Introduction

to
Communication
Sciences and Disorders
The Scientific Basis of Clinical Practice
 Introduction
to
Communication
Sciences and Disorders
The Scientific Basis of Clinical Practice

Gary Weismer, PhD

David K. Brown, PhD
5521 Ruffin Road
San Diego, CA 92123

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Library of Congress Cataloging-in-Publication Data

Names: Weismer, Gary, (Professor Emeritus), author. | Brown, David K. (Professor of audiology),
author.
Title: Introduction to communication sciences and disorders : the
scientific basis of clinical practice / Gary Weismer, David K. Brown.
Description: San Diego, CA : Plural Publishing, Inc., [2021] | Includes
bibliographical references and index.
Identifiers: LCCN 2019029827 | ISBN 9781597562973 (paperback) | ISBN
1597562971 (paperback)
Subjects: MESH: Communication Disorders | Voice Disorders | Hearing
Disorders | Language Development | Speech — physiology |
Hearing — physiology
Classification: LCC RC423 | NLM WL 340.2 | DDC 616.85/5 — dc23
LC record available at https://lccn.loc.gov/2019029827
Contents
Preface xv
Acknowledgments xvii
Reviewers xix

1 Introduction to Communication Sciences 1

and Disorders
Introduction:  Communication Sciences and Disorders as a Discipline 1
Communication Sciences and Disorders:  The Whole Is Greater 2
Than the Sum of Its Parts
An Interdisciplinary Field 3
Translational Research 4
Does the Basic Science Work? Does the Clinic Work? 6
Evidence-Based Practice 7
A Typical Undergraduate Curriculum 10
Who Are the Professionals in Communication Sciences and Disorders? 10
Preparation for, and the Profession of, Speech-Language Pathology 10
Preparation for, and the Profession of, Audiology 12
Order of Chapters in the Text 13
Chapter Summary 14
References 14

2 The Nervous System:  Language, Speech, and

17
Hearing Structures and Processes
Introduction 17
Central and Peripheral Nervous Systems 17
The Neuron 18
The Synapse 21
Tour of Gross Neuroanatomy 21
Frontal Lobe 22
Occipital Lobe 23
Temporal Lobe 23
Parietal Lobe 24
Hidden Cortex 24
Subcortical Nuclei 24
Brainstem, Cerebellum, and Spinal Cord 26
The Auditory Pathways 27

v
vi Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

The Dominant Hemisphere and the Perisylvian Language Areas 28

Arcuate Fasciculus (Dorsal Stream) and Ventral Stream 30
Functional Magnetic Resonance Imaging and Speech and Language 31
Brain Activity
Functional Magnetic Resonance Imaging 31
Diffusion Tensor Imaging 32
Chapter Summary 33
References 34

3 Language Science 35
Introduction 35
What Is Language? 35
Language:  A Conventional System 36
Language:  A Dynamic System 36
Language Is Generative 37
Language Uses Mental Representations 37
Language Is Localized in the Brain 38
Components of Language 38
Form 38
Social Use of Language (Pragmatics) 42
Language and Cognitive Processes 42
Why 43
How 43
When 43
Chapter Summary 44
References 44

4 Communication in a Multicultural Society 45

Introduction 45
Why It Matters 47
Difference Versus Disorder 47
Standardized Testing and Language Difference Versus Disorder 48
Accent, Dialect, and Culture 50
Accent 50
Dialect 51
Code Switching 52
Foreign Accent 53
Bilingualism and Multilingualism 54
Chapter Summary 55
References 55

5 Preverbal Foundations of Speech and 57

Language Development
Introduction 57
Preparatory Notes on Developmental Chronologies 58
0 to 3 Months:  Expression (Production) 58
0 to 3 Months:  Perception and Comprehension 60
3 to 8 Months:  Production 61
3 to 8 Months:  Perception and Comprehension 63
 Contents vii

8 to 12 Months:  Production 65
8 to 12 Months:  Perception and Comprehension 65
Gesture and Preverbal Language Development 66
Chapter Summary 66
References 67

6 Typical Language Development 69

Introduction 69
12 to 18 Months 71
18 to 24 Months 71
Three Years (36 Months) 72
Multiword Utterances, Grammatical Morphology 72
Expanding Utterance Length:  A Measure of Linguistic Sophistication 74
Grammatical Morphology 76
Typical Language Development in School Years 77
Metalinguistic Skills 77
Pragmatic Skill:  Discourse 78
Complex Sentences 81
Sample Transcript 81
Chapter Summary 83
References 83

7 Pediatric Language Disorders I 85

Introduction 85
Specific Language Impairment/Developmental Language Disorder 85
Language Characteristics of Children with SLI/DLD 86
Summary of the Language Disorder in SLI/DLD 88
What Is The Cause of SLI/DLD? 88
The Role of Genetics in SLI/DLD 88
Language Delay and Autism Spectrum Disorder 89
Language Characteristics in ASD 89
Language Delay and Hearing Impairment 92
Epidemiology of Hearing Loss 92
Language Characteristics in Hearing Impairment 92
Speech and Language Development and Hearing Impairment 93
Chapter Summary 94
References 95

8 Pediatric Language Disorders II 99

Introduction 99
Criteria for a Diagnosis of ID 99
Down Syndrome (DS): General Characteristics 100
Epidemiology and the DS Phenotype 101
Language Characteristics in DS 102
Fragile X Syndrome: General Characteristics 104
Epidemiology of FXS 106
Language Characteristics in FXS 106
Chapter Summary 109
References 109
viii Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

9 Language Disorders in Adults 111

Introduction 111
Review of Concepts for the Role of The Nervous System In Speech, 111
Language, and Hearing
Cerebral Hemispheres 111
Lateralization of Speech and Language Functions 112
Language Expression and Comprehension Are Represented in 112
Different Cortical Regions of the Left Hemisphere
Connections Between Different Regions of the Brain 112
Perisylvian Speech and Language Areas of the Brain 112
Adult Language Disorders:  Aphasia 114
Classification of Aphasia 114
Aphasia Due to Stroke:  A Summary 122
Traumatic Brain Injury and Aphasia 124
Nature of Brain Injury in TBI 124
Language Impairment in TBI 125
Dementia 126
Brain Pathology in Dementia 126
Language Disorders in Dementia 127
Chapter Summary 128
References 128

10 Speech Science I 131

Introduction 131
The Speech Mechanism:  A Three-Component Description 131
Respiratory System Component (Power Supply for Speech) 131
The Respiratory System and Vegetative Breathing 133
Speech Breathing 134
Clinical Applications:  An Example 137
The Larynx (Sound Source for Speech) 138
Laryngeal Cartilages 138
Laryngeal Muscles and Membranes 139
Phonation 141
Characteristics of Phonation 142
Clinical Applications:  An Example 145
Upper Airway (Consonants and Vowels) 145
Muscles of the Vocal Tract 146
Vocal Tract Shape and Vocalic Production 146
Velopharyngeal Mechanism 147
Valving in the Vocal Tract and the Formation of Speech Sounds 149
Coarticulation 149
Clinical Applications:  An Example 149
Chapter Summary 150
References 151

11 Speech Science II 153

Introduction 153
The Theory of Speech Acoustics 154
The Sound Source 154
 Contents ix

The Sound Filter 154

Vowel Sounds Result From the Combination of Source and 155
Filter Acoustics
Resonant Frequencies of Vowels Are Called Formants:  Spectrograms 156
The Tube Model of Human Vocal Tract Makes Interesting Predictions 158
and Suggests Interesting Problems
A Spectrogram Shows Formant Frequencies and Much More 158
Speech Synthesis 159
Speech Recognition 159
Speech Acoustics and Assistive Listening Devices 159
Speech Perception 160
The Perception of Speech:  Special Mechanisms? 160
The Perception of Speech:  Auditory Theories 162
Motor Theory and Auditory Theory:  A Summary 163
Top-Down Influences:  It Is Not All About Speech Sounds 163
Speech Intelligibility 165
Chapter Summary 166
References 166

12 Phonetics 169
Introduction 169
International Phonetic Alphabet 170
Vowels and Their Phonetic Symbols 170
Consonants and Their Phonetic Symbols 174
Clinical Implications of Phonetic Transcription 176
Chapter Summary 177
References 178

13 Typical Phonological Development 179

Introduction 179
Phonetic and Phonological Development:  General Considerations 180
Phonetic and Phonological Development 180
Phonetic Development 181
Phonological Development 181
Typical Speech Sound Development 181
Determination of Speech Sound Mastery in Typically Developing Children
183
Possible Explanations for the Typical Sequence of Speech Sound Mastery 183
Phonological Processes and Speech Sound Development 186
Phonological Development and Word Learning 188
Chapter Summary 188
References 188

14 Motor Speech Disorders in Adults 191

Introduction 191
Classification of Motor Speech Disorders 191
Dysarthria 193
Subtypes of Dysarthria 193
The Mayo Clinic Classification System for Motor Speech Disorders 193
x Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

The Dysarthrias:  A Summary 201

Apraxia of Speech 203
Chapter Summary 203
References 204

15 Pediatric Speech Disorders I 205

Introduction 205
Speech Delay 206
Diagnosis of Speech Delay 207
Quantitative Measures of Speech Delay and Speech Intelligibility 208
Speech Delay:  Phonetic, Phonological, or Both? 209
Additional Considerations in Speech Delay and Residual and 210
Persistent Speech Sound Errors
Speech Delay and Genetics 211
Childhood Apraxia of Speech 211
CAS Compared With Adult Apraxia of Speech (AAS) 212
CAS:  Prevalence and General Characteristics 214
CAS:  Speech Characteristics 214
CAS and Overlap With Other Developmental Delays 215
CAS and Genetics 215
Chapter Summary 216
References 217

16 Pediatric Speech Disorders II 219

Introduction 219
Childhood Motor Speech Disorders:  Cerebral Palsy 220
Subtypes of Cerebral Palsy 220
Dysarthria in Cerebral Palsy 221
Childhood Motor Speech Disorders:  Traumatic Brain Injury 224
and Tumors
Traumatic Brain Injury 224
Brain Tumors 225
Treatment Options and Considerations 226
Chapter Summary 227
References 227

17 Fluency Disorders 229

Introduction 229
Incidence and Prevalence of Stuttering 229
Genetic Studies 231
Diagnosis of Developmental Stuttering 231
The Natural History of Developmental Stuttering 231
Stage I:  Typical Dysfluencies 232
Stage II:  Borderline Stuttering 232
Stage III:  Beginning Stuttering 233
Stage IV:  Intermediate Stuttering 233
Stage V:  Advanced Stuttering 233
Recovery of Fluency 234
Possible Causes of Stuttering 234
 Contents xi

Psychogenic Theories 234

Learning Theories 235
Biological Theories 235
Acquired (Neurogenic) Stuttering 238
Symptoms of Neurogenic Stuttering Compared With 238
Developmental Stuttering
Treatment Considerations 239
Chapter Summary 239
References 240

18 Voice Disorders 243

Introduction 243
Epidemiology of Voice Disorders 243
Initial Steps in the Diagnosis of Voice Disorders 244
Case History 244
Perceptual Evaluation of the Voice 244
Viewing the Vocal Folds 244
Measurement of Basic Voice Parameters 245
Classification/Types of Voice Disorders 247
The Hypo-Hyperfunctional Continuum 248
Phonotrauma 249
Organic Voice Disorders 252
Functional Voice Disorders 252
Neurological Voice Disorders 254
Pediatric Voice Disorders 257
Prevalence of Childhood Voice Disorders 257
Types of Childhood Voice Disorders 257
Treatment of Childhood Voice Disorders 257
Chapter Summary 258
References 258

19 Craniofacial Anomalies 261

Introduction 261
Definition and Origins of Craniofacial Anomalies 261
Embryological Development of the Upper Lip and Associated 261
Structures
Embryological Errors and Clefting:  Clefts of the Lip 264
Embryological Errors and Clefting:  Clefts of the Palate 265
Cleft Lip With or Without a Cleft Palate; Cleft Palate Only 266
(Isolated Cleft Palate)
Epidemiology of Clefting 267
Speech Production in CL/P and CPO 267
Diagnosis of VPI 269
VPI and Hypernasality 270
VPI, Consonant Articulation, and Speech Intelligibility 270
Clefting and Syndromes 272
Cleft Palate:  Other Considerations 273
Chapter Summary 274
References 275
xii Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

20 Swallowing 277
Introduction 277
Anatomy of Swallowing 277
Esophagus 277
Stomach 278
The Act of Swallowing 278
Oral Preparatory Phase 280
Oral Transport Phase 280
Pharyngeal Phase 280
Esophageal Phase 282
Overlap of Phases 282
Breathing and Swallowing 282
Nervous System Control of Swallowing 283
Role of the Peripheral Nervous System 283
Role of the Central Nervous System 283
Variables That Influence Swallowing 284
Bolus Characteristics 284
Development 285
Age 286
Measurement and Analysis of Swallowing 286
Videofluoroscopy 286
Endoscopy 287
Client Self-Report 287
Health Care Team for Individuals With Swallowing Disorders 288
Chapter Summary 289
References 290

21 Hearing Science I:  Acoustics and Psychoacoustics 293

Introduction 293
Oscillation 294
Waveform 295
Spectrum 295
Waveform and Spectrum 295
Resonance 297
Psychoacoustics 297
Pitch 298
Loudness 299
Sound Quality 299
Chapter Summary 300
References 300

2
2 Hearing Science II:  Anatomy and Physiology
301
Introduction 301
Temporal Bone 301
Peripheral Anatomy of the Ear 303
Outer Ear (Conductive Mechanism) 303
Middle Ear 305
Inner Ear (Sensorineural Mechanism) 307
Chapter Summary 314
References 314
 Contents xiii

23 Diseases of the Auditory System and 317

Diagnostic Audiology
Introduction 317
Hearing Evaluation 317
Case History 318
Otoscopy 318
Immittance 319
Tympanometry 320
Acoustic Reflex Threshold 323
Audiometric Testing 324
Physiological Responses 327
Vestibular Assessment 332
Audiometric Results 334
Type, Degree, and Configuration of Loss 335
Hearing and Balance Disorders 337
Patient Examples 337
Chapter Summary 341
References 341

24 Assistive Listening Devices 343

Introduction 343
Hearing Aids 343
Steps in Selecting and Fitting a Hearing Aid 343
Types of Hearing Aids 345
Hearing Aid Components 348
Auditory Implantable Devices 349
Bone-Anchored Implant 350
Middle Ear Implant 351
Cochlear Implant 354
Chapter Summary 355
Hearing Aids 355
Auditory Implantable Devices 356
References 356

25 Aural Habilitation and Rehabilitation 359

Introduction 359
Aural Habilitation 360
Assessment of Communication Needs in Children 360
Pediatric Intervention 362
Components of a
Family-Centered Intervention 364
Auditory Training in Aural Habilitation 365
Communication Options 365
Outcome Measures for Children 367
Aural Rehabilitation 367
Assessment of Communication Needs in Adults 367
Adult Intervention 368
Auditory Training in Aural Rehabilitation 368
Communication Strategies 369
Speechreading 369
xiv Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Outcome Measures for Adults 370

Group Aural Rehabilitation 371
Chapter Summary 372
Aural Habilitation 372
Aural Rehabilitation 372
References 373

Index 375
Preface
Introduction to Communication Sciences and Disorders: The Scientific Basis of Clinical Practice is a
textbook designed and written for undergraduate students who enroll in a course that lays out
the scientific foundations for the clinical disciplines of speech-language pathology and audiol-
ogy. The great majority of departments in our field that offer an undergraduate major have
a regularly taught introductory course among their course offerings. Introductory courses in
any field, whether in psychology, anthropology, linguistics, or communication sciences and
disorders (hereafter, CS&D), are survey courses in which nearly all aspects of a field are pre-
sented. For academic disciplines that have many aspects — and most do — breadth of coverage
takes precedence over depth of coverage. Simplification of complicated material is inevitable,
and long-standing, ongoing debates in a field cannot be described in detail. An introductory
course in CS&D is subject to these characteristics, and these constraints. That being said, we
have attempted to provide a carefully measured depth in each chapter, in the hope of con-
veying the sense of excitement in the continuing expansion of the scientific basis of clinical
practice in CS&D.
This textbook is organized with a general plan of matching individual chapters to indi-
vidual lectures, or perhaps to one-and-one-half lectures. The textbook is written to give the
instructor the option of not including selected chapters in the classroom lectures, or not
assigning them as required reading material, if that is desired. For example, there are two
chapters that present information on pediatric language disorders, and two chapters that pres-
ent information on pediatric speech sound disorders. For each pair of chapters, one chapter
presents information on two or three disorders, and the other presents information on two or
three other disorders. An instructor who decides to present examples of a particular pediatric
language or speech sound disorder can surely choose one chapter for a lecture and assign
(or not) the other chapter for reading. The same can be said of several other chapters in the
textbook. In this sense, we believe the textbook is a flexible instructional companion for both
instructors and students.
The graduate training of speech-language pathologists (SLPs) and audiologists (AuDs) is
a significant mission of CS&D departments. Communication Sciences and Disorders is, at its
core, a clinical discipline. But if a clinical endeavor is to be disciplined, the core must include
material that supports and motivates clinical practice with knowledge that has emerged from
the research laboratory. This text is primarily concerned with the scientific basis of clinical
practice, the former being a first step to qualify for the latter professional skill.
Clinical information is not ignored in the textbook. In fact, all chapters that present the
nature of language, speech, and hearing disorders include some information on diagnosis
and treatment of communication disorders. In some chapters, this information is integrated
with the presentation of the main material, in others a brief section describes clinical issues
relevant to the communication disorder(s) under discussion. A fixed formula is not used for
the inclusion of clinical information in various chapters of the textbook; rather, in each chapter
that presents information on communication disorders, the clinical information is placed in
the location that seemed (in our opinion) to make the most sense.

xv
xvi Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Curricula in departments of CS&D are structured to include classes on typical and dis-
ordered language, on typical and disordered speech, and on typical and disordered hearing.
This is to say that language, speech, and hearing occupy three different categories of course-
work. The categories are organized more for the structure of a curriculum, rather than a belief
that language, speech, and hearing processes are separate. They are not. The integrated nature
of language, speech, and hearing processes, whether typical (normal) or disordered, is known
by all clinicians and scientists concerned with communication sciences and disorders. For
example, a child who is seen in the clinic for a delay in the mastery of speech sounds often has
delays in language acquisition as well, and is at risk for reading delays. Similarly, an Ameri-
can child who is born deaf may have delays in oral language development but have typical
language development in American Sign Language (ASL).
This textbook follows the approach of separating language, speech, and hearing chapters.
But we ask students to keep in mind that this is a teaching decision (much like the organiza-
tion of courses, as stated earlier), not a statement that the areas are separate. Language chap-
ters are presented first, followed by speech chapters and then hearing chapters; this sequence
is arbitrary. One of us (GW) taught the introductory course in the University of Wisconsin–
Madison CS&D department for 20 years, changing the order of the language, speech, and
hearing categories several times to see if one sequence was more effective than others; the
order did not seem to make a difference.
The textbook covers a lot of information; this is a necessary feature of a text designed to
be the primary reading material for a survey course in communication sciences and disorders.
Some areas of the field may be mentioned only briefly, which does not mean we believe they
do not merit careful discussion. Decisions were made to limit discussion of certain areas to a
minimum to accommodate the goal of a compact textbook.
Two final comments are in order. First, the use of pronouns is an efficient and straight-
forward way to construct sentences in a textbook with frequent references to people. In cases
(which constitutes most of the uses) we have chosen to limit pronouns to “he” and “she,” and
to alternate between the use of the two when the reference is to a person who is (for example),
a clinician or person seeking services. Second, the pattern and extent of citations vary across
chapters. Every effort has been made to provide interested students and instructors with up-
to-date references, and with review papers that provide overviews of the current state of both
the research and clinical aspects of a topic under study.
We hope the textbook and the course are effective in creating an enhanced understanding
of the importance of successful communication, and of the need to understand the impact of
a communication disorder on every aspect of an individual’s life.

Happy learning!
Acknowledgments
Kalie Koscielak, Valerie Johns, and Angie Singh, we are indebted to you for years of support
and encouragement.

