true prevalence of the disorder (Perkins &
Lieberman, 2012).
Etiology
A variety of biological and socio-​environmental risk fac-
tors interact dynamically to contribute to the develop-
ment of schizophrenia (Uher, 2014; van Os & Kapur,
2009). Family history of schizophrenia is a significant
risk factor, indicating a role for genetic vulnerability.
Although in the general population the risk of someone
Schizophrenia 437
developing schizophrenia is approximately 1%, this risk
is increased to 10% for people with a first-​degree relative
who has the disorder and to 50% for people with an iden-
tical twin (McGuffin, Owen, & Farmer, 1996). However,
exposure to psychological trauma in childhood and other
adversities increases the risk of developing schizophre-
nia (Okkels, Trabjerg, Arendt, & Pedersen, 2017; Varese
et al., 2012), and shared trauma within families, as well
as between identical versus fraternal twins, may explain
some of the family associations in the development of the
disorder that have traditionally been ascribed to genetic
factors (Fosse, Joseph, & Riochardson, 2015).
The risk of schizophrenia is also increased by a vari-
ety of perinatal complications. Maternal infection (Brown
et al., 2004), starvation (Hoek, Brown, & Susser, 1998), and
exposure to stressful events (Khashan et al., 2008) are all
associated with increased risk of schizophrenia. Obstetric
complications such as anoxia or forceps delivery also signif-
icantly increase the chances of developing schizophrenia
(Cannon, Jones, & Murray, 2002). Socio-​environmental
factors associated with increased risk of schizophrenia
include being born and raised in an urban setting (Saha
et al., 2005), immigration from another country (Cantor-​
Graae, Zolkowska, & McNeil, 2005), poverty and lower
social class (Eaton, 1994), and ethnic or cultural minor-
ity status (Boydell et  al., 2001). Cannabis use, especially
before age 15  years, has been linked to the subsequent
development of schizophrenia, and onset at an earlier age,
in several national birth cohort studies (Miller et al., 2009;
Radhakrishnan, Wilkinson, & D’Souza, 2014).
The combined effects of biological and socio-​
environmental risk factors for schizophrenia have led to
the general theory that schizophrenia is a neurodevelop-
mental disorder (Allin & Murray, 2002; Weinberger &
Marenco, 2003). Altered brain development early in life
is hypothesized to interact with subsequent environmen-
tal stress to result in the disorder emerging in late adoles-
cence or early adulthood. Neurodevelopmental theories
of the etiology of schizophrenia are compatible with the
stress–​vulnerability model, which proposes that the course
of the disorder is influenced by a similar dynamic inter-
action between biological and environmental factors
(Nuechterlein & Dawson, 1984; Zubin & Spring, 1977).
PURPOSES OF ASSESSMENT
Assessment in schizophrenia serves a number of distinct
purposes. First, because the diagnosis of a schizophrenia
438 Schizophrenia and Personality Disorders
spectrum disorder has important treatment implications,
especially with regard to pharmacological management, a
careful assessment is necessary to ensure accurate identi-
fication of the disorder. Aside from undetected substance
abuse or medical conditions that can lead to common
symptoms of schizophrenia, there is a great overlap with
the symptoms of bipolar disorder and major depression.
The primary distinction between schizophrenia and
mood disorders is made based on the course and co-​
occurrence of different symptoms (e.g., the absence of
psychotic symptoms in people with a mood disorder when
depression or mania are absent), which requires accurate
historical information and sound clinical judgment.
Second, assessment serves a critical purpose in identi-
fying treatment needs and informing treatment planning.
Although it was once thought that schizophrenia led to irre-
versible deterioration (Kraepelin, 1919/​1971), it is now clear
that comprehensive interventions, grounded in a wide-​
ranging and thorough assessment, can dramatically improve
outcomes. In addition to the complex of symptoms present
in schizophrenia, and its impact on role functioning, social
relationships, and self-​care, other comorbidities are often
present, including psychiatric, substance abuse, and medi-
cal disorders. In this chapter, we focus mainly on the assess-
ment of symptoms and functioning for treatment planning,
with only brief attention to comorbid substance abuse.
Third, assessment is necessary in order to monitor the
effects of treatments. Ongoing evaluation of targeted areas
for treatment is critical in order to know whether alterna-
tive approaches are necessary and when treatment goals
have been achieved. Numerous different treatments may
impact on specific symptoms and areas of functioning,
and thus many alternatives exist if treatment targets have
not improved sufficiently.
In light of the sometimes pervasive nature of the defi-
cits in schizophrenia, it is not surprising to observe that
assessment of many other domains may be critical to the
development of an accurate diagnosis and treatment plan
in schizophrenia. Although important, they are beyond
the scope of this chapter. For example, we do not cover the
assessment of cognitive impairment (Sharma & Harvey,
2000), but at a minimum recommend employing a brief
cognitive screen to evaluate cognitive functioning (Gold,
Queern, Iannone, & Buchanan, 1999; Keefe et al., 2004),
followed up by a more comprehensive neuropsychological
assessment if prominent deficits are identified. We also do
not describe the assessment of medical disorders, but con-
sidering the high rates of medical comorbidity in schizo-
phrenia (Janssen, McGinty, Azrin, Juliano-​Bult, & Daumit,
2015), we recommend arranging for all clients to have a
physical examination. Similarly, we do not address the
assessment of health risk behaviors, such as smoking (Evins
et  al., 2014)  and unprotected sex (Carey, Carey, Maisto,
Gordon, & Vanable, 2001), but due to the high rate of nico-
tine addiction and infectious diseases in this population, we
recommend routine assessment of these and other health-​
related behaviors (e.g., diet) in all clients using standard
approaches developed for the general population.
ASSESSMENT FOR DIAGNOSIS
Diagnostic assessment for schizophrenia spectrum dis-
orders involves obtaining a broad range of information
that includes subjective states (e.g., hallucinations and
delusions); behavioral observation (e.g., blunted affect
and bizarre behavior); and reports about functioning in
areas such as social relationships, work or school, and self-​
care. Because the diagnosis of schizophrenia in DSM-​5
requires ascertaining whether the duration of impaired
functioning has been 6  months or longer, historical
information must also be obtained. Although much of
the information required to establish a diagnosis can be
obtained by directly interviewing the client, the lack of
insight characteristic of the illness (Amador & Gorman,
1998)  often necessitates obtaining supplementary infor-
mation. Such information can usually be obtained from
relatives, other treatment providers, and medical records,
and it is most useful for determining the presence of psy-
chotic symptoms or problems in functioning.
Historically, the diagnosis of schizophrenia was unre-
liable (Matarazzo, 1983)  before objective criteria were
established by DSM-​III (APA, 1980), and the disorder
was frequently overdiagnosed (Kuriansky, Deming, &
Gurland, 1974). With the clearer specification of diag-
nostic criteria for schizophrenia in the DSM series, more
reliable diagnostic assessment became possible. However,
even with these objective criteria, the reliability of diag-
noses is greatest when it is established using a structured
clinical interview to probe for symptoms in a systematic
fashion. The ratings of the psychometric properties of
these interviews are presented in Table 20.1.
The most widely used standardized instrument
for diagnostic interviewing is the Structured Clinical
Interview for DSM-​ 5 (SCID-​ 5; First, Williams, Karg,
& Spitzer, 2015a, 2015b). The SCID has demonstrated
excellent reliability and validity for the diagnosis of schizo-
phrenia, although considerable training and clinical

TABLE 20.1  Ratings of Instruments Used for Diagnosis
Internal Inter-​Rater Test–​Retest
Instrument Norms Consistency Reliability Reliability
DIS E NA E E
M.I.N.I. E E E E
SCID E NA E E
Comorbidities
CSDS E E E E
CAP-​S G E E E
Note:  DIS  =  Diagnostic Interview Schedule; M.I.N.I.  =  Mini-​International Neuropsychiatric Interview; SCID  =  Structured Clinical Interview for
DSM-​IV; CSDS = Calgary Depression Scale for Schizophrenia; CAPS-​S = Clinician Administered Rating Scale for Post-​Traumatic Stress Disorder–​
Schizophrenia; A = Adequate; G = Good; E = Excellent; NA = Not Applicable.
interviewing experience are required to administer it, and
it is time-​consuming to conduct, often requiring 1 or 2
or more hours to complete. The SCID is very compre-
hensive, permits a variety of psychiatric diagnoses to be
made from the same interview, and is most often used as
a research instrument. Shorter versions of earlier versions
of the SCID have been developed, such as the PRIME
MD (Spitzer et al., 1994), but their reliability and valid-
ity for assessing relatively low-​frequency disorders such
as schizophrenia remain uncertain. An alternative to the
SCID, the Mini-​International Neuropsychiatric Interview
(MINI; Sheehan et al., 1998), is much briefer, acceptable
to patients, and can easily be used in most clinical office
settings, although its sensitivity and specificity with psy-
chosis are not as strong as those of the SCID (Amorim,
Lecrubier, Weiller, Hergueta, & Sheehan, 1998).
Two broad diagnostic measures have been developed
that can be administered by lay persons with training. The
Diagnostic Interview Schedule (DIS) (Robins, 1995) was
designed primarily for use in large-​scale epidemiological
research studies, and it lacks the sensitivity and specific-
ity necessary for use in clinical settings. The DIS requires
less training to learn than the SCID, and it can usually
be administered in less than 1 hour, but it also has dem-
onstrated lower reliability and validity (Malgady, Lloyd,
& Tryon, 1992). A more recent alternative to the DIS is
the World Health Organization (WHO) World Mental
Health (WMH) Composite International Diagnostic
Interview (CIDI) (Kessler & Ustün, 2004), which is a
refinement and expansion of the original CIDI (Robins
et  al., 1988)  that was based on the DIS. The original
CIDI was designed to align with ICD diagnoses to permit
international research but did not include a section on
psychosis. The WHO WMH-​CIDI does include a section
on psychosis, but validity studies often omit that diagnosis
Schizophrenia 439
Content Construct Validity Clinical Highly
Validity Validity Generalization Utility Recommended
E G G A
E G G E
E E E A ✓
E E E E ✓
E E E E ✓
because of its low frequency (Haro et  al., 2006), so the
sensitivity and specificity of the measure for schizophrenia
are difficult to determine. An intensive training program is
offered by the developers.
It is well established that cultural factors can influ-
ence the interpretation of, reaction to, and expression of
common symptoms in schizophrenia (Jacob, Johnson,
Prince, Bhugra, & David, 2007; Jenkins & Barrett,
2004). Efforts have focused on establishing a framework
for organizing cultural information pertaining to estab-
lishing a psychiatric diagnosis, such as the Outline for
Cultural Formulation in DSM-​IV (APA, 1994). More
recently, work has focused on establishing standardized
guidelines for obtaining and understanding culturally
relevant information obtained in the context of diag-
nostic assessment, including the Cultural Formulation
Interview (CFI) presented in DSM-​5 (Lewis-​Fernández
et al., 2014). Although progress in this area is promising,
the available data on the CFI indicate that it is too pre-
liminary to incorporate in the current review (Aggarwal
et  al., 2014; Aggarwal, Nicasio, DeSilva, Boiler, &
Lewis-​Fernández, 2013).
Assessment of Co-​occurring Disorders
Comorbidities are common in schizophrenia, with rates
of co-​occurring substance abuse, depression, and PTSD
being most prevalent (Buckley, Miller, Lehrer, & Castle,
2009). Typically, the identification of a co-​occurring disor-
der in schizophrenia relies on the clinical acumen of the
assessor, often guided by the specificity of instruments such
as the SCID, which permits the diagnosis of several inde-
pendent disorders based on multiple modules conducted
in a single interview. However, discerning whether a
symptom reflects schizophrenia or another disorder can be
440 Schizophrenia and Personality Disorders
complicated and requires clinical judgment. When does
social anxiety become paranoia? Is hearing the voice of a
deceased loved one a reflection of grief or a hallucination?
The growing recognition of the prevalence of comor-
bidities has prompted the development of scales designed
to diagnose co-​occurring disorders in the presence of schizo-
phrenia. These scales are particularly useful in clarifying
the diagnostic picture when symptoms of two or more
disorders may present similarly. Two of the most com-
monly used scales are the Calgary Scale for Depression
in Schizophrenia (CSDS) (Addington, Addington, &
Maticka-​Tyndale, 1993) and the Clinicians Administered
PTSD Scale–​Schizophrenia (CAPS-​S) (Gearon, Bellack,
& Tenhula, 2004). The CSDS is designed to permit
assessment of depressive symptoms independent from
positive, negative, and extrapyramidal symptoms in peo-
ple with schizophrenia, using a nine-​item semi-​structured
interview. Items are scored on a 0 to 3 scale, with a total
score greater than 6 having 82% specificity and 85% sensi-
tivity for predicting the presence of a major depressive epi-
sode (Addington, Addington, & Maticka-​Tyndale, 1994).
Trauma rates are high in individuals with serious psychi-
atric illness (Goodman, Rosenberg, Mueser, & Drake,
1997; Monahan, Vesselinov, Robbins, & Appelbaum,
2017), raising the likelihood that many of these individu-
als are experiencing symptoms of PTSD (Grubaugh et al.,
2011). To permit more accurate diagnosis of PTSD in per-
sons with schizophrenia, Gearon et al. revised the word-
ing of items to the original CAPS (Blake et al., 1995) by
reducing the reading level, adding behavioral definitions
and anchors, and providing probe examples more relevant
to the lives of individuals diagnosed with a more serious
psychiatric illness. The CAPS-​S has strong psychomet-
ric properties, and it can be a useful tool in determining
whether individuals presenting with psychotic symptoms
also have concurrent PTSD.
Overall Evaluation
Schizophrenia is a complex illness to diagnose that over-
laps with many other major mental illnesses, especially
major mood disorders. Although in the clinic and hospital
setting most schizophrenia diagnoses are made based on a
clinical interview, research instruments such as the SCID
and MINI are reliable and well-​validated tools to improve
diagnostic accuracy. Comorbidities in schizophrenia are
common; more recent work has involved developing
instruments that can be used to diagnose common comor-
bidities in schizophrenia.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
In this section, we describe the assessment of symptoms,
medication adherence, community functioning, subjec-
tive appraisal, family attitudes, and comorbid substance
abuse for the purposes of case conceptualization and
treatment planning. The ratings of the psychometric
properties of these tools are presented in Table 20.2. As
we describe subsequently, many of these same assessment
tools can also be used to monitor symptoms and evaluate
treatment outcomes.
Symptoms
Two semi-​ structured interview instruments with well-​
established evidence of reliability and validity are widely
used for the assessment of symptoms of schizophre-
nia:  the Brief Psychiatric Rating Scale (BPRS; Lukoff,
Nuechterlein, & Ventura, 1986; Overall & Gorham,
1962)  and the Positive and Negative Syndrome Scale
(PANSS; Kay, Opler, & Fiszbein, 1987). The BPRS and
PANSS cover a broad range of symptoms commonly pres-
ent in schizophrenia. The instruments include specific
interview probes, clearly elucidated descriptions of target
symptoms, and behaviorally anchored 5-​to 7-​point ratings
scales for scoring the presence and severity of symptoms.
The PANSS includes 30 items, of which the first 18 were
drawn from the original version of the BPRS (Overall
& Gorham, 1962). Following the development of the
PANSS, an additional 6 items were developed for the
BPRS, referred to as the Expanded BPRS (Lukoff et al.,
1986). Each of these measures requires 25 to 40 minutes
to complete.
The BPRS was designed as a general psychiatric rating
scale for the broad range of symptoms present in severe
mental illnesses, whereas the PANSS was developed to
specifically tap the symptoms of schizophrenia. Factor
analyses of the BPRS have most frequently identified
either four or five symptom dimensions (Long & Brekke,
1999; Mueser, Curran, & McHugo, 1997; Shafer, 2005),
corresponding to thought disorder, anergia (negative
symptoms), anxiety–​depression, disorganization, and acti-
vation. As expected, because of the overlap in symptoms
between the BPRS and the PANSS, very similar factor
structures have been identified for the PANSS (Mueser
et  al., 1997; van der Gaag et  al., 2006; Velligan et  al.,
2005; Wallwork, Fortgang, Hashimoto, Weinberger, &
Dickinson, 2012).
TABLE 20.2  Ratings of Instruments Used for Case Conceptualization and Treatment Planning
Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Symptoms
BPRS A G E A A G E A ✓
PANSS A G E A A E E A ✓
SANS A G E A A E E A
CAINS E E E E E E E G
BNSS E E E E E E E E
BASIS-​R G G NA A G G G G
CSI G G NA A G G G G
Medication Adherence
ROMI A A G A A A A A ✓
DAI A A NA A G G G G
Community Functioning
CASIG A A E A E A G A ✓
CAN A G E G E G E G ✓
ILSS A G G A G A A A ✓
MCAS A A G A A G G A
QLS A E E E A G E A ✓
SAFE A G G A A A E A
SAS-​II A G E A A G E A
SBS A E E E A A A A
SFS A G E A G G E A ✓
SF-​36 E G NA A A G E A
SLOF A G G G E E E G
MIRECC-​GAF A E E NR E E E E ✓
Subjective Appraisal
MHRM A G NA A A A A A
QOLI E G NA A G E E A ✓
RAS A G NA A G A E A ✓
TL-​30S A G NA A A A E A
IMR (Client) E G NA E E E G E ✓
SSMI G G NA E E E E G
ISMI G G NA E E E E G
SS G E NA E G E G E
PSYRATS E E E E E E E E ✓
Family Attitudes
PRS A G NA A A A A A
BAS A G NA NR G G A G ✓
Substance Abuse
ASI E G E A E E E A ✓
AUDIT E G NA A G G E A
DAST E G NA A A A E A
MAST E G NA A A A E A
SATS A NA E A A G G A ✓
TLFB E NA E A A G E A ✓

Note: BPRS = Brief Psychiatric Rating Scale; PANSS = Positive and Negative Syndrome Scale; SANS = Scale for Assessment of Negative Symptoms;
CAINS = Clinical Assessment Interview for Negative Symptoms; BNSS = Brief Negative Symptoms Scale; BASIS-​R = Revised Behavior and Symptom
Identification Scale; CSI = Colorado Symptom Index; ROMI = Rating of Medication Influences; DAI = Drug Attitudes Inventory; CASIG = Client’s
Assessment of Strengths, Interests and Goals (both client and informant versions); CAN = Camberwell Assessment of Need (both clinician and client
versions); ILSS = Independent Living Skills Survey (both client and informant versions); MCAS = Multnomah Community Ability Scale; QLS = Quality
of Life Scale; SAFE = Social Adaptive Functions Scale; SAS-​ll = Social Adjustment Scale; SBS = Social Behavior Scale; SFS = Social Functioning
Scale; SF-​36 = Short Form-​36 Health Survey; SLOF = Specific Level of Functioning; MIRECC-​GAF = Mental Illness Research Education and Clinical
Center Global Assessment of Functioning; MHRM = Mental Health Recovery Measure; QOLI = Quality of Life Interview; RAS = Recovery Assessment
Scale; TL-​30S = Quality of Life Interview Self-​Administered Short Form; IMR = Illness Management and Recovery; SSMI = Self Stigma of Mental
Illness; ISMI = Internalized Stigma of Mental Illness; SS = Stigma Scale; PSYRATS = Psychotic Symptom Rating Scale; PRS = Patient Rejection Scale;
BAS = Burden Assessment Scale; ASI = Alcohol Severity Inventory; ADUIT = Alcohol Use Identification Test; DAST = Drug Abuse Screening Test;
MAST = Michigan Alcoholism Screening Test; SATS = Substance Abuse Treatment Scale; TLFB = Timeline Followback Calendar; A = Adequate;
G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.
442 Schizophrenia and Personality Disorders
As the presence of negative symptoms in schizophre-
nia has become increasingly prominent in conceptualiza-
tions of the disorder (Tandon et al., 2009), there has been
a concomitant emphasis on enhancing accurate measure
of this symptom constellation. The primary scales in use
for negative symptoms are assessor administered in a
semi-​structured interview, although self-​report measures
are emerging (Dollfus, Mach, & Morello, 2015). The
Scale for the Assessment of Negative Symptoms (SANS;
Andreasen, 1984; Mueser, Sayers, Schooler, Mance, &
Haas, 1994; Vadhan, Serper, Harvey, Chou, & Cancro,
2001)  was designed to capture core negative symptoms
using both individual and global items. The SANS covers
five domains—​affective flattening or blunting, alogia, avo-
lition/​apathy, anhedonia/​asociality, and inattention—​and
within each domain separate symptoms are rated from
0 (absent) to 5 (severe). One factor analysis indicated a
three-​factor solution composed of blunted affect, apathy–​
anhedonia, and alogia–​ inattention (Sayers, Curran, &
Mueser, 1996).
Two more recent negative symptoms measures are the
Clinical Assessment Interview for Negative Symptoms
(CAINS; Kring, Gur, Blanchard, Horan, & Reise,
2013)  and the Brief Negative Symptoms Scale (BNSS;
Kirkpatrick et  al., 2011). The CAINS was designed to
address limitations of existing negative symptom instru-
ments and to evaluate the need for the five consensus
negative symptom subdomains (represented, for example,
in the SANS, described previously). Intensive scale refine-
ment with iterative trials across multiple samples yielded
a shorter, more focused negative symptom assessment
instrument. The final 13-​item CAINS contains a moti-
vation/​pleasure factor defined by 9 items and a 4-​item
expression factor. The final CAINS has good psycho-
metric properties, including evidence of strong conver-
gent validity reflected in association with clinician-​rated
real-​world functioning and patient-​rated quality of life
(Kring et al., 2013). The CAINS requires approximately
25 minutes for administration and can be administered
reliably in nonacademic clinical settings by bachelor-​and
master-​ educated raters. There is an extensive training
manual as well as training videos available on the Internet
(Carpenter, Blanchard, & Kirkpatrick, 2016).
The BNSS is a semi-​structured interview that includes
the five domains assessed in the SANS as well as an addi-
tional item, lack of normal distress. The BNSS consists of
13 items and has demonstrated excellent psychometric
properties (Kirkpatrick et al., 2011; Strauss et al., 2012),
with administration of the scale typically requiring less
than 15 minutes. Items in the anhedonia, avolition, and
asociality subscales distinguish objective behavior from
subjective experience and consummatory from appeti-
tive anhedonia. The BNSS has a similar factor structure
to the CAINS, with one factor consisting of pleasure and
motivation items, and the other including blunted affect
and alogia items; the lack of normal distress item loading
on the two BNSS factors is inconsistent. With training,
the BNSS can be administered by bachelor degree raters
if they have experience with people with schizophrenia
(Carpenter et al., 2016). Training videos are available.
Conducting the symptom assessments mentioned in
the preceding paragraphs is labor-​intensive because they
require the interviewer be trained to adequate levels of
reliability, and the scales themselves can often require
more than 30 minutes to administer. Health services
researchers have addressed these obstacles by designing
broad symptom self-​ report measures intended for use
with general psychiatric populations, such as the Revised
Behavior and Symptom Identification Scale (BASIS-​R;
Eisen, Normand, Belanger, Spiro, & Esch, 2004) and the
Modified Colorado Symptom Index (Conrad et al., 2001),
even evaluating whether computer administration of such
self-​report measures can yield useful results (Chinman,
Young, Schell, Hassell, & Mintz, 2004). Initial data are
promising, insofar as subscales on the BASIS-​R have
been found to discriminate psychotic from nonpsychotic
groups in outpatient and inpatient samples, and some of
the subscales indicate sensitivity to change (Jerrell, 2005;
Niv, Cohen, Mintz, Ventura, & Young, 2007). Chinman
et al. (2014) reported that results on BASIS-​R computer-​
administered assessments and interviews were highly
correlated.
Three caveats are warranted in considering the use of
self-​report and/​or computer administration of symptom
measures such as the BASIS-​R in persons with schizophre-
nia, however. First, these measures have not been widely
used in typical clinical settings, so their day-​to-​day use
may require some revision of procedures or interpretation
of data, especially with regard to comparison samples of
individuals diagnosed with schizophrenia. Second, even
with self or computer administration, professional efforts
are required to orient clients to the assessment, answer
questions, and ensure that individuals comprehend the
task sufficiently to respond accurately. Third, many peo-
ple with schizophrenia lead economically disadvantaged
lives and may have limited prior experience with comput-
ers. Thus, orienting them to the computer assessment of
symptoms in the office may entail teaching them how to
work the computer (how to use a mouse, what to do if the
monitor screen freezes, etc.) and being available while the

assessment is being conducted. The professional time and
effort required to ensure the respondent can complete the
task successfully should not be underestimated; of course,
personnel assisting with these tasks do not require gradu-
ate training.
Medication Adherence
For many individuals with schizophrenia, regular medi-
cation taking reduces symptoms; thus, monitoring adher-
ence with prescribed medication regimens is a critical
aspect of treatment. However, research indicates that
both self-​reports and collateral reports of medication
adherence are not especially accurate (Pratt, Mueser,
Driscoll, Wolfe, & Bartels, 2006). Clinically, reports of
nonadherence are typically assumed to be more accurate
than reports of adherence. Although nonadherence to
antipsychotic medication is often identified as a problem
(Dolder et al., 2004), it is important to note that reviews
of prescription studies with nonpsychiatric populations
report noncompliance rates of at least 30%. Not taking
medications as prescribed is a common problem, regard-
less of the medical condition (Blackwell, 1976).
Clinicians working with persons with schizophre-
nia should assess at least two dimensions of adherence:
(a) actual level of medication taking and (b) reasons for
any nonadherence, as they may lend themselves to dif-
ferent interventions. Unfortunately, assessing medication-​
taking behavior accurately is notoriously difficult across
medical populations (Osterberg & Blaschke, 2005).
Although pill counts and electronic pill bottles with cap
sensors have been used in scientific investigations as the
“gold standard” for assessing adherence, the norm in non-​
research settings is still to rely on client self-​report based
on questions asked frequently and nonjudgmentally,
beginning with statements such as “I know it must be dif-
ficult to take all your medications regularly. How often
do you miss taking them?” (Osterberg & Blaschke, 2005).
To supplement reports of medication adherence, estab-
lishing reasons for nonadherence and general attitudes
toward psychiatric mediation can be very useful. The
Rating of Medication Influences (ROMI) scale (Weiden
et al., 1994) includes 20 self-​report items assessing reasons
for nonadherence that have been prospectively linked to
nonadherence (Yamada et al., 2006). The ROMI is divided
into two subscales that separate reasons for adherence
(Reasons for Compliance) from reasons for nonadherence
(Reasons for Noncompliance), and it assesses a broad
range of factors influencing a client’s personal decisions
about adherence. Factor analyses revealed a three-​factor
Schizophrenia 443
structure within the Reasons for Compliance scale and a
five-​factor structure for the Reasons for Noncompliance
scale. These two subscales have been found to correlate
moderately with the Drug Attitudes Inventory (DAI) (.56
for Reasons for Compliance and  –​.47 for Reasons for
Noncompliance). The DAI is available in 30-​item (DAI-​
30; Hogan, Awad, & Eastwood, 1983) and 10-​item (DAI-​
10; Stjernswärd, Persson, Nielsen, Tuninger, & Levander,
2013)  self-​report formats, which are highly correlated;
both versions include items reflecting positive and nega-
tive attitudes toward psychiatric medications. Identifying
specific reasons for medication nonadherence is critical
because unique responses will call for different interven-
tions: Someone who reports that he or she has difficulty
physically obtaining the medication needs a different kind
of assistance than someone who describes feeling embar-
rassed about taking the medication.
Community Functioning
Impaired adjustments in the areas of social, role, and self-​
care functioning are the hallmarks of schizophrenia, and
an accurate assessment is critical to treatment planning.
Unfortunately, assessment of each of these functioning
domains presents challenges to the clinician in terms of
both precise definitions of adequate “adjustment” and the
use of clients as informants of their own functioning. For
example, the domain of social functioning is complex,
and it may include a broad range of only weakly intercor-
related dimensions, such as number of regular social con-
tacts, number of “friends,” satisfaction with friendships,
reciprocity of friendships, initiation of social contacts,
romantic involvement, degree of contact and satisfac-
tion with family relationships, social skill competence,
and engagement in leisure and recreational activities.
Aside from the sheer number of potentially important
dimensions of social functioning, clients are not always
accurate in their perceptions of how well they function
compared to others, highlighting the value of obtaining
collateral reports from people who know the client, such
as relatives or (for clients with frequent contact with pro-
fessional or paraprofessional staff) mental health work-
ers (Bowie, Reichenberg, Patterson, Heaton, & Harvey,
2006). Furthermore, the definition of “adequate” social
adjustment is elusive, even in nonpsychiatric populations.
In a society that values independent functioning, are
adult offspring who continue to live with their parents less
socially adjusted? What about persons who are divorced or
never married—​are their community functioning levels
necessarily less?
444 Schizophrenia and Personality Disorders
There is no consensus instrument used to assess com-
munity functioning in schizophrenia. Most published
measures of community functioning used with persons
with schizophrenia are dimensional, with one to several
items assessing different domains of functioning (e.g.,
social support and independent living). The scales vary
in their length (from as few as 12 to as many as 70 items
with multiple prompts for each one), level of training
required for the assessment administrator, relative empha-
sis on global life domains (e.g., social support) versus spe-
cific instrumental skills (e.g., ability to do laundry or ride
the bus), whether original development of the scale was
directed more for researchers (e.g., the Social Adjustment
Scale-​II) or practitioners (e.g., the Client Assessment of
Strengths, Interests, and Goals), and whether the scales
emphasize objective or subjective aspects of function-
ing. There is no one scale that will meet every need.
Clinicians will do best to review the scales discussed here
and determine which assess the domains of most interest
for a particular client.
Scales of wide use in the assessment of community
functioning in schizophrenia include the Camberwell
Assessment of Need (CAN); the Social Adjustment
Scale-​II (SAS-​ II); the Quality of Life Scale (QLS);
the Social Functioning Scale (SFS); the Independent
Living Scale Survey (ILSS); the Client Assessment of
Strengths, Interests, and Goals (CASIG); the Short Form-​
36 (SF-​36); the Multnomah Community Ability Scale
(MCAS); the Social Behavior Schedule (SBS); the Social
Adaptive Function Scale (SAFE); the Specific Level of
Functioning (SLOF) Assessment Scale; and the Mental
Illness Research, Education, and Clinical Center Global
Assessment of Functioning (MIRECC-​GAF).
The CAN (Slade, Loftus, Phelan, Thornicroft, &
Wykes, 1999)  evaluates functioning across 22 areas of
need, including substance use; symptoms such as psy-
chotic symptoms or psychological distress; and areas of
psychosocial functioning such as living situation, food,
money management, social relationships, intimate rela-
tionships, child care, safety to self and others, and ability
to use transportation. A number of versions of the CAN
have been developed, including a research and clinical
version (Phelan et  al., 1995), staff-​administered and cli-
ent self-​rated versions (Reininghaus et  al., 2013), and a
short version (Andresen, Caputi, & Oades, 2000), and the
instrument has been translated into many languages. In
addition, adapted versions of the CAN have been devel-
oped for special mental health populations, including
older clients, persons using forensic mental health ser-
vices, clients with intellectual disability, and mothers or
pregnant persons. Generally, the CAN has been shown
to have high test–​ test and inter-​rater (between clini-
cians) reliability and good validity (McCrone et al., 2005;
Phelan et  al., 1995; Reininghaus et  al., 2013), and it is
increasingly being used across a range of clinical contexts
(Medeiros-​Ferreira et al., 2016; Slade, 2012).
The SAS-​II is a semi-​structured client interview, which
is a schizophrenia-​specific modification of an instrument
widely used in depressive samples (Weissman & Bothwell,
1976). The validity of the SAS-​II for use with outpatients
with schizophrenia has been previously demonstrated
(Jaeger, Berns, & Czobor, 2003; Schooler, Hogarty, &
Weissman, 1979). Measures of global adjustment in work/​
student role, household functioning, extended kin role,
social and leisure activities, intimate relationships, well-​
being, and overall adjustment are rated on a 1 to 7 scale,
based on specific responses to a series of questions in each
domain. The SAS-​II was primarily designed as a research
interview, and thus substantial training is required to
administer it with high reliability.
The QLS (Heinrichs, Hanlon, & Carpenter, 1984) con-
tains 21 items and is designed to assess the deficit syndrome
concept in individuals with schizophrenia. It measures
four domains—​ interpersonal functioning, instrumental
role functioning, intrapsychic factors (e.g., motivation and
curiosity), and possession of common objects/​participation
in common activities—​and also yields a total score. It has
been found to be sensitive to change from participating in
psychosocial interventions (Glynn et al., 2002). A confir-
matory factor analysis of the QLS was recently published
that mainly replicated the first three factors (interpersonal
functioning, instrumental role functioning, and intrapsy-
chic foundations) with 16 of the 21 items (Mueser et al.,
2017). The authors proposed renaming the intrapsychic
factor as “motivation” because the motivation item loaded
highest on this factor. Two abbreviated versions of the QLS
have been developed that include 5 (Ritsner, Kurs, Ratner,
& Gibel, 2005)  and 7 (Bilker et  al., 2003)  items, which
have been found to be strongly correlated with the total
QLS score. Similar to the SAS-​II, the QLS was designed
as a research interview and is not practical for use in most
routine clinical settings.
The SFS (Birchwood, Smith, Cochrane, Wetton, &
Copestake, 1990)  is a 20-​minute interview assessing the
following domains of functioning: social engagement and
withdrawal, interpersonal communication, independence
performance, socially appropriate behaviors, indepen-
dence competence, and occupation. Scales are normed
in each of the categories, and the breadth of topics con-
tains most of the items relevant to psychiatric populations.

The ILSS (Cyr, Toupin, Lesage, & Valiquette, 1994;
Wallace, Liberman, Tauber, & Wallace, 2000) is an inter-
view including 70 items asked of the client assessing a
range of instrumental skills required for independent liv-
ing:  appearance and clothing, personal hygiene, care of
personal possessions, food preparation and storage, health
maintenance, money management, transportation, lei-
sure and community, and job seeking and job mainte-
nance. Both client (self)-​rated and staff-​rated versions of
the scale exist. It is particularly targeted at identifying
specific skills required for community functioning (e.g.,
doing laundry and managing money).
The CASIG (Lecomte, Wallace, Caron, Perreault, &
Lecomte, 2004; Wallace, Lecomte, Wilde, & Liberman,
2001) is also available in both client and informant inter-
view formats. Nine areas of social and independent living
skills (health management, money management, food
preparation, vocational, transportation, friends, leisure,
personal hygiene, and care of personal possessions) are
assessed from four to nine dichotomous items. Items are
designed to assess performance rather than ability or moti-
vation. The informant and client versions are moderately
highly correlated.
The RAND Short Form-​ 36 Health Survey (SF-​ 36;
https:// ​ w ww.rand.org/ ​ h ealth/ ​ s urveys_ ​ t ools/ ​ m os/ ​ m os_​
core_​36item.html) is a modification of the SF-​36 (Ware,
Kosinski, & Keller, 1994) and is designed to assess func-
tioning in a broad range of medical and psychiatric popu-
lations. It can be administered by interviews in person or
over the phone. The RAND 36-​Item Health Survey taps
eight health concepts: physical functioning, bodily pain,
role limitations due to physical health problem, roles
limitations due to personal or emotional problems, emo-
tional well-​being, social functioning, energy/​fatigue, and
general health perceptions. It also includes a single item
that provides an indication of perceived change in health.
Scores can be summed for both a total and within specific
domains. Note that the scale does not specifically address
instrumental skills that might be related to capacity to
function independently in a psychiatric population (e.g.,
skill in riding the bus).
The MCAS (Barker, Barron, & McFarlane, 1994;
Corbière et  al., 2002; Hendryx, Dyck, McBride, &
Whitbeck, 2001)  is an informant-​based scale designed
to be completed by a staff member who is familiar with
the client’s functioning in the community. The scale
includes 17 items rated on 5-​point Likert scales, covering
the domains of interference with functioning, adjustment
to living, social competence, and community integra-
tion. A modification of this scale has been developed with
Schizophrenia 445
interview probes (Dickerson, Origoni, Pater, Friedman, &
Kordonski, 2003).
The SBS (Lima, Goncalves, Pereira, & Lovisi, 2006;
Wykes & Sturt, 1986) is an informant-​rated instrument
designed for the inpatient setting to be completed by
staff members. The SBS contains 30 items, most rated
on 5-​point or 6-​point Likert scales, pertaining to dimen-
sions of adjustment in an intensive treatment setting,
such as communication skills, symptomatic behavior,
and self-​harming behavior. The SBS can also be used
with outpatients, as long as an informant can be identi-
fied who is knowledgeable about the person’s day-​to-​day
functioning.
The SAFE (Harvey et al., 1997) is an informant-​rated
instrument that is completed by staff members who are
familiar with the client’s daily functioning. The scale
includes 17 items rated on 5-​point Likert scales, with
subscales corresponding to instrumental and self-​ care,
impulse control, and social functions. The SAFE was
originally developed for older persons with severe men-
tal illness, although most of the items are applicable to
younger clients.
The SLOF (Schneider & Struening, 1983)  is a 43-​
item measure on which assessors rate the following
domains: physical functioning, personal care skills, inter-
personal relationships, social acceptability (i.e., socially
appropriate or inappropriate behavior), engagement in
activities, and work skills. Items are rated on 1-​to 5-​point
Likert scales, with higher scores reflecting better com-
munity functioning. SLOF scores have been found to be
significantly related to performance of “real-​world” self-​
maintenance activities (Harvey et al., 2011).
In contrast to the previously mentioned commu-
nity functioning scales, MIRECC-​ GAF (Niv, Cohen,
Sullivan, & Young, 2007) ratings are not typically based
on information obtained in a single interview but, rather,
on all observations and information available to the
treatment team during the specified assessment period.
An extension of the original Global Assessment Scale
introduced with DSM III (APA, 1980), the MIRECC-​
GAF measures occupational functioning, social func-
tioning, and symptom severity on three 1-​to 100-​point
subscales. Similar to the standard clinician-​administered
GAF, lower scores on the modified version indicate more
impairment in that domain, and higher scores indicate
better occupational and social functioning and fewer
symptoms. All MIRECC-​GAF subscales are divided into
10 equal intervals and include criteria for scoring within
each interval. The scale has demonstrated good conver-
gent validity.
446 Schizophrenia and Personality Disorders
Subjective Appraisal
In addition to obtaining expert assessments, there is an
increasing interest in the field in measuring the client’s
own attitude toward his or her illness, as well as the indi-
vidual’s subjective appraisal of his or her circumstances
(living situation, safety, budget, etc.) and his or her
symptoms. In many ways, this focus reflects the growing
influence of the recovery movement in mental health.
Recovery from a serious and persisting psychiatric ill-
ness has been defined by the President’s New Freedom
Commission on Mental Health (2003) as
the process by which people are able to live, work,
learn, and participate fully in their communities. For
some individuals, recovery is the ability to live a fulfill-
ing and productive life despite a disability. For others,
recovery implies the reduction or complete remission
of symptoms. . . . Science has shown that having hope
plays an integral role in an individual’s recovery. (p. 7)
With regard to assessment, this recovery focus highlights
two necessary domains of measurement—​recovery atti-
tudes and satisfaction with life circumstances.
In a factor analysis of clients’ responses to a series of
items reflecting recovery orientations, Resnick, Rosenheck,
and Lehman (2004) identified four domains that can be
viewed as aspects of this process: life satisfaction, hope and
optimism, knowledge of mental illness, and empower-
ment. Assessing recovery attitudes is a new area of inves-
tigation, but there are now several tools to identify factors
related to recovery in schizophrenia (Cavelti, Kvrgic,
Beck, Kossowsky, & Vauth, 2012). Generally, these tools
can divided into two categories—​ones assessing positive
aspects of the recovery process and ones assessing negative
self-​assessments related to a diagnosis of schizophrenia or
another significant mental illness.
With regard to capturing a positive recovery orien-
tation, one of the widely used measures is the Mental
Health Recovery Measure (MHRM; Young & Bullock,
2005). The MHRM is a behaviorally anchored self-​report
measure designed for use with persons who have serious
and persistent mental illnesses, such as recurrent major
depression, bipolar disorder, or schizophrenia. The item
content of the MHRM and its subscales is based on a spe-
cific conceptual model of mental health recovery that is
grounded in the experiences of persons with psychiatric
disabilities (Young & Ensing, 1999). The 30-​item version
of the MHRM contains the following subscales: overcom-
ing; self-​ empowerment; learning and self-​ redefinition;
basic functioning; overall well-​ being; new potentials;
advocacy/​enrichment; spirituality in the recovery process;
and higher order activities, including advocacy, coping
with stigma, and financial quality of life. Items are rated
on 5-​point Likert scales. Relatively recently, a 10-​item
version of the measure (MHRM-​10) was developed that
had a single factor and was found to have high internal
reliability (Armstrong, Cohen, Hellemann, Reist, &
Young, 2014).
Another widely used measure of recovery is the
Recovery Assessment Scale (RAS; Giffort, Schmook,
Woody, Vollendorf, & Gervain, 1995; Ralph, Kidder, &
Phillips, 2000). The RAS includes 41 items, rated on 5-​
point Likert scales, pertaining to different dimensions of
recovery. A factor analysis indicated that the RAS taps the
following factors:  hope, meaningful life, quality of life,
symptoms, and empowerment (Corrigan, Salzer, Ralph,
Sangster, & Keck, 2004). There is limited evidence sug-
gesting some sensitivity of the RAS to treatment-​related
change (Corrigan, 2006). The Illness Management
and Recovery (IMR) scale (Mueser & Gingerich, 2005;
Mueser et al., 2005) is a 15-​item scale with self-​report and
clinician versions that was originally designed to capture
outcomes from the Illness Management and Recovery
Module (Mueser & Gingerich, 2005). However, the scale
is now used widely to assess recovery-​oriented actions
and successes (e.g., achieving personal goals, sustaining
community tenure, and managing substance use prob-
lems well) (Sklar, Sarkin, Gilmer, & Groessl, 2012). The
psychometric qualities have been found to be moder-
ate to strong (Färdig, Lewander, Fredriksson, & Melin,
2011; Hasson-​Ohayon, Roe, & Kravetz, 2008; McGuire,
Kean, Bonfils, Presnell, & Salyers, 2014; Salyers, Godfrey,
Mueser, & Labriola, 2007). A  variety of other recovery-​
oriented measures have been developed (for a review, see
Sklar, Groessl, O’Connell, Davidson, & Aarons, 2013),
but they are not covered here because their psychometric
properties are still being evaluated.
As mentioned previously, the individual can also
develop negative self-​assessments related to a diagnosis
of schizophrenia or another significant mental health
disorder. There has been much recent interest in devel-
oping measures to assess these negative self-​appraisals,
which have been labeled self-​stigma or internalized
stigma. Self-​stigma is a particular concern because it has
been linked to poorer psychosocial treatment adherence
(Fung, Tsang, & Corrigan, 2008)  and higher rates of
depression (Ritsher, Otilingam, & Grajales, 2003) in indi-
viduals diagnosed with schizophrenia. The Self-​Stigma of
Mental Illness Scale (SSMI; Corrigan, Watson, & Barr,

2006) contains 40 items, with 10 items representing each
of the four constructs in the self-​stigma model of Watson,
Corrigan, Larson, and Sells (2007): stereotype awareness,
stereotype agreement, stereotype self-​ concurrence, and
self-​esteem decrement. Order of items within each sub-
scale is randomized to diminish order effects. Clients are
asked to respond to each item using a 9-​point agreement
scale from “strongly disagree” to “strongly agree.” A short
form is also available.
The Internalized Stigma of Mental Illness (ISMI)
scale (Ritsher et  al., 2003)  contains 29 items that
assess individuals’ subjective experiences of internal-
ized stigma. In addition to producing an overall score,
the ISMI contains five subscales: alienation, stereotype
endorsement, discrimination experience, social with-
drawal, and stigma resistance. Both total and subscale
scores are calculated as a mean, with possible total and
subscale scores ranging from 1 to 4 and higher scores
indicating greater self-​stigma. The Stigma Scale (SS;
King et al., 2007) contains 28 items, each self-​rated on
a 5-​point Likert scale from “strongly agree” to “strongly
disagree” with good test–​retest (over 2 weeks) reliability.
The SS has three factors corresponding to discrimina-
tion, disclosure, and potential positive aspects of mental
illness, and it has been shown to be negatively correlated
with global self-​esteem.
A complementary aspect of subjective appraisal is the
client’s own evaluation of his or her satisfaction with the
circumstances of his or her life in areas such as living
situation and family relations. The original widely used
instrument for this type of assessment was the Lehman
Quality of Life Interview (Lehman, Kernan, & Postrado,
1995), a 183-​item instrument requiring 45 minutes to
administer that asks participants to rate their satisfaction
with various facets of their life on a scale from 1 to 7. The
Quality of Life Interview Self-​Administered Short Form
(TL-​30S) is a validated briefer (30-​item) 15-​minute ver-
sion that is based on correlation coefficients between
the brief and full version scales (Lehman, 2006). The
brief version provides measures of satisfaction with liv-
ing situation, social relations/​ network, finances, and
employment, and it includes both objective and sub-
jective items; the subjective appraisal items are of most
interest here.
In addition to judgments about the impact of a psy-
chiatric illness on one’s sense of self (either positive
or negative) and one’s life satisfaction, a more person-​
centered approach to assessment in schizophrenia has
also highlighted the importance of understanding the cli-
ent’s level of distress ensuing from symptoms. Those with
Schizophrenia 447
lived experience of the symptoms of schizophrenia do not
necessarily find them distressing (Baumeister, Sedgwick,
Howes, & Peters, 2017). For example, some individuals
experience internal voices that they judge to be benign or
even helpful, and they may reject the idea that these expe-
riences reflect the presence of a disorder. Thus, it can be
helpful for clinicians to distinguish between the presence
of a symptom and the distress the experience causes the
client. The Psychotic Symptom Rating Scale (PSYRATS;
Haddock, McCarron, Tarrier, & Faragher, 1999)  is a
semi-​structured 17-​item interview that assesses multiple
subjective dimensions of hallucinations and delusions. In
contrast to other psychotic symptom measures, details are
elicited by the respondent on several unique subjective
aspects of delusions and hallucinations (e.g., perceived
intensity, controllability, preoccupation, and distress) on
a 0 to 4 scale, with higher scores indicating more diffi-
culty. It has been found to have excellent psychometric
properties.
Family Attitudes
Work conducted in England in the 1950s through the
1970s (Brown, Birley, & Wing, 1972; Brown, Monck,
Carstairs, & Wing, 1962)  demonstrated that family atti-
tudes reflective of high levels of distress measured at the
time of a loved one’s psychotic relapse tended to predict
greater rates of subsequent relapse, especially if the rela-
tive and client had more than 35 hours of contact per
week. This high level of family distress has been labeled
“high expressed emotion” (EE), and the relationship
between high EE and subsequent relapse is among the
most potent predictors of outcome in schizophrenia
(Butzlaff & Hooley, 1998). EE is reflected in critical com-
ments or tone or reported extreme self-​sacrificing behav-
ior during a semi-​structured interview (the Camberwell
Family Interview) at the time of the initial relapse (Leff &
Vaughn, 1985), and it is likely evidenced in actual interac-
tions with the client (Mueser et al., 1993; Strachan, Leff,
Goldstein, Doane, & Burtt, 1986).
The measurement of EE requires an extensive
research assessment and scoring procedure, which is out-
side the time capacities of most clinicians. However, clini-
cians can be alert to signs of extreme distress, criticism,
and self-​sacrificing behavior on the part of the relative at
the time of a relapse and can consider a referral for an
evidenced-​based family intervention if these are observed.
These might be reflected, for example, in frequent calls
to the clinic for assistance, repeated complaints about
the client, or tearfulness in a relative. Hooley and Parker
448 Schizophrenia and Personality Disorders

(2006) suggested that one feasible method for assess- Comorbid Substance Abuse
ing EE is to ask clients how critical their relative is of
The assessment of co-​occurring substance use disorders
them. In a sample of clients with depression, Hooley and
may have important treatment planning implications for
Teasdale (1989) simply asked clients to rate how critical
clients with schizophrenia. Approximately 50% of persons
they thought their spouse was of them using a 10-​point
with schizophrenia develop a substance use disorder at
Likert-​type scale. Clients’ perceptions of their partner’s
some point in their illness, and most estimates of the point
criticism level (assessed during the index hospitalization)
prevalence of substance use disorders range between 25%
was highly predictive (r = –​.64) of client relapse over the
and 35% (Mueser, Bennett, & Kushner, 1995; Regier
course of a 9-​month follow-​up. Although this result has
et  al., 1990; Thoma & Daum, 2013). The treatment of
not been replicated in schizophrenia, the method war-
co-​occurring substance abuse is important because of its
rants more consideration and may have special utility for
deleterious effects on the course and outcome of schizo-
busy clinicians.
phrenia (Drake & Brunette, 1998) and the emergence of
An alternative measure to ratings of perceived criti-
effective treatment models that integrated services for the
cism is the Patient Rejection Scale (PRS; Kreisman et al.,
two disorders (Drake, O’Neal, & Wallach, 2008; Mueser,
1988; Kreisman, Simmens, & Joy, 1979). This 24-​item
Noordsy, Drake, & Fox, 2003).
scale consists of both positively and negatively worded
A number of brief screening instruments may be
items reflecting feelings of love and acceptance, criti-
used to detect substance abuse problems in schizophre-
cism, disappointment, and rejection; it can be considered
nia (Carey, 2002). Although some research suggests
an analogue of the critical comments and hostility factors
that instruments developed for measuring substance
comprising the concept of EE. Presumably, families high
abuse in the general population may be insensitive to
in rejecting attitudes would benefit from participation in
it in people with schizophrenia (Corse, Hirschinger, &
targeted interventions such as education or stress manage-
Zanis, 1995; Wolford et al., 1999), several measures have
ment. However, clinicians using the PRS should be aware
been demonstrated to have acceptable reliability and
that some of the items may be distressing for relatives to
validity, including the Alcohol Use Identification Test
rate (e.g., “I wish (the patient) had never been born”) and
(Dawe, Seinen, & Kavanagh, 2000; Maisto, Carey, Carey,
that a short debriefing with relatives after they complete
Gordon, & Gleason, 2000; Saunders, Aasland, Babor, De
the scale may be in order.
La Fuente, & Grant, 1993; Seinen, Dawe, Kavanagh, &
The impact of caregiving on the families of individu-
Bahr, 2000), the Michigan Alcoholism Screening Test
als with serious psychiatric illnesses is of concern. There
(McHugo, Paskus, & Drake, 1993; Searles, Alterman, &
is no consensus measure of family burden, and many of
Purtill, 1990; Selzer, 1971; Wolford et al., 1999), and the
the measures used with families of individuals diagnosed
Drug Abuse Screening Test (Maisto et al., 2000; Skinner,
with schizophrenia were developed for use in other dis-
1982; Wolford et al., 1999). In addition, the Dartmouth
orders (e.g., the Zarit Burden Scale; Zarit, Reever, &
Assessment of Lifestyle Instrument was developed spe-
Bach-​Peterson, 1980)  or are interview based and quite
cifically to detect alcohol, cannabis, and cocaine use dis-
intensive to administer, such as the Family Experiences
orders in persons with severe mental illness, and scores
Interview Schedule (FEIS; Tessler & Gamache, 1996).
have shown good reliability and validity in this population
One measure that appears to have good potential to cap-
(Batalla et al., 2013; Ford, 2003; Rosenberg et al., 1998).
ture burden in the families of the seriously mentally ill is
Diagnoses of substance use disorders in clients with
the Burden Assessment Scale (BAS; Reinhard, Gubman,
schizophrenia can also be reliably measured with the
Horwitz, & Minsky, 1994). The BAS is a 19-​item self-​
SCID-​5 (First et al., 2015a, 2015b). Although there is a
report measure that has subjective and objective burden
tendency for clients with schizophrenia to have low sub-
dimensions and has demonstrated good psychometric
scale scores on the Addiction Severity Index (ASI), which
properties. The BAS may have particular value because
was developed for the general population (McLellan et al.,
it does not require interviewer training and is designed
1992), there is evidence that the ASI can nevertheless
to focus on the experience of burden, and it is not con-
provide valid and reliable measures of the consequences
founded with issues of coping or skill in illness manage-
of substance use (Corse et  al., 1995). Limited work has
ment. There is some evidence supporting the validity of
been conducted indicating that measures of expectancies
the BAS across different cultures (Chakrabortya, Bhatia,
and reasons for substance use developed for the general
Anderson, Nimgaonkar, & Deshpande, 2013; Talwar &
population may be valid in persons with schizophrenia
Matheiken, 2010).

(Carey & Carey, 1995; Laudet, Magura, Vogel, & Knight,
2004; Mueser, Nishith, Tracy, DeGirolamo, & Molinaro,
1995), although currently the research is too preliminary
to make firm recommendations. Mueser and colleagues
(2003) provide detailed standardized assessment tools of
substance use in persons with severe mental illness for
treatment planning purposes, although rigorous psycho-
metric evaluation remains to be conducted.
The Substance Abuse Treatment Scale (SATS;
McHugo, Drake, Burton, & Ackerson, 1995; Mueser,
Drake, et  al., 1995; Mueser et  al., 2003)  is an 8-​point
behaviorally anchored scale designed to measure moti-
vation for substance abuse treatment in persons with
severe mental illness. The SATS is based on the stages of
treatment model (Mueser et al., 2003; Osher & Kofoed,
1989), which was adapted from the transtheoretical stages
of change model (Prochaska & DiClemente, 1984). The
stages of treatment include engagement (establishing a
therapeutic relationship with the client), persuasion (moti-
vating the person to work on substance abuse problems),
active treatment (helping the person reduce substance use
and/​or attain abstinence), and relapse prevention (helping
the client prevent substance abuse relapses). Because the
client’s stage of treatment has implications for treatment
planning (e.g., in the engagement stage, the clinician
focuses on establishing rapport and meeting with the cli-
ent regularly, whereas in the active treatment stage the
focus is on changing substance use behavior), the SATS
is clinically useful.
The Timeline Followback (TLFB) Calendar (Sobell
& Sobell, 1992) is an instrument for quantifying substance
use during the past 6 months and obtaining information
about patterns of use that can be useful in treatment plan-
ning. The primary dependent variable studied has been
the number of days of drinking to intoxication and the
number of days of drug use. The TLFB has been adapted
for use with persons with severe mental illness (Mueser,
Drake, et  al., 1995; Mueser et  al., 2003), with research
supporting its reliability and validity (Carey, Carey,
Maisto, & Henson, 2004), although there is evidence of
underreporting compared to laboratory tests (Bahorik,
Newhill, Queen, & Eack, 2014).
Overall Evaluation
A wide range of validated instruments have been devel-
oped for case conceptualization and treatment planning
regarding the domains of symptoms, community function-
ing, and comorbid substance abuse in schizophrenia. The
most strongly validated measures for each of these areas
Schizophrenia 449
involve either semi-​structured interviews or informant-​
based ratings, which is consistent with the poor insight
many clients with schizophrenia have into their illness
(Amador & Gorman, 1998). There are fewer choices
for treatment planning-​related assessment of medication
adherence, subjective appraisal, and family attitudes, but
there is at least one psychometrically sound instrument for
each domain that is practical for use in clinical settings.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
Symptoms
The BPRS, PANSS, and SANS administered by inter-
view have demonstrated sensitivity to change following
treatment and are suitable for monitoring the effects of
interventions on symptoms. Many research studies have
utilized the BPRS or PANSS as frequently as every 2
weeks during times of psychotic exacerbation to deter-
mine when symptoms return to baseline. The CAINS
and BNSS are newer measures, so their sensitivity to
change is less certain. Self-​reported symptoms on scales
such as the BASIS-​R and the Colorado Symptom Index
tend to measure global distress and not specific dimen-
sions of symptoms as with interview measures; therefore,
their clinical utility for monitoring the effects of treat-
ment on symptoms is not established. The ratings of the
psychometric properties of these tools are presented in
Table 20.3.
The Clinical Global Impression Scale (Guy, 1976;
Haro et  al., 2003)  has been widely used to assess symp-
tom change, especially in pharmaceutical studies. The
scale has three items, the first two being rated on 7-​point
Likert scales and of most relevance here. These items
assess severity of illness (from “normal” to “extremely
ill”) and global improvement from baseline (“very much
improved” to “very much worse”). There is a third effi-
cacy item, typically referring to the hypothesized effect of
a pharmaceutical agent, that is rated on a 4-​point scale.
Although the three ratings are brief, they are typically
made after extended clinical assessments and/​or contact
with clients and require that assessors have known the cli-
ent since the baseline period.
Medication Adherence
Although a range of instruments have been developed to
measure medication adherence, none have a consistent
450 Schizophrenia and Personality Disorders

TABLE 20.3  Rating of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Symptoms
BPRS A G E A A G E E A ✓
CGI A NA E A A A E E A ✓
PANSS A G E A A E E E A ✓
SANS A G E A A E E A A ✓
Community Functioning
CASIG A A E A E A G G A ✓
ILSS A G G A G A A G A ✓
MCAS A A G A A G G G A ✓
QLS A G E A A G E E A
SAFE A G G A A A E G A
SAS-​II A G E A A G E E A
SBS A A G A A A A G A
SFS A G E A G G E G A ✓
SF-​36 E G NA A A G E A A
MIRECC-​GAF A E E NR E E E E E ✓
Subjective Appraisal
MHRM A G NA A A A A A A
QOLI E G NA A G E E A A
RAS A G NA A G A E A A ✓
TL-​30S A G NA A A A G A A
PSYRATS E E E E E E E NR E ✓
IMR (Client) E G NA E E E G NR E ✓
Family Attitudes
PRS A G NA A A A A A A
BAS A G NA NR G G A G G ✓
Substance Abuse
ASI E G E A E E E G A ✓
AUS A NA E A A A E E A ✓
DUS A NA E A A A E E A ✓
SATS A NA E A A A E E A ✓
TLFB E NA E A A G E E A

Note: BPRS = Brief Psychiatric Rating Scale; CGI = Clinical Global Impression Scale; PANSS = Positive and Negative Syndrome Scale; SANS = Scale
for Assessment of Negative Symptoms; CASIG  =  Client’s Assessment of Strengths, Interests and Goals (both client and informant versions);
ILSS = Independent Living Skills Survey (both client and informant versions); MCAS = Multnomah Community Ability Scale; QLS = Quality of Life
Scale; SAFE = Social Adaptive Functions Scale; SAS-​II = Social Adjustment Scale-​II; SBS = Social Behavior Scale; SFS = Social Functioning Scale;
SF-​36 = Short Form-​36 Health Survey; MIRECC-​GAF = Mental Illness Research Education and Clinical Center Global Assessment of Functioning;
MHRM = Mental Health Recovery Measure; QOLI = Quality of Life Interview; RAS = Recovery Assessment Scale; TL-​30S = Quality of Life Interview
Self-​Administered Short Form; PSYRATS  =  Psychotic Symptom Rating Scale; IMR  =  Illness Management and Recovery; PRS  =  Patient Rejection
Scale; BAS = Burden Assessment Scale; ASI = Alcohol Severity Inventory; AUS = Alcohol Use Scale; DUS = Drug Use Scale; SATS = Substance Abuse
Treatment Scale; TLFB = Timeline Followback Calendar; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

track record for demonstrating sensitivity to change.
Most interventions that have been evaluated in research
trials for improving medication adherence employ either
pill counts or electronic pill bottles with cap sensors
(Zygmunt, Olfson, Boyer, & Mechanic, 2002). More
recently, a form of aripiprazole tablets with a sensor to
permit external monitoring of pill ingestion has been
approved by the FDA, but it is not clear how this will be
used in typical clinical practice, and whether consum-
ers will agree to its use. However, there are significant
problems with validity of data obtained by self-​report of
medication adherence so these kinds of automatic sen-
sors may have some appeal.
Community Functioning
The GAF, based on the widely used Global Assessment
Scale (Endicott, Spitzer, Fleiss, & Cohen, 1976), is
a single rating scale for evaluating a person’s psycho-
logical, social, and occupational functioning on a
 Schizophrenia 451

hypothetical continuum of mental illness—​ mental Family Attitudes

health, which ranges from 1 (most ill) to 100 (most
The Camberwell Family Interview (CFI) was developed
healthy). The scale provides defining characteristics,
primarily as a measure of negative family affect for cli-
including both symptoms and functioning, for each
ents who have recently experienced a symptom relapse,
10-​point interval between 1 and 100. Scores have been
and it has been evaluated as a predictor of subsequent
reported to be reliable and correlated with symptom
relapse and rehospitalization (Butzlaff & Hooley, 1998).
measures, especially with repeated assessments, and
Research evaluating changes in negative family affect
they have been found to have high inter-​rater reliabil-
measured on the CFI indicates modest sensitivity to
ity (Pedersen, Hagtvet, & Karterud, 2007; Söderberg,
treatment-​related change (Hogarty et al., 1991). However,
Tungström, & Armelius, 2005; Startup, Jackson, &
the extensive time required to administer the CFI makes
Pearce, 2002). As discussed previously, the MIRECC-​
it impractical for monitoring the effects of family inter-
GAF extends the GAF rating framework to include
vention in clinical settings. Client measures of perceived
occupational and social functioning as well as symp-
relative criticism have not been reported in schizophrenia
tom severity, so it can also be a useful tool for assessing
to date. The Patient Rejection Scale has been found to
changes in adaptive functioning.
be predictive of relapse in schizophrenia (Kreisman et al.,
The client-​based interview instruments of community
1988) and is sensitive to the effects of participation in fam-
functioning reviewed in the previous section on assess-
ily interventions (Mueser et  al., 2001). As a measure of
ment for treatment planning (including the SAS-​II, QLS,
family burden, the BAS has several advantages, including
ILSS, SFS, CASIG, and SLOF) are sensitive to change
ease of administration and interpretation.
and suitable for the purposes of monitoring treatment
effects. Similarly, the informant-​based instruments have
demonstrated sensitivity to change and are appropriate Substance Abuse
for treatment monitoring (including CASIG, MCAS, The Alcohol Use Scale (AUD) and Drug Use Scale
SBS, and SAFE). However, these measures would rarely (DUS) are 5-​point rating scales completed by clinicians to
be used more frequently than quarterly because changes rate substance use problems over the past 6 months, based
in social and community functioning typically lag behind on all available information (Drake et al., 1990; Mueser,
symptom changes and require relatively long periods of Drake, et al., 1995; Mueser et al., 2003). Both scales were
time to occur (e.g., to find a job, rent an apartment, or developed to reflect DSM-​IV criteria pertaining to sub-
develop a friendship). stance abuse and dependence. Both have specific ratings
corresponding to 1 = no substance use, 2 = use but not
Subjective Appraisal abuse, 3 = abuse, 4 = dependence, and 5 = dependence
and substance use-​related institutionalization (e.g., hospi-
Most of the self-​appraisal measures discussed in the treat- talizations and incarcerations). The AUS and DUS have
ment planning section (MHRM, RAS, QOLI, and TL-​ high sensitivity to change and are appropriate for moni-
30s) have been proposed for ongoing monitoring and toring treatment outcomes, although the scales have not
assessment of treatment outcomes, although data on been revised to reflect changes in DSM-​5 criteria for sub-
their use in this way are limited. Investigations on inter- stance use disorders. Similarly, the SATS and TLFB have
ventions to reduce self-​ stigma in persons with schizo- demonstrated sensitivity to treatment-​ related change.
phrenia are just being developed (Lucksted et al., 2011; The Alcohol Severity Inventory (ASI) is also sensitive to
Russinova et al., 2014), so the capacity for this variable to change following treatment, although clients with mod-
change over time is unknown. Reducing distress result- erate substance abuse severity tend to have floor effects
ing from psychotic symptoms is a treatment goal in many (Corse et al., 1995).
cognitive–​behavioral therapy for psychosis studies, and
the PSYRATS has been shown to be sensitive to change
Overall Evaluation
in some of these trials (Mehl, Werner, & Lincoln, 2015).
Because subjective appraisal and quality of life tend to be Similar to assessment for the purposes of treatment plan-
stable over relatively long periods of time, and their sensi- ning, a wide range of psychometrically sound instruments
tivity to change is often uncertain, most of these measures are available for monitoring and evaluating the effects of
would best be administered no more frequently than once treatment on symptoms, community functioning, and
every 6 months. comorbid substance abuse in schizophrenia. In contrast,
452 Schizophrenia and Personality Disorders
there are more limited, but nevertheless clinically suitable,
choices for measuring family attitudes. Aside from the
PSYRATS, measures of subjective appraisal and quality of
life appear to be less sensitive to treatment-​related change,
although it is not clear that this reflects limitations in the
measures or the high stability of these appraisals over time.
Currently, there are no scientifically validated (and hence
recommended) measures of medication adherence that
can be used for the purposes of routine treatment moni-
toring, and clinicians are advised to combine client self-​
report with observational measures such as pill counts or
use of electronic pill bottles with cap sensors.
CONCLUSIONS AND FUTURE DIRECTIONS
Because schizophrenia can affect so many different areas
of life functioning, assessment is necessarily complex and
spans a broad range of different domains. Furthermore,
because impaired insight into the illness is a common
feature of schizophrenia, the most sensitive measures
of functioning usually require either standardized inter-
views or informant ratings. With these considerations,
well-​validated measures have been developed for diagnos-
ing schizophrenia and for both treatment planning and
monitoring treatment effects in the domains of symptoms,
community functioning, family attitudes, and substance
abuse. Although some useful tools are available, more
work is needed to develop and evaluate instruments of
subjective appraisal and medication adherence that are
sensitive to the effects of treatment.
In addition to the importance of developing measures
for some domains that are more sensitive to change, there
is a strong need for measures that can be implemented
in routine clinical settings by competent clinicians with-
out requiring extensive training. With the exception of
self-​report measures of subjective appraisal, the strongest
measures for assessment in schizophrenia have been
developed in the context of research studies and validated
with trained clinicians. Only limited evidence supports
the utility of these instruments in the routine practice of
treating clients with schizophrenia, and time constraints
often prevent a thorough assessment that would lead to
comprehensive treatment.
A related problem is the relative paucity of measures
that provide a comprehensive, integrated assessment
across the broad range of domains of functioning that
are often impaired, or for which there are often needs,
in schizophrenia. Most of the measures described previ-
ously only assess one or two of the broad range of domains
affected in schizophrenia, necessitating the use of mul-
tiple assessment tools to develop a comprehensive picture
of the client and his or her needs. The development of
more fully integrated measures that cover a broader range
of functioning in schizophrenia could improve the com-
prehensiveness of assessment and the effectiveness of
treatment planning; CAN scales and the IMR scales are
exemplars of such measures.
One field that holds promise for increasing the effi-
ciency, and perhaps even effectiveness, of treatment plan-
ning and monitoring is the use of client-​facing technology
(Treisman et al., 2016). Although there were initial con-
cerns about lack of access to smartphones and computer
access in this population, recent surveys indicate that
many individuals diagnosed with schizophrenia do have
access to smartphones (Miller, Stewart, Schrimsher,
Peeples, & Buckley, 2015; Record et al., 2016), whereas
other studies have circumvented this problem by provid-
ing low-​cost computers, when needed, to facilitate partici-
pation in online educational and support interventions
(Rotondi et  al., 2005). With regard to assessment, there
is particular interest in the field in determining whether
careful real-​ time monitoring of medication adherence
and early warning signs might reduce rehospitaliza-
tions (Granholm, Ben-​Zeev, Link, Bradshaw, & Holden,
2012; Španiel, Vohlídka, Hrdlička, et al., 2008; Španiel,
Vohlídka, Kožený, et al., 2008). The early data from these
studies are mixed; there are many issues to resolve in mov-
ing from concept to effective clinical intervention, but it
is likely that technological tools will improve the capacity
to monitor and intervene more effectively with individu-
als diagnosed with schizophrenia in the coming years.
Finally, there is a need to develop assessment and
treatment planning methods that strive to reconcile and
integrate the perspectives of treatment providers and
clients with schizophrenia. Shared decision-​ making
between clients and providers has been growing in men-
tal health services (Fenton, 2003; Hamann, Leucht, &
Kissling, 2003) and is an important value espoused by the
President’s New Freedom Commission on Mental Health
(2003). Models of shared decision-​ making have been
proposed for prescribing medication (Deegan & Drake,
2006), and there is a need for further work to develop
such approaches that span the full range of functioning in
schizophrenia. Shared decision-​making approaches have
the potential to both integrate different perspectives on
functioning and set informed treatment priorities based
on client preferences. Such approaches are critical con-
sidering the ever-​growing array of effective medications
and rehabilitation approaches for schizophrenia.
 Schizophrenia 453

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 21
Personality Disorders
Stephanie L. Rojas
Thomas A. Widiger
This chapter is concerned with an evidence-​based assess-
ment for personality disorder. It is organized into three
sections: instruments for the diagnosis of personality disor-
ders, for case conceptualization and treatment planning,
and for treatment monitoring and outcome. For the pur-
poses of this chapter, the focus is on personality disorders;
other chapters in this volume provide useful resources for
assessing other aspects of the client with a personality dis-
order. The chapter begins with a brief discussion of the
nature of personality disorder.
NATURE OF THE DISORDER
Personality is one’s characteristic manner of thinking, feel-
ing, behaving, and relating to others. Personality traits are
typically perceived to be integral to each person’s sense of
self because they involve what persons value, what they
do, and what they are like most every day throughout
much of their lives. According to the fifth edition of the
Diagnostic and Statistical Manual of Mental Disorders
(DSM-​ 5; American Psychiatric Association [APA],
2013a), it is “when personality traits are inflexible and
maladaptive and cause significant functional impairment
or subjective distress [that] they constitute Personality
Disorders” (p. 647).
The current edition of the DSM, DSM-​ 5 (APA,
2013a), retained in Section II (the section for the official
diagnoses) everything from DSM-​IV (APA, 1994) regard-
ing personality disorders. Included in Section III of DSM-​
5, however, for “emerging measures and models” (APA,
2013a, p. 729), is a proposed hybrid model within which
personality disorders are said to involve a combination of
deficits in the sense of self and interpersonal relatedness
(Criterion A) along with maladaptive personality traits
464
(Criterion B). Although this conundrum is not addressed
in the context of evidence-​based assessment of personality
disorders, this chapter does address assessment measures
that can be used for both Section II and Section III for
personality disorder diagnoses.
The 10 personality disorders retained in DSM-​ 5
Section II are the paranoid, schizoid, and schizotypal
(placed within an odd–​eccentric cluster); the histrionic,
antisocial, borderline, and narcissistic (placed within a
dramatic–​emotional cluster); and the avoidant, depen-
dent, and obsessive–​ compulsive (placed within an
anxious–​avoidant cluster). By definition, personality
disorders must be evident since adolescence or young
adulthood and have been relatively chronic and stable
throughout adult life. As such, they often predate the
occurrence of other mental disorders, such as a mood,
anxiety, or substance use disorder. It is estimated that
approximately 15% of adults in the United States meet
diagnostic criteria for at least one personality disorder
(APA, 2013a). Although the comorbid presence of a per-
sonality disorder is likely to have an important impact on
the course and treatment of other forms of psychopathol-
ogy (Links & Eynan, 2013), the prevalence of personality
disorder is generally underestimated in clinical practice,
due in part to the failure to provide systematic or compre-
hensive assessments of personality disorder symptomatol-
ogy (Miller, Few, & Widiger, 2012).
One change for the personality disorders in DSM-​5
was the loss of the multiaxial system of DSM-​IV-​TR (APA,
2000), wherein personality disorders had been placed on
a separate diagnostic axis. The reason for the multiaxial
system was the fundamental differences between the per-
sonality disorders and other forms of psychopathology.
Personality disorders will typically predate the occurrence
of other mental disorders of adulthood and may in fact
 Personality Disorders 465

have contributed to their etiology as well as their future Most DSM-​5 mental disorders can be diagnosed sim-
course and treatment. In summary, it is possible that the ply through an assessment of current functioning. One
loss of the multiaxial system will further diminish the need not inquire as to the person’s functioning 15 years
assessment of personality disorders in clinical practice. ago to assess whether or not the person currently has a
Personality disorders are highly comorbid with one major depressive disorder. However, an assessment of
another (Clark, 2007; Trull, Scheiderer, & Tomko, 2012). current functioning can be highly misleading when diag-
Patients who meet the DSM-​5 diagnostic criteria for one nosing a personality disorder, particularly if the person is
personality disorder are likely to meet the diagnostic crite- currently suffering from, or is in treatment for, a mood,
ria for another. DSM-​5 noted that “prevalence estimates anxiety, or other comorbid mental disorder. One needs
for the different clusters suggest 5.7% for Cluster A [odd–​ to distinguish the effect of these other mental disorder on
eccentric], 1.5% for Cluster B [dramatic–​emotional], 6% the patient’s current functioning from the characteristic
for Custer C [anxious–​avoidant], and 9.1% for any person- manner of thinking, feeling, and relating to others that
ality disorder, indicating frequent co-​occurrence of disor- predated their onset.
ders from different clusters” (APA, 2013a, p. 646). DSM-​5 The most commonly used and preferred method for
instructs clinicians that all diagnoses should be recorded the diagnosis of a personality disorder in general clinical
because it can be important to consider, for example, the practice is an unstructured clinical interview (Westen,
presence of antisocial traits in someone with a borderline 1997). However, studies have consistently indicated that
personality disorder or the presence of paranoid traits in assessments based on unstructured clinical interviews do
someone with a dependent personality disorder. However, not consider all of the necessary or important diagnostic
the extent of diagnostic co-​occurrence is at times so exten- criteria (Garb, 2005). Personality disorder assessments
sive that many researchers prefer a more dimensional or based on unstructured clinical interviews are often unre-
profile description of personality (Clark, 2007; Skodol, liable (Miller et  al., 2012). Clinicians may base their
2012; Trull et al., 2012; Widiger & Trull, 2007). diagnosis on a subjective impression or focus on just
A primary purpose of a diagnosis is to suggest a specific one or two diagnostic criteria that they consider to be
etiology and pathology for which a particular treatment sufficient (Samuel & Bucher, 2017). The diagnosis of a
would ameliorate the condition (First & Tasman, 2006). particular personality disorder may even be governed by
However, many of the disorders in DSM-​5, including the the particular theoretical interests of the clinician as well
personality disorders, may not in fact have single etiolo- as gender and cultural biases (Garb, 2005; Oltmanns &
gies or even specific pathologies (Kupfer, First, & Regier, Powers, 2012).
2002). Research has suggested the DSM-​ 5 Section II The preferred method for diagnosing personality
personality disorders are typically constellations of mal- disorders in research is the semi-​ structured interview
adaptive personality traits resulting from multiple genetic (Segal & Coolidge, 2007; Skodol, 2014; Widiger & Boyd,
dispositions that are interacting with a variety of nega- 2009; Zimmerman, 2003). Semi-​ structured interviews
tive environmental experiences (Paris, 2012; Widiger & have several advantages over unstructured interviews
Trull, 2007). (McDermut & Zimmerman, 2008; Miller et  al., 2012).
Semi-​structured interviews ensure and document that a
systematic and comprehensive assessment of each per-
ASSESSMENT FOR DIAGNOSIS sonality disorder diagnostic criterion has been made. This
documentation can be particularly helpful in situations
Personality disorders can be among the most difficult to in which the credibility or validity of the assessment might
assess. Personality includes one’s characteristic sense of be questioned, such as forensic or disability evaluations.
self, typically involving distortions in self-​image (Millon, Semi-​ structured interviews provide specific, carefully
2011). Dependent persons can be excessively self-​ selected questions for the assessment of each diagnostic
effacing and even self-​denigrating, narcissistic persons criterion, the application of which increases the likeli-
can be grandiose and arrogant, and paranoid persons hood that assessments will be consistent across interview-
can be highly suspicious and mistrustful. As a result, sim- ers. Therefore, semi-​structured interviews provide more
ply seeking self-​reported information from persons who reliable and valid results across interviewers and time
are characterized, in part, by distortions in self-​image (Miller et  al., 2012; Segal & Coolidge, 2007; Widiger
can complicate a valid assessment (Miller et  al., 2012; & Boyd, 2009; Wood, Garb, Lilienfeld, & Nezworski,
Widiger & Boyd, 2009). 2002). In addition, the manuals that often accompany a
466 Schizophrenia and Personality Disorders
semi-​structured interview frequently provide a consider-
able amount of helpful information for understanding
the rationale of each diagnostic criterion, for interpret-
ing vague or inconsistent symptoms, and for resolving
diagnostic ambiguities (e.g., Loranger, 1999; Widiger,
Mangine, Corbitt, Ellis, & Thomas, 1995).
Concerns regarding problems with semi-​ structured
interviews (e.g., time-​ consuming and less flexibility)
should not dissuade clinicians from their use (Segal &
Coolidge, 2007; Widiger & Samuel, 2005; Zimmerman,
2003). For example, the diagnosis of intellectual disability
typically requires a time-​consuming and structured assess-
ment battery that includes the assessment of both intel-
lectual and adaptive functioning. Yet few clinicians object
to these requirements or would risk making such a diag-
nosis on the basis of an unstructured interview (Widiger
& Clark, 2000). It is not unreasonable to expect clinicians
to utilize similarly rigorous assessment methodologies for
the assessment of personality disorders, especially when
these disorders and traits are related to significant func-
tional impairment (e.g., Skodol et  al., 2002)  and have
important implications for treatment utilization (e.g.,
Miller, Pilkonis, & Mulvey, 2006)  and outcomes (e.g.,
Skodol, 2008). However, it is also unrealistic to expect
clinicians to have the time to assess all the diagnostic
criteria for the personality disorders (Mullins-​ Sweatt,
Lengel, & DeShong, 2016), typically requiring 2 hours
(Widiger & Boyd, 2009). Therefore, it is recommended
that one first administer a self-​report inventory to identify
the most likely personality disorders to be present, fol-
lowed by a semi-​structured interview to document the
presence of their respective diagnostic criteria (Widiger
& Samuel, 2005).
A variety of self-​report inventories and interviews that
would be useful to clinicians for assessing abnormal per-
sonality functioning have been developed. A  complete
summary of all these potential instruments is beyond the
scope of this chapter, but several extensive reviews exist
(e.g., Clark & Harrison, 2001; Furnham, Milner, Akhtar,
& De Fruyt, 2014; McDermut & Zimmerman, 2005;
Miller et  al., 2012; Rogers, 2001; Segal & Coolidge,
2007; Widiger & Boyd, 2009). There are five semi-​
structured interviews designed to assess the 10 DSM-​5
Section II personality disorders: (a) Diagnostic Interview
for DSM-​IV Personality Disorders (DIPD-​IV; Zanarini,
Frankenburg, Chauncey, & Gunderson, 1987; Zanarini,
Frankenburg, Sickel, & Young, 1996), (b)  International
Personality Disorder Examination (IPDE; Loranger,
1999), (c)  Personality Disorder Interview-​ IV (PDI-​ IV;
Widiger et  al., 1995), (d)  Structured Clinical Interview
for DSM-​ 5 Personality Disorders (SCID-​ 5-​PD; First,
Williams, Benjamin, & Spitzer, 2016), and (e) Structured
Interview for DSM-​IV Personality Disorders (SIDP-​IV;
Pfohl, Blum, & Zimmerman, 1997). In addition, the
Shedler–​Westen Assessment Procedure-​200 (SWAP-​200)
is a clinician rating form of 200 items, drawn from the psy-
choanalytic and personality disorder literature (Shedler,
2015). SWAP-​200 items are not ranked on the basis of
an administration of a series of questions; instead, the
SWAP-​200 “relies on clinicians to do what clinicians do
well:  observe and describe individual patients or clients
they know” (Shedler, 2015, p. 228).
There are eight traditional self-​report inventories for the
assessment of the DSM-​5 Section II (i.e., DSM-​IV) per-
sonality disorders:  (a) Coolidge Axis II Inventory (CATI;
Coolidge 1992); (b)  Minnesota Multiphasic Personality
Inventory-​ 2 (MMPI-​ 2) personality disorder scales devel-
oped originally by Morey, Waugh, and Blashfield (1985)
but revised for the MMPI-​ 2 by Colligan, Morey, and
Offord (1994); (c) Millon Clinical Multiaxial Inventory-​IV
(Millon, Grossman, & Millon, 2015); (d) OMNI Personality
Inventory (OMNI; Loranger, 2001); (e)  Personality
Diagnostic Questionnaire-​4 (PDQ-​4; Bagby & Farvolden,
2004); (f) Personality Assessment Inventory (PAI; Morey &
Boggs, 2004); (g) Schedule for Nonadaptive and Adaptive
Personality–​2nd Edition (SNAP-​2; Clark, Simms, Wu, &
Casillas, 2014); and (h)  Wisconsin Personality Disorders
Inventory-​IV (WISPI-​IV; Klein et  al., 1993). These eight
inventories contain items that assess for the respective
diagnostic criteria of each personality disorder. There are
also two self-​report inventories that assess for Section III
maladaptive personality traits that have also been keyed for
the DSM-​5 Section II personality disorders: (a) Five Factor
Model Personality Disorder scales (FFMPD; Widiger,
Lynam, Miller, & Oltmanns, 2012)  and (b)  Personality
Inventory for DSM-​5 (PID-​5; Krueger, Derringer, Markon,
Watson, & Skodol, 2012).
Table 21.1 provides a comparative listing of these
instruments, using the rating system of this text (see
Chapter  1). The first five instruments in the table (i.e.,
DIPD, IPDE, PDI-​IV, SCID-​5-​PD, and SIDP-​IV) are
the five semi-​structured interviews, presented in alpha-
betical order and followed by the SWAP-​200 clinician rat-
ing form. The next eight instruments are the traditional
self-​report inventories (i.e., CATI, MCMI-​IV, MMPI-​2,
OMNI, PAI, PDQ-​4, SNAP-​2, and WISPI-​IV), followed
by the two trait-​based self-​report inventories (i.e., FFMPD
and PID-​5), again presented in alphabetical order. Rather
than provide summary details on each of these measures
in turn, the following sections focus on the psychometric
 Personality Disorders 467

TABLE 21.1  Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Semi-​Structured Interviews
DIPD NR G E A G G G A ✓
IPDE A G E A G E G A ✓
PDI-​IV NR G E A G A G A ✓
SCID-​5-​PD NR G E A G E G A ✓
SIDP-​IV NR G E A G E G A ✓
Clinician Ratings
SWAP-​200 NR G A NR A A NR A
Traditional Self-​Report Inventories
CATI A G NA A A A NR G
MCMI-​IV E G NA A A A A A
MMPI-​2 E G NA A A A A G
OMNI G G NA A A A NR G
PAI E G NA A A A NR A
PDQ-​4 NR A NA A G A G G
SNAP-​2 A G NA A A A NR G
WISPI-​IV A G NA A A A NR G
Trait-​Based Self-​Report Inventories
FFMPD NR E NA NR E E NR E ✓
PID-​5 NR E NA A G E NR E ✓

Note: DIPD = Diagnostic Interview for Personality Disorders; IPDE = International Personality Disorders Examination; PDI-​IV = Personality
Disorder Interview-​IV; SCID-​5-​PD = Structured Clinical Interview for DSM-​5 Personality Disorders; SIDP-​IV = Structured Interview for DSM-​
IV Personality Disorders; SWAP-​200 = Shedler–​Westen Assessment Procedure; CATI = Coolidge Axis II Inventory; MCMI-​IV = Millon Clinical
Multiaxial Inventory-​IV; MMPI-​2 = Minnesota Multiphasic Personality Inventory-​2; OMNI = Omni Personality Inventory; PAI = Personality
Assessment Inventory; PDQ-​4  =  Personality Diagnostic Questionnaire-​4; SNAP-​2  =  Schedule for Nonadaptive and Adaptive Personality-​2;
WISPI-​IV = Wisconsin Personality Disorders Inventory; FFMPD = Five Factor Model Personality Disorder scales; PID-​5 = Personality Inventory
for DSM-​5; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

properties rated in the table and provide comparisons
among instruments for each property.
Norms
Four of the five semi-​ structured interviews and the
SWAP-​200 were rated as not reported for normative data
because normative data have not been provided within
their test manuals (Kaye & Shea, 2000; Rogers, 2001;
Widiger & Samuel, 2005). Normative data have not been
obtained, in part, because of the substantial cost of con-
ducting an epidemiological study with a semi-​structured
interview administered by professional clinicians. There
are published studies in which mean values and preva-
lence rates have been provided, and one can compare
one’s findings with these published values (e.g., for mean
SWAP-​200 scores obtained in a clinical data set, see
Westen & Shedler, 2003). However, these values can vary
considerably across clinical settings, and one cannot con-
sider these findings to actually represent normative data
(i.e., a representative sample obtained from a designated
population; Clark, 2007). The one potential exception
might be the IPDE, a version of which was adminis-
tered in 14 mental health centers located in 11 differ-
ent countries of North America, Europe, Africa, and Asia
(Loranger, 1999). However, the individual results across
countries for each disorder were never published.
With regard to the eight traditional self-​report inven-
tories, the test manuals for the MCMI-​IV (Millon et al.,
2015), OMNI (Loranger, 1999), PAI (Morey, 1991),
CATI (Coolidge & Merwin, 1992), WISPI-​ IV (Klein
et  al., 1993), and SNAP-​2 (Clark et  al., 2014)  provide
information concerning normative data. Colligan et  al.
(1994) provide substantial information concerning the
normative data for the MMPI-​ 2 personality disorder
scales, although for unclear reasons, test manuals for the
MMPI-​2 refer only in passing to the Morey et al. (1985)
personality disorder scales (e.g., Derksen, 2006). A rating
of not reported for normative data was provided for the
PDQ-​4 because the PDQ-​4 has been treated in a man-
ner comparable to the semi-​structured interviews (i.e.,
little attention given to providing normative information;
468 Schizophrenia and Personality Disorders

Bagby & Farvolden, 2004). Normative data have not yet study in which they administered both the IPDE and
been provided for the FFMPD and PID-​5. SCID-​ II to the same 100 inpatients of a personality
disorders treatment unit. Both interviews were adminis-
tered blind to one another on the same day (one in the
Reliability
morning and the other in the afternoon). This study has
Reliability can concern internal consistency, inter-​rater never been replicated or extended to comparisons of
agreement, and test–​retest agreement (Kurtz, McCrae, other semi-​structured interviews, nor has anyone ever
Terracciano, & Yamagata, 2011). It should also be empha- compared the results of the same semi-​structured inter-
sized that the internal consistency of scores on an instru- view administered at different times to the same patients.
ment is a reflection of the construct being assessed. The Nevertheless, there remains the importance of obtaining
DSM-​5 Section II personality disorders are constellations inter-​rater reliability studies with independently adminis-
of maladaptive personality traits, and these syndromal tered interviews. Indeed, one of the results of the DSM-​5
assortments of traits can complicate obtaining accu- field traits was the poor inter-​rater reliability obtained for
rate estimates of internal consistency when the traits do antisocial personality disorder and, at one site, for border-
not themselves correlate highly with one another. For line (Regier et  al., 2013). This poor reliability was due
example, antisocial personality disorder includes traits of in part to the absence of a semi-​structured interview but
antagonism and disinhibition, whereas schizoid is con- likely also reflects the fact that different persons inter-
fined largely to traits of introversion. As a result, scores viewed the patients at different times.
on scales to assess DSM-​5 Section II antisocial will often The test–​retest reliability of scores for a variety of mea-
have poorer internal consistency compared to scales to sures has been rated as “adequate” because the neces-
assess schizoid. The FFMPD and PID-​5 were rated as sary research to understand the findings has not yet been
excellent for their assessment of the maladaptive person- conducted. It is possible that some instruments should
ality trait scales; however, internal consistency estimates be rated as inadequate, but additional research would
will at times decrease when these scales are combined for be necessary before this judgment is provided. Consider,
the respective DSM-​5 Section II syndromes. for example, a study by Piersma (1987, 1989)  that illus-
All five of the semi-​structured interviews were rated as trates well a point that may apply to other measures. He
excellent with respect to inter-​rater reliability (inter-​rater reported substantial changes in MCMI assessments across
reliability is not relevant to the self-​report inventories). brief inpatient hospitalizations. Test–​retest kappa was only
The major strength of these instruments is their provision .11 for the borderline diagnosis, .09 for compulsive, .01
of explicit and systematic assessments of each personality for passive–​aggressive, and .27 for schizotypal. One could
disorder diagnostic criterion contributing to their obtain- conclude that clinical treatment resulted in significant
ment of good to excellent inter-​rater reliability in most changes to personality functioning, as personality disor-
studies (Furnham et al., 2014; Miller et al., 2012; Segal ders are responsive to treatment (Leichsenring & Leibing,
& Coolidge, 2007; Widiger & Boyd, 2009). Nevertheless, 2003; Perry & Bond, 2000). However, inconsistent with
it is also worth noting that the reliability data that are this explanation is the fact that the treatment was quite
reported in most studies have been confined to the agree- brief and was focused on mood, anxiety, and other forms of
ment in the coding of respondents’ answers to interview psychopathology. Perhaps most problematic to the hypoth-
questions. This might not be the more important or fun- esis of a valid change in personality was the additional find-
damental concern with respect to the reliability of a per- ing of significant increases in the histrionic and narcissistic
sonality disorder assessment (Clark & Harrison, 2001). Of personality disorder scales (Piersma, 1989). If the inpatient
greater importance would be studies addressing whether hospitalization did, in fact, contribute to a remission of
semi-​structured interviews are being administered reli- borderline and compulsive symptoms, it should perhaps
ably across different research or clinical sites (Segal & take responsibility as well for contributing to the creation
Coolidge, 2007). For example, are some interviewers of histrionic and narcissistic personality disorders. Piersma
providing substantially more follow-​up queries than other (1989) concluded, instead, that the self-​report inventory
interviewers? Do patients respond to the same open-​ assessment “is not able to measure long-​term personal-
ended questions in a consistent manner at different times? ity characteristics (‘trait’ characteristics) independent of
The reason that such research has not been con- symptomatology (‘state’ characteristics)” (p. 91).
ducted is largely the cost. Skodol, Oldham, Rosnick, It is perhaps unfair to single out the MCMI-​IV with
Kellman, and Hyler (1991) conducted an impressive respect to this problem, as it is possible, if not likely, that

comparable results would occur for the other self-​report
inventories and even the semi-​structured interviews. A sig-
nificant problem for all of the self-​report inventories is
the absence of directions, within the instructions to the
respondents, to describe one’s characteristic manner of
functioning before the occurrence of any current diag-
nostic disorder (previously identified as Axis I disorders).
The instructions for the MCMI-​IV even refer explicitly
to describing one’s current problems. As a result, many
respondents are probably answering personality disorder
items with respect to their current mood, anxiety, or other
psychopathology.
Semi-​structured interviews have the potential of being
relatively less susceptible to confusing a personality disor-
der with other psychopathology compared to self-​report
inventories (Segal & Coolidge, 2007; Widiger & Boyd,
2009), but they are not immune. An interviewer can eas-
ily fail to appreciate the extent to which patients’ self-​
descriptions are being distorted by mood, anxiety, distress,
or other situational factors. In fact, results equivalent to
those reported by Piersma (1987, 1989)  were obtained
in a study that was purportedly documenting the resil-
ience of semi-​structured interviews to mood state distor-
tions. Loranger et al. (1991) compared IPDE assessments
obtained at the beginning of an inpatient admission to
those obtained 1 week to 6  months later and reported
“a significant reduction in the mean number of criteria
met on all of the personality disorders except schizoid and
antisocial” (p. 726). It is unlikely that 1 week to 6 months
of treatment that was focused largely on mood, anxiety,
and other forms of psychopathology resulted in the extent
of changes to personality that were obtained. In fact, com-
parable to the findings of Piersma (1989), twice as many
patients (eight) were diagnosed with a histrionic person-
ality disorder at discharge than were diagnosed with this
personality disorder at admission.
Further complicating an understanding of instability
in personality disorder assessments is the suggestion that
the changes on these measures may reflect actual fluctua-
tions in personality. Comparable changes have occurred
with respect to the assessment of such traits as neuroti-
cism within treatment-​seeking individuals. To the extent
that neuroticism is a disposition to experience and express
negative affect, increases (and decreases) in the expres-
sion of these moods could be understood as fluctuating
expressions of (and changes to) the personality trait of
neuroticism. Costa, Bagby, Herbst, and McCrae (2005)
argued that “rather than regard these depression-​caused
changes in assessed personality trait levels as a distortion,
we interpret them as accurate reflections of the current
Personality Disorders 469
condition of the individual” (p.  45). One’s level of neu-
roticism will not simply remain flat and stable no matter
what is happening within one’s life. Fluctuations in lev-
els of agreeableness and extraversion, and other domains
of personality, will also occur in response to situational
changes. In summary, further research is needed to
understand instability in personality trait and personality
disorder scores.
Content Validity
A rating of good was provided for all five of the semi-​
structured interviews with respect to content validity.
A  strength of all five semi-​structured interviews is their
explicit effort to obtain a systematic and comprehensive
assessment of the DSM-​5 Section II personality disor-
der criterion sets. A rating of excellent was not provided
because none of the authors of the measures obtained
quantitative ratings for the extent to which the interview
questions adequately covered the content. However, the
face validity of the questions does appear to be excellent.
Age of Onset
An important limitation of the semi-​structured interviews
is the extent to which each adheres to the requirement
that the personality disorder symptomatology has an age
of onset in late adolescence or young adulthood. All of
the interviews focus their initial, if not their entire, assess-
ment on the previous 2 to 5 years. The SCID-​5-​PD (First
et al., 2016) requires that each diagnostic criterion be evi-
dent over a 5-​year period, whereas the DIPD (Zanarini
et al., 1987) focuses its assessment on the previous 2 years
(Widiger, 2005). The PDI-​IV (Widiger et  al., 1995), in
contrast, encourages the interviewer to document that
each diagnostic criterion considered to be present has
been evident since young adulthood but does not provide
an explicit set of questions to do so. The IPDE (Loranger,
1999) is the most explicit in its requirements, but it is also
more liberal, as it requires that only one diagnostic crite-
rion for a respective personality disorder be present since
the age of 25 years; all of the others can be evident only
within the past few years.
The assumption with the DIPD, for example, is that
if the behavior has been evident during the previous
2 years, then it is likely to have been present before the
onset of other psychopathology and evident since young
adulthood. However, this can often be a false and highly
problematic assumption. For example, the DIPD was
used in the widely published Collaborative Longitudinal
470 Schizophrenia and Personality Disorders
Personality Disorders Study (CLPS; Gunderson et  al.,
2000). CLPS reported many cases of sudden, dramatic
remissions soon after the study began. For example, 23 of
160 persons (14%) diagnosed with borderline personality
disorder at the study’s baseline assessment met criteria for
two or fewer of the nine diagnostic criteria just 6 months
later (Gunderson et  al., 2003). Gunderson et  al. (2003)
concluded that only 1 of these 18 persons had been inac-
curately diagnosed at baseline; the rest were considered
to be valid instances of sudden and dramatic remission.
However, it is difficult to imagine so many persons who
met the diagnostic criteria for borderline personality dis-
order since late childhood and who continued to manifest
these symptoms throughout their adult life experienced,
apparently for the first time, dramatic changes in person-
ality functioning soon after the onset of the study. For
example, the diagnoses included one person whose origi-
nal symptoms were determined to be secondary to the use
of a stimulant for weight reduction. For other cases, “the
changes involved gaining relief from severely stressful sit-
uations they were in at or before the baseline assessment”
(p. 115), including the resolution of a traumatic divorce
or custody battle. To the extent that these cases of remis-
sion represent invalid baseline assessments, the test–​retest
reliability of the interview assessments should perhaps be
rated as less than adequate.
DSM-​5 Section II Criterion Sets
Whereas all five of the semi-​ structured interviews are
coordinated explicitly with the respective DSM-​5 Section
II diagnostic criterion sets, this is not the case for the
SWAP-​200 or for most of the self-​report inventories. These
instruments vary considerably in the extent to which they
are coordinated with the current DSM-​5 Section II. The
CATI (Coolidge & Merwin, 1992) and the PAI (Morey &
Boggs, 2004) were constructed in reference to the DSM-​
III-​R criterion sets (APA, 1987) and have not since been
revised. The Morey et  al. (1985) MMPI-​2 items were
selected on the basis of the DSM-​III criterion sets (APA,
1980), and Somwaru and Ben-​Porath (1995) developed
MMPI-​2 personality disorder scales that are coordinated
with DSM-​IV-​TR (Hicklin & Widiger, 2000). It is inter-
esting to note that both Somwaru and Ben-​Porath and
Morey et al. used quantitative ratings by multiple judges
for the selection of items from the same pool (i.e., can
be described as “excellent”), yet the two efforts yielded a
different item pool selection (Hicklin & Widiger, 2000).
Deviating from the DSM, however, might not be a disad-
vantage in all cases. For example, many of the SWAP-​200
items concern symptoms, features, or traits that are out-
side of the respective DSM-​5 criterion sets, which might
in fact be considered a strength (Shedler, 2015) if it then
provides a more valid personality disorder assessment.
Content validity for the PID-​ 5 was rated as good
because multiple judges were involved in the assignment
of the trait scales to respective personality disorder con-
structs (Krueger et al., 2012), although the precise nature
of this process has not been explicitly described. Content
validity for the FFMPD scales was rated as excellent
because multiple judges and quantitative ratings were
obtained for these trait scales. Scales were selected in part
on the basis of surveys of researchers (Lynam & Widiger,
2001) and surveys of clinicians (Samuel & Widiger, 2004).
Construct Validity
The “investigation of a test’s construct validity is not
essentially different from the general scientific procedures
for developing and confirming theories” (Cronbach &
Meehl, 1955, p. 300). Construct validity subsumes other
forms of validity and concerns the extent to which the
scientific findings for the measure produce the expected
theoretical findings for the respective construct (Strauss &
Smith, 2009). Ratings of construct validity, for this text, are
based on the extent to which there is replicated evidence
of predictive validity, concurrent validity, and convergent
and discriminant validity, as well as a measure’s ability to
provide incremental validity with respect to other clini-
cal data. The IPDE, SCID-​5-​PD, and SIDP-​IV were pro-
vided with excellent ratings for construct validity, in part
because these three instruments have been used most
extensively in personality disorder research. Much of what
is published concerning the etiology, pathology, course,
and treatment of personality disorders has been based on
studies using one of these three instruments. The DIPD
similarly was the instrument used in the heavily published
CLPS project (Gunderson et al., 2000). The PDI-​IV has
been used in a number of studies but not nearly as fre-
quently as the other four semi-​structured interviews.
Most of the instruments have demonstrated evidence
of problematic discriminant validity, but this likely reflects
the absence of adequate discriminant validity with regard
to the personality disorder constructs themselves (Clark,
2007; Lynam & Widiger, 2001; Miller et al., 2012; Trull
& Durrett, 2005). A valid assessment of an individual per-
sonality disorder should obtain weak discriminant validity
with respect to other near-​neighbor personality disorder
constructs. For example, to the extent that borderline per-
sonality disorder does in fact overlap substantially with

dependent personality disorder (e.g., both involve fears
of separation and abandonment), then valid scales that
assess borderline personality disorder should correlate
with scales that assess dependent personality disorder.
In fact, the scales of some personality disorder self-​report
inventories (e.g., the MCMI-​IV and MMPI-​2) include
substantial item overlap in order to compel the obtain-
ment of a particular degree and direction of co-​occurrence
that would be consistent with theoretical expectations.
The PID-​ 5, similarly, uses the same maladaptive trait
scales for different personality disorders (APA, 2013a).
The FFMPD has scales specific to each personality dis-
order. For example, there are different anxiousness scales
for the schizotypal (i.e., Social Anxiousness), borderline
(i.e., Anxious Uncertainty), dependent (i.e., Relationship
Anxiety), avoidant (i.e., Evaluation Apprehension), and
obsessive–​compulsive (i.e., Excessive Worry) personality
disorders. Each scale was constructed to assess how anx-
iousness is expressed differently for each personality dis-
order (Widiger et  al., 2012). However, no study has yet
attempted to demonstrate that these scales do in fact have
adequate discriminant validity.
SWAP-​ 200 assessments have consistently obtained
better discriminant validity compared to personality
disorder semi-​structured interviews (Shedler & Westen,
2004), but this could reflect the fact that clinicians
administering the SWAP-​200 are artifactually required
to provide a distribution of ratings that diminishes sub-
stantially the likelihood of obtaining diagnostic co-​
occurrence (Block, 2008; Wood, Garb, Nezworski, &
Koren, 2007). For example, Westen and Shedler (1999)
required clinicians to identify half of the personality dis-
order symptoms as being absent and only eight SWAP-​
200 items could be given the highest rankings, no matter
the actual opinions of the clinicians or the symptoms
that were in fact present (similar constraints were placed
on the other ratings).
Only a few studies have examined the convergent
validity among the personality disorder semi-​structured
interviews (O’Boyle & Self, 1990; Pilkonis et  al., 1995;
Skodol et al., 1991). Of these studies, only two involved
the administration of interview schedules to the same
patients (O’Boyle & Self, 1990; Skodol et  al., 1991),
and all three were confined to just two of the five semi-​
structured interviews. The most comprehensive study
was conducted by Skodol et  al., summarized previously
with respect to inter-​rater reliability. Skodol et al. reported
weak convergent validity for the categorical diagnoses
(e.g., κ = .14 for schizoid) but good convergent validity for
dimensional ratings (e.g., κ = .58 for schizoid).
Personality Disorders 471
Saylor and Widiger (2008) converted some of the
five DSM-​5 Section II semi-​structured interviews per-
sonality disorder assessments into self-​report inventories
in order to examine the convergence of the instru-
ments in regard to the content of the interviews (i.e.,
variation in what questions are asked) rather than with
respect to their administration or scoring (e.g., variation
in follow-​up questions). The inventories demonstrated
substantial convergent validity in regard to total scores
but some divergence regarding individual diagnostic
criteria. For example, for antisocial impulsivity or fail-
ure to plan ahead, the DIPD demonstrated significantly
lower convergence with the other four interviews and
did not obtain significant convergence with the SNAP
and PDQ-​4. This lack of convergence may have been
due to content specific to the DIPD (Widiger & Lowe,
2010). The DIPD items contain queries such as “Since
the age of 15, have you changed jobs,” “Since the age
of 15, have you moved,” and “Since the age of 15, have
you gone from close relationship to close relationship”
(Zanarini et al., 1996). These queries are related to the
presence of changes in job, residence, or relationship,
respectively. These questions do not examine if the
changes are excessive in frequency or even dysfunc-
tional, or whether there is a failure to plan ahead, as
included within the respective DSM-​5 Section II diag-
nostic criterion.
Several studies have been published on the con-
vergence of personality disorder semi-​ structured
interviews with self-​report inventories, as well as the
convergent validity among self-​ report inventories.
Miller et  al. (2012) tabulated the findings from 25 of
these studies. In comparison to correlations between
self-​report inventories, the correlations between self-​
report and semi-​ structured interviews were substan-
tially lower. Miller et al. reported that the decrease in
convergent validity of semi-​structured interviews with
the self-​report inventories indicates that the method of
assessing personality disorders can have a significant
effect on the resultant diagnoses. Additional research
is required regarding the relative validity of semi-​struc-
tured and self-​ report assessment (Widiger & Boyd,
2009). Rojas and Widiger (2017) examined the PID-​5
coverage of DSM criteria as assessed by the CATI and
PDQ-​4+. The authors reported good coverage of the
DSM-​IV-​TR diagnostic criteria by the PID-​5 for the
antisocial, borderline, avoidant, dependent, and narcis-
sistic personality disorders. However, coverage could
be improved for some criteria of obsessive–​compulsive
personality disorder.
472 Schizophrenia and Personality Disorders
Validity Generalization
Validity generalization concerns whether the instrument
has been shown to be equally valid across different popu-
lations. Considered in this chapter is generalization across
age, gender, and culture/​ethnicity.
Age
The DSM-​ 5 notes that personality disorder traits are
often recognizable by adolescence or early adulthood.
However, with the exception of conduct disorder as an
antecedent of adult antisocial personality disorder, very
little is known about the childhood antecedents of the
DSM-​5 Section II personality disorders (De Fruyt & De
Clercq, 2014). The DSM-​5 cautions clinicians that per-
sonality disorder features in childhood will often resolve
as the individual enters adulthood. In addition, the DSM-​
5 Section II criterion sets were written for adults, and it
is not at all clear whether they translate well to children.
For example, many children will act in a dependent fash-
ion that will have little to do with a personality disorder,
and some adolescents will display borderline personality
disorder symptomatology that should perhaps be under-
stood as part of a normative identity crisis rather than a
personality disorder. In line with this research, many of
the instruments reviewed are indicated for use with indi-
viduals aged 18 years or older. However, Westen, Shedler,
Durrett, Glass, and Martens (2003) diagnosed adolescents
with personality disorders using the SWAP-​200, and a
version of the PID-​5 is available for children aged 11 to
17 years (APA, 2013b).
The same point can be made for the assessment of
personality disorders among older adults. A  significant
amount of research has been conducted on personality
disorders among older adults (Oltmanns & Balsis, 2011),
but this research has also been shown to be rather prob-
lematic. For example, estimates of the prevalence of per-
sonality disorders among older adults are generally higher
than is obtained among middle-​ aged adults, which is
fundamentally inconsistent with the DSM-​5 diagnostic
system. It is quite possible that maladaptive personality
can develop as one ages (Widiger & Seidlitz, 2002), but
DSM-​5 does not currently recognize the occurrence of an
adult onset for a personality disorder; therefore, the preva-
lence rate should decrease as the population ages (unless
those with personality disorders have a much lower rate
of mortality). The difficulty perhaps lies, again, with the
failure (discussed previously) of the existing instruments
to adequately address age of onset and temporal stability
throughout adult life (Oltmanns & Balsis, 2011). In addi-
tion, some of the diagnostic criteria may again have a
different meaning within an older adult population. For
example, the dependent personality disorder diagnostic
criteria of being unrealistically preoccupied with fears of
being left to care for oneself, or feeling uncomfortable or
helpless when alone because of exaggerated fears of being
unable to care for oneself, were written to assess depen-
dency in middle-​aged persons who are otherwise fully
capable of caring for themselves. They would clearly have
a much different meaning for a person who is experienc-
ing a decline in physical ability due to aging. Therefore,
caution should be noted when attempting to diagnose a
personality disorder in an older adult.
Gender
The topic of gender in relation to personality disorders has
often been examined. Many of the personality disorders
have a differential prevalence rate across the sexes, and
some appear to involve maladaptive variants of gender-​
related personality traits (APA, 2013a). The suggestion
that these differential sex prevalence rates reflect gender
biases has been among the more difficult and heated
diagnostic issues (Widiger, 2007). Concerns regarding
gender bias have been examined regarding the concep-
tualization of personality disorders, diagnostic criteria
wording and application, thresholds for diagnosis, clini-
cal presentation, research sampling, self-​awareness and
openness of patients, and the items included in self-​report
measures (Morey, Alexander, & Boggs, 2005; Oltmanns
& Powers, 2012).
However, research has not demonstrated a significant
bias within the DSM-​5 diagnostic criteria (Boggs et  al.,
2005; Jane, Oltmanns, South, & Turkheimer, 2007).
Research has indicated that the gender differences of the
personality disorders appear to be consistent with norma-
tive difference in general personality structure between
genders (Lynam & Widiger, 2007). Note, however, that
research has indicated gender biases in clinical judgments
and self-​report inventories (Miller et  al., 2012; Widiger
& Boyd, 2009). When systematic assessments of diagnos-
tic criteria sets are provided, as occurs with the admin-
istration of a semi-​structured interview, there appears to
be a considerable decrease in gender-​biased assessments
(Miller et al., 2012).
In regard to gender biases in self-​report inventories, the
MMPI-​2 and the MCMI-​IV personality disorder inven-
tories include gender-​related items that are keyed in the
direction of adaptive rather than maladaptive functioning.

An item need not assess for dysfunction to contribute to
a valid assessment of personality disorders. For example,
items assessing for gregariousness can identify histrionic
persons, items assessing for confidence can identify
narcissistic persons, and items assessing conscientious-
ness can identify obsessive–​compulsive persons (Millon
et  al., 2015). Items keyed in the direction of adaptive,
rather than maladaptive, functioning can be helpful in
countering the tendency of some respondents to deny or
minimize personality disorder symptomatology. However,
these items will not be useful in differentiating abnormal
from normal personality functioning, and they are likely
to contribute to an overdiagnosis of personality disorders
in normal or minimally dysfunctional populations, such
as encountered in student counseling centers, child cus-
tody disputes, or personnel selection (Boyle & Le Dean,
2000). When these items are related to the sex or gender
of respondents, as many are in the case of the histrionic,
dependent, narcissistic, and obsessive–​ compulsive per-
sonality disorder scales of the MCMI-​III (Millon, Davis,
Millon, & Grossman, 2009) and the MMPI-​2 (Colligan
et al., 1994), they may contribute to gender biased assess-
ments (Oltmanns & Powers, 2012). The PDQ-​ 4 was
provided a good rating because all of its items are keyed
in a maladaptive direction and therefore do not demon-
strate the gender bias evident within the MMPI-​2 and the
MCMI-​III (Lindsay, Sankis, & Widiger, 2000).
Culture and Ethnicity
There is considerable literature on the impact of gen-
der on the assessment of personality disorders, but there
is limited research on the impact of ethnicity or culture,
despite the social and theoretical significance of this area
of research (Ryder, Sunohara, & Kirmayer, 2015). Ryder
et al. (2015) reported that research examining culture and
personality disorder contains a variety of long-​standing
methodological and conceptual issues. The authors noted
that the databases examining culture and personality dis-
orders are sparse and the research often does not focus on
true “culture.” Studies often indicate “broad differences
using ‘Western’ constructs and rarely test their explana-
tions” (p. 40).
Items within self-​report inventories are generally writ-
ten from the perspective of a member of the dominant
ethnic/​cultural group, and such items may not have the
same meaning or implications when provided to mem-
bers of a minority ethnic group (Okazaki & Sue, 2016).
Hindering the effort of psychologists to identify (a)  the
cultural contexts in which assessment techniques should
Personality Disorders 473
be interpreted differently or (b)  the adjustments in test
interpretation that should be made across different ethnic
groups is the absence of sufficient research on the mecha-
nisms for cultural or ethnic group differences. Much of
the existing research has been confined to the reporting of
group differences, without an assessment of the purported
mechanism by which the differences could be explained
or understood (Okazaki & Sue, 2016).
As an example of this line of research, studies have
reported the obtainment of significantly higher scores by
African Americans (compared to European Americans)
on Cluster A  personality disorders. Gibbs et  al. (2013)
demonstrated that in a nationally representative com-
munity sample, African Americans were less likely than
European Americans to be diagnosed with avoidant or
dependent personality disorder but were more likely to
be diagnosed with paranoid or schizoid personality disor-
der. The authors indicated the higher rates of paranoid
or schizoid personality disorders could be due to an
accurate increase in symptom prevalence due to adverse
social environment (e.g., discrimination) as well as a pos-
sible inaccurate increase in symptom prevalence due to
interviewers pathologizing healthy coping strategies (e.g.,
understandable mistrust, skepticism, and suspicion out-
siders) or by a failure to appreciate the meaning of (for
instance) suspiciousness in persons who have a history
of being discriminated against or victimized. In addi-
tion, Manseau and Case (2014) demonstrated that both
Hispanics and non-​ Hispanic Blacks were treated less
frequently in an outpatient mental health setting for per-
sonality disorders. However, this disparity was not neces-
sarily reflective of lower incidence rates for personality
disorder diagnoses for Hispanics and non-​Hispanic Blacks.
Manseau and Case indicated that the treatment rates in
this sample could be due to a variety of factors, such as
language barriers, immigration status, patient treatment
preferences, poverty, insurance status, and hospital loca-
tion. Wu et al. (2013) examined Asian Americans, Native
Hawaiians/​ Pacific Islanders, and “mixed-​ race” patients
and found that mixed-​race patients were more likely to
have a personality disorder diagnosis.
Ryder et al. (2015) argued that a dimensional model,
similar to DSM-​5 Section III, could aid in understand-
ing the links between culture and personality disorder.
If the traits demonstrate cross-​ cultural replicability, a
dimensional model would aid in identifying problematic
patterns of personality traits. The traits assessed by the
PID-​5 and FFMPD scales are related conceptually and
empirically to the five-​factor model of general personal-
ity structure (Krueger & Markon, 2014; Widiger et  al.,
474 Schizophrenia and Personality Disorders

2012), which has substantial empirical support for its self-​report inventories, they also require little time on
cross-​cultural application (Allik, 2005). In addition, these the part of the clinician to administer, although they do
maladaptive traits should be examined in context, related vary in the amount of time it can take to score them. The
to local norms, and examined for consequences, which CATI, MMPI-​2, PDQ-​4, and SNAP-​2 must be scored by
requires acknowledgment of the individual’s experience hand (computer scoring systems for the MMPI-​2 do not
beyond dimensional or categorical classifications. include the Morey et al. [1985] scales). One can purchase
a computer scoring system for the OMNI and WISPI-​IV
at an added expense. The PDQ-​4 is the briefest of these
Clinical Utility
self-​report inventories, consisting of only 99 items, and it
Clinical utility concerns ease of usage, communication, is perhaps the most frequently used self-​report inventory
and treatment formulation (Mullins-​Sweatt et al., 2016). in clinical research because it is much shorter than the
Here, emphasis is given to ease of usage and communi- alternative measures. In contrast, the MCMI-​IV is exceed-
cation; treatment planning is discussed in the next sec- ingly difficult to score by hand; a computer scoring system
tion. Administration of a semi-​structured interview will be is available, but it is relatively expensive.
important in clinical situations in which the credibility or The SWAP-​ 200 requires considerably less time to
validity of the assessment might be questioned, such as a complete compared to a semi-​structured interview, as its
forensic or a disability evaluation. The administration of items are rated on the basis of whatever information is
a semi-​structured interview will document that the assess- available to the clinician. No questions are required to be
ment was reasonably comprehensive, replicable, and administered to rank the items. It was for this reason that
objective (Miller et al., 2012). However, semi-​structured the SWAP-​200 was provided a rating of adequate for clini-
interviews require, on average, 2 hours to be administered, cal utility. However, the SWAP-​200 includes more than
which is not realistic (or useful) in clinical practice. Note twice as many items (i.e., 200) as the entire set of DSM-​
that this is a reflection of the constructs being assessed, not 5 Section II personality disorder diagnostic criteria (i.e.,
the instrument providing the assessment. Therefore, the 96). If clinicians routinely fail to consider systematically
routine administration of a semi-​structured interview may the diagnostic criteria currently included within DSM-​
be impractical for general clinical practice. 5 (Garb, 2005), it might not be realistic to expect them
As noted previously, the amount of time required for to assess systematically or carefully a patient with a set of
the administration of a semi-​structured interview can also items that is twice as long.
be reduced substantially by first administering and scor- As suggested previously, the utility of an assessment
ing a self-​report inventory (Miller et al., 2012; Widiger & measure is limited by the utility of the construct being
Boyd, 2009). The administration of the interview could assessed. Verheul (2005) systematically reviewed various
then be confined to the personality disorder scales that components of clinical utility for the personality disor-
were significantly elevated on the self-​report inventory. In der diagnostic categories and suggested that the hetero-
fact, the SCID-​II (First & Gibbon, 2004) and the IPDE geneity of diagnostic membership, the lack of precision
(Loranger, 1999)  include screening measures precisely in description, the excessive diagnostic co-​occurrence,
for this purpose. However, if a self-​report inventory is to the reliance on the “not otherwise specified” wastebas-
be administered, it is preferable to administer one that was ket diagnosis, and the unstable and arbitrary diagnostic
constructed to provide a comprehensive and valid assess- boundaries are sources of considerable frustration for
ment (e.g., PDQ-​4), and for which there is empirical clinicians. Verheul stated, “Overall, the categorical sys-
support for its validity to assess the personality disorders, tem has the least evidence for clinical utility, especially
rather than simply a measure developed for the purpose with respect to coverage, reliability, subtlety, and clini-
of brief screening. cal decision-​making” (p.  295). The DSM-​5 Section III
The CATI, MMPI-​2, OMNI, PDQ-​4, SNAP-​2, and dimensional trait model assessed by the PID-​5 and the
WISPI-​IV traditional self-​report inventories all received FFMPD scales provide more individualized and pre-
a rating of good with respect to clinical utility. Self-​ cise personality profiles and an increased homogeneity
report inventories can be very useful in alerting a clini- of trait constructs that improve considerably the clini-
cian to maladaptive personality functioning that might cal utility of personality disorder assessments (Mullins-​
otherwise have been missed due to false expectations Sweatt & Lengel, 2012). Indeed, studies have directly
or assumptions, such as failing to notice antisocial per- compared the clinical utility as assessed by clinicians
sonality traits in female patients (Miller et al., 2012). As for the DSM-​5 Section II diagnostic categories and the

FFM dimensional trait model. Across a series of studies,
clinicians have considered the FFM trait model to be
preferable to the diagnostic categories for communica-
tion with patients and for ease of usage (Mullins-​Sweatt
& Lengel, 2012). Similar results have been obtained for
the DSM-​5 Section III dimensional trait model (Morey,
Skodol, & Oldham, 2014). Therefore, the FFMPD and
PID-​5 trait-​based self-​report inventories received scores
of excellent.
Overall Evaluation
The strongest statement that can be made in a review
of instruments for the diagnosis of personality disorder
is that there are clearly quite a number of alternative
measures readily available. Regrettably, no single mea-
sure stands out as being clearly preferable to all others.
Semi-​ structured interviews are strongly preferred over
self-​report inventories in research due to their relatively
greater resilience to distortions secondary to comor-
bid disorders (Widiger & Boyd, 2009). However, there
appears to be no clear advantage of one semi-​structured
interview relative to another. The IPDE has more inter-
national application, but its clinical value is limited
by the fact that it requires considerably more time to
administer. The SCID-​II and DIPD are relatively more
straightforward to administer in comparison to the SIDP-​
IV and the PDI-​IV, but the latter could be said to be more
sophisticated in their assessment. Researchers are recom-
mended to obtain copies of at least three of the existing
semi-​structured interviews and base their selection, in
part, on which instrument appears to be best suited for
their particular research needs and interests.
Clinicians are generally recommended to administer
a self-​report inventory first as a screening measure, iden-
tifying which one to four personality disorders should be
emphasized during a subsequent follow-​up interview and
which can be safely ignored. Brief screening measures
can be used for this purpose, but there might be little
advantage to using a screening instrument in preference
to an inventory that was constructed to provide a com-
prehensive and valid assessment. Most of the self-​report
inventories listed in Table 21.1 can be used for this pur-
pose. The PAI is limited by the absence of scales for all
of the personality disorders; quite a number of problems
occur for the MCMI-​IV with respect to test–​retest reli-
ability, gender bias, problematic cut-​off points, and cost;
the OMNI is not as widely used as the other traditional
self-​report measures; the PDQ-​4 is perhaps the weakest
measure with respect to validity (in large part due to its
Personality Disorders 475
brevity); and validity generalization is unavailable for the
others. The FFMPD and PID-​5 (trait-​based self-​report
inventories) can be said to be highly recommended due
to their excellent ratings of internal consistency, con-
struct validity, clinical utility, and positive content validity
scores. These measures are outlined further in the follow-
ing section.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
There are numerous texts with suggestions for the treat-
ment of personality disorders (e.g., Clarkin, Fonagy, &
Gabbard, 2010; First & Tasman, 2006; Oldham, Skodol,
& Bender, 2005; Paris, 2015; Perry, 2014; Widiger, 2012).
Case conceptualization and treatment planning with these
texts are guided by the presence of personality disorders
diagnosed with one or more of the instruments discussed
previously. These texts are based largely on clinical experi-
ences and theoretical speculations. There are few empiri-
cally validated manuals for the treatment of personality
disorders. The American Psychiatric Association has pub-
lished empirically based guidelines for the treatment of
individual mental disorders. Guidelines, however, have
been published for only borderline personality  disorder
(APA, 2001), due in large part to the fact that there is cur-
rently insufficient research to develop empirically based
guidelines for the treatment of dependent, avoidant, obses-
sive–​compulsive, and other personality disorders.
This section is for assessment measures that could be
used to augment diagnostic information to yield a psy-
chological case conceptualization that can be used to
guide decisions on treatment planning beyond that which
is provided simply by a personality disorder diagnosis.
Clinicians do not treat all at once an entire DSM-​5 per-
sonality disorder syndrome, such as borderline. Clinicians
treat individual components of each syndrome (Paris,
2006), such as the dysregulated anger, fragility, anxious
uncertainty, affective dysregulation, oppositionality, and/​
or manipulativeness of persons diagnosed with borderline
personality disorder. Existing measures of the DSM-​ 5
Section II personality disorders do not provide scales for
the assessments of these components (with the excep-
tion of the PAI for the borderline and antisocial person-
ality disorders). However, scales for their assessment are
available in the Dimensional Assessment of Personality
Pathology-​ Basic Questionnaire (DAPP-​ BQ; Livesley &
Jackson, 2009)  and the SNAP-​2 (Clark et  al., 2014), as
well as more recently developed measures of maladaptive
476 Schizophrenia and Personality Disorders

TABLE 21.2  Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

CAT-​PD E A NA NR E E A G
DAPP-​BQ G E NA G E E E E
FFMPD NR E NA NR E E NR E ✓
PID-​5 NR G NA A G E NR E ✓
SNAP-​2 E E NA G G G G E

Note: CAT-​PD = Computerized Adaptive Test of Personality Disorder; DAPP-​BQ = Dimensional Assessment of Personality Psychopathology–​

Basic Questionnaire; FFMPD = Five Factor Model Personality Disorder scales; PID-​5 = Personality Inventory for DSM-​5; SNAP-​2 = Schedule for
Nonadaptive and Adaptive Personality-​2; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

personality traits, including the FFMPD scales (Widiger
et al., 2012), the Computerized Adaptive Test–​Personality
Disorder (CAT-​PD; Simms et  al., 2011), and the PID-​5
(Krueger et al., 2012).
The DAPP-​BQ (Livesley & Jackson, 2009)  includes
18 trait scales (e.g., anxiousness, self-​ harm, intimacy
problems, social avoidance, passive opposition, and inter-
personal disesteem) subsumed within four higher order
domains of emotional dysregulation, dissocial, inhibit-
edness, and compulsivity that align well with the neu-
roticism, antagonism, introversion, and conscientiousness
domains of the FFM, respectively (Clark & Livesley,
2002). The SNAP-​2 (Clark et al., 2014) includes 12 trait
scales (e.g., self-​harm, entitlement, eccentric perceptions,
workaholism, detachment, and manipulation) that are
grouped into the three higher order domains of negative
affectivity, positive affectivity, and constraint that align
well with the neuroticism, extraversion, and conscien-
tiousness domains of the FFM, respectively (Watson,
Clark, & Harkness, 1994). However, factor analyses of the
12 SNAP scales do not appear to yield a three-​factor struc-
ture. Joint factor analyses of the DAPP-​BQ and the SNAP
yield the four-​factor structure (Clark, Livesley, Schroeder,
& Irish, 1996).
The PID-​ 5 provides the official assessment of the
dimensional trait model included within Section III of
the DSM-​5 (APA, 2013a). This dimensional trait model
was first developed through nominations of 37 maladap-
tive traits from DSM-​ 5 work group members regard-
ing respective personality disorders included within
DSM-​ IV-​
TR (APA, 2000; Krueger et  al., 2012). The
number of scales was eventually reduced from 37 to 25
on the basis of factor analyses of the respective scales
within each domain (Krueger et  al., 2012), including
such scales as Anxiousness, Attention-​Seeking, Hostility,
and Suspiciousness. The 25 PID-​5 scales are organized
into five domains of negative affectivity, detachment,
antagonism, disinhibition, and psychoticism that are
explicitly aligned with the FFM (APA, 2013a, p. 773).
Table 21.2 provides a summary of the psychometric
properties of the PID-​5. A variety of reviews are available
that have examined the validity of the PID-​5 as well as the
DSM-​5 Section III trait model (Al-​Dajani, Gralnick, &
Bagby, 2016; Furnham et al., 2014; Hopwood & Sellbom,
2013; Krueger & Markon, 2014; Morey, Benson, Busch,
& Skodol, 2015). These reviews have indicated good
internal consistency, adequate test–​retest reliability, good
content validity, and excellent construct validity. Research
has indicated good to excellent coverage of the variance
within each respective personality disorder (Rojas &
Widiger, 2017). Bach, Markon, Simonsen, and Krueger
(2015) provided a theoretical rationale for the use of
the PID-​5 in clinical practice. Bach et al. demonstrated
how DSM-​5 Section III can aid in case conceptualiza-
tion as well as treatment planning through six case study
examples. Morey, Skodol, and Oldham (2014) compared
directly clinicians’ impressions of the DSM-​5 Section III
trait model for use in treatment planning in comparison
to the DSM-​5 Section II personality disorder syndromes.
The clinicians consistently preferred the trait model.
Al-​Dajani et al., however, suggested that future research
should provide clinicians with a standardized scoring
method, methods of examining profile accuracy, and
a recognized normative sample to effectively interpret
scores.
The CAT-​PD (Simms et  al., 2011)  contains 33 trait
scales organized within five domains of negative emo-
tionality, detachment, antagonism, disconstraint, and
psychoticism that were aligned with the five domains
proposed for DSM-​5 by Widiger and Simonsen (2005)
and, as indicated by Wright and Simms (2014), with the
FFM. The scales of the CAT-​PD are very similar to those
of the PID-​5. In fact, all but three of the PID-​5 scales
are included in the CAT-​PD. The CAT-​PD has more

coverage, in that it includes 33 scales relative to the 25
of the PID-​5, although the CAT-​PD does not appear to
have scales comparable to the PID-​5 Attention-​Seeking,
Perseveration, or Distractibility scales. The PID-​5, in turn,
does not appear to have scales comparable to the CAT-​
PD Cognitive Problems, Domineering, Exhibitionism,
Fantasy Proneness, Health Anxiety, Rudeness, Self-​Harm,
Norm-​Violation, or Workaholism scales.
Psychometric ratings for the CAT-​PD are provided in
Table 21.2. Existing research suggests adequate internal
consistency, excellent coverage of domains included,
adequate convergent and discriminant validity compared
to other trait-​based measures, and adequate generaliza-
tion across different age and gender groups (Crego &
Widiger, 2016; Simms et  al., 2011; Williams & Simms,
2016; Wright & Simms, 2014). Temporal stability of the
domains has not yet been reported. A rating of good was
provided for clinical utility due to the coverage of the
CAT-​PD of largely the same traits as covered by the PID-​
5, albeit no explicit study regarding its clinical utility has
yet been performed.
The FFMPD consists of eight self-​report measures
constructed to assess the DSM-​ 5 Section II personal-
ity disorders from the perspective of the FFM, yielding
a total of 99 scales organized conceptually and empiri-
cally within the five domains of the FFM (Lynam, 2012;
Widiger et al., 2012). Researchers and clinicians can use
a subset of the scales to assess for a particular personality
disorder from the perspective of the FFM (e.g., border-
line; Mullins-​Sweatt et al., 2012) or select scales from a
domain of the FFM (e.g., agreeableness vs. antagonism)
to assess for its maladaptive variants (e.g., Gullibility and
Subservience from agreeableness and Callousness and
Manipulativeness from antagonism).
Each of the FFMPD instruments was constructed by
first identifying which facets of the FFM (as provided
within the NEO Personality Inventory-​Revised [NEO PI-​
R]; Costa & McCrae, 1992)  are most relevant for each
respective personality disorder on the basis of research-
ers’ descriptions of each respective personality disorder
in terms of the FFM (i.e., Lynam & Widiger, 2001),
clinicians’ descriptions of each personality disorder (i.e.,
Samuel & Widiger, 2004), and FFM personality disorder
research (e.g., Samuel & Widiger, 2008). Scales were
then constructed to assess the maladaptive variants of
each facet that were specific to each personality disorder
(e.g., Perfectionism, Workaholism, Punctiliousness, and
Doggedness as maladaptive variants of conscientiousness
for the Five-​ Factor Obsessive–​ Compulsive Inventory;
Samuel, Riddell, Lynam, Miller, & Widiger, 2012).
Personality Disorders 477
Ratings of the psychometric properties of the FFMPD are
presented in Table 21.2. The FFMPD scales were initially
validated by demonstrating convergence with both their
respective parent FFM facet scale and alternative mea-
sures of the respective personality disorder (e.g., Mullins-​
Sweatt et  al., 2012). Finally, each of the measures was
shown to have incremental validity over alternative mea-
sures of these personality disorders (e.g., Samuel et  al.,
2012). Additional validation studies have since been pub-
lished (Bagby & Widiger, in press). These studies have
indicated excellent internal consistency, content validity,
and construct validity as measures of both the FFM and
the respective personality disorder. Crego and Widiger
(2016) demonstrated convergent and discriminant valid-
ity for 36 of the FFMPD scales with the PID-​5 and CAT-​
PD. No studies have yet assessed for test–​retest reliability.
A  number of studies have also indicated that clinicians
consider the constructs assessed by these measures to have
excellent clinical utility relative to the DSM-​5 Section II
personality disorder syndromes with respect to treatment
planning (Mullins-​Sweatt & Lengel, 2012).
A strength of the FFMPD and PID-​5 relative to many
other DSM-​ 5 Section II self-​report inventories is that
through use of the subscales, clinicians or researchers
are able to dismantle the heterogeneous syndromes into
more distinctive component parts. For example, as noted
previously, research has indicated that when treating a
personality disorder, clinicians do not address the entire
personality structure with each intervention (Paris, 2006).
Clinicians focus instead on underlying components,
such as the dysregulated anger, fragility, or the opposi-
tional behavior of an individual diagnosed with border-
line personality disorder. These components are assessed
independently and specifically by the scales of the FFBI
(Mullins-​ Sweatt et  al., 2012), providing considerably
greater utility in clinical practice than that provided by
the more global measures of borderline personality disor-
der (Mullins-​Sweatt & Lengel, 2012).
Overall Evaluation
Recommendations for instruments that would augment
treatment planning and case conceptualization are hin-
dered by the absence of much controlled clinical trials
of manually guided treatment programs for personality
disorders. The general recommendation is for the use
of measures of maladaptive personality structure, coor-
dinated with the DSM-​5 Section II personality disorder
syndromes, which could thereby provide scales for the
assessment of the more precise personality disorder traits
478 Schizophrenia and Personality Disorders

that are a focus of treatment. An advantage of the CAT-​ characteristic manner of thinking, feeling, and relat-
PD, DAPP-​ BQ, FFMPD, PID-​ 5, and SNAP is their ing to others only with respect to the previous week or
assessment of the more precise components. The CAT-​ month. However, a limitation of this proposal is that it
PD, FFMPD, and PID-​5 also contain conceptual and is not really clear what period of time should be speci-
empirical coordination with all five domains of the FFM, fied to accurately document that a maladaptive person-
thereby allowing what is known about the course, etiology, ality trait is now within remission or no longer present.
and outcomes of FFM traits to be applied to the clinical Personality traits vary in the frequency with which they are
assessment. The FFMPD and PID-​5 are highly recom- evident within any particular period of time. Borderline
mended because they also include algorithms to assess self-​destructiveness must be evident for at least 5 years to
a respective personality disorder, with a considerable indicate its presence on the SCID-​5-​PD, but it is unclear
body of research supporting these algorithms (Krueger how long it should not be present to indicate its absence.
& Markon, 2014; Widiger et  al., 2012). These scoring If persons must display self-​destructiveness over a 5-​year
algorithms allow researchers and clinicians to relate their period to indicate the presence of borderline suicidality,
findings for a respective personality disorder to the FFM. perhaps they should also evidence the absence of self-​
destructiveness over a 5-​year period to indicate the suc-
cessful treatment of this borderline suicidality.
ASSESSMENT FOR TREATMENT MONITORING An additional limitation of most of the existing person-
AND TREATMENT OUTCOME ality disorder semi-​structured interviews and traditional
self-​report inventories for the purpose of treatment moni-
This section presents assessment measures and strategies toring and outcome assessment is that they are not well
that can be used to (a) track the progress of treatment and differentiated with respect to the facets or components
(b) evaluate the overall effect of treatment on symptoms, of each personality disorder. What is evident from the
diagnosis, and general functioning. The semi-​structured limited amount of research on the treatment of personal-
interviews and traditional self-​report inventories consid- ity disorders is that this treatment rarely involves a com-
ered within the first section could, again, provide a natu- prehensive or complete cure of the personality disorder
ral choice as treatment outcome measures. However, a (Leichsenring & Leibing, 2003; Perry & Bond, 2000).
significant disadvantage of most of the personality disor- What appears to occur is the resolution of some traits but
der semi-​structured interviews and traditional self-​report the maintenance or continuation of other traits. This sug-
inventories is that they were constructed to assess long-​ gests better utility for measures that assess for the underly-
term functioning, including functioning before the onset ing components of each personality syndrome. Research
of treatment, and may not accurately reflect current on the effectiveness of treatments often focuses on mea-
changes in functioning. For this reason, these instruments surable, behaviorally based outcomes (self-​harm, suicidal
are not included in Table 21.3. thoughts, etc.) rather than other aspects of personality
The semi-​ structured interviews and traditional self-​ disorder symptomology (O’Connell & Dowling, 2014).
report measures could, hypothetically, be modified Effective change occurs with respect to the components
to assess only current or recent functioning, specify- rather than the entire global construct. For example, one
ing, for instance, that the persons should describe their of the empirically supported treatments for borderline

TABLE 21.3  Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

CAT-​PD E A NA NR E E A G G ✓
DAPP-​BQ G E NA G E E E E E ✓
FFMPD NR E NA NR E E NR E E ✓
PID-​5 NR G NA A G E NR E E ✓
SNAP-​2 E E NA G G G G E E ✓

Note:  CAT-​PD  =  Computerized Adaptive Test of Personality Disorder; DAPP-​BQ  =  Dimensional Assessment of Personality Psychopathology–​
Basic Questionnaire; FFMPD = Five Factor Model Personality Disorder scales; PID-​5 = Personality Inventory for DSM-​5; SNAP-​2 = Schedule for
Nonadaptive and Adaptive Personality-​2; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

personality  disorder  (APA, 2001)  is dialectical behavior
therapy (DBT; Linehan, 2015). Research has demon-
strated that DBT is an effective treatment for many of the
components of this personality disorder. DBT has been
particularly effective with respect to decreasing parasui-
cidal behavior, anger hostility, hopelessness, anxiety, and
distress symptoms (Linehan, 2015).
In Section III of the DSM-​5, there are Criterion A and
Criterion B for the personality disorders. For the self
and interpersonal relatedness impairments of Criterion
A, the Level of Personality Functioning Scale (LPFS;
APA, 2013a, p. 775; Bender, Morey, & Skodol, 2011) has
been used in a few studies (e.g., Few et al., 2013; Keeley,
Flanagan, & McCluskey 2014; Morey, Bender, & Skodol,
2013; Zimmerman et  al., 2015). The LPFS provides a
broad assessment of disturbances in self and interpersonal
functioning through a clinician rating form. However,
note that the LPFS does not provide an assessment of
the Criterion A disturbances that are specific to each per-
sonality disorder. For example, moderate impairment in
identity is suggested within the LPFS by “depends exces-
sively on others for identity definition, with compromised
boundary delineation,” “vulnerable self-​esteem controlled
by exaggerated concern about external evaluation, with a
wish for approval,” and “threats to self-​esteem may engen-
der strong emotions such as rage or shame” (APA, 2013a,
p. 776). The LPFS severe impairments are suggestive of
impairments in Section III described for the borderline,
narcissistic, and schizotypal personality disorders, but
they are not particularly indicative of impairments for the
obsessive–​compulsive.
There are also two self-​ report inventories that have
been used as proxy measures for Criterion A: the General
Assessment of Personality Disorders (GAPD; Berghuis,
Kamphuis, Verheul, Larstone, & Livesley, 2013)  and
the Severity Indices for Personality Problems (SIPP-​118;
Verheul et al., 2008). The GAPD includes 19 scales, 15 of
which concern self-​pathology and 4 concern interpersonal
deficits. The SIPP-​118 has 16 scales, organized in the ini-
tial validation study (Verheul et al., 2008) into five domains
of self-​control, identity integration, relational capacities,
responsibility, and social concordance. The GAPD and
SIPP-​118 have both been used to assess for Criterion A (e.g.,
Bastiaansen, De Fruyt, Rossi, Schotte, & Hofmans, 2013;
Berghuis, Kamphuis, & Verheul, 2014; Berghuis et  al.,
2013). However, neither of these measures provides an
explicit assessment of the self and interpersonal dysfunctions
specified for the six personality disorders in Section III.
Regarding the maladaptive traits of Criterion B of
Section III, as previously noted, the CAT-​PD, FFMPD,
Personality Disorders 479
and PID-​ 5 provide precise assessment of a variety of
components that construct the personality disorders (dis-
cussed previously). A strength of the CAT-​PD, FFMPD,
and PID-​5 measures is their coordination with the five
domains of the FFM, thereby allowing what is known
about the course, etiology, and outcomes of FFM traits
to be applied to the clinical assessment. The DAPP-​BQ
(Livesley & Jackson, 2009) and the SNAP-​2 (Clark et al.,
2014) are also clinically useful measures of specific com-
ponents of personality disorder. As previously indicated,
the DAPP-​BQ and the SNAP-​2 were constructed in a
similar manner to provide assessments of the fundamental
dimensions of maladaptive personality functioning that
cut across and define the existing diagnostic categories.
Overall Evaluation
The primary goal for the treatment of a personality dis-
order would naturally be the remission of the personal-
ity disorder. As such, the appropriate treatment outcome
measure might then be a diagnostic measure. However,
many existing instruments are limited in this regard
because they have not yet been modified to assess change
in long-​standing personality traits. An additional limita-
tion is that treatment of personality disorders does not
appear to address the global personality structure, focus-
ing instead on more specific personality traits and com-
ponents of the personality disorders. In this regard, the
CAT-​PD, DAPP-​BQ, FFMPD, PID-​5, and the SNAP-​2
are likely to be better suited as treatment outcome mea-
sures and are highly recommended. Clinicians should
consider these instruments and select which appears to be
best suited to their particular clinical population.
CONCLUSIONS AND FUTURE DIRECTIONS
A considerable amount of attention and research has been
devoted to the assessment and diagnosis of the DSM-​5
Section II personality disorders. Although this chapter
identifies 18 distinct instruments developed that pro-
vide assessments of these personality disorders, a variety
of additional assessments exist. The variety of measures
available is a testament to both the complexity and inter-
est in personality disorder assessment and, regrettably,
potential limitations of each of the existing instruments.
If one instrument was clearly preferable to another, there
would be no need or interest in so many alternative mea-
sures. It is perhaps time to devote research attention to
more direct comparisons of the reliability and validity of
480 Schizophrenia and Personality Disorders
the alternative measures in order to begin to separate the
wheat from the chaff. However, in the absence of a gold
standard for what constitutes an unambiguously valid cri-
terion, comparative research can be difficult to conduct.
It will also be important for future studies to devote
more attention to the construction of measures that could
be used to augment diagnostic information that could
guide decisions on treatment planning and treatment out-
come assessment beyond that which is provided simply by
a personality disorder diagnosis. Progress in such research
is hindered by the virtual absence of studies devoted to
the development and validation of empirically supported
treatments for specific personality disorders. Research on
treatment of personality disorders focuses on borderline,
whereas no randomized controlled or open trial studies
have been conducted on the paranoid, schizoid, schizo-
typal, dependent, narcissistic, or histrionic personality dis-
orders (Leahy & McGinn, 2012).
Hand in hand with the development of such treatment
research, it will be necessary to (a) tackle the thorny issue
of what constitutes successful treatment of personality
disorders and (b) develop, based on this formulation, and
implement measures that are designed to be sensitive to
treatment effects in a clinical setting. The successful treat-
ment of a personality disorder will not be the construction
of an ideal personality structure. One is unlikely to change
a “Theodore Bundy” into a “Mother Teresa.” On the other
hand, given the substantial public health care costs that
can be associated with some of the more dysfunctional per-
sonality disorders (e.g., costs to victims and to law enforce-
ment agencies of persons with an antisocial personality
disorder, and the costs of the many brief hospitalizations of
persons with borderline personality disorder), even mod-
erate improvements in personality functioning can have
substantial personal, social, and public health care ben-
efits (Linehan, 2015). Measures more specifically suited to
these important benefits of personality disorder treatment
need further implementation in a clinical setting.
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 Part VII

Couple Distress and Sexual Disorders

 22
Couple Distress
Douglas K. Snyder
Richard E. Heyman
Stephen N. Haynes
Christina Balderrama-​Durbin
Assessment of couple distress shares basic principles
of assessing individuals—​ namely that (a)  the content
of assessment methods be empirically linked to target
problems, treatment goals, and constructs hypothesized
to be functionally related; (b)  measures and methods
be reliable, valid, and cost-​effective; and (c)  findings be
linked within a theoretical or conceptual framework of
the presumed causes of difficulties, as well as to clini-
cal intervention or prevention. However, couple assess-
ment differs from individual assessment in that couple
assessment strategies (a)  focus specifically on relation-
ship processes and the interactions between individuals;
(b) provide an opportunity for direct observation of target
complaints involving communication and other interper-
sonal exchanges; and (c)  must be sensitive to potential
challenges unique to establishing a collaborative alliance
when assessing highly distressed or antagonistic partners,
particularly in a conjoint context. Similar to the assess-
ment process itself, our discussion of strategies for assess-
ing couple distress is necessarily selective—​emphasizing
dimensions empirically related to couple distress, iden-
tifying alternative methods and strategies for obtaining
relevant assessment data, and highlighting specific tech-
niques within each method.
We begin this chapter by defining couple distress and
noting its prevalence and comorbidity with emotional,
behavioral, and physical health problems of individu-
als in both clinical and community populations. Both
brief screening measures and clinical methods are pre-
sented for diagnosing couple distress in clinical as well as
research applications. The bulk of the chapter is devoted
489
to conceptualizing and assessing couple distress for the
purpose of planning and evaluating treatment. Toward
this end, we review empirical findings regarding behav-
ioral, cognitive, and affective components of couple
distress and specific techniques derived from clinical
interview, behavioral observation, and self-​report meth-
ods. In most cases, these same assessment methods and
instruments are relevant to evaluating treatment progress
and outcomes. We conclude with general recommenda-
tions for assessing couple distress and directions for future
research.
CONCEPTUALIZING COUPLE
RELATIONSHIP DISTRESS
Defining Couple Distress
The fifth edition of the Diagnostic and Statistical Manual
of Mental Disorders (DSM-​ 5; American Psychiatric
Association, 2013)  contains criteria for relationship dis-
tress with spouse or intimate partner to be used when
(a)  the major clinical focus is the subjective experience
of problematic quality in the relationship or (b) the prob-
lematic quality is affecting the course, prognosis, or treat-
ment of a mental or other medical disorder. Potentially
impaired couple functioning criteria include behav-
ioral (e.g., conflict resolution difficulty, withdrawal, and
aggression), cognitive (e.g., chronic negative attributions
or dismissal), or affective (e.g., chronic sadness, apathy,
or anger) domains. The proposed criteria for partner
490 Couple Distress and Sexual Disorders
relational problem in the forthcoming 11th edition of the
International Classification of Disease (ICD-​11; World
Health Organization, 2016)  are similar but more expli-
cated (see Heyman, Slep, & Foran, 2015); for example,
whereas the DSM-​5’s criteria address adverse impacts in
behavioral, cognitive, and affective domains (with exam-
ples), ICD-​11’s criteria include adverse impacts on behav-
ior, cognition, emotion, physical health, interpersonal
interaction, and major life role activities. The DSM-​5 (as
with prior editions) consigns relational problems to the
appendix on Other Conditions and Problems That May
Be a Focus of Clinical Attention or That May Otherwise
Affect the Diagnosis, Course, Prognosis, or Treatment
of a Patient’s Mental Disorder. As discussed in depth
by Heyman and Slep (in press), (a)  the DSM excludes
problems beyond the individual for guild, rather than for
definitional, reasons; (b) decisions regarding the boundary
between normality and pathology are made regularly—​
for both individuals and their behaviors in key contexts
such as relationships; (c) the DSM’s “harm criterion” is
an important innovation that can be used to delineate
the boundary for clinically significant individual and rela-
tional problems; and (d) diagnostic criteria for relational
problems, although not perfect, would still be useful in
operationalizing problems that, as with individual prob-
lems, cause pain, injury, an important loss of freedom,
or death.
Nonetheless, diagnostic systems still do not overtly
recognize subthreshold deficiencies that couples often
present as a focus of concern, including those that detract
from optimal individual or relationship well-​being. These
include deficits in feelings of security and closeness,
shared values, trust, joy, love, physical intimacy, and simi-
lar positive emotions that individuals typically value in
their intimate relationships. Not all such deficits necessar-
ily culminate in “clinically significant” impaired function-
ing or emotional and behavioral symptoms as traditionally
conceived; yet, frequently, these deficits are experienced
as insidious and may culminate in partners’ disillusion or
their dissolution of the relationship. The most positive fea-
tures of the DSM’s conceptualization of partner relational
problems are its emphasis on the interactions between
partners and its recognition that relational problems are
frequently associated with individual symptoms in one or
both partners.
Prevalence and Comorbid Conditions
Clinical interventions targeting couple distress continue
to gain in stature as vital components of mental health
services. Three factors contribute to this growing recogni-
tion: (a) the prevalence of couple distress in both commu-
nity and clinic samples; (b) the impact of couple distress
on both the emotional and the physical well-​being of
adult partners and their offspring; and (c) increased evi-
dence of the effectiveness of couple therapy, not only in
treating couple distress and related relationship problems
but also as a primary or adjunct treatment for a variety
of individual emotional, behavioral, or physical health
disorders (Fischer, Baucom, & Cohen, 2016; Lebow,
Chambers, Christensen, & Johnson, 2012; Roddy,
Nowlan, Doss, & Christensen, 2016; Snyder, Castellani,
& Whisman, 2006).
Couple distress is a prevalent finding in both com-
munity epidemiological studies and research involving
clinical samples. In the United States, the most salient
indicator of couple distress remains a divorce rate of 40%
to 50% among married couples (Kreider & Ellis, 2011),
with about half of these occurring within the first 7 years of
marriage. Independent of divorce, many, if not most, mar-
riages experience periods of significant turmoil that place
partners at risk for dissatisfaction, dissolution, or symp-
tom development (e.g., depression or anxiety); roughly
one-​third of married persons report being in a distressed
relationship (Whisman, Beach, & Snyder, 2008). Data on
the effects of stigma, prejudice, and multiple social stress-
ors experienced by lesbian, gay, and bisexual populations
suggest that same-​sex couples may experience additional
challenges (Meyer, 2003).
In a previous national survey, the most frequently
cited causes of acute emotional distress were couple rela-
tionship problems, including divorce, separation, and
other relationship strains (Swindle, Heller, Pescosolido,
& Kikuzawa, 2000). Couple distress covaries with over-
all life dissatisfaction even more strongly than does dis-
tress in other domains, such as health, work, or children
(Fleeson, 2004). Other studies have indicated that persons
in distressed couple relationships are overrepresented
among individuals seeking mental health services, regard-
less of whether or not they report couple distress as their
primary complaint (Lin, Goering, Offord, Campbell, &
Boyle, 1996). In a study of 800 employee assistance pro-
gram (EAP) clients, 65% rated family problems as “con-
siderable” or “extreme” (Shumway, Wampler, Dersch, &
Arredondo, 2004).
Findings from various national surveys have indicated
that compared to happily married persons, maritally dis-
tressed partners are significantly more likely to have a
mood disorder, anxiety disorder, or substance use disor-
der (McShall & Johnson, 2015; Whisman, 1999, 2007).
 Couple Distress 491

Additional findings from an epidemiological survey in
Ontario, Canada, showed that even when controlling for
distress in relationships with relatives and close friends,
couple distress was significantly correlated with major
depression, generalized anxiety disorder, social and sim-
ple phobia, panic disorder, and alcohol dependence or
abuse (Whisman, Sheldon, & Goering, 2000). Moreover,
couple distress—​particularly negative communication—​
has direct adverse effects on cardiovascular, endocrine,
immune, neurosensory, and other physiological systems
that, in turn, contribute to physical health problems
(Robles, Slatcher, Trombello, & McGinn, 2014). Nor are
the effects of couple distress confined to the adult partners.
Couple distress has been related to a wide range of delete-
rious effects on children, including depression, anxiety,
withdrawal, poor social competence, health problems,
poor academic performance, and a variety of other con-
cerns (Bernet, Wamboldt, & Narrow, 2016; Cummings &
Davies, 2010; Hetherington, Bridges, & Insabella, 1998;
Vaez, Indran, Abdollahi, Jurahi, & Mansor, 2015).
In brief, couple distress has a markedly high preva-
lence; has a strong linkage to emotional, behavioral, and
health problems in the adult partners and their offspring;
and is among the most frequent primary or secondary
concerns reported by individuals seeking assistance from
mental health professionals.
Etiological Considerations and Implications
for Assessment
As noted previously, both the aforementioned comorbidity
findings and clinical observations suggest that couple dis-
tress likely results from, as well as contributes to, emotional
and behavioral problems in one or both partners as well
as their children. However, as a relational (vs. individual)
disorder, understanding a given couple’s distress requires
extending beyond individual considerations to pursue a
broader assessment of the relational and socioecological
context in which couple distress emerges. Snyder, Cavell,
Heffer, and Mangrum (1995) proposed a multitrait, mul-
tilevel assessment model for assessing couple and family
distress comprising five overlapping construct domains
(cognitive, affective, behavioral, interpersonal, and struc-
tural/​developmental) operating at five system levels (indi-
viduals, dyads, the nuclear family, the extended family, and
community/​cultural systems). Table 22.1 (from Abbott &
Snyder, 2010) provides a modest sampling of specific con-
structs relevant to each domain at each system level.