Susan Ellis Weismer had a profound influence on the shaping of Chapters 3, 5, 6, 7, and 8.
Professor Ellis Weismer read and reread successive drafts of these chapters, each time making
spot-on suggestions for revision. We cannot thank her enough.

Once again, as it is with previous textbooks, Maury Aaseng’s beautiful artwork is a defining
feature of this textbook. Thanks, Maury.

Thanks to Professor Susan Thibeault, and Eileen Peterson, for their gracious offer and prepa-
ration of images for Chapter 18.

Thanks to Denny and Shelley Weismer for the photo of Friday, their African gray.

Thanks to Professor Jenny Hoit for her enormous and generous influence on several parts of
this textbook.

Anna Ollinger read drafts of several chapters and made excellent suggestions for clarification
of concepts and organization.

Thanks to Professor Steven Kramer for his influence on the audiology portions of this textbook.

The people named are not responsible for any errors that may exist in the textbook; whatever
errors exist are solely our responsibility.

xvii
Reviewers
Plural Publishing, Inc., and the authors would like to thank the following reviewers for taking
the time to provide their valuable feedback during the development process:
Gretchen Bennett, MA, CCC-SLP
NYS Licensed Speech-Language Pathologist
Coordinator of Speech-Language Clinical
Services
Clinical Associate Professor/Supervisor
SUNY at Buffalo Speech-Language and
Hearing Clinic
Kate Bunton, PhD, CCC-SLP
Associate Professor
Speech, Language, and Hearing Sciences
University of Arizona
Jaime Fatás-Cabeza, MMA
Associate Professor
Director of Translation and Interpretation
Department of Spanish and Portuguese
University of Arizona
Vicki L. Hammen, PhD, CCC-SLP
Professor and Program Director
Communication Disorders
Indiana State University
Jennifer M. Hatfield, MHS, CCC-SLP
Speech-Language Pathologist
Clinical Assistant Professor
Indiana University, South Bend
Rachel Kasthurirathne, MA, CCC-SLP
Indiana University, Bloomington
Breanna Krueger, PhD, CCC-SLP
University of Wyoming
Florence Lim-Hardjono, MA, PhD
(ABD), CCC-SLP
Mount Vernon Nazarene University
Avinash Mishra, PhD, CCC-SLP
University of Connecticut
Elisabeth A. Mlawski, PhD, CCC-SLP
Assistant Professor
Monmouth University
Nikki Murphy, MS, CCC-SLP
University of Nevada, Reno
Kelly S. Teegardin, MS, CCC-SLP, LSLS
Cert AVT
Instructor I
Communication Sciences and Disorders
University of South Florida
Angela Van Sickle, PhD, CCC-SLP
Texas Tech University Health Sciences
Center
Jason A. Whitfield, PhD, CCC-SLP
Bowling Green State University
xix
For Susan

For Dianne

Introduction to Communication
Sciences and Disorders
We would build a profession independent
of medicine or psychology or speech,
based in colleges and public schools.
— Van Riper, 1981
Introduction: Communication
Sciences and Disorders
as a Discipline
This is how Charles Van Riper, one of the pioneers of
the field of Communication Sciences and Disorders,
remembered the early 20th-century beginnings of the
discipline. From the time he began to speak as a child,
Van Riper had a severe stuttering problem. In young
adulthood, he continued to stutter and desperately
sought a “scientific” explanation for his problem. He
reasoned that if an explanation could be identified
through a program of systematic discovery — a pro-
gram of scientific research — treatment methods would
follow from the explanations, perhaps leading to a cure
for stuttering.
Van Riper interacted with a small group of indi-
viduals, several of whom were also people who stut-
tered; jointly they decided to break away from the
1
domination of medical and Freudian perspectives on
speech disorders. In 1925, approximately 25 individuals
established an independent society called the American
Academy of Speech Correction. This society was intended
as a research organization. One of the charter members
of this organization was Dr. Sara Mae Stinchfield, who
was the first person in the United States to be awarded
a PhD (from the University of Wisconsin) in the field
of Speech Pathology. In 1929, the organization changed
its name to the American Society for the Study of Disorders
of Speech. The word “Study” in the organization’s new
name highlighted the scientific goals of the group. This
contrasted with the more practical but (in the opinion
of some of the founding members of that society) less
lofty goal of treating Communication Sciences and Dis-
orders. “Speech teachers,” or people who attempted
to help individuals with problems such as stuttering,
articulation disorders, language delay, speech and lan-
guage problems associated with neurological disease,
or unintelligible speech resulting from absence or loss
of hearing, were well known in society but certainly
not professional mainstays in schools and hospitals.
The newly minted American Society for the Study
of Disorders of Speech struggled a bit because of small
membership and some disagreements among mem-
bers. As recounted by Van Riper (1981), several of the
1
2 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
influential members wanted the group to focus on sci-
entific investigation of stuttering, but others saw the
world of Communication Sciences and Disorders more
broadly. Pauline Camp, who was serving as the head of
speech correction in the State of Wisconsin, proposed
that the field could grow by establishing speech cor-
rection clinics in universities. These clinics would train
future “speech correctionists” as well as scientists inter-
ested in the nature and cause of speech disorders. As
trained clinicians found employment in public schools
and demonstrated their ability to help children with
speech problems, the need for additional trained pro-
fessionals would increase, and the American Society
for the Study of Disorders of Speech would grow.
Camp’s proposed strategy for growing the pro-
fession was right on target. University programs were
developed, with the training of “service providers”
(clinicians) and scientists conducted in the same envi-
ronment. The guiding principle of this training concept
was the presence of clinicians and scientists in a com-
mon environment, teaching each other and enhancing
their respective knowledge and performance. Scien-
tists formulated more specific and worthy research
questions by obtaining information about the clinical
details of communication problems in actual patients,
and clinicians sharpened their diagnostic procedures
and practice techniques by learning from the research.
This training model has persisted until the present day,
and has been successful.
In 1934, the young speech organization, much
larger than it was in 1930, was reconstituted under a
third name: the American Speech Correction Association.
This name stuck until 1947, when the association was
renamed the American Speech and Hearing Association,
or ASHA. In 1978, the group was renamed the Ameri-
can Speech-Language-Hearing Association, to recognize
the equivalent importance of language function (as
compared to the act of producing speech, or the ability
to hear) in the understanding of normal and disorder-
ed communication function. The association has
retained this name to this day but is still referred to
as “ASHA.”
As of 2018, ASHA reported a membership (including
student members) of 203,945 individuals (https://www​
.asha.org/uploadedFiles/2018-Member-Counts​.pdf).
Among the members of ASHA are 12,480 who
have their primary training in Audiology and practice
as Clinical Audiologists. Many of these professionals
are also members of the American Academy of Audiol-
ogy (AAA), an organization whose mission is to define
the training and practice guidelines for professionals
who work as clinical audiologists (https://www.audi-
ology.org/about-us/academy-information). AAA was
founded in 1988, in recognition of the need for an orga-
nization whose primary purpose would be serving the
profession of Clinical Audiology. Many of the 12,000+
Audiologists who are members of ASHA are also mem-
bers of the American Academy of Audiology.
There is a difference between the perspectives of
ASHA and AAA on the right to practice Clinical Audi-
ology. ASHA currently argues that a Clinical Audiolo-
gist must have a Certificate of Clinical Competence in
Audiology (CCC-A), issued by ASHA, as the proper
credential for the practice of audiology. AAA’s posi-
tion is that the CCC-A is not necessary for the practice
of audiology; what is required is that students-in-
training in audiology have a sequence of courses that
is recognized as the foundation for training profes-
sional audiologists, and that a year of professional
work (much like an internship) follows the completion
of the coursework training. In the view of AAA, this
training prepares the student for state licensure as a
Clinical Audiologist, which when obtained provides
the “legal” right to practice clinical audiology. The
different perspectives on the credentials needed by
trainees to practice clinical audiology are complicated;
readers are encouraged to visit https://www.audiology​
.org/publications-resources/document-library/audi-
ology-licensure-vs-certification. There is a concerted
effort among several different associations, including
ASHA and AAA, to resolve these different perspec-
tives (https://www.asha.org/uploadedFiles/Aligned-
Sense-of-Purpose-for-the-Audiology-Profession.pdf).
Communication Sciences and
Disorders: The Whole Is Greater
Than the Sum of Its Parts
When Van Riper remembered the early vision of a dis-
cipline “independent of medicine or psychology or
speech,” he was not thinking of abandoning the con-
tent of these other fields of study. Rather, he imagined
an academic and clinical field with a separate identity,
forged from the concepts and facts of medicine, psy-
chology, and other disciplines, but clearly something
different and new — a field with its own identity, able
to stand on its own merits. It is comically ironic (to
this author, at least) that over the past 10 to 15 years,
two buzzwords on college campuses have been “inter-
disciplinary research” and “translational research.”
The field of Communication Sciences and Disorders
embraced these two activities — in fact, defined itself by
an interdisciplinary and translation mentality — long
before they became fashionable and fundable claims in
university settings.
 1  Introduction to Communication Sciences and Disorders
An Interdisciplinary Field
Communication Sciences and Disorders is a field prac-
ticed and studied by individuals with expertise in a
variety of academic and clinical disciplines. It is truly
interdisciplinary, the product (but not merely the sum)
of many different areas of knowledge. Speech is pro-
duced by moving structures of the respiratory system,
larynx, and vocal tract (the latter sometimes referred
to as the “upper articulators,” including the tongue,
lips, and jaw). Scientists and clinicians who are inter-
ested in communication disorders must understand
the anatomy (structure) and physiology (function) of
these body parts. When a person speaks, air pressures
and flows are generated throughout the speech mech-
anism, and an acoustic signal (what you hear when
someone talks) is emitted from the lips and/or nose.
An understanding of these aerodynamic and acoustic
phenomena of speech requires at least a foundation of
knowledge of basic physics.
When the acoustic signal emerges from the talk-
er’s mouth (or nose), it is metaphorically “aimed” at
another person who receives it through his or her audi-
tory mechanism. This makes it clear that the anatomy
and physiology of the auditory system must be mas-
tered by the person specializing in Communication
Sciences and Disorders. As with the process of speech
production, hearing and comprehending acoustic sig-
nals involve complex mechanisms understood prop-
erly only with a decent amount of knowledge in the
areas of anatomy, physiology, and physics (and other
areas as well).
Of course, when talkers produce speech, they want
to communicate a message. The nature and structure
of the message — what is being communicated, and
the form it takes when it is spoken — is determined by
linguistic-cognitive processes. For example, linguistic-
cognitive processes are set into motion by the simple
act of asking someone to have coffee. An idea must be
developed and structured in linguistic terms according
to the intent and wishes of the person doing the ask-
ing. The idea is something like, “I want to spend time
with this person and suggesting we have coffee at a
comfortable café seems like a good approach,” but the
manner in which this “want” is structured as a message
can vary wildly, depending on many factors. “Would
you like to have coffee?” “Hey, how ’bout we grab
some coffee?” “I’m really sleepy, let’s stop at Completely
Wired and get some coffee.” “I’d really like to talk to
you over coffee.” “Let’s have a no-obligation date over
coffee.” “Coffee?” These different ways to convey the
same message reflect variation in underlying cognitive
processes and linguistic structure, both of which are
3
critical to language usage. The clinician and scientist
in Communication Sciences and Disorders deal with
disorders of language structure and usage, and must
therefore have expertise in the broad areas of hearing,
cognition, and linguistics.
The term “cognitive-linguistic” refers
to psychological processes applied to
the use of language forms. “Cogni-
tion” refers to several psychological processes,
including memory; executive function (e.g.,
planning behavior, connecting current behavior
with future consequences); the development,
refinement, and stabilization of mental represen-
tations; brain computation speeds; and transfer
of information from one type of memory (e.g.,
short-term memory) to another (e.g., long-term
memory). These various aspects of cognition are
listed here as separate processes but in fact may
overlap and in some cases be different reflections
of a single psychological process. “Linguistic”
refers to any aspect of language form — sounds,
words, sentences, tone of voice, and so forth. The
term “cognitive-linguistic” is used here to indi-
cate that the psychological processes previously
listed (among others) are applied to language
forms and therefore to communication. The
same cognitive processes are applied to other
forms of knowledge, as well (such as spatial
reasoning or mathematics).
We are not done. Because speech and language
develop throughout infancy and childhood and may
change throughout the lifetime and especially in old
age, expertise in Communication Sciences and Disor-
ders requires a solid knowledge of child development
and aging. Most obvious, perhaps, is the need to have
a broad and deep expertise concerning the many dis-
eases and conditions associated with speech, hearing,
and language disorders. Extensive medical knowledge
is absolutely necessary to function as an effective spe-
cialist in Communication Sciences and Disorders. This
knowledge ranges from how surgeries on structures of
(for example) the brain, tongue, and ear affect speech,
hearing, and language function, to how pharmaceutical
interventions (such as drugs for Parkinson’s disease, or
schizophrenia, or even chronic arthritis) may change a
patient’s ability to communicate.
Finally, legal and technical issues are relevant to the
profession of Communication Sciences and Disorders.
4 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

These issues concern a person’s right to receive the Table 1–1.  Some Areas of Knowledge Required
proper services when he or she has a speech, hearing, for People to be Effective Professionals in the Field of
or language disorder, as well as the requirements for Communication Sciences and Disorders
professional accreditation as someone who can pro-
vide services or train people to provide services, or the Neuroscience
requirement of extensive training in research to mentor Brain anatomy (structure)
students who intend to devote their careers to research. Brain physiology (function)
Our field has been fortunate to have professional lead- Neuropharmacology (chemicals and their role in
ers who can lay claim to both clinical and research brain function)
expertise. Motor control (how brain controls movement)
Table 1–1 provides a partial summary of the areas Sensory function (how brain processes sensation)
of knowledge and, in many cases, expertise, required
of the professional in Communication Sciences and Anatomy and Physiology of the Speech Mechanism
Disorders. This list includes the areas previously men- (muscles, ligaments, membranes, cartilages, etc.,
associated with the respiratory, laryngeal, and upper
tioned and adds a few more for good measure. There
airway system, which collectively are called the
are (at least) two ways to react to this list. One is to
“speech mechanism”)
feel intimidated by the need to know so much about so
many areas. The other is to look at the combination of Anatomy and Physiology of the Hearing Mechanism
these different types of knowledge as something spe- (bones, membranes, ligaments, special structures of
cial, as an opportunity to be informed about many dif- the ear)
ferent areas of study and, most importantly, to employ Child Development
an integrated and synthesized fund of this information
in an understanding of the most human of behaviors, Aging
communication. Of course, a single individual is not Diseases of the Head, Neck, Respiratory System,
likely to be an accomplished expert in each of these Auditory System, and Brain
areas, but a commitment to learn the basic principles
of each of the disciplines listed in Table 1–1, to use this Syndromes
knowledge when providing clinical services to a per- Physics
son with a communication disorder, to function as an Aerodynamics
effective member of a clinical or research team, or to
Acoustics
develop an answer to a research question, is genuinely
Movement
exciting. Communication Sciences and Disorders is the
original, lifelong learning discipline.1 Cognition
Memory and Processing
Planning
Translational Research Manipulation and Use of Symbols

Researchers and clinicians are often trained in the same Linguistics

department and yet do not interact professionally to a Phonetics and Phonology
significant degree. This has been a concern in various Morphology
branches of medicine, as well as in departments such Syntax
as Psychology, and Communication Sciences and Dis- Semantics
orders. Many scientists in these professions are trained Pragmatics
to do something they understand as “basic science.”
In basic science, research questions are asked for the
sake of improving the knowledge base in a field, or to
address purely theoretical questions. An assumption of not need to be motivated or prompted by immediate
this approach to research has been that basic science, clinical concerns; any improvement in knowledge of
if done well, will eventually have an effect on clinical the world must have implications for the betterment
practice. In this way of thinking, “basic science” does of humankind.

1
As a university professor in Communication Sciences and Disorders, I more than once told students that it was hard to believe someone was
willing to pay me to come to my office every day, learn new things in many different areas, and use this information in my research, in the
classroom, and in mentoring teaching (one-on-one instruction, as with graduate students training to be researchers).
 1  Introduction to Communication Sciences and Disorders
Let’s consider an example of a possible link between
basic science and clinical application. A fair number of
scientists have investigated birdsong and its relation-
ship to the evolution of human language (reviews can
be found in Fitch, 2000, 2006, and Deacon, 1998). Much
of this work has been funded by a federal agency, the
National Institutes of Health (NIH), whose primary
mission is to sponsor research that ultimately improves
health care in the United States. The research on bird-
song (and vocalizations produced by other, nonhuman
species) has been “sold” to the federal agency by claim-
ing potential links between, on the one hand, an under-
standing of why and how birds sing, and on the other
hand, a better understanding of speech and language
capabilities in humans. The link between birdsong and
human communication is evolutionary, in which bird-
song is a “step” along the evolutionary path to human
vocalization for purposes of communication. The rea-
soning is extended by arguing that a better understand-
ing of the basic “mechanisms” of vocal communication,
which can be studied in birds using techniques that
cannot be used in humans,2 should eventually lead to a
better understanding of the partial or complete failure
of similar mechanisms in humans. A better understand-
ing of disease-related problems in human vocalization
should, this reasoning concludes, result in better ways
to diagnose and treat human vocalization disorders.
Basic science such as work on birdsong has been
criticized for occupying federal funds that might be
used to fund “applied” research. “Applied science” is
research with more immediate clinical consequences,
research with less distance between the results of a
study and its potential use in clinical settings. For
example, funding could be provided for a research
program in which participants with healthy voices are
enrolled in a vocal exercise regime (like the kind of
warm-up exercises used by many professional singers)
and compared to a group of participants who do not
engage in this exercise (a “control group”). The applied
research question is, do nonspeech vocal exercises gen-
eralize, or translate, to the use of the voice in everyday
speech? Perhaps the effect of the vocal exercise could
be evaluated by having listeners judge the quality of
participants’ voices, with the critical comparison being
the “goodness” (pleasing quality?) of voices pre- versus
postexercise. This is basic, nonclinical research — non-
clinical because the participants do not have voice dis-
orders — but a positive result, where exercise produces
a more pleasing voice, points more directly to a specific
clinical application in patients with voice problems.
2 
 uch as creating a small area of brain damage to see how it affects the development of birdsong, or depriving a newborn bird of exposure
S
to his or her species’ song to determine if, as the baby bird matures, the song develops in the same way as in birds who are exposed to their
song from birth.
5
The relatively new buzzword for applied sci-
ence is “translational research,” or research in which
the results of basic science can be translated relatively
quickly to clinical application. The hypothetical vocal
exercise study is one example of translational research;
many others have been proposed (see Ludlow et al.,
2008; Raymer et al., 2008). The National Institutes of
Health (NIH), the federal agency having the mission
of funding and setting priorities for health-care-related
research activities in the United States, published in
2008 the following text on its website concerning trans-
lational research:
To improve human health, scientific discoveries must
be translated into practical applications. Such dis-
coveries typically begin at “the bench” with basic
research — in which scientists study disease at a molec-
ular or cellular level — then progress to the clinical
level, or the patient’s “bedside.”
Scientists are increasingly aware that this bench-
to-bedside approach to translational research is a two-
way street. Basic scientists provide clinicians with new
tools for use in patients and for assessment of their
impact, and clinical researchers make novel observa-
tions about the nature and progression of disease that
often stimulate basic science. See https://nexus.od.nih​
.gov/all/2016/03/25/nihs-commitment-to-basic-sci​
ence/ for a summary of the benefits of funding both
kinds of research.
The National Institute on Deafness and Other Com-
munication Disorders (NIDCD), the NIH institute that
is the primary funder of research in Communication
Sciences and Disorders, has a specific funding program
for translational research (as of 2017). This funding
mechanism is called the Research Grants for Translating
Basic Research into Clinical Tools. The stated objective and
requirements of these grants are as follows:
[T]o provide support for research studies that trans-
late basic research findings into better clinical tools for
human health. The application should seek to trans-
late basic behavioral or biological research findings,
which are known to be directly connected to a human
clinical condition, to a practical clinical impact. Tools
or technologies advanced through this FOA [Funding
Opportunity Announcement] must overcome existing
obstacles and should provide improvements in the
diagnosis, treatment or prevention of a disease process.
For the purposes of this FOA, the basic science advance-
6 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
ment must have previously demonstrated potential for
clinical impact and the connection to a human clinical
condition must be clearly established. The research
must be focused on a disease/disorder within one or
more of the NIDCD scientific mission areas: hearing,
balance, smell, taste, voice, speech, or language.
Research conducted under this FOA is expected to
include human subjects. Preclinical studies in animal
models are allowed only for a candidate therapeutic
that has previously demonstrated potential for the
treatment of communication disorders. The scope of
this FOA allows for a range of activities encouraging the
translation of basic research findings to practical impact
on the diagnosis, treatment, and prevention of deafness
and other communication disorders. [https://grants​
.nih.gov/grants/guide/pa-files/PAR-17-184.html]
The first statement presents the issue of “trans-
lational research” with molecular or cellular work as
the basic science, but basic science exists at the behav-
ioral level of analysis, as well. This is why the NIDCD
description mentions a “range of activities” in its mis-
sion to fund translational research in Communication
Sciences and Disorders.
Both of these NIH statements imply that it is the
basic scientist’s obligation to show how laboratory
results can be “translated” to clinical settings. This is in
contrast to earlier models of the basic science/applied
science dichotomy, in which the basic scientist might
have said, “I’ll do the bench work (very basic science)
and down the road, perhaps way down the road, clini-
cians can figure out how to use my findings when they
diagnose and treat patients.” In this view, the clinician,
not the scientist, has the primary responsibility for
translating the basic science to clinical application. The
second paragraph of the statement sounds remarkably
similar to the concept, described previously, of train-
ing “speech correctionists” in university settings where
clinical practice informs the direction of research pro-
grams, and research findings enhance clinical practice.
Pauline Camp suggested this concept in 1934, and our
discipline has been guided by the “two-way street”
philosophy since that time. As a field, we have under-
stood the potential value of “translational research” for
a long time.
Does the Basic Science Work?
Does the Clinic Work?
It is all well and good to claim that people in the field
of Communication Sciences and Disorders understood
the value of interdisciplinary work, and practiced
translational research well before the concept was so
christened and attained the status of an official move-
ment on 21st-century university campuses and in gov-
ernment funding agencies. It is quite another thing to
claim scientific success as the result of interdisciplinary
efforts, or to show that basic science has indeed been
translated to clinical application. A major goal of this
text is to present introductory information on normal
and disordered communication processes in a way that
highlights previous, and the latest, scientific findings
that have emerged from interdisciplinary thinking. For
the time being, the reader is asked to trust the claim
that the growth of the scientific basis of normal com-
munication processes, and Communication Sciences
and Disorders, has been nothing short of spectacular
over the last 50 years. None of this would have been
possible if speech, language, and hearing scientists
had not been open to the influences and thinking of
scientists in areas such as linguistics, physiology,
neuroscience, and psychology (among others). Most
importantly, the openness of these scientists to the
experience and knowledge of clinical speech-language
pathologists and audiologists has made a huge differ-
ence to the growth of the scientific knowledge base in
normal and disordered communication.
It is not a goal of this text to present detailed
information on therapy (management) techniques for
persons with speech, language, and/or hearing disor-
ders. Readers will learn a great deal about speech, lan-
guage, and hearing disorders, but a full treatment of
clinical processes and procedures is a topic for a more
advanced course of study, typically in graduate pro-
grams (see later in the chapter).
An aspect of the clinical process that is discussed
throughout this text is the diagnosis of speech, lan-
guage, and/or hearing disorders. Technically, diagno-
sis involves the identification and determination of the
nature and cause of a disorder. Notice the inclusion
of “nature” in this definition. Proper techniques must
be employed to describe a disorder and to document
the characteristics of a communication disorder that
make it different from other communication disorders.
A good part of this text is therefore devoted to descrip-
tions of how we know a specific speech, language,
and/or hearing disorder is “x” and not “y.”
This text does not shy away from controversies in
our field about the nature and causes of certain com-
munication disorders. As in any health-care-related
field, many diagnoses remain unclear and are the
subject of ongoing debate. In the best of all worlds
(sorry,Voltaire), we would welcome absolute certainty
concerning the diagnosis of human diseases and con-
ditions. The world-as-is, however, does not allow such
certainty, but let’s not regard the gray areas as defeats;
they are opportunities. Uncertainty and controversy
have always been the engines of scientific advance-
ment. Not knowing, or disagreement about what we
 1  Introduction to Communication Sciences and Disorders
do know, pushes science forward. Diagnosis, then,
is a critical part of the scientific underpinnings of a
health-care-related discipline such as Communication
Sciences and Disorders. In many cases, questions con-
cerning clinical diagnosis and the basic science founda-
tion of our field are completely intertwined.
The second part of the heading for this section asks,
“Does the Clinic Work?” Do speech-language patholo-
gists and audiologists make a difference in the lives of
people with communication disorders? Although this
text does not present detailed information about treat-
ment of communication disorders, there is widespread
evidence for treatment success.
It is important for the reader to know that many
of the services offered by clinicians in our field have
been documented as being effective. In the absence
of such documentation, the entire enterprise of train-
ing clinicians to treat communication disorders could
be questioned. Fortunately, our interdisciplinary and
translational approach to understanding communica-
tion disorders has produced diagnosis and manage-
ment techniques that are effective for many patients.
A selective sampling of publications in which this
clinical success is reviewed includes results for voice
therapy (Angadi, Croke, & Stemple, 2017; Desjardins,
Halstead, Cooke, & Bonilha, 2017; Ramig &Verdolini,
1998; Ruotsalainen, Sellman, Lehto, Jauhiainen, &
Verbeek, 2007), hearing disorders (Ferguson, Kitter-
ick, Chong, Edmonson-Jones, Barker, & Hoare, 2017;
Kaldo-Sandström, Larsen, & Andersson, 2004; Mendel
2007), stuttering (Baxter et al., 2015; R. Ingham, J.C.
Ingham, Bothe, Wang, & Kilgo, 2015; Tasko, McClean,
& Runyan, 2007), childhood articulatory disorders
(Gierut, 1998; Wren, Harding, Goldbart, & Roulstone,
2018), and childhood language disorders (Law, Garrett,
& Nye, 2008; Tyler, Lewis, Haskill, & Tolbert (2003).
Students who obtain undergraduate and graduate
degrees in our field learn the scientific basis and tech-
nical details of these successful clinical strategies. This
is not to say that we have conquered all, or even many,
of the communication disorders affecting people
around the world. Indeed, there is a substantial amount
of disagreement concerning precisely what constitutes
therapy “success” for people with communication
disorders, and a specific therapy technique may work
for some patients but not others. But the articles listed
previously show a pattern of success for many com-
munication disorders; continuing research will add to
this list.
Evidence-Based Practice
Although this text does not present detailed informa-
tion on management (treatment) of communication
7
disorders, the concept of evidence-based practice (EBP)
and its role in speech, language, and/or hearing ther-
apy is integral to an understanding of how knowledge
of typical and disordered communication is related to
treatment of communication disorders.
EBP, a movement with roots in the medical world,
takes as its central concept that any treatment approach
should be supported by scientifically based evidence
of the treatment’s effectiveness (the term “efficacy”
is often used to refer to effectiveness of a therapy
procedure, but the technical sense of “efficacy” is an
experimental demonstration that a particular clinical
technique shows promise as an effective management
tool; it is like a first step in the determination of a treat-
ment’s real-world effectiveness). The need to formalize
such a notion may at first glance seem surprising, for
should a treatment not be administered in the absence
of solid evidence that it works? Again, in the best of all
worlds this would be so, but in much of medicine and
behavioral sciences, including Communication Sciences
and Disorders, the effectiveness of treatments is often
unknown or only partially supported by research data.
EBP must be based on proper outcome measures.
Evidence for the success of a therapeutic approach
requires the measurement of one or more variables
after (or sometimes during) the treatment. Outcome
measures should have the best possible face validity,
meaning that the measures provide good indices of
the phenomena they are supposed to represent. An
example from basketball helps to understand face
validity of outcome measures. If an outcome measure
is desired for a player’s in-game shooting accuracy fol-
lowing several months of intense practice of nongame,
unguarded shooting, the percentage of shots made
over 100 attempts has good face validity if the measure
is taken during games. The measure has much poorer
face validity if the measure is taken over 100 shots
attempted during multiple games of HORSE. Shoot-
ing percentage during games is a much better outcome
measure for “real-world” shooting as compared to
shooting percentage during games of HORSE.
An example from health care, closer to the con-
cerns of this textbook, is one of drug treatment for epi-
lepsy for which there may be the potential for multiple
outcome measures with face validities that are only
subtly different. The question is, after 6 months of drug
treatment, are there fewer seizures as reported by the
patient (one potential outcome measure)? As reported
by the patient, are there no seizures over the same time
period (a second potential outcome variable)? After
6 months of drug treatment, can a seizure be induced in
the clinical setting by very bright flashing lights (a third
potential outcome variable)? Or, after 6 months, are the
blood levels of the drug in the “correct” range based
on values reported in the scientific literature (a fourth
8 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

potential outcome variable)? At first glance, the first Levels of Evidence

two outcome measures have the best face validity — the
Level I and II evidence are usually based on large
best evidence for reduction of seizures is a report from
numbers of participants to generate the most reli-
a patient that seizure episodes have been reduced or
able statistical results. In Table 1–2, Level I evidence
eliminated. Some clinicians and scientists, however,
is summarized as “systematic reviews” or “meta-
may think that patient-reported data are unreliable
analyses” of RCTs. An RCT is an experiment in which
because they are subject to the notorious uncertainties
each individual from an initial, large pool of partici-
of memory or even a patient’s misrepresentation of sei-
pants is randomly assigned to one of two (or more)
zure history. Measures such as inducement of a seizure
treatments. Ideally, neither the experimenters nor the
by flashing lights or drug blood levels are regarded as
participants have knowledge about which treatment
more objective (and have a clearly quantitative basis)
has been assigned to any participant in the study. The
and therefore may seem more reliable than the patient
participants (and in many cases, the experimenters)
reports of seizure history. Yet, from the perspective of
are “blind” to which participants have been assigned
the patient, inducement of a seizure in a controlled
to which treatments, and the participants are “blind”
clinical setting or “good” drug blood levels mean very
to the status of their treatment condition (real treat-
little when he or she is losing consciousness two or
ment group, or placebo group). This is an example of a
three times a week or even having many episodes of
“double-blind” experiment.
preseizure activity.
In Table 1–2, Level I evidence is summarized as
The choice of a proper outcome measure (or mea-
“systematic reviews” or “meta-analyses” of RCTs.
sures) is not straightforward and is often the subject
A systematic review is the organization and evaluation
of considerable debate. The debate is lively and even
of data from many different, individual RCTs, and a
heated when the behaviors of speech, language, and
“meta-analysis” is a quantitative (statistical) analysis
hearing disorders are evaluated for their response to
of the data from many such studies. A meta-analysis of
therapy. Readers may want to keep this in mind when
the results of many different studies can only be done
considering the concept of EBP.
when the data from each study are sufficiently compa-
The concept of EBP has taken on a life of its own
rable — as when the same pretreatment and outcome
as an academic discipline, and there is no end to the
measures were used in the different studies (such as
debate about precisely what serves as “good” scientific
number of seizures per week), the same blinding con-
evidence for the efficacy of a treatment. Table 1–2 pre­
ditions, the same dosage levels, and so forth.
sents a six-level EBP model of “goodness” of evidence,
Level II evidence is the result from a single RCT.
with the “best” evidence at the top (Level I) and the
Level II evidence is high-level scientific evidence but
worst at the bottom (Level VI). This simplified model
is not as trustworthy as having many different dem-
of EBP serves the purposes of this discussion well and
onstrations, from different laboratories and different
has been presented several times in the Communica-
scientists, of the same outcome. In other words, when
tion Sciences and Disorders literature (Dodd, 2007;
Level II evidence is replicated several times, Level I evi-
Dollaghan, 2004; Moodie, Kothari, Bagatto, Seewald,
dence has been produced.
Miller, & Scollie, 2011).

Table 1–2.  Levels of Evidence Applied to Evidence- Level I and II Evidence in Communication Sci-
Based Practice: A Simplified Model ences and Disorders.  In Communication Sciences
and Disorders, it is relatively difficult to obtain Level
Level I Systematic reviews and meta-analyses of I and II evidence. How easy is it to find, for example,
randomized controlled trials (RCTs) 100 people who have a similar stuttering problem, or
100 people who have had a stroke and who have very
Level II A single RCT
similar problems with expressing or comprehending
Level III Nonrandomized, controlled (well-designed) speech? How easy is it to find 100 children with autism,
treatment studies who all have the same communication challenges and
similar characteristics in noncommunication domains?
Level IV Nonexperimental studies
In each of these cases, the answer is: Not easy at all.
Level V Case reports and/or narrative literature In addition, it is unusual for different laboratories that
reviews study communication disorders, and even a single
communication disorder such as stuttering (as one
Level VI Expert/authority opinion
example), to use the same measure of stuttering fre-
 1  Introduction to Communication Sciences and Disorders
quency (perhaps number of stuttered words per 100
words produced). For these reasons and others, RCTs
are unusual in our field.
Many RCTs in medical fields contrast an experi-
mental group that receives a trial drug for a condition
or disease, and a control group that receives a placebo.
Both groups take pills on a schedule, but do not know
if they are taking the experimental medication or sugar
pills. Such experiments in Communication Sciences
and Disorders raise an ethical question: how do you
withhold treatment from a group of individuals with a
communication disorder?
RCTs are unusual in our field. They are difficult
to execute because of many factors, not the least of
which is assembling an initial participant pool, with
the same kind and degree of speech/language/hearing
challenges, from which random assignment to different
treatment types is possible. Perhaps this explains why
some introductory texts in Communication Sciences
and Disorders (e.g., Justice & Redle, 2014) choose to
talk broadly about EBP from sources external to scien-
tific pursuits. These sources include patient values and
preferences, and clinician expertise (Sackett, Rosen-
berg, Gray, Haynes, & Richardson, 1996). These factors
are considered jointly with scientific data as contribu-
tions to EBP in the life of a speech-language patholo-
gist or audiologist. The absence of solid Level I and II
“high-level” evidence in our field places greater weight
on the other factors (patient preference, clinical experi-
ence) in treatment decisions made by speech-language
pathologists and audiologists.
Level III Evidence.  The description of Level III evi-
dence in Table 1–2 is “non-randomized, controlled
(well-designed) treatment studies.” As in the case of
RCTs, two groups are typically studied and compared,
one receiving Treatment X, the other Treatment Y (or
no treatment). Level III evidence does not involve ran-
domization from a pool of eligible subjects but must be
well controlled in other ways.
Studies that produce Level III evidence are rela-
tively common in the communication sciences and dis-
orders literature. Level III evidence often comes from
studies with a relatively small number (e.g., 10 to 20)
of participants in each group, certainly smaller than the
group numbers in (for example) drug trials. In addi-
tion to the absence of randomization of participants to
treatment conditions, the relatively small number of
participants in Level III studies renders them less pow-
erful statistically and, therefore, less “valued” than RCTs.
Level IV Evidence.  Level IV evidence is produced
when a study is performed in the absence of proper
9
experimental controls. The lack of a control group
whose performance can be compared to an experimen-
tal group is a common problem in experiments that
align with Level IV evidence.
Level IV-type evidence is found in in the speech,
language, and hearing literature. Treatments are
applied to a group of individuals with communication
disorders, in the absence of proper controls. People
with communication disorders improve following the
treatment, and a conclusion is reached that the specific
treatment is to be valued for its positive effect on the
communication impairment. In the absence of controls,
however, any form of treatment, not the specific treat-
ment employed, may have improved the communica-
tion skills of a group of persons with a communication
impairment.
Levels V and VI Evidence.  Levels V and VI are types
of evidence considered to be poor support for a treat-
ment approach in any field. Case reports, which con-
sider the outcome of a specific treatment applied to
a single patient, or to a series of patients with similar
characteristics, lack controls and cannot be generalized
to a larger group of patients. The absence of experimen-
tal controls and the study of only a single or few indi-
viduals contribute heavily to the evaluation of this kind
of evidence as “poor quality.” Even so, case reports
are common in the health care literature, including
the treatment literature in Communication Sciences
and Disorders.
An argument can be made that case reports
gain value when they are organized and synthesized
in a single publication, with conclusions drawn from
the careful analysis of results across reports. The
problem with this line of thinking is that the primary
problem of lack of experimental controls in each case
report is not solved by accumulating many case stud-
ies. The shared flaw of most case studies, of no experi-
mental controls, means that a summary of many cases
for the purpose of providing evidence to support
a treatment approach is a summary of many flawed
experiments.
Another type of Level V evidence is the narrative
literature review. Narrative literature reviews are pub-
lications in which a large number of research papers,
most often those that provide Level III evidence, are
organized and evaluated for the purpose of drawing
qualitative conclusions about a focused issue. Narrative
reviews are popular in Communication Sciences and
Disorders and are published in leading journals. Narra-
tive reviews have poor evidence quality for the purpose
of supporting a treatment approach, because ultimately
they are position papers, like editorials, with a primary
10 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
aim of persuading readers that their conclusion(s) is
(are) preferable to alternate conclusions.3
The narrative review and its aim to persuade by
summaries of existing research findings and theoretical
issues, is a more scholarly version of the lowest evi-
dence level, that of expert/authority opinion. Anyone
can have an opinion that is stated as the likely truth.
When “anyone” turns out to be an authority in a disci-
pline, and asks that his or her position be accepted not
on the basis of published data but on his or her author-
ity, the evidence has little or no value.
The concept of EBP is firmly grounded in the inter-
action and co-dependency of laboratory experiments
and clinical practice. Scientists construct experiments
to generate results in support of proper diagnosis and
effective clinical management, and clinicians apply the
findings to their patients and evaluate their real-world
results. On the basis of those clinical results, scientists
may adjust their experiments to provide additional and
improved data for EBP.
A Typical Undergraduate
Curriculum
Table 1–3 shows the undergraduate, major curricu-
lum in Communication Sciences and Disorders at
the University of Wisconsin–Madison. This sequence
of courses is more or less representative of curricula
in any department in the United States that offers an
undergraduate degree in our field (some variation will
occur from department to department). The course for
which this text was written is shown in parentheses
because it is not a requirement in the UW–Madison
department for an undergraduate major in the field.
Rather, this course is taken each semester by a large
number of students to satisfy a breadth requirement in
the College of Letters and Science. Many students who
choose to major in Communication Sciences and Disor-
ders at UW–Madison do take the introductory course,
and in many cases, the exposure to the field provided
by the class is the reason they choose Communication
Sciences and Disorders as their major.
A group of courses in the curriculum (Speech Sci-
ence; Hearing Science; Neural Bases of Speech, Hear-
ing, and Language; Speech Acoustics and Perception;
Language Development in Children and Adolescents;
the Phonetic Transcription module of Phonological
Development and Disorders) establishes a solid sci-
entific foundation for normal (typical) processes of
communication. Other courses (the second part of
3 
 he author feels free to point to the evidentiary weakness of narrative reviews because he has published several of them. Conversely, narrative
T
reviews may organize the literature in a way that is useful for clinicians and scientists as they pursue their professional goals.
Phonological Development and Disorders; Voice, Cra-
niofacial, and Fluency Disorders; parts of Neural Bases
of Speech, Language, and Hearing Disorders; Auditory
Rehabilitation; Child Language Disorders: Assessment
and Intervention) provide basic information on the
classification, causes, and nature of the many diseases
and conditions associated with communication disor-
ders. Some curricula may have a course called “Pre-
clinical Observation,” in which students are introduced
to the clinical process by observing clinical sessions,
rather than being directly involved in diagnosing or
treating communication disorders.
Who Are the Professionals
in Communication Sciences
and Disorders?
Students obtain undergraduate and graduate degrees
in preparation for a job. In the field of Communication
Sciences and Disorders, this preparation is for employ-
ment as a speech-language pathologist or audiologist
in an educational or health care setting. Or, a student
may prepare for a career as a professor in a college or
university setting. At the undergraduate level, training
is not differentiated across these different career paths.
Nearly everyone who intends to be a professional in
Communication Sciences and Disorders learns a com-
mon scientific foundation for the field, as summarized
in Table 1–3.
Preparation for, and the Profession
of, Speech-Language Pathology
The requirements to practice as a speech-language
pathologist (SLP) include coursework that furnishes
a knowledge base specified by ASHA, completion of
a master’s degree, a clinical fellowship, and success-
ful performance on a national exam. The information
presented here is based on ASHA’s published certifi-
cation standards as of 2014, as well as some revisions
and amendments to these standards published in 2016.
ASHA documents are available at https://www.asha.org
Students finishing an undergraduate major in
Communication Sciences and Disorders apply to mas-
ter’s degree training programs in the fall semester of
their senior year (or later, if they decide to take a year
or two off before beginning graduate school). There
are currently over 200 such training programs in the