TABLE 22.1   Sample Assessment Constructs Across Domains and Levels of Individual, Couple, and Family Functioning

Extended System
Dyad (Couple, (Family of Origin,
Individual Parent–​Child) Nuclear Family System Friends) Culture/​Community

Cognitive Intelligence; memory Cognitions regarding Shared or co-​ Intergenerational Prevailing societal and
functions; thought self and other constructed patterns of thinking cultural beliefs and
content; thought in relationship; meanings within and believing; co-​ attitudes; ways of
quality; analytic expectancies, the system; family constructed meaning thinking associated
skills; cognitive attributions, ideology or paradigm; shared by therapist with particular
distortions; schemas; attentional biases, thought sequences and family or other religious or ethnic
capacity for self-​ and goals in the between members significant friends or groups that are
reflection and relationship. contributing to family. germane to the
insight. family functioning. family or individual.
Affective/​emotional Mood; affective range, Predominant emotional Family emotional Emotional themes Prevailing emotional
intensity, and themes or patterns themes of fear, and patterns in sentiment in
valence; emotional in the relationship; shame, guilt, extended system; the community,
lability and cohesion; range or rejection; intergenerational culture, and society;
reactivity. of emotional system properties emotional legacies; cultural norms and
expression; of cohesion patterns of fusion or mores regarding
commitment and or emotional differentiation across the expression of
satisfaction in disaffection; generations. emotion.
the relationship; emotional
emotional content atmosphere in the
during conflict; home—​including
acceptance and humor, joy, love, and
forgiveness. affection as well as
conflict and hostility.
(Continued)
492 Couple Distress and Sexual Disorders

TABLE 22.1  Continued

Extended System
Dyad (Couple, (Family of Origin,
Individual Parent–​Child) Nuclear Family System Friends) Culture/​Community

Behavioral Capacity for self-​ Recursive behavioral Repetitive behavioral Behavioral patterns Cultural norms and
control; impulsivity; sequences displayed patterns or sequences displayed by the mores of behavior;
aggressiveness; in the relationship; used to influence extended system behaviors which
capacity to defer behavioral repertoire; family structure (significant friends, are prescribed or
gratification; reinforcement and power; shared family of origin, proscribed by the
substance abuse; contingencies; recreation and other therapist) used larger society.
overall health, strategies used to pleasant activities. to influence the
energy, and drive. control other’s structure and
behavior. behaviors of the
extended system.
Interpersonal/​ Characteristic ways Quality and frequency Information flow in Degree to which Information that is
communication of communicating of the dyad’s the family system; information is shared communicated to the
and interacting communication; paradoxical with and received family or individual
across relationships speaking and messages; family from significant by the community
or personality (e.g., listening skills; system boundaries, others outside the or culture in which
shy, gregarious, how couples share hierarchy, and nuclear family they live; how the
narcissistic, information, express organization; how system or dyad; family or individual
dependent, feelings, and resolve the family system the permeability of communicates their
controlling, conflict. uses information boundaries and the needs and mobilizes
avoidant). regarding its own degree to which the resources.
functioning; family family or couple is
decision-​making receptive to outside
strategies. influences.
Structural/​ All aspects of History of the Changes in the family Developmental changes The cultural and political
developmental physiological relationship and how system over time; across generations; history of the society
and psychosocial it has evolved over current stage in the significant historical in which the family
development; personal time; congruence of family life cycle; events influencing or individual lives;
history that influences partners’ cognitions, stressors related current system current political and
current functioning—​ affect, and behavior. to child-​rearing; functioning (e.g. economic changes;
including psychosocial congruence in death, illness, divorce, congruence of the
stressors; intrapersonal needs, beliefs, and abuse); congruence individual’s or couple’s
consistency of behaviors across family of beliefs and values values with those of
cognitions, affect, and members. across extended social the larger community.
behavior. support systems.

Source: From B. V. Abbott and D. K. Snyder (2010). Couple distress. In M. M. Antony & D. H. Barlow (Eds.), Handbook of Assessment and Treatment
Planning for Psychological Disorders (2nd ed., pp. 439–​476). New York, NY: Guilford Press. Copyright 2010 by Guilford Press. Reprinted with permission
of The Guilford Press.

The relevance of any specific facet of this model to
relationship distress for either partner varies dramati-
cally across couples; hence, although providing guid-
ance regarding initial areas of inquiry from a nomothetic
perspective, the relation of any specific facet to relation-
ship distress for a given individual or couple needs to
be determined from a functional analytic approach and
applied idiographically (Haynes, Mumma, & Pinson,
2009; Haynes, O’Brien, & Kaholokula, 2011). Moreover,
interactive effects occur within domains across lev-
els, within levels across domains, and across levels and
domains. For example, individual differences in emotion
regulation could significantly impact how partners inter-
act when disclosing personal information or attempting to
resolve conflict. Later in this chapter, we highlight more
salient components of this assessment model operating
primarily at the dyadic level as they relate to case concep-
tualization and treatment planning.

ASSESSMENT FOR DIAGNOSIS
A diagnosis of couple distress is based, in part, on the
subjective evaluation of dissatisfaction by one or both
partners with the overall quality of their relationship. By
comparison, relationship dysfunction may be determined
by external evaluations of partners’ objective interactions.
Although subjective and external evaluations frequently
converge, partners may report being satisfied with a rela-
tionship that—​by outsiders’ evaluations—​would be rated
as dysfunctional due to observed deficits in conflict reso-
lution, emotional expressiveness, management of rela-
tionship tasks involving finances or children, interactions
with extended family, and so forth; similarly, partners may
report dissatisfaction with a relationship that to outsiders
appears characterized by effective patterns of interacting
in these and other domains. Discrepancies between part-
ners’ subjective reports and outside observers’ evaluations
may result, in part, from differences in raters’ personal
values, developmental stage, gender, ethnicity, or cultural
perspective (Haynes, Kaholokula, & Tanaka-​Matsumi, in
press) or from a lack of opportunity to observe relatively
infrequent behaviors (e.g., incidents of physical or emo-
tional abuse). To complicate matters, partners themselves
may diverge in their appraisals—​either because of actual
differences in subjective experiences or because of differ-
ences in ability or willingness to convey these experiences.
Some clients may be more forthcoming when responding
to a questionnaire (Whisman & Snyder, 2007)  or when
interviewed individually rather than conjointly with their
partner.
Assessment measures and methods intended to iden-
tify couple distress should be both sensitive (i.e., able to
detect its presence at some operationalized threshold) and
TABLE 22.2   Ratings of Instruments Used for Screening and Diagnosis
Internal Inter-​Rater Test–​Retest
Instrument Norms Consistency Reliability Reliability
SDI-​MD-​PA NR NA E NR
DAS-​7 NR A NA NR
MSI-​B E E NA E E
CSI-​4 A E NA NR
RMICS E E A NR
RCISS E NR A NR
Note: SDI-​MD-​PA = Structured Diagnostic Interview for Marital Distress and Partner Aggression; DAS-​7 = Dyadic Adjustment Scale–​7-​item version;
MSI-​B = Marital Satisfaction Inventory-​Brief; CSI-​4 = Couple Satisfaction Index Scale–​4-​item version; RMICS = Rapid Marital Interaction Coding
System; RCISS = Rapid Couples Interaction Scoring System; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.
Couple Distress 493
specific (i.e., able to distinguish couple distress from other
related or comorbid conditions). For screening purposes,
a brief structured interview may be used to assess over-
all relationship distress and partner violence. Heyman,
Feldbau-​Kohn, Ehrensaft, Langhinrichsen-​Rohling, and
O’Leary (2001) developed a structured diagnostic inter-
view for couple distress (Structured Diagnostic Interview
for Marital Distress and Partner Aggression [SDI-​MD-​
PA]), and Heyman, Slep, Snarr, and Foran (2013) devel-
oped a set of structured diagnostic interviews for partner
physical, emotional, and sexual abuse, all patterned after
the Structured Clinical Interview for the DSM (First,
Gibbon, Spitzer, & Williams, 1997). An initial evalua-
tion of the relationship distress structured interview dem-
onstrated high inter-​rater reliability; moreover, partners’
responses to items presented in this interview showed a
high correspondence with the same items given in the
form of a questionnaire (Table 22.2).
The emphasis on partners’ subjective evaluations of
couple distress has led to development of numerous self-​
report measures of relationship satisfaction and global
affect. There is considerable convergence across mea-
sures purporting to assess such constructs as marital “qual-
ity,” “satisfaction,” “adjustment,” “happiness,” “cohesion,”
“consensus,” “intimacy,” and the like, with correlations
between measures often approaching the upper bounds
of their reliability. Differentiation among such constructs
at a theoretical level often fails to achieve the same opera-
tional distinction at the item-​content level (for an excel-
lent discussion of this issue, see Fincham & Bradbury,
1987). Hence, selection among such measures should
be guided by careful examination of item content (i.e.,
content validity) and empirical findings regarding both
convergent and discriminant validity.
Content Construct Validity Clinical Highly
Validity Validity Generalization Utility Recommended
G G G G ✓
G G NR G
G G G ✓
E G NR G ✓
A G G A ✓
A G G A
494 Couple Distress and Sexual Disorders
Relatively short measures of overall relationship satis-
faction may be useful as diagnostic and screening strate-
gies for couple distress. The most frequently used global
measure of relationship satisfaction in couple research
is the Dyadic Adjustment Scale (DAS; Spanier, 1976),
a 32-​item instrument purporting to differentiate among
four related subscales reflecting cohesion, satisfaction,
consensus, and affectional expression. For abbreviated
screening measures of couple distress, several alterna-
tives are available, including a brief (7-​ item) version
of the DAS (Hunsley, Best, Lefebvre, & Vito, 2001;
Sharpley & Rogers, 1984). More recent global measures
of relationship sentiment include a 10-​ item screening
scale (Marital Satisfaction Inventory-​Brief form [MSI-​B];
Whisman, Snyder, & Beach, 2009)  derived from the
Marital Satisfaction Inventory-​Revised (MSI-​R; Snyder,
1997) and a set of three Couple Satisfaction Index (CSI)
scales constructed using item response theory comprising
32, 16, and 4 items each (Funk & Rogge, 2007).
Despite its widespread use, a review of psychometric
properties reveals important limitations to the DAS. Factor
analyses have failed to replicate its four subscales (Crane,
Busby, & Larson, 1991), and the reliability of the affec-
tional expression subscale is weak. There is no evidence
that the full-​length DAS and similar longer global scales
offer incremental validity above the briefer and more
recent MSI-​B and CSI scales that offer higher precision
of measurement and greater sensitivity for detecting dif-
ferences in relationship satisfaction (Balderrama-​Durbin,
Snyder, & Balsis, 2015).
Because partners frequently present for treatment
together, clinicians have the rare opportunity to observe
the reciprocal social determinants of problem behaviors
without venturing outside the therapy office. Structured
observations constitute a useful assessment method
because they minimize inferences needed to assess behav-
ior, can facilitate formal or informal functional analysis,
can provide an additional method of assessment in a
multimethod strategy (e.g., integrated with interview and
questionnaires), and can facilitate the observation of oth-
erwise difficult to observe behaviors (Haynes et al., 2011;
Heyman & Slep, 2004). We discuss analog behavioral
observation of couple interactions and describe specific
observational coding systems at greater length in the fol-
lowing section on case conceptualization and treatment
planning. However, for purposes of initial screening and
diagnosis, we advocate two approaches to assessing part-
ners’ descriptions of relationship problems, expression of
positive and negative feelings, and efforts to resolve con-
flicts and reach decisions—​the Rapid Marital Interaction
Coding System (RMICS; Heyman, 2004) and the Rapid
Couples Interaction Scoring System (RCISS; Krokoff,
Gottman, & Hass, 1989). Even when not formally cod-
ing couples’ interactions, clinicians’ familiarity with the
behavioral indicators for specific communication pat-
terns previously demonstrated to covary with relationship
accord or distress should facilitate empirically informed
screening of partners’ verbal and nonverbal exchanges.
When a couple presents for therapy with primary
complaints of dissatisfaction in the relationship, screening
for the mere presence of couple distress is unnecessary.
However, there are numerous other situations in which
the practitioner may need to screen for relationship dis-
tress as a contributing or exacerbating factor in patients’
presenting complaints, including mental health profes-
sionals treating individual emotional or behavioral diffi-
culties; physicians evaluating the interpersonal context of
such somatic complaints as fatigue, chronic headaches,
sleep disturbance, alcohol misuse, or difficulties at work;
or emergency room personnel confronting persons with
severe relationship distress culminating in physical vio-
lence and injuries. We advocate a sequential strategy of
progressively more detailed assessment when indicators of
relationship distress emerge (cf. Abbott & Snyder, 2010,
pp. 468–​469):
1. Clinical inquiry as to whether relationship prob-
lems contribute to individual difficulties such as
feeling depressed or anxious, having difficulty
sleeping, abusing alcohol or other substances, or
feeling less able to deal with such stresses as work,
children and family, or health concerns.
2. Alternatively, use of an initial brief screening
measure (e.g., the Couple Satisfaction Index
Scale–​4-​item version [CSI-​4], Dyadic Adjustment
Scale–​7-​item version [DAS-​7], or MSI-​B) having
evidence of both internal consistency and construct
validity.
3. For individuals reporting moderate to high levels of
global relationship distress, following up with more
detailed assessment strategies such as semi-​struc-
tured interviews, analogue behavioral observation,
and multidimensional relationship satisfaction
questionnaires to differentiate among levels and
sources of distress.
Overall Evaluation
When screening for either clinical or research purposes,
we advocate assessment strategies favoring sensitivity over

specificity to minimize the likelihood of overlooking
potential factors contributing to individual or relationship
distress. This implies the initial use of broad screening
items in clinical inquiry or brief self-​report measures with
strong psychometric support—​ along with direct obser-
vation of partner interactions whenever possible—​ and
subsequent use of more extensive narrowband or mul-
tidimensional measures described in the following sec-
tion on treatment planning to pinpoint specific sources
of concern. Initial assessment findings indicating overall
relationship distress need to be followed by idiographic
functional analytic assessment strategies to delineate the
manner in which individual and relationship concerns
affect each other and relate to situational factors (Haynes
et al., 2009).
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
Conceptualizing couple distress for the purpose of plan-
ning treatment requires extending beyond global senti-
ment to assess specific sources and levels of relationship
difficulties, their individual and broader socioecologi-
cal determinants, and their potential responsiveness to
various clinical interventions. We begin our consider-
ation of assessing couple relationships for case concep-
tualization and treatment planning with a discussion
of construct domains particularly relevant to couple
distress—​ including relationship behaviors, cognitions,
and affect—​as well as individual and broader cultural fac-
tors. We follow this with a discussion of various assessment
strategies and methods for evaluating specific constructs
in these domains.
Domains to Target When Evaluating
Couple Distress
Relationship Behaviors
Research examining behavioral components of couple
distress has emphasized two domains:  (a) the rates and
reciprocity of positive and negative behaviors exchanged
between partners (see a review by Salazar, 2015)  and
(b)  communication behaviors related to both emotional
expression and decision-​making. Regarding the former,
distressed partners, compared with nondistressed partners,
(a)  are more hostile; (b)  start their conversations more
hostilely and maintain this hostility during the course
of the conversation; (c)  are more likely to reciprocate
Couple Distress 495
and escalate their partners’ hostility; (d) are less likely to
edit their behavior during conflict, resulting in longer
negative reciprocity loops; (e) emit less positive behavior;
(f) suffer more ill health effects from their conflicts; and
(g) are more likely to show demand ↔ withdraw patterns
(Heyman, 2001). Findings suggest a stronger linkage
for negativity, compared to positivity, to overall couple
distress.
Given the inevitability of disagreements arising in
long-​term relationships, numerous studies have focused
on specific communication behaviors that exacerbate or
impede the resolution of couple conflicts. Most notable
among these are difficulties in articulating thoughts and
feelings related to specific relationship concerns and defi-
cits in decision-​making strategies for containing, reduc-
ing, or eliminating conflict. Gottman (1994) observed that
expression of criticism and contempt, along with defen-
siveness and withdrawal, predicted long-​term distress and
risk for relationship dissolution. Christensen and Heavey
(1990) found that distressed couples were more likely
than nondistressed couples to demonstrate a demand ↔
withdraw pattern in which one person attempts to engage
the partner in relationship exchange and that partner
withdraws, with respective approach and retreat behaviors
progressively intensifying.
Given findings regarding the prominence of negativ-
ity, conflict, and ineffective decision-​ making strategies
as correlates of relationship distress, couple assessment
must address specific questions regarding relationship
behaviors, especially communication behaviors. We list
these here, along with sample assessment methods; in
subsequent sections specifying interview, observational,
and self-​report strategies for assessing couple distress, we
describe these and related methods in greater detail:
1. How frequent and intense are the couple’s conflicts?
How rapidly do initial disagreements escalate into
major arguments? For how long do conflicts persist
without resolution? Both interview and self-​report
measures may yield useful information regarding
rates and intensity of negative exchanges as well as
patterns of conflict engagement. Commonly used
self-​
report measures specific to communication
include the Communication Patterns Questionnaire
(CPQ; Christensen, 1987; Crenshaw, Christensen,
Baucom, Epstein, & Baucom, 2016; see Table
22.3). Couples’ conflict-​resolution patterns may be
observed directly by instructing partners to discuss
problems of their own choosing representative of
both moderate and high disagreement and then
496 Couple Distress and Sexual Disorders

TABLE 22.3   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly

Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Interviews
RQI A A G NR A A G A
Self-​Report Measures
Specific Relationship Behaviors
FAPBI A G NA NR E G A A
CPQ NR G NA A NR G G G
CTS2 NR G NA A A A A G ✓
DCI E G NA G E G G G
Relationship Cognitions
RAM NR G NA G A G NR G
Multidimensional Inventories
MSI-​R E G NA G E E G E ✓
ENRICH G G NA A G A A A
Observational Measures
Affect
BARS A NR A NR A A NR A
SPAFF G NR A G A G G A ✓
Communication (Demand/​Withdraw)
CRS G A G NR A G G A
Communication (Affect)
CRAC G G G A A G G A ✓
IDCS NR NR A NR A G A A
KPI G NR G NR A G E A
Communication (Problem Solving)
COMFI NR NR A NR A A A A
CST G NR G NR A G E A ✓
DISC NR NR A NR A NR A A
LIFE G NR G NR A G A A
VTCS NR NR A NR A G A A
Communication (Power/​Affect)
SCID NR NR A NR A A G A ✓
Support/​Intimacy
SSICS NR NR G NR A G A A ✓
CIBRS U E G NR G G A A

Note: RQI = Relationship Quality Interview; FAPBI = Frequency and Acceptability of Partner Behavior Inventory; CPQ = Communication Patterns
Questionnaire; CTS2 = Conflict Tactics Scale-​Revised; DCI = Dyadic Coping Inventory; RAM = Relationship Attribution Measure; MSI-​R = Marital
Satisfaction Inventory-​Revised; ENRICH = Evaluating and Nurturing Relationship Issues, Communication, Happiness; BARS = Behavioral Affective
Rating System; SPAFF = Specific Affect Coding System; CRS = Conflict Rating System; CRAC = Clinical Rating of Adult Communication Scale;
IDCS = Interactional Dimensions Coding System; KPI = Kategoriensystem für Partnerschaftliche Interaktion; COMFI = Codebook of Marital and
Family Interaction; CST = Communication Skills Test; DISC = Dyadic Interaction Scoring Code; LIFE = Living in Family Environments Coding
System; VTCS = Verbal Tactics Coding Scheme; SCID = System for Coding Interactions in Dyads; SSICS = Social Support Interaction Coding System;
CIBRS = Couples’ Intimate Behavior Rating System; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.

either formally or informally coding these interac-
tions using one of the behavioral coding systems
described later in this chapter.
2. What are common sources of relationship con-
flict? For example, interactions regarding finances,
children, sexual intimacy, use of leisure time, or
household tasks; involvement with others, includ-
ing extended family, friends, or coworkers; and
differences in preferences or core values? In addi-
tion to the clinical interview, numerous self-​report
measures sample sources of distress across a vari-
ety of relationship domains. Among those having
evidence of both reliability and construct validity
are the Frequency and Acceptability of Partner
Behavior Inventory (FAPBI; Doss & Christensen,
2006)  and the MSI-​ R (Snyder, 1997), both of

which are described in greater detail later, along
with other self-​report measures.
3. What resources and deficits do partners dem-
onstrate in problem-​ identification and conflict-​
resolution strategies? Do they engage couple issues
at adaptive levels (i.e., neither avoiding nor dwell-
ing on relationship concerns)? Do partners balance
their expression of feelings with decision-​making
strategies? Are problem-​resolution efforts hindered
by inflexibility or imbalances in power? Do part-
ners offer each other support when confronting
stressors from within or outside their relationship
(e.g., chronic medical or psychological illness of
one partner)? As noted by others (e.g., Bradbury,
Rogge, & Lawrence, 2001; Cutrona, 1996), most
of the interactional tasks developed for use in
couple research have emphasized problem solv-
ing and conflict resolution to the exclusion of tasks
designed to elicit more positive relationship behav-
iors, such as emotional or strategic support. Hence,
when designing interaction tasks for couples, both
clinicians and researchers should include tasks spe-
cifically designed to sample potential positive as
well as negative exchanges. For example, couples
might be asked to discuss a time when one partner’s
feelings were hurt by someone outside the relation-
ship (e.g., a friend or coworker) in order to assess
behaviors expressing understanding and caring,
although few templates with these foci have been
developed and psychometrically evaluated (for an
exception, see Mitchell et al., 2008).
Relationship Cognitions
Social learning models of couple distress have expanded
to emphasize the role of cognitive processes in mediat-
ing the impact of specific behaviors on relationship func-
tioning (Baucom, Epstein, Kirby, & LaTaillade, 2015).
Research in this domain has focused on such factors as
selective attention; attributions for positive and negative
relationship events; and specific relationship assump-
tions, standards, and expectancies. For example, find-
ings indicate that distressed couples often exhibit a bias
toward selectively attending to negative partner behav-
iors and relationship events and ignoring or minimizing
positive events (Sillars, Roberts, Leonard, & Dun, 2000).
Compared to nondistressed couples, distressed partners
also tend to blame each other for problems and to attri-
bute each other’s negative behaviors to broad and stable
traits (Bradbury & Fincham, 1990). Initial negative attri-
butions predict relationship deterioration during the first
Couple Distress 497
4 years of marriage (Lavner, Bradbury, & Karney, 2012).
Distressed couples are also more likely to have unrealis-
tic standards and assumptions about how relationships
should work and lower expectancies regarding a partner’s
willingness or ability to change his or her behavior in
some desired manner (Epstein & Baucom, 2002). Based
on these findings, assessment of relationship cognitions
should emphasize the following questions:
1. Do partners demonstrate an ability to accurately
observe and report both positive and negative rela-
tionship events? For example, partners’ descriptions
and interpretations of couple interactions observed
directly in therapy can be compared to the clini-
cian’s own assessment of these same exchanges.
Partners’ response-​sets when completing self-​report
relationship measures can also be assessed; for
example, the Conventionalization (CNV) scale on
the MSI-​R (Snyder, 1997) assesses the tendency to
distort relationship appraisals in an overly positive
direction.
2. What interpretation or meaning do partners impart
to relationship events? Clinical interviews are
particularly useful for eliciting partners’ subjec-
tive interpretations of their own and each other’s
behaviors; such interpretations and attributions
also frequently are expressed during conflict-​
resolution or other interactional tasks. To what
extent are partners’ negative relationship behaviors
attributed to stable, negative aspects of the partner
versus external or transient events? Self-​report mea-
sures assessing relationship attributions include the
Relationship Attribution Measure (RAM; Fincham
& Bradbury, 1992).
3. What beliefs and expectancies do partners hold
regarding both their own and the other person’s
ability and willingness to change in a manner
anticipated to be helpful to their relationship?
What standards do they hold for relationships
generally?
Relationship Affect
Similar to findings regarding behavior exchange, research
indicates that distressed couples are distinguished from
nondistressed couples by higher overall rates, dura-
tion, and reciprocity of negative relationship affect and,
to a lesser extent, by lower rates of positive relationship
affect. Nondistressed couples show less reciprocity of
positive affect, reflecting partners’ willingness or ability
to express positive sentiment spontaneously independent
498 Couple Distress and Sexual Disorders

of their partner’s affect (Gottman, 1999). By contrast, in reports of distress across most or all domains of
partners’ influence on each other’s negative affect has relationship functioning assessed using self-​report.
been reported for both proximal and distal outcomes. In research applications, ratings of affect by part-
For example, Pasch, Bradbury, and Davila (1997) found ners observing their videotaped interactions may
that partners’ negative mood prior to discussion of a per- provide an additional means of assessing sentiment
sonal issue predicted lower levels of emotional support override. For example, in a study of the effects of
they provided to the other during their exchange. From relationship sentiment override on couples’ percep-
a longitudinal perspective, couples who divorce are dis- tions, partners used an affect-​rating dial to indicate
tinguished from those who remain married by partners’ how positively or negatively they felt during a previ-
initial levels of negative affect and by a stronger linkage of ously videotaped interaction and how they thought
initial negativity to the other person’s negative affect over their partner felt during the interaction (Hawkins,
time (Cook et al., 1995). Gottman (1999) determined that Carrère, & Gottman, 2002).
the single best predictor of couples’ eventual divorce was
the amount of contempt partners expressed in videotaped
Comorbid Individual Distress
interactions. Hence, assessment of couple distress should
evaluate the following: As noted previously when discussing comorbid condi-
tions, there is growing evidence that relationship difficul-
1. To what extent do partners express and reciprocate ties covary with, contribute to, and result from individual
negative and positive feelings about their relation- emotional and behavioral disorders (Lebow et al., 2012;
ship and toward each other? Partners’ reciprocity Snyder & Whisman, 2003). Both clinician reports and
of affect is best evaluated using either structured treatment outcome studies suggest that individual diffi-
or unstructured interactions and coded (either for- culties render couple therapy more difficult or less effec-
mally or informally) using one of the behavioral tive (Allgood & Crane, 1991; Christensen et  al., 2004;
observation systems described later in this section. Dalgleish et  al., 2015; Knobloch-​ Fedders, Pinsof, &
Although much of the couple literature emphasizes Haase, 2015; Northey, 2002; Rowe, Doss, Hsueh, Libet,
negative emotions, positive emotions such as smil- & Mitchell, 2011; Sher, Baucom, & Larus, 1990; Snyder,
ing, laughter, expressions of appreciation or respect, Mangrum, & Wills, 1993; Whisman, Dixon, & Johnson,
comfort or soothing, mutual support or coping, and 1997). Hence, when evaluating couple distress, additional
similar expressions are equally important to assess attention should be given to disorders of individual emo-
through observation or clinical inquiry. tional or behavioral functioning to address the extent to
2. What ability does each partner have to express his which either partner exhibits individual emotional or
or her feelings in a modulated manner? Problems behavioral difficulties potentially contributing to, exacer-
with emotion self-​ regulation may be observed bating, or resulting in part from couple distress. Given the
either in overcontrol of emotions (e.g., an inability association of couple distress with affective disorders and
to access, label, or express either positive or nega- alcohol use, initial interviews of couples should include
tive feelings) or in undercontrol of emotions (e.g., questions regarding suicidality and alcohol or other sub-
the rapid escalation of anger into intense negativ- stance use, as well as brief screening for previous treat-
ity approaching rage, progression of tearfulness ment of emotional or behavioral disorders.
into sobbing, or deterioration in quality of thought When clinical interview suggests potential interac-
secondary to emotional overload). Unregulated tion of relationship and individual dysfunction, focused
negativity culminating in either verbal or physical and brief measures such as those for depression, anxi-
aggression can be assessed through self-​or partner ety, alcohol misuse, or other clinical disorders should
report using the revised version of the Conflict be considered—​ for example, the Beck Depression
Tactics Scale (CTS2; Straus, Hamby, Boney-​ Inventory-​II (BDI-​II; Beck, Steer, & Brown, 1996), the
McCoy, & Sugarman, 1996). Alcohol Use Disorders Identification Test (AUDIT;
3. To what extent does partners’ negative affect gener- Babor, Higgins-​ Biddle, Saunders, & Monteiro, 2001),
alize across occasions? Generalization of negative the Beck Anxiety Inventory (BAI; Beck, Epstein, Brown,
affect can be observed in partners’ inability to shift & Steer, 1988), the Generalized Anxiety Disorder scale
from negative to either neutral or positive affect (GAS-​7; Spitzer, Kroenke, Williams, & Lowe, 2006), or
during the interview or in interactional tasks, or the Symptom Checklist-​90-​Revised (SCL-​90-​R; Derogatis

& Savitz, 1999). It is equally important to assess couples’
strengths and resources across intrapersonal, relationship,
and broader social system levels. These include partners’
ability to limit the impact of individual or couple dysfunc-
tion despite overwhelming stressors, or containing the
generalization of distress to other family members.
Finally, establishing the direction and strength of causal
relations among individual and relationship disorders, as
well as their linkage to situational stressors or buffers, is
crucial for determining both the content and the sequenc-
ing of clinical interventions. This includes the linkage of
adult relationship conflict to child behavior problems. In
many cases, such functional relations are reciprocal—​
supporting interventions at either end of the causal chain.
Cultural Differences in Couple Distress
Consistent with our conceptual framework, cultural dif-
ferences in the development, subjective experience, overt
expression, and treatment of couple distress are critical to
evaluate. By this we refer not only to cross-​national differ-
ences in couples’ relationships but also to cross-​cultural
differences within nationality and consideration of nontra-
ditional relationships including gay and lesbian couples.
There can be important differences among couples as a
function of their race/​ethnicity, culture, religious orien-
tation, economic level, and age. These dimensions can
affect the importance of the couple relationship to a part-
ner’s quality of life, their expectancies regarding marital
and parenting roles, typical patterns of verbal and nonver-
bal communication and decision-​making within the fam-
ily, the behaviors that are considered distressing, sources
of relationship conflict, the type of external stressors faced
by a family, and the ways that partners respond to couple
distress and divorce (e.g., Diener, Gohm, Suh, & Oishi,
2000; Gohm, Oishi, Darlington, & Diener, 1998; Jones
& Chao, 1997; Kline et al., 2012; Lam et al., 2015). For
example, Haynes and colleagues (1992) found that parent-
ing, extended family, and sex were less strongly related to
marital satisfaction whereas health of the spouse and other
forms of affection were more important factors in marital
satisfaction in older (i.e., older than age 55  years) com-
pared to younger couples. Similarly, Bhugra and De Silva
(2000) suggested that relationships with extended fam-
ily members might be more important in some cultures.
Also, when partners are from different cultures, cultural
differences and conflicts can be a source of relationship
dissatisfaction (e.g., Baltas & Steptoe, 2000). An important
implication of such findings is that measures shown to be
valid for one population may be less so for another.
Couple Distress 499
Culturally sensitive assessment in couple/​ family,
forensic, intellectual, school, and psychiatric contexts has
been the topic of hundreds of articles and book chapters,
which have highlighted cross-​cultural similarities and dif-
ferences in behavior, sources of distress, values, and beliefs
(e.g., Lim, 2015). Implications for couple assessment
from cross-​cultural research are consistent with the idio-
graphic approach to assessment emphasized previously in
this chapter, particularly sensitivity to and respect for indi-
vidual differences in the factors that affect a couple’s rela-
tionship satisfaction and treatment goals. Because norms
for measures can differ across cultures, case formulation,
treatment planning, and treatment outcome monitoring
may benefit from greater attention to elements within
scales than to scale scores when a self-​report instrument is
used to assess couples who differ in potentially important
ways from the original development sample.
Assessment Strategies and Methods for Evaluating
Couple Distress
Assessment strategies for evaluating relationships vary
across the clinical interview, observational methods, and
self-​and other-​report measures. In the sections that follow,
we discuss empirically supported techniques within each
of these assessment strategies. Although specific techniques
within any method could target diverse facets of individual,
dyadic, or broader system functioning, we emphasize those
more commonly used when assessing couple distress.
The Clinical Interview
The pretreatment clinical interview is the first step in
assessing couples. It can aid in identifying a couple’s
behavior problems and strengths, help specify a couple’s
treatment goals, and be used to acquire data that are useful
for treatment outcome evaluation. The assessment inter-
view can also serve to strengthen the couple–​clinician
relationship, identify barriers to treatment, and increase
the chance that the couple will participate in subsequent
assessment and treatment tasks. Furthermore, it is the
primary means of gaining a couple’s informed consent
about the assessment–​treatment process. Data from initial
assessment interviews also guide the clinician’s decisions
about which additional assessment strategies may be most
useful; for example, Gordis, Margolin, and John (2001)
used an interview to select topics for discussion during
an analogue behavioral observation of couple communi-
cation patterns. Perhaps most important, the assessment
interview can provide a rich source of hypotheses about
500 Couple Distress and Sexual Disorders
factors that may contribute to the couple’s distress. These
hypotheses contribute to the case formulation, which in
turn affects decisions about the best treatment strategy for
a particular couple.
The interview can also be used to gather informa-
tion on multiple levels, in multiple domains, and across
multiple response modes in couple assessment. It can
provide information on the specific behavioral interac-
tions of the couple, including behavioral exchanges and
violence; problem-​solving skills, sources of disagreement,
areas of satisfaction and dissatisfaction, and each partner’s
thoughts, beliefs, and attitudes; and their feelings and
emotions regarding the partner and the relationship. The
couple assessment interview can also provide information
on cultural and family system factors and other events that
might affect the couple’s functioning, treatment goals, and
response to treatment. These factors might include inter-
actions with extended family members, other relationship
problems within the nuclear family (e.g., between parents
and children), economic stressors, and health challenges.
The initial assessment interview can also provide informa-
tion on potentially important causal variables for couple
distress at an individual level, such as a partner’s substance
use, mood disorder, or problematic personality traits.
Moreover, the clinical interview can be especially use-
ful in identifying functional relations that may account for
relationship difficulties. The functional relations of great-
est interest in couple assessment are those that are relevant
to problem behaviors, feelings, and relationship enhance-
ment. Identifying functional relations allows the assessor
to hypothesize about “why” a partner is unhappy or what
behavioral sequences lead to angry exchanges. Clinicians
are interested, for example, in finding out what triggers a
couple’s arguments and what communication patterns lead
to their escalation. What does one partner do, or not do,
that leads the other partner to feel unappreciated or angry?
In the previous section on screening and diagnosis, we
discussed a brief structured interview for identifying over-
all relationship distress and partner aggression. Various
formats for organizing and conducting more extensive
assessment interviews with couples have been proposed
(cf., Abbott & Snyder, 2010; Epstein & Baucom, 2002;
Gottman, 1999; Karpel, 1994; L’Abate, 1994). For exam-
ple, Karpel suggested a four-​part evaluation that includes
an initial meeting with the couple together, followed by
separate sessions with each partner individually and then
an additional conjoint meeting with the couple. Abbott
and Snyder recommended an extended initial assess-
ment interview lasting approximately 2 hours in which
the following goals are stated at the outset: (a) first getting
to know each partner as an individual separate from the
marriage; (b)  understanding the structure and organiza-
tion of the marriage; (c) learning about current relation-
ship difficulties, their development, and previous efforts
to address these; and (d) reaching an informed decision
together about whether to proceed with couple therapy
and, if so, discussing respective expectations.
Despite many strengths of the assessment interview, a
major drawback is that few of the comprehensive formats
have undergone rigorous psychometric evaluation. All
have face validity, but most have little empirical evidence
regarding their temporal reliability, internal consistency,
inter-​rater agreement, content validity, convergent valid-
ity, sources of error, and generalizability across sources
of individual differences such as ethnicity and age. One
recent exception is the Relationship Quality Interview
(RQI; Lawrence et al., 2011), a semi-​structured interview
designed to obtain objective ratings in various domains
of couple functioning, including (a) quality of emotional
intimacy, (b)  quality of the couple’s sexual relationship,
(c)  quality of support transactions, (d)  the couple’s abil-
ity to share power, and (e) conflict/​problem-​solving inter-
actions. The RQI has demonstrated good reliability and
validity in samples of both married and dating couples.
The clinical literature reflects considerable diver-
gence on the issue of whether initial assessment of couple
distress should be conducted with partners conjointly
or should also include individual interviews with part-
ners separately. Arguments for the latter include con-
siderations of both veridicality and safety, particularly
when assessing such sensitive issues as intimate partner
violence (IPV), substance abuse, or sexual interactions
(Haynes, Jensen, Wise, & Sherman, 1981; Whisman &
Snyder, 2007). Research indicates that couples experi-
encing IPV often do not spontaneously disclose IPV in
early interviews due to embarrassment, minimization, or
fear of retribution (Ehrensaft & Vivian, 1996), but they
do disclose when asked directly (sometimes disclosing in
the interview when they did not on an IPV questionnaire
(e.g., O’Leary, Vivian, & Malone, 1992). Moreover, risks
of retaliatory aggression against one partner by disclosing
the other’s violence in conjoint interview argue for the
importance of conducting inquiries concerning IPV in
individual interviews.
Arguments against individual interviews when assessing
couple distress emphasize potential difficulties in conjoint
therapy if one partner has disclosed information to the ther-
apist about which the other partner remains uninformed.
Of particular concern are disclosures regarding IPV
(Aldarondo & Straus, 1994; Rathus & Feindler, 2004) and
 Couple Distress 501

sexual infidelity (Snyder & Doss, 2005; Whisman &
Wagers, 2005). Hence, if separate interviews are conducted
with partners as a prelude to conjoint couple therapy, the
interviewing clinician needs to be explicit with both part-
ners ahead of time regarding conditions under which infor-
mation disclosed by one partner will be shared with the
other and also any criteria for selecting among individual,
conjoint, or alternative treatment modalities.
Observational Methods
As noted previously, couple assessment offers the unique
opportunity to observe partners’ communication and
other interpersonal exchanges directly. Like interviews
and self-​report methods, analogue behavioral observa-
tion (ABO) describes a method of data collection; spe-
cifically, it involves a situation designed, manipulated,
or constrained by a clinician that elicits both verbal and
nonverbal behaviors of interest, such as motor actions,
verbalized attributions, affect, and observable facial and
other behavioral reactions (Heyman & Slep, 2004). We
previously identified both the RMICS and the RCISS as
rapid observational methods particularly useful for ini-
tial screening and diagnosis of couple distress. Detailed
descriptions and psychometric reviews of additional
couple coding systems have been published previously
(Heyman, 2001; Kerig & Baucom, 2004). Although these
systems vary widely, in general they reflect six major a
priori classes of targeted behaviors:
1. Affect (e.g., humor, affection, anger, criticism, con-
tempt, sadness, and anxiety):  Examples include
the Behavioral Affective Rating System (BARS;
Johnson, 2002)  and the Specific Affect Coding
System (SPAFF; Gottman, McCoy, Coan, &
Collier, 1996; Shapiro & Gottman, 2004).
2. Behavioral engagement (e.g., demands, pressures
for change, withdrawal, and avoidance): An exam-
ple is the Conflict Rating System (CRS; Heavey,
Christensen, & Malamuth, 1995).
3. General communication skills (e.g., involvement, ver-
bal and nonverbal negativity and positivity, and infor-
mation and problem description): Examples include
the Clinician Rating of Adult Communication
(CRAC; Basco, Birchler, Kalal, Talbott, & Slater,
1991), the Interactional Dimensions Coding
System (IDCS; Kline et  al., 2004), and the
Kategoriensystem für Partnerschaftliche Interaktion
(KPI; Hahlweg, 2004).
4. Problem solving (e.g., self-​ disclosure, validation,
facilitation, and interruption):  Examples include
the Codebook of Marital and Family Interaction
(COMFI; Notarius, Pellegrini, & Martin, 1991),
the Communication Skills Test (CST; Floyd,
2004), the Dyadic Interaction Scoring Code
(DISC; Filsinger, 1983), the Living in Family
Environments (LIFE) coding system (Hops, Davis,
& Longoria, 1995), and the Verbal Tactics Coding
Scheme (VTCS; Sillars, 1982).
5. Power (e.g., verbal aggression, coercion, and
attempts to control):  An example is the System
for Coding Interactions in Dyads (SCID; Malik &
Lindahl, 2004).
6. Support/​ intimacy (e.g., emotional and tangible
support, and attentiveness):  Examples are the
Social Support Interaction Coding System (SSICS;
Pasch, Harris, Sullivan, & Bradbury, 2004)  and
the Couples’ Intimate Behavior Rating System
(CIBRS; Mitchell et al., 2008).
Psychometric characteristics for the 16 couple coding
systems summarized in Tables 22.2 through 22.4 indicate

TABLE 22.4   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation

Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly

Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

DAS A G NA G A A G G A
CSI-​16 A E NA NR E G NR E G ✓
MSI-​B E E NA E E G G E G ✓
MSI-​R E G NA G E E G G E ✓
RMICS E E A NR A G G A A ✓
GAS NA A NA NR G G NR A A

Note:  DAS  =  Dyadic Adjustment Scale; CSI-​16  =  Couple Satisfaction Index Scale–​16-​item version; MSI-​B  =  Marital Satisfaction Inventory-​Brief;
MSI-​R = Marital Satisfaction Inventory-​Revised; RMICS = Rapid Marital Interaction Coding System; GAS = Goal Attainment Scaling; A = Adequate;
G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.
502 Couple Distress and Sexual Disorders
considerable variability in the extent to which informa-
tion regarding reliability, validity, and treatment sensitivity
for each system has been accrued. For example, only 4 of
16 coding systems report data concerning internal consis-
tency, although this likely reflects systems’ emphasis on
specific behaviors rather than broader constructs. When
superordinate classes of behavior (e.g., positive or nega-
tive) are of interest, internal consistency should be evalu-
ated by using either Cronbach’s alpha or indices derived
from factor analysis (Heyman, Eddy, Weiss, & Vivian,
1995). (See also Haynes, 2001, for an overview of critical
dimensions of psychometric evaluation of ABO methods.)
Stable estimates of behavioral frequencies may
require extended observation depending on the base rate
of their occurrence—​for example, as few as 2 minutes
for frequent behaviors but 30 minutes or longer for infre-
quent behaviors (Heyman et  al., 2001). Inter-​rater reli-
ability for nearly all coding systems reviewed here was
adequate or better following coder training, although
the more comprehensive or complicated the system, the
more difficult it is to obtain high inter-​rater reliability.
Few studies have been conducted on the temporal stabil-
ity of observed couple behaviors across tasks or settings.
However, the limited evidence suggests that couples’
interactions do not vary significantly based on topic diffi-
culty (Sanford, 2003) but are influenced by setting (e.g.,
home vs. clinic or research laboratory) and length of
marriage (with longer married couples exhibiting more
enduring patterns; Gottman & Levenson, 1999; Lord,
1999; Wieder & Weiss, 1980).
Although varying in their emphasis, each of the couple
coding systems reviewed here clearly assesses constructs
related to communication and other domains of partner
interaction relevant to relationship functioning and cou-
ple distress. Many of the coding systems can trace their
origins—​directly or indirectly—​to a single source:  the
Family Interaction Coding System (Patterson, Ray, Shaw,
& Cobb, 1969; Reid, 1978), which was developed from nat-
uralistic observations of family members’ behaviors in the
home. Nearly all coding systems have accrued evidence
of discriminative validity and relatedness to independent
measures of similar constructs, and only the most recently
developed systems have yet to accrue evidence of valid-
ity generalization. Pre-​and post-​treatment data for couple
behavioral coding systems are limited, in part because
of fewer funded clinical trials of couple therapy during
the past two decades. However, the Marital Interaction
Coding System (MICS) and Couples Interaction Scoring
System (CISS) have evidence of treatment sensitivity; it
is reasonable to infer that their quicker versions (RMICS
and RCISS) and coding systems that measure similar con-
structs (i.e., most of the communication-​oriented systems)
would demonstrate similar levels of treatment sensitivity.
Concerns have been raised about the clinical utility of
ABO (e.g., Mash & Foster, 2001) because nearly all cod-
ing systems require extensive observer training to reach
adequate levels of interobserver agreement. Even after
observers are certified as being able to code data reliably, a
great deal of energy is required to maintain reliability (e.g.,
weekly meetings with regular feedback on agreement).
Thus, even if clinicians expended a great deal of time
learning a system to the point of mastery (i.e., meeting the
reliability criterion), their reliability would naturally decay
without ongoing efforts to maintain agreement. Such a
requirement is likely not reasonable for most clinicians.
However, even if not striving to code behavioral
observations in the manner required for scientific study
of couple interactions, the empirically informed use of
behavioral observations should be standard in clinicians’
assessment of couple distress. That is, collecting com-
munication samples is an important part of couple clini-
cal assessment because “communication is the common
pathway to relationship dysfunction because it is the com-
mon pathway for getting what you want in relationships.
Nearly all relationship-​relevant conflicts, emotions, and
neuroses are played out via observable communication—​
either verbally or nonverbally” (Heyman, 2001, p. 6).
If questionnaire or interview assessments suggest
that an interactive task may place one or both partners
in danger (e.g., if there is a history of serious physical or
emotional IPV, indications of severe power or control
dynamics, or threats conveyed to the assessor), ABO would
be contraindicated. However, if it seems reasonable that it
is safe to proceed, then the clinician should hypothesize
which classes of behaviors seem most highly connected
to the target problems. Wherever possible, ABOs should
be video-​recorded so that the sample can be reviewed
later with an eye toward a class of behaviors other than
what was the assessor’s primary focus during the in vivo
ABO. Furthermore, unless the clinician can rule out a
plausible connection between conflict communication
and the couple’s problems, we recommend that a con-
flict communication ABO be collected. Based on findings
from observational research with couples, Heyman (2001)
suggested that clinicians use behavioral observations in
assessing couple distress to address the following:
1. How does the conversation start? Does the level of
anger escalate? What happens when it does? Does
the couple enter repetitive negative loops?

2. Do partners indicate afterward that what occurred
during the conversations is typical? Is their behavior
stable across two or more discussions?
3. Do partners’ behaviors differ when it is one part-
ner’s topic versus the other’s? Do they label the
other person or the communication process as the
problem?
4. What other communication behaviors—​ either
positive (e.g., support and empathic reflection)
or negative (e.g., criticism, sneers, and turning
away)—​ appear functionally related to partners’
ability to discuss relationship issues effectively?
Self-​and Other-​Report Methods
The rationale underlying self-​report methods in couple
assessment is that such methods (a)  are convenient and
relatively easy to administer; (b) are capable of generating
a wealth of information across a broad range of domains
and levels of functioning germane to clinical assessment
or research objectives, including those listed in Table 22.1;
(c) lend themselves to collection of data from large nor-
mative samples that can serve as a reference for interpret-
ing data from individual respondents; (d) allow disclosure
about events and subjective experiences that respondents
may be reluctant to discuss with an interviewer or in the
presence of their partner; and (e) can provide important
data concerning internal phenomena opaque to observa-
tional approaches, including thoughts and feelings, values
and attitudes, expectations and attributions, and satisfac-
tion and commitment.
However, the limitations of traditional self-​report mea-
sures also bear noting. Specifically, data from self-​report
instruments can (a) reflect bias in self-​and other-​reporting
in either a favorable or an unfavorable direction, (b)  be
affected by differences in stimulus interpretation and
errors in recollection of specific events, (c) inadvertently
influence respondents’ non-​test behavior in unintended
ways (e.g., by sensitizing respondents and increasing their
reactivity to specific issues), and (d)  typically provide
few fine-​grained details concerning moment-​to-​moment
interactions compared with ABOs.
We describe here, and summarize in Table 22.3,
a small subset of self-​report instruments selected on
the basis of their potential clinical utility and at least
moderate evidence of reliability and validity. In some
domains (e.g., relationship cognitions and affect), well-​
validated measures are few. Additional measures iden-
tified in previous reviews (Epstein & Baucom, 2002;
Sayers & Sarwer, 1998; Snyder, Heyman, Haynes,
Couple Distress 503
Carlson, & Balderrama-​Durbin, in press) or in compre-
hensive bibliographies of self-​report couple and fam-
ily measures (e.g., Corcoran & Fischer, 2000; Davis,
Yarber, Bauserman, Schreer, & Davis, 1998; Hamilton
& Carr, 2016; L’Abate & Bagarozzi, 1993; Touliatos,
Perlmutter, Straus, & Holden, 2001)  may be consid-
ered as additional clinical resources; however, the data
they generate should generally be regarded as similar
to data generated from other self-​reports derived from
interview—​namely as subject to various potential biases
of observation, recollection, interpretation, and motiva-
tions to present oneself or one’s partner in a favorable or
unfavorable light.
A variety of self-​report measures have been developed
to assess couples’ behavioral exchanges including com-
munication, verbal and physical aggression, and physical
intimacy. The FAPBI (Doss & Christensen, 2006) assesses
20 positive and negative behaviors in four domains (affec-
tion, closeness, demands, and relationship violations)
and possesses excellent psychometric characteristics. As
a clinical tool, the FAPBI has the potential to delineate
relative strengths and weaknesses in the relationship—​
transforming diffuse negative complaints into specific
requests for positive change.
Among self-​ report measures specifically targeting
partners’ communication, two that have demonstrated
good reliability and validity are the CPQ (Christensen,
1987)  and the Marital Communication Inventory
(Bienvenu, 1970). The CPQ was designed to measure
the temporal sequence of couples’ interactions by solic-
iting partners’ perceptions of their communication pat-
terns before, during, and following conflict. Scores on the
CPQ can be used to assess characteristics of the demand
↔ withdraw pattern frequently observed among distressed
couples. A more recent measure assessing both commu-
nication and coping, the Dyadic Coping Inventory (DCI;
Bodenmann, 2008; Randall, Hilpert, Jimenez-​ Arista,
Walsh, & Bodenmann, 2016), contains 37 items assessing
(a) one’s own coping, (b) one’s perception of one’s part-
ner’s stress communication, (c) supportive dyadic coping,
and (d)  negative dyadic coping, in close relationships
when one or both partners are stressed.
Assessing relationship aggression by self-​report mea-
sures assumes particular importance because of some
individuals’ reluctance to disclose the nature or extent
of such aggression during an initial conjoint interview.
By far the most widely used measure of couples’ aggres-
sion is the CTS2 (Straus et al., 1996), assessing various
modes of conflict resolution (reasoning, verbal aggres-
sion, and physical aggression), as well as levels of sexual
504 Couple Distress and Sexual Disorders
coercion and physical injury. A measure of psychological
aggression demonstrating strong psychometric properties
and gaining increasing support is the Multidimensional
Measure of Emotional Abuse (MMEA; Murphy &
Hoover, 1999). An additional measure of relationship
aggression, the Aggression (AGG) scale of the MSI-​R
(Snyder, 1997), comprises 10 items reflecting psychologi-
cal and physical aggression experienced from one’s part-
ner. Advantages of the AGG scale as a screening measure
include its relative brevity and its inclusion in a multidi-
mensional measure of couples’ relationships (the MSI-​R)
described later.
Previously, we noted the importance of evaluating
partners’ attributions for relationship events. The RAM
(Fincham & Bradbury, 1992)  presents hypothetical
situations and asks respondents to generate responsi-
bility attributions indicating the extent to which the
partner intentionally behaved negatively, was selfishly
motivated, and was blameworthy for the event. Both
causal and responsibility attributions assessed by the
RAM have evidence of good internal consistency and
test–​retest reliability, as well as convergence with part-
ners’ self-​reported overall relationship satisfaction and
observed affect.
For purposes of case conceptualization and treatment
planning, well-​constructed multidimensional measures
of couple functioning are useful for discriminating
among various sources of relationship strength, con-
flict, satisfaction, and goals. Widely used in both clini-
cal and research settings is the MSI-​R (Snyder, 1997), a
150-​item inventory designed to identify both the nature
and the intensity of relationship distress in distinct
areas of interaction. The MSI-​R includes two validity
scales, one global scale, and 10 specific scales assessing
relationship satisfaction in such areas as affective and
problem-​ solving communication, aggression, leisure
time together, finances, the sexual relationship, role
orientation, family of origin, and interactions regarding
children. More than 30 years of research has supported
the reliability and construct validity of the MSI-​R scale
scores (Snyder et  al., 2004). The instrument boasts a
large representative national sample, evidence of good
internal consistency and test–​retest reliability, and evi-
dence of excellent sensitivity to treatment change. The
Global Distress Subscale (GDS) of the MSI-​R has been
shown to predict couples’ likelihood of divorce 4  years
following therapy (Snyder, 1997). A  validation study
using a national sample of 60 marital therapists sup-
ported the overall accuracy and clinical utility of the
computerized interpretive report for this instrument
(Hoover & Snyder, 1991). Recent studies suggest the
potential utility of Spanish, German, Italian, French,
Chinese, Korean, and Arabic adaptations of the MSI-​R
for cross-​cultural application with both clinic and com-
munity couples (Antonelli, Dettore, Lasagni, Snyder, &
Balderrama-​Durbin, 2014; Balderrama-​Durbin, Snyder,
& Semmar, 2011; Brodard et al., 2015; Gasbarrini et al.,
2015; Kwon & Choi, 1999; Lou, Lin, Chen, Balderrama-​
Durbin, & Snyder, 2016; Reig-​Ferrer, Cepeda-​Benito, &
Snyder, 2004), as well as use of the original English ver-
sion with nontraditional (e.g., gay and lesbian) couples
(Means-​Christensen, Snyder, & Negy, 2003).
Additional multidimensional measures obtaining
fairly widespread use are the PREPARE and ENRICH
inventories (Fowers & Olson, 1989, 1992; Olson &
Olson, 1999), developed for use with premarital and
married couples, respectively. Both of these measures
include 165 items in 20 domains reflecting personal-
ity (e.g., assertiveness and self-​ confidence), intraper-
sonal issues (e.g., marriage expectations and spiritual
beliefs), interpersonal issues (e.g., communication and
closeness), and external issues (e.g., family and friends).
A  computerized interpretive report identifies areas of
“strength” and “potential growth” and directs respon-
dents to specific items reflecting potential concerns. The
ENRICH inventory has a good normative sample and
has ample evidence supporting both the reliability and
the validity of scores on its subscales.
Overall Evaluation
Couples presenting for therapy vary widely in both the
content and the underlying causes of their individual and
relationship problems, as well as their treatment goals.
Conceptualizing partners’ distress and planning effective
treatment require careful assessment of behavioral, cogni-
tive, and affective components of relationship functioning
conducted across multiple modalities and using multiple
methods, including interview, ABO, and self-​report mea-
sures. Effective intervention depends on assimilating
assessment findings within an overarching theoretical
framework linking individual and relationship difficulties
to presumed etiologies as well as to clinical intervention.
Toward this end, assessment of couple distress requires
going beyond nomothetic conclusions derived from stan-
dardized measures of relationship functioning to integrate
idiographic findings from multiple sources and methods
in a functional analytic approach (Haynes et al., 2009).

ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
In principle, assessment strategies relevant to case concep-
tualization and treatment planning are also germane to
monitoring treatment progress and evaluating outcome.
It would be difficult to imagine adequate assessment of
partners’ changes in individual and relationship function-
ing not including clinical inquiry about alterations in
behavioral, cognitive, and affective domains outside of
treatment sessions; repeated ABOs to track the acquisition
and use of targeted communication skills; and integration
of self-​report measures profiling changes across diverse
domains and providing information in sensitive areas.
Several caveats moderate this general conclusion.
First, the use of repeated assessments to evaluate changes
attributable to treatment requires that measures dem-
onstrate temporal reliability in the absence of clinical
intervention. Although obvious as a precondition for
interpreting change, information regarding the tempo-
ral reliability of couple-​based assessment techniques is
remarkably sparse. Second, treatment effects are best
assessed by using measures both relevant and specific
to aspects of individual and relationship functioning tar-
geted by clinical interventions. Finally, treatment moni-
toring across sessions imposes pragmatic constraints on
measures’ length, thus suggesting enhanced utility for
measures that have evidence of score reliability and valid-
ity and are distinguished by their brevity (e.g., the MSI-​B
or CSI-​16 as a measure of global affect or the FAPBI to
assess more specific dyadic behaviors). Table 22.4 pro-
vides ratings on several relevant instruments.
Changes in individualized treatment goals can be
quantified using goal attainment scaling (GAS; Kiresuk,
Smith, & Cardillo, 1994)  as described previously for
use in couple therapy by Whisman and Snyder (1997).
When adopting the GAS method, the issues that will
be the focus of treatment are first identified, and then
each problem is translated into one or more goals. The
expected level of outcome is then specified for each goal,
along with the “somewhat more” and “much more” than
expected levels of outcome, as well as the “somewhat
less” and “much less” than expected levels. Each level of
outcome is assigned a value on a 5-​point measurement
scale ranging from –​2 for much less than expected level
of outcome to +2 for much more than expected level of
outcome. Levels of outcome can then be rated during or
following treatment, and the ratings across goals can be
averaged to provide a summary score for evaluating the
Couple Distress 505
degree to which treatment helped the couple attain their
own individualized goals.
Overall Evaluation
Gains or deterioration in individual and relationship
functioning should be evaluated using techniques sensi-
tive and specific to treatment effects across assessment
modalities incorporating interview, behavioral observa-
tion, and self-​report methods. Conclusions drawn from
nomothetic approaches (e.g., the DAS or MSI-​R) should
be complemented by idiographic methods, ideally incor-
porating observational assessment as well as GAS or simi-
lar procedures.
CONCLUSIONS AND FUTURE DIRECTIONS
Recommendations for Assessing Couple Distress
Assessment strategies and specific methods for assessing
couple distress will necessarily be tailored to partners’
unique constellation of presenting difficulties, as well as
specific resources of both the couple and the clinician.
However, regardless of the specific context, the following
recommendations for assessing couple distress will apply:
1. Given empirical findings linking couple distress to
individual disorders and their respective impact in
moderating treatment outcome, assessment of couple
functioning should be standard practice when treat-
ing individuals. Screening for couple distress when
assessing individuals may involve a brief interview for-
mat shown to relate to relevant indicators of couple
interactions (e.g., the SDI-​MD-​PA or the RQI) or a
brief self-​report measure that has exhibited prior evi-
dence of discriminative validity (e.g., the MSI-​B or
the CSI-​4). Similarly, when treating couples, part-
ners should be screened for individual emotional or
behavioral difficulties that may contribute to, exacer-
bate, or partially result from couple distress.
2. Assessment foci should progress from broad to
narrow—​first identifying relationship concerns at
the broader construct level and then examining
more specific facets of couple distress and its cor-
relates using a finer-​grained analysis. The specific
assessment methods described in this review vary
considerably in their overall breadth or focus within
any specific construct domain and, hence, will vary
both in their applicability across couples and in
506 Couple Distress and Sexual Disorders
their placement in a sequential exploratory assess-
ment process.
3. Within clinical settings, certain domains should
always be assessed with every couple either because
of their robust linkage to relationship difficulties
(e.g., communication processes that involve emo-
tional expressiveness, problem discussions, posi-
tive exchanges, and decision-​making) or because
the specific behaviors, if present, have particularly
adverse impact on couple functioning (e.g., physi-
cal aggression or substance abuse).
4. Couple assessment should integrate findings across
multiple assessment methods and domains. Self-​
and other-​report measures can complement find-
ings from interview or behavioral observation and
generate data across diverse domains both centrally
or conceptually related to the couple’s difficul-
ties and treatment goals, or across those domains
potentially more challenging to assess because of
their sensitive nature or their not being amenable
to direct observation. However, caution should be
exercised when adopting self-​or other-​report mea-
sures in the assessment of couple distress. Despite
their proliferation, most measures of couple func-
tioning described in the literature have not under-
gone careful psychometric evaluation. Among
those instruments for which some evidence con-
cerning reliability and validity has been garnered,
evidence often exists only for overall scores and not
at the level of subscales or smaller units of analysis
at which interpretations may be made.
5. At the same time, assessment of couple distress
should be parsimonious. This objective can be facili-
tated by choosing evaluation strategies and modali-
ties that complement each other and by following
a sequential approach that uses increasingly nar-
rowband measures to target problem areas that have
been identified by other assessment techniques.
6. Psychometric characteristics of any assessment
measure—​whether from interview, ABO, or self-​
report method—​are conditional upon the specific
population and purpose for which that assess-
ment method was developed. Given that nearly
all measures of couple distress were developed
and tested on White, middle-​ class, heterosexual
married couples, their relevance to and utility for
assessing ethnic minority couples, gay and lesbian
couples, older couples, and low-​income couples is
unknown. This caveat extends to content-​as well
as criterion-​related validity. Hence, any assessment
measure demonstrating evidence of validity with
some couples may be less valid, in part or in whole,
for any given couple, thus further underscoring the
importance of drawing upon multiple indicators
across multiple methods for assessing any specific
construct.
7. Given the dynamic and conditional nature of
couple distress and its causes, assessment should be
ongoing throughout the therapy process.
Recommendations for Further Research
Future directions for assessment research germane to the
field generally also apply to research in assessing couple
distress specifically, including the need for greater atten-
tion to (a)  psychometric characteristics of measures;
(b) factors moderating reliability and validity across popu-
lations differing in sociocultural characteristics as well
as in clinical functioning; (c)  the assessment process,
including initial articulation of assessment goals, selec-
tion of assessment method and instruments, and methods
of interpreting data and providing feedback; and (d) the
functional utility of assessment findings in enhancing
treatment effectiveness (Hayes, Nelson, & Jarrett, 1987).
In considering the implications of these directives
for the assessment of couple distress, considerably more
research is needed before a comprehensive, empirically
based couple assessment protocol can be advocated. For
example, despite the ubiquitous use of couple assessment
interviews, scant research has been conducted to assess
their psychometric features. Observational methods,
although a rich resource for generating and testing clini-
cal hypotheses, are less frequently used in clinical settings
and present significant challenges to their reliable and
valid application in everyday practice. Questionnaires—​
despite their ease of administration and potential utility in
generating a wealth of data—​frequently suffer from inad-
equate empirical development and, at best, comprise only
part of a multimethod assessment strategy.
We recommend, as a research roadmap, that clinical
researchers consider adapting the Institute of Medicine
stages of intervention research cycle (Mrazek & Haggerty,
1994). Stage 1 involves identifying the disorder and mea-
suring its prevalence. Despite being so basic a need, there
currently exists no gold standard for discriminating distressed
from nondistressed couples; the questionnaires most fre-
quently used for such classifications are of limited sensitivity
and specificity (Heyman et al., 2001). Stage 2 involves delin-
eating specific risk and protective factors. As noted previ-
ously, some replicated factors have been identified, although

this research could be sharpened by defining groups more
carefully (via Stage 1). Stage 3 (efficacy trials) would involve
tightly controlled trials of the efficacy of a multimethod
assessment in clinical practice. Stage 4 (effectiveness trials)
would involve controlled trials of the outcome of this assess-
ment in more real-​world clinical environments. Only then
would testing broad-​scale dissemination (Stage 5) of empiri-
cally based couple assessment be appropriate.
This research roadmap reflects an ambitious agenda
unlikely to be met by any single investigator or group of
investigators. However, progress toward evidence-​based
assessment of couple distress will be enhanced by research
on specific components targeting more notable gaps in the
empirical literature along the lines recommended here:
1. Greater attention should be given to expanding the
empirical support for promising assessment instru-
ments already detailed in the literature than to the
initial (and frequently truncated) development of
new measures. Proposals for new measures should be
accompanied by compelling evidence for their incre-
mental utility and validity and a commitment to pro-
grammatic research to examine their generalizability
across diverse populations and assessment contexts.
2. Research needs to delineate optimal structured
and semi-​ structured interview formats for assess-
ing couples. Such research should address (a)  issues
of content validity across populations and settings,
(b)  organizational strategies for screening across
diverse system levels and construct domains relevant
to couple functioning (similar to branching strategies
for the Structured Clinical Interview for the DSM
[First et al., 1997] and related structured interviews for
individual disorders), (c) relative strengths and limita-
tions to assessing partners separately versus conjointly,
(d)  factors promoting the disclosure and accuracy of
verbal reports, (e) relation of interview findings to com-
plementary assessment methods (as in generating rel-
evant tasks for ABO), and (f) the interview’s special role
in deriving functional analytic case conceptualization.
3. Although laboratory-​based behavioral observation
of couple interaction has considerably advanced
our understanding of couple distress, generaliza-
tion of these techniques to more common clini-
cal settings has lagged behind. Hence, researchers
should develop more clinically useful methods of
observation and macro-​ level coding systems for
quantifying observational data that promote their
routine adoption in clinical contexts while preserv-
ing their psychometric fidelity.
Couple Distress 507
4. Research needs to attend to the influences of cul-
ture at several levels. First, there has been little
attention to developing measures directly assess-
ing domains specific to relationship functioning
at the community or cultural level (e.g., cultural
standards or norms regarding emotional expres-
siveness, balance of decision-​making influence, or
boundaries governing the interaction of partners
with extended family or others in the community).
Hence, assessment of such constructs currently
depends almost exclusively on the clinical inter-
view, with no clear guidelines regarding either the
content or the format of questions. Second, consid-
erably more research needs to examine the moder-
ating effects of sociocultural factors on measures of
couple functioning, including the impact of such
factors as ethnicity, age, socioeconomic status, or
sexual orientation. Third, work needs to proceed
on adapting established measures to alternative
languages. In the United States, the failure to adapt
existing instruments to Spanish or to examine the
psychometric characteristics of extant adaptations
is particularly striking given that (a) Hispanics are
among the largest and fastest-​growing ethnic minor-
ity group and (b) among U.S. Hispanic adults aged
18 to 64 years, 28% have either limited or no ability
to speak English (Snyder et al., 2004).
Adapting existing measures to alternative contexts
(i.e., differing from the original development sample in
language, culture, or specific aspects of the relationship
such as sexual orientation) should proceed only when
theoretical or clinical formulations suggest that the con-
struct being measured does not differ substantially across
the new application. Detailed discussions of both con-
ceptual and methodological issues relevant to adapting
tests to alternative languages or culture exist elsewhere
(e.g., Butcher, 1996; Geisinger, 1994; Haynes et  al.,
2016; Van Widenfelt, Treffers, de Beurs, Siebelink, &
Koudijs, 2005). Because clinicians and researchers may
fail to recognize the inherent cultural biases of their con-
ceptualization of couple processes, the appropriateness
of using or adapting tests cross-​culturally should be evalu-
ated following careful empirical scrutiny examining each
of the following:
• Linguistic equivalence including grammatical, lexi-
cal, and idiomatic considerations
• Psychological equivalence of items across the source
and target cultures
508 Couple Distress and Sexual Disorders
• Functional equivalence indicating the congruence
of external correlates in concurrent and predictive
criterion-​related validation studies of the measure
across applications
• Scalar equivalence ensuring not only that the slope
of regression lines delineating test–​ criterion rela-
tions be parallel (indicating functional equivalence)
but also that they have comparable metrics and ori-
gins (zero points) in both cultures
Finally, research needs to examine the process, as well
as the content, of couple assessment. For example, little
is known regarding the impact of decisions about the tim-
ing or sequence of specific assessment methods, the role
of the couple in determining assessment objectives, or
the provision of clinical feedback on either the content
of assessment findings or their subsequent effect on clini-
cal interventions. Recent studies suggest that systematic
monitoring and feedback in couple therapy may enhance
treatment outcomes (Halford et  al., 2012; Pepping,
Halford, & Doss, 2015). Similarly, additional studies
are needed to examine the psychometric equivalence
of Internet administration of paper-​and-​pencil question-
naires used in couple research (Brock, Barry, Lawrence,
Dey, & Rolffs, 2012).
Although assessment of couples has shown dramatic
gains in both its conceptual and empirical underpinnings
during the past 35 years, much more remains to be discov-
ered. Both clinicians and researchers need to avail them-
selves of recent advances in assessing couple distress and
collaborate in promoting further development of empiri-
cally based assessment methods.
ACKNOWLEDGMENTS
Portions of this chapter were adapted from Snyder,
Heyman, and Haynes (2005). Richard Heyman’s work
on this chapter was supported by the National Institute of
Dental and Craniofacial Research grant UH2DE025980.
The authors express their appreciation to Brian Abbott,
Danielle Mitnick, and Dawn Yoshioka for their contribu-
tions to Tables 22.1 through 22.4.
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 23
Sexual Dysfunction
Natalie O. Rosen
Maria Glowacka
Marta Meana
Yitzchak M. Binik
The question of assessment in sexuality has always been
a complex one. Arguably more than with other phenom-
ena covered in the Diagnostic and Statistical Manual of
Mental Disorders (DSM), the classification of sexuality
has been complicated by changing notions of normality,
the subjective nature of the sexual experience, gender dif-
ferences, and significant social, economic, and political
investment from parties with opposing ideologies. The
past two decades have evidenced a series of challenges to
extant definitions of sexual dysfunction in general and,
specifically, to the legitimacy of certain dysfunctions. The
DSM-​ IV-​
TR (American Psychiatric Association [APA],
2000) classification was critiqued for (a) medicalizing sex-
uality by discounting the diversity of sexual expression in
favor of categorical distinctions between health and disor-
der (Tiefer, 2002), (b) using an androcentric conceptual-
ization of the sexual response that inadequately accounts
for female sexuality (Basson et al., 2004), (c) ignoring ques-
tions of sexual and relationship satisfaction (Byers, 1999),
and (d) decontextualizing the sexual experience (Laumann
& Mahay, 2002). The validity of specific dysfunctions has
also been questioned (Basson, 2002; Binik, 2005; Reissing,
Binik, Khalife, Cohen, & Amsel, 2004), with theoretical
and empirical challenges resulting in the removal of sexual
aversion disorder, and the combining of female hypoactive
sexual desire disorder and female sexual arousal disorder
into a new diagnosis of female sexual interest/​arousal dis-
order (FSIAD), as well as dyspareunia and vaginismus into
genito-​pelvic pain/​penetration disorder (GPPPD) in the
DSM-​5 (APA, 2013). Male dyspareunia was also excluded
from the DSM-​5 due to insufficient data.
515
Our aim in this chapter is not to determine what rises
to the level of a disorder and what does not. Rather, we
aim to describe and discuss different ways of measuring
subjective and physiological sexual phenomena related
to global sexual function as well as to the seven sexual
dysfunctions defined in the DSM-​ 5:  delayed ejacula-
tion, erectile disorder, female orgasmic disorder, female
sexual interest/​arousal disorder, genito-​pelvic pain/​pen-
etration disorder, male hypoactive sexual desire disorder,
and premature (early) ejaculation. After a brief descrip-
tion of the nature of these sexual problems, we describe
global sexual function measures suitable for the purposes
of diagnosis, case conceptualization and treatment plan-
ning, and treatment monitoring and outcome. A descrip-
tion of assessments specific to each of the aforementioned
sexual dysfunctions follows, concluding with a discussion
of future directions.
THE NATURE OF SEXUAL DYSFUNCTION
One of the reasons clinicians and researchers debate the
very notion of sexual dysfunction is the ubiquity of sex-
ual complaints in our society. Despite wide variation in
prevalence rates for all sexual dysfunctions depending on
the population and methodology in question (Simons &
Carey, 2001), the numbers remain staggering. With gen-
eral prevalence figures for sexual problems reported to be
as high as 40% in women and 28% in men (Hendrickx,
Gijs, & Enzlin, 2014; Laumann, Paik, & Rosen, 1999;
Shifren, Monz, Russo, Segreti, & Johannes, 2008), sexual
516 Couple Distress and Sexual Disorders
difficulties seem close to normative. Once relegated strictly
to sex therapists and sexologists, the assessment of sexual
function is increasingly considered an integral part of an
overall health assessment (Parish, 2006). However, it is
important to distinguish a fleeting sexual complaint from
a more pervasive problem. Most people will experience
difficulty with sex at some point in their lives. The DSM-​5
restricts diagnosis to cases characterized by a persistence of
the problem (at least 6 months) and significant associated
distress for the individual or couple. Indeed, prevalence
estimates drop to 12% to 20% for women and 11% for men
when considering both persistence and associated distress
(Christensen et al., 2011; Hendrickx et al., 2014; Shifren
et  al., 2008). Furthermore, another population-​ based
study (Prevalence of Female Sexual Problems Associated
with Distress and Determinants of Treatment Seeking
[PRESIDE]) reported that the vast majority of sexual prob-
lems with a 1-​month duration (>72%) did not persist to
6 months (Shifren et al., 2008). It is notable that the preva-
lence of sexual problems can vary considerably across cul-
tures, further highlighting the importance of contextual
factors (Laumann et al., 2005).
The DSM-​5 further classifies sexual dysfunctions as
generalized or situational (with the exception of GPPPD)
and lifelong or acquired, and it specifies the current sever-
ity as mild, moderate, or severe. Exclusion criteria include
problems that are better explained by a nonsexual mental
disorder; medical conditions and/​or use of substances;
or severe relationship distress, partner violence, or other
stressors. To better address the degree of medical and
nonmedical correlates, several associated features are now
listed for consideration in the diagnosis, including part-
ner factors, relationship factors, individual vulnerabilities,
cultural or religious factors, and medical factors.
The exact determination of the DSM-​ 5 inclusion/​
exclusion criterion relating specifically to etiology is par-
ticularly complicated in any individual case. It is often
difficult to determine whether the sexual problem ema-
nates from psychological disturbances alone or whether
there is organic involvement. Considering that the sexual
response necessarily involves both peripheral and central
nervous system activity, and that it is usually experienced
in an intrapersonal, interpersonal, and cultural context,
one could argue that every sexual problem either origi-
nates from or is perpetuated by both psychological and
physiological factors.
The overall organization of the sexual dysfunctions
in the DSM-​5 is alphabetical and includes seven dys-
functions relating to sexual desire, arousal, orgasm, and
pain. There are no dysfunctions listed that relate to the
period immediately following sexual activity, although
this may change in future editions given growing support
for the existence of persistent sexual arousal syndrome in
women (Facelle, Sadeghi-​Nejad, & Goldmeier, 2013).
The comorbidity of sexual dysfunctions other than the
presenting one is very common (Hendrickx et al., 2014).
A  problem at any stage of sexual response is likely to
engender difficulties at other stages. A  brief description
of the known features of each of the sexual dysfunctions
listed in the DSM-​5 follows.
Delayed Ejaculation
Previously referred to as male orgasmic disorder, delayed
ejaculation (DE) presents as delayed, infrequent, or
absent ejaculation in 75% to 100% of partnered sexual
activity occasions. Population prevalence estimates
range from less than 1% to 2% (Christensen et al., 2011;
Hendrickx, Gijs, & Enzlin, 2013). The most common
physiological etiologies are select disease processes associ-
ated with aging, such as heart disease and benign prostatic
hyperplasia/​lower urinary tract symptoms, although pelvic
surgeries, diabetes, neurological disturbances, antidepres-
sants, and alpha blockers have also been linked to DE.
Theorized psychosocial etiologic pathways include fear,
performance anxiety, hostility, guilt, low desire for the
partner, lack of confidence, and inadequate stimulation
(Rowland et al., 2010). Idiosyncratic and vigorous mastur-
batory styles may also negatively impact ejaculation.
Erectile Disorder
Erectile disorder (ED) is diagnosed when at least one
of the following criteria is met during 75% to 100% of
sexual activity encounters:  (1) difficulty obtaining an
erection, (2)  difficulty maintaining an erection, or (3)  a
decrease in erectile rigidity. Almost 15% of men in the
British National Survey of Sexual Attitudes and Lifestyles
(NATSAL) study reported difficulty getting or maintain-
ing an erection (Mitchell et al., 2013). In two other large
studies, approximately 5% of men reported distressing
ED (Christensen et  al., 2011; Hendrickx et  al., 2013).
The prevalence and severity of ED increase with age;
however, older men are typically less distressed in com-
parison to younger or middle-​aged men (Rosen, Miner,
& Wincze, 2014).
Vascular and neurological diseases or damage are
associated with ED, as are lifestyle behaviors (e.g., smok-
ing, alcohol abuse, and inactivity) that affect the vascu-
larization and innervation necessary for erection and/​or
 Sexual Dysfunction 517

the stamina to sustain the physical exertion of penetra- sexual desire disorder (MHSDD), a desire discrepancy
tion (Rosen, Miner, et al., 2014). Some antidepressants, between partners is not alone sufficient for a diagnosis.
antihypertensives, and drugs that block the conversion of There are no population-​based studies that have exam-
testosterone into dihydrotestosterone (DHT), commonly ined the prevalence of this new disorder. The NATSAL
used to treat male pattern hair loss and benign prostatic study reported that 40.6% of women lacked interest in
hyperplasia (Shamloul & Ghanem, 2013), have also sex. However, when the criterion of 6-​month duration
been implicated. Psychosocially, performance demands, was included, the prevalence declined to 10.2% (Mercer
arousal underestimation, negative affect during sex, self-​ et al., 2003). The prevalence rate of arousal difficulties is
critical attributions, depressive symptoms, and relation- estimated to be between 10.9% and 31.2% (Brotto, Bitzer,
ship problems have all been linked to ED (Rosen, Miner, Laan, Leiblum, & Luria, 2010). Cultural variations in
et al., 2014). the prevalence of arousal and desire difficulties have also
been noted (Laumann et al., 2005).
Sexual desire and arousal are influenced by a com-
Female Orgasmic Disorder
bination of biological, psychological, and contextual
A diagnosis of female orgasmic disorder (FOD) requires a factors (Laan & Both, 2008; Toates, 2009). Biologically,
delay in, infrequency of, or absence of orgasm or a reduced difficulties with desire and arousal have been linked to
intensity of orgasmic sensations during 75% to 100% of endocrine factors, medical illnesses, and medical treat-
sexual activity encounters. Because of the wide variation ments that impact hormones or the menstrual cycle
in the type or intensity of stimulation that triggers orgasm, (Brotto et al., 2010). There is mixed evidence related to
clinicians are left to judge whether the woman’s orgasmic the role of androgen levels in problems with sexual desire
capacity is less than expected for her age, sexual experi- in women (Davis, Davison, Donath, & Bell, 2005; Davis,
ence, and stimulation received. A review of several stud- Worsley, Miller, Parish, & Santoro, 2016; Santoro et al.,
ies reported that the prevalence of FOD is approximately 2005). Similar to MHSDD, negative mood states, trau-
3% to 34%, varying widely across studies and cultures matic experiences, body image concerns, relationship fac-
(Graham, 2010; Laumann et  al., 2005). Approximately tors, and pressure from various cultural norms have been
half of women with orgasm difficulties do not report asso- linked to arousal and desire problems (Brotto et al., 2010).
ciated distress (Shifren et al., 2008). A diagnosis of FOD
should not be made if lack of orgasm is solely dependent
Genito-​Pelvic Pain/​Penetration Disorder
on inadequate sexual stimulation; however, epidemiology
studies rarely take into account the source of stimulation GPPPD is defined as recurrent or persistent difficulty
(Graham, 2014). Neurophysiological and vascular disrup- with at least one of the following: (a) vaginal penetration
tions, thyroid problems, pelvic nerve damage, and spinal during intercourse, (b) vulvovaginal or pelvic pain during
cord injury, as well as side effects from serotonin reuptake penetration or attempts, (c) marked fear or anxiety about
inhibitors have been implicated in the development of vulvovaginal or pelvic pain, or (d) tensing of pelvic floor
FOD. Psychosocial etiologic factors are more common muscles during penetration attempts. Studies indicate
than physiological factors and include fear of losing con- that 14% to 34% of younger women and 6.5% to 45% of
trol, relationship quality, and socioeconomic status and older women suffer from pain during sexual intercourse
educational level (Graham, 2014). (van Lankveld et al., 2010). The Global Study of Sexual
Attitudes and Behaviours, which spanned 29 countries,
reported that 2% to 8.6% of women experienced frequent
Female Sexual Interest/​Arousal Disorder
pain during sex; however, this study did not take into
FSIAD is defined as absent or reduced sexual interest/​ account distress (Laumann et al., 2005). Although there
arousal based on meeting three or more of the following are no population-​based studies of GPPPD specifically,
criteria: lack of or reduced (a) interest in sexual activity, previous studies  that accounted for clinical distress indi-
(b) sexual thoughts/​fantasies, (c) initiations of sexual activ- cated the prevalence of dyspareunia to be 3% and vagi-
ity or being unreceptive to partner initiations, (d) excite- nismus to be 0.4% (Christensen et  al., 2011; Hendrickx
ment or pleasure during 75% to 100% of sexual activity et al., 2014). Male genital pain has been removed from
events, (e)  interest/​arousal in the context of any sexual the DSM-​5 due to insufficient research, despite grow-
cues, or (f)  genital or nongenital sensations during 75% ing evidence of men experiencing pain during erection,
to 100% of sexual activity events. As with male hypoactive ejaculation, and receptive anal intercourse (Bergeron,
518 Couple Distress and Sexual Disorders
Rosen, & Pukall, 2014). The prevalence of male dyspa-
reunia remains unclear, but it is estimated to range from
1% to 15% (Christensen et al., 2011; Clemens, Meenan,
O’Keeffe, Rosetti, Gao, & Calhoun, 2005).
Biologically, GPPPD can arise from congenital mal-
formations of the genital tract, acute and chronic diseases,
nonspecific inflammatory or nerve dysfunction processes,
such as vestibulodynia, postmenopausal decreases in
estrogen, and iatrogenic damage from genital surgeries/​
procedures (Bergeron, Corsini-​ Munt, Aerts, Rancourt,
& Rosen, 2015). Psychological factors associated with
GPPPD include pain catastrophizing, fear of and
hypervigilance to pain, lower self-​efficacy, anxiety, and
depression. In addition, women who suffer from sexual,
physical, or psychological abuse have an increased likeli-
hood of developing genito-​pelvic pain (Harlow & Stewart,
2005). Recent research has highlighted a number of inter-
personal factors associated with greater pain and poorer
adjustment, such as partner response to the pain and
couple communication (Rosen, Bergeron, et al., 2014).
Male Hypoactive Sexual Desire Disorder
MHSDD is defined as persistent or recurrent absence
or deficiency of sexual thoughts/​fantasies and desire for
sexual activity. The prevalence rates vary substantially
across studies but are estimated to be between 15% and
25% (Brotto, 2010; Lewis et al., 2010). Unfortunately, dis-
tress is rarely assessed in studies of male desire. In a large
study that did account for clinically significant distress,
only 1.6% of men met the DSM-​IV-​TR diagnostic criteria
for MHSDD (Hendrickx et al., 2013).
It is worth noting that men may be reluctant to report
low desire for a variety of reasons, including adherence to
cultural norms (Meana & Steiner, 2014). It is imperative
to tease apart true MHSDD from desire that fails to rise to
a partner’s wishes or to a societal, oppressive ideal. Barring
age, medical conditions, pain syndromes, or medication
side effects, the most often cited biological factor impli-
cated in MHSDD has been hormones. Administration
of exogenous testosterone has shown effects in the desire
of hypogonadal men with erectile dysfunction; however,
increased testosterone positively impacts energy and
mood, which may improve desire (Khera et  al., 2011).
Furthermore, it is unlikely that testosterone replace-
ment would improve desire in eugonadal men (Meana
& Steiner, 2014). Thus, testosterone may not be as impor-
tant to the etiology of MHSDD as was previously thought.
Psychosocially, many negative emotional states and
life experiences have been linked to low desire in men,
including stress, depression, anxiety, cognitive set, self-​
esteem, trauma, cultural norms, and relational and finan-
cial difficulties (for a review, see Meana & Steiner, 2014).
Premature (Early) Ejaculation
Premature (early) ejaculation (PE) is defined as persistent
or recurrent ejaculation within 1 minute following vagi-
nal penetration and before the person wishes it on 75%
to 100% of partnered sexual activity occasions. Men who
engage in nonvaginal sexual activity may meet the diagno-
sis for PE, but the specific duration criteria are unknown.
In this case, the onus is on the clinician to judge whether
conditions described are adequate for most men to delay
ejaculation until desired. Two large studies of Danish and
American men reported a prevalence of 7% or 8% for dis-
tressing PE based on DSM-​IV-​TR criteria (Christensen
et al., 2011; Patrick et al., 2005). The addition of the 1-​
minute criterion to the DSM-​5 diagnosis is likely to sig-
nificantly impact prevalence estimates (Althof, 2014).
In fact, a multinational consultation team composed of
more than 200 experts estimated that the prevalence of
PE, using the more stringent duration criteria, is only 1%
to 3% (Rowland et al., 2010).
In addition to innate physiological predispositions
to ejaculate quickly; genitourinary, cardiovascular, and
neurologic diseases; prostatitis/​chronic pelvic pain syn-
drome; and erectile dysfunction have also been impli-
cated. Psychosocial factors hypothesized to contribute to
PE include negative mood states, performance anxiety,
unrealistic expectancies, sexual misinformation, poor
sexual skills and sensory awareness, maladaptive arousal
patterns, and relational problems (Althof et  al., 2014;
Perelman, 2006).
PURPOSES OF ASSESSMENT
The latest edition of the Handbook of Sexuality-​Related
Measures (Fisher, Davis, Yarber, & Davis, 2011)  con-
tains 218 self-​administered questionnaires that relate to
sexuality. The comprehensiveness of this reference text is
deceiving, however, because it creates the impression that
the field of human sexuality is rich in assessment tools. In
terms of sexual function and its clinical assessment, this is
not always the case.
Only a small subset of the measures in the Handbook
focuses on sexual function and possesses adequate psy-
chometric properties. The assessment of sexual function
using extensively validated instruments has grown in the
 Sexual Dysfunction 519

TABLE 23.1   Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly

Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Global Sexual Function

For Use with Men, Women, and Couples
GRISS G G NA A A G G A
For Use with Women Only
BISF-​W A A NA A A A A A
FSFI G E NA A G G G A ✓
MFSQ G A NA A G G G A ✓
SFQ G G NA A E G G A ✓
SDM A NA L NR A A NR A
For Use with Men Only
BMSFI A G NA A G A A A
IIEF G G NA A G G G A ✓
MSHQ G G NA A G A NR A
Dysfunction-​Specific
SIDI-​F A E NA A G A A A
IIEF-​5 G G NA A G G A A ✓
MSHQ-​EjD A G NA A A A G A
IPE G A NA A G A G A
PEDT G A NA A G A G A

Note: GRISS = Golombok–​Rust Inventory of Sexual Satisfaction; BISF-​W = Brief Index of Sexual Functioning for Women; FSFI = Female Sexual
Function Index; MFSQ = McCoy Female Sexuality Questionnaire; SFQ = Sexual Function Questionnaire; SDM = Structured Diagnostic Method;
BMSFI = Brief Male Sexual Function Inventory; IIEF/​IIEF-​5 = International Index of Erectile Function; MSHQ/​MSHQ-​EjD = Male Sexual Health
Questionnaire/​–​Ejaculation Short Form; SIDI-​F = Sexual Interest and Desire Inventory; IPE = Index of Premature Ejaculation; PEDT = Premature
Ejaculation Diagnostic Tool; L = Less Than Adequate; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

past decade as a consequence of the emerging need to
assess outcomes in pharmaceutical clinical trials (Daker-​
White, 2002). This chapter is limited to the description
and evaluation of measures that (a)  aim to assess sexual
function in clinically useful ways and (b) have adequate
or better psychometric properties. The list of measures
covered could arguably have been longer because the
multifactorial conceptualization of sexual problems
could conceivably include assessments of myriad aspects
of an individual’s life. Our choice was guided by objective
indices of reliability and validity, and by our subjective
assessment of a measure’s promise of clinical utility. We
first present multidimensional measures of global sexual
function or related constructs (satisfaction, distress, and
relationship adjustment) adequate for diagnosis, case
conceptualization, and treatment monitoring. This is
followed by a discussion of assessment tools specific to
each of the sexual dysfunctions. Some of the measures
selected are applicable to men, women, and/​or couples,
whereas others are gender-​specific. Critical evaluations of
the psychometric properties of all measures (global and
dysfunction-​ specific) by assessment purpose (diagnosis,
case conceptualization, and treatment monitoring) are
provided in Tables 23.1 and listed in the order in which
they appear in the text.
GLOBAL ASSESSMENT OF SEXUAL FUNCTION
Concerns about the growing medicalization of the field
have engendered appeals for integrative conceptualiza-
tions of sexual dysfunctions that encompass individual,
family of origin, relational, social, and cultural factors
(Binik & Hall, 2014). This multifactorial approach, how-
ever, represents a daunting challenge to assessment and
treatment because it requires the simultaneous consid-
eration of multiple factors. It also calls for assessment of
other mental disorders or medical conditions that may
impact on sexual function and for assessment of the
comorbidity of other sexual dysfunctions in the client and
his or her partner.
The assessment of global sexual function generally
involves a clinical interview and/​or self-​administered
questionnaires, depending on the context of the evalu-
ation. General practitioners who want to screen for
sexual dysfunction in the context of a busy medical
520 Couple Distress and Sexual Disorders
practice may depend primarily on brief screening ques-
tionnaires. Sex therapists and other mental health
professionals more directly involved in the treatment
of sexual dysfunction will almost invariably start with
an extended clinical interview, possibly followed by
questionnaires.
Assessment for Diagnosis
There is no diagnostic category of global sexual dysfunc-
tion because there is no such diagnosis. The “diagnostic”
assessment of global sexual function is thus conducted for
one of two reasons: to get a general sense of the person’s
sexual adjustment multidimensionally defined as func-
tion, satisfaction, distress, and relationship quality, or as a
screen for the existence of a specific dysfunction that will
then be investigated further. Although the DSM-​5 has
enhanced specificity of the diagnostic criteria for sexual
disorders, several still depend heavily on clinician judg-
ment, rendering the clinical interview an essential diag-
nostic tool. Self-​report measures of global sexual function
and specific dysfunctions are generally considered diag-
nostic adjuncts.
Clinical Interview
The clinical interview remains the mainstay of sexual
dysfunction diagnostic assessment. Clinician judgment
is central to the determination of whether a client meets
DSM-​5 criteria for sexual dysfunction. However, there
is no widely used, standardized interview that has been
psychometrically validated, as is the case for other men-
tal disorders. The Structured Clinical Interview for
DSM-​5 Disorders (SCID-​5) does not cover the sexual
dysfunctions (First, Williams, Karg, & Spitzer, 2015).
Several authors have proposed clinical interview out-
lines and recommendations about coverage of topics
and process (e.g., Maurice, 1999; McConaghy, 2003;
Wincze & Weisberg, 2015)  and also for the specific
dysfunctions (Binik & Hall, 2014; Levine, Risen, &
Althof, 2016).
Briefly, the clinical interview typically starts with the
individual describing the nature of the problem and the
reasons for seeking treatment at the time. Following an
open-​ended characterization of the difficulty, the clini-
cian might start asking more operationally specific ques-
tions about the extent of the problem and the conditions
under which it occurs. This is ideally followed by ques-
tions covering the myriad biological, psychological, and
social problems that might be implicated, paying attention
to the four “P’s”—​that is, predisposing, precipitating, per-
petuating, and protective factors.
From a broadly biological perspective, it is important
to assess and take into account age, general health status
(e.g., body mass index, energy levels, and sense of physical
well-​being), lifestyle factors (e.g., diet, cigarette smoking,
alcohol use, and exercise), life transitions (e.g., menopause
and childbirth), hormone levels, chronic pain syndromes
(e.g., vulvodynia and interstitial cystitis), vascular diseases
(e.g., hypertension, atherosclerosis, and impaired cardiac
function), conditions that affect nervous system function
(e.g., diabetes and neuropathy), and pelvic or perineum
trauma. It is also important to assess for the potentially iat-
rogenic influence of surgeries that may interfere with the
musculature and innervation of the genital area, as well as
its cosmetic appearance. Antidepressants, antipsychotics,
and antihypertensives can also have a deleterious effect
on desire, arousal, and orgasm, and should be inquired
about. Often, assessment of many of these factors will
require referral to the appropriate medical or other health
professional (e.g., a physiotherapist).
In terms of individual psychological factors, depres-
sion and anxiety are often comorbid with sexual dys-
function. Treatment for sexual difficulties that does not
simultaneously target mood disturbances and anxiety (if
present) is unlikely to meet with much success. Substance
abuse disorders can also have a major impact on sexual
functioning, as can certain maladaptive cognitive sets and
negative emotional reactions that interfere with sexual
function, although they may not rise to the level of a dis-
order. These may arise from past trauma, negative experi-
ences, or learned sexual scripts. Often, individuals simply
lack knowledge of physiology or of sexual techniques.
From a relational/​social perspective, family of origin
attitudes regarding sexuality can be instated early on
and create the conditions for the development of sexual
dysfunction. The importance of assessing the quality of
the individual’s current relationship cannot be stressed
enough. Although sexual difficulties can occur in the hap-
piest of relationships, couple disharmony can be a cause
and/​or consequence of sexual problems and needs to be
addressed. Relational issues important to assess include
anger, distrust, discrepancies in drive and preferences,
communication, and physical attraction. The way in
which a relationship partner responds to the sexual dif-
ficulty both inside and outside of a sexual context can
also have implications for the individuals’ and couples’
sexual functioning. It is usually recommended that both
partners be interviewed together and/​ or separately to
gather as much information as possible. The comorbidity

of partner sexual dysfunction is common and crucial to
assess. Finally, ethnocultural and religious attitudes and
beliefs are important as they can be implicated in the
development and maintenance of sexual difficulties. Also,
these beliefs need to be respected in order to successfully
treat the individual or the couple.
In summary, the presence of any one or combination
of the aforementioned factors does not necessarily result
in dysfunction. Failing to assess for them, however, may
interfere with otherwise reasonable treatment efforts.
Although the unstructured clinical interview undeniably
provides maximum flexibility to explore the specifics of
an individual’s sexual problem and profile, the addition
of a shorter, structured interview and/​or self-​administered
questionnaires may enhance the accuracy and utility of
the overall assessment.
Self-​Report Measures of Global Sexual Function
Table 23.1 provides a listing of self-​report measures of
global sexual function helpful in diagnostic assessment.
The first two of these measures are designed to be appli-
cable to men, women, and couples, whereas the rest are
gender-​specific. It is worth noting that many of these
measures are quite heteronormative, and adaptations and
validations with diverse sexual identities are required.
A description of these measures follows.
The Golombok–​Rust Inventory of Sexual Satisfaction
(GRISS; Rust & Golombok, 1985, 1986, 1998)  is a
56-​item self-​
report measure of sexual function and
of relationship quality in heterosexual relationships.
Female-​specific dimensions (28 items) pertain to orgas-
mic difficulties, vaginismus, nonsensuality, avoidance,
and dissatisfaction. Male-​specific dimensions (28 items)
pertain to erectile dysfunction, PE, nonsensuality, avoid-
ance, and dissatisfaction. The two common dimensions
pertain to infrequency and noncommunication. Items
are responded to on 5-​ point adjectival scales. Scores
on the 12 dimensions are transformed into standard-
ized scores and can be plotted to provide a profile. The
GRISS also provides a global score indicative of overall
relationship quality and the couple’s sexual function that
can be useful in case conceptualization and treatment
planning. Although there is some support for its use as a
diagnostic tool, the GRISS was designed primarily as an
evaluation tool for sex and couple therapy and for cross-​
treatment efficacy comparisons. Its clinical utility lies in
its ease of administration (approximately 10 minutes to
complete) and its simultaneous assessment of both sexual
function and relationship quality.
Sexual Dysfunction 521
The Brief Index of Sexual Functioning for Women
(BISF-​W; Rosen, Taylor, & Leiblum, 1998; Taylor, Rosen,
& Leiblum, 1994) is a 22-​item scale developed to measure
global sexual function for the purposes of large-​scale clini-
cal trials. A scoring algorithm provides an overall score for
sexual function and on seven dimensions: thoughts/​desire,
arousal, frequency of sexual activity, receptivity/​initiation,
pleasure/​orgasm, relationship satisfaction, and problems
affecting sexual function. Items are responded to in a vari-
ety of formats, it takes 15 to 20 minutes to administer, and
some dimensions and the overall score have been shown
to be sensitive to treatment (Rosen et  al., 2006; Shifren
et al., 2000).
The Female Sexual Function Index (FSFI; Rosen
et  al., 2000)  is a brief, 19-​item self-​report measure of
female sexual function yielding a total score as well
as scores on five domains:  desire, arousal, lubrication,
orgasm, satisfaction, and pain. Items are responded to on
5-​or 6-​point adjectival scales and in reference to the past 4
weeks. The FSFI takes approximately 15 minutes to com-
plete. Cross-​validation of this instrument has supported
its use as a screening tool or diagnostic aid, but not as the
sole basis of diagnosis (Meston, 2003; Wiegel, Meston,
& Rosen, 2005). Because it does not address questions of
onset, duration, etiological or maintaining factors, or situ-
ational specifics, it is not as useful in the conceptualiza-
tion of cases and treatment planning as in screening and
measurement of treatment outcome. Data indicate that it
can detect treatment-​related changes (Derogatis, 2008).
Recent recommendations have suggested modifications
to the FSFI when it is administered to women who are
sexually inactive (Yule, Davison, & Brotto, 2011), and a 6-​
item version has been validated for use as a rapid screener
for female sexual dysfunction (Isidori et al., 2010).
The McCoy Female Sexuality Questionnaire (MFSQ;
McCoy & Matyas, 1998) is a 19-​item measure that assesses
a woman’s general level of sexual interest and response in
the preceding 4 weeks. It was designed to serve as a diag-
nostic aid and to measure changes in sexual functioning
over time. The first 11 questions relate to general sexual
enjoyment, arousal, interest, satisfaction with partner, and
feelings of attractiveness; the remaining 8 questions cover
intercourse frequency and enjoyment, orgasm frequency
and pleasure, lubrication, pain with intercourse, and the
impact of the partner’s erectile difficulties. Most items are
answered on a 7-​point adjectival scale. Time to administer
is approximately 10 minutes. The MFSQ has primarily
been used with menopausal women, but there is support
for its use as a valid measure of dysfunction in women
aged 18 to 65 years (Rellini et al., 2005).
522 Couple Distress and Sexual Disorders
The Sexual Function Questionnaire (SFQ; Quirk
et al., 2002; Quirk, Haughie, & Symonds, 2005) is a 34-​
item self-​report instrument developed to assess female
sexual function and sexual satisfaction in sexual pharma-
cology clinical trials. The eight specific dimensions tar-
geted are desire, arousal–​sensation, arousal–​lubrication,
subjective arousal, enjoyment, orgasm, pain, and partner
relationship. The SFQ specifically distinguishes between
subjective and genital aspects of arousal. It takes 15 to 20
minutes to complete, with items answered in reference to
the preceding 4 weeks on 5-​point adjectival scales. The
4-​week reference period makes the measure suitable for
the tracking of treatment progress, although no data sup-
porting its use for treatment outcome have yet been made
available.
The Structured Diagnostic Method (SDM; Utian
et  al., 2005)  was designed to help health care providers
who are not sexuality experts determine a diagnosis of
female sexual dysfunction in postmenopausal women.
The SDM consists of four self-​report measures, followed
by a clinical interview. The four questionnaires are admin-
istered in the following order: Life Satisfaction Checklist
(Fugl-​Meyer, Lodnert, Bränholm, & Fugl-​Meyer, 1997),
the first seven of nine questions in the sexual compo-
nent of the Medical History Questionnaire (Pfeiffer &
Davis, 1972), the Female Sexual Distress Scale (FSDS;
Derogatis, Rosen, Leiblum, Burnett, & Heiman, 2002),
and the SFQ (Quirk et al., 2002). The combination cov-
ers overall life satisfaction (including sexual), decline in
sexual function as well as its onset, sexually related dis-
tress, and sexual function. The measures are followed by a
structured interview based on a guide to diagnostic assign-
ment outlined by Utian and colleagues. The administra-
tion of the SDM is lengthy and not suitable for primary
care clinic use, but it can be clinically useful in both clini-
cal trials and sex therapy practice. The authors have not
provided an algorithm or guidelines to combine results
from the measures and interview to arrive at a diagnosis.
The Brief Male Sexual Function Inventory (BMSFI;
O’Leary et al., 1995) is an 11-​item measure of male sexual
function covering sexual drive, erection, and ejaculation;
subjective problem assessment of drive, erection, and
ejaculation; and overall satisfaction. Responses are given
on 5-​point adjectival scales in reference to the last 30 days,
with higher scores indicating better function. The more
recent validation of this measure suggests that it is most
efficacious as a unidimensional tool for general screening
purposes (Mykletun, Dahl, O’Leary, & Fossa, 2005). The
measure was intended to be suitable for men in same-​sex
or other-​sex relationships.
The International Index of Erectile Function (IIEF;
Rosen et  al., 1997)  is a brief self-​administered measure
of erectile function designed to detect treatment-​related
changes in patients with erectile dysfunction, although it
is also a useful diagnostic adjunct. The 15 items address
five domains of sexual function: erectile function, orgas-
mic function, sexual desire, intercourse, and overall satis-
faction. Response options consist of 5-​or 6-​point adjectival
scales, and the time reference is the prior 4 weeks. It takes
less than 15 minutes to complete and is easy to administer
in most settings. Recent recommendations have suggested
modifications to the IIEF when it is administered to men
who are sexually inactive (Yule et al., 2011) and men who
have sex with men (Coyne et  al, 2010). The IIEF has
been validated in many languages.
The Male Sexual Health Questionnaire (MSHQ;
Rosen et  al., 2004)  is a 25-​item self-​administered mea-
sure designed specifically to assess sexual function and
satisfaction in aging men with urogenital concerns
often associated with heart disease, prostate cancer, and
benign prostatic hyperplasia/​ lower urinary tract symp-
toms. Disorders of ejaculation are common in men with
these age-​related physical problems, yet erectile function
measures such as the IIEF do not focus specifically on
problems such as delayed or retrograde ejaculation and
diminished sensation, force, or pleasure. The MSHQ
thus addresses three domains of sexual function: erection,
ejaculation, and satisfaction with the sexual relationship.
Assessment for Case Conceptualization and
Treatment Planning
Again, the richest tool for case conceptualization and
treatment planning is the clinical interview, with its
capacity to investigate multiple areas of functioning both
in the client and in the partner. One important area to
assess in the formulation of a treatment plan is the exis-
tence of other mental disorders. Other chapters in this
text elaborate on the assessment of these and thus will not
be covered here. The other area crucial to case concep-
tualization and treatment planning is the assessment of
the nonsexual aspects of the client’s primary relationship
(see also Chapter 22). Table 23.2 provides a listing of self-​
report measures suitable as adjuncts in case conceptual-
ization and treatment planning.
Ideally, the assessment of sexual function should
include the client’s partner if he or she has one and if the
partner is willing to participate. There are multiple func-
tions to partner assessment, including a general assess-
ment of relationship adjustment, the partner’s perception
 Sexual Dysfunction 523

TABLE 23.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly

Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Global Sexual Function

For Use with Men, Women, and Couples
GRISS G G NA A G G G A ✓
DAS G G NA A G G G A ✓
CSI A E NA NR A A G A
DSFI G A NA A A G G A
ISS G E NA A A A A A
GMSEX G E NA G A G G A
NSSS A E NA A G A A A
For Use with Women Only
SSS-​W G G NA A G A A A
FSDS G G NA A G G A A ✓
Dysfunction-​Specific
SDI A G NA A G A A A
PFSF G G NA A G A G A ✓
SIDI-​F G E NA A G A A A

Note: GRISS = Golombok–​Rust Inventory of Sexual Satisfaction; DAS = Dyadic Adjustment Scale; CSI = Couple Satisfaction Index; DSFI = Derogatis
Sexual Functioning Inventory; ISS = Index of Sexual Satisfaction; GMSEX = Global Measure of Sexual Satisfaction; NSSS = New Sexual Satisfaction
Scale; SSS-​W = Sexual Satisfaction Scale for Women; FSDS = Female Sexual Distress Scale; SDI = Sexual Desire Inventory; PFSF = Profile of
Female Sexual Function; SIDI-​F = Sexual Interest and Desire Inventory; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not
Reported.

of and responses to the sexual difficulty, and the presence
of partner sexual dysfunction. This couple assessment can
be enhanced with self-​administered measures of relation-
ship adjustment.
The Dyadic Adjustment Scale (DAS; Spanier, 1976) is
the most widely used instrument for the measurement
of relationship quality. It consists of 32 items in a vari-
ety of response formats that are summed to create a total
score ranging from 0 to 151, with a score of 26.5 or lower
indicating clinical distress. There are also four subscales,
which can be used independently because scores on these
have also shown good reliability and validity:  Dyadic
Consensus (13 items), Dyadic Satisfaction (10 items),
Dyadic Cohesion (5 items), and Affective Expression (4
items). Total DAS scores have been shown to discrimi-
nate between distressed and nondistressed couples and to
identify at-​risk marriages. The measure has also been used
with gay and lesbian couples (Kurdek, 1992). It is easy
to administer (10–​15 minutes) and provides information
about the relationship context within which the sexual
dysfunction exists. A  well-​ validated short-​
form version
(Revised-​DAS; Busby, Christensen, Crane, & Larson,
1995) consisting of 14 items is also available.
A limitation to the DAS and the Revised-​DAS is that
they are only valid for couples who are married or living
together. The Couple Satisfaction Index (CSI; Funk &
Rogge, 2007) was developed using item response theory
and was found to have greater precision of measurement
and enhanced power for detecting differences in relation-
ship satisfaction compared to the DAS. The CSI can be
used in dating, common-​law, or married couples. It con-
sists of 32 items in a variety of response formats that are
summed for a total score ranging from 0 to 161, with a
score of 104.5 or lower indicating clinical distress. Two
shorter versions, the CSI-​ 16 and the CSI-​ 4, are also
available.
Because of the multidimensionality of most measures
of global sexual function, many are appropriate for use
in case conceptualization and treatment planning. Of the
measures already covered in the preceding diagnosis sec-
tion, the GRISS can be useful because it covers corol-
lary cognitions and behaviors, as well as satisfaction and
relationship quality. Measures of sexual satisfaction and
sexual distress can be invaluable in case conceptualiza-
tion and the holistic measurement of treatment outcome,
regardless of the presenting sexual dysfunction. Other
measures include those discussed next.
The Derogatis Sexual Functioning Inventory (DSFI;
Derogatis, 1998; Derogatis & Melisaratos, 1979)  is a
multidimensional measure that assesses constructs asso-
ciated with sexual functioning and general well-​being.
It consists of 254 items arranged into 10 subscales. The
524 Couple Distress and Sexual Disorders
response format is a mixture of yes/​no answers and mul-
tipoint adjectival scales. The 10 dimensions addressed by
the scales are information, experiences, drive, attitudes,
psychological symptoms, affect, gender role definition,
fantasy, body image, and sexual satisfaction. Each scale
provides a separate score, and the linear combination of
the 10 scales yields the Sexual Functioning Index. A sec-
ond global score, the Global Sexual Satisfaction Score,
assesses the individual’s subjective perception of his or
her sexual function. The psychometric soundness of the
measure varies by subscale; thus, it is important to review
relevant research prior to interpreting the results of any
given subscale.
The Index of Sexual Satisfaction (ISS; Hudson, 1998;
Hudson, Harrison, & Crossup, 1981)  is a 25-​item self-​
report measure of dissatisfaction in the sexual aspects of a
couple’s relationship from the perspective of the respon-
dent. In the original measure, items were responded to
on 5-​point adjectival scales describing relative frequency.
The newer version has 7-​point scales and minor item revi-
sions. The measure has been validated in various popu-
lations (Santos-​Iglesias et  al., 2009; Vieira, Pechorro, &
Diniz, 2008).
The Sexual Satisfaction Scale for Women (SSS-​W;
Meston & Trapnell, 2005) has 30 items that are responded
to on 5-​point scales anchored at “strongly agree” and
“strongly disagree” in reference to the respondent’s cur-
rent situation. The detailed breakdown of satisfaction into
separate components (communication, compatibility,
contentment, relational concern, and personal concern)
may be particularly helpful in clarifying the sometimes
confusing relationship between satisfaction/​distress and
sexual difficulties in women.
The Global Measure of Sexual Satisfaction (GMSEX;
Lawrance & Byers, 1995) is a brief five-​item measure of
an individual’s overall positive and negative evaluation of
the sexual relationship. It consists of five word pairs that
are descriptive of the respondent’s sex life and rated on 7-​
point bipolar scales. It is a component of the Interpersonal
Exchange Model of Sexual Satisfaction questionnaire but
can be used independently. It can be completed in less
than 5 minutes and can be used with all genders and sex-
ual orientations.
The New Sexual Satisfaction Scale (NSSS; Štulhofer,
Buško, & Brouillard, 2010) has 20 items that are responded
to on 5-​point scales and across five conceptual dimensions
(sexual sensations, sexual awareness and focus, sexual
exchange, emotional closeness, and sexual activity). Two
subscales are an ego-​centered subscale, which measures
satisfaction with personal experiences and sensations, and
the partner-​and sexual activity-​centered subscale, which
measures satisfaction with one’s partner and sexual activ-
ity. A  short form (NSSS-​S) consists of 12 items and has
similar reliability and validity as the long form (Štulhofer,
Buško, & Brouillard, 2011). The measure is not limited to
a particular sexual orientation, relationship status, gender,
or culture but may be particularly useful for women who
include their partner’s sexual satisfaction in the assess-
ment of their own sexual satisfaction (Mark, Herbenick,
Fortenberry, Sanders, & Reece, 2014; McClelland, 2011).
The Quality of Sex Inventory (QSI; Shaw & Rogge,
2016) is a promising new measure that assesses sexual sat-
isfaction and sexual dissatisfaction as distinct components
of sexual quality. It was developed using item response
theory and has demonstrated increased precision and
power compared to other measures of sexual satisfaction
while retaining strong convergent and construct validity
characteristics. It consists of two 12-​item subscales that are
responded to on 5-​point scales. The short form consists of
two 6-​item subscales.
The FSDS (Derogatis et al., 2002) is designed to mea-
sure sexually related distress in women. It consists of 12
items that describe distressing feelings or problems related
to one’s sexuality or sexual relationships. The items are
responded to on 5-​ point adjectival scales anchored at
“never” and “always” in reference to the past 30  days.
A  revised version (FSDS-​R) added a 13th item to assess
distress related to low sexual desire (Derogatis, Clayton,
Lewis-​ D’Agostino, Wunderlich, & Fu, 2008). Cut-​ off
scores for clinical distress have been published for both
versions (Derogatis et al., 2002, 2008). The measure takes
3 to 5 minutes to complete. Although developed and vali-
dated with women only, the items of the FSDS are gender
neutral. It has been administered to men and is currently
under validation (Santos-​Iglesias, Danko, Robinson, &
Walker, 2016). Currently, men’s results must be inter-
preted with caution because more research is required
to confirm the validity of the FSDS in this population.
The ascertainment of distress over sexual difficulties can
be integral to case conceptualization and treatment plan-
ning, and the FSDS has been shown to be sensitive to
treatment changes.
Assessment for Treatment Monitoring
and Treatment Outcome
Treatment monitoring and outcome is the one assessment
purpose for which the clinical interview is not optimal.
This assessment purpose requires the quantification that
only standardized measurement can provide. Fortunately,
 Sexual Dysfunction 525

the recent explosion in clinical trials for pharmacothera-
peutic agents targeting sexual dysfunction has resulted
in the development of a number of measures designed
specifically for the assessment of treatment monitoring
and outcome. Table 23.3 provides a listing of measures
suitable to treatment monitoring and the assessment of
treatment outcome.
In terms of measures applicable to men, women, and
couples, there are data to support that the GRISS and
the ISS can detect changes attributable to treatment
effects.
The Changes in Sexual Functioning Questionnaire
(CSFQ and CSFQ-​14:  Clayton, McGarvey, & Clavet,
1997; Clayton, McGarvey, Clavet, & Piazza, 1997;
Keller, McGarvey, & Clayton, 2006)  can be clinician
administered as a structured interview (CSFQ-​I) or self-​
administered as a gender-​specific questionnaire (CSFQ-​F
or CSFQ-​M). It measures five dimensions of sexual func-
tioning (frequency of sexual activity, sexual desire, plea-
sure, arousal, and orgasmic capacity), as well as comorbid
conditions, current medications, alcohol and substance
use, and relationship status. The first 21 items apply to
both men and women and are followed by 36 male-​specific
and 35 female-​specific items, answered primarily on 5-​
point Likert-​type scales. Scores on the CSFQ have been
found to be more valid and reliable in female than in
male samples, and most of the available psychometric
data derive from the self-​administered version. An abbre-
viated short-​form version also exists; the CSFQ-​14 also has
gender-​specific versions and is self-​administered. It yields
scores for three scales corresponding to desire, arousal,
and orgasm, as well as for the five scales in the original
long form. The CSFQ-​14 scores appear to improve on the
reliability and validity of the long form, especially with
regard to men. The addition of a short form enhances its
clinical utility because it can be administered quickly in
busy practices and is amenable to immediate clinician
feedback. Although designed with psychiatric patients
in mind, the CSFQ has also been tested in nonclinical
populations and has been found suitable for general use.
In terms of measures specific to female sexual dysfunc-
tion, the BISF-​W, FSDS, and FSFI have all been found
to be sensitive to treatment effects (Derogatis, 2008;
Safarinejad, Hosseini, Asgari, Dadkhah, & Taghva, 2010).
Thus, these measures can be used for treatment monitor-
ing and outcome. In terms of measures specific to male

TABLE 23.3   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation

Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly

Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Global Sexual Function

For Use with Men, Women, and Couples
GRISS G G NA A G G G G A ✓
ISS G E NA A A A A A A
CSFQ/​CSFQ-​14 G A NA A A G G A A ✓
For Use with Women Only
BISF-​W A A NA A A A A A A
FSFI G E NA A G G G G A ✓
MFSQ G A NA A G G G A A ✓
FSDS G G NA A G G A G A ✓
For Use with Men Only
IIEF G G NA A G G G G A ✓
Dysfunction-​Specific
SDI A G NA A G A A A A
IIEF-​5 G G NA A G G A G A
EHS A NA NA A NR G G G A
QEQ G G NA A G A A G A
IPE G A NA A G A A A A
PEP G NR NA A G A A A A

Note: GRISS = Golombok–​Rust Inventory of Sexual Satisfaction; ISS = Index of Sexual Satisfaction; CSFQ/​CSFQ-​14 = Changes in Sexual Function
Questionnaire; BISF-​W = Brief Index of Sexual Functioning for Women; FSFI = Female Sexual Function Index; MFSQ = McCoy Female Sexuality
Questionnaire; FSDS  =  Female Sexual Distress Scale; IIEF/​IIEF-​5  =  International Index of Erectile Function; SDI  =  Sexual Desire Inventory;
EHS = Erection Hardness Score; QEQ = Quality of Erection Questionnaire; IPE = Index of Premature Ejaculation; PEP = Premature Ejaculation
Profile; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.
526 Couple Distress and Sexual Disorders
sexual dysfunction, the IIEF has demonstrated treatment
sensitivity (Derogatis, 2008).
DYSFUNCTION-​S PECIFIC ASSESSMENT
The assessment of any one sexual dysfunction is largely
dependent on the clinical interview. However, the
administration of one or more of the aforementioned
self-​administered measures of global sexual function that
contain a domain pertinent to the dysfunction in question
can be a useful adjunct. Selecting a subset of items from
an instrument can be useful for standardizing the manner
in which particular symptoms are assessed, but it warrants
caution because the psychometric adequacy (of the select
items) would be unknown. Dysfunction-​specific measures
are described in this section, and they are included in
Tables 23.1 to 23.3 as appropriate. A growing number of
dysfunction-​specific measures have been developed dur-
ing the past decade with the advancement of clinical trials
for new medications. When a client presents with symp-
toms of a specific dysfunction, assessment can combine
a clinical interview with self-​report measures and may
involve physiological assessment strategies as appropriate.
Although only a few psychophysiological measures have
been validated for the assessment of sexual dysfunction,
they are discussed briefly to introduce the reader to pos-
sible additions to the multidisciplinary assessment tool kit.
Delayed Ejaculation
Most global sexual function measures inquire about the
occurrence of orgasm and satisfaction with ejaculatory
latency and sensation, but instruments designed specifi-
cally for male sexual dysfunction tend to more adequately
investigate the range of problems that fall under DE. The
IIEF and the BSFI contain one question addressing the
occurrence of and difficulty with ejaculation. The IIEF
adds one more item on the pleasurable sensation of
orgasm, and the BSFI-​M asks directly about satisfaction
with the amount of ejaculate emitted. The best coverage
of orgasmic problems in men, however, is provided by the
MSHQ and the MSHQ-​Ejaculation (MSHQ-​EjD; Rosen
et al., 2007). The MSHQ has seven questions devoted to
ejaculation, its occurrence, delay, volume, force, pain or
discomfort, and pleasure, as well as the occurrence of ret-
rograde ejaculation. Although the MSHQ was designed
for aging men, it can be useful for patients of any age who
report orgasm problems. The MSHQ-​EjD is a four-​item
measure consisting of three ejaculatory function items
and one ejaculatory bother item. This briefer version of
the MSHQ can be used for assessing the diagnosis and
treatment outcomes of DE within an everyday clinical set-
ting, and it can be used with heterosexual, bisexual, and
gay men.
Retrograde ejaculation and emission phase disorders
will likely have a physiological cause; thus, a careful med-
ical history and referral to a physician are important to
assess for potential disease or other biological processes (for
a list of these, see Segraves & Segraves, 1993). Whether
or not biological factors are implicated, a psychosexual
history is necessary to assess psychological and relational
factors contributing to the problem or consequential to it
because this history can be helpful for the purpose of case
conceptualization and treatment planning.
Erectile Disorder
The comprehensive assessment of ED requires a thorough
clinical interview that includes both medical and psycho-
sexual history, physical examination, and laboratory test-
ing. More specialized diagnostic tests may be indicated in
some cases, and these may include Doppler ultrasound
and nocturnal penile tumescence tests (NPT). Self-​report
measures can be helpful in the diagnosis of the problem,
although they are rarely sufficient. General sexual func-
tion measures that inquire about ED are the CSFQ and
the GRISS. Male-​specific measures that explore the exis-
tence and diagnosis of ED in more detail are the BSFI-​
M and the IIEF-​5. Measures specific to ED that track
treatment outcomes are the IIEF, Erectile Hardness
Score (EHS), and the Quality of Erection Questionnaire
(QEQ). In addition, a recently validated measure exists
for assessing ED in men who do not engage in intercourse
(Yuan et  al., 2014); however, this measure requires fur-
ther study. Finally, using the Female Assessment of Male
Erectile Dysfunction Detection Scale, female partners
appear to be able to accurately identify ED, supporting
the integration of a couples-​based approach to the diag-
nosis and treatment of ED (Rubio-​Aurioles et al., 2009).
The IIEF-​5 (Rosen, Cappelleri, Smith, Lipsky, & Pena,
1999) consists of five items from the IIEF that specifically
measure erectile function and intercourse satisfaction.
This measure is also sometimes referred to as the Sexual
Health Inventory for Men. It is easy to administer in the
context of busy general practices, although it does not pro-
vide information about other aspects of the person’s sexual
function. It was designed to tag erectile difficulties and
track treatment-​related changes. The response options are
on 5-​point adjectival scales, and the reference period is

6 months. The IIEF-​5 can be modified for administration
to men who are sexually inactive (Yule et al., 2011).
The EHS (Goldstein et al., 1998) is a one-​item mea-
sure that asks the patient to rate the hardness of his erec-
tion. This measure is useful in monitoring treatment
outcome over regular time points (i.e., across sexual
encounters), both in office and at home. The response
options range from 0 (Penis does not enlarge) to 4 (Penis is
completely hard and fully rigid).
The QEQ (Porst et  al., 2007)  is a six-​item measure
that assesses satisfaction with the quality of erections, spe-
cifically in men who are concerned by their erectile func-
tion. It can be used to monitor treatment-​related changes
in satisfaction with erection quality. The response options
are on 5-​point adjectival scales, and the reference period
is the previous 4 weeks.
Specialized techniques to assess for ED include
NPT, penile strain gauges, the RigiScan Monitor, and
the Doppler ultrasound. The most commonly used
psychophysiologic procedure in the diagnosis of ED is
NPT, based on the assumption that the erections during
the rapid eye movement phase of the sleep cycle rule out
substantial organic etiology. Usually measured in sleep
labs with penile strain gauges that measure circumfer-
ential changes, NPT has demonstrated both valid-
ity and clinical utility (Ghanem & Shamloul, 2008).
The RigiScan Monitor, a small computerized device,
improves on NPT by addressing the issue of rigidity, in
addition to tumescence and duration of erectile episodes
(Meuleman, Hatzichristou, Rosen, & Sadovsky, 2010).
Thermal imaging technology rapidly produces thermal
images indicating the average temperature of less than 1
millimeter of skin with a precision of 0.07°C (Kukkonen,
Binik, Amsel, & Carrier, 2007). Thermal imaging is
significantly associated with self-​reported arousal, has
shown evidence of good test–​retest reliability, and has
been used to distinguish between men with and men
without ED (Kukkonen, Binik, Amsel, & Carrier, 2010;
Sarin, Amsel, & Binik, 2014). Finally, intracavernosal
injection testing and penile duplex ultrasonography have
been found clinically useful in the detection of arterial
inflow abnormalities and venoocclusions (Shamloul &
Ghanem, 2013).
Once ED has been adequately diagnosed, case con-
ceptualization can be greatly enhanced by a sexual, medi-
cal, and psychosocial history to assess for general sexual
functioning; medical, pharmacologic, surgical, and life-
style risk factors; as well as relationship and general psy-
chological well-​being. The physical examination should
focus on genitourinary, neurologic, and cardiovascular
Sexual Dysfunction 527
systems, with laboratory tests focused on endocrine dys-
function (Hatzimouratidis et al., 2010).
Female Orgasmic Disorder
Within a clinical interview, women with lifelong orgas-
mic difficulty will typically report either never having had
an orgasm or difficulty attaining one. Alternately, they
may complain of having lost orgasmic capacity over time
or a lack of pleasure or intensity during orgasm, or even
not knowing whether or not they have had an orgasm.
Almost all of the self-​administered measures of general
and female-​specific sexual function covered in this chap-
ter inquire directly about orgasm and can be helpful in
indicating a potential problem. Although most of the
questions embedded in these global sexual function ques-
tionnaires are not sufficient to establish a nuanced clinical
picture of the many variations possible in female orgas-
mic difficulty, question 15 on the Female Sexual Distress
Scale/​Desire Arousal Orgasm correlates well with clini-
cian diagnosis and has been suggested as an appropriate
tool for evaluating treatment benefit in FOD (Dickstein,
Goldstein, Tkachenko, & Kreppner, 2013). The clinical
interview remains the best diagnostic tool for the assess-
ment of orgasmic difficulties in women. Mah and Binik’s
(2002) Orgasm Rating Scale (ORS) is an interesting
addition to the assessment of orgasm for both men and
women. It is not designed to assess anorgasmia per se but,
rather, the cognitive–​affective and sensory components
of orgasm. This measure may be useful in identifying
determinants of orgasmic pleasure as part of a treatment
program for women or men who are not completely anor-
gasmic. In terms of psychophysiological instruments, the
GenitoSensory Analyzer (GSA) is a quantitative sensory
testing tool that measures the vibratory and thermal sen-
sations of the vagina and clitoris. The GSA has shown
promise for assessing and diagnosing FOD (Helpman,
Greenstein, Hartoov, & Abramov, 2009), but it has similar
constraints as those mentioned for the psychophysiologi-
cal instruments used to assess FSIAD.
Female Sexual Interest/​Arousal Disorder
A clinical interview for FSIAD should include questions
about the frequency and intensity of sexual interest, sex-
ual thoughts, past and current responses to sexual stim-
uli, relationship factors, and physical sensations related
to sexual activity. The following measures for assessing
FSIAD were developed for the diagnosis of hypoactive
sexual desire disorder (HSDD) and female sexual arousal
528 Couple Distress and Sexual Disorders
disorder (FSAD), which were replaced with FSIAD in the
DSM-​5. It will take time for clinically relevant measures
for FSIAD to be developed and validated; in the mean-
time, we must rely on previous tools.
In terms of self-​administered measures, the CSFQ,
BISF-​ W, and MFSQ all inquire about sexual interest
and arousal in general terms, but the inquiry is limited
to one or a few questions. The CSFQ and BISF-​W also
contain questions about comorbid conditions that might
impact desire and arousal, such as relationship status and
use of medications and other substances. The FSFI has
two questions about sexual desire, four questions about
general sexual arousal, and four about lubrication. The
FSFI appears to be valid for use in women with FSIAD
(Opperman, Benson, & Milhausen, 2013). The SFQ
has eight questions devoted to arousal and six questions
to assess desire. An adapted version of the SFQ (SFQ-​28;
Symonds et al., 2012) has been validated in women with
HSDD and FSAD, suggesting that it may be appropri-
ate for those with FSIAD. The Sexual Desire Inventory
(SDI) and the Decreased Sexual Desire Screener (DSDS;
Clayton et al., 2009) have been validated in women with
HSDD and could be used to assess problems with desire;
however, arousal is not assessed in these measures.
The Profile of Female Sexual Function (PFSF;
Derogatis et  al., 2004; McHorney et  al. 2004)  is a 37-​
item self-​report instrument that was designed to assess
symptoms of HSDD. It covers seven domains:  desire,
arousal, orgasm, pleasure, sexual concerns, responsive-
ness, and self-​image. A brief version—​the Brief-​Profile of
Female Sexual Function (B-​PFSF)—​has been validated
in postmenopausal women and includes 5 items from the
PFSF and 2 items from the Personal Distress Scale (Rust
et al., 2007).
The Sexual Interest and Desire Inventory (SIDI-​F;
Clayton et  al., 2006)  is a clinician-​administered instru-
ment designed to quantify the severity of symptoms in pre-
menopausal women diagnosed with HSDD and to track
symptom changes in response to treatment. The 13 items
cover relationship–​sexual, receptivity, initiation, desire–​
frequency, affection, desire–​ satisfaction, desire–​
distress,
thoughts–​ positive, erotica, arousal–​ frequency, arousal–​
ease, arousal–​continuation, and orgasm. The SIDI-​F was
initially validated in samples of women with HSDD or
FSAD (Clayton et al., 2010). Compared to the measures
described previously, this scale is briefer and shows higher
specificity in assessing the severity and frequency of desire
and arousal symptoms. Past studies have excluded women
with comorbid HSDD and FSAD; thus, further research
is required to establish the validity and reliability of scores
on this measure in women diagnosed with FSIAD.
A physical examination that includes examining
the pelvic floor muscle and vagina for possible atrophy,
infections, or pain could be included in the assessment
(Brotto & Luria, 2014). Unlike the clinical assessment
of male erectile dysfunction, the assessment of female
sexual interest and arousal has historically relied almost
exclusively on self-​report. The experience of sexual desire
may emerge subsequent to sexual arousal initiated by a
sexually meaningful stimulus rather than always preced-
ing arousal (Laan & Both, 2008). This discovery and oth-
ers have stimulated research focused on objective genital
arousal assessment instruments.
Attempts to measure lubrication, clitoral engorge-
ment, and uterine contractions have met with little suc-
cess for a variety of reasons (see Meston, 2000; Prause &
Janssen, 2006). Vaginal blood flow has been most ame-
nable to measurement, and the most frequently used
instrument is the vaginal photoplethysmograph (VPP),
a tampon-​like, light-​emitting device that measures vaso-
congestion via the amount of light reflected back from
the vaginal walls. However, VPP results do not necessar-
ily represent vaginal wall engorgement, and associations
with self-​reported arousal have been weak (Chivers, Seto,
Lalumière, Laan, & Grimbos, 2010; Prause & Janssen,
2006). The labial thermistor clip is a surface temperature
probe fastened to the labia minora (Janssen, 2001; Payne
& Binik, 2006). The thermistor clip is associated with self-​
reported arousal, and there is evidence for discriminant
validity (Kukkonen, 2015). Thermal imaging (described
previously in the section on assessments specific to ED)
has been successfully used to measure arousal in com-
munity samples and in women reporting pain during
intercourse (Cherner & Reissing, 2013; Kukkonen et al.,
2010). Magnetic resonance imaging is now also being
applied to the measurement of genital vasocongestion, as
well as brain activation during sexual arousal (Maravilla,
2006). A recent review reported that laser Doppler imag-
ing, which measures superficial blood flow in the geni-
tal area using an infrared laser beam, provides the most
valid and reliable psychophysiological data on female
sexual arousal (Kukkonen, 2015). It is the only tool that
measures direct blood flow, and it appears to distinguish
between women with and those without sexual dysfunc-
tion (Boyer, Pukall, & Chamberlain, 2013). Furthermore,
there is support for its discriminant validity and test–​retest
reliability (Waxman & Pukall, 2009). The clinical utility
of all these instruments is constrained by the necessity of
 Sexual Dysfunction 529

sexual arousal induction, equipment, trained technicians, approximately 20–​25 minutes). There are three supple-
and, sometimes, interpretive problems. mental scales (additional pain descriptors, coping styles,
and romantic partner factors) that take 10 minutes each
to complete. There is also a screener version composed of
Genito-​Pelvic Pain/​Penetration Disorder
38 items containing all the descriptive questions from the
An understanding of GPPPD requires the assessment full version as well as items selected from each of the sub-
of sexual function and of pain. Self-​administered sexual scales. The authors of the VPAQ found support for con-
function measures, such as the CSFQ, GRISS, MFSQ, struct, convergent, and discriminant validity, as well as the
and BISF-​W, contain one question to assess the existence internal consistency of scores on the measure. Although
and frequency of pain with intercourse. The SFQ and the further research is required, the VPAQ is the first measure
FSFI have questions related to frequency and intensity of specific to the assessment of genital pain and shows prom-
the pain, and the SFQ includes a question regarding wor- ise as a useful tool for the evaluation of GPPPD.
rying about pain. Scores on both the FSFI and the SFQ The clinical interview for GPPPD should contain
have been found to have good discriminant validity in the questions on the history, onset, location, quality, duration,
assessment of chronic vulvar pain (Legocki, Aikens, Sen, and intensity of the pain because these pain character-
Haefner, & Reed, 2013). A  measure of sexual distress, istics have been found to have discriminant validity in
such as the FSDS (Derogatis et al., 2002), should also be the differentiation of pain subtypes (Meana et al., 1997).
included in the assessment of GPPPD. Other details that should be queried are the experience
General pain measures found to be useful in the con- of pain in nonsexual contexts, cognitive distortions, fac-
ceptualization and treatment planning of GPPPD are the tors that might reduce or exacerbate pain symptoms, and
McGill Pain Questionnaire (MPQ; Melzack, 1975), the any previous treatment attempts and associated outcomes
Pain Catastrophizing Scale (PCS; Sullivan, Bishop, & (Bergeron et  al., 2014). The impact of the pain on sex-
Pivik, 1995), as well as visual analogue scales and pain dia- ual activity, relationships, and psychological function-
ries (Payne, Bergeron, Khalife, & Binik, 2006). In addition ing is also important to cover. As previously mentioned,
to a large number of studies attesting to the reliability and the diagnosis of GPPPD does not apply to men. Sexual
validity of the MPQ scores for a wide range of pain experi- functioning measures for men do not include questions
ences, it has been shown to distinguish between different about pain, which has probably contributed to the dearth
subtypes of GPPPD (Meana, Binik, Khalife, & Cohen, of research on this problem. The pain measures described
1997). The PCS, another widely validated general pain previously and the clinical interview information are
measure, is useful for determining the amount of pain-​ likely relevant for the assessment of pain in men as well,
related distress and in formulating cognitive treatment and they would involve adaptation to the male context of
strategies. Pain-​related distress is particularly germane to pain during penetrative activities or ejaculation.
women who catastrophize about their intercourse pain A physical examination that aims to replicate the pain
and who experience pelvic floor muscle dysfunction dur- experienced with attempted penetration is a necessary
ing intercourse (Pukall, Binik, Khalife, Amsel, & Abbott, component of assessment. The physical examination
2002; Reissing et al., 2004). Consistent with a biopsycho- should include a cotton-​swab palpation of the vulva and
social model of genito-​pelvic pain, partner responses to a pelvic examination, during which the woman is asked
the pain significantly impact women’s pain experience to rate the intensity of the pain. An instrument called the
(Rosen, Bergeron, Sadikaj, & Delisle, 2015) and should vulvalgesiometer was developed to standardize palpation
be considered in the assessment of GPPPD. pressure and discriminates between women with and
The Vulvar Pain Assessment Questionnaire Inventory those without GPPPD (Pukall, Young, Roberts, Sutton,
(VPAQ; Dargie, Holden, & Pukall, 2016)  is a novel & Smith, 2007; Tu, Fitzgerald, Todd, Todd, & Harden,
63-​item assessment tool developed to measure biopsy- 2007). The palpation serves to both locate the pain pre-
chosocial aspects of vulvar pain. The VPAQ contains cisely and establish the sensitivity of the hyperalgesic
descriptive questions about pain characteristics and asso- area, if one is identified. Assessment of vulvar or pelvic
ciated symptoms, as well as the following subscales: pain diseases is another important goal of medical referral. For
severity, emotional response, cognitive response, life example, the assessment of pelvic floor tonicity has gained
interference, sexual functioning interference, and self-​ wider acceptance because it has been shown to discrimi-
stimulation/​penetration interference (completion time of nate between women with and those without GPPPD
530 Couple Distress and Sexual Disorders
(Reissing, Brown, Lord, Binik, & Khalife, 2005). Recently,
transperineal four-​dimensional ultrasound (consisting of a
probe applied to the surface of the perineum) has been
used as a pain-​free measure of pelvic floor tonicity in
women with a specific type of GPPPD (Morin, Bergeron,
Khalifé, Mayrand, & Binik, 2014).
Male Hypoactive Sexual Desire Disorder
MHSDD is perhaps the most difficult sexual dysfunc-
tion to diagnose in men because it is not anchored in the
absence of an expected discrete event (e.g., erection and
orgasm). Diagnostic assessment is usually based on the
presenting complaint of distress about desire level, taking
into account natural discrepancies between members of a
couple. In addition to the clinical interview, an operation-
alization of the severity of the problem can be facilitated
by self-​administered measures. Global sexual function
measures that have domains specific to desire are the
CFSQ, DSFI, GRISS, BSFI-​M, and IIEF. The advantage
of these multidimensional measures of desire is that they
may also be helpful for the purpose of case conceptualiza-
tion because they provide information on the existence of
comorbid sexual dysfunctions, can also be administered
to the partner, and, in some cases, provide information
about relationship quality and satisfaction. However,
there is only one desire-​specific self-​administered mea-
sure for men with acceptable psychometric properties and
clinical utility—​the SDI. The SDI can also be used in
combination with the FSDS to evaluate distress related to
low desire, as the wording in the FSDS is gender-​neutral.
However, the FSDS still requires validation in men.
The SDI (Spector, Carey, & Steinberg, 1996) is a 14-​
item self-​report measure of dyadic and solitary desire for
use with men and women. Its focus is primarily on cog-
nitive rather than behavioral dimensions of desire. Each
item is responded to according to the intensity of feeling or
frequency of occurrence on 7-​or 8-​point adjectival scales
and yields scores for dyadic desire and solitary desire, as
well as a total score. Because of its cognitive emphasis,
it can be particularly useful in cognitive–​behavioral case
conceptualizations.
In the absence of psychological, relational, situ-
ational, or disease-​related factors that could account for
a decline in desire, clinicians are increasingly turning to
the assessment of sex hormone levels as aids in the case
conceptualization and treatment planning of MHSDD.
Links have been found between sexual desire and vari-
ous hormones in men, including testosterone; however,
it is important to note that no single hormone level has
been found to be predictive of low desire (Rubio-​Aurioles
& Bivalacqua, 2013).
Premature (Early) Ejaculation
The assessment of PE has been complicated by variations
in what is considered a normal ejaculatory latency by
expert opinions and by the patient himself. In clinical tri-
als, intravaginal ejaculation latency time (IELT) is usually
assessed by means of a stopwatch; however, this is not a
viable assessment technique in clinical practice. Because
PE depends not only on objective measurement but also
on patient distress, most clinicians do not use IELT cut-​
off points to assess PE. Assessment usually relies more on
clinical impression and patient distress gathered from the
clinical interview (Perelman, 2006). The GRISS contains
a subscale for PE, and it can be used for diagnosis of PE.
There are also two recently developed self-​administered
measures designed for diagnosing PE that include patient
distress and can also be used for assessing treatment out-
comes: the Index of Premature Ejaculation (IPE; Althof
et  al., 2006)  and the Premature Ejaculation Diagnostic
Tool (PEDT; Symonds et  al., 2007). The Premature
Ejaculation Profile (PEP; Patrick et  al., 2005)  was
designed specifically for monitoring treatment outcomes
in men with PE. Note that the IPE, PEDT, and PEP were
created based on DSM-​IV-​TR criteria for PE, which did
not include specific criteria on the frequency and dura-
tion of PE symptoms, nor on ejaculatory latency of less
than 1 minute after penetration.
The IPE (Althof et al., 2006) consists of 10 items that
assess subjective aspects of the overall experience of PE
from the patient perspective. The tool was designed both
for diagnosis and as a more encompassing alternative to
single-​ item patient-​
reported treatment outcomes. The
response items are on 5-​point adjectival scales, and the
reference period is the past 4 weeks.
The PEDT (Symonds et  al., 2007)  is a five-​item
measure that captures the main elements of the DSM-​
IV-​TR criteria for premature ejaculation. This measure
was designed to be a validated, brief tool to standard-
ize the diagnosis of the absence or presence of PE in
clinical trials. The response items are on 4-​point scales
and ask about the patient’s general experience with
intercourse.
The PEP (Patrick et  al., 2005)  consists of four items
and can be used in three different ways: for examining the
PE domains separately, as an overall index score, and as a
profile score (Patrick et al., 2009). It was designed specifi-
cally for monitoring treatment outcomes in men with PE.