Table 1–3.  The Undergraduate Curriculum for a Major in Communication Sciences and Disorders
at University of Wisconsin–Madison
Course
(Introduction to Communication Sciences
and Disorders)
Speech Anatomy and Physiology (speech
science)
Hearing Anatomy and Physiology (hearing
science)
Neural Bases of Speech, Language, and
Hearing Disorders
Language Development in Children and
Adolescents
Speech Acoustics and Perception
Phonological Development and Disorders
Voice, Craniofacial, and Fluency Disorders
Introduction to Audiology
Preclinical Observation
Auditory Rehabilitation
Child Language Disorders: Assessment
and Intervention
United States, as well as about 10 in Canada. Clinical
training programs, either established or under devel-
opment and based closely or more generally on the
ASHA model, are available in Australia, Brazil, Bel-
gium, China, England, Finland, Germany, Hong Kong,
Ireland, Italy, the Netherlands, New Zealand, Scot-
land, South Africa, South Korea, Sweden, and Taiwan,
among others.
Many opportunities exist to find a program that
fits an individual student’s needs. Master’s degree
training typically includes 2 years of advanced course-
1  Introduction to Communication Sciences and Disorders 11
Comments
Survey of field
Anatomy and physiology of speech mechanism
(respiratory system, larynx, upper articulators)
Anatomy and physiology of hearing mechanism;
basic acoustics
Basic neuroanatomy and diseases of nervous system
that affect communication
Typical language development from infancy through
adulthood, with information on atypical language
development
Speech acoustics, speech perception, role of speech
acoustics in understanding articulation processes
and understanding the speech signal
Basic phonetics; typical development of the speech
sound systems of languages; definition, causes, and
nature of developmental speech sound disorders
Classification, causes, and nature of disorders of
the larynx (voice disorders), syndromes and other
related genetic/embryological disorders affecting
the speech mechanism, and fluency disorders such
as developmental stuttering
Hearing science, approaches to evaluation of
auditory disorders, interpretation of frequently used
hearing tests
Introduction to clinical issues via lectures and
observation of clinical interactions
Principles and techniques for auditory training of
individuals with hearing impairment
Child language disorders in various populations,
their classification, nature, and causes, plus the
scientific basis of assessment
work designed to build on the foundation developed by
the undergraduate course of study. Coursework at the
undergraduate and master’s degree levels is designed
to meet certain training standards established by ASHA
(for American universities) or Speech-Language and
Audiology Canada (SAC, for Canadian universities).
A critical component of training at the master’s level
is direct clinical experience in the diagnosis and treat-
ment of speech-language disorders. ASHA standards
require students to obtain 400 hours of direct clinical
experience by the end of their master’s program. The
12 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

knowledge and skills derived from coursework and
clinical experience are one component of eligibility for
certification by ASHA.
ASHA sets certification standards for students in
training, and develops other documents and standards
for professional SLPs (described in full detail at https://
www.asha.org/Certification/2014-Speech-Language-
Pathology-Certification-Standards/). The steps toward
clinical certification are summarized in Table 1–4.
SLPs work in a variety of settings. Hospital clinics,
private medical practices, public and private schools,
rehabilitation centers, and nursing homes are common
work sites for SLPs. SLPs also work in private practice,
setting up businesses that offer on-site diagnosis and
therapy (like a physician’s private practice) or contract-
ing their services to other sites. A significant number of
SLPs work in university settings, supervising the train-
ing activities of future SLPs. Finally, SLPs who earn a
PhD typically work on a university faculty where they
teach and do research. These individuals — probably
like your instructor in this course — continue their
schooling past their master’s training for (on average)
between 3 and 5 years to earn the PhD degree. At most
universities, faculty members are expected to perform
and publish research, provide classroom instruction
at the undergraduate and graduate levels, serve on
committees, and mentor students in laboratory or clini-
cal settings.
SLPs diagnosis and treat a wide variety of speech
and language problems. These clinical activities range
from early intervention with a child who has delayed
language development or is showing an early form of
stuttering, to diagnoses and treatment of voice prob-
lems, or to serving as a member of a team of health care
professionals who provide services to children with cleft
palates. There are too many areas of professional speech-
language pathology involvement to mention here, but
most are discussed in this text. The scope of speech-
language pathology practice is published at https://
www.asha.org/policy/SP2016-00343/ (2016 revision).
Preparation for, and the
Profession of, Audiology
This is a professional doctorate, analogous to the profes-
sional doctoral degree required for the practice of (for
example) optometry and pharmacy.4
At the current time (based on 2012 standards),
an individual enrolled in an AuD program and who
seeks the Certificate of Clinical Competence in the area
of Audiology (CCC-A) must obtain a minimum of 75
credit hours of postbaccalaureate (graduate-school)
study. Like the master’s degree in Speech-Language
Pathology, students enrolled in an AuD program take
academic courses and are engaged in clinical practica.

Table 1–4.  Steps to Obtaining Certificate of Clinical Competence in Speech-

Language Pathology (CCC-SLP) or Audiology (CCC-A)

CCC-SLP Undergraduate degree (or equivalent) in accredited university program →

Clinical master’s degree from accredited university program (2 years of
coursework + total of 400 hours of supervised clinical training) →
Clinical Fellowship Year (36 weeks, full-time clinical work, supervised by
professional who already holds CCC-SLP) →
Pass national exam

CCC-A Undergraduate degree (or equivalent) in accredited university program →

AuD degree from accredited university program (3 years of coursework
+ 1 year of full-time, clinical practice, supervised by professional who
already holds CCC-A) →
Pass national exam

4 
 he reader may wonder if there has been a similar movement among SLPs to require a professional doctorate in speech-language pathology
T
for clinical practice. There have been several attempts to specify standards and training objectives for something that might be called the
“SplD”— Doctor of Speech-Language Pathology — but the movement has never been sufficiently focused or persuasive to prompt a serious
consideration of abandoning the clinical master’s degree in favor of a professional doctorate as the “entry-level” degree to practice clinical
speech-language pathology. Professional doctorates in Speech-Language Pathology are offered at some universities. One model for this degree
and its requirements is the program at the University of Pittsburgh (https://www.shrs.pitt.edu/CScD).
 1  Introduction to Communication Sciences and Disorders
The clinical practica in an AuD program are designed
to prepare students to diagnose and treat hearing and
balance disorders, and to counsel patients about these
disorders and their ongoing management. Unlike mas-
ter’s-level training for SLPs, the final year of the AuD
program is spent in full-time clinical practice under the
supervision of an individual who has the CCC-A. In
total, AuD students obtain a minimum of 1,820 hours
of clinical practicum before they receive the degree.5
Full details of ASHA requirements for earning
an AuD are published at https://www.asha.org/Cert​
ification/2012-Audiology-Certification-Standards/
The AuD program typically requires 3 or 4 years
of postbaccalaureate study, including the final year of
full-time clinical practice. Currently, there are approxi-
mately 75 AuD programs in the United States.
Audiologists work in many of the same settings as
SLPs, with some exceptions. For example, audiologists
may work for hearing aid companies, contributing to
the design and use of hearing aids and dispensing them
to patients. The fitting of hearing aids is done by find-
ing the best style and amplification characteristics for
the specific characteristics of a patient’s hearing loss;
an important component of the AuD training involves
Pauline Camps’ 1934 plan to train
SLPs for work in the public schools
looked like prophecy when, in 1975,
Public Law 94-142 was enacted. Public Law 94-142
is now called the Individuals with Disabilities Educa-
tion Act (IDEA) and is linked with the Americans
with Disabilities (ADA) act, both originally formal-
ized as laws in 1990. These laws had the specific
purpose of protecting the rights of children with
disabilities (and their parents) and guarantee-
ing access to a public education and the special
services required to make that education effective.
Specifically, the law had four purposes: (a) “to
assure that all children with disabilities have avail-
able to them . . . a free appropriate public education
which emphasizes special education and related
services designed to meet their unique needs,”
(b) “to assure that the rights of children with
disabilities and their parents . . . are protected,”
(c) “to assist States and localities to provide for the
education of all children with disabilities,” and
(d) “to assess and assure the effectiveness of efforts
5 
 he difference between this requirement for an AuD degree, and the degree requirement for clinical training of SLPs is more logistical than
T
substantial. As described in the text, students who complete an accredited master’s degree in speech-language pathology must have a 36-week,
full-time clinical experience before they are eligible for the CCC-SLP. This experience is obtained after the degree is completed, usually in the
form of a job. AuD programs incorporate this requirement into their degree programs.
13
hearing aid fitting (see Chapter 24). Audiologists are
also regularly employed by otologists (physicians who
deal with diseases of the ear). In addition to testing
hearing and fitting hearing aids, audiologists assess bal-
ance problems (the mechanisms for balance and hear-
ing are closely related), help patients manage excessive
production of earwax, and train people with hearing
loss to enhance their communication skills. The full
scope of practice for persons with an AuD is published
at https://www.asha.org/policy/SP2004-00192/
Order of Chapters in the Text
This text is organized into three general areas: lan-
guage, speech, and hearing. Each of these general areas
is initiated with a chapter (or two) on normal processes.
These normal processes are presented to support an
instructional philosophy that disordered language,
speech, or hearing are understood best by reference to
“normal” processes and behavior.
Two important aspects of the material in this text
should be kept in mind when reading the chapters.
Although the text is arranged in the order of language,
to educate all children with disabilities.” The law
provides that each child with a disability who
attends public school be provided with an Indi-
vidualized Education Program (“IEP” in the jargon
of school officials) designed by a team of special-
ists. These specialists include (among others such
as occupational therapists, physical therapists, and
special education teachers) SLPs and audiologists.
To meet the needs of children with disabilities,
these professionals must be employed by public
school systems. The specifics of IDEA have
undergone some changes since the original 1975
enactment of the law, but children with disabilities
are still guaranteed, by law, a public education and
specially designed educational plan. Public school
systems in the United States therefore offer many
employment opportunities for SLPs and audiolo-
gists. More information on PL 94-142, its history,
and specifics, can be obtained by typing in “IDEA”
in any search engine on the Web. The curious Web
surfer will find the roots of PL94-142, ADA, and
IDEA in the Civil Rights Act of 1964.
14 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
speech, and hearing , the sequencing of material and
the content of each chapter is somewhat arbitrary. The
separation of Communication Sciences and Disorders
into language versus speech versus hearing disorders,
and the separation of their normal processes, is not real-
istic for real-world clinical and scientific settings. The
material in this textbook is separated in this way for
instructional purposes, but the reader should keep in
mind the interconnected processes and disorders of the
three areas. When appropriate, the reader is reminded
of these interconnections.
Chapter Summary
Communication Sciences and Disorders was formal-
ized as an academic discipline in the 1920s and 1930s,
and has enjoyed enormous growth since that time.
The field grew because of its interdisciplinary
roots and interactions but forged a separate identity.
The field is also committed to taking the results of
laboratory research and “translating” them to the clinic
for both diagnostic (determining what the problem is)
and treatment purposes.
Clinical and academic degrees are available in the
areas of speech-language pathology and audiology.
Most of the regulations that govern the training
and conduct of professionals in Communication Sci-
ences and Disorders are developed and overseen by
the American Speech-Language-Hearing Association
(ASHA).
This text is written to introduce students to Com-
munication Sciences and Disorders; the text surveys a
wide range of normal processes of language, speech,
and hearing, and the way in which these processes
can be affected by disease and/or conditions to affect
communication.
In this textbook, emphasis is placed on what we
know about normal (typical) communication pro-
cesses as well as the nature of language, speech, and
hearing disorders that affect an individual’s ability to
communicate.
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The Nervous System:
Language, Speech, and Hearing
Structures and Processes
Introduction
This chapter presents an overview of the nervous sys-
tem, and how it functions in language, speech, and
hearing. The chapter has been written specifically to
support brain-related material covered in subsequent
chapters. Students interested in detailed presentations
on brain anatomy and function, including informa-
tion relevant to speech, language, and hearing, are
encouraged to consult the outstanding texts by Kandel,
Schwartz, Jessell, Siegelbaum, and Hudspeth (2012),
and Bear, Connors, and Paradiso (2015). Additional
information on brain function for speech, hearing,
and language can be found in Kent (1997), Bhatnagar
(2013), and Hoit and Weismer (2016).
In the current chapter, the anatomy and physiology
of the basic unit of the nervous system — the neuron — is
presented first. A quick tour of gross neuroanatomy fol-
lows. The topic of gross neuroanatomy applies to the
structural components of the nervous system. The term
neurophysiology denotes the study of brain function.
Knowledge of both neuroanatomy and neurophysi-
2
ology is relevant to the role of the nervous system in
speech, hearing, and language. Selected, examples of
neuroanatomical and neurophysiological topics that
are matched — that is, function associated with specific
structures — are presented in Table 2–1.
Central and Peripheral
Nervous Systems
The nervous system includes all neural tissue in the
body. The nervous system has two subcomponents, the
central nervous system and the peripheral nervous system.
The central nervous system (CNS) includes the cerebral
hemispheres and their contents — the “brain” housed
inside the skull — and the entire mass of tissue beneath
the hemispheres (including the cerebellum, brainstem,
and spinal cord: see later in chapter). The periph-
eral nervous system (PNS) includes the many nerves
extending from the CNS to innervate (control the func-
tion of) various parts of the body. For example, nerves
in the foot run up the leg and into your spinal cord; this
17
18 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Table 2–1.  Selected Examples of Neuroanatomy and Neurophysiology Topics
in the Study of the Nervous System
Neuroanatomy
Structure of neuron membrane
Structure of nerve attachment to
muscle
Clusters of cells in brainstem that
send nerve fibers to muscles of the
tongue
Relative volume of auditory cortex in
left versus right hemisphere of brain
Note.  The examples are meant to clarify the difference between the two aspects of studying
the nervous system.
nerve is part of the PNS. When the fibers of the nerve
enter the spinal cord, they are in the CNS. Figure 2–1
provides an image of these two broad components of
the nervous system; structures labeled “nerves” are part
of the PNS, the remaining neural structures are part of
the CNS. Figure 2–2 shows a simple way to understand
the distinction between the CNS and PNS.
The Neuron
Figure 2–3 shows a schematic drawing of two neu-
rons. The neuron is the basic cell unit of the nervous
system. The neuron has a cell body, with a nucleus
at its center. This cell body issues a long fiber called
an axon.
When a brain is removed from an organ donor,
fixed in a special solution, and dissected, two shades of
tissue are seen. These two types of tissue are called the
gray matter and the white matter of the brain. Gray mat-
ter consists of clusters of cell bodies, and white matter
is composed of bundles of axons.
Groups of cell bodies in in the nervous system are
organized together for a specific function. Similarly,
bundles of axons are pathways that connect groups of
such specialized cell bodies in one part of the nervous
system to another group of cell bodies elsewhere in the
nervous system. The concepts of gray matter and white
matter are critical to understanding both the anatomy
and physiology of the brain.
Neurophysiology
Nature of electrical impulses
conducted by neurons
Release of neurotransmitter and its
effect on muscle fibers
Movement of tongue when part of
these brainstem cells are affected by
disease
Observation via functional brain
imaging of difference between left
hemisphere and right hemisphere
auditory cortex when speech is
presented to listener
Nervous System Cells
Neurons are not the only cell type
in the nervous system. The nonsignaling cells
serve the purpose of providing structural and
metabolic support to neurons. What is meant
by “nonsignaling”? Neurons communicate with
each other; they pass information from one
neuron to other neurons. The nonsignaling cells
in the CNS do not transmit information in the
brain but nonetheless have critical functions.
Most of these cells are called glial cells, and they
are more numerous than neurons. Glia is the
Greek word meaning “glue,” a fitting name for
cells that hold neurons together. Glial cells also
support neurons by “feeding” them with nutri-
ents and oxygen. Some tumors of the brain have
their beginnings in these glial cells, rather than
in the neurons.
Axons have a whitish appearance because they
are covered with a substance called myelin. Myelin
functions like an electrical insulator, allowing axons
to conduct electrical impulses at high speeds. Some
axons, fewer than myelinated axons, lack myelin and
conduct electrical impulses at relatively slow speeds.
Axons may lose myelin as a result of disease, as in mul-
tiple sclerosis.
 2  The Nervous System:  Language, Speech, and Hearing Structures and Processes 19

Cerebrum
Diencephalon
Midbrain (mesencephalon)
Cerebellum
Pons
Cranial Medulla
Nerves

Spinal cord
Cervical
nerves

Thoracic
nerves

Lumbar
nerves

Sacral
nerves

Coccygeal
nerve

Figure 2–1.  The divisions between the central nervous system (CNS) and
peripheral nervous system (PNS). Structures of the CNS include the cerebrum
(cerebral hemispheres), the diencephalon, the brainstem (midbrain, pons,
and medulla), the cerebellum, and the spinal cord. Structures shown in the
PNS include the cranial nerves (red and light green ) and the spinal nerves.
The cranial nerves emerge from the brainstem; the spinal nerves emerge
from the spinal cord. See text for additional details.
20 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Nervous System

CNS PNS

Cerebral hemispheres Nerves to and from brainstem

Brainstem Cerebellum Nerves to and from spinal cord

Spinal cord Sensory receptors and motor endplates

Figure 2–2.  Simple summary of the components of the CNS and PNS.

Dendrites Axon terminals

Cell body

Nucleus

Axon Synaptic cleft

Figure 2–3.  Two neurons. The image shows the cell bodies and their nuclei, axons, dendrites, axon terminals,
and a single synapse.

Figure 2–3 shows spiny-like projections from the
cell bodies of the two neurons. At the ends of the axons,
there are long projections ending in button-like struc-
tures. The spiny projections are called dendrites, and the
projections from the end of the axons are called terminal
buttons (or simply, terminal segments). Both projections
are specialized structures that allow information to be
received or sent to other neurons; they are the places
where one neuron “talks” to another.
Neurons conduct electrical impulses that originate
in the cell body and travel like electrical current down
the axon to the terminal buttons. When the electrical
energy reaches the projections at the end of the axon,
a small amount of a chemical substance, called a neu-
rotransmitter, is released into the space between two
or more axons. A portion of the chemical is deposited
on the dendrites of another neuron’s cell body, which
causes the membrane to change its electrical proper-
ties. If everything goes well (and it usually does), the
changes in the membrane’s properties cause this neu-
ron’s cell body to “fire” an impulse, which repeats the
process of conducting electrical energy down the axon
and releasing more chemical to affect another neuron’s
cell body. Neurons talk to each other in this electro-
 2  The Nervous System:  Language, Speech, and Hearing Structures and Processes
Myelin Trivia
Here are two interesting myelin facts
for your next trivia contest. First, many axons
that conduct pain and temperature impulses from
various parts of the body to the CNS are unmyelin-
ated. The relatively slow “conduction time” of
these pathways explains why reactions to extreme
temperatures and painful stimuli often seem to
take a long time. Most of us have experienced this
when touching something very hot but apparently
not realizing it for a second or two. Second, there
are specific processes that “wrap” myelin around
neurons, a process that has a long course of devel-
chemical way: electrical energy turned into chemical
energy, turned again into electrical energy, and so forth.
The transfer of information in the nervous system
depends critically on this chain of events. Diseases that
affect either the dendrites or the terminal buttons can
have a significant effect on information transfer within
the PNS and/or CNS and, therefore, on the behavioral
function of human beings.
The Synapse
As illustrated in Figure 2–3, a synapse is the space
between the projections at the end of the axon (ter-
minal buttons) and the spiny projections (dendrites)
from the cell body of an adjacent neuron. The synapse
also includes connections between the terminal but-
tons and dendrites, as illustrated by the dashed lines
in Figure 2–3. Thus, the termination of the axon and
dendrites of an adjacent cell body are joined together,
linking them as a unit.
Figure 2–3 does not do justice to the incredibly com-
plicated structure and function of synapses throughout
the nervous system. Two observations illustrate this
complexity. First, within the CNS there are between 10
and 100 billion neurons. It really is not important if the
actual number is 10, 20, 70, or 100 billion, it is sufficient
to note the tremendous number of neurons packed
into a relatively small space. With so many neurons in
such a small volume, the size of the synaptic “spaces”
between adjacent neurons is very, very tiny (roughly 20
nanometers, or 20/1,000,000,000th of a meter). The cell
body of a single neuron is contacted by the projections
from many axons, and the terminal buttons of one neu-
ron contact the dendrites of multiple cell bodies. The
pattern of connections among the huge number of neu-
rons within the CNS is highly overlapped and dense.
21
opment, continuing well into the later teenage
and young adult years. Perhaps this explains why
toddlers seem to react so slowly to events that look
as if they should be painful. Just about everyone
has seen a small child fall to the ground and
hesitate for what seems like a very long time before
crying. One interpretation of the hesitation is that
the child is waiting for an adult’s reaction, to see if
she should be crying. Another interpretation is that
the pain information moves at a slow rate in the
toddler’s nervous system because of the relative
lack of myelinization.
Second, the transmission of information between
neurons depends on several different neurotransmit-
ters, which are critical for normal brain function. When
there is too much or too little of a specific neurotrans-
mitter, signs of neurological disease may appear. Com-
munication problems in neurological disease can be
related to deficiencies or excesses of neurotransmitters.
Tour of Gross Neuroanatomy
Gross anatomy is the study of the large-structure
components of a human body part. What follows is a
brief tour of the gross anatomy of the human nervous
system.
Figure 2–4 shows the cerebral hemispheres of
the CNS as seen from above. The front of the cerebral
hemispheres is to the left of the image. From this van-
tage point, the cerebral hemispheres are seen to con-
sist of two symmetrical halves. These halves are the
right (top of image) and left (bottom of image) cere-
bral hemispheres. The right and left hemispheres are
grossly symmetrical, but in certain cases, parts of one
side are bigger or differently shaped than the analo-
gous part on the other side. More importantly, perhaps,
the two halves of the brain are not symmetrical in their
functions. The left hemisphere is specialized for certain
functions and the right hemisphere for other functions.
Some of these specializations are discussed in greater
detail later in this chapter.
The visible tissue in Figure 2–4 is the cortex. The
cortex is composed of densely-packed cell bodies — ​
gray matter — that perform the most complex functions
of an organism. The highly developed and extensive
cortical tissue in humans is responsible for the wide
range of human abilities that are far more sophisticated
than the abilities of non-humans.
22 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Gyri Sulci

Right Hemisphere

Left Hemisphere

Figure 2–4.  View from above of a fixed human brain, with the front of the
brain to the left of the image. Note the two hemispheres of the brain (right hemi-
sphere, top half of image, left hemisphere, lower half of image). The gyri are the
hills of tissue, the sulci the fissures (grooves) between the gyri.

The two hemispheres are connected by a massive Frontal Lobe

bundle of axons (white matter) called the corpus cal-
losum. Axons arising from cortical cells in one hemi-
sphere travel to the other hemisphere where they make
synapses with other cortical cells. There are roughly
200 million axons in the corpus callosum; the connec-
tions between hemispheres are fine-grained and dense.
One hand knows what the other hand is doing.
The surface of the brain appears as thick, humped
ridges separated by deep fissures. The ridges are called
gyri (singular = gyrus), and the fissures are called sulci
(singular = sulcus) or fissures. The gyri and sulci give
the cortex its characteristic appearance.
Humans have much more cortical tissue than even
the most advanced primates, such as chimpanzees.
As suggested previously, the volume and complexity
of human cortical tissue constitute one reason for the
huge cognitive “edge” we enjoy relative to other mem-
bers of the animal kingdom. This edge almost certainly
includes, and perhaps is defined by, our ability to use
speech and language in creative and novel ways.
Figure 2–5 shows an artist’s rendition of a side
view of the left hemisphere of the brain, plus parts of
the brainstem and spinal cord (discussed later). Both
hemispheres have four lobes, including the frontal,
parietal, temporal, and occipital lobes. The same four
lobes can also be identified in the right hemisphere.
The frontal lobe, as suggested by its name, is the front
part of the cerebral hemispheres. It is separated from
the more back part of the brain by a long, deep sulcus
running down the side of the brain. This central sul-
cus is a dividing line between the front and back of the
brain. The frontal lobe is separated from the temporal
lobe below by the sylvian fissure (also called the lateral
sulcus, see Figure 2–5).
The frontal lobe has many functions, including
executive function. Executive function includes the skill
of planning actions, connecting current behavior with
future consequences of that behavior, and imposing
organization on the tasks of everyday life. Diseases that
affect the areas of the frontal lobe that control executive
function have a major impact on behavior, including
communication.
The frontal lobe contains a gyrus, directly in front
of the central sulcus, called the primary motor cortex
(Figure 2–5, shaded blue). This gyrus extends from the
top of the brain to the sylvian fissure and contains the
cell bodies of neurons that control muscle contractions
in all parts of the body. The arrangement of these cells
is systematic, from the top to bottom of the primary
motor cortex. Muscles toward the bottom of the body,
such as the lower leg and foot, are controlled by cells
 2  The Nervous System:  Language, Speech, and Hearing Structures and Processes 23

Central sulcus

Parietal lobe
Frontal lobe

Occipital lobe
Temporal lobe

Sylvian
fissure

Pons Cerebellum

Medulla
oblongata

Spinal cord

Figure 2–5.  Side view of the left hemisphere, showing the four
lobes as well as the brainstem, cerebellum, and upper part of spinal
cord.

at the top of the primary motor cortex. Muscles of the
face, tongue, and lips, on the other hand, are controlled
by cells at the bottom of the primary motor cortex, close
to the sylvian fissure. The top-to-bottom arrangement
of cells in the primary motor cortex is therefore an
inverted representation of muscles in the body. This
systematic arrangement of cells in the primary motor
cortex is called somatotopic representation.
Other parts of the frontal lobe take part in the plan-
ning of action. Even a simple action, such as reaching
for a doorknob to open a door, requires a complex and
properly sequenced set of muscular contractions. The
force of contraction and the timing of the sequence of
muscles to be used must be based on a plan. The frontal
lobe plays a major role in the learning and activation of
these plans. Such plans are essential to speech produc-
tion. To speak the word “production,” the contraction
patterns of the many muscles of the head, neck, and
respiratory system must be planned for accurate articu-
lation of speech sounds, their sequencing, and prosody
of the three-syllable utterance. A disorder called apraxia
of speech affects this planning of speech sequences and
may have an underlying cause of damage to the frontal
lobe of the left hemisphere.
Broca’s area is also located in the frontal lobe. Bro-
ca’s area is just in front of the primary motor cortex (see
previous description). It is known to be a “speech cen-
ter” of the brain, containing tissue that is essential for
speech production. Broca’s area is discussed in greater
detail in the section, “The Dominant Hemisphere and
the Perisylvian Language Areas.”
Occipital Lobe
The occipital lobe forms the back of each cerebral hemi-
sphere. The occipital lobe has front boundaries with
both the parietal and temporal lobes (see Figure 2–5).
The sulci (plural of sulcus) separating the occipital lobe
from the parietal and temporal lobes are not as easily
seen as the more dramatic central sulcus and sylvian
fissure. The primary function of the occipital lobe is to
process visual stimuli.
Temporal Lobe
The temporal lobe forms much of the lateral (side) part
of the cerebral hemispheres and is separated from the
frontal and parietal lobes by the sylvian fissure. The
temporal lobe plays an important role in hearing. In
Figure 2–5, three gyri of the temporal lobe can be seen,
24 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
each one oriented more or less horizontally, with a
slight upward tilt from the forward tip of the lobe to
the back boundary adjoining the occipital lobe. The
top-most gyrus contains the primary auditory cortex (see
Figure 2–5), which contains neurons that receive audi-
tory impulses originating in the sensory end organ of
the ear (called the cochlea, covered in more detail in
Chapter 22).
The temporal lobe also plays an important role in
the lexicon (words and their meanings stored in the
cerebral hemispheres) and in the relations between
words. It also is important to aspects of speech and
language perception. The temporal lobe also plays an
important role in memory and emotion.
Parietal Lobe
The parietal lobe extends from the central sulcus back
to the front boundary of the occipital lobe. A portion of
the parietal lobe is separated from the temporal lobe by
the sylvian fissure. The parietal lobe shares boundaries
with the other three lobes of the cerebral hemispheres.
The parietal lobe contains a gyrus, immediately
in back of the central sulcus, called the primary sensory
cortex (Figure 2–5, shaded yellow). This gyrus parallels
the course of the primary motor cortex of the frontal
lobe, extending from the top of the brain to the sylvian
fissure. The cell bodies of the primary sensory cortex
can be thought of as the final station in the brain for the
collection of tactile (touch) information (other types of
sensory information also find their way to the primary
sensory cortex). Like the primary motor cortex, cells in
the primary sensory cortex are arranged somatotopi-
cally, with touch information from the lower part of
the body represented at the top of the gyrus, and touch
information from the face, tongue, and lips represented
toward the bottom of the sensory cortex.
In addition to the primary function of touch sen-
sation, the parietal lobe integrates large amounts of
sensory data and plays an important role in coordinat-
ing various sources of information critical to cognitive
functions, including language. Extensive connections
exist between the parietal lobe and each of the other
three lobes, allowing the integration of visual, auditory,
and touch sensations, as well as motor control informa-
tion. This integration is fundamental for higher-level
control and cognitive functions.
Hidden Cortex
The four lobes in each hemisphere are seen easily on
the surface of the brain. There is more to the cortex than
just these surface features, however, and especially so
in humans. The evolution of the human brain required
fitting the enormous computing power of cortical neu-
rons into a relatively small space (the skull). Clearly,
there is room for just so much area on the surfaces
shown in Figure 2–5.
Human evolution took a novel approach to pack-
ing more cortex into this small space by “burying”
millions of cortical cells in the deep sulci separating
the many gyri that define the surface of the brain. In a
“fixed” brain (one that has been hardened somewhat
with a special solution, prior to removal from the skull),
like the one shown in Figures 2–4 and 2–5, adjacent gyri
can be pulled apart to reveal previously hidden, inte-
rior walls of cortical cells. The cortex is not simply the
surface of the brain and its thickness of cell bodies, but
also the cell bodies buried within the deep sulci of the
human brain. When a human brain is compared to that
of other animals, a striking feature is the greater com-
plexity and much deeper sulci of the human version.
In so-called lower animals, the surface of the brain may
look positively smooth compared to the human brain.
The smoothness reflects the absence of deep sulci and,
therefore, the absence of extra cortical cells.
In the human brain, there is also hidden cortex
beneath the temporal, frontal, and parietal lobes. In a
fixed human brain, the front end of the temporal lobe
can be pulled away from the rest of the brain to expose
additional cortical gyri. These gyri make up the insular
cortex (or, simply, the insula). Many scientists believe
the insular cortex plays an important role in speech, as
well as in memory and emotional functions.
Subcortical Nuclei
Figure 2–6 shows a view of the cerebral hemispheres
in which the cortical surface and white matter in the
cerebral hemispheres have been made transparent,
revealing structures inside the hemispheres. As previ-
ously described, clusters of cell bodies within the brain
are called nuclei; the structures shown in Figure 2–6 are
several of the subcortical nuclei (below the cortex, within
the hemispheres).
Subcortical nuclei include the basal ganglia (some-
times called the basal nuclei) and the thalamus. The basal
ganglia include five separate nuclei, which for simplic-
ity are shown in Figure 2–6 as a single, but complex,
structure.
The basal ganglia play an important role in con-
trol of movement, including movements of the speech
mechanism. Damage to the basal ganglia may impair
a person’s ability to produce speech. In addition, the
basal ganglia play a role in language. Although the lan-
 2  The Nervous System:  Language, Speech, and Hearing Structures and Processes 25

Basal ganglia

Thalamus

Figure 2–6.  Selected subcortical nuclei, contained within the cere-

bral hemispheres. Structures of the basal ganglia and thalamus are
included in this picture.

guage ability of humans is often thought of as powered
by cortical cells, the basal ganglia and cortex are exten-
sively interconnected and communicate with each
other. Many scientists believe these subcortical nuclei
have an important role in human communication.
The thalamus, the egg-like structure in the middle
of the hemispheres (shaded pale red in Figure 2–6), is a
collection of nuclei that serves as the main connection
between the basal ganglia and cortex. It is also the main
“relay station” for the transmission of sensory events
(e.g., touch, vision, auditory) from the outside world
to the cortex.

The Basal Ganglia and Parkinson’s Disease

Various neurological diseases, such as Parkinson’s disease,
Tourette’s syndrome, and Huntington’s disease, are known to be related
to damage to structures of the basal ganglia. In Parkinson’s disease, for
example, patients show several signs (evidence of a disease that can be
observed on clinical examination), including rigid (stiff) limbs, slow or
absent movement, and tremors. These signs are evidence of disruption
of basal ganglia physiology, mostly having to do with a deficiency of a
neurotransmitter called dopamine. Some of the lost dopamine can be
replaced with drugs. Another form of therapy involves insertion of a tiny
electrode in the brain to provide electrical stimulation to structures in the
basal ganglia. The therapeutic procedure, called deep brain stimulation
(DBS), often provides some relief from the signs noted above.
26 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Figure 2–7 shows another view of the brain that
illustrates the relationship of subcortical to cortical
structures. This is a frontal cut through the cerebral
hemispheres of a human brain, as if the hemispheres
are facing you and cut through to separate them into
front and back halves; the interior of the brain is
exposed as the front or “face” of the back half.
Figure 2–7 shows the difference between gray and
white matter in the cerebral hemispheres. The deep sul-
cus in the middle and toward the top of the image is the
dividing line between the left and right hemispheres of
the brain. Note the grayish, top layer of the brain, hav-
ing a thickness somewhat like the rind of a watermelon.
Note also the deep sulci in which the gray matter forms
interior “walls” of cortex. Immediately below the rind
of cortical cell bodies there is whitish tissue — the white
matter of the brain. These are bundles of axons — fiber
tracts — running between different groups of cell bod-
ies throughout the CNS. Any “chunk” of white matter
within the cerebral hemispheres is a densely interwo-
ven mesh of all these different connections.
The individual structures and their names are not
the point of Figure 2–7. Rather, the image presents a
good orientation to the distinction between gray and
white matter. In addition, it shows the cortical gray
matter as well as the subcortical gray matter (subcorti-
cal nuclei). Finally, the image provides a good look at
the dense network of white matter within the cerebral
hemispheres.
Brainstem, Cerebellum,
and Spinal Cord
The part of the central nervous system extending below
the cerebral hemispheres includes the brainstem, cer-
ebellum, and spinal cord. These parts of the brain also
play important roles in communication and its disorders.
Brainstem
In Figure 2–5, a stalk-like structure descends from the
cerebral hemispheres. Its top part is the brainstem; its
downward continuation is the spinal cord. The brain-
stem is divided into three major parts, including the
midbrain (hidden in Figure 2–5 by the lower edges of
the temporal lobe), pons, and medulla. The brainstem
serves a host of functions including regulation of blood
pressure, breathing, production of saliva and perspira-
tion, and level of consciousness. Very serious damage
to the brainstem is, in most cases, not consistent with
the maintenance of life.