The response items are on 5-​point scales, and the refer-
ence period varies depending on each item.
The clinical interview should assess whether the PE
is likely to be attributable to psychological traits, distress,
psychosexual skills deficits, relationship problems, and/​or
physical illness or injury (Althof, 2014). Metz and Pryor
(2000) provided a useful decision tree for the aforemen-
tioned classifications and potential etiologic pathways.
Perelman (2006) stressed the importance of assessing
whether the patient is able to detect premonitory sensa-
tions (bodily changes reflecting arousal/​impending ejac-
ulation) because this is necessary in order to choose to
ejaculate or to delay ejaculation.
CONCLUSIONS AND FUTURE DIRECTIONS
The multidimensionality of sexual function and its prob-
lems poses a formidable challenge to both research and
clinical practice. With lengthy laundry lists of potential
etiologies for all the sexual dysfunctions, the isolation
of any one predominating factor or even of a reasonably
articulated system of interdependent factors is exceedingly
difficult. It is against this backdrop of complexity that cli-
nicians are left to diagnose, conceptualize, and treat. No
single measure of sexual function can provide sufficient
information regarding the affective, cognitive, behavioral,
relational, and social contexts within which the sexual dif-
ficulties have arisen or are perpetuated. Only the clinical
interview has the flexibility to encompass an individual
client’s specific circumstances, yet it is compromised by
potential reliability and validity deficiencies and by the
fact that instrumental details affecting the sexual difficul-
ties tend to emerge long after the initial intake. For this
reason, assessment needs to be an integrated component
of treatment at all stages, to track efficacy and to revise
strategies as information and conditions change.
Despite their limitations, self-​administered measures
and psychophysiological tests can be useful in diagnosis,
case conceptualization, and the monitoring of treatment
progress. The clinical interview does not lend itself well
to repeat administrations or to the operationalization of
changes in sexual function. Indeed, the U.S. Food and
Drug Administration requires the use of psychometri-
cally valid tools in clinical trials of new drug treatments.
Regardless of complexities in the etiology and mainte-
nance of sexual difficulties, simple measures of drive,
frequency, pleasure, or pain can indicate improvement,
stasis, or deterioration. Elaboration on the meaning of the
changes can follow, but their quantification is essential
Sexual Dysfunction 531
to the client’s and the clinician’s evaluation of progress.
Self-​administered measures are also integral to screening
of sexual function in health care settings. After decades of
urging the medical profession to attend to sexual health
as a primary component of an overall health assessment,
sex researchers have made great strides toward providing
them with the tools to do so accurately.
Certainly there is more work to be done, and many
sexual function measures require additional psychomet-
ric validation. There is a paucity of independent valida-
tion and data supporting long-​term test–​retest reliability,
validity generalization, treatment sensitivity, and clinical
benefit. Achieving high psychometric standards is an
important research goal that will increase our confidence
in the continued use of these measures and encourage
other disciplines to engage in the assessment of sexual
function. The concerning move toward medicalization
has had the unexpected benefit of promoting the devel-
opment of clinically useful measures for use in clinical
trials. We must remain vigilant that the originating drive
for the development of these measures does not result in
reductionist assessment tools that miss the forest for the
trees or that neglect to address the specific concerns of
minority populations.
Most sexual function measures are penile–​ vaginal
intercourse centered and validated with predominantly
Caucasian, heterosexual, abled populations. There have
been recent developments on how to administer some
tools to individuals who are currently sexually inactive, as
well as validation for use of tools across sexual orientations
(Coyne et  al., 2010; Štulhofer et  al., 2010; Yule et  al.,
2011). There is little research on culturally informed
assessment and treatment for sexual difficulties over and
above concerns about high-​risk behaviors (Lewis, 2004).
Cultural norms are important to prevent sexual function
measures from pathologizing groups that fall outside of
mainstream expectations. The cross-​national validation of
some sexual function measures designed for clinical trials
and Laumann et al.’s (2006) work on the sexual well-​being
of older adults in 29 countries are good examples of this
culturally informed direction. The sexual health of indi-
viduals with disabilities or chronic illness has also been
neglected. The norming of existing measures, as well as
the development and validation of measures specific to
ethnocultural groups, sexual minorities, and individuals
with disabilities, is long overdue.
Finally, note that the much needed corrective trend
toward the investigation of female sexual dysfunction
may now need to be matched by one that revisits the
complexity of male sexual function. There are now many
532 Couple Distress and Sexual Disorders
more measures for the assessment of female than of male
sexual function. The “age of Viagra” may have reduced
male sexual function to a medically produced erection.
Although the male sexual response may be more predict-
able than the female one, we risk simplifying and doing a
disservice to male sexual function.
In conclusion, sexual health as defined by the World
Health Organization is a state of physical, emotional,
mental, and social well-​being related to sexuality, which
is respectful and free of coercion and discrimination
(Edwards & Coleman, 2004). Clearly, this encompasses
much more than the absence of dysfunction, but it does
includes dysfunction. Our endeavors to develop effective
assessment strategies are instrumental in the promotion of
sexual health. We cannot address problems without the
proper tools to identity them. Ensuring that these strate-
gies are both accurate and inclusive is essential.
ACKNOWLEDGMENTS
The authors thank Nicole Snowball and Kayla Mooney
for their assistance in preparing this chapter.
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 Part VIII

Health-​Related Problems
 24
Eating Disorders
Robyn Sysko
Sara Alavi
This chapter presents the most commonly used and well-​
validated eating disorder assessments for the purposes of
diagnosis, case conceptualization and treatment plan-
ning, and treatment monitoring and treatment outcome.
General information is also presented as an introduction
to the topic of assessment, including the criteria for an
eating disorder diagnosis, prevalence and incidence of
eating disorders, common comorbidities, treatment out-
comes, and etiology of the disorders. Although structured
or semi-​structured interviews or self-​report questionnaires
are often used in research studies, and have demonstrated
their value for studying the nature of eating disorders
in research, the assessments also have promise as clini-
cal tools. As such, this chapter provides information for
practitioners interested in using these measures in clinical
practice.
NATURE OF EATING DISORDERS
The fifth edition of the Diagnostic and Statistical Manual
for Mental Disorders (DSM-​ 5; American Psychiatric
Association [APA], 2013)  introduced several changes to
the chapter on feeding and eating disorders. An important
decision in DSM-​5 was to combine conditions previously
listed in both the Eating Disorders and the Feeding and
Eating Disorders of Infancy or Early Childhood sections
into a single section, thereby including pica, rumination
disorder, and a new category of avoidant/​restrictive food
intake disorder (ARFID). Given the focus of this chap-
ter on eating disorders, notable alterations to criteria for
anorexia nervosa (AN), bulimia nervosa (BN), binge eat-
ing disorder (BED), and revisions to residual category for
eating disorders are briefly described here.
541
Eating Disorder Categories
Anorexia Nervosa
The DSM-​5 criteria for AN differ from earlier categoriza-
tions in several ways, although the hallmark of AN contin-
ues to be the presence of a significantly low body weight.
The description of this symptom was altered to eliminate
the term “refusal” from DSM-​ IV (APA, 1994), which
avoids a perception that individuals with AN are making
a conscious choice, and also focuses on the importance
of altered energy intake through reduced food intake
and/​or increased physical activity (APA, 2013). An exam-
ple of percent ideal body weight is not provided, which
requires clinicians to determine whether an individual’s
weight is low given age, sex, and developmental trajectory.
Individuals with AN are also expected to demonstrate a
fear of gaining weight; DSM-​5 accommodates individu-
als who deny this criterion, but their overt behavior (e.g.,
avoidance of high-​calorie foods and reluctance to con-
sume a range of foods) must be consistent with fear. A dis-
turbance in shape or weight was retained in the diagnosis,
but a “persistent lack of recognition” of the seriousness of
low weight was offered as a clarification of the phenom-
enon. The greatest change from the DSM-​IV criteria for
AN was eliminating the requirement for amenorrhea.
Individuals who do not regularly engage in binge eating
or purging behaviors (i.e., self-​induced vomiting and laxa-
tive or diuretic abuse) continue to be classified as having
AN-​restricting type (AN-​R), and those reporting binge eat-
ing or purging are diagnosed with AN-​binge-​eating/​purg-
ing (AN-​B/​P) type. Some studies have noted an increase
in rates of individuals diagnosed with AN, which likely
results from cases previously placed in the residual not
otherwise specified category in DSM-​ IV moving to a
542 Health-Related Problems
formal category under DSM-​5, including one retrospec-
tive study that noted an increase of 14% in diagnoses of
AN in a clinical sample after applying DSM-​5 criteria
(Gualandi, Simoni, Manzato, & Scanelli, 2016).
Bulimia Nervosa
Changes to the criteria for BN in DSM-​5 were modest.
Diagnostic criteria require that individuals report recurrent
episodes of binge eating and inappropriate compensatory
behavior (e.g., self-​induced vomiting, fasting, and exces-
sive exercise). On the basis of a literature review (Wilson
& Sysko, 2009), the required frequency of these episodes
was lowered from at least twice weekly in DSM-​IV to once
weekly over a 3-​month period in DSM-​5, and people meet-
ing diagnostic criteria are required to experience an undue
influence of shape and weight on their self-​evaluation. An
episode of binge eating is characterized by consuming a
large amount of food and the experience of a loss of control
over eating. A reapplication of DSM-​5 criteria to a clinical
sample identified a 2.4% increase in the rate of BN diagno-
ses (Gualandi et al., 2016). The classification of individuals
with BN with either the purging or the nonpurging type
was considered to be of limited utility and frequently not
employed (Peat, Mitchell, Hoek, & Wonderlich, 2009);
therefore, this subtyping scheme was eliminated.
Binge Eating Disorder
A major shift in DSM-​5 was the formal recognition of BED
as a diagnosis. Individuals with BED experience recurrent
episodes of binge eating, at least once weekly over a 3-​month
period, parallel with the criterion for BN, in the absence
of compensatory behaviors. To be diagnosed with BED,
individuals must experience distress over their binge eating
episodes, have binge eating episodes characterized by eat-
ing large amounts of food during a short time and a sense
of loss of control during the episode, and report three of the
following:  eating until feeling uncomfortably full; eating
large amounts of food when not physically hungry; eating
much more rapidly than normal; eating alone because of
embarrassment; and feeling disgusted, depressed, or guilty
after overeating. Obesity, or the presence of excess body
weight, is listed as a general medical condition and not an
eating disorder within the DSM-​5 system.
Residual Categories
Two new residual categories in DSM-​5 divide the group
with clinically significant eating pathology formerly
identified with DSM-​ IV eating disorder not otherwise
specified (EDNOS), namely other specified feeding and
eating disorder (OSFED) and unspecified feeding and
eating disorder (UFED). The OSFED category includes
the five example clinical presentations of atypical anorexia
nervosa, subthreshold binge eating disorder, purging dis-
order, and night eating syndrome. All other individuals
are classified within the UFED category. Several stud-
ies examined changes in prevalence of residual diagno-
ses post-​DSM-​ 5 criteria, with the general observation
that rates of residual diagnoses are substantially reduced
(Caudle, Pang, Mancuso, Castle, & Newton, 2015; Keel,
Brown, Holm-​ Denoma, & Bodell, 2011; Machado,
Gonçalves, & Hoek, 2013; Mustelin et al., 2016; Ornstein
et al., 2013).
Prevalence
In comparison to other psychiatric diagnoses, such as
major depression or substance abuse, eating disorders are
relatively rare among the population. The prevalence of
eating disorders in the general population appears to be
increasing, although this may be a result of the recently
broadened diagnostic criteria (Lindvall Dahlgren &
Wisting, 2016; Qian et al., 2013). A meta-​analysis includ-
ing data from 15 global epidemiological studies of the
general population reported the lifetime prevalence of
BED as the highest (2.2%), followed by BN (0.81%) and
AN (0.21%), using the DSM-​IV scheme (Qian et  al.,
2013). Eating disorders are more common when consid-
ering only adolescents, with the highest incidence rate
in females aged 15 to 19  years at 109.2 per 100,000 in
a year, comprising approximately 40% of all cases of AN
(Smink, van Hoeken, & Hoek, 2012). In adolescents, the
point prevalence of BED is the highest (3.7% females,
0.5% males), followed by AN (1.2% females, 0.1% males)
and BN (0.6% females, 0.1% males) (Smink, van Hoeken,
Oldehinkel, & Hoek, 2014). Estimates of the prevalence
of BED among the general population are typically
higher than those of AN and BN (Cossrow et  al., 2016;
Kessler et al., 2013; Smink et al., 2012). Based on DSM-​5
criteria, the 12-​month BED prevalence estimate is 1.6%
(2.0% and 1.2% in women and men, respectively). As
expected with the broader diagnostic criteria, this estimate
is higher than the estimate based on DSM-​IV-​TR (1.2%;
APA, 2000). Similarly, the lifetime prevalence of BED as
determined by DSM-​5 criteria is 2.0% (2.6% and 1.5% in
women and men, respectively) compared to the DSM-​IV-​
based estimate of 2.07% (Cossrow et al., 2016). The gap
between women and men in prevalence rates for BED is

significantly smaller than that of AN and BN, with several
studies showing that BED is roughly as common in men
as it is in women (Lewinsohn, Seeley, Moerk, & Striegel-​
Moore, 2002; Mond & Hay, 2007; Streigel-​Moore et al.,
2009). However, among samples of obese individuals,
prevalence estimates can be up to 8% (Striegel-​Moore &
Franko, 2003).
Culture and Sex Differences
Although eating disorders are often considered to be cul-
turally bound syndromes, AN has been documented in
every region of the world (Keel & Klump, 2003). In addi-
tion, the prevalence of AN is similar in Western and non-​
Western countries; therefore, AN does not appear to occur
solely, or even more frequently, in Western countries
(Keel & Klump, 2003). Although BN has been observed
outside of Western countries, Western cultural influences
appear to play a more significant role in the development
of this disorder, and an increase in the incidence of BN
was also observed during the latter half of the twentieth
century (Keel & Klump, 2003).
Although epidemiological studies consistently esti-
mate eating disorders in males to occur at a lower fre-
quency than for females, more recent data have found
smaller discrepancies in the rates between genders,
including a 3:1 ratio of women to men with either AN
or BN (Hudson, Hiripi, Pope, & Kessler, 2007). Several
important gender differences should be taken into con-
sideration when interpreting these findings, such as the
attribution of this increase in estimates among males with
AN or BN to (a) an actual rise in numbers of cases, (b) less
gender bias in the diagnostic criteria, or (c)  a greater
awareness of eating disorders in males (Hildebrandt &
Craigen, 2015). Body image disturbances in males typi-
cally present in one of two dimensions: muscularity and
body fat. Men and boys who are preoccupied with achiev-
ing thinness with limited muscularity concerns more
easily map onto the existing criteria for classic eating
disorders related to the drive for thinness. On the other
hand, men and boys who have an extreme desire for mus-
cularity are more likely to have symptoms of muscle dys-
morphia, a subtype of body dysmorphic disorder in males
that has been termed “reverse anorexia.” The defining
feature of muscle dysmorphia is a drive for leanness and
muscularity and not a desire for thinness (Hildebrandt &
Craigen, 2015; Hildebrandt, Schlundt, Langenbucher, &
Chung, 2006; Pope, Gruber, Choi, Olivardia, & Phillips,
1997). Differences in core motivation for the achieve-
ment of a physical ideal not based on thinness have led
Eating Disorders 543
to suggestions that the symptoms of body image distur-
bance in males could manifest very differently from those
observed in females (Hildebrandt et al., 2011). Along with
a shared body image disturbance, behavioral symptoms in
males with AN and muscle dysmorphia include both diet
and exercise disturbances (Murray et al., 2012), but these
conditions differ in that in muscle dysmorphia, the pri-
mary disturbance relates to body image, whereas for AN
and other eating disorders, the primary disturbance is eat-
ing pathology (Hildebrandt & Craigen, 2015). Males with
an excessive drive for muscularity often engage in the use,
and sometimes abuse, of illicit substances called appear-
ance and performance enhancing drugs (APEDs) such as
anabolic steroids to further control their physical appear-
ance (Pope, Kanayama, & Hudson, 2012). Understanding
the distinct motivations for weight and shape control in
men and boys that drive their impairment is necessary
before we can adequately assess eating disorder sympto-
mology in this half of the population.
Etiology, Comorbidities, Prognosis, and Treatment
The etiology of eating disorders is complex; however,
some biological, environmental, and psychosocial factors
may increase an individual’s risk for developing these dis-
orders. The interaction of biological (e.g., hormones) and
psychological changes in adolescence likely influences
the development of these disorders because the major-
ity of individuals experience the onset of eating disorders
near puberty, and a greater proportion of young women
are affected by eating disorders. In addition, social influ-
ences, such as peers, can affect beliefs about shape and
weight or dieting (Jones & Crawford, 2006), and cultural
influences, including the influence of mass media, can
produce increases in body dissatisfaction and eating distur-
bances (Becker, Burwell, Gilman, Herzog, & Hamburg,
2002). Genetic factors may also predispose individuals to
the development of eating disorders; however, there are
currently no specific genes that are consistently identi-
fied as specific to patients with eating disorders. Thus,
biological, social, cultural, genetic, and other variables
likely influence the etiology of eating disorders, but it is
not known whether different factors are responsible for
the development of these disorders and maintenance of
symptoms or if an interaction of these factors is a better
explanation.
Comorbid psychiatric diagnoses are common
among treatment-​seeking patients with eating disorders.
Prevalence rates of a lifetime anxiety disorder range from
approximately 33% to 72% of patients with AN-​R, 55%
544 Health-Related Problems
of patients with AN-​B/​P, 41% to 75% of patients with BN
(Godart, Flament, Perdereau, & Jeammet, 2002), and
29% of patients with BED (Wilfley, Friedman, et  al.,
2000). Rates of lifetime major depressive disorder range
from 9.5% to 64.7% of patients with AN-​R, 50% to 71.3%
of patients with AN-​B/​P, 20% to 80% of patients with
BN (Godart et al., 2007), and 58% of patients with BED
(Wilfley, Friedman, et al., 2000). Some data suggest that
comorbid depressive symptoms improve with success-
ful treatment, as statistically significant improvements
in mood symptoms have been observed among inpa-
tients with AN receiving nutritional rehabilitation and
psychotherapy after weight restoration (Meehan, Loeb,
Roberto, & Attia, 2006) and patients with BN after treat-
ment with cognitive–​behavioral therapy (CBT; Wilson &
Fairburn, 2002).
The prognosis for individuals with eating disorders
varies across diagnostic categories. Anorexia nervosa has
the highest mortality rate of all psychiatric disorders, and
few treatments, psychological or pharmacological, have
been found to be particularly effective for patients with
AN (Zipfel, Giel, Bulik, Hay, & Schmidt, 2015). One
study reported the expected long-​term course and out-
come of patients with AN as follows: 27.5% experienced
a good outcome, 25.3% had an intermediate outcome,
39.6% had a poor outcome, and 7.7% had died (Fichter,
Quadflieg, & Hedlund, 2006). Individuals with AN who
are younger or receive treatment after a short duration of
illness may experience better treatment outcomes com-
pared to adults with a longer course of illness (Forsberg &
Lock, 2015; Herpertz-​Dahlmann et al., 2001).
Two forms of treatment, CBT and antidepressant med-
ication, have been found to be helpful for the treatment
of BN. Patients treated with CBT typically experience a
reduction in binge eating and purging of 80% or more,
and approximately 30% of patients are abstinent from
binge eating and purging at the end of treatment (National
Institute for Clinical Excellence, 2004). Antidepressant
medications are consistently superior to placebo in phar-
macological treatment studies for BN, and median reduc-
tions of up to 70% have been observed for symptoms of
binge eating and vomiting (Agras, 1997; Bacaltchuk &
Hay, 2003; Shapiro et al., 2007). The selective serotonin
reuptake inhibitor fluoxetine is the only drug approved by
the U.S. Food and Drug Administration for the treatment
of bulimia nervosa, with the most effective dose identified
as 60 mg/​day (Fluoxetine Bulimia Nervosa Collaborative
Study Group, 1992). Despite the availability of effective
treatments, the symptoms of BN can be chronic for some
individuals, with recovery rates (not fulfilling diagnostic
criteria of any eating disorder) of approximately 50% for
both DSM-​5 and DSM-​IV BN documented after 6 years
of follow-​up (Castellini et  al., 2011)  and approximately
30% of patients with BN experiencing recurrent episodes
of binge eating and purging more than a decade after pre-
sentation for their disorder (Keel, Mitchell, Miller, Davis,
& Crow, 1999).
Research suggests more encouraging outcomes among
patients with BED because reductions in binge eating
are observed in response to a variety of treatments (CBT,
interpersonal psychotherapy, and behavioral weight loss;
Wilson, Wilfley, Agras, & Bryson, 2010), which are main-
tained over at least 1  year (Ricca et  al., 2001; Wilson
et al., 2010). CBT is currently considered to be the treat-
ment of choice for BED. Although psychological treat-
ments for BED have been shown to successfully reduce
binge eating and associated psychological symptoms, no
significant degree of weight loss is observed among these
patients either in the short term or the long term (Wilson
et al., 2010; Wonderlich, de Zwaan, Mitchell, Peterson,
& Crow, 2003). For individuals with BED, a majority
of whom are overweight or obese, this failure to achieve
weight loss can be associated with significant morbidity
and mortality (National Task Force on the Prevention and
Treatment of Obesity, 2000).
PURPOSES OF ASSESSMENT
Regardless of the particular purpose for a clinical evalu-
ation, assessments for eating disorders must consider the
wide range of symptoms experienced by patients with AN,
BN, BED, and residual forms of eating disorders. These
symptoms can include restraint over eating; binge eat-
ing and purging; concerns about shape and weight; and
obsessions and compulsions about food, eating, shape,
and weight. In the following paragraphs, a number of the
challenges involved in accurately and fully assessing an
individual with an eating disorder are described.
The assessment of binge eating, which is a core eating
disturbance experienced by individuals with AN-​B/​P, BN,
and BED, is perhaps the most difficult construct to mea-
sure accurately. To receive a diagnosis of BN or BED that
is consistent with DSM-​5, an individual must describe
binge episodes in which he or she consumes an objectively
large amount of food and experiences a sense of loss of
control over eating (objective bulimic episode [OBE]; see
the description of the Eating Disorder Examination pre-
sented later). This definition of binge eating was partially
derived from eating behavior experiments conducted in

laboratory settings, in which patients with BN were asked
to binge eat and were provided with a large multi-​item
meal. Patients demonstrated a significant disturbance in
the total amount of calories consumed during the binge
episode (mean of between 3,352 and 4,477 kcal), as
opposed to a specific type of food or a specific macronutri-
ent group (Kissileff, Walsh, Kral, & Cassidy, 1986; Walsh,
Kissileff, Cassidy, & Dantzic, 1989). Similarly, other stud-
ies have observed disturbances in total consumption dur-
ing a binge episode for individuals with BED, although
BED patients generally consume fewer calories than do
patients with BN (Walsh & Boudreau, 2003).
Thus, although laboratory data help provide some
objective measure of binge eating, there are no explicit
criteria for the amount of food needed to constitute a
binge episode in DSM-​ 5 (e.g., consumption of 1,500
calories per sitting). As a result, many of the assess-
ments described in the chapter employ standards stem-
ming from judgments of experts in the field (e.g., Eating
Disorder Examination), the judgment of the interviewer
(e.g., Structured Clinical Interview for DSM-​5), or the
self-​report of the patient (e.g., Eating Disorder Diagnostic
Scale). The way in which an instrument assesses binge
eating is described throughout the chapter so that the
reader can weigh the advantages and disadvantages of
each method for determining the presence of absence of
binge episodes.
In addition, caution should be exercised when select-
ing measures to use for eating disorders. Many measures
of eating disorder symptoms or body image do not assess
fundamental behavioral disturbances, such as binge
eating, or address issues relevant to men (Thompson,
Roehrig, Cafri, & Heinberg, 2005). Men may report that
commonly used measures ask questions that are not appli-
cable to their experience of shape or weight disturbance
(e.g., “Have you felt excessively large and rounded?”),
and readers are directed to measures developed specifi-
cally for the purpose of assessing men with eating disor-
ders, including the Male Body Attitudes Scale (Tylka,
Bergeron, & Schwartz, 2005), the Muscle Dysmorphic
Disorder Inventory (Hildebrandt, Langenbucher, &
Schlundt, 2004), and the Muscle Dysmorphia Inventory
(Rhea, Lantz, & Cornelius, 2004). Because this chapter
focuses on the routine clinical assessment of eating disor-
ders, and the prevalence of eating disorders among men
is low, these measures are not covered here in detail.
Second, professionals utilizing the measures described in
this chapter should be aware that not all assessments are
validated for children or adolescents (Thompson et  al.,
2005), and care should be taken to utilize assessments
Eating Disorders 545
that have been developed specifically for children or
adolescents for younger individuals. A  comprehensive
review of the diagnosis of feeding and eating disorders in
children and adolescents is available (Schvey, Eddy, &
Tanofsky-​Kraff, 2015).
The assessments described in the following three
sections focus specifically on eating disorder symptoms.
Other features have been shown to be either risk factors
for the development of eating disorders or symptoms oth-
erwise associated with eating disorders, including perfec-
tionism, body dissatisfaction, exercise, impulse regulation,
and thin-​ideal internalization. Instruments are available
that measure these constructs and can be employed
along with other measures (e.g., Body Esteem Scale
[Franzoi & Shields,  1984], Eating Disorder Inventory-​2
[Garner,  1991], Eating Pathology Symptoms Inventory
[Forbush et  al.,  2013], Ideal-​ Body Stereotype Scale-​
Revised [Stice & Bearman,  2001], and Satisfaction and
Dissatisfaction with Body Parts Scale [Berscheid, Walster,
& Bohmstedt, 1973]).
Clinicians may also be interested in measuring the
general psychological or psychosocial functioning of eat-
ing disorder patients, interpersonal functioning, or the
patient’s family context. A  number of treatment studies
(Agras, Crow, et al., 2000; Agras, Walsh, Fairburn, Wilson,
& Kraemer, 2000; Halmi et  al., 2005; Wilfley et  al.,
2002) assessed general psychological functioning pre-​and
post-​treatment using the Social Adjustment Scale (SAS;
Weissman & Bothwell, 1976), others (Agras, Walsh, et al.,
2000; Walsh, Fairburn, Mickley, Sysko, & Parides, 2004;
Wilfley et  al., 2002)  employed the Symptom Checklist
(53 or 90 items; Derogatis, Lipman, & Covi, 1973), and
yet others (Walsh et  al., 2006)  used the Quality of Life
Enjoyment and Satisfaction Questionnaire (Endicott,
Nee, Harrison, & Blumenthal, 1993). Interpersonal func-
tioning has been frequently measured using the Inventory
of Interpersonal Problems (IIP; Horowitz, Rosenberg,
Baer, Ureno, & Villasenor, 1988) in treatment studies for
BN (Agras, Crow, et al., 2000; Agras, Walsh, et al., 2000;
Carter et al., 2003) or BED (Devlin et al., 2005; Wilfley
et  al., 2002). Studies of the Maudsley form of family
therapy (Lock, 2015; Lock, Agras, Dare, & Le Grange,
2002), a useful treatment for adolescents with AN, have
measured family functioning in a number of ways, includ-
ing the Standardized Clinical Family Interview (Kinston
& Loader, 1984, as cited in Le Grange, Eisler, Dare,
& Russell, 1992), video recordings of interviews to rate
expressed emotion (Vaughn & Leff, 1976, as cited in Le
Grange et  al., 1992), and the Family Adaptability and
Cohesion Evaluation Scales (Olson, Sprenkle, & Russell,
546 Health-Related Problems

1979; Olson, Portner, & Lavee, 1985, as cited in Le Grange semi-​ structured interview that is considered to be the
et al., 1992), the Family Environment Scale (Moos, 1974; “gold standard” of measurement for eating disorders
Moos & Moos, 1994, as cited in Lock, Agras, Bryson, (Wilson, 1993). The EDE provides a comprehensive
& Kraemer, 2005), the Parent Adolescent Relationship description of the psychopathology associated with AN,
Questionnaire (Robin, Koepke, & Moye, 1990, as cited BN, and BED; allows for DSM-​5 eating disorder diagno-
in Robin et al., 1999), and the Family Assessment Device ses to be assigned; and is publicly available (http://​www.
(Epstein, Baldwin, & Bishop, 1983, as cited in Gowers credo-​oxford.com/​pdfs/​EDE_​17.0D.pdf).
et al., 2007, and Le Grange et al., 2016). The format of the EDE is assessor based, such that
Although data on the aforementioned related con- consistent scoring of the EDE items is achieved by a
structs can provide useful information about patients with synthesis of information provided by the interviewee and
eating disorders, the most salient aspect of diagnosis, case the assessors’ understanding of the terms and constructs
conceptualization and treatment planning, and treat- as defined by the assessment (Fairburn & Cooper, 1993;
ment outcome is knowledge of a patient’s eating disorder Fairburn et al., 2014; Wilson, 1993). To become proficient
symptoms. Only the assessment of specific eating disorder in administering the interview, it is necessary to complete
symptoms can generate DSM-​5 diagnoses, and the diag- comprehensive training. Training includes mastery of
nosis assigned to a given patient subsequently helps deter- the interview format, co-​ rating interviews, and receiv-
mine the most efficacious treatments for that patient. The ing supervision from an individual previously trained in
research evaluating eating disorder treatments to date has administering the EDE. Although methods for complet-
stratified patients on the basis of their diagnosis; therefore,
ing EDE training vary and there is no standardized proto-
these studies allow clinicians to use empirically supported col, training potential assessors on randomized controlled
treatments in routine practice when eating disorder symp- trials (e.g., Wilson et al., 2010) and at large academic cen-
toms are measured. ters (e.g., Columbia University Medical Center) required
approximately 20 to 30 hours of (a) watching training vid-
eos (~8 hours), (b) carefully reading the EDE interview
ASSESSMENT FOR DIAGNOSIS and chapter describing administration (~2 hours), (c) co-​
rating existing taped EDE interviews and reviewing with
In this section, we focus on assessment tools used to a supervisor (~3–​6 hours), (d)  observing approximately
formulate eating disorder diagnoses, including AN, BN, three EDEs (~3 hours), (e)  completing one to three
BED, or OSFED/​UFED. One important measurement EDEs with a trained observer (~1–​3 hours), (f) conduct-
issue relevant to the diagnosis of eating disorders, regard- ing an independent EDE and receiving feedback from a
less of assessment method, is the measurement of body trained interviewer (~1–​3 hours), and (g)  any necessary
weight. Weight is crucial in differentiating between diag- remediation (~1–​ 5 hours). Trained EDE interviewers
noses such as AN-​B/​P versus BN because similar bulimic make determinations about the severity of eating disorder
symptoms are present in both disorders. To assign the symptoms and rate the amounts of food that qualify for dif-
diagnosis of AN-​B/​P, the individual must be at a signifi- ferent types of overeating (see the later discussion of four
cantly low weight, which requires obtaining the patient’s types of overeating), which is particularly important for
weight and, subsequently, using either tables of ideal diagnosing BN and BED.
body weight (e.g., Metropolitan Life Insurance, 1959) or Because the EDE assesses eating disorder symptoms
a calculation of body mass index (BMI; weight in kg/​ over a significant period of time (3 or 6  months), the
height in m2) or BMI percentile in the case of younger Timeline Followback (TLFB) method is used. For the
patients (https://​nccd.cdc.gov/​dnpabmi/​calculator.aspx). EDE TLFB, the interviewer presents the patient with a
Thus, in conjunction with any data from interviews or calendar showing the 3-​or 6-​month period covered by
self-​
report questionnaires, a measurement of weight the EDE and, with the patient, identifies events in each
must be obtained to assign an accurate eating disorder month that might have disrupted the patient’s normal
diagnosis. eating routine and other notable events (e.g., vacations,
Both semi-​structured interviews and self-​report ques- birthdays, and parties). These events are written on
tionnaires are available for use in formulating a diagnosis. the calendar so that the patient can refer back to them
Perhaps the most commonly used assessment instrument throughout the interview. The TLFB procedure was
is the Eating Disorder Examination (EDE, current ver- originally developed to retrospectively measure alcohol
sion 17.0D; Fairburn, Cooper, & O’Connor, 2014), a consumption (Maisto, Sobell, Cooper, & Sobell, 1982),

and it helps orient patients to the time period being
assessed and provides contextual information during
the interview.
The EDE has four subscales (Restraint, Eating
Concern, Shape Concern, and Weight Concern) and a
global score, and it includes items with either frequency
or severity ratings. Severity items on the EDE are rated on
a scale from 0 to 6, where a 1 is assigned if the feature is
“barely present,” a 5 is assigned when the symptom does
not qualify for the most severe rating (6), and a 3 is used
as the midpoint between 0 and 6 (Fairburn & Cooper,
1993). Four different types of overeating are assessed by
the EDE, including (a)  objective bulimic episodes, or
the consumption of an objectively large amount of food
while experiencing a sense of loss of control; (b) subjec-
tive bulimic episodes, or experiencing loss of control
while consuming smaller amounts of food that are viewed
by the individual as excessive; (c) objective overeating, or
eating an objectively large amount of food without loss of
control; and (d)  subjective overeating, or eating a small
amount of food without a sense of loss of control, which
the individual believes is excessive (Fairburn & Cooper,
1993). The designation of an amount of food that consti-
tutes an “objectively large” amount of food during a binge
episode is determined by the EDE interviewer; how-
ever, an appendix to the EDE was developed by experts
in the field to standardize amounts constituting OBEs.
For example, the consumption of two full meals (each
with two or more courses), or three main courses (e.g.,
three Big Macs), or more than 1 pint of ice cream, or five
donuts would all be considered large when rating OBEs
on the EDE.
A version of the EDE suitable for the assessment of
children and adolescents (child EDE; ChEDE) has been
developed by Bryant-​Waugh, Cooper, Taylor, and Lask
(1996), and a few studies have evaluated this form of the
TABLE 24.1   Ratings of Instruments Used for Diagnosis
Internal Inter-​Rater
Instrument Norms Consistency Reliability
EDE, versions 12–​17 G A E A
SCID-​IV A NA G L
EDA-​5 NA NR NR
EDE-​Q (version 4.0 E G NA
or 6.0)
EDDS for DSM-​IV G G NA
Note: EDE = Eating Disorder Examination; SCID-​IV = Structured Clinical Interview for DSM-​IV; EDA-​5 = Eating Disorder Assessment for DSM-​5;
EDE-​Q = Eating Disorder Examination Questionnaire; EDDS = Eating Disorder Diagnostic Scale; L = Less Than Adequate; A = Adequate; G = Good;
E = Excellent; NR = Not Reported; NA = Not Applicable.
Eating Disorders 547
measure (e.g., Decaluwe & Braet, 2004; Glasofer et  al.,
2007; Hilbert et  al., 2013; Tanofsky-​Kraff et  al., 2003;
Watkins, Frampton, Lask, & Bryant-​Waugh, 2005). To
make the assessment more appropriate for younger chil-
dren, the ChEDE uses modified language and a sort task
to evaluate the importance of shape and weight (Bryant-​
Waugh et al., 1996). Training in the use of the ChEDE to
diagnose eating disorders among younger patients (aged
7–​14  years) has been described (Tanofsky-​ Kraff et  al.,
2007). After BED was added to DSM-​5, recent versions
of the ChEDE now include BED as a diagnostic category
(see Schvey et al., 2015).
Whereas the EDE is used in numerous treatment stud-
ies to diagnose patients with eating disorders, only a few
studies have examined the validity of diagnoses generated
by EDE. The EDE does successfully distinguish between
patients with BN and individuals without BN who are
preoccupied with shape and weight (Wilson & Smith,
1989). Comparisons of the diagnoses generated by the
EDE and the self-​report version of the EDE (EDE-​Q) are
described in the following paragraphs. Summary psycho-
metric data for the use of the EDE for diagnostic purposes
are provided in Table 24.1; comparable data on the EDE
for other assessment purposes are reported in subsequent
tables. Berg, Peterson, Frazier, and Crow (2012) offer an
excellent review of data pertinent to the EDE, and in
addition to articles referenced previously, data for ratings
made in Table 24.1 were obtained from the following
studies: Grilo, Masheb, Lozano-​Blanco, and Barry (2004);
Jennings and Phillips (2017); Rizvi, Peterson, Crow, and
Agras (2000); Rosen, Vara, Wendt, and Leitenberg (1990);
and Wilfley, Schwartz, Spurrell, and Fairburn (2000).
Despite the common use of the instrument in research
settings, there are many obstacles for administering the
EDE in routine clinical practice. Clinicians may not have
completed the extensive training required to administer
Test–​Retest Content Construct Validity Clinical Highly
Reliability Validity Validity Generalization Utility Recommended
E A E A ✓
E A E A ✓
A G A A NR
L E NR E A
A G A A A ✓
548 Health-Related Problems
the EDE, and the amount of time needed to administer
the EDE (~1 or 2 hours) is significant, which makes the
EDE less practical for private practice settings. However,
the EDE can be clinically useful for developing a detailed
understanding of a range of eating disorder symptoms
(Wilson, 1993), and it is also helpful for case conceptu-
alization and monitoring of treatment outcome—​issues
that are discussed later.
The Structured Clinical Interview for DSM-​ 5 sures. In contrast to the EDE, which requires extensive
(SCID-​5; First, Williams, Karg, & Spitzer, 2015)  pro-
vides an updated means for assessing DSM-​5 diagnostic
criteria for AN, BN, BED, and OSFED. For this version
of the interview, the SCID-​5 is available exclusively for
purchase through American Psychiatric Publishing, and
psychometric data are not currently available for eating
disorders. The SCID-​IV (SCID; First, Spitzer, Gibbon,
& Williams, 2002) was used in numerous studies of eat-
ing disorders, in some cases to diagnose comorbid Axis
I psychopathology (e.g., Agras, Crow, et al., 2000) and in
others to provide eating disorder diagnoses (e.g., Engel
et  al., 2005; Grilo & Masheb, 2005). When using the
SCID, clinicians must determine what constitutes a
large amount of food to classify binge eating episodes.
Although the SCID-​ IV was employed frequently in
research on eating disorders, there are limited data
specifically examining the psychometric properties of
the version of the instrument for DSM-​IV diagnoses.
Previous versions of the SCID (SCID for DSM-​III-​R;
APA, 1987)  found acceptable kappa coefficients and
test–​retest reliabilities for the eating disorder modules
(Segal, Hersen, & van Hasselt, 1994). The data for the
inter-​rater reliability of DSM-​IV eating disorder diagno-
ses are consistent with those of previous versions, with
a good κ value (.77); however, the test–​retest reliability
estimates for DSM-​IV eating disorder diagnoses (correla-
tion = .64) are not consistent with a rating of acceptable
(minimum correlation over several days or weeks = .70;
Zanarini et  al., 2000). The prior version of the SCID-​
IV does have at least acceptable psychometric data for
norms, and construct validity for eating disorder diagno-
ses, and is thus included in Table 24.1.
The SCID, like the EDE, requires significant train-
ing for interviewers (~20–​30 hours), and it can be time-​
consuming to complete the entire instrument. However,
the SCID only assesses the diagnostic criteria for eating
disorders and not associated eating disorder pathology.
As such, administering only the SCID eating disorder
modules to generate diagnoses is not particularly time-​
consuming, but given the limited availability and nota-
ble burden of training in the SCID, and cost of the
instrument, it is unlikely that the measure is suitable for
routine community-​based practice.
The Eating Disorder Assessment (EDA-​5; Sysko et al.,
2015)  is an electronic assessment (available for free at
http://​www.eda5.org) developed to focus specifically on
the comprehensive assessment of all DSM-​5 feeding and
eating disorders. The EDA-​5 diverges in several important
ways from previously mentioned interview-​ based mea-
training and an extended amount of time to administer,
the EDA-​5 can be administered with limited training and
in a brief time period to reduce participant burden. The
SCID-​5 (First et al., 2015) assesses the presence of an eat-
ing disorder, but it does not evaluate pica or rumination
disorder, and the module on ARFID is optional; it also
fails to precisely determine the individual’s BMI or fre-
quencies of a range of behavioral disturbances, such as
objective and subjective binge eating episodes (Glasofer,
Sysko, & Walsh, 2015). Two studies examined the utility
of the EDA-​5 in treatment-​seeking adults across multiple
sites (for details, see Sysko et  al., 2015). The first study
compared the diagnostic validity of the EDA-​5 to the EDE
and measured test–​retest reliability of diagnoses from the
new measure. The EDA-​5 and the EDE showed high
rates of agreement (κ = .74 across diagnoses, n = 64), with
a range of κ = .65 for OSFED/​UFED to κ = .90 for BED.
For a random subgroup of participants, a new interviewer
readministered the EDA-​5 at 7 to 14  days following the
first assessment. Across diagnoses, the test–​retest κ coef-
ficient was .87, and diagnostic agreement was achieved
in 19 of 21 cases (90.5%). Because feedback from inter-
viewers highlighted the complexity of the interview’s skip
rules, an electronic application (“app”) version of the
EDA-​5 was created. A second study compared the EDA-​5
app to clinician interview and found a high rate of agree-
ment between diagnosis by EDA-​5 and clinician interview
(κ = .83 across diagnoses, n = 71). Across individual diag-
nostic categories, κ ranged from .56 for OSFED/​UFED to
.94 for BED. The EDA-​5 required significantly less time
to complete than the EDE, and the app version of the
EDA-​5 significantly shortened the length of time needed
to administer the interview, from an average of 19.3 ±
5.6 minutes (range, 5–​34 minutes) to 14.0 ± 6.2 minutes
(range, 5–​30 minutes). Given the encouraging results of
these preliminary investigations, the EDA-​5 is included
in Table 24.1; however, further validation and replication
studies are warranted.
Several self-​report questionnaires are also available
to provide clinicians with a means for assigning eat-
ing disorder diagnoses; however, limited information is

available about updated DSM-​5 versions of these assess-
ments and the psychometrics relevant to diagnosis with
updated instruments. The most commonly used mea-
sures were developed in an effort to generate eating dis-
order diagnoses while circumventing the need for costly
or time-​ consuming interviews (Stice, Telch, & Rizvi,
2000). Although self-​report measures are brief and do not
require specific clinician training, there are also some
issues that clinicians should consider before utilizing
these assessments, including the need to obtain scoring
algorithms and the costs of the questionnaires (Peterson
& Mitchell, 2005).
The Eating Disorder Examination Questionnaire
(EDE-​ Q, current version 6.0; http://​www.credo-​oxford.
com/​pdfs/​EDE-​Q_​6.0.pdf; Fairburn & Beglin, 2008)  is
a 38-​item self-​report version of the EDE designed to be
completed in 15 minutes. Similar to the EDE, the EDE-​
Q includes four subscales (Restraint, Eating Concern,
Shape Concern, and Weight Concern) and uses a com-
bination of frequency items (e.g., objective bulimic epi-
sodes and vomiting) and severity items rated on a scale of
0 to 6 to assess the 28-​day period before the completion
of the questionnaire (Fairburn & Beglin, 2008). A child
version of the EDE-​Q has also been developed (ChEDE-​
Q; Decaluwe, 1999). The EDE-​Q is listed in Table 24.1,
although the data on test–​retest reliability are generally
less than acceptable, with some variability (e.g., Rose,
Vaewsorn, Rosselli-​Navarra, & Wilson, 2013). However,
research on this questionnaire has found it to demonstrate
acceptable treatment sensitivity and clinical utility; good
internal consistency; and excellent norms, content valid-
ity, and validity generalization.
Several studies compared the EDE and EDE-​Q for
diagnosis, including for DSM-​IV AN in comparison to
clinical interview, which was considered to be the stan-
dard for diagnosis (Wolk, Loeb, & Walsh, 2005). By clini-
cal interview, 100% of patients were diagnosed with AN
and 66.7% of these patients were diagnosed with AN-​B/​P,
with corresponding percentages for the EDE and EDE-​Q
of 71.7% and 86.7% of patients diagnosed with AN and
79% and 71% of the subsample diagnosed with AN-​B/​P,
respectively (Wolk et al., 2005). Because all of the patients
in the study met criteria for low weight and amenorrhea,
the authors indicated that the discrepancies between the
diagnosis of AN with the EDE and that with the EDE-​
Q were related to the severity items, and specifically
Criterion B of the AN diagnostic criteria, or the fear of
gaining weight or becoming fat (Wolk et al., 2005). Thus,
to better evaluate this criterion, clinicians interested in
using either the EDE or the EDE-​Q to diagnose AN
Eating Disorders 549
should consider gathering additional data from patients
about the fear of gaining weight or becoming fat. The
EDE-​Q should not be used as the only method of diagnos-
ing BN. In a study of women seeking treatment for sub-
stance abuse, the EDE-​Q underassessed the rate of BN
when strict DSM-​IV criteria were applied, but it overdi-
agnosed individuals as having BN when the criteria were
slightly relaxed (Black & Wilson, 1996). More recently,
several studies (Berg, Peterson, et  al., 2012; Mancuso
et  al., 2015)  utilized the EDE/​ EDE-​ Q or EDE-​ Q to
compare DSM-​IV to DSM-​5 criteria, and they suggested
that more individuals met diagnostic criteria for a full-​
threshold eating disorder under DSM-​5 criteria, result-
ing in a reduction of the relative prevalence of residual
eating disorder diagnoses. However, the EDE-​Q does not
evaluate several of the diagnostic criteria for DSM-​5 (e.g.,
lack of recognition of the seriousness of low body weight;
Mancuso et al., 2015), and there is moderate diagnostic
concordance between the EDE and EDE-​Q (Berg, Stiles-​
Shields, et al., 2012), which limits the ability to use the
measure for the purpose of diagnosis.
The Eating Disorder Diagnostic Scale (EDDS; Stice
et  al., 2000)  is a 22-​item self-​report scale that can gen-
erate possible diagnoses for AN, BN, and BED and an
overall composite score for eating disorder symptoms.
The EDDS was developed for the purposes of diagnos-
ing eating disorders in etiological research, for use in
research that requires frequent measurements, or for
identification of individuals with eating disorders in
clinical practice (e.g., primary care; Stice et al., 2000). It
includes questions rated on a Likert scale, dichotomous
response questions, questions about symptom frequency,
and open-​ended questions. In addition, to improve on
some of the difficulties inherent in assessing binge eat-
ing by self-​report, the EDDS does not include the word
“binge”; instead, binge eating is described solely in behav-
ioral terms (Peterson & Mitchell, 2005). Two studies have
examined the reliability and validity of the EDDS scores
for DSM-​IV diagnoses (Stice et  al., 2000; Stice, Fisher,
& Martinez, 2004), other studies have used the EDDS to
measure treatment sensitivity (Stice, Orjada, & Tristan,
2006; Stice & Ragan, 2002), and information about psy-
chometric properties of the scale is provided in Table
24.1. The EDDS is psychometrically sound for DSM-​IV
and appropriate for clinical practice. The measure is brief
and can be completed quickly; therefore, the EDDS can
also be helpful in evaluating patients with other psychiat-
ric disorders where eating disorders are likely to co-​occur
(e.g., major depression, anxiety disorders, and substance
use disorders). A revised version of the original EDDS was
550 Health-Related Problems

developed to fit the diagnostic changes in the DSM-​5 for The measurement of body weight is an essential ele-
eating disorders, but it is currently under development ment of case conceptualization and treatment planning
and has not yet been validated. because, as described previously, body weight differen-
tiates patients with AN-​B/​P from individuals with BN,
and it informs clinicians about the type of treatment
Overall Evaluation
that will be most effective. For example, for individuals
Additional information about the assignment of DSM-​5 with BN, fluoxetine at 60 mg is an effective treatment,
diagnoses is needed before an instrument can be recom- and it produces significant reductions in binge eating
mended. One assessment, the EDA-​5, has some psycho- and purging behaviors (Fluoxetine Bulimia Nervosa
metric data, and two other tools, the EDE and EDDS, Collaborative Study Group, 1992; Goldstein, Wilson,
have consistently strong supporting psychometric data for Thompson, Potvin, & Rampey, 1995). Conversely, no
use in the diagnosis of DSM-​IV eating disorders. However, significant benefits have been observed for individuals
clinicians should consider confirming diagnoses gener- with AN-​B/​P receiving fluoxetine at 60 mg in comparison
ated by the EDDS to ensure that the patient has binge to placebo for the acute treatment of AN (Attia, Haiman,
eating episodes that satisfy DSM criteria. Other measures, Walsh, & Flater, 1998) or for preventing relapse (Walsh
such as the SCID and EDE-​Q, are widely used in eat- et al., 2006).
ing disorders research, but test–​retest reliability estimates Patients with AN, BN, or BED should be referred
are not adequate. Because of their ease of use, self-​report for a medical evaluation before the start of treatment
measures hold some promise for being used in clinical set- and at regular intervals throughout the course of treat-
tings, but current psychometric evidence is limited. The ment. The medical assessments described here are
scarcity of instruments with adequate test–​retest reliabil- based on the recommendations of experts in the field
ity and possible reasons for difficulties in assessing eating (e.g., Crow & Swigart, 2005; National Task Force on the
disorder symptoms over time are discussed in the conclu- Prevention and Treatment of Obesity, 2000). Patients at
sions/​future directions section. a low weight (e.g., AN-​R and AN-​B/​P) should receive a
complete blood count, an electrolyte battery, an elec-
trocardiogram, liver function tests, and a dual-​energy
ASSESSMENT FOR CASE CONCEPTUALIZATION X-​ray absorptiometry (DEXA; Crow & Swigart, 2005) to
AND TREATMENT PLANNING evaluate risk for complications associated with low body
weight (e.g., low heart rate, hypotension, and hypona-
Assessment instruments can also provide clinically tremia; Commission on Adolescent Eating Disorders,
meaningful information for clinicians to guide case con- 2017). Inpatient treatment may be necessary for indi-
ceptualization and treatment planning. Some of the afore- viduals with AN at a low weight in order to restore body
mentioned instruments (e.g., EDE and EDE-​Q) measure weight and allow for the close monitoring of medical
a broad spectrum of symptoms, which can allow the clini- complications that may emerge during the refeeding
cian to determine the severity of a patient’s eating disorder. process. For patients with binge eating and purging
A significant amount of treatment planning is dependent behaviors (e.g., AN-​B/​P and BN), an electrolyte battery
on the eating disorder and type of treatment to be deliv- and a dental evaluation should be completed because
ered; therefore, careful consideration must be given to individuals who purge are at risk for electrolyte distur-
the choice of assessments for this purpose. In addition, as bances, including potassium depletion (Crow & Swigart,
described previously, many patients with eating disorders 2005). The majority of individuals presenting with BED
experience comorbid disorders. As such, screening assess- are at a weight classified as overweight (BMI > 25 kg/​m2)
ments for depression, anxiety, and substance use should or obese (BMI > 30 kg/​m2). As such, patients with BED
also be considered for eating-​disordered patients. The data should be assessed for the serious medical sequelae (e.g.,
from these measures and the presence or absence of co-​ type 2 diabetes) associated with higher body weights as
occurring psychiatric symptoms should then be used in the outlined by the National Task Force on the Prevention
development of a case formulation. Readers are encour- and Treatment of Obesity (2000).
aged to refer to the chapters on assessments for depression, In this chapter, assessments for treatment planning
anxiety, and substance abuse in this volume to determine and case conceptualization for individuals with eating
the most clinically relevant and psychometrically sound disorders are discussed in the context of empirically
measures to evaluate comorbid symptoms. supported treatments, specifically CBT. Continuing

assessment and evaluation of progress throughout treat-
ment are essential components of CBT because adjust-
ments can be made by the clinician based on the data
provided by the measures. Research studies of CBT
for BN (Fairburn, Marcus, & Wilson, 1993; Fairburn,
2008) have used assessments not only to guide treatment
but also to better understand mechanisms of change dur-
ing treatment. Thus, the remainder of this section pres-
ents measures that can be employed during the delivery
of CBT for eating disorders.
As described previously, the EDE and EDE-​Q mea-
sure a wide range of eating disorder symptoms. These
instruments are particularly helpful in case conceptu-
alization for CBT because they assess dietary restraint,
bulimic behaviors (binge eating and purging), and shape
and weight concerns, all of which are targets of CBT (see
Table 24.2 for summary psychometric ratings). The util-
ity of the EDE and EDE-​Q is particularly relevant in the
delivery of CBT for BN, where patients need to eliminate
binge eating and purging behaviors, establish a pattern
of regular eating, identify alternative activities, and learn
problem-​solving strategies. In addition, dietary restraint
is addressed through the development of regular eating
and exposure to forbidden foods, and shape and weight
concerns are targeted through cognitive restructuring and
behavioral experiments. Research has demonstrated that
the reduction in dietary restraint as early as the fourth
week of CBT for BN mediates post-​ treatment reduc-
tions in binge eating and vomiting (Wilson, Fairburn,
Agras, Walsh, & Kraemer, 2002), and change in purging
behavior after 4 weeks of CBT predicts symptom levels
at 8-​month follow-​up (Fairburn, Agras, Walsh, Wilson, &
Stice, 2004). Thus, clinicians could use the EDE-​Q dur-
ing the first month of CBT for BN to monitor levels of
dietary restraint and frequency of purging, which would
provide important information about whether improve-
ments should be expected with continued CBT. The
clinician would then have objective data informing the
TABLE 24.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planning
Internal Inter-​Rater
Instrument Norms Consistency Reliability
EDE, versions 12–​16 G A E A
EDE-​Q, versions 4 and 6 E G NA
BSQ A E NA
BCQ A E NA
Note: EDE = Eating Disorder Examination; EDE-​Q = Eating Disorder Examination Questionnaire; BSQ = Body Shape Questionnaire; BCQ = Body
Checking Questionnaire; L = Less Than Adequate; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.
Eating Disorders 551
decision to continue delivering CBT for BN or to begin
using another treatment strategy (e.g., switching to inter-
personal psychotherapy or beginning antidepressant
medication).
Another important means of assessment throughout
CBT is self-​monitoring, which is an integral part of CBT
for eating disorders. Patients begin self-​monitoring after
the first session of CBT; as such, the monitoring records
can help with case conceptualization or treatment
planning because they provide information about the
patient’s baseline eating disorder symptoms. The moni-
toring typically involves recording circumstances associ-
ated with binge eating and purging, such as antecedent
and consequent events, and general descriptions of food
intake. Self-​monitoring can also focus on other behaviors
typical of patients with eating disorders, including body
checking or avoidance (Fairburn, Cooper, & Shafran,
2003). Wilson and Vitousek (1999) reviewed research
on self-​monitoring in the treatment of eating disorders
and identified a number of important advantages to this
form of measurement. Because these records are com-
pleted closer to the time when the behaviors occur, the
likelihood that the records are affected by problems
of retrospective recall is reduced (Wilson & Vitousek,
1999). Thus, assessing eating disorder symptoms imme-
diately after they occur may increase the accuracy of
self-​reported binge eating or restricting behaviors on
self-​monitoring records in comparison to other forms of
assessment (e.g., EDE).
The possibility that symptoms can be measured more
accurately without a time delay has been explored using
ecologic momentary assessment (EMA; Engel et al., 2016,
Farchaus & Corte, 2003; Smyth et al., 2001). In general,
EMA involves recording events multiple times during
a day on monitoring records, a hand-​held computer, or
smartphone. Patients can be instructed to record at spe-
cific times of day (e.g., just after waking), when signaled
by a pager, alarm on a watch, or hand-​held computer, or
Test–​Retest Content Construct Validity Clinical Highly
Reliability Validity Validity Generalization Utility Recommended
E A E A ✓
L E NR E A
A G A A A
A G A A A
552 Health-Related Problems
when a specific event occurs (e.g., binge eating; Farchaus
& Corte, 2003). In the assessment of eating disorders,
EMA has been used to measure mood, stressors, eating
behavior, dietary restraint, binge eating, antecedents of
binge eating, exercise inappropriate compensatory behav-
iors, and other related variables among individual with
eating disorders (Engel et  al., 2016; Farchaus & Corte,
2003; Le Grange, Gorin, Catley, & Stone, 2001; Smyth
et al., 2001). Ecological momentary assessment has also
been examined as an alternative to self-​monitoring in
CBT for binge eating disorder, where patients record
mood, events, thoughts, and eating behaviors; however,
the use of EMA did not provide any additional benefit
to standard CBT (Le Grange, Gorin, Dymek, & Stone,
2002). Thus, like self-​monitoring, EMA may be useful in
treatment planning and conceptualization, but additional
data are needed.
Self-​monitoring also provides information about the
temporal pattern of eating behaviors, such as the obser-
vation that binge eating is more likely to occur during
the afternoon or evening and that episodes of binge eat-
ing are often preceded by negative mood states, which
can be used to inform the therapeutic process (Wilson &
Vitousek, 1999). For example, if the monitoring records
indicate that a patient is experiencing difficulties with
binge eating in the afternoons, after avoiding eating dur-
ing the morning, the CBT therapist will help the patient
consume additional meals or snacks earlier in the day and
schedule activities that are inconsistent with binge eating
during the afternoon. Self-​monitoring may also serve a cru-
cial role in the process of early response observed among
patients with BN treated with CBT (Wilson et al., 1999),
as some of the improvements observed in the first few
weeks of CBT for BN (e.g., Fairburn et al., 2004; Wilson
et al., 2002) may be attributable to the awareness of eating
behavior and patterns of eating through self-​monitoring.
Although self-​monitoring records are very useful clini-
cally, this form of measurement is not included in Table
24.2 because studies have not established norms for self-​
monitoring, it is not possible to measure internal consis-
tency, content validity is not applicable, and inter-​rater
reliability is not helpful in clinical practice. In addition,
test–​retest reliability of self-​monitoring records is difficult
to establish because patterns of eating behavior are con-
stantly changing among individuals with eating disorders
(Hildebrandt & Latner, 2006).
Thus, self-​monitoring is an integral and useful part of
CBT for eating disorders. However, even when patients
are instructed in the appropriate methods for completing
self-​monitoring records, there are indications that self-​
monitoring may not provide entirely accurate information
about the amount of food consumed. Patients have been
shown to report similar meal patterns on 24-​hour self-​
report interviews and the EDE (Bartholome, Raymond,
Lee, Peterson, & Warren, 2006); however, patients
may exaggerate the size of binge episodes when self-​
monitoring (Hadigan, Walsh, Devlin, LaChaussee, &
Kissileff, 1992). Therefore, when evaluating monitoring
records, clinicians should attend to the overall pattern of
meals, snacks, and binge episodes rather than the total
amount of food eaten.
The diagnostic criteria for both AN and BN include
specific disturbances in body image, which can also be
observed among individuals with BED or EDNOS.
The Body Shape Questionnaire (BSQ; Cooper, Taylor,
Cooper, & Fairburn, 1987) is a 34-​item self-​report ques-
tionnaire that provides an overall measure of concerns
about shape, weight, and body image. The BSQ allows
clinicians to assess the need for interventions addressing
distortions in the perception of shape or weight among
individuals with AN, BN, EDNOS, or BED. Although
there are many existing assessments measuring body
image concerns (for more information, see Thompson
et  al., 2005), the BSQ is highly recommended because
it is both psychometrically sound (see Table 24.2) and
straightforward for patients to complete. In addition to
articles referenced in the text, data for ratings in Table
24.2 for the BSQ were obtained from Evans and Dolan
(1993) and Rosen, Jones, Ramirez, and Waxman (1996).
The BSQ also includes two questions that specifically
assess body checking and avoidance behaviors. The behav-
iors measured by the BSQ are avoiding wearing clothes
that make the person particularly aware of body shape and
pinching areas of the body to determine how much fat there
is. Williamson, Muller, Reas, and Thaw (1999) suggested
that preoccupation with shape and weight is increased by
the selective attention focused on a disliked part of the
body that occurs in body checking and avoidance. A study
by Shafran, Fairburn, Robinson, and Lask (2004) sup-
ported this hypothesis by demonstrating increases in pre-
occupation with shape and weight after body checking.
Thus, checking and avoidance can be important targets
for treatment because these behaviors reinforce negative
beliefs about shape and weight and may also maintain eat-
ing disorder symptoms. The most recent version of CBT
for eating disorders (Fairburn et al., 2003) asks patients to
monitor these behaviors during treatment, and the clini-
cian intervenes to reduce body checking and avoidance
(Fairburn, 2006). The Body Checking Questionnaire
(BCQ; Reas, Whisenhunt, Netemeyer, & Williamson,
2002) is a 23-​item measure designed to assess body check-
ing behaviors. The importance of body checking in the

maintenance of symptoms of AN (Fairburn, Shafran, &
Cooper, 1999)  and the psychometric soundness of the
measure justify its inclusion in this chapter. A version of
the BCQ specific to males has also been developed and
initially validated since the original version of this chapter
(see Hildebrandt, Walker, Alfano, Delinsky, & Bannon,
2010). Information about the BCQ is provided in Table
24.2, including data from Calugi, Dalle Grave, Ghisi, and
Sanavio (2006) and Reas, White, and Grilo (2006).
A recently developed self-​ report questionnaire, the
45-​item Eating Pathology Symptoms Inventory (EPSI;
Forbush et al., 2013), also assesses eating disorder dimen-
sions relevant to treatment outcome. A total of eight sub-
scales can be measured with the EPSI, including Body
Dissatisfaction (dissatisfaction with body weight and/​or
shape), Binge Eating (eating large amounts of food and
associated cognitive symptoms), Cognitive Restraint (cog-
nitive attempts to limit or avoid eating, whether or not
successful), Purging (self-​induced vomiting, laxative use,
diuretic use, and diet pill use), Muscle Building (desire
for increased muscularity and muscle-​building supple-
ment use), Restricting (efforts to avoid or reduce food con-
sumption), Excessive Exercise (intense and/​or compulsive
physical exercise), and Negative Attitudes Toward Obesity
(negative attitudes toward overweight or obese individu-
als). Given that the EPSI is not yet widely used, it is not
included in the table; however, the psychometric proper-
ties of scores on the measure based on initial testing are
promising (see also Forbush & Berg, 2015). Specifically,
scores on the EPSI have demonstrated good to excel-
lent internal consistency across samples of men, women,
obese participants, and psychiatric patients with and with-
out eating disorders (Forbush, Wildes, & Hunt, 2014;
Forbush et al., 2013). For test–​retest reliability estimates,
scores on most of the EPSI subscales exceeded .70, except
for the Cognitive Restraint scale (.61). Discriminant valid-
ity for the EPSI scores was found between individuals with
eating disorders and (a)  general psychiatric outpatients
(Forbush et al., 2013) and (b) college students (Forbush
et al., 2013, 2014). In college samples, convergent valid-
ity was also observed, with the EPSI subscale scores more
strongly related to scores on measures of similar than dis-
similar areas. Thus, extant data suggest initial support for
the validity of the EPSI and the potential for use in case
conceptualization and treatment planning.
CBT for eating disorders involves the use of assess-
ments to determine whether the areas of interpersonal
functioning, perfectionism, core low self-​ esteem, or
mood intolerance should be addressed during treatment.
Fairburn et  al. (2003) proposed that for some patients,
these areas are barriers to change because they serve as
Eating Disorders 553
additional maintaining processes that interact with the
eating disorder maintaining mechanisms usually targeted
by CBT for BN (Fairburn et al., 1993; e.g., overevaluation
of shape and weight, dietary restraint, and binge eating
and compensatory behavior). A number of measures can
be used by clinicians to gather data about these areas to
inform treatment in the expanded form of CBT (Fairburn,
2008). Examples of relevant instruments include the Beck
Depression Inventory-​II (BDI-​II; Beck, Steer, & Brown,
1996), the Rosenberg Self-​Esteem Scale (RSE; Rosenberg,
1979), the Inventory of Interpersonal Problems (IIP;
Horowitz et  al., 1988), and the Dysfunctional Attitude
Scale (DAS; Weissman & Beck, 1978).
Overall Evaluation
Similar to the assessments used to diagnose eating disor-
ders, there are a handful of measures specific to eating
disorders that have sufficient empirical support to allow
them to serve as clinical tools for treatment conceptu-
alization and planning. These measures are especially
appropriate for treatment planning in CBT because the
CBT model includes strategies designed to affect the
areas assessed by these measures (e.g., dietary restraint
and overvaluation of shape and weight). However, these
instruments are also likely to be of use for other treatment
approaches that have the goal of achieving reductions in
eating disorder symptoms (e.g., Maudsley family therapy
and psychopharmacological treatment).
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
Very few measures have been designed and used for track-
ing and evaluating the impact of treatments for eating dis-
orders. The EDE is the most commonly used assessment
for measuring treatment outcome for patients with eat-
ing disorders, including studies of AN (e.g., Pike, Walsh,
Vitousek, Wilson, & Bauer, 2003; Walsh et al., 2006), BN
(e.g., Agras, Crow, et al., 2000; Agras, Walsh, et al., 2000;
Walsh et al., 2004), and BED (e.g., Devlin et al., 2005;
Wilfley et  al., 2002; Wilson et  al., 2010). However, as
described previously, the EDE is time-​consuming and
requires extensive training of interviewers, which make
the instrument less practical for multiple assessments of
outcome. As such, a number of studies have investigated
whether the EDE-​Q can be substituted for the EDE in
measuring treatment outcome for patients with eating dis-
orders, many of which are summarized in the review by
Berg, Peterson, et al. (2012).
554 Health-Related Problems

The first comparison of the EDE and the EDE-​Q
(Fairburn & Beglin, 1994)  examined the agreement
between the measures among a sample of women from
the community (n  =  243) and a sample of women
with eating disorders (n  =  23 patients with BN, n  =  13
patients with AN). Across the two instruments, OBEs,
self-​induced vomiting, and laxative misuse were highly
correlated, with the data on self-​induced vomiting being
the most highly correlated between EDE and EDE-​Q
for both samples. When comparing the scores obtained
for the EDE and EDE-​Q subscales, the agreement was
greatest for the restraint and weight concern subscales.
A number of studies have since compared the EDE and
the EDE-​Q in women seeking treatment for substance
abuse (Black & Wilson, 1996), obese patients with BED
(Wilfley, Schwartz, Spurrell, & Fairburn, 1997), obese
bariatric surgery candidates (Kalarchian, Wilson, Brolin,
& Bradley, 2000), patients with BED (Grilo, Masheb,
& Wilson, 2001a, 2001b), women with AN (Wolk et al.,
2005), and women with BN (Carter, Aime, & Mills,
2001; Sysko, Walsh, & Fairburn, 2005). A  general pat-
tern of results has emerged among these studies, in which
the behavioral features (e.g., self-​induced vomiting) and
clearly defined concepts (e.g., dietary restraint) are most
highly correlated between EDE and EDE-​Q (Black &
Wilson, 1996; Wilfley et  al., 1997; Wolk et  al., 2005).
Greater discrepancies have been observed between the
EDE and the EDE-​Q for complex concepts such as binge
eating (Black & Wilson, 1996; Carter et al., 2001; Grilo
et al., 2001a; Wilfley et al., 1997), and significantly higher
levels of pathology have been observed on the EDE-​Q
subscales in comparison to the EDE (Kalarchian et  al.,
2000; Wilfley et  al., 1997). High levels of convergence
between the EDE and the EDE-​Q for the assessment
of binge eating can be produced with the addition of a
brief (one page) instruction sheet to the EDE-​Q providing
detail definitions and examples of binge eating (Goldfein,
Devlin, & Kamenetz, 2005). The results of two studies
examining the ChEDE and the ChEDE-​Q among obese
children and adolescents with AN found a similar pattern
of results, with higher levels of eating disorder pathology
observed on the questionnaire measure (Decaluwe &
Braet, 2004; Passi, Bryson, & Lock, 2003).
When the EDE and the EDE-​Q were compared for
the measurement of change in a study of patients with BN,
the change in compensatory behaviors over the course of
the study was highly correlated, but the change in binge
eating (OBE and subjective bulimic episode [SBE]) and
attitudinal features (e.g., importance of shape and weight)
were more discrepant (Sysko, Walsh, & Fairburn, 2005).
The authors concluded that although both instruments
assess change, it is not possible to evaluate which measure
provides greater validity in assessing eating disorder pathol-
ogy. Thus, Sysko et al. recommended that clinicians and
researchers should consistently use one measure (EDE or
EDE-​Q) rather than switching back and forth between
measures or viewing the measures as interchangeable.
Because patients with AN often experience obsessive
thoughts and compulsions related to eating disorder symp-
toms, a number of studies evaluating treatments for AN
have evaluated change using the Yale–​Brown–​Cornell
Eating Disorder Scale (YBC-​ EDS; Attia et  al., 1998;
Kaye et  al., 2001; Mazure, Halmi, Sunday, Romano,
& Einhorn, 1994; Walsh et  al., 2006). The YBC-​EDS
includes a 65-​item symptom checklist assessing 18 cat-
egories (e.g., food/​ eating/​weight and shape/​ clothing/​
hoarding/​exercise preoccupations, and eating/​food/​binge
eating/​purging/​somatic rituals). In addition, 19 questions
measuring specific symptoms are asked, and a total score
is calculated by summing 8 items assessing preoccupa-
tions and rituals. Summary psychometric information
about the YBC-​EDS is provided in Table 24.3.
Any of the three measures described previously in the
context of measuring overall treatment outcome can also

TABLE 24.3   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

EDE, versions G A E A E A E A A ✓
12–​16
EDE-​Q, versions E G NA L E NR E A A
4 and 6
YBC-​EDS A G E NR G A G G A

Note: EDE = Eating Disorder Examination; EDE-​Q = Eating Disorder Examination Questionnaire; YBC-​EDS = Yale–​Brown–​Cornell Eating Disorder
Scale; L = Less Than Adequate; A = Adequate; G = Good; E = Excellent; NR = Not Reported; NA = Not Applicable.

be used to evaluate progress during treatment. Because
the EDE and the EDE-​Q both assess eating-​disordered
behaviors over a 28-​day period, these measures are ideal
for evaluating change on a monthly basis. Clinicians
interested in changes in symptoms on a weekly basis
can use self-​monitoring records to determine progress in
treatment.
Overall Evaluation
The overall evaluation of measures assessing treatment
monitoring and treatment outcome is consistent with
the conclusions of the two previous sections. Only the
EDE and YBC-​EDS can be included in Table 24.3 as
assessments that work, and although these instruments
are widely used in research, they may be less practical for
use by clinicians. Both are semi-​structured interviews that
require extensive training, and the amount of time needed
to administer the EDE or the YBC-​EDS can be consider-
able. Thus, the development of more efficient assessment
tools is an important goal for furthering the assessment of
treatment monitoring and outcome evaluation.
CONCLUSIONS AND FUTURE DIRECTIONS
The assessments described in this chapter are among
the most widely used in the field of eating disorders.
However, only a small number of measures can be clas-
sified as having extensive supporting psychometric evi-
dence. Commonly used research strategies, such as the
use of laboratory meal situations, can provide an objective
measure of eating behavior but are simply not feasible in
clinical practice (Wilson, 1993).
Although some variability in symptoms over time is to
be expected, ratings for test–​retest reliability are subopti-
mal for the instruments described in this chapter. Mond,
Hay, Rodgers, Owen, and Beaumont (2004) conducted the
longest evaluation of the stability of eating disorder assess-
ment over time, giving the EDE-​Q a mean of 303.2 days
apart. The authors found that “although the cognitive and
personality dimensions of eating disorder psychopathol-
ogy are relatively stable, eating-​disordered behaviors such
as binge eating and use of exercise as a means of weight
control are liable to fluctuate considerably in intensity
and severity over time” (p.  200). Symptom reactivity in
eating-​disordered behaviors has also been observed with
other forms of assessment, with a study by Hildebrandt
and Latner (2006) demonstrating a significant decrease in
OBEs and a concurrent increase in SBEs among women
Eating Disorders 555
with BN and BED after 7 days of self-​monitoring and no
additional treatment intervention. These studies suggest
that the core eating-​disordered behavior of binge eating
may oscillate and be significantly reactive to nonspecific
interventions, rendering the evaluation of binge eating
over a long period of time quite difficult.
One measurement issue that affects the accuracy and
reliability of scores on most eating disorder instruments is
the frequent reliance on a single questionnaire or inter-
view item to assess a particular behavior or symptom.
For example, most measures have only one question for
quantifying the number of binge eating episodes dur-
ing a specified period. This can provide important and
meaningful information for the purpose of diagnosis (e.g.,
whether a patient meets criteria for BN), treatment con-
ceptualization (e.g., are binge eating episodes decreasing
over time), and treatment outcome (e.g., has a clinically
meaningful change been observed). However, the reli-
ance on a single item increases measurement error and
decreases the overall statistical power to detect changes
across time or between groups (Viswanathan, 2005).
Given the poor test–​retest reliability observed for scores
on some measures, it may be useful to determine if reli-
ability could be improved by using multiple indicators for
each behavior or symptom. Beyond this, future research
should focus on attempting to examine DSM-​5 diagno-
ses, design new measures, and refine existing measures
in order to provide scientifically sound assessment tools
available to clinicians.
ACKNOWLEDGMENT
We thank G. Terence Wilson, PhD, who served as a con-
sultant on the version of this chapter from the first edi-
tion and provided guidance about the initial content of
the chapter.
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 25
Insomnia Disorder
Charles M. Morin
Simon Beaulieu-​Bonneau
Kristin Maich
Colleen E. Carney
Sleep complaints are extremely common in clinical prac-
tice. They may present as a clinical feature or symptom
of another co-​occurring disorder, or they may represent a
sleep–​wake disorder. There are multiple types of sleep–​wake
disorders, which may involve, for example, trouble sleeping
at night (insomnia), problems with breathing during sleep
(sleep apnea), or abnormal events during sleep (night-
mares). Insomnia is by far the most prevalent of all sleep
disorders and the one most likely to be encountered in clini-
cal practice by psychologists and other mental health prac-
titioners. Although some of the basic assessment procedures
and methodologies are similar across sleep–​wake disorders,
this chapter focuses on the assessment of insomnia (Arnedt,
Conroy, Posner, & Aloia, 2006; Morgenthaler et al., 2007;
Sateia, Doghramji, Hauri, & Morin, 2000; Schutte-​Rodin,
Broch, Buysse, Dorsey, & Sateia, 2008). After describing
the main clinical features and diagnostic criteria of insom-
nia disorder, along with a summary of its epidemiology and
public health significance, we review assessment strategies
and measures of insomnia-​related complaints in the context
of making a diagnosis and developing a case conceptualiza-
tion for treatment planning, as well as for monitoring treat-
ment and assessing outcome.
NATURE AND SIGNIFICANCE
OF INSOMNIA DISORDER
Clinical Features and Diagnostic Criteria
Insomnia is characterized by both nocturnal and diurnal
symptoms. The predominant feature is dissatisfaction
563
with sleep quality or duration, with complaints of diffi-
culties initiating or maintaining sleep. The three classic
nocturnal insomnia symptoms involve problems initiating
sleep at bedtime, trouble staying asleep with middle of
the night awakenings and difficulty going back to sleep,
or waking up too early in the morning with an inability to
return to sleep (American Academy of Sleep Medicine,
2014; American Psychiatric Association, 2013). Insomnia
complaints are typically accompanied by significant dis-
tress or impairments of daytime functioning that involve
daytime fatigue, cognitive impairments (e.g., attention
and memory), and mood disturbances (e.g., irritabil-
ity and dysphoria); these are often the primary concerns
prompting clients to seek insomnia treatment. To make
the diagnosis of insomnia disorder, these difficulties must
be present 3 nights or more per week and last for more
than 3 months. Sleep difficulties that are less frequent or
of shorter durations may still require clinical attention
before they reach disorder status.
The conceptualization of insomnia has evolved during
the past two decades from being viewed predominantly
as a symptom of another psychiatric disorder to being
recognized as a disorder on its own. Indeed, important
changes were made to the diagnostic criteria of insom-
nia in the fifth edition of the Diagnostic and Statistical
Manual of Mental Disorders (DSM-​ 5; American
Psychiatric Association, 2013)  and the third edition
of the International Classification of Sleep Disorders
(ICSD; American Academy of Sleep Medicine, 2014).
For instance, the most important change introduced in
both classifications is that there is no longer a distinction
564 Health-Related Problems
made between primary insomnia and insomnia secondary
to another psychiatric or medical disorder. Such comor-
bidities, when present, only need to be listed, but there
is no requirement to make a causal attribution to deter-
mine whether insomnia is primary or secondary. This
departure from previous nosologies was predicated on the
recognition that when insomnia is comorbid with another
disorder (e.g., major depression), it is often difficult to
determine which condition is the cause and which is the
consequence, and also on evidence that the direction
of this relationship may change over time (Reynolds &
Redline, 2010). It was also based on increasing evidence
that treatment outcome is more favorable when treating
both insomnia and the comorbid condition (e.g., depres-
sion, anxiety, and pain) concurrently than when treating
either condition alone.
Epidemiology and Public Health Significance
Population-​based estimates indicate that between 6% and
12% of adults meet criteria for an insomnia disorder dur-
ing the course of a year, and an additional 15% to 20%
of adults report subsyndromal insomnia (Morin, LeBlanc,
et al., 2011; Ohayon, 2002; Roth et al., 2006). Insomnia
is more prevalent among women, middle-​aged and older
adults, shift workers, and individuals with medical or psy-
chiatric disorders. Difficulties initiating sleep are more
common among young adults, and problems maintain-
ing sleep are more frequent among middle-​aged and older
adults. The incidence of insomnia is higher among first-​
degree family members (daughter and mother) than in
the general population (Dauvilliers et  al., 2005), but it
remains unclear whether this link is inherited through a
genetic predisposition, learned by observations of parental
models, or a by-​product of another psychopathology.
The onset of insomnia can occur at any time in life, but
the first episode is most common in young adulthood. It is
often precipitated by stressful life events, such as a separa-
tion, occupational or family stress, and interpersonal con-
flicts (Bastien, Vallières, & Morin, 2004; Ellis, Gehrman,
Espie, Riemann, & Perlis, 2012). In some cases, insomnia
begins in childhood, in the absence of psychological or
medical problems, and persists throughout adulthood.
Insomnia is a common problem among women during
menopause and often persists even after other symptoms
(e.g., hot flashes) have subsided either naturally or with
hormonal replacement therapy. Insomnia may also have a
late-​life onset, which needs to be distinguished from nor-
mal (age-​related) changes in sleep; such late-​life onset is
often associated with other health-​related problems.
Potential risk factors for insomnia include demo-
graphic factors (e.g., female gender and advancing age),
psychological factors (e.g., a worry-​prone cognitive style),
hyperarousal, and a personal or familial history of insom-
nia (Jarrin, Chen, Ivers, & Morin, 2014; LeBlanc et al.,
2009). For most individuals, insomnia is transient in
nature, lasting a few days and resolving itself once the ini-
tial precipitating event has subsided. For others, perhaps
those more vulnerable to sleep disturbances due to risk
factors just mentioned, insomnia may persist long after
the initial triggering event has disappeared; other fac-
tors, such as spending excessive amounts of time in bed
or repeated napping during the day, would then perpetu-
ate sleep disturbances (Spielman & Glovinsky, 1991). It
is particularly important to identify these perpetuating
factors when planning treatment. The course of insom-
nia may also be intermittent, with repeated brief episodes
of sleep difficulties following a close association with the
occurrence of stressful events. Longitudinal studies have
shown that chronicity rates may range from 45% to 75%
for follow-​ups of 1 to 7 years (Buysse et al., 2008; Morin,
Bélanger, et al., 2009; Morphy, Dunn, Lewis, Boardman,
& Croft, 2007). Even in chronic insomnia, there is often
significant night-​to-​night variability in sleep patterns, with
an occasional restful night’s sleep intertwined with several
nights of poor sleep (Vallières, Ivers, Bastien, Beaulieu-​
Bonneau, & Morin, 2005).
The prognosis for insomnia varies across individuals
and is probably mediated by a combination of biologi-
cally related predisposing factors and psychological and
behavioral perpetuating factors. It may also be compli-
cated by the presence of comorbid psychiatric or medical
disorders. Persistent insomnia is not a benign problem and
often produces adverse effects on an individual’s life, on
his or her family, and on society at large. For example,
persistent insomnia is associated with reduced quality of
life, decreased work productivity, increased absenteeism,
and higher rates of health care utilization (Daley et  al.,
2009; Simon & VonKorff, 1997; Sivertsen et  al., 2006).
Increasing evidence suggests associations between chronic
insomnia and long-​term negative health outcomes such as
increased risk of depression, disability, hypertension, and
even mortality (Baglioni et al., 2011; Fernandez-​Mendoza
et  al., 2012; Laugsand, Vatten, Platou, & Janszky, 2011;
Suka, Yoshida, & Sugimori, 2003; Vgontzas et al., 2010).
Insomnia is often comorbid with other psychiatric
and medical conditions, most frequently depression,
anxiety, and pain (Baglioni et al., 2011; Taylor, Lichstein,
Durrence, Reidel, & Bush, 2005; Taylor et  al., 2007).
This high comorbidity may add to the complexity and

challenges of making an accurate diagnosis. Nonetheless,
it is essential to consider these comorbid conditions when
assessing insomnia, particularly for planning treatment.
PURPOSES OF ASSESSMENT
The 24-​ hour nature of insomnia (i.e., nocturnal and
daytime symptoms), combined with some discrepancies
between the subjective and objective measurements of
sleep/​wakefulness, makes this condition particularly chal-
lenging for clinical assessment. In addition, sometimes
insomnia is the presenting complaint, but there may be
another sleep disorder unknown to the client. For these
reasons, the assessment of insomnia should be multidi-
mensional and involve a multitrait, multimethod assess-
ment paradigm that takes into consideration nighttime
(sleep) and daytime dimensions (fatigue, mood, and cog-
nition), along with subjective, behavioral, and physiologi-
cal measures. In the following sections, we highlight the
main strategies to consider for assessing insomnia in the
context of diagnosis, treatment planning, and monitoring
treatment progress/​outcome (Schutte-​Rodin et al., 2008).
ASSESSMENT FOR DIAGNOSIS
The diagnosis of insomnia is derived primarily from a
detailed clinical evaluation of the client’s subjective
complaint (Arnedt et al., 2006; Sateia et al., 2000; Wyatt,
Cvengros, & Ong, 2012). The sleep history should cover
the type of complaint (initial, middle, or late insomnia),
its duration (acute vs. chronic), and course (recurrent or
persistent); typical sleep schedule (bedtime and arising
time); functional analysis of precipitating, perpetuating,
and alleviating factors; perceived consequences and func-
tional impairments; and the presence of medical, psychi-
atric, or environmental contributing factors. A complete
history of alcohol and drug use and prescribed and over-​
the-​counter medications is also essential, as is a history of
previous treatments and outcome (Buysse, Ancoli-​Israel,
TABLE 25.1   Ratings of Instruments Used for Diagnosis
Internal Inter-​Rater Test–​Retest
Instrument Norms Consistency Reliability Reliability
DSISD NR NA G NR
Polysomnography NR NA E G
Note: DSISD = Duke Structured Interview for Sleep Disorders. A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.
Insomnia Disorder 565
Edinger, Lichstein, & Morin, 2006; Morin & Espie,
2003; Schutte-​ Rodin et  al., 2008). Several assessment
options are available to assist the clinician in conducting
the initial evaluation of insomnia; they are presented in
Table 25.1.
Clinical Interviews
The Insomnia Diagnostic Interview (IDI), also called the
Insomnia Interview Schedule (Morin, 1993), was devel-
oped to assist clinicians in conducting a semi-​structured
interview. Topics covered by this interview include typical
sleep–​wake schedules; the nature, frequency, and severity
of insomnia symptoms; daytime consequences of insom-
nia; the history of the sleep problem; overview of predispos-
ing, precipitating, and perpetuating factors; sleep-​related
behaviors (e.g., napping and strategies to manage insom-
nia symptoms or consequences); environmental factors
and life habits (e.g., work schedule, bedroom organiza-
tion, use of caffeine, and exercise); current and past use
of medication and other sleep aid; medical history; and
screening questions for other sleep disorders. The IDI
has been used extensively in clinical research studies to
assist in the initial diagnosis of insomnia and to facilitate
treatment planning. It has also been adapted for use with
several clinical populations presenting comorbid condi-
tions such as cancer (Savard, Simard, Ivers, & Morin,
2005)  and brain injury (Ouellet, Beaulieu-​Bonneau, &
Morin, 2012). Despite its clinical usefulness to gather sys-
tematic information, there are no psychometric data on
either reliability or validity, and for this reason the IDI
is not included in Table 25.1. In addition, more recent
structured interviews have been developed to specifically
address the diagnosis of insomnia.
The Duke Structured Interview for Sleep Disorders
(DSISD; Edinger, Wyatt, et al., 2009) was first developed
to assess for the presence of sleep disorders according
to criteria from the DSM-​IV-​TR (American Psychiatric
Association, 2000) and the ICSD-​2 (American Academy
of Sleep Medicine, 2005). It is a comprehensive interview
that includes a screening questionnaire to streamline the
Content Construct Validity Clinical Highly
Validity Validity Generalization Utility Recommended
E E A E ✓
A A E A
566 Health-Related Problems
interview and shorten the administration time, verbatim
questions for each diagnosis, a scoring table for yes/​no
responses to remind interviewers of the criteria and aid
in decision-​ making, and a ranking table of diagnoses
with ICSD-​2 and DSM-​IV-​TR codes. Importantly, this
interview carefully leads the clinician through insomnia
diagnostic possibilities but also through other sleep dis-
orders that may be comorbid or may actually explain the
insomnia complaint. A  typical DSISD interview takes
approximately 1 hour to administer. It may be especially
helpful for those with less experience in diagnosing sleep
disorders.
Because the DSISD uses diagnostic criteria, it has
excellent face validity and content/​ construct validity.
There is evidence for reliability as well, with moderate
to good inter-​rater agreement for the DSM categories of
primary insomnia (r  =  .46), breathing-​related sleep dis-
order (r = .75), circadian rhythm disorder (r = .44), dys-
somnia not otherwise specified (r  =  .42), and insomnia
related to mental (r = .57) and medical disorder (r = .44)
(Carney et  al., 2008). However, some diagnoses in the
interview were associated with poor inter-​rater agreement,
mainly from the ICSD-​2 (e.g., paradoxical insomnia).
Subsequent field studies suggested that some insomnia
subtypes were not particularly valid or reliable (Edinger
et  al., 2011), and they were subsequently dropped from
DSM-​ 5. Issues of reliability and validity in structured
interviews are difficult because the measure can only be
as reliable and valid as the diagnostic categories on which
it is based. The DSISD has been used in a number of clin-
ical trials to establish the presence of an insomnia diagno-
sis and to rule out other sleep disorders (Edinger, Olsen,
et al., 2009; Harvey et al., 2014; Talbot et al., 2014). An
updated version for DSM-​5 and ICSD-​3 is available by
contacting the first author of the interview.
Polysomnography
Polysomnography (PSG) involves the monitoring of simul-
taneous physiologic channels for the purposes of charac-
terizing the onset of sleep and its stages. PSG channels
include electroencephalography (EEG), electrooculog-
raphy, and electromyography indices that measure brain
activity, eye movements, and muscle tone. Several addi-
tional channels for monitoring breathing and leg move-
ments are typically used to diagnose other sleep disorders,
such as sleep apnea and periodic limb movements during
sleep. Most often, PSG monitoring takes place in a sleep
laboratory, but it can also be conducted on an ambula-
tory basis in the client’s home. There are standardized
rules for scoring the array of PSG indices, including sleep
stages, the onset of sleep, and breathing-​and movement-​
related events (Berry et  al., 2012). Although clinicians
often assume that overnight sleep studies involving PSG
are necessary for insomnia assessment, PSG is not recom-
mended as part of routine clinical practice for insomnia
(Schutte-​Rodin et al., 2008). The reason why PSG is not
commonly used in insomnia assessment is that the valid-
ity for insomnia may be dubious (Littner et al., 2003). For
example, in chronic insomnia, arousal may become con-
ditioned/​associated with the bed, so having someone sleep
in a different environment (e.g., the sleep lab) may undo
the arousal–​bed association and obfuscate the insomnia
complaint temporarily. The characteristics of the lab may
have the reverse effect—​that is, the noise and discomfort
could worsen insomnia symptoms; in either case, PSG can
interfere with the assessment of the problem it is intended
to measure. There may be reliability issues associated with
PSG because it typically assesses sleep in one night or per-
haps two, but sleep is thought to be variable across nights,
so this limited sampling may not reflect the sleep of the
client overall. In addition, EEG activity scored according
to consensus rules may not correlate with the subjective
experience/​complaint of the insomnia sufferer (Kaplan
et  al., 2016; Krystal, Edinger, Wohlgemuth, & Marsh,
2002). Given that insomnia is a subjective disorder, the
lack of correspondence between PSG and subjective
experience is a significant shortcoming of PSG. In addi-
tion, given that there are not hard quantitative rules for
defining insomnia, PSG is not an essential component of
clinical insomnia assessment except when other sleep dis-
orders may be suspected.
Overall Evaluation
In summary, a detailed and systematic clinical evalu-
ation of insomnia and its related symptoms is the most
important assessment strategy for making an initial diag-
nosis of insomnia. This clinical evaluation can and should
be complemented with other assessment strategies to be
described in the next sections.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
Conceptual Models of Insomnia
There are several conceptual models of insomnia that all
view hyperarousal as a core feature of this sleep disorder.
 Insomnia Disorder 567

Some models emphasize behavioral factors, whereas oth-
ers stress cognitive factors, and still others focus on cor-
tical arousal (Espie, 2002; Harvey, 2002; Morin, 1993;
Perlis, Ellis, Kloss, & Riemann, 2016). The 3P model
(Spielman & Glovinsky, 1991)  is an integrative model
that outlines three key contributing factors to insomnia,
namely predisposing, precipitating, and perpetuating fac-
tors. Predisposing factors enhance the vulnerability to
develop insomnia; these include increasing age, female
gender, an anxiety-​prone personality style, and physiologi-
cal hyperarousal. The mere presence of these risk factors
is usually not enough to trigger insomnia; there needs to
be some precipitating event, typically a stressful life event
(e.g., an accident, a separation, death of a loved one,
and occupational stress), to bring about acute sleep dis-
turbances. Whereas otherwise good sleepers will resume
normal sleep after these precipitating events have disap-
peared, individuals who are more prone or vulnerable to
suffer from insomnia will often continue to experience
sleep disturbances even after the initial triggering event
is no longer present. When insomnia becomes a chronic
problem, there are several psychological and behavioral
factors that contribute to the perpetuation of sleep difficul-
ties over time. Among these are classic psychological/​cog-
nitive factors such as sleep-​specific performance anxiety,
the fear of not sleeping, apprehension about the potential
consequences of insomnia, and maladaptive sleep habits
(e.g., spending excessive amounts of time in bed, main-
taining irregular sleep schedules, and using stimulants to
stay awake). It is here that the case formulation becomes
extremely helpful in identifying the factors contributing
to the perpetuation of insomnia and the factors that must
be targeted in treatment.
Case Formulation
Case formulation is an iterative, client-​centered approach
to assessment and treatment (Persons, 2012). Case formula-
tion is essential to a good treatment plan because it considers
who to treat and when to treat them (e.g., diagnostic consid-
erations), the treatment targets (e.g., perpetuating factors for
the insomnia), and the behavioral strategies that will be used
to address these targets (Manber & Carney, 2015). Manber
and Carney recommended collecting the following informa-
tion on clients to organize the case formulation: (a) factors
associated with poor homeostatic sleep drive, (b) factors asso-
ciated with poor circadian functioning, (c) factors associated
with hyperarousal, (d) unhealthy sleep behaviors, (e) medi-
cations that may impact sleep and alertness, (f) comorbidi-
ties that may worsen sleep, and (g) environmental or other
factors that may affect the sleep complaint or impact the
delivery of cognitive–​ behavioral therapy for insomnia
(CBT-​I). Tables 25.2 and 25.3 provide examples of instru-
ments that assess for each of these domains. As illustrated in
Table 25.3, central to this approach is a thorough clinical
interview, the use of sleep diary monitoring, the testing of
hypotheses derived from the formulation, and the evaluation
of treatment outcomes. The clinician hypothesizes about the
most important targets for treatment (i.e., those with a high
negative impact on sleep regulation) and shares this hypoth-
esis with the client, as well as a suggested plan for addressing
the problem. Clinician and client then collaborate on the

TABLE 25.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Consensus NR NA NA NA E E NR E ✓
Sleep Diary
DBAS-​16 A A NA A A A NR G ✓
PSAS NR G NA G A G A A
SBSRS NR G NA G A A NR A
SAMI A G NA A A NR NR A
SPS A G NA NR A NR NR A
APS A G NA NR A A NR A
FIRST A G NA G A NR A A
GSES A A NA NR A NR NR A

Notes: Psychometric ratings are based on the original English version of the instrument only.
DBAS  =  Dysfunctional Beliefs and Attitudes About Sleep Scale; PSAS  =  Pre-​Sleep Arousal Scale; SBSRS  =  Sleep-​Behavior Self-​Rating Scale;
SAMI = Sleep Associated Monitoring Index; SPS = Sleep Preoccupation Scale; APS = Arousal Predisposition Scale; FIRST = Ford Insomnia Response
to Stress Test; GSES = Glasgow Sleep Effort Scale; A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.
568 Health-Related Problems
TABLE 25.3   Case Formulation Assessment Domains, Sources, and Treatment Implications
Perpetuating Factors How to Assess
1. What factors may be Examine diary for napping, add all the time
negatively impacting spent in bed in the 24-​hour period to
the homeostatic determine if it far exceeds the average total
drive for deep sleep? sleep time.
Clinical interview: Query activity levels, time
into bed and out of bed, nap attempts,
dozing.
2. What factors may be Examine diary for a variability of 1 hour
negatively impacting or more between the earliest and latest
the biological clock? bedtime, wake time, and arising time.
Clinical interview: Query whether there is an
early (advanced sleep phase or early bird
tendency) or late (delayed sleep phase
or night owl tendency) chronotype, and
whether the client is able to schedule sleep
opportunities that match this tendency.
Actigraphs may be helpful for assessing
rare, irregular rest/​activity patterns in the
24-​hour period.
3. What factors may Clinical interview: Query whether there is
be associated with increased alertness upon getting into the
increased arousal? bed (e.g., conditioned arousal).
Sleep diary evidence of increased sleep effort
(e.g., increased time in bed to increase the
likelihood of sleep, use of sleep aides).
Is the mean DBAS-​16 score 4 or above
(i.e., do they have beliefs about sleep that
are target-​worthy)?
Is there an elevation on the Glasgow Sleep
Effort Scale, suggestive of a maladaptive
belief that one has to exert effort to sleep?
Is there a tendency toward monitoring
for sleep-​related threats on the Sleep
Associated Monitoring Index or the Sleep
Preoccupation Scale? Are there increased
scores suggestive of hyperarousal on the
Arousal Predisposition Scale and/​or the
Pre-​Sleep Arousal Scale?
4. What unhealthy Sleep diary to track excessive or consumption
sleep behaviors may late in the day of caffeine, alcohol, drugs,
be affecting sleep and cigarettes.
and/​or alertness? Insomnia Diagnostic Interview and/​or clinical
interview to assess for behaviors such as
nocturnal eating, late, vigorous exercise, etc.
5. What medications Sleep diary to track sleep medication use.
could be affecting Interview to assess for contingent (i.e., prn)
the client’s sleep use of sleep or anxiety medications,
and/​or alertness? safety behaviors, and daytime effects of
the medication. Assess for medications
other than sleep or anxiety pills that can
interfere with sleep (e.g., antidepressant
medications).
Cognitive Behavioral Strategies to Consider
Sleep restriction therapy (i.e., decrease time spent in bed to match
current average total sleep time).
Stimulus control (i.e., no napping, set arise time 7 days per week, do
not go to bed until sleepy).
Sleep hygiene (i.e., exercise).
Sleep restriction therapy (i.e., consider chronotype when setting sleep
schedule).
Stimulus control (i.e., set arise time 7 days per week).
Sleep hygiene (i.e., limit exposure to blue light in the evening and
increase blue light exposure during the day for input to the clock).
Stimulus control (i.e., go to bed only when sleepy, get out of bed when
unable to sleep, set arise time 7 days per week, no naps, refrain from
wakeful activities in bed).
Cognitive therapy (i.e., challenge belief that sleep effort is helpful for
sleep and the fear of not sleeping, explore whether particular beliefs
on the DBAS-​16 are sleep-​interfering, test whether sleep monitoring
or sleep-​preoccupation behaviors are helpful or sleep-​interfering).
Relaxation therapy to decrease hyperarousal.
Counter-​arousal techniques (e.g., Pennebaker writing intervention
[Harvey & Farrell, 2003] or structured problem solving [Carney &
Waters, 2006]) to address hyperarousal.
MBTI (Ong et al., 2014) to address hyperarousal.
Sleep hygiene (i.e., decrease use of caffeine, alcohol, drugs, cigarettes;
limit exposure to blue light in the evening; exercise but not close to
bedtime; refrain from nocturnal eating).
Signed release to review medical history and to collaborate with
prescriber to eliminate contingent use of sleep medication and to
discuss options for an optimal, efficacious sleep medication.
Psychoeducation about the effects of sleep medication.
Cognitive therapy to test whether sleep mechanisms are still
functioning in the client.
Proceed with CBT-​I and then, if consistent with client goals,
implement taper.
Consider whether adaptations to CBT-​I are necessary for safety
(e.g., restricting sleep to a lesser degree in those on sedating
medications or asking them to refrain from getting out of bed in the
middle of the night if there is a concern for falls).

TABLE 25.3  Continued
Perpetuating Factors How to Assess
6. What comorbidities Structured interview such as the Duke
impact the client’s Structured Interview for Sleep Disorders or
sleep and/​or Insomnia Diagnostic Interview to assess for
alertness and how? signs of other sleep disorders. Follow-​up with
referral for polysomnography if other sleep
disorders are suspected (e.g., sleep apnea).
Clinical interview to assess for medical and
psychiatric conditions, and treatment
strategies (e.g., sleep apnea diagnosis but
difficult adjustment to CPAP treatment,
or chronic pain with ambivalence toward
using pain management strategies).
Self-​report measures to track comorbid
symptoms such as depression (BDI-​II,
PHQ-​9), anxiety, (STAI and BAI), and
fatigue (FSS or MFI)
7. What other factors Insomnia Diagnostic Interview and/​or
are there to consider? clinical interview to assess other factors
(e.g., current sleep environment, mental/​
cognitive status, and readiness for change).
Note: BAI = Beck Anxiety Inventory; BDI-​II = Beck Depression Inventory-​II; CBT-​I = Cognitive–​Behavioral Therapy for Insomnia; CPAP = Continuous
Positive Airway Pressure; DBAS-​16 = Dysfunctional Beliefs and Attitudes About Sleep Scale; FSS = Fatigue Severity Scale; MBTI = Mindfulness-​Based
Therapy for Insomnia; MFI = Multidimensional Fatigue Inventory; PHQ-​9 = Patient Health Questionnaire; STAI = State–​Trait Anxiety Inventory.
course and agree to track progress so that they can evaluate if
the plan needs to be altered.
Self-​Report Measures
Having the client complete a sleep diary each morning is
an essential component of insomnia assessment both for
diagnosis and for treatment planning/​tracking. Although
there are different models of sleep diaries available in
the literature, the Consensus Sleep Diary (CSD; Carney
et al., 2012) was developed in consultation with a group
of 25 leading experts to provide a standardized diary. The
CSD is a prospective tool completed upon awakening that
queries the subjective experience of the previous night.
Core items include the time the client got into bed, the
estimated amount of time it took to fall asleep, the num-
ber of awakenings and total estimated length of awaken-
ings during the night, the last time that the client woke
up for the day, the time at which the client got out of
bed, and a 5-​point Likert rated subjective sleep quality.
Insomnia Disorder 569
Cognitive Behavioral Strategies to Consider
Consider whether adaptations to CBT-​I are necessary (e.g., adding a
fatigue module with chronic illnesses such as cancer, or restricting
sleep to a lesser degree with panic disorder or disorders associated
with excessive daytime sleepiness).
Refer for treatment of other disorder and work with client on adherence
to the treatment of the other disorder.
In cases of a low readiness for behavior change or medical/​psychiatric
crisis, consider motivational interviewing to explore whether it is the
right time to initiate CBT-​I. Discuss benefits and drawbacks to other
approaches, including relaxation as a monotherapy, medication, MBTI.
Troubleshooting adaptations for current environment or referral for
social supports to improve housing situation.
Adaptation/​simplification of materials (e.g., sleep diaries and handouts)
for the cognitive/​reading level of the client.
Given the subjective nature of insomnia disorder, the
sleep diary represents an essential tool to obtain the cli-
ent’s perception of the problem. Establishing reliability
and validity data for this measure is difficult. For example,
we would not anticipate that there would be high test–​
retest reliability because sleep is quite variable across
nights, particularly among individuals with insomnia.
Sleep is a construct defined by what measure is selected,
so in PSG, sleep is defined as electrical activity, whereas
in actigraphy it is defined by movement patterns; thus, we
would not expect high correlation with other measures of
slightly differing constructs. Despite the subjectivity of the
diary, the stability and clinical value of this measure are
optimal when the diary is completed soon after wakening
and for at least a 2-​week period (Wohlgemuth, Edinger,
Fins, & Sullivan, 1999). Good evidence for validity has
been obtained when CSD indices were compared against
objective (i.e., actigraph) indices (Maich, Lachowski, &
Carney, 2016). There is evidence for diagnostic valid-
ity for establishing an insomnia diagnosis (Natale et  al.,
570 Health-Related Problems
2015); for example, there is strong specificity evidence
for CSD indices of sleep-​onset latency, wakefulness after
sleep onset, number of awakenings, and sleep efficiency
(Maich et al., 2016). There is only moderate sensitivity for
the same indices (Maich et al., 2016), but this may relate
to the difficulty in deriving suitable quantitative criteria
for insomnia (Lineberger, Carney, Edinger, & Means,
2006) rather than to the properties of the CSD. Although
some clinicians worry about whether clients can complete
diary measures, this diary was created with client-​directed
input via focus groups (Carney et  al., 2012), and there
is a high reported rate of completion of the diary as well
(Maich et al., 2016). Readability analyses suggest the core
diary is written at a third-​grade reading level (Carney
et al., 2012).
The Dysfunctional Beliefs and Attitudes About Sleep
Scale (DBAS) is a self-​report questionnaire that assesses
unhelpful cognitions related to sleep, insomnia, and day-
time consequences of insomnia. The initial version con-
tains 30 items that are categorized into five themes:  (a)
misconceptions about the causes of insomnia (e.g., “I
believe insomnia is essentially the result of a chemical
imbalance”), (b)  misattribution or amplification of the
consequences of insomnia (e.g., “Without an adequate
night’s sleep, I can hardly function the next day”), (c) unre-
alistic expectations about sleep (e.g., “I need 8 hours of
sleep to feel refreshed and function well during the day”),
(d) misconceptions about sleep-​promoting practices (e.g.,
“When I  don’t get proper amount of sleep on a given
night, I need to catch up on the next day by napping or on
the next night by sleeping longer”), and (e) lack of control
or unpredictability of sleep (e.g., “I am worried that I may
lose control over my abilities to sleep”). Respondents rate
the extent to which they endorse each item on a Likert-​
type scale (0 = strongly disagree to 10 = strongly agree).
A total score is derived by averaging item scores (the score
of item 23 is reversed), with higher scores suggesting a
higher level of dysfunctional sleep-​related cognitions. In
place of using formal scoring of this instrument, clini-
cians may use it in practice simply to identify unhelpful
sleep beliefs that should be targeted during the course of
therapy. Although the original DBAS contains 30 items
(Morin, 1993), an abbreviated 16-​item version has also
been validated (Morin, Vallieres, & Ivers, 2007), and a
24-​item adaptation is available for use with children
(Gregory et al., 2009). Only the DBAS-​16 is included in
Table 25.2 because of its stronger psychometric proper-
ties and shorter format. The factor structure is consis-
tent with the longer version: (a) perceived consequences
of insomnia, (b)  worry/​ helplessness about insomnia,
(c) sleep expectations, and (d) medication (Morin et al.,
2007). The DBAS has been shown to be sensitive to treat-
ment change with CBT-​I (Edinger, Wohlgemuth, Radtke,
Marsh, & Quillian, 2001; Eidelman et al., 2016).
The Pre-​ Sleep Arousal Scale (PSAS) (Nicassio,
Mendlowitz, Fussell, & Petras, 1985)  is a 16-​item self-​
report measure of the state of arousal just before sleep.
There are two summed PSAS subscales measuring
somatic and cognitive states of pre-​sleep arousal. The
original validation article by Nicassio and colleagues
(1985) reported good internal consistency and test–​retest
reliability for PSAS scores. There is also good evidence
for convergent validity because scores on the somatic and
cognitive subscales correlate moderately with anxiety, self-​
identification as a poor sleeper, sleep-​onset latency, total
sleep time, and awakenings from sleep. The PSAS scores
distinguish between good sleepers and those with insom-
nia, particularly on the basis of the cognitive subscale
score (Nicassio et al., 1985). This scale was also validated
with a community sample, and there was good evidence
for a two-​factor model with a shortened version of the
scale (Jansson-​Frojmark & Norell-​Clarke, 2012). Further
research is needed to determine if the scales need to be
modified based on these results.
The Sleep Behavior Self-​ Rating Scale (SBSRS;
Kazarian, Howe, & Csapo, 1979)  measures the fre-
quency of sleep-​ incompatible behaviors in the bed-
room. It includes 20 items that are rated on a 5-​point
scale (i.e., ranging from 1  =  never to 5  =  very often).
Eighteen items are duplicates, with one set of 9 items
referring to activities engaged in during the day and the
other 9 items pertaining to the same behaviors engaged
in around sleeping time. The total score is the sum of
the 20 items, with higher scores suggesting greater degree
of sleep-​incompatible behaviors. Its internal consistency
was found to be adequate in the original study (α = .72 to
.76), and the test–​retest reliability was high (r = .88 for two
administrations separated by 2 or 3 weeks). In addition,
the SBSRS scores differentiated between poor and good
sleepers (as defined on the basis of sleep-​onset latency)
and showed adequate discriminant validity with anxiety
and depression measures. Although the SBSRS can be
a useful tool to identify target behaviors to change with
stimulus control procedures during insomnia treatment,
psychometric data are limited to just one study. Moreover,
because the scale was developed in 1979, additional sleep-​
incompatible behaviors, more relevant to the advent of
modern technology, should be added to the scale (e.g.,
using a smartphone or tablet in bed and working on a
computer in the bedroom).

The Sleep Associated Monitoring Index (SAMI;
Semler & Harvey, 2004) is a 30-​item questionnaire assess-
ing nighttime and daytime monitoring for sleep-​related
threat, a key component of Harvey’s cognitive model of
insomnia (Harvey, 2002). A  factor analysis yielded eight
factors:  (a) pre-​sleep monitoring for body sensations
consistent with falling asleep, (b)  pre-​ sleep monitor-
ing for body sensations inconsistent with falling asleep,
(c)  pre-​sleep monitoring the environment, (d)  pre-​sleep
monitoring the clock, (e) calculation of time, (f) waking
monitoring for body sensations, (g)  daytime monitoring
for body sensations, and (h) daytime monitoring of func-
tioning. Each item is rated on a 5-​point scale (1 = not at
all to 5 = all the time). Eight subscale scores and a total
score can be derived by adding up scores of individual
items. Psychometric properties reported in Table 25.2
are derived from the initial validation study (Semler &
Harvey, 2004).
The Sleep Preoccupation Scale (SPS; Ellis, Mitchell,
& Hogh, 2007)  was developed as a measure of the day-
time cognitive processes related to sleep (e.g., “My
memory appears to be worse after a bad night’s sleep”
and “I am more irritable after a bad night’s sleep”). It is
composed of 22 items, each answered on a 6-​point rat-
ing scale (0 = never to 6 = all the time) representing the
frequency of cognitions related to daytime consequences
of sleep patterns. The SPS has two subscales, one for cog-
nitive/​behavioral consequences and the other for affec-
tive consequences. Based on the initial validation study,
poor sleepers reported significantly greater levels of cog-
nitive/​behavioral and affective preoccupations compared
to good sleepers. Psychometric properties of the SPS
have not been studied independently from the initial
development study.
The Arousal Predisposition Scale (APS; Coren,
1988)  is a 12-​ item questionnaire assessing cognitive
arousability (e.g., “I get excited easily” and “I can be
emotionally moved by what other people consider simple
things”). It is distinct from the PSAS because it focuses
on cognitive arousability as a long-​ term, stable trait
rather than as a pre-​sleep state. The respondent rates on
a 5-​point scale (1 = never to 5 = always) how each item
describes his or her typical behaviors. The summation
of the 12 items yields the APS total score. The psycho-
metric qualities of the APS have been documented in
several studies (Coren, 1988, 1990; Coren & Mah, 1993;
Hicks, Conti, & Nellis, 1992; Saliba, Henderson, Deane,
& Mahar, 1998).
The Ford Insomnia Response to Stress Test (FIRST;
Drake, Richardson, Roehrs, Scofield, & Roth, 2004)  is
Insomnia Disorder 571
a self-​reported measure of an individual’s vulnerability
to stress-​related sleep disturbance and hyperousal. The
questionnaire includes nine items representing common
stressful situations, and the respondent has to rate on a
4-​point scale (from 1 = not likely to 4 = very likely) the
likelihood of experiencing sleep difficulties in response
to these situations (e.g., before an important meeting the
next day or after an argument). A total score ranging from
9 to 36 is obtained by adding up the nine item scores,
with higher scores suggesting greater sleep reactivity. The
psychometric properties of the FIRST have been docu-
mented in the original validation article (Drake et  al.,
2004)  and in at least one further study (Jarrin, Chen,
Ivers, Drake, & Morin, 2016). It has also been shown that
the vulnerability to stress-​related sleep disturbances, as
assessed by the FIRST, has a strong familial aggregation
(Drake, Scofield, & Roth, 2008).
The Glasgow Sleep Effort Scale (GSES; Broomfield
& Espie, 2005) assesses cognitive and behavioral compo-
nents of sleep effort and control, both at sleep onset and
after nighttime awakenings. Because sleep is an involun-
tary process, excessive effort to control sleep initiation
has been proposed as a potential cognitive factor contrib-
uting to the maintenance and exacerbation of insomnia.
The GSES contains seven items (e.g., “I feel I should be
able to control my sleep” and “I put too much effort into
sleep when it should come naturally”) rated on a 3-​point
scale (0  =  not at all, 1  =  to some extent, and 2  =  very
much), with the period of reference being the past week
(the GSES is therefore a measure of state rather than
trait). The total score is the summation of the seven
items, with a score of 3 or more suggesting high sleep
effort (Broomfield & Espie, 2005). A  pilot version of
the GSES was first used in two studies (Broomfield &
Espie, 2003, 2005), and the scale was then formally vali-
dated (Broomfield & Espie, 2005) and further used with
both insomnia and good sleeper samples (Hertenstein
et al., 2015).
Overall Evaluation
Of all assessment strategies described in this section,
the case conceptualization and the sleep diary represent
essential assessment strategies for initial evaluation and
diagnosis of insomnia. The remaining measures are help-
ful for gaining a better understanding of factors predispos-
ing to or potentially contributing to perpetuate insomnia.
They can be used for specific client needs or when other
assessments suggest that more information in one or
another area might be helpful in case formulation.
572 Health-Related Problems

ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
A comprehensive assessment of treatment progress and
outcome following treatment should include assessment
of nocturnal sleep–​wake parameters and insomnia symp-
toms, as well as assessment of several dimensions of day-
time functioning including fatigue, and also mood and
psychological symptoms. Ideally, some measures of day-
time performance and cognitive functioning should also
be conducted, but there is currently a lack of adequate
measures for this dimension. Ratings of instruments
reviewed in this section are presented in Table 25.4.
Assessment of Sleep/​Insomnia
The Consensus Sleep Diary, described previously, is
essential to treatment monitoring. The CSD is used to
derive daily averages of several sleep–​wake parameters,
including time to fall asleep, time awake after sleep
onset, total sleep time, and sleep efficiency. These indi-
ces are then used to inform treatment decisions and to
track whether hypotheses about how to correct the sleep
problem are correct. For example, the CSD is central
to developing the sleep scheduling component of sleep
restriction therapy in CBT-​I. The calculated mean total
sleep time is used to derive the time-​in-​bed prescription,
and then in subsequent weeks, the CSD is used to assess
for adherence (i.e., Does the mean time in bed match the
time-​in-​bed prescription?) as well as outcome (i.e., Does
mean sleep efficiency normalize?). The CSD is also used
to determine when the second phase of sleep restriction
therapy (i.e., sleep extension) occurs (i.e., Is the mean
sleep efficiency greater than 90%). In addition, the CSD
is used in CBT-​I to test beliefs the client has about his
or her sleep system. For example, sleep tracked on the
CSD may reveal that all-​or-​none statements about “not
sleeping” were inaccurate, or assumptions that naps are
not actually sleep disruptive can be evaluated by examin-
ing sleep after naps or no naps. The CSD is central to
hypothesis testing in treatment. The CSD has good treat-
ment sensitivity in detecting improvement after CBT-​I
(Lichstein et al., 2013).
The Insomnia Severity Index (ISI; Bastien, Vallières,
& Morin, 2001; Morin, 1993) is a seven-​item measure of
perceived insomnia severity assessing initial, middle, and
late insomnia; satisfaction with sleep; sleep-​related preoc-
cupation; and the impact and noticeability of sleep dif-
ficulties. Each item is rated on a 5-​point scale, and the
summation of the items yields a total score ranging from 0
to 28. The following interpretation guidelines are recom-
mended for the total score: 0 to 7 = absence of insomnia, 8
to 14 = subthreshold insomnia symptoms, 15 to 21 = mod-
erate insomnia, and 22 to 28 = severe insomnia. Cut-​off
scores of 10 in community samples and 14 in primary care
clinics have been recommended to detect insomnia, and
a change score of 8 points has been suggested to define a
positive treatment response (Gagnon, Belanger, Ivers, &
Morin, 2013; Morin, Belleville, Belanger, & Ivers, 2011).
Scores on the ISI have been shown in several studies to

TABLE 25.4   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Consensus NR NA NA NA E E NR E E ✓
Sleep Diary
ISI A E NA NR A G E E A ✓
PSQI A G NA A G A G G A
Actigraphy NR NA NA G A NR NR G G
FSS A G NA G G G G G G ✓
MFI A G NA G G G G G G ✓
BAI NR E NA NR A A A A A
STAI NR G NA NR G A G G G ✓
BDI-​II NR G NA NR A A A A A ✓
PHQ-​9 NR G NA A G A G G E

Notes: Psychometric ratings are based on the original English version of the instruments only; for BAI, BDI-​II, FSS, MFI, PHQ-​9, and STAI, ratings are
based on studies on insomnia samples only.

ISI  =  Insomnia Severity Index; PSQI  =  Pittsburgh Sleep Quality Index; FSS  =  Fatigue Severity Scale; MFI  =  Multidimensional Fatigue Inventory;
BAI = Beck Anxiety Inventory; STAI = State–​Trait Anxiety Inventory; BDI-​II = Beck Depression Inventory-​II; PHQ-​9 = Patient Health Questionnaire;
A = Adequate; G = Good; E = Excellent; NA = Not Applicable; NR = Not Reported.

be sensitive to therapeutic changes (Harvey et al., 2014;
Morin et al., 2004; Morin, Beaulieu-​Bonneau, LeBlanc,
& Savard, 2005; Morin, Vallières, et  al., 2009). In addi-
tion to a patient-​completed version, there are two parallel
versions of the ISI: one completed by a significant other
(usually a spouse) and one completed by a clinician.
These versions can be useful to assess changes with treat-
ment. An extended version of the ISI includes questions
pertaining to the perceived impact of sleep difficulties
on six specific domains of daytime functioning:  mood,
fatigue, concentration/​memory, quality of life, interper-
sonal relationships, and social or leisure activities. Studies
have demonstrated the validity and clinical utility of
the ISI in various populations, including cancer clients
(Savard, Savard, Simard, & Ivers, 2005)  and individuals
with sickle cell disease (Moscou-​Jackson, Allen, Smith, &
Haywood, 2016), and as a web-​based measure (Thorndike
et al., 2011).
The Pittsburgh Sleep Quality Index (PSQI; Buysse,
Reynolds, Monk, Berman, & Kupfer, 1989) is a 19-​item
measure that queries several aspects of subjective sleep
quality, efficiency, duration, as well as symptoms of sev-
eral other sleep disorders (e.g., nightmares) and sources
of sleep disruptions (e.g., bedpartner’s snoring). There are
several subscales of the PSQI, but the most widely used
index is an overall global sleep quality score that has a cut-​
off score of 5. It is a widely used tool in sleep research, but
the construct of sleep quality remains poorly defined. The
PSQI is a generic measure of sleep rather than an insom-
nia measure per se; indeed, there are a number of content
items related to different sleep problems subsumed under
the generic “poor sleep quality” in the PSQI, including
restless legs syndrome, nightmares, and insomnia. Despite
the inclusion of content items related to a variety of sleep
disorders, the PSQI is not effective at detecting other
sleep disorders (Nishiyama et al., 2014). There are stud-
ies suggesting that the overall PSQI sleep quality score
is measuring something different (e.g., anxiety/​distress)
from sleep diaries and/​or actigraphy in those with comor-
bid psychiatric disorders (Dorheim, Bondevik, Eberhard-​
Gran, & Bjorvatn, 2009; Hartmann, Carney, Lachowski,
& Edinger, 2015). Some authors have argued that the
overall PSQI score may be considered an index of distress
about sleep quality more than anything else, particularly
in those with comorbid diagnoses, and should be used
with caution (Crawford & Ong, 2015). The PSQI scores
have good test–​retest reliability (Backhaus, Junghanns,
Broocks, Riemann, & Hohagen, 2002), although this
decreases when using a time frame of a few weeks for
retrospective reporting. The standard time frame for
Insomnia Disorder 573
completing the PSQI is the past month; using a 1-​week
reference period increases the correlation between the
diaries and the PSQI (Wohlgemuth et al., 1999).
Wrist actigraphy uses a small portable device that
records movement, and light with some devices, for an
extended period of time (days to weeks) to estimate sleep,
circadian rhythm, and motor activity. The actigraph is usu-
ally worn as a watch on the nondominant wrist. Movement
data captured by the accelerometer of the actigraph are
transformed with mathematical algorithms into estimates
of sleep parameters (e.g., total sleep time, sleep latency,
and wake after sleep onset). Actigraphy does not measure
sleep directly as does polysomnography, nor the subjective
experience of sleep as do sleep diaries, but rather assesses
sleep patterns (sleep and wake periods) through move-
ment data. Actigraphy generally has high specificity in
detecting sleep but low specificity in detecting wake, often
underestimating sleep onset latency and wake after sleep
onset. As such, it is fairly reliable in estimating global
sleep–​wake parameters, such as total sleep time and sleep
efficiency, but much less accurate in estimating more dis-
crete sleep–​wake parameters, such as sleep onset latency
and time awake after sleep onset. Nonetheless, actigra-
phy is especially useful for evaluating circadian rhythms
(Morgenthaler et  al., 2007)—​that is, typical sleep–​wake
schedule (bedtime, arising time, and nap time)—​and for
examining night-​to-​night variability. It has also been used
in clinical studies for documenting treatment adherence
and, occasionally, for documenting treatment outcome
in clinical trials of CBT-​I. Although it is a useful tool in
research studies on insomnia and circadian rhythm sleep
disorders, its use in clinical settings is fairly limited due to
its cost. In recent years, sleep-​tracking devices using accel-
erometry have become increasingly available, affordable,
and popular. However, the vast majority of these devices
have been developed commercially without supporting
evidence for reliability and validity (Lee & Finkelstein,
2015). Although a potentially useful complement to self-​
report and PSG measures, actigraphy devices and algo-
rithms are not all equivalent, and there may be significant
variability in the reliability and validity of sleep–​wake data
derived from different devices.
Fatigue Assessment
In addition to assessing sleep, it is important to assess for
daytime problems associated with insomnia. Daytime
problems, the most common of which is fatigue, are
often the primary complaint of people seeking treatment
for insomnia. That is, they are concerned about waking
574 Health-Related Problems
up at night because of the feared negative consequences
on daytime functioning (e.g., fatigue). Although sev-
eral scales are available for fatigue measurement, the
Fatigue Severity Scale and the Multidimensional Fatigue
Inventory are most often used in the insomnia literature.
The Fatigue Severity Scale (FSS; Krupp, LaRocca,
Muir-​Nash, & Steinberg, 1989)  is a nine-​item question-
naire assessing the subjective severity of fatigue symptoms
on a 7-​point Likert scale over the past week. It is brief
(estimated 2 or 3 minutes to complete) and requires mini-
mal training to administer, score, and interpret (Hewlett,
Dures, & Almeida, 2011). The scale has strong face valid-
ity because items explicitly ask the respondent to rate the
severity of his or her fatigue symptoms. The scale is scored
by calculating the mean score of all nine items. A cut-​off
score greater than 3 is indicative of significant fatigue
(Herlofson & Larsen, 2002; Hossain, Reinish, Kayumov,
Bhuiya, & Shapiro, 2003; Krupp et al., 1989; Lichstein,
Means, Noe, & Aguillard, 1997; Schwartz, Jandorf, &
Krupp, 1993). The main criticism of the FSS is that it
is a unidimensional scale, whereas fatigue is regarded as
having multiple components. Indeed, the FSS focuses
primarily on physical fatigue, as indicated by its defini-
tion of fatigue:  a “sense of tiredness, lack of energy, or
total body give-​out.” The FSS psychometrics are strong
and reflect the participant’s perception of the impact of
his or her fatigue symptom experience over the past week
(Herlofson & Larsen, 2002; Hossain et al., 2003; Krupp
et  al., 1989; Schwartz et  al., 1993). Perhaps one of the
reasons why this scale performs well without containing
the multiple domains is that there is not one domain of
fatigue that consistently characterizes all insomnia cli-
ents. There is evidence of clinical utility for treatment
tracking, although there is not always an improvement
in fatigue even when there is sleep improvement after
CBT-​I. Although this may be a shortcoming of the scale,
it is also possible that CBT-​I alleviates sleep problems but
does not adequately address fatigue.
The Multidimensional Fatigue Inventory (MFI;
Smets, Garssen, Bonke, & De Haes, 1995) assesses several
dimensions of fatigue: general, physical, mental, reduced
motivation, and reduced activity. The MFI is a 20-​item
instrument with a score on each dimension ranging from 5
to 20 points, indicating no fatigue to extreme fatigue. The
MFI is a well-​validated questionnaire that has been used
for several diseases and disorders, including cancer (Meek
et al., 2000) and chronic fatigue syndrome (Weatherley-​
Jones et  al., 2004). Evaluating the treatment sensitivity
of the inventory is a challenge. There is a lack of corre-
spondence between fatigue reporting and objective sleep
disturbance, and there appears to be a cognitive factor that
accounts for the reporting of fatigue in insomnia (Riedel
& Lichstein, 2000). This observation is consistent with
neuropsychological models of central fatigue, which posit
a prominent role of appraisal of the personal resources
needed for a task (Chaudhuri & Behan, 2004). Thus, it
is possible that treatments that do not target this appraisal
process will not result in a meaningful decrease in fatigue
symptoms. If this is true, it is unreasonable to expect an
assessment tool to detect a difference that is unlikely to
occur in treatment.
One alternative to the MFI and FSS is the Flinders
Fatigue Scale (Gradisar et al., 2007), a scale proposed to
detect treatment differences in fatigue. However, scores
on the scale were shown to relate to changes on the PSQI,
a scale confounded by anxiety and distress (Hartmann
et  al., 2015). Thus, it is unclear if the Flinders Fatigue
Scale is detecting changes in distress rather than changes
in fatigue.
Assessment of Psychological/​Mood Symptoms
The Beck Anxiety Inventory (BAI; Beck, Epstein, Brown,
& Steer, 1988) is a 21-​item self-​report measure (i.e., over
the past week) of anxiety symptom severity and is a rec-
ommended instrument for use in insomnia (Buysse et al.,
2006). The BAI is widely used in insomnia research
(Harvey & Greenall, 2003; Morin, Belleville, et al., 2011),
and it has sound psychometrics in anxiety-​disordered cli-
ents; however, the BAI has been criticized for its content
validity because of its high number of autonomic symp-
toms. The somatic items of the BAI have poor specificity
because they overestimate anxiety severity and may mis-
categorize those without clinical levels of anxiety if they
have medical conditions (Wetherell & Gatz, 2005)  or
sleep-​
disordered breathing (Sanford, Bush, Stone,
Lichstein, & Aguillard, 2008). In a large-​scale psychomet-
ric evaluation of those with an insomnia disorder diag-
nosis, Carney, Moss, Harris, Edinger, and Krystal (2011)
cautioned against the use of the BAI cut-​offs with insom-
nia clients because the cut-​off scores were associated with
suboptimal sensitivity and specificity, and several items
failed to discriminate those with an anxiety disorder from
those without. The overall score may be useful as an
index of anxiety symptom severity because the BAI total
score differentiates those with insomnia with and without
an anxiety disorder diagnosis. The reliability of the score
in an insomnia sample has been reported to be similarly
high to that in anxiety disorder investigations (Cronbach’s
α = .89; Carney et al., 2011). Despite some concern over

the BAI cut-​offs for those with insomnia, it continues to be
a widely used tracking tool for anxiety symptoms.
The Spielberger State–​Trait Anxiety Inventory (STAI;
Spielberger, 1983)  is a widely used 20-​item self-​report,
retrospective measure designed to assess general levels of
anxiety. The initial iteration of the test (Form X, published
in 1970) was popular in clinical research. Scores on the
revised Form Y (Spielberger, 1983) are significantly cor-
related with the original measure scores, but this form has
improved psychometric properties (Oei, Evans, & Crook,
1990). The STAI has been criticized for not being able
to adequately differentiate between anxiety and depres-
sion (Bieling, Antony, & Swinson, 1998; Gros, Antony,
Simms, & McCabe, 2007). The STAI has been used
across many insomnia studies, but we are not aware of any
psychometric evaluations of the properties of the STAI in
those with insomnia or other sleep disorders.
The Beck Depression Inventory, Second Edition
(BDI-​II; Beck, Steer, & Brown, 1996) is one of the most
commonly used measures of dysphoric symptoms. It has
strong psychometric properties in samples of depressed
individuals but variable support in medical populations,
perhaps due to the lack of depression-​specific (i.e., discrim-
inating) items. An investigation of the BDI-​II in insomnia
sufferers (Carney, Ulmer, Edinger, Krystal, & Knauss,
2009) found good internal consistency (α = .82) in those
with clinical levels of insomnia without depression and
excellent internal consistency in those with diagnoses of
insomnia and major depressive disorder (α = .90). There
is some concern with the use of the mild BDI-​II cut-​off
(BDI-​II ≥ 14)  because the BDI-​II can overclassify those
with insomnia as having mild depression (Carney et  al.,
2009), probably because several of its items overlap with
the research diagnostic criteria (Edinger et  al., 2004)  for
insomnia (e.g., insomnia, fatigue, and concentration prob-
lems). Although there may be concern for use of this scale
with the mild depression cut-​off, the cut-​off of BDI-​II ≥
17 has good accuracy support for correctly identifying
depressed clients. The BDI-​II is useful for capturing mood
improvements after CBT-​I (Bastien, Morin, Ouellet, Blais,
& Bouchard, 2004), although the overlap with insomnia
symptoms makes it difficult to determine if this scale is
capturing sleep improvement or mood improvement.
The Patient Health Questionnaire-​9 (PHQ-​9; Kroenke,
Spitzer, & Williams, 2001) is among the most widely used
screening measures for depression in primary care facili-
ties (Zhong, Gelaye, Fann, Sanchez, & Williams, 2014).
The nine items of this diagnostic measure reflect the
DSM-​IV-​defined criteria for depressive disorders. Each
item is rated on a Likert-​type scale (0–​3); thus, the authors
Insomnia Disorder 575
suggest that the PHQ-​9 may establish depression diagno-
sis as well as provide information with regard to symptom
severity (Kroenke et al., 2001). Administration and scor-
ing are brief (~3 minutes), and little training is required
for interpretation for those familiar with the criteria for
diagnosing depressive disorders. Although the PHQ-​9 has
been used in a number of insomnia studies, there appear
to be no studies evaluating the psychometric properties
of the PHQ-​9 within insomnia or other sleep-​disordered
populations.
Overall Evaluation
Essential assessment strategies for monitoring treatment
progress and outcome should include the daily sleep diary
(CSD) and the ISI, as well as some measures of daytime
symptoms, such as fatigue as well as anxiety and depres-
sive symptomatology. Although there is some evidence
supporting the use of anxiety and depression scales in
those with insomnia, more research on the psychomet-
ric properties of these scales is needed. Other assessment
methods, such as actigraphy, are useful for research pur-
poses and in cases wherein a circadian rhythm disorder
may be present, but they may not be necessary for routine
clinical use. In addition, many with insomnia complain
about cognitive impairments affecting their attention and
concentration, but to date, there is no adequate measure
to reliably capture such deficits or detect changes in these
domains with insomnia treatment.
CRITICAL ISSUES IN ASSESSING INSOMNIA
Barriers and Challenges
Despite the wide range of measures available, clinicians
face a number of challenges when assessing sleep/​insom-
nia complaints. The most important one derives from the
fact that the diagnosis of insomnia is based solely on the
client’s subjective complaint of difficulties initiating and/​
or maintaining sleep and the resulting daytime impair-
ments. What is considered a long time to fall asleep or
spent awake at night, too short amount of sleep, or poor
sleep quality may vary widely across individuals. DSM-​5
criteria indicate a cut-​point of 20 to 30 minutes to define
sleep onset and sleep maintenance insomnia, but this is
not part of the formal diagnostic criteria. Furthermore,
such criteria are quite arbitrary. Because there are age-​
related, “normal” changes in sleep patterns, being awake
for 30 minutes at night is not necessarily perceived to
576 Health-Related Problems
be problematic by an older adult, whereas it is typically
perceived as bothersome by a 30-​ year-​
old individual.
Likewise, because of individual differences in sleep
needs, there is no cut-​point to how much sleep is too short
amount of sleep. Hence, the lack of quantitative criteria to
define insomnia contributes to a significant heterogeneity
of clinical profiles when working with individuals with an
insomnia disorder.
A related problem is that there are often important dis-
crepancies between a person’s perception of being awake
or asleep and objective recordings of sleep derived from
PSG or actigraphy. Most people tend to overestimate the
time they take to fall asleep and to underestimate the time
they sleep at night relative to objective measurements, but
this discrepancy is more pronounced in some individu-
als with insomnia. This phenomenon, also called sleep
state misperception, can only be identified when objec-
tive sleep recording (i.e., PSG) is available, which is rarely
the case in clinical practice. Therefore, clinicians should
usually take at face value the information reported during
the interview and in the client’s sleep diary. Reports of fre-
quent sleepless nights may be an indication of significant
sleep state misperception because such phenomenon is
rare even among the most severe cases of insomnia.
A similar paradox is that individuals with insomnia
often report significant impairments of daytime function-
ing, but objective evaluation of performance, when avail-
able, usually reveals fairly mild and selective deficits (e.g.,
attention) (Fortier-​ Brochu, Beaulieu-​ Bonneau, Ivers,
& Morin, 2012). In general, individuals with insomnia
tend to perceive their sleep and daytime functioning as
more impaired relative to how it can be objectively mea-
sured, which may reflect a generalized faulty appraisal of
sleep and daytime functioning among individuals with
insomnia. Notwithstanding these discrepancies, insomnia
complaints must be taken seriously because they carry
significant long-​term negative mental and physical health
outcomes.
The high rate of comorbidity between insomnia and
other psychiatric disorders can also pose some assess-
ment challenges, although this is less of a problem now
that DSM-​5 has eliminated the need to ascertain whether
insomnia is primary in nature or secondary to another dis-
order. Because of the overlap of several symptoms (e.g.,
sleep difficulties, decreased energy, and poor concentra-
tion) in insomnia, anxiety, and depression, it is sometimes
difficult for clinicians to determine whether insomnia is
simply a clinical symptom or feature of another disorder
(e.g., generalized anxiety disorder or major depression),
a disorder of its own, or a co-​occurring condition. The
literature is now fairly clear that insomnia can present in
any of these three forms and, temporally, it can precede,
accompany, or follow the occurrence of another psychi-
atric disorder. Most sleep experts are also in agreement
that when an insomnia disorder is comorbid with another
psychiatric or even medical (pain) condition, treatment
should target both conditions without reference to which
disorder may have occurred first (Manber et al., 2008). Of
course, treatment may proceed sequentially and take into
account what may be considered the most critical and
urgent condition in need of treatment.
Streamlining Assessment for Clinical Decision-​Making
Despite the previously mentioned challenges, there are
a number of assessment strategies that can guide clini-
cians in their evaluation of insomnia in clinical practice.
First, the diagnosis of insomnia is derived primarily from
a detailed clinical evaluation of the client’s subjective
complaints. Thus, a detailed and comprehensive sleep-​
focused interview remains the most important assessment
component. Completed in parallel with a case formula-
tion, this assessment should cover the type of complaints,
their duration, and their course; perceived consequences
and impairments; typical sleep schedules; precipitating
and perpetuating factors; and the presence of medical
and psychiatric contributing factors with a history of pre-
scribed and over-​the-​counter medications. Second, the
use of a sleep diary is essential to document the nature,
frequency, and severity of insomnia; identify behavioral
and scheduling factors that may perpetuate insomnia;
and monitor treatment compliance and progress. Third,
although there are multiple measures that may comple-
ment the assessment of insomnia, if a single instrument
is to be used to minimize burden, the ISI provides a
quick assessment of perceived insomnia severity and its
impact on daytime functioning and is a useful measure
to monitor treatment progress and outcome. Additional
measures of fatigue, anxiety, and depressive symptom-
atology can provide useful complementary information,
particularly in view of the high co-​occurrence of insom-
nia and psychological symptoms. A more comprehensive
psychological evaluation may be necessary for clients with
suspected psychiatric disorders. Although PSG is not indi-
cated for the routine evaluation of insomnia, it is essen-
tial to diagnose other sleep disorders (e.g., sleep apnea)
and clinicians should refer their clients for such evalua-
tion whenever another sleep disorder is suspected. PSG
should also be considered when a client is unresponsive
to treatment.