White matter

Caudate

Thalamus

Putamen
Globus pallidus Subthalamic nucleus
Substantia nigra

Figure 2–7.  Image of brain structures as if the brain is cut into front and back
halves; the perspective is looking toward the “face” of the back half. Gray and white
matter is shown, including the gray matter of the cortex and of subcortical nuclei.
White matter is seen directly below the cortex, and surrounding the subcortical nuclei.
 2  The Nervous System:  Language, Speech, and Hearing Structures and Processes
The brainstem also contains motor neurons — neu-
rons specialized for motor control, such as muscle con-
traction — that control muscles in the head and neck.
There are also sensory neurons that receive sensation
from head and neck structures. The cell bodies of
these neurons are organized into dense, small nuclei in
various parts of the brainstem. The motor neurons in
the brainstem nuclei receive commands from cortical
motor neurons, and together the cortical and brainstem
motor neurons exert control over muscles of the larynx,
throat, tongue, lips, and jaw. The motor neurons in the
brainstem send out fiber tracts that exit the CNS as cra-
nial nerves (see Figure 2–1). The term “cranial” nerve is
used to distinguish these from nerves running to and
from the spinal cord (“spinal” nerves), as explained
later in this chapter.
There are 12 paired cranial nerves (CNs). They are
referred to by Roman numerals (e.g, CN V; CN XII) as
well as by their names (e.g., CN V = trigeminal nerve;
CN XII = hypoglossal nerve). Five of the cranial nerves
carry information from brainstem motoneurons to
muscles of the head and neck that control movements
of the jaw, tongue, soft palate, pharynx, and larynx
during speech. One of the nerves serves the sense of
hearing, and another nerve plays a role in breathing
during speech.
The brainstem and the cranial nerves attached to
it play a critical role in the control of the speech mecha-
nism and in hearing. Damage to brainstem nuclei or
the cranial nerves results in weakness or paralysis of
speech muscles as well as loss of sensation in head and
neck structures.
Cerebellum
The cerebellum is the large mass of tissue immediately
behind the brainstem (see Figure 2–5). It is recognizable
in fixed brain preparations because of its size, unusual
appearance — somewhat like a cauliflower — relative
to other surface features, and because of its location
at the back and base of the cerebral hemispheres. Like
the cerebral hemispheres, the cerebellum contains gray
and white matter.
The cerebellum has extensive connections with the
cerebral cortex, brainstem, spinal cord, and basal gan-
glia.1 The cerebellum has been likened to a computer
that integrates vast amounts of information about mus-
cle contraction, signals coming into the brain from the
outside world including the body surface, the location
of the head relative to the body, and the general state
of brain activity. This integration produces the smooth,
1 
 onnections between the cerebellum and basal ganglia have not always been included in neuroanatomy textbooks, but research in the past
C
10 years has identified these connections (Bostum, Dum, & Strick, 2010, 2018).
27
coordinated movement of everyday life, from walking
to making a jump shot while surrounded by nine other
players. The cerebellum is important for other brain
functions as well, but its role in movement coordina-
tion is very prominent. Patients with diseases of the
cerebellum often lose the ability to produce smooth
movement patterns.
Spinal Cord
The spinal cord extends from the bottom of the brain-
stem down the back, terminating a little below the
waist. The spinal cord contains cell bodies that control
muscles of the arms, legs, chest, and other parts of the
torso, as well as cell bodies that receive sensory infor-
mation from those structures. The nerves that run to
and from the spinal cord are called, not surprisingly,
spinal nerves. Of primary importance for the purposes
of this text are the spinal nerves that serve muscles and
structures of the respiratory system. These muscles
are located between the ribs, in the abdomen, and in
the neck. Because the respiratory system plays a criti-
cal role as the “power supply” for speech production
(Chapter 10), damage to cell bodies within the spinal
cord or to the spinal nerves can result in speech breath-
ing problems.
The Auditory Pathways
The nervous system pathway that connects the sen-
sory organ for hearing to the auditory cortex is special-
ized for auditory analysis. The auditory pathways are
shown schematically in Figure 2–8.
The bilateral, auditory pathways begin in the
cochlea (marked number 1 on Figure 2–8), which is
the sensory end organ of hearing. “Bilateral” means the
pathways are the same on both sides of the head. The
auditory nerve (CN VIII) (number 2) emerges from
the cochlea and transmits auditory information to the
brainstem. The nerve enters the CNS, and its fibers
make synapses with several nuclei in the lower brain-
stem (numbers 3 and 4). At brainstem location #4, the
pathways make an interesting turn.
Roughly 75% of the ascending fibers cross over to
the other side of the brainstem (red pathway) where they
make a synapse with another nucleus; the remaining
25% of the fibers (green pathway) make synapses with
cells of the corresponding nucleus on the side of entry
in the brainstem. As the auditory fibers ascend, they
make synapses in more brainstem nuclei (represented
28 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
3
2
Auditory
nerve
Cochlea
1
Figure 2–8.  A simplified view of the peripheral and central auditory
pathways, from cochlea to cortex.
by number 5) before ascending to the thalamus (num-
ber 6). The final destination of the auditory pathway is
the auditory cortex (number 7).
At each succeeding level along the auditory path-
way, the analysis of the auditory information becomes
more complex and sophisticated. The crossing of audi-
tory fibers from one side of the brainstem to the other
(point number 4 in Figure 2–8) means that auditory
analysis in the cortex of one hemisphere is primarily
from the ear on the opposite side.
The Dominant Hemisphere and
the Perisylvian Language Areas
The concept of specialization of function is that within the
brain there are certain clusters of cells and their con-
Auditory
cortex
7
nections to other clusters of cells that are specialized
or even dedicated to certain functions, behaviors, or
processes. Two well-known examples of such special-
ization are the gyri in the left frontal lobe called Broca’s
area, and the area of tissue in the top gyrus of the left
temporal lobe and perhaps extending to a small area
of the parietal lobe called Wernicke’s area. These two
areas of a preserved human brain are shown in the left
image of Figure 2–9. The central sulcus (see Figure 2–5)
is shown for orientation.
Broca’s area is thought to be specialized for the
production of speech, and Wernicke’s area for the recep-
tion (comprehension) of speech and language. Of par-
ticular importance is the specialization of these areas in
the left hemisphere of the brain. Broca’s and Wernicke’s
areas are therefore not only specialized, they are also
lateralized. Lateralization of function is the term used to
 2  The Nervous System:  Language, Speech, and Hearing Structures and Processes
Central sulcus
Wernicke’s area
Broca’s area
Broca’s area
Figure 2–9.  Left, Broca’s area and Wernicke’s are shown on a preserved brain; the central sulcus is shown as a land-
mark separating the frontal and parietal lobes. Right, two pathways connecting Wernicke’s and Broca’s areas — the arcuate
fasciculus and the ventral stream.
denote brain tissue specialized for a specific function,
but only on one side of the brain. According to research
estimates, approximately 90% of humans have speech
and language functions lateralized to the left hemi-
sphere (Bear, Connors, & Paradiso, 2016).
How was this specialization and lateralization of
function for speech and language discovered? Paul
Broca (1824–1880), a 19th-century French physician
who followed up on similar work of other physicians,
had a patient who suffered brain damage resulting
from syphilis and was almost completely unable to
produce speech. The patient’s only speech consisted of
one syllable, “tan,” which he repeated over and over.
The patient seemed to understand speech well. Broca
suggested the lesion, wherever it was in the brain,
affected speech production, but not speech perception
and language comprehension. “Lesion,” from the Latin
alaedere (“injury”), means damaged or destroyed tissue.
Following the patient’s death, an autopsy showed
a large lesion in the lower part of the left frontal lobe,
adjacent to and just forward of the primary motor cor-
tex. The location of this lesion is indicated in Figure 2–9
as “Broca’s area.” Broca, as well as other physicians,
saw additional patients with the same lesion location
and the same speech symptoms. Broca concluded that
this part of the brain was specialized for the articula-
tion of speech. The lateralization of this speech articula-
tion center to the left hemisphere was discovered in the
following way: patients whose brains showed lesions
in the same location as Broca’s area, but in the right
hemisphere, did not have speech articulation deficits.
The brain was therefore not specialized for articula-
29
Arcuate fasciculus
Wernicke’s
area
Ventral stream
tion in a symmetrical way. For these reasons, the term
“Broca’s area” is reserved for the left hemisphere.
A similar story can be told for Wernicke’s area. Carl
Wernicke (1848–1905) was a Prussian (his birthplace
now part of Poland) physician who was interested in
the relationship between brain function and speech
and language. Wernicke published a book in 1874 in
which he described a link between lesions in the top
gyrus of the left temporal lobe, close to where the tem-
poral lobe meets the parietal lobe, and difficulty com-
prehending speech and language but little difficulty
articulating speech. However, the speech produced by
these patients often conveyed jumbled ideas and even
jargon — speech that sounded like strings of words but
lacked meaning. The lesion location described by Wer-
nicke (Wernicke’s area) is indicated in the left image of
Figure 2–9
Wernicke’s area was thought of as the language
comprehension center of the brain. Like the lateralized
function of Broca’s area, the language comprehension
problems emerged with damage to the left hemisphere.
Damage to the same location in the right hemisphere
did not result in language comprehension problems.
Research to the present day confirms, in general
ways, the specialization of Broca’s area for speech artic-
ulation and Wernicke’s area for language comprehen-
sion. In the great majority of humans, this specialization
is lateralized to the left hemisphere. The left hemisphere
is often referred to as the dominant hemisphere because it
houses the specialization for speech and language.
There is a good deal of controversy concerning
the specifics of Broca’s and Wernicke’s areas, including
30 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
their exact boundaries and the restriction of one area to
speech articulation (Broca’s) and the other to language
comprehension (Wernicke’s). For example, damage to
Broca’s area may result in certain language comprehen-
sion problems, and damage to Wernicke’s area can pro-
duce problems with speech articulation. More is said
about these issues in Chapter 9.
Arcuate Fasciculus (Dorsal
Stream) and Ventral Stream
Not surprisingly, Wernicke’s area and Broca’s area are
connected by thick bundles of axons. One tract, shown
on the right side of Figure 2–9, is called the arcuate fas-
ciculus (“fasciculus” is a bundle of fibers; “arcuate” is
descriptive of the arch-like configuration of the tract).
The arcuate fasciculus connects cell bodies in Wer-
nicke’s area to cell bodies in Broca’s area. The tract in
Figure 2–9 is superimposed on the surface of the left
hemisphere but actually runs deep (beneath) to the
cortex within the temporal, parietal, and frontal lobes.
A fiber tract that connects Broca’s and Wernicke’s
areas seems to make perfect sense. For example, our
ability to repeat what someone says must involve some
auditory analysis of speech, in and around Wernicke’s
area, and the transfer of that analysis to Broca’s area
where the heard speech is readied for production. In
fact, scientists have argued that the arcuate fasciculus
is the pathway for connecting the auditory analysis
of incoming speech sounds (Wernicke’s area) to the
articulatory characteristics that produced the sound
(Broca’s area). The arcuate fasciculus is discussed fur-
ther in Chapter 9.
Speech and Language, Together Always
Readers may notice the use of “speech”
and “language” as different components of the
communication process (see Chapter 3). To some
extent they are. “Speech” usually refers to the
planning and production of the sound sequences
that form words. “Language” refers to the repre-
sentations and the “public” usage of those symbols
to communicate. Some examples of differences
between speech and language are (a) a stroke
survivor who produces speech with no errors but
with no meaning — the speech sounds and words
are correct but the use of the words does not fit the
situation (such as a response to a specific question)
and are combined in meaningless ways (as in the
Speech perception must lead to meaning, how-
ever, so the arcuate fasciculus cannot account for link-
ing sounds to words; it is mainly for the identification
of speech sounds. The ventral stream pathway runs
between Wernicke’s area and cortical regions adja-
cent to (or in) Broca’s area, and is thought to connect
sounds with word meanings. The arcuate fasciculus
is considered as the “upper loop” (dorsal stream) con-
necting auditory analysis areas in the temporal lobe to
articulatory areas (Broca’s area) in the frontal lobe. The
ventral stream runs between Wernicke’s areas and the
lower part of the temporal lobe before it connects to
frontal lobe regions in and around Broca’s area. The
upper-loop/lower-loop model of integrating auditory
analysis with articulation (upper loop) and auditory
analysis with meaning (lower loop) is called the dual-
stream model (Fridriksson et al., 2018).
Notice in Figure 2–9 how the arcuate fasciculus
(dorsal stream) and ventral stream form a flattened
loop around the sylvian fissure. In a landmark study on
brain activity and speech and language, the Canadian
neurosurgeon Wilder Penfield (1891–1976) used electri-
cal currents to stimulate the cortex in and around the
tissue enclosed in this flattened loop. The patients on
the operating table were having tissue excised because
of severe epilepsy. Penfield was able to stimulate the
perisylvian areas with electrical currents while the
brain was exposed. Penfield found that almost any
stimulus around the sylvian fissure of the left hemi-
sphere evoked some form of language behavior in his
awake patients (Penfield & Roberts, 1959). Autopsies of
patients who had suffered strokes and who had speech
and language problems also revealed frequent damage
in this loop of tissue. The part of the cerebral hemi-
previous example of damage to Wernicke’s area;
(b) a 9-year old child with cerebral palsy who
has difficulty producing clear speech sounds as a
result of a speech motor disorder, but who has an
age-appropriate vocabulary, sequences words for
sentences like a typically developing 9-year-old
child, and comprehends speech perfectly; and
(c) a typically developing 4-year-old child who
has age-appropriate speech production but has
not mastered morphemes, the minimal units of
meaning discussed in Chapter 3. Of course, speech
and language skills interact, but examples like
those presented show how they can be separable.
 2  The Nervous System:  Language, Speech, and Hearing Structures and Processes 31

spheres enclosed within the dorsal and ventral streams Functional Magnetic
is referred to as the perisylvian cortex (“peri” being a Resonance Imaging
prefix meaning “around” or “enclosing”).2 The peri-
sylvian cortex is assumed to be important to normal Magnetic resonance imaging (MRI) is a technique that
speech and language functioning, and damage to this was developed in the 1970s and 1980s to produce very
region of the brain is likely to result in a communica- detailed images of body structures. A strong magnetic
tion impairment, ranging from mild to severe depend- field surrounding the body part of interest reacts to
ing on the extent of the damage. properties of biological tissue that affect the magnetic
field. These reactions are reconstructed as an image hav-
ing exquisite detail. Figure 2–10 shows an MR image
Functional Magnetic Resonance of the right side of the head and neck. The image was
Imaging and Speech and programmed to show structures of the medial (inside)
Language Brain Activity wall of the left hemisphere, as if the other hemisphere
has been removed from the view. The gyri and fissures
The identification of speech and language areas of the that define the surface and thickness of the cortex are
brain is often based on an approach of linking parts of easy to see, as is the white matter below the cortex. The
the brain with specific functions. A patient is seen, her cerebellum, midbrain, pons, and medulla of the brain-
symptoms documented, and if the patient passes away stem, and the cervical (neck) part of the spinal cord are
her brain may be autopsied to locate lesions that might also imaged clearly. The thick, arch-like band of white
explain the symptoms. If a sufficient number of patients matter just below the cortical tissue and in the center
are studied with the same symptoms and lesion loca- of the image is the corpus callosum, the fiber tract that
tion, the damaged part of the brain is thought to be connects the two hemispheres.
critical to the normal behavior compromised by the
neurological disease. For example, if patients who have
suffered strokes share a common symptom of read-
ing problems, and later autopsies reveal that all these
patients had lesions in the same part of the parietal
lobe, that part of the brain is thought to be critical to
normal reading ability.
This approach to identifying functions of the brain
is limited. It is unusual to find a sufficiently large group
of patients with exactly the same symptoms, and pre-
cisely the same lesion location. Thus, the ability to
generalize between lesion locations and brain func-
tion is limited by the lack of a sufficiently large sample
of cases to “prove” the point that brain structure “x”
causes behavior “y.”
The last half-century has seen a technological rev-
olution in the ability to generate images of the brain
in living individuals. This revolution includes imag-
ing techniques to identify specific brain structures and
make precise measures of their length, width, volume,
and tissue type. Enhancements of these techniques
are also available to monitor the activity of specific
brain structures as a person performs different tasks.
This chapter closes with a brief discussion of how one
technique to monitor brain activity during speech and
language tasks has enhanced understanding of speech Figure 2–10.  MR image of the medial surface of a cere-
and language functions of the brain. bral hemisphere, brainstem, and spinal cord.

2
 The term “perisylvian language areas” typically refers to the tissue in the left, speech- and language-dominant hemisphere. This is consistent
with the facts in a general way, but of course, when you start digging it is more complicated. For example, the arcuate fasciculus (dorsal stream)
is thought to be strongly lateralized to the left hemisphere. In contrast, the ventral stream, which connects auditory analysis to word meaning, is
thought to be active in both hemispheres (Fridriksson et al., 2018).
32 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

About 30 years ago, MRI technology was enhanced
to monitor brain activity as an individual performed a
task. The technology is called functional MRI (abbre-
viated as fMRI). fMRI shows which parts of the brain
“light up” for different tasks. Neurons use more oxy-
genated blood when active, as compared with resting.
Neurons in a region of more heavily oxygenated blood
emit a different magnetic signal compared with neu-
rons in a less heavily oxygenated blood region. With
the proper equipment and software, an MRI scanner
can detect these oxygen differences and show locations
in the brain that are presumed active during the perfor-
mance of specific tasks.
A lesson learned from fMRI studies of speech
and language behavior is that many areas of the brain
“light up” for these tasks. Broca’s and Wernicke’s cor-
tical areas are far from the complete story of how the
brain functions for human communication. Figure 2–11
shows data from multiple studies on brain region acti-
vation for oral language tasks (i.e., speech production)
(Ardila, Bernal, & Rosselli, 2016a). The surface of the
left hemisphere is shown on the left, the medial wall of
the left hemisphere is shown on the right.
On the surface of the left hemisphere, Broca’s area
is active for oral language (purple) but frontal lobe
regions adjacent to but more forward than Broca’s area
are also active (red). The blue areas include not only
the motor cortex in the frontal lobe (gyrus immediately
anterior to the central fissure) but cortical tissue in the
region of Wernicke’s area. Activity is also seen on the
middle wall of the left hemisphere, both in cortical and
subcortical structures.
The “big picture” conclusion from these analyses
is that the brain areas that “control” speech production
(or, perhaps more generally, language expression) are
more widespread than Broca’s area. The same conclu-
sion has been reached about Wernicke’s area — more
brain regions are active for language comprehen-
sion than the region around the upper temporal lobe
(Ardila, Bernal, & Rosselli, 2016b). Because these dif-
ferent areas “light up” together during communication
behavior, it appears they are connected as a network.
It is the network that is important, not simply brain
centers such as Broca’s and Wernicke’s areas.
Diffusion Tensor Imaging
If communication is controlled by a network in which
clusters of cell bodies (such as in the cortex) are con-
nected, it follows that the proper connections — fiber
tracts — must exist. Computed tomography (CT), MRI,
and fMRI images show gray and white matter but
do not show specific fiber tracts that connect specific
groups of cell bodies such as Wernicke’s and Broca’s
areas. An MR technique called diffusion tensor imag-
ing (DTI) creates images of specific fiber tracts (such as
the arcuate fasciculus) that connect cell bodies.

Figure 2–11.  Summary of areas of cerebral cortex of left hemisphere that are active during oral language. Note activ-
ity in multiple areas. See text for additional details. Reproduced with permission from Ardila, A., Bernal, B., & Rosselli, M.
(2016a). How localized are language brain areas? A review of Brodmann areas involvement in oral language. Archives of
Clinical Neuropsychology, 31, 112–122.
 2  The Nervous System:  Language, Speech, and Hearing Structures and Processes
At least two important lessons have been learned
from DTI research. First, the necessary connections
exist. Second, certain brain diseases have as much or
more damage in the fiber tracts as they do in cortical
structures. In these diseases, the disruption of connec-
tions is as important to the disease process as is dam-
age to gray matter. A good example is Alzheimer’s
disease, in which dementia is a primary symptom.
Dementia is almost always associated with a communi-
cation disorder. The presence of white matter disease in
dementia-associated communication disorders shows
that the planning, production, and comprehension of
language are dependent as much on the connections
(white matter) between nuclei and cortical cell bodies
as they are on the cell bodies themselves (gray matter).
This recently acquired knowledge lends further sup-
port to the idea of a brain network for the production
and perception of speech and language.
Chapter Summary
The nervous system includes the CNS and PNS.
The CNS includes the cerebral hemisphere and its
contents, the brainstem, cerebellum, and spinal cord;
the PNS includes all the nerves connected to the brain-
stem and spinal cord, these nerves carrying information
from the CNS to different parts of the body (motor), or
conveying information from different parts of the body
to the CNS (sensory).
The basic cellular unit of the nervous system is a
neuron. The neuron has a cell body and an axon. Clus-
ters of cell bodies make up the gray matter of the brain,
and bundles of axons the white matter.
The basic function of a neuron is to conduct elec-
trical impulses from the cell body via its axon to other
axons; neurons communicate with other neurons at
synapses, where electrical energy is converted into
chemical energy and then back into electrical energy.
The electrical energy of one neuron causes a neu-
rotransmitter to be released at the end of its axon,
which affects the cell body of another neuron by caus-
ing it to “fire” (that is, conduct an electrical impulse).
The surface of the cerebral hemispheres shows
ridges (gyri) and deep fissures (sulci); the surface is
called the cortex, a thick layer consisting of gray mat-
ter that cover the cerebral hemispheres somewhat like
the rind of a watermelon.
Many millions of neuron cell bodies are packed
into a relatively small volume in the human brain,
partly by “hiding” additional cortical surfaces in the
walls of the sulci.
33
Clusters of cell bodies within the cerebral hemi-
spheres but below the cortex are called subcortical
nuclei; the cortex and subcortical nuclei are connected
by fiber tracts.
Both cerebral hemispheres are organized into four
lobes, the frontal, parietal, occipital, and temporal lobe.
The left hemisphere is specialized for speech and lan-
guage in about 90% of people.
Broca’s area, in the frontal lobe, appears to be
strongly associated with the production of speech,
and Wernicke’s area, mainly in the temporal lobe but
also involving a small region of parietal cortex, is
strongly associated with comprehension of speech/
language.
The specialization of these areas in the left, and
not right, hemispheres was originally discovered in
patients who had suffered strokes; damage in one of
these areas in the left hemisphere resulted in speech
and language problems, whereas damage to the same
areas in the right hemisphere did not have the same
effect on communication abilities.
In the left hemisphere, cortical tissue surrounding
the sylvian fissure (perisylvian language areas) plays
a prominent role in speech and language. This tissue
includes Broca’s and Wernicke’s areas, other parts of
the cortex, and fiber tracts that connect different corti-
cal areas.
The brainstem is part of the CNS that contains
nuclei for the control of head and neck muscles — that
is, the muscles that control speech articulation and
phonation; the brainstem also contains nuclei for sen-
sation from head and neck structures.
The spinal cord contains analogous nuclei, for
the control of muscular contraction of, and sensation
from, respiratory structures and other important body
structures (such as the arms and legs); the spinal cord
is important for breathing in general, and breathing for
speech in particular.
The basal ganglia, a group of subcortical nuclei,
play an important role in movement.
The thalamus, a subcortical nucleus consisting of
many smaller nuclei, is the main sensory relay to the
cortex; the information from almost all sensory stimuli
makes a final synapse in the thalamus before being sent
to the cortex.
The cerebellum communicates with all parts of the
brain and is important for coordination of movement.
Modern techniques of imaging the brain allow for
precise identification of the size and activity levels of
specific brain structures. Studies using these techniques
suggest that the function of the brain is very complex,
and that a network of many different brain structures
is involved in speech and language function.
34 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
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Ardila, A., Bernal, B., & Rosselli, M. (2016a). How localized
are language brain areas? A review of Brodmann areas
involvement in oral language. Archives of Clinical Neuro-
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Ardila, A., Bernal, B., & Rosselli, M. (2016b). How extended is
Wernicke’s area? Meta-analytic connectivity study of BA20
and integrative proposal. Neuroscience Journal, https://doi.
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ence: Exploring the brain (4th ed.). Philadelphia, PA: Wolters
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den, C., Basilakos, A., . . . Bonilha, L. (2018). Anatomy of
aphasia revisited. Brain, 14, 848–862.
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Language Science
Introduction
What is language? In lay terms, it is the “thing” we
use to communicate. Ask the average person on the
street this question, and he or she may respond, “You
know, it’s the words, the sentences, stuff like that.” And
indeed, it would be difficult to argue with this answer,
because the words and sentences and stuff like that are
all clearly important parts of language. Why is lan-
guage so much more than stuff like that?
For those of us who as children had a typical his-
tory of speech and language development and who
have been fortunate enough to avoid illnesses associ-
ated with communication disorders, language does
not seem like a very big deal, at least in its daily use.
For humans, language is a bit like bipedal locomotion,
sleeping, and enjoying chocolate cake: it comes natu-
rally and seems like it should not be any other way. We
are all aware, at some level (often implicit), of the pro-
found way in which language defines us as a species.
After all, you do not hear zoo animals asking each other
for another piece of chocolate cake. Because speech and
language are so intertwined with being human and are
so natural for us, we sometimes run the risk of treating
speech and language as our old, uninteresting friend,
someone we know everything about and who does not
surprise us.
When the author was a doctoral student at Univer-
sity of Wisconsin (UW)–Madison, he visited his home
on the East Coast after his first semester, full of (what
3
he thought of as) the wonder of speech and language
production, perception, and comprehension. One of
his brothers asked him, “So, exactly what is it that you
are studying?” When the author answered this ques-
tion with an excruciatingly boring monologue about
the intricacies of tongue movement, the nature of the
speech acoustic signal, the fascinating changes in air
pressures and air flows within the speech mechanism,
and their role in producing a series of speech sounds
to create words and convey meaning, his brother
responded, “I don’t get it, what’s the big deal, you open
your mouth and you talk.”
Indeed, you do just “open your mouth and talk,”
or at least most of us do. For those who cannot, how-
ever, either because of developmental problems or as a
result of a stroke, a degenerative neurological disease,
or a structural problem within the speech and/or audi-
tory mechanism, the deficit or loss of this natural ability
has devastating consequences. It is precisely because
language is so naturally human that its disruption is
such a big deal.
What Is Language?
Language is studied by scientists from many differ-
ent disciplines, including speech-language pathology,
linguistics, cognitive psychology, general medicine,
neuroscience, computer science, and even engineer-
ing. Individual scientists may disagree on the details
35
36 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
of exactly what they study as “language,” but we can
offer a fairly broad and noncontroversial definition to
organize our discussion of language science.
Language is a conventional, dynamic, and genera-
tive system of components; the relationships between
these components are used to express ideas, feelings,
and facts in communication with other people. Lan-
guage also uses mental representations to guide lin-
guistic behavior. And, in a general sense, language
is controlled by a network of specific, connected
regions of the brain. Each of these claims is discussed
briefly, below.
Language:  A Conventional System
Language is conventional because, to a large extent, its
use is based on arbitrary specifications and rules. The
arbitrary characteristic of language components is not
a problem, provided that a group of people agree on
their use for communication. People adopt and agree
upon arbitrary language characteristics as conventions
to be followed for maximum benefit to the group using
them. In this case, the benefit is communication.
The most obvious (but hardly the only) example
of the arbitrary nature of language usage is found in
words and their meanings. Different words are used in
different languages to mean the same thing. Speakers
of English understand the sequence of sounds form-
ing the word “home” because they have agreed, even
if implicitly, on its meaning as a place where people
live. There is nothing in the sequence of an “h,” “o,”
and “m” sounds that captures the concept of a place
of your own, where you eat, sleep, and raise children,
any more so than the sequence of a “k,” “ah,” “s,” and
“ah” (“casa”: Spanish), or “j,” “ee,” and “p” (“jeep”:
Korean). Users of an imaginary language may call the
place where you live a “glerkin”; if everyone agreed
on this use, “glerkin” would induce exactly the same
warm feelings as “home,” “casa,” and “jeep.”
Words are not the only arbitrary characteristic of
languages. The phonetic contrasts used to make differ-
ences in word meanings vary widely across languages
(see Chapter 12), as does word order within a sentence.
In English, for example, the subject-verb-object word
order is required (“The dog chased the rabbit,” not
“chased the rabbit the dog” or “rabbit the dog chased”).
In Russian, word order for these kinds of sentences is
optional, unless the larger conversational context of the
sentence requires a specific order. Even social uses of
language may be arbitrary. For example, the charac-
teristics of conversational turn-taking vary quite a bit
across different ethnicities and cultures. In some cul-
tures, it is imperative as an indicator of good manners
for a listener to wait until the speaker has paused suffi-
ciently for the talking turn to shift to the listener. Other
cultures may allow lots of verbal interruptions, indeed
may encourage them in a kind of Darwinian struggle to
be heard, with no suggestion of lack of manners.
Language is conventional. One language’s con-
ventions are no better or worse than those of another
language. When a group of people agree to a set of
conventions, whatever they might be, communication
happens. English is referred to a great deal through-
out the following discussion, but only because it is
the language of instruction for this course. Examples
from other languages are provided to emphasize spe-
cific points.
Language:  A Dynamic System
Language is said to be dynamic because it changes
over time; language evolves. Language usage is not
the same from generation to generation, or even within
generations as individuals move through stages of life.
The claim of language as an evolving system is easy
to verify by, for example, comparing dialog from films
or TV shows from the 1950s to those of the present.
Certain aspects of language — usually words — may
become more or less “extinct” over time, certain oth-
ers are adaptable and are rarely pushed to the margins
by contemporary culture. For example, if a sophomore
attending college in 2018 was asked if he wanted to
attend a football game and responded, “That would
be swell,” other sophomores overhearing the response
may ask where this student’s spaceship is parked and
how it escaped the gravitational pull of his home planet.
On the other hand, if the student said “cool,” few of
his contemporaries would take notice. The interesting
thing about these two words is that “swell” succumbed
to linguistic evolutionary pressures after frequent use
in the 1950s (watch a Leave it to Beaver or Father Knows
Best rerun, you will probably hear the word used in
a context similar to the one given above). “Cool,” on
the other hand, adapted and maintained its usefulness,
beginning its widespread usage in English as a marker
of the beatnik/jazz culture of the early 1950s and then
making its way through hippie culture, hair bands,
the frighteningly empty 1980s, and all the way to the
present. Cool is cool, then and now. Somewhere in
between these extremes along the continuum of verbal
viability, we used copasetic, groovy, far out, solid, tight,
rad, and awesome, to mean basically the same thing. For
an interesting dissection of the origins of “cool” as we
now understand it to mean hip, good, great, and many
other shades of “okay,” see the Slate column (http://
www​ . slate.com/articles/life/cool_story/2013/10/

cool_the_etymology_and_history_of_the_concept_​
of_coolness.html) on the long history and evolution of
the word.
Language is also dynamic because it is used as
a group marker to indicate, “I belong to this group”
without saying so explicitly. High school students and
young college-age students typically sound different
from their parents, instructors, and other adults from
whom they are one or two generations removed. That
is to say, high school students, within the same broad
culture (e.g., American culture), have subtly different
accents and not-so-subtle differences in dialect from
their parents and grandparents. Everything from the
choice of specific words to prosody is often used as a
group marker. A 55-year-old male and 20-year-old male
may both use the word “cool” as a response without
attracting attention, but the 55-year-old who explains
how he likes to fish by saying, “That’s how I roll on
the weekend” will attract attention because of the mis-
match between his age and language usage; so, too, the
contemporary 20-year-old who says, “I’m attending a
rock and roll concert tonight.”
The dynamic nature of language is inextricably
tied in with cultural shifts. When your author was
a teenager, certain words spoken in public created a
major, scandalous incident. The open-air utterance of
at least one of these words suggested a deep charac-
ter flaw on the part of the speaker, like dipping your
face into a mound of mashed potatoes and shouting,
“Look, no hands!” at an upscale restaurant to which
your future in-laws have taken you to get to know you
better. In contemporary culture, those words — and
in particular, that one — have more or less entered the
mainstream as judged by their frequent use in public,
on TV shows, and in films, from the mouths of people
from all generations.
An interesting, mostly nontechnical survey of lan-
guage evolution is found in David Crystal’s The Stories
of English (2004).
Language Is Generative
Speech and language define the human species. The
thoughtful reader may question this claim by pointing
to various animal languages or in some cases an appar-
ent animal ability to produce speech. Honey bees have
an elaborate communication system for guiding their
fellow workers to sources of food, chimps have been
taught rudimentary sign-language skills, and African
Grey parrots in captivity learn and produce an enor-
mous number of phrases over the course of their 50-
1
Dr. Irene Pepperberg has claimed the famous, late African Grey, Alex invented new phrases by combining previously unrelated words.
3  Language Science 37
or 60-year life span. How are these examples different
from human communication?
Human language differs from animal languages
by virtue of its creative and consistently novel char-
acteristics. Humans take a small number of language
rules and use them to combine and recombine words
to produce interesting and, typically, never-before-
heard or -spoken utterances. This is the generative
nature of human language, its ability to produce new
utterances by applying conventional rules and word
meanings to the needs of a communication goal. Afri-
can Grey parrots produce lots of different utterances,
apparently because of their outstanding mimicry and
memory skills, but evidence for their ability to gener-
ate novel phrases is scant to nonexistent.1 The evidence
for novel phrase production is somewhat more compel-
ling in primates who have been taught sign language
and who have been reported to combine individual
signs in unique ways to achieve communication goals.
Nevertheless, even if one accepts these reports as accu-
rate (and not everyone does), the tremendous effort
required to teach primates sign language is in stark
contrast to the human infant/early toddler’s ability to
generate new and useful phrases with a small set of
words in the absence of formal instruction; to a signifi-
cant degree, it just happens. Certainly it “just happens”
for little humans in an environment rich with linguis-
tic stimulation; put a chimp in the same rich linguistic
environment and she will not produce spontaneous
two- or three-word utterances, vocal or signed, around
2 years of age. There is something radically different
about the human child’s language capabilities and
potential from those of a primate, even one who has
been intensively instructed.
The generative nature of human language is often
taken as a proof for its genetic legacy. Clearly, if the
generative nature of language is what makes it pecu-
liarly human, the human genome must have a lot to
do with our language ability (Fisher & Vernes, 2015;
Fisher, 2017). But it would be a mistake to discount
environmental influences on human language devel-
opment and skills. Human language characteristics
reflect an interaction between the environment and
the human genetic endowment for sophisticated lin-
guistic behavior.
Language Uses Mental
Representations
Language learning and usage are based on the develop-
ment and manipulation of mental representations. This
38 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
is a central idea in much of contemporary cognitive
psychology, an idea we will adhere to in this chapter,
even though there are scientists who do not believe in
mental representations. A mental representation is an
idea or image in the mind that has information content.
Many language scientists believe there are mental rep-
resentations of the sounds that are used contrastively
in a language. According to this view, in English there
is a mental representation of the vowel category “ee”
(in phonetic symbols, /i/), which can replace other
vowel categories in various syllable forms to create
alternative word meanings. For example, the vowel in
the word “heat” distinguishes the word for a temper-
ature-based concept from the word “hat”; the words
differ only by the vowel separating the “h” from the
“t.” The mental representation of “ee” is built up and
stabilized by exposure to the language.
In contrast, in English there is presumably no men-
tal representation — or at least not a linguistic one — for
the vowel “ee” produced with the lips rounded. This
is because an “ee”-like vowel made with rounded lips
does not distinguish words in English. “Heat” spoken
in English with the lips spread (the typical production)
or with the lips rounded would strike a listener as the
same word, even if the rounded version sounds odd
or like a poor attempt to imitate a foreign accent (such
as Swedish). The rounded “ee” is one of the variants of
the mentally represented category of “ee” in the Eng-
lish-speaker’s mind. This means it is recognized as a
member of the “ee” phoneme, albeit one with a slightly
different sound. A similar example can be made for
semantic categories. Language users have a mental
representation for the category “dog,” which is devel-
oped from exposure and contact with many dogs. This
mental representation contributes to a listener under-
standing of the kind of animal that has just relieved
himself on the front lawn when someone says, “A dog
just made a mess on our lawn.” This mental representa-
tion and its connection to language prevent the listener
from imagining the offending animal to be, say, a lion,
a horse, a cat, or some other type of animal with fur,
primarily quadrupedal locomotion, a tail, and so forth.
The mental representations for language units are
thought to be powered by a variety of psychological
processes. These processes create, maintain, adjust, and
store the representations.
Language Is Localized in the Brain
There is good evidence that speech and language capa-
bilities are controlled by a specific network of brain
regions and their connections. In classical terms, lan-
guage is said to be “localized” in the nervous system.
When neuroscientists talk about “localized function,”
they refer to a region or regions of the brain, and con-
nections between these regions, in which the tissue
is specialized for a specific function, or at least has
developed a critical role in a specific function. There
are many debates about brain localization for specific
functions, and especially in the case of speech and
language. It is safe to conclude, however, that in the
overwhelming majority of people, language is local-
ized to tissue in the left hemisphere of the brain. We
know about the localization of speech and language
from natural diseases (e.g., stroke) that affect specific
parts of the brain, from brain imaging studies of speech
and language activities, and from surgical procedures
in which parts of the brain are stimulated or rendered
nonfunctional for a brief (not permanent) time. Left-
hemisphere brain localization for speech and language
is yet another argument for the species-specific nature
of speech and language. The brain regions associated
with speech and language are discussed in greater
detail in Chapter 2.
Components of Language
Language is made up of well-defined components
which are grouped into three categories. These catego-
ries are form, content, and use.
Form
The form category includes the components of lan-
guage that are referred to as “structural.” The three
subcategories of form are phonology, morphology,
and syntax.
Phonology
Phonology is the study of the sound system of a lan-
guage. The phonological component of a language
includes all the sounds used by a language (the phonetic
inventory), the phoneme categories of the language (the
sounds that are “contrastive”), and the rules for sound
sequences that can create words (phonotactic rules).
Phonetic Inventory and Phonemes. Imagine an
expedition to Madison, Wisconsin, from some far-
away planet where the language is entirely different
from English. These space travelers have a scientific
tradition of language study, like our own, and resolve
to gather information on the native tongue of Madiso-
nians. Like any good phonetician, the space travelers
use their highly evolved recording instruments which

have become a permanent part of their brains; their
ears serve as microphones, covered by only weakly
effective, cartilaginous windscreens to collect a large
speech sample from several native speakers. Because
there is a coffee shop on every corner of Madison, Wis-
consin, they have no trouble finding people willing to
talk at length and provide an extensive sampling of
the sounds used in their language. The space travelers
examine the collected speech samples carefully, using
narrow phonetic transcription to identify every sound
heard in the recordings. “Narrow” transcription means
they record very fine details of the sound production.
These aliens have superhuman skills in phonetic tran-
scription — they will get it right.
When the space travelers have finished their tran-
scriptions and analyzed them, they construct a chart
showing all the sounds they have transcribed. The chart
is a record of the phonetic inventory of the language
spoken in Madison, Wisconsin. The chart records about
a dozen vowel sounds, as well as glides, stops, frica-
tives, and affricates (see Chapter 12). An interesting
feature of their analysis is the case of stop consonants
(such as “p,” “t,” “k”), for which the space travelers
find very small but noticeable differences for a specific
sound. A good example is the “t” sound, which some-
times sounds as if it is produced with a strong burst of
air; they transcribed this sound from words like “top,”
“type,” and “attack,” but they do not know the words
yet, they are just listening to the sounds. At other times
the “t” sounds as if it lacks this burst (words like “mitt”
and “stop.” They also record a stop sound that sounds
as if the speaker suddenly closed the vocal folds for a
short time before suddenly releasing a puff of air. This
sound resembles “t” in some ways, especially ones
without a burst of air, but the space travelers have suffi-
ciently good transcription skills and can hear the sound
as slightly different from the other “t” sounds.
When the phonetic inventory is established, the
space travelers must determine which of those sounds
function as phonemes. A phoneme can be defined as a
speech sound category that can change the meaning of
a word, when it is exchanged for another speech sound
category. The most straightforward example of this
sound exchange is when they both appear in exactly
the same location within the words. Two simple exam-
ples will make this definition clear. In English, the “k”
and “g” sounds are both phonemes, because they can
change the meaning of a word when substituted for
each other. The word “duck,” for example, is changed
to “dug” simply by exchanging the word-final “k” with
a “g.” Native speakers of English above the age of 6 or
7 years know that these are two different words — they
have different meanings. Similarly, “girl” and “curl”
are distinguished in meaning by the exchange of the
3  Language Science 39
“g” and “k.” To offer an example with another sound
pair, in English the “s” and “sh” sounds are phonemes,
as easily shown by such word pairs as “so”-“show”
and “sip”-“ship.” The space-traveling phoneticians
learn the changes in word meanings with these sound
exchanges by asking the humans what the words mean
when the sounds are exchanged; this is how they learn
the phonemes of Madison English — identifying the
sounds from the phonetic inventory that result in the
change of a word meaning.
The space travelers jet off to Amsterdam, in the
Netherlands, to identify the phonetic inventory and
phonemes of the local Dutch dialect. They use the same
methodology as in Madison — sitting in coffeehouses
and engaging people in conversations, to determine if
the phonetic patterns of Dutch are the same or different
from those in English. Dutch, they learn, has the “k”
and “s” sounds but these do not contrast with “g” and
“sh,” respectively. Although these sounds may some-
times be heard in Amsterdam Dutch, there are no “k”-
“g” or “s”-“sh” exchanges in Dutch that change word
meanings. That is, “g” and “sh” do not function as pho-
nemes in Dutch. When they occur, they are phonetic
variants of the “k” and “s” phonemes.
Consideration of these examples leads to an inter-
esting insight: the phonetic inventory and phonemes
of a language are not the same thing. Here is another
example, based on the space travelers’ recording of
Madison English “t” sounds. In a word such as “light,”
the space travelers may hear the word-final “t” pro-
duced with (a) no burst of air, (b) a burst of air, or (c) a
sound made as if the vocal folds were being closed
tightly for a brief time, and then released. These pho-
netic variants can be heard with training, yet the word
“light” can be spoken with each of the variants with-
out changing its meaning. The variants are separate
entries in the phonetic inventory but are all versions of
the phoneme category “t.” Phonetic variants of a single
phoneme category are called allophones. Languages dif-
fer widely in their phonetic inventories as well as in the
way those sounds are used as phonemes.
Here is a very important point. Phonemes are the
minimal sound unit that can change word meaning,
but phonemes have no meaning of their own. Pho-
nemes are therefore not the minimal unit of meaning
in languages. Minimal units of meaning are discussed
in the section titled, “Morphemes.”
Phonotactic Rules. Phonotactic rules specify the
allowable sequences of phonemes for word formation,
as illustrated by the three following examples. First, in
English, words cannot start with a velar nasal sound
(the sound at the end of the English word in “sang”),
but they can in several languages of the world (e.g.,
40 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Burmese: Ladefoged, 2001). Second, English allows
syllables to be initiated by a fricative followed by a
stop (as in the word “stop”), but many languages (e.g.,
Japanese: Avery & Ehrlich, 1992) do not allow syllables
initiated by consonant clusters (such as the “st” in
“stop”) to initiate syllables. Third, English syllables can
take a variety of forms for words, including ones that
end with a final consonant (CVC [consonant-vowel-
consonant] form, as in the word “kick”). In Mandarin
Chinese, however, all syllables end in vowels — there
are no CVC, or closed syllable forms (i.e., syllables
“closed” with a consonant2). These examples illus-
trate phonotactic rules (also known among linguists as
phonotactic constraints) in different languages, or restric-
tions on the sequences of sounds that are permitted to
form words.
Morphology
Morphemes are the smallest meaningful units in lan-
guage. Morphology is the study of the rules applying
to morphemes and how they are used and modified
in communication. There are free morphemes and bound
morphemes. Table 3–1 shows examples of both types.
A free morpheme is a minimal unit of meaning that
stands alone; words such as “dog,” “wait,” “run,”
“hoot,” and “giraffe” are examples of free morphemes.
A bound morpheme is a minimal unit of meaning that
cannot stand alone but must be attached to a free mor-
pheme to implement its meaning. As shown in Table
3–1, the plural “s” is a bound morpheme whose mean-
ing is “more than one” when attached to a free mor-
pheme such as “dog.” Similarly, the past tense “ed”
is a bound morpheme whose meaning is “occurred in
the past” when attached to a free morpheme such as
Table 3–1.  Free Morphemes and Bound Morphemes
Free Morphemes Bound Morphemes
dog -s
wait -ed
perfect im-
certain un-; -ly; -ty
run -ing
laugh -able
fool -ish
2
 There is an exception to this phonotactic rule in Mandarin: CV (consonant-vowel) syllables can end in the velar nasal sound mentioned in
the text.
“wait.” The words “dogs” (dog + s) and “waited” (wait
+ ed) therefore consist of two morphemes, one free
and one bound. Other familiar bound morphemes in
English include “-ing” (running), “-er” (taller), “-able”
(laughable), “pre-” (prenuptial), “un-” (unusual), and
“-ish” (foolish).
Morphemes are important in language develop-
ment, showing a typical pattern (on average) of mas-
tery as children develop and gain levels of language
sophistication. Morphemes also have significance in
certain delays and disorders of language development,
as discussed in Chapters 7 and 8.
Syntax
Syntax specifies the rules for ordering of words to form
“legal” sentences. For example, in English, “The cat ate
the mouse” is a legal sentence, whereas “Ate mouse the
cat” is not, because the verb must follow the subject of
the sentence. This is true for English even though the
meaning of “Ate mouse the cat” can be worked out. As
noted, some languages have very strict rules about the
positions of verbs, adjectives, and nouns in sentences,
whereas others do not.
Another example of a syntactical rule in English
is the requirement for noun phrases to link with adjec-
tives by means of the “to be” verb and its variants.
“John is happy” is legal, “John happy” is not.
Content
The content component of language refers to meaning.
Morphemes have already been identified as the mini-
mal units of meaning in language, but here we are con-
cerned with the nature and organization of all meaning
units. The branch of language science concerned with
meaning is called semantics.
Semantics includes not only the meaning of words,
and how sets of words may be similar or different,
but also the meaning of phrases. As noted earlier, words
and their meanings are established arbitrarily and
become useful when the linguistic community agrees
on the correspondence between them. Semanticists are
interested in how speakers employ and organize the
words they produce, and how listeners interpret those
words. Readers may wonder, “Why should there be a
difference in the meanings of a word or phrase when
users of a language agree on them?” This is one of the
many interesting aspects of semantics — that language
users may agree in general on semantics but differ on
specifics.
 3  Language Science 41