CONCLUSIONS AND FUTURE DIRECTIONS
Insomnia is a prevalent condition brought to the atten-
tion of clinicians, either as an independent disorder or,
more frequently, as a condition coexisting with another
psychiatric disorder. A wide array of assessment strategies
and methods are available to assist in the assessment of
insomnia disorder. Most of these have been developed
and validated in the context of research studies, but they
can also facilitate the clinical decision-​making process.
Some instruments are better suited for diagnosis or treat-
ment planning, whereas others are better indicated for
treatment monitoring or for assessing outcomes. Their
clinical utility, availability, and cost, as well as their psy-
chometric properties, are critical factors likely to guide
the selection and use of some of these tools in clinical
practice.
Despite progress made in standardizing insomnia
assessment in research, there are still important barri-
ers and challenges to effective assessment of insomnia
in clinical practice. There are several evidenced-​based
therapies for insomnia, but insomnia often remains
underrecognized and undertreated in clinical practice.
Brief and valid screening tools are needed to identify
individuals requiring treatment. There is a definite need
for more practical, user-​ friendly assessment methods
that can be used at the point of care. Additional research
is also warranted to develop new assessment strategies
to better understand the contribution of different factors
(e.g., hyperarousal) to insomnia and characterize differ-
ent phenotypes of insomnia. In view of the significant
discrepancies between subjective and objective measures
of sleep and daytime impairments, additional research is
also needed to develop and validate insomnia-​specific
measures that are sensitive and better suited to docu-
ment the daytime impairments (e.g., fatigue and cog-
nitive impairments) that often prompt individuals with
insomnia to seek treatment. Specific assessment instru-
ments are necessary to document more precisely the
impact of insomnia therapies on several aspects of day-
time functioning, such as fatigue, quality of life, psycho-
logical well-​being, and cognitive functioning (attention/​
concentration). A  significant challenge for the future
will be to develop an assessment tool to optimize treat-
ment algorithms and ensure evidence-​based therapies
are matched to specific insomnia phenotypes. Finally,
given that insomnia is a frequent complaint associated
with several other psychological conditions, the develop-
ment of an instrument that could be used transdiagnosti-
cally would be very helpful.
Insomnia Disorder 577
ACKNOWLEDGMENTS
Preparation of this chapter was supported by research
grants from the National Institute of Mental Health
(MH091053) and the Canadian Institutes of Health
Research (MT-​42504; No. 353509).
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 26
Child and Adolescent Pain
C. Meghan McMurtry
Patrick J. McGrath
The International Association for the Study of Pain
defines pain as “an unpleasant sensory and emotional expe-
rience associated with actual or potential tissue damage, or
described in terms of such damage” (Merskey & Bogduk,
1994, p.  210, emphasis added). The definition goes on
to assert that pain is always subjective. This definition is
very widely accepted and serves as the starting point for all
pain assessment. Pain is common throughout childhood.
There has been an explosion of research in the scientific
study of pain and its measurement in children and youth.
One of the most important findings has been that pain
is much more complex than was thought 60  years ago.
The beginning of the modern era of pain research can
be marked by Melzack and Wall’s (1965) seminal paper
proposing the gate control theory of pain. They posited
that pain was modulated by “gates” in the spinal cord,
by descending signals from the brain, and by peripheral
stimulation. More recently, both peripheral and central
sensitization have been described (Taddio & Katz, 2005;
Woolf, 2011). In effect, our bodies have a memory for
pain so that one experience of pain can trigger more
pain during later experiences (Taddio, Katz, Illersich, &
Koren, 1997). Rather than “getting used to” pain, we (and
children and adolescents) can actually become more sen-
sitive to it (Fradet, McGrath, Kay, Adams, & Luke, 1990;
Woolf, 2011). As explored later, there are significant nega-
tive sequelae from unmanaged pain. Unfortunately, many
children and adolescents continue to suffer from inade-
quately treated acute and chronic/​recurrent pain (Perquin
et al., 2000; Stevens et al., 2011).
Pain measurement is the application of a metric to a
specific aspect of pain. Assessment is much broader than
measurement and includes the selection of what aspects
of pain to measure and what measures to use (McGrath &
Unruh, 1987). Often, the focus is pain intensity; however,
583
intensity alone fails to capture the overall experience of
pain. The Pediatric Initiative on Methods, Measurement,
and Pain Assessment in Clinical Trials (PedIMMPACT;
McGrath et al., 2008) recommended that in addition to
pain intensity, several other domains should be consid-
ered, including satisfaction with treatment, symptoms and
adverse events, physical recovery, emotional response, role
functioning, sleep, and economic factors. One strategy to
capture the relevant domains is to use a standard battery
of questions (e.g., Eccleston et  al., 2005). Alternatively,
one can select specific measures for each aspect of the
pain experience that is to be measured. Regardless, the
first step in the effective management of pain in children
and adolescents is an evidence-​based assessment.
In this chapter, we provide recommendations for
assessment tools that have demonstrated utility and feasi-
bility in clinical settings or hold promise as clinical assess-
ment tools. Assessment tools in pediatric pain can be
thought of as self-​report, behavioral (observational), physi-
ological, or some combination. Because pain is always a
subjective experience, self-​report has been referred to as
the “gold standard” in pain assessment (Twycross, Voepel-​
Lewis, Vincent, Franck, & von Baeyer, 2015). However,
self-​report tools have a number of limitations (e.g., Craig,
Lilley, & Gilbert, 1996; Twycross et al., 2015; von Baeyer,
2013). For example, these tools require sophisticated cog-
nitive and communication abilities, and ratings on them
are likely influenced by self-​interest (Craig et  al., 1996;
von Baeyer, 2006, 2013). A child who knows that medi-
cation will be given by needle may underreport pain to
avoid the needle (Eland & Anderson, 1977). Ideally, a
thorough pain assessment would utilize a combination of
behavioral and self-​report tools. Unfortunately, in clinical
practice this is often not feasible. Self-​report might best
be considered the “primary” but not exclusive source of
584 Health-Related Problems

information in verbal individuals (von Baeyer, 2013). parental responses and peer support) factors that influ-
Many self-​ report tools are quick and cost-​ effective to ence pain experience and expression. Measurement and
administer in clinical settings. Thus, they have received assessment of pain in children and adolescents must be
the most research attention, and many have undergone considered within a developmental context. First, there
rigorous psychometric testing. Therefore, we focus our are developmental factors in the occurrence of differ-
review on self-​report tools. When relevant, we also discuss ent pains (King et  al., 2011). For example, recurrent
parental proxy reports. For a review of observational mea- abdominal pain is more common in younger than older
sures of pediatric pain, the reader is directed to Chorney children, headache is more common in older children,
and McMurtry (2013). Researchers have used physiologi- and migraine increases sharply after puberty, especially in
cal methods (e.g., heart rate and vagal tone) for measur- females (King et  al., 2011; Unruh & Campbell, 1999).
ing pain in very young children (infants in particular), but Second, development limits children’s understanding of
these methods are rarely used in clinical care outside of pain. An 18-​month-​old child is unlikely to understand
neonatal intensive care units and no single measure cap- why he or she should receive a needle for a vaccination,
turing pain has been identified (Brummelte, Oberlander, whereas an 11-​ year-​
old child can understand. Third,
& Craig, 2013). Furthermore, physiologically based development is a limiting factor in the use of self-​report
assessments (e.g., heart rate) may reflect other biological measures. Many children younger than 5 or 6  years of
states (e.g., arousal) rather than pain. This chapter focuses age cannot consistently use self-​report measures for pain
on the assessment of pain in children between the ages or show response biases such as endorsing the extremes
of 3 and 18  years without severe cognitive impairment. of a scale (Chambers & Johnston, 2002; von Baeyer,
The assessment of pain in cognitively impaired children is 2013). Conversely, older children may inhibit behavioral
beyond the scope of this chapter, and the reader is referred responses to pain and thus make observational measures
to Oberlander and Symons (2006) and Belew and col- less useful. In this chapter, although we focus on measures
leagues (2013). Because assessment of pain in infants is that have demonstrated validity across a broad age range
quite specialized, it is not covered in this chapter (see Lee (from 3 through 18 years), we have kept developmental
& Stevens, 2013). factors in mind while formulating our recommendations.
Our discussion of the pediatric pain assessment lit- Pain in children and adolescents can arise from medi-
erature is tailored to mental health professionals such cal procedures such as needles or surgery and can also
as clinical and health psychologists, social workers, and be caused by disease or trauma. Some diseases, such as
psychiatrists working with children who suffer from pain. sickle cell disease or juvenile rheumatoid arthritis, fre-
The role of mental health practitioners in pediatric pain quently cause pain, but the amount of pain often does
assessment is multifaceted and varies from setting to set- not correspond to the severity of the underlying disease.
ting. However, mental health practitioners are united by The origin of pain may also be unknown—​a large propor-
a focus that extends beyond assessing simple pain percep- tion of children who attend pediatric chronic pain clin-
tion. They also examine the effects of pain on the func- ics suffer from pain of unknown origin. When the cause
tioning of youth and their families across domains, such as of pain cannot be ascertained, it is often assumed to be
physical, emotional, and social role functioning, because the result of psychological factors. This is an unfortunate
the nature of pain requires assessment beyond simplistic and pernicious strategy because it alienates patients who
pain intensity. believe they are being blamed for their pain and that they
are being told their pain “is all in their head.” This “leap
to the head,” as Wall (1989) called it, is not scientifically
THE NATURE OF PAIN justified because there is seldom any positive evidence
of psychological causation. However, psychological fac-
The World Health Organization (WHO, 1948)  defines tors are important in the experience of pain regardless
health as “a state of complete physical, mental and social of etiology.
well-​being and not merely the absence of disease or infir- Pain may also be categorized in terms of its time
mity.” This definition is consistent with a biopsychosocial course, such as acute, recurrent, or chronic. Acute pain
model of pain that captures the complex, bidirectional can be divided into short sharp pain that may last a few
relations among biological (e.g., genetics and biochemi- seconds to a few minutes or longer lasting acute pain that
cals such as endorphins), psychological (e.g., self-​efficacy, may last from hours to days. Postoperative pain and pain
anxiety, and depression), and social (e.g., caregiver/​ from injuries are the most common longer lasting acute
 Child and Adolescent Pain 585

pain. Examples of short sharp pain include pain from
everyday accidents such as stubbing a toe or skinning a
knee. Clinical short sharp pain is typically from medi-
cal procedures, such as needles. Vaccinations by needle
are common for all children, and children with chronic
illnesses such as cancer or diabetes undergo other types
of needle procedures (e.g., insulin injections, venipunc-
tures, bone marrow aspirations, and lumbar punctures).
Unmanaged pain and fear during medical procedures
are associated with negative short-​and long-​term conse-
quences, including longer procedure times, use of physi-
cal restraint during the procedure, injuries, increased
pain and distress during future procedures, and negative
memories of the event, and can contribute to the develop-
ment of significant needle fear (McMurtry et  al., 2015;
Taddio et al., 1997).
Chronic pain is typically defined as pain that lasts
more than 3 months (Merskey & Bogduk, 1994). It may
be persistent or recurrent (episodic), in which there are
bouts of pain interspersed with either pain-​free or low-​
pain periods. Chronic pain is common in youth. Median
prevalence rates differ depending on the type of pain
and range from 11% to 38%, with the most common
including headaches, abdominal pain, back pain, and
musculoskeletal pain (King et  al., 2011). Chronic pain
is associated with impairments in functioning (school,
social, and physical) and increased risk of internaliz-
ing symptoms (Dick & Pillai Riddell, 2010; Forgeron
et  al., 2010; Huguet & Miró, 2008; Varni et  al., 1996).
Approximately 5% of youth with chronic pain are moder-
ately to severely impaired (Huguet & Miró, 2008). Youth
with chronic pain are at increased risk of continuing to
have pain as adults (Brna, Dooley, Gordon, & Dewan,
2005; Walker, Dengler-​Crish, Rippel, & Bruehl, 2010).
The economic costs of chronic pain are enormous: Direct
health care costs due to adult chronic pain are estimated
at $6 billion per year in Canada (M. E. Lynch, 2011) and
more than $260 billion in the United States (Gaskin &
Richard, 2011). There is less literature on costs of pediat-
ric chronic pain; however, Groenewald, Essner, Wright,
Fesinmeyer, and Palermo (2014) studied a sample of
American adolescents presenting for initial evaluation at
interdisciplinary pain treatment programs and extrapo-
lated the annual costs of moderate to severe chronic pain
to $19.5 billion.
ASSESSMENT FOR DIAGNOSIS
As mentioned previously, most clinical short sharp pain
is iatrogenic and of known cause (e.g., from a needle
or a surgical procedure). Pain and related fear regard-
ing needle procedures should be managed using phar-
macological (e.g., topical anesthetics), physical (e.g.,
sitting in an upright position), and psychological (e.g.,
distraction) strategies; based on a series of systematic
reviews, a comprehensive clinical practice guideline
for the management of vaccination-​related pain and
fear has been published (Taddio et  al., 2015). With
respect to the diagnosis of recurrent and chronic pain,
there are several parameters of pain that are useful to
consider, including pain intensity, localization, quality,
frequency, and duration. Table 26.1 provides summary
information on measures designed to assess some of
these constructs.
Pain Intensity
Sensory intensity is often one of the first dimensions of
pain assessed by clinicians. It is vital for clinicians to
obtain quantitative ratings of intensity in order to under-
stand the extent of children’s pain. However, reliance
on pain intensity is an oversimplification of a complex
experience and should not on its own determine clinical

TABLE 26.1   Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Pieces of Hurt Tool NA NA NA NA A G G G ✓

The Oucher NA NA NA NA G G G G
FPS-​R NA NA NA NA A G E G ✓
Visual analogue scales NA NA NA NA NA A G A
Numerical rating scale NA NA NA A A G G G ✓
APPT NA NA NA A G G E A ✓

Note: FPS-​R = Faces Pain Scale-​Revised; APPT = Adolescent Pediatric Pain Tool; A = Adequate; G = Good; E = Excellent; NA = Not Applicable.
586 Health-Related Problems
care (Schiavenato & Craig, 2010; Voepel-​Lewis, 2011;
von Baeyer, 2013). Although pain intensity measures are
discussed in this section, these measures are also valu-
able for treatment planning and monitoring treatment
effectiveness. These tools are all single-​item measures of
a subjective and ever-​fluctuating state; therefore, conven-
tional indices of reliability are not generally applicable.
In general, a pain-​free state is the norm. Norms for pain-
ful conditions have little meaning because pain problems
vary considerably. The typical intensity, duration, and
frequency of pain that produces a given level of func-
tional disability would be of interest but have not been
researched. Clinicians and parents make these judgments
without good normative data. For example, the judgment
that it is not “normal” for a 14-​year-​old girl with headache
pain to miss 4 days of school each month is likely statisti-
cally true. But, how severe might the pain have to be to
make school absence typical and thus normative (even if
it is not helpful)?
Pieces of Hurt Tool
The Pieces of Hurt Tool (sometimes called the Poker
Chip Tool; Hester, 1979) is a concrete ordinal rating tool.
This tool consists of four plastic poker chips that represent
“pieces of hurt.” When the tool is administered, the child
is asked, “Did/​does it hurt?” If the child says “no,” a score
of zero is recorded. If the child says “yes,” he or she is
asked to indicate pain intensity by selecting between one
and four poker chips, with one chip representing “a little
hurt” and four chips representing “the most hurt.” The
number of chips selected is the child’s score.
Psychometric data indicate that the Pieces of Hurt
Tool score provides a valid self-​report measure of child
pain intensity (Stinson, Kavanaugh, Yamada, Gill, &
Stevens, 2006). It has adequate content validity (Hester,
1979)  and good construct validity. It has been shown to
correlate strongly with other self-​report and observational
pain intensity measures (Beyer & Aradine, 1987, 1988;
Gharaibeh & Abu-​Saad, 2002; Goodenough et al., 1997;
Hester, 1979; Suraseranivongse et al., 2005). Evidence of
discriminant validity includes low correlations with two
measures of fear (Beyer & Aradine, 1988). The Pieces of
Hurt Tool has been studied with children between the ages
of 3 and 18 years (Stinson, Kavanagh, et al., 2006) and has
been used with hospitalized children (Beyer & Aradine,
1987, 1988)  and children with postoperative pain
(Aradine, Beyer, & Tompkins, 1988; Suraseranivongse
et  al., 2005), as well as children undergoing venipunc-
tures (Gharaibeh & Abu-​Saad, 2002) and immunizations
(Goodenough et al., 1997; Hester, 1979). The Pieces of
Hurt Tool has been translated and validated for use with
children in Thailand (Suraseranivongse et al., 2005) and
Jordan (Gharaibeh & Abu-​Saad, 2002).
Advantages of the Pieces of Hurt Tool include that
it is scored on a concrete ordinal rating scale. This type
of scale is appealing for use with children because con-
crete representations (poker chips) enhance children’s
ability to understand the concept of levels of hurt/​pain
(Stinson, Kavanagh, et al., 2006). Disadvantages include
the need to sterilize the chips after each use and its 0 to
4 rating scale differs from the 0 to 10 scale widely used in
health settings. We recommend it for use with children
between the ages of 3 and 7  years suffering from acute
pain, as it requires further testing in preschool-​aged chil-
dren and children with chronic pain (Stinson, Kavanagh,
et al., 2006).
The Oucher
The Oucher (Beyer, 1984) consists of two separate scales
in a poster format:  a 0-​to-​100 numerical scale for older
children and a photographic faces scale for younger chil-
dren that is scored from 0 to 5. The original Oucher photo-
graphic scale shows the face of a 4-​year-​old Caucasian boy
in increasing levels of discomfort, from “no hurt” to “the
biggest hurt you could ever have.” African American and
Hispanic versions of the Oucher are available (Villarruel
& Denyes, 1991), and a modified Asian version of the
Oucher (with a numerical scale that ranges from 0 to
10) has also been developed (Yeh, 2005). Finally, a First
Nations version has been developed but little information
on the psychometrics is available (Shapiro, 1997).
Extensive psychometric research has been carried
out on the Oucher (Stinson, Kavanagh, et  al., 2006;
Tomlinson, von Baeyer, Stinson, & Sung, 2010). Belter,
McIntosh, Finch, and Saylor (1988) assessed the Oucher
score’s reliability by asking young children to rate the
intensity of pain depicted in various cartoon scenes and
found low to moderate levels of test–​ retest reliability.
Luffy and Grove (2003) also obtained ratings of test–​retest
reliability on the African American version by asking
children to rate the pain they experienced from two past
medical procedures/​treatments (r  =  .70). The concep-
tual framework behind the Oucher was clearly defined
and informed each step in its creation (Beyer, Denyes,
& Villarruel, 1992). Three to 7-​year-​old children show
strong agreement with the order of the six original photo-
graphs (Beyer & Aradine, 1986). Content validity has also
been established for the African American, Hispanic, and

Asian versions (Villarrruel & Denyes, 1991; Yeh, 2005).
The construct validity of the original Oucher is supported
by strong and positive correlations with a visual analogue
scale of pain in a group of hospitalized children (Beyer
& Aradine, 1988). Evidence for discriminant validity is
provided by low correlations with two measures of chil-
dren’s fears (Beyer & Aradine, 1988). Similar evidence
of convergent and discriminant validity has been found
for the African American, Hispanic, and Asian versions
(Beyer & Knott, 1998; Yeh, 2005). There is evidence to
support the use of the Oucher with hospitalized children
(Beyer & Aradine, 1987, 1988)  and children suffering
from postoperative pain (Beyer & Knott, 1998; Ramritu,
2000). It has been validated with Caucasian, African
American, and Hispanic children between the ages of
3 and 12  years (Beyer & Knott, 1998). Patients seem to
prefer the Oucher over a word-​graphic scale (Ramritu,
2000) but the Wong–​Baker FACES scale over the Oucher
(Luffy & Grove, 2003).
One of the main advantages of the Oucher is that it is
culturally sensitive. On the other hand, versions other than
the Asian version depict male children, and there is some
informal evidence that female children may have difficulty
relating to the photographs of male children (Beyer et al.,
1992). As of 2009, the Oucher has been downloadable from
http://​oucher.org. We recommend the numerical scale of
the Oucher for use with children between the ages of 5 and
12  years because it requires further psychometric testing
with very young children (i.e., ages 3 and 4 years; Stinson,
Kavanagh, et al., 2006; Tomlinson et al., 2010). We also sug-
gest that the photographic scale of the Oucher may be used
with children between 3 and 6 years old who are not able to
use the numerical scale. Although there are recommended
tasks to determine which version a child should use (e.g.,
counting to 100 and sequencing shapes; Beyer et al., 1992),
they are often not practical in clinical settings.
Faces Pain Scale-​Revised
The early development of the ability to recognize facial
expressions of emotion may make it easier for children to
use scales with faces (Bieri, Reeve, Champion, Addicoat,
& Ziegler, 1990). However, to use a faces scale, children
are still required to match their internal feelings of pain to
a given face on the scale (Hicks, von Baeyer, Spafford, van
Korlaar, & Goodenough, 2001). Based on the Faces Pain
Scale developed by Bieri and colleagues (1990), the Faces
Pain Scale-​Revised (FPS-​R; Hicks et  al, 2001)  is scored
from 0 to 10 and shows a series of six faces ranging from
a neutral face showing “no pain” to a face showing “very
Child and Adolescent Pain 587
much pain.” The child is asked to rate his or her pain by
indicating which face shows how much pain (hurt) he or
she has. Substantial evidence supports the psychometrics
of the FPS-​R (Stinson, Kavanagh, et al., 2006; Tomlinson
et al., 2010; von Baeyer, 2013).
The faces for the original version of the scale were
based on children’s drawings of increasing pain expres-
sions (Bieri et al., 1990). The six faces for the FPS-​R were
produced through a magnitude production task with
adults (Hicks et al., 2001). The FPS-​R has generally shown
strong convergent validity with other self-​report measures
of pain intensity (Hicks et al., 2001; Miró & Huguet, 2004;
Newman et al., 2005). Discriminant validity of the FPS-​
R has been supported by comparisons with pain affect
(Miró & Huguet, 2004) and between vignettes (Stanford,
Chambers, & Craig, 2006). Parents’ ratings using the FPS-​
R have been found to correlate significantly to their chil-
dren’s self-​report scores (e.g., Wood et al., 2004). Acceptable
test–​retest reliability in response to hypothetical events was
demonstrated by Miró and Huguet (2004). The FPS-​R
has been used with numerous different samples, includ-
ing children between 4 and 19 years old (e.g., Hicks et al.,
2001; Newman et al., 2005; Saudan et al., 2008; Taddio,
Kaur Soin, Schuh, Koren, & Scolnik, 2005). The FPS-​R
has been used with nonclinical samples (Hicks et al., 2001;
Miró & Huguet, 2004) and numerous samples undergo-
ing various medical procedures (Hicks et al., 2001; Lister
et  al., 2006; Migdal, Chudzynska-​Pomianowska, Vause,
Henry, & Lazar, 2005; Miró & Huguet, 2004; Newman
et al., 2005; Saudan et al., 2008; Wood et al., 2004).
Advantages of the FPS-​R include its strong psychomet-
rics, quickness and ease of administration, and its avail-
ability (free for clinical and research use at https://​www.
iasp-​pain.org/​FPSR). The FPS-​R has been translated into
more than 30 languages. Versions that have been validated
include French (Wood et al., 2004), Thai (Newman et al.,
2005), and Catalan (Miró & Huguet, 2004). One must
be cautious in administering the FPS-​R and similar scales
to young children (i.e., ages 4–​6 years) because children
of this age have been found to use the extreme ends
of the scale (Arts et  al., 1994). Finally, the FPS-​R may
not have high acceptability because children, parents,
and nurses have indicated preference for more cartoon-​
like scales that have a smiling no pain face (Chambers,
Hardial, Craig, Court, & Montgomery, 2005). However,
in a comparison with a nonfacial scale of pain intensity,
the majority of schoolchildren and children in hospital
preferred the FPS-​R (Miró & Huguet, 2004). Overall, we
recommend the FPS-​R for clinical use in assessing pain
intensity in children between 4 and 12 years of age.
588 Health-Related Problems
The Wong–​Baker FACES Pain Scale (Wong & Baker,
1988)  is another widely used, psychometrically sound,
single-​item, self-​report measure of pain intensity (Stinson,
Kavanagh, et al., 2006; Tomlinson et al., 2010; von Baeyer,
2013). It contains six cartoon-​like faces that, in contrast to
the FPS-​R, range from a smiling “no hurt” face to a face
with tears for the “hurts worst” face. Parents, children, and
nurses have indicated a preference for the Wong–​Baker
FACES Pain Scale over other faces scales (Chambers
et al., 2005). However, scales with a smiling no pain face
have been shown to confound affect with pain inten-
sity (Chambers & Craig, 1998; Chambers, Giesbrecht,
Craig, Bennett, & Huntsman, 1999). Children report-
ing their pain on faces scales with a smiling no pain face
endorse higher pain ratings than on scales with a neutral
face anchor (Chambers et al., 1999). Although these dif-
ferences in ratings are statistically significant, it is not
clear whether these differences affect the clinical care of
children, and debate continues on this and whether the
scale measures fear or not (Chambers et al., 2005; Garra,
Singer, Domingo, & Thode, 2013).
Visual Analogue Scales
Usually, visual analogue scales (VAS) consist of a 10-​cm
horizontal line drawn on a piece of paper, with stops
(anchors) placed at each end of the line (Wewers & Lowe,
1990). The anchors are labeled from, for example, “no
pain” to “the most extreme pain,” and the child is asked
to point or make a mark on the line to represent his or her
current level of pain intensity. The recordings are typically
measured in millimeters, yielding scores that range from
0 to 100. The minimum clinically significant difference
on 10-​cm VAS for child pain intensity is 10 mm (Powell,
Kelly, & Williams, 2001). There are many versions of the
VAS available that differ in the terminology they use for
the anchors, presence or absence of divisions along the
line, units of measurement, length, and orientation of the
scale (Stinson, Kavanagh, et al., 2006).
Table 26.1 summarizes the psychometric testing of VAS
for child pain intensity (Stinson, Kavanagh, et  al., 2006;
von Baeyer, 2013). In a study that examined children’s
ratings of past medical procedures/​treatments, Luffy and
Grove (2003) found that only 45% of children rated their
pain intensity within 10 mm above or below their original
rating. However, more research on children’s recalled pain
intensity is needed before any conclusions about the test–​
retest reliability of VAS can be drawn. Convergent validity
is supported by moderate to strong correlations with other
child-​reported pain intensity measures (Beyer & Aradine,
1987, 1988; Migdal et al., 2005). In terms of discriminant
validity, VAS have been found to have low correlations
with two measures of fear (Beyer & Aradine, 1988). VAS
have been used successfully with children in acute and
chronic pain (Beales, Keen, & Lennox-​Holt, 1983; Beyer
& Aradine, 1987, 1988; Migdal et al., 2005; Powell et al.,
2001). Child preference data on VAS compared to other
self-​report measures are equivocal (Berntson & Svensson,
2001; Luffy & Grove, 2003).
VAS are quick and easy to use. They can be easily
and affordably photocopied for use (as long as line length
remains constant). Another advantage is that they allow
for measurement of pain on an interval scale, which
allows for greater sensitivity (Champion, Goodenough,
von Baeyer, & Thomas, 1998). One of the main disadvan-
tages of VAS is that clinicians must be careful to ensure
that children (especially younger children) understand
the instructions for their use. These scales require chil-
dren to seriate their perceptions from small to large, and
this ability does not appear until children are approxi-
mately 7 years of age (Shields, Palermo, Powers, Grewe, &
Smith, 2003). For this reason, we recommend the use of
VAS with children older than the age of 8 years (Stinson,
Kavanagh, et al., 2006).
Numerical Rating Scales
Numerical rating scales (NRS; or verbal numerical scales
[VNS] if delivered verbally) are probably the most fre-
quently used scales and are well established for children
8 years old or older (von Baeyer, 2013; von Baeyer et al.,
2009). For example, von Baeyer and colleagues (2009)
presented analyses from three different data sets support-
ing the use of NRS in postoperative pain and vaccination
pain in terms of concurrent validity with the VAS and
the FPS-​R. Although the age range was 7 to 17 years, the
authors recommended use in children 8 year old or older
(von Baeyer et  al., 2009). Miró and Huguet (2009) also
demonstrated concurrent validity and discriminant valid-
ity in healthy schoolchildren and children post-​surgery.
Bailey, Daoust, Doyon-​ Trottier, Dauphin-​ Pierre, and
Gravel (2010) reported data gathered from 8-​to 17-​year-​
old children in the emergency department that supported
test–​test reliability and content validity of the VNS; partic-
ipants significantly preferred the VNS to a VAS and a ver-
bal descriptor rating scale. Ruskin and colleagues (2014)
presented evidence of discriminant validity of the VNS for
assessing pain intensity in youth with chronic pain. We
recommend the NRS (VNS) for use with children 8 years
old or older.

Pain Localization
The location of a child’s pain is an important assessment
parameter. In clinical practice, children are often asked
to tell or point to where they feel pain. These informal
methods have limitations. Children may not have enough
anatomical knowledge to accurately express where they
hurt and/​or may be hesitant to point to their pain sites
(Savedra, Tesler, Holzemer, Wilkie, & Ward, 1989).
These methods do not preserve empirical documenta-
tion of children’s responses. Body outline tools have been
developed to aid in the assessment of pain localization.
However, they have not received nearly as much research
attention as measures of intensity in the pediatric pain
literature.
Eland Color Tool
The Eland Color Tool (Eland & Anderson, 1977)  is a
measure of child pain intensity and localization. To use
this tool, the child is asked to choose four crayon colors to
represent “no hurt,” “a little hurt,” “more hurt,” and “worst
hurt.” The child then selects the color that represents his
or her level of pain and is asked to color in a body outline
wherever he or she hurts. In an unpublished study, 98% of
hospitalized children between the ages of 4 and 10 years
could place a mark on this tool that coincided with their
pathology, surgical procedure, or another painful event
that occurred during hospitalization (Eland & Anderson,
1977). A  modified version of the Eland Color Tool has
been used successfully in a sample of children with devel-
opmental delays (Benini et al., 2004). The advantage of
the Eland Color Tool is that it allows clinicians to assess
children’s self-​reported pain, localization, and intensity.
In our clinical experience, this tool has proven to be very
appealing to young children, who are often eager to use
a favorite activity (coloring) to communicate about their
pain. Because the Eland Color Tool has not undergone
rigorous psychometric testing to date, it must be inter-
preted with caution.
Adolescent Pediatric Pain Tool
The Adolescent Pediatric Pain Tool (APPT; Savedra,
Holzemer, Tesler, & Wilkie, 1993) is a self-​report multi-
dimensional pain measure that can be used to assess pain
intensity, localization, and quality. It is divided into three
separate components: a body outline, a word-​graphic rat-
ing scale, and a qualitative descriptive word list. The body
outline is made up of two line drawings showing the front
Child and Adolescent Pain 589
and back of the body. The word-​graphic rating scale is a
10-​cm VAS with five pain intensity anchors (“no pain,”
“little pain,” “medium pain,” “large pain,” and “worst pain
possible”). The word list is composed of 67 words that
describe the sensory, affective, evaluative, and temporal
dimensions of pain. Both the body outline and the word
list are based on a widely used adult pain assessment mea-
sure, the McGill Pain Questionnaire (Melzack, 1983).
Adolescents indicate the location of their current pain on
the body outline, rate their current pain intensity on the
word-​graphic rating scale, and highlight words describing
their current pain experience.
The APPT has undergone rigorous psychometric test-
ing with both healthy and hospitalized children from a
wide range of ethnic backgrounds between the ages of
8 and 17  years. The development of the APPT is docu-
mented in a series of published studies (Savedra et  al.,
1989; Tesler et  al., 1991; Wilkie et  al., 1990)  that pro-
vide good evidence for the content validity of each of its
three components. Evidence for the convergent validity
of the body outline component of the APPT is supplied
by a study in which hospitalized children’s markings on
the body outline were found to match nurses’ observa-
tions and/​or medical records (Savedra et al., 1989). The
word-​graphic rating scale has also shown evidence of con-
vergent validity through moderate to strong correlations
with other scales (Tesler et al., 1991). Scores on the word
list component of the APPT have shown weak to mod-
erate but significant correlations with pain intensity and
number of pain sites; these results provide some limited
support for its convergent validity (Wilkie et  al., 1990).
Children may underselect descriptors consistent with
neuropathic pain when asked to choose from the APPT
list in comparison to when they are asked to report sensa-
tions in an affected body part generally (Ho, Curtis, &
Clarke, 2015). Test–​retest reliability has been supported
for all three components (Savedra et  al., 1993; Tesler
et al., 1991; Wilkie et al., 1990). The originally intended
age range was 8 to 17 years; however, the APPT has been
used with individuals ranging from to 2 to 68 years of age
(Fernandes, De Campos, Batalha, Perdigão, & Jacob,
2014). Younger children may not be able to understand
some of the words in the word list and may have difficulty
with left/​right reversal of body outline drawings (Savedra
et  al., 1989, 1993; Wilkie et  al., 1990). The APPT has
been used with youth with sickle cell disease, cancer,
HIV, undergoing venipuncture or immunization, and in
the postoperative context (Fernandes et al., 2014).
Average administration time for the APPT is approxi-
mately 3 to 6 minutes (Savedra et al., 1993). The tool is
590 Health-Related Problems
easily reproducible, provided that the correct scaling of
the word-​graphic rating scale is preserved. Scoring the
tool requires placing a clear plastic template over the
completed body outline to measure the number of sepa-
rate locations marked by the child; measuring the child’s
mark on the word-​graphic rating scale with a ruler; and
calculating total and percentage sensory, affective, and
evaluative subscale scores for the word list. The multi-
step scoring procedure may limit the APPT’s feasibility in
some busy clinical settings. Although no child preference
data appear to be available for the complete APPT, child
preference was taken into account during the develop-
ment of the word-​graphic rating scale (Tesler et al., 1991).
The main advantage of the APPT is that it measures three
important dimensions of pain (location, intensity, and
quality). The body outline component of the APPT is
the only pediatric pain tool of its kind with evidence to
support its reliability and validity. It provides a measure
of pain location in children who may not have enough
anatomical knowledge to indicate the location of their
pain verbally or who may be hesitant to point to their pain
sites (Savedra et  al., 1989). The body outline also pro-
vides empirical documentation that can be used to track
changes in children’s pain location over time. A  recent
systematic review of the APPT concluded that the APPT
has support for use with hospitalized children between 8
and 17  years of age, with further work needed for other
populations (Fernandes et al., 2014).
Pain Quality
The quality of pain is important for clinical description
and/​or diagnosis because it may give an indication of
the type of pain or particular disease causing the pain.
For example, burning pain is a part of the diagnosis of
neuropathic pain, pounding headache is one part of the
criteria for migraine, steady headache is a component of
a tension-​type headache diagnosis, and pain in the flank
radiating to the groin is indicative of kidney stones. There
are no particular measures for children and adolescents
that have been mapped to specific disorders. Currently,
the APPT word list is the only tool assessing pain quality
that has undergone extensive psychometric testing with
children, and we recommend it for that purpose.
Pain Frequency and Duration
Pain frequency and duration are important dimen-
sions of the pain experience to take into account when
formulating diagnoses. Diagnoses for chronic and recur-
rent pain conditions depend on the time course of the
symptoms; as noted previously, chronic pain typically has
to last for 3 months or more. In painful conditions seen by
other specialists (e.g., gastroenterologists), there are simi-
lar requirements; for example, functional abdominal pain
requires that the symptoms must occur at least 4 times
per month for at least 2  months (Hyams et  al., 2016).
Pain diaries are used to augment diagnostic information
provided via interview and questionnaires. Pain diaries
are discussed in more detail in the Assessment for Case
Conceptualization and Treatment Planning section.
Overall Evaluation
To make accurate diagnoses in children and adolescents
suffering from pain, clinicians must, at the minimum,
assess the perceptual dimensions of pain, including inten-
sity, localization, quality, duration, and frequency. The
Pieces of Hurt Tool, FPS-​R, VAS, numerical rating scales,
and the Oucher have all undergone rigorous psychomet-
ric testing, and we recommend their use in clinical set-
tings for the assessment of pain intensity in preschool and
school-​aged children. We also recommend VAS and the
word-​graphic rating scale of the APPT for the measure-
ment of pain intensity in older children and adolescents.
For pain localization, we recommend the APPT body out-
line tool with older children and adolescents. For younger
children, the Eland Color Tool may be useful for measur-
ing pain intensity and localization. However, this measure
has not undergone rigorous psychometric testing to date.
For pain quality, we recommend the APPT word list for
older children and adolescents. Unfortunately, we know
of no similar measure that has been validated for use with
younger children. We recommend pain diaries for the
assessment of pain frequency and duration for the pur-
poses of diagnosis, with parental proxy-​report for younger
children.
ASSESSMENT FOR CASE CONCEPTUALIZATION
AND TREATMENT PLANNING
Mental health practitioners will typically not be involved
in case conceptualization or treatment planning for chil-
dren undergoing isolated acutely painful procedures or
injuries. The exception is a child who develops severe
anxiety of and fear during certain painful procedures,
such as vaccination by needle injection. In this case,
 Child and Adolescent Pain 591

TABLE 26.2   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

FDI G E NA A A E G G ✓
PedsQL 4.0 E A NA A G E E A
PCS-​C A A NA A A A G G ✓

Note:  FDI  =  Functional Disability Inventory; PedsQL 4.0  =  Pediatric Quality of Life Inventory Generic Core Scales; PCS-​C  =  Pain
Catastrophizing Scale for Children; A = Adequate; G = Good; E = Excellent; NA = Not Applicable.

the assessment typically focuses on the anxiety and fear Pain Diaries
associated with the painful procedure rather than on the
Paper-​and-​pencil pain diaries (for an example, see Table 26.3)
pain itself. (For a clinical practice guideline on high lev-
combine numerical ratings with a calendar to allow for the
els of needle fear across the lifespan, see McMurtry et al.
assessment of pain over time. Diaries are commonly used for
[2016].) Most pediatric pain assessments by mental health
continuing or episodic pain such as headache, abdominal
practitioners are with children suffering from recurrent or
pain, or neuropathic pain. Although diaries are commonly
chronic pain. To obtain a full case conceptualization for
used in clinical contexts, they have not been the focus of
a child or adolescent suffering from recurrent or chronic
pain, clinicians must assess basic pain perception param-
eters, such as pain intensity and frequency, over time. It
is also important for clinicians to assess the impact of the TABLE 26.3  
Pain Diary of a Fictional 10-​Year-​Old Child
child’s pain on his or her day-​to-​day functioning to define with Chronic Headaches
targets for intervention. Finally, there are a number of Name: Jamie Trisco
psychological factors related to pain that clinicians should
consider when conceptualizing cases and formulating Rating What
(0 = No Pain Happened
treatment plans. These psychological factors include pain to 5 = Severe Before the What Did
catastrophizing, fear of pain, as well as general anxiety and Date Time Pain) Headache You Do
depression. Table 26.2 provides summary information on
Monday Breakfast 0
measures designed to assess some of these constructs.
Lunch 0
Dinner 4 Late dinner Took 2
ibuprofen
Pain Frequency and Duration Bedtime 0
Information about pain frequency and duration augments Tuesday Breakfast 3 Woke up with Took 2
headache ibuprofen
basic diagnostic information and allows mental health Lunch 4 Took 2
professionals to form full psychological case conceptual- ibuprofen
izations and plan treatments for children suffering from Dinner 3 Slept for
1 hour
recurrent or chronic pain. By working with children and
Bedtime 1
their families to document pain frequency and duration, Wednesday Breakfast 0
clinicians gain insight into possible patterns in children’s Lunch 5 Late lunch Took 2
pain experiences. For example, a child with recurrent ibuprofen,
abdominal pain may report severe pain twice per week, slept for
1 hour
on Mondays and Wednesdays during a challenging class Dinner 2 Slept for
at school. This might indicate a link between the child’s 1 hour
abdominal pain and academic stress and suggest that Bedtime 1
psychological strategies targeting the management of
Note:  This diary suggests the possibility that headaches are triggered by
academic stress may help decrease this child’s pain. Pain
delays in eating and are made somewhat better by ibuprofen and by sleep.
diaries are the best method for investigating potential pat- A  lengthier observation period might support these ideas, and specific
terns in children’s pain experiences. manipulations could confirm them.
592 Health-Related Problems
thorough psychometric testing. Research conducted to date
suggests that children who are queried retrospectively about
their pain tend to overreport pain in comparison with data
from prospective pain diaries (Andrasik, Burke, Attanasio,
& Rosenblum, 1985; van den Brink, Bandell-​Hoekstra, &
Abu-​Saad, 2001). For this reason, pain diaries help clinicians
obtain a more accurate picture of children’s pain experi-
ences over time. Pain diaries are most typically time-​based
and require the child and/​or parent to make a rating three or
four times a day. More frequent reporting by the respondents
will increase the precision of the diary but will also increase
the burden on the respondents and likely decrease compli-
ance. Event-​based diaries are an alternative to time-​based
diaries. In this style of diary, respondents are asked to record
the beginning and end of pain episodes. Event-​based diaries
have the advantage of being able to determine the duration
of pain episodes more accurately but also carry the risk of
being unable to distinguish between the absence of pain and
the absence of reporting. Whether the parent, child, or both
fill out the diary will depend on the developmental level of
the child. There is evidence to suggest that there is a positive
relation between child report and parental proxy report of the
intensity of the child’s pain (Andrasik et al., 1985; Richardson,
McGrath, Cunningham, & Humphreys, 1983; Vetter,
Bridgewater, Ascherman, Madan-​Swain, & McGwin, 2014);
however, parents’ and children’s pain frequency ratings may
differ under some circumstances, including younger child
age (Vetter et  al., 2014). Furthermore, pain experienced at
school is unlikely to be recorded by a parent unless it is of
sufficient severity that the child has to leave school. Similarly,
mild pain may not result in behavior that is evident to parents
even when it is present.
We recommend that clinicians routinely use paper-​
and-​pencil pain diaries to inform their case conceptual-
izations and treatment plans for children suffering from
chronic or recurrent pain. Electronic diaries (via programs
run on smartphones, tablets, or computers) are becoming
more popular as well; a recent review on e-​diaries for head-
ache recommended improvement in their development
and testing, including assessing psychometric properties
(Stinson et al., 2013). These e-​diaries have several advan-
tages over paper-​and-​pencil diaries. Compliance appears
to be improved with e-​diaries in that respondents are
more likely to complete electronic diary recordings and
to make these recordings at the time when pain occurs
(rather than recalling the pain experience later and mak-
ing the recording retrospectively; Lewandowski, Palermo,
Kirchner, & Drotar, 2009; Palermo, Valenzuela, & Stork,
2004). The usability of an electronic chronic pain diary
was demonstrated in a small sample of adolescents with
juvenile arthritis (Stinson, Petroz, et  al., 2006). Further
research with larger samples of children is needed before
we can determine whether the advantages of these tools
over paper-​and-​pencil diaries outweigh their cost.
Physical, Social, and Role Functioning
In accordance with the biopsychosocial model of health
and the International Classification of Functioning,
Disability and Health (ICF; WHO, 2001), clinicians
need to assess how pain impacts children’s physical,
social, and role functioning in completing a full case
conceptualization and treatment plan. When assessing
physical functioning, clinicians should always include
a measure of sleep because it is often disrupted in chil-
dren with chronic or recurrent pain (e.g., Walters &
Williamson, 1999). It is beyond the scope of this chapter
to discuss pediatric sleep assessment in detail; for recom-
mendations, see Mindell and Owens (2015) and de la
Vega and Miró (2013). Appetite and weight are two other
aspects of physical functioning that should be assessed.
This does not usually require formal assessment mea-
sures. In children, role functioning is often synonymous
with academic functioning because school is the “job” of
children. In children with chronic or recurrent pain, it is
also important to assess the extent to which children are
taking on a “sick role” in their family and demonstrating
lower functioning in their other roles (e.g., social).
Functional Disability Inventory
The Functional Disability Inventory (FDI) is a 15-​item
global measure of children’s physical and psychosocial
functioning that has both self-​and parent-​report compo-
nents (Walker & Greene, 1991). Respondents are asked
to indicate the perceived difficulty the child has had
performing various activities (e.g., walking to the bath-
room) in the previous few days. The response scale has
the following options, scored 0 to 4 and summed across
items: “no trouble,” “a little trouble,” “some trouble,” “a
lot of trouble,” and “impossible.” Total scores range from
0 to 60 for both self-​and parent-​report forms, with higher
scores indicating greater disability. Healthy children have
been found to score on average between 2 and 3.5 on
the FDI (Walker & Greene, 1991). Kashikar-​Zuck et al.
(2011) distinguished four levels of disability correspond-
ing to the following scores:  no/​minimal (0–​12), moder-
ate (13–​29), and severe (≥30); they found support for two
factors (physically strenuous activities and non-​physically
strenuous daily activities).

Three major studies have been conducted to exam-
ine the psychometric properties and clinical utility of the
FDI (Claar & Walker, 2006; Kashikar-​Zuck et al., 2011;
Walker & Greene, 1991), and many other studies have
employed the FDI as an assessment or treatment outcome
measure. The internal consistency of the FDI has ranged
from good to excellent for both child and parent versions
(Walker & Greene, 1991). Adequate test–​retest reliability
of the FDI has been supported (Claar & Walker, 2006;
Walker & Greene, 1991). The FDI was developed based
on adult measures of functional disability and pilot tested
for usability with children and adolescents (Walker &
Greene, 1991). Cross-​informant (parent–​child) correla-
tions on the FDI have ranged from moderate to strong
(Reid, McGrath, & Lang, 2005; Walker & Greene, 1991).
Concurrent and convergent validity of the FDI have been
established by its moderate to strong relationships with
other measures of child health and well-​being (Claar &
Walker, 2006; Kashikar-​ Zuck, Vaught, Goldschneider,
Graham, & Miller, 2002; A.  M. Lynch, Kashikar-​Zuck,
Goldschneider, & Jones, 2006; Palermo & Kiska, 2005;
Walker & Greene, 1991; Walker, Smith, Garber, & Claar,
2005). Discriminant validity of the FDI has been sup-
ported through negative correlations with measures that
would not be expected to be closely related to functional
disability (Claar, Walker, & Smith, 1999) and through its
ability to distinguish between groups of youth expected
to have different levels of perceived disability (Walker &
Greene, 1991; Walker, Guite, Duke, Barnard, & Greene,
1998). There is also evidence that scores on the FDI have
incremental validity over other clinical measures in pre-
dicting the severity of sleep–​wake problems (Palermo &
Kiska, 2005), number of days a child spent in bed due to
illness, and school absences (Walker & Greene, 1991). In
addition, significant correlations between baseline scores
on the FDI and subsequent measures of illness behav-
ior (e.g., school absence, bed days, pain, and depressive
symptoms) support the predictive validity of this instru-
ment (Claar & Walker, 2006; Walker & Greene, 1991).
The FDI has very good validity generalization. It has
been translated into Arabic (Madi & Clinton, 2014) and
German (Offenbächer et  al., 2016). The FDI has been
administered to children as young as age 6 years and adults
up to age 23 years, with the majority of the studies con-
ducted with children between ages 8 and 17 years. There
is evidence that girls may report greater disability com-
pared to boys (Claar & Walker, 2006; Walker & Greene,
1991; but see Kashikar-​Zuck et al., 2011). The FDI has
been used to assess disability in many different clinical
populations, including children with recurrent abdominal
Child and Adolescent Pain 593
pain (Campo et al., 2004; Claar & Walker, 2006; Walker
& Greene, 1991), chronic back pain (Lynch et al., 2006),
burns (Barnum, Synder, Rapoff, Mani, & Thompson,
1998), complex regional pain syndrome (Eccleston,
Crombez, Scotford, Clinch, & Connell, 2004), juvenile
idiopathic musculoskeletal pain (Eccleston et al., 2004),
fibromyalgia (Kashikar-​ Zuck et  al., 2002; Reid et  al.,
2005), recurrent headache (Palermo & Kiska, 2005), and
sickle cell disease (Peterson & Palermo, 2004). The FDI
has also been used with adolescents following oral surgery
(Gidron, McGrath, & Goodday, 1995), outpatients with
minor health complaints (Walker & Greene, 1991), and
healthy controls (Walker & Greene, 1991).
An advantage of the FDI is that it is easy and relatively
quick to administer. Furthermore, the tool has been used
with a number of different populations, shows good psy-
chometric properties, and scores associated with levels of
disability have been calculated in chronic pain popula-
tions (Kashikar-​Zuck et  al., 2011). Use of the measure
may allow both children and parents to express the level
of disruption that the child’s health problems are creat-
ing for the child’s daily functioning. A  disadvantage is
that it has primarily been used with Caucasian children,
although some research suggests no differences due to
ethnicity (Kashikar-​Zuck et al., 2011). Further work needs
to establish the use of the measure with children and
adolescents of different ethnic backgrounds. In addition,
there have been inconsistent relationships between scores
on the FDI and socioeconomic status (Claar & Walker,
2006; Peterson & Palermo, 2004; Walker & Greene,
1991). Despite these limitations, there is sufficient psy-
chometric support to recommend the use of the FDI to
measure children’s physical and psychosocial functioning
in clinical settings.
The Pediatric Quality of Life Inventory Generic
Core Scales
The Pediatric Quality of Life Inventory (PedsQL) is a
23-​item modular instrument measuring health-​ related
quality of life (HRQOL), which can be defined as “an
individual’s subjective perception of his or her function-
ing and emotional state vis-​à-​vis the effects of disease
and treatment” (Connelly & Rapoff, 2006, p. 698). The
PedsQL 4.0 Generic Core Scales (PedsQL 4.0; Varni,
Seid, & Kurtin, 2001)  were designed to measure child
physical, mental, and social health dimensions, as well
as role (school) functioning. The measure is made up of
parallel child self-​report and parent proxy-​report formats.
The parent proxy-​reports measure parents’ perceptions of
594 Health-Related Problems
their children’s HRQOL. Child self-​reports include ages
5 to 7 years (young child), 8 to 12 years (child), and 13 to
18 years (adolescent). Parent proxy-​reports include ages 2
to 4 years (toddler), 5 to 7 years (young child), 8 to 12 years
(child), and 13 to 18 years (adolescent). Respondents indi-
cate the extent to which the child is having problems in
each of the four areas of functioning using a Likert scale.
A 5-​point scale is used for the child self-​report forms (ages
8–​18 years) and the parent proxy-​report forms. To increase
ease of use for young children, a simplified 3-​point scale is
used. The young child self-​report form is also anchored to
a faces scale ranging from happy to sad. Items are reverse-​
scored and converted into a 0-​to-​100 scale, with higher
scores indicating better HRQOL. The measure yields
scores on Physical Functioning, Emotional Functioning,
Social Functioning, and School Functioning, as well as a
Physical Health Summary Score, a Psychosocial Health
Summary Score, and a Total Score.
A large volume of empirical evidence supports
the psychometric properties of the PedsQL 4.0. The
PedsQL 4.0 was designed to measure the core health
dimensions outlined by WHO (1948). Items for the
original instrument were created based on a literature
search, interviews with children with cancer and their
families, and discussions with clinicians (Varni, Seid,
& Rode, 1999). This most recent version is the result
of a number of iterations that have occurred since the
publication of the original instrument (Varni et  al.,
1999). Measures of central tendency and distribution
are available for total and scale scores in large samples
of youth with chronic and acute health conditions, as
well as samples of healthy children (Connelly & Rapoff,
2006; Powers, Patton, Hommel, & Hershey, 2004; Tran
et al., 2015; Varni, Burwinkle, Limbers, & Szer, 2007;
Varni et al., 2001, 2015; Varni, Seid, Knight, Uzark, &
Szer, 2002). Internal consistency has been reported to
be at least adequate (Connelly & Rapoff, 2006; Varni
et  al., 2001, 2007). Two-​week test–​retest reliability of
the Total Scale score has also been reported as adequate
(Connelly & Rapoff, 2006). There is good evidence for
the construct validity of the PedsQL 4.0 (e.g., scores are
lower in samples of children with chronic pain condi-
tions and acute health conditions than in samples of
healthy children; Connelly & Rapoff, 2006; Powers
et al., 2004; Varni et al., 2001, 2007, 2015). Empirical
evidence supports the use of the PedsQL 4.0 with a wide
age range (2–​18 years). It is the only generic pediatric
quality of life measure to span such a wide age range
that has undergone rigorous psychometric testing (Eiser
& Morse, 2001). The PedsQL 4.0 is appropriate for use
with both healthy children and children with a wide
variety of acute and chronic illnesses (e.g., Varni et al.,
2001). This measure has been tested with samples of
children from different ethnic backgrounds and their
parents in both English and Spanish, and ratings pro-
vided in both languages have been found to be equiva-
lent (Varni et al., 2001). Translations in a wide range of
other languages are also available (Varni, 2016), includ-
ing Norwegian, Dutch, German, and Chinese versions
that have all been validated by independent groups of
authors (Bastiaansen, Koot, Bongers, Varni, & Verhulst,
2004; Chan, Chow, & Lo, 2005; Felder-​Puig et  al.,
2004; Reinfjell, Diseth, Veenstra, & Vikan, 2006).
Because the PedsQL 4.0 is a generic HRQOL mea-
sure, it gives researchers and clinicians the ability to
conduct comparisons across acute and chronic health
conditions, as well as benchmark against healthy popu-
lation norms (Varni et  al., 2002). However, the generic
nature of this instrument may make it necessary to
administer supplementary disease-​specific assessments to
address the full range of functioning in some children
with pain (Eiser & Morse, 2001). PedsQL disease-​specific
modules are currently available for arthritis, asthma,
brain tumor, rheumatology, diabetes, cancer, cerebral
palsy, and cardiac conditions, among others. One of the
main advantages of the PedsQL 4.0 is that it includes
complementary child and parent proxy-​ report forms.
Although patient self-​report is considered the standard for
measuring perceived HRQOL, it is parents’ perception of
their children’s HRQOL that influences health care utili-
zation (Varni & Setoguchi, 1992). Correlations between
child and parent ratings are in the moderate range, sug-
gesting that it is important to obtain both the child’s and
the parent’s perspective (e.g., Powers et  al., 2004; Varni
et  al., 2007). Another advantage of the PedsQL is that
it provides a multidimensional quality of life assessment
with a quick administration time (<5 minutes) and rela-
tively simple scoring procedure. This makes it practical
for use in clinical settings. The PedsQL also has a use-
ful website (http://​www.pedsql.org) that provides detailed
information about administration and scoring, along
with an extensive reference list. The main disadvantage
of the PedsQL 4.0 is that large noncommercial organiza-
tions such as hospitals and health care systems must pay
a license fee to use it (conditions of use are detailed on
the website). Although clinicians must take this practi-
cal consideration into account, we believe that there is
enough evidence for the clinical utility of this measure
to recommend its use as part of multidimensional pain
assessments.

The Adult Response to Child Symptoms Scale
The Illness Behavior Encouragement Scale (IBES;
Walker & Zeman, 1992)  was designed to measure par-
ents’ encouragement of their children’s sick-​role behav-
ior. Sick-​role behavior (which is synonymous with “illness
behavior”) can be defined as behavior that suggests illness,
such as complaining about physical symptoms like pain or
refusing to complete daily tasks such as attending school
due to pain (Brace, Smith, McCauley, & Sherry, 2000).
Parents who attend to or reward their children’s sick-​role
behavior may unintentionally reinforce it (Walker &
Zeman, 1992). The Adult Response to Child Symptoms
(ARCS) was initially designed to expand the IBES and
measure parental protective, minimizing, and encourag-
ing/​monitoring behaviors (Van Slyke & Walker, 2006).
The ARCS consists of parallel parent-​and child-​report
forms. The parent-​report form asks parents to indicate
the frequency with which they respond to their children’s
symptoms in particular ways—​for example, “How often
do you let your child stay home from school when he/​
she has [symptom].” Similarly, the child-​report form asks
children to indicate the frequency with which their par-
ents respond to their (the children’s) symptoms in particu-
lar ways. Both forms are scored on a 5-​point Likert scale
ranging from 0 (“never”) to 4 (“always”). Subscale scores
are obtained by summing and averaging the items, with
higher scores indicating more parental encouragement of
the symptom in question.
Until recently, only one (Protect) of the three subscales
formally underwent psychometric evaluation (Walker,
Levy, & Whitehead, 2006; reviewed in Noel, Palermo,
et al., 2015; Noel et al., 2016). The Protect subscale has
shown convergent validity with child symptomatology,
disability, and health care costs (Claar, Guite, Kaczynski,
& Logan, 2010; Walker et al., 2006). The ARCS (or par-
ticular subscales) has been used with 8-​to 17-​year-​olds
with functional abdominal pain (Walker et  al., 2006),
inflammatory bowel disease (Noel, Palermo, et al., 2015),
musculoskeletal pain (Guite, McCue, Sherker, Sherry,
& Rose, 2011), and various types of chronic pain (Claar
et al., 2010; Noel, Palermo, et al., 2015). A four-​factor sub-
scale structure of the measure has recently been proposed
for children:  Protect, Monitor, Minimize, and Distract;
in contrast, a five-​factor subscale structure of the measure
has been proposed for adolescents with the additional sub-
scale of Solicitousness (Noel, Palermo, et al., 2015).
Advantages of the ARCS include its straightforward
scoring procedure and parallel parent-​and child-​report
forms, which allow clinicians to compare parent and
Child and Adolescent Pain 595
child reports. Unfortunately, the Protect subscale (and to
a lesser extent, the new Monitor subscale) is the aspect
that is most often included in research due to question-
able psychometrics of the other subscales (Noel et  al.,
2016). In our clinical experience, the ARCS (and the
IBES prior to that) has proven very useful for identifying
ways in which parents may show problematic responses to
their children’s pain and related sick-​role behavior (and
thus provide explicit treatment targets). Until further psy-
chometric testing is completed, we suggest that this mea-
sure may be used with caution in clinical contexts.
Psychological Factors Related to Pain
Pain catastrophizing can be defined as “an exaggerated
negative orientation” toward pain (Sullivan, Bishop, &
Pivik, 1995, p. 524). Pain catastrophizing has been found
to be related to somatic complaints, pain severity, and
functional disability as well as lower pain acceptance in
youth (Huguet, Eccleston, Miró, & Gauntlett-​Gilbert,
2008; Tran et  al., 2015; Vervoort, Goubert, Eccleston,
Bijttebier, & Crombez, 2006; Weiss et al., 2013), and it
can be assessed as a part of the treatment planning pro-
cess. The Pain Catastrophizing Scale for Children (PCS-​
C; Crombez et  al., 2003)  was adapted from the Pain
Catastrophizing Scale (Sullivan et al., 1995). The PCS-​C
is a 13-​item self-​report measure, with each item depict-
ing various feelings or thoughts one might have while in
pain. The child responds to each statement by choosing
an intensity rating:  “not at all,” “mildly,” “moderately,”
“severely,” or “extremely.” The items represent three
related dimensions: rumination, magnification, and help-
lessness. Total scores on the PCS-​C range from 0 to 52,
with higher scores indicating higher levels of pain cata-
strophizing. The initial validation study for the PCS-​C
showed evidence of at least adequate internal consistency,
criterion validity, construct validity, and validity general-
ization (Crombez et al., 2003). Later work has also found
evidence for at least adequate internal consistency and
test–​retest reliability (Parkerson et al., 2013; Pielech et al.,
2014). The PCS-​C has been used with healthy children,
children with inflammatory bowel disease, postoperative
children, and children with chronic pain between the ages
of 8 and 19 years (Crombez et al., 2003; Noel, Rabbitts,
Tai, & Palermo, 2015; Parkerson et  al., 2013; Pielech
et  al., 2014; Tran et  al., 2015; Wojtowicz, Greenley,
Gumidyala, Rosen, & Williams, 2014). Some advantages
of the PCS-​C are its relative brevity, ease of administra-
tion, and initial psychometric data. Furthermore, Pielech
and colleagues (2014) derived reference points with a
596 Health-Related Problems
sample of almost 700 youth with chronic pain:  low (0–​
14), moderate (15–​25), and high (≥26). A French version
of the scale has also been developed, although limited
psychometric information is available (Tremblay et  al.,
2008). There is also a parent-​report version of the PCS-​C
(herein PCS-​P). The PCS-​P has been used with parents of
8-​to 18-​year-​old healthy schoolchildren, children follow-
ing surgery, and youth with chronic pain (Cunningham
et  al., 2014; Goubert, Eccleston, Vervoort, Jordan, &
Crombez, 2006; Noel, Rabbitts, et al., 2015). Results have
provided evidence of both adequate internal consistency
and construct validity (Goubert et al., 2006; Pielech et al.,
2014). Parental catastrophizing about their child’s pain
has also been shown to predict parental mental health
beyond their child’s pain intensity (Goubert et al., 2006).
Fear of pain is another psychological factor that has
been shown to predict disability in adult chronic pain
patients (McCracken, Zayfert, & Gross, 1992). An
influential model of pain is the Fear Avoidance Model
(Asmundson, Noel, Petter, & Parkerson, 2012; Simons &
Kaczynski, 2012; Vlaeyen, Kole-​Snijders, Boeren, & Van
Eek, 1995). Recently, measures targeting pain-​ related
fear have been developed: the Pediatric Pain Fear Scale
(Huguet, McGrath, & Pardos, 2011; developed with 6-​to
16-​year-​old healthy and also youth with chronic pain in
Spain), the Fear of Pain Questionnaire (Simons, Sieberg,
Carpino, Logan, & Berde, 2011; developed with 8-​to 17-​
year-​old youth with chronic pain in the United States),
and the Child Pain Anxiety Symptoms Scale (Pagé, Fuss,
Martin, Escobar, & Katz, 2010; developed with healthy
youth in Canada). Based on a citation count, currently,
the Fear of Pain Questionnaire (FOPQ) appears to be
the most popular and will be reviewed briefly here; it is
also the only one of the three included in a recent meta-​
analysis of fear-​ avoidance and pain intensity (Kroska,
2016). There are both child-​and parent-​report versions of
the FOPQ (FOPQ-​C and FOPQ-​P, respectively), which
were developed using four strong adult chronic pain mea-
sures, clinical expertise, and family feedback (Simons
et al., 2011). The FOPQ-​C has 24 items representing Fear
of Pain and Avoidance of Activities, whereas the FOPQ-​P
has 23 items and has an additional School Avoidance sub-
scale (Simons et  al., 2011). Responses on both versions
are provided on a 5-​point Likert scale (“strongly disagree”
to “strongly agree”). In the initial development and vali-
dation study, the FOPQ-​C and FOPQ-​P were used with
8-​to 17-​year-​old youth with chronic pain and their par-
ents; the measures showed internal consistency and con-
struct validity (positive relations with functional disability,
pain, health care utilization, somatic symptoms, anxiety
symptoms, and catastrophizing; Simons et  al., 2011).
Although scores did not vary by pain duration, diagnosis,
or gender, there was an inverse relationship for both mea-
sures and socioeconomic status. There was some lack of
stability of the measures over a 1-​month period (decrease
but no treatment), but this was accompanied by decreases
in functional disability (Simon et  al., 2011). Later work
has supported the use of the FOPQ-​C with youth with
chronic headaches (Simons, Pielech, Capucci, & Lebel,
2014). The FOPQ-​C and FOPQ-​P are promising mea-
sures and are suggested for clinical use with a caution that
further psychometric investigation is needed.
Two other psychological factors that clinicians should
take into account during case conceptualization and
treatment planning are depression and anxiety. Symptoms
of both depression and anxiety have been found at
increased rates in children with recurrent pain (Palermo,
2000; Tran, Jastrowski Mano, Anderson Khan, Davies, &
Hainsworth, 2016). The reader is referred to Chapters 6
and 11 in this volume on child and adolescent depres-
sion and anxiety disorders for information on assessment
of these factors.
There have been relatively more recent attempts to
create multicomponent assessment measures to capture
correlates of pain in youth:  the Bath Adolescent Pain
Questionnaire (BAPQ; Eccleston et al., 2005), the Bath
Adolescent Pain Questionnaire Parent version (BAPQ-​P;
Eccleston, McCracken, Jordan, & Sleed, 2007), and the
Pain Experience Questionnaire (PEQ [German], child
and parent versions; Hermann, Hohmeister, Zohsel,
Tuttas, & Flor, 2008). The BAPQ and BAPQ-​P contain
61 items and are scored into seven subscales:  physi-
cal functioning, social functioning, depression, general
anxiety, pain-​specific anxiety, development, and family
functioning. The initial validation study of the BAPQ
with 11-​to 18-​year-​olds from a rheumatology clinic and
a chronic pain clinic showed adequate internal consis-
tency, good stability/​test–​retest reliability, and good con-
struct validity (Eccleston et al., 2005). Since the original
validation study, we are aware of no other targeted psy-
chometric studies, although studies have been published
using the measure or, more commonly, selected sub-
scales (e.g., Caes, Fisher, Clinch, Tobias, & Eccleston,
2015; Cohen, Vowles, & Eccleston, 2010; Fales, Essner,
Harris, & Palermo, 2014). The initial validation study of
the BAPQ-​P was conducted on the parents of the youth
in the Eccleston et al. (2005) sample; the results provided
evidence of adequate internal consistency, good temporal
stability (except for pain-​specific anxiety), and good con-
struct validity (Eccleston et  al., 2007). These measures
 Child and Adolescent Pain 597

appear promising but await further psychometric assess- The FOPQs (parent and child versions) are also promis-
ment on the full package. ing instruments. Readers are directed to other chapters in
this volume for recommendations on the assessment of
anxiety and depression.
Overall Evaluation

There are a number of factors that clinicians must take

into account in forming case conceptualizations and
planning treatments for children with chronic or recur-
rent pain. Detailed information about pain frequency
and duration should be collected with a pain diary. Pain
diaries are invaluable assessment tools because they allow
clinicians to identify possible patterns in pain symptoms
and target their interventions accordingly. Assessments of
the child’s physical, social, and role functioning are also
essential components of treatment planning. We recom-
mend the use of the FDI for the assessment of physical
and psychosocial functioning in older children between
the ages of 8 and 17  years. We also recommend the
PedsQL 4.0 for the assessment of physical, emotional,
social, and school functioning for children and adoles-
cents from age 2 through 18  years. For the assessment
of problematic parental responses to children’s sick-​role
behavior, we suggest that clinicians consider the parent-​
and child-​report forms of the ARCS for children 8 years
old or older and the parent-​report form of the ARCS for
children younger than 8 years. Results of the ARCS must
be interpreted with caution because further evaluation of
the psychometric properties of this measure is needed.
We recommend that clinicians assess for sleep problems
in children with chronic or recurrent pain. Psychological
factors such as pain catastrophizing, fear of pain, as well
as general depression and anxiety should also be assessed
before treatment plans are formulated. For pain catastro-
phizing, we recommend that clinicians use the PCS-​C.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
The measures chosen for assessment of treatment moni-
toring and outcome for a given youth will reflect the areas
of functioning identified during case conceptualization as
major problem areas (e.g., poor school attendance, fear of
pain, depression, anxiety, and sleep). Assessment for treat-
ment monitoring and outcome must also include pain
perception parameters such as pain intensity, duration,
and frequency. Pain diaries that track when each inter-
vention was implemented and the resulting pain levels
are especially useful for tracking progress. However, more
research is needed to formally document the treatment
sensitivity of various pain diary formats. Table 26.4 pres-
ents ratings for instruments relevant for use in treatment
monitoring and treatment outcome evaluation.
Each of the pain intensity measures we recommended
for formulating diagnoses has some evidence of treatment
sensitivity. Specifically, there are some data to suggest
that the Pieces of Hurt Tool is responsive to changes in
pain intensity following surgery (Beyer & Aradine, 1987).
Similarly, there is evidence to suggest that the Oucher
is responsive to changes in pain following surgery and
analgesic administration (Aradine et  al., 1988; Beyer &
Aradine, 1987; Beyer & Knott, 1998; Ramritu, 2000).
There is also good evidence for the treatment sensitiv-
ity of the FPS-​R, including pre–​post needle differences

TABLE 26.4   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Treatment Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Sensitivity Recommended

Pieces of Hurt Tool NA NA NA NA A G G G A ✓

The Oucher NA NA NA NA G G A G G
FPS-​R NA NA NA NA A G E G E ✓
Visual analogue NA NA NA NA NA A G A G
scales
Numerical rating NA NA NA A A G G G G ✓
scales
APPT NA NA NA A G G E A G ✓
FDI G E NA A A E G G E ✓
PedsQL 4.0 E A NA A G G G A E

Note: FPS-​R = Faces Pain Scale-​Revised; APPT = Adolescent Pediatric Pain Tool; FDI = Functional Disability Inventory; PedsQL 4.0 = Pediatric Quality
of Life Inventory Generic Core Scales; A = Adequate; G = Good; E = Excellent; NA = Not Applicable.
598 Health-Related Problems
in pain and group differences between children receiv-
ing two different types of vaccines (Wood et  al., 2004).
Children’s pain ratings on the FPS-​R have also reflected
significant differences between treatment with lidocaine
versus placebo for needle pain (Taddio et al., 2005) and
two different types of tonsillectomy surgery (Lister et al.,
2006). Although the evidence for the treatment sensitivity
of VAS is not as strong as it is for the FPS-​R, these mea-
sures have also been shown to be responsive to changes
in child pain intensity following the administration of
analgesic medications (Aradine et  al., 1988)  and topical
anesthetics (Migdal et al., 2005). Bailey and colleagues’
(2010) data supported treatment responsivity of the 0 to
10 VNS and showed that even a 1-​point difference was
clinically significant.
In terms of pain localization, preliminary evidence
for the treatment sensitivity of the Eland Color Tool was
demonstrated in a small sample of kindergarten children
undergoing injections (Eland, 1982). The treatment sen-
sitivity of all three components of the APPT is supported
in two surgical studies (Savedra, Tesler, Holzemer, Wilkie,
& Ward, 1990; Savedra et al., 1993). Another study also
provides limited support for sensitivity of the APPT to
treatment (Jacob, Hockenberry, & Mueller, 2008; word
descriptors only).
Unfortunately, some children and adolescents with
chronic pain may not experience significant decreases
in pain intensity over the course of treatment; however,
they may show dramatic improvement in their overall
coping and functioning. For this reason, it is important
for clinicians to include measures of overall functioning
and quality of life in their treatment monitoring plans.
The treatment sensitivity of two such measures, the
FDI and the PedsQL 4.0, has received some empirical
support. Eccleston, Malleson, Clinch, Connell, and
Sourbut (2003) found that following residential treat-
ment, FDI scores for adolescents with chronic pain
significantly declined immediately after treatment and
3  months post-​ treatment compared with baseline. In
another study, Walker and Greene (1991) showed that
the FDI scores of children who had received medical
treatment for their abdominal pain of organic etiology
declined after treatment. More recent investigations in
chronic pain populations have also supported the FDI’s
response to treatment (e.g., Cunningham et  al., 2016;
Holm, Ljungman, Åsenlöf, Linton, & Söderlund, 2015).
A  number of studies support the treatment sensitivity of
the PedsQL 4.0. In a study conducted with children visit-
ing an orthopedic clinic for treatment of fractures, quality
of life scores were significantly lower at the initial clinic
visit than at a follow-​up phone call 6 to 8  months later
(Varni et al., 2002). In another study, children with recur-
rent headaches showed significant improvements on the
Total Scale, Physical Health Summary, and Psychosocial
Health Summary scores following a cognitive–​behavioral
intervention (Connelly & Rapoff, 2006). Scores also
improved following an intensive rehabilitation program
for chronic pain (Benore, D’Auria, Banez, Worley, &
Tang, 2015). Significant improvements in Total Scale
scores following cognitive–​ behavioral treatment were
reported in a study of children with recurrent abdomi-
nal pain (Youssef et  al., 2004). The ARCS subscales of
Protect and Monitor (but not Minimize or Distract)
showed responsiveness to treatment in children; similarly,
the subscales of Protect and Monitor (but not Minimize,
Distract, or Solicitousness) showed treatment responsivity
in adolescents (Noel et al., 2016).
Overall Evaluation
The choice of measures for treatment monitoring and
treatment outcome should flow from information gath-
ered during diagnosis, case conceptualization, and treat-
ment planning. It is important for clinicians to monitor
basic pain perception parameters, as well as overall func-
tioning and quality of life in youth suffering from pain.
Of the pain intensity measures discussed previously, the
FPS-​R has received the most empirical support for its
treatment sensitivity. There is some less rigorous evidence
for the treatment sensitivity of the Pieces of Hurt Tool, the
Oucher, NRS (VNS), VAS, and the APPT. In terms of
overall functioning and quality of life, there is adequate
evidence for the sensitivity of the FDI and good evi-
dence for the sensitivity of the PedsQL 4.0. More data are
needed on the treatment sensitivity of the PCS-​C, PCS-​P,
FOPQ-​C, FOPQ-​P, and the ARCS.
CONCLUSIONS AND FUTURE DIRECTIONS
Assessment of pain requires an understanding of pain
intensity, localization, quality, frequency, and duration.
However, these dimensions are only part of the puzzle
when we seek to understand a child’s or adolescent’s total
experience of pain. For example, two young people with
the same chronic pain condition and similar pain inten-
sity, localization, frequency, and duration can have very
different levels of functional ability. Psychological fac-
tors, such as the presence of symptoms of depression or
anxiety, as well as a person’s specific orientation to pain

(e.g., pain catastrophizing and fear of pain) are important
pieces to take into account. For youth, it is also impor-
tant to consider parents’ orientation and behavior toward
their children’s pain (e.g., unintentional encouragement
of illness behavior). The biopsychosocial model and the
WHO’s (2001) ICF provide ideal frameworks for assess-
ment when working with children or adolescents who suf-
fer from chronic/​recurrent pain because they go beyond a
disease-​based model to focus on overall health, functional
ability, and quality of life. As reflected in our recommen-
dations, we believe that it is just as important to assess
the impact of children’s pain on their physical, social,
and role functioning as it is to assess the basic perceptual
parameters of their pain.
There are several areas in which child and adolescent
pain assessment tools need to be developed, including
pain quality and location. However, in general, future
research should focus on establishing the psychometrics
and feasibility of existing assessment tools rather than add-
ing to the list of tools already available. This is particularly
true for measures of pain intensity, a construct for which
there are numerous tools, all of which have gaps in their
psychometric data. Some of the pain intensity measures
we have discussed in our review have been applied pri-
marily to assess the intensity of acute pain. Their appli-
cation in the assessment of chronic pain deserves further
study. Although there has been valuable research on the
measurement of various aspects of pain in children, insuf-
ficient attention has been paid to the development and
validation of measures suitable for everyday clinical use.
There is also a dearth of research on clinical issues such as
interpretability of assessment tools and levels of clinically
significant pain and pain reduction (e.g., when a child
believes he or she would need pharmacological interven-
tion; Lavigne, 2016; Voepel-​Lewis, 2011). Developed by
the U.S. Department of Health and Human Services, the
Patient-​Reported Outcomes Measurement Information
System (PROMIS) measures are an important set of tools
designed to allow comparisons across a variety of health
conditions (http://​www.healthmeasures.net). These
PROMIS measures should continue to be investigated
in the near future. In addition, as can be seen through-
out this chapter, much of the literature focuses on risk
factors in chronic pain. There have been recent calls for
incorporating consideration of resiliency resources as well
for factors such as optimism, pain self-​efficacy, and pain
acceptance (Bursch, Tsao, Meldrum, & Zeltzer, 2006;
Cousins, Kalapurakkel, Cohen, & Simons, 2015; Cousins,
Tomlinson, Cohen, & McMurtry, 2016; McCracken,
Gauntlett-​Gilbert, Eccleston, 2010; Tomlinson, Cousins,
Child and Adolescent Pain 599
McMurtry, & Cohen, 2017). During the next 10 years of
research on pediatric pain, we hope to see further explora-
tion of these types of factors to further inform our under-
standing and treatment of chronic pain.
Patient health registries, which are large-​scale, multi-
site collections of standardized patient experiences and
outcomes, have become critical components of modern
health care and research. With electronic data collection,
rapid updating of data and feedback to individual practitio-
ners and clinics is now very feasible. Linkage with admin-
istrative databases can be useful to answer some questions.
Registries are useful for clinical tracking, for quality assur-
ance, and for research. The Quebec Pain Registry (http://​
www.quebecpainregistry.com) is a good example of a pain
registry in which data for close to 10,000 patients with
chronic pain are available to researchers. The Stanford
Pain Management Clinic has developed an open-​source
registry software system called CHOIR (Collaborative
Health Outcomes Information Registry; https://​choir.
stanford.edu) that is freely available to other clinics with
modest costs for maintenance. The Pediatric version,
Peds-​CHOIR (Bhandari et al., 2016), has been thought-
fully built and allows for customization for specific clinics.
The Stanford group is continuing to expand the function-
ality of the software. Widespread adoption of this type of
architecture is warranted because it would allow for indi-
vidual tracking by patients and their families, benchmark-
ing of clinic success, and large-​scale studies that would
otherwise be so expensive as to be impossible. Clinical
trials can be a built-​in component of patient health regis-
tries (James, Rao, & Granger, 2016) so that trials can be
more efficient and more inclusive. Nelson and colleagues
(2016) have detailed how patient health registries can be
enhanced by strong participation of patients and families
in their development and functioning. These registries
can transform health care and facilitate research. A good
example of maximal patient involvement and use of a
registry is the Swedish Rheumatology Quality Register
(Eriksson, Askling, & Arkema, 2014; Forsberg et al., 2015;
Nelson et al., 2016), in which patients can access a patient
portal and track their own progress. A short YouTube video
(www.youtube.com/​watch?v=8F-​mjAzylBQ) explains this
aspect of the registry.
The growth of evidence-​based clinical practice in pedi-
atric pain depends on the use of psychometrically sound
assessment tools. Close collaboration between clinicians
practicing in busy clinics and pain measurement scientists
is needed to ensure that the measures and assessments
that are developed are easy to use and yield information
that clinicians find helpful in clinical decision-​making for
600 Health-Related Problems
diagnosis, case formulation, and evaluation of treatments.
The integration of appropriate measures into routine care
will be invaluable for ensuring that each child is given the
most effective treatment.
ACKNOWLEDGMENTS
The current version of this chapter is based on a previous
chapter by Moon, McMurtry, and McGrath. We grate-
fully acknowledge Dr. Erin C. Moon for her leadership in
writing the initial version of the chapter.
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 27
Chronic Pain in Adults
Thomas Hadjistavropoulos
Natasha L. Gallant
Michelle M. Gagnon
THE NATURE OF PAIN IN ADULTS
Pain is widely regarded as a psychological experience that
incorporates both physical and emotional components
(Hadjistavropoulos et al., 2011; Melzack & Wall, 1965).
This is recognized in the formally adopted definition of
pain, which states that pain is “an unpleasant sensory and
emotional experience associated with actual or potential
tissue damage, or described in terms of such damage”
(Merskey & Bogduk, 1994, p.  210). The most widely
accepted theory of pain, the gate control theory (Melzack
& Wall, 1965), along with more recent related formula-
tions (Melzack, 1999), provides descriptions of the ways
ascending inputs from the body can interact with input
from the brain (e.g., thoughts, attributions, and attention)
to determine the intensity, unpleasantness, and psychoso-
cial consequences of the overall pain experience.
In addition to this main theory, a number of biopsy-
chosocial formulations of pain have been developed
(e.g., Fordyce, 1976; Sullivan, Adams, & Sullivan, 2004;
Vlaeyen & Linton, 2000). These formulations are consis-
tent with the gate control theory; well supported by empir-
ical research; and elaborate on the manner in which
cognitive, social (including situational and cultural), and
psychological factors interact with biological influences
(e.g., extent of tissue damage) to determine the overall
experience of pain (e.g., Gatchel, Peng, Peters, Fuchs, &
Turk, 2007; Lumley et al., 2011). One of these biopsycho-
social formulations, the communications model of pain
(e.g., Hadjistavropoulos et  al., 2011; Prkachin & Craig,
1995), is most relevant to assessment. This model consid-
ers pain and its communication as a three-​step process: (a)
608
the internal experience, (b)  the encoding of pain in
expressive behavior, and (c)  the decoding of expressive
behavior by observers who could potentially intervene to
palliate the pain. The process of pain assessment can be
conceptualized within the communications framework of
pain (Hadjistavropoulos & Craig, 2002).
Step 1: The Internal Experience
In Step 1, the internal experience of pain is determined,
consistent with the gate control theory, through the
interplay of biological components (e.g., extent of tissue
damage and brain activity), psychosocial influences, and
situational contexts. A variety of emotional responses (e.g.,
anger and fear) have been associated with pain responses
(Hale & Hadjistavropoulos, 1997). The biological corre-
lates of pain have been demonstrated in numerous brain
imaging studies and consist of both serial and parallel levels
of brain activation (Casey & Bushnell, 2000). Similarly, as
an example of social influences, it has been demonstrated
that research participants, who were exposed to a pain
stimulus, reported different levels of pain when they were
exposed to confederates modeling low versus high pain
tolerance (Craig, 1978; Craig & Weiss, 1972). Research
with children has also shown that children whose parents
were taught to interact in a pain-​promoting way during a
pain task reported more pain than did children whose par-
ents were not given such instruction (Chambers, Craig,
& Bennett, 2002). Accordingly, a comprehensive under-
standing of the internal experience of pain should include
evaluation of not only its intensity and quality but also any
social, psychological, and cognitive influences.

Step 2: The Encoding of Pain in Expressive Behavior
There are two possible modes of pain expression: verbal
report and nonverbal behavior (e.g., reflexive withdrawal
of a limb, paralinguistic vocalizations, and grimaces). The
verbal report of pain is heavily reliant on mediation from
cognitive executive functions, whereas nonverbal pain
expressions are largely the result of reflexive automatic-
ity. These modes of pain expression reflect less than fully
overlapping components of the pain experience and are
not always highly correlated (Labus, Keefe, & Jensen,
2003). Nonverbal expressions tap the more immediate
reactions to the pain, whereas verbal reports follow central
processing of the painful stimulation. A  comprehensive
assessment of pain should take into account both verbal
and nonverbal responses.
Step 3: The Decoding of Pain by Observers
Verbal expressions are more easily understood by observ-
ers, whereas nonverbal expressions are more difficult to
decode (e.g., they may be mistaken as signs of other types
of distress). Importantly, however, situational character-
istics and potential secondary gain could result in the
underreporting or overreporting of pain. The comprehen-
sive assessment of pain should focus on the decoding of
the various dimensions of the experience. As a result of
the pain decoding, observers often take measures to palli-
ate the pain experience or otherwise provide comfort, but
occasionally they can exacerbate it (e.g., in the context of
a physical confrontation).
Chronic Pain: Prevalence and Consequences
Approximately 30% of adults experience chronic pain
(Tsang et al., 2008), but this proportion varies by country
(e.g., Breivik, Collett, Ventafridda, Cohen, & Gallacher,
2006; Institute of Medicine, 2011; Moulin, Clark,
Speechley, & Morley-​Forster, 2002)  and as a function
of study methodology. On average, females and older
persons are reported as having relatively higher rates of
chronic pain (Moulin et  al., 2002; Tsang et  al., 2008).
Demographic disparities also exist, with members of eth-
nic minority groups being at increased risk for inadequate
pain control (Campbell & Edwards, 2012).
The most common chronic pain locations include the
back (accounting for approximately 40% of cases) and the
knees, with arthritis, herniated disks, and traumatic injury
being the most common causes (Breivik et  al., 2006;
Moulin et al., 2002; Tsang et al., 2008). Chronic pain is
Chronic Pain in Adults 609
associated with a variety of psychosocial and health conse-
quences, including, but not limited to, difficulty holding
gainful employment, sleep problems, interference with
sexual functioning, depression, anxiety, marital distress,
and social isolation (e.g., Breivik et al., 2006; Fine, 2011;
Kroenke et  al., 2013; Tsang et  al., 2008). Interventions
designed to improve pain and its consequences rely on
adequate pain assessment, but thorough assessments
of pain and its sequelae are frequently not conducted.
Breivik and colleagues, for example, found that of the
people who visited their physician about their chronic
pain, only 9% reported that a pain scale was administered
to determine the extent of the pain reported.
PURPOSES OF ASSESSMENT
Given the multiple effects of pain, there are several
important domains that need to be covered during the
assessment process. Key assessment domains are summa-
rized in Table 27.1. Assessment of general psychological
functioning is important to pursue with pain patients.
Such assessment can be accomplished with a variety of
tools that are discussed in other chapters of this volume.
The primary goal of this chapter is to cover key measures
that are specifically focused on facets of the pain expe-
rience. A multitude of psychometrically validated assess-
ment tools for pain have been developed. In this chapter,
we discuss some of the most commonly used tools that
cover key domains of assessment. Some of these tools are
unidimensional and/​or brief and could be used in general
practice contexts, such as at acute and primary care facili-
ties and hospitals, as long as the administering staff have
appropriate training in their use and interpretation. More
complex assessment tools or batteries would require the
involvement of a well-​trained health professional (e.g.,
clinical psychologist) and are usually used as part of spe-
cialized tertiary care or psychological consultations.
ASSESSMENT FOR DIAGNOSIS
The diagnoses of physical conditions (e.g., arthritis and
musculoskeletal injury) that accompany pain must be
made by physicians and other allied health professionals.
Nonetheless, psychologists can sometimes provide infor-
mation that can facilitate the medical diagnosis (e.g., by
providing systematic information on pain qualities and
temporal characteristics of pain). Moreover, psychologists
610 Health-Related Problems
TABLE 27.1   Central Pain Assessment Domains
• Description of the pain and any related presenting issues
(e.g., nature and intensity of pain, inability to perform occupational
duties due to pain, pain-​related sleep interference)
• Verbal and nonverbal behaviors related to pain
• Establishment of a time frame for the pain and its course
(e.g., onset, precipitants, fluctuation over time, possible contributors
to fluctuations)
• Antecedents of pain flare-​ups
• Physical (e.g., excessive physical activity, specific movements)
• Psychological/​situational (e.g., general stress, insomnia)
• Consequences of pain flare-​ups
• Physical (e.g., inability to engage in certain movements)
• Behavioral/​psychological/​social (e.g., going for massage therapy,
irritability, others offering to help, changes in routines, changes
in mood)
• Comorbidities
• Physical (e.g., coronary heart disease)
• Psychological (e.g., major depression, post-​traumatic stress
disorder)
• Litigation/​compensation issues
• Coping/​pain management efforts
• Physical (e.g., using over-​the-​counter medication, application of
heat or cold)
• Psychosocial (e.g., distraction, trying to stay busy with friends,
coping self-​statements)
• History and lifestyle factors
• Personal history
• Current stressors
• Educational/​occupational history
• Brief health history
• Current social supports
• Hobbies, exercise habits, health-​promoting behaviors
• Substance use
• Goals/​plans for the future
• Past and current treatment history
• Past history of psychological problems
• Client goals, concerns and expectations about therapy
Note: This list of clinical interview domains is not meant to be exhaustive
but only intended to highlight key domains that are typically covered dur-
ing an interview with a pain patient.
Source: From Hadjistavropoulos, T. (2015). Pain assessment and manage-
ment in older adults. In P. A. Lichtenberg & B. T. Mast (Eds.), APA hand-
book of clinical geropsychology (pp. 413–​439). Washington, DC: American
Psychological Association. Reproduced with permission.
can play a key role in the determination of pain-​related
Diagnostic and Statistical Manual of Mental Disorders,
fifth edition (DSM-​5; American Psychiatric Association
[APA], 2013) diagnoses as well as mental health comor-
bidities that may accompany pain. Finally, evaluation of
disability and quality of life can also be a key component
of the psychological assessment of the person with pain.
The DSM-​5 diagnostic approach has changed sub-
stantially from the previous edition of the DSM system
(DSM-​IV-​TR; APA, 2000), with better recognition that
the physical and psychological elements of pain are
integrated. That is, compared to previous editions of the
DSM system, the DSM-​5 appropriately does not encour-
age separate estimation of the physical and psychological
components of pain. Specifically, in the DSM-​5, somatic
symptom disorder replaced somatization symptom dis-
order, undifferentiated somatoform disorder, and pain
disorder, although some people with pain can still be
diagnosed with psychological factors affecting other medi-
cal conditions.
To be diagnosed with somatic symptom disorder, an
individual must present with somatic symptoms that are
either very distressing or cause a significant disruption
in functioning as well as disproportionate cognitive and
emotional reactions. These problems must be persistent
(typically more than 6  months) for the diagnosis to be
made. The somatic symptoms need not be “physically
unexplained” for the diagnosis. That is, a physician’s
report indicating the “physically unexplained” nature of
the symptoms would not be necessary to support such a
diagnosis.
To facilitate determination of pain qualities, temporal
characteristics, extent of the disruption in functioning,
and the severity of the cognitive and emotional sequelae
of pain, a variety of psychometric tools can complement
information from the clinical interview. Before discuss-
ing specific tools within these content categories, we
briefly describe the West Haven–​Yale Multidimensional
Pain Inventory (MPI; Kerns, Turk, & Rudy, 1985). This
multidimensional tool, developed within a cognitive–​
behavioral framework, covers many domains of function-
ing. It includes 52 items and yields 12 specific subscales.
Individual item responses can range from 0 (i.e., not at
all or never) to 6 (i.e., yes, very much, or very frequently).
Higher scores indicate worse outcomes for some of the
scales (e.g., pain interference, negative mood, and pun-
ishing responses) and better outcomes for other scales
(e.g., perceived life control and distracting responses).
Although we discuss the MPI in more detail in the follow-
ing section, given the relevance of the MPI in case con-
ceptualization, we note here that there are three sections
of the MPI. The first MPI section covers pain intensity,
pain-​related interference with activity, perception of life
control, affective distress, and social support. The second
section evaluates the person’s perceptions of significant
others’ responses to the pain and the extent to which
these responses are punishing, solicitous, or distracting.
The third section provides information about the ability
to engage in household chores, outdoor activities, activi-
ties away from home, and social activities. Data from the
MPI can make significant contributions to the diagnostic
 Chronic Pain in Adults 611

TABLE 27.2   Ratings of Instruments Used for Diagnosis

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Brief Pain Inventory–​Short Form A G NA A A G E A ✓

McGill Pain Questionnaire A A NA A E G E G ✓
Short-​Form McGill Pain A A NA A E G E G
Questionnaire
Medical Outcomes Study 36-​Item E G NA A A G E A
Short-​Form Health Survey
Neuropathic Pain Scale A A NA A A A A A
Pain Catastrophizing Scale G G NA A A E E G ✓
Pain Diary A NA NA A NA G E A
Pain Patient Profile G G NA A A A A G
Roland–​Morris Disability A G NA A A G G A
Questionnaire
West Haven–​Yale Multidimensional A G NA A A G G E ✓
Pain Inventory
Western Ontario and McMaster E G NA A G G E A
Osteoarthritis Index

Note: A = Adequate; G = Good; E = Excellent; NA = Not Applicable.

conceptualization because most diagnostic pain assess-
ments include evaluations of pain intensity, pain-​related
interference with functioning, as well as frequency, dura-
tion, and severity of pain complaints, and most of these
dimensions, albeit not all, are covered by the MPI.
Table 27.2 provides psychometric information on the
MPI and other assessment tools that can facilitate diagno-
sis. It is noted that there is a certain degree of subjectivity
when evaluating psychometric dimensions of assessment
tools on the psychometric tables included in this chap-
ter. As such, it is possible that other raters might make
somewhat different determinations. We recommend that
clinicians consult the literature to make their own final
judgments.
Pain Intensity, Interference, Temporal
Characteristics, and Pain Qualities
Very brief, single-​item rating tools can be used for assess-
ment of pain intensity and interference. These tools may
be most suitable for monitoring of treatment progress and
are reviewed in the following section. In this section, we
focus on more comprehensive tools.
The Brief Pain Inventory (BPI; Cleeland, 1989, 1990,
1991; Cleeland & Ryan, 1994)  is a widely used clinical
tool that covers several dimensions. It is available in both
long (BPI) and short (BPI-​SF) forms (Cleeland, 2009).
The BPI comprises 32 items assessing pain intensity and
pain interference (tapping dimensions such as general
activity, mood, enjoyment of life, sleep, and work) during
the past week. In addition to several descriptive questions,
the BPI includes an item about the respondent’s pain that
day, a drawing of the human body (for marking the areas
corresponding to the respondent’s pain), and open-​ended
questions about pain treatments as well as potential con-
tributors to pain.
The BPI-​SF, which is composed of nine items and
usually takes less than 5 minutes to complete, is more
widely used in clinical and research settings compared
to the BPI, and most psychometric evaluations of the
instrument have involved the short form of the tool rather
than the long form (Cleeland, 2009). Compared to the
BPI, the BPI-​SF does not include additional descriptive
questions (other than the item on pain relief treatment
or medication), and it assesses pain in the past 24 hours
rather than in the past week (Cleeland, 2009). Internal
consistency for scores on the BPI-​ SF pain intensity
and pain interference scales ranges from good to excel-
lent (e.g., Kapstad, Rokne, & Stavem, 2010). BPI-​SF
norms are available for both patients with cancer pain
and patients with chronic non-​cancer pain (e.g., Hølen,
Lydersen, Klepstad, Loge, & Kaasa, 2008). The tool has
been validated with a variety of pain patient populations
(e.g., cancer, fibromyalgia, neuromuscular pain, neuro-
pathic pain, osteoarthritis, and surgical and procedural
pain; Cleeland, 2009). The construct validity of the BPI-​
SF is also well supported (e.g., Kapstad et  al., 2010).
A two-​factor structure of the tool has been demonstrated
across several studies (i.e., pain intensity and pain inter-
ference; Cleeland, 2009), with evidence for a three-​factor
612 Health-Related Problems
structure for the BPI found in one study (i.e., pain inten-
sity, activity interference, and affective interference;
Atkinson et al., 2011).
Pain diaries can also be used to collect additional
information about the duration and frequency of pain and
pain-​related exacerbations. Pain diaries, paper or elec-
tronic, can be used to evaluate pain fluctuations to deter-
mine if a person meets such criteria as recurrent pain,
chronic pain, or breakthrough pain (i.e., transitory flare-​
ups of pain during pain management therapy; Portenoy &
Hagen, 1990). Pain ratings obtained through pain diaries
appear to have adequate validity (e.g., they are responsive
to the effects of pain treatments, correlate with measures
of recalled averaged pain, and show adequate variance;
see Jensen & Karoly, 2011). Data collected from elec-
tronic and paper versions of pain diaries are comparable
in assessing pain (e.g., Jamison et al., 2001). Drawbacks
associated with pain diaries can include respondent bur-
den, missing data, and biased sampling (Jensen, 2010).
As indicated previously, psychological assessment data
could inform diagnoses made by physicians. For example,
tools such as the Neuropathic Pain Scale (NPS; Galer &
Jensen, 1997) are designed to help diagnose neuropathic
pain (i.e., pain due to nervous system damage), and ques-
tionnaires such as the McGill Pain Questionnaire (MPQ;
Melzack, 1975)  could also clarify qualities of pain that
may be diagnostic.
The NPS comprises two global ratings (intensity and
unpleasantness), with specific ratings addressing the loca-
tion (deep or surface) and quality of the pain (sharp, hot,
dull, cold, sensitive, or itchy). One additional item que-
ries the temporal characteristics of the pain (constant
with intermittent increases, intermittent, or constant
with fluctuation). Rog, Nurmikko, Friede, and Young
(2007) reported satisfactory internal consistency and test–​
retest correlation coefficients for NPS scores. A series of
composite scores for the NPS have been proposed (i.e.,
NPS Composite Score [NPS 10], NPS Total Descriptor
Score [NPS  8], NPS Nonallodynic Score [NPS NA],
and NPS 4 Score [NPS 4]; Galer, Jensen, Ma, Davies, &
Rowbotham, 2002), although further validation of these
scores is needed. The NPS items have been shown to
discriminate between different types of neuropathic pain
conditions. Galer and Jensen (1997) found, for example,
that compared to patients with other specific neuropathic
pain conditions, patients with post-​ herpetic neuralgia
described their pain as significantly sharper, more sensi-
tive, itchier, and less cold. Fishbain and colleagues (2008)
have also reported initial evidence that the NPS can dis-
criminate between neuropathic and non-​ neuropathic
pain conditions. In addition, the NPS has been shown
to detect changes in pain due to treatment effects (e.g.,
Jensen et al., 2005).
The MPQ is commonly used to assess specific qualities
of the pain that may have diagnostic value. It comprises 78
pain descriptors corresponding to four dimensions:  sen-
sory (e.g., burning and tingling), affective (e.g., terrifying
and vicious), evaluative (e.g., annoying and intense), and
miscellaneous (e.g., tight and squeezing). Categories of
two to six pain descriptors (e.g., “tender, taut, rasping,
splitting” and “tiring, exhausting”) make up the 20 sub-
classes, with each corresponding to one of the four dimen-
sions. A pain rating index is calculated based on the sum
of the rank values of each word (determined by each
word’s position within its category). The number of words
chosen also represents an MPQ index, as does the num-
ber of word categories endorsed. In addition, respondents
rate the present intensity of their pain on a 0 to 5 scale
and mark their pain sites on a human drawing. Patients
with similar pain conditions consistently choose similar
pain-​related words (e.g., Dubuisson & Melzack, 1976;
Graham, Bond, Gerkovitch, & Cook, 1980), and the
MPQ has strong discriminative capacity across pain con-
ditions (Katz & Melzack, 2011). Test–​retest stability for
the MPQ is difficult to estimate given that many types of
pain tend to fluctuate over time (Katz & Melzack, 2011);
however, Roche, Klestov, and Heim (2003) indicated that
MPQ scores did not significantly change over a 6-​year
period in patients with rheumatoid arthritis. With some
inconsistencies in the literature (see Katz & Melzack,
2011), the three-​factor structure (i.e., sensory, affective,
and evaluative) of the MPQ words has been confirmed in
a number of well-​conducted studies (e.g., Lowe, Walker,
& McCallum, 1991; Turk, Rudy, & Salovey, 1985).
A short version of the MPQ (SF-​ MPQ; Melzack,
1987)  is also available. The tool consists of 15 descrip-
tors (e.g., fearful, aching, and heavy) rated on a 4-​point
scale ranging from “none” to “severe.” With few excep-
tions, a two-​factor structure of the SF-​MPQ (i.e., sensory
and affective) has been confirmed (e.g., Beattie, Dowda,
& Feuerstein, 2004). Similar to the MPQ, the SF-​MPQ
has been shown to contribute to formulating a diagnosis.
Droz and Howard (2011) demonstrated, for example, that
certain MPQ items had diagnostic value in excluding
(but not predicting) pelvic pain-​related diagnoses. That is,
the descriptors “cramping,” “aching,” and “hot-​burning”
could provide evidence that could  aid in the  ruling out
of certain diagnoses such as endometriosis. Another ver-
sion of the tool, the SF-​MPQ-​2 (Dworkin et  al., 2009),
is an expanded and revised version of the SF-​MPQ. The

expansion involved the addition of 7 descriptors that cap-
ture the qualities of neuropathic pain (i.e., dull, electric-​
shock, cold-​freezing, pain caused by light touch, itching,
tingling or pins and needles, and numbness) to the 15
descriptors of non-​neuropathic pain included in the SF-​
MPQ. The descriptors are rated on an 11-​point numeric
rating scale, with “none” and “worst possible” labels at
opposite ends of the scale. Dworkin and colleagues dem-
onstrated that the SF-​MPQ-​2 scores were highly reliable
and valid, with a four-​factor solution being supported (i.e.,
continuous pain, intermittent pain, predominantly neu-
ropathic pain, and affective descriptors). Dworkin et  al.
suggested that the tool can contribute to discrimination
between neuropathic and non-​neuropathic pain.
Emotional Distress and Catastrophic Thinking
Assessment of possible psychological comorbidities (e.g.,
depression) is important, and the assessment approaches
described in other chapters in this volume for such
comorbidities should be used. Moreover, in order to make
a diagnosis of somatic symptom disorder, it is important
to demonstrate that emotional distress and beliefs that
accompany pain are excessive or exaggerated. Measures
of emotional functioning tapping into depression, anxiety,
and related dimensions are typically valuable (e.g., the
Beck Depression Inventory-​II [BDI-​II; Beck, Steer, Ball,
& Ranieri, 1996] and the Profile of Mood States [POMS;
McNair, Lorr, & Droppleman, 1971]). Because the BDI-​
II and the POMS are not specifically developed for assess-
ing people experiencing pain, they are not reviewed in
this chapter. Of note, norms for individuals with chronic
pain are available for the BDI-​II (e.g., Harris & D’Eon,
2008). Clinicians should be aware that the inclusion of
somatic items in some tools, including the BDI-​II, could
lead to artificially inflated scores in patients who have
somatic symptoms due to causes unrelated to depression
or other psychological disorders.
The Pain Patient Profile (P3; Tollison & Langley,
1995) is a 44-​item measure designed to identify emotional
distress associated with pain through a depression scale,
an anxiety scale, and a somatization scale. Factor ana-
lytic research has not supported this three-​factor structure
(McGuire, Hogan, & Morrison, 2008), but more research
is needed before a final conclusion can be reached on
this point. The P3 includes a validity scale to assess for
random responding, reading comprehension problems,
and magnification of symptoms (e.g., McGuire, Harvey,
& Shores, 2001; McGuire & Shores, 2001). The tool
could potentially assist in the detection of malingering in
Chronic Pain in Adults 613
clinical pain settings, although the assessment of malin-
gering represents a complicated and controversial area of
practice. Construct validity support for the P3 has been
provided (Willoughby, Hailey, & Wheeler, 1999), but the
extent of the research literature is limited.
The Pain Catastrophizing Scale (PCS; Sullivan,
Bishop, & Pivik, 1995) may be useful in determining the
extent to which responses to pain are excessive and exag-
gerated. The PCS, aimed at assessing catastrophic beliefs
related to pain, is a 13-​item instrument that taps into three
dimensions of pain catastrophizing: rumination, helpless-
ness, and magnification (Sullivan, 2009; Sullivan et  al.,
1995). The total and subscale scores have been found to
be internally consistent (Sullivan, 2009). The three-​factor
structure of the PCS has received research support across
clinical and nonclinical populations (e.g., Van Damme,
Crombez, Bijttebier, Goubert, & Van Houdenhove,
2002); a two-​factor structure of the PCS (i.e., rumination
and powerlessness; Chibnall & Tait, 2005) was found to
be the best fit when administered to an ethnically diverse
subsample, but these findings require additional confir-
mation (DeGood & Cook, 2011). High scores on the PCS
have been associated with a variety of negative outcomes,
including more intense pain, disability, depression, and
anxiety; more prolonged hospital stays; and increased use
of analgesic medication (Sullivan, 2009).
Measures of illness-​ related worry (e.g., the Revised
Illness Perception Questionnaire [IPQ-​ R]; Moss-​ Morris
et  al., 2002)  can also be helpful in assessing the person
with pain. The IPQ-​R and its subscales have been normed
for acute and chronic pain patients (Moss-​Morris et  al.,
2002). Scores indicative of significantly elevated emotional
distress (compared to norms derived of patients with simi-
lar chronic pain problems) would provide evidence that
is consistent with a somatic symptom disorder diagnosis.
As indicated previously, another pain-​related DSM-​5
diagnosis is psychological factors affecting other medi-
cal conditions. According to the DSM-​5, the psychologi-
cal factors in this diagnosis are not necessarily excessive
and a diagnosed medical condition is normally present,
so the clinician can determine whether psychological
factors have significant clinical effects on the pain con-
dition. For example, if anxiety and psychological stress
are present, based on pain diaries (discussed previously)
and other clinical information, a psychologist may deter-
mine that stress may precipitate migraine headaches. This
DSM-​5 diagnosis would be appropriate under such cir-
cumstances. The specific assessment tools to evaluate the
intensity of psychological contributors to pain would vary
as a function of the type of contributor.
614 Health-Related Problems

Disability and Quality of Life The WOMAC is a 24-​item self-​report tool developed
for use among patients with osteoarthritis of their lower
A pain assessment can often involve a determination of
extremity (i.e., hips and knees). It comprises three dimen-
disability and an evaluation of quality of life. Although the
sions:  pain, stiffness, and physical function. A  recent
determination of disability is frequently based on func-
systematic review of the WOMAC showed acceptable
tional assessments conducted by physiotherapists, certain
internal consistency for scores on the pain and stiffness
self-​report tools, including the BPI and the MPI (dis-
scales and excellent internal consistency for scores on the
cussed previously), can be used by patients to self-​report
physical function scale (Gandek, 2015). Test–​retest sta-
impairment on a variety of domains.
bility for scores on the scales has been acceptable for a
A more general measure of quality of life, the Medical
period of up to 3 weeks (Gandek, 2015), although scores
Outcomes Study 36-​Item Short-​Form Health Survey (SF-​
on the stiffness scale have demonstrated below accept-
36; Ware & Sherbourne, 1992), yields subscale scores in
able test–​retest reliability (e.g., Jinks, Jordan, & Croft,
the areas of Physical Functioning, Social Functioning,
2002). The validity of the WOMAC is well supported
Role–​ Physical, Role–​Emotional, Bodily Pain, General
(e.g., Bellamy et  al., 1988a, 1998b; Gandek, 2015), and
Health, Vitality, and Mental Health. This measure can
WOMAC scores are responsive to changes over time
be completed through self-​report or administered by a
(e.g., Kapstad et al., 2010; O’Connor & Dworkin, 2011;
trained interviewer. With few exceptions, internal consis-
Ostendorf et al., 2004). For the most part, the WOMAC
tency estimates for the SF-​36 subscale scores range from
and RMDQ have been found to be more sensitive to
good to excellent (Ware & Gandek, 1998). Test–​retest cor-
change than generic health-​related quality of life instru-
relations vary across subscales, with most subscale scores
ments for patients with a specific pain-​related condition
associated with values of at least .70 over a period of sev-
(O’Connor & Dworkin, 2011).
eral days to several weeks (e.g., Marx, Menezes, Horovitz,
Jones, & Warren, 2003). The SF-​36 has been validated
and normed for use across multiple countries and among Malingering
diverse socioeconomic groups (e.g., Gandek, Sinclair,
Clinicians may be asked to evaluate the possibility that
Kosinski, & Ware, 2004; Hopman et  al., 2000; Turner-​
a patient is malingering. This is a highly controversial
Bowker, Bartley, & Ware, 2002; Wagner et al., 1998; Ware
assessment task given the significant limitations of assess-
& Gandek, 1998).
ment instruments, the difficulty in identifying criterion
groups to conduct relevant research, and the lack of con-
Condition-​Specific Measures clusive evidence differentiating psychological profiles of
The Roland–​Morris Disability Questionnaire (RMDQ; litigation/​compensation patients and patients not involved
Roland & Morris, 1983)  and the Western Ontario and in litigation (Turk & Robinson, 2011). Generally, clini-
McMaster Osteoarthritis Index (WOMAC; Bellamy, cians addressing questions related to malingering and sec-
Buchanan, Goldsmith, Campbell, & Stitt, 1988a, ondary gain rely on a variety of sources of information,
1988b) are examples of condition-​specific measures. The including previous history, collateral sources of informa-
RMDQ is a 24-​item self-​report measure designed specifi- tion, performance on tasks of physical functioning, medi-
cally for the assessment of daily life activities in back pain cal reports, observations during the interview and in other
patients through a yes/​no response format (e.g., “Because unobtrusive situations, self-​ reports, and validity scales
of my back pain, I am not doing any of the jobs that I usu- of tools such as the Minnesota Multiphasic Personality
ally do around the house”). There is evidence that the Inventory-​2 (MMPI-​ 2 ; Butcher, Dahlstrom, Graham,
scores on the measure have good internal consistency Tellegen, & Kaemmer, 1989) and MMPI-​ 2–​Restructured
(e.g., Hsieh, Philips, Adams, & Pope, 1992), with the Form (MMPI-​ 2 -​
R F; Ben-​
P orath & Tellegen, 2008;
construct validity of scores being supported by associa- Tellegen & Ben-​P orath, 2008), with each of these sources
tions with measures of disability, physical function, and of information contributing to conclusions about the
pain ratings (Roland & Fairbank, 2000). However, the credibility of the report (Turk & Robinson, 2011). Given
extent to which the construct that is being measured is the risk of false positives and false negatives resulting from
unidimensional or multidimensional has not been defini- these types of assessments and the potentially devastat-
tively determined (e.g., Grotle, Wilkens, Garratt, Scheel, ing consequences of incorrect conclusions, clinicians are
& Storheim, 2013; Magnussen, Lygren, Strand, Hagen, advised to approach these types of assessments with a great
& Breivik, 2015). deal of caution.
 Chronic Pain in Adults 615

Overall Evaluation key dimensions of functioning (see Table 27.1). Of these

dimensions, affective distress, social support, pain descrip-
The diagnosis of pain-​related conditions (e.g., osteoar-
tors, and functional capability are believed to be central
thritis and sacroiliac joint dysfunction) falls outside the
in assessing chronic pain (Mikail, DuBreuil, & D’Eon,
scope of psychological practice. Formulating the DSM-​5
1993). In addition, behavioral observations noted dur-
diagnoses of somatic symptom disorder and psychologi-
ing the interview (e.g., demonstrative pain behaviors or
cal factors affecting other medical conditions, however,
a defensive interactional style) may also be useful for
does fall within the scope of psychological practice and
case conceptualization purposes. Although standardized
can be aided with various tools designed to evaluate the
observational systems have been developed and applied
extent to which pain-​related distress is excessive or exag-
in research studies for conditions such as low back pain
gerated, especially when interpreted within the context
(e.g., Keefe, Somers, Williams, & Smith, 2011), more
of norms for patients with comparable pain conditions.
work is needed before such systems can be used systemati-
When used in the context of multidisciplinary teams, an
cally and routinely as part of the clinical assessment of the
array of psychometrically strong questionnaires can be
chronic pain patient (e.g., developing norms for specific
used in facilitating diagnoses (e.g., neuropathic pain).
patient groups).
Generally, these tools (e.g., the NPS) focus on the assess-
Prior to discussing tools designed to assess key dimen-
ment of pain qualities. Diagnostic assessments also focus
sions for case conceptualization and treatment planning,
on the determination of disability, which can be assessed
we return to the MPI. As indicated in the section on diag-
with a variety of self-​report instruments (e.g., the RMDQ).
nosis, the first section of the 52-​item MPI yields infor-
Ideally, however, results obtained with these tools should
mation about pain intensity/​ interference and affective
be considered within the context of multidisciplinary
distress, and the third section contains subscales capturing
assessments that include clinical interviews, medical
engagement in household chores, outdoor activity, and
examinations, and functional capacity evaluations. Given
social activity. It is important to also note that in the sec-
the subjectivity involved in the experience of pain, clini-
ond section, the MPI provides information on significant
cians are frequently called upon to provide an opinion
other support and responses from significant others (nega-
about the likelihood that a pain patient may be malinger-
tive, solicitous, and distracting) that is critical for case
ing. Such determinations concerning malingering can be
conceptualization. Numerous studies have supported the
highly controversial given the high rate of false positives
validity and reliability of the scores on this part of the tool
and false negatives of existing assessment approaches.
(e.g., Kerns et al., 1985; Turk & Rudy, 1988). Given the
Finally, although the tests selected would vary depending
wide range of psychosocial issues assessed by the tool, it is
on the patient, clinician, and circumstances of the assess-
especially good for case conceptualization. Importantly,
ment (e.g., referral question and whether neuropathic
based on a cluster analysis of the scores of the scales,
pain is suspected), a suitable brief battery might consist
Turk and Rudy (1988, 1990)  identified and then cross-​
of the BPI and brief tools designed to assess psychological
validated three unique profiles or subgroups for patients
responses to pain (e.g., a depression and anxiety scale).
with chronic pain that they labeled as dysfunctional (high
The BPI, combined with such brief tools, would tap pain
scores on pain severity, life interference, and emotional
intensity, pain-​related interference/​disability, and psycho-
distress, but low scores on perceived control and activity),
logical distress that accompanies pain. The MPI is also a
interpersonally distressed (low levels of social support in
useful multidimensional tool, but it is relatively long and
addition to the aspects that comprise the dysfunctional
involves more complex scoring. For this reason, we tend to
profile), and minimizers/​adaptive copers (low levels of
use the MPI as part of more comprehensive assessments.
pain, interference, and distress, but high levels of life con-
trol and activity). Patients classified as having a dysfunc-
tional profile, for example, displayed more pain behaviors,
ASSESSMENT FOR CASE CONCEPTUALIZATION consumed more analgesic medication, spent more time in
AND TREATMENT PLANNING bed, and were more likely to be unemployed compared to
patients with other profiles. Patients in the dysfunctional
A presenting pain condition must be conceptualized and interpersonally distressed groups showed more non-
within the overall context of a patient’s life circum- verbal pain behavior compared to those in the adaptive
stances. As such, a comprehensive assessment should coping group. Overall, patients classified as interperson-
include a detailed clinical interview tapping across all ally distressed are considered to have the greatest need for
616 Health-Related Problems

TABLE 27.3   Ratings of Instruments Used for Case Conceptualization and Treatment Planning

Internal Inter-​Rater Test–​Retest Content Construct Validity Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Utility Recommended

Chronic Pain Coping Inventory G G NA A A G E A

Chronic Pain Coping Inventory-​42 G A NA A A G G A
Coping Strategies Questionnaire A A NA A A G E A ✓
Fear-​Avoidance Beliefs A G NA A A E A A
Questionnaire
Pain Anxiety Symptoms Scale G G NA A A E G A ✓
Pain Anxiety Symptoms Scale-​20 G G NA A A G G A ✓
Pain Beliefs and Perceptions A A NA A A G A A
Inventory
Pain Beliefs Questionnaire G A NA A A A A A
Pain Catastrophizing Scale G G NA A A E E G ✓
Pain Diary A NA NA A NA G E A ✓
West Haven–​Yale Multidimensional A G NA A A G G E ✓
Pain Inventory
Tampa Scale of Kinesiophobia A A NA A A G A A
Tampa Scale of Kinesiophobia-​11 A A NA A A G A A

Note: A = Adequate; G = Good; E = Excellent; NA = Not Applicable.

psychological treatment (e.g., Turk, Okifuji, Sinclair, &
Starz, 2005; Verra et al., 2012). This type of multidimen-
sional classification has been supported in the literature
and can help clinicians tailor treatment strategies (e.g.,
Verra et al., 2012).
A 61-​item version with modified instructions (MPI-​
M; Okifuji, Turk, & Eveleigh, 1999), which specifies the
meaning of the term “significant other,” is also available.
The MPI-​M has been demonstrated to improve upon the
accuracy of classifying respondents into one of the three
primary subgroups (Okifuji, Turk, & Everleigh, 1999).
Nonetheless, Broderick, Junghaenel, and Turk (2004)
characterized the classifications as state-​like rather than
trait-​like because these classifications did not appear to be
stable across time. Supporting Broderick et  al.’s conclu-
sion, McKillop and Nielson (2011) also found evidence of
MPI profile instability among some of their participants.
Table 27.3 summarizes psychometric information on the
MPI and other tools that can be used for case conceptual-
ization and treatment planning.
Integrating Assessment Information Obtained
for Diagnostic Purposes
conceptualization and treatment planning (e.g., psycho-
logical comorbidities would point toward specific treat-
ment directions). To best conceptualize the pain and to
plan psychological treatment, a good understanding of
the diagnosis, the antecedents and consequences of pain,
coping strategies (including avoidance), client expecta-
tions, fluctuations in the pain, the impact of the social
environment, and extent of catastrophic and other cogni-
tions/​beliefs about pain, as well as anxiety, depression, and
related comorbidities, is needed.
Antecedents, Consequences, and Temporal Patterns
Diaries can be used to collect information about temporal
patterns as well as the antecedents and consequences of
the pain experience. Knowledge derived from these dia-
ries could guide treatment planning by pointing toward
psychosocial and other contributors to pain exacerbations
(e.g., stress or use of a particular chair). Important conse-
quences of the pain condition could also be identified and
represent potential targets of treatment (e.g., solicitous
encouragement by family to avoid potentially beneficial
physical activity).

The assessment for case conceptualization will build

upon the results of the diagnostic assessment. The diag-
nosis, along with a better understanding of the extent
of disability, overall quality of life, pain intensity, pain
qualities, and the like, will play a key role in the case
Pain-​Related Cognitions/​Beliefs
Cognitions and beliefs that may exacerbate the pain con-
dition and have potential implications for outcome should
also be assessed. A key dimension is catastrophic thinking
 Chronic Pain in Adults 617

about pain, which is a predictor of a variety of negative Coping Strategies

outcomes. For example, pain-​related catastrophizing has
Coping strategies can be influential with regard to pain-​
been shown to predict disability even after controlling for
related disability and outcomes. Generally, diverting atten-
pain intensity, depression, and anxiety (Sullivan & Neish,
tion, reinterpreting sensations, and coping self-​statements
1998). As such, the PCS would be especially useful for
have been found to be positively related to adjustment,
case conceptualization.
whereas praying and hoping have been found to be asso-
In addition to catastrophizing, other types of mal-
ciated with poorer adjustment (e.g., Ashby & Lenhart,
adaptive pain beliefs have been implicated in pain
1994; DeGood & Cook, 2011).
and chronicity (e.g., Geisser, Robinson, & Riley, 1999;
The Coping Strategies Questionnaire (CSQ;
Jensen & Karoly, 1992; Lamé, Peters, Vlaeyen, Kleef, &
Rosentiel & Keefe, 1983) is a 48-​item self-​report question-
Patijn, 2005). The 16-​item Pain Beliefs and Perceptions
naire that is based on a cognitive–​behavioral framework.
Inventory (PBAPI; Williams & Thorn, 1989) can be a use-
It includes both cognitive (diverting attention, reinterpret-
ful instrument for the evaluation of such beliefs. Although
ing pain sensations, coping self-​statements, ignoring pain
William and Thorn initially proposed that the tool is com-
sensations, praying or hoping, and catastrophizing) and
posed of three factors representing time, mystery (e.g.,
behavioral (increasing activity) coping strategies. The
“I don’t know enough about my pain”), and self-​blame
CSQ also includes two additional items assessing the
(e.g., “I am the cause of my pain”), other investigators
respondents’ perceived ability to control or decrease their
(Herda, Siegeris, & Basler, 1994; Morley & Wilkinson,
pain. Rosentiel and Keefe (1983) reported that, with the
1995) have reported results that support the splitting of the
exception of the increasing pain behaviors subscale, all
time factor into two parts: time constancy (e.g., “It seems
subscales yielded scores that had satisfactory internal con-
like I  wake up with pain and I  go to sleep with pain”)
sistencies. Both five-​factor (Swartzman, Gwadry, Shapiro
and time permanency (e.g., “My pain is here to stay”).
& Teasell, 1994; Tuttle, Shutty, & DeGood, 1991) and six
Beyond the United States, where the tool was developed
factor structures (Riley & Robinson, 1997; Robinson et al.,
(Williams, Robinson, & Geisser, 1994), scores on the
1997) for the CSQ have been supported. Shorter, revised
PBAPI have been validated in several countries, including
versions—​the CSQ-​R (Riley & Robinson, 1997) and the
England (Morley & Wilkinson, 1995), Germany (Herda
CSQ 24 (Harland & Georgieff, 2003)—​have also been
et al., 1994), and Norway (Dysvik, Lindstrøm, Eikeland,
developed, with initial support for their psychometric
& Natvig, 2004). Most investigations have provided con-
properties (e.g., DeGood & Cook, 2011). The shorter
struct validity support for the PBAPI (Williams & Keefe,
versions, however, have not been evaluated as much as
1991; Williams & Thorn, 1989; Williams et  al., 1994),
the original version.
although the mystery subscale has been described as
The Chronic Pain Coping Inventory (CPCI; Jensen,
being similar to the construct of catastrophizing (DeGood
Turner, Romano, & Strom, 1995)  is an alternative to
& Cook, 2011). Moreover, low internal consistency val-
the CSQ and was developed to assess behavioral coping
ues for scores on the mystery subscale have been reported
dimensions often targeted for change in multidisciplinary
(Dysvik et al., 2004).
pain treatment. The CPCI, available in a self-​report ver-
The Pain Beliefs Questionnaire (PBQ; Edwards,
sion as well as a significant-​other version, consists of 65
Pearce, Turner-​ Stokes, & Jones, 1992)  assesses beliefs
items and has the following eight subscales:  guarding,
about the cause and treatment of pain. Respondents rate
resting, asking for assistance, relaxation, task persistence,
how much they agree (ranging from “always” to “never”)
exercise/​stretch, coping self-​statements, and seeking social
with 20 statements. Factor analytic investigations have
supports. Respondents report the frequency with which
confirmed that the questionnaire is composed of two
they have used various strategies to cope with pain during
scales: Organic Beliefs (e.g., “Persistent pain is the result of
the past week. An additional pacing scale has been devel-
damage to tissues of the body”) and Psychological Beliefs
oped for use with the CPCI (Nielson, Jensen, & Hill,
(“Being anxious makes persistent pain worse”; Edwards
2001) and, when used, increases the length of the scale
et  al., 1992). Scores on these scales have been demon-
by 6 items (DeGood & Cook, 2011). Internal consistency
strated to have adequate internal consistency (Walsh &
values for scores for each of the CPCI subscales, includ-
Radcliffe, 2002). Some construct validity support has also
ing the additional pacing scale, range from adequate to
been presented in the research literature (e.g., Baird &
excellent (e.g., Jensen et  al., 1995; Nielson et  al., 2001;
Haslam, 2013; Walsh & Radcliffe, 2002).
618 Health-Related Problems

Romano, Jensen, & Turner, 2003). Test–​retest correla- four subscales:  fearful appraisal of pain, cognitive anxi-
tions for scores on these subscales range from .60 to .90 ety, physiological symptoms, and escape and avoidance
over periods of 2 weeks to 1 month (Jensen et al., 1995; behavior. Internal consistency for scores on each of the
Romano et al., 2003). Over a period of several weeks to four PASS subscales ranges from adequate to good, and
several months, however, Nielson et  al. reported lower for the PASS total score, it is excellent (McCracken &
levels of stability for scores on the CPCI, with test–​retestDhingra, 2002). Factor analytic investigations have pro-
correlations ranging from .47 to .78. vided support for a four-​factor (Osman, Barrios, Osman,
Norms for the CPCI are available for chronic non-​ Schneekloth, & Troutman, 1994) and five-​factor (Larsen,
cancer pain populations (e.g., Jensen et  al., 1995; Taylor, & Asmundson, 1997)  structure. Evidence for
Romano et al., 2003; Truchon & Côté, 2005), but more construct validity is provided by significant correlations
research investigating the use of the CPCI among specific between the PASS and measures of anxiety, disability,
pain populations (e.g., neuropathic, procedural, and sur- pain, and physical capacity (Burns, Mullen, Hidgon,
gical procedures) is warranted. Factor analytic investiga- Wei, & Lansky, 2000; McCracken & Dhingra, 2002;
tions (Hadjistavropoulos, MacLeod, & Asmundson, 1999; McCracken, Gross, Aikens, & Carnrike, 1996). Two
Jensen et  al., 1995; Tan, Nguyen, Anderson, Jensen, & other studies demonstrated the incremental validity of the
Thornby, 2005)  have confirmed the presence of the PASS over and above measures of pain severity, anxiety,
original eight CPCI subscales. Support for the CPCI’s depression, and emotional distress (Burns et  al., 2000;
construct validity has also been demonstrated through McCracken et al., 1992).
significant associations with other indices of coping strate- A 20-​item version of the PASS (PASS-​20; McCracken
gies, as well as with measures of functioning and disability & Dhingra, 2002), composed of the same four subscales
(Hadjistavropoulos et al., 1999; Jensen et al., 1995; Tan, of the PASS, is also available. Internal consistency for
Jensen, Robinson-​ Whelen, Thornby, & Monga, 2001; scores on each subscale generally ranges from adequate
Tan et  al., 2005; Truchon & Côté, 2005). A  42-​ item to good (e.g., Abrams, Carleton, & Admundson, 2007;
version of the tool, the CPCI-​42, is also available (e.g., McCracken & Dhingra, 2002), and the four-​factor struc-
Romano et  al., 2003). The CPCI-​42 has been normed ture has been confirmed (e.g., Abrams et  al., 2007).
among chronic non-​cancer pain populations (e.g., Ersek, Correlations between the PASS-​20 and the original ver-
Turner, & Kemp, 2006; Romano et al., 2003). Although sion provide construct validity support (McCracken
initial evidence for the validity of scores on the CPCI-​42 & Dhingra, 2002). Patterns of association between the
has been provided (Romano et al., 2003), more research PASS-​20 and relevant measures (e.g., pain, pain-​related
is warranted. anxiety/​fear, and anxiety) provide additional construct
validity support (Abrams et al., 2007).
The Tampa Scale of Kinesiophobia (TKS; Miller,
Pain-​Related Anxiety/​Avoidance
Kori, & Todd, 1991)  is a 17-​item measure for assessing
Many chronic pain patients display pain-​related fear and fear of movement (e.g., “It is really not safe for a person
avoidance that, when excessive, can interfere with recov- with a condition like mine to be physically active”) and
ery because it could lead patients to avoid potentially injury/​re-​injury (e.g., “Pain always means I have injured
beneficial activity (e.g., physiotherapy exercises) and my body”) in patients with a variety of musculoskeletal
activity that could enhance their psychological function- pain conditions. Internal consistency for TKS total scores
ing. Instruments assessing fear/​avoidance could facilitate is at least satisfactory (e.g., Roelofs, Goubert, Peters,
both case conceptualization and treatment planning. Vlaeyen, & Crombez, 2012; Swinkels-​Meewisse et  al.,
Regarding the latter, for example, exposure procedures 2003). Some studies have reported good test–​retest sta-
have been used with some success in overcoming pain-​ bility of scores on the TKS over a 24-​hour period (e.g.,
related fear and avoidance (e.g., Leeuw et al., 2008; Woods Swinkels-​Meewisse et al., 2003), although studies examin-
& Asmundson, 2008), although it is not certain whether ing a longer test–​retest period are needed. The tool has
the addition of exposure enhances outcomes within a also been validated for use among Swedish (Lundberg,
comprehensive multidisciplinary treatment program. Styf, & Carlsson, 2004)  and Dutch (Swinkels-​Meewisse
The Pain Anxiety Symptoms Scale (PASS; et  al., 2003)  populations. The TKS has been normed
McCracken, Zayfert, & Gross, 1992)  is a self-​ report for several chronic pain populations, including low
measure of pain-​related fear/​anxiety among persons with back pain and fibromyalgia (e.g., Roelofs et  al., 2012).
chronic pain conditions. The 40-​item measure includes Confirmatory factor analyses have provided evidence for

a two-​factor structure:  somatic focus (TKS-​SF), which
reflects a belief in underlying and serious medical prob-
lems, and the view that activity (TKS-​AA) may result in
(re)injury or increased pain (Clark, Kori, & Brockel,
1996). Low to moderate associations between the TKS
and measures of pain-​related constructs (e.g., intensity,
catastrophizing, and disability) provide construct validity
support (Swinkels-​Meewisse et  al., 2003; Woby, Roach,
Urmston, & Watson, 2005). Woby and colleagues, for
instance, demonstrated that after controlling for pain
intensity, reductions on the TKS predicted reductions in
disability. An 11-​item version of the TSK is also available
(TSK-​11; Woby et al., 2005) and has similar psychometric
properties to the original version (e.g., Tkachuk & Harris,
2012; Woby et al., 2005). Norms are available for general
and specific chronic pain populations (e.g., Tkachuk &
Harris, 2012; Walton & Elliott, 2013).
The Fear-​
Avoidance Beliefs Questionnaire
(FABQ; Waddell, Newton, Henderson, Somerville,
& Main, 1993)  is a 16-​item instrument that covers two
domains:  fear-​avoidance beliefs about work (e.g., “My
work makes or might make my pain worse”; FABQ-​W)
and fear-​avoidance beliefs about physical activity (e.g.,
“I should not do physical activities that might harm my
back”; FABQ-​PA). Scores for both subscales have been
found to have good internal consistency (Cleland et al.,
2008; Swinkels-​ Meewisse et  al., 2003; Waddell et  al.,
1993), and with some exceptions, the literature shows
test–​retest correlations of over .70 for a period of up to
several weeks (e.g., Inrig, Amey, Borthwick, & Beaton,
2012; Swinkels-​Meewisse et  al., 2003). Norms are avail-
able for injured workers (e.g., Inrig et al., 2012) and for
those referred to a medical clinic for low back pain (e.g.,
Swinkels-​Meewisse et al., 2003), neck pain (e.g., Cleland
et al., 2008), and shoulder pain (e.g., Mintken, Cleland,
Whitman, & George, 2010). Although several studies
have provided construct validity support for the FABQ
(e.g., Swinkels-​Meewisse et  al., 2003), construct validity
for the FABQ-​W has generally been more robust than that
of the FABQ-​PA (Cleland et al., 2008; Inrig et al., 2012;
Mintken et al., 2010). Evidence of this construct validity
support was based on associations with indices of dimen-
sions such as pain, disability, and days of work missed.
Overall Evaluation
The area of adult pain assessment is rich in measures that
can facilitate case conceptualization and treatment plan-
ning. Tools such as the CPCI, MPI, and PASS build upon
the information collected from the part of the assessment
Chronic Pain in Adults 619
intended to facilitate diagnosis. Coping strategies, pain-​
related beliefs and attitudes, social support/​ reactions,
pain-​related anxiety, and avoidance are all important to
assess for case conceptualization. Pain diaries have an
important role to play both in case conceptualization
(e.g., providing a better understanding of the antecedents
and consequences of a pain problem) and in treatment
monitoring. Information collected from assessment tools
must be contextualized, however, through information on
the circumstances of the individual patient that can be
obtained with clinical interviews.
ASSESSMENT FOR TREATMENT MONITORING
AND TREATMENT OUTCOME
Ongoing assessments of pain intensity, pain-​related dis-
ability, and affective symptoms/​psychological distress that
may accompany the pain experience are critical for treat-
ment monitoring and outcome evaluation. Brevity of tools
is important in order to minimize burden to the patient
when monitoring treatment progress. As such, unidimen-
sional pain intensity tools (e.g., a numeric 0–​10 scale) as
well as brief multidimensional tools (e.g., the BPI-​SF)
provide the most parsimonious assessment options for
ongoing monitoring.
Common unidimensional tools include numeric rat-
ing scales (NRS; e.g., an 11-​point scale, which ranges from
0 to 10 and is anchored by polar opposites such as “no
pain” and “extreme pain”), visual analogue scales (VAS;
e.g., a 10-​cm line anchored by similar polar opposites as
the NRS), and verbal rating scales (VRS; i.e., where spe-
cific words are used to describe pain intensity [e.g., “no
pain,” “mild pain,” “moderate pain,” and “severe pain”] or
pain unpleasantness [e.g., “not unpleasant,” “tolerable,”
“intolerable,” and “agonizing”]). The validity of these
tools has been demonstrated through correlations with
other pain measures and changes in response to treat-
ment (Jensen, Karoly, & Braver, 1986; Kremer, Atkinson,
& Ignelzi, 1981), although only the VAS appears to have
ratio measurement qualities, at least for group data (see
Jensen & Karoly, 2011). Most of these tools show at least
adequate sensitivity to change (e.g., Jensen & Karoly,
2011). Of note, some respondents, including some older
adults, have been shown to have difficulty with VAS com-
pletion (e.g., Gauthier & Gagliese, 2011; Jensen et  al.,
1986); in these cases, NRS and VRS may be more appro-
priate. Unidimensional tools, which can easily be used
at each session, can be supplemented with intermittent
administration of the BPI. The frequency of intermittent
620 Health-Related Problems

TABLE 27.4   Ratings of Instruments Used for Treatment Monitoring and Treatment Outcome Evaluation
Internal Inter-​Rater Test–​Retest Content Construct Validity Treatment Clinical Highly
Instrument Norms Consistency Reliability Reliability Validity Validity Generalization Sensitivity Utility Recommended

Brief Pain Inventory–​ A G NA A A G E G A ✓

Short Form
Medical Outcomes E G NA A A G E G A
Study 36-​Item
Short-​Form
Health Survey
Neuropathic Pain A A NA A A A A A A
Scale
Numeric Rating Scale G NA NA A A G E E E ✓
Pain Catastrophizing G G NA A A E E E G ✓
Scale
Pain Diary A NA NA A NA G E A A ✓
Verbal Rating Scale A NA NA A A G E A A
Visual Analogue A NA NA A A G E G G ✓
Scale
West Haven–​Yale A G NA A A G G G E ✓
Multidimensional
Pain Inventory

Note: A = Adequate; G = Good; E = Excellent; NA = Not Applicable.

administration should be determined based on the
expected duration of treatment (e.g., every 2 or 3 ses-
sions); generally, evaluated psychological treatment pro-
grams tend to range between 8 and 12 sessions (e.g., Kerns
et al., 2014; Trafton et al., 2012; Turner et al., 2016).
The BPI intensity and interference domains have
been recommended as outcome measures for clini-
cal trials involving pain by the Initiative for Methods,
Measurement and Pain Assessment in Clinical Trials
(IMMPACT) consensus panel (http://​www.immpact.
org; Turk et al., 2003). Given the brevity and comprehen-
siveness of the BPI-​SF, we also consider it to be a highly
recommended tool for ongoing evaluation, along with
ongoing use of pain diaries. In addition to pain intensity
and interference, the BPI-​SF provides an indication of
functional ability, affective distress, pain location, and
response to treatment. Depending on problem areas iden-
tified during the assessment, brief tools (e.g., BDI-​II) eval-
uating these areas (e.g., depression, anxiety, catastrophic
thinking, pain-​related anxiety, and avoidance) could also
be included intermittently, with the frequency deter-
mined based on the expected duration of the treatment.
In terms of a more comprehensive multidimensional tool,
the MPI is sensitive to change, but given its length, we are
more inclined to recommend it as an outcome measure
rather than as a tool for assessing progress on an ongo-
ing basis (e.g., Flavell, Carrafa, Thomsa, & Disler, 1996).
The MPI, and other tools that may be added depending
on the specific patient, can also be supplemented with a
pain-​related quality of life assessment (e.g., SF-​36). Data
from such measures can contribute to the evaluation of
the psychological component of the treatment and the
multidisciplinary treatment as a whole. Of course, deter-
mination of whether an individual meets diagnostic cri-
teria for the pain-​related DSM-​5 diagnoses would also be
of interest from a therapy outcome standpoint. This can
be accomplished, in part, with readministration of the
tools discussed in the diagnostic section. Table 27.4 sum-
marizes our assessment of the psychometric properties of
various tools that can be used for the evaluation of treat-
ment and its outcomes.
Overall Evaluation
For the purposes of ongoing treatment monitoring, it is
important to use tools that are brief, sensitive to change,
and easy to administer. The BPI-​SF meets these criteria
and covers several functional domains. A variety of quick-​
to-​complete tools (e.g., NRS and VAS) can be used to
assess monitoring of progress from week to week. Diaries
kept by the client for ongoing monitoring can also be
examined by the treatment provider on a weekly basis.
Depending on specific issues identified as targets for
treatment, during the initial assessment, other tools can
be added, but in order to reduce burden for the client,
we do not recommend weekly administration. Instead,
such tools can be used intermittently, with the frequency
of administration determined based on the expected

duration of treatment. For the purposes of the final out-
come evaluation, a more detailed battery could be used
that might involve readministration of some tools used
during the initial diagnostic and case conceptualization
assessments (e.g., to help determine whether the client
still meets DSM-​5 diagnostic criteria). The MPI, which
is sensitive to change, could also be administered as an
outcome measure.
CONCLUSIONS AND FUTURE DIRECTIONS
Pain is a multidimensional, subjective experience, and
its effective assessment requires evaluation of a variety
of domains, including pain intensity, pain qualities (e.g.,
burning and dull), functional abilities, affective responses,
beliefs/​attitudes about pain, social support, coping skills,
and other key domains (see Table 27.1). Research has
established that with regard to chronic pain, psychologi-
cal predictors of outcome are often more important than
physical ones (e.g., van der Hulst, Vollenbroek-​Hutten,
& Ijzerman, 2005), thus making the psychological assess-
ment of the chronic pain patient of critical importance.
Given that psychologists do not diagnose painful physi-
cal conditions (e.g., osteoarthritis and rotator cuff tear),
information derived from the psychological assessment
must be integrated with information obtained and inter-
preted by other professionals (e.g., physicians and physical
therapists).
There are several special situations, not detailed in this
chapter, in which a more specialized approach to assess-
ment may be required. For example, specific pain assess-
ment tools have been developed for persons with severe
limitations in ability to communicate due to conditions
such as progressive dementia or head injury (for a review,
see Hadjistavropoulos, Breau, & Craig, 2011). As a sec-
ond example, patients who are intubated are also unable
to self-​report their pain verbally and require a specialized
approach (see Herr et  al., 2006). Generally, the assess-
ment of adult patients with limited ability to communicate
their pain can be achieved with standardized observa-
tional tools. An example is the Pain Assessment Checklist
for Seniors with Limited Ability to Communicate-II
(PACSLAC-​ II; Chan, Hadjistavropoulos, Williams, &
Lints-​Martindale, 2014), which has been developed for
people with dementia.
In terms of future directions, there is encouraging
initial evidence that technological developments (e.g.,
electronic diaries and the possibility of completing pain
assessment tools from a remote location) will lead to
Chronic Pain in Adults 621
significant advances in pain assessment (Marceau, Link,
Jamison, & Carolan, 2007). Digital approaches allow for
the possibility of a time stamp that can help the clinician
ensure that a tool was completed the way it was supposed
to be completed, as opposed to being completed either
retrospectively or prospectively (Turk & Melzack, 2011).
Moreover, it has been suggested that the development of
item response theory, which has certain advantages over
classical test theory, has the potential of helping refine
existing assessment tools (e.g., increasing predictive abil-
ity by using fewer items; Turk & Melzack, 2011). Finally,
more specialized normative information is needed for a
wider range of cultural groups (e.g., persons of Indigenous
ancestry and older adults) because such norms are cur-
rently unavailable for a wide range of tools pertinent to
pain assessment. It is our hope that the field of pain assess-
ment will advance in these and other exciting directions.
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 Assessment Instrument Index
Tables, figures, and boxes are indicated by an italic t, f, and b following the page number.
Achenbach System of Empirically Based Assessment
(ASEBA),  54–​55, 55t, 77t, 78, 81, 82t, 85t, 86, 87
body image scales,  35
Direct Observation Form (DOF),  57, 77t, 81, 82t
Teacher Report Form (TRF),  54, 55t, 57, 59, 60t, 110–​111
Actigraphy, 572t, 573, 576
Activity Schedule,  138
Addiction Severity Index (ASI),  251–​252, 397, 448
DSM-​5 (ASI-​5),  389, 390t
Addiction Severity Index-​Gambling Severity Index
(ASI-​GSI),  419–​420, 420t, 423, 424, 424t, 426
Addiction Severity Inventory (ASI),  450t, 451
30-​day (ASI-​6),  367, 372–​373, 372t
ADHD Rating Scale-​5,  51, 51t, 59, 60t
Adolescent Pediatric Pain Tool (APPT),  589–​590, 597t, 598
Adolescent Substance Abuse Goal Commitment
(ASAGC), 394
Adolescent Symptom Inventory,  35
Adult ADHD Rating Scale,  62
Adult Suicide Ideation Questionnaire (ASIQ),  196t, 199
Affect Intensity Measure (AIM),  138t, 140
Aggression (AGG) scale,  504
Agoraphobic Cognitions Questionnaire (ACQ),  274, 274t, 276,
279, 280t, 281
Alanine aminotransferase (ALT),  399t, 400
Albany Panic and Phobia Questionnaire (APPQ),  274, 274t,
277–​278, 280t, 281
Alcohol, Smoking, and Substance Involvement Screening Test
(ASSIST),  385, 386–​387, 386t, 388
Alcohol Craving Questionnaire (ACQ),  396
Jellinik (JACQ),  390t, 396
present moment (ACQ-​Now),  390t, 396
Revised (ACQ-​R),  390t, 396
Alcohol Dependence Scale (ADS),  386t, 387, 448
Alcohol Expectancies Questionnaire (AEQ),  396
Alcoholic Abstinence Self-​Efficacy Scale (AASE),  391t, 397
Alcoholic Anonymous Affiliation Scale (AAS),  399t
Alcoholic Anonymous Involvement Scale (AAI),  399t
Alcohol Reduction Strategies–​Current Confidence (ARS-​CC),  397
Alcohol Severity Inventory (ASI),  441t
Alcohol-​Specific Role-​Play Test,  399t
Alcohol Treatment Outcome Measure (ATOM),  399t, 400
Consequences of Drinking (ATOM-​C),  400, 402
Research (ATOM-​R),  400
Alcohol Urge Questionnaire (AUQ),  390t, 396, 397
Alcohol Use Disorder and Associated Disabilities Interview
Schedule (AUDADIS),  389, 391
DSM-​5 (AUDADIS-​5),  386t, 388
Alcohol Use Disorders Identification Test (AUDIT),  386t, 387,
388, 398, 422, 423, 441t, 448, 498
Alcohol Use Inventory (AUI),  390t, 393
Alcohol Use Scale (AUS),  450t, 451
Alexian Brothers Assessment of Self-​Injury (ABASI),  205
Altman Self-​Rating Mania scale (ASRM),  181t, 182, 184
American Society of Addiction Medicine Patient Placement
Criteria (ASAM PPC),  390t, 392
Antisocial Process Screening Device (APSD),  82t, 84
Anxiety Control Questionnaire (ACQ-​CON),  280–​281, 280t
Anxiety Disorders Interview Schedule (ADIS),  270–​272, 271t,
279, 280t
Child and Parent Versions (ADIS-​C/​P),  221–​222, 221t, 225,
226, 227t
Child and Parent Versions, Clinician Rating Scale (ADIS-​C/​P:
CRS), 232t
Child and Parent Versions, DSM-​IV (ADIS C/​P-​IV),  232t, 233
DSM-​5 (ADIS-​5),  246–​247, 270–​272, 271t, 298, 336t, 338
DSM-​IV (ADIS-​IV),  246–​247, 246t, 297t, 298, 304t, 305,
315–​316, 315t, 336t, 338
Lifetime Version for DSM-​5 (ADIS-​5L),  135, 136t
Revised (ADIS-​R),  271, 273
630 Assessment Instrument Index
Anxiety Sensitivity Index (ASI),  251–​252, 274–​275, 274t,
279, 280t
3rd edition (ASI-​3),  248t, 252, 257, 274, 274t, 275, 279, 280t
ARCS (Adult Response to Child Symptoms),  595, 597
Protect and Monitor subscales,  597t, 598
Arousal Predisposition Scale (APS),  567t, 571
Aspartate aminotransferase (AST),  399t, 400
Attentional Control Scale (ACS),  138t, 140
Attention-​Deficit Disorder Evaluation Scale-​4
(ADDES-​4),  51t, 52
Barkley Adult ADHD Rating Scale-​IV (BAARS-​IV),  61–​62
Barkley Functional Impairment Scale (BFIS),  62
BASC Student Observation System (BASC-​SOS),  77t, 80, 82t
Bath Adolescent Pain Questionnaire (BAPQ),  591t, 596–​597
Parent (BAPQ-​P),  591t, 596–​597
Bech–​Rafaelsen Mania Scale (MAS),  181t, 182, 184
Beck Anxiety Inventory (BAI),  300–​301, 300t, 304t, 305, 498,
572t, 574–​575
Beck Depression Inventory-​II (BDI-​II),  157, 158t, 164t, 300t,
301, 304t, 305, 553, 572t, 575, 613, 620, 620t
Beck Scale for Suicidal Ideation (BSI, BSS, BSSI),  196t, 197,
199, 200, 201
Behavioral Affective Rating System (BARS),  496t, 501
Behavioral and Emotional Rating Scale (BERS),  114, 114t, 116
Behavioral Approach Test (BAT),  227t, 252, 254, 255t, 256,
278, 279, 282–​283
Behavioral Avoidance Task/​Social Evaluative Task/​Parent–​Youth
Interaction Task (BAT/​SET/​PYIT),  232t
Behavioral Coding System (BCS),  58, 60, 77t, 79, 85t, 86, 87
Behavioral Observation of Students in Schools (BOSS),  57–​58
Behavior and Symptom Identification Scale (BASIS)
32 item (BASIS-​32),  344
Revised (BASIS-​R),  441t, 442, 449
Behavior Assessment System for Children (BASC)
2nd ed. (BASC-​2),  56
3rd ed. (BASC-​3),  55–​56, 55t, 77t, 78, 81, 82t, 86
3rd ed. Flex Monitor (BSC-​3 Flex Monitor),  59
Student Observation System (BASC-​SOS),  77t, 80, 82t
Berkeley Puppet Interview (BPI),  111, 113
Bipolar Spectrum Disorder Scale (BSDS),  178
Body Checking Questionnaire (BCQ),  551t, 552–​553
Body Sensations Questionnaire (BSQ),  274, 274t, 275–​276,
279, 280t, 281
Body Shape Questionnaire (BSQ),  551t, 552
Brief Addiction Monitor (BAM),  398, 399t, 402
Brief Comprehensive Effects of Alcohol Scale
(B-​CEOA),  390t, 396
Brief Fear of Negative Evaluation Scale (BFNE),  248t, 250–​251
Brief Impairment Scale (BIS),  114, 114t, 116
Brief Index of Sexual Functioning for Women (BISF-​W),  519t,
521, 525, 525t, 528, 529
Brief Male Sexual Function Inventory (BMSFI),  519t, 522
Brief Negative Symptoms Scale (BNSS),  441t, 442, 449
Brief Pain Inventory (BPI),  611–​612, 614, 615, 619–​620
Short Form (BPI-​SF),  611–​612, 611t, 615, 619–​620, 620t
Brief Psychiatric Rating Scale (BPRS),  440, 441t, 449, 450t
Brief QoL BD,  181t, 183–​184
Brief Reasons for Living Inventory (BRFL),  202, 202t
Brief Sexual Function Inventory-​M (BSFI-​M),  526, 530
Brief Social Phobia Scale (BSPS),  255t, 256
Brief Trauma Questionnaire (BTQ),  342t, 343
Brief Young Adult Alcohol Consequences Questionnaire
(B-​YAACQ),  390t, 394, 397, 399t
Brown Assessment of Beliefs Scale (BABS),  315t, 316
Brown–​Peterson Recovery Progress Inventory (B-​PRI),  399t
Burden Assessment Scale (BAS),  441t, 448, 450t, 451
CAGE,  385–​386, 386t, 387, 388
Calgary Depression Scale for Schizophrenia (CSDS),  439t, 440
Camberwell Assessment of Need (CAN),  441t, 444
Camberwell Family Interview (CFI),  181, 447, 451
Canadian Problem Gambling Index-​Problem Gambling
Severity Index (CPGI-​PGSI),  413t, 417, 418, 419, 420t
Carbohydrate-​deficient transferrin (CDT),  385, 386t, 399t,
400, 401
Center for Epidemiological Studies–​Depression Scale
(CES-​D),  157–​158, 158t, 162, 163, 164t, 165
Revised (CESD-​R),  158, 158t
Changes in Sexual Functioning Questionnaire (CSFQ),  525,
525t, 528, 529
CSFQ-​14,  525, 525t
Child and Adolescent Functional Assessment Scale
(CAFAS),  22, 55t, 57, 59, 60t, 77t, 81, 85t, 86, 114,
114t, 116, 118
Child and Adolescent Psychiatric Assessment (CAPA),  53, 113,
115, 116
Child Anxiety Impact Scale (CAIS),  230–​231, 232t, 233
Child Behavior Checklist (CBCL),  54, 55t, 57, 59, 60t, 117
Internalizing Scale (CBCL-​I),  232–​233, 232t
Child Global Assessment Scale (CGAS, C-​GAS),  77t, 81, 85t,
86, 113, 114t, 117–​118, 118t, 119
Childhood Anxiety Sensitivity Index (CASI),  221t, 226
DSM-​5 (CASI-​5),  78
Childhood Trauma Questionnaire,  115–​116
Children of Alcoholics Screening Test (CAST),  394
Children’s Depression Inventory (CDI),  118, 118t
Children’s Depression Rating Scale –​Revised (CDRS-​R),  117,
118, 118t
Children’s Organizational Skills Scale (COSS),  55t, 57, 60, 60t
Child Suicide Potential Scales (CSPS),  197t, 200
Child World Health Organization Disability Assessment Scale
(C-​WHO-​DAS),  115
Chronic Pain Coping Inventory (CPCI),  616t, 617–​618, 619
42-​item (CPCA-​42),  616t, 618
Circumscribed Fear Measure,  250
Client Assessment of Strengths, Interests, and Goals
(CASIG), 441t, 444, 445, 450t, 451
Clinical Assessment Interview for Negative Symptoms
(CAINS), 441t, 442, 449
Clinical Global Impression (CGI),  449, 450t
Improvement (CGI-​I),  117, 119
Severity (CGI-​S),  117, 119
Clinical Institute Withdrawal Assessment for Alcohol
(CIWA-​AR),  389, 390t, 397
Clinical Rating of Adult Communication Scale
(CRAC), 496t, 501
Clinician-​Administered PTSD Scale (CAPS),  343, 345
DSM-​5 (CAPS-​5),  336–​337, 336t, 341, 346t, 347
DSM-​IV (CAPS-​IV),  336–​337, 336t, 346t

Clinician Administered Rating Scale for Mania (CARS-​M),  182
Clinician Administered Rating Scale for Post-​Traumatic Stress
Disorder–​Schizophrenia (CAPS-​S),  439t, 440
Cocaine Negative Consequences Checklist (CNCC),  366t, 372
Cocaine Related Assessment of Coping Skills (CRACS),  371
Self-​Efficacy (CRACS-​SE),  366t
Codebook of Marital and Family Interaction
(COMFI), 496t, 501
Cognitive Avoidance Questionnaire (CAQ),  300t, 303,
304t, 305
Cognitive–​Behavioral Analysis System of Psychotherapy
(CBASP), 133
Cognitive Lifetime Drinking Inventory (CLDH),  393
College Student Reasons for Living Inventory
(CSRLI), 202t, 203
Colorado Symptom Index,  449
Columbia Impairment Scale (CIS),  113–​114, 114t
Columbia–​Suicide Severity Rating Scale (C-​SSRS),  196t,
197–​198, 204, 205
Combat Exposure Scale,7-​item, 343–​344
Communication Patterns Questionnaire (CPQ),  495,
496t, 503
Communication Skills Test (CST),  496t, 501
Compliance Test (CT),  77t, 80, 85t
Composite International Diagnostic Interview (CIDI),  156,
157, 336t, 338–​339, 362t, 364
CIDI 65+, 156
Comprehensive Effects of Alcohol Scale (CEOA),  390t,
396, 397
Brief (B-​CEOA),  390t, 396
Computerized Adaptive Test–​Personality Disorder (CAT-​
PD),  476–​477, 476t, 478t, 479
Concordia Lifetime Drinking Questionnaire (CLDQ),  393
Conflict Rating System (CRS),  496t, 501
Conflict Tactics Scale–​Revised (CTS  2), 496t, 498, 503–​504
Conners  3, 52, 54, 55t, 56, 59, 60t
DSM-​IV-​TR Symptom Scales,  51t, 52
Conners Adult ADHD Diagnostic Interview for DSM-​IV
(CAADID-​IV),  62
Conners Rating Scales,3rd ed. (CRS-​3), 77t, 78
Consensus Sleep Diary (CSD),  567t, 569–​570, 572, 572t, 575
Conventionalization (CNV) scale,  497
Coolidge Axis II Inventory (CATI),  466, 467, 467t, 470,
471, 474
Coping Strategies Questionnaire (CSQ),  616t, 617
Cornell Scale for Depression in Dementia (CSDD),  158t,
161–​162, 163, 164t, 165
Couple Satisfaction Index (CSI),  441t, 493t, 494, 523, 523t
4-​item (CSI-​4),  78, 493t, 494
16-​item (CSI-​16),  501t, 505
DSM-​IV (CSI-​IV),  56
Couples Interaction Scoring System (CISS),  502
Couples’ Intimate Behavior Rating System (CIBRS),  496t, 501
Cultural Formulation Interview (CFI),  439, 451
Daily Record of Dysfunctional Thoughts,  139
Dartmouth Assessment of Lifestyle Instrument,  448
Decreased Sexual Desire Screener (DSDS),  528
Deliberate Self-​Harm Inventory (DSHI),  196t, 199
Dementia Mood Assessment Scale (DMAS),  158t, 162, 165
Assessment Instrument Index 631
Dental Anxiety Inventory (DAI),  248t, 249, 255, 255t, 441t, 442
10-​item (DAI-​10),  442
30-​item (DAI-​30),  442
Dental Cognitions Questionnaire,  249
Dental Fears Survey,  249
Deployment Risk and Resilience Inventory (DRRI),  344
Deployment Risk and Resilience Inventory-​2 (DRRI-​2),  344
Depression Anxiety Stress Scales (DASS),  142–​143, 144t
Derogatis Sexual Functioning Inventory (DSFI),  523–​524,
523t, 530
Diagnostic Interview for ADHD in Adults (DIVA  2.0), 62
Diagnostic Interview for Children and Adolescents
(DICA), 77t, 79, 81–​82, 221t, 222, 227t, 232t
Diagnostic Interview for Gambling Schedule (DIGS),  413t,
415, 418, 420t, 421
DSM-​IV,  416
Diagnostic Interview for Personality Disorders (DIPD),  466,
467t, 469–​470, 471, 475
Diagnostic Interview Schedule (DIS),  364, 439, 439t
Diagnostic Interview Schedule for Children (DISC),  496t, 501
DSM-​IV,  51t, 52, 77t, 79, 81–​82, 221t, 222, 227t, 232t
Dimensional Assessment of Personality Pathology-​Basic
Questionnaire (DAPP-​BQ),  475–​476, 476t, 478t, 479
Dimension Obsessive Compulsive Scale (DOCS),  322t, 324
Direct Observation Form (DOF), ASEBA,  57, 77t, 81, 82t
Disgust Emotion Scale,  251
Disgust Scale (DS),  248t
Revised (DS-​R),  251
Dog Phobia Questionnaire,  250
Drinker Inventory of Consequences (DrInC),  390t, 393, 399t,
400, 401
Drinking Context Scale (DCS),  390t
Drinking Motives Questionnaire–​Revised (DMQ-​R),  390t, 396
Drinking Patterns Questionnaire (DPQ),  390t
Drinking Refusal Self-​Efficacy Questionnaire
(DRSEQ), 390t, 397
Revised (DRSEQ-​R),  391t, 397
Drinking Self-​Monitoring Log (DMSL),  391t
Drinking Triggers Inventory (DTI),  370
Drug Abstinence Self-​Efficacy Scale (DASE),  370
Drug Abuse Screening Test (DAST),  362t, 363, 365, 423,
441t, 448
Drug-​Taking Confidence Questionnaire (DTCQ),  366t, 370
Drug Use Scale (DUS),  450t, 451
Drug Use Screening Inventory (DUSI),  362t, 363, 365, 386t, 387
Duke Structured Interview for Sleep Disorders
(DSISD),  565–​566, 565t
Dyadic Adjustment Scale (DAS),  493t, 494, 501t, 505, 523, 523t
7-​item (DAS-​7), 493t, 494
Dyadic Couples Inventory (DCI),  496t, 503
Dyadic Parent-​Child Interaction Coding System (DPICS),  77t,
79–​80, 85t, 86, 87
Dysfunctional Attitude Scale (DAS),  180, 553
Dysfunctional Beliefs and Attitudes about Sleep Scale
(DBAS), 570
16-​item (DBAS-​16),  567t, 568t, 570
Early Childhood Inventory-​5 (ECI-​5),  78
Eating Disorder Assessment for DSM-​5 (EDA-​5),  547t,
548, 550
632 Assessment Instrument Index
Eating Disorder Diagnostic Scale (EDDS), DSM-​IV,  547t,
549–​550
Eating Disorder Examination Questionnaire (EDE-​Q)
versions  4.0, 6.0, 547t, 549, 550, 551, 551t, 553–​555, 554t
versions  12-​16, 550, 551, 551t, 553–​555, 554t
versions  12-​17, 546–​548, 547t, 550
Eating Pathology Symptoms Inventory (EPSI),  551t, 553
Eland Color Tool,  589, 590, 598
Emetophobia Questionnaire,  250
Emotion Regulation Questionnaire (ERQ),  138t, 140
Erection Hardness Score (EHS),  525t, 526, 527
Ethyl gluconic (EtG),  399t, 400
Ethyl sulfate (EtS),  399t, 400
Evaluating and Nurturing Relationship Issues
(ENRICH), 496t, 504
Experiences Questionnaire (EQ),  138t, 139–​140
Eyberg Childhood Behavior Inventory/​(Sutter-​Eyberg Child
Behavior Inventory-​Revised (ECBI/​SESBI-​R),  77t, 78,
82t, 85t, 86
Eyberg Childhood Behavior Inventory-​5/​Child & Adolescent
Symptom Inventory-​5 (ECBI-​5/​CASI-​54),  77t, 78, 82t,
85t, 86, 87
Faces Pain Scale-​Revised (FPS-​R),  585t, 587–​588, 590,
597–​598, 597t
Family Accommodation Scale–​Anxiety (FASA),  227t
Family Accommodation Scale–​Child Report
(FASA-​CR),  227t, 231
Family Adaptability and Cohesion Evaluation Scales
(FACES-​III),  545–​546
Family Assessment Device (FAD),  179t, 181
Family History Research Diagnostic Criteria
(FHRDC), 116, 394
Family History Screen,  116
Family Informant Schedule,  116
Family Interview for Genetic Studies,  116
Family Tree Questionnaire (FTQ),  394, 397
Fast Alcohol Screening Test (FAST),  385, 386, 386t, 387
Father’s Alcoholism, Short Michigan Alcoholism Screening Test
(F-​MAST),  394
Fatty acid ethyl esters (FAEE),  399t, 400
Fear-​Avoidance Beliefs Questionnaire (FABQ),  616t, 619
Fear of Pain Questionnaire (FOPQ),  591t, 596, 597
Fear of Spiders Questionnaire (FSQ),  248t, 249, 254,
255, 255t
Fear Questionnaire (FQ),  274, 274t, 276–​277, 279, 280t, 281
Fear Survey Schedule (FSS),  248, 572t, 574
Children-​Revised (FSSC-​R),  221t, 223, 232t
Children-​Revised Short Form (FSSC-​R-​SF),  224
Female Experiences Interview Schedule (FEIS),  448
Female Sexual Distress Scale (FSDS),  523t, 524, 525t, 530
Female Sexual Function Index (FSFI),  521, 525, 525t,
528, 529
5-​Hydroxytryptophol (5-​HTOL),  399t, 400
Five Factor Model Personality Disorder scales
(FFMPD),  466, 467t, 468, 470, 471, 473–​475,
476, 476t, 477, 478t, 479
Flinders Fatigue Scale,  574
Ford Insomnia Response to Stress Test (FIRST),  567t, 571
Form  90, 390t, 392, 395, 398, 399t, 401
Frequency and Acceptability of Partner Behavior Inventory
(FAPBI),  496–​497, 496t, 503, 505
Frost Multidimensional Perfectionism Scale (FMPS),  138t,
139, 248t, 252
Functional Assessment of Self-​Mutilation (FASM),  202,
202t, 203
Functional Disability Inventory (FDI),  591t, 592–​593, 597,
597t, 598
Gamblers’ Beliefs Questionnaire (GBQ),  424t, 426
Gambling Abstinence Self-​Efficacy Scale (GASS),  420t, 422,
423, 424t, 425
Gambling Behavior Inventory (GBI),  413t, 417, 418
Gambling Cognitions Inventory (GCI),  424t
Gambling Functional Assessment (GFA),  422
Revised (GFA-​R),  420t, 422
Gambling Motives Questionnaire (GMQ),  420t, 421
Financial Motives (GMQ-​F),  420t
Gambling Treatment Outcome Monitoring System
(GAMTOMS),  158–​159, 158t, 163, 420–​421, 420t,
423, 424–​425, 424t, 426
Discharge Questionnaire (GAMTOMS-​D),  424, 424t
DSM-​IV Screen (GAMTOMS-​DSM),  413t, 416, 417, 418
Follow-​up questionnaire (GAMTOMS-​F),  424, 424t
γ-​glutamyl transferase (GGT),  386, 386t, 399t, 400, 401
General Alcoholics Anonymous Tools of Recovery Scale
(GAATOR), 399t
General Assessment of Personality Disorders (GAPD),  479
General Behavior Inventory (GBI),  174t, 177–​178
Generalized Anxiety Disorder Questionnaire-​IV
(GAD-​Q-​IV,  297–​298, 297t
Generalized Anxiety Disorder Scale (GAS-​7),  498
GenitoSensory Analyzer (GSA),  527
Geriatric Depression Rating Scale (GDRS),  158t, 160–​161,
164–​165, 164t
Geriatric Depression Scale (GDS),  164t
Geriatric Mental State Schedule (GMS),  155t, 156–​157,
158t, 160
AGECAT (GMS/​AGECAT),  155t, 156–​157
GMS-​DS,  158t, 160, 162–​163, 164, 165
GET.ON PAPP,  282
Giner transdermal alcohol sensor (Giner TAS),  399t
Glasgow Sleep Effort Scale (GSES),  567t, 571
Global Appraisal of Individual Needs (GAIN)
90 day (GAIN-​M)M,  372t, 373, 375
Gain Short Screener (GAIN-​GSS),  385, 386t, 387, 388
Initial Interview (GAIN-​I),  362t, 364–​365, 366t, 367–​368
Short Screener (GAIN-​SS),  365
Web-​based Assessment Building System (GAIN-​ABS),  364
Global Assessment of Functioning (GAF),  450–​451
Global Measure of Sexual Satisfaction (GMSEX),  523t, 524
Goal Attainment Scaling (GAS),  143, 144t, 501t, 505
Golombok-​Rust Inventory of Sexual Satisfaction (GRISS),  519t,
521, 523, 523t, 525t, 526, 529, 530
Hamilton Rating Scale for Depression (HRSD),  160, 164
Harkavy Asnis Suicide Scale (HASS),  197t, 200
Harvard Trauma Questionnaire (HTQ),  345
Health and Behavior Questionnaire (HBQ), McArthur,  111
Helping Alliance Questionnaire, Revised (HAq-​II),  144, 144t

5-​Hydroxytryptophol (5-​HTOL),  399t, 400
Hypomania Checklist (HCL-​32),  178
Hypomanic Personality Scale (HPS),  178
Illness Behavior Encouragement Scale (IBES),  595
Illness Intrusiveness Rating Scale (IIRS),  255t, 257
Illness Management and Recovery (IMR),  441t, 446, 450t, 452
Illness Perception Questionnaire–​Revised (IPQ-​R),  613
Impact of Event Scale-​Revised (IES-​R),  336t, 339, 346t
Impaired Control Scale,  399t
Impairment Rating Scale (IRS),  55t, 57, 59–​60, 60t
Important People and Activities interview (IPA),  391t, 397
Important People measure (IP-​5),  397
Independent Living Scale Survey (ILSS),  441t, 444, 445,
450t, 451
Index of Dental Fear and Anxiety,  249
Index of Premature Ejaculation (IPE),  519t, 525t, 530
Index of Sexual Satisfaction (ISS),  523t, 524, 525t
Indices of Problems (IDS),  390t
Insight and Treatment Attitudes Questionnaire,  180
Insomnia Diagnostic Interview (IDI),  565
Insomnia Severity Index (ISI),  572–​573, 572t, 575, 576
Interactional Dimensions Coding System (IDCS),  496t, 501
Internal State Scale (ISS),  183
International Index of Erectile Function (IIEF),  519t, 522,
525t, 526, 530
5-​item (IIIEF-​5),  519t, 525t, 526–​527
International Personality Disorder Examination (IPDE),  466,
467, 467t, 468, 469, 470, 475
International Stigma of Mental Illness (ISMI),  441t, 447
Interpretation of Intrusions Inventory (III),  318–​319, 319t, 321
Intolerance of Uncertainty Scale (IUS),  300t, 301–​302, 304t, 305
Inventory of Callous–​Unemotional Traits (ICU),  82t, 84
Inventory of Depression and Anxiety Symptoms (IDAS),  179
Inventory of Depressive Symptomatology (IDS),  136, 161, 165
Clinician-​rated (IDS-​C),  161
Self-​report (IDS-​SR),  161
Inventory of Drinking Situations (IDS),  390t, 396, 397
Inventory of Drinking Situations,42-​item (IDS-​42), 396
Inventory of Drug Taking Situations (IDTS),  366t, 370
Inventory of Drug Use Consequences (IDUC),  366t, 368, 372t,
373, 375
Inventory of Gambling Situations (IGS),  420t, 421, 423
Inventory of Interpersonal Problems (IIP),  553
Inventory of Motivations for Suicide Attempts (IMSA),  205–​206
Inventory of Statements about Self-​Injury (ISAS),  202t, 203
IOWA, 59, 60t
Jellinik Alcohol Craving Questionnaire (JACQ),  390t, 396
Kategoriensystem für Partnerschaftliche Interaktion
(KPI), 496t, 501
Kiddie Schedule for Affective Disorders and Schizophrenia for
School-​Age Children (K-​SADS),  52–​53, 106–​107, 106t,
112, 117, 118, 118t, 177, 179, 221t, 222, 227t, 232t
Present and Lifetime Version (K-​SADS-​PL),  174t, 177
Leeds Dependence Questionnaire (LDQ),  399t
Liebowitz Social Anxiety Scale (LSAS),  255t, 256
Life Events Checklist (LEC),  342t, 343
Assessment Instrument Index 633
Life Situation Survey (LSS),  399t
Life Stress Interview (LSI),  115, 116
Life Stressor Checklist-​Revised (LSC-​R),  342t, 343
Life Stressors and Social Resources Inventory (LISRES),  390t
Lifetime Drinking History (LDH),  390t, 393
Living in Family Environments (LIFE),  496t, 501
Male Sexual Health Questionnaire (MSHQ),  519t, 522, 526
Male Sexual Health Questionnaire–​Ejaculation Short
Form(MSHQ-​EjD),  519t, 526
Marijuana Problems Scale (MPS),  366t, 368–​369, 372t, 373
Marijuana Withdrawal Checklist (MWC),  362t, 364
Marital Interaction Coding System (MICS),  502
Marital Satisfaction Inventory–​Brief (MSI-​B),  493t, 494,
501t, 505
Marital Satisfaction Inventory–​Revised (MSI-​R),  413t, 415–​416,
418, 420t, 496–​497, 496t, 497, 501t, 504
3-​Month Version (NODS-​3),  424t, 425
Maudsley Addiction Profile (MAP),  399t
Maudsley Obsessional Compulsive Inventory (MOCI),  323
McArthur Health and Behavior Questionnaire (HBQ),  111
McCoy Female Sexuality Questionnaire (MFSQ),  519t, 521,
525t, 528, 529
McGill Pain Questionnaire (MPQ),  611t, 612
Short Form (SF-​MPQ),  611t, 612–​613
Short Form-​2 (SF-​MPQ-​2),  611t, 612–​613
Mean corpuscular volume (MCV),  386, 386t, 399t, 400
Medical Fear Survey,  249
Mental Health Recovery Measure (MHRM),  441t, 444, 445,
446, 450t, 451
Mental Illness Research Educational and Clinical
Center Global Assessment of Functioning
(MIRECC-​GAF),  441t, 444, 445, 450t, 451
Millon Clinical Multiaxial Inventory-​IV (MCMI–​IV),  466,
467, 467t, 468–​469, 471, 472–​473, 474, 475
Mini International Neuropsychiatric Interview  6.0 (M.I.N.I.),
362t, 363–​364, 365, 389, 391, 439, 439t
Mini-​Mental State Examination,  163
Minnesota Multiphasic Personality Inventory-​2 (MMPI-​2),  35,
466, 467, 467t, 470, 471, 472–​473, 474, 614
Mississippi Scale for Combat-​Related PTSD (Mississippi
Scale), 336t, 339–​340
Mobility Inventory for Agoraphobia (MI),  274, 274t, 277, 280t, 281
Modified Scale for Suicide Ideation (MSSI),  196t, 199
Montgomery-​Åsberg Depression Rating Scale (MADRS),  158t,
161, 164t, 165
Mood and Feelings Questionnaire (MFQ),  106t, 109, 110, 112,
117, 118, 118t
Shorter (SMFQ),  519t, 522, 528, 529
Mood Disorder Questionnaire (MDQ),  174t, 178
Mood Spectrum Self-​Reports (MOODS-​SR),  178, 529
Mother’s Alcoholism, Short Michigan Alcoholism Screening
Test (M-​SMAST),  394
Multi-​Attitude Suicide Tendency Scale for Adolescents
(MAST), 202t, 203, 386t, 387, 388, 390t, 393, 441t, 448
Multidimensional Anxiety Scale for Children (MASC),  221t,
223–​224, 227t, 232t
Revised (MASC-​2),  223, 224, 226
Revised, Parallel Version for Parent (MASC-​2-​2-​P),  224
Revised, Self-​Report Version for Child (MASC-​2-​SR),  224
634 Assessment Instrument Index
Multidimensional Fatigue Inventory (MFI),  572t, 574
Multidimensional Measure of Emotional Abuse
(MMEA), 504
Multidimensional Pain Inventory-​M (MPI), West Haven–​
Yale,  610–​611, 611t, 615–​616, 616t, 619, 620, 620t
61-​item, Modified instructions (MPI-​M),  616, 616t
Multnomah Community Ability Scale (MCAS),  441t, 444,
445, 450t, 451
Mutilation Questionnaire,  249
National Comorbidity Survey Replication (NCS–​R),  131, 153,
243, 266, 331
National Epidemiological Survey on Alcohol and Related
Conditions (NESARC),  360, 382
III (NESARC-​III),  381, 382
National Opinion Research Center DSM-​IV Screen for
Gambling Problems (NODS)
Preoccupation, Escape, Risked relationships, and Chasing
(NODS-​PERC),  417
National Opinion Research Center DSM-​IV Screen for
Gambling Problems, Control, Lying, and Preoccupation
(NODS-​CLiP),  415–​416, 417
National Vietnam Veterans Readjustment Study (NVVRS),  331
Negative Problem Orientation Questionnaire (NPOQ),  300t,
303, 304t, 305
Neurobehavioral Cognitive Status Examination
(COGNISTAT), 163
Neuropathic Pain Scale (NPS),  611t, 612, 615, 620t
Neuropsychiatric Inventory (NPI),  162
New Sexual Satisfaction Scale (NSSS),  523t, 524
Non-​Suicidal Self-​Injury-​Assessment Tool (NSSI-​AT),  206
Non-​Suicidal Self-​Injury Disorder Scale (NSSID),  205
Numerical rating scales (NRS),  585t, 588, 597t, 619, 620t
Objective Opiate Withdrawal Scale,  364
Obsessive Beliefs Questionnaire (OBQ),  318, 319t, 321
Obsessive-​Compulsive Drinking Scale (OCDS),  390t, 395
Obsessive-​Compulsive Inventory-​Revised (OCI-​R),  322t, 323
OMNI Personality Inventory (OMNI),  466, 467, 467t, 474, 475
Orgasm Rating Scale (ORS),  527
Outcome Questionnaire-​45 (OQ-​45),  137, 143, 144t
Padua Inventory-​Revised (PI-​R),  322t, 323
Pain Anxiety Symptoms Scale (PASS),  616t, 618, 619
20-​item (PASS-​20),  616t, 618
Pain Beliefs and Perceptions Inventory (PBAPI),  616t, 617
Pain Beliefs Questionnaire (PBQ),  616t, 617
Pain Catastrophizing Scale (PCS),  529, 611t, 613, 616t,
617, 620t
Children (PCS-​C),  591t, 595–​596, 597
Pain diaries,  591–​592, 591t, 611t, 612, 616, 616t, 619, 620, 620t
Pain Experience Questionnaire (PEQ),  591t, 596
Pain Patient Profile (P  3), 611t, 613
Panic Disorder Severity Scale (PDSS),  271t, 273, 280, 280t
Self-​Report (PDSS-​SR),  273
Parent Daily Report (PDR),  85t, 86
Parent’s Consumer Satisfaction Questionnaire (PCSQ),  85t, 86
Parent-​Young Mania Rating scale (P-​YMRS),  178–​179
Pathological Gambling Modification, Yale–​Brown Obsessive-​
Compulsive Scale (PC-​YBOCS),  424t, 426
Patient Health Questionnaire-​9 (PHQ-​9),  135–​136, 136t, 138,
158t, 159, 162, 163–​164, 164t, 165, 572t, 575
Patient Rejection Scale (PRS),  441t, 448, 450t, 451
Pediatric Anxiety Rating Scale (PARS),  226, 230
Pediatric Quality of Life Inventory Generic Core Scales
(PedsQL  4.0), 591t, 593–​594
Penn Alcohol Craving Scale (PACS),  390t, 395
Preoccupation, 390t, 396
Penn State Worry Questionnaire (PSWQ),  299–​300, 300t,
304, 304t
Past Week (PSWQ-​PW),  304, 304t
Perceived Criticism Scale (PCS),  181
Perseverative Thinking Questionnaire (PTQ),  138t, 139
Personality Assessment Inventory (PAI),  466, 467, 467t,
470, 475
Personality Diagnostic Questionnaire-​4 (PDQ-​4),  466, 467–​468,
467t, 471, 473, 474, 475
Personality Disorder Interview-​IV (PDI-​IV),  466, 467t, 469, 475
Personality Inventory for DSM-​5 (PID-​5),  466, 467t, 468, 470,
471, 472, 473–​475, 476, 476t, 477, 478t, 479
Phosphatidylethanol (PEth),  386, 386t, 388, 399t, 400
Pieces of Hurt Tool,  585t, 586, 590, 597, 597t
Pittsburgh Sleep Quality Index (PSQI),  180, 572t, 573
Pleasant Events Schedule (PES),  138, 138t, 597t, 598
Poker Chip Tool (Pieces of Hurt),  585t, 586, 590, 597, 597t
Polysomnography (PSG),  565t, 566, 576
Positive and Negative Syndrome Scale (PANSS),  440, 441t,
449, 450t
Posttraumatic Diagnostic Scale for DSM-​5 (PDS-​5),  336t,
340, 346t
Posttraumatic Diagnostic Scale for DSM-​IV (PDS-​IV),  336t,
340, 346t
Posttraumatic Stress Disorder Checklist (PCL)
Civilian (PCL-​C),  341
DSM-​5 (PCL-​5),  336t, 340–​341, 346t
DSM-​IV (PCL-​IV),  336t, 340–​341, 346t
Military (PCL-​M),  341
Specific (PCL-​S),  341
Posttraumatic Stress Related Functioning Inventory,  344
Prediction of Alcohol Withdrawal Severity (PAWSS),  386t
Premature Ejaculation Diagnostic Tool (PEDT),  519t, 530
Premature Ejaculation Profile (PEP),  525t, 530–​531
PREPARE, 504
Preschool Age Psychiatric Assessment (PAPA),  106, 106t,
107–​108, 112, 113, 115, 116
Present State Exam (PSE),  156
Pre-​Sleep Arousal Scale (PSAS),  567t, 570
Primary Care-​PTSD screen (PC-​PTSD),  347
DSM-​5 (PC-​PTSD-​5),  347
Problem and Pathological Gambling Measure (PPGM),  413t,
417–​418
Processes of Change questionnaire (POC),  366t, 371
10-​item,  366t
Profile of Female Sexual Functions (PFSF),  523t, 528
Profile of Mood States (POMS),  613
PROMIS,  110, 398, 399t, 402
Protective Behavioral Strategies Survey (PBSS),  399t, 401
Psychiatric Diagnostic Screening Questionnaire (PDSQ),  386t
Psychiatric Research Interview for Substance and Mental
Disorders (PRISM),  386t, 388

Psychosocial Schedule for School Age Children-​Revised
(PSS-​R),  114–​115, 116
Psychotic Symptom Rating Scale (PSYRATS),  441t, 447, 450t,
451, 452
PTSD Symptom Scale Interview (PSSI-​I),  338, 347
DSM-​5 (PSSI-​5),  336t, 338
DSM-​IV (PSSI-​IV),  336t, 338
Quality of Erection Questionnaire (QEQ),  525t, 526, 527
Quality of Life Interview Self-​Administered Short Form
(TL-​30S),  441t, 447, 450t, 451
Quality of Life Inventory (QOLI),  300t, 301, 304t, 305, 441t,
450t, 451
Quality of Life Questionnaire (QLQ),  300t, 301, 304t, 305
Quality of Life Scale (QLS),  441t, 444, 450t, 451
Quality of Sex Inventory (QSI),  524
Quantity–​Frequency Measures (Q-​F measures),  390t
Quick Inventory of Depressive Symptomatology Self-​Rated
(QIDS-​SR),  135–​136, 136t, 142, 144t
Rapid Alcohol Problems Screen-​4 (RAPS-​4),  386t
Rapid Couple Interaction Scoring Systems (RCISS),  493t, 494,
500, 502
Rapid Marital Interaction Coding System (RMICS),  493t, 494,
500, 502
Rating of Medication Influences Scale (ROMI),  441t, 442
Readiness to Change Questionnaire (RCQ),  390t, 394
Reasons for Drinking Questionnaire (RFDQ),  396
Reasons for Living Inventory (RFL),  202, 202t
Adult (RFL-​A),  202–​203, 202t
Older Adult (RFL-​OA),  202t, 203
Young Adults (RFL-​YA),  202t, 203
Reasons for Suicide Attempts Questionnaire (RSAQ),  202t, 203
Recovery Assessment Scale (RAS),  441t, 446, 450t, 451
Recovery Attitude and Treatment Evaluator
(RAATE), 390t, 397
Relationship Attribution Measure (RAM),  496t, 497, 504
Relationship Quality Interview (RQI),  496t, 500
Revised Behavior and Symptom Identification Scale
(BASIS-​R),  441t, 442, 449
Revised Children’s Anxiety and Depression Scale
(RCADS), 226
Revised Children’s Manifest Anxiety Scale (RCMAS),  221t,
223, 227t, 228
2 (RCMAS-​2),  224, 226
2 (RCMAS-​2), Defensiveness Scale,  233, 234
Lie Scale,  232t, 233–​234
Revised Edition of the School Observation Coding System
(REDSOCS), 77t, 80, 85t, 86
Revised Helping Alliance Questionnaire (HAq-​II),  144, 144t
Revised Padua Inventory (PI-​R),  322t, 323
Reynolds Adolescent Depression Scale (RADS),  106t, 109, 110,
112, 117, 118, 118t
Reynolds Child Depression Scale (RCDS),  106t, 109, 110,
112, 117, 118, 118t
Roland–​Morris Disability Questionnaire (RMDQ),  611t,
614, 615
Rosenberg Self-​Esteem Scale (RSE),  553
Rutgers Alcohol Problem Index (RAPI),  390t, 393, 397,
399t, 400
Assessment Instrument Index 635
Scale for Assessment of Negative Symptoms (SANS),  441t, 442,
449, 450t
Scale for Suicide Ideation (SSI),  196t, 197t, 198–​199, 200
Scale for Suicide Ideation–​Worse (SSI-​W),  196t, 199
Scale to Assess Unawareness of Mental Disorder (SUMD),  180
Schedule for Affective Disorders and Schizophrenia
(SADS), 155t, 156, 157, 158t, 160, 174t, 175–​176, 179
Change Mania Scale (SADS-​C),  181t, 182, 184
Schedule for Assessment of Insight–​Expanded Version
(SAI-​E),  179t, 180
Schedule for Nonadaptive and Adaptive Personality-​2nd edition
(SNAP-​2),  466, 467, 467t, 474, 475–​476, 476t, 478t, 479
Schedule of Compulsions, Obsessions, and Pathological
Impulses (SCOPI),  322t, 324
School Refusal Assessment Scale (SRAS),  227t, 228
Revised (SRAS-​R),  228
Screen for Child Anxiety-​Related Emotional Disorders
(SCARED), 221t, 223–​224
Secure Continuous Remote Alcohol Monitor (SCRAM),  399t
Self-​Administered Alcoholism Screening Test (SAAST),  386t
Self-​Efficacy to Control a Panic Attack Questionnaire
(SE-​CPAQ),  281–​282
Self-​Harm Behavior Questionnaire (SHBQ),  196t, 199
Self-​Harm Inventory (SHI),  196t, 200
Self-​Injurious Thoughts and Behaviors Interview
(SITBI),  196–​197, 196t, 197t, 200, 201, 202t
Self-​Injury Questionnaire (SIQ),  197t, 200
Children (SIQ-​JR),  197t, 200
Self-​Monitoring (SM),  227t
Self-​Report Manic Inventory (SRMI),  181t, 182–​183, 184
Self-​Stigma of Mental Illness Scale (SSMI),  441t, 446–​447
Semistructured Assessment for Genetics of Alcoholism
(SSAGA), 386t, 388, 389, 391
Sense of Hyper-​Positive Self Scale (SHPSS),  181t, 183
Session Alliance Inventory (SAI),  144, 144t
Severity Indices for Personality Problems (SIPP-​118),  479
Severity of Dependence Scale (SDS),  366–​367, 366t
Sexual Desire Inventory (SDI),  523t, 525t, 528, 530
Sexual Interest and Desire Inventory-​Female (SIDI-​F),  519t,
523t, 528
Sexual Satisfaction Scale for Women (SSS-​W),  523t, 524
Shedler–​Western Assessment Procedure-​200 (SWAP-​200),  466,
467, 467t, 470, 471, 472, 474
Sheehan Disability Scale,  344
Sheehan-​Suicidality Tracking Scale (S-​STS),  196t, 198, 204, 205
Short Alcohol Withdrawal Scale (SAWS),  389, 390t
Shorter Mood and Feelings Questionnaire (SMFQ),  519t, 522,
528, 529
Short Form Health Survey (SFHS)
12-​item (SF-​12),  389, 390t, 397, 399t, 401
36-​item (SF-​36),  163, 344, 389, 390t, 397, 399t, 401, 441t,
444, 445, 450t, 614, 620, 620t
Short Form-​McGill Pain Questionnaire (SF-​MPQ),  611t,
612–​613
2 (SF-​MPQ-​2),  611t, 612–​613
Short Inventory of Problems (SIP),  390t, 393, 399t, 400
Alcohol and Drugs (SIP-​AD),  366t, 368, 372t, 373
Short Michigan Alcoholism Screening Test (SMAST),  394
Father’s Alcoholism (F-​MAST),  394
Mother’s Alcoholism (M-​SMAST),  394
636 Assessment Instrument Index
Short Screening Scale for PTSDS, seven-​item,  347
Simple Screening Instrument for Alcohol and Other Drugs
(SSI-​AOD),  386t, 387
Simple Screening Instrument for Substance Abuse
(SSI-​SA),  386t, 387
Situational Confidence Questionnaire (SCQ),  391t, 396
Situational Confidence Questionnaire for Gambling
(SCQG), 420t, 422
SKAMP, 59
Sleep-​Associated Monitoring Index (SAMI),  567t, 571
Sleep-​Behavior Self-​Rating Scale (SBSRS),  567t, 570
Snaith–​Hamilton Pleasure Scale (SHAPS),  138–​139, 138t
Snake Questionnaire (SNAQ),  248t, 249, 255, 255t
Social Adaptive Function Scale (SAFE),  254, 441t, 444, 445,
450t, 451
Social Adjustment Inventory for Children and Adolescents
(SAICA),  114, 114t, 116, 118t
Social Adjustment Scale (SAS-​II),  441t, 444, 450t, 451
Social Adjustment Scale–​Self-​Report (SAS-​SR),  138t, 140
Social Anxiety Scale for Children–​Revised (SASC-​R),  221t,
224–​225
Social Behavior Schedule (SBS),  441t, 444, 445, 450t, 451
Social Evaluative Task/​Parent-​Youth Interaction Task
(SET/​PYIT),  227t
Social Functioning Scale (SFS),  441t, 444, 450t, 451
Social Performance Rating Scale (SPRS),  248t, 253
Social Phobia and Anxiety Inventory (SPAI),  248t, 250, 255, 255t
Social Phobia and Anxiety Inventory for Children
(SPAIC), 221t, 224, 227t, 232t
Social Phobia Inventory (SPIN),  248t, 250, 254, 255, 255t
Social Support Interaction Coding System (SSICS),  496t, 501
South Oaks Gambling Screen (SOGS),  413t, 414–​415, 418,
419, 420t, 423
3-​month (SOGS-​3),  414, 424t, 425
past-​year (SOGS-​R),  413t, 414–​415
SPAN, 347
Specific Affect Coding System (SPAFF),  496t, 501
Specific Level of Functioning (SLOF),  441t, 444, 445
Spence Children’s Anxiety Scale (SCAS),  221t, 223–​224,
227t, 232t
Spielberger State Anxiety Inventory (STAI),  572t, 575
Stages of Change Readiness and Treatment Eagerness Scale
(SOCRATES), 390t, 394, 399t, 400, 401
State-​Trait Anxiety Inventory for Children (STAIC),  221t,
223, 232t
Stigma Scale (SS),  441t, 447
Storm Fear Questionnaire,  250
Strengths and Difficulties Questionnaire (SDQ),  52
Stressful Life Events Screening Questionnaire
(SLESQ), 342t, 343
Stressful Life Events Screening Schedule (SLES),  115, 116
Structured Clinical Interview for DSM (SCID),  155–​156,
155t, 157, 174–​175, 174t, 176, 179, 279, 280t, 389, 391,
496t, 501
Axis II disorders (SCID-​II),  475
Clinical Version (SCID-​CV),  158t, 160
DSM-​5 (SCID-​5),  135, 136t, 247, 271t, 272–​273, 336t,
337–​338, 346t, 362t, 363, 386t, 388, 413t, 438–​439,
439t, 448, 520, 548, 550
Clinical Trials Version (SCID-​5-​CT),  272
Clinical Version (SCID-​5-​CV),  272, 298–​299
Personality Disorders (SCID-​5-​PD),  135, 136t, 466, 467t,
469, 470, 478
Research Version (SCID-​5-​RV),  272, 413t
DSM-​IV (SCID-​IV),  246, 246t, 247, 315t, 316, 336t, 337–​338,
346t, 547t, 548, 550
DSM-​IV-​TR,  175
DSM-​IV-​TR for Axis I Disorders, Patient Edition
(SCID-​I/​P),  297t, 299, 304t
Structured Clinical Interview for DSM-​IV Childhood
Diagnoses (KID-​SCID),  272
Structured Clinical Interview for Pathological Gambling
(SCI-​PG),  413t, 415, 418
Structured Diagnostic Interview for Marital Distress and Partner
Aggression (SDI-​MD-​PA),  493, 493t
Structured Diagnostic Method (SDM),  519t, 522
Structured Interview for DSM-​IV Personality Disorders
(SIDP-​IV),  466, 467t, 470, 475
Subjective Opiate Withdrawal Scale,  364
Subjective Units of Distress Scale (SUDS),  278
Substance Abuse Treatment Scale (SATS),  441t, 449, 450t, 451
Substance Dependence Severity Scale (SDSS),  362t, 364,
366t, 367, 372, 386t
Substance Use Beliefs Questionnaire (SUBQ),  366t, 369
Suicidal Behaviors Questionnaire (SBQ),  196t, 199
4-​item,  196t, 199
SBQ-​R,  196t, 197t, 199, 200
Suicide Attempt Self-​Injury Interview (SASII),  196t, 197, 201,
202t, 203, 204
Suicide Behaviors Interview (SBI),  197t, 200
Suicide Ideation Scale (SIS),  196t, 199
Suicide Probability Scale (SPS),  567t, 571
Symptom Checklist-​90 (SCL-​90),  35
Revised (SCL-​90-​R),  498
Tampa Scale of Kinesiophobia (TKS),  616t, 618–​619
11-​item (TKS-​11),  616t, 619
Activity (TKS-​AA),  619
Somatic Focus (TKS-​SF),  619
Teacher Report Form (TRF), ASEBA,  54, 55t, 57, 59, 60t, 77t,
110–​111
Temperament Evaluation of Memphis, Pisa, Paris, and San
Diego (TEMPS),  178
Temptation and Restraint Inventory (TRI),  390t, 395
Temptations to Gamble Scale (TGS),  420t, 421, 422
The Oucher,  585t, 586–​587, 597, 597t
Therapy Attitude Inventory (TAI),  85t, 86
Timeline Followback Interview (TLFB),  372t, 373, 390t, 392,
393, 395, 397, 398, 399t, 401, 420t, 421, 423–​424, 424t,
441t, 449, 450t, 451
Top Problems,  143, 145
Youth, 41
Traumatic Events Questionnaire (TEQ),  342t
Traumatic Life Events Questionnaire (TLEQ),  342t, 343
Traumatic Stress Schedule (TSS),  342t, 343
Treatment Ambivalence Questionnaire (TAQ),  253–​254
UCLA PTSD index,  115–​116
University of Rhode Island Change Assessment (URICA),  390t,
394, 397, 399t, 400, 401

Urge-​Specific Questionnaire and General Change Strategies
Questionnaire (USS/​GSC),  366t, 371
Vancouver Obsessive Compulsive Inventory (VOCI),  322t, 323
Vanderbilt ADHD Diagnostic Parent and Teacher Rating
Scales, 55t, 56
Verbal rating scale (VRS),  620, 620t
Verbal Tactics Coding Scheme (VTCS),  496t, 501
Vineland Adaptive Behavior Scales, Second Edition
(VABS-​II),  55t, 56–​57
Visual analogue scales (VAS),  585t, 588, 590, 597t, 598, 619, 620t
Vulvar Pain Assessment Questionnaire Inventory (VPAQ),  529
Washington University WASH-​U-​KSADS. See Kiddie Schedule
for Affective Disorders and Schizophrenia for School-​
Age Children (K-​SADS)
Western Ontario and McMaster Osteoarthritis Index
(WOMAC), 611t, 614
West Haven–​Yale Multidimensional Pain Inventory
(MPI),  610–​611, 611t, 615–​616, 616t, 619, 620, 620t
61-​item, Modified instructions (MPI-​M),  616, 616t
Why Worry-​II (WW-​II),  300t, 302, 304t, 305
Willingly Approached Set of Statistically Unlike Pursuits
(WASSUP), 181t, 183
Wisconsin Personality Disorders Inventory-​IV (WISPI-​IV),  466,
467, 467t, 474
Assessment Instrument Index 637
World Health Organization Disability Adjustment Scale 2.0
(WHODAS 2.0), 137–​138, 138t, 140, 344
World Health Organization Quality of Life Survey–​BREF
(WHOQOL-​BREF),  399t
World Health Organization World Mental Health Composition
International Diagnostic Interview
(WHO WMH-​CIDI),  439
Worry and Anxiety Questionnaire (WAQ),  297, 297t, 304t
Yale–​Brown–​Cornell Eating Disorder Scale
(YBC-​EDS),  554, 554t
Yale–​Brown Obsessive-​Compulsive Scale
(Y-​BOCS),  322–​323, 322t
Pathological Gambling Modification
(PC-​YBOCS),  424t, 426
Symptom Checklist (Y-​BOCSC-​SC),  314, 315t
Yale Interactive Kinetic Environment Software
(YIKES), 229, 233
Young Adult Alcohol Consequences Questionnaire
(YAACQ), 390t, 393–​394, 399t, 400
Young Mania Rating Scale (YMRS),  181–​182, 181t, 184
Youth Self-​Report (YSR),  54–​55, 110–​111
Youth Severity Rating (YSR),  233
Youth Top Problems,  41
Zung Self-​rating Depression Scale (SDS),  158t, 159
 Author Index

Aabech, H. S.,  53 Acevedo, A.,  161

Aakhus, E.,  161 Achenbach, T. M.,  4, 9, 19, 33, 34, 35, 38, 49, 54, 55, 57, 78,
Aaroe, L. A.,  24 81, 87, 88, 104, 110, 111, 113, 232, 233
Aarons, G. A.,  19, 24, 446 Acheson, D. T.,  269
Aaronson, C.,  244 Achim, A. M.,  436
Aaronson, N. K.,  614 Achtrari, C.,  517
Aasland, O. G.,  448 Ackerman, B.,  104
Abbas, M.,  18, 24 Ackermann, K.,  385
Abbiati, I.,  521 Ackerson, T.,  449, 451
Abbott, B. V.,  491, 494, 500, 504, 507 Ackerson, T. H.,  449
Abbott, F. V.,  529 Acosta, D.,  157
Abbott, L. K.,  583 Acosta, M. C.,  360
Abbott, M. J.,  222, 254 Acquadro, C.,  614
Abdel-​Malak, B.,  134 Adaikan, P. G.,  518
Abdo, C.,  516, 518 Adair, C. E.,  437
Abdollahi, A.,  491 Adams, A.,  614
Abel, A.,  142 Adams, B. G.,  331, 332
Abel, K. M.,  437 Adams, H.,  608
Abela, J. R. Z.,  200 Adams, P.,  120
Abelskov, K.,  159, 161 Adams, S.,  583
Abelson, J. M.,  174 Adamson, S. J.,  392
Abikoff, H.,  57, 60 Addicoat, L.,  586, 587
Abitbol, V.,  583, 587, 598 Addington, D.,  440, 444
Ablow, J. C.,  111, 113 Addington, J.,  440, 444
Aboyans, V.,  193 Addis, M.,  199
Abraham, I. L.,  162 Addis, M. E.,  132, 133, 253, 272
Abraham, L.,  528, 530 Ade, M.,  158, 159
Abramov, L.,  527 Aderka, I.,  142
Abramowitz, J. S.,  251, 252, 268, 312, 313, 315, 317, 318, 319, Aderka, I. M.,  256
320, 323, 324, 325 Adjei, A., 59
Abrams, D. B.,  365, 369, 370, 371, 373 Adkins, B. J.,  413
Abrams, M. P.,  618 Adkins, J. W.,  339
Abrams, R. C.,  161, 165 Adler, A. B.,  334, 347
Abramson, L. Y.,  100, 177, 178 Adler, L., 62
Abu-​Saad, H.,  586 Adler, L. A.,  61
Abu-​Saad, H. H.,  587, 592 Admundson, G. J. G.,  618
640 author Index

Adolfsson, R.,  178 Allan, N. P.,  218, 280

Adson D.,  426 Allan, W. D.,  200
Aerts, L.,  518 Allardyce, J.,  437
Aeschlimann, A.,  616 Allen, A. J.,  59
Afifi, T. O.,  414, 417 Allen, B.,  252
Aggarwal, N. K.,  439 Allen, J.,  573
Aggen, S. H.,  244 Allen, J. L.,  219
Agosto, C.,  589 Allen, J. P.,  397, 401, 422
Agras, W. S.,  282, 544, 545, 546, 547, 548, 551, 552, 553 Allen, L. B.,  275, 279, 280, 281
Agrawal, A.,  361 Allen, N. B.,  383
Agrawal, S.,  392 Allen, R. R.,  620
Aguado, J.,  180 Allgood, S. M.,  498
Aguilar, A.,  281 Allik, J.,  474
Aguillard, N.,  574 Allin, M.,  437
Aguillard, R. N.,  574 Alloy, L. B.,  177, 178
Ahmeti-​Pronaj, A.,  4 Allsworth, J. E.,  517
AhnAllen, C. G.,  199 Almeida, C.,  574
Aikens, J.,  618 Almirall, D.,  103
Aikens, J. E.,  529 Almquist, J., 19
Aime, A.,  545 Aloia, M. S.,  563, 565
Aime, A. A.,  554 Alonso, J.,  193, 195, 201, 330, 609, 614
Aivadyan, C.,  388 Alonso, P.,  267
Ajdacic, V.,  564 Alpers, G. W.,  270
Akehurst, R., 61 Alpert, J. E.,  199
Akhtar, R.,  466, 468, 476 Alphs, L. D.,  198
Akiskal, H.,  178 Altamura, A. C.,  244
Akiskal, H. S.,  175, 176, 177, 178, 184, 295 Alterman, A.,  367
Akiskal, K. K.,  178 Alterman, A. I.,  367, 373, 389, 392, 397, 448
Alaatin, E.,  219 Alterman, I. S.,  162, 165
Alabi, D.,  202 Althof, S.,  521, 522, 530
Alahi, P.,  183 Althof, S. E.,  518, 520, 526, 530, 531
Albano, A. M.,  222, 223, 228, 233, 271 Altis, D.,  175, 176
Albert, P. S.,  174 Altman, E. G.,  182, 183
Alberts, N.,  598 Altoè, G.,  275
Alcaine, O.,  133, 294, 296 Altshuler, K. Z.,  17
Alcántara, C.,  345 Altshuler, L.,  174, 183
Alda, J. A.,  179 Aluwahlia, S.,  81, 86, 113
Al-​Dajani, N.,  476 Alvarez, J.,  330
Aldarondo, E.,  500–​501 Alvarez, K.,  228
Alden, L. E.,  3, 23, 252, xi Alvarez, W.,  338
Alderson, R. M.,  53 Alves, P. C. G.,  4
Aldinger, M.,  244 Alvir, J., 58
Aldridge, D.,  205 Alwyn, T.,  385
Aldridge, J. W.,  134 Amador, X. F.,  38, 180, 438, 449
Aldridge, T.,  392 Aman, M. G.,  86, 225, 226
Alegria, M.,  115 Amar, E.,  527
Alegría, M.,  439 Amaria, K.,  588
Alessi, C.,  563, 573 Amaya-​Jackson, L.,  23–​24
Alexander, G. M.,  472 Ambrosini, P.,  81, 86, 113
Alexander, L. D.,  249 Ambrosini, P. J.,  107, 222
Alexopoulos, G. S.,  134, 153, 154, 161, 165 Ameis, N.,  197, 200
Alfano, C. A.,  252 Ames, D.,  157
Alfano, L.,  553 Ames, M., 62
Algorta, G. P.,  52, 109, 182, 198 Amey, B.,  619
Ali, J.,  295 Amir, N.,  220, 323
Alicea Rodríguez, A.,  61 Ammerman, Y.,  423
Alkin, T.,  273, 275 Amorim, P.,  363, 439
Alkozei, A.,  252 Amsbary, M.,  381
Allan, C. L.,  158 Amsel, R.,  515, 527, 528, 529
Allan, J.,  162 Anand, V., 63
 author Index 641

Anastasi, A.,  9, 177 Antshel, K. M.,  57

Anastasiades, P.,  279 Apolone, G.,  614
Anastassiades, T.,  614 Appelbaum, P. S.,  440
Anastopoulos, A. D.,  50, 51, 63 Applegate, B.,  48, 83, 119
Anaya, Y.,  114 April, L. M.,  101, 107
Ancoli-​Israel, S.,  565, 569, 570, 574 Apter, A.,  200, 203
an der Heiden, W.,  436 Aradine, C.,  597, 598
Andersen, M.,  161, 165 Aradine, C. R.,  586, 587, 588, 597
Anderson, C.,  425, 448 Araga, M.,  179
Anderson, C. M.,  451, 452 Araya, M.,  345
Anderson, D.,  322 Arbabzadeh-​Bouchez, S.,  339, 439
Anderson, D. A.,  19, 401 Arbelaez, C.,  100–​101
Anderson, E. R.,  250 Arbisi, P.,  177
Anderson, J.,  361 Arbisi, P. A.,  xi
Anderson, J. E.,  583 Arbuckle, T. Y.,  393
Anderson, K. G.,  361 Arch, J. J.,  280
Anderson, K. O.,  618 Arean, P. A.,  341
Anderson, L. R.,  396 Arends, W.,  269
Anderson, M. L.,  620 Arendt, M.,  279, 437
Anderson, V., 52 Arensman, E.,  154
Anderson, W. M.,  566 Argeriou, M.,  367
Anderson Khan, K.,  596 Argyle, M.,  253
Andersson, A.,  385 Arias, B.,  247, 251
Andersson, G.,  116, 154, 268, 276, 281 Arias-​Carrión, O.,  270
Ando, K. B.,  573 Arkema, E. V.,  599
Andrade, J.,  395 Armani, A.,  178
Andrade, L. H.,  330 Armelius, B. A.,  451
Andrasik, F.,  592 Armey, M. F.,  205, 206
Andrea, H.,  479 Armfield, J. M.,  249
Andreas, S.,  156 Armor, D. J.,  393
Andreasen, N. C.,  116, 176, 394, 442 Armour, C.,  341
Andresen, R.,  444 Armstrong, J. M.,  111
Andreski, P.,  331 Armstrong, K. J.,  52
Andrews, B. P.,  337 Armstrong, N. P.,  446
Andrews, G.,  268, 293, 294, 295, 339 Arnau, R. C.,  153, 159
Andrews, J.,  117 Arndt, S.,  268
Andrews, R. K.,  115 Arnedt, J. T.,  563, 565
Andrews, T.,  199 Arnesen, H.,  272
Aneshensel, C. S.,  103 Arnett, A. B.,  50
Ang, R. P.,  55, 224 Arnkoff, D. B.,  269
Angell, K. E.,  100 Arnold, E. B.,  226
Angelucci, J., 88 Arnold, E. M.,  196
Angerious, M.,  448 Arnold, L. E.,  86
Angermeyer, M.,  193, 195, 201, 332 Arnow, B.,  136
Angermeyer, M. C.,  331, 437, 609 Arntz, A.,  251
Anglin, M. D.,  361 Aronson, M. J.,  364
Angold, A.,  47, 50, 53, 73, 100, 101, 102, 104, 105, 106, 107, Arora, P.,  20, 23
108, 109, 110, 113, 115, 218, 219, 225, 230 Arredondo, R.,  490
Angst, F.,  184, 616 Arrindell, W. A.,  276
Angst, J.,  178, 184, 564 Arterberry, B. J.,  384
Annis, H. M.,  370, 396 Arthaud, T. J.,  52
Anthenelli, R. M.,  360 Arts, S. E.,  587
Anthony, J. C.,  153, 338 Arvilommi, P.,  178
Antipova, A. V.,  268, 275 Asarnow, J.,  200
Anton, R. F.,  395 Asarnow, J. R.,  117
Antonelli, P.,  504 Åsberg, M.,  161, 165
Antonietti, J. P.,  504 Asboe, D.,  522, 531
Antony, M.,  139 Ascher, B. H.,  107
Antony, M. M.,  139, 143, 242, 244–​245, 246, 248, 249, 250, Ascherman, L. I.,  592
251, 252, 253, 255, 256, 257, 269, 273, 275, 277, 575, 591 Åsenlöf, P.,  598
642 author Index

Asgari, M. A.,  525 Badour, C. L.,  330

Ashbaugh, A.,  250 Badura, A.,  203
Ashby, J. S.,  617 Baer, B. A.,  545, 553
Asher, M. K.,  371 Baer, L.,  316
Asherson, P.,  47, 48, 61 Bagarozzi, D. A.,  503
Ashikaga, T.,  435 Bagby, R. M.,  10, 103, 160, 164, 466, 468, 469, 476, 477
Ashman, S. B.,  180 Bagdy, G.,  268
Askling, J.,  599 Bagge, C. L.,  110, 199, 200, 203, 206
Asmundson, G. J.,  618 Baglioni, C.,  564, 571
Asmundson, G. J. G.,  245, 302, 585, 591, 595, 596, 618 Bagner, D. M.,  80, 86
Asnis, G. M.,  200 Baguley, T., 10
Aspland, H., 81 Bahorik, A. L.,  449
Assari, S.,  180 Bahr, M.,  448
Asscher, J. J.,  84 Bähr, T.,  275
Atala, K. D.,  316 Bailey, B.,  588, 598
Atkins, D. C.,  305, 498, 508 Bailey, D.,  566
Atkinson, J. H.,  619 Bailey, K.,  272
Atkinson, S. D.,  117 Bailey-​Kloch, M.,  417
Atkinson, T. M.,  612 Bailin, A., 23
Attanasio, V.,  592 Baillargeon, L.,  564, 573
Attia, E.,  544, 545, 550, 552, 554 Bair, M. J.,  609
Au, A., 4 Baird, A. J.,  617
Au, J. R.,  20, 22 Bajunirwe, F.,  385
Aubry, J.,  178 Baker, A. S.,  165
Aubry, J.-​M.,  178 Baker, C. M.,  588
Aubry, T.,  437 Baker, D. G.,  332
Aucoin, K. J.,  73, 76 Baker, F. M.,  160, 164
Augenstein, T. M.,  38, 104, 106, 119 Baker, L. A.,  180
Augimeri, L. K.,  88 Baker, M. T.,  202, 203
August, G. J.,  53 Baker, P. N.,  437
Auriacombe, M.,  381 Baker, S. L.,  256
Austin, D.,  276, 281 Baker, S. R.,  256
Austin, D. W.,  280 Baker-​Dennis, A.,  546
Austin, J. L.,  422 Baker-​Ericzen, M.,  120
Austin, K.,  224 Bakhiyi, C. L.,  202
Avenevoli, S.,  100, 105, 218 Bala, D. A.,  56, 57
Averill, P.,  276, 277–​278 Balach, L.,  223
Awad, A. G.,  443 Baldacci, H. B.,  223
Axelson, D.,  102, 108, 176, 177 Balderrama-​Durbin, C.,  494, 503, 504
Axelson, D. A.,  106, 107, 110 Balderson, B. H.,  620
Ayers, C. R.,  250, 280 Baldessarini, R.,  174
Aykes, K., 48 Baldessarini, R. J.,  173, 174, 175–​176, 193
Azizian, A.,  49, 50 Baldwin, L. M.,  115, 181, 546
Azorin, J. M.,  182 Baldwin, R. C.,  154
Azrin, S. T.,  438 Ball, R.,  157, 613
Azur, M., 3 Ball, S. A.,  544
Ball, W. A.,  183
Bäärnhielm, S.,  439 Ballash, N. G.,  280, 281
Babcock, T. F.,  61 Balsis, S.,  472, 494
Babor, F. F.,  364 Baltas, Z.,  499
Babor, T.,  422 Baltrus, P.,  131
Babor, T. F.,  156, 387, 439, 448, 498 Banaji, M. R.,  37, 206
Baca-​García, E.,  197 Bancroft, J.,  521
Bacaltchuk, J.,  544 Bandell-​Hoekstra, E. N. G.,  592
Bach, B.,  476 Bandelow, B.,  243
Bachar, J. R.,  153 Banez, G. A.,  598
Bach-​Peterson, J.,  448 Bangs, M. E.,  117
Bacio, G.,  395 Bank, L., 86
Backhaus, J.,  573 Bankier, B.,  273
 author Index 643

Bannon, E. E.,  397 Barry, R. A.,  500, 508

Bannon, K.,  553 Barry, T. D.,  49
Baptista, C. A.,  243 Barsevick, A.,  574
Barbe, R. P.,  102 Bartels, S. J.,  443
Barber, B.,  522 Bartholome, L. T.,  552
Barber, J.,  144 Bartko, D.,  136
Barber, J. P.,  142, 277 Bartley, B. J.,  614
Barber, L. L.,  383 Basch, E.,  612
Barbery, V.,  200 Baschnagel, J. S.,  339
Barca, M. L.,  161, 162 Basco, M. R.,  17, 18, 22, 156, 161, 165, 270, 501
Barch, D. M.,  5, 107, 108, 113 Basile, J.,  102
Barclay, R.,  162 Basile, K.,  229
Bard, D. E.,  53, 56 Basler, H. D.,  617
Barder, H. E.,  436 Basoglu, M.,  282
Bar-​Haim, Y.,  220, 231 Basson, R.,  515, 528
Barkauskas, D. A.,  332 Basta, M.,  564
Barker, S.,  445 Bastiaansen, D.,  594
Barker, W.,  161 Bastiaansen, L.,  479
Barker, W. W.,  161 Bastien, C.,  573
Barkley, R., 61 Bastien, C. H.,  564, 572, 575
Barkley, R. A.,  4, 47, 50, 54, 58, 61, 62, 63, 78, 87 Batalden, P. B.,  599
Barlow, D.,  269, 271, 315, 521 Batalha, L.,  589, 590
Barlow, D. H.,  3–​4, 5, 135, 143, 203, 204, 219, 221–​222, 228, 243, Batalla, A.,  448
246, 251, 256, 266, 267, 268, 269, 270, 271, 272, 273, 274, 275, Batelaan, N. M.,  266
277–​278, 279, 280, 281, 282, 294, 295, 298, 315, 333, 337, 338 Bateman, A.,  204
Barnard, J. A.,  593 Bates, J. E.,  72
Barnes, G.,  416 Bates, M. P.,  114
Barnett, K.,  596 Battaglia, M.,  250
Barnett, N. P.,  397, 402 Battagliese, G.,  564
Barnett, V.,  17, 18, 22, 156, 270 Batterham, P. J.,  199
Barney, C. C.,  584 Batty, G. D.,  437
Barnow, S.,  244 Batty, M., 22
Barnum, D. D.,  593 Baucom, B.,  499, 501
Baron, D. A.,  374 Baucom, B. R.,  495
Baron, S. H.,  374 Baucom, D. H.,  313, 490, 495, 497, 498, 500, 501, 503, 508
Baroncelli, A., 84 Bauer, D., 84
Barr, L.,  446–​447 Bauer, J.,  268, 553
Barr, T.,  199 Bauer, M.,  178
Barraclough, C.,  436 Bauer, M. S.,  174, 183
Barrada, J.,  281 Bauer, N. S.,  63
Barrantes-​Vidal, N.,  178 Bauermeister, J. J.,  73
Barré, P. E.,  257 Baugher, M.,  116
Barrera, M.,  132 Baumann, B. L.,  21, 23
Barrera, T. L.,  243 Baumeister, D.,  447
Barrett, B.,  546 Baumeister, S. E.,  244
Barrett, P.,  220 Baumgaertal, A., 56
Barrett, P. M.,  226 Baumrind, N.,  330
Barrett, R. J.,  439 Bauserman, R.,  503
Barretto, K. M.,  330, 337 Baxter, M. L.,  518
Barrios, F. X.,  199, 200, 202, 203, 250, 618 Bay, R. C.,  165
Barrios, V.,  222, 275, 279, 280, 281 Bayon, V.,  569–​570
Barrocas, A. L.,  200 Beach, S. R. H.,  490, 494
Barron, N.,  445 Beale, E. E.,  206
Barrs, K. L.,  199 Beales, J. G.,  588
Barry, A. E.,  9 Beamon, T.,  153
Barry, C. T.,  50, 54, 55, 73, 74, 76, 79, 80, 81, 82, 84, 87–​88 Beard, C.,  275
Barry, D. T.,  547 Beardslee, W.,  117
Barry, K.,  199 Bearman, S. K.,  7, 23, 40, 41, 545
Barry, M. J.,  522 Bearman, S. R.,  143, 145
644 author Index

Beaton, D.,  619 Bellivier, F.,  174

Beattie, E.,  159, 162 Bellon, K. K.,  194
Beattie, P. F.,  612 Belotti, R.,  244
Beattie, S. G.,  3 Belsky, D. W.,  61
Beauchaine, T. P.,  305 Belter, R. W.,  18, 586
Beaudett, M. S.,  451 Beltran, I.,  383
Beaudoin, S.,  297, 305 Ben-​Abdallah, A.,  413
Beaulieu, Y.,  596 Benatti, B.,  244
Beaulieu-​Bonneau, S.,  564, 565, 566, 573, 576 Benazzi, F.,  178
Beaumont, P. J. V.,  555 Bender, D.,  272, 299, 470, 548
Beautrais, A.,  193, 195, 199, 201, 332 Bender, D. S.,  466, 475, 479
Beazley, M. B.,  244, 252, 253 Bender, M. B.,  59
Bech, P.,  160, 161, 165, 182 Bender, M. E.,  333, 334
Beck, A.,  110, 224 Bender, P. K.,  219
Beck, A. T.,  113, 132, 133, 136, 138, 139, 157, 180, 198, 199, Bendo, C. B.,  594
200, 204, 276, 293–​294, 300, 301, 312, 338, 340, 347, 498, Benini, F.,  589
553, 574, 575, 613 Benjamin, B.,  587, 598
Beck, E.-​M.,  446 Benjamin, L. S.,  466, 467, 469
Beck, J.,  110, 224, 396 Bennett, M.,  448
Beck, J. G.,  339, xi Bennett, S.,  588
Beck, J. S.,  139, 141–​142 Bennett, S. M.,  608
Beck, L.,  53, 56 Bennett-​Levy, J.,  294
Beck, S.,  199 Benningfield, M. M.,  22
Becker, A.,  543 Benoit, K.,  219, 252
Becker, E. M.,  19, 20, 24 Benore, E.,  598
Becker, K. D.,  xi Ben-​Porath, Y. S.,  35, 470, 609, 614
Becker, S. P.,  48 Benson, K. T.,  476
Beckham, J. C.,  330, 331 Benson, L. E.,  528
Beckman, A.,  198 Bentall, R. P.,  180, 437
Beckner, V. L.,  132 Bent-​Hansen, J.,  161, 165
Bedard-​Gilligan, M.,  334 Bentley, K.,  201
Bedics, J. D.,  305 Bentley, K. H.,  203
Bedoya, D. D.,  24, 177 Benton, S. A.,  3
Bedoya, L.,  385–​386 Ben-​Zeev, D.,  452
Beekman, A. T.,  141, 266, 295 Berardo, C. G.,  436
Beekman, A. T. F.,  131, 154 Berde, C.,  596
Beer, D. A.,  316 Beresford, T.,  174
Beesdo, K.,  266, 267, 270, 293, 294, 295 Berg, E.,  256
Begaz, T.,  426 Berg, K. C.,  547, 548, 549, 553
Begg, M. D.,  437 Berg, S.,  154, 157
Beglin, S. J.,  549, 554 Berger, C.,  614
Behan, P. O.,  574 Bergeron, D.,  545
Behar, E.,  133, 294, 296 Bergeron, L.,  108
Behn, J.,  115 Bergeron, S.,  517–​518, 529, 530
Beidas, R. S.,  12, 21, 23, 24, 42, 142 Berghout, C.,  479
Beidel, D. C.,  218, 224, 229, 233, 250, 252, 253 Berghuis, H.,  479
Beil, T. L.,  155 Bergin, A. E.,  vii
Bejerot, S.,  47, 48 Berglund, P.,  132, 173, 204, 243, 267, 272–​273, 294, 296, 313,
Bekker, E. M.,  61 331, 343
Belanger, A. J.,  442 Berglund, P. A.,  542
Belanger, L.,  564, 566, 570, 572, 573, 574 Bergly, T. H.,  394
Bélanger, L.,  564 Bergman, R. L.,  222, 230
Belden, A.,  111 Berg-​Nielsen, T. S.,  107, 108
Belden, A. C.,  101, 107, 108, 109 Bergström, J.,  268
Belew, J. L.,  584 Bergstrom, M. K.,  24
Bell, R.,  339 Berk, M.,  177, 178, 200
Bell, R. J.,  517 Berking, M.,  282
Bellack, A. S.,  440, 447, 451 Berkman, L. F.,  163
Bellamy, N.,  614, 620 Berkman, N. D.,  544
Belleville, G.,  572, 574 Berlim, M. T.,  199
 author Index 645

Berlin, H. A.,  312 Biederman, J.,  219

Berliner, L.,  21, 23 Biehn, T. L.,  341
Berman, A. L.,  193, 195 Bieling, P. J.,  3, 23, 143, 252, 575, xi
Berman, N.,  324, 325 Bienvenu, M. J.,  503
Berman, N. C.,  252, 268 Bieri, D.,  587
Berman, S. L.,  219, 231 Bierman, K. L.,  78
Berman, S. R.,  573 Biggs, B.,  595
Bernal, G.,  117 Biggs, J. T.,  181, 182
Bernardo, M.,  448 Biggs, M.,  440
Bernd, L.,  163 Biggs, M. M.,  17
Berndtsson, Å.,  436 Bijttebier, P.,  84, 595, 613
Bernert, R. A.,  194, 205 Bilder, R. M.,  113
Bernet, W.,  491 Bilker, W.,  160
Bernhard, B.,  178 Bilker, W. B.,  444
Bernier, A.,  596 Billiard, M.,  564
Berninger, A.,  332 Billington, D. R.,  18, 24
Berns, S.,  498 Binik, Y. M.,  257, 515, 517, 520, 527, 528, 529, 530
Berns, S. B.,  40 Binkoff, J. A.,  370
Berns, S. M.,  444 Birchler, G. R.,  501
Bernstein, A.,  10, 111, 133, 274, 280 Birchwood, M.,  436, 444
Bernstein, A. D.,  12 Bird, H.,  79, 81, 83, 86, 87, 113
Bernstein, B. H.,  585 Bird, H. R.,  81, 103, 108, 113, 114, 115
Bernstein, D. A.,  282 Bird, V.,  159
Bernstein, I. H.,  10, 109 Birley, J. L. T.,  156, 157, 447
Berntson, L.,  588 Birmaher, B.,  53, 100–​101, 102, 106, 107, 108, 109, 110, 115,
Berridge, K. C.,  134 116, 176, 177, 178, 182, 223, 225
Berry, D. T. R.,  61 Birmaher, B. J.,  177
Berry, K.,  142 Bishop, D. S.,  115, 181, 546
Berry, R. B.,  566 Bishop, S. B.,  199
Berscheid, E.,  545 Bishop, S. R.,  529, 595, 613
Bertholet, N.,  385 Bitran, S.,  281
Berthoz, S.,  544 Bittencourt, J.,  304
Bertoni, A.,  504 Bittner, A.,  218
Bertrand, J.,  302 Bitzer, J.,  517
Berv, D. A.,  178 Bivalacqua, T. J.,  530
Besel, K.,  370 Bixler, E. O.,  564
Besnard, A.,  182 Bizzini, V.,  178
Besset, A.,  564 Bjerkeset, O.,  178
Bessmer, J., 80 Björgvinsson, T.,  275
Best, D.,  366 Bjorvatn, B.,  573
Best, M.,  494 Black, C. L.,  178
Betthauser, L. M.,  194 Black, C. M. D.,  549, 554
Beusterien, K., 61 Blackwell, A.,  47, 48
Beutler, L. E.,  vii Blackwell, B.,  443
Beyer, J.,  597, 598 Blackwood, D.,  268
Beyer, J. E.,  586, 587, 588, 597 Blader, J. C.,  176
Bhandari, R. P.,  599 Blaine, J.,  364, 367, 388
Bhatia, T.,  448 Blair, K.,  444
Bhattacharya, R. K.,  518 Blair, R. J. R.,  76
Bhave, S. V.,  385, 400, 402 Blais, F.,  302
Bhugra, D.,  439, 499 Blais, F. C.,  575
Bhui, K.,  392 Blais, M. A.,  199, 275
Bhuiya, P.,  574 Blake, D. D.,  336, 337, 340, 343, 440
Bhuiyan, N.,  79, 80 Blanchard, E.,  271
Bhuyan, N.,  389 Blanchard, E. B.,  337, 338, 340, 425
Bianchi, K. N.,  251 Blanchard, J.,  158
Bickerton, W. L.,  117, 118 Blanchard, J. J.,  442
Bickman, L.,  17, 18, 22, 23, 24, 56 Blanchard, K. A.,  368, 373
Biddle-​Higgins, J. C.,  387 Blanco, C.,  176, 252, 253, 415, 426, 473
Bieber, C.,  392 Bland, S.,  197, 204
646 author Index

Blane, H. T.,  396 Boisvert, J.-​M.,  302

Blankenship, S.,  109 Boisvert, J. M.,  305
Blankenstein, N.,  276 Boivin, M., 72
Blanton, H.,  206 Boivin, M. K.,  250
Blaschke, T.,  443 Bolano, C.,  112, 113, 119
Blasco-​Fontecilla, H.,  197 Bolhofner, K.,  177
Blashfield, R. K.,  387, 466, 467, 470, 474 Bollini, P.,  345
Blaszczynski, A.,  423 Bölte, S.,  56, 62
Blaya, C.,  268 Bolton, J. M.,  332
Blazer, D.,  153 Bolwig, T. G.,  182
Blazer, D. G.,  153, 294, 295, 473 Bonanno, G. A.,  334
Blechert, J.,  256, 268 Bonar, E. E.,  397
Bledsoe, S. E.,  18, 23 Bond, D.,  551, 552
Blehar, M. C.,  116 Bond, M.,  468, 478
Bleiberg, J.,  332 Bond, S. S.,  612
Bleuler, E.,  435 Bondevik, G. T.,  573
Blick, G.,  518 Bondolfi, G.,  178
Bliese, P. D.,  347 Boness, C. L.,  388
Bloch, M. H.,  220, 231 Boney-​McCoy, S.,  344, 498, 503–​504
Bloch, P.,  451 Bonfils, K.,  446
Block, J.,  471 Bongers, I. L.,  594
Block, R. I.,  269 Bonke, B.,  574
Bloomquist, M. L.,  81 Bonn, K.,  159, 163
Blount, R. L.,  5 Bonnet, M. H.,  575
Blow, F.,  199 Boolell, M.,  522
Blow, F. C.,  180, 359 Boomsma, D. I.,  52
Blum, N.,  466 Boon, E.,  543
Blume, S. B.,  414, 415, 419 Boonstra, A. M.,  61
Blumenthal, M. D.,  153 Booth, B. M.,  359
Blumenthal, R.,  451, 545 Booth, M.,  361
Boardman, H. F.,  564 Bootzin, R. R.,  575
Bobes, J.,  367 Bopagoda, K.,  332
Bobes Bascarán, T.,  367 Borden, J. W.,  250
Bodell, L. P.,  542 Borenstein, M.,  451
Bodenmann, G.,  503, 504 Borgaro, S., 17
Bodin, S. D.,  74, 76, 84 Borges, G.,  193, 195, 201, 204, 381
Boe, H.,  142 Borkovec, T. D.,  133, 282, 293, 294, 296, 299, 300, 303,
Boeding, S. E.,  313 304, 305
Boehlecke, B.,  563, 573 Born, C.,  178
Boehnke, J. R.,  22, 24 Bornstein, R. F.,  177
Boeren, R. G.,  596 Borschmann, R.,  437
Boergers, J.,  202 Borszcz, G. S.,  608
Bogardis, J.,  392 Borthwick, C.,  619
Bogart, K.,  322–​323 Bortolomasi, M.,  387
Bogduk, N.,  583, 585, 608 Borus, J.,  175, 247, 272, 299, 316
Bögels, S. M.,  250, 252 Borza, T.,  161
Boggs, C.,  466, 470, 472 Bosanac, P.,  436, 549
Boggs, C. D.,  472 Bosch, J.,  344
Boggs, S. R.,  79, 80, 86 Boschen, M. J.,  250
Bogie, N.,  223 Bosley, H. G.,  145
Bohl, J.,  423 Bosma, H.,  159, 163
Bohman, S.,  276, 281 Bossuyt, P. M.,  37
Bohmstedt, G.,  545 Bossuyt, P. M. M.,  11
Bohn, M. J.,  396 Bostic, J. Q.,  17, 18, 22, 156, 270
Bohn, P.,  269 Boström, K. B.,  136
Bohnena, A. M.,  583 Both, S.,  517
Bohnenkamp, J. H.,  22 Bothwell, S.,  140, 444, 545
Böhnke, J. R.,  479 Bottesi, G.,  275
Boiler, M.,  439 Botticello, A. L.,  103
Boiman, E.,  180 Botzet, A.,  415, 416, 417, 420, 424
 author Index 647

Bouchard, C.,  415, 528 Braver, E. R.,  332

Bouchard, S.,  282, 575 Braver, S.,  619
Boudewyns, P.,  340 Breau, L.,  621
Boudreau, G.,  545 Breaux, R. P.,  47
Bouman, T. K.,  282 Breckenridge, J.,  156
Boundy, M.,  574 Breda, C.,  18, 22
Bourgon, G.,  3, 23, xi Bredemeier, K.,  132
Bourne, L.,  272 Breen, R. B.,  419
Bourque, J.,  437 Breier, A.,  435
Bourrillon, A.,  583, 587, 598 Breiner, J. L.,  80
Bourtress, K.,  383 Breivik, H.,  609
Boustani, M., xi Breivik, K.,  614
Bouton, M. E.,  219, 269 Brekke, J. S.,  435, 440
Bouvard, M.,  276 Bremmer, M. A.,  295
Bovin, M. J.,  330, 333, 334, 335, 337, 341, 347 Brendgen, M., 72
Bowden, C. L.,  182 Brener, L.,  392
Bowen, R.,  272 Brennan, J., 76
Bower, S.,  175 Brennan, P. A.,  243
Bowie, C. R.,  443 Brenner, L. A.,  194
Bowlby, J.,  219 Brensinger, C. M.,  444
Boxmeyer, C. L.,  54 Brent, D.,  53, 100–​101, 107, 114–​115, 116, 117, 177
Boyce, P.,  153 Brent, D. A.,  101, 102, 106, 107, 110, 113, 115, 194, 195, 197,
Boyce, W. T.,  111 204, 223, 593
Boyd, B. L.,  199 Breshears, R. E.,  194
Boyd, J.,  451 Breslau, J.,  330, 345
Boyd, M. R.,  24 Breslau, N.,  331, 339, 343, 345, 347
Boyd, S. E.,  465, 466, 468, 469, 471, 472, 474, 475 Bresnahan, M.,  437
Boydell, J.,  437 Brestan, E. V.,  86
Boyer, C. A.,  450 Brett, E. I.,  417
Boyer, R.,  295 Brewer, J. A.,  134
Boyer, S. C.,  528 Brewer, J. L.,  199
Boyle, G. J.,  473 Brewin, C. R.,  330, 333
Boyle, M. H.,  108, 490 Breyer, J.,  415, 416, 417, 420, 424
Brabender, V. M.,  3 Brickman, A.,  174
Brace, M. J.,  595 Bridge, J.,  116, 177, 593
Brackbill, R. M.,  332 Bridge, J. A.,  102
Bracken, B. A.,  9 Bridges, M.,  491
Bradbury, T. N.,  493, 497, 498, 501, 504 Bridgewater, C. L.,  592
Bradizza, C. M.,  383 Briggs-​Gowan, M.,  49
Bradley, A. M.,  385 Bright, A.,  545, 553
Bradley, B.,  371 Bright, P.,  274, 275–​276, 281, 282
Bradley, B. P.,  220 Brighton, H.,  34, 35
Bradley, J., 22 Brill, P.,  392
Bradley, K. A.,  341, 386 Brillon, P.,  302, 305
Bradley, L.,  554 Brink, T. L.,  158, 159
Bradshaw, K. R.,  452 Brioschi, R.,  616
Braet, C.,  117, 547, 554 Britt, M.,  156, 160
Braham, L.,  18, 24 Britton, P. C.,  203
Brailey, K.,  332 Brna, P.,  585
Brame, B. U.,  72 Broadbent, J. M.,  71, 75
Brams, M., 59 Broch, L.,  563, 565
Bramson, R.,  153, 159 Brock, R. L.,  86, 500, 508
Brandenburg, N.,  620 Brockel, J.,  619
Bränholm, I. B.,  522 Brodard, F.,  504
Brar, S.,  253 Brodaty, H.,  153, 159, 162
Brasic, J.,  81, 86, 113 Broderick, J. E.,  616
Braun, M.,  268 Brodersen, A. M.,  159, 161
Braünig, P.,  182, 183 Brodsky, B. S.,  332
Braunstein, G. D.,  521 Brody, D. J.,  132
Brausch, A. M.,  199 Broe, G. A.,  158
648 author Index

Broekman, T.,  277 Brummelte, S.,  584

Broidy, L. M.,  72 Brunette, M. F.,  437, 448
Brolin, R. E.,  554 Bruni, B.,  118
Bromet, E. J.,  193, 195, 201, 331 Bruns, D. E.,  37
Broocks, A.,  573 Brunsden, V., 10
Brookman-​Frazee, L.,  120 Brunt, S.,  276, 281
Brooks, G. W.,  435 Bryan, A.,  197
Brooks, R.,  566 Bryan, C.,  197, 546
Brooks, S. J.,  106, 108, 109, 110, 117 Bryan, C. J.,  199, 204
Broome, K. M.,  370 Bryant, B.,  253
Broomfield, N. M.,  571 Bryant, D., 72
Brotman, M.,  112 Bryant, F. B.,  140
Brotman, M. A.,  112 Bryant, J.,  392
Brotto, L.,  515, 521, 522, 527, 528, 531 Bryant, R. A.,  330, 331, 333
Brotto, L. A.,  517, 518 Bryant, S. L.,  202
Brouillard, P.,  524, 531 Bryant-​Waugh, R.,  547
Brovedani, P., 59 Bryant-​Waugh, R. J.,  547
Brown, A. S.,  437 Bryson, S.,  546
Brown, C.,  142, 177, 275, 521, 528, 530 Bryson, S. W.,  544, 545, 546, 553, 554
Brown, C. H.,  113 Bucci, S.,  142
Brown, E. J.,  252 Buchan, G.,  366, 373
Brown, F.,  296 Buchana, M.,  442
Brown, G.,  199, 300, 301, 338, 340, 347, 498, 574 Buchanan, J.,  159, 164
Brown, G. K.,  113, 136, 157, 194, 195, 197, 199, 204, 205, 301, Buchanan, R. W.,  438, 442
498, 553, 575 Buchanan, W. W.,  614
Brown, G. K., Jr.,  198 Bucher, M. A.,  465
Brown, G. W.,  447 Buchholz, A.,  392
Brown, J., 3 Bucholz, K.,  381, 416
Brown, J. M.,  392 Bucholz, K. K.,  364, 388, 394
Brown, K.,  109 Buckley, A. F.,  280, 281
Brown, K. M.,  100 Buckley, P. F.,  439, 452
Brown, L. M.,  220 Budney, A.,  381
Brown, L. S.,  373 Budney, A. J.,  364, 368, 373, 374
Brown, M. T.,  583 Budney. A. J.,  369
Brown, M. Z.,  196, 197, 203, 204 Buergener, F.,  244, 252, 253
Brown, N. V.,  86 Buerger, A.,  547
Brown, P. J.,  251, 343 Bufferd, S. J.,  102, 107, 108, 119
Brown, S.,  361 Bufka, L. F.,  3
Brown, S. A.,  396, 415 Bugarski-​Kirola, D.,  436
Brown, T.,  271, 315 Buhr, K.,  297, 302
Brown, T. A.,  135, 143, 221–​222, 246–​247, 251, 267, 268, 269, Buhrman, M.,  276, 281
270, 271–​272, 273, 274, 275, 277, 279, 280, 281, 283, 294, Bui, E.,  133
295, 296, 298, 305, 315, 316, 338, 542 Buick, D.,  613
Brown, T. E.,  52 Buis, T.,  133, 139
Brown, W. C.,  360 Buitelaar, J. K.,  61
Browne, N.,  371 Bujold, A.,  425
Brown-​Jacobsen, A. M.,  224 Bukowski, W. M.,  302
Brownley, J.,  417 Bukstein, O. G.,  86
Brownley, K. A.,  544 Bukumiric, Z.,  160
Brown T. A.,  242 Bulik, C. M.,  544
Brozovich, F.,  254 Bullock, W. A.,  446
Brubakk, A. M.,  107 Bunde, M.,  500
Bruce, B. K.,  595 Bunford, N., 53
Bruce, M. L.,  159 Bunnell, B. E.,  250
Bruce, S. E.,  267 Burchett, B.,  473
Bruchmüller, K.,  20, 39 Burdick, K.,  178
Bruehl, S.,  585 Burg, M. M.,  330
Bruer, E. H.,  198 Burge, D.,  113, 115
Bruffaerts, R.,  542 Burgers, D. E.,  38, 74, 104, 119
Brugha, T. S.,  331, 339, 439 Burgess, N.,  333
 author Index 649

Burgess Moser, M.,  498 Cadeddu, M.,  178

Burke, A. K.,  332 Cadigan, J. M.,  384
Burke, E. J.,  592 Cadoret, R.,  388
Burke, J.,  156, 364, 439 Caes, L.,  596
Burke, J. D.,  73 Cafri, G.,  545
Burke, J. R.,  153 Cahalan, D.,  393
Burke, R. H.,  394 Cahill, B. S.,  157
Burke, R. S.,  415 Cahill, S. P.,  325
Burke, W. J.,  162 Cai, L.,  107, 110
Burlingame, G. M.,  4, 137, 143 Cairney, J., 5
Burnett, A.,  522, 524, 529 Calabrese, J.,  176
Burns, B. J.,  17, 113, 118 Calabrese, J. R.,  24, 176, 177, 178, 181, 182
Burns, C. T.,  161 Calabresse, J. R.,  178
Burns, G. L.,  48, 50, 51, 323 Calamari, J. E.,  324
Burns, J. W.,  615, 618, 620 Calati, R.,  202
Burns, K.,  343 Calder, A. J.,  75, 83–​84
Burns, P.,  526 Calhoun, C. D.,  4, 24
Burns, T.,  444 Calhoun, E. A.,  518
Burrows-​Mclean, L.,  57, 59 Calhoun, P. S.,  331, 341
Bursch, B.,  599 Calhoun, S.,  564
Burstein, M.,  100, 218 Callahan, C.,  163
Burt, S. A.,  72 Callahan, J. L.,  392
Burton, H. L.,  449 Callahan, S. T.,  542
Burton, S.,  417 Callcott, P.,  281
Burtt, C.,  447 Calmes, C.,  451
Burwell, R.,  543 Calugi, S.,  553
Burwinkle, T. M.,  594 Calvo, M.,  274
Busby, D. M.,  494, 523 Calvocoressi, L.,  220, 231
Busch, A. B.,  360 Calzada, E., 86
Busch, A. J.,  476 Camacho, M.,  178
Bush, A. J.,  564, 574 Camara, W. J.,  33
Bush, K. R.,  341, 386 Cameron, L. D.,  613
Bushmakin, A. G.,  528 Cameron, R. P.,  347
Bushnell, M. C.,  608 Camilleri, A. C.,  392
Buskens, E.,  614 Campbell, C. D.,  19
Buško, V.,  524, 531 Campbell, C. M.,  609
Busschbach, J. J. V.,  479 Campbell, D.,  229, 490
Bussing, R.,  59, 435 Campbell, F.,  588
Buster, J. E.,  521 Campbell, J.,  614
Butcher, J. N.,  507, 614 Campbell, K.,  435
Butler, G.,  294 Campbell, L.,  316
Butler, M.,  200 Campbell, L. A.,  246–​247, 267, 271–​272, 283, 296, 298,
Butterfield, M. I.,  437 305, 338
Butzlaff, R. L.,  447, 451 Campbell, M.,  584
Bux, D. A.,  368, 373 Campbell, S.,  153, 154
Buysse, D.,  563, 565 Campbell, W. K.,  415
Buysse, D. J.,  564, 565, 569, 570, 573, 574 Campbell-​Sills, L.,  250
Buysse, D. J., III,  180 Camper, P.,  199
Byerly, M. J.,  138–​139 Campo, J. V.,  593
Byers, E. S.,  515, 524 Campus, A.,  178
Byford, S.,  117, 118 Camuri, G.,  244
Bystritsky, A.,  269, 275, 277, 278, 279 Cancro, R.,  442
Canino, G.,  73, 75, 83, 103, 113, 114, 115
Caballo, V. E.,  247, 251 Canino, G. J.,  115
Cabrera, O.,  347 Cannon, T. D.,  437
Cacciola, J.,  367 Cano, A.,  608
Cacciola, J. S.,  367, 373, 389, 392, 397 Can Serefoglu, E.,  518
Caci, H.,  47, 48 Cantor-​Graae, E.,  437
Caciola, J. S.,  373 Cantwell, D. P.,  105
Caddell, J. M.,  333, 334, 337, 339, 343–​344 Cao, C.,  341
650 author Index

Capaldi, D., 74 Carter, M.,  451

Capaldi, D. M.,  74 Carter, M. M.,  251, 252, 275, 279
Cappelleri, J. C.,  526, 528 Carter, R.,  218
Capron, D. W.,  280 Carter, R. M.,  295, 296
Capucci, S.,  596 Carusi, D. A.,  162
Caputi, P.,  444 Carvalho, A. F.,  178
Caputo, G. C.,  274, 275–​276, 277, 281, 282 Carver, C.,  183
Carbonari, J.,  397 Carver, C. S.,  174, 178, 183
Carbonari, J. P.,  370, 397 Casares, M. J.,  367
Carbonneau, C.,  297 Casas-​Brugué, M.,  47, 48
Carbray, J. A.,  178 Case, B. G.,  473
Cardenas, S. J.,  252 Casement, M. D.,  345
Cardillo, J. E.,  143, 505 Caserta, D. A.,  59
Cardin, D.,  203 Casey, D. M.,  417
Cardish, R. J.,  204 Casey, K. L.,  608
Cardone, L.,  499 Casey, L. M.,  281
Carek, P. J.,  347 Cashel, M.,  175
Carey, K. B.,  383, 394, 396, 422, 438, 448, 449 Cashel, M. L.,  19, 20
Carey, M. P.,  223, 394, 396, 438, 448, 449, 515, 530 Cashman, L.,  340
Carey, S.,  132, 137 Cashman-​McGrath, L.,  298
Carlander, B.,  564 Casillas, A.,  466, 467, 475, 476, 479
Carlbring, P.,  276, 281 Caspi, A.,  61, 71, 75, 116, 436
Carleton, R. N.,  245, 250, 251, 302, 618 Caspi, Y.,  343
Carli, G.,  589 Caspi-​Yavin, Y.,  345
Carlino, A. R.,  102 Cassano, G. B.,  38, 178
Carlson, C.,  503 Cassidy, E.,  413
Carlson, G. A.,  33, 102, 107, 108, 119, 176 Cassidy, J.,  294
Carlson, M.,  158 Cassidy, K. A.,  180
Carlson, P. J.,  269 Cassidy, S. M.,  545
Carlsson, S. G.,  618 Cassin, S. E.,  252
Carmen Viana, M.,  331 Casson, P. R.,  521
Carmichael, D. H.,  233 Castarlenas, E., 24
Carmody, T.,  102, 117 Castellani, A. M.,  490, 497, 501
Carmody, T. J.,  136, 138–​139 Castellini, G.,  544
Carneiro, A. H. S.,  178 Castellví, P.,  448
Carney, C. E.,  565, 566, 567, 568t, 569, 570, 573, 574, 575 Castle, D.,  436, 542
Carnrike, C. L. M.,  618 Castle, D. J.,  439, 549
Carolan, S.,  621 Castle, N.,  162
Caron, J.,  445 Castonguay, L. G.,  vii
Carosella, A.,  393 Castro, C. A.,  206, 332, 333, 347
Carpenter, K. M.,  364, 367, 388 Catalan, J.,  522, 531
Carpenter, W. T.,  442 Catalano, R. F.,  73
Carpenter, W. T. J.,  444 Cataldo, M. F.,  72
Carpenter-​Song, E.,  33 Catania, J.,  522
Carpentier, P. J.,  47, 48 Catania, J. A.,  526
Carper, M. M.,  231 Catchpoole, R.,  20, 22
Carpino, E.,  596 Cather, C.,  438
Carr, A.,  503 Catley, D.,  552
Carr, D. B.,  620 Caudle, H.,  542
Carrafa, G. P.,  620 Cauffman, E., 74
Carrère, S.,  498 Cavaco-​Paulo, A.,  374
Carrier, L.,  161 Cavanaugh, S. V.,  157
Carrier, S.,  527, 528 Cavell, T. A.,  491
Carrieri, K. L.,  448 Cavelti, M.,  446
Carroll, A. E.,  63 Cecil, C. A.,  76
Carroll, B. J.,  109 Çelebi, F.,  243
Carstairs, G. M.,  447 Cella, D.,  21, 49, 110
Carta, M. G.,  178 Cepeda-​Benito, A.,  504, 507
Carter, J. C.,  545, 550, 552, 554 Cerny, J. A.,  282
Carter, K.,  294, 302 Ceroni, D.,  587
 author Index 651

Cervena, K.,  564 Chen, J.,  81, 516, 518

Cha, C. B.,  332 Chen, J. Y.,  113
Chadwick, P.,  120, 141 Chen, M.,  332
Chaikelson, J. S.,  393 Chen, M. C.,  134
Chainhop, P.,  586 Chen, V. V.,  19, 20, 24
Chakrabortya, S.,  448 Chen, X.,  332
Chamberlain, P.,  72, 74, 81, 86 Cheng, D. M.,  385
Chamberlain, S. M.,  528 Chenoweth, L.,  159, 162
Chambers, A. L.,  490, 498 Chentsova-​Dutton, Y. E.,  103
Chambers, C. T.,  584, 585, 587, 588, 608 Cherkin, D. C.,  620
Chambers, W.,  106 Cherner, R. A.,  528
Chambers C. T.,  591 Chevron, E. S.,  134
Chambless, D. L.,  244, 251, 252, 253, 274, 275–​276, 277, 279, Chey, T.,  331
281, 282–​283, 301, vii Chhean, D.,  337
Champion, G.,  587 Chiang, A.,  565
Champion, G. D.,  586, 587, 588 Chiang, B.,  244, 253
Champoux, M.,  219 Chiang, C. N.,  374
Chan, A. W.,  393 Chibnall, J. T.,  613
Chan, J. A.,  3 Chick, G.,  102
Chan, L. F.,  594 Chikaraishi, C.,  443
Chan, S.,  621 Chikoore, M.,  18, 24
Chandrasekhar, C.,  316 Chilcoat, H. D.,  343
Chaney, B. H.,  9 Childs, J. D.,  619
Chang, B.,  201 Childs, R. A.,  18
Chang, B. P. I.,  145 Chiles, J. A.,  199, 202
Chang, J. P.,  22 Chinman, M.,  442
Chang, M.,  158 Chiu, H.,  157
Chant, D.,  437 Chiu, H. F.,  42
Chanthavanich, P. A.,  587 Chiu, W. T.,  131, 266, 267, 542
Chao, C. M.,  499 Chivers, M. L.,  528
Chapman, H.,  397 Chmielewski, M.,  10, 179
Chapman, J.,  178 Cho, Y.,  276
Chapman, L. J.,  178 Choi, K. M.,  504
Chapman, T. F.,  116 Choi, P.,  543
Charak, R.,  341 Choi, S., 21
Charalambous, A.,  180 Choi, S. W.,  21, 110
Chard, K.,  334 Choi, T. K.,  281
Chard, K. M.,  334, 344 Choo, E.,  588
Charlson, M.,  153, 154 Chopra, H. P.,  154
Charney, D. S.,  314, 322, 336, 440 Chorney, J. M.,  584
Charney, M. E.,  340, 345 Chorpita, B.,  227, 231
Charter, R. A.,  10 Chorpita, B. F.,  4, 7, 12, 18, 40, 41, 111, 118, 143, 145, 227,
Charvoz, L.,  504 228, 249, 272, 295, xi
Chassin, L.,  382, 383 Chotpitayasunondh, T.,  587
Chatterji, S.,  137, 138, 337 Chou, C.-​P.,  158
Chaudhry, B. R.,  11 Chou, J. C.,  442
Chaudhuri, A.,  574 Chou, P. S.,  381
Chauncey, D. L.,  466, 469 Chou, S. P.,  295, 330, 331, 332, 334, 362, 363, 381, 382, 384,
Chavarria, E. A.,  9 388, 389
Chavez, L.,  114 Choukas-​Bradley, S.,  4, 24
Chavira, D. A.,  272 Chow, C. W.,  199
Cheetham, A.,  383 Chow, S. M.,  594
Chelminski, I.,  161, 165, 178 Chrestman, K. R.,  343
Chelonis, J., 57 Christ, M. A. G.,  72
Chen, C.,  504 Christensen, A.,  490, 495, 496–​497, 498, 501, 501, 503, 508
Chen, C. S.,  180 Christensen, B. S.,  516, 517, 518
Chen, D., 74 Christensen, C.,  523
Chen, E.,  269 Christensen, H.,  153, 199
Chen, H.-​C.,  178 Christian, R. E.,  84
Chen, I. Y.,  564, 571 Christon, L. M.,  4, 17, 24
652 author Index

Christova, P.,  336 Clemens, J. Q.,  518

Chronis, A. M.,  57, 59 Clevenger, W., 59
Chronis-​Tuscano, A.,  103 Clifford, P. R.,  397
Chu, A.,  381 Clinch, J.,  583, 593, 596, 598
Chu, B. C.,  117 Clinton, M.,  593
Chuang, S.,  175 Cloitre, M.,  330
Chudzynska-​Pomianowska, E.,  587, 588, 598 Cloninger, C. R.,  388
Chumbler, N.,  609 Cloud, R.,  370
Chung, T.,  381, 543 Clouse, G.,  137, 143
Church, A. S.,  3 Clum, G. A.,  199
Churchill, E.,  250 Clyti, N.,  583, 587, 598
Chuu, A.,  389 Coan, J.,  501
Chuy, I. L.,  160 Cobb, J. A.,  502
Ciaravino, S.,  230 Coburn, G.,  592
Cicchetti, D.,  218 Cocco, K. M.,  422
Cicchetti, D. V.,  10, 56, 57 Cochet, B.,  174
Ciechanowski, P.,  163, 341 Cochrane, K. J.,  364
Ciechomski, L.,  280 Cochrane, R.,  444
Cienfuegos, A.,  442 Cockerham, M. S.,  364, 367, 388
Cillessen, A. H. N.,  72 Coderch, L.,  374
Ciompi, L.,  435 Coffey, S. F.,  339
Cipriano, N.,  226 Coffield, A. B.,  384
Cisin, I. H.,  393 Coghill, D.,  56, 62, 63
Cisler, J. M.,  242 Coghill, R. C.,  598
Cisler, R. A.,  401 Cohen, A. B.,  325
Ciucci, E., 84 Cohen, A. N.,  435, 442, 445, 446
Claar, R. L.,  592, 593, 595 Cohen, B. E.,  330
Claiborn, C. D.,  17 Cohen, D.,  515, 528, 529
Clapp, J. D.,  339 Cohen, D. J.,  218
Clark, A.,  546 Cohen, H. W.,  332
Clark, A. J.,  609 Cohen, J.,  5, 334, 344, 450
Clark, C. H.,  180 Cohen, J. L.,  608
Clark, D.,  275 Cohen, L. L.,  5, 596, 599
Clark, D. A.,  3, 23, 294, 301, 313, xi Cohen, L. R.,  545, 553
Clark, D. B.,  250, 269 Cohen, M. J.,  490
Clark, D. C.,  157 Cohen, R.,  609
Clark, D. M.,  256, 269, 279, 333 Cohen, R. M.,  162, 165
Clark, E.,  117 Coie, J. D.,  72
Clark, F.,  158 Coifman, K. G.,  139–​140
Clark, K. A.,  101 Colby, S. M.,  369, 370, 371, 373
Clark, L. A.,  10, 143, 179, 218, 268, 465, 466, 467, 468, 470, Colder, C. R.,  382, 383, 393
475, 476, 479 Colditz, J.,  397
Clark, M. E.,  619 Cole, B.,  612
Clark, R. E.,  449, 451 Cole, D. A.,  107, 109, 110, 199
Clark, S. W.,  471 Cole, J. C.,  160
Clark, W. B.,  393 Colebunders, R.,  522, 531
Clarke, D. E.,  468 Coleman, E.,  532
Clarke, G.,  117 Coles, C. D.,  56
Clarke, G. N.,  117, 223 Coles, M.,  325
Clarke, H. W.,  589 Coles, M. E.,  316, 323
Clarke, J. C.,  219, 247, 251 Colledge, E., 76
Clarkin, J. F.,  475 Collett, B.,  609
Clary, C.,  243 Collett, B. R.,  113, 114, 118
Clavet, G. J.,  525 Collier, H.,  501
Clayton, A.,  524 Colligan, R. C.,  466, 467, 473
Clayton, A. H.,  525, 528 Collimore, K. C.,  250, 251
Cleeland, C. S.,  611 Collins, J. F.,  339
Cleland, J. A.,  619 Collins, K. A.,  251
Cleland, P.,  366, 373 Collins, P.,  421
Clemans, T. A.,  194 Collins, R.,  296
 author Index 653

Collins, R. L.,  395 Copeland, J.,  157, 160, 161, 165, 400

Collins, S.,  527 Copeland, J. R. M.,  156, 157, 160, 162–​163, 164, 165
Collishaw, S.,  101, 107 Copeland, W.,  107, 218
Collshaw, S.,  100, 101 Copeland, W. E.,  73, 100, 101, 102, 107
Colman, I.,  206, 419 Copestake, S.,  444
Combs, A.,  620 Coplan, J. D.,  269
Comer, S. D.,  383 Corbett, K.,  401
Comijs, H. C.,  154, 161 Corbière, M.,  445
Compton, S.,  204 Corbitt, E. M.,  466, 469
Compton, W.,  382 Corcoran, C.,  343
Compton, W. M.,  364, 413, 416 Corcoran, D. L.,  61
Comtois, K. A.,  196, 197, 203, 204 Corcoran, K.,  503
Cone, E. J.,  374 Coren, S.,  571
Cone, J. D.,  11 Coric, V.,  198
Conger, R. E.,  78 Cormier, W. H.,  78
Connell, H.,  583, 593, 596, 598 Corn, K. J.,  267
Connelly, M.,  593, 594, 598 Cornelius, A. E.,  545
Connelly, M. A.,  588 Corneliussen, S. J.,  548
Conner, K. R.,  206 Cornell, A. H.,  74, 76
Conner, M.,  145 Cornell, J.,  301, 344
Conners, C. K.,  50, 52, 53, 56, 62, 78 Cornoni-​Huntley, J.,  163
Conners, K.,  222 Corona, G.,  518
Connolly, M. B.,  142 Correll, C. U.,  176, 437
Connolly, N. P.,  243 Corretti, G.,  178
Connor, D. F.,  59 Corrigan, P.,  447
Connor, J. P.,  395 Corrigan, P. W.,  446–​447
Connor, K. M.,  250 Corse, S. J.,  448, 451
Connors, E. H.,  20, 23 Corsini-​Munt, S.,  518
Connors, G. J.,  397 Corte, C. M.,  551, 552
Connor-​Smith, J. K.,  117 Cortese, S., 48
Conover, N. C.,  103 Coryell, W.,  154, 175, 176, 268, 394
Conrad, K. J.,  442 Cossrow, N.,  542
Conradt, J.,  218, 243 Costa, P. J.,  469
Conroy, D. A.,  563, 565 Costa, P. T.,  477
Constable, G.,  180 Costello, A. J.,  103, 108
Constantino, M. J.,  298 Costello, E.,  305
Conte, H. R.,  200 Costello, E. J.,  47, 50, 100, 101, 102, 107, 108, 109, 110, 113,
Conti, P. A.,  571 115, 218, 219, 225, 230
Conway, M.,  297, 302 Costello, J.,  53, 73, 101, 218
Conwell, Y.,  193, 198, 199, 206 Côté, D.,  619
Cook, A. J.,  613, 617, 620 Cote, G.,  282
Cook, E. H.,  225, 226 Cote, J.,  196
Cook, J.,  332, 498 Cotter, A. N.,  598
Cook, J. M.,  341 Cottler, L.,  364
Cook, M. R.,  612 Cottler, L. B.,  413, 416
Cook, S. C.,  109 Cotton, C. R.,  199, 203
Cook, S. M.,  392 Cotton, D.,  528
Cook, T. G.,  373 Cotton, S. M.,  177
Cooke, R. G.,  183 Cottraux, J.,  276
Coolidge, F. L.,  157, 465, 466, 467, 468, 469, 470 Coughenour, L.,  438
Coon, D. W.,  526 Cougle, J. R.,  269
Cooney, N.,  365, 370 Court, A.,  546
Cooney, N. J.,  402 Court, C.,  587, 588
Cooney, N. L.,  397 Courtet, P.,  196, 202
Coons, M. J.,  250 Courtney, K. E.,  395
Cooper, A. M.,  546–​547 Cousins, L. A.,  599
Cooper, J. E.,  156, 157 Couyoumdjian, A.,  275
Cooper, M. L.,  383, 396, 421 Covi, L.,  545
Cooper, P. J.,  252, 547, 552 Cowart, M.,  252
Cooper, Z.,  546, 547, 551, 552, 553 Cowart, M. J,  220
654 author Index

Cowles, M. L.,  199 Crow, S. J.,  544, 545, 547, 548, 549, 553
Cowlishaw, S.,  425 Crowell, J.,  13n1
Cox, A.,  106, 107 Crowther, J. H.,  205, 206
Cox, A. L.,  332 Cruise, K.,  76, 84
Cox, B. J.,  143, 252, 275, 276, 277, 332, 414, 417 Cruise, K. R.,  76
Cox, J.,  570 Crump, R.,  116
Coyne, J. C.,  154 Cruz, C. F.,  374
Coyne, K.,  522, 531 Cruz, D.,  332
Coyne, K. S.,  612–​613 Cruz, M. S.,  367
Coyne, P. J.,  621 Csapo, K. G.,  570
Craddock, S. G.,  361 Cuadras, D.,  267
Craig, A. D.,  134 Cuellar, A. K.,  178, 180
Craig, F., 56 Cuellar, J., 86
Craig, K. D.,  583, 584, 586, 587, 588, 608, 621 Cui, L.,  218
Craigen, K.,  543 Cui, W.,  526
Craighead, W. E.,  132, 137, 142 Cuijpers, P.,  116, 154, 394
Crane, C.,  135 Culhane, M. A.,  344
Crane, D. R.,  494, 498, 523 Cully, M.,  223
Craney, J. L.,  177 Culpepper, L.,  273
Crapanzano, A. M.,  73 Cuming, S.,  254
Craske, M.,  269, 278 Cummings, E. M.,  491
Craske, M. G.,  266, 267, 268, 269, 270, 274, 275, 276, 277–​278, Cummings, J. L.,  162
279, 280, 281, 282, 293, 294 Cungi, C.,  276
Crawford, J. K.,  543 Cunningham, H.,  446
Crawford, M. J.,  392 Cunningham, M. J.,  587, 598
Crawford, M. R.,  570, 573, 587 Cunningham, N. R.,  596, 598
Crawford, S.,  517 Cunningham, P. B.,  86
Crawshaw, V. B.,  115 Cunningham, S. J.,  592
Creamer, M.,  334, 339 Cunningham-​Williams, R. M.,  413, 416
Creasey, H.,  158 Curran, P.,  382, 383
Crego, C.,  477 Curran, P. J.,  440, 442
Crenshaw, A. O, Christensen, A.,  495 Currie, S.,  417
Creswell, C.,  252 Currie, S. R.,  417, 427
Crews, T. M.,  394 Currier, G. W.,  194, 205
Crick, N. R.,  72–​73, 74 Curry, J.,  117
Crippa, J. A. S.,  243, 247, 250 Curtain, S. C.,  155
Crisler, M. E.,  54 Curtin, L.,  369, 373
Crismon, M. L.,  440 Curtis, C. G.,  589
Crits-​Christoph, P.,  142, 183 Curtis, G. C.,  243
Crocker, A. G.,  437, 445 Curtis, L.,  20, 23
Crocker, N., 56 Cusack, K.,  338
Crockford, D. N.,  413, 417 Cusack, K. J.,  341
Croft, P.,  614 Cushing, P. J.,  72
Croft, P. R.,  564 Cuthbert, B., 99
Cromarty, P.,  281 Cuthbert, B. N.,  145
Crombez, G.,  593, 595, 596, 613, 618 Cutler, R.,  612
Cronbach, L. J.,  206, 470 Cutrona, C.,  497
Crone, D. A.,  24 Cutshall, C.,  248
Crook, C., 86 Cvengros, J. A.,  565
Crook, G. M.,  397, 575 Cyr, M.,  444
Crosby, R.,  551, 552 Czaja, J.,  547
Crosby, R. D.,  546, 548, 551, 552 Czlapinski, R.,  615, 620
Croskerry, P., 33 Czobor, P.,  444
Cross, S., 22 Czuba, K. J.,  18, 24
Cross, S. E.,  499
Cross, W., 23 Dadds, M. R.,  76, 84, 88, 220, 233
Crossup, P. C.,  524 Dadkhah, F.,  525
Croudace, T.,  444 D’Agostino, R.,  521
Croughan, J.,  156, 176 Dahl, A. A.,  522
Crow, S.,  544, 545, 548, 550 Dahl, R. E.,  134
 author Index 655

Dahlagaard, K. K.,  199 Davidson, K.,  583

Dahlgaard, J.,  135 Davidson, L.,  446
Dahlmeier, J.,  200 Davidson, M.,  445
Dahlstrom, W. G.,  614 Davies, C.,  280
Daker-​White, G.,  519 Davies, D.,  17, 18, 22, 156, 270
Dakroub, H.,  200 Davies, M.,  114, 115, 175, 178, 194, 196, 247, 272, 299, 316
Daleiden, E. L.,  12, 22, 118, 220 Davies, P. S.,  612
Daley, D.,  53, 144 Davies, P. T.,  491
Daley, D. C.,  398 Davies, W. H.,  594, 595, 596
Daley, M.,  564 Davila, J.,  498
Dalgleish, T.,  4, 220, 333 Davis, A. C.,  21, 23
Dalgleish, T. L.,  498 Davis, B.,  501
Dallaire, D. H.,  219 Davis, C. M.,  503, 518
Dalle Grave, R.,  553 Davis, C. S.,  396
Dalman, C.,  436 Davis, D. C.,  35
Dalrymple, K.,  178 Davis, G. C.,  331, 343, 522
Dammen, T.,  272 Davis, H.,  340
Dampier, C., 40 Davis, J. M.,  182, 183
Dancu, C. V.,  250, 253, 338 Davis, M., 59
Dandreaux, D. M.,  75 Davis, M. L.,  312
Dane, H. A.,  74, 76 Davis, R.,  473
Dang, J.,  160 Davis, S.,  219, 528
D’Angelo, E. J.,  106 Davis, S. L.,  503, 518
Daniel, D. G.,  442 Davis, S. R.,  517
Daniel, F.,  162 Davis, T.,  205, 249
Daniels, J. B.,  339 Davis, T. E.,  225, 243
Danielson, C. K.,  176, 178 Davis, T. L.,  544
Danis, B.,  74, 88 Davison, J.,  521, 522, 527, 531
Danish, S.,  361 Davison, S. L.,  517
Danko, A.,  524 Davison, T. E.,  162
Dantzic, S.,  545 Daviss, B.,  110
Danzig, A. P.,  107, 108 Dawe, S.,  448
Daoust, R.,  588, 598 Dawes, R. M.,  38
Dar, R.,  322 Dawson, D. A.,  295, 296, 382
Dare, C.,  545, 546 Dawson, M. E.,  437
Dargie, E.,  528 Daza, P.,  276, 277–​278
Darke, S.,  360, 366 Deacon, B.,  252, 275
Darkes, J.,  362, 384, 396 Deacon, B. J.,  242, 252, 268, 317, 318, 323, 324, 325
Darlington, J.,  499 Deagle, E. A.,  271
Daruwala, S. E.,  254 Dean, K.,  437
Darwin, W. D.,  374 De Andrade, A. R. V.,  18, 22, 23
Dasher, R.,  296 Deane, F. P.,  571
da Silva Freitas, M. C.,  247 DeAntonio, M.,  175
das Nair, R.,  18, 24 de Araujo, M.,  366
Datta, J.,  516 de Arellano, M.,  338
Dattilio, F.,  144 Dearing, K. F.,  73
Datto, C. J.,  163 Deaton, W. L.,  203
Daum, I.,  437, 448 De Backer, V.,  117
Daumit, G. L.,  438 de Bejczy, A.,  385
Dauphin-​Pierre, S.,  588, 598 de Beurs, D. P.,  199
D’Auria, A.,  598 de Beurs, E.,  295, 301, 507
Dauser, C.,  220, 231 De Beurs, E.,  282
Dauvilliers, Y.,  564 de Bie, R. A.,  616
Davey, C. G.,  177 De Brito, S. A.,  76
David, A. S.,  180, 436, 439 de Bruin, E. I.,  52
David, B.,  250 Decaluwe, V.,  547, 549, 554
David A.,  180 De Campos, C.,  589, 590
David Rudd, M.,  204 DeCaria, C. M.,  426
Davidson, J.,  24, 138, 139, 347 Dechant, K.,  421
Davidson, J. R. T.,  250, 256, 334, 336, 337 Deckert, J.,  268, 270
656 author Index

De Clercq, B.,  472 Delong, L. K.,  19

DeCola, J.,  269 De Los Reyes, A.,  38, 49, 87, 104, 119, 254
DeCola, J. P.,  269, 279 DelPorto-​Bedoya, D.,  178
De Cort, K.,  269 Demaray, M. K.,  19
De Cuyper, S.,  117 de Matos, K. J. N.,  178
Deeg, D. J.,  295 Dembo, R., 84
Deeg, D. J. H.,  154 Demers, L.,  162, 165
Deegan, P. E.,  452 Demeter, C.,  24, 36, 177, 178, 233
Deep, D.,  554 Demeter, C. A.,  177, 182
DeForge, B.,  451 Demier, O.,  131
DeFries, J. C.,  50 Deming, W. E.,  438
De Fruyt, F.,  466, 468, 472, 476, 479 Demler, O.,  62, 132, 173, 243, 267, 272–​273, 294, 313,
DeGarmo, D. S.,  86 331, 343
Degenhardt, L.,  101 De Moura, M. A.,  50
DeGeorge, D. P.,  178 Demyttenaere, K.,  338
de Girolamo, G.,  339, 439 De Nadai, A. S.,  225–​226
DeGirolamo, J.,  449 Dengler-​Crish, C. M.,  585
DeGood, D. E.,  613, 617 Denicoff, K. D.,  180
de Graaf, R.,  131, 266, 338 de Nijs, P. F. A.,  52
DeGrazia, J. M.,  180 Denis, C. M.,  367, 389
de Groot, M. H.,  199 Dennehy, E.,  440
deGruy, F. V,  3rd, 439 Dennis, J. P.,  199
de Haan, L.,  440 Dennis, M. L.,  364, 365, 367–​368, 373, 374, 385–​386
De Haes, J. C.,  574 de Noord, I.,  61
De Henauw, S.,  115 Denyes, M.,  586, 587
De Hert, M.,  181 Denys, D. A. J. P.,  19
Dehoust, M.,  156 D’Eon, J. L.,  613, 615
Dehoust, M. C.,  156 DePaulo, R.,  176
Deighton, J., 21 DePhilippis, D.,  397
Deitz, A. C.,  542 Depp, C. A.,  152
De Jong, C. A. J.,  392 Depue, R. A.,  177
de Jong, G. M.,  282 Dere, J.,  103
de Jong, J. R.,  618 Derks, E. M.,  52
De Jong, J. T.,  345 Derksen, J. J.,  467
de Jong, P. J.,  249, 250, 251 Derogatis, L.,  515, 528
de Jongh, A.,  249 Derogatis, L. R.,  35, 498–​499, 521, 522, 523, 524, 525, 526,
Dejos-​Conant, V.,  583, 587, 598 528, 529, 545
de Keijser, J.,  199 Derringer, J.,  466, 470, 476
Dekker, M. C.,  104 Derryberry, D.,  140
Dekker, M. C. J.,  52 Dersch, C.,  490
Dekovic, M., 84 DeRubeis, R. J.,  132
de la Cámara, C.,  157 Desai, R.,  330
de la Fuente, J. R.,  422, 448 Deschênes, S. S.,  297
de la Osa, N.,  84, 108 DeShong, H. L.,  11, 466, 474
de la Vega, R.,  24, 592 Deshpande, S. N.,  448
DelBello, M. P.,  177 De Silva, P.,  320, 499
Del-​Ben, C.,  247 De Silva, R.,  439
Del Ben, K.,  341 de Sousa Gurgel, W.,  178
Del Boca, F. K.,  362, 384, 398 Des Rosiers, P.,  161
Delfabbro, P. H.,  425 Dettore, D.,  504
Del-​Favero, J.,  268 Deveci, E.,  243
Delgado, P.,  314, 322 Devenand, D. P.,  153
Deliberto, T. L.,  193, 206 Deveney, C. M.,  102
de Lijster, J. M.,  243 de Vente, W.,  250
de Lima Osório, F.,  243, 247 Devineni, B.,  178
Delinsky, S.,  553 Devins, G. M.,  257
Delisle, I.,  518, 529 Devlin, M. J.,  545, 552, 554
Delisle, M. M.,  203 De Vriendt, T.,  115
Dell’Osso, B.,  244 de Waal, M. W. M.,  161
Dell’Osso, L.,  38, 178 DeWalt, D. A.,  40, 110
 author Index 657

Dewan, T.,  585 Diseth, T. H.,  594

De Weert-​van Oene, G. H.,  392 Dishion, T. J.,  74, 85, 87, 382
Dewees, E.,  183 Disler, P. B.,  620
Deweese, B. N.,  56 Disney, E. R.,  180
Dewey, M.,  157 Distasio, J.,  437
Dewey, M. E.,  156, 157 Distinto, M.,  198
DeWitt, E. M.,  110 Dixon, A. E.,  498
Dexter-​Mazza, E. T.,  193 Dixon, D. J.,  10
Dey, A. N.,  369 Dixon, L. B.,  452
Dey, J.,  508 Dixon, M. R.,  422
de Zwaan, M.,  544 Dixon-​Woods, M.,  599
Dhert, W. J.,  614 Dizner-​Golab, A.,  392
Dhingra, L.,  618 Djukic, M.,  400
Día, J.,  157 Doane, J. A.,  447
Diamond, A.,  142 Dobbins, T.,  101
Diamond, G. M.,  117 Dobie, D. J.,  341
Diamond, G. S.,  117 Dobson, K. S.,  3, 156
Díaz Mesa, E. M.,  367 Doctoroff, G., 23
Di Bernardo, M.,  544 Dodd, A. L.,  52
DiBonaventura, M.,  153 Dodd, S.,  178
Dick, B. D.,  585 Dodds, N.,  397
Dick, D. M.,  361 Dodds, N. E.,  398
Dickerson, F. B.,  436, 445 Dodge, K. A.,  72–​73, 74, 85
Dickerson, M.,  418 Doersch, A.,  423
Dickinson, D.,  440 Doffing, M.,  53, 56
Dickson, N.,  71, 75 Doffing, M. A.,  56
Dickstein, B. D.,  334 Doghramji, K.,  563, 575
Dickstein, D. P.,  181 Döhnert, M.,  17, 22
Dickstein, J. B.,  527 Dohrenwend, B. P.,  331
Dickstein, S.,  177 Dolan, B.,  552
DiClemente, C.,  394 Dolan, C. C.,  479
DiClemente, C. C.,  370, 371, 394, 397, 420, 449 Dolan, C. V.,  52
Diefenbach, G. J.,  323 Dolan, R.,  272, 299
Diehr, P.,  163 Dolan, R. T.,  295
Dieleman, G. C.,  243 Dolan, S. L.,  371, vii
Diener, E.,  140, 499 Dolan-​Sewell, R.,  470
Dierckx, B.,  243 Dolder, C. R.,  443
Dierker, L.,  111 Dollfus, S.,  442
Dierker, L. C.,  223 Dölling, K.,  17, 22
DiFilippo, S.,  159, 164 Domenech, J. M.,  84, 108
Di Gasbarro, I.,  182, 183 Domènech, J. P.,  108
DiGrande, L.,  332 Domingo, A.,  588
Dill, D. L.,  420 Domschke, K.,  268
Dillon, H. R.,  572 Donaldson, D.,  202
Di Lorenzo, C.,  590 Donath, S.,  517
Dilsaver, S. C.,  182 Donato, S.,  504
Dilts, S. L.,  360, 361 Dong, K. A.,  206
Dime-​Meenan, S.,  174 Dong, N.,  109
Dimidjian, S.,  117, 132 Donison, D.,  254
DiNapoli, E. A.,  572 Donker, T.,  154
DiNardo, P.,  246, 271, 315, 316 Donner-​Banzhoff, N.,  392
DiNardo, P. A.,  221–​222, 243, 246–​247, 271–​272, 296, Donovan, D.,  401
298, 338 Donovan, D. M.,  359, 361
Dineen, K.,  117 Donovan, J. E.,  250
Diniz, A.,  524 Doody, R.,  155
Dinos, S.,  447 Doolan, M., 86
Dinwiddie, S. H.,  388, 394 Dooley, J.,  585
Dirks, M., 49 Dore, G. M.,  392
Dirmaier, J.,  392 Dorheim, S. K.,  573
di Ruffano, L. F.,  11 Dorsey, C.,  563, 565
658 author Index