Big Bits of Language

The example in text of the bound morpheme “-able” in the
word “laughable” (which transforms the verb “laugh” to an adjective as
in, “His novel is laughable” or as in “What a laughable novel”) offers an
opportunity to illustrate the complex nature of morphology, and the tricky
relationship in English between orthography (the printed representation
of a word) and its spoken version. In “laughable,” the same orthographic
sequence (able) is also a free morpheme, but pronounced differently:
“uh-bl” when it functions as a bound morpheme, “ay-bl” for the free
morpheme; the meaning of both the bound and free versions is essentially
the same. In “laughable,” the addition of the bound morpheme changes
the verb (laugh can also be a noun) to mean, “able to evoke laughter
(or laughs).” When the free morpheme “able” (“ay-bl”) is added to the
free morpheme “laugh,” note how its pronunciation changes from the
free-morpheme version. If you told someone, “I’m uh-bl (able) to meet
that deadline,” you would receive a strange look; your listener might not
understand what you mean. You may get an equally strange look if you
said, “That’s laugh-ay-bl,” but in this case, your listener is likely to know
what you mean, even if recognizing there is something wrong with your
pronunciation. These changes in sound when morphemes are combined
are called morphophonemic alternations. They are often rule based (the same
change from “ay” to “uh” occurs for words such as “portable,” “notable,”
“changeable,” and “stackable”). A nicely complicated example of morpho-
phonemic alternation is the spoken versions of the words “harmony”
expanded to “harmonic,” “harmonious,” and “harmonizing.” As the
morphology changes, notice how the sound “ee” after the “n” in the “base”
morpheme (“harmony”) changes to “ih” in “harmonic,” back to “ee” in
“harmonious,” and to “eye” in “harmonizing”; in “harmonious” the sound
after “m” changes to “oh.” An additional piece of this morphology puzzle is
that the stressed syllable in each word (bolded in the orthographic repre-
sentation that follows) depends on the morphological structure. These shifts
in stress can affect the pronunciation of the vowel following the “n.”
The phonetic transcriptions of this sequence of morphophonemic
alternations have been included with a guide to sound symbols that are
different from English orthography.

harmony /hɑrməni/ phonetic symbol /ɑ/ = “ah”; /i/ =

“ee”; /ə/ = very short “uh” (schwa)
harmonic /hɑrmɑnIk/ phonetic symbol /I/ = “ih”
harmonious /hɑrmoniəs/ phonetic symbol /o/ = “oh”
harmonizing /hɑrmənɑIzIŋ/ phonetic symbol /ɑI/ = “eye;
/ŋ/ = “ing”

Some scientists believe these subtle differences in
word meanings can wreak havoc in certain communi-
cation settings. For example, most people would agree
on the general meaning of the word “fine” as a response
to the question, “How do I look?,” but the more spe-
cific interpretation of the response may depend on the
gender of the question-asker (Tannen, 1994). A more
subtle example, one in the arena of the social use of
language (discussed later in this chapter), is the mean-
ing of a word such as “adorable.” The obvious content
of this word is clear, as applied to a child, perhaps, or
a small, cuddly pet, but a deeper level of meaning may
42 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
be implied by the gender of the speaker. Semanticists,
therefore, explore all sorts of meaning aspects of words
and phrases, and the nuance of meanings depending
on who is speaking, the context of the conversation,
and so forth (Tannen, 1994).
In speech and language development, vocabulary
is of interest as children begin to understand the hierar-
chical structures of meaning. “Hierarchical” means that
certain meanings are subsumed, or embedded, within
larger meanings, like subcategories of more general
categories. At an early stage of development, “dog”
may mean only Muffy, the family dog, but as the child
accumulates life and language experience, “dog” takes
on a more global lexical status. “Dog” may include
any of those sniffing four-legged creatures attached to
humans by a rope, and especially that nasty slobbering
Spike who scares poor Muffy when they meet on the
street. Lexical (vocabulary) development is covered in
more detail in Chapter 6.
Social Use of Language
(Pragmatics)
Social use of language is distinguished from the form
and content components of language partly because
it does not have easily identified units (such as pho-
nemes, morphemes, words) or rules (as in the case of
syntax), and partly because it concerns communica-
tion on the “big stage” of social interaction. Social use
of language is sometimes discussed under the term
pragmatics, sometimes under the term speech acts. Even
if units and rules of language pragmatics are hard to
specify because they are less obvious than the units and
rules for form and syntax, language pragmatics is not
random or unguided by convention. For the following
discussion, the term “pragmatics” will be used to des-
ignate the social use of language.
Pragmatics often involves aspects of communica-
tion that are implicit to the language user’s communi-
cation skills. People know successful communication
when they see it, but if asked to identify characteristics
of successful communication, they are not necessar-
ily able to verbalize them in explicit terms. Never-
theless, pragmatics are an essential part of successful
communication.
Conversations are maintained between two or
more people by observing these implicit rules. Speak-
ers engaged in a conversation cooperate to maintain it
by sticking to the topic under discussion or using the
appropriate means to change the topic, by observing
turn-taking rules, and by speaking in a voice appro-
priate to the setting (e.g., not overly loud). Coopera-
tion and politeness in conversation seem like obvious
requirements for communication success, but we all
know people who have trouble with these require-
ments. It is as if these individuals do not recognize
the mismatch between their conversational techniques
and those of the majority of people with whom they
communicate. Pragmatics, like other aspects of lan-
guage, must be learned. These learned pragmatics
skills can be undone by certain neurological diseases.
The deterioration of pragmatics skills is part of a lan-
guage disorder.
Pragmatics is a complex, culture-bound aspect
of language. The domain of pragmatics extends well
past actual spoken conversation to such things as body
language, gestures, patterns of eye contact during con-
versation, distances between speakers engaged in a
conversation, and choice of vocabulary. For example,
the simple act of waving a friendly goodbye to some-
one with an open hand, fingers spread, and palm facing
the person may be interpreted in Greece as an insult. In
certain cultures, the way in which someone leaves a
room after concluding a conversation with a superior
(a boss, a teacher, a parent) may differ in accordance
with pragmatic rules (e.g., backing out of a room ver-
sus turning and leaving). Just as pragmatic rules may
be variable across different cultures, where cultures
are defined geographically, the rules may vary within
cultures according to age group, ethnic and racial back-
ground, and so forth.
Language and Cognitive
Processes
This chapter reviews the components of language
as separate entities. The presentation seems to make
sense ​— an adult can accept the idea of phonemes,
morphemes, words, syntax, and even pragmatics as
components of language. The definition of these com-
ponents, however, does not include discussion of how
the components interact in both language development
and communication among people with well-devel-
oped language skills (e.g., individuals at least 5 years
of age). It also does not discuss why language develops
so rapidly, how language develops, and when compo-
nents of language and their interactions are mastered
throughout language development. Each of these is
considered in turn in the following sections.
As with the components of language, the why,
how, and when of language development and mas-
tery are not independent. The discussion of “how” and
“when” is expanded in Chapter 6. These questions are
important because they have direct implications for the
understanding, diagnosis, and treatment of speech and
language disorders.

Why
The question of why language develops, and so rap-
idly, is answered in different ways depending on
(among other things) the initial premise of the ques-
tion. If the premise is the existence of an innate speech
and language property of the human brain, language
develops because it is driven by brain tissue dedicated
to it. In this view, there is a human brain mechanism
for speech and language, different from the commu-
nication brain mechanism of any other animal. At
some point in the first year of life, the mechanism is
“turned on,” to initiate speech and language develop-
ment. Language advances so rapidly from first words
through morphology, vocabulary, and sentence struc-
ture (syntax), presumably because it is coded to do so
by this mechanism. This view has been championed by
the famous linguist Noam Chomsky (Chomsky, 1957,
1975). He called this brain mechanism a language acqui-
sition device (LAD).
The idea of an innate, human-specific language
mechanism has been disputed and rejected by many
scientists. One compelling argument against an innate
mechanism for language is the large variability among
typically developing children in the rate of language
learning. Across typically developing children, first
words may be spoken over a wide range of months;
at 2 years of age, there is significant variability across
children in vocabulary size and utterance length (e.g.,
single word versus multiword utterances). If an innate
mechanism guides language development, why is
there so much age variability among children in the
mastery of language development?
Many scientists argue that the human brain does
not need a specialized mechanism for language devel-
opment. The brain has an extraordinary number of
interconnections between its approximately 100 billion
neurons (brain cells that transmit information); the
brain can function like a supercomputer. The mastery
of language is powered by this massive biological com-
puting ability, which processes an enormous volume
of speech and language data, organizes patterns, and
learns from these data how to use language compo-
nents for effective communication (see Kidd, Donnelly,
& Christiansen, 2018, for a review of these issues).
How
As discussed more completely in Chapters 5 and 6,
language development moves from a preverbal stage
(prior to first words) through simple language skills
(single words, “dog”), which are later expanded into
multiword utterances (“dog eat”) to use and mastery
3  Language Science 43
of bound morphemes (“want”-“wanted”), through
more sophisticated syntax, and on through more com-
plex levels of language usage. Development of the
form, content, and usage (pragmatics) components
of language are most notable between ages 1 and 9 or
10 years, with especially rapid advances in the first
five years after the first word. Included in this rapid
advance is complete mastery of the sound system of
language by no later than 8 or 9 years of age. The suc-
ceeding levels of language development overlap in
time; vocabulary, for example, grows rapidly as utter-
ance length (multiword sentences) expands.
Language development includes both compre-
hension and production (expression) skills. Language
comprehension and expression are interdependent
processes in language development. Comprehension
and expression can also be understood as partially (or
sometimes wholly) independent. For example, in the
preverbal stage of language development, comprehen-
sion skills are more advanced than skills of expression.
The preverbal stage for expression is largely phonetic
(as in babbling), rather than phonemic (because there
are no true words), but comprehension of language
and sophisticated speech perception skills for phone-
mic contrasts are present. For example, a 6-month-old
infant is typically on the verge of comprehending her
first words but is (on average) an additional 6 months
away from producing a first word.
Language development proceeds well into the
teenage years, and even into adulthood (e.g., expan-
sion of vocabulary, or understanding the meaning of
subtle language use as in humor). Reading skills, as
one example of language development, are affected
significantly by language comprehension skills. The
development of language may therefore be influenced
by cross-modality skills (in this case, auditory and
visual modalities, see Hogan, Adlof, & Alonzo, 2014).
When
The “when” of language development is different for
each child. Average-age benchmarks for mastery of dif-
ferent components of speech and language are sum-
marized here and discussed more fully in Chapters 5,
6, and 13.
First words are expected around 1 year of age, a
50-word vocabulary at 18 months of age, two-word
utterances at age 2 years, longer utterances between
the ages of 2 and 3 years, as well as the comprehen-
sion and expression of adjectives, verbs, and free mor-
phemes. Bound morphemes are usually mastered by
age 4 or 5, and longer, more complex utterances from
age 5 years onward. Complete mastery of phonol-
44 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
ogy ranges between the ages of 5 and 8 years. Finally,
production and comprehension of complex language
usage — jokes, irony, and other abstract language phe-
nomena — may not be mastered before the teenage
years. These age benchmarks for language components
and the very large variation across children in the time
of their appearance are discussed more fully in Chap-
ters 5 and 6.
This short summary of “when” is introduced in
this chapter because of the systematic nature of lan-
guage development across childhood years. Why are
first utterances single words? Why are most of these
initial words nouns? Why does vocabulary develop-
ment accelerate dramatically when two-word utter-
ances appear in the child’s expressive skills? A person
who subscribes to Chomsky’s position imagines these
sequential elaborations of language form, content, and
usage as a set of switches that are turned on throughout
development. The switches are a characteristic of the
language-acquisition device.
A person who views learning as the basis for lan-
guage development is interested in the development
of cognitive skills as a foundation for increasingly
sophisticated language skills. Nonlanguage cognitive
skills (memory, organization, speed of processing, and
so forth) mature throughout childhood. If nonlinguis-
tic cognitive skills are employed to power the devel-
opment of language skills, the schedule for increasing
language sophistication can proceed in parallel with
and, in fact, influence, nonlanguage cognition, which
in turn influences language development. Brain devel-
opment continues well into childhood and the teenage
years, providing increasing brain power to develop
very sophisticated language skills. In this view, spe-
cial brain mechanisms are not required for language
development.
Chapter Summary
Human language is unique not only because of its con-
ventional, dynamic, and generative nature, but also
because it seems to require and make use of specific
brain regions.
It is convenient to separate the components of lan-
guage into the categories of form, content, and use.
Form includes the phonological, morphological,
and syntactic components of language, content the
semantic component, and use the pragmatic compo-
nent (social use of language).
Both comprehension and expression (production)
of speech and language development are important
skills in the mastery of communication.
One view of speech and language development
is that there is a language acquisition device specific
to the human brain, that the device “turns on” around
1 year of age and initiates a series of increasingly
sophisticated language steps.
Another view is that language development is
guided by cognitive processes (e.g., memory, process-
ing speed, attention) that become increasingly skilled
and complex with development.
These cognitive processes are not specific to lan-
guage but are well suited to the organization and
manipulation of the massive amount of speech and
language data to which a child is exposed.
Three questions can be asked about the develop-
ment of language: why, how, and when.
“Why” is answered by language in the service of
communication: language develops to serve a critical
need of humans, to communicate complex ideas and
actions with flexible use of semantics, sentences, and
pragmatics.
“How” language develops is by starting out very
simply (babbling and first words) and adding new lay-
ers of complexity to language skills as a child develops.
“When” language develops refers to an age-related
sequence of steps of language mastery at succeeding
levels of complexity; mastery of each stage of language
proceeds through systematic phases for the “average,”
typically developing child, but from child to child there
is substantial variation in the ages at which mastery of
a specific aspect of language is accomplished.
References
Avery, P., & Ehrlich, S. (1992). Teaching American English pro-
nunciation. Oxford, UK: Oxford University Press.
Chomsky, N. (1957). Syntactic structures. The Hague, Nether-
lands: Mouton.
Chomsky, N. (1975). Reflections on language. London, UK:
Fontana.
Crystal, D. (2004). The stories of English. New York, NY: Over-
look Press.
Fisher, S. E. (2017). Evolution of language: Lessons from the
genome. Psychonomic Bulletin and Review, 24, 34–40.
Fisher, S. E., & Vernes, S. C. (2015). Genetics and the language
sciences. Annual Review of Linguistics, 1, 289–310.
Hogan, T. P., Adlof, S. M., & Alonzo, C. N. (2014). On the
importance of listening comprehension. International Jour-
nal of Speech Language Pathology, 16, 199–207.
Kidd, E., Donnelly, S., & Christiansen, M. H. (2018). Individ-
ual differences in language acquisition and processing.
Trends in Cognitive Sciences, 22, 154–169.
Ladefoged, P. (2001). Vowels and consonants. An introduction to
the sounds of languages. Oxford, UK: Blackwell.
Tannen, D. (1994). Gender and discourse. New York, NY: Oxford
University Press.

Communication in a
Multicultural Society
Introduction
If asked to define “culture,” how would you respond?
“Culture” is a concept most people understand but
find it difficult to define in precise terms. Here are a
few (admittedly academic) definitions of “culture”
selected from a search on the Internet:
n “a set of learned beliefs, values and behaviors;
the way of life shared by members of a society”
n “The accumulated habits, attitudes, and beliefs
of a group of people that define for them their
general behavior and way of life”
n “understandings, patterns of behavior, practices,
values, and symbol systems that are acquired,
preserved, and transmitted by a group of
people . . . ”
n “Learned behavior of a group of people, which
includes their belief systems and languages,
their social relationships, their institutions and
organizations . . . ”
These four statements define culture in similar
ways. The common threads among them are that cul-
ture is learned, shared among a group of people, and
determines the way they behave and construct their
4
societies. It is easy to see how communication, and
more specifically speech and language, fit with these
concepts of culture. The first two definitions imply
the major role of communication in culture with the
phrases, “a set of learned behaviors . . . ,” “way of life
shared by members of society . . . ,” and “accumulated
habits . . . that define for them their general behavior
and life.” The final two definitions make an explicit link
between culture and communication by saying that
culture consists of “symbol systems that are acquired,
preserved, and transmitted by a group of people . . . ,”
and, “includes their . . . languages . . . ” (emphasis added).
Language, as shown in Chapter 3 is a conventional set
of symbols used by members of a community to com-
municate. “Conventional,” in this description of lan-
guage, means “arbitrary” but agreed upon by members
of a group.
Consider the following anecdote, from the author’s
experience. I came to Madison, Wisconsin, in August
1972, never having ventured west of State College,
Pennsylvania, where I earned my undergraduate and
master’s degrees. When admitted to the doctoral pro-
gram at University of Wisconsin–Madison, I was fortu-
nate enough to have been awarded a fellowship. This
award required me to fill out some paperwork at a uni-
versity administration building, which after arriving
45
46 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
in town I located (with difficulty). I walked into the
lobby and had no idea where to go, but there, at an
information desk, sat an obviously sightless gentle-
man, wearing dark glasses, who was likely to know
where I should go.
I approached him and asked, “Can you tell me
where I can find Window 20?”
He responded, “Walk down the hallway and turn
right at the bubbler.”
A bubbler? I had no idea what a “bubbler” was,
but I imagined a decorative, in-ground water feature — ​
I knew water must be involved — perhaps with small
stone figures of angels or ducks bathing in gently per-
colating water emerging from an elegant spout in its
center. I walked down the long hall and saw nothing
so peaceful or watery, not even anything vaguely close
to this image that had popped into my head when the
gentleman said, “bubbler.”
Back at the information desk, head bowed and
feeling, well, incompetent, I said to the gentleman,
“Okay, I’m really sorry, I don’t see a bubbler or maybe
I don’t even know what that is.”
The sightless man, who I would learn through
repeated contacts over the next several years was not a
smiler, grinned ever so slightly and said, “Son, where
are you from?”
“Philadelphia, sir.”
He allowed the grin to turn a tad more obvious and
said, “Down the hall, right at the drinking fountain.”
I immediately, of course, made the connection
between “bubbler” and “drinking fountain.”1 I had
never heard the word “bubbler” used in this way,
even the term “drinking fountain” was slightly for-
eign sounding; in Philadelphia, we called these things
“water fountains.” The point is not that the use of
the term “bubbler” was an impossible hurdle to my
understanding of Wisconsin talk — like most adults,
I learned what this new label meant after a single trial.
Rather, this strange spoken label for “water fountain”
made me feel — different. Over the next several weeks,
I would have this same experience many times, learn-
ing terms such as “stop-and-go light” and “hoser” as
alternate expressions for the vocabulary items I used to
designate a traffic signal