Dorsey, C. M.,  575 Duhem, S.,  276

Dorsey, S.,  21, 23 Duke, M.,  593
Doss, B. D.,  490, 496–​497, 498, 501, 503, 508 Dulcan, M.,  79, 87, 108
Dougherty, D. M.,  402 Dulcan, M. K.,  52, 79, 83, 103, 108, 222
Dougherty, L. R.,  102, 107, 108, 119 Dumenci, L.,  19, 33, 34, 38, 57
Douglas, K. V.,  19 Dun, T.,  497
Douglas, S. R.,  18, 22, 23 Dunbar, D.,  545, 553
Doumani, S.,  247 Dunbar, G. C.,  363, 439
Dounchis, J. Z.,  544 Duncko, R.,  251
Dour, H. J.,  206 Dunlop, B. W.,  132, 137
Dow, M. G.,  199, 277 Dunn, A. L.,  599
Dowda, M.,  612 Dunn, D., 59
Dowdall, D.,  301 Dunn, G.,  444
Dowling, M.,  478 Dunn, K. M.,  564
Dowling, N.,  425 Dunn, T. J.,  10
Downey, D. L.,  202 Dunn, V. K.,  159
Downey, M. M.,  12, 24, 42, 142 Dunne, M. P.,  394
Downie, F.,  246 Dunner, D. L.,  175, 176
Downs, S. M.,  63 DuPaul, G. J.,  50, 51, 58
Downs, W. R.,  202, 203 DuPont, R. L.,  296
Doyle, A. E.,  48 Dupuy, J.-​B.,  305
Doyon-​Trottier, E.,  588, 598 Dura, J. R.,  156, 160
Dozois, D. J.,  23 Durbin, C. E.,  108
Dozois, D. J. A.,  3, 156, 251, xi Dures, E.,  574
Drabick, D. A.,  38, 104, 119 Durham, T. A.,  341
Drabick, D. A. G.,  49, 50, 74 Durlak, J. A.,  22
Draganac-​Cardona, L.,  60 Durning, P.,  80, 86
Draisma, S.,  178 Du Rocher Schudlich, T. D.,  181
Drake, C. L.,  571 Durrant, J. D.,  269
Drake, K.,  451 Durrence, H. H.,  564
Drake, R. E.,  440, 448, 449, 451, 452 Durrett, C.,  472
Drancourt, N.,  174 Durrett, C. A.,  470
Drapalski, A.,  451 Dvorak, R. D.,  369
Drapeau, M.,  19, 20 Dworkin, R. H.,  583, 612–​613, 614, 620
Drapeua, M., xi Dyck, D. G.,  445
Drapkin, M. L.,  397 Dyck, I. R.,  267, 295, 466
Drigo, P.,  589 Dymek, M.,  552
Driscoll, M.,  443 Dymond, S.,  422
Drobes, D. J.,  339 Dyson, M.,  108
Droppleman, L. F.,  613 Dyson, M. W.,  108
Drotar, D.,  592 Dysvik, E.,  617
Droz, J.,  612 Dzankovic, S.,  500
Drukker, M.,  437
Drummond, C.,  369 Eack, S. M.,  449
D’Souza, D. C.,  437 Eardley, I.,  527
Duara, R.,  161 Earleywine, M.,  158
Duarte, C.,  114 Eastwood, R.,  443
Duberstein, P.,  198 Eaton, C. A.,  365, 372
Duberstein, P. R.,  203 Eaton, W. W.,  158, 243, 295, 296, 437
Dubicka, B.,  33, 102, 106, 117, 118 Eaves, L. J.,  268, 294
DuBreuil, S. C.,  615 Ebenfeld, L.,  282
Dubuis, V.,  178 Eberhard-​Gran, M.,  573
Dubuisson, D.,  612 Ebert, L.,  23–​24
Duck, S.,  608 Ebesutani, C.,  111, 251
Dudley, R.,  142 Ebmeier, K. P.,  158
Duff, C. T.,  53 Ebner-​Priemer, U. W.,  24
Dufour, M. C.,  382 Eccleston, C.,  583, 593, 595, 596, 598, 599
Dugan, T. M.,  63 Echandia, A., 56
Dugas, M. J.,  30, 294, 295, 296, 297, 299, 301, 302, 303, 305 Eckblad, M.,  178
DuHamel, K.,  341 Eckenrode, J.,  195
 author Index 659

Edbrooke-​Childs, J.,  21 Elhai, J. D.,  331, 341

Eddy, J. M.,  502 Elizur, A.,  203
Eddy, K. T.,  545, 547 Ellard, J.,  392
Edelbrock, C.,  81, 103, 108 Ellard, K. K.,  132
Edelen, M. O.,  159, 164 Ellery, M.,  421
Edelmann, R. J.,  256 Elliott, J. M.,  619
Edelstein, B. A.,  203 Elliott, P.,  334
Edens, J. F.,  400 Ellis, C. G.,  466, 469
Edge, M. D.,  174 Ellis, J.,  202, 571
Edinger, J. D.,  565, 566, 569, 570, 573, 574, 575, 576 Ellis, J. G.,  564, 567
Edmondson, D.,  330 Ellis, M., 74
Edmundson, M.,  475, 477 Ellis, M. L.,  73
Edwards, D.,  80, 86 Ellis, R.,  490
Edwards, J.,  419 Ellison, N.,  250
Edwards, L. C.,  617 El Masri, M.,  345
Edwards, M. C.,  57 Elvins, R.,  102
Edwards, N. M.,  384 Elwood, L. S.,  251
Edwards, R. R.,  609 Elwyn, G.,  392
Edwards, V.,  546 Embretson, S. E.,  206
Edwards, W. M.,  532 Emery, E. E.,  154
Edwin, D.,  176 Emery, G.,  132, 133, 138, 139
Efron, D., 52 Emmelkamp, P.,  323
Egan, S. J.,  252 Emmelkamp, P. M.,  347
Egede, L. E.,  437, 440 Emmerich, A.,  110
Egeland, B.,  219 Emmons, R. A.,  140
Egeland, J.,  243 Emslie, G.,  117, 204
Egger, H.,  102, 218 Emslie, G. J.,  17, 102, 105, 109, 112, 113, 115, 117
Egger, H. L.,  47, 100, 104, 106, 107, 108, 218 Endicott, J.,  116, 156, 160, 175, 176, 180, 184, 243, 388, 394,
Ehlers, A.,  139, 268, 269, 281, 282, 333 450, 545
Ehmann, M.,  106, 107, 593 Engdahl, B. E.,  336
Ehrenreich May, J.,  225–​226 Engedal, K.,  161, 162
Ehrensaft, M.,  500 Engel, C. C.,  332
Ehrensaft, M. K.,  493, 502, 506 Engel, S. G.,  548, 551, 552
Ehring, T.,  139, 339, 347 Engels, R.,  111
Ehrman, R. N.,  366, 373 Enns, M. W.,  143, 417
Eich, D.,  564 Ensing, D. S.,  446
Eich, W.,  392 Enzlin, P.,  515, 516, 517, 518
Eidelman, P.,  21, 566, 570, 573 Epler, A. J.,  341
Eifert, G. H.,  269, 280 Epping-​Jordan, J.,  138
Eikeland, O. J.,  617 Epstein, A. M.,  266
Eikenaes, I.,  243 Epstein, E. E.,  392
Einhorn, A. M. J.,  554 Epstein, J. N.,  62
Eiraldi, R., 57 Epstein, M. H.,  114
Eisemann, M.,  112 Epstein, N.,  300, 301, 497, 498, 574
Eisen, A. R.,  222, 228, 230 Epstein, N. B.,  115, 181, 495, 500, 503, 546
Eisen, J. L.,  267, 316 Epstein, R. A.,  22
Eisen, S.,  442 Erbacci, A.,  569–​570
Eisen, S. V.,  344, 420 Erder, M. H.,  542
Eisenstadt, T. H.,  86 Erens, B.,  517
Eiser, C.,  594 Erhardt, D., 62
Eisler, I.,  545, 546 Erickson, D. B.,  86
Ekeberg, O.,  272 Erickson, T.,  298
Ekeblad, A.,  144 Erickson, T. M.,  299, 300
Ekenga, C. C.,  332 Ericsson, K. A.,  426
Ekselius, L.,  136, 276 Eriksson, J. K.,  599
Eland, J. M.,  583, 589 Erisman, S. M.,  281
Elbogen, E. B.,  330 Erkanli, A.,  47, 50, 100, 104, 107, 218, 225, 230
Elderkin-​Thompson, V.,  153 Eron, L. D.,  115
Eley, T. C.,  218, 219, 268 Ersek, M.,  162, 618
el-​Guebaly, N.,  363, 413, 417, 418, 421, 427 Erskine, H. E.,  101
660 author Index

Ertekin, B. A.,  243 Falbo, J.,  279, 281

Ertekin, E.,  243 Falco, M., 19
Esbjørn, B. H.,  219 Fales, J. L.,  596
Esch, D.,  442 Falissard, B.,  182
Eschstruth, A.,  479 Falk, A.,  230
Escobar, E. M.,  596 Falkenström, F.,  144
Eshleman, S.,  295 Faller, S.,  367
Espejo, E.,  250 Falsetti, S.,  338
Espie, C. A.,  564, 565, 567, 571, 575 Falzon, L.,  330
Esposito, K.,  521 Fang, Q.,  110
Essau, C., 84 Fann, J. R.,  575
Essau, C. A.,  100, 113, 218, 226, 243 Fanti, K., 84
Essex, M. J.,  111 Fanti, K. A.,  76, 84
Essner, B.,  595 Faragher, E. B.,  447
Essner, B. S.,  585, 596 Faraone, S., 62
Essock, S., 5 Faraone, S. V.,  219
Essock, S. M.,  437 Faravelli, C.,  266, 544
Estes, A. M.,  74, 80, 87 Farber, G. K.,  113
Etain, B.,  174 Farber, P. D.,  393
Etienne, N.,  204 Farchaus, S. K.,  551, 552
Evans, C.,  552 Farchione, T. J.,  275, 279, 280, 281
Evans, D. A.,  163 Färdig, R.,  446
Evans, D. R.,  174 Farfel, M. R.,  332
Evans, L.,  277, 575 Fargas, A.,  449
Evans, L. D.,  344 Farkas, G., 50
Evans, L. K.,  161 Farmer, A. E.,  437
Evans, S. C.,  11 Farmer, M. E.,  174, 448
Evans, S. W.,  53 Farmer, R. F.,  383
Eveleigh, D. J.,  616 Farr, D.,  177
Evensen, J. H.,  436 Farrell, A.,  361
Everard, L.,  436 Farrell, C.,  568t
Evins, A. E.,  438 Fartacek, R.,  194, 205
Ewing, J. A.,  385, 387 Farvolden, P.,  257, 466, 468
Exner-​Cortens, D.,  206 Fava, J. S.,  371
Eyberg, S.,  80, 86 Fava, M.,  199, 275
Eyberg, S. M.,  59, 78, 79, 80, 86 Fawcett, J. A.,  193
Eyde, L. D.,  18 Fawley-​King, K.,  120
Eynan, R.,  464 Fayyad, R.,  243
Eysenck, H. J.,  218, 268, vii Fazel, S.,  436
Eysenck, M.,  274 Federico, M.,  198
Eysenck, M. W.,  218 Fedor, S.,  206
Ezpeleta, L.,  84, 108, 179, 219 Fedoroff, I.,  366, 373
Feehan, C.,  110, 117, 118
Fabbri, M.,  569–​570 Feeling, N.,  331
Fabiano, G. A.,  52, 53, 54, 55, 56, 57, 59, 60, 63–​64 Feeney, G. F.,  395
Fabricant, L. E.,  313 Feeney, T.,  385–​386
Facelle, T. M.,  516 Feeny, N. C.,  35
Fagiolini, A.,  178 Fehm, L.,  243, 244
Fagiolini, A. M.,  180 Feifel, D.,  220
Fai Ho, K.,  530 Feige, B.,  564, 571
Failla, S.,  339 Feijoo-​Lorza, R.,  153–​154
Fair, D., 48 Feindler, E. L.,  500–​501
Fairbank, J.,  115, 117, 614 Feinstein, A. B.,  599
Fairbank, J. A.,  23–​24, 331, 333, 334, 337, 343–​344 Feinstein, B. A.,  334
Fairbrother, N.,  319 Feldbau-​Kohn, S. R.,  493, 502, 506
Fairburn, C. G.,  544, 545, 546, 547, 549, 551, 552, 553, 554 Felder-​Puig, R.,  594
Fairchild, G.,  48, 75, 83–​84 Feldman, B. M.,  586, 592
Fajkowska, M.,  140 Feldman, R.,  220, 221
Fakhry, F., 33 Feng, G. C.,  10
Fala, N. C.,  397 Fennell, M.,  294
 author Index 661

Fenske, K.,  270 Fischer, M. S.,  313, 490

Fenton, K. A.,  517 Fischer, S., 11
Fenton, W. S.,  436, 452 Fischmann, D.,  199
Fentz, H. N.,  279 Fishbain, D. A.,  612
Ferdeghini, F.,  521 Fisher, A. J.,  4, 145
Ferdinand, R. F.,  52, 104 Fisher, D. G.,  394
Ferdinando, S.,  112 Fisher, E.,  596
Ferenschak, M. P.,  334 Fisher, H. L.,  436
Ferentzy, P.,  421 Fisher, M.,  549
Fergusson, D. M.,  74, 225, 269 Fisher, P.,  52, 74, 79, 81, 83, 86, 87, 102, 108–​109, 113, 222
Ferland, F.,  415 Fisher, P. W.,  105, 106, 107, 115
Fernandes, A. M.,  589, 590 Fisher, R. J.,  587
Fernandes, M. M.,  374 Fisher, T. D.,  518
Fernandez, K. C.,  250 Fister, S. M.,  11
Fernandez, M., 59 Fiszbein, A.,  440
Fernandez-​Egea, E.,  448 Fitzgerald, C. M.,  529
Fernandez-​Mendoza, J.,  180, 564 Fitzgerald, T. D.,  608
Ferrari, P., 22 Fitzpatrick, K. K.,  199
Ferri, C. P.,  366 Fitzpatrick, M.,  19, 20, 24, xi
Ferrier, A. G.,  401 Flaherty, J. F.,  180
Ferris, J.,  414, 417 Flament, M. F.,  544
Ferro, T.,  104 Flanagan, E. H.,  387, 479
Ferster, C. B.,  132 Flanagan, K. D.,  73
Fesinmeyer, M. D.,  585 Flannery, B. A.,  389, 395–​396
Feske, U.,  275, 301 Flannery-​Schroeder, E.,  232, 233
Feuerstein, M.,  612 Flater, S.,  550, 554
Feurer, I. D.,  56 Flaum, M.,  180
Few, L. R.,  464, 465, 466, 468, 470, 471, 472, 474, 479 Flavell, H. A.,  620
Fichter, M. M.,  544 Fleeson, W.,  196, 490
Fidaner, H.,  273 Fleischmann, R. L.,  314, 322
Field, A. P.,  219, 220 Fleiss, J. L.,  156, 160, 245, 450
Field, N.,  516 Flekkoy, K.,  180
Figueira, M. L.,  332 Fleming, A. P.,  80
Fihn, S. D.,  386 Fleming, I., 22
Filho, A. S.,  247 Fleming, J. E.,  108
Filsinger, E. E.,  501 Fletcher, K.,  178, 180
Finch, A. E.,  17 Flett, G. L.,  203
Finch, A. J.,  223, 586 Fliege, H.,  199
Fincham, F. D.,  493, 497, 504 Flinn, L.,  18, 24
Findler, M.,  343 Flor, H.,  340, 596
Findling, R. L.,  24, 35, 36, 59, 75, 86, 102, 107, 108, 109, 110, Flora, D. B.,  48
176, 177, 178, 181, 182, 233 Flottemesch, T. J.,  384
Fine, P. G.,  609 Flowers, S. R.,  592, 593
Fingerhut, R.,  180 Floyd, F. J.,  499, 501
Finkelstein, J.,  573 Flury, L.,  383
Finkelstein, J. S.,  517 Flynn, C.,  53, 107, 177
Finley, G. A.,  583 Flynn, E.,  157
Finn, C. T.,  206, 332 Flynn, L.,  178
Finney, J. W.,  359, 361, 425 Flynn, M.,  115
Fins, A. I.,  569, 573 Foa, E.,  250
Finsaas, M.,  101 Foa, E. B.,  256, 313, 323, 333, 334, 338, 340, 344
Firestone, P., 59 Fokkema, M.,  199
First, M.,  272, 316, 337 Foley, D. L.,  218, 267
First, M. B.,  21, 135, 155, 175, 246, 247, 270, 272, 273, 279, Follette, W.,  321
298, 299, 316, 337, 363, 388, 389–​391, 416, 422, 438, 448, Folstein, M. F.,  163
465, 466, 469, 474, 475, 493, 507, 520, 548 Folstein, S. E.,  163, 176
Fischer, B. A.,  442 Fonagy, P.,  204, 475, 479
Fischer, G.,  197, 200 Fonseca, E.,  367
Fischer, J.,  503 Fontana, A.,  332
Fischer, L. R.,  159 Fontenelle, L. F.,  267
662 author Index

Foran, H. M.,  116, 490, 493 Franklin, J. C.,  204

Forbes, C.,  451 Franklin, M. E.,  313
Forbes, D.,  334 Franko, D. L.,  543
Forbes, E. E.,  109, 110, 118, 134 Franks, A.,  144
Forbush, K. T.,  545, 553 Franz, M.,  332
Ford, G.,  250 Franzoi, S. L.,  545
Ford, G. T.,  276, 301 Frasquilho, D.,  332
Ford, J. M.,  134 Frasure-​Smith, N.,  154
Ford, P.,  448 Frazer, D. R.,  84
Ford, S. M.,  256 Frazier, P.,  547, 549
Ford, T.,  47, 50, 100, 108 Frazier, T. W.,  12, 37, 40, 41, 59, 177, 178, 182
Fordyce, W. E.,  608 Fredman, S. J.,  335
Forehand, R.,  72, 79, 80, 86, 107, 110 Fredrick, J.,  159, 163
Forehand, R. L.,  58, 60, 72, 78, 86 Fredrikson, M.,  249
Foreman, K.,  193 Fredriksson, A.,  446
Forgatch, M. S.,  86 Freed, S.,  269
Forgeron, P. A.,  585 Freedy, J. R.,  347
Forman, E., 21 Freeman, A. J.,  198
Forman, S.,  542 Freeman, K. A.,  193
Formea, G.,  323 Freeman, R.,  175
Forsberg, H. H.,  599 Freeston, M.,  281
Forsberg, S.,  544 Freeston, M. H.,  295, 297, 299, 301, 302, 303, 305
Forsyth, J. P.,  193, 269, 274, 280, 281 Freidenberg, B.,  425
Fortenberry, J. D.,  524 Freire, R. C.,  270
Fortgang, R.,  440 Freitas, T. H.,  178
Fortier-​Brochu, E.,  566, 573, 576 French, A., 61
Fortune, E. E.,  415 French, D.,  282
Fossa, S. D.,  522 French, L.,  142
Fosse, R.,  437 Fresco, D. M.,  132, 133, 134, 136, 139–​140, 251, 296, 298
Foster, F. M.,  393 Freudenheim, J. L.,  393
Foster, S. L.,  11, 502 Frey, E.,  594
Fothergill, C. D.,  120, 141 Frey, R. M.,  394–​395
Fountoulakis, K. N.,  268 Freyberger, H. J.,  156, 295
Fourcroy, J.,  515 Frick, P. J.,  48, 50, 54, 55, 71, 72, 73, 74, 75–​76, 79, 80, 81, 82,
Fournier, A.-​A.,  132 84, 85, 86, 87–​88
Fowers, B.,  504 Friede, T.,  612
Fowler, D.,  436 Friedman, B. K.,  445
Fowler, F. J.,  522 Friedman, L.,  563, 573
Fowler, J. C.,  193 Friedman, M. A.,  544
Fowles, D. C.,  269 Friedman, M. J.,  330, 331, 333, 334, 344
Fox, E.,  282 Friedman, S.,  332
Fox, K. R.,  201 Friedmann, M. S.,  181
Fox, L. W.,  101 Friedrichs, A.,  392
Fox, M. L.,  448, 449 Friend, J. M.,  332
Foxwell, A. A.,  102 Friend, R.,  250
Fraccaro, R. L.,  224 Friis, S.,  272, 436
Fradet, C.,  583 Friman, P. C.,  52
Fraguas, D.,  176 Frisch, G. R.,  415, 416, 417, 427
Frampton, I.,  547 Frisch, M.,  516, 517, 518
Frances, A.,  278, 443 Frisch, M. B.,  301, 344
Franchi, M., 84 Fristad, M.,  109
Franciosi, J. P.,  594 Fristad, M. A.,  102, 108, 176, 182
Francis, S. E.,  227 Fritz, J. M.,  619
Franck, L. S.,  583 Fromme, K.,  396
Franco, C.,  414, 415, 425 Frost, R.,  322–​323, 325
Franco, X.,  225 Frost, R. O.,  139, 252, 318
Frank, E.,  140, 174, 178, 179, 180, 273 Frueh, B. C.,  341, 437, 440
Frank, M. J.,  134 Fruscione, M.,  612
Frankenburg, F. R.,  272, 466, 469, 471 Frye, A.,  7, 40, 41, 143, 145
Franklin, J.,  201 Frynta, D.,  249
 author Index 663

Ftanou, M.,  199 Gallo, J. J.,  153, 154

Fu, Y.,  524 Gallop, R.,  142
Fuchs, P. N.,  608 Gallop, R. J.,  204
Fugl-​Meyer, A. R.,  522 Gallops, M. S.,  244
Fugl-​Meyer, K.,  515 Galloway-​Long, H. S.,  48
Fugl-​Meyer, K. S.,  518, 522 Galper, D. I.,  3
Fuhr, K.,  178 Galvan, T.,  181
Fujita, H.,  443 Gamache, G.,  448
Fukao, A.,  330 Gamaldo, C. E.,  566
Fulford, D.,  183 Gameroff, M. J.,  18, 23
Fullerton, C. S.,  334 Gamma, A.,  178, 184, 564
Fulop, N.,  392 Gammaitoni, A. R.,  612
Fulton, C. L.,  161 Gammon, G. D.,  115
Fulton, J. J.,  331 Gandek, B.,  614
Funderburk, B.,  80, 86 Ganguli, R.,  452
Funderburk, F.,  256 Gans, J., 19
Fung, D. S. S.,  55 Gansicke, M.,  295
Fung, K. M. T.,  446 Gao, B.,  526
Fung, T.,  418 Gao, S. Y.,  518
Funk, B.,  282 Garb, H.,  465, 474
Funk, J.,  494 Garb, H. N.,  33, 217, 465, 471
Funk, J. L.,  523 Garber, G.,  109
Funk, R.,  364, 367–​368, 373, 374 Garber, J.,  100, 107, 110, 111, 115, 116, 593
Furman, J. M.,  269 García, M.,  524
Furmark, T.,  243 García-​Nieto, R.,  197
Furnham, A.,  466, 468, 476 García-​Palacios, A.,  281
Furr, R. M.,  196 García-​Portilla, P.,  367
Furtado, S.,  417 Garcia-​Rizo, C.,  448
Furukawa, T. A.,  266, 273 Garcia-​Torner, S.,  56
Fuss, S.,  595, 596 Gardner, E., 57
Fussell, J. J.,  570 Gardner, F., 81
Fydrich, T.,  244, 252, 253, 301 Garey, L.,  396
Fyer, A.,  268 Garibaldi, G.,  436
Fyer, A. J.,  116, 243, 244, 256 Garland, A. F.,  18, 19, 24, 33, 108, 120
Garner, D. M.,  545
Gabbard, G. O.,  475 Garner, L.,  275
Gaboury, A.,  425 Garofalo, A.,  3, 21
Gabrielle, M.,  154 Garra, G.,  588
Gadner, H.,  594 Garrard, J.,  159
Gadow, K. D.,  35, 49, 50, 56, 59, 78, 86, 111, 225 Garratt, A. M.,  614
Gaffrey, M. S.,  101, 107, 108 Garre-​lmo, J.,  153–​154
Gagliese, L.,  619 Garssen, B.,  574
Gagne, C.,  451 Gartner, A. F.,  469
Gagnon, C.,  572 Garvan, C. W.,  59
Gagnon, D. D.,  530 Garvey, M., 99
Gagnon, F.,  295, 299, 301, 302, 305 Garza, M. J.,  199
Gahm, G. A.,  199 Garzotto, N.,  387
Gajewski, V. L.,  17 Gasbarrini, M. F.,  504
Gale, C. R.,  437 Gaskin, D. J.,  585
Gale, J.,  117 Gasquet, I.,  338
Galea, S.,  332 Gastfriend, D. R.,  391, 392
Galer, B. S.,  612 Gaston, J. E.,  254
Galione, J. N.,  178 Gatchel, R. J.,  608
Gallacher, D.,  609 Gates, P.,  400
Gallagher, D.,  156 Gathercoal, K. A.,  19
Gallagher, M. W.,  334, 341 Gatsonis, C. A.,  37
Gallagher, R.,  57, 60, 274, 275–​276, 281, 282 Gatward, R.,  108
Gallasch, J.,  574 Gatz, M.,  152, 154, 157, 159, 163, 574
Gallelli, K.,  341 Gau, J. M.,  383
Gallo, E. F.,  48 Gau, S. S.,  56, 62
664 author Index

Gaudet, A.,  30, 302, 305 Gibbon, M.,  175, 246, 247, 272, 273, 299, 316, 337, 416, 474,
Gauntlett-​Gilbert, J.,  595, 599 493, 507, 548
Gauthier, J.,  282 Gibbons, R. D.,  157
Gauthier, L. R.,  619 Gibbs, T. A.,  473
Gauthier, S.,  161 Gibel, A.,  444
Gavin, D. R.,  363 Giddens, J. M.,  194, 198, 204
Gavin, L.,  107 Gidron, Y.,  593
Gay, H.,  423 Giel, K. E.,  544
Gaynes, B. N.,  155 Giesbrecht, K.,  588
Gearity, J.,  108 Gifford, J.,  202
Gearon, J. S.,  440 Gifford, S.,  253
Gebauer, L.,  417 Giffort, D.,  446
Geddes, J. R.,  158 Gijs, L.,  515, 516, 517, 518
Gee, B.,  436 Gilbert, C.,  527
Geer, J. H.,  248 Gilbert, C. A.,  583
Gehrman, P.,  564 Gilbert, K.,  499, 501
Geisinger, K. F.,  507 Gilbertson, M. W.,  335
Geisser, M. E.,  617 Gilbody, S., 4
Gelaye, B.,  575 Gilbody, S. M.,  19, 20
Gelder, M.,  279 Giles, D. E.,  161
Gelenberg, A. J.,  180, 198 Gill, L., 22
Gellatly, R., xi Gill, N.,  586, 587, 588
Geller, B.,  101, 177 Gillet, C.,  385
Gent, C. L.,  81 Gillham, J.,  107
Gentilello, L. M.,  392 Gillihan, S. J.,  334
Genty, C.,  196 Gillis, M.,  250
George, L. K.,  294, 295 Gillis, M. M.,  276, 301
George, S. Z.,  619 Gilman, S.,  543
Georgieff, K.,  617 Gilman, S. E.,  345
Georgiou, G., 76 Gilmer, T.,  446
Georgiou, S., 84 Gilroy, M.,  546
Georgopoulos, A. P.,  336 Gilson, K.,  280
Geraci, M.,  269 Giltay, E. J.,  141, 152, 153
Gerard, S.,  182 Gingell, C.,  517, 531
Gerardi, R. J.,  338 Gingerich, S.,  446
Gerber, S.,  178 Ginn, N. C.,  79, 80
Gerber-​Werder, R.,  184 Ginsburg, G.,  230
Gere, M.,  223 Ginsburg, G. S.,  233
Gere, M. K.,  223 Gipson, D. S.,  40
Gerkovitch, M. M.,  612 Giugliano, D.,  521
Gerritsen, D. L.,  161 Giuliano, F.,  527, 530
Gerrity, E.,  342 Giuliano, K. C.,  59
Gerschler, A.,  156 Gizer, I.,  383
Gersing, K. R.,  473 Gladis, M.,  142
Gerstein, D.,  415 Gladman, M., 55
Gerstein, D. R.,  415 Glascoe, T., 22
Gervain, M.,  446 Glasgow, R. E.,  24
Gervais, N. J.,  305 Glasofer, D. R.,  547, 548
Gervasoni, N.,  178 Glass, A.,  439
Gex-​Fabry, M.,  178 Glass, C. R.,  269
Ghaemi, S. N.,  173, 174, 178, 179, 180 Glass, L., 56
Ghanem, H.,  517, 527 Glass, S.,  472
Gharaibeh, M.,  586 Glasser, D. B.,  517, 531
Ghelani, K., 48 Glasziou, P.,  37, 38, 39
Ghisi, M.,  275, 553 Glasziou, P. P.,  32, 37
Ghoneim, M.,  269 Glatt, S. J.,  268
Ghuman, H., 47 Gleacher, A.,  18, 22, 23
Ghuman, J., 47 Gleacher, A. A.,  22, 24
Gibb, B.,  100, 101, 115 Gleason, J. R.,  448
Gleaves, D. H.,  504, 507
 author Index 665

Gleghorn, A.,  361 Goldstein, R. B.,  296, 330, 331, 332, 334, 362, 363, 381, 382,
Glenn, C. R.,  200, 202, 203, 204, 206 384, 388, 389
Glick, H.,  183 Goldstein, S. W.,  527
Glick, I. D.,  451 Golinelli, D.,  275, 277
Glisson, C., 24 Golmaryami, F. N.,  84
Gloster, A. T.,  266, 267, 270, 281 Golombok, S.,  521, 528
Glover, D.,  269 Golshan, S.,  443
Glover, D. L.,  435 Gomes, A. C.,  374
Glovinsky, P. B.,  564, 567 Gomez, R.,  50, 51
Glowacka, M.,  518 Gonçalves, S.,  445, 542
Glozier, N.,  564 Gonda, X.,  268
Glynn, S. M.,  435, 444 Gonder-​Frederick, L. A.,  573
Gnagy, E. M.,  57, 59 Gong, X.,  332
Gnam, W. H.,  204 Gonzalez, A.,  278
Gobber, D.,  589 Gonzalez, H. M.,  154
Godart, N. T.,  544 González, R. A.,  61
Godbout, C.,  282 Gonzalez, T.,  499, 501
Godfrey, J. L.,  446 Goodday, R.,  593
Godley, M. D.,  373 Goodenough, B.,  586, 587, 588
Goel, R.,  437 Goodie, A. S.,  415
Goepel, K. A.,  254 Gooding, P.,  204
Goering, P.,  437, 490, 491 Goodman, D. W.,  61
Goetter, E.,  133 Goodman, J. T.,  59
Goetz, R.,  115 Goodman, K. L.,  104
Goetz, R. R.,  269 Goodman, L.,  343
Goff, D. C.,  438 Goodman, L. A.,  437, 440
Goh, M. T.-​T.,  196 Goodman, M. J.,  384
Gohm, C. L.,  499 Goodman, R.,  35, 47, 52, 73, 100, 107, 108, 112
Gold, D. P.,  393 Goodman, S. H.,  75, 83, 118
Gold, E. B.,  517 Goodman, W. K.,  220, 312, 314, 322
Gold, J. M.,  5, 438, 442 Goodstein, J. L.,  202
Gold, R.,  394 Goodwin, F.,  175
Goldberg, H. M.,  333 Goodwin, F. K.,  174, 180, 448
Goldberg, L. R.,  476 Goodwin, R. D.,  269
Goldberg, T. E.,  438 Goodyear, R. K.,  17
Golder, S.,  370 Goodyer, I.,  117, 118
Goldfein, J. A.,  545, 554 Goodyer, I. M.,  75, 83–​84, 102
Goldfischer, E. R.,  528 Goossens, L.,  547
Goldfried, M. R.,  227 Goossens, M. E.,  618
Goldin, P. R.,  254 Goplerud, E.,  177
Golding, E.,  364 Gordis, E. B.,  117, 499–​500
Golding, J., 50 Gordon, C. M.,  438, 448
Goldman, D.,  443 Gordon, K.,  585
Goldman, M. S.,  396 Gordon, M., 57
Goldmeier, D.,  516, 528 Gore, K. L.,  252, 279
Goldschmidt, A.,  547 Gorecki, A.,  392
Goldschneider, K.,  596 Gorg, N.,  142
Goldschneider, K. R.,  593, 598 Gorham, D. R.,  440
Goldsmith, C. H.,  614 Gorin, A.,  552
Goldsmith, H.,  279 Gorman, J. G.,  244
Goldsmith, H. H.,  111 Gorman, J. M.,  180, 269, 294, 438, 449, vii, xi
Goldstein, A. J.,  301 Gornbein, J.,  162
Goldstein, B. I.,  106, 107 Gorsuch, R. L.,  338, 340, 346
Goldstein, B. L.,  101 Gosselin, P.,  295, 297, 302, 303
Goldstein, D. J.,  550 Gossop, M.,  366, 371, 389
Goldstein, I.,  527, 528 Gotlib, I. H.,  113, 132, 133, 134
Goldstein, J. M.,  437 Gottman, J. M.,  494, 495, 498, 500, 501, 502
Goldstein, L. H.,  111 Goubert, L.,  595, 596, 608, 613, 618
Goldstein, M. G.,  394 Gould, M.,  194, 195
Goldstein, M. J.,  180, 436, 447 Gould, M. S.,  81, 86, 113, 196
666 author Index

Goulding, J.,  199 Green, L.,  371

Gourlay, A. J.,  156, 160 Green, M. F.,  5, 247, 436
Govoni, R.,  415, 416, 417, 427 Green, P., 24
Gower, P.,  142 Green, R. S.,  365
Gowers, S.,  19, 20, 24 Green, S. M.,  48, 49, 83, 176, 177
Gowers, S. G.,  546 Green, S. T.,  574
Goyette, C. H.,  50 Greenall, E.,  574
Grabowski, L., 88 Greenbaum, P. E.,  84
Graceffo, R. A.,  18–​19 Greenberg, G., 59
Gracely, E. J.,  275–​276, 277, 281, 282 Greenberg, L. S.,  144
Gracey, K. A.,  22 Greenberg, P. E.,  132
Gracious, B. L.,  24, 176, 177, 178 Greenberg, R. S.,  587
Gradisar, M.,  574 Greenberger, D.,  139
Gradus, J. L.,  332 Greene, J. W.,  592, 593, 598
Gräfe, K.,  272 Greene, M. C.,  394, 395
Graff, F. S.,  392 Greenfield, B. L.,  397
Gragg, R. A.,  585 Greenhill, L. L.,  59, 204
Gragnani, A.,  275 Greenley, R. N.,  595
Graham, C.,  612 Greeno, C.,  174
Graham, C. A.,  517 Greenstein, A.,  527
Graham, D. P.,  155 Greenwald, D. P.,  451
Graham, J. M.,  396 Greenwald, S.,  113
Graham, J. R.,  614 Greer, T. L.,  138–​139
Graham, P.,  156, 157 Grégoire, J. P.,  564
Graham, T. B.,  593 Gregory, A. M.,  218, 570
Grajales, M.,  446, 447 Gregory, J. D.,  333
Gralnick, T. M.,  476 Greist, J.,  322
Granero, R.,  84, 108 Greist, J. H.,  198, 204, 466, 467
Granger, C. B.,  599 Grekin, E. R.,  382
Granholm, E.,  452 Grekin, R. S.,  86
Granlund, M.,  56, 62 Gresham, F. M.,  84
Grannemann, B. D.,  138–​139 Gress, J. L.,  576
Granot, M.,  517 Grewe, S. D.,  588
Grant, B.,  332 Griesel, D.,  340
Grant, B. F.,  295, 296, 330, 331, 332, 334, 362, 363, 381, 382, Griest, D. L.,  72, 80, 86
384, 388, 389, 413 Griez, E.,  268, 269
Grant, D. M.,  339 Griez, E. J.,  268, 269
Grant, J.,  414, 417 Griffin, M. G.,  340
Grant, J. E.,  412, 414, 415, 416, 426 Griffiths, A.,  546
Grant, M.,  422, 448 Griffiths, G.,  444
Grant J. E.,  426 Griffiths, P.,  296, 366
Grapentine, W. L.,  201 Griffiths-​Jones, H. M.,  157
Gratch, J., 34 Grills, A. E.,  222
Grattan, E.,  117, 118 Grilo, C. M.,  19, 243, 472, 547, 548, 553, 554
Gratz, K. L.,  199, 206 Grimbos, T.,  528
Graugaard, C.,  516, 517, 518 Grisham, J. R.,  199, 267, 271, 276, 283
Gravel, J.,  588, 598 Grissom, G.,  367, 448
Gravenstein, S.,  437 Grissom, G. R.,  392
Gray, C. L.,  334 Grizenko, N., 60
Gray, J. A.,  133 Grizenko-​Vida, M.,  60
Gray, J. A. M.,  xi Grob, M. C.,  420
Gray, J. R.,  134 Grochocinski, V.,  273
Gray, K.,  162 Groenewald, C. B.,  585
Gray, M. J.,  343 Groessl, E.,  446
Gray, S.,  330 Groessl, E. J.,  446
Grayson, D. A.,  158 Gronbæk, M.,  516, 517, 518
Greden, J. F.,  132 Groom, M. J.,  53
Green, B.,  343 Gros, D. F.,  245, 575
Green, J. D.,  330, 333, 337 Groschwitz, R.,  197, 200
Green, J. G.,  105 Gross, J. J.,  132, 140, 254
 author Index 667

Gross, R.,  347 Guy, W.,  449

Gross, R. T.,  596, 618 Guyer, M. E.,  339, 439
Grosscup, S. J.,  138 Gwadry, F. G.,  617
Grossman, D.,  599 Gwaltney, C. J.,  198, 204
Grossman, R.,  426
Grossman, S.,  59, 466, 467, 473 Haaga, D.,  250
Grotle, M.,  614 Haaga, D. A.,  276
Grove, S. K.,  586, 588 Haaga, D. A. F.,  301
Grove, W. M.,  175, 176 Haas, G.,  447
Grover, K. E.,  199 Haas, G. L.,  442, 452
Grover, K. W.,  278 Haase, C. M.,  498
Grover, P. J.,  102 Haberer, J. E.,  385
Groves, M., 61 Habing, B.,  367
Grubaugh, A. L.,  341, 437, 440 Habrat, B.,  392
Gruber, A. J.,  543 Habre, W.,  587
Gruber, J.,  183 Hack, S.,  452
Gruber, M. J.,  105 Hackmann, A.,  279, 294
Gruber, R., 58 Hadash, Y.,  133
Grunebaum, M. F.,  332 Haddock, G.,  447
Grunewald, M.,  17, 22 Hadigan, C. M.,  552
Gual, A.,  387 Hadjistavropoulos, H. D.,  618
Gualandi, M.,  542 Hadjistavropoulos, T.,  608, 621
Guay, B.,  573 Hadler, J. L.,  332
Gubman, G. D.,  448 Hadley, T.,  154
Gudmundsen, G.,  117 Hadwin, J. A.,  220
Gueorguieva, R.,  389 Haefner, H. K.,  529
Guerra, N. G.,  115 Haeny, A. M.,  387
Guerreiro, D. F.,  332 Häfner, H.,  436, 437
Guertin, T.,  202 Hagen, E. M.,  614
Guess, H. A.,  522 Hagen, N. A.,  612
Guillaume, S.,  196, 202 Hagen, R.,  394
Guimond, T.,  204 Haggard, P.,  180
Guinta, D., 59 Haggerty, R. J.,  506
Guite, J. W.,  592, 593, 595 Hagopian, L. P.,  228
Gullion, C. M.,  161, 165 Hagtvet, K. A.,  451
Gulliver, S. B.,  344, 369, 370, 371, 373 Hahlweg, K.,  501, 504, 507
Gulmann, N.,  159, 161 Hahn, A.,  595
Gumidyala, A.,  595 Hahn, S. R.,  439
Gunawardane, N.,  178 Haidt, J.,  251
Gunawardena, C. N.,  332 Haigh, E. A. P.,  136
Gunderson, J. G.,  243, 299, 466, 469, 470, 472, 548 Hailey, B. J.,  613
Gunduz-​Bruce, H.,  437 Haiman, C.,  550, 554
Gunlicks-​Stoessel, M.,  103 Haine-​Schlagel, R.,  120
Gunnar, M.,  219 Hainsworth, K. R.,  594, 595, 596
Gunning-​Dixon, F. M.,  134 Hair, L. P.,  331
Guo, T., 42 Hajcak, G.,  323
Guo, Y.,  526 Hakstain, A.,  318
Gupta, S., 59 Halberstam, B.,  332
Gur, R. C.,  444 Hale, C. J.,  608
Gur, R. E.,  442, 444 Hale, L.,  324, 325
Gurland, B. J.,  156, 160, 438 Haley, C. L.,  109
Gursky, D. M.,  274, 280 Halford, W. K.,  508
Gusnard, D. A.,  134 Halikas, J. A.,  392
Gustafsson, J.,  436 Hall, C., 22
Gustave, J.,  332 Hall, C. L.,  53
Gustavsson, P.,  136 Hall, K. S.,  520
Guterstam, J.,  385 Hall, M. N.,  414
Gutierrez, J.,  178 Hall, S. M.,  394
Gutierrez, P. M.,  110, 199, 200, 203 Hall, W.,  366, 394
Guttman, R. D.,  257 Halladay, A.,  225, 226
668 author Index
Haller, D.,  360
Haller, M.,  383
Hallett, V.,  226
Hallgren, K. A.,  397
Halmi, K. A.,  545, 548, 553, 554
Halperin, J. M.,  47
Halpern, J. M.,  334
Ham, L. S.,  396
Hamann, J.,  452
Hambrick, E. P.,  59
Hamburg, P.,  543
Hamby, S. L.,  344, 498, 503–​504
Hameed, A.,  198
Hamilton, A. B.,  435
Hamilton, E.,  503
Hamilton, J.,  107
Hamilton, J. P.,  134
Hamilton, M.,  138–​139, 160, 164
Hammen, C.,  113, 115, 243
Hammer, R.,  203
Hammerle, M., 61
Hammerton, G.,  107
Hammond, M.,  86, 160, 161, 164
Han, S.,  332
Hancock, P.,  162
Hancox, R. J.,  71, 75
Handelsman, L.,  364
Handleman, J., 84
Handley, E.,  383
Hando, J.,  366
Handwerk, M., 19
Handwerk, M. L.,  52
Hanekamp, M.,  174
Hanf, C., 79
Hankin, B. L.,  100, 200
Hanley, J. A.,  182
Hanlon, P. J.,  203
Hanlon, T. E.,  444
Hannan, C., 20
Hannan, S. M.,  334
Hansen, N. B.,  17, 137, 143
Hanson, K., 72
Hanssen-​Bauer, K.,  55
Hansson, T.,  385
Hantouche, E.,  178
Hantson, J., 60
Haraburda, C. M.,  203
Harap, S. T.,  279, 281
Harden, N.,  529
Harder, V. S.,  57
Hardeveld, F.,  131
Hardial, J.,  587, 588
Harding, C. M.,  435, 437
Harding, G.,  612–​613
Harding, K.,  177
Harding, S. M.,  566
Hardoy, M. C.,  178
Hare, R. D.,  84
Har-​Even, D.,  203
Hargis, M. B.,  113, 118
Hargreaves, D.,  138–​139
Haring, C. T.,  102
Harkavy-​Friedman, J.,  116
Harkavy Friedman, J. M. H.,  200
Harkin, B.,  145
Harkness, A. R.,  476
Harkness, K.,  103
Harkness, K. L.,  115
Harland, N. J.,  617
Harllee, L. M.,  393
Harlow, B. L.,  518
Harmon, C.,  20, 37, 145
Harned, M. S.,  204, 334
Haro, J. M.,  180, 339, 439, 449
Haroon, E.,  154
Harper, A.,  199
Harpin, V., 59
Harpole, J. K.,  251
Harrigan, S.,  157
Harrington, H.,  436
Harrington, K.,  219
Harrington, R.,  33, 106, 107, 110, 111, 113, 117
Harris, A. L.,  574
Harris, C. A.,  613, 619
Harris, E. C.,  436
Harris, J.,  574
Harris, K. M.,  196
Harris, K. W.,  501
Harris, M.,  220
Harris, M. A.,  596
Harrison, D.,  583
Harrison, D. F.,  524
Harrison, J. A.,  466, 468
Harrison, M. A. M.,  156
Harrison, T. E.,  595
Harrison, W.,  545
Harshfield, G.,  278
Hart, E. L.,  48, 110
Hart, T. A.,  251
Hartdagen, S. E.,  74
Harter, M., 38
Härter, M.,  156, 392
Hartley, J.,  414, 415, 425
Hartman, N. S.,  251
Hartman, S.,  499, 501
Hartmann, A. S.,  547
Hartmann, J. A.,  573, 574
Hartnick, C. J.,  587, 598
Hartoov, J.,  527
Harvey, A.,  180
Harvey, A. G.,  566, 567, 568t, 570, 571, 573, 574, 613
Harvey, E. A.,  47
Harvey, P.,  438
Harvey, P. D.,  17, 436, 438, 442, 443, 445
Harvey, W., 60
Harwood, D. G.,  161
Harwood, J. E. F.,  194
Harwood, M. K.,  396
Hashimoto, R.,  440
Hasin, D.,  388
 author Index 669

Hasin, D. S.,  295, 296, 364, 367, 381, 382, 384, 388, 389 Heape, C. L.,  471
Hasking, P.,  195, 199 Heard, H. L.,  196, 197, 204
Hasking, P. A.,  397 Heath, A.,  268
Haslam, R.,  617 Heath, A. C.,  111, 268, 294, 394
Hass, J. P.,  593 Heather, N.,  394, 396
Hass, S. D.,  494 Heaton, R. K.,  443, 445
Hasselbad, V., 37 Heavey, C. L.,  495, 501, 501
Hassell, J.,  442 Hebebrand, J.,  544
Hasson-​Ohayon, I.,  446 Hebert, E. A.,  302
Hastie, T., 33 Hedegaard, H.,  155
Hastings, J. E.,  249 Hedeker, D.,  182, 183
Hatcher, N. M.,  56 Hedeker, D. R.,  182
Hatcher, R. L.,  144 Hedges, L. V.,  37
Hatfield, D. R.,  19, 20, 145 Hedlund, S.,  544
Hatgis, C.,  272 Heeren, T.,  332
Hathaway, J., 19 Heeren, T. J.,  154
Hatzichristou, D.,  527 Heffelfinger, A.,  109, 111
Hatzimouratidis, K.,  527 Heffelfinger, A. K.,  100
Hatzipetrou, L.,  20, 22 Heffer, R. W.,  491
Hauger, R.,  174 Hegeman, I. M.,  218
Haughie, S.,  522 Hegeman, J. M.,  152, 153, 161
Haukka, J.,  174, 175 Heidenreich, T.,  244
Haupt, D.,  250 Heilä, H.,  198, 200
Hauri, P. J.,  563 Heilman, N.,  499
Havassy, B. E.,  394 Heim, H. M.,  612
Haw, C.,  332 Heiman, J.,  521, 522, 524, 529
Hawes, D. J.,  76, 84, 88 Heiman, J. R.,  522
Hawken, L. S.,  24 Heimberg, R.,  252, 254, 325
Hawkins, E. J.,  5, 37, 143, 144, 145 Heimberg, R. G.,  133, 134, 139, 223, 228, 247, 251, 252, 275,
Hawkins, J. D.,  73 293, 294, 295, 296, 298
Hawkins, J. M.,  180 Hein, D.,  272
Hawkins, M. W.,  498 Heinberg, L. J.,  545
Hawkins, W.,  117 Heindel, W.,  268
Hawks, R. L.,  374 Heinrichs, D. W.,  444
Hawley, K. M.,  19, 20, 24, 33, 103 Heinrichs, N.,  243, 256
Hawley, L. L.,  255 Heinssen, R., 99
Hawley, P. H.,  72, 73 Heinssen, R. K.,  435
Hawton, K.,  332, 436 Heinze, S.,  281
Hay, D. F.,  73 Heisel, M. J.,  203
Hay, P.,  544 Hellemann, G.,  446
Hay, P. J.,  543, 555 Heller, K.,  490
Hay, P. P.,  544 Heller, T., 80
Hayes, J. P.,  333 Heller, T. L.,  80
Hayes, R. D.,  518 Hellstrom. K.,  228
Hayes, S.,  508 Helpman, L.,  527
Hayes, S. C.,  119–​120, 226, 506 Helstrom, A. M. Y.,  383
Haynes, B., 32 Helzer, J. E.,  156, 364, 439
Haynes, R. B.,  37, 38, 39, xi Hemmelgarn, A., 24
Haynes, S. N.,  4, 11, 139, 142, 343, 492, 493, 494, 495, 499, Henderson, A. S.,  153, 156, 294
500, 502, 503, 504, 507 Henderson, I.,  619
Hayward, C.,  267, 268 Henderson, R. D.,  571
Hayward, P.,  444 Hendrickse, W.,  17, 18, 22, 156, 270
Haywood, C.,  573 Hendrickx, L.,  515, 516, 517, 518
Hazard, E.,  178 Hendriks, G. J.,  277
Hazebroek-​Kampschreur, A. A. J. M.,  583 Hendriksen, S.,  20, 39, 387
Hazell, P., 52 Hendrix, E., 24
He, J.,  100, 218 Hendryx, M.,  445
He, J.-​P.,  180 Henggeler, S. W.,  86
Head, J.,  158 Henin, A.,  219, 232, 233
Healy, D. J.,  199 Heninger, G. R.,  314, 322
670 author Index

Henningfield, J. E.,  396 Hidgon, L. J.,  618

Henrich, C. C.,  72, 73 Hiebert, B.,  282
Henriques, G. R.,  204 Higa-​McMillan, C.,  22
Henry, C.,  174 Higa-​McMillan, C. K.,  20, 22, 111, 227
Henry, D. B.,  178 Higgins, S. T.,  368, 373, 374
Henry, E.,  587, 588, 598 Higgins-​Biddle, J. C.,  498
Henry, J.,  220 Hijman, R.,  440
Henson, J. M.,  401, 449 Hilbert, A.,  547
Herald-​Brown, S. L.,  115 Hildebrandt, T.,  543, 545, 548, 552, 553, 555
Herbenick, D.,  524 Hill, C. L.,  314, 322
Herbst, J. H.,  469 Hill, J. L.,  162, 165
Herda, C.,  617 Hill, K. A.,  20, 22
Hergueta, T.,  364, 439 Hill, L. C.,  24
Herjanic, B.,  106 Hill, M.,  415
Herlofson, K.,  574 Hill, M. L.,  617, 618
Herman, B. K.,  542 Hill, N. L.,  84
Herman, D. S.,  338, 340, 341 Hillemeier, M. M.,  50
Hermann, C.,  593, 596 Hiller, M. L.,  370
Hermann, E.,  20, 39, 387 Hilpert, P.,  503
Hermann, R. C.,  3 Himelhoch, S. S.,  417
Hermans, D.,  269 Hinrichsen, G. A.,  154
Hermes, H.,  231 Hinshaw, S. P.,  74, 80
Hernandez, B.,  566 Hinton, D.,  345
Hernandez, E.,  269 Hinton, D. E.,  337
Hernandez-​Ferrandiz, M.,  153–​154 Hinton, K. E.,  102
Herpertz, S.,  544 Hipwell, A. E.,  73
Herpertz-​Dahlmann, B.,  544 Hiripi, E.,  62, 543
Herr, K.,  621 Hirschfeld, R. M.,  174, 176
Herrell, R. K.,  331, 341 Hirschfeld, R. M. A.,  178
Herrmann, N.,  154 Hirschinger, N. B.,  448, 451
Herrmann-​Lingen, C.,  272 Hirshfeld-​Becker D. R.,  219
Herschell, A., 86 Hirshkowitz, M.,  566
Herschell, A. D.,  21, 23 Hirshman, J.,  566
Hersen, M.,  155–​156, 160, 226, 548 Ho, E. S.,  589
Hershey, A. D.,  594 Ho, K. F.,  530
Hertenstein, E.,  571 Hoagwood, K.,  18, 22, 23, 24
Hervas, A., 59 Hoagwood, K. E.,  7, 24, 40, 41, 143, 145
Herzig, J.,  469 Hobbs, M. J.,  293, 294
Herzog, D.,  543 Hock, M.,  275
Herzog, R.,  156 Hockenberry, M.,  598
Herzog, W.,  272 Hodgekins, J.,  436
Hesselbrock, V. M.,  388 Hodges, K.,  22, 57, 81, 86, 88, 108, 114
Hessler, M. J.,  100 Hodgins, D. C.,  412, 413, 414, 415, 417, 418, 421, 422, 423,
Hester, N. O.,  586 425, 426, 427
Hetherington, E. M.,  491 Hodgins, S.,  436
Hettema, J. M.,  244, 267, 294 Hodgkins, D.,  364, 367–​368
Heun, R.,  156, 295 Hodgkins, P., 61
Heussen, N.,  544 Hodgson, R.,  323, 385
Heuts, P. H.,  618 Hoehn-​Saric, R.,  256
Hewage, C.,  332 Hoek, H. W.,  437, 542
Hewlett, S.,  574 Hoekstra, J.,  323
Heyerdahl, S., 55 Hoeppner, S. S.,  438
Heyman, R. E.,  13n1, 116, 490, 493, 494, 495, 501, 502, Hoerger, M.,  340
503, 506 Hoff, A.,  223
Heyne, D.,  228 Hoffart, A.,  279
Hickie, I.,  153 Hoffer, M.,  253
Hicklin, J.,  470 Hoffman, A. R.,  566
Hicks, C. L.,  587 Hoffman, D.,  448
Hicks, R.,  113 Hoffman, J.,  203
Hicks, R. A.,  571 Hoffman, K.,  109
 author Index 671

Hoffman, N. G.,  392 Hoogduin, C.,  277

Hoffman, S.,  142 Hoogerheide, K. N.,  104
Hoffman, T.,  440 Hoogstraten, J.,  249
Hoffmann, E.,  397 Hooker, D. J.,  17
Hoffmann, J.,  415 Hooley, J. M.,  181, 447–​448, 451
Höfler, M.,  266, 267, 270, 295 Hoover, C.,  177
Hofmann, S. G.,  243, 247, 251, 256, 275 Hoover, D. W.,  504
Hofmans, J.,  479 Hoover, S. A.,  504
Hogan, M.,  177 Hope, D. A.,  252, 396
Hogan, M. J.,  613 Hope, T.,  202
Hogan, T. P.,  32, 443 Hopman, W. M.,  614
Hogarty, G.,  444 Hops, H.,  117, 501
Hogarty, G. E.,  451 Hoptman, M. J.,  134
Hoge, C. W.,  206, 331, 332, 333, 334, 341, 347 Hopwood, C. J.,  19, 476
Hoge, E. A.,  133 Horan, W. P.,  442
Hogh, H.,  571 Horn, J. L.,  387, 393
Hohagen, F.,  573 Horn, W. F.,  59
Hohmeister, J.,  596 Hornbrook, M.,  117
Hohoff, C.,  268 Horne, R.,  613
Holaway, R. M.,  295 Hornyak, R.,  136
Holden, G. W.,  503 Horon, R.,  199
Holden, J. L.,  452 Horovitz, L.,  614
Holden, R. R.,  203, 528 Horowitz, J. L.,  100, 111
Holder, D.,  116 Horowitz, L.,  545, 553
Hølen, J. C.,  611 Horowitz, M. J.,  338, 339
Holi, M. M.,  198, 200 Horton, L.,  193
Holland, J.,  570 Horvath, A. O.,  144
Hollander, E.,  426 Horvath, C., 3
Hollander, J. E.,  204 Horvitz-​Lennon, M.,  443
Hollifield, M.,  332 Horwitz, A. V.,  448
Hollis, C.,  22, 53 Horwitz, S. M.,  24, 102, 108, 176
Holloman, G.,  206 Horwood, L. J.,  74, 269
Hollomby, D. J.,  257 Höschl, C.,  452
Hollon, S. D.,  132, 134, 180 Hoskinson, K.,  180
Holloway, F.,  444 Hossain, J. L.,  574
Holm, S.,  598 Hosseini, S. Y.,  525
Holman, E.,  194 Hou, W., 59
Holmbeck, G. N.,  5 Houck, P. R.,  273
Holmberg, E. B.,  196, 197, 200, 202 Hougaard, E.,  279
Holm-​Denoma, J.,  542 Hough, R. L.,  33, 108, 331, 337
Holmes, C.,  174 House, A. O.,  19, 20
Holmes, M. K.,  174 Houts, R., 61
Holmqvist, R.,  144 Hoven, C., 81
Holodniy, M.,  620 Hovens, J. G.,  141
Holowka, D. W.,  302, 337 Howard, A. L.,  74
Holt, P.,  294 Howard, C.,  361
Holub, A.,  421, 426 Howard, F. M.,  612
Holzemer, W.,  589, 598 Howard, L. M.,  437
Holzemer, W. L.,  589, 590, 598 Howe, M. G.,  570
Holzer, C.,  178 Howell, C. T,  104
Holzman, S. B.,  389 Howell, C. T.,  49, 87, 88
Hom, M. A.,  194, 205 Howes, O.,  447
Homa, K.,  599 Hoyer, J.,  281, 295, 296
Hommel, K. A.,  594 Hoyle, R. H.,  140
Hommer, R. E.,  102 Hoza, B.,  52, 53
Honeycutt, A. A.,  86 Hrdlička, J.,  452
Hong, J. J.,  142 Hser, Y. I.,  361
Hong, M.,  178 Hsieh, C.,  614
Hood, H.,  244 Hsu, F. P.,  396
Hood, H. K.,  249 Hsu, J. L.,  343
672 author Index

Hsu, K. J.,  275 Huss, M.,  59, 61

Hsu, L. K. G.,  554 Hussong, A.,  382, 383
Hsu, L. M.,  4 Husted, J.,  466, 467
Hsu, M.-​A.,  162 Huston, L.,  219
Hsueh, A. C.,  498 Huta, V.,  252, 257
Hu, C. Q.,  42 Hutchinson, T. A.,  257
Hu, Q.,  542 Hutchison, S. L.,  18
Huang, B.,  295, 296, 388 Huth-​Bocks, A. C.,  200
Huang, C.,  109 Huybrechts, I.,  115
Huang, L., 60 Hvidsten, K.,  527
Huang, V.,  158, 159 Hwang, I.,  201, 332, 416
Huang, X.,  527 Hyams, J. S.,  590
Hubbard, J. A.,  72, 73 Hyde, C. J.,  11
Hubbard, R. L.,  361 Hyer, L.,  340
Hubley, S.,  117 Hyler, S. E.,  468, 471
Hudec, K. L.,  53 Hyman, R. B.,  200
Hudson, J. I.,  35, 542, 543 Hynd, G. W.,  74
Hudson, J. L.,  217, 218, 229, 294
Hudson, W. W.,  524 Iacono, W. G.,  361
Hudziak, J. J.,  52, 111 Iafrate, R.,  504
Huesmann, L. R.,  115 Ialongo, N., 59
Huestis, M. A.,  374 Ialongo, N. S.,  59
Huestis, S. E.,  599 Iannone, V. N.,  438
Hueston, W. J.,  347 Ibanez, A.,  415, 426
Huffman, J. C.,  206 Ibrahim, H. M.,  136
Hugdahl, K.,  256 Ierullo, M. D.,  244, 253
Hugelshofer, D. S.,  347 Ignacio, R. V.,  180
Hughes, C. W.,  17, 105, 117 Ignelzi, R. J.,  619
Hughes, D.,  294, 295 Ii, Y. B.,  385
Hughes, D. C.,  153 Ijzerman, M. J.,  621
Hughes, E. K.,  546 Ilardi, S. S.,  142
Hughes, H. M.,  21, 106 Ille, T.,  160
Hughes, J.,  200 Illersich, A. L.,  583, 585
Hughes, J. R.,  364 Imel, Z.,  332
Hughes, S. O.,  370, 397 Imel, Z. E.,  334
Hügle, B.,  593 In-​Albon, T.,  20, 39, 387
Hugues, M.,  295 Inderbitzen-​Nolan, H. M.,  250
Huguet, A.,  584, 585, 587, 588, 592, 595, 596 Indran, R.,  491
Huijding, J.,  249 Inn, A.,  396
Hull, J.,  154 Inoue, K.,  268
Hullett, C.,  389 Inrig, T.,  619
Humayan, A.,  138–​139 Insabella, G. M.,  491
Hummelen, B.,  243 Insel, T., 99
Humphreys, P.,  592 Insel, T. R.,  145, 219
Hunfeld, J. A. M.,  583 Inskip, H. M.,  436
Hunsley, J.,  3, 4, 11, 12, 19, 20, 21, 23, 24, 32, 34, 40, 41, 119, Intaprasert, S., 59
494, vii, xi Ionita, F., xi
Hunt, C.,  295 Ionita, G.,  19, 20, 24
Hunt, P.,  385 Irish, S. L.,  476
Hunt, T. K.,  553 Irurtia, M. J.,  247, 251
Hunter, J. E.,  11 Irwig, L. M.,  37
Huntsman, E.,  588 Irwin, D. E.,  110
Huntzinger, R. M.,  228 Irwin, M. R.,  160
Huppert, J. D.,  10, 256, 323, 325 Isaacs, A. D.,  156, 157
Hurl, K., 4 Isaacs, L.,  117
Hurlbert, M. S.,  108 Isaksson, A.,  385
Hurlbut, S. C.,  451 Isenhart, C. E.,  396, 400
Husebye, T.,  272 Isidori, A.,  521
Huska, J. A.,  338, 340, 341 Isometsä, E.,  178
Husky, M.,  196 Isometsä, E. T.,  199
 author Index 673

Israelski, D.,  620 Jamison, R. N.,  612, 621

Issakidis, C.,  295 Janardhan Reddy, Y.,  316
Ivanoff, A.,  202 Janavs, J.,  439
Ivanova, M. Y.,  4, 19, 33, 34, 38 Janavs, J.,  363, 389, 461
Ivers, H.,  564, 565, 570, 571, 572, 573, 574, 576 Jandorf, L.,  574
Ivey, A. Z.,  200 Jane, J. S.,  472
Iwenofu, L., 48 Jang, S. J.,  202
Iyengar, S.,  102 Janicak, P.,  182
Iyer, S. P.,  48 Janicak, P. L.,  182
Iza, M.,  253 Janis, I. B.,  193
Izard, C.,  104 Jannini, E.,  516, 518, 521
Izmirian, S.,  20, 22 Jansen, P. W.,  111
Janssen, E.,  521, 528
Jablensky, A.,  11, 437 Janssen, E. M.,  438
Jaccard, J.,  206 Janssen, J.,  154
Jacka, F. N.,  178 Janssens, J.,  111
Jackson, A.,  425 Jansson, M.,  154
Jackson, D.,  475, 479 Jansson-​Frojmark, M.,  570
Jackson, E.,  343 Janszky, I.,  564
Jackson, J.,  159 Januzzi, J. L.,  273
Jackson, K.,  12, 24, 42, 142 Janz, T.,  295
Jackson, K. M.,  382 Jaquett, C.,  196
Jackson, M.,  451 Jardine, R.,  268
Jackson, P. L.,  608 Jarrett, M. A.,  48
Jackson, R. J.,  268 Jarrett, R. B.,  119–​120, 161, 165, 226, 506
Jackson, R. L.,  175, 182 Jarrin, D. C.,  564, 571
Jacob, E.,  589, 590, 598 Jasin, S. E.,  277, 281, 282
Jacob, K.,  272 Jasiukaitis, P.,  365
Jacob, K. S.,  439 Jastrowski Mano, K. E.,  594, 595, 596
Jacob, R. G.,  250, 269 Jay, M. S.,  542
Jacobs, B., 86 Jayaram, G.,  452
Jacobs, D. G.,  193 Jaycox, L.,  340
Jacobs, G. A.,  338, 340, 346 Jazaieri, H.,  254
Jacobs, J.,  80, 86 Jeammet, P.,  544
Jacobs, J. R.,  86
Jean-​Louis, G.,  178
Jacobs, M.,  218
Jefferson, A. L.,  157
Jacobson, C. M.,  195
Jefferson, J. W.,  198, 204
Jacobson, N. S.,  40, 132, 133, 253, 305
Jefferson, S.,  425
Jacoby, R. J.,  312, 317
Jellinek, M. S.,  114
Jacomb, P. A.,  153
Jenkins, J. H.,  439
Jacques, C.,  415
Jenkins, M. M.,  24, 33, 34, 35, 176
Jaeger, J.,  444
Jenkins-​Guarnieri, M. A.,  347
Jaeger, S.,  17, 22, 564
Jennings, K. M.,  547
Jafarpour, S.,  269
Jensen, B.,  500
Jaffe, A.,  394
Jensen, D.,  177
Jaffe, J. H.,  361
Jensen, M.,  618
Jäger, N.,  593
Jensen, M. B.,  279
Jager-​Hyman, S.,  177, 194, 205
Jensen, M. P.,  609, 612, 615, 617, 618, 619, 620
Jagpal, A.,  598
Jensen, N. K.,  392
Jahng, S.,  360
Jensen, P.,  79, 83, 87
Jain, R., 59
Jensen, P. S.,  75, 79, 87, 103, 108, 118
Jain, U., 48
Jakobsen, H.,  244 Jensen-​Doss, A.,  4, 12, 17, 19, 20, 21, 24, 33, xi
Jakupcak, M.,  332, 334 Jenson, M. R.,  392
James, G.,  33, 278 Jenson, W. R.,  117
James, L. M.,  336 Jeon, Y.-​H.,  159
James, S.,  599 Jeon, Y. H.,  162
Jamieson, C.,  530 Jerrell, J. M.,  442
Jamieson, E.,  114 Jerrett, I.,  200
Jamison, C.,  160, 164 Jerrett, I. M. A.,  200
674 author Index

Jerstad, S.,  415, 416, 417, 420, 424 Jones, N. P.,  133

Jeste, D. V.,  152, 153, 443 Jones, P. B.,  437
Jewell, J., 19 Jones, R. R.,  78
Jiang, H.,  61, 176, 545 Jones, R. T.,  332
Jimenez, M.,  199 Jones, S.,  183
Jimenez-​Arista, L. E.,  503 Jones, S. M.,  72, 73
Jimenez-​Camargo, L. A.,  54 Jones, T.,  202
Jimenez-​Murcia, S.,  414, 417 Jongeling, B., 52
Jin, R.,  132, 173, 180, 243, 266, 267, 272–​273, 294, 313, 330, Jonkers, C. C. M.,  159, 163
331, 339, 343, 439, 564 Joober, R., 60
Jinks, C.,  614 Joosten, E. A. G.,  392
Jitendra, A. K.,  58 Jordan, A.,  583, 596
Johannes, C. B.,  515, 516, 517 Jordan, B. K.,  331, 337
Johannes, L. M.,  60 Jordan, K.,  614
Johannessen, J. O.,  436 Jorgensen, P. M.,  244
Johansson, B.,  154, 157 Jorm, A. F.,  153, 158
John, B.,  385 Joseph, D. L.,  250
John, K.,  113, 115 Joseph, J.,  437
John, O. P.,  140 Joseph, J. I.,  497, 501
John, R. S.,  499–​500 Joseph, R. E.,  374
John, U.,  244, 270 Joseph, S.,  333
Johnson, A. M.,  517 Jovanovic, T.,  336
Johnson, B.,  498 Joy, V. D.,  448
Johnson, B. D.,  361 Jozefiak, T.,  107
Johnson, B. H.,  256 Judd, L. L.,  174, 184, 448
Johnson, B. N.,  132, 137 Judez, J.,  108
Johnson, D. E.,  62 Juhari, R.,  491
Johnson, H. S.,  250 Juhasz, G.,  268
Johnson, J. E.,  365, 372 Juliano-​Bult, D.,  438
Johnson, J. G.,  439 Julien, D.,  499, 501
Johnson, M. D.,  490, 501 Júlíusdóttir, G., 22
Johnson, M. H.,  182 Jung, J.,  330, 331, 332, 334, 362, 363, 381, 382, 384, 389
Johnson, R.,  415 Junghaenel, D. U.,  616
Johnson, S.,  144, 437, 439 Junghanns, K.,  573
Johnson, S. L.,  174, 178, 179, 180, 181, 183 Juniper, K.,  586
Johnson, S. M.,  490, 498 Juniper, K. H.,  587
Johnson, T. E.,  422 Juster, H. R.,  252
Johnston, A.,  18, 24, 574 Juzwin, K. R.,  205
Johnston, C.,  3, 19, 20, 24, 49, 50, 59, 584, xi
Johnston, D. W.,  277 Kaasa, S.,  611
Johnston, K. L.,  397, 398 Kaat, A. J.,  225, 226
Joiner, T.,  199 Kabacoff, R. I.,  155–​156, 160, 181
Joiner, T. E.,  193, 194, 195, 198, 199, 205 Kabat-​Zinn, J.,  135
Joiner, T. E. J.,  199 Kable, J. A.,  56
Jolly, J.,  110, 224 Kachin, K. E.,  298
Jones, A.,  552, 617 Kackley, N.,  402
Jones, A. C.,  499 Kaczynski, K.,  595–​596
Jones, A. M.,  225–​226 Kaczynski, K. J.,  595, 596
Jones, B. A.,  593 Kadden, R.,  365, 370, 397, 423
Jones, D.,  114 Kaelin, A.,  587
Jones, D. C.,  543 Kaemmer, B.,  614
Jones, D. J.,  86 Kaess, M.,  197, 200
Jones, E. C.,  614 Kagan, E. R.,  231
Jones, J.,  220, 231 Kagan, J.,  177
Jones, J. D.,  220, 231, 383 Kahler, C. W.,  393, 394
Jones, J. M.,  102 Kahn, J. S.,  117
Jones, J. W.,  394 Kahn, R. E.,  75–​76, 84
Jones, K. G.,  516 Kahneman, D., 33
Jones, M., 22 Kaholokula, J. K.,  139, 142, 493, 507
Jones, N.,  24, 225, 226 Kaholokula, K.,  492, 494
 author Index 675

Kakuma, T.,  154 Karney, B. R.,  497

Kalal, B.,  501 Karoly, P.,  612, 617, 619
Kalali, A., 33 Karpel, M. A.,  500
Kalapurakkel, S.,  599 Karpenko, V., 60
Kalarchian, M. A.,  554 Karterud, S.,  451
Kalas, C.,  106, 107, 593 Karyotaki, E.,  116
Kalas, R.,  103, 108 Kashani, J. H.,  200
Kalayam, B.,  154 Kashdan, T. B.,  281
Kaldo, V.,  281 Kashikar-​Zuck, S.,  592, 593, 596, 598
Kali, J.,  381 Kashner, R. M.,  105
Kalista, T.,  576 Kashner, T. M.,  17
Kaloupek, D. G.,  334, 335, 336, 337, 340, 343, 346, 440 Kasius, M. C.,  104
Kalsekar, A.,  564 Kaslow, N. J.,  3, 117
Kamali, M.,  180 Kasper, L. J.,  53
Kamath, S. A.,  449 Katerelos, M.,  255
Kamenetz, C.,  554 Katerndahl, D. A.,  267
Kamerman, J. D.,  396 Katon, W.,  295, 341
Kamijima, K.,  273 Katz, I. R.,  163
Kaminer, Y.,  394 Katz, J.,  421, 583, 585, 595, 596, 612
Kaminski, K. M.,  115 Katz, M. M.,  175
Kammerer, N.,  343 Katz, N. P.,  612
Kamphaus, R. W.,  50, 54, 55, 56, 59, 79, 80, 81, 82, 87–​88 Katzelnick, D. J.,  198
Kamphuis, J. H.,  479 Kauffman, B. Y.,  338, 340
Kampman, M.,  277 Kaufman, E. R.,  218
Kanai, T.,  273 Kaufman, J.,  53, 107, 177, 223
Kanayama, G.,  543 Kaufmann, C. A.,  116
Kanba, S.,  443 Kaur Soin, H.,  585, 587, 598
Kane, J.,  451 Kavanagh, D. J.,  395, 448
Kane, J. M.,  180, 435, 437 Kavanagh, T.,  586, 587, 588
Kane, R.,  332 Kay, D. W. K.,  156
Kang, H.,  339 Kay, J.,  583
Kang, H. K.,  332 Kay, S. R.,  440
Kang, J.,  174 Kaye, A. L.,  467
Kang, J.-​H.,  531 Kaye, W. H.,  554
Kanof, P. D.,  364 Kayed, N. S.,  107
Kao, G. S.,  56 Kaysen, D.,  334
Kapczinski, F.,  243 Kayumov, L.,  574
Kapen, S.,  566 Kazak, A. E.,  5
Kaplan, A. S.,  343, 545, 550, 552, 554 Kazantzis, N.,  144
Kaplan, D.,  396 Kazarian, S. S.,  570
Kaplan, G. M. D.,  200 Kazdin, A. E.,  4, 5, 7, 41, 59, 87, 105, 139, 177, 200, 233
Kaplan, H. B.,  387 Kean, J.,  446
Kaplan, J. S.,  269 Keane, T. M.,  333, 334, 335, 336, 337, 338, 339, 340, 341, 342,
Kaplan, K.,  382 343–​344, 345, 346, 440
Kaplan, K. A.,  566 Keaney, F.,  389
Kaprio, J.,  174, 175, 542 Kearney, C. A.,  228
Kapstad, H.,  611, 614 Keck, L.,  446
Kapur, S.,  436, 437 Keck, P. E.,  180
Kapur, V.,  563, 573 Keck, P. E., Jr.,  178
Karalunas, S. L.,  48 Keefe, F. J.,  608, 609, 615, 617
Karam, E.,  609 Keefe, R. S.,  436
Karam, E. G.,  331 Keefe, R. S. E.,  438
Karantzas, G.,  162 Keel, P. K.,  542, 543, 544
Karataraki, M.,  564 Keeler, G.,  104, 218, 219
Karel, M. J.,  152, 159, 163 Keeley, J.,  479
Karg, R. S.,  135, 155, 175, 247, 270, 272, 279, 298, 337, 363, Keeley, J. W.,  11, 387
388, 389–​391, 416, 422, 438, 448, 520, 548 Keen, J. H.,  588
Karkowski, L. M.,  174 Keen, S. M.,  341
Karlov, L.,  543 Keenan, K., 73
Karlsson, L.,  198, 200 Keenan, M.,  435
676 author Index

Kehle, T. J.,  117 Keyes, K. M.,  331

Kehle-​Forbes, S.,  347 Keys, D. J.,  253
Keijsers, G.,  277 Khaled, N.,  345
Keith, S. J.,  174, 448, 451 Khalife, S.,  515, 528, 529, 530
Keitner, G. I.,  181 Khalifeh, H.,  437
Kellar, I.,  145 Khalsa, S. R.,  277
Kelleher, M. J.,  156, 160 Khan, K. A.,  594, 595
Keller, A.,  525 Khandker, M.,  318, 319
Keller, A. B.,  437 Khashan, A. S.,  437
Keller, M.,  117, 175 Khavari, K. A.,  393
Keller, M. B.,  136, 175, 176, 180, 184, 267, 273, 294, 295, 470 Khawaja, N. G.,  302
Keller, S. D.,  389, 445 Khayrallah, M., 59
Keller, W. R.,  442 Khera, M.,  518
Kellett, J. M.,  156, 160 Khetarpal, S.,  223
Kelley, K., 10 Kichic, R.,  323
Kelley, M. L.,  202 Kidder, K.,  446
Kelley, S. D.,  18, 22 Kiecolt-​Glaser, J. K.,  156, 160
Kellman, H. D.,  468, 471 Kiel, J. T.,  203
Kelly, A.-​M.,  588 Kiernan, R. J.,  163
Kelly, H. S.,  104 Kieseppa, T.,  174, 175
Kelly, J. F.,  394, 395 Kikuzawa, S.,  490
Kelly, S.,  392 Kilbourne, A. M.,  180, 339
Kelsoe, J.,  178 Killen, J. D.,  267, 268
Kelvin, R.,  117, 118 Kilpatrick, D.,  330
Kemp, C. A.,  618 Kilpatrick, D. G.,  331, 338
Kemp, N.,  254 Kim, B.,  281
Kemp, R.,  180 Kim, E. D.,  526
Kempe, P. T.,  276 Kim, H.,  256
Kemper, C. J.,  275 Kim, J. B.,  278
Kenardy, J. A.,  277 Kim, J. H.,  278
Kendall, P. C.,  9, 23, 105, 180, 223, 230, 231, 232, 233 Kim, K. L.,  181
Kendall, T.,  176 Kim, L. J.,  396
Kendell, R., 11 Kim, M.,  444
Kendler, K. S.,  112, 174, 244, 267, 268, 294, 295, 383, 436 Kim, P. Y.,  206
Kennard, B. D.,  102, 109, 112, 113, 115 Kim, S., 56
Kennedy, C.,  138 Kim, S. W.,  414, 415, 416, 426
Kennedy, S.,  133, 139 Kim, Y. W.,  281
Kent, L.,  110 Kimbrel, N. A.,  344
Keortge, S.,  323 Kimerling, R.,  330, 339, 343, 347
Keough, M. E.,  269, 283 Kimonis, E. R.,  71, 72, 73, 74, 76, 84
Keramari, E.,  180 Kinderman, P.,  180
Kerig, P. K.,  501 King, A., 34
Kerkhof, A. J. F. M.,  199 King, C. A.,  132, 200
Kern, R. S.,  436 King, D. W.,  339, 340, 344
Kernan, E.,  447 King, J.,  102
Kerns, R., 3 King, K.,  250
Kerns, R. D.,  610, 615, 620 King, K. M.,  80
Kerr, D. C. R.,  200 King, L. A.,  339, 340, 344
Kerr, P. S.,  203 King, M.,  447
Kersten, P.,  18, 24 King, N. J.,  219, 223, 227, 231
Keshavan, M.,  436, 442 King, S.,  584, 585
Keski-​Rahkonen, A.,  35, 542 Kinney, P. J.,  279, 281
Kessel, E. M.,  102 Kinosian, B.,  183
Kessler, F.,  367 Kinston, W.,  545
Kessler, R.,  156, 313, 339 Kirby, A.,  566
Kessler, R. C.,  62, 105, 131, 132, 153, 173, 174, 180, 194, 201, Kirby, J. S.,  497
204, 243, 245, 266, 267, 272–​273, 294, 295, 296, 331, 332, Kircanski, K.,  266
338, 339, 343, 347, 416, 439, 542, 543, 564 Kirchmann, H.,  22, 24
Kewley, E.,  588 Kirchner, H. L.,  592
Key, T.,  621 Kiresuk, T. J.,  143, 505
 author Index 677

Kirisci, L.,  250, 363, 387 Knight, T. S.,  594, 598

Kirkpatrick, B.,  442 Knobloch-​Fedders, L. M.,  498
Kirkpatrick, J.,  522 Knott, C. B.,  587, 597
Kirmayer, L. J.,  439, 473 Knott, K.,  154, 163
Kiropoulos, L. A.,  280 Knottnerus, J. A.,  159, 163
Kirouac, C.,  301 Knouse, L., 61
Kishna, M. A.,  59 Knouse, L. E.,  61
Kisiel, C.,  23–​24 Knowles, K.,  340
Kiska, R.,  593 Knudsen, H. C.,  444
Kissileff, H. R.,  545, 552 Ko, C. H.,  180
Kissling, W.,  452 Kobak, K.,  322
Kitajima, T.,  573 Kober, H.,  134
Kite, B. A.,  401 Kocalevent, R.-​D.,  199
Kivimäki, M.,  158 Koch, W. J.,  251–​252
Kiviruusu, O.,  198, 200 Kochanska, G., 86
Kivlahan, D. R.,  341 Kodituwakku, P.,  332
Kizer, A.,  174 Koenen, K. C.,  331, 335, 345
Kjeldgaard, K. M.,  159, 161 Koepke, T.,  546
Klahn, J. A.,  394 Koerner, K., 21
Klapp, B. F.,  199 Koerner, N.,  30, 250, 295, 302
Klaric, S. H.,  108 Koffel, E.,  179
Kleef, M. V.,  617 Kofoed, L. L.,  449
Kleespies, P. M.,  193, 199 Kogan, J. N.,  18, 179
Kleiman, E.,  201 Köhler, C. A.,  178
Kleiman, E. M.,  206 Kohler, C. G.,  444
Klein, B.,  280 Kohls, N.,  593
Klein, D.,  177 Kohn, R.,  154
Klein, D. F.,  116, 244, 269 Kohout, F. J.,  163
Klein, D. N.,  101, 102, 104, 107, 108, 116, 118, 119, 136, 177 Kojima, M.,  573
Klein, J. B.,  17 Kok, B. C.,  331
Klein, M. H.,  466, 467 Kok, R. M.,  152, 153, 161
Kleinknecht, R. A.,  249, 251 Kolb, L. C.,  337, 338, 340
Kleinman, M.,  196 Kole-​Snijders, A. M.,  596
Klepac, R. K.,  249 Kolko, D.,  116
Klepstad, P.,  611 Kolko, D. J.,  21, 23
Klerman, G. L.,  134 Kollenstam, C.,  281
Klestov, A. C.,  612 Kollins, S. H.,  59, 60
Klieger, D. M.,  249 Komproe, I. H.,  345
Kliem, S.,  204 Konick, L. C.,  199, 200
Klimek, P.,  548 Koochaki, P.,  528
Klimes-​Dougan, B.,  201 Koocher, G. P.,  3, 21, 32, 53
Kline, G. H.,  499, 501 Kooij, J. J. S.,  47, 48, 61, 62
Kline, S. L.,  499 Koopmans, R. T. C. M.,  161
Klingaman, E. A.,  452 Koot, H. M.,  104, 594
Klonsky, E. D.,  195, 202, 203, 205, 206 Koppenhaver, J.,  373
Kloosterman, P. H.,  245, 246 Kopper, B. A.,  199, 200, 202, 203
Klorman, R.,  249 Korathu-​Larson, P. A.,  20, 22
Klosko, J. S.,  282 Kordonski, W. M.,  445
Kloss, J. D.,  567 Koren, D.,  471
Klugman, J.,  178 Koren, G.,  583, 585, 587, 598
Klump, K. L.,  543 Koretz, D.,  132
Klysner, R.,  161, 165 Kori, S.,  618
Knapp, E.,  389 Kori, S. H.,  619
Knapskog, A. B.,  161 Korman, L.,  204
Knauss, F.,  575 Kornblith, S. J.,  451
Knee, C. R.,  383 Kørner, A.,  159, 161
Knight, E. L.,  449 Korotitsch, W.,  143
Knight, J.,  344 Korslund, K. E.,  204
Knight, J. A.,  199 Korsnes, M.,  161
Knight, K.,  370 Korten, A. E.,  153
678 author Index

Kosfelder, J.,  204 Kröger, C.,  204

Kosinski, M.,  344, 445, 614 Krokoff, L. J.,  494
Kosinski, M., Jr.,  389 Krokstad, S.,  564
Koslow, S. H.,  175 Kroll, L.,  110
Kossowsky, J.,  446 Kroner, D. G.,  203
Kostanjsek, N.,  138, 337 Kronish, I. M.,  330
Kosty, D. B.,  383 Kroska, E. B.,  596
Kotler, J. S.,  88 Krueger, R. F.,  119, 466, 470, 473, 476, 478
Kotov, R.,  179, 268, 275 Krüger, S.,  182, 183
Kotte, A.,  20, 22 Krukowski, R. A.,  38
Koudijs, E.,  507 Krull, J. L.,  206
Kouimtsidis, C.,  369 Krumholz, L. S.,  5, 102
Kovac, S. H.,  202 Krupitsky, E.,  389
Kovacs, M.,  100–​101, 103, 106, 109, 110, 198, 223 Krupp, L. B.,  574
Koven, L. P.,  203 Kruse, M.,  19, 24
Kowalski, P.,  256 Krystal, A. D.,  566, 569, 570, 574, 575
Kowatch, R. A.,  102, 108, 117, 176 Krystal, J. H.,  389
Koyuncu, A.,  243 Kryszak, E.,  397
Kozak, M. J.,  313, 323 Ktasafanas, E.,  436
Kožený, J.,  452 Kubany, E. S.,  11, 343
Kraaij, V.,  154 Kuch, K.,  276
Kraemer, H.,  551, 552 Kuhl, E. A.,  468
Kraemer, H. C.,  37, 38, 42, 111, 113, 267, 268, 346, 468, 545, Kuhn, L.,  437
546, 548, 553 Kukkonen, T. M.,  527, 528
Kraemer, S.,  180 Kulka, R. A.,  331, 337
Kraepelin, E.,  435, 438 Kulkarni, G.,  153
Krägeloh, C. U.,  18, 24 Kumar, A.,  153
Krahn, D. D.,  396 Kumar, G.,  200
Kraiprasit, K.,  586 Kumar, V.,  269
Kral, J. G.,  545 Kun, P.,  332
Kralovec, K.,  194, 205 Kundey, S.,  104
Kramer, A. C.,  200 Kunik, M. E.,  155
Kramer, M.,  566 Kuntsche, E.,  383
Krämer, M.,  256 Kuo, J. R.,  252
Kramer, T. L.,  17, 113, 118 Kuo, T. F.,  576
Kramp, P.,  182 Kupersmidt, J., 72
Krane, E. J.,  599 Kupfer, D. J.,  111, 113, 178, 180, 223, 465, 468, 573
Kranzler, H. R.,  383 Kupper, R. J.,  59
Krasnow, A. D.,  272 Kuramoto, S. J.,  468
Kratochvil, C., 59 Kurdek, L. A.,  523
Kraus, S. W.,  397 Kuriansky, J. B.,  438
Krause, P.,  295 Kurlowicz, L. H.,  161
Krauss, G. E.,  340 Kurs, R.,  444
Krauss, S.,  177 Kurtin, P. S.,  593, 594
Kravetz, S.,  446 Kurtines, W. M.,  233
Krebs, E.,  609 Kurtz, J.,  468
Krebs, P. M.,  394 Kurtz, M. M.,  444
Kreider, R. M.,  490 Kurtz, S. M. S.,  80, 87
Kreisman, D.,  451 Kushner, H.,  367, 419, 424, 448, 518
Kreisman, D. E.,  448 Kushner, M. G.,  448
Kremer, E.,  619 Kuskowski, M. A.,  382
Kreppner, W.,  527 Kutash, K., 4
Kreyenbuhl, J.,  417, 452 Kutcher, S.,  106, 108, 109, 110, 117
Kring, A. M.,  442 Kutter, C. J.,  341
Krinsley, K. E.,  341 Kuyken, W.,  4, 120, 135, 141, 142
Krishnamurthy, R., 3 Kvaal, K.,  161
Krishnan, R. R.,  256 Kvaal, S. A.,  617
Kroenke, K.,  136, 159, 162, 163, 164, 165, 337, 439, 498, Kvernmo, S.,  55, 112
575, 609 Kvrgic, S.,  446
Kroeze, S.,  269 Kwapil, T. R.,  178
 author Index 679

Kwon, J. H.,  504 Landau, S., 86

Kyngdon, A.,  418 Landová, E.,  249
Kyrios, M.,  324 Lane, S. P.,  388
Lang, A. J.,  269, 279, 280, 281
Laan, E.,  517, 522, 528 Lang, B. A.,  593
L’Abate, L.,  500, 503 Lang, N.,  160
Laberg, J. C.,  256 Lang, P. J.,  248, 249
Laberge, B.,  282 Langberg, J. M.,  48
Labouvie, E.,  394–​395, 552 Lange, A.,  282
Labouvie, E. W.,  368, 373, 393, 400 Langenbucher, J.,  543, 545
Labrecque, J.,  301 Langenbucher, J. W.,  381, 543
LaBrie, R.,  416, 417 Langer, A.,  500
Labriola, S.,  446 Langer, D. A.,  117
Labus, J. S.,  609 Langer, J. K.,  10, 244
Lachance, N.,  425 Langer, M. M.,  110
Lachance, S.,  297 Langer, S.,  595
Lachar, D.,  50–​51 Langer, S. L.,  598
LaChaussee, J. L.,  552 Langhinrichsen-​Rohling, J.,  493, 502, 506
Lachowski, A.,  573, 574 Langley, A. K.,  223, 230
Lachowski, A. M.,  569, 570 Langley, J.,  206, 613
Lack, L.,  574 Langlois, F.,  302, 303, 305
Laconti, A.,  402 Langner, R.,  323
Lacro, J. P.,  443 Langsrud, O., 55
Ladd, B. O.,  397 Langston, J. W.,  163
Ladd, G. W.,  115 Lansford, J. E.,  85
Ladouceur, R.,  295, 297, 299, 301, 302, 303, 305, 414, 415, Lansky, D.,  618
417, 418, 423, 425 Lantz, C. D.,  545
Lafontaine, M. F.,  498 Lapidus, K. A. B.,  312
La Greca, A. M.,  5, 219, 224, 225 Lapidus, S.,  393
Lahart, C.,  139, 252 Lapp, W. M.,  395
Lahey, B. B.,  48, 49, 57, 59, 72, 73, 74, 75, 83, 103, 110, 118, Laptook, R.,  108
119, 176, 177 Laranjeira, R. R.,  366
Lai, J.,  110 Larken, S. M.,  72
Lai, J. K.,  543 Larkin, E. J.,  247
Laje, G.,  176 Larner, A. J.,  162
Lajnef, M.,  174 LaRocca, N. G.,  574
Lakoma, M. D.,  105 Larsen, D. K.,  618
Laks, J.,  161 Larsen, J. P.,  574
Laliberte, S.,  596 Larsen, R. J.,  140
Lalloo, C.,  588 Larson, G. E.,  332
Lalumière, M. L.,  528 Larson, J. E.,  447
Lam, B. C. P.,  499 Larson, J. H.,  494, 523
Lam, D.,  180, 184 Larsson, H.,  112
Lam, D. H.,  180, 183 Larsson, M. H.,  144
Lamanna, A. L.,  56 Larstone, R.,  479
Lambe, L.,  421 LaRue, R. H.,  84
Lamber, M. J.,  vii, xi Larus, J. M.,  498
Lambert, E. W.,  56 Lasagni, I.,  504
Lambert, M.,  508 Lash, T. L.,  332
Lambert, M. C.,  51 Lask, B.,  547, 552
Lambert, M. J.,  4, 5, 17, 18, 19, 20, 37, 120, 137, 143, 144, 145, Lask, B. D.,  547
281, 282 Laska, K.,  334
Lamé, I. E.,  617 Lasser, R. A.,  61
Lamers, F.,  159, 163 Last, C.,  223
Lamis, D.,  202 Laszik, A.,  268
Lamis, D. A.,  203 LaTaillade, J. J.,  497
Lamoureux, B. E.,  136 Latas, M.,  160
Lampert, C.,  175 Lataster, T.,  437
Lancaster, S., 55 Latham, A. E.,  154
Lance, C. E.,  415 Latham, P.,  395
680 author Index

Lathan, C. E.,  332 Lee, H.-​C. B.,  277

Latimer, E.,  445 Lee, H.-​J.,  206
Latimer, E. A.,  437 Lee, J.,  573
Latner, J.,  552, 555 Lee, M.,  383, 414, 415, 425
Lau, A. S.,  33 Lee, M. D.,  194, 201, 205, 206
Lau, N.,  7, 40, 41, 143, 145 Lee, M. R.,  382
Laudenslager, M. L.,  269 Lee, R.,  332
Laudet, A. B.,  449 Lee, S.,  51, 59, 180, 609
Laugesen, N.,  30, 302 Lee, S.-​H.,  281
Laugsand, L. E.,  564 Lee, S. S.,  50, 552
Laumann, E. O.,  515, 517, 518, 531 Lee, S. Y.,  278
Lauritzen, L.,  159, 161 Lee, T. C.,  251
Lauterbach, D.,  339, 343 Lee, Y. Y.,  101
Lauth, B.,  22, 223 Leech, A.,  117, 118
Lavee, Y.,  546 Leese, M.,  444
Lavelle, J.,  345 Leeuw, I.,  256
Lavender, J. M.,  551, 552 Leeuw, M.,  618
Lavene, D.,  612 Lefebvre, M.,  494
Lavigne, J. V.,  17, 599 Leff, H. S.,  344
Lavner, J. A.,  497 Leff, J.,  447, 545
Lavori, P. W.,  176, 180, 337, 340 Leff, J. P.,  447
Lavretsky, H.,  153 Leff, S. S.,  88
Law, M. K.,  196 Leffingwell, T. R.,  402
Lawing, K.,  76, 84 Leffler, J. M.,  21, 106
Lawler, E.,  332 Leger, D.,  569–​570
Lawrance, K. A.,  524 Léger, E.,  301, 305
Lawrence, E.,  497, 500, 508 Legerstee, J. S.,  243
Lawrence, S. M.,  398 Legocki, L. J.,  529
Lawrinson, P.,  400 Le Grange, D.,  545, 546, 548, 549, 552, 553
Lawson, J.,  219 Lehman, A.,  447
Lawson, W. B.,  473 Lehman, A. F.,  446, 447
Lawyer, S. R.,  257 Lehman, C.,  316
Lazar, J.,  587, 588, 598 Lehman, C. L.,  246–​247, 267, 271–​272, 296, 298, 338
Lazarou, C., 76 Lehmann, S.,  616
Lazarus, L. W.,  160 Lehr, D.,  282
Lazary, J.,  268 Lehrer, D. S.,  439
Leahy, R. L.,  174, 480 Leibenluft, E.,  102, 112, 174, 180
Leary, M. R.,  140, 250, 251 Leiberg, S.,  323
Lebel, A.,  596 Leibing, E.,  468, 478
Leblanc, G.,  301 Leiblum, S.,  515, 517, 521, 522, 524, 528, 529
LeBlanc, J.,  573 Leiblum, S. R.,  521
LeBlanc, M.,  564, 573 Leichsenring, F.,  468, 478
LeBlanc, N. J.,  345 Leirer, V. O.,  158, 159
Leblanc, R.,  302 Leisen, M. B.,  343
Leblond, J.,  415 Leising, D.,  479
Lebow, J.,  549, 553 Leistner-​Segal, S.,  268
Lebow, J. L.,  490, 498 Leitenberg, H.,  547
Lebowitz, E. R.,  220, 221, 229, 231 Lejuez, C. W.,  419
Lecavalier, L.,  225, 226 Lemanek, K. L.,  5
Leckman, J. F.,  220, 221, 231 Lemery-​Chalfant, K.,  111
Lecomte, J.,  445 Lemsky, C.,  499
Lecomte, T.,  445 Lenderking, W. R.,  522
Lecrubier, Y.,  295, 363, 389, 439 Lengel, G. J.,  11, 466, 474, 477
Le Dean, L.,  473 Lenhart, R. S.,  617
Lederer, A. S.,  229 Lennon, S.,  269
Ledley, D. R.,  252, 275 Lennox, R.,  368, 374
Lee, C. M.,  3 Lennox-​Holt, P. J.,  588
Lee, D. J.,  337 Lenox, M. S.,  173, 174
Lee, D. L.,  60 Lenze, E. J.,  10
Lee, G. Y.,  584 Lenze, S.,  101, 117
 author Index 681

Lenze, S. N.,  101, 117 Lewis-​D’Agostino, D. J.,  528

Lenzenweger, M. F.,  469 Lewis-​Fernández, R.,  334, 345, 439
Leo, G. I.,  366, 373, 392 Li, F., 74
Leon, A. C.,  154, 175, 176 Li, Q.,  198
Leonard, K. E.,  396, 497 Li, T.,  542
Leontjevas, R.,  161 Li, T. K.,  383
Leopold, D. R.,  48 Li, Y.,  251
Leppämäki, S.,  178 Li, Z.,  159, 162
Lerew, D. R.,  268 Liao, D.,  564
Lerner, D., 3 Liberman, R. P.,  247, 444, 445
Lesage, A. D.,  444, 445 Liberzon, I.,  335
Lesher, E. L.,  159 Libet, J.,  498
Lesieur, H. R.,  414, 415, 419 Lichstein, K. L.,  564, 565, 566, 569, 570, 572, 574
Leskin, G. A.,  340 Lichtash, Y.,  133
Lesperance, F.,  154 Lichtenberg, P. A.,  160
Lestarevic, M.,  160 Lichtenstein, D. P.,  19
Lester, D.,  113 Lichtenstein, J.,  294
Lester, H.,  436 Lichtenstein, P.,  112
Lester, K. J.,  220 Lickiss, L.,  202
Letarte, H.,  302 Liddle, P. F.,  436
Lett, N. J.,  80 Lieb, R.,  244, 266, 267, 270
Leucht, S.,  452 Lieberman, J. A.,  437
Leung, A. W.,  252 Liebmann, M.,  279, 281
Levander, S.,  443 Liebowitz, M.,  251
Levene, K. S.,  88 Liebowitz, M. R.,  247, 251, 256, 294
Levenson, R. W.,  502 Lietti, L.,  244
Leventhal, E. A.,  153 Lieverse, R.,  437
Leventhal, H.,  153 Lijmer, J. G.,  37
Leventhal, N.,  154 Lilienfeld, S. O.,  73, 217, 337, 465
Leverich, G. S.,  180 Lilley, C. M.,  583
Levin, F. R.,  61 Lim, K. Y.,  278
Levin, K.,  343 Lim, R. F.,  499
Levin, M. J.,  160 Lim, S.,  193
Levine, J. G.,  612 Lima, L. A.,  445
Levine, S. B.,  520 Lima, M. S.,  268
Levine, S. Z.,  436 Limbers, C. A.,  594
Levinson, B.,  531 Limkittikul, K.,  587
Levinson, C. A.,  244, 251 Lin, C.,  504
Levitt, A.,  383 Lin, E.,  490
Levy, F., 47 Linardatos, E.,  136
Levy, R. L.,  595, 598 Lincoln, A. K.,  332
Levy, S. R. A.,  22 Lincoln, T. M.,  451
Lewander, T.,  446 Lindahl, K. M.,  501
Lewandowski, A. S.,  592 Lindblad, S.,  599
Lewczyk, C. M.,  108 Lindefors, N.,  268
Lewin, A. B.,  225–​226 Lindenboim, N.,  204
Lewin, M.,  276, 282 Lindsay, D. W.,  74
Lewinsohn, P.,  117 Lindsay, K. A.,  473
Lewinsohn, P. M.,  100, 101, 105, 107, 109, 110, 113, 116, 117, Lindsley, C. B.,  585
118, 132, 138, 154, 383, 543 Lindstrom, T. C.,  617
Lewis, B.,  220 Lindvall Dahlgren, C.,  542
Lewis, C. C.,  18, 19, 20, 24 Lindwall, R.,  228
Lewis, E. L.,  275, 279 Lineberger, M. D.,  566, 570
Lewis, G.,  158 Linehan, M. M.,  196, 197, 199, 202, 203, 204, 479
Lewis, J. E.,  612 Link, C.,  621
Lewis, L. J.,  531 Link, P.,  620
Lewis, M.,  564 Link, P. C.,  452
Lewis, R. W.,  518 Links, P. S.,  204, 464
Lewis, S. M.,  336 Linnerroth, P.,  321
Lewis-​D’Agostino, D.,  524 Linton, S. J.,  598, 608
682 author Index

Lints-​Martindale, A.,  621 Loken, E. K.,  244

Linz, M.,  295 Lolekha, R.,  587
Linzer, M.,  439 Lombardo, T. W.,  343
Lipman, R. S.,  545 Loney, B. R.,  73, 74, 76, 79, 88
Lipp, O. V.,  220 Loney, J.,  49, 50, 59
Lipsitz, J. D.,  243, 256 Long, J. D.,  440
Lipsky, J.,  526 Longabaugh, R.,  393, 397, 401
Lipton, M.,  333 Longoria, N.,  501
Lish, J. D.,  174 Lonigan, C. J.,  218, 223
Liss, A.,  244 Lonnqvis, J.,  174, 175
Lissek, S.,  133 Lonsdorf, T. B.,  268
Lister, M. T.,  587, 598 Lopez, A. D.,  435
Litt, M.,  397 Lopez, M., 59
Litten, R. Z.,  385 Lopez, N.,  225
Little, T. D.,  72, 73 López-​Antón, R.,  157
Littlefield, A. K.,  206, 382, 387 Lopez-​Ibor, I.,  180
Littman, A. B.,  273 Lopez-​Pousa, S.,  153–​154
Littman-​Sharp, N.,  421 López-​Solà, C.,  267
Littner, M.,  566 LoPiccolo, C.,  174
Litz, B. T.,  334, 338, 340, 341, 343 Lorah, K. S.,  58
Liu, E.,  421 Loranger, A. W.,  466, 467, 469, 474
Liu, F., 24 Lorber, M. F.,  10
Liu, H., 21 Lord, C.,  13n1
Liu, P.,  341 Lord, C. C.,  502
Liu, S.,  252 Lord, M. J.,  530
Liu, X.,  552 Lorr, M.,  613
Liu, Y., 40 Losardo, D.,  324, 325
Liu, Z.,  162 Lo Sauro, C.,  544
Livesley, J.,  479 Losilla, J. M.,  108
Livesley, W. J.,  475, 476, 479 Lotan, G.,  280
Ljungman, G.,  598 Lou, Y.,  504
Llera, S. J.,  133 Loughran, M.,  598
Llerena, K.,  436 Loureiro, S. R.,  243, 247, 250
Lloyd, D.,  334 Lovibond, P. F.,  142, 143
Lloyd, E. E.,  202 Lovibond, S. H.,  142, 143
Lloyd, H.,  439 Lovisi, G. M.,  445
Lloyd-​Richardson, E.,  202 Low, L.-​F.,  159
Lo, S. K.,  594 Lowe, B.,  498
Loader, P.,  545 Löwe, B.,  272
Lobbrecht, J.,  334 Lowe, J. R.,  471
Lobo, A.,  157 Lowe, N. K.,  588, 612
Lochman, J. E.,  54, 76 Lowe, P. A.,  224
Lock, J.,  544, 545, 546, 554 Lozano, R.,  193
Lock, J. E.,  545 Lozano-​Blanco, C.,  547
Locke, B. Z.,  174, 448 Lozano-​Gattego, M.,  153–​154
Lockwood, P. L.,  76 Lu, F.,  60, 439
Lodnert, G.,  522 Lu, R.-​B.,  178
Loeb, K. L.,  544, 549, 552, 554 Luangxay, K.,  587
Loeber, R.,  48, 49, 72, 73, 74, 83, 176, 177 Lubman, D. I.,  383
Lof, E.,  385 Luborsky, L.,  41, 144, 367, vii
Loftus, L.,  444 Luby, J.,  101, 102, 108–​109, 111, 113, 117
Löfving, S.,  436 Luby, J. L.,  100, 101, 107, 108, 109, 111, 117
Logan, D.,  595–​596 Lucas, A.,  593
Logan, D. E.,  592, 593, 595 Lucas, C.,  19, 79, 87, 102, 108–​109, 222
Loge, J. H.,  611 Lucas, C. P.,  52, 79, 83, 113
LoGerfo, J.,  159, 163 Lucas, G. M.,  34
Logue, E.,  136 Lucas, S.,  12, 24, 42, 142
Lohr, J. M.,  251 Lucko, A.,  160
Lohr, K. N.,  544 Luckoor, R.,  448
Loisequx-​Meunier, M. N.,  385 Lucksted, A.,  451
 author Index 683

Luczak, S.,  402 Maciosek, M. V.,  384

Ludewig, D.,  174 Mack, J. L.,  161, 162
Lue, T. F.,  527 Mack, K. P.,  330
Luepke, L.,  159 Mackay, P. W.,  339
Luffy, R.,  586, 588 Mackey, S. C.,  599
Lugo-​Candelas, C. I.,  47 MacKillop, J.,  395, 415, 479
Lukasiewicz, M.,  182 Mackin, P., 33
Luke, B.,  583 MacKinnon, A.,  158
Lukens, E.,  114–​115 MacKinnon, A. J.,  153, 199
Lukoff, D.,  440 MacKinnon, D. F.,  176
Lum, O.,  158, 159 Mackinnon, S. P.,  421
Lumley, M. A.,  608 MacLeod, A. M.,  134
Lumpkin, P. W.,  222, 233 MacLeod, F. K.,  618
Lundberg, M. K.,  618 MacLeod, J.,  229
Lunde, M.,  161, 165 MacNevin, R. C.,  584, 585
Lungu, A.,  204 MacPhillamy, D. J.,  138
Lunnen, K. M.,  35 Maczuga, S., 50
Lunney, C.,  337 Madan-​Swain, A.,  592
Luo, J.,  545, 553 Madden, P. A.,  394
Luria, M.,  517, 528 Madi, D.,  593
Lushene, R.,  338, 340, 346 Madison, H.,  363
Lusky, J. A.,  115 Maercker, A.,  330
Luterek, J. A.,  298 Magalhaes, P. V.,  243
Lutz, J.,  275 Magaro, P. A.,  182
Lutz, J. G.,  58 Magee, E. A.,  18
Lutz, W.,  22, 24 Magee, J. C.,  573
Luxton, D. D.,  199 Magee, W. J.,  243
Lydersen, S.,  611 Maggs, J. L.,  361
Lygren, H.,  614 Magnus, B., 40
Lyketsos, G.,  165 Magnussen, L. H.,  614
Lynam, D. R.,  466, 470, 471, 472, 473–​474, 475, 476, 477, 478 Magnusson, A.,  180
Lynch, A. D.,  19, 33, 34 Magruder, K.,  339
Lynch, A. M.,  593 Magruder, K. M.,  347
Lynch, F.,  117 Maguen, S.,  344, 566
Lynch, K. G.,  394 Magura, S.,  449
Lynch, M. E.,  585 Mah, A. C.,  20, 22
Lynch, S. P.,  574 Mah, K.,  527
Lynch-​Jordan, A.,  596 Mah, K. B.,  571
Lynch-​Jordan, A. M.,  592, 593, 598 Mahar, D.,  571
Lyne, A., 60 Mahay, J.,  515
Lyneham, H. J.,  222 Mahdi, S.,  56, 62
Lynn, L. L.,  35 Mahon, K.,  178
Lynskey, M. T.,  74 Mahoney, A. E. J.,  302
Lyon, A. R.,  18, 19, 20, 21, 23, 24 Maich, K. H.,  569, 570
Lyubomirsky, S.,  133 Maidenberg, E.,  269, 278
Maier, S. F.,  269
Ma, H.,  133, 139, 140 Maier, W.,  156, 295
Ma, T.,  612 Maihoefer, C.,  397
Maalouf, F. T.,  101, 102, 113 Main, C. J.,  619
Maas, J. W.,  175 Maislin, G.,  161
MacCabe, J. H.,  436 Maisto, S. A.,  383, 394, 438, 448, 449, 546–​547
MacCauley, C.,  437 Maixner, S. M.,  162
MacDonald, A. J.,  584, 585 Majdandžić, M.,  250
Macdonald, J., 22 Makarchuk, K.,  413, 421, 422, 423, 427
MacDonald, K.,  220 Makris G. S.,  252
MacDowall, W.,  517 Malamuth, N. M.,  501, 501
Mach, C.,  442 Malas, K. L.,  337
Machado, P. P.,  542 Malgady, R.,  439
Machado, S.,  270 Malik, N. M.,  501
Machan, J. T.,  273 Malleson, P. N.,  598
684 author Index

Mallett, J.,  156 Marchand, A.,  301

Mallin, R.,  384 Marchione, K.,  282
Mallinger, A. G.,  180 Marchione, N.,  282
Mallon, J. C.,  177 Marcopulos, B. A.,  160
Mallory, L. J.,  564 Marcus, B. H.,  394
Mallory, R., 59 Marcus, C. L.,  566
Malloy, P. F.,  337 Marcus, D. K.,  49
Malmberg, B.,  154 Marcus, M. D.,  551, 553
Malone, J.,  500 Marder, S. M.,  442
Malone, T.,  386 Marder, S. R.,  5, 435, 444
Mammel, K. A.,  542 Marenco, S.,  437
Mammen, O.,  275 Margari, F., 56
Manber, R.,  567, 576 Margari, L., 56
Mance, R. M.,  442 Margola, D.,  504
Mancill, R. B.,  267 Margolin, G.,  499–​500
Mancini, C.,  254, 257 Margolis, R. L.,  452
Mancuso, S.,  542 Margraf, J.,  20, 39, 274, 279, 282, 387
Mancuso, S. G.,  549 Margulies, D. M.,  102
Mandalia, S.,  522, 531 Mari, E.,  426
Mandell, D. S.,  12, 24, 42, 142 Maric, M.,  232
Manders, W. A.,  84 Marin, C. E.,  220, 231
Mandrusiak, M.,  195 Marin, N. W.,  279
Maneeton, B., 59 Marinkovic, J.,  160
Maneeton, N., 59 Marinos, V.,  180
Manfredi, A., 59 Marion, M. S.,  202
Manfro, G. G.,  268 Mark, K. P.,  524
Mangine, S.,  466, 469 Markiewicz, J. M.,  23–​24
Mangrum, L. F.,  491, 498 Markman, H. J.,  499, 501
Mani, M. M.,  593 Markon, K.,  476
Manicavasagar, V.,  180 Markon, K. E.,  11, 473, 476, 478
Manley, C.,  392 Markon, K. F.,  466, 470, 476
Mann, C.,  269, 279 Markovic, N.,  393
Mann, J. J.,  113, 198, 278, 332 Marks, D. J.,  62
Mann, K.,  385 Marks, I. M.,  274, 276, 277, 282
Mann, R. E.,  394 Markvart, V.,  160
Manne, S. L.,  341 Marlatt, G. A.,  359, 361
Mannelli, P.,  473 Marlowe, J. H.,  86
Mannucci, E.,  544 Marmar, C.,  339
Mannuzza, S.,  116, 243, 244, 256 Marmar, C. R.,  331, 334, 337, 344
Mann-​Wrobel, M. C.,  347 Marmarosh, C.,  547
Manohar, U.,  499 Marnane, C.,  331
Manos, M. J.,  59 Marques, L.,  345
Manseau, M.,  473 Marriott, M., 22
Mansfield, A.,  272 Marrocco, F. A.,  196
Mansley, C.,  413 Marrs-​Garcia, A.,  9
Mansor, M.,  491 Mars, B.,  107
Mantar, A.,  275 Marsden, J.,  366, 371
Mantere, O.,  178 Marsee, M. A.,  72, 73, 76, 84
Manworren, R.,  621 Marsh, G. R.,  566, 570
Manzato, E.,  542 Marsh, L.,  161
Mao, L.,  198 Marshall, A.,  333
Maples, J.,  415 Marshall, E. J.,  389
Maples, M. R.,  203 Marshall, J. R.,  393
Maples, S.,  479 Marshall, M.,  436
Maradeix, B.,  385 Marshall, M. B.,  160, 164
Maravilla, K. R.,  528 Marshall, R.,  331
Marc, L. G.,  159 Marshall, S. A.,  48
Marceau, L. D.,  621 Martel, M. M.,  48, 49, 50
March, J.,  115, 117, 223 Martell, C.,  117
March, J. S.,  117, 217, 222, 223, 224 Martell, C., Jr.,  132
 author Index 685

Martell, C. R.,  132, 133 Mattia, J. I.,  174, 273, 296

Martell, R.,  425 Mattick, R. P.,  247, 251
Marten, P.,  139, 252 Mattis, S. G.,  225
Martens, A.,  472 Mattson, M. E.,  397, 401
Martens, M. P.,  384, 401 Mattson, S. N.,  56
Martens, P. J.,  417 Matuschek, T.,  17, 22
Marti, M.,  374 Matyas, J. R.,  521
Martin, A. L.,  596 Matzner, F.,  272
Martin, C. S.,  381, 395, 402 Maughan, B.,  73, 100, 101
Martin, G.,  199, 370 Maurice, W. L.,  520
Martin, G. E.,  195 Mavandadi, S.,  383
Martin, L.,  501 Mavissakalian, M.,  277, 278
Martin, L. Y.,  244 Maxwell, S. E.,  109
Martin, M.,  528, 530 May, A. M.,  202, 203, 206
Martin, N.,  268 May, J.,  395
Martin, N. C.,  107, 110 May, K.,  530
Martin, N. G.,  268, 394 May, R. K.,  415, 422, 426
Martin, R. A.,  365, 369, 370, 371, 372, 373 May, R. S.,  198
Martin, R. R.,  203 Mayer, L. S.,  165
Martínez, A.,  524 Mayes, T. L.,  102, 109, 112, 113, 115
Martinez, E.,  549 Maynard, C.,  341
Martinez, J.,  268 Mayrand, M. H.,  530
Martinez, J. A.,  382 Mayzner-​Zawadzka, E.,  392
Martinez, J. M.,  269 Mazelis, R.,  343
Marting, L. N.,  614 Mazer, N. A.,  521
Martino, S.,  384 Maziade, M.,  436
Martire, L. M.,  154 Mazure, C.,  314, 322
Martoni, M.,  569–​570 Mazure, C. M.,  554
Marttunen, M.,  198, 200 Mazza, J.,  113
Maruish, M.,  504, 507 Mazza, J. J.,  200
Marx, B. P.,  331, 333, 334, 335, 336, 337, 340, 341, 343, 347 McAlister, B., 19
Marx, R. G.,  614 McAllister, T.,  183
Mascagni, T.,  595 McArthur, D.,  200
Maser, J.,  184, 342 McBride, D.,  445
Maser, J. D.,  175, 176, 295 McBurnett, K.,  51, 84
Mash, E. J.,  3, 4, 21, 24, 32, 50, 54, 226, 502, vii McCabe, K., 86
Masheb, R. M.,  547, 548, 554 McCabe, K. M.,  33
Masi, G., 59 McCabe, M. P.,  162
Maslow, C.,  113 McCabe, R.,  444
Mason, T.,  551, 552 McCabe, R. E.,  244, 245, 250, 251, 252, 253, 255, 256, 273,
Massat, I.,  268 545, 575
Massetti, G. M.,  52, 53, 54, 55, 56, 60, 63–​64 McCaffery, K. J.,  11
Massion, A. O.,  294 McCaffery, M.,  621
Masson, C. L.,  365 McCallum, R. C.,  612
Mastanduno, M. P.,  599 McCarney, S. B.,  52
Mastrocinque, C., 38 McCarron, J.,  447
Matalí, J. L.,  179 McCarthy, K. S.,  277
Matarazzo, B. B.,  194 McCarthy, W. J.,  361
Matarazzo, J. D.,  438 McCarty, C. A.,  63, 109
Matera, E., 56 McCarty, D.,  397
Matheiken, S. T.,  448 McCaslin, S. E.,  344, 566
Mathews, A.,  479 McCauley, C.,  251
Mathews, A. M.,  274, 276, 277 McCauley, E.,  117, 595
Mathur, S. R., Jr.,  24 McCauley Ohannessian, C. M.,  394
Maticka-​Tyndale, E.,  440 Mcclearn, G. E.,  154
Matt, G. E.,  545, 553 McClelland, S. I.,  524
Matt, L. M.,  139–​140 McClure, K. S.,  138, 142
Matters, M. D.,  442 McCluskey, D. L.,  479
Matthey, S.,  105 McCombes, S.,  20, 22
Matthias, A.,  338 McConaghy, N.,  520
686 author Index

McConaha, C.,  554 McGuffin, P.,  110, 437

McConaughy, S. H.,  49, 55, 57, 81, 87, 88, 104 McGuire, A. B.,  446
McConnaughy, E. A.,  394 McGuire, B. E.,  613
McCord, J., 85 McGurk, D.,  332
McCormack, J.,  437 McGurk, S. R.,  436, 444
McCormick, J. C.,  588 McGwin, G. L.,  592
McCormick, R. A.,  413 McHale, J. P.,  80
McCoy, K.,  501 McHorney, C. A.,  528
McCoy, K. J. M.,  200 McHugh, P. R.,  163
McCoy, M. G.,  74 McHugh, R. K.,  204
McCoy, N. L.,  521 McHugo, G.,  343
McCracken, J.,  222, 230 McHugo, G. J.,  440, 448, 449, 451
McCracken, J. T.,  226 McInerney, M.,  586
McCracken, L. M.,  583, 596, 599, 618 McInnes, A.,  426
McCrady, B. S.,  392, 394–​395 McInnis, M. G.,  176, 180
McCrae, R. R.,  468, 469, 477 McIntosh, J. A.,  586
McCraw, K. S.,  250 McKay, D.,  318, 324
McCraw, S.,  178 McKay, J. R.,  373, 392, 394, 397
McCreadie, R.,  437 McKee, D. R.,  203
McCready, J.,  414, 417 McKendrick, M. W.,  574
McCrone, P.,  444 McKenzie, K.,  437
McCrory, E. J.,  76 McKiernan, P.,  370
McCue, R. L.,  595 McKillop, J. M.,  616
McCullough, J. J. P.,  133 McKinnon, A., 4
McCullough, S.,  522, 531 McLaren, S.,  202
McDade, M.,  197 McLaughlin, K. D.,  360
McDavid, J. D.,  471 McLean, C. P.,  256, 338, 340
McDermott, P. A.,  373 McLean, D. B.,  522
McDermut, W.,  465, 466 McLean, P. D.,  251
McDermut, W. H.,  181 McLellan, A. T.,  367, 392, 419, 424, 448
McDevitt-​Murphy, M.,  339 McLeod, B. D.,  4, 17, 24
McDonald, N.,  220 McLeod, D. R.,  256
McDonald, S. D.,  251, 341 McMahon, C. G.,  516, 518
McDonald-​Scott, P.,  175, 176 McMahon, F. J.,  176
McDonell, M. B.,  386 McMahon, R. J.,  58, 60, 71, 72, 74, 76, 78, 79, 80, 82, 84, 85,
McDougle, C. J.,  220 86, 87–​88
McElroy, S. L.,  180 McMahon, R. P.,  442
McEvoy, P. M.,  302 McMain, S. F.,  204
McFadden, A.,  572 McMakin, D. L.,  109, 110, 118
McFall, M.,  332, 341 McMann, M. R.,  21, 53
McFall, M. E.,  337, 339 McManus, F.,  142
McFarlane, B.,  445 McManus, S.,  517
McGarvey, E. L.,  525 McManus, T.,  199
McGee, R.,  100 McMurray, J.,  136
McGinn, L. K.,  480 McMurtry, C. M.,  584, 585, 591, 599
McGinn, M. M.,  491 McNair, D. M.,  613
McGinty, E. E.,  438 McNally, R. J.,  251–​252, 274, 275, 280
McGlashan, T. H.,  243, 272, 436, 466, 470 McNamara, G.,  361
McGlinchey, J. B.,  40, 305 McNamara, N. K.,  177, 182
McGonagle, K. A.,  295 McNamee, R.,  437
McGorry, P. D.,  177 McNaughton, N.,  133
McGough, J. J.,  61 McNeil, B. J.,  182
McGovern, A. R.,  134 McNeil, C. B.,  86
McGrath, A. M.,  52 McNeil, D. W.,  275, 281
McGrath, D. S.,  421 McNeil, T. F.,  437
McGrath, J.,  437 McNiel, D. E.,  280, 281
McGrath, P.,  588, 592 McNulty, P.,  530
McGrath, P. B.,  252, 268 McQuaid, J.,  267
McGrath, P. J.,  59, 583, 584, 585, 586, 592, 593, 596 McRee, B.,  362, 384
McGrath, R. E.,  11 McShall, J. R.,  490
 author Index 687

McTaggart, S.,  107 Mérette, C.,  436, 564, 573

Meader, N.,  159 Merikangas, K. R.,  100, 105, 131, 132, 180, 218, 223, 243, 267,
Meadows, E. A.,  138, 142 272–​273, 294, 313
Meagher, M. W.,  153, 159 Merkel, S.,  621
Meana, M.,  518, 529 Merkitch, K. G.,  178
Means, M. K.,  566, 570, 574 Merkouris, S.,  425
Means-​Christensen, A. J.,  504 Merrill, J. E.,  369
Measelle, J. R.,  111, 113 Merskey, H.,  583, 585, 608
Mechanic, D.,  450 Mertens, G.,  595
Mechanic, M. B.,  340 Merwin, M. M.,  467, 470
Medeiros-​Ferreira, L.,  444 Mesholam, R. I.,  160
Medina-​Mora, M. E.,  11 Messer, J., 73
Medoff, D. R.,  417, 452 Messer, S. C.,  108, 109, 110
Medrano, G. R.,  594, 595 Messick, S., 11
Meehan, K. G.,  544 Meston, C.,  521
Meehan, T.,  20, 22 Meston, C. M.,  521, 524, 528
Meehl, P. E.,  35, 206, 470 Metz, M. E.,  531
Meek, P. M.,  574 Metzger, D.,  367, 373, 419, 424, 448
Meeker, K.,  159, 163 Metzger, L. J.,  335
Meeks, T. W.,  153 Metzger, R. L.,  299, 304
Mee-​Lee, D.,  391, 392 Metzler, C. W.,  86
Meenan, R. T.,  518 Metzler, T.,  344
Mega, M.,  162 Metzler, T. J.,  566
Mehl, S.,  451 Meuleman, E. J. H.,  527
Meier, E.,  422 Meuret, A. E.,  268, 275
Meier, M. H.,  436 Meyer, A.,  244
Meijer, J.,  268 Meyer, A. H.,  281
Melamed, B. G.,  249 Meyer, D. A.,  181, 182
Melartin, T. K.,  199 Meyer, E. C.,  344
Meldrum, M.,  599 Meyer, G. J.,  11, 119
Melendez, G., 35 Meyer, I.,  490
Melhem, N. A.,  110 Meyer, P.-​A.,  587
Melin, L.,  446 Meyer, R. E.,  198
Melisaratos, N.,  523 Meyer, T. D.,  178
Melle, I.,  436 Meyer, T. J.,  299, 304
Mellenbergh, G. J.,  249 Meyers, A. W.,  421, 422, 426
Meller, S.,  479 Meyers, B. S.,  153, 154
Melli, G.,  275 Meyers, D. C.,  22
Mellor, D.,  162 Mezuk, B.,  436
Mellor-​Clark, J.,  22 Mezzani, B.,  544
Melnick, S., 80 Michael, R., 76
Meltzer, H.,  73, 100, 108, 193 Michaelis, S.,  243
Melzack, R.,  529, 583, 589, 608, 612–​613, 621 Michaels, S. M.,  110
Méndez, S.,  374 Michalak, E. E.,  180, 183
Mendlowicz, M.,  178 Michalakeas, A.,  180
Mendlowicz, M. V.,  257 Michalec, E.,  369, 370
Mendlowitz, D. R.,  570 Michalec, E. M.,  369
Mendonca, J. D.,  203 Michel, B. D.,  196, 197, 200, 202
Mendoza, T. R.,  612 Michelson, L.,  277, 278
Menezes, A.,  614 Michelson, L. K.,  282
Mennin, D. S.,  132, 133, 134, 139, 296, 298 Michopoulos, V.,  336
Menon, V.,  134 Mickley, D.,  545, 553
Mensinger, J. L.,  394 Midanik, L.,  393
Menzies, R. G.,  219, 244, 320 Midanik, L. T.,  393
Mercer, C. H.,  516, 517 Middleton, H.,  279
Mercer-​McFadden, C.,  449, 451 Miele, G.,  388
Merchán-​Naranjo, J.,  176 Miele, G. M.,  364, 367, 388
Mercier, C.,  445 Migdal, M.,  587, 588, 598
Mercier, E.,  267 Miguez, M.,  178
Merckelbach, H.,  223, 249, 251 Mihelish, G. L.,  452
688 author Index

Mihura, J. L.,  18–​19 Ming, E. E.,  542

Mikail, S.,  3, xi Miniati, M.,  178
Mikail, S. F.,  23, 615 Minichiello, M.,  162
Miklowitz, D. J.,  179, 180, 181 Minsky, S.,  448
Milanak, M. E.,  331 Mintken, P. E.,  619
Miles, S. R.,  387 Mintz, J.,  247, 442, 444
Miles-​McLean, H.,  417 Miranda, J.,  118
Milhausen, R. R.,  528 Mirch, M. C.,  547
Milich, R., 59 Miró, J.,  24, 585, 587, 588, 592, 595
Miller, A. L.,  200 Miron, L. R.,  334
Miller, B. A.,  387 Mishra, A.,  522
Miller, B. J.,  439, 452 Misiuta, I. E.,  452
Miller, C. J.,  178 Mitchell, A. E.,  497, 498, 501
Miller, C. L.,  160, 164 Mitchell, A. J.,  159
Miller, E.,  230, 330 Mitchell, C. C.,  59
Miller, F. G.,  60 Mitchell, D. G. V.,  76
Miller, I. W.,  181, 199, 205, 206 Mitchell, J.,  280, 545, 551, 552
Miller, J. C.,  422, 593 Mitchell, J. E.,  542, 544, 545, 548, 549, 553
Miller, J. D.,  415, 464, 465, 466, 468, 470, 471, 472, 473–​474, Mitchell, K.,  571
475, 476, 477, 478, 479 Mitchell, K. J.,  62
Miller, J. Y.,  73 Mitchell, K. R.,  516
Miller, K. A.,  200 Mitchell, K. S.,  330, 337
Miller, K. B.,  544 Mitchell, M. A.,  198
Miller, K. K.,  517 Mitchell, P.,  153
Miller, L. L.,  50 Miville, M. L.,  3
Miller, L. M.,  339 Miyahara, S.,  181
Miller, L. S.,  72 Mizruchi, M. S.,  200
Miller, M.,  332 Mizuno, T.,  573
Miller, M. B.,  178 Mneimne, M.,  196
Miller, M. L.,  299, 304 Moak, D. H.,  395
Miller, M. W.,  330, 331, 335 Moberg, P. J.,  160
Miller, N. V.,  50 Modecki, K., 76
Miller, O. J.,  275 Modell, J. G.,  198
Miller, P. M.,  384 Moeci, P.,  177
Miller, P. P.,  267 Moerk, K. C.,  543
Miller, P. R.,  296 Moffitt, M., 24
Miller, R.,  437 Moffitt, T. E.,  61, 71, 75, 83, 84, 100, 116, 436
Miller, R. P.,  618 Mofidi, A.,  269
Miller, T. L.,  17, 113, 118 Mogg, K.,  220
Miller, W. R.,  369, 392, 393, 394, 396, 397, 398 Mojtabai, R., 19
Miller, W. S.,  368, 373 Mokros, H. B.,  109
Millner, A. J.,  194, 201, 205, 206 Moldavsky, M., 22
Millon, C.,  466, 467, 473 Molina, B. S.,  86
Millon, T.,  465, 466, 467, 473 Molina, S.,  294, 300
Mills, J. S.,  545, 554 Molinari, V. A.,  155
Mills, K.,  334 Molinaro, M.,  449
Milne, B. J.,  116 Mollard, E.,  276
Milner, K. K.,  199 Mollica, R. F.,  345
Milner, R.,  466, 468, 476 Monahan, J.,  38, 440
Milo, L.,  136 Monahan, K. C.,  74
Milone, A., 59 Monck, E. M.,  447
Milosevic, I.,  253 Mond, J. M.,  543, 555
Milrod, B. L.,  277 Mones, R. L.,  598
Milstein, I.,  203 Money, R.,  273, 280
Miltenberger, R.,  551, 552 Monga, T. N.,  618
Mimiaga, M. J.,  61 Monk, K.,  106, 107
Mindell, J. A.,  592 Monk, T.,  180
Mineka, S.,  219, 269, 270, 312 Monk, T. H.,  180, 573
Miner, M.,  516, 517 Monkul, E. S.,  273
Miner, M. M.,  518 Monon, J.,  586
 author Index 689

Monroe, S. M.,  115 Morrison, A.,  254

Monson, C. M.,  330, 335, 344 Morrison, L. L.,  202
Montapaneewat, T.,  586 Morrison, T. G.,  613
Monteiro, M. G.,  387, 498 Morriss, R.,  180
Montes, K. S.,  422 Morris-​Yates, A.,  294
Montgomery, C.,  587, 588 Morrow, C. E.,  204
Montgomery, M. A.,  370 Morse, R.,  594
Montgomery, R. P.,  397 Mortensen, P. B.,  437
Montgomery, S.,  161, 165 Morzorati, S. L.,  383
Montgomery, W.,  180 Moscou-​Jackson, G.,  573
Monti, P. M.,  365, 369, 370, 371, 373 Moscovitch, D.,  244, 253
Montorsi, F.,  527 Moscovitch, D. A.,  242, 243
Monz, B. U.,  515, 516, 517 Moses, E.,  269
Mooney, P.,  114 Mosovich, S.,  426
Moore, A.,  110, 117 Moss, H. B.,  385
Moore, B. A.,  364, 369, 373, 374 Moss, T. G.,  574
Moore, J.,  102 Moss-​Morris, R.,  613
Moore, K. A.,  178 Mostkoff, K.,  196
Moore, M. C.,  280 Motivala, S. J.,  160
Moore, M. T.,  133, 139, 140 Motlová, L.,  452
Moore, T. C.,  382 Motoca, L. M.,  227
Moos, B.,  546 Mott, M.,  361
Moos, R.,  546 Mott, T.,  443
Moos, R. H.,  359, 361 Mottram, P.,  160, 161, 165
Mora, C. A.,  343–​344 Moulin, D. E.,  609
Mora, P. A.,  153 Mours, J. M.,  19
Moran, P.,  437 Moussavi, S.,  137
Moran, S.,  417 Moye, A.,  546
Morano, S.,  521 Moye, A. W.,  546
Moras, K.,  271, 338 Moylan, A.,  277
Moreci, P.,  53, 107 Mrakotsky, C.,  100, 109
Moreira, E.,  517 Mrazek, P. J.,  506
Moreira, E. D.,  518 Mroczek, D.,  156
Morello, R.,  442 Muehlenkamp, J.,  422
Morency, L.-​P.,  34 Muehlenkamp, J. J.,  197, 199, 203
Moreno, C.,  176 Mueller, B.,  598
Morey, L. C.,  19, 466, 467, 470, 472, 473, 474, 475, 476, Mueller, C. W.,  22
479, 548 Mueller, J.,  163
Morgan, C. M.,  547 Mueller, M.,  294
Morgan, P. L.,  50 Mueller, T. I.,  154, 371
Morgan, S. T.,  199 Mueser, K. T.,  435, 436, 437, 440, 442, 443, 444, 445, 446,
Morgan, T. J.,  368, 373, 392 447, 448, 449, 451
Morgan, T. S.,  599 Muffler, J.,  361
Morgenstern, J.,  368, 373, 394–​395 Mufson, L.,  18, 23, 103
Morgenthaler, T.,  563, 573 Muhrer, E.,  112
Morin, C. M.,  563, 564, 565, 566, 567, 569, 570, 571, 572, 573, Muir, W.,  268
574, 575, 576 Muir-​Nash, J.,  574
Morin, M.,  530 Mulders, A.,  161
Morina, N.,  334, 339 Mullen, J. T.,  618
Morissette, S. B.,  281, 344 Muller, B.,  544
Morley, S.,  138–​139, 617 Muller, C.,  435
Morley-​Forster, P. K.,  609 Müller, H.,  156, 392
Morosini, P. L.,  178 Muller, S. L.,  552
Morphy, H.,  564 Mullican, C., 4
Morris, A. S.,  76, 84 Mullins-​Sweatt, S. N.,  11, 466, 474, 475, 477
Morris, D. D.,  182 Mulvey, E., 74
Morris, D. W.,  138–​139 Mulvey, E. P.,  466
Morris, M.,  530 Mumma, G. H.,  492, 495, 504
Morris, R. W.,  614 Munck, I. M.,  416
Morris, T. L.,  224, 229, 233 Munck, L. A.,  219
690 author Index

Mundayat, R.,  530 Nagin, D. S.,  72

Mundle, G.,  385 Nagy, L. M.,  336, 440
Mundt, J. C.,  198, 204 Nail, L. M.,  574
Muniz, R., 61 Najavits, L.,  144, 334
Munkes, J.,  385 Najavits, L. M.,  360
Muñoz, L. C.,  73, 74, 76, 84 Najmi, S.,  332
Muñoz, R. F.,  132, 138 Nakaji, P.,  396
Muñoz Centifanti, L. C.,  73, 76 Nakamura, B. J.,  22, 111
Munroe-​Blum, H.,  114 Nakano, Y.,  273
Muntaner, C.,  158 Nakayama, M.,  573
Muratori, F.,  118 Nakonezny, P. A.,  102, 138–​139
Muratori, P., 59 Napper, L. E.,  394
Muray, E.,  444 Nappi, R. E.,  521, 528
Muris, P.,  219, 223, 224, 249 Naragon-​Gainey, K.,  133, 179
Murphy, C. M.,  504 Naranjo, C. A.,  389
Murphy, J. G.,  402 Nardi, A. E.,  270
Murphy, J. M.,  114 Narrow, W. E.,  468, 491
Murphy, K. R.,  58, 61 Nasrallah, H. A.,  436, 442
Murphy, M.,  117 Natale, V.,  569–​570
Murphy, M. T.,  282 Nath, S. R.,  9
Murphy, S.,  103, 415 Nathan, J. S.,  33
Murphy, T. K.,  225–​226 Nathan, P. E.,  vii, xi
Murray, A. M.,  204 Natvig, G. K.,  617
Murray, C.,  49, 50 Naugle, A.,  321
Murray, C. J.,  193 Navarro, J. B.,  108
Murray, C. J. L.,  435 Navarro-​Haro, M.,  281
Murray, D. W.,  59, 60 Navarro-​Pastor, J. B.,  444
Murray, G.,  180, 183 Neacsiu, A. D.,  204
Murray, J.,  498 Neal, A. M.,  229
Murray, R.,  437 Neal, C. D.,  156
Murray, R. M.,  437 Neale, M. C.,  267, 294, 383
Murray, S. B.,  543 Neas, B.,  53, 56
Murray-​Gregory, A.,  197, 204 Neckelmann, D.,  564
Murray-​Gregory, A. M.,  204 Nedeljkovic, S. S.,  612
Murru, A.,  178 Nee, J.,  545
Musa, M.,  120, 141 Neer, S. M.,  223
Musser, E.,  363 Negy, C.,  504, 507
Musser, E. D.,  48 Neigh, G. N.,  154
Mustafa, H.,  499 Neighbors, C.,  383
Mustelin, L.,  542 Neighbors, C. J.,  365, 372, 394–​395
Mustillo, S.,  218 Neish N.,  617
Muthén, B. O.,  153 Nelles, W. B.,  220
Muti, P.,  393 Nellis, T.,  571
Myers, C. D.,  617 Nelson, A. L.,  250
Myers, F. S.,  180 Nelson, C. A.,  318, 319
Myers, J.,  112, 383 Nelson, C. B.,  295
Myers, J. K.,  158 Nelson, C. M.,  24
Myers, K.,  63, 106, 109, 110, 112, 117 Nelson, E. C.,  599
Myers, K. M.,  113, 114, 118 Nelson, J. R.,  24
Myers, M.,  361 Nelson, K. G.,  397
Myers, M. G.,  369, 370, 371, 373 Nelson, M. M.,  79, 80
Mykletun, A.,  522, 564 Nelson, R. O.,  119–​120, 226, 506
Nelson, S. E.,  382
Nácar, D.,  249 Nelson-​Gray, R. O.,  120, 230
Nachtigall, L.,  528 Nematollahi, S.,  389
Nadeem, E.,  22, 24 Nemeth, C. L.,  154
Nadorff, M.,  203 Nemoto, N.,  443
Nagamoto, H. T.,  194 Neradilek, M. B.,  162
Nagata, T.,  554 Neria, Y.,  332
Naghavi, M.,  193 Nesci, J. B.,  549
 author Index 691

Nesheim, L.,  382 Nishith, P.,  449

Ness, R.,  364 Nishiyama, T.,  573
Netemeyer, R.,  552 Nissen, C.,  564, 571
Neufeld, E.,  203 Niv, N.,  442, 445
Neumann, C. S.,  182 Nixon, R. D. V.,  86, 334
Neuner, B.,  392 Nochajski, T. H.,  393
Neville, K.,  588 Nock, M.,  204
Newby, J. M.,  4 Nock, M. K.,  37, 80, 87, 193, 194, 195, 196, 197, 200, 201, 202,
Newcomb, K.,  80, 86 203, 204, 205, 206, 332
Newcombe, P. A.,  281 Nocon, A.,  266, 267, 270
Newcorn, J. H.,  59, 60 Noda, Y.,  273
Newcorn, J. M. D.,  200 Noe, S. L.,  574
Newhill, C. E.,  449, 452 Noel, M.,  585, 591, 595, 596, 598
Newhouse, P. A.,  162, 165 Noestlinger, C.,  522, 531
Newman, C. J.,  587 Nolan, E. E.,  59
Newman, E.,  341 Nolen, W. A.,  131, 178
Newman, J. P.,  158 Nolen-​Hoeksema, S.,  133
Newman, M. G.,  133, 277, 298 Noordsy, D. L.,  448, 449, 451
Newth, S.,  319 Noortman, D.,  269
Newton, J. R.,  549 Norcross, J. C.,  3, 21, 32, 53, 144, 394, 420, vii, xii
Newton, M.,  619 Nordahl, H. M.,  394
Newton, P. E.,  10 Nordbrock, E., 59
Newton, R.,  542 Nordstokke, D. W.,  224
Neylan, T. C.,  344, 566 Norell-​Clarke, A.,  570
Neyman, I.,  160 Noriega-​Dimitri, R.,  276, 282
Nezu, A. M.,  138, 142 Norman, G. R.,  5
Nezworski, M. T.,  465, 471 Norman, K.,  220
Ng, M.,  102 Norman, W. H.,  199
Ng, M. Y.,  4, 5, 7, 40, 41, 143, 145 Normand, S. L.,  442
Nguyen, D.,  518 Norrholm, S. D.,  336
Nguyen, H. T.,  153 Norris, F.,  343
Nguyen, L.,  442 Norris, M. P.,  153, 155, 159
Nguyen, Q.,  618 North, C. S.,  364
Nguyen, T. A.,  132 Northey, W. F.,  498
Niaura, R. S.,  395 Norton, M. A.,  302
Nicasio, A.,  439 Norton, P. J.,  243, 252, 274, 396
Nicasio, A. V.,  439 Notarius, C. I.,  501
Nicassio, P. M.,  570 Nothen, M.,  268
Nicholl, J. P.,  574 Novák, T.,  452
Nicholls, T. L.,  437 Novick, D.,  180, 449
Nicholson, J. M.,  52 Novy, D. M.,  276, 277–​278
Nickerson, A.,  142 Novy, P. L.,  364, 368, 373
Nicolaou, D. C.,  280 Nowakowski, M.,  252
Nicolosi, A.,  517 Nowlan, K. M.,  490
Nielsen, R.,  443 Nowlin, C.,  114
Nielsen, S. L.,  20, 143, 144, 145, 202 Nuechterlein, K. H.,  5, 436, 437, 440
Nielson, W. R.,  615, 616, 617, 618, 620 Nunnally, J. C.,  10
Nieuwsma, J. A.,  347 Nurko, S.,  594
Nievergelt, C. M.,  332 Nurmikko, T. J.,  612
Nigg, J., 48 Nurnberger, J. I.,  116, 388
Nigg, J. T.,  48, 49, 50, 80 Nusslock, R.,  177
Nightingale-​Teresi, J.,  102 Nyutu, P. N.,  203
Nikolas, M.,  49, 50
Niles, B. L.,  341 Oades, L. G.,  444
Niles, J. K.,  332 Oakman, J.,  257
Nilsen, T. S.,  112 Obasi, E. M.,  202
Nilsson-​Ihrfelt, E.,  281 Oberlander, T. F.,  584
Nimgaonkar, V. L.,  448 Oberth, C., 74
Nishida, N.,  268 Obiols, J. E.,  444
Nishimura, Y.,  268 O’Boyle, M.,  471
692 author Index

O’Brien, B. S.,  74, 84 Olivardia, R.,  543

O’Brien, C. P.,  367, 373, 381, 392 Oliver, D.,  436
O’Brien, G.,  271 Ollendick, T.,  24, 36, 222, 233, 249, 252
O’Brien, G. T.,  338 Ollendick, T. H.,  217, 218, 219, 220, 222, 223, 224, 225, 226,
O’Brien, W. H.,  139, 142, 492, 494 227, 228, 229, 231, 232, 233, 243, vii
O’Carroll, P. W.,  193 Olmsted, M.,  545, 550, 552, 554
Ochoa, S.,  449 Olmsted, M. P.,  545
Ocio, S.,  178 Olsen, M. K.,  565, 566
O’Connell, B.,  478 Olson, A. K.,  504
O’Connell, M.,  446 Olson, D.,  504
O’Conner, D.,  162 Olson, D. H.,  504, 545–​546
O’Connor, A. B.,  614 Olson, R. K.,  50
O’Connor, D. W.,  156, 159 Olsson, G.,  108
O’Connor, E. A.,  155 Oltmanns, T. F.,  465, 466, 471, 472, 473–​474, 475, 476, 477, 478
O’Connor, J.,  418 Omer, H.,  231
O’Connor, M.,  546 O’Neal, E.,  448
O’Connor, R. C.,  332 Onega, L. L.,  162
O’Connor, R. M.,  421 O’Neill, S., 47
O’Connor, S.,  383 Ong, C. J.,  565
Odgers, C. L.,  71, 75 Ong, J. C.,  567, 573
O’Doherty, J. P.,  133 Ong, M.-​L.,  12, 21, 40, 41
O’Donnell, P., 19 Onishi, J.,  159
O’Donohue, W.,  249 Onnela, J.-​P.,  206
O’Donovan, M. C.,  268 Onur, E.,  273
Oei, T. P.,  277, 281, 397, 575 Onwuameze, O. E.,  153
Ofek, H.,  200 Ooi, Y. P.,  55
Offenbächer, M.,  593 Oostendorp, R. A. B.,  618, 619
Offord, D. R.,  108, 490 Opjordsmoen, S.,  180
Offord, K. P.,  466, 467, 473 Opler, L. A.,  440
Ogland-​Hand, S.,  152, 159, 163 Opperman, E. A.,  528
Ogles, B. M.,  19, 20, 35, 40, 145, 281, 282 Oppo, A.,  178
Ogliari, A.,  244, 250 Oquendo, M.,  194
O’Hara, M. W.,  86, 179 Oquendo, M. A.,  113, 194, 195, 197, 204, 332, 473
Ohayon, M. M.,  564 Orazem, R. J.,  340
Ohlsson, H.,  436 Orbach, I.,  203
Öhman, A.,  268 Orcutt, H. K.,  334
Ohrmann, P.,  268 Oremus, M.,  162, 165
Oishi, S.,  499 Orengo, C. A.,  155
Ojserkis, R. A.,  133 Origoni, A.,  436
Okamura, K. H.,  22 Origoni, A. E.,  445
Okazaki, S.,  473 O’Riley, A. A.,  157
O’Keefe Rosetti, M. C.,  518 Orjada, K.,  549
Okifuji, A.,  616 Ornstein, R. M.,  542
Okkels, N.,  437 Orr, S. P.,  335, 337, 340
Okuda, M.,  312, 473 Orsillo, S.,  139
Olaleye, D. O.,  612 Orsillo, S. M.,  139, 250, 255, 281
Olatunji, B.,  324, 325 Osborn, D.,  437
Olatunji, B. O.,  133, 242, 250, 251, 312 Osborn, D. P. J.,  437
Oldani, L.,  244 Osher, F. C.,  437, 449, 451
Oldehinkel, A. J.,  542 Osler, M.,  516, 517, 518
Oldham, J. M.,  466, 468, 471, 475, 476 Oslin, D.,  383
O’Leary, K. D.,  493, 500, 502, 506 Oslin, D. W.,  154
O’Leary, M.,  522, 526 Osma, J.,  281
O’Leary, M. P.,  522 Osman, A.,  110, 199, 200, 202, 203, 250, 618
Oleka, N.,  612 Osman, J.,  202
Olfson, M.,  120, 176, 253, 450 Osman, J. R.,  202, 203, 250, 618
Olié, E.,  196 Osório, F. L.,  250
Olin, S.,  18, 22, 23 Öst, L. G.,  222, 228, 243, 249, 256, 276, 281
Olin, S. S.,  22, 24 Ostacher, M. J.,  199
Olino, T. M.,  107, 108, 109, 110, 118, 119 Ostendorf, M.,  614
 author Index 693

Osterberg, L.,  443 Papp, L. A.,  269, 273, 280

Osterloh, I. H.,  522 Paprocki, C. M.,  313
Ostrander, R., 53 Paradiso, S.,  153
Otavio Torres, L.,  518 Pardini, D. A.,  76
Otilingam, P. G.,  446, 447 Pardos, J.,  596
O’Toole, M.,  133, 139 Parellada, E.,  448
O’Toole, M. S.,  279 Parellada, M.,  176
Otowa, T.,  268 Parent, J.,  86, 278
Otten, R.,  111 Parides, M.,  545, 550, 552, 554
Otto, M. W.,  61, 179, 180, 181, 199, 267, 275, 280 Parides, M. K.,  545, 553
Ou, C.-​S.,  178 Paris, J.,  465, 475, 477
Oude Voshaar, R.,  277 Parish, S. J.,  516, 517
Ouellet, M. C.,  565, 575 Park, J. M.,  206, 332
Ouimette, P.,  347 Park, S. G.,  452
Ouimette, P. C.,  104 Parker, E. H.,  73
Outcalt, S.,  609 Parker, G.,  153, 178, 180
Overall, J. E.,  440 Parker, H. A.,  332, 447–​448
Overington, L.,  19, 20, 24, xi Parker, J.,  416
Overland, S.,  564 Parker, J. D.,  276, 415
Owen, C.,  555 Parker, J. D. A.,  62, 222
Owen, M. J.,  437 Parker, L.,  584, 585
Owens, J.,  563, 573 Parker, S.,  252
Owens, J. A.,  343, 592 Parkerson, H. A.,  595, 596
Owens, J. S.,  53, 60 Parrella, M.,  445
Ownby, R. L.,  161 Parry, C.,  389
Oxman, T. E.,  448 Parry, G. J.,  574
Parslow, R. A.,  156
Pacchiarotti, I.,  175–​176 Partonen, T.,  174, 175
Pace, K.,  435 Parzer, P.,  197, 200
Pachas, G. N.,  438 Pasalich, D. S.,  76
Packard, T., 59 Pasch, L. A.,  498, 501
Padesky, C.,  142 Pasco, J. A.,  178
Padesky, C. A.,  139 Pascoe, J. M.,  59
Padma-​Nathan, H.,  527 Paskus, T. S.,  448
Pagano, M.,  267 Pasquale, L. E.,  116
Pagano, M. E.,  114, 273 Passchier, J.,  583
Page, A.,  195, 199 Passetti, F.,  447
Pagé, M. G.,  595, 596 Passi, V. A.,  554
Pagura, J.,  332 Patarnello, M.,  118
Paik, A.,  515, 517, 531 Patel, A. B.,  344
Paionni, A.,  544 Patel, V.,  137
Palao, D.,  178 Pater, A.,  445
Palazzo, C.,  244 Pathak, D.,  269
Palermo, T. M.,  585, 588, 592, 593, 595, 596, 598 Patjin, J.,  617
Palinkas, L. A.,  118 Patrick, D. L.,  530
Pallesen, K. J.,  135 Patterson, D. A.,  370
Pallesen, S.,  564 Patterson, G. R.,  72, 74, 78, 83, 86, 502
Palmer, A.,  415 Patterson, K.,  545, 553, viii
Palmieri, P. A.,  331 Patterson, M. B.,  161, 162
Palyo, S. A.,  339 Patterson, T. L.,  443, 445
Panak, W. F.,  203 Patton, G.,  101
Panayiotou, G., 76 Patton, S. R.,  594
Pané-​Farré, C. A.,  270 Paul, L.,  437, 440
Pang, C.,  542 Paul, S. M.,  589, 590
Pangallo, B. A.,  117 Paulitzki, J. R.,  244, 253
Panichelli-​Mindel, S. M.,  232, 233 Paulosky, C. A.,  19
Pantelis, C.,  267 Paulus, M. P.,  134
Panza, K. E.,  220, 231 Pautsch, J.,  101, 108, 117
Papadimitropoulos, E.,  614 Pavao, J.,  330
Papish-​David, R.,  178 Pavlickova, H.,  180
694 author Index

Pavuluri, M. N.,  178 Perkins, D. O.,  437, 443

Pawaskar, M.,  542 Perlis, M. L.,  564, 567
Paykel, E.,  160 Perlmutter, B. F.,  503
Payne, I. R.,  281, 282 Perquin, C. W.,  583
Payne, K. A.,  528, 529 Perrault, A.,  162, 165
Paz Yepes, M.,  197 Perreault, M.,  445
Pearce, E.,  451 Perrin, E.,  182
Pearce, S. A.,  617 Perrin, S.,  223, 233
Pearlson, G. D.,  452 Perry, D.,  334
Pearson, C.,  295 Perry, J. C.,  468, 475, 478
Pearson, M. R.,  401 Perry, K.,  340
Peasley, C. E.,  294 Perry, K. L.,  244, 252, 253
Peat, C.,  542 Persons, J. B.,  21, 24, 132, 138, 139, 142, 567
Pechansky, F.,  367 Persson, K.,  443
Pechorro, P.,  524 Pescosolido, B.,  490
Peden, N.,  413, 422, 425 Pescosolido, M. F.,  181
Peden, N. E.,  421 Pestreich, L., 61
Pedersen, B. V.,  516, 517, 518 Petcharatana, S.,  586
Pedersen, C. B.,  437 Peterman, J.,  223
Pedersen, E. R.,  334 Peterman, J. S.,  231
Pedersen, G.,  451 Petermann, F.,  218, 243
Pedersen, M. G.,  437 Peters, D. K.,  199
Pedersen, N. L.,  154 Peters, E.,  447
Pederson, N.,  157 Peters, K.,  153
Pedrelli, P.,  199 Peters, L.,  254, 339
Pedwell, G., 22 Peters, M.,  251
Peed, S., 86 Peters, M. L.,  251, 608, 617, 618
Peeples, D.,  452 Peters, R.,  367, 419, 424, 448
Peirce, R. S.,  393 Peterson, C.,  544
Pejovic, S.,  564 Peterson, C. B.,  547, 549, 552, 553
Pelham, W. E.,  52, 53, 54, 55, 56, 57, 59, 60, 63–​64 Peterson, C. C.,  593
Pelissolo, A.,  243 Peterson, D. R.,  3
Pelkonen, M.,  198, 200 Peterson, E.,  331
Pellegrini, D.,  501 Peterson, E. L.,  339, 347
Pelletier, M.-​H.,  282 Peterson, J. L.,  182, 183
Pelletier, O.,  303 Peterson, M., 19
Pemble, M. K.,  280, 281 Peterson, R.,  275
Pena, B. M.,  526 Peterson, R. A.,  251, 274, 280
Pendergast, L. L.,  177, 178 Petkova, E.,  60, 545, 552
Penelo, E., 84 Petras, L.,  570
Peng, J.,  526 Petretto, D. R.,  198
Peng, Y. B.,  608 Petrie, K. J.,  613
Penk, W. E.,  193 Petrocchi, N.,  275
Penn, D. L.,  435 Petrovski, P.,  105
Pennington, B. F.,  48, 50 Petroz, G. C.,  586, 592
Penninx, B. W.,  141, 266 Petry, N.,  423
Penninx, B. W. J. H.,  159, 163 Petry, N. M.,  412, 413, 414, 416, 417, 419, 423
Pepler, D. J.,  88 Petrycki, S.,  117
Pepping, C. A.,  508 Petter, M.,  596
Peradotto, D., 59 Pettersson, A.,  136
Perdereau, F.,  544 Pettinati, H. M.,  395–​396
Perdigao, A.,  589, 590 Pettit, G. S.,  72, 74
Pereira, B. B.,  445 Pettit, J. W.,  199
Perel, J.,  593 Petukhova, M.,  153, 267, 416
Perelman, M. A.,  518, 530, 531 Pétursson, H., 22
Perez-​Olivas, G.,  220 Peugh, J.,  596
Perez-​Rodriguez, M.,  178 Pfaff, D. W.,  543
Peris, T.,  230 Pfeffer, C. R.,  200
Peristeris, A.,  180 Pfeffer, C. R. M. D.,  200
Perkins, A.,  163 Pfeiffer, E.,  522
 author Index 695

Pfister, H.,  295, 296 Pirkis, J.,  199

Pfohl, B.,  466 Pisano, S., 59
Phares, V.,  226 Pissmiller, D.,  363
Phelan, E.,  159, 163 Pisterman, S., 59
Phelan, M.,  444 Pitanti, M.,  198
Phelps, J. R.,  179 Pitch, A., 48
Philips, R.,  614 Pitman, R. K.,  335, 337
Phillips, B. M.,  218 Pittman, B.,  389
Phillips, D.,  446 Pitts, T. E.,  471
Phillips, G.,  371 Pivik, J.,  529, 595, 613
Phillips, K. A.,  295, 316, 543 Planche, F.,  385
Phillips, K. E.,  547 Plassman, B. L.,  153
Phillips, L. J.,  161 Platou, C.,  564
Phillips, S. D.,  17, 113, 118 Plener, P. L.,  197, 200
Philyaw, A., 57 Pliszka, S. R.,  48
Photos, V. I.,  196, 197, 200, 202 Plöderl, M.,  194, 205
Piacentini, J.,  79, 87, 223, 230 Plotkin, D.,  268
Piacentini, J. C.,  222, 230 Ploubidis, G. B.,  516
Piasere, O.,  387 Plutchik, R.,  200
Piatosa, M. J.,  436 Plutchik, R. P. D.,  200
Piazza, L.,  525 Poe, M. P.,  438
Piazza-​Gardner, A. K.,  9 Pogge, D. L.,  17
Picchi, L.,  118 Pohl, J. F.,  594
Piccinelli, M.,  387 Pokorny, A. D.,  387
Piccirillo, M. L.,  250 Polák, J.,  249
Pich, V.,  337 Polan, J. J.,  278
Pickering, T.,  278 Polanczyk, G., 73
Pickles, A.,  108, 109, 110 Pole, M.,  200
Pickrel, S. G.,  86 Pole, N.,  335
Pielech, M.,  595–​596 Polen, M.,  117
Pier, C.,  280 Polich, J. M.,  393
Pierce, C. D.,  114 Poling, J.,  384
Pierce-​Sandner, S.,  612–​613 Poliquin, S.,  614
Piersma, H. L.,  468, 469 Politis, A.,  165
Pierson, H.,  620 Pollack, L.,  522
Pies, R. W.,  178 Pollack, L. M.,  526
Piet, J.,  135 Pollack, L. O.,  545, 553
Pieters, G.,  181 Pollack, M. H.,  199, 275, 280, 337
Pietrzak, R. H.,  331, 332, 341 Pollard, C. A.,  267
Pignone, M. P.,  155 Pollard, H. J.,  267
Pike, C. T.,  132 Pollock, M.,  22, 24
Pike, K. M.,  553 Pols, H.,  268
Pilkonis, P. A.,  21, 107, 109, 110, 118, 397, 398, 466, 471 Ponniah, K.,  18, 23
Pillai Riddell, R.,  585 Pope, H. G.,  180, 543
Pilver, C.,  330 Pope, M.,  157
Pina, A. A.,  219, 222, 233 Pope, M. H.,  614
Pincus, D., 78 Popovich, S., 59
Pincus, H. A.,  102 Pornprasertmanit, S., 10
Pinderhughes, E. E.,  76 Porst, H.,  526, 527
Pine, D.,  268 Portenoy, R. K.,  612
Pine, D. S,  220 Porter, C. A.,  275, 281
Pine, D. S.,  99, 101, 102, 113, 217, 266, 267, 270 Porter, E.,  279
Pini, S., 38 Porter, K.,  338
Pinninti, N. R.,  363 Porter, L. S.,  608
Pinsof, W. M.,  498 Portman, M. E.,  293–​294
Pinson, C.,  492, 495, 504 Portner, L.,  546
Pinto, A.,  200, 220 Posner, D. A.,  563, 565
Piotrowski, C., 18 Posner, J., 48
Pippingsköld, M.,  178 Posner, K.,  113, 194, 195, 197, 198, 204
Piquero, A. R.,  83 Post, R. M.,  180
696 author Index

Posternak, M. A.,  161, 165 Priore, R. L.,  393

Postrado, L.,  447 Prkachin, K. M.,  608
Pot, A. M.,  22 Prochaska, J. O.,  371, 394, 420, 449
Potenza, M. A.,  414, 416 Proctor, E., 24
Potenza, M. N.,  415, 423, 426 Proctor, S. P.,  332
Potter, C.,  252 Proietti, J. M.,  471
Potter, G. G.,  153 Proksch, K.,  594
Potter, J. F.,  162 Protopapa, J.,  115
Potter, R.,  107 Proud, L.,  106
Potter, W. Z.,  174 Provencher, M.,  297, 305
Potts, E.,  104 Provencher, M. D.,  297
Potts, N. L. S.,  256 Prusoff, B. A.,  115
Potvin, J. H.,  550 Pryor, J. L.,  530, 531
Poulin, F.,  72, 85 Przeworski, A.,  298
Poulton, R.,  116, 244, 268 Pucci, M. L.,  61
Powchik, P.,  445 Pucci, N. C.,  59
Powell, C. K.,  22 Puddy, R. W.,  59
Powell, C. V.,  588 Puente, A. E.,  33
Powell, N. P.,  54 Puig-​Antich, J.,  106, 114–​115
Power, T. J.,  50, 51 Pukall, C. F.,  517, 528, 529
Powers, A. D.,  465, 473 Pukall, C. P.,  517–​518, 529
Powers, D. V.,  157 Pullmann, M.,  21, 23
Powers, J. D.,  588 Purcell Baerga, P.,  61
Powers, K.,  361 Purdon, C.,  252, 253, 257
Powers, M. B.,  276, 312, 334, 340 Purdon, C. L.,  252
Powers, S. W.,  80, 594 Purington, A.,  206
Powers, W. J.,  134 Purnine, D. M.,  394
Powis, B.,  366 Pursell, C.,  228
Poythress, N. G.,  84 Purtill, J. J.,  448
Poznanski, E. O.,  109 Puttler, L., 59
Pozza, C.,  521 Pyke, R.,  528
Prakash, A.,  117 Pynoos, R. S.,  334
Pratt, L. A.,  132
Pratt, S. A.,  438 Qian, J.,  542
Pratt, S. I.,  443, 444 Qin, P.,  332
Prause, N.,  528 Quadflieg, N.,  544
Prendergast, M.,  106, 107 Queen, C. C.,  449
Prescott, C. A.,  294, 383 Queern, C.,  438
Presnell, J.,  446 Querido, J.,  80, 86
Presskreischer, B.,  199 Quickfall, J.,  417
Prestwich, A.,  145 Quillian, R. E.,  570
Preti, A.,  198 Quilty, L. C.,  257
Preuitt, L.,  153 Quinn, H., 40
Prezant, D. J.,  332 Quinn, K., 99
Price, J., 86 Quintero, J. M.,  134, 139
Price, L. H.,  220, 314, 322 Quirk, F. H.,  522
Price, M.,  24, 177
Price, M. J.,  76, 84, 88 Raabe, A.,  396
Price, R. A.,  174 Raadal, M.,  256
Price-​Munn, N.,  108 Raat, H.,  111
Priebe, S.,  334, 339, 444 Rabalais, A. E.,  341
Prien, R. F.,  174 Rabbitts, J. A.,  596
Prigerson, H. G.,  154 Rabian, B.,  109, 222, 232
Prihoda, T.,  440 Rabinovitz, B. B.,  47
Prince, M.,  157 Rabinowitz, J.,  38, 104, 119, 436
Prince, M. J.,  439 Rabins, P. V.,  153
Prins, A.,  347 Rachman, S.,  219, 244, 318, 319, 323
Prins, P. J. M.,  84, 232 Racine, N.,  585
Prinstein, M.,  40, 41 Racine, Y.,  108
Prinstein, M. J.,  12, 201, 203, 205, 206, 219 Radcliffe, A. M.,  608
 author Index 697

Radcliffe, J. C.,  617 Rasmusson, A. M.,  333, 335

Radhakrishnan, R.,  437 Rastegar, D. A.,  389
Radloff, L. S.,  157, 158, 162, 163, 165 Ratcliff, K. S.,  156
Radomsky, A.,  318, 324 Ratheesh, A.,  177
Radonovich, K. J.,  368, 373 Rathouz, P. J.,  75, 119
Radouco-​Thomas, M.,  573 Rathus, J. H.,  200, 500–​501
Radovic, A.,  230 Ratner, Y.,  444
Radtke, R. A.,  570 Rauch, S.,  338
Rae, D. S.,  108, 174, 448 Rauch, S. L.,  206
Raevuori, A.,  542 Raue, P. J.,  159
Rafaelsen, O. J.,  182 Raust, A.,  174
Rafat, B.,  269 Ravaldi, C.,  544
Ragan, J.,  549 Ravie Kishore, V.,  316
Raichle, M. E.,  134 Ravindran, A. V.,  160, 162–​163, 164, 165
Raines, A. M.,  280 Rawson, H. E.,  117
Raishevich, N.,  243 Ray, J., 74
Raizman, P. S.,  545 Ray, J. V.,  74, 75–​76, 84, 88
Rajab, M. H.,  199 Ray, L. A.,  395
Rajad, M. H.,  199 Ray, R. S.,  502
Rajendran, K., 47 Ray, W. J.,  303
Rakowski, W.,  394 Rayfield, A. D.,  86
Raleigh, K. L.,  59 Raykov, T.,  445
Ralevski, E.,  243 Raymond, E.,  436
Ralph, R.,  446 Raymond, N. C.,  552
Ralph, R. O.,  446 Raymond, S. A.,  612
Ramchandani, V. A.,  383 Ray-​Sannerud, B. N.,  204
Ramirez, A.,  114 Razdan, V.,  112
Ramirez, E.,  552 Razzetti, E.,  275
Ramirez, L. F.,  413 Rddel, H.,  275
Ramírez, R.,  114 Read, J. P.,  339, 369, 393, 394
Rampey, A. H.,  550 Ready, R. E.,  18, 19
Ramritu, P. L.,  587, 597 Realini, J. P.,  267
Ramsden, S. R.,  73 Ream, G.,  437
Ramsey, E., 84 Reardon, G.,  451
Ramtvedt, B. E.,  53 Reas, D. L.,  552, 553
Rancourt, K.,  518 Reay, B., 4
Randall, A. K.,  503 Rebouças, D. B.,  178
Randall, J., 86 Record, E. J.,  452
Randall, J. R.,  206 Redd, W. H.,  341
Randall, M.,  392 Reddell, T.,  250
Range, L. M.,  199, 202, 203 Redline, S.,  564, 566
Ranieri, W.,  613 Redmond, G. P.,  521
Ranieri, W. F.,  157, 199 Reece, M.,  524
Ranseen, J. D.,  61 Reed, B. D.,  529
Rao, P. A.,  252 Reed, C.,  182
Rao, S. V.,  599 Reed, G. M.,  11, 330
Rao, U.,  53, 107, 113, 115, 177 Reed, M.,  178
Rapado-​Castro, M.,  176 Reed, M. A.,  140
Rapaport, M. H.,  243 Reed, M. L.,  81
Rapee, R.,  220, 269, 271 Reese, H. E.,  280
Rapee, R. M.,  217, 218, 219, 222, 229, 243, 244, 251, 254, 269, Reeve, B., 21
274, 275, 277–​278, 280, 294, 296, 338 Reeve, R.,  587
Rapee, R. R.,  219 Reever, K.,  448
Rapkin, B.,  443 Reeves, E.,  102
Rapoff, M. A.,  585, 593, 594, 598 Reger, M. A.,  199
Rapp, S. R.,  156, 160 Regier, D. A.,  448, 465, 468
Rappaport, D.,  389 Rehm, J.,  138, 337, 382, 389
Rash, C. J.,  339 Reich, T.,  116, 394
Rasmussen, F.,  437 Reich, W.,  79, 106, 108, 222
Rasmussen, S. A.,  314, 316, 322 Reichenberg, A.,  436, 443
698 author Index

Reichman, J. T.,  276 Ricard, N.,  445

Reid, G. J.,  593 Ricca, V.,  544
Reid, J. B.,  74, 78, 81, 86, 502 Riccardi, C. J.,  269
Reid, J. C.,  200 Rice, J.,  394
Reid, R.,  50, 51, 599 Rice, J. P.,  175, 176
Reidel, B. W.,  564 Rich, A. R.,  442
Reider, A., 24 Richard, D. C. S.,  11
Reidy, B. L.,  181 Richard, P.,  585
Reif, A.,  270 Richards, A.,  566
Reig-​Ferrer, A.,  504 Richards, H.,  108, 574
Reigier, D. A.,  174 Richards, J.,  276, 281
Reilly-​Harrington, N. A.,  179, 180 Richardson, G.,  571
Rein, Z.,  544 Richardson, G. M.,  592
Reinelt, E.,  244 Richardson, W. S.,  37, 38, 39, xi
Reinert, D. F.,  422 Richichi, E. A.,  256
Reinfjell, T.,  594 Richmond, B. O.,  223, 224, 233
Reinhard, S. C.,  448 Richters, J. E.,  79, 87, 104, 177
Reinholdt-​Dunne, M. L.,  219 Riddell, A. B.,  477
Reininghaus, U.,  444 Riebel, J.,  21, 106
Reinish, L. W.,  574 Riedel, B. W.,  564, 574
Reis, B. F.,  117 Rieger, E.,  543
Reise, S. P.,  21, 110, 251, 442 Riemann, D.,  564, 571, 573
Reiss, D. J.,  451 Riemann, D. W.,  567
Reiss, S.,  251, 274, 275, 280 Riemer, M.,  17, 18, 22
Reissing, E. D.,  515, 528, 530 Rietschel, M.,  268
Reist, C.,  446 Rifkin, A.,  451
Reitsma, J. B.,  37 Rifkin, L. S.,  275
Rele, K.,  449 Riggs, D. S.,  338, 340
Rellini, A. H.,  521 Rihmer, Z.,  268
Remijsen, M.,  440 Riley, A.,  522
Remschmidt, H.,  544 Riley, J. L.,  617
Ren, Z.,  542 Riley, W., 21
Renna, M. E.,  134, 139 Riley, W. T.,  21, 24, 110
Rescorla, L. A.,  4, 35, 54, 55, 57, 78, 110, 113 Rimehaug, T.,  107
Resick, P. A.,  333, 340, 344 Rinaldi, S.,  115
Resnick, H. S.,  330, 331 Ringeisen, H., 4
Resnick, I.,  392 Ringham, R.,  547
Resnick, S. G.,  446 Ringle, V.,  22, 24
Rettew, D. C.,  19, 33, 34 Ringoot, A. P.,  111
Rettew, J. B.,  470 Rintelmann, J.,  117
Retzlaff, P. J.,  301, 344 Rintelmann, J. W.,  102
Reuterskiöld, L.,  222 Riochardson, K.,  437
Revicki, D. A.,  612–​613 Riolo, S. A.,  132
Reyes, R. U.,  446 Rippel, S.,  585
Reyes Ayllon, A. R.,  437 Risen, C. B.,  520
Reynaud, M.,  385 Riso, L. P.,  104
Reynolds, C.,  157 Rissmiller, D. J.,  157
Reynolds, C. F.,  180 Rith-​Najarian, L.,  227
Reynolds, C. F,  3rd, 564, 573 Ritsher, J. B.,  359, 446, 447
Reynolds, C. R.,  55, 56, 59, 80, 81, 223, 224, 233 Ritsner, M.,  444
Reynolds, G. L.,  394 Ritter, M.,  133, 134, 139
Reynolds, W. M.,  109, 110, 113, 117, 199, 200 Ritterband, L. M.,  573
Reznick, J. S.,  218 Rivera-​Medina, C.,  117
Rhea, D. J.,  545 Riviere, L. A.,  331, 341
Rhéaume, J.,  302, 305, 325 Rizvi, S. L.,  547, 549
Rheaume, N.,  415 Rizzo, M.,  159
Rhebergen, D.,  266 Ro, E.,  500
Rhew, I.,  117 Roach, N. K.,  619
Rhode, P.,  116, 117 Robbins, J. M.,  17, 113, 118
Ribeiro, J. D.,  201 Robbins, P. C.,  440
 author Index 699

Robbins, S. J.,  366, 373 Rogers, E. S.,  451

Roberson-​Nay, R.,  112, 250 Rogers, H. J.,  494
Roberto, C. A.,  544 Rogers, J. R.,  203
Roberts, A. L.,  345 Rogers, R.,  175, 182, 247, 466, 467
Roberts, C.,  102, 117, 118, 546 Rogge, R.,  494, 497
Roberts, J.,  202 Rogge, R. D.,  523, 524
Roberts, J. E.,  476 Rohde, L. A.,  48, 73
Roberts, L. J.,  40, 497 Rohde, P.,  101, 107, 118, 154
Roberts, M., 86 Rohlof, H.,  439
Roberts, M. C.,  11, 59 Rohsenow, D. J.,  365, 369, 370, 371, 372, 373
Roberts, M. J.,  529 Roinås, E., 53
Roberts, M. L.,  24 Rojas, S. L.,  471, 476
Roberts, M. W.,  80 Rokne, B.,  611, 614
Roberts, R. E.,  105, 109, 175 Roland, M.,  614
Robertson, B.,  59, 60 Roland, M. O.,  614
Robichaud, M.,  30, 294, 295, 296, 297, 299, 302, 303 Rolffs, J.,  508
Robin, A. L.,  546 Rollnick, S.,  369, 394
Robinaugh, D. J.,  133, 345 Rolnick, S. J.,  159
Robins, E.,  156, 176 Rom, D., 33
Robins, L.,  416 Romagnoli, G.,  118
Robins, L. N.,  83, 156, 364, 439 Romaní, R.,  444
Robinson, D.,  437 Romano, J. M.,  617, 618
Robinson, D. G.,  435, 437 Romano, S. J.,  554
Robinson, E., 80 Ronan, G. F.,  138, 142
Robinson, G.,  281 Ronneberg, U.,  180
Robinson, J.,  524 Rooney, M. T.,  108
Robinson, J. P.,  5, 614 Roper, M.,  79, 87
Robinson, M. E.,  617 Rorty, M.,  551, 552
Robinson, P.,  552 Rosario, P. G.,  370
Robinson, T. E.,  134 Rose, J. B.,  595
Robinson-​Whelen, S.,  618 Rose, J. S.,  549
Robles, R., 11 Rose, K.,  426
Robles, T. F.,  491 Rose, R.,  275, 279, 280, 281
Robson, E.,  419 Rose, R. D.,  280
Roccaforte, W. H.,  162 Rose, S.,  331
Rocha, H. L.,  373, 374 Rose, T. L.,  158, 159
Roche, P. A.,  612 Rosen, A.,  595
Rockert, W.,  545, 550, 552, 554 Rosen, D. S.,  542
Rockhill, C. M.,  63 Rosen, G.,  402
Roddy, M. K.,  490 Rosen, J. C.,  547, 552
Rode, C. A.,  594 Rosen, N. O.,  517–​518, 529
Rodebaugh, T. L.,  10, 244, 247, 250, 251 Rosen, R.,  521, 522, 524, 529, 530
Rodebaugh, T. M.,  295 Rosen, R. C.,  330, 337, 515, 516, 517, 521, 522, 526, 527
Rodenberg, C.,  528 Rosenbaum, J.,  219
Rodgers, B.,  153, 555 Rosenbaum, J. F.,  180
Rodriguez, B. F.,  273 Rosenberg, H.,  397, 418
Rodriguez, D.,  277 Rosenberg, M.,  553
Rodriguez, E.,  219 Rosenberg, N. K.,  279
Rodriguez, L. M.,  383 Rosenberg, S. D.,  437, 440, 448
Rodriguez, P.,  337, 341 Rosenberg, S. E.,  545, 553
Rodríguez Cardona, J.,  61 Rosenberg, W. M. C.,  xi
Roe, D.,  446 Rosenberger, P.,  615, 620
Roehrig, M.,  545 Rosenberg-​Thompson, S.,  162
Roehrs, T.,  571 Rosenblate, R.,  139, 252
Roelofs, J.,  224, 618 Rosenbloom, B.,  592
Roemer, L.,  139, 250, 255, 276, 281 Rosenblum, E. L.,  592
Roerecke, M.,  382 Rosenfeld, B. D.,  612
Roffman, R. A.,  368, 369, 373 Rosenfeld, R.,  322, 466, 467
Rog, D. J.,  612 Rosenfield, D.,  275
Rogers, E.,  499 Rosengren, D.,  162
700 author Index

Rosenheck, R.,  332 Ruan, W. J.,  295, 296, 382, 388

Rosenheck, R. A.,  435, 437, 446 Rubel, J.,  22, 24
Rosenquist, K. J.,  178 Rubin, D. C.,  140
Rosenstock, J. B.,  452 Rubinow, D. R.,  174
Rosenthal, N. E.,  174 Rubinstein, K. J.,  364
Rosenthal, R., 11 Rubio-​Aurioles, E.,  526, 530
Rosentiel, A. K.,  617 Rubio-​Stipec, M.,  103
Roset, R., 24 Rubonis, A. V.,  370
Rosh, J. R.,  598 Rucci, P.,  178, 273
Rosnick, L.,  468, 471 Rück, C.,  268
Rosof-​Williams, J.,  17 Rudd, M. D.,  195, 199
Rosomoff, H. L.,  612 Rudenko, A. A.,  389
Rosomoff, R. S.,  612 Rudolph, K.,  113, 115
Ross, H. E.,  247, 363 Rudolph, K. D.,  115
Ross, J.,  360 Rudy, T. E.,  610, 612, 615
Rossberg, J. I.,  436 Ruggero, C.,  178
Rossell, S. L.,  549 Ruggero, C. J.,  179
Rosselli-​Navarra, F.,  549 Ruggiero, K. J.,  341
Rosselló, J.,  117 Rugle, L.,  417
Rossi, G.,  479 Ruscio, A. M.,  266, 267
Rossi, J. S.,  394 Rush, A.,  272
Rossi, S. R.,  394 Rush, A. J.,  17, 18, 22, 102, 105, 117, 136, 156, 161, 165, 270
Rossier, J.,  504 Rush, J. A.,  132, 133, 138, 139
Rossler, W.,  564 Rushe, R.,  498
Rost, C.,  422 Rushe, T.,  156
Roszell, D. K.,  337 Ruskin, D.,  588
Rotella, B., 60 Russell, C. S.,  545–​546
Rotella, C. M.,  544 Russell, G., 50
Roth, C.,  116 Russell, G. F. M.,  545, 546
Roth, D.,  257 Russell, J.,  543
Roth, T.,  564, 571 Russell, L.,  343
Roth, W. T.,  268, 275, 282 Russell, M.,  393, 421
Rothbaum, A. O.,  479 Russinova, Z.,  451
Rothbaum, B. O.,  333, 338 Russo, A. M.,  413
Rothman, M.,  530 Russo, D. C.,  72
Rothrock, N., 21 Russo, J.,  267
Rotondi, A. J.,  452 Russo, P. A.,  515, 516, 517
Rotterman, J. H.,  476 Rust, G.,  131
Rotunda, R.,  267 Rust, J.,  521, 528
Rouget, B. W.,  178 Rutherford, M. J.,  373
Rounsaville, B.,  272 Rutherford, R. B.,  24
Rounsaville, B. J.,  134, 384, 414, 416 Rutter, D.,  392
Rourke, K. M.,  364 Rutter, M.,  50, 106, 107, 116
Rousseau, C.,  330 Ruuttu, T.,  198, 200
Rowa, K.,  242, 244–​245, 248, 252, 253, 257 Ryan, C. E.,  181
Rowbotham, M. C.,  612 Ryan, C. F.,  155–​156, 160
Rowe, B. H.,  206 Ryan, K. M.,  611
Rowe, L. S.,  498 Ryan, L., 60
Rowe, M.,  269, 276, 279, 282 Ryan, M.,  595–​596
Rowe, R., 73 Ryan, N.,  53, 107, 177
Rowland, D.,  516, 518 Ryan, N. D.,  115
Rowland, D. L.,  530 Ryan, S.,  220
Rowland, M. D.,  86 Ryan, S. M.,  269
Roy, L.,  437 Ryan, T.,  361
Roy, M.,  18–​19 Rychtarik, R. G.,  397
Roy, M. A.,  436 Ryder, A.,  103
Roy-​Byrne, P.,  250, 275, 277 Ryder, A. G.,  103, 160, 164, 473
Roy-​Byrne, P. P.,  267, 295 Rygwall, R.,  318, 319
Rozenman, M.,  220 Ryser, G.,  114
Rozin, P.,  251 Ryu, S.,  499
 author Index 701

Saadi, E.,  437 Sanders, S.,  524

Saavedra, L.,  225 Sanderson, W. C.,  243
Saavedra, L. M.,  217, 222, 223, 226, 233 Sandoval, J., 56
Sacco, W. P.,  159 Sanford, K.,  502
Sachs, G. S.,  180, 181 Sanford, M.,  108, 114
Sachs-​Ericsson, N.,  269 Sanford, S. D.,  574
Sackett, D. L.,  xi Sangster, Y.,  446
Sadeghi-​Nejad, H.,  516 Sanislow, C.,  272, 299, 470, 548
Sadikaj, G.,  518, 529 Sanislow, C. A.,  19, 243, 472
Sadler, I. J.,  617 Sankis, L. M.,  473
Sadovsky, R.,  527 Sano, N.,  256
Saelens, B. E.,  545, 553 San Pedro-​Salcedo, M. G.,  576
Saettoni, M., 38 Sansone, L. A.,  200
Safarinejad, M. R.,  525 Sansone, R. A.,  200
Safavi, R.,  180 Santiago, P. N.,  334
Safran, J. D.,  133, 253–​254 Santoro, N.,  517
Safren, S. A.,  61 Santos, A. B.,  86
Sagnier, P. P.,  522 Santos, J. C.,  332
Saha, C., 63 Santos-​Iglesias, P.,  524
Saha, S.,  437 Santostefano, A. M.,  230
Saha, T. D.,  330, 331, 332, 334, 381, 382, 384, 388, 389 Santucci, L.,  5, 102
Saitz, R.,  385 Sanz, M.,  180
Sáiz, P. A.,  367 Sapin, H.,  182
Sajatovic, M.,  180 Saps, M.,  590
Saks, E. R.,  435 Sareen, J.,  332, 417
Saladin, M. E.,  339 Sarin, S.,  527
Salary, C. B.,  102 Sarkin, A.,  446
Salazar, I. C.,  247, 251 Sarmiento, T. L.,  116
Salazar, L. R.,  495 Sarwer, D. B.,  503
Salekin, K. L.,  182 Sateia, M.,  563, 565
Sales, C. M. D.,  4 Sateia, M. J.,  563
Sales, P. M. G.,  178 Sattler, A. F.,  19
Saliba, A. J.,  571 Saudan, S.,  587
Saliba, D.,  159, 164 Sauer-​Zavala, S.,  4, 475, 477
Salisbury, H.,  49, 50 Saulnier, C. A.,  56
Salkovskis, P. M.,  278, 279, 312, 320, 323 Saunders, A. E.,  199
Salovey, P.,  612 Saunders, E. F.,  180
Salters-​Pedneault, K.,  281 Saunders, E. F. H.,  24
Salum, G. A.,  268 Saunders, J.,  422
Salyers, M. P.,  437, 446 Saunders, J. B.,  387, 448, 498
Salzer, M.,  446 Sauter, F. M.,  228
Samar, R.,  316 Savard, J.,  564, 565, 573
Samet, J. H.,  385 Savard, M. H.,  573
Samet, S.,  388 Savard, P.,  30, 302, 305
Sampaio, D.,  332 Savedra, M. C.,  589, 590, 598
Sampler, R. E.,  344 Savitz, K. L.,  498–​499
Sampson, N.,  201, 332 Sawchuck, C.,  318
Sampson, N. A.,  153, 180, 201, 267, 330, 416 Sawchuk, C. N.,  250, 251
Samuel, D. B.,  19, 465, 466, 467, 470, 477 Sawyer, S. M.,  546
Samuels, L.,  422 Sax, K. W.,  180
San, L.,  179 Saxena, S., 11
Sanavio, E.,  553 Sayal, K.,  22, 47, 53
Sánchez, A.,  524 Sayers, S.,  383
Sanchez, S. E.,  575 Sayers, S. L.,  442, 447, 503
Sanchez-​Moreno, J.,  178 Sayette, M. A.,  395
Sánchez-​Rodríguez, E.,  24 Saylor, C. F.,  586
Sandberg, S.,  219 Saylor, D. K.,  573
Sanddal, N. D.,  193 Saylor, K. I.,  471
Sander, J. B.,  110 Saz, P.,  157
Sanders, A.,  389 Sbrocco, T.,  275, 279
702 author Index

Scahill, L.,  225, 226, 231 Schneiderman, A. I.,  332

Scaini, S.,  244, 250 Schneiderman, J.,  389
Scanelli, G.,  542 Schneier, F.,  252
Scanlan, J.,  219 Schneier, F. R.,  247, 251
Scazufca, M.,  157 Schnell, S. V.,  81
Schackman, B. R.,  19 Schnelle, J. F.,  162
Schadel, W. G.,  395 Schnicke, M. K.,  344
Schaefer, C. A.,  437 Schniering, C. A.,  217, 218
Schaefer, E.,  272, 299, 344 Schnoll, S. H.,  360
Schaefer, E. S.,  115 Schnurr, P.,  343
Schaefer, K., 19 Schnurr, P. P.,  334, 335, 336, 337, 340, 341, 343
Schaefer, L.,  360 Schoenfeld, D. A.,  438
Schaerer, L.,  178 Schoenfelder, E. N.,  63
Schafer, A. B.,  159 Schoenmakers, N.,  249
Schalling, M.,  268 Schoenwald, S. K.,  118
Scharfstein, L.,  220, 231, 252 Schohn, M.,  347
Scharfstein, L. A.,  220, 231 Scholle, S. H.,  3
Schatte, D. J.,  199 Schönfeld, S.,  139
Schaumberg, D. A.,  587, 598 Schooler, N.,  444
Schecter, J.,  108 Schooler, N. R.,  435, 437, 442, 451
Scheel, I.,  614 Schork, N. J.,  332
Scheel, K.,  203 Schotte, C.,  479
Scheftner, W. A.,  176 Schotte, C. K. W.,  19
Scheiderer, E. M.,  465 Schouten, E.,  251
Schell, T.,  442 Schreer, G.,  503
Schellenberg, B. J.,  421 Schreiber, J. E.,  111
Schellenberg, F.,  385 Schrijvers, A. J.,  614
Schene, A. H.,  444 Schrimsher, J.,  452
Schermelleh-​Engel, K.,  244 Schroeder, J.,  436
Schertzer, S.,  182, 183 Schroeder, M. L.,  476
Schettler, P. J.,  184 Schruers, K.,  269
Schiavenato, M.,  586 Schruers, K. R.,  268, 269
Schiffer, B.,  436 Schry, A. R.,  250, 331
Schilpzand, E. J.,  52 Schuckalo, S. G.,  598
Schimmack, U.,  49, 50 Schuckit, M.,  361, 381
Schinke, S. P.,  394 Schuckit, M. A.,  360, 362, 382, 383, 388
Schipper, E.,  56, 62 Schuh, S.,  585, 587, 598
Schlenger, W. E.,  331, 337 Schulenberg, J.,  361
Schlesser, M. A.,  161 Schuller, D. R.,  160, 164
Schloredt, K.,  117 Schultz, L. R.,  347
Schlundt, D.,  543 Schultz, S., 24
Schlundt, D. G.,  545 Schulz, E. G.,  57
Schmaly, K.,  163 Schulz, H.,  156
Schmidt, A. B.,  176 Schulz, R.,  154
Schmidt, C. W.,  452 Schumacher, J. A.,  206
Schmidt, F. L.,  11 Schumm, J.,  334
Schmidt, N. B.,  199, 268, 274, 275, 280, 283 Schutte-​Rodin, S.,  563, 565
Schmidt, N. L.,  111 Schvey, N. A.,  545
Schmidt, U.,  544 Schwab-​Stone, M.,  75, 108
Schmidt-​Lackner, S.,  175 Schwab-​Stone, M. D.,  118
Schmitt, S.,  528 Schwab-​Stone, M. E.,  52, 79, 83, 103, 108, 222
Schmitz, J.,  256 Schwahn, C.,  244
Schmitz, M.,  566 Schwan, R.,  385
Schmollinger, J.,  199 Schwantes, S. A.,  584
Schmook, A.,  446 Schwartz, A. L.,  574
Schneekloth, R.,  618 Schwartz, D., 72
Schneider, J., 50 Schwartz, J.,  49, 50
Schneider, L. C.,  445 Schwartz, J. E.,  574
Schneider, M.,  543 Schwartz, J. P.,  545
Schneider, S.,  20, 39, 274, 279, 387 Schwartz, K. T. G.,  112, 113, 119
 author Index 703

Schwartz, M. B.,  547, 554 Semler, C. N.,  571

Schwartz, S.,  24, 163 Semmar, Y.,  504
Schwartz, S. A.,  315 Sen, A.,  529
Schwienfurth, L. A. B.,  436 Sengun, S.,  282
Sciberras, E., 52 Sengupta, A.,  451
Scofield, H.,  571 Sensky, T.,  392
Scogin, F.,  160, 164, 572 Sepulveda, J. E.,  103
Scolnik, D.,  585, 587, 598 Serafini, L. T.,  232
Scotford, A.,  593 Serfaty, M.,  447
Scott, C. K.,  364, 367–​368, 373 Serper, M. R.,  442
Scott, C. S.,  368, 374 Serpi, T.,  339
Scott, J.,  178, 180, 591 Serrano, E.,  179
Scott, K. M.,  331 Seshadri, R., 17
Scott, M.,  113 Seth, S., 63
Scott, S., 86 Seto, M. C.,  528
Scott, T. M.,  24 Setoguchi, Y.,  594
Scotti, J.,  275 Sevy, S.,  437
Scotti, J. R.,  341 Sexton, K. A.,  302, 303
Scott-​Sheldon, L. A.,  396 Seymour, K.,  181
Sculling, R. B.,  10 Shabsigh, R.,  521
Seagraves, R. T.,  528 Shafer, A.,  440
Searles, J. S.,  448 Shaffer, D.,  52, 79, 81, 83, 86, 108, 113, 118, 222
Sears, M. R.,  116 Shaffer, H. J.,  414, 416, 417
Sebastian, C. L.,  76 Shaffer, J. A.,  330
Sechrest, L., 5 Shaffer, M. L.,  564
Seckinger, R. A.,  38 Shafran, R.,  252, 318, 320, 551, 552, 553
Secunda, S. K.,  175 Shah, V.,  585
Sedgwick, O.,  447 Shahly, V.,  542
Sedlácková, K.,  249 Shalev, A. Y.,  333
Sedway, J. A.,  544 Sham, P.,  180, 183
Seedat, S.,  331 Shamir-​Essakow, G.,  219
Seeley, J.,  117 Shamloul, R.,  517, 527
Seeley, J. R.,  101, 105, 107, 109, 110, 116, 117, 118, 383, 543 Shamoian, C. A.,  161, 165
Seftel, A. D.,  522, 526 Shanahan, L.,  100, 101, 102, 107
Segal, D. L.,  155–​156, 157, 160, 465, 466, 468, 469, 548 Shane, P.,  365
Segal, S., 59 Shaner, A.,  247
Segal, Z.,  567 Shapiro, A. F.,  501
Segal, Z. V.,  133, 134, 139, 140, 253–​254 Shapiro, A. P.,  617
Segraves, K.,  526 Shapiro, C.,  586
Segraves, R. T.,  526 Shapiro, C. M.,  574
Segraves, T.,  518 Shapiro, D.,  278
Segreti, A.,  515, 516, 517 Shapiro, E. S.,  57–​58
Sehner, S.,  156 Shapiro, J. R.,  544
Seid, M.,  593, 594, 598 Shapiro, R. W.,  176
Seidlitz, L.,  472 Shapiro, S.,  567
Seidman, E., 4 Sharma, T.,  438
Seim, R. W.,  334 Sharp, C.,  200
Seinen, A.,  448 Sharpe, L.,  156, 160
Seirup, J. K.,  134 Sharpless, B. A.,  277
Selbæk, G.,  161, 162 Sharpley, C. F.,  494
Self, D.,  471 Sharrock, R.,  279
Self, M. M.,  594 Shaver, P. R.,  5
Seligman, L. D.,  217, 223, 225 Shaw, A. M.,  524
Sellbom, M.,  35, 476 Shaw, B. F.,  132, 133, 138, 139, 276, 277
Sellers, E. M.,  389 Shaw, D. A.,  502
Sellers, R.,  107 Shaw, D. S.,  134
Sellman, J. D.,  392 Shaw, J.,  447
Sells, M.,  447 Shaw, S. D.,  10
Selzer, M. L.,  387, 394, 448 Shaw-​Hegwer, J.,  347
Semenzin, M.,  387 Shea, M. T.,  19, 243, 467, 472, 548
704 author Index

Shea, T.,  295, 470 Shon, S.,  440

Shear, K.,  266, 267 Shores, E. A.,  613
Shear, M.,  275 Shores-​Wilson, K.,  440
Shear, M. K.,  174, 273, 278, 280 Short, E. J.,  59
Shearin, E.,  199 Shuchter, S. R.,  154
Shedler, J.,  466, 467, 470, 471, 472 Shugar, G.,  182, 183
Sheeber, L. B.,  117 Shulman, G. L.,  134
Sheehan, D.,  363 Shulman, M.,  615, 620
Sheehan, D. V.,  194, 198, 204, 257, 344, 389, 439 Shulman, R. J.,  590, 594
Sheehan, I. S.,  198, 204 Shumway, S. T.,  490
Sheehan, K. H.,  194, 363, 389, 439 Shutty, M. S.,  617
Sheehan, M. F.,  389 Si, X.,  108
Sheehy, M. J.,  401 Sica, C.,  275
Sheeran, P.,  145 Sickel, A. E.,  466, 471
Sheffield, R. L.,  497, 501 Siebelink, B. M.,  507
Sheikh, J. I.,  158, 347 Sieberg, C. B.,  596
Sheldon, C. T.,  491 Siegel, P. T.,  546
Sheldon, T. A.,  19, 20 Siegel, S. J.,  444
Sheldrick, R. C.,  9 Siegeris, K.,  617
Shelton, K. K.,  76 Siegert, R. J.,  18, 24
Shelton, R. C.,  199 Siegle, G.,  133
Shelton, T. L.,  63 Siegle, G. J.,  132
Shemmassian, S. K.,  50 Sierra, J. C.,  524
Shen, S.,  114, 194, 195, 197, 204 Sigman, M.,  220
Shenoy, R.,  107, 108 Sigman, R.,  381
Shepard, J.,  382 Sikand, A.,  546
Shepherd, K.,  133 Sikirica, V.,  59, 60
Shepherd, K. A.,  139–​140 Sil, S.,  596
Sher, K.,  382, 383 Silbaugh-​Cowdin, J.,  21, 23
Sher, K. J.,  382, 383, 384, 387, 388, 394 Silbersweig, D.,  153, 154
Sher, T. G.,  498 Silén, Y.,  542
Sherbourne, C.,  275, 277 Sillars, A.,  497
Sherbourne, C. D.,  163, 267, 389, 614 Sillars, A. L.,  501
Sher-​Censor, E.,  115 Silove, D.,  331
Sherdell, L.,  134 Silva, P., 75
Sherker, J. L.,  595 Silva, P. A.,  100
Sherman, D.,  500 Silva, S.,  117
Sherman, K. J.,  620 Silverman, D.,  195
Sherman, R. E.,  143 Silverman, M. M.,  193, 194, 195
Sherry, D.,  595 Silverman, W.,  225
Sherry, D. D.,  595 Silverman, W. K.,  109, 217, 218, 219, 220, 221, 222, 223, 225,
Sherwood, A.,  250 226, 227, 228, 229, 230, 231, 232, 233, 271
Sheu, W. J.,  393 Silverthorn, P.,  73, 75, 76
Shibuya, K.,  193 Simard, S.,  565, 573
Shic, F.,  229 Simmel, C., 80
Shield, K. D.,  389 Simmens, S. J.,  219, 448
Shields, B. J.,  588 Simmons, A.,  401
Shields, S. A.,  545 Simmons, J.,  269, 279
Shiffman, S.,  395, 402 Simmons, M.,  106
Shiffrin, T. P.,  115 Simmons, T., 56
Shifren, J. L.,  515, 516, 517, 521 Simms, L. J.,  466, 467, 475, 476, 477, 479, 575
Shikatani, B.,  252 Simon, D., 38
Shim, R. S.,  131 Simon, G. E.,  564
Shimabukuro, S., 22 Simon, H. A.,  426
Shimokawa, K.,  18, 20, 120, 143 Simon, J. A.,  521
Shin, L. M.,  335 Simon, N. M.,  133, 199, 280
Shindel, A. W.,  518 Simon, R.,  193
Shin Y. C.,  426 Simone, M., 56
Shiwach, R.,  156 Simoni, M.,  542
Sholomskas, D. E.,  273, 280 Simonoff, E.,  106, 107
 author Index 705

Simons, J. S.,  369, 515 Smart, D. W.,  18, 20, 143, 144, 145

Simons, L. E.,  595–​596, 599 Smeets, F.,  437
Simons, R. F.,  73 Smeets, R. J.,  618
Simonsen, E.,  476 Smets, E. M.,  574
Simpson, D. D.,  370 Smider, N.,  111, 113
Simpson, E. E.,  368, 373 Smink, F. R.,  542
Simpson, H. B.,  312 Smit, F.,  394
Simpson, L. E.,  498 Smit, J. H.,  295
Simpson, M.,  400 Smith, A.,  143, 385, 505
Simpson, S. G.,  116, 176 Smith, A. E.,  384
Simpson, T. L.,  334 Smith, A. M.,  19, 20, 24
Sinclair, J. D.,  616 Smith, B. L.,  3
Sinclair, S. J.,  614 Smith, B. N.,  344
Singer, A. J.,  588 Smith, C.,  158, 421
Singer, B.,  vii Smith, C. A.,  593
Singer, J.,  107, 108 Smith, D.,  107, 337, 547
Singh, A. L.,  119 Smith, D. E.,  339
Singh, J. P.,  84 Smith, G.,  419
Single, E.,  414 Smith, G. A.,  588
Singleton, E. G.,  396 Smith, G. T.,  10, 11, 361, 470
Siqueland, L.,  117, 142, 144 Smith, I.,  367, 448
Sirbu, C., III,  243 Smith, J.,  444
Sireling, L.,  160 Smith, K. B.,  529
Sirota, A. D.,  369 Smith, M.,  388
Sisitsky, T.,  132 Smith, M. D.,  522, 526
Sisson, M.,  522 Smith, M. S.,  595
Sit, L.,  612 Smith, M. T.,  573
Sitarenios, G., 62 Smith, M. W.,  330
Sivertsen, B.,  564 Smith, N.,  180
Skaret, E.,  256 Smith, R. D.,  256
Skarphedinsson, G.,  223 Smith, S. J.,  615
Skeem, J.,  76, 84 Smith, S. M.,  330, 331, 332, 334, 362, 363
Skinner, H.,  422 Smith, S. S.,  156, 160
Skinner, H. A.,  363, 387, 393, 448 Smith, V. C.,  102
Skinner, J. B.,  421 Smitherman, T. A.,  257
Skinner, W.,  392 Smith-​Jackson, E. E.,  180
Skjulsvik, T.,  22, 144 Smithmyer, C. M.,  73
Sklar, M.,  446 Smits, J. A.,  276, 280
Sklar, S. M.,  370 Smits, J. J.,  312
Skodol, A.,  272 Smolenski, D. J.,  347
Skodol, A. E.,  19, 243, 272, 299, 465, 466, 468, 470, 471, 472, Smolla, N.,  108
475, 476, 479 Smoller, J. W.,  113
Skoog, G.,  313 Smyth, J.,  551, 552
Skoog, I.,  313 Smyth, N. J.,  202
Skoutas, C.,  180 Snaith, R. P.,  138–​139
Slade, K.,  37, 145 Snarr, J. D.,  493
Slade, M.,  444 Snell, J., 51
Slatcher, R. B.,  491 Snell, L. D.,  385, 400, 402
Slater, A.,  501 Snider, E. C.,  392
Slater, J. F.,  177 Snow, A. L.,  155, 162
Slattery, P., 22 Snowden, M.,  159, 163
Slavens, S.,  250 Snowdon, J.,  162
Slavin, L., 22 Snyder, A. Z.,  134
Slawsby, E. A.,  612 Snyder, C. R.,  593
Sleed, M.,  583, 596 Snyder, D. K.,  490, 491, 493, 494, 496–​497, 498, 500, 501, 503,
Slep, A. M. S.,  116, 490, 493, 494 504, 505, 507
Sloan, D. M.,  334, 335, 337 Snyder, K. S.,  436
Slutske, W. S.,  394, 413 Sobell, D. P.,  394
Smalbrugge, M.,  161 Sobell, L. C.,  366, 373, 392, 393, 394, 449, 546–​547
Smart, D.,  120 Sobell, M. B.,  366, 373, 392, 393, 394, 449, 546–​547
706 author Index
Sochting, I.,  322
Soczynska, J. K.,  178
Sodano, R.,  414, 415, 425
Söderberg, P.,  451
Söderlund, A.,  598
Söderpalm, B.,  383
Söderpalm Gordh, A. H.,  383
Sokol, M. S.,  554
Solanto, M. V.,  48, 58, 62
Solberg, L. I.,  384
Solhan, M. B.,  360
Solheim, E.,  107, 108
Sollman, M. J.,  61
Solomon, D.,  154
Solomon, D. A.,  181, 184
Solomon, G. M. D.,  200
Solomon, S.,  342
Solstad, K.,  161, 165
Somasundaram, D.,  345
Somayaji, V.,  522
Somers, T. J.,  269, 281, 615
Somerville, D.,  619
Somwaru, D. P.,  470
Song, W.,  526
Songer, D. A.,  200
Sonntag, R.,  281
Sonuga-​Barke, E. J. S.,  48
Soobiah, C.,  592
Sookman, D.,  324
Sorbero, M. J.,  18
Sorensen, H. T.,  332
Sorenson, J. L.,  365
Sorgen, K.,  341
Soriano-​Mas, C.,  267
Sorrell, J. T.,  620
Souery, D.,  268
Sourbut, C.,  598
South, S. C.,  472
Southam-​Gerow, M.,  232, 233
Southam-​Gerow, M. A.,  117, 249
Southwick, S. M.,  331, 332
Soutullo, C.,  177
Souza, F. G. d. M.,  178
Souza-​Formigoni, M. L.,  367
Spafford, P. A.,  587
Spagrud, L. J.,  588
Španiel, F.,  452
Spanier, G. B.,  494, 523
Sparrow, E., 62
Sparrow, S. S.,  56, 57
Speckart, G. R.,  361
Specker, S.,  416, 421
Spector, I. P.,  530
Speechley, M.,  609
Speisman, B. B.,  313
Spence, S. H.,  223, 244
Spencer, H.,  330
Spencer, T. J.,  61
Spenner, K.,  547
Spetzler, R. F.,  396
Spiegel, D.,  334
Spiegel, D. A.,  273, 281
Spiegelhalder, K.,  564, 571
Spielberger, C. D.,  223, 338, 340, 346, 575
Spielman, A. J.,  564, 567
Spies, C. D.,  392
Spies, M.,  392
Spijker, J.,  131, 266
Spilka, M. J.,  3
Spinhoven, P.,  154
Spinner, M.,  114
Spira, J. L.,  332
Spirito, A.,  19, 201, 202
Spiro, A. R.,  442
Spitzer, A., 81
Spitzer, R.,  272, 316, 337
Spitzer, R. L.,  116, 135, 136, 155, 156, 159, 160, 162, 163, 165,
175, 176, 178, 245, 246, 247, 270, 272, 279, 298, 299, 316,
337, 363, 388, 389–​391, 394, 416, 422, 438, 439, 448, 450,
466, 469, 493, 498, 507, 520, 548, 575
Spitznagel, E.,  100, 108, 109, 111
Spitznagel, E. L.,  413, 416
Spoont, M. R.,  177, 347
Spracklen, K. M.,  74
Sprafkin, J.,  35, 49, 50, 56, 59, 78
Sprafkin, J. N.,  111
Sprenkle, D. H.,  545–​546
Sprich, S., 61
Spring, B.,  437
Spring, M. B.,  452
Spruyt, A.,  269
Spurrell, E. B.,  545, 547, 553, 554
Sroufe, L. A.,  219
Staal, J. B.,  616
Stadelmann, S.,  17, 22
Staehler, B. A.,  396
Staff, J., 50
Stafford, J.,  330
Staghezza, B., 81
Staghezza, G.,  113
Stahl, D.,  369
Staiano, A.,  590
Stalets, M.,  109
Staley, D.,  363
Stallings, C.,  436
Stallings, M. C.,  383
Stallings, P.,  222
Stallvik, M.,  394
Stambul, H. B.,  393
Stanford, E. A.,  587
Stang, P. E.,  331, 564
Stangier, U.,  244
Stanick, C. F.,  19, 20, 24
Stanley, B.,  113, 194, 195, 197, 204, 205
Stanley, M. A.,  250, 276, 277–​278, 293, 294
Stansbrey, R. J.,  177, 182
Stansfeld, S. A.,  158
Stanton, W., 75
Stapleton, L. M.,  110
Starcevic, V.,  160, 293–​294
 author Index 707

Stark, K. D.,  110, 117, 220, 231 Stevens, B. J.,  583, 584, 586, 592
Starr, L. R.,  243 Stevens, L.,  415, 426
Startup, H. M.,  299, 300 Stevens, L. H.,  385–​386
Startup, M.,  451 Stevens, S.,  447
Starz, T. W.,  616 Stevenson, J.,  220
Statham, D. J.,  395 Stewart, A.,  452
Stavem, K.,  611, 614 Stewart, D.,  371, 389
Stea, J. N.,  412, 418 Stewart, E. G.,  518
Stecher, V.,  527 Stewart, G. W.,  294
Stechuchak, K. M.,  565, 566 Stewart, M. O.,  132, 134
Steel, Z.,  331 Stewart, R. E.,  12, 24, 42, 142
Steele, C.,  165 Stewart, S. H.,  251, 274, 275, 281, 396, 421, 425
Steenbergh, T. A.,  422, 426 Stice, E.,  545, 549, 551, 552
Steenkamp, M. M.,  334, 347 Stiles-​Shields, E. C.,  549, 553
Steenweg-​de Graaff, J.,  111 Stinchfield, R.,  413, 414, 415, 416, 417, 420, 421, 424, 427
Steer, R. A.,  136, 157, 199, 200, 300, 301, 338, 340, 347, 498, Stinson, F. S.,  295, 296, 382, 413
553, 574, 575, 613 Stinson, J.,  583
Steers, W. D.,  527 Stinson, J. N.,  585, 586, 587, 588, 592
Stefanick, M. L.,  566 Stitt, L.,  614
Steffanowski, A.,  22, 24 Stjernswärd, S.,  443
Steffans, D. C.,  153 St. John, N. J.,  195
Stegemann, S. K.,  282 Stober, J.,  139
Steger, M. F.,  281 Stöber, J.,  303, 304
Steiger, H.,  548 Stockings, E. A.,  101
Steiger, J. H.,  340 Stokes, J., 17
Stein, B. D.,  18, 230 Stoll, A. L.,  180
Stein, D. J.,  331 Stone, A.,  21, 552
Stein, M. A.,  60 Stone, K. C.,  574
Stein, M. B.,  134, 250, 257, 267, 272, 275, 277, 294, 332 Stone, L. L.,  111
Stein, M. T.,  272 Stone, W. L.,  224
Stein, R. I.,  544, 545, 553 Stoop, T. B.,  330, 337
Steinberg, A. D.,  574 Stopsack, M.,  244
Steinberg, K.,  423 Storch, E. A.,  225–​226, 313
Steinberg, L.,  74, 530 Storheim, K.,  614
Steinberg, M.,  165 Stork, P. P.,  592
Steinberg, M. A.,  414, 416 Storms, G.,  181
Steiner, D. A.,  160 Stout, A. O.,  21, 53
Steiner, E. T.,  518 Stout, R. L.,  295, 397, 466, 470
Steingart, A.,  154 Stouthamer-​Loeber, M.,  49, 74, 176
Steinhausen, H. C.,  244 Stouthard, M. E. A.,  249
Steinley, D.,  382 Stover, A. M.,  21, 110
Steinman, K. J.,  361 Stoyanova, M.,  275, 279, 280, 281
Steinmetz, J.,  156 Strachan, A. M.,  447
Steketee, G.,  253, 282–​283, 313, 318, 321, 322–​323 Strakowski, S. M.,  180
Steketee, S.,  318 Strand, L. I.,  614
Stelk, W., 4 Strand, V. C.,  116
Stelniki, A. M.,  224 Strang, J.,  366, 389
Stender, J. P.,  270 Straus, M.,  500–​501
Stepanski, E. J.,  566, 575 Straus, M. A.,  344, 498, 503–​504
Stephan, S. H.,  20, 23 Straus, S. E.,  37, 38, 39
Stephen, S.,  574 Strauss, B. M.,  22, 24
Stephens, R. S.,  368, 369, 373 Strauss, D. H.,  180
Stephenson, R.,  301 Strauss, G. P.,  442
Steps, T.,  570 Strauss, J. S.,  435
Steptoe, A.,  499 Strauss, M. E.,  10, 470
Sterba, S. K.,  108, 205, 206 Street, A. E.,  330
Stern, E. R.,  312 Street, G. P.,  313
Stern, S. L.,  182 Strehle, J.,  156
Sternberger, L.,  323 Streim, J.,  159, 164
Stevens, B.,  586, 587, 588 Streiner, D.,  586, 592
708 author Index

Streiner, D. L.,  5, 10, 204 Surís, A., 17

Striegel-​Moore, R. H.,  543 Surman, C., 61
Stringaris, A.,  48, 52, 73, 100, 101, 102, 112 Suslow, T.,  268
Strober, M.,  175 Susman, V. L.,  469
Ströhle, A.,  281 Susser, E.,  437
Strom, S. E.,  617, 618 Susser, E. S.,  437
Stromeyer, S. L.,  54 Susskind, D.,  33, 39
Strong, D. R.,  393, 394, 419 Susskind, R.,  33, 39
Stroot, E. A.,  396 Sutton, K. S.,  529
Strosahl, K.,  199 Sutton, S. W.,  20
Struening, E. L.,  445 Suvak, M.,  334
Strumpf, N. E.,  161 Suvak, M. K.,  275, 335
Strunk, D. R.,  132, 134 Suyasa, M.,  162
Stuart, G. L.,  277 Suzuki, S.,  573
Stuart, S. P.,  vii Suzuki, T.,  499
Stucky, B.,  110 Suzuki, Y.,  159
Stukenberg, K. W.,  156, 160 Sveen, T. H.,  107, 108
Štulhofer, A.,  524, 531 Svensson, E.,  588
Sturt, E.,  445 Svensson, L.,  228
Styan, G.,  254 Sverd, J., 59
Styer, D. M.,  205 Swain, N. R.,  74
Styf, J.,  618 Swanke, J., 21
Su, J.,  220 Swann, A.,  175
Su, J. C.,  499 Swann, A. C.,  182
Su, T. P.,  374 Swannell, S. V.,  195
Suchday, S.,  275 Swanson, J., 59
Suchowersky, O.,  417 Swanson, J. M.,  59
Suddath, R. L.,  180 Swanson, S. A.,  218, 549, 553
Sue, S.,  473 Swartz, H. A.,  174, 180
Sugarman, D. B.,  344, 498, 503–​504 Swartz, M.,  295
Sugawana, Y.,  381 Swartz, M. S.,  437, 473
Sugaya, N.,  268 Swartzman, L. C.,  617
Sugimori, H.,  564 Sweeney, L., 86
Suh, E.,  499 Swendsen, J.,  100, 196, 218
Suh, S. Y.,  281 Swets, J. A.,  38
Suka, M.,  564 Swette, L.,  402
Sukhodolsky, D. G.,  226 Swift, J. K.,  392
Suling, A.,  156 Swift, R. M.,  371, 402
Sulla, E. M.,  53 Swigart, S.,  550
Sullivan, C. P.,  330 Swindle, R.,  490
Sullivan, G.,  445 Swinkels, R. A. H. M.,  618, 619
Sullivan, J.,  109, 111 Swinkels, S. H. N.,  61
Sullivan, J. T.,  389 Swinkels-​Meewisse, E. J. C. M.,  618, 619
Sullivan, K.,  222 Swinson, R.,  247
Sullivan, K. T.,  501 Swinson, R. P.,  143, 244, 246, 250, 252, 253, 256, 257, 276,
Sullivan, M. E.,  608 277, 575
Sullivan, M. J. L.,  529, 595, 596, 608, 613, 617 Sykora, K.,  389
Sullivan, R. J.,  569, 573 Sylva, K., 86
Summerfeldt, L.,  244 Symonds, T.,  522, 527, 528, 530
Summerfeldt, L. J.,  245, 246, 253, 257 Symons, F. J.,  584
Sunday, S. R.,  554 Symons, J.,  522
Sunderland, T.,  162, 165 Sysko, R.,  542, 545, 547, 548, 553, 554
Sundet, K. S.,  53 Szatmari, P.,  108, 114
Sundquist, J. O.,  436 Szer, I. S.,  594, 598
Sundquist, K.,  436 Szymanski, J.,  249
Sung, L.,  586, 587, 588
Sunohara, M.,  473 Tabakoff, B.,  385, 400, 402
Suominen, K.,  178 Tabb, L. C.,  117
Suppiger, A.,  20, 39, 387 Taber, J. I.,  413
Suraseranivongse, S.,  586 Tabrizi, M.,  115
 author Index 709

Tabscott, J. A.,  160 Telch, C. F.,  549

Taddio, A.,  583, 585, 587, 591, 598 Telch, M. J.,  276
Taft, C.,  333 Tellegen, A.,  609, 614
Taft, C. T.,  330, 340 Tenenhouse, A.,  614
Taghizadeh, P.,  200 Ten Have, T.,  154, 204
Taghva, A.,  525 Ten Have, T. R.,  394
Tai, G.,  596 Tenhula, W. N.,  440
Tait, G.,  586, 592 Tenney, N. H.,  19
Tait, R. C.,  613 Tenore, K.,  275
Takacs, L.,  385, 400, 402 Terdal, L. G.,  4, 226
Takwoingi, Y.,  178 ter Horst, G.,  249
Talajic, M.,  154 Teriot, P. N.,  162, 165
Talbot, F.,  276 Terracciano, A.,  468
Talbot, L.,  566, 570, 573 Terranova, A. M.,  73
Talbot, L. S.,  566 Terrell, H. K.,  422
Talbott, R.,  501 Terry, D. L.,  396
Talwar, P.,  448 Terry, J.,  479
Tan, G.,  618 Ter-​Stepanian, M.,  60
Tanaka-​Matsumi, J.,  493, 507 Tesler, M.,  589, 598
Tanay, G.,  133, 280 Tesler, M. D.,  589, 590, 598
Tandon, A.,  137 Tessari, E.,  387
Tandon, M.,  108 Tessler, R.,  448
Tandon, R.,  436, 442 Testa, S.,  282
Tang, A.,  598 Thapar, A.,  101, 107, 110
Tang, Y.,  134 Thapar, A. K.,  101, 107
Tanghoj, P.,  161, 165 Thase, M.,  133
Tannenbaum, L. E.,  72 Thase, M. E.,  180
Tannock, R.,  48, 59 Thaw, J. M.,  552
Tanofsky-​Kraff, M.,  545, 547 Thayer, J. F.,  256
Tansella, M.,  387 Theim, K. R.,  547
Tapia, M.,  524 Thennarasu, K.,  316
Targum, S. D.,  33 Theologou, A.,  180
Tarraf, W.,  154 Thibault, P.,  596
Tarrier, N.,  204, 447 Thibodeau, N.,  302, 305
Tarter, R.,  363 Thissen, D.,  40, 110
Tarter, R. E.,  387 Thissen, D. M.,  251
Tarver, D. J.,  337, 339 Thode, H. C.,  588
Tasca, G. A.,  498 Thom, B.,  385
Tasman, A.,  465, 475 Thoma, P.,  437, 448
Taub, J.,  11, 38 Thomas, C.,  21, 142
Tauber, R.,  445 Thomas, G.,  551, 552
Tay, L. K.,  176 Thomas, G. V.,  466, 469
Taylor, C. B.,  267, 268, 277, 282 Thomas, H. M.,  56
Taylor, C. L.,  547 Thomas, J. G.,  196
Taylor, D. J.,  564 Thomas, J. L.,  206, 331, 332
Taylor, E. B.,  177 Thomas, K. J.,  574
Taylor, J.,  22, 103 Thomas, R.,  267
Taylor, J. E.,  521 Thomas, R. G.,  337, 340
Taylor, J. F.,  521 Thomas, S.,  425
Taylor, K.,  204 Thomas, S. A.,  38, 104, 119, 254
Taylor, K. L.,  334, 337, 339, 343–​344 Thomas, S. E.,  384
Taylor, M. J.,  552 Thomas, S. J.,  572
Taylor, S.,  251–​252, 268, 274, 275, 318, 322, 618 Thomas, W.,  588
Taylor, W., 3 Thomas, Y. F.,  473
Tazeau, Y. N.,  3 Thomason, C., 59
Teachman, B. A.,  250 Thomassin, K.,  5, 102
Teague, G. B.,  451 Thompson, B., 9
Teasdale, J. D.,  133, 134, 135, 139, 140, 181, 448 Thompson, J. K.,  545
Teasell, R. W.,  617 Thompson, L.,  156
Teeple, M.,  389 Thompson, R.,  163, 593
710 author Index
Thompson, V. L.,  550
Thompson-​Hollands, J.,  4
Thomsa, C. H.,  620
Thomson, A.,  277
Thordarson, D.,  318, 322
Thordarson, D. S.,  318
Thorn, B. E.,  617
Thornby, J.,  618
Thornby, J. I.,  618
Thorndike, F. P.,  573
Thorndike, R. M.,  249
Thornicroft, G.,  444
Thornton, L. C.,  74, 75–​76, 84
Thorpe, L. E.,  332
Thygesen, K.,  413
Tiano, S.,  203
Tibbetts, S. G.,  83
Tibboel, D.,  584
Tibshirani, R., 33
Tidwell, M.,  416
Tiedemann, G. L.,  86
Tiefer, L.,  515
Tiemeier, H.,  111
Tien, A.,  158
Tierney, A.,  447
Tiet, Q. Q.,  72, 347
Tiffany, S. T.,  395, 396
Tillman, R.,  101, 107, 117
Timbremont, B.,  117
Timko, C.,  361
Timmons-​Mitchell, J.,  59
Timpano, K. R.,  269
Tinsley, R.,  269
Tirado, A.,  439
Tirrell, A.,  587, 598
Titus, J. C.,  364, 367–​368
Tkachenko, N.,  527
Tkachuk, G. A.,  619
Toates, F.,  517
Tobias, J. H.,  596
Toce, M.,  415
Toce-​Gerstein, M.,  415
Todd, D.,  618
Todd, F.,  529
Todd, K.,  529
Tohen, M.,  182
Tolin, D. F.,  251, 323, 325
Tollison, D.,  613
Tomaro, J.,  19, 20, 24
Tomaszewski, K. J.,  206
Tomenson, B.,  154
Tomko, R. L.,  360, 465
Tomlinson, D.,  586, 587, 588
Tomlinson, M.,  18, 22, 23
Tomlinson, R. M.,  599
Tompkins, J.,  597, 598
Tompkins, M. A.,  132, 138, 139
Tondo, L.,  174
Toneatto, T.,  421, 423, 426
Toner, B. B.,  182, 183
Tonetti, L.,  569–​570
Tonigan, J. S.,  368, 373, 392, 393, 394, 397
Tonigan, S.,  397
Topf, R.,  594
Toplak, M. E.,  48
Tor, S.,  345
Torgersen, S.,  223
Torrens, J.,  517
Touchon, J.,  564
Touliatos, J.,  503
Toupin, J.,  444
Touyz, S. W.,  86, 543
Towheed, T.,  614
Towle, L. H.,  156, 364, 439
Townsend, L.,  178
Towsley, G.,  162
Trabjerg, B.,  437
Tracy, J. I.,  449
Trafton, J. A.,  620
Trainor, K.,  156
Trajkovic, G.,  160
Tram, J. M.,  109
Tran, G. Q.,  282–​283
Tran, K. K.,  203
Tran, S. T.,  594, 595, 596, 598
Trapanatto, M.,  589
Trapnell, P.,  524
Trask, E.,  120
Trauer, T., 22
Trautman, K.,  388
Trautman, K. D.,  364, 367, 388
Treanor, M.,  281
Treat, T. A.,  277
Treboux, D.,  13n1
Treece, C.,  466, 467
Treffers, A.,  507
Treisman, G. J.,  452
Treloar, C.,  392
Tremblay, I.,  596
Tremblay, M.,  297
Tremblay, R. E.,  72
Tremblay, S.,  425
Trepanier, K. L.,  252
Treuer, T.,  180
Trevisan, M.,  393
Trexler, L.,  113
Trezise, L.,  279
Trigwell, P.,  138–​139
Tristan, J.,  549
Trivedi, M. H.,  136, 138–​139, 161, 165
Trombello, J. M.,  491
Troutman, J. A.,  618
Trower, P.,  253
Truax, P.,  305
Truchon, M.,  619
Trufan, S. J.,  220
Truglia, E.,  266
Trull, T. I.,  360
Trull, T. J.,  24, 465, 470
Trumbetta, S. L.,  437
 author Index 711

Truong, T.,  345 Undurraga, J.,  175–​176

Tryon, W.,  439 Ung, D.,  226
Tsai, J.,  103, 341 Ungerer, J. A.,  219
Tsai, W. J., Jr.,  374 Ungvari, G. S.,  42
Tsai, Y., 59 Unruh, A.,  583
Tsang, A.,  609 Unruh, A. M.,  584
Tsang, H. W. H.,  446 Unsicker, J.,  364, 367–​368
Tsao, J. C.,  268, 270 Unützer, J.,  163
Tsao, J. C. I.,  599 Urbano, R. C.,  119
Tsao, J. W.,  332 Urbina, S.,  177
Tsao, L. I.,  374 Ureno, G.,  545, 553
Tsemberis, S.,  437 Urmston, M.,  619
Tu, F.,  529 Urosevic, S.,  177
Tu, X.,  142 Ursano, R. J.,  334
Tucker, J. A.,  393 Ustun, B.,  137
Tuckwell, V.,  157 Ustün, T. B.,  138, 245, 273, 337, 338, 439
Tükel, R.,  243 Usui, W. M.,  280, 281
Tulloch, T. G.,  302 Utens, E. M.,  243
Tully, E. C.,  361 Utian, W. H.,  522
Tulshi, D. S.,  362, 363 Uzark, K.,  594, 598
Tungström, S.,  451
Tuninger, E.,  443 Vacca, I.,  198
Tural, Ü.,  273 Vaccaro, D.,  361
Turcotte, J.,  30, 302, 305 Vaccaro, P.,  521
Turgay, A., 61 Vacha-​Haase, T.,  9, xi
Turk, C. L.,  251, 296, 298 Vadhan, N. P.,  442
Turk, D. C.,  583, 608, 610, 612–​613, 614, 615, 616, 620, 621 Vaewsorn, A.,  549
Turkheimer, E.,  472 Vaez, E.,  491
Turnbull, O.,  180 Vagg, P. R.,  338, 340, 346
Turner, B. J.,  206 Vahia, I. V.,  153
Turner, J. A.,  617, 618, 620 Vail, A., 33
Turner, J. B.,  204, 331 Valadez, C.,  397
Turner, K.,  343, 435 Valenti, M.,  175–​176
Turner, L. V.,  4 Valentine, A. Z.,  53
Turner, N. E.,  370, 414, 417, 421 Valentiner, D. P.,  250
Turner, R. J.,  103 Valenzuela, D.,  592
Turner, S. M.,  218, 224, 229, 233, 250, 253 Valeri, S. M.,  109
Turner-​Bowker, D. M.,  614 Valiquette, C. A.,  444
Turner-​Stokes, L.,  617 Valkenburg, A. J.,  584
Turon-​Estrada, A.,  153–​154 Valla, J. P.,  108
Turse, N. A.,  331 Vallières, A.,  564, 570, 572, 573
Turvey, C. L.,  156 Valtonen, H.,  178
Tuschen-​Caffier, B.,  256 Vana, J. E.,  393
Tuttas, M. L.,  596 Vanable, P. A.,  438
Tuttle, D. H.,  617 Vanaelst, B.,  115
Twamley, E. W.,  445 van Ameringen, M.,  257
Twycross, A.,  583 Van Ameringen, M.,  254
Tyler, L., 84 Van Audenhove, C.,  181
Tylka, T. L.,  545 van Balkom, A. J.,  276, 295
Tynelius, P.,  437 van Beek, N.,  268
Tyson, R.,  498 van Boeijen, C. A.,  276
van Breukelen, G. J.,  618
Uddin, L. Q.,  134 Van Citters, A. D.,  599
Uebelacker, L. A.,  181 van Daal, C.,  111
Uher, R.,  437 Van Dam, D.,  347
Uhlmansiek, M. H.,  340 Van Dam, N. T.,  158
Ulmer, C.,  575 Van Damme, S.,  613
Ulrich, R. F.,  50, 451 VandeCreek, L., 3
Umegaki, H.,  159 van den Berg, B.,  178
Umphress, V. J.,  137, 143 van den Brink, M.,  592
712 author Index

van den Brink, W.,  178 Varker, T.,  334

van den Hout, M. A.,  269 Varney, S. M.,  369
Vander Bilt, J.,  273, 414 Varni, J. W.,  585, 593, 594, 598
van der Ende, J.,  104, 111, 177 Vasa, R. A.,  102
van der Gaag, M.,  440 Vasey, M. W.,  220
Vanderhallen, I.,  251 Vasterling, J. J.,  332, 333, 344
van der Hulst, M.,  621 Vatten, L. J.,  564
Van der Kroft, P. J. A.,  479 Vaughn, A. J.,  52, 53
van der Laan, P. H.,  84 Vaughn, B. V.,  566
van der Mast, R. C.,  152, 153, 161 Vaughn, C.,  447
van der Maten, M.,  111 Vaughn, G. E.,  545
Van der Staak, C. P. F.,  392 Vaught, M. H.,  593
Vander Stoep, A.,  63 Vause, E.,  587, 588, 598
van der Velden, A. M.,  135 Vauth, R.,  446
van der Weijden, T.,  392 Vázquez, G.,  174
van der Woudon, J. C.,  583 Vázquez-​Barquero, J. L.,  444
Vandrey, R. G.,  364 Veague, H. B.,  18, 19
van Duijn, C. M.,  52 Veale, D.,  250, 251
van Dulmen, M.,  133, 139, 140 Vedel, E.,  347
van Dyck, R.,  276, 282 Veenstra, M.,  594
Van Dyke, C.,  163 Veerbeek, M. A.,  22
Van Eek, H.,  596 Vela-​Bueno, A.,  564
van Eijk, J. T. M.,  159, 163 Velamoor, V. R.,  203
van Goozen, S. H. M.,  75, 83–​84 Veldhuizen, S.,  437
van Hasselt, V. B.,  155–​156, 160, 548 Velex-​Borras, J.,  59
van Hoeken, D.,  542 Vélez-​Pastrana, M. C.,  61
van Hooren, S.,  161 Velicer, W. F.,  371, 394
Van Horn, Y.,  72 Vella, L.,  445
Van Houdenhove, B.,  613 Velligan, D.,  440
Van Hulle, C.,  119 Venta, A.,  200
Van Hulle, C. A.,  111, 119 Ventafridda, V.,  609
Van Humbeeck, G.,  181 Ventura, J.,  135, 247, 440, 442
van Korlaar, I.,  587 Ventura, T.,  157
van Lankveld, J. D. M.,  517 Verbeek, A. L. M.,  618, 619
van Megen, H. J. G. M.,  19 Verbout, A. J.,  614
van Meijel, B.,  440 Verbraak, M.,  277
Van Meter, A.,  5, 12, 24, 35, 36, 40, 41, 42, 233 Verburg, K.,  268
Van Meter, A. R.,  198 Verdeli, H.,  18, 23, 120
van Minnen, A.,  334 Verdes, E.,  137
van Ommeren, M.,  330, 331, 345 Verga, B. G.,  598
van Oppen, P.,  141, 276, 323 Verheul, R.,  474, 479
van Os, J.,  437 Verhulst, B.,  383
van Overveld, M.,  251 Verhulst, F. C.,  52, 104, 177, 243, 594
van Reekum, R.,  162 Vermeersch, D. A.,  4, 137, 143, 144, 145
van Rooijen, L.,  387, 394 Vermes, D.,  253
Van Ryzin, M. J.,  382 Vernberg, E. M.,  59, 219
van Schaik, D. J.,  141 Vernon, S. W.,  175
Van Slyke, D. A.,  595 Vernooij-​Dassen, M. J. F. J.,  161
van Stel, H. F.,  614 Verra, M. L.,  616
Van Straten, A.,  154 Verstraeten, K.,  595
van Suijlekom-​Smitd, L. W. A.,  583 Vertommen, H.,  181
van Tilburg, M.,  590 Vervoort, T.,  595, 596
van Tilburg, W.,  295 Vesselinov, R.,  440
van Widenfelt, B. M.,  228, 507 Vetter, T. R.,  592
van Zaane, J.,  178 Vgontzas, A. N.,  564
Vapnik, T.,  278 Vickers, K.,  269
Vara, L.,  547 Victor, S. E.,  205
Varese, F.,  180, 437 Victor, T. W.,  542
Varga, M.,  180 Vida, S.,  161, 162, 165
Varghese, M.,  157 Vidaver, R. M.,  448
 author Index 713

Viding, E., 76 Vries, P. J.,  56, 62

Viding, E. M.,  71, 74, 75 Vuchinich, R. E.,  393
Viechtbauer, W.,  37, 437 Vuorilehto, M. S.,  199
Vieira, R. X.,  524
Vielhauer, M.,  343 Waara, J.,  281
Vieta, E.,  175–​176, 178, 182 Waddell, G.,  619
Vignozzi, L.,  521 Waddell, M.,  271
Vikan, A.,  594 Waddell, M. T.,  338
Vilalta-​Franch, J.,  153–​154 Wade, J. H.,  447
Vilardaga, J. C. P.,  280 Wade, M.,  347
Villabø, M.,  223 Wade, T. D.,  35, 252
Villabø, M. A.,  223 Wade, W. A.,  277
Villagran, J.,  178 Wadkins, M., 23
Villañueva, M.,  301, 344 Wadsworth, M. E.,  111
Villarruel, A.,  586, 587 Wagers, T. P.,  501
Villasenor, V. S.,  545, 553 Wagner, A.,  196, 197
Vincent, C.,  583 Wagner, A. K.,  614
Vinogradov, A.,  275 Wagner, E.,  163
Vinokur, A.,  387, 394 Wagner, G.,  522
Virtue, C.,  200 Wagner, H. R.,  153, 330, 331
Virues-​Ortega, J.,  4 Wahl, K.,  139
Visser, J. H.,  104 Wahler, R. G.,  78
Visser, S.,  276 Wakschlag, L. S.,  49, 74, 88
Viswanathan, M.,  555 Walco, G. A.,  583
Vitaro, F., 72 Waldinger, M. D.,  516, 518
Vitiello, B.,  59, 102, 117 Waldman, I. D.,  75, 83, 119
Vito, D.,  494 Waldron, S. A.,  585
Vitousek, K. B.,  553 Walfish, S., 19
Vitousek, K. M.,  551, 552 Walker, B. L.,  574
Vivian, D.,  13n1, 500, 502 Walker, D. C.,  553
Vlaeyen, J. W.,  596, 617, 618 Walker, E. A.,  341
Vlaeyen, J. W. S.,  608, 618, 619 Walker, G. M.,  53
Voderholzer, U.,  564 Walker, H. M.,  84
Voepel-​Lewis, T.,  500, 583, 586 Walker, L.,  524, 593
Vogel, H. S.,  449 Walker, L. S.,  585, 592, 593, 595, 598
Vogt, D.,  344 Walker, M.,  415, 423
Vogt, D. S.,  344 Walker, R. L.,  202
Vohlídka, P.,  452 Walker, R. S. W.,  199
Vojta, C.,  183 Walker, S. N.,  612
Volberg, R. A.,  415, 416, 417, 418 Walkup, J. T.,  204
Volkert, J.,  156 Wall, P. D.,  583, 584, 608
Vollenbroek-​Hutten, M. M. R.,  621 Wallace, C. J.,  445
Vollendorf, C.,  446 Wallace, D. P.,  224, 595
Volpe, R. J.,  58 Wallace, J.,  445
Volpicelli, J. R.,  395–​396 Wallace, R. B.,  156
Vona, P. L.,  230 Wallach, M. A.,  448
von Baeyer, C. L.,  583, 584, 586, 587, 588, 598 Wallier, J.,  544
Voncken, M. J.,  250, 252 Walls, M. M.,  249
Vonderlin, E.,  197, 200 Wallwork, R. S.,  440
von Eye, A.,  48 Walsh, B. T.,  542, 545, 547, 548, 549, 550, 551, 552, 553, 554
von Knorring, A. L.,  108 Walsh, B. W.,  197
Von Korff, M.,  564, 609 Walsh, C.,  114
Von Ungern-​Sternberg, B. S.,  587 Walsh, D. A.,  617
Vorstenbosch, V.,  250 Walsh, J. A.,  50
Voshaar, R. C. O.,  22 Walsh, K. J.,  503
Vostanis, P.,  110, 117, 118 Walsh, L.,  12, 24, 42, 142
Votta-​Bleeker, E.,  585 Walsh, M. A.,  178
Vowles, K. E.,  596 Walsh, M. M.,  88
Vrana, S.,  343 Walster, E.,  545
Vrana, S. R.,  251, 339 Walter, B.,  104
714 author Index

Walter, O. B.,  199 Waters, A. M.,  220

Walters, A. S.,  592 Waters, E. B.,  13n1
Walters, E.,  331, 343 Waters, W. F.,  568t
Walters, E. E.,  62, 131, 173, 243, 266, 267, 272–​273, 294, Watkins, B.,  547
295, 313 Watkins, E. R.,  132, 133
Walther, L.,  385 Watkins, L. E.,  330
Walton, D.,  619 Watkins, M. W.,  51
Walton, M. A.,  359 Watson, A. C.,  446–​447
Walzer, E. A.,  180 Watson, D.,  10, 143, 179, 218, 248, 250, 268, 323, 324, 466,
Wamboldt, F. S.,  107 470, 476
Wamboldt, M. Z.,  107, 491 Watson, L. C.,  155
Wampler, R. S.,  490 Watson, P. J.,  619
Wan, Y.,  542 Watson, R.,  447
Wanberg, K. W.,  393 Watson, S. B.,  343
Wandersman, A., 22 Wattar, U.,  135
Wang, A.,  517 Watters, C. A.,  103
Wang, G., 42 Watts, F. N.,  279
Wang, L.,  59, 341 Waugh, C. E.,  134
Wang, M.,  38, 104, 119 Waugh, M. H.,  466, 467, 470, 474
Wang, M.-​C.,  203 Waxman, S.,  552
Wang, N.,  414, 415, 425 Waxman, S. E.,  528
Wang, P., 99 Waxmonsky, J. G.,  60
Wang, P. P.,  60 Wayland-​Smith, D.,  17
Wang, P. S.,  132, 204 Weatherley-​Jones, E.,  574
Wang, R.,  341 Weatherly, J. N.,  422
Wang, S.,  153, 252, 253, 473 Weathers, F.,  337, 339, 343
Wang, T.,  273, 531 Weathers, F. W.,  331, 334, 336, 337, 338, 339, 340, 341, 343, 440
Wang, W. L.,  374 Weaver, T.,  392
Wang, Y. C.,  499 Webb, R. T.,  437
Ward, A.,  118 Webb, T. L.,  145
Ward, D. E.,  41 Webber, M. P.,  332
Ward, D. M.,  86 Weber, J.,  134
Ward, J. A.,  589, 590, 598 Weber, S.,  417
Wardenaar, K. J.,  161 Weber Rouget, B.,  178
Ware, A. L.,  56 Webster, I., 59
Ware, J. E.,  163, 344, 389, 445, 614 Webster-​Stratton, C.,  74, 81, 86
Wareham, J., 84 Wedervang-​Jensen, T.,  159, 161
Warman, M.,  232, 233 Wedig, M. M.,  193
Warner, M.,  155 Weedman, R. D.,  392
Warner, V.,  115 Weeks, J. W.,  245, 251
Warnick, E.,  220, 231 Weems, C.,  218
Warren, C. S.,  552 Weems, C. F.,  218, 219, 220, 222, 225, 233
Warren, K. A.,  443 Weems, C. G.,  233
Warren, R. F.,  614 Weerarathnege, K.,  332
Warren, S. L.,  219 Weersing, V. R.,  101, 112, 113, 119, 220
Warschburger, P.,  547 Weerts, T. C.,  249, 282
Warshaw, M. G.,  294, 295 Wehr, T. A.,  174
Waschbusch, D. A.,  57, 59, 60, 73 Wei, C.,  223
Washburn, J. J.,  24, 33, 35, 176, 205 Wei, J.,  251
Wasserman, D. A.,  365, 394 Wei, J. M.,  618
Wasserman, G. A.,  72 Weidacker, K.,  139
Wasserman, J. D.,  9 Weiden, P.,  443
Wasserstein, J., 62 Weight, D. G.,  281, 282
Wasserstein, S. B.,  225 Weijmar Schultz, W.,  515
Wassick, S.,  177 Weijmar Schultz, W. C. M.,  517
Watanabe, H. K.,  79, 87 Weil, J., 88
Watanabe, K.,  443 Weiller, E.,  363, 364, 389, 439
Watanabe, M.,  609 Weinberg, W. A.,  117
Watanabe, N.,  273 Weinberger, D. R.,  437, 440
Waternaux, C.,  552 Weiner, A.,  200
 author Index 715

Weinfurt, K. P.,  53, 140 Wespes, E.,  527

Weinman, J.,  613 Wessa, M.,  340
Weinraub, M.,  219 Wesselmann, U.,  517
Weinrott, M. R.,  86 West, J. A.,  180
Weinstein, J. N.,  599 West, R.,  369
Weinstock, J.,  417, 421 West, S. A.,  180
Weinstock, L. M.,  181 Westbrook, D.,  294
Weintraub, S.,  102 Westefeld, J. S.,  203
Weis, S.,  17, 22 Westen, D.,  11, 465, 467, 471, 472
Weisberg, R. B.,  267, 273, 520 Westenberg, H. G. M.,  19
Weisler, R. H.,  250 Westerberg, M. W.,  228
Weisman, A. Y.,  436 Westerberg, V. S.,  396
Weisman, N. M.,  158 Westermeyer, J.,  382
Weisman, S. J.,  594, 595 Westervelt, A.,  103
Weiss, B.,  109, 117 Westling, B. E.,  276
Weiss, D.,  339 Westphal, J.,  365
Weiss, D. S.,  331, 337 Westra, H. A.,  251
Weiss, G.,  517 Wetherell, J. L.,  574
Weiss, K. E.,  595 Wetton, S.,  444
Weiss, L. T.,  599 Wetzler, S.,  200
Weiss, M., 59 Wewers, M. E.,  588
Weiss, M. D.,  50, 60 Whaley, S. E.,  220
Weiss, M. G.,  439 Wheatley, M. V.,  162
Weiss, R. D.,  360 Wheaton, M. G.,  252, 268, 313, 324, 325
Weiss, R. L.,  502 Wheeler, J.,  498
Weiss, S. M.,  608 Wheeler, L. C.,  613
Weissenburger, J. E.,  161 Whelan, J. P.,  421, 422, 426
Weissman, A.,  113, 180, 198 Whipple, J. L.,  37, 143, 144, 145
Weissman, A. N.,  553 Whisenhunt, B. L.,  552
Weissman, M.,  178, 444 Whisman, M. A.,  200, 490, 491, 493, 494, 498, 500, 501, 505
Weissman, M. M.,  18, 23, 120, 134, 140, 444, 545 Whitbeck, J.,  445
Weisz, J.,  101, 113, 115 White, H. R.,  393, 400
Weisz, J. R.,  4, 5, 7, 17, 40, 41, 102, 103, 109, 111, 117, 118, White, J.,  498
143, 145 White, K. S.,  269, 277, 279, 280, 281
Weitz, E.,  116 White, L.,  445
Weizman, T.,  200 White, M.,  364, 367–​368, 592
Welburn, K.,  160, 162–​163, 164, 165 White, M. A.,  553
Welch, R. R.,  544, 545, 553 White, M. T.,  595–​596
Welham, J.,  437 White, S. F.,  84
Weller, E. B.,  108, 182 White, S. W.,  250
Weller, R. A.,  108, 182 White, S. W., III,  225
Wellings, K.,  516, 517 Whiteford, H. A.,  101
Wells, A.,  294, 296, 302 Whitehead, W. E.,  595
Wells, C.,  341 Whitehouse, W. G.,  177
Wells, K.,  117, 204 Whiteside, S. P.,  19, 224, 317
Wells, K. C.,  60, 72, 80, 88 Whitfield, K.,  154
Wells, S. Y.,  333 Whitfield-​Gabrieli, S.,  134
Wells A.,  256 Whitley, B. E.,  163
Welsh, D.,  199 Whitley, E.,  437
Welsh-​Bohmer, K. A.,  153 Whitlock, E. P.,  155
Welte, J.,  416, 476 Whitlock, J.,  195, 206
Weltzin, T. E.,  554 Whitman, J. M.,  619
Wendt, S.,  547 Whitmer, A. J.,  133, 134
Wengel, S. P.,  162 Whitmer, K.,  574
Wenzel, K.,  479 Whittington, C.,  144
Wenzel, K. R.,  417 Whooley, M. A.,  330
Wenzel, R.,  202 Whybrow, P. C.,  174, 183
Werner, D.,  451 Wicherts, J. M.,  334
Wertenberger, E.,  204 Wichstrøm, L.,  107, 108
Wertz, J. S.,  368, 369 Wicker, P. A.,  527
716 author Index

Wickramaratne, P.,  18, 23, 120 Williams, R. J.,  417, 418

Wicks, S.,  436 Williams, S. E.,  595
Wickwire, E. M.,  415 Williams, S. L.,  278, 279, 281
Widiger, T. A.,  464, 465, 466, 467, 468, 469, 470, 471, 472, Williams, T. F.,  477
473–​474, 475, 476, 477, 478 Williams, V.,  442
Wiebe, S. A.,  498 Williamson, D. A.,  552
Wieczorek, W.,  416 Williamson, D. E.,  115
Wieder, G. B.,  502 Williamson, D. J.,  198
Wiederman, M. W.,  200 Williamson, G. M.,  592
Wiegel, M.,  521 Williford, W. O.,  174
Wiersma, D.,  440 Willoughby, F. W.,  400
Wiersma, J. E.,  141 Willoughby, M., 72
Wigal, S. B.,  59 Willoughby, M. T.,  59
Wigal, T., 59 Willoughby, S. G.,  613
Wight, R. G.,  103 Wills, R. M.,  498
Wightman, J., 4 Wills, T. A.,  361
Wilberg, T.,  243 Wilner, N.,  338
Wilcox, H.,  113 Wilson, A. C.,  592, 593
Wilcox, M.,  344 Wilson, G. T.,  542, 544, 545, 546, 547, 548, 549, 551, 552, 553,
Wilcox, R.,  158 554, 555
Wild, J.,  621 Wilson, J. P.,  340
Wilde, J.,  445 Wilson, K.,  160, 161, 165
Wildes, J. E.,  545, 553 Wilson, K. A.,  301
Wiley, J. F.,  230 Wilson, L. C.,  344
Wilfley, D. E.,  544, 545, 546, 547, 553, 554 Wilson, M. G.,  550
Wilhelm, E. M.,  268 Wilson, S. B.,  218
Wilhelm, F. H.,  268 Wilson, W.,  256
Wilhelm, K.,  153 Wincze, J.,  516, 517, 521
Wilhelm, S.,  313, 318, 321, 324 Wincze, J. P.,  520
Wilk, J. E.,  206, 331, 341 Windle, M.,  421
Wilkens, P.,  614 Winefield, A. H.,  425
Wilkie, D.,  589, 598 Winemiller, D.,  499
Wilkie, D. J.,  589, 590, 598 Wing, J.,  156, 364, 439
Wilkinson, L.,  617 Wing, J. K.,  156, 157, 447
Wilkinson, P.,  102, 106, 117, 118 Winograd, R. P.,  384
Wilkinson, S. T.,  437 Winokur, G.,  116, 394
Willcutt, E. G.,  48, 50 Winslow, R.,  17, 105
Williams, A.,  588 Winter, M. R.,  385
Williams, B.,  159, 163 Winters, A., 73
Williams, C.,  277, 281, 282 Winters, K.,  387
Williams, D.,  193, 195, 201 Winters, K. C.,  19, 414, 415, 416, 417, 420, 421, 424
Williams, D. A.,  615, 617 Winters, N. C.,  106, 109, 110, 112, 113, 114, 117, 118
Williams, D. R.,  201, 332 Winters, R.,  180
Williams, J.,  272, 273, 316, 337, 621 Winterstein, A. G.,  435
Williams, J. B.,  175, 270, 272, 279, 337, 388, 416, 439, 466, Wirshing, D. A.,  444
469, 575 Wirshing, W. C.,  444
Williams, J. B. W.,  135, 136, 155, 159, 162, 163, 165, 175, 178, Wirtz, P. W.,  397
246, 247, 298, 299, 363, 389–​391, 416, 422, 438, 448, 493, Wisco, B.,  133
498, 507, 520, 548 Wisco, B. E.,  330, 331
Williams, J. M. G.,  133, 134, 139, 140 Wise, E.,  500
Williams, J. R.,  161 Wisniewski, S. R.,  179, 180, 181
Williams, J. W.,  136, 337, 347 Wisting, L.,  542
Williams, K.,  528 Witkiewitz, K., 76
Williams, L. J.,  178 Witt, E. A.,  542
Williams, L. L.,  220 Witt, K.,  436
Williams, M.,  177, 587, 598 Wittchen, H. U.,  153, 156, 175, 243, 244, 247, 266, 267, 270,
Williams, M. A.,  575 281, 294, 295, 296, 364, 439
Williams, N. A.,  382 Witte, B.,  17, 18, 22, 156, 270
Williams, N. J.,  24 Witte, S.,  272
Williams, N. L.,  251 Witte, T.,  195
 author Index 717

Witte, T. K.,  198, 199 Worley, K., 56

Witten, D., 33 Worley, S.,  598
Witter, J.,  620 Wormdal, A. K.,  107
Wittmann, W. W.,  22, 24 Wormnes, B.,  256
Woby, S. R.,  619 Worsley, R.,  517
Woerner, M.,  451 Wotring, J., 81
Wohlfahrt, H.,  17, 105 Woznica, A.,  269
Wohlgemuth, W. K.,  566, 569, 570, 573 Wright, A. C.,  476
Wojtowicz, A.,  595 Wright, C. V.,  3
Wolf, E. J.,  330, 331, 337 Wright, D.,  585
Wolf, S.,  383 Wright, K.,  180, 183
Wolf (Adelv Unegv Waya), S.,  370 Wright, K. M.,  347
Wolfe, B. E.,  227 Wrightsman, L. S.,  5
Wolfe, J.,  330, 343 Wu, C., 59
Wolfe, R.,  443 Wu, C. C.,  180
Wolff, P. L.,  218 Wu, K.,  323, 324
Wolford, G. L.,  448 Wu, K. D.,  466, 467, 475, 476, 479
Wolfson, C.,  162, 165 Wu, L.,  473
Wolfstetter-​Kausch, H.,  177 Wu, M.,  59, 542
Wolitzky-​Taylor, K. B.,  133 Wu, T. F.,  499
Wolk, S.,  120, 545 Wu, Y.-​S.,  178
Wolk, S. L.,  549, 554 Wulfert, E.,  414, 415, 425
Wolke, D.,  101 Wullaert, R.,  117
Wolpe, J.,  248, 278 Wunderlich, G.,  524, 528
Wolpert, M.,  21, 22 Wunderlich, G. R.,  528
Wolraich, M. L.,  53, 56 Wuyek, L. A.,  273
Wonderlich, S.,  551, 552 Wyatt, J. K.,  565, 566, 567
Wonderlich, S. A.,  542, 544, 548, 551, 552 Wyatt, R. J.,  437
Wong, C. M.,  426 Wykes, T.,  444, 445
Wong, D. G.,  526 Wynne, H.,  413, 414, 417
Wong, D. L.,  588
Wong, G.,  184 Xia, Y.,  567
Wong, J.,  252 Xiang, Y. T.,  42
Wong, M. M.,  22, 57 Xiao, L., 42
Wong, N.,  252 Xie, H.,  451
Wongpakaran, N.,  162 Xie, S. X.,  204
Wongpakaran, T.,  162 Xu, D.,  435
Woo, B., 55 Xu, S., 10
Wood, A.,  110, 117 Xue, S.,  251
Wood, C.,  583, 587, 598 Xue, Y., 81
Wood, J., 3
Wood, J. J.,  222, 225–​226 Yagelka, J. R.,  442
Wood, J. M.,  217, 465, 471 Yakovenko, I.,  413
Wood, M. M.,  394 Yale, S. A.,  180
Wood, S.,  162 Yamada, J.,  583, 586, 587, 588
Woodruff-​Borden, J.,  280, 281 Yamada, K.,  443
Woods, C. M.,  247, 250, 251, 253 Yamagata, S.,  468
Woods, M. G.,  340 Yamamoto, I.,  273
Woods, M. P.,  618 Yamauchi, K.,  443
Woods, S. W.,  218, 273, 280 Yanchar, S.,  137, 143
Woodson, B. T.,  566 Yang, B.,  199
Woodward, L. J.,  225 Yang, F.,  158
Woody, C.,  446 Yang, J. C.,  278
Woody, G. E.,  367 Yang, S. J.,  180
Woody, S.,  251 Yanovski, J. A.,  547
Woolf, C. J.,  583 Yanovski, S. Z.,  547
Woolston, J.,  220, 231 Yao, L.,  332
Woottiluk, P., 59 Yao, S.-​.,  276
Wootton, J. M.,  76, 84 Yarber, W. L.,  503, 518
Worhunsky, P. D.,  134 Yarema, K. T.,  162
718 author Index

Yarnold, P. R.,  53, 140 Yu, L.,  107, 109, 110, 118, 397, 398
Yasuda, S.,  268 Yu, L. N. H.,  302
Yates, B. T.,  11, 38 Yu, N.,  414, 417
Yazdi, K.,  194, 205 Yu, S.,  103
Ybarra, M.,  158 Yu, Z.,  609
Ye, J.,  131 Yuan, N.,  343
Yeager, D. E.,  347 Yuan, Y.,  526
Yee, A. M.,  109, 182 Yucel, M.,  383
Yeh, C.-​H.,  586, 587 Yücel, M.,  448
Yeh, K. H.,  499 Yuen, G. S.,  134
Yeh, M.,  33, 86 Yüksel, Ç.,  243
Yeh, M. L.,  180 Yule, M.,  521, 522, 527, 531
Yehuda, R.,  543 Yule, W.,  233
Yemez, B.,  275 Yurgil, K. A.,  332
Yen, C. F.,  180 Yusof, N.,  224
Yen, J. Y.,  180
Yen, S.,  470 Zabala, J., 24
Yeo, M.,  546 Zaccario, M., 17
Yershova, K. V.,  113, 194, 195, 197, 204 Zacchello, F.,  589
Yesavage, J. A.,  158, 159 Zack, M.,  421
Yiend, J.,  160 Zagoory-​Sharon, O.,  220
Yoerger, K., 83 Zajecka, J.,  178
Yolken, R.,  436 Zalta, A. K.,  199
Yonkers, K. A.,  267, 294 Zammit, G. K.,  469
Yook, K.,  281 Zanarini, M. C.,  272, 299, 466, 469, 471, 548
Yook, K.-​H.,  281 Zane, G.,  278
Yoon, G.,  382 Zang, Y.,  338, 340
York-​Cooler, C.,  116 Zaninelli, R.,  415, 426
Yoshida, E.,  268 Zanis, D.,  392, 448, 451
Yoshida, K.,  564 Zarate, R.,  269
You, S. D.,  35 Zarin, D.,  272
Young, A. H.,  33 Zarit, S.,  448
Young, A. S.,  442, 445, 446 Zarkov, Z.,  180
Young, B.,  586 Zasepa, E., 4
Young, C. A.,  612 Zaslavsky, A. M.,  105, 153, 267
Young, D.,  178 Zayfert, C.,  596, 618
Young, J., 57 Zazzali, J. L.,  3
Young, J. F.,  200 Zebb, B. J.,  280
Young, K.,  397 Zeigler, H.,  526
Young, K. M.,  397 Zeiss, A. M.,  138, 154
Young, L.,  257, 466, 471 Zeitzer, L.,  583
Young, M. E.,  181 Zelazny, J.,  117
Young, R. A.,  529 Zeller, P. J.,  175
Young, R. C.,  153, 154, 161, 165, 181, 182, 469 Zeltzer, L. K.,  599
Young, R. M.,  395, 397 Zeman, J. L.,  595
Young, S. L.,  446 Zeman, L. D.,  21
Young Ahn, T.,  516, 518 Zen, A. L.,  330
Young-​McCaughon, S.,  204 Zenilman, J.,  387
Youngren, M. A.,  138 Zera, M., 73
Youngstrom, E.,  24, 36, 75, 104, 176, 233 Zetsche, U.,  139
Youngstrom, E. A.,  4, 5, 12, 21, 24, 32, 33, 34, 35, 36f, 37, Zhang, B.,  341
40, 41, 42, 52, 102, 107, 108, 109, 110, 176, 177, 178, 181, Zhang, C.,  251
182, 198 Zhang, H.,  330, 331, 332, 334, 362, 363, 381, 382, 384, 389
Youngstrom, J. K.,  12, 24, 33, 35, 36, 40, 41, 75, 176, 233 Zhang, J.,  251, 341
Young-​Wolff, K. C.,  383 Zhang, Q.,  117
Yount, D.,  162, 165 Zhang, S.,  499
Yount, S., 21 Zhang, W.,  332
Youssef, N. N.,  598 Zhang, Z.,  526
Yu, B. H.,  278 Zhao, S.,  174, 295, 296, 330
Yu, D.,  542 Zheng, Y., 74
 author Index 719

Zhong, J.,  338, 340 Zohsel, K.,  596

Zhong, Q.,  575 Zolkowska, K.,  437
Zhou, C.,  63, 595 Zoller, J. S.,  347
Ziegler, J.,  587 Zonderman, A. B.,  153
Ziegler, J. B,  587 Zuardi, A. W.,  243
Ziegler, J. B.,  586 Zubin, J.,  437
Ziegler, V. E.,  181, 182 Zubritsky, C.,  154
Zieldorff, C.,  243 Zucchi, T.,  544
Zimering, R. T.,  333, 334, 343–​344 Zucker, B. G.,  275
Zimerman, B.,  177 Zucker, R. A.,  361, 382
Zimmerman, J.,  200, 479 Zuckerman, S. P. D.,  200
Zimmerman, M.,  105, 161, 165, 174, 178, 273, 296, 465, 466 Zuellig, A. R.,  298
Zimmermann, R. P.,  19 Zung, W. W. K.,  159
Zinbarg, R.,  269, 270, 312 Zúñiga-​Lagares, A.,  444
Zinbarg, R. E.,  268, 274, 275 Zupan, B. A.,  80
Zinser, M. C.,  178 Zvolensky, M. J.,  252, 268, 269, 274, 275, 278, 281
Zinzow, H. M.,  437, 440 Zweben, A.,  397, 401
Zipfel, S.,  272, 544 Zwick, W. R.,  369
Zisook, S.,  154 Zygmunt, A.,  443, 450
Zoccolillo, M., 73 Zywiak, W.,  397
Zoellner, L. A.,  334 Zywiak, W. H.,  365, 372
 Subject Index
Tables, figures, and boxes are indicated by an italic t, f, and b following the page number.
AAI. See Alcoholic Anonymous Involvement Scale
AAS. See Alcoholic Anonymous Affiliation Scale
AASE. See Alcoholic Abstinence Self-​Efficacy Scale
ABASI. See Alexian Brothers Assessment of Self-​Injury
Achenbach System of Empirically Based Assessment
(ASEBA),  54–​55, 55t, 77t, 78, 81, 82t, 85t, 86, 87
body image scales,  35
Direct Observation Form (DOF),  57, 77t, 81, 82t
Teacher Report Form (TRF),  54, 55t, 57, 59, 60t, 110–​111
ACQ. See Agoraphobic Cognitions Questionnaire; Alcohol
Craving Questionnaire
ACQ-​CON. See Anxiety Control Questionnaire
ACQ-​Now. See Alcohol Craving
Questionnaire–​present moment
ACQ-​R. See Alcohol Craving Questionnaire–​Revised
ACS. See Attentional Control Scale
Actigraphy, 572t, 573, 576
Activity Schedule,  138
ADDES-​4. See Attention-​Deficit Disorder Evaluation Scale-​4
Addiction center (brain),  360–​361
Addiction Severity Index (ASI),  251–​252, 397, 448
DSM-​5 (ASI-​5),  389, 390t
Addiction Severity Index-​Gambling Severity Index
(ASI-​GSI),  419–​420, 420t, 423, 424, 424t, 426
Addiction Severity Inventory (ASI),  450t, 451
30-​day (ASI-​6),  367, 372–​373, 372t
ADHD Rating Scale-​5,  51, 51t, 59, 60t
ADIS. See Anxiety Disorders Interview Schedule
ADIS-​5. See Anxiety Disorders Interview Schedule–​DSM-​5
ADIS-​5L. See Anxiety Disorders Interview Schedule–​Lifetime
Version for DSM-​5
ADIS-​C/​P. See Anxiety Disorders Interview Schedule–​Child
and Parent Versions
ADIS-​C/​P: CRS. See Anxiety Disorders Interview Schedule–​
Child and Parent Versions, Clinician Rating Scale
ADIS C/​P-​IV. See Anxiety Disorders Interview Schedule–​Child
and Parent Versions, DSM-​IV
ADIS-​IV. See Anxiety Disorders Interview Schedule–​DSM-​IV
ADIS-​R. See also Anxiety Disorders Interview Schedule–​Revised
Adolescent Pediatric Pain Tool (APPT),  589–​590, 597t, 598
Adolescent Substance Abuse Goal Commitment (ASAGC),  394
Adolescent Symptom Inventory,  35
ADS. See Alcohol Dependence Scale
Adult ADHD Rating Scale,  62
Adult Suicide Ideation Questionnaire (ASIQ),  196t, 199
AEQ. See Alcohol Expectancies Questionnaire
Affect Intensity Measure (AIM),  138t, 140
AGG. See Aggression scale
Aggression. See also specific disorders
conduct problems,  72
Aggression (AGG) scale,  504
Agoraphobia,  266–​284. See also Panic disorder and agoraphobia
assessment, case conceptualization and treatment
planning,  273–​279, 274t
assessment, diagnosis,  270–​273, 271t
assessment, purpose,  270
assessment, treatment monitoring and
outcome,  279–​283, 280t
conclusions and future directions,  283–​284
nature,  266–​270
Agoraphobic Cognitions Questionnaire (ACQ),  274, 274t, 276,
279, 280t, 281
AIM. See Affect Intensity Measure
Alanine aminotransferase (ALT),  399t, 400
Albany Panic and Phobia Questionnaire (APPQ),  274, 274t,
277–​278, 280t, 281
722 subject Index

Alcohol, Smoking, and Substance Involvement Screening Test FHRDS, 394

(ASSIST),  385, 386–​387, 386t, 388 Form  90, 390t, 392, 395
Alcohol Craving Questionnaire (ACQ),  396 F-​SMAST,  394
Jellinik (JACQ),  390t, 396 FTQ, 394, 397
present moment (ACQ-​Now),  390t, 396 high-​risk drinking situations,  396
Revised (ACQ-​R),  390t, 396 IDS, 390t, 396, 397
Alcohol Dependence Scale (ADS),  386t, 387, 448 IDS-​42,  396
Alcohol Expectancies Questionnaire (AEQ),  396 IP-​5,  397
Alcoholic Abstinence Self-​Efficacy Scale (AASE),  391t, 397 IPA, 391t, 397
Alcoholic Anonymous Affiliation Scale (AAS),  399t JACQ, 390t, 396
Alcoholic Anonymous Involvement Scale (AAI),  399t LDH, 390t, 393
Alcohol Reduction Strategies–​Current Confidence level of care determination,  391–​392
(ARS-​CC),  397 LISRES, 390t
Alcohol Severity Inventory (ASI),  441t MAST, 390t, 393
Alcohol-​Specific Role-​Play Test,  399t medical/​health screening,  389
Alcohol Treatment Outcome Measure (ATOM),  399t, 400 M.I.N.I., 389, 391
Consequences of Drinking (ATOM-​C),  400, 402 M-​SMAST,  394
Research (ATOM-​R),  400 OCDS, 390t, 395
Alcohol Urge Questionnaire (AUQ),  390t, 396, 397 overall evaluation,  397
Alcohol use disorder (AUD),  372t, 373–​374, 381–​402 PACS -​Penn,  390t, 395
assessment, case conceptualization and treatment PACS -​Preoccupation,  390t, 396
planning,  388–​397, 390t–​391t Q-​F measures,  390t
AASE, 391t, 397 RAATE, 390t, 397
ACQ, 396 RAPI, 390t, 393, 397
ACQ-​Now,  390t RCQ, 390t, 394
ACQ-​R,  390t, 396 relapse situations,  396
AEQ, 396 RFDQ, 396
alcohol outcome expectancies,  396 SAWS, 389, 390t
ARS-​CC,  397 SCID, 389, 391
ASAGC, 394 SCQ, 391t, 396
ASAM PPC,  390t, 392 SF-​12,  389, 390t, 397
ASI, 397 SF-​36,  389, 390t, 397
ASI-​5,  389, 390t SIP, 390t, 393
AUC, 397 SMAST, 394
AUDADIS, 389, 391 social network,  397
AUI, 390t, 393 SOCRATES, 390t, 394
AUQ, 390t, 396 SSAGA, 389, 391
B-​CEOA,  390t, 396 TLFB, 390t, 392, 393, 395, 397
B-​YAACQ,  390t, 394, 397 treatment history,  395
CAST, 394 treatment preference,  392
CEOA, 390t, 396, 397 TRI, 390t, 395
change, readiness for,  394–​395 URICA, 390t, 394, 397
CIWA-​Ar,  389, 390t, 397 YAACQ, 390t, 393–​394
CLDH, 393 assessment, case identification and diagnosis,  384–​388, 386t
CLDQ, 393 ADS, 386t, 387
comorbid psychopathology,  389–​391 ASSIST,  385, 386–​387, 386t, 388
consequences of drinking,  393–​394 AUDADIS-​5,  386t, 388
consumption patterns,  392–​393 AUDIT, 386t, 387, 388
craving,  395–​396 CAGE,  385–​386, 386t, 387, 388
DCS, 390t case identification,  384–​387
detoxification need,  389 CDT, 385, 386t
DMQ-​R,  390t, 396 diagnosis,  387–​388
DMSL, 390t DUSI-​R,  386t, 387
DPQ, 390t FAST,  385, 386, 386t, 387
DrInC, 390t, 393 GAIN-​GSS,  385, 386t, 387, 388
drinking goals,  395 GGT, 386, 386t
drinking self-​efficacy,  396–​397 MAST, 386t, 387, 388
DRSEQ, 390t, 397 MCV, 386, 386t
DRSEQ-​R,  391t, 397 overall evaluation,  388
family history, alcoholism,  394 PAWSS, 386t
 subject Index 723

PDSQ, 386t with bipolar disorder,  382

PEth,  386, 386t, 388 with borderline personality disorder,  382
PRISM, 386t, 388 conclusions and future directions,  402
RAPS-​4,  386t depression with,  382
SAAST-​R,  386t generalized anxiety disorder with,  382
SCID-​5,  386t, 388 nature,  381–​384
SDSS, 386t comorbidities, 382
SSAGA, 386t, 388 course/​prognosis,  382
SSI-​AOD (SSI-​SA),  386t, 387 etiology,  382–​384
assessment, purpose,  384 prevalence/​incidence,  381–​382
assessment, treatment monitoring and outcome,  397–​402, 399t with PTSD,  332
AAI, 399t PTSD with,  382
AA involvement/​12-​step affiliation, 399t, 401 with substance use disorders, other,  382
AAS, 399t Alcohol Use Disorder and Associated Disabilities Interview
Alcohol-​Specific Role-​Play Test,  399t Schedule (AUDADIS),  389, 391
ALT, 399t, 400 DSM-​5 (AUDADIS-​5),  386t, 388
AST, 399t, 400 Alcohol Use Disorders Identification Test (AUDIT),  386t, 387,
ATOM, 399t, 400 388, 398, 422, 423, 441t, 448, 498
ATOM-​C,  400, 402 Alcohol Use Inventory (AUI),  390t, 393
ATOM-​R,  400 Alcohol Use Scale (AUS),  450t, 451
AUDIT, 398 Alcohol withdrawal syndrome (AWS),  389
BAM,  398, 399t, 402 Alexian Brothers Assessment of Self-​Injury (ABASI),  205
biological measures,  398–​400 ALT. See Alanine aminotransferase
B-​PRI,  399t Altman Self-​Rating Mania scale (ASRM),  181t, 182, 184
B-​YAACQ,  399t American Society of Addiction Medicine Patient Placement
CDT, 399t, 400, 401 Criteria (ASAM PPC),  390t, 392
consequences of drinking,  400 Anorexia nervosa,  541–​542. See also Eating disorders
consumption patterns,  398 Antisocial Process Screening Device (APSD),  82t, 84
coping skills,  401 Anxiety Control Questionnaire (ACQ-​CON), 
DrInC, 399t, 400, 401 280–​281, 280t
EtG, 399t, 400 Anxiety disorders, children and adolescents,  217–​234
EtS, 399t, 400 assessment, case conceptualization and treatment
FAEE, 399t, 400 planning,  226–​232, 227t
5-​HTOL,  399t, 400 ADIS-​C/​P,  227t
Form  90, 398, 399t, 401 BAT, 227t
GAATOR, 399t behavioral observations,  228–​229
GGT, 399t, 400, 401 CAIS,  230–​231
Giner TAS,  399t DICA, 227t
Impaired Control Scale,  399t DISC-​IV,  227t
LLS, 399t family accommodation,  231
MAP, 398, 399t FASA-​CR,  231
MCV, 399t, 400 FASA/​FASA-​CR,  227t
overall evaluation,  401–​402 impaired but not diagnosed,  230–​231
PBSS, 399t, 401 K-​SADS,  227t
PEth, 399t, 400 MASC, 227t
PROMIS,  398, 399t, 402 overall evaluation,  231
quality of life,  400–​401 PARS, 230
RAPI, 399t, 400 prescriptive treatment strategies,  227t, 228
readiness for change,  400 RCMAS, 227t, 228
SCRAM, 399t SCAS, 227t
SF-​12,  399t, 401 self-​monitoring,  229–​230
SF-​36,  399t, 401 semi-​structured and structured diagnostic interview
SIP, 399t, 400 schedules, 227
SOCRATES, 399t, 400, 401 SET/​PYIT,  227t
sweat, 399t SM, 227t
TLFB,  398, 399t, 401 SPAIC, 227t
transdermal monitoring,  399t SRAS, 227t, 228
URICA, 399t, 400, 401 SRAS-​R,  228
WHOQOL-​BREF,  399t treatment utility, demonstrating,  230
YAACQ, 399t, 400 YIKES, 229
724 subject Index

Anxiety disorders, children and adolescents (continued) Anxiety disorders, with PTSD,  332
assessment, diagnosis,  221–​226, 221t Anxiety Disorders Interview Schedule (ADIS),  270–​272, 271t,
ADIS-​C/​P,  221–​222, 221t, 225, 226 279, 280t
with autism, comorbid,  225–​226 Child and Parent Versions (ADIS-​C/​P),  221–​222, 221t, 225,
CASI, 221t, 226 226, 227t
comorbidities,  225–​226 Child and Parent Versions, Clinician Rating Scale
conceptual and practical issues,  225–​226 (ADIS-​C/​P: CRS),  232t
DICA, 221t, 222 Child and Parent Versions, DSM-​IV
differential diagnosis,  225 (ADIS C/​P-​IV),  232t, 233
DISC-​IV,  221t, 222 DSM-​5 (ADIS-​5),  246–​247, 270–​272, 271t, 298, 336t, 338
FSSC-​R,  221t, 223 DSM-​IV (ADIS-​IV),  246–​247, 246t, 297t, 298, 304t, 305,
FSSC-​R-​R-​SF,  224 315–​316, 315t, 336t, 338
K-​SADS,  221t, 222 Lifetime Version for DSM-​5 (ADIS-​5L),  135, 136t
MASC, 221t, 223–​224 Revised (ADIS-​R),  271, 273
MASC-​2,  224, 226 Anxiety Sensitivity Index (ASI),  251–​252, 274–​275, 274t,
MASC-​2-​2-​P,  224 279, 280t
MASC-​2-​SR,  224 3rd edition (ASI-​3),  248t, 252, 257, 274, 274t, 275, 279, 280t
overall evaluation,  226 APA Presidential Task Force on Evidence-​Based Practice,  17
PARS, 226 APPQ. See Albany Panic and Phobia Questionnaire
rating scales,  223–​225 APPT. See Adolescent Pediatric Pain Tool
rating scales, discriminant validity,  223–​224 APS. See Arousal Predisposition Scale
rating scales, specific anxiety disorders,  224–​225 APSD. See Antisocial Process Screening Device
rating scales, youth self-​rated, updated,  224 ARCS. See Adult Response to Child Symptoms
RCADS, 226 ARCS (Adult Response to Child Symptoms),  595, 597
RCMA, 221t, 223 Protect and Monitor subscales,  597t, 598
RCMAS-​2,  224, 226 Arousal Predisposition Scale (APS),  567t, 571
SASC-​R,  221t, 224–​225 ARS-​CC. See Alcohol Reduction Strategies–​Current
SCARED, 221t, 223–​224 Confidence
SCAS, 221t, 223–​224 ASAGC. See Adolescent Substance Abuse Goal Commitment
semistructured and structured diagnostic interview ASAM PPC. See American Society of Addiction Medicine
schedules,  221–​222 Patient Placement Criteria
SPAIC, 221t, 224 ASEBA. See Achenbach System of Empirically Based
STAIC, 221t, 223 Assessment
assessment, treatment monitoring and outcome,  231–​234, 232t ASEBA-​DOF. See Achenbach System of Empirically Based
ADIS-​C/​P: CRS,  232t Assessment–​Direct Observation Form
ADIS C/​P-​IV,  232t, 233 ASEBA-​TRF. See Achenbach System of Empirically Based
BAT/​SET/​PYIT,  232t Assessment–​Teacher Report Form
behavioral observations,  233 ASI. See Addiction Severity Index; Addiction Severity Inventory;
CAIS, 232t, 233 Alcohol Severity Inventory; Anxiety Sensitivity Index
CBCL-​I,  232–​233, 232t ASI-​3. See Anxiety Sensitivity Index, 3rd edition
conceptual and practical issues,  233–​234 ASI-​5. See Addiction Severity Index DSM-​5
DICA, 232t ASI-​6. See Addiction Severity Inventory, 30-​day
DISC-​IV,  232t ASI-​GSI. See Addiction Severity Index-​Gambling Severity Index
FSSC-​R,  232t ASIQ. See Adult Suicide Ideation Questionnaire
K-​SADS,  232t Aspartate aminotransferase (AST),  399t, 400
MASC, 232t ASRM. See Altman Self-​Rating Mania scale
normative data use,  233 Assessment. See also specific disorders
overall evaluation,  234 accurate, importance,  xii
rating scales,  232–​233 application of measurement,  32
RCMAS-​2 Defensiveness Scale,  233, 234 definition, 32
RCMAS Lie Scale,  232t, 233–​234 prerequisite, xii
reporting biases,  233–​234 purposes,  6–​7
SCAS, 232t research–​practice gap,  18
SPAIC, 232t ASSIST. See Alcohol, Smoking, and Substance Involvement
STAIC, 232t Screening Test
YIKES, 233 AST. See Aspartate aminotransferase
YSR, 233 ATOM. See Alcohol Treatment Outcome Measure
conclusions and future directions,  234 ATOM-​C. See Alcohol Treatment Outcome Measure–​
nature,  217–​221 Consequences of Drinking
prevalence benchmarks,  34t ATOM-​R. See Alcohol Treatment Outcome Measure–​Research
 subject Index 725

Attentional Control Scale (ACS),  138t, 140 assessment, purposes,  49

Attention-​Deficit Disorder Evaluation Scale-​4 assessment, treatment monitoring and evaluation,  58–​61, 60t
(ADDES-​4),  51t, 52 ADHD Rating Scale-​5,  59, 60t
Attention-​deficit hyperactivity disorder (ADHD),  47–​64 ASEBA, CBCL,  59, 60t
age of referral,  47 ASEBA, TRF,  59, 60t
assessment, case conceptualization and treatment ASEBA CBCL,  59, 60t
planning,  53–​58, 55t BASC-​3 Flex Monitor,  59
ASEBA,  54–​55, 55t BCS, 60
ASEBA CBCL,  54, 55t, 57 broadband checklists,  59, 60t
ASEBA-​DOF,  57 CAFAS, 59, 60t
ASEBA TRF,  54, 55t, 57 Conners  3, 59, 60t
BASC-​3,  55–​56, 55t COSS, 60, 60t
BCS, 58, 60 impairment measures,  59–​60, 60t
BOSS,  57–​58 instrument ratings,  60t
broadband checklists,  54–​56, 55t IOWA, 59, 60t
CAFAS, 55t, 57 IRS,  59–​60, 60t
Conners  3, 54, 55t, 56 narrowband checklists,  59, 60t
COSS, 55t, 57 observational measures,  60
CSI-​IV,  56 overall evaluation,  60–​61
DOF, 57 overview of measures,  59–​61, 60t
impairment measures,  56–​57 SKAMP, 59
instrument ratings,  55t Weiss,  59–​60, 60t
IRS, 55t, 57 assumptions, underlying,  49
observational measures,  57–​58 conclusions and future directions,  62–​64
overall evaluation,  58 with conduct problems,  73
overview of measures,  54–​58 controversy, 47
VABS-​II,  55t, 56–​57 definition, 48
Vanderbilt ADHD Diagnostic Parent and Teacher Rating identification, benefits and challenges,  47
Scales, 55t, 56 lifespan perspective,  47
YSR,  54–​55 nature, 48
assessment, for diagnosis,  49–​53, 51t prevalence, 47
ADDES-​4,  51t, 52 prevalence benchmarks,  34t
ADHD Rating Scale-​5,  51, 51t, 59, 60t AUDADIS. See Alcohol Use Disorder and Associated
CAPA, 53 Disabilities Interview Schedule
combinatorial methods,  50 AUDADIS-​5. See Alcohol Use Disorder and Associated
Conners 3, 52 Disabilities Interview Schedule DSM-​5
Conners  3, DSM-​IV-​TR Symptom Scales, 51t, 52 AUDIT. See Alcohol Use Disorders Identification Test
developmentally appropriate symptoms,  50 AUI. See Alcohol Use Inventory
DISC-​IV,  51t, 52 AUQ. See Alcohol Urge Questionnaire
DSM-​5 criteria,  49–​50 AUS. See Alcohol Use Scale
gender and ethnicity,  50 Autism, with anxiety disorders,  225–​226
instrument ratings,  51, 51t Away and Back thresholds,  40
K-​SADS,  52–​53
measures overview,  51–​53, 51t BAARS-​IV. See Barkley Adult ADHD Rating Scale-​IV
narrowband checklists,  51–​52, 51t BABS. See Brown Assessment of Beliefs Scale
non-​useful measures,  53 Back definition,  40
older assessment measures problems,  50–​51 BAI. See Beck Anxiety Inventory
“or”/​“and” rules,  50 BAM. See Brief Addiction Monitor
overall evaluation,  53 BAPQ. See Bath Adolescent Pain Questionnaire
rater/​source variance,  50 BAPQ-​P. See Bath Adolescent Pain Questionnaire–​Parent
SDQ, 52 Barkley Adult ADHD Rating Scale-​IV (BAARS-​IV),  61–​62
structured interviews,  51t, 52–​53 Barkley Functional Impairment Scale (BFIS),  62
“working hypothesis,”  50 BARS. See Behavioral Affective Rating System
assessment, in adulthood,  61–​62 BAS. See Burden Assessment Scale
Adult ADHD Rating Scale,  62 BASC-​2. See Behavior Assessment System for Children, 2nd ed.
BAARS-​IV,  61–​62 BASC-​3. See Behavior Assessment System for Children, 3rd ed.
BFIS, 62 BASC-​SOS. See BASC Student Observation System;
CAADID-​IV,  62 Behavior Assessment System for Children–​Student
DIVA 2.0, 62 Observation System
assessment, in children,  48–​49 BASC Student Observation System (BASC-​SOS),  77t, 80, 82t
726 subject Index

BASIS-​32. See Behavior and Symptom Identification children and adolescents,  176–​177
Scale–​32 item GBI, 174t, 177–​178
BASIS-​R. See Behavior and Symptom Identification HCL-​32,  178
Scale–​Revised; Revised Behavior and Symptom HPS, 178
Identification Scale IDAS, 179
BAT. See Behavioral Approach Test K-​SADS,  177, 179
Bath Adolescent Pain Questionnaire (BAPQ),  591t, 596–​597 K-​SADS-​PL,  174t, 177
Parent (BAPQ-​P),  591t, 596–​597 MDQ, 174t, 178
BAT/​SET/​PYIT. See Behavioral Avoidance Task/​Social MOODS-​SR,  178
Evaluative Task/​Parent–​Youth Interaction Task overall evaluation,  179
B-​CEOA. See Brief Comprehensive Effects of Alcohol Scale; P-​YMRS,  178–​179
Comprehensive Effects of Alcohol Scale–​Brief SADS, 174t, 175–​176, 179
BCQ. See Body Checking Questionnaire SCID,  174–​175, 174t, 176, 179
BCS. See Behavioral Coding System SCID for DSM-​IV-​TR,  175
BDI-​II. See Beck Depression Inventory-​II self-​report measures,  177–​179
Bech–​Rafaelsen Mania Scale (MAS),  181t, 182, 184 TEMPS, 178
Beck Anxiety Inventory (BAI),  300–​301, 300t, 304t, 305, 498, WASH-​U-​KSADS,  177
572t, 574–​575 assessment, treatment monitoring and
Beck Depression Inventory-​II (BDI-​II),  157, 158t, 164t, 300t, outcomes,  181–​184, 181t
301, 304t, 305, 553, 572t, 575, 613, 620, 620t ASRM, 181t, 182, 184
Beck Scale for Suicidal Ideation (BSI, BSS, BSSI),  196t, 197, Brief QoL BD,  181t, 183–​184
199, 200, 201 ISS, 183
Behavioral Affective Rating System (BARS),  496t, 501 MAS, 181t, 182, 184
Behavioral and Emotional Rating Scale (BERS),  114, 114t, 116 overall evaluation,  184
Behavioral Approach Test (BAT),  227t, 252, 254, 255t, 256, SADS-​C,  181t, 182, 184
278, 279, 282–​283 self-​report measures,  182–​184
Behavioral Avoidance Task/​Social Evaluative Task/​Parent–​Youth SHPSS, 181t, 183
Interaction Task (BAT/​SET/​PYIT),  232t SRMI, 181t, 182–​183, 184
Behavioral Coding System (BCS),  58, 60, 77t, 79, 85t, 86, 87 WASSUP, 181t, 183
Behavioral Observation of Students in Schools (BOSS),  57–​58 YMRS,  181–​182, 181t, 184
Behavior and Symptom Identification Scale (BASIS) conclusions and future directions,  184
32 item (BASIS-​32),  344 definition, 173
Revised (BASIS-​R),  441t, 442, 449 heritability, 174
Behavior Assessment System for Children (BASC) nature,  173–​174
2nd ed. (BASC-​2),  56 prevalence,  173–​174
3rd ed. (BASC-​3),  55–​56, 55t, 77t, 78, 81, 82t, 86 Bipolar Spectrum Disorder Scale (BSDS),  178
3rd ed. Flex Monitor (BSC-​3 Flex Monitor),  59 BIS. See Brief Impairment Scale
Student Observation System (BASC-​SOS),  77t, 80, 82t BISF-​W. See Brief Index of Sexual Functioning for Women
Behavior change therapy,  40 BMSFI. See Brief Male Sexual Function Inventory
Berkeley Puppet Interview (BPI),  111, 113 BNSS. See Brief Negative Symptoms Scale
BERS. See Behavioral and Emotional Rating Scale Body Checking Questionnaire (BCQ),  551t, 552–​553
BFIS. See Barkley Functional Impairment Scale Body Sensations Questionnaire (BSQ),  274, 274t, 275–​276,
BFNE. See Brief Fear of Negative Evaluation Scale 279, 280t, 281
Binge eating disorder,  542. See also Eating disorders Body Shape Questionnaire (BSQ),  551t, 552
Bipolar disorder,  173–​184 Borderline personality disorder (BPD), alcohol use disorder
alcohol use disorder with,  382 with, 382
assessment, case conceptualization and treatment BOSS. See Behavioral Observation of Students in Schools
planning,  179–​181, 179t BPI. See Berkeley Puppet Interview; Brief Pain Inventory
DAS, 180 BPI-​SF. See Brief Pain Inventory–​Short Form
FAD, 179t, 181 B-​PRI. See Brown–​Peterson Recovery Progress Inventory
Insight and Treatment Attitudes Questionnaire,  180 BPRS. See Brief Psychiatric Rating Scale
overall evaluation,  181 BRFL. See Brief Reasons for Living Inventory
PCS, 181 Brief Addiction Monitor (BAM),  398, 399t, 402
PSQI, 180 Brief Comprehensive Effects of Alcohol Scale
SAI-​E,  179t, 180 (B-​CEOA),  390t, 396
SUMD, 180 Brief Fear of Negative Evaluation Scale (BFNE),  248t, 250–​251
assessment, diagnosis,  174–​179, 174t Brief Impairment Scale (BIS),  114, 114t, 116
bipolar I, adults,  175 Brief Index of Sexual Functioning for Women (BISF-​W),  519t,
bipolar II, adults,  175–​176 521, 525, 525t, 528, 529
BSDS, 178 Brief Male Sexual Function Inventory (BMSFI),  519t, 522

Brief Negative Symptoms Scale (BNSS),  441t, 442, 449
Brief Pain Inventory (BPI),  611–​612, 614, 615, 619–​620
Short Form (BPI-​SF),  611–​612, 611t, 615, 619–​620, 620t
Brief Psychiatric Rating Scale (BPRS),  440, 441t, 449, 450t
Brief QoL BD,  181t, 183–​184
Brief Reasons for Living Inventory (BRFL),  202, 202t
Brief Sexual Function Inventory-​M (BSFI-​M),  526, 530
Brief Social Phobia Scale (BSPS),  255t, 256
Brief Trauma Questionnaire (BTQ),  342t, 343
Brief Young Adult Alcohol Consequences Questionnaire
(B-​YAACQ),  390t, 394, 397, 399t
Brown Assessment of Beliefs Scale (BABS),  315t, 316
Brown–​Peterson Recovery Progress Inventory (B-​PRI),  399t
BSC-​3 Flex Monitor. See Behavior Assessment System for
Children, 3rd ed. Flex Monitor
BSDS. See Bipolar Spectrum Disorder Scale
BSFI-​M. See Brief Sexual Function Inventory-​M
BSI. See Beck Scale for Suicidal Ideation
BSPS. See Brief Social Phobia Scale
BSQ. See Body Sensations Questionnaire; Body Shape
Questionnaire
BSS. See Beck Scale for Suicidal Ideation
BSSI. See Beck Scale for Suicidal Ideation
BTQ. See Brief Trauma Questionnaire
Bulimia nervosa,  542. See also Eating disorders
Burden Assessment Scale (BAS),  441t, 448, 450t, 451
B-​YAACQ. See Brief Young Adult Alcohol Consequences
Questionnaire
CAADID-​IV. See Conners Adult ADHD Diagnostic Interview
for DSM-​IV
CAFAS. See Child and Adolescent Functional
Assessment Scale
CAGE,  385–​386, 386t, 387, 388
CAINS. See Clinical Assessment Interview for Negative
Symptoms
CAIS. See Child Anxiety Impact Scale
Calgary Depression Scale for Schizophrenia (CSDS),  439t, 440
Camberwell Assessment of Need (CAN),  441t, 444
Camberwell Family Interview (CFI),  181, 447, 451
CAN. See Camberwell Assessment of Need
Canadian Problem Gambling Index-​Problem Gambling
Severity Index (CPGI-​PGSI),  413t, 417, 418, 419, 420t
CAPA. See Child and Adolescent Psychiatric Assessment
CAPS. See Clinician-​Administered PTSD Scale
CAPS-​5. See Clinician-​Administered PTSD Scale, DSM-​5
CAPS-​IV. See Clinician-​Administered PTSD Scale, DSM-​IV
CAPS-​S. See Clinician Administered Rating Scale for Post-​
Traumatic Stress Disorder–​Schizophrenia
CAQ. See Cognitive Avoidance Questionnaire
Carbohydrate-​deficient transferrin (CDT),  385, 386t, 399t,
400, 401
CARS-​M. See Clinician Administered Rating Scale for Mania
CASI. See Childhood Anxiety Sensitivity Index
CASI-​5. See Childhood Anxiety Sensitivity Index, DSM-​5
CASIG. See Client Assessment of Strengths, Interests,
and Goals
CAST. See Children of Alcoholics Screening Test
CATI. See Coolidge Axis II Inventory
CAT-​PD. See Computerized Adaptive Test–​Personality Disorder
subject Index 727
CBASP. See Cognitive–​Behavioral Analysis System of
Psychotherapy
CBCL. See Child Behavior Checklist
CBCL-​I. See Child Behavior Checklist–​Internalizing Scale
CDI. See Children’s Depression Inventory
CDRS-​R. See Children’s Depression Rating Scale–​Revised
CDT. See Carbohydrate-​deficient transferrin
Center for Epidemiological Studies–​Depression Scale
(CES-​D),  157–​158, 158t, 162, 163, 164t, 165
Revised (CESD-​R),  158, 158t
CEOA. See Comprehensive Effects of Alcohol Scale
CES-​D. See Center for Epidemiological
Studies–​Depression Scale
CESD-​R. See Center for Epidemiological Studies–​Depression
Scale–​Revised
CFI. See Camberwell Family Interview; Cultural Formulation
Interview
C-​GAS. See Child Global Assessment Scale
CGAS. See Child Global Assessment Scale
CGI. See Clinical Global Impression
CGI-​I. See Clinical Global Impression–​Improvement
CGI-​S. See Clinical Global Impression–​Severity
Changes in Sexual Functioning Questionnaire (CSFQ),  525,
525t, 528, 529
CSFQ-​14,  525, 525t
Child and Adolescent Functional Assessment Scale (CAFAS),  22,
55t, 57, 59, 60t, 77t, 81, 85t, 86, 114, 114t, 116, 118
Child and Adolescent Psychiatric Assessment (CAPA),  53, 113,
115, 116
Child Anxiety Impact Scale (CAIS),  230–​231, 232t, 233
Child Behavior Checklist (CBCL),  54, 55t, 57, 59, 60t, 117
Internalizing Scale (CBCL-​I),  232–​233, 232t
Child Global Assessment Scale (CGAS, C-​GAS),  77t, 81, 85t,
86, 113, 114t, 117–​118, 118t, 119
Childhood Anxiety Sensitivity Index (CASI),  221t, 226
DSM-​5 (CASI-​5),  78
Childhood Trauma Questionnaire,  115–​116
Child Outcomes Research Consortium (CORC),  22
Children of Alcoholics Screening Test (CAST),  394
Children’s Depression Inventory (CDI),  118, 118t
Children’s Depression Rating Scale –​Revised (CDRS-​R),  117,
118, 118t
Children’s Organizational Skills Scale (COSS),  55t, 57, 60, 60t
Child Suicide Potential Scales (CSPS),  197t, 200
Child World Health Organization Disability Assessment Scale
(C-​WHO-​DAS),  115
Chronic pain, adults,  608–​621. See also Pain, chronic, adult
Chronic Pain Coping Inventory (CPCI),  616t, 617–​618, 619
42-​item (CPCI-​42),  616t, 618
CIBRS. See Couples’ Intimate Behavior Rating System
CIDI. See Composite International Diagnostic Interview
Circumscribed Fear Measure,  250
CIS. See Columbia Impairment Scale
CISS. See Couples Interaction Scoring System
CIWA-​AR. See Clinical Institute Withdrawal Assessment for
Alcohol
CLDH. See Cognitive Lifetime Drinking Inventory
CLDQ. See Concordia Lifetime Drinking Questionnaire
Client Assessment of Strengths, Interests, and Goals
(CASIG), 441t, 444, 445, 450t, 451
728 subject Index

Clinical Assessment Interview for Negative Symptoms APSD, 82t, 84

(CAINS), 441t, 442, 449 ASEBA, 82t
Clinical Global Impression (CGI),  449, 450t BASC-​3,  82t
Improvement (CGI-​I),  117, 119 behavioral observations,  82t
Severity (CGI-​S),  117, 119 callous and unemotional traits,  83–​84, 85
Clinical Institute Withdrawal Assessment for Alcohol (CIWA-​ definition, operational,  83
AR),  389, 390t, 397 developmental pathways,  82–​83
Clinical Rating of Adult Communication Scale ECBI/​SESBI-​R,  82t
(CRAC), 496t, 501 ECI-​5/​CASI-​5,  82t
Clinical utility,  9b, 11–​12 functional behavioral assessment,  84
Clinician-​Administered PTSD Scale (CAPS),  343, 345 ICU, 82t, 84
DSM-​5 (CAPS-​5),  336–​337, 336t, 341, 346t, 347 overall evaluation,  85
DSM-​IV (CAPS-​IV),  336–​337, 336t, 346t rating scales,  82t, 84
Clinician Administered Rating Scale for Mania (CARS-​M),  182 structured interviews,  82t
Clinician Administered Rating Scale for Post-​Traumatic Stress assessment, diagnosis,  76–​82, 77t
Disorder–​Schizophrenia (CAPS-​S),  439t, 440 ASEBA, 77t, 78, 81
CNCC. See Cocaine Negative Consequences Checklist ASEBA-​DOF,  77t, 81
CNV. See Conventionalization (CNV) scale BASC-​3,  77t, 78, 81
Cocaine Negative Consequences Checklist (CNCC),  366t, 372 BASC-​SOS,  77t, 80
Cocaine Related Assessment of Coping Skills (CRACS),  371 BCS, 77t, 79
Self-​Efficacy (CRACS-​SE),  366t behavioral observation,  77t, 79–​81
Codebook of Marital and Family Interaction behavior rating scales,  77–​78, 77t
(COMFI), 496t, 501 CAFAS, 77t, 81
COGNISTAT. See Neurobehavioral Cognitive Status CASI-​5,  78
Examination CGAS, 77t, 81
Cognitive Avoidance Questionnaire (CAQ),  300t, 303, Compliance Test,  77t, 80
304t, 305 CRS-​3,  77t, 78
Cognitive–​Behavioral Analysis System of Psychotherapy CSI-​4,  78
(CBASP), 133, 134 DICA, 77t, 79, 81–​82
Cognitive Lifetime Drinking Inventory (CLDH),  393 DISC-​IV,  77t, 79, 81–​82
Cohen’s d effect,  40 DPICS, 77t, 79–​80
Collaborative Longitudinal Personality Disorders Study DSM-​5,  72
(CLPS), 470 DSM-​IV-​TR,  77t, 81
Collateral informants,  38 ECBI-​5/​CASI-​54,  77t, 78
College Student Reasons for Living Inventory ECBI/​SESBI-​R,  77t, 78
(CSRLI), 202t, 203 ECI-​5,  78
Colorado Symptom Index,  449 factor analysis,  72
Columbia Impairment Scale (CIS),  113–​114, 114t functional impairment,  77t, 81
Columbia–​Suicide Severity Rating Scale (C-​SSRS),  196t, instrument ratings,  77t
197–​198, 204, 205 interviews, 77t, 78–​79
Combat Exposure Scale,7-​item, 343–​344 overall evaluation,  77t, 81–​82
COMFI. See Codebook of Marital and Family Interaction REDSOCS, 77t, 80
Communication Patterns Questionnaire (CPQ),  495, 496t, 503 assessment, treatment monitoring and outcomes,  85–​87, 85t
Communication Skills Test (CST),  496t, 501 ASEBA, 85t, 86, 87
Compliance Test (CT),  77t, 80, 85t BASC-​3,  86
Composite International Diagnostic Interview (CIDI),  156, BCS, 85t, 86, 87
157, 336t, 338–​339, 362t, 364 CAFAS, 85t, 86
CIDI 65+, 156 CGAS, 85t, 86
Comprehensive Effects of Alcohol Scale (CEOA),  390t, CT, 85t
396, 397 DPICS, 85t, 86, 87
Brief (B-​CEOA),  390t, 396 ECBI/​SESBI-​R,  85t, 86, 87
Computerized Adaptive Test–​Personality Disorder (CAT-​ ECI-​5/​CASI-​5,  85t
PD),  476–​477, 476t, 478t, 479 PCSQ, 85t, 86
Concordia Lifetime Drinking Questionnaire (CLDQ),  393 PDR, 85t, 86
Conduct problems, child and adolescent,  71–​89 REDSOCS, 85t, 86
ADHD with,  73 TAI, 85t, 86
aggression, 72 callous and unemotional traits,  75–​76, 83–​84, 85
assessment, case conceptualization and treatment conclusions and future directions,  87–​89
planning,  82–​85, 82t nature,  71–​76
age of symptom onset,  83 aggression,  72–​73
 subject Index 729

causal theories,  74–​76 relationship behaviors,  495–​497

childhood-​ vs. adolescent-​onset,  75–​76 relationship cognitions,  497
conduct disorder,  72 RMICS, 500, 502
co-​occurring problems in adjustment,  73–​74 RQI, 496t, 500
epidemiology, 73 SCID, 496t, 501
oppositional defiant disorder,  72 self-​ and other-​report methods,  503–​504
risks with, multiple,  74 SPAFF, 496t, 501
types and severity,  71–​73 SSICS, 496t, 501
noncompliance, 72, 80 strategies and methods,  499–​504
substance abuse with,  73–​74 VTCS, 496t, 501
Conflict Rating System (CRS),  496t, 501 assessment, diagnosis,  493–​495, 493t
Conflict Tactics Scale–​Revised (CTS  2), 496t, 498, 503–​504 CSI and CSI-​4,  493t, 494
Conners  3, 52, 54, 55t, 56, 59, 60t DAS and DAS-​7,  493t, 494
DSM-​IV-​TR Symptom Scales,  51t, 52 MSI-​B,  493t, 494
Conners Adult ADHD Diagnostic Interview for DSM-​IV RCISS, 493t, 494
(CAADID-​IV),  62 RMICS, 493t, 494
Conners Rating Scales,3rd ed. (CRS-​3), 77t, 78 SDI-​MD-​PA,  493, 493t
Consensus Sleep Diary (CSD),  567t, 569–​570, 572, 572t, 575 assessment, treatment monitoring and outcome,  501t, 505
Contextualized Feedback System (CFS),  22 CSI-​16,  501t, 505
Conventionalization (CNV) scale,  497 DAS, 501t, 505
Coolidge Axis II Inventory (CATI),  466, 467, 467t, 470, FAPBI, 505
471, 474 GAS, 501t, 505
Coping Strategies Questionnaire (CSQ),  616t, 617 MSI-​B,  501t, 505
Cornell Scale for Depression in Dementia (CSDD),  158t, MSI-​R,  501t, 504
161–​162, 163, 164t, 165 conclusions and future directions
COSS. See Children’s Organizational Skills Scale assessing,  505–​506
Couple distress,  489–​508 further research,  506–​508
assessment, case conceptualization and treatment nature,  489–​491
planning,  495–​504, 496t definition,  489–​490
AUDIT, 498 etiology,  491–​492, 491t–​492t
BAI, 498 prevalence and comorbidities,  490–​491
BARS, 496t, 501 sample assessment constructs,  491, 491t–​492t
CIBRS, 496t, 501 Couple Satisfaction Index (CSI),  441t, 493t, 494, 523, 523t
CISS, 502 4-​item (CSI-​4),  78, 493t, 494
clinical interview,  499–​501 16-​item (CSI-​16),  501t, 505
COMFI, 496t, 501 DSM-​IV (CSI-​IV),  56
CPQ,  495, 496t, 503 Couples Interaction Scoring System (CISS),  502
CRAC, 496t, 501 Couples’ Intimate Behavior Rating System (CIBRS),  496t, 501
CRS, 496t, 501 CPCI-​42. See Chronic Pain Coping Inventory, 42-​item
CST, 496t, 501 CPCI. See Chronic Pain Coping Inventory
CTS  2, 496t, 498, 503–​504 CPGI-​PGSI. See Canadian Problem Gambling Index-​Problem
cultural differences,  499 Gambling Severity Index
DCI, 496t, 503 CPQ. See Communication Patterns Questionnaire
DISC, 496t, 501 CRAC. See Clinical Rating of Adult Communication Scale
distress, comorbid individual,  498–​499 CRACS. See Cocaine Related Assessment of Coping Skills
ENRICH, 496t, 504 CRACS-​SE. See Cocaine Related Assessment of Coping
FAPBI,  496–​497, 496t, 503 Skills–​Self-​Efficacy
GAS-​7,  498 Criteria, ratings,  7
IDCS, 496t, 501 CRS. See Conflict Rating System
KPI, 496t, 501 CRS-​3. See Conners Rating Scales, 3rd ed.
LIFE, 496t, 501 CSD. See Consensus Sleep Diary
MICS, 502 CSDD. See Cornell Scale for Depression in Dementia
MMEA, 504 CSDS. See Calgary Depression Scale for Schizophrenia
MSI-​R,  496–​497, 496t, 497, 504 CSFQ. See Changes in Sexual Functioning Questionnaire
observational methods,  501–​503 CSFQ-​14, 14–​item, Changes in Sexual Functioning
overall evaluation,  504 Questionnaire
PREPARE, 504 CSI. See Couple Satisfaction Index
RAM, 496t, 497, 504 CSI-​4. See Couple Satisfaction Index, 4-​item version
RCISS, 500, 502 CSI-​16. See Couple Satisfaction Index, 16-​item version
relationship affect,  497–​498 CSI-​IV. See Couple Satisfaction Index, DSM-​IV
730 subject Index

CSPS. See Child Suicide Potential Scales ERQ, 138t, 140

CSQ. See Coping Strategies Questionnaire FMPS, 138t, 139
CSRLI. See College Student Reasons for Living Inventory interpersonal mechanisms,  140
C-​SSRS. See Columbia–​Suicide Severity Rating Scale OQ-​45,  137
CST. See Communication Skills Test origins,  140–​141
CT. See Compliance Test overall evaluation,  142
CTS2. See Conflict Tactics Scale–​Revised PES, 138, 138t
Cultural Formulation Interview (CFI),  439, 451 PHQ-​9,  138
C-​WHO-​DAS. See Child World Health Organization Disability precipitants, 140
Assessment Scale psychological mechanisms,  138–​140
PTQ, 138t, 139
DAI. See Dental Anxiety Inventory SAS-​SR,  138t, 140
DAI-​10. See Dental Anxiety Inventory, 10-​item SHAPS,  138–​139, 138t
DAI-​30. See Dental Anxiety Inventory, 30-​item symptoms/​disorders/​problems,  137–​138
Daily Record of Dysfunctional Thoughts,  139 treatment plan,  142
DAPP-​BQ. See Dimensional Assessment of Personality WHODAS  2.0, 137–​138, 138t, 140
Pathology-​Basic Questionnaire assessment, diagnosis,  135–​137, 136t
Dartmouth Assessment of Lifestyle Instrument,  448 ADIS-​5L,  135, 136t
DAS. See Dyadic Adjustment Scale; Dysfunctional overall evaluation,  136–​137
Attitude Scale PHQ-​9,  135–​136, 136t
DAS-​7. See Dyadic Adjustment Scale, 7-​item QIDS-​SR,  135–​136, 136t
DASE. See Drug Abstinence Self-​Efficacy Scale SCID-​5,  135, 136t
DASS. See Depression Anxiety Stress Scales SCID-​5-​PD,  135, 136t
DAST. See Drug Abuse Screening Test self-​report measures,  135–​136
DBAS. See Dysfunctional Beliefs and Attitudes about semi-​structured interviews,  135
Sleep Scale assessment, purpose,  135
DBAS-​16. See Dysfunctional Beliefs and Attitudes about Sleep assessment, treatment monitoring and
Scale, 16-​item outcome,  142–​145, 144t
DCI. See Dyadic Couples Inventory DASS,  142–​143, 144t
DCS. See Drinking Context Scale elements of therapy,  143–​144
Decreased Sexual Desire Screener (DSDS),  528 GAS, 143, 144t
Default network (DN),  134 HAq-​II,  144, 144t
d effect, Cohen’s,  40 monitoring outcome,  142–​143
Delayed ejaculation (DE),  516, 526 monitoring process,  143–​144
Deliberate Self-​Harm Inventory (DSHI),  196t, 199 OQ-​45,  143, 144t
Dementia Mood Assessment Scale (DMAS),  158t, 162, 165 overall evaluation,  144–​145
Dental Anxiety Inventory (DAI),  248t, 249, 255, 255t, 441t, 442 psychological mechanisms,  144
10-​item (DAI-​10),  442 QIDS-​SR,  142, 144t
30-​item (DAI-​30),  442 SAI, 144, 144t
Dental Cognitions Questionnaire,  249 therapeutic relationship,  144
Dental Fears Survey,  249 Top Problems,  143
Deployment Risk and Resilience Inventory (DRRI),  344 conclusions and future directions,  145
Deployment Risk and Resilience Inventory-​2 (DRRI-​2),  344 nature of major depressive disorder,  131–​135
Depression behavioral models,  132
alcohol use disorder with,  382 cognitive content models,  132–​133
with OCD,  313 cognitive process models,  133
with PTSD,  331 diagnostic criteria,  131
Depression, adult,  131–​145 emotion models,  133–​134
assessment, case conceptualization and treatment epidemiology,  131–​132
planning,  137–​142, 138t interpersonal models,  134
ACS, 138t, 140 relapse prevention models,  134–​135
Activity Schedule,  138 theories of depression,  132–​135
AIM, 138t, 140 Depression, children and adolescents,  99–​120
behavioral mechanisms,  138–​139 assessment, case conceptualization and treatment
case conceptualization,  137–​141 planning,  112–​116, 114t
case conceptualization, developing initial,  141–​142, 141f BERS,  114, 114t, 116
cognitive mechanisms,  139–​140 BIS,  114, 114t, 116
Daily Record of Dysfunctional Thoughts,  139 CAFAS,  114, 114t, 116
emotion-​focused mechanisms,  140 CAPA,  113, 115, 116
EQ, 138t, 139–​140 C-​GAS,  113, 114t
 subject Index 731

Childhood Trauma Questionnaire,  115–​116 K-​SADS,  117, 118, 118t

CIS,  113–​114, 114t MFQ,  117, 118, 118t
comorbid psychopathology,  112 overall evaluation,  118–​119
C-​WHO-​DAS,  115 psychosocial functioning,  117–​118
diagnostic interviews,  112–​113 RADS,  117, 118, 118t
family history, psychopathology,  116 RCDS,  117, 118, 118t
Family History Research and Diagnostic Criteria,  116 SAICA, 118t
Family History Screen,  116 clinical utility and construct validity,  99
Family Informant Schedule,  116 conclusions and future directions,  119–​120
Family Interview for Genetic Studies,  116 DSM-​5 changes,  99
LSI, 115, 116 DSM-​5 DMDD,  102
overall evaluation,  116 future research, issues,  119–​120
PAPA,  113, 115, 116 nature,  99–​102
PSS-​R,  114–​115, 116 comorbidities, 100
psychosocial functioning,  113–​115, 114t course,  100–​101
ratings scales,  113 functional impairment,  100
SAICA,  114, 114t, 116 prevalence, 100
severity, initial,  112 psychopathology,  99–​100
SLES, 115, 116 treatment,  101–​102
stressful life events,  115–​116 Depression, late life,  152–​166
UCLA PTSD index,  115–​116 assessment, case conceptualization and treatment
assessment, diagnosis,  105–​112, 106t planning,  157–​163, 158t
ARI, 112 BDI-​II,  157, 158t
BDI-​Y,  110 CES-​D,  157–​158, 158t, 162
BPI, 111 CESD-​R,  158, 158t
CAPA,  106, 106t, 107, 112 clinician rating scales,  160–​161
CBCL,  110–​111 COGNISTAT, 163
CDI, 106t, 109, 110, 112 CSDD, 158t, 161–​162, 163
CDRS-​R,  106t, 109 depression in dementia measures,  161–​162
CSI-​4,  111 DMAS, 158t, 162
DICA,  106, 106t, 108 GDRS, 158t, 160–​161
DISC-​IV,  106t, 108, 112 GDS,  158–​159, 158t
DMDD,  111–​112 GMS, 158t, 160
ECI-​4,  111 GMS-​DS,  158t, 160, 162–​163
fully structured interviews,  105, 108–​109 HRSD, 160
HBQ, 111 IDS, 158t, 161
K-​SADS,  106–​107, 106t, 112 MADRS, 158t, 161
MFQ, 106t, 109, 110, 112 Mini-​Mental State Examination,  163
overall evaluation,  112 NPI, 162
PAPA,  106, 106t, 107–​108, 112 overall evaluation,  162–​163
PROMIS network,  110 PHQ-​9,  158t, 159, 162
RADS, 106t, 109, 110, 112 SADS, 158t, 160
rating scales,  105, 109–​111 SCID-​CV,  158t, 160
RCDS, 106t, 109, 110, 112 SDS, 158t, 159
semi-​structured interviews,  105, 106–​108 self-​report measures,  157–​159
TRF,  110–​111 SF-​36,  163
YSR,  110–​111 structured interviews,  159–​160
assessment, purposes,  102–​105 assessment, diagnosis,  155–​157, 155t
attenuation effect,  104 CIDI, 156, 157
information source,  103–​104 CIDI 65+, 156
psychometric considerations,  104–​105 GMS, 155t, 156–​157
assessment, strategy,  99 GMS/​AGECAT,  155t, 156–​157
assessment, treatment monitoring and overall evaluation,  157
outcomes,  117–​119, 118t PSE, 156
CAFAS, 118 SADS, 155t, 156, 157
CBCL, 117 SCID,  155–​156, 155t, 157
CDI, 118, 118t structured interviews,  155–​157, 155t
C-​GAS,  117–​118, 118t, 119 assessment, purposes,  155
CGI-​I,  117, 119 assessment, treatment monitoring and
CSRS-​R,  117, 118, 118t outcomes,  163–​165, 164t
732 subject Index
Depression, late life (continued)
BDI-​II,  164t
CES-​D,  163, 164t, 165
clinician rating scales,  164–​165
CSDD, 164t, 165
depression in dementia measures,  165
DMAS, 165
GDRS,  164–​165, 164t
GDS, 163
GMS-​DS,  164, 165
HRSD, 164
IDS, 165
MADRS, 164t, 165
overall evaluation,  165
PHQ-​9,  163–​164, 164t, 165
self-​report measures,  163–​164
structured interviews,  164
conclusions and future directions,  165–​166
definition, 152
differential diagnosis, comorbidities,  152
nature,  152–​154
prevalence, 153
underreporting, 152
Depression Anxiety Stress Scales (DASS),  142–​143, 144t
Derogatis Sexual Functioning Inventory (DSFI),  523–​524,
523t, 530
Diagnosis as usual,  33
Diagnostic assessment. See also specific disorders
research–​practice gap,  18–​19
Diagnostic Interview for ADHD in Adults (DIVA  2.0), 62
Diagnostic Interview for Children and Adolescents
(DICA), 77t, 79, 81–​82, 221t, 222, 227t, 232t
Diagnostic Interview for Gambling Schedule (DIGS),  413t,
415, 418, 420t, 421
DSM-​IV,  416
Diagnostic Interview for Personality Disorders (DIPD),  466,
467t, 469–​470, 471, 475
Diagnostic Interview Schedule (DIS),  364, 439, 439t
Diagnostic Interview Schedule for Children
(DISC), 496t, 501
DSM-​IV,  51t, 52, 77t, 79, 81–​82, 221t, 222, 227t, 232t
Diagnostic likelihood ratio (DLR),  37
DICA. See Diagnostic Interview for Children and Adolescents
DIGS. See Diagnostic Interview for Gambling Schedule
DIGS DSM-​IV. See Diagnostic Interview for Gambling
Schedule (DIGS) DSM-​IV
Dimensional Assessment of Personality Pathology-​Basic
Questionnaire (DAPP-​BQ),  475–​476, 476t, 478t, 479
Dimension Obsessive Compulsive Scale (DOCS),  322t, 324
DIPD. See Diagnostic Interview for Personality Disorders
Direct Observation Form (DOF), ASEBA,  57, 77t, 81, 82t
DIS. See Diagnostic Interview Schedule
DISC. See Diagnostic Interview Schedule for Children
DISCDSM-​IV. See Diagnostic Interview Schedule for
Children, DSM-​IV
Disgust Emotion Scale,  251
Disgust Scale (DS),  248t
Revised (DS-​R),  251
Disruptive mood dysregulation disorder (DMDD),  99, 102. See
also Depression, children and adolescents
Dissemination, EBA,  17–​25. See also Evidence-​based
assessment (EBA), dissemination and implementation
DIVA2.0. See Diagnostic Interview for ADHD in Adults
DMAS. See Dementia Mood Assessment Scale
DMQ-​R. See Drinking Motives Questionnaire–​Revised
DMSL. See Drinking Self-​Monitoring Log
DOCS. See Dimension Obsessive Compulsive Scale
DOF, ASEBA. See Direct Observation Form
Dog Phobia Questionnaire,  250
DPICS. See Dyadic Parent-​Child Interaction Coding System
DPQ. See Drinking Patterns Questionnaire
DrInC. See Drinker Inventory of Consequences
Drinker Inventory of Consequences (DrInC),  390t, 393, 399t,
400, 401
Drinking Context Scale (DCS),  390t
Drinking Motives Questionnaire–​Revised (DMQ-​R),  390t, 396
Drinking Patterns Questionnaire (DPQ),  390t
Drinking Refusal Self-​Efficacy Questionnaire
(DRSEQ), 390t, 397
Revised (DRSEQ-​R),  391t, 397
Drinking Self-​Monitoring Log (DMSL),  391t
Drinking Triggers Inventory (DTI),  370
DRRI. See Deployment Risk and Resilience Inventory
DRRI-​2. See Deployment Risk and Resilience Inventory-​2
DRSEQ. See Drinking Refusal Self-​Efficacy Questionnaire
DRSEQ-​R. See Drinking Refusal Self-​Efficacy
Questionnaire–​Revised
Drug Abstinence Self-​Efficacy Scale (DASE),  370
Drug Abuse Screening Test (DAST),  362t, 363, 365, 423,
441t, 448
Drug-​Taking Confidence Questionnaire (DTCQ),  366t, 370
Drug Use Scale (DUS),  450t, 451
Drug Use Screening Inventory (DUSI),  362t, 363, 365,
386t, 387
DS. See Disgust Scale
DSDS. See Decreased Sexual Desire Screener
DSFI. See Derogatis Sexual Functioning Inventory
DSHI. See Deliberate Self-​Harm Inventory
DSISD. See Duke Structured Interview for Sleep Disorders
DS-​R. See Disgust Scale–​Revised
DTCQ. See Drug-​Taking Confidence Questionnaire
DTI. See Drinking Triggers Inventory
Duke Structured Interview for Sleep Disorders
(DSISD),  565–​566, 565t
DUS. See Drug Use Scale
DUSI. See Drug Use Screening Inventory
Dyadic Adjustment Scale (DAS),  493t, 494, 501t, 505, 523, 523t
7-​item (DAS-​7),  493t, 494
Dyadic Couples Inventory (DCI),  496t, 503
Dyadic Parent-​Child Interaction Coding System (DPICS),  77t,
79–​80, 85t, 86, 87
Dysfunctional Attitude Scale (DAS),  180, 553
Dysfunctional Beliefs and Attitudes about Sleep Scale
(DBAS), 570
16-​item (DBAS-​16),  567t, 568t, 570
Early Childhood Inventory-​5 (ECI-​5),  78
Eating Disorder Assessment for DSM-​5 (EDA-​5),  547t, 548, 550
Eating Disorder Diagnostic Scale (EDDS), DSM-​IV,  547t,
549–​550
 subject Index 733

Eating Disorder Examination Questionnaire (EDE-​Q) EPSI. See Eating Pathology Symptoms Inventory
versions  4.0, 6.0, 547t, 549, 550, 551, 551t, 553–​555, 554t EQ. See Experiences Questionnaire
versions  12-​16, 550, 551, 551t, 553–​555, 554t Erectile disorder (ED),  516–​517, 526–​527
versions  12-​17, 546–​548, 547t, 550 Erection Hardness Score (EHS),  525t, 526, 527
Eating disorders,  541–​555 ERQ. See Emotion Regulation Questionnaire
assessment, case conceptualization and treatment EtG. See Ethyl gluconic
planning,  550–​553, 551t Ethyl gluconic (EtG),  399t, 400
BCQ, 551t, 552–​553 Ethyl sulfate (EtS),  399t, 400
BDI-​II,  553 EtS. See Ethyl sulfate
BSQ, 551t, 552 Evaluating and Nurturing Relationship Issues
DAS, 553 (ENRICH), 496t, 504
EDE, versions  12-​16, 550, 551, 551t Evidence-​based assessment (EBA)
EDE-​Q, versions  4.0, 6.0, 550, 551, 551t APA core competency,  23
EPSI, 551t, 553 background,  xi–​xii
IIP, 553 criteria development,  3–​13
RSE, 553 assessment purposes,  6–​7
assessment, diagnosis,  546–​550, 547t criteria ratings,  7
EDA-​5,  547t, 548, 550 final thoughts,  12–​13
EDDS for DSM-​IV,  547t, 549–​550 “good-​enough” principle,  5–​6
EDE, versions  12-​17, 546–​548, 547t, 550 norms,  7–​9, 8b
EDE-​Q,  v 4.0, 6.0, 547t, 549, 550 psychometric properties,  7
overall evaluation,  550 rating criteria,  7
SCID-​5,  548, 550 reliability, 8b, 9–​10
SCID-​IV,  547t, 548, 550 sensitivity, treatment,  9b, 10–​11
assessment, purposes,  544–​546 utility, clinical,  9b, 11–​12
assessment, treatment monitoring and validity, 8b, 10–​11
outcomes,  553–​555, 554t literature, recent,  xi
EDE, versions  12-​16, 553–​555, 554t Evidence-​based assessment (EBA), clinical intervention and
EDE-​Q,  v 4.0, 6.0, 553–​555, 554t outcome improvement,  32–​42
YBC-​EDS,  554, 554t 3 P’s,  32
conclusions and future directions,  555 assessment, 32
nature,  541–​544 application of measurement,  32
anorexia nervosa,  541–​542 cost, additional,  41–​42
binge eating disorder,  542 diagnosis and treatment formulation as usual,  33
bulimia nervosa,  542 EBA  2.0, 32–​33, 37, 39, 42
comorbidities,  543–​544 prediction phase,  35–​38, 35f
culture and sex differences,  543 preparation phase,  33–​34, 34t
etiology, 543 prescription phase,  38–​40
prevalence,  542–​543 collateral informants, add,  38
prognosis, 544 focused constructs, assess more,  38
residual categories,  542 more intensive testing, other,  39
treatment, 544 semi-​structured diagnostic interviews,  38–​39
Eating Pathology Symptoms Inventory (EPSI),  551t, 553 treatment planning and goal setting,  39–​40
EBA  2.0, 32–​33, 37, 39, 42 treatment monitoring and outcome
ECBI-​5/​CASI-​54. See Eyberg Childhood Behavior Inventory-​5/​ idiographic goal setting,  41
Child & Adolescent Symptom Inventory-​5 maintenance monitoring,  41
ECBI/​SESBI-​R. See Eyberg Childhood Behavior Inventory/​ nomothetic goal setting,  40–​41
(Sutter-​Eyberg Child Behavior Inventory-​Revised process measurement,  41
ECI-​5. See Early Childhood Inventory-​5 Evidence-​based assessment (EBA), dissemination and
Ecological momentary assessment (EMA) implementation,  17–​25
eating disorders,  551–​552 APA Presidential Task Force on Evidence-​Based Practice,  17
self-​injurious thoughts and behavior,  205 assessment practice improvement efforts,  20–​23
EDA-​5. See Eating Disorder Assessment for DSM-​5 dissemination, 21
EDDS. See Eating Disorder Diagnostic Scale, DSM-​IV organizational-​level implementation,  21–​22
EDE-​Q. See Eating Disorder Examination Questionnaire system-​level,  22–​23
EHS. See Erection Hardness Score training, 21
Eland Color Tool,  589, 590, 598 future directions,  23–​25
Emetophobia Questionnaire,  250 history, 17
Emotion Regulation Questionnaire (ERQ),  138t, 140 monitoring and feedback systems,  17–​18, 20, 22
ENRICH. See Evaluating and Nurturing Relationship Issues progress monitoring,  17
734 subject Index
Evidence-​based assessment (EBA), dissemination and
implementation (continued)
public health improvement,  17
research–​practice gap,  18–​20
in assessment,  18
causes, 20
in diagnostic assessment,  18–​19
in progress monitoring,  19–​20
Evidence-​based practice (EBP),  xi
Evidence-​based practice in psychology (EBPP),  17
Evidence-​based treatment (EBT),  22, vii–​viii
Experiences Questionnaire (EQ),  138t, 139–​140
Exposure and response prevention (ERP),  312
Expressed emotion (EE) theory,  180–​181
Externalizing problems, prevalence benchmarks,  34t
Eyberg Childhood Behavior Inventory-​5/​Child & Adolescent
Symptom Inventory-​5 (ECBI-​5/​CASI-​54),  77t, 78, 82t,
85t, 86, 87
Eyberg Childhood Behavior Inventory/​(Sutter-​Eyberg Child
Behavior Inventory-​Revised (ECBI/​SESBI-​R),  77t, 78,
82t, 85t, 86
FABQ. See Fear-​Avoidance Beliefs Questionnaire
FACES-​III. See Family Adaptability and Cohesion
Evaluation Scales
Faces Pain Scale-​Revised (FPS-​R),  585t, 587–​588, 590,
597–​598, 597t
FAD. See Family Assessment Device
FAEE. See Fatty acid ethyl esters
Family Accommodation Scale–​Anxiety (FASA),  227t
Family Accommodation Scale–​Child Report
(FASA-​CR),  227t, 231
Family Adaptability and Cohesion Evaluation Scales
(FACES-​III),  545–​546
Family Assessment Device (FAD),  179t, 181
Family History Research Diagnostic Criteria
(FHRDC), 116, 394
Family History Screen,  116
Family Informant Schedule,  116
Family Interview for Genetic Studies,  116
Family Tree Questionnaire (FTQ),  394, 397
Fantasies, 315
FAPBI. See Frequency and Acceptability of Partner Behavior
Inventory
FASA. See Family Accommodation Scale–​Anxiety
FASA-​CR. See Family Accommodation Scale–​Child Report
FASM. See Functional Assessment of Self-​Mutilation
FAST. See Fast Alcohol Screening Test
Fast Alcohol Screening Test (FAST),  385, 386, 386t, 387
Father’s Alcoholism, Short Michigan Alcoholism Screening Test
(F-​MAST),  394
Fatty acid ethyl esters (FAEE),  399t, 400
FDI. See Functional Disability Inventory
Fear-​Avoidance Beliefs Questionnaire (FABQ),  616t, 619
Fear of Pain Questionnaire (FOPQ),  591t, 596, 597
Fear of Spiders Questionnaire (FSQ),  248t, 249, 254, 255, 255t
Fear Questionnaire (FQ),  274, 274t, 276–​277, 279, 280t, 281
Fear Survey Schedule (FSS),  248, 572t, 574
Children-​Revised (FSSC-​R),  221t, 223, 232t
Children-​Revised Short Form (FSSC-​R-​SF),  224
FEIS. See Female Experiences Interview Schedule
Female Experiences Interview Schedule (FEIS),  448
Female orgasmic disorder (FOD),  517, 527
Female Sexual Distress Scale (FSDS),  523t, 524, 525t, 530
Female Sexual Function Index (FSFI),  521, 525, 525t, 528, 529
Female sexual interest/​arousal disorder (FSIAD),  517, 527–​529
FFMPD. See Five Factor Model Personality Disorder scales
FHRDC. See Family History Research Diagnostic Criteria
FIRST. See Ford Insomnia Response to Stress Test
5-​HTOL. See 5-​Hydroxytryptophol
5-​Hydroxytryptophol (5-​HTOL),  399t, 400
Five Factor Model Personality Disorder scales (FFMPD),  466,
467t, 468, 470, 471, 473–​475, 476, 476t, 477, 478t, 479
Flinders Fatigue Scale,  574
F-​MAST. See Father’s Alcoholism, Short Michigan Alcoholism
Screening Test; Short Michigan Alcoholism Screening
Test–​Father’s Alcoholism
FMPS. See Frost Multidimensional Perfectionism Scale
Focused constructs,  38
FOPQ. See Fear of Pain Questionnaire
Ford Insomnia Response to Stress Test (FIRST),  567t, 571
Form  90, 390t, 392, 395, 398, 399t, 401
FPS-​R. See Faces Pain Scale-​Revised
FQ. See Fear Questionnaire
Frequency and Acceptability of Partner Behavior Inventory
(FAPBI),  496–​497, 496t, 503, 505
Frost Multidimensional Perfectionism Scale (FMPS),  138t,
139, 248t, 252
FSDS. See Female Sexual Distress Scale
FSFI. See Female Sexual Function Index
FSQ. See Fear of Spiders Questionnaire
FSS. See Fear Survey Schedule
FSSC-​R. See Fear Survey Schedule–​Children-​Revised
FSSC-​R-​SF. See Fear Survey Schedule–​Children-​Revised
Short Form
FTQ. See Family Tree Questionnaire
Functional assessment,  317
Functional Assessment of Self-​Mutilation (FASM),  202,
202t, 203
Functional Disability Inventory (FDI),  591t, 592–​593, 597,
597t, 598
GAATOR. See General Alcoholics Anonymous Tools of
Recovery Scale
GAD-​Q-​IV. See Generalized Anxiety Disorder Questionnaire-​IV
GAF. See Global Assessment of Functioning
GAIN-​ABS. See Global Appraisal of Individual Needs–​Web-​
based Assessment Building System
GAIN-​GSS. See Global Appraisal of Individual Needs–​Gain
Short Screener
GAIN-​I. See Global Appraisal of Individual Needs–​Initial
Interview
GAIN-​M. See Global Appraisal of Individual Needs,90 day M
GAIN-​SS. See Global Appraisal of Individual Needs–​Short
Screener
Gamblers’ Beliefs Questionnaire (GBQ),  424t, 426
Gambling Abstinence Self-​Efficacy Scale (GASS),  420t, 422,
423, 424t, 425
Gambling Behavior Inventory (GBI),  413t, 417, 418
Gambling Cognitions Inventory (GCI),  424t
 subject Index 735

Gambling disorders,  412–​427 SOGS-​3,  424t, 425

assessment, case conceptualization and treatment therapeutic mechanisms,  425
planning,  418–​423, 420t TLFB,  423–​424, 424t
ASI-​GSI,  419–​420, 420t, 423 urges, 426
associations and circumstances,  421–​422 comorbidities, 413
AUDIT, 422, 423 conclusions and future directions,  426–​427
comorbidities, 422 definition, 412
CPGI-​PGSI,  419, 420t DSM-​5,  412
DAST, 423 nature,  412–​413
DIGS, 420t, 421 types, 412
domains, important,  419, 419t Gambling Functional Assessment (GFA),  422
gambling frequency,  421 Revised (GFA-​R),  420t, 422
GAMTOMS,  420–​421, 420t, 423 Gambling Motives Questionnaire (GMQ),  420t, 421
GASS, 420t, 422, 423 Financial Motives (GMQ-​F),  420t
GFA, 422 Gambling Treatment Outcome Monitoring System
GFA-​R,  420t, 422 (GAMTOMS),  158–​159, 158t, 163, 420–​421, 420t, 423,
GMQ, 420t, 421 424–​425, 424t, 426
GMQ-​F,  420t Discharge Questionnaire (GAMTOMS-​D),  424, 424t
IGS, 420t, 421, 423 DSM-​IV Screen (GAMTOMS-​DSM),  413t, 416, 417, 418
NODS, 420t Follow-​up questionnaire (GAMTOMS-​F),  424, 424t
omnibus instruments,  419–​421, 419t γ-​glutamyl transferase (GGT),  386, 386t, 399t, 400, 401
overall evaluation,  422–​423 GAMTOMS. See Gambling Treatment Outcome
SCQG, 420t, 422 Monitoring System
self-​efficacy,  422 GAMTOMS-​D. See Gambling Treatment Outcome
severity of problem,  419–​420 Monitoring System–​Discharge Questionnaire
SOGS,  419, 420t, 423 GAMTOMS-​DSM. See Gambling Treatment Outcome
TGS, 420t, 421, 422 Monitoring System–​DSM-​IV Screen
TLFB, 420t, 421 GAMTOMS-​F. See Gambling Treatment Outcome Monitoring
treatment, 422 System–​Follow-​up questionnaire
assessment, diagnosis,  413–​418, 413t GAPD. See General Assessment of Personality Disorders
CPGI-​PGSI,  413t, 417, 418 GAS. See Goal Attainment Scaling
DIGS-​DSM,  413t, 415, 418 GAS-​7. See Generalized Anxiety Disorder Scale
GAMTOMS-​DSM,  413t, 416, 417, 418 GASS. See Gambling Abstinence Self-​Efficacy Scale
GBI, 413t, 417, 418 GBI. See Gambling Behavior Inventory; General Behavior
NODS, 413t, 415–​416, 418 Inventory
NODS-​CLiP,  415–​416, 417 GBQ. See Gamblers’ Beliefs Questionnaire
NODS-​PERC,  417 GCI. See Gambling Cognitions Inventory
PPGM, 413t, 417–​418 GDRS. See Geriatric Depression Rating Scale
SCID-​5,  413t GDS. See Geriatric Depression Scale
SCID-​5-​RV,  413t General Alcoholics Anonymous Tools of Recovery Scale
SCI-​PG,  413t, 415, 418 (GAATOR), 399t
SOGS, 413t, 414–​415, 418 General Assessment of Personality Disorders (GAPD),  479
SOGS-​3,  414 General Behavior Inventory (GBI),  174t, 177–​178
SOGS-​R,  413t, 414–​415 Generalized anxiety disorder (GAD),  293–​306
assessment, treatment monitoring and alcohol use disorder with,  382
outcome,  423–​426, 424t assessment, case conceptualization and treatment
ASI-​GSI,  424, 424t, 426 planning,  299–​303, 300t
cognitive distortions, coping skills, and anxiety, depression, and quality of life,  300–​301
self-​efficacy,  425–​426 BAI,  300–​301, 300t
gambling behavior,  423–​424 BDI-​II,  300t, 301
gambling-​related consequences,  424–​425 CAQ, 300t, 303
GAMTOMS,  424–​425, 424t, 426 cognitive processes,  301–​303
GAMTOMS-​D,  424, 424t IUS, 300t, 301–​302
GAMTOMS-​F,  424, 424t NPOQ, 300t, 303
GASS, 424t, 425 overall evaluation,  303
GBQ, 424t, 426 PSWQ,  299–​300, 300t
GCI, 424t QLQ, 300t, 301
NODS-​3,  424t, 425 QOLI, 300t, 301
overall evaluations,  426 worry severity measure,  299–​300
PC-​YBOCS,  424t, 426 WW-​II,  300t, 302
736 subject Index

Generalized anxiety disorder (GAD) (continued) 90 day (GAIN-​M)M,  372t, 373, 375

assessment, diagnosis,  296–​299, 297t Gain Short Screener (GAIN-​GSS),  385, 386t, 387, 388
ADIS-​5,  298 Initial Interview (GAIN-​I),  362t, 364–​365, 366t, 367–​368
ADIS-​IV,  297t, 298 Short Screener (GAIN-​SS),  365
GAD-​Q,  297–​298, 297t Web-​based Assessment Building System (GAIN-​ABS),  364
overall evaluation,  299 Global Assessment of Functioning (GAF),  450–​451
SCID-​5-​CV,  298–​299 Global Measure of Sexual Satisfaction (GMSEX),  523t, 524
SCID-​I/​P,  297t, 299 GMQ. See Gambling Motives Questionnaire
self-​report measures,  297–​298 GMQ-​F. See Gambling Motives Questionnaire–​Financial
semi-​structured interviews,  298–​299 Motives
WAQ, 297, 297t GMS. See Geriatric Mental State Schedule
assessment, purposes,  296 GMS/​AGECAT. See Geriatric Mental State
assessment, treatment monitoring and Schedule–​AGECAT
outcome,  303–​305, 304t GMS-​DS. See Geriatric Mental State Schedule DS
ADIS-​IV,  304t, 305 GMSEX. See Global Measure of Sexual Satisfaction
BAI, 304t, 305 Goal Attainment Scaling (GAS),  143, 144t, 501t, 505
BDI-​II,  304t, 305 Goal setting,  39–​40
CAQ, 304t, 305 idiographic, 41
IUS, 304t, 305 nomothetic,  40–​41
NPOQ, 304t, 305 Golombok-​Rust Inventory of Sexual Satisfaction (GRISS),  519t,
overall evaluation,  305 521, 523, 523t, 525t, 526, 529, 530
PSWQ, 304, 304t “Good-​enough” principle,  5–​6
PSWQ-​PW,  304, 304t GRISS. See Golombok-​Rust Inventory of Sexual Satisfaction
QLQ, 304t, 305 GSA. See GenitoSensory Analyzer
QOLI, 304t, 305 GSES. See Glasgow Sleep Effort Scale
SCID-​I/​P,  304t
self-​monitoring booklet,  304–​305, 304t Hamilton Rating Scale for Depression (HRSD),  160, 164
treatment monitoring,  304–​305 HAq-​II. See Helping Alliance Questionnaire, Revised; Revised
treatment outcome,  305 Helping Alliance Questionnaire
WAQ, 304t Harkavy Asnis Suicide Scale (HASS),  197t, 200
WW-​II,  304t, 305 Harvard Trauma Questionnaire (HTQ),  345
conclusions and future directions,  306 HASS. See Harkavy Asnis Suicide Scale
nature,  293–​296 HBQ. See McArthur Health and Behavior Questionnaire
comorbidity and cost,  295–​296 HCL-​32. See Hypomania Checklist
diagnostic criteria, history,  293–​294 Health and Behavior Questionnaire (HBQ), McArthur,  111
etiology,  294–​295 Helping Alliance Questionnaire, Revised (HAq-​II),  144, 144t
onset and course,  294 HPS. See Hypomanic Personality Scale
prevalence, sex differences, and age,  295 HRSD. See Hamilton Rating Scale for Depression
prevalence benchmarks,  34t HTQ. See Harvard Trauma Questionnaire
Generalized Anxiety Disorder Questionnaire-​IV 5-​Hydroxytryptophol (5-​HTOL),  399t, 400
(GAD-​Q-​IV,  297–​298, 297t Hypomania Checklist (HCL-​32),  178
Generalized Anxiety Disorder Scale (GAS-​7),  498 Hypomanic Personality Scale (HPS),  178
Genito-​pelvic pain/​penetration disorder (GPPPD),  517–​518,
529–​530 IBES. See Illness Behavior Encouragement Scale
GenitoSensory Analyzer (GSA),  527 ICU. See Inventory of Callous–​Unemotional Traits
Geriatric Depression Rating Scale (GDRS),  158t, 160–​161, IDAS. See Inventory of Depression and Anxiety Symptoms
164–​165, 164t IDCS. See Interactional Dimensions Coding System
Geriatric Depression Scale (GDS),  164t IDI. See Insomnia Diagnostic Interview
Geriatric Mental State Schedule (GMS),  155t, 156–​157, Idiographic goal setting,  41
158t, 160 IDS. See Indices of Problems; Inventory of Depressive
AGECAT (GMS/​AGECAT),  155t, 156–​157 Symptomatology; Inventory of Drinking Situations
GMS-​DS,  158t, 160, 162–​163, 164, 165 IDS-​42. See Inventory of Drinking Situations, 42-​item
GET.ON PAPP,  282 IDS-​C. See Inventory of Depressive
GFA. See Gambling Functional Assessment Symptomatology–​Clinician-​rated
GFA-​R. See Gambling Functional Assessment–​Revised IDS-​SR. See Inventory of Depressive
GGT. See γ-​glutamyl transferase Symptomatology–​Self-​Report
Giner TAS. See Giner transdermal alcohol sensor IDTS. See Inventory of Drug Taking Situations
Giner transdermal alcohol sensor (Giner TAS),  399t IDUC. See Inventory of Drug Use Consequences
Glasgow Sleep Effort Scale (GSES),  567t, 571 IES-​R. See Impact of Event Scale-​Revised
Global Appraisal of Individual Needs (GAIN) IGS. See Inventory of Gambling Situations

IIEF. See International Index of Erectile Function
IIEF-​5. See International Index of Erectile Function, 5-​item
III. See Interpretation of Intrusions Inventory
IIP. See Inventory of Interpersonal Problems
IIRS. See Illness Intrusiveness Rating Scale
Illness Behavior Encouragement Scale (IBES),  595
Illness Intrusiveness Rating Scale (IIRS),  255t, 257
Illness Management and Recovery (IMR),  441t, 446, 450t, 452
Illness Perception Questionnaire–​Revised (IPQ-​R),  613
ILSS. See Independent Living Scale Survey
Impact of Event Scale-​Revised (IES-​R),  336t, 339, 346t
Impaired Control Scale,  399t
Impairment Rating Scale (IRS),  55t, 57, 59–​60, 60t
Implementation, EBA,  17–​25. See also Evidence-​based
assessment (EBA), dissemination and implementation
Important People and Activities interview (IPA),  391t, 397
Important People measure (IP-​5),  397
IMR. See Illness Management and Recovery
IMSA. See Inventory of Motivations for Suicide Attempts
Independent Living Scale Survey (ILSS),  441t, 444, 445,
450t, 451
Index of Dental Fear and Anxiety,  249
Index of Premature Ejaculation (IPE),  519t, 525t, 530
Index of Sexual Satisfaction (ISS),  523t, 524, 525t
Indices of Problems (IDS),  390t
Insight and Treatment Attitudes Questionnaire,  180
Insomnia Diagnostic Interview (IDI),  565
Insomnia disorder,  563–​577
assessment, case conceptualization and treatment
planning,  566–​571, 567t
APS, 567t, 571
case formulation,  567–​569, 568t–​569t
conceptual models,  566–​567
CSD, 567t, 569–​570
DBAS-​16,  567t, 570
FIRST, 567t, 571
GSES, 567t, 571
overall evaluation,  571
PSAS, 567t, 570
SAMI, 567t, 571
SBSRS, 567t, 570
self-​report measures,  569–​571
SPS, 567t, 571
assessment, diagnosis,  565–​566, 565t
clinical interviews,  565–​566
DSISD,  565–​566, 565t
IDI, 565
overall evaluation,  566
polysomnography, 565t, 566
assessment, purposes,  565
assessment, treatment monitoring and
outcomes,  572–​575, 572t
actigraphy, 572t, 573
BAI, 572t, 574–​575
BDI-​II,  572t, 575
CSD,  572, 572t, 575
fatigue,  573–​574
Flinders Fatigue Scale,  574
FSS, 572t, 574
ISI,  572–​573, 572t, 575
subject Index 737
MFI, 572t, 574
overall evaluation,  575
PHQ-​9,  572t, 575
PSQI, 572t, 573
psychological/​mood symptoms,  574–​575
sleep/​insomnia,  572–​573
STAI, 572t, 575
conclusions and future directions,  577
critical issues
actigraphy, 576
barriers and challenges,  575–​576
ISI, 576
PSG, 576
streamlining, for clinical decision-​making,  576
nature and significance,  563–​565
clinical features and diagnostic criteria,  563–​564
epidemiology and public health,  564–​565
Insomnia Severity Index (ISI),  572–​573, 572t, 575, 576
Interactional Dimensions Coding System (IDCS),  496t, 501
Internal State Scale (ISS),  183
International Index of Erectile Function (IIEF),  519t, 522,
525t, 526, 530
5-​item (IIIEF-​5),  519t, 525t, 526–​527
International Personality Disorder Examination (IPDE),  466,
467, 467t, 468, 469, 470, 475
International Stigma of Mental Illness (ISMI),  441t, 447
Interpretation of Intrusions Inventory (III),  318–​319, 319t, 321
Intolerance of uncertainty (IU),  301–​302
Intolerance of Uncertainty Scale (IUS),  300t, 301–​302,
304t, 305
Intravaginal ejaculation latency time (IELT),  530
Inventory of Callous–​Unemotional Traits (ICU),  82t, 84
Inventory of Depression and Anxiety Symptoms (IDAS),  179
Inventory of Depressive Symptomatology (IDS),  136, 161, 165
Clinician-​rated (IDS-​C),  161
Self-​report (IDS-​SR),  161
Inventory of Drinking Situations (IDS),  390t, 396, 397
Inventory of Drinking Situations,42-​item (IDS-​42), 396
Inventory of Drug Taking Situations (IDTS),  366t, 370
Inventory of Drug Use Consequences (IDUC),  366t, 368, 372t,
373, 375
Inventory of Gambling Situations (IGS),  420t, 421, 423
Inventory of Interpersonal Problems (IIP),  553
Inventory of Motivations for Suicide Attempts (IMSA),  205–​206
Inventory of Statements about Self-​Injury (ISAS),  202t, 203
IOWA, 59, 60t
IP-​5. See Important People measure
IPA. See Important People and Activities interview
IPDE. See International Personality Disorder Examination
IPE. See Index of Premature Ejaculation
IPQ-​R. See Illness Perception Questionnaire–​Revised
IRS. See Impairment Rating Scale
ISAS. See Inventory of Statements about Self-​Injury
ISI. See Insomnia Severity Index
ISMI. See International Stigma of Mental Illness
ISS. See Index of Sexual Satisfaction; Internal State Scale
IUS. See Intolerance of Uncertainty Scale
JACQ. See Jellinik Alcohol Craving Questionnaire
Jellinik Alcohol Craving Questionnaire (JACQ),  390t, 396
738 subject Index
Kategoriensystem für Partnerschaftliche Interaktion
(KPI), 496t, 501
Kiddie Schedule for Affective Disorders and Schizophrenia for
School-​Age Children (K-​SADS),  52–​53, 106–​107, 106t,
112, 117, 118, 118t, 177, 179, 221t, 222, 227t, 232t
Present and Lifetime Version (K-​SADS-​PL),  174t, 177
KID-​SCID. See Structured Clinical Interview for DSM-​IV
Childhood Diagnoses
KPI. See Kategoriensystem für Partnerschaftliche Interaktion
K-​SADS. See Kiddie Schedule for Affective Disorders and
Schizophrenia for School-​Age Children
K-​SADS-​PL. See Kiddie Schedule for Affective Disorders and
Schizophrenia for School-​Age Children–​Present and
Lifetime Version
Labial thermistor clip,  528
LDH. See Lifetime Drinking History
LDQ. See Leeds Dependence Questionnaire
LEC. See Life Events Checklist
Leeds Dependence Questionnaire (LDQ),  399t
Liebowitz Social Anxiety Scale (LSAS),  255t, 256
LIFE. See Living in Family Environments
Life Events Checklist (LEC),  342t, 343
Life Situation Survey (LSS),  399t
Life Stress Interview (LSI),  115, 116
Life Stressor Checklist-​Revised (LSC-​R),  342t, 343
Life Stressors and Social Resources Inventory (LISRES),  390t
Lifetime Drinking History (LDH),  390t, 393
LISRES. See Life Stressors and Social Resources Inventory
Living in Family Environments (LIFE),  496t, 501
LSAS. See Liebowitz Social Anxiety Scale
LSC-​R. See Life Stressor Checklist-​Revised
LSI. See Life Stress Interview
LSS. See Life Situation Survey
MADRS. See Montgomery-​Åsberg Depression Rating Scale
Maintenance monitoring,  41
Major Depressive Disorder (MDD). See Depression, children
and adolescents
Male hypoactive sexual desire disorder (MHSDD),  518, 530
Male Sexual Health Questionnaire (MSHQ),  519t, 522, 526
Male Sexual Health Questionnaire–​Ejaculation Short
Form(MSHQ-​EjD),  519t, 526
MAP. See Maudsley Addiction Profile
Marijuana Problems Scale (MPS),  366t, 368–​369, 372t, 373
Marijuana Withdrawal Checklist (MWC),  362t, 364
Marital Interaction Coding System (MICS),  502
Marital Satisfaction Inventory–​Brief (MSI-​B),  493t, 494,
501t, 505
Marital Satisfaction Inventory–​Revised (MSI-​R),  413t, 415–​416,
418, 420t, 496–​497, 496t, 497, 501t, 504
3-​Month Version (NODS-​3),  424t, 425
MAS. See Bech–​Rafaelsen Mania Scale
MASC. See Multidimensional Anxiety Scale for Children
MASC-​2. See Multidimensional Anxiety Scale for
Children–​Revised
MASC-​2-​2-​P. See Multidimensional Anxiety Scale for
Children–​Revised, Parallel Version for Parent
MASC-​2-​SR. See Multidimensional Anxiety Scale for
Children–​Revised, Self-​Report Version for Child
MAST. See Multi-​Attitude Suicide Tendency Scale for
Adolescents
Maudsley Addiction Profile (MAP),  399t
Maudsley Obsessional Compulsive Inventory (MOCI),  323
McArthur Health and Behavior Questionnaire (HBQ),  111
MCAS. See Multnomah Community Ability Scale
McCoy Female Sexuality Questionnaire (MFSQ),  519t, 521,
525t, 528, 529
McGill Pain Questionnaire (MPQ),  611t, 612
Short Form (SF-​MPQ),  611t, 612–​613
Short Form-​2 (SF-​MPQ-​2),  611t, 612–​613
MCMI–​IV. See Millon Clinical Multiaxial Inventory-​IV
MCV. See Mean corpuscular volume
MDQ. See Mood Disorder Questionnaire
Mean corpuscular volume (MCV),  386, 386t, 399t, 400
Medical Fear Survey,  249
Memories
situationally accessible,  331
verbally accessible,  331
Mental Health Recovery Measure (MHRM),  441t, 444, 445,
446, 450t, 451
Mental Illness Research Educational and Clinical Center Global
Assessment of Functioning (MIRECC-​GAF),  441t,
444, 445, 450t, 451
MFI. See Multidimensional Fatigue Inventory
MFQ. See Mood and Feelings Questionnaire
MFSQ. See McCoy Female Sexuality Questionnaire
MHRM. See Mental Health Recovery Measure
MI. See Mobility Inventory for Agoraphobia
MICS. See Marital Interaction Coding System
Millon Clinical Multiaxial Inventory-​IV (MCMI–​IV),  466,
467, 467t, 468–​469, 471, 472–​473, 474, 475
M.I.N.I. See Mini International Neuropsychiatric Interview6.0
Mini International Neuropsychiatric Interview  6.0 (M.I.N.I.),
362t, 363–​364, 365, 389, 391, 439, 439t
Minimally important differences (MID) method,  40
Mini-​Mental State Examination,  163
Minnesota Multiphasic Personality Inventory (MMPI-​2), body
image scales,  35
Minnesota Multiphasic Personality Inventory-​2 (MMPI-​2),  35,
466, 467, 467t, 470, 471, 472–​473, 474, 614
MIRECC-​GAF. See Mental Illness Research Educational and
Clinical Center Global Assessment of Functioning
Mississippi Scale. See Mississippi Scale for
Combat-​Related PTSD
Mississippi Scale for Combat-​Related PTSD (Mississippi
Scale), 336t, 339–​340
MMEA. See Multidimensional Measure of Emotional Abuse
MMPI-​2. See Minnesota Multiphasic Personality Inventory-​2
Mobility Inventory for Agoraphobia (MI),  274, 274t, 277, 280t, 281
MOCI. See Maudsley Obsessional Compulsive Inventory
Modified Scale for Suicide Ideation (MSSI),  196t, 199
Monitoring. See also specific disorders
maintenance, 41
progress, research–​assessment gap,  18
treatment,  40–​43 (See also Treatment monitoring and outcome)
Monitoring and feedback systems (MFSs),  17–​18, 20, 21
Contextualized Feedback System,  22
Montgomery-​Åsberg Depression Rating Scale (MADRS),  158t,
161, 164t, 165

Mood and Feelings Questionnaire (MFQ),  106t, 109, 110, 112,
117, 118, 118t
Shorter (SMFQ),  519t, 522, 528, 529
Mood Disorder Questionnaire (MDQ),  174t, 178
Mood disorders
prevalence benchmarks,  34t
with PTSD,  332
Mood Spectrum Self-​Reports (MOODS-​SR),  178, 529
MOODS-​SR. See Mood Spectrum Self-​Reports
Mother’s Alcoholism, Short Michigan Alcoholism Screening
Test (M-​SMAST),  394
MPI. See Multidimensional Pain Inventory-​M, West Haven–​Yale;
West Haven–​Yale Multidimensional Pain Inventory
MPI-​M. See Multidimensional Pain Inventory-​M, West
Haven–​Yale,61-​item, Modified instructions; West
Haven–​Yale Multidimensional Pain Inventory, 61-​item,
Modified instructions
MPQ. See McGill Pain Questionnaire
MPS. See Marijuana Problems Scale
MSHQ. See Male Sexual Health Questionnaire
MSHQ-​EjD. See Male Sexual Health Questionnaire–​
Ejaculation Short Form
MSI-​B. See Marital Satisfaction Inventory–​Brief
MSI-​R. See Marital Satisfaction Inventory–​Revised
MSI-​R NODS-​3. See Marital Satisfaction Inventory–​Revised,
3-​Month Version
M-​SMAST. See Mother’s Alcoholism, Short Michigan
Alcoholism Screening Test; Short Michigan Alcoholism
Screening Test–​Mother’s Alcoholism
MSSI. See Modified Scale for Suicide Ideation
Multi-​Attitude Suicide Tendency Scale for Adolescents
(MAST), 202t, 203, 386t, 387, 388, 390t, 393, 441t, 448
Multidimensional Anxiety Scale for Children (MASC),  221t,
223–​224, 227t, 232t
Revised (MASC-​2),  223, 224, 226
Revised, Parallel Version for Parent (MASC-​2-​2-​P),  224
Revised, Self-​Report Version for Child (MASC-​2-​SR),  224
Multidimensional Fatigue Inventory (MFI),  572t, 574
Multidimensional Measure of Emotional Abuse (MMEA),  504
Multidimensional Pain Inventory-​M (MPI), West
Haven–​Yale,  610–​611, 611t, 615–​616 616t, 619, 620, 620t
61-​item, Modified instructions (MPI-​M),  616, 616t
Multnomah Community Ability Scale (MCAS),  441t, 444,
445, 450t, 451
Mutilation Questionnaire,  249
MWC. See Marijuana Withdrawal Checklist
National Comorbidity Survey Replication (NCS–​R),  131, 153,
243, 266, 331
National Epidemiological Survey on Alcohol and Related
Conditions (NESARC),  360, 382
III (NESARC-​III),  381, 382
National Opinion Research Center DSM-​IV Screen for
Gambling Problems (NODS)
Preoccupation, Escape, Risked relationships, and Chasing
(NODS-​PERC),  417
National Opinion Research Center DSM-​IV Screen for
Gambling Problems, Control, Lying, and Preoccupation
(NODS-​CLiP),  415–​416, 417
National Vietnam Veterans Readjustment Study (NVVRS),  331
subject Index 739
NCS–​R. See National Comorbidity Survey Replication
Negative predictive value (NPV),  385
Negative Problem Orientation Questionnaire (NPOQ),  300t,
303, 304t, 305
NESARC. See National Epidemiological Survey on Alcohol
and Related Conditions
NESARC-​III. See National Epidemiological Survey on Alcohol
and Related Conditions III
Neurobehavioral Cognitive Status Examination
(COGNISTAT), 163
Neuropathic Pain Scale (NPS),  611t, 612, 615, 620t
Neuropsychiatric Inventory (NPI),  162
New Sexual Satisfaction Scale (NSSS),  523t, 524
Nocturnal penile tumescence tests (NPT),  526
NODS-​CLiP. See National Opinion Research Center DSM-​IV
Screen for Gambling Problems, Control, Lying, and
Preoccupation
NODS-​PERC. See National Opinion Research Center DSM-​IV
Screen for Gambling Problems–​Preoccupation, Escape,
Risked relationships, and Chasing
Nomograms, probability,  35
Nomothetic goal setting,  40–​41
Non-​Suicidal Self-​Injury-​Assessment Tool (NSSI-​AT),  206
Non-​Suicidal Self-​Injury Disorder Scale (NSSID),  205
Norm-​referenced measures,  40
Norms,  7–​9, 8b
NPI. See Neuropsychiatric Inventory
NPOQ. See Negative Problem Orientation Questionnaire
NPS. See Neuropathic Pain Scale
NRS. See Numerical rating scales
NSSI-​AT. See Non-​Suicidal Self-​Injury-​Assessment Tool
NSSID. See Non-​Suicidal Self-​Injury Disorder Scale
NSSS. See New Sexual Satisfaction Scale
Numerical rating scales (NRS),  585t, 588, 597t, 619, 620t
NVVRS. See National Vietnam Veterans Readjustment Study
Objective Opiate Withdrawal Scale,  364
OBQ. See Obsessive Beliefs Questionnaire
Obsessions,  314–​315
Obsessive Beliefs Questionnaire (OBQ),  318, 319t, 321
Obsessive-​compulsive disorder (OCD),  311–​325
assessment, case conceptualization and treatment
planning,  317–​321, 319t
behavioral ritual responses,  319–​320
case conceptualization,  320, 321f
cognitive features,  318–​319, 318t
dysfunctional beliefs,  318–​319, 318t
external triggers,  317
feared consequences,  318
functional assessment,  317
III,  318–​319, 319t, 321
intrusive thoughts,  317
mental ritual responses,  320
OBQ,  318, 319t, 321
obsessional stimuli,  317
overall evaluation,  321
passive avoidance responses,  319
practical considerations,  320–​321
responses to obsessional distress,  319–​320
self-​monitoring,  320
740 subject Index

Obsessive-​compulsive disorder (OCD) (continued) BAPQ-​P,  591t, 596–​597

assessment, diagnosis,  314–​317, 315t FDI, 591t, 592–​593, 597
ADIS-​IV,  315–​316, 315t FOPQ, 591t, 596, 597
BABS, 315t, 316 functioning, physical, social, and role,  592–​595
general description of problem,  314 IBES, 595
overall evaluation,  317 overall evaluation,  597
practical considerations,  316–​317 pain diaries,  591–​592, 591t
SCID-​IV,  315t, 316 pain frequency and duration,  591–​592
senselessness of symptoms, insight,  316 PCS-​C,  591t, 595–​596, 597
standardized diagnostic assessment,  315–​316 PedsQL  4.0, 591t, 593–​594
symptom checklist,  314 PEQ, 591t, 596
symptoms vs. other phenomena,  314–​315 psychological factors,  595–​597
Y-​BOCSC-​SC,  314, 315t assessment, diagnosis,  585–​590, 585t
assessment, purposes,  313 APPT,  589–​590
assessment, treatment monitoring and Eland Color Tool,  589, 590
outcomes,  322–​325, 322t FPS-​R,  585t, 587–​588, 590
DOCS, 322t, 324 NRS, 585t, 588
interview measures,  322 The Oucher,  585t, 586–​587
OCI-​R,  322t, 323 overall evaluation,  589
overall evaluation,  324–​325 pain frequency and duration,  589
PI-​R,  322t, 323 pain intensity,  585–​588
practical considerations,  324 pain quality,  589
SCOPI, 322t, 324 Pieces of Hurt Tool,  585t, 586, 590
self-​report measures,  322–​324 VAS, 585t, 588, 590
VOCI, 322t, 323 assessment, treatment monitoring and
Y-​BOCS,  322–​323, 322t outcomes,  597–​598, 597t
cognitive-​behavioral models,  312–​313 APPT, 597t, 598
conclusions and future directions,  325 ARCs, Protect and Monitor subscales,  597t, 598
conditioning models,  312 Eland Color Tool,  598
depression with,  313 FDI, 597t, 598
exposure and response prevention,  312 FPS-​R,  597–​598, 597t
nature,  311–​313 NRS, 597t
associated features,  313 The Oucher,  597, 597t
biological models,  312 overall evaluation,  598
definition,  311–​312 PedsQL  4.0, 597t, 598
epidemiology, course, and prognosis,  313 Pieces of Hurt Tool,  597, 597t
etiological models and treatment,  312–​313 VAS, 597t, 598
psychological models,  312–​313 CHOIR, 599
Obsessive-​Compulsive Drinking Scale (OCDS),  390t, 395 conclusions and future directions,  598–​599
Obsessive-​Compulsive Inventory-​Revised (OCI-​R),  322t, 323 definition, 583
OCDS. See Obsessive-​Compulsive Drinking Scale nature,  584–​585
OCI-​R. See Obsessive-​Compulsive Inventory-​Revised acute,  584–​585
OMNI. See OMNI Personality Inventory chronic, 585
OMNI Personality Inventory (OMNI),  466, 467, 467t, 474, 475 definition, 584
OQ-​45. See Outcome Questionnaire-​45 etiology, 584
Orgasm Rating Scale (ORS),  527 pain measurement, defined,  583
ORS. See Orgasm Rating Scale Peds-​CHOIR,  599
Outcome monitoring,  17. See also specific disorders PROMIS, 599
Outcome Questionnaire-​45 (OQ-​45),  137, 143, 144t research, modern era,  583
self-​report,  583–​584
P3. See Pain Patient Profile Pain, chronic, adult,  608–​621
PACS. See Penn Alcohol Craving Scale assessment, case conceptualization and treatment
Padua Inventory-​Revised (PI-​R),  322t, 323 planning,  615–​619, 616t
PAI. See Personality Assessment Inventory antecedents and consequences,  616
Pain, child and adolescent,  583–​600 anxiety/​avoidance, pain-​related,  618–​619
assessment, case conceptualization and treatment cognitions/​beliefs, pain-​related,  616–​617
planning,  590–​597, 591t coping strategies,  617–​618
ARCS, 595, 597 CPCI-​42,  616t, 618
BAPQ, 591t, 596–​597 CPCI, 616t, 617–​618, 619
 subject Index 741

CSQ, 616t, 617 internal experience,  608

FABQ, 616t, 619 prevalence and consequences,  609
integrating assessment information,  616 Pain Anxiety Symptoms Scale (PASS),  616t, 618, 619
MPI,  615–​616 616t, 619 20-​item (PASS-​20),  616t, 618
MPI-​M,  616 616t Pain Beliefs and Perceptions Inventory (PBAPI),  616t, 617
overall evaluation,  619 Pain Beliefs Questionnaire (PBQ),  616t, 617
pain diary,  616, 616t, 619 Pain Catastrophizing Scale (PCS),  529, 611t, 613, 616t,
PASS, 616t, 618, 619 617, 620t
PASS-​20,  616t, 618 Children (PCS-​C),  591t, 595–​596, 597
PBAPI, 616t, 617 Pain diaries,  591–​592, 591t, 611t, 612, 616, 616t, 619, 620, 620t
PBQ, 616t, 617 Pain Experience Questionnaire (PEQ),  591t, 596
PCS, 616t, 617 Pain Patient Profile (P  3), 611t, 613
temporal patterns,  616 Panic, prevalence benchmarks,  34t
TKS, 616t, 618–​619 Panic disorder and agoraphobia,  266–​284
TKS-​11,  616t, 619 assessment, case conceptualization and treatment
assessment, diagnosis,  609–​615, 611t planning,  273–​279, 274t
BDS-​II,  613 ACQ,  274, 274t, 276, 279
BPI-​SF,  611–​612, 611t, 615 APPQ,  274, 274t, 277–​278
central assessment domains,  609, 610t ASI,  274–​275, 274t, 279
condition-​specific measures,  614 ASI-​3,  274, 274t, 275, 279
disability and quality of life,  614 BAT, 278, 279
DSM-​5,  610 behavioral approach tests,  278
emotional distress and catastrophic thinking,  613 BSQ,  274, 274t, 275–​276, 279
IPQ-​R,  613 FQ,  274, 274t, 276–​277, 279
malingering, 614 MI,  274, 274t, 277
MMPI-​2,  614 overall evaluation,  279
MPI,  610–​611, 611t, 615 physiological measures,  278–​279
MPQ, 611t, 612 self-​report instruments,  273–​278
NPS, 611t, 612, 615 SUDS, 278
overall evaluation,  615 in vivo cognition measures,  279
P  3, 611t, 613 assessment, diagnosis,  270–​273, 271t
pain diary,  611t, 612 ADIS and ADIS-​5,  270–​272, 271t
pain intensity and interference,  611–​613 ADIS-​R,  271, 273
PCS, 611t, 613 anxiety disorders interview schedule,  270–​272
POMS, 613 KID-​SCID,  272
RMDQ, 611t, 614, 615 overall evaluation,  273
SF-​36,  614 PDSS, 271t, 273
SF-​MPQ,  611t, 612–​613 PDSS-​SR,  273
SF-​MPQ-​2,  611t, 612–​613 SCID-​5,  271t, 272–​273
temporal characteristics and qualities,  611–​613 SCID-​5-​CT,  272
WOMAC, 611t, 614 SCID-​5-​CV,  272
assessment, purposes,  609, 610t SCID-​5-​RV,  272
assessment, treatment monitoring and assessment, purpose,  270
outcome,  619–​621, 620t assessment, treatment monitoring and
BDI, 620, 620t outcome,  279–​283, 280t
BPI-​SF,  619–​620, 620t ACQ, 280t, 281
MPI, 620, 620t ACQ-​CON,  280–​281, 280t
NPS, 620t ADIS, 279, 280t
NRS, 619, 620t APPQ, 280t, 281
overall evaluation,  620–​621 ASI, 280t
pain diary,  620, 620t ASI-​3,  280t
PCS, 620t BATs,  282–​283
SF-​36,  620, 620t BSQ, 280t, 281
VAS, 619, 620t FQ, 280t, 281
VRS, 620, 620t GET.ON PAPP,  282
conclusions and future directions,  621 interviews,  279–​280
nature,  608–​609 MI, 280t, 281
decoding, observer,  609 PDSS, 280, 280t
encoding, expressive behavior,  609 SCID, 279, 280t
742 subject Index

Panic disorder and agoraphobia (continued) Penn State Worry Questionnaire (PSWQ),  299–​300, 300t,
SE-​CPAQ,  281–​282 304, 304t
self-​report instruments,  280–​282 Past Week (PSWQ-​PW),  304, 304t
conclusions and future directions,  283–​284 PEP. See Premature Ejaculation Profile
nature,  266–​270 PEQ. See Pain Experience Questionnaire
anxiety sensitivity,  268 Perceived Criticism Scale (PCS),  181
etiology,  267–​269 Perseverative Thinking Questionnaire (PTQ),  138t, 139
genetics,  267–​268 Personality Assessment Inventory (PAI),  466, 467, 467t, 470, 475
maintenance factors,  269–​270 Personality Diagnostic Questionnaire-​4 (PDQ-​4),  466, 467–​468,
mental illness and abuse history,  268–​269 467t, 471, 473, 474, 475
neuroticism, 268 Personality Disorder Interview-​IV (PDI-​IV),  466, 467t,
presenting features,  266–​267 469, 475
Panic Disorder Severity Scale (PDSS),  271t, 273, 280, 280t Personality disorders,  464–​480
Self-​Report (PDSS-​SR),  273 assessment, case conceptualization and treatment
PANSS. See Positive and Negative Syndrome Scale planning,  475–​478, 476t
PAPA. See Preschool Age Psychiatric Assessment CAT-​PD,  476–​477, 476t
Parent Daily Report (PDR),  85t, 86 DAPP-​BQ,  475–​476, 476t
Parent’s Consumer Satisfaction Questionnaire (PCSQ),  85t, 86 FFMPD,  476, 476t, 477
Parent-​Young Mania Rating scale (P-​YMRS),  178–​179 PID-​5,  476, 476t, 477
PARS. See Pediatric Anxiety Rating Scale SNAP-​2,  475–​476, 476t
PASS. See Pain Anxiety Symptoms Scale assessment, diagnosis,  465–​475, 467t
PASS-​20. See Pain Anxiety Symptoms Scale, 20-​item age, 472
Pathological Gambling Modification, Yale–​Brown Obsessive-​ age of onset,  469–​470
Compulsive Scale (PC-​YBOCS),  424t, 426 CATI,  466, 467, 467t, 470, 471, 474
Patient Health Questionnaire-​9 (PHQ-​9),  135–​136, 136t, 138, clinical utility,  474–​475
158t, 159, 162, 163–​164, 164t, 165, 572t, 575 culture and ethnicity,  473–​474
Patient Rejection Scale (PRS),  441t, 448, 450t, 451 DIPD and DIPD-​IV,  466, 467t, 469–​470, 471, 475
PAWSS. See Prediction of Alcohol Withdrawal Severity DSM-​5 section II criterion sets,  470
PBAPI. See Pain Beliefs and Perceptions Inventory FFMPD,  466, 467t, 468, 470, 471, 473–​475
PBQ. See Pain Beliefs Questionnaire gender,  472–​473
PBSS. See Protective Behavioral Strategies Survey IPDE,  466, 467, 467t, 468, 469, 470, 475
PCL-​5. See Posttraumatic Stress Disorder Checklist–​DSM-​5 MCMI-​IV,  466, 467, 467t, 468–​469, 471, 472–​473,
PCL-​C. See Posttraumatic Stress Disorder Checklist–​Civilian 474, 475
PCL-​IV. See Posttraumatic Stress Disorder Checklist–​DSM-​IV MMPI-​2,  466, 467, 467t, 470, 471, 472–​473, 474
PCL-​M. See Posttraumatic Stress Disorder Checklist–​Military norms,  467–​468
PCL-​S. See Posttraumatic Stress Disorder Checklist–​Specific OMNI,  466, 467, 467t, 474, 475
PC-​PTSD. See Primary Care-​PTSD screen overall evaluation,  475
PC-​PTSD-​5. See Primary Care-​PTSD screen, DSM-​5 PAI,  466, 467, 467t, 470, 475
PCS. See Pain Catastrophizing Scale; Perceived Criticism Scale PDI-​IV,  466, 467t, 469, 475
PCS-​C. See Pain Catastrophizing Scale–​Children PDQ-​4,  466, 467–​468, 467t, 471, 473, 474, 475
PCSQ. See Parent’s Consumer Satisfaction Questionnaire PID-​5,  466, 467t, 468, 470, 471, 472, 473–​475
PC-​YBOCS. See Pathological Gambling Modification, Yale–​Brown reliability, 468
Obsessive-​Compulsive Scale; Yale-​Brown Obsessive-​ SCID-​5-​PD,  466, 467t, 469, 470
Compulsive Scale-​Pathological Gambling Modification SCID-​II,  475
PDI-​IV. See Personality Disorder Interview-​IV self-​report inventories and interviews,  466
PDQ-​4. See Personality Diagnostic Questionnaire-​4 semi-​structured interviews,  465–​466
PDR. See Parent Daily Report SIDP-​IV,  466, 467t, 470, 475
PDS-​5. See Posttraumatic Diagnostic Scale for DSM-​5 SNAP-​2,  466, 467, 467t, 474
PDS-​IV. See Posttraumatic Diagnostic Scale for DSM-​IV SWAP-​200,  466, 467, 467t, 470, 471, 472, 474
PDSQ. See Psychiatric Diagnostic Screening Questionnaire unstructured interviews,  465
PDSS. See Panic Disorder Severity Scale validity, construct,  469–​470
PDSS-​SR. See Panic Disorder Severity Scale–​Self-​Report validity, content,  468–​469
Pediatric Anxiety Rating Scale (PARS),  226, 230 validity, generalization,  472–​474
Pediatric Quality of Life Inventory Generic Core Scales WISPI-​IV,  466, 467, 467t, 474
(PedsQL  4.0), 591t, 593–​594 assessment, treatment monitoring and
PedsQL4.0. See Pediatric Quality of Life Inventory Generic outcome,  478–​479, 478t
Core Scales CAT-​PD,  478t, 479
PEDT. See Premature Ejaculation Diagnostic Tool DAPP-​BQ,  478t, 479
Penn Alcohol Craving Scale (PACS),  390t, 395 FFMPD, 478t, 479
Preoccupation, 390t, 396 GAPD, 479
 subject Index 743

PID-​5,  478t, 479 ADIS-​IV,  246–​247, 246t

SCID-​5-​PD,  478 overall evaluation,  247
SIPP-​118,  479 SCID-​5,  247
SNAP-​2,  478t, 479 SCID-​IV,  246, 246t, 247
conclusions and future directions,  479–​480 assessment, purpose,  244–​245
nature,  464–​465 assessment, treatment monitoring and
comorbidities, 465 outcomes,  255–​257, 255t
DSM-​5,  464–​465 ASIS-​3,  257
Personality Inventory for DSM-​5 (PID-​5),  466, 467t, 468, 470, BAT, 255t, 256
471, 472, 473–​475, 476, 476t, 477, 478t, 479 behavioral indicators of treatment progress,  256
PES. See Pleasant Events Schedule BSPS, 255t, 256
PEth. See Phosphatidylethanol DAI, 255, 255t
PFSF. See Profile of Female Sexual Functions FSQ, 255, 255t
Phobia, specific, and social anxiety disorder,  242–​258 functional impairment and quality of life,  257
assessment, case conceptualization and treatment IIRS, 255t, 257
planning,  248–​254, 248t interview measures of symptom severity,  256
anxiety sensitivity,  251–​252 LSAS, 255t, 256
ASI,  251–​252 overall evaluation,  257
ASI-​3,  248t, 252 physiological indications of treatment progress,  256–​257
BAT, 252, 254 self-​report measures of severity,  255
behavioral assessment,  252 SNAQ, 255, 255t
BFNE, 248t, 250–​251 SPAI, 255, 255t
Circumscribed Fear Measure,  250 SPIN, 255, 255t
DAI, 248t, 249 conclusions and future directions,  257–​258, 258t
Dental Cognitions Questionnaire,  249 nature,  242–​244
Dental Fears Survey,  249 diagnostic considerations,  242–​243
Disgust Emotion Scale,  251 epidemiology and descriptive psychopathology,  243–​244
disgust sensitivity,  251 etiology, 244
Dog Phobia Questionnaire,  250 prevalence benchmarks,  34t
DS, 248t sample assessment protocol,  257, 258t
DS-​R,  251 Phosphatidylethanol (PEth),  386, 386t, 388, 399t, 400
Emetophobia Questionnaire,  250 PHQ-​9. See Patient Health Questionnaire-​9
FMPS, 248t, 252 PID-​5. See Personality Inventory for DSM-​5
FSQ, 248t, 249, 254 Pieces of Hurt Tool,  585t, 586, 590, 597, 597t
FSS, 248 PI-​R. See Padua Inventory-​Revised; Revised Padua Inventory
Index of Dental Fear and Anxiety,  249 Pittsburgh Sleep Quality Index (PSQI),  180, 572t, 573
Medical Fear Survey,  249 Planning, treatment,  39–​40. See also specific disorders
Mutilation Questionnaire,  249 Pleasant Events Schedule (PES),  138, 138t, 597t, 598
overall evaluation,  254 POC. See Processes of Change questionnaire
perfectionism, 252 Poker Chip Tool (Pieces of Hurt),  585t, 586, 590, 597, 597t
SAFE, 254 Polysomnography (PSG),  565t, 566, 576
safety behaviors,  254 POMS. See Profile of Mood States
self-​report measures of related dimensions,  251–​252 Positive and Negative Syndrome Scale (PANSS),  440, 441t,
self-​report measures of severity and phenomenology, 449, 450t
related dimensions,  251–​252 Positive predictive value (PPV),  385
self-​report measures of severity and phenomenology, Posttraumatic Diagnostic Scale for DSM-​5 (PDS-​5),  336t,
SAD,  250–​251 340, 346t
self-​report measures of severity and phenomenology, Posttraumatic Diagnostic Scale for DSM-​IV (PDS-​IV),  336t,
specific phobia,  248–​250 340, 346t
skills deficits assessment,  252–​253 Post-​traumatic stress disorder (PTSD),  329–​348
SNAQ, 248t, 249 after disasters, recent,  329, 331–​332
SPAI, 248t, 250 alcohol use disorder with,  332, 382
SPIN, 248t, 250, 254 anxiety disorders with,  332
SPRS, 248t, 253 assessment, case conceptualization and treatment
Storm Fear Questionnaire,  250 planning,  342–​345, 342t
TAQ,  253–​254 BASIS-​32,  344
treatment history, treatment concerns, and CBT BTQ, 342t, 343
suitability,  253–​254 CAPS, 343, 345
assessment, diagnosis,  245–​247, 246t Combat Exposure Scale,7-​item, 343–​344
ADIS-​5,  246–​247 cultural considerations,  345
744 subject Index

Post-​traumatic stress disorder (PTSD) (continued) conclusions and future directions,  347–​348
developmental factors and age of trauma,  344–​345 disaster management,  329
DRRI, 344 major depressive disorder with,  331
DRRI-​2,  344 mood disorders with,  332
functioning, 344 nature,  329–​334
HTQ, 345 associated features,  330
LEC, 342t, 343 comorbidities,  332–​333
LSC-​R,  342t, 343 diagnostic considerations,  329–​330
overall evaluation,  345 epidemiological evidence,  330–​332
Posttraumatic Stress Related Functioning Inventory,  344 etiology, 333
SF-​36,  344 treatment and prognosis,  334
Sheehan Disability Scale,  344 prevalence benchmarks,  34t
single vs. multiple trauma,  343–​344 substance use disorder with,  332
SLESQ, 342t, 343 suicidal behaviors with,  332
TEQ, 342t traumatic brain injury with,  332–​333
TLEQ, 342t, 343 Posttraumatic Stress Disorder Checklist (PCL)
TSS, 342t, 343 Civilian (PCL-​C),  341
type of trauma,  342–​343 DSM-​5 (PCL-​5),  336t, 340–​341, 346t
WHODAS 2.0, 344 DSM-​IV (PCL-​IV),  336t, 340–​341, 346t
assessment, diagnosis,  336–​342, 336t Military (PCL-​M),  341
ADIS-​5,  336t, 338 Specific (PCL-​S),  341
ADIS-​IV,  336t, 338 Posttraumatic Stress Related Functioning Inventory,  344
CAPS-​5,  336–​337, 336t, 341 PPGM. See Problem and Pathological Gambling Measure
CAPS-​IV,  336–​337, 336t Precision Medicine Initiative,  23
CIDI, 336t, 338–​339 Prediction of Alcohol Withdrawal Severity (PAWSS),  386t
IES-​R,  336t, 339 Prediction phase, EBA,  35–​38, 35f
Mississippi Scale for Combat-​Related PTSD,  336t, Premature (early) ejaculation (PE),  518, 530–​531
339–​340 Premature Ejaculation Diagnostic Tool (PEDT),  519t, 530
overall evaluation,  341–​342 Premature Ejaculation Profile (PEP),  525t, 530–​531
PCL-​5,  336t, 340–​341 Premenstrual dysphoric disorder,  99. See also Depression,
PCL-​IV,  336t, 340–​341 children and adolescents
PDS-​5,  336t, 340 Preparation phase, EBA,  33–​34, 34t
PDS-​IV,  336t, 340 PREPARE, 504
PSSI-​5,  336t, 338 Preschool Age Psychiatric Assessment (PAPA),  106, 106t, 107–​108,
PSS-​I-​IV,  336t, 338 112, 113, 115, 116
SCID-​5,  336t, 337–​338 Prescription phase, EBA,  38–​40
SCID-​IV,  336t, 337–​338 collateral informants, add,  38
self-​report measures,  339–​341 focused constructs, assess more,  38
structured diagnostic interviews,  336–​339 more intensive testing, other,  39
assessment, overview,  334–​336 semi-​structured diagnostic interviews,  38–​39
biologically based,  335–​336 treatment planning and goal setting,  39–​40
history, 334 Present State Exam (PSE),  156
multimethod approaches,  334–​335 Presidential Task Force on Evidence-​Based Practice, APA,  17
assessment, treatment monitoring and Pre-​Sleep Arousal Scale (PSAS),  567t, 570
outcomes,  345–​347, 346t prevalence benchmarks,  34t
CAPS-​5,  346t, 347 Primary Care-​PTSD screen (PC-​PTSD),  347
CAPS-​IV,  346t DSM-​5 (PC-​PTSD-​5),  347
IES-​R,  346t PRISM. See Psychiatric Research Interview for Substance and
overall evaluation,  347 Mental Disorders
PCL-​5,  346t Problem and Pathological Gambling Measure (PPGM),  413t,
PCL-​IV,  346t 417–​418
PC-​PTSD,  347 Processes of Change questionnaire (POC),  366t, 371
PC-​PTSD-​5,  347 10-​item,  366t
PDS-​5,  346t Process measurement,  41. See also specific disorders
PDS-​IV,  346t Profile of Female Sexual Functions (PFSF),  523t, 528
SCID-​5,  346t Profile of Mood States (POMS),  613
SCID-​IV,  346t Progress monitoring. See also specific disorders
screening, 347 EBA for,  17
Short Screening Scale for PTSDS, seven-​item,  347 research–​practice gap,  19–​20
SPAN, 347 PROMIS,  21, 110, 398, 399t, 402

Protective Behavioral Strategies Survey (PBSS),  399t, 401
Provider Feedback Data Parties,  22
PRS. See Patient Rejection Scale
PSAS. See Pre-​Sleep Arousal Scale
PSE. See Present State Exam
PSG. See Polysomnography
PSQI. See Pittsburgh Sleep Quality Index
PSSI-​5. See PTSD Symptom Scale Interview, DSM-​5
PSSI-​I. See PTSD Symptom Scale Interview
PSSI-​IV. See PTSD Symptom Scale Interview, DSM-​IV
PSS-​R. See Psychosocial Schedule for School Age
Children-​Revised
PSWQ. See Penn State Worry Questionnaire
PSWQ-​PW. See Penn State Worry Questionnaire–​Past Week
Psychiatric Diagnostic Screening Questionnaire (PDSQ),  386t
Psychiatric Research Interview for Substance and Mental
Disorders (PRISM),  386t, 388
Psychometric properties,  7
Psychosocial Schedule for School Age Children-​Revised
(PSS-​R),  114–​115, 116
Psychotic Symptom Rating Scale (PSYRATS),  441t, 447, 450t,
451, 452
PSYRATS. See Psychotic Symptom Rating Scale
PTQ. See Perseverative Thinking Questionnaire
PTSD Symptom Scale Interview (PSSI-​I),  338, 347
DSM-​5 (PSSI-​5),  336t, 338
DSM-​IV (PSSI-​IV),  336t, 338
Purposes, assessment,  6–​7. See also specific disorders
P-​YMRS. See Parent-​Young Mania Rating scale
QEQ. See Quality of Erection Questionnaire
Q-​F measures. See Quantity–​Frequency Measures
QIDS-​SR. See Quick Inventory of Depressive Symptomatology
Self-​Rated
QLQ. See Quality of Life Questionnaire
QLS. See Quality of Life Scale
QOLI. See Quality of Life Inventory
QSI. See Quality of Sex Inventory
Quality of Erection Questionnaire (QEQ),  525t, 526, 527
Quality of Life Interview Self-​Administered Short Form
(TL-​30S),  441t, 447, 450t, 451
Quality of Life Inventory (QOLI),  300t, 301, 304t, 305, 441t,
450t, 451
Quality of Life Questionnaire (QLQ),  300t, 301, 304t, 305
Quality of Life Scale (QLS),  441t, 444, 450t, 451
Quality of Sex Inventory (QSI),  524
Quantity–​Frequency Measures (Q-​F measures),  390t
Quick Inventory of Depressive Symptomatology Self-​Rated
(QIDS-​SR),  135–​136, 136t, 142, 144t
RAATE. See Recovery Attitude and Treatment Evaluator
RADS. See Reynolds Adolescent Depression Scale
RAM. See Relationship Attribution Measure
RAPI. See Rutgers Alcohol Problem Index
Rapid Alcohol Problems Screen-​4 (RAPS-​4),  386t
Rapid Couple Interaction Scoring Systems (RCISS),  493t, 494,
500, 502
Rapid Marital Interaction Coding System (RMICS),  493t, 494,
500, 502
RAPS-​4. See Rapid Alcohol Problems Screen-​4
subject Index 745
RAS. See Recovery Assessment Scale
Rating criteria,  7. See also specific disorders
Rating of Medication Influences Scale (ROMI),  441t, 442
RCADS. See Revised Children’s Anxiety and Depression Scale
RCDS. See Reynolds Child Depression Scale
RCISS. See also Rapid Couple Interaction Scoring Systems
RCMAS. See Revised Children’s Manifest Anxiety Scale
RCMAS-​2. See Revised Children’s Manifest Anxiety Scale,2
RCQ. See Readiness to Change Questionnaire
Readiness to Change Questionnaire (RCQ),  390t, 394
Reasons for Drinking Questionnaire (RFDQ),  396
Reasons for Living Inventory (RFL),  202, 202t
Adult (RFL-​A),  202–​203, 202t
Older Adult (RFL-​OA),  202t, 203
Young Adulits (RFL-​YA),  202t, 203
Reasons for Suicide Attempts Questionnaire (RSAQ),  202t, 203
Recovery Assessment Scale (RAS),  441t, 446, 450t, 451
Recovery Attitude and Treatment Evaluator (RAATE),  390t, 397
REDSOCS. See Revised Edition of the School Observation
Coding System
Relationship Attribution Measure (RAM),  496t, 497, 504
Relationship Quality Interview (RQI),  496t, 500
Reliability, 8b, 9–​10
Reliable change index (RCI),  40
Repetitive behaviors,  315. See also Obsessive-​compulsive
disorder (OCD)
Research–​practice gap,  18–​20
assessment, 18
causes, 20
diagnostic assessment,  18–​19
progress monitoring,  19–​20
Revised Behavior and Symptom Identification Scale (BASIS-​
R), 441t, 442, 449
Revised Children’s Anxiety and Depression Scale
(RCADS), 226
Revised Children’s Manifest Anxiety Scale (RCMAS),  221t,
223, 227t, 228
2 (RCMAS-​2),  224, 226
2 (RCMAS-​2), Defensiveness Scale,  233, 234
Lie Scale,  232t, 233–​234
Revised Edition of the School Observation Coding System
(REDSOCS), 77t, 80, 85t, 86
Revised Helping Alliance Questionnaire (HAq-​II),  144, 144t
Revised Padua Inventory (PI-​R),  322t, 323
Reynolds Adolescent Depression Scale (RADS),  106t, 109, 110,
112, 117, 118, 118t
Reynolds Child Depression Scale (RCDS),  106t, 109, 110,
112, 117, 118, 118t
RFDQ. See Reasons for Drinking Questionnaire
RFL. See Reasons for Living Inventory
RFL-​A. See Reasons for Living Inventory–​Adolescents
RFL-​OA. See Reasons for Living Inventory–​Older Adult
RFL-​YA. See Reasons for Living Inventory–​Young Adults
RMDQ. See Roland–​Morris Disability Questionnaire
RMICS. See Rapid Marital Interaction Coding System
Roland–​Morris Disability Questionnaire (RMDQ),  611t,
614, 615
ROMI. See Rating of Medication Influences Scale
Rosenberg Self-​Esteem Scale (RSE),  553
RQI. See Relationship Quality Interview
746 subject Index

RSAQ. See Reasons for Suicide Attempts Questionnaire CSI, 441t

RSE. See Rosenberg Self-​Esteem Scale DAI, 441t, 442
Rutgers Alcohol Problem Index (RAPI),  390t, 393, 397, DAI-​10,  442
399t, 400 DAI-​30,  442
Dartmouth Assessment of Lifestyle Instrument,  448
SAAST. See Self-​Administered Alcoholism Screening Test DAST, 441t, 448
SADS. See Schedule for Affective Disorders and Schizophrenia family attitudes,  447–​448
SADS-​C. See Schedule for Affective Disorders and FEIS, 448
Schizophrenia–​Change Mania Scale ILSS, 441t, 444, 445
SAFE. See Social Adaptive Function Scale IMR, 441t, 446
SAI. See Session Alliance Inventory ISMI, 441t, 447
SAICA. See Social Adjustment Inventory for Children and MAST, 441t, 448
Adolescents MCAS, 441t, 444, 445
SAI-​E. See Schedule for Assessment of Insight–​Expanded medication adherence,  443
Version MHRM, 441t, 446
Salience network (SN),  134 MIRECC-​GAF,  441t, 444, 445
SAMI. See Sleep-​Associated Monitoring Index overall evaluation,  449
SANS. See Scale for Assessment of Negative Symptoms PANSS, 440, 441t
SASC-​R. See Social Anxiety Scale for Children–​Revised PRS, 441t, 448
SAS-​II. See Social Adjustment Scale PSYRATS, 441t, 447
SASII. See Suicide Attempt Self-​Injury Interview QLS, 441t, 444
SAS-​SR. See Social Adjustment Scale–​Self-​Report QOLI, 441t
SATS. See Substance Abuse Treatment Scale RAS, 441t, 446
SAWS. See Short Alcohol Withdrawal Scale ROMI, 441t, 442
SBI. See Suicide Behaviors Interview SAFE, 441t, 444, 445
SBQ. See Suicidal Behaviors Questionnaire SANS, 441t, 442
SBQ-​R. See Suicidal Behaviors Questionnaire–​Revised SAS-​II,  441t, 444
SBS. See Social Behavior Schedule SATS, 441t, 449
SBSRS. See Sleep-​Behavior Self-​Rating Scale SBS, 441t, 444, 445
Scale for Assessment of Negative Symptoms (SANS),  441t, 442, SCID-​5,  448
449, 450t SF-​36,  441t, 444, 445
Scale for Suicide Ideation (SSI),  196t, 197t, 198–​199, 200 SFS, 441t, 444
Scale for Suicide Ideation–​Worse (SSI-​W),  196t, 199 SLOF, 441t, 444, 445
Scale to Assess Unawareness of Mental Disorder (SUMD),  180 SS, 441t
SCARED. See Screen for Child Anxiety-​Related Emotional SSMI, 441t, 446–​447
Disorders subjective appraisal,  446–​447
SCAS. See Spence Children’s Anxiety Scale substance abuse, comorbid,  448–​449
Schedule for Affective Disorders and Schizophrenia symptoms,  440–​443
(SADS), 155t, 156, 157, 158t, 160, 174t, 175–​176, 179 TL-​30S,  441t, 447
Change Mania Scale (SADS-​C),  181t, 182, 184 TLFB, 441t, 449
Schedule for Assessment of Insight–​Expanded Version assessment, diagnosis,  438–​440, 439t
(SAI-​E),  179t, 180 CAPS-​S,  439t, 440
Schedule for Nonadaptive and Adaptive Personality-​2nd edition CFI, 439
(SNAP-​2),  466, 467, 467t, 474, 475–​476, 476t, 478t, 479 co-​occurring disorders,  439–​440
Schedule of Compulsions, Obsessions, and Pathological CSDS, 439t, 440
Impulses (SCOPI),  322t, 324 DIS, 439, 439t
Schizophrenia,  435–​452 M.I.N.I., 439, 439t
assessment, case conceptualization and treatment overall evaluation,  440
planning,  440–​449, 441t SCID-​5,  438–​439, 439t
ADS, 448 WHO SMH-​CIDI,  439
ASI, 441t, 448 assessment, purposes,  437–​438
AUDIT, 441t, 448 assessment, treatment monitoring and
BAS, 441t, 448 outcomes,  449–​452, 450t
BASIS-​R,  441t, 442 ASI, 450t, 451
BNSS, 441t, 442 AUS, 450t, 451
BPRS, 440, 441t BAS, 450t, 451
CAINS, 441t, 442 BASIS-​R,  449
CAN, 441t, 444 BNSS, 449
CASIG, 441t, 444, 445 BPRS, 449, 450t
community functioning,  443–​445 CAINS, 449
 subject Index 747

CASIG, 450t, 451 SCID-​I/​P. See Structured Clinical Interview for DSM, DSM-​IV-​

CFI, 451 TR for Axis I Disorders, Patient Edition
CGI, 449, 450t SCID-​IV. See Structured Clinical Interview for DSM, DSM-​IV
Colorado Symptom Index,  449 SCID-​IV-​TR. See Structured Clinical Interview for DSM,
community functioning,  450–​451 DSM-​IV-​TR
DUS, 450t, 451 SCI-​PG. See Structured Clinical Interview for Pathological
family attitudes,  451 Gambling
GAF,  450–​451 SCL-​90. See Symptom Checklist-​90; Symptom Checklist 90
ILSS, 450t, 451 (SCL-​90)
IMR, 450t, 452 SCL-​90-​R. See Symptom Checklist-​90–​Revised
MCAS, 450t, 451 SCOPI. See Schedule of Compulsions, Obsessions, and
medication adherence,  449–​450 Pathological Impulses
MHRM, 450t, 451 SCQ. See Situational Confidence Questionnaire
MIRECC-​GAF,  450t, 451 SCQG. See Situational Confidence Questionnaire for
overall evaluation,  451–​452 Gambling
PANSS, 449, 450t SCRAM. See Secure Continuous Remote Alcohol Monitor
Patient Rejection Scale,  451 Screen for Child Anxiety-​Related Emotional Disorders
PRS, 450t (SCARED), 221t, 223–​224
PSYRATS, 450t, 451, 452 SDI. See Sexual Desire Inventory
QLS, 450t, 451 SDI-​MD-​PA. See Structured Diagnostic Interview for Marital
QOLI, 450t, 451 Distress and Partner Aggression
RAS, 450t, 451 SDM. See Structured Diagnostic Method
SAFE, 450t, 451 SDQ. See Strengths and Difficulties Questionnaire
SANS, 449, 450t SDS. See Severity of Dependence Scale; Zung Self-​rating
SAS-​II,  450t, 451 Depression Scale
SATS, 450t, 451 SDSS. See Substance Dependence Severity Scale
SBS, 450t, 451 SE-​CPAQ. See Self-​Efficacy to Control a Panic Attack
SF-​36,  450t Questionnaire
SFS, 450t, 451 Secure Continuous Remote Alcohol Monitor (SCRAM),  399t
subjective appraisal,  451 Self-​Administered Alcoholism Screening Test (SAAST),  386t
substance abuse, comorbid,  451 Self-​Efficacy to Control a Panic Attack Questionnaire
symptoms, 449 (SE-​CPAQ),  281–​282
TL-​30S,  450t, 451 Self-​Harm Behavior Questionnaire (SHBQ),  196t, 199
TLFB, 450t, 451 Self-​Harm Inventory (SHI),  196t, 200
conclusions and future directions,  452 Self-​injurious thoughts and behaviors (SITB),  193–​206
DSM-​5 and ICD-​10,  435–​436 assessment, case conceptualization and treatment
nature,  435–​437 planning,  201–​204, 202t
epidemiology, 437 BRFL, 202, 202t
etiology, 437 CSRLI, 202t, 203
history, modern conceptualization,  435 FASM,  202, 202t, 203
symptoms and associated impairments,  436–​437 ISAS, 202t, 203
neurodevelopmental disorder,  437 MAST, 202t, 203
stress-​vulnerability model,  437 overall evaluation,  203–​204
substance abuse with,  448–​449, 451 RFL, 202, 202t
School Refusal Assessment Scale (SRAS),  227t, 228 RFL-​A,  202–​203, 202t
Revised (SRAS-​R),  228 RFL-​OA,  202t, 203
SCID. See Structured Clinical Interview for DSM RFL-​YA,  202t, 203
SCID-​5. See Structured Clinical Interview for DSM, DSM-​5 RSAQ, 202t, 203
SCID-​5-​CT. See Structured Clinical Interview for DSM, SASII,  201, 202t, 203
DSM-​5–​Clinical Trials Version self-​report measures,  202–​203
SCID-​5-​CV. See Structured Clinical Interview for DSM, SITBI, 201, 202t
DSM-​5–​Clinical Version structured and semi-​structured interviews,  201–​202
SCID-​5-​PD. See Structured Clinical Interview for DSM, assessment, diagnosis, adults,  196–​200, 196t
DSM-​5–​Personality Disorders ASIQ, 196t, 199
SCID-​5-​RV. See Structured Clinical Interview for DSM, BSI, 196t, 199
DSM-​5–​Research Version C-​SSRS,  196t, 197–​198
SCID-​CV. See Structured Clinical Interview for DSM, DSHI, 196t, 199
Clinical Version MSSI, 196t, 199
SCID-​II. See Structured Clinical Interview for DSM, Axis II SASII, 196t, 197
disorders SBQ, 196t, 199
748 subject Index

Self-​injurious thoughts and behaviors (SITB) (continued) Session Alliance Inventory (SAI),  144, 144t
SBQ (4-​item),  196t, 199 SET/​PYIT. See Social Evaluative Task/​Parent-​Youth
SBQ-​R,  196t, 199 Interaction Task
self-​report measures,  199–​200 Severity Indices for Personality Problems (SIPP-​118),  479
SHBQ, 196t, 199 Severity of Dependence Scale (SDS),  366–​367, 366t
SHI, 196t, 200 Sexual Desire Inventory (SDI),  523t, 525t, 528, 530
SIS, 196t, 199 Sexual dysfunction,  515–​532
SITBI,  196–​197, 196t assessment, case conceptualization and treatment
SSI, 196t, 198–​199 planning,  522–​524, 523t
SSI-​W,  196t, 199 CSI, 523, 523t
S-​STS,  196t, 198 DAS, 523, 523t
structured and semi-​structured interviews,  196–​199 DSFI,  523–​524, 523t
assessment, diagnosis, children and adolescents,  197t, FSDS, 523t, 524
200–​201 GMSEX, 523t, 524
BSI, 197t, 200 GRISS, 523, 523t
CSPS, 197t, 200 ISS, 523t, 524
HASS, 197t, 200 NSSS, 523t, 524
SBI, 197t, 200 PFSF, 523t, 528
SBQ-​R,  197t, 200 QSI, 524
SIQ, 197t, 200 SDI, 523t, 528, 530
SIQ-​JR,  197t, 200 SIDI-​F,  523t, 528
SITBI, 197t, 200 SSS-​W,  523t, 524
SSI, 197t, 200 assessment, diagnosis,  519t, 520–​522
assessment, diagnosis, overall evaluation,  201 BISF-​W,  519t, 521
assessment, purpose,  195 BMSFI, 519t, 522
assessment, treatment monitoring and clinical interview,  520–​521
outcomes,  204–​205m196tm197t FSFI, 521
C-​SSRS,  204 GRISS, 519t, 521
overall evaluation,  196t, 197t, 204–​205 IIEF, 519t, 522
SASII, 204 IIEF-​5,  519t, 526–​527
S-​STS,  204 IPE, 519t, 530
clinical recommendations and research questions,  205b MFSQ, 519t, 521
conclusions and future directions,  205–​206 MSHQ, 519t, 522
ABASI, 205 MSHQ-​EjD,  519t, 526
C-​SSRS,  205 PEDT, 519t, 530
IMSA,  205–​206 PEP,  530–​531
NSSI-​AT,  206 SCID-​5,  520
NSSID, 205 SDM, 519t, 522
S-​STS,  205 self-​report measures, global sexual function,  521–​522
ecological momentary assessment studies,  205 SFQ, 519t, 522
nature,  193–​196 SIDI-​F,  519t, 528
classification and measurement,  193–​195 assessment, purposes,  518
direct assessment,  195–​196 assessment, treatment monitoring and
prevalence and conditional probability,  195 outcomes,  524–​526, 525t
with PTSD,  332 BISF-​W,  525, 525t
Self-​Injurious Thoughts and Behaviors Interview CSFQ/​CSFQ-​14,  525, 525t
(SITBI),  196–​197, 196t, 197t, 200, 201, 202t EHS, 525t
Self-​Injury Questionnaire (SIQ),  197t, 200 FSDS, 525t
Children (SIQ-​JR),  197t, 200 FSFI, 525, 525t
Self-​Monitoring (SM),  227t GRISS, 525t
Self-​Report Manic Inventory (SRMI),  181t, 182–​183, 184 IIEF, 525t, 526
Self-​Stigma of Mental Illness Scale (SSMI),  441t, 446–​447 IIEF-​5,  525t
Semistructured Assessment for Genetics of Alcoholism IPE, 525t
(SSAGA), 386t, 388, 389, 391 ISS, 525t
Semi-​structured diagnostic interviews,  38–​39. See also specific MFSQ, 525t
disorders PEP, 525t
Sense of Hyper-​Positive Self Scale (SHPSS),  181t, 183 QEQ, 525t
Sensitivity, treatment,  9b, 10–​11 SDI, 525t
Serotonin, OCD and,  312 conclusions and future directions,  531–​532
 subject Index 749

dysfunction-​specific assessment,  526–​531 Shedler–​Western Assessment Procedure-​200 (SWAP-​200),  466,

BISF-​W,  528, 529 467, 467t, 470, 471, 472, 474
BSFI-​M,  526, 530 Sheehan Disability Scale,  344
CFSQ, 530 Sheehan-​Suicidality Tracking Scale (S-​STS),  196t, 198, 204, 205
CSFQ, 528, 529 SHI. See Self-​Harm Inventory
delayed ejaculation,  526 Short Alcohol Withdrawal Scale (SAWS),  389, 390t
DSDS, 528 Shorter Mood and Feelings Questionnaire (SMFQ),  519t, 522,
DSFI, 530 528, 529
EHS, 526, 527 Short Form Health Survey (SFHS)
erectile disorder,  526–​527 12-​item (SF-​12),  389, 390t, 397, 399t, 401
female orgasmic disorder,  527 36-​item (SF-​36),  163, 344, 389, 390t, 397, 399t, 401, 441t,
female sexual interest/​arousal disorder,  527–​529 444, 445, 450t, 614, 620, 620t
FSDS, 530 Short Form-​McGill Pain Questionnaire (SF-​MPQ),  611t,
FSFI, 528, 529 612–​613
genito-​pelvic pain/​penetration disorder,  529–​530 2 (SF-​MPQ-​2),  611t, 612–​613
GRISS,  526, 529, 530 Short Inventory of Problems (SIP),  390t, 393, 399t, 400
GSA, 527 Alcohol and Drugs (SIP-​AD),  366t, 368, 372t, 373
IIEF, 526, 530 Short Michigan Alcoholism Screening Test (SMAST),  394
IIEF-​5,  526–​527 Father’s Alcoholism (F-​MAST),  394
IPE, 530 Mother’s Alcoholism (M-​SMAST),  394
male hypoactive sexual desire disorder,  530 Short Screening Scale for PTSDS, seven-​item,  347
MFSQ, 528, 529 SHPSS. See Sense of Hyper-​Positive Self Scale
MPQ, 529 SIDI-​F. See Sexual Interest and Desire Inventory-​Female
MSHQ, 526 SIDP-​IV. See Structured Interview for DSM-​IV Personality
MSHQ-​EjD,  526 Disorders
ORS, 527 Simple Screening Instrument for Alcohol and Other Drugs
PCS, 529 (SSI-​AOD),  386t, 387
PEDT, 530 Simple Screening Instrument for Substance Abuse
PEP,  530–​531 (SSI-​SA),  386t, 387
PFSF, 528 SIP. See Short Inventory of Problems
premature (early) ejaculation,  530–​531 SIP-​AD. See Short Inventory of Problems–​Alcohol and Drugs
QEQ, 526, 527 SIPP-​118. See Severity Indices for Personality Problems
SDI, 528, 530 SIQ. See Self-​Injury Questionnaire
SFQ, 528, 529 SIQ-​JR. See Self-​Injury Questionnaire–​Children
SIDI-​F,  528 SIS. See Suicide Ideation Scale
VPAQ, 529 SITBI. See Self-​Injurious Thoughts and Behaviors Interview
global assessment,  519–​520 Situational Confidence Questionnaire (SCQ),  391t, 396
nature,  515–​518 Situational Confidence Questionnaire for Gambling
delayed ejaculation,  516 (SCQG), 420t, 422
DSM-​5,  516 Situationally accessible memories (SAM),  331
erectile disorder,  516–​517 SKAMP, 59
female orgasmic disorder,  517 Sleep-​Associated Monitoring Index (SAMI),  567t, 571
female sexual interest/​arousal disorder,  517 Sleep-​Behavior Self-​Rating Scale (SBSRS),  567t, 570
genito-​pelvic pain/​penetration disorder,  517–​518 SLES. See Stressful Life Events Screening Schedule
male hypoactive sexual desire disorder,  518 SLESQ. See Stressful Life Events Screening Questionnaire
premature (early) ejaculation,  518 SLOF. See Specific Level of Functioning
Sexual Interest and Desire Inventory-​Female (SIDI-​F),  519t, SM. See Self-​Monitoring
523t, 528 SMAST. See Short Michigan Alcoholism Screening Test
Sexual Satisfaction Scale for Women SMFQ. See Mood and Feelings Questionnaire–​Shorter; Shorter
(SSS-​W),  523t, 524 Mood and Feelings Questionnaire
SF-​12. See Short Form Health Survey, 12-​item Snaith–​Hamilton Pleasure Scale (SHAPS),  138–​139, 138t
SF-​36. See Short Form Health Survey, 36-​item Snake Questionnaire (SNAQ),  248t, 249, 255, 255t
SF-​MPQ. See McGill Pain Questionnaire–​Short Form; Short SNAP-​2. See Schedule for Nonadaptive and Adaptive
Form-​McGill Pain Questionnaire Personality-​2nd edition
SF-​MPQ-​2. See McGill Pain Questionnaire–​Short Form-​2; SNAQ. See Snake Questionnaire
Short Form-​McGill Pain Questionnaire,2 Social Adaptive Function Scale (SAFE),  254, 441t, 444, 445,
SFS. See Social Functioning Scale 450t, 451
SHAPS. See Snaith–​Hamilton Pleasure Scale Social Adjustment Inventory for Children and Adolescents
SHBQ. See Self-​Harm Behavior Questionnaire (SAICA),  114, 114t, 116, 118t
750 subject Index
Social Adjustment Scale (SAS-​II),  441t, 444, 450t, 451
Social Adjustment Scale–​Self-​Report (SAS-​SR),  138t, 140
Social anxiety disorder,  242–​258. See also Phobia, specific, and
social anxiety disorder
assessment, case conceptualization and treatment
planning,  248–​254, 248t
assessment, diagnosis,  245–​247, 246t
assessment, purpose,  244–​245
assessment, treatment monitoring and
outcomes,  255–​257, 255t
conclusions and future directions,  257–​258, 258t
nature,  242–​244
prevalence benchmarks,  34t
sample assessment protocol,  257, 258t
Social Anxiety Scale for Children–​Revised (SASC-​R),  221t,
224–​225
Social Behavior Schedule (SBS),  441t, 444, 445, 450t, 451
Social Evaluative Task/​Parent-​Youth Interaction Task (SET/​
PYIT), 227t
Social Functioning Scale (SFS),  441t, 444, 450t, 451
Social Performance Rating Scale (SPRS),  248t, 253
Social Phobia and Anxiety Inventory (SPAI),  248t, 250,
255, 255t
Social Phobia and Anxiety Inventory for Children
(SPAIC), 221t, 224, 227t, 232t
Social Phobia Inventory (SPIN),  248t, 250, 254, 255, 255t
Social Support Interaction Coding System (SSICS),  496t, 501
SOCRATES. See Stages of Change Readiness and Treatment
Eagerness Scale
SOGS. See South Oaks Gambling Screen
SOGS-​3. See South Oaks Gambling Screen, 3-​month
SOGS-​R. See South Oaks Gambling Screen, past-​year
South Oaks Gambling Screen (SOGS),  413t, 414–​415, 418,
419, 420t, 423
3-​month (SOGS-​3),  414, 424t, 425
past-​year (SOGS-​R),  413t, 414–​415
SPAFF. See Specific Affect Coding System
SPAI. See Social Phobia and Anxiety Inventory
SPAIC. See Social Phobia and Anxiety Inventory for Children
SPAN, 347
Specific Affect Coding System (SPAFF),  496t, 501
Specific Level of Functioning (SLOF),  441t, 444, 445
Spence Children’s Anxiety Scale (SCAS),  221t, 223–​224,
227t, 232t
Spielberger State Anxiety Inventory (STAI),  572t, 575
SPIN. See Social Phobia Inventory
SPRS. See Social Performance Rating Scale
SPS. See Suicide Probability Scale
SRAS. See School Refusal Assessment Scale
SRAS-​R. See School Refusal Assessment Scale–​Revised
SRMI. See Self-​Report Manic Inventory
SS. See Stigma Scale
SSAGA. See Semistructured Assessment for Genetics of
Alcoholism
SSI. See Scale for Suicide Ideation
SSI-​AOD. See Simple Screening Instrument for Alcohol and
Other Drugs
SSICS. See Social Support Interaction Coding System
SSI-​SA. See Simple Screening Instrument for Substance Abuse
SSI-​W. See Scale for Suicide Ideation–​Worse
SSMI. See Self-​Stigma of Mental Illness Scale
SSS-​W. See Sexual Satisfaction Scale for Women
S-​STS. See Sheehan-​Suicidality Tracking Scale
Stages of Change Readiness and Treatment Eagerness Scale
(SOCRATES), 390t, 394, 399t, 400, 401
STAI. See Spielberger State Anxiety Inventory
STAIC. See State-​Trait Anxiety Inventory for Children
Standard deviations (SDs), Away and Back thresholds,  40
State-​Trait Anxiety Inventory for Children (STAIC),  221t,
223, 232t
Stigma Scale (SS),  441t, 447
Storm Fear Questionnaire,  250
Strengths and Difficulties Questionnaire (SDQ),  52
Stressful Life Events Screening Questionnaire
(SLESQ), 342t, 343
Stressful Life Events Screening Schedule (SLES),  115, 116
Stress-​vulnerability model,  437
Structured Clinical Interview for DSM (SCID),  155–​156,
155t, 157, 174–​175, 174t, 176, 179, 279, 280t, 389, 391,
496t, 501
Axis II disorders (SCID-​II),  475
Clinical Version (SCID-​CV),  158t, 160
DSM-​5 (SCID-​5),  135, 136t, 247, 271t, 272–​273, 336t,
337–​338, 346t, 362t, 363, 386t, 388, 413t, 438–​439,
439t, 448, 520, 548, 550
Clinical Trials Version (SCID-​5-​CT),  272
Clinical Version (SCID-​5-​CV),  272, 298–​299
Personality Disorders (SCID-​5-​PD),  135, 136t, 466, 467t,
469, 470, 478
Research Version (SCID-​5-​RV),  272, 413t
DSM-​IV (SCID-​IV),  246, 246t, 247, 315t, 316, 336t,
337–​338, 346t, 547t, 548, 550
DSM-​IV-​TR,  175
DSM-​IV-​TR for Axis I Disorders, Patient Edition
(SCID-​I/​P),  297t, 299, 304t
Structured Clinical Interview for DSM-​IV Childhood
Diagnoses (KID-​SCID),  272
Structured Clinical Interview for Pathological Gambling
(SCI-​PG),  413t, 415, 418
Structured Diagnostic Interview for Marital Distress and Partner
Aggression (SDI-​MD-​PA),  493, 493t
Structured Diagnostic Method (SDM),  519t, 522
Structured Interview for DSM-​IV Personality Disorders
(SIDP-​IV),  466, 467t, 470, 475
Subjective Opiate Withdrawal Scale,  364
Subjective Units of Distress (SUDS)
panic disorder and agoraphobia,  278, 279, 282
PTSD, 346
Subjective Units of Distress Scale (SUDS),  278
SUBQ. See Substance Use Beliefs Questionnaire
Substance Abuse Treatment Scale (SATS),  441t, 449,
450t, 451
Substance Dependence Severity Scale (SDSS),  362t, 364,
366t, 367, 372, 386t
Substance Use Beliefs Questionnaire (SUBQ),  366t, 369
Substance use disorders (SUDs),  359–​375
alcohol use disorder with,  382
assessment, case conceptualization and treatment
planning,  365–​372, 366t
AASE, 366t, 370
 subject Index 751

ASI-​6,  366t, 367, 372 GAIN,90 day M, 372t, 373, 375

CEQ, 366t, 369, 372 IDUC, 372t, 373, 375
CNCC, 369 MPS, 372t, 373
CNCC-​75,  369 overall evaluation,  374–​375
CNCC-​87,  366t, 369, 372 SIP-​AD,  372t, 373
cocaine expectancies,  369–​370 TLFB, 372t, 373
Cocaine Related Assessment of Coping Skills,  371 urine and hair toxicology analyses,  372t, 373–​374
coping skills,  371 conclusions and future directions,  375
CRACS-​SE,  366t with conduct problems,  73–​74
DASE, 370 nature,  359–​361
DCQ, 370 addiction center,  360–​361
DTCQ, 366t, 370 comorbidities,  359–​360
DTI, 370 ethnicity and geography,  360
expected effects of use,  369 gender and race,  360
GAIN-​I,  366t, 367–​368 prevalence, 360
GSC, 366t, 371 prevalence benchmarks,  34t
high-​risk situations,  370 with PTSD,  332
honest reporting, increasing,  365–​366 with schizophrenia,  448–​449, 451
IDTC, 368 SUDS. See Subjective Units of Distress Scale
IDTS, 366t, 370 Suicidal behaviors. See Self-​injurious thoughts and
IDUC, 366t, 368 behaviors (SITB)
MPS, 366t, 368–​369 Suicidal Behaviors Questionnaire (SBQ),  196t, 199
negative consequences of use,  368–​369 4-​item,  196t, 199
overall evaluation,  371–​372 SBQ-​R,  196t, 197t, 199, 200
POC, 366t, 371 Suicide Attempt Self-​Injury Interview (SASII),  196t, 197, 201,
POC-​10 items,  366t 202t, 203, 204
rationale, instrument selection,  365 Suicide Behaviors Interview (SBI),  197t, 200
relapse prevention,  370–​371 Suicide Ideation Scale (SIS),  196t, 199
SDS,  366–​367, 366t Suicide Probability Scale (SPS),  567t, 571
SDSS, 366t, 367, 372 SUMD. See Scale to Assess Unawareness of Mental Disorder
self-​efficacy,  370–​371 SWAP-​200. See Shedler–​Western Assessment Procedure-​200
SIP-​AD,  366t, 368 Symptom Checklist-​90 (SCL-​90),  35
SUBQ, 366t, 369 Revised (SCL-​90-​R),  498
use severity and psychosocial functioning,  366–​368
USS, 366t, 371 TAI. See Therapy Attitude Inventory
assessment, diagnosis,  362–​365, 362t Tampa Scale of Kinesiophobia (TKS),  616t, 618–​619
CIDI, 362t, 364 11-​item (TKS-​11),  616t, 619
DAST, 362t, 363, 365 Activity (TKS-​AA),  619
diagnostic instruments,  363–​365 Somatic Focus (TKS-​SF),  619
DIS, 364 TAQ. See Treatment Ambivalence Questionnaire
DSM-​5,  362 Teacher Report Form (TRF), ASEBA,  54, 55t, 57, 59, 60t, 77t,
DUSI-​R,  362t, 363, 365 110–​111
GAIN-​ABS,  364 Temperament Evaluation of Memphis, Pisa, Paris, and San
GAIN-​I,  362t, 364–​365 Diego (TEMPS),  178
GAIN-​SS,  365 TEMPS. See Temperament Evaluation of Memphis, Pisa, Paris,
M.I.N.I., 362t, 363–​364, 365 and San Diego
MWC, 362t, 364 Temptation and Restraint Inventory (TRI),  390t, 395
Objective Opiate Withdrawal Scale,  364 Temptations to Gamble Scale (TGS),  420t, 421, 422
overall evaluation,  365 TEQ. See Traumatic Events Questionnaire
SCID-​5,  362t, 363 TGS. See Temptations to Gamble Scale
screening measures,  362–​363 The Oucher,  585t, 586–​587, 597, 597t
SDSS, 362t, 364 Therapy Attitude Inventory (TAI),  85t, 86
Subjective Opiate Withdrawal Scale,  364 Tics, 315. See also Obsessive-​compulsive disorder (OCD)
assessment, purpose,  361 Timeline Followback Interview (TLFB),  372t, 373, 390t, 392,
assessment, treatment monitoring and 393, 395, 397, 398, 399t, 401, 420t, 421, 423–​424, 424t,
outcomes,  372–​375, 372t 441t, 449, 450t, 451
areas of life function,  372–​373 TKS. See Tampa Scale of Kinesiophobia
ASI-​6, 30-​day,  367, 372–​373, 372t TKS-​11. See Tampa Scale of Kinesiophobia, 11-​item
consequences of drug or alcohol use,  373–​374 TKS-​AA. See Tampa Scale of Kinesiophobia–​Activity
drug and alcohol use frequencies,  373 TKS-​SF. See Tampa Scale of Kinesiophobia–​Somatic Focus
752 subject Index
TL-​30S. See Quality of Life Interview Self-​Administered Short Form
TLEQ. See Traumatic Life Events Questionnaire
TLFB. See Timeline Followback Interview
Top Problems,  143, 145
Youth, 41
Training, diagnostic assessment,  18–​19
Traumatic brain injury (TBI), with PTSD,  332–​333
Traumatic Events Questionnaire (TEQ),  342t
Traumatic Life Events Questionnaire (TLEQ),  342t, 343
Traumatic Stress Schedule (TSS),  342t, 343
Treatment Ambivalence Questionnaire (TAQ),  253–​254
Treatment formulation as usual,  33
Treatment monitoring and outcome,  40–​43. See also specific
disorders
idiographic goal setting,  41
impact vs. use,  xi
maintenance monitoring,  41
nomothetic goal setting,  40–​41
process measurement,  41
Treatment planning,  39–​40
TRF. See Teacher Report Form, ASEBA
TRI. See Temptation and Restraint Inventory
TSS. See Traumatic Stress Schedule
UCLA PTSD index,  115–​116
University of Rhode Island Change Assessment (URICA),  390t,
394, 397, 399t, 400, 401
Urge-​Specific Questionnaire and General Change Strategies
Questionnaire (USS/​GSC),  366t, 371
URICA. See University of Rhode Island Change Assessment
USS/​GSC. See Urge-​Specific Questionnaire and General
Change Strategies Questionnaire
Utility, clinical,  9b, 11–​12
VABS-​II. See Vineland Adaptive Behavior Scales, Second Edition
Vaginal photoplethysmograph (VPP),  528
Validity, 8b, 10–​11
Vancouver Obsessive Compulsive Inventory (VOCI),  322t, 323
Vanderbilt ADHD Diagnostic Parent and Teacher Rating
Scales, 55t, 56
VAS. See Visual analogue scales
Verbally accessible memories (VAM),  331
Verbal rating scale (VRS),  620, 620t
Verbal Tactics Coding Scheme (VTCS),  496t, 501
Vineland Adaptive Behavior Scales, Second Edition
(VABS-​II),  55t, 56–​57
Visual analogue scales (VAS),  585t, 588, 590, 597t, 598,
619, 620t
VOCI. See Vancouver Obsessive Compulsive Inventory
VPAQ. See Vulvar Pain Assessment Questionnaire Inventory
VRS. See Verbal rating scale
VTCS. See Verbal Tactics Coding Scheme
Vulvar Pain Assessment Questionnaire Inventory (VPAQ),  529
WAQ. See Worry and Anxiety Questionnaire
Washington University WASH-​U-​KSADS. See Kiddie Schedule
for Affective Disorders and Schizophrenia for School-​
Age Children (K-​SADS)
WASSUP. See Willingly Approached Set of Statistically Unlike
Pursuits
Western Ontario and McMaster Osteoarthritis Index
(WOMAC), 611t, 614
West Haven–​Yale Multidimensional Pain Inventory
(MPI),  610–​611, 611t, 615–​616, 616t, 619, 620, 620t
61-​item, Modified instructions (MPI-​M),  616, 616t
WHODAS2.0. See World Health Organization Disability
Adjustment Scale 2.0
WHOQOL-​BREF. See World Health Organization Quality of
Life Survey–​BREF
WHO WMH-​CIDI. See World Health Organization World
Mental Health Composition International Diagnostic
Interview
Why Worry-​II (WW-​II),  300t, 302, 304t, 305
Willingly Approached Set of Statistically Unlike Pursuits
(WASSUP), 181t, 183
Wisconsin Personality Disorders Inventory-​IV (WISPI-​IV),  466,
467, 467t, 474
WISPI-​IV. See Wisconsin Personality Disorders Inventory-​IV
WOMAC. See Western Ontario and McMaster
Osteoarthritis Index
World Health Organization Disability Adjustment Scale2.0
(WHODAS 2.0), 137–​138, 138t, 140, 344
World Health Organization Quality of Life Survey–​BREF
(WHOQOL-​BREF),  399t
World Health Organization World Mental Health
Composition International Diagnostic Interview (WHO
WMH-​CIDI),  439
Worry and Anxiety Questionnaire (WAQ),  297, 297t, 304t
WW-​II. See Why Worry-​II
YAACQ. See Young Adult Alcohol Consequences
Questionnaire
Yale–​Brown–​Cornell Eating Disorder Scale
(YBC-​EDS),  554, 554t
Yale–​Brown Obsessive-​Compulsive Scale
(Y-​BOCS),  322–​323, 322t
Pathological Gambling Modification (PC-​YBOCS),  424t, 426
Symptom Checklist (Y-​BOCSC-​SC),  314, 315t
Yale Interactive Kinetic Environment Software
(YIKES), 229, 233
YBC-​EDS. See Yale–​Brown–​Cornell Eating Disorder Scale
Y-​BOCS. See Yale–​Brown Obsessive-​Compulsive Scale
Y-​BOCSC-​SC. See Yale–​Brown Obsessive-​Compulsive
Scale-​Symptom Checklist
YIKES. See Yale Interactive Kinetic Environment Software
YMRS. See Young Mania Rating Scale
Young Adult Alcohol Consequences Questionnaire
(YAACQ), 390t, 393–​394, 399t, 400
Young Mania Rating Scale (YMRS),  181–​182, 181t, 184
Youth Self-​Report (YSR),  54–​55, 110–​111
Youth Severity Rating (YSR),  233
Youth Top Problems,  41
Youth Top Problems approach,  40
YSR. See Youth Self-​Report; Youth Severity Rating
Zung Self-​rating Depression Scale (SDS),  158t, 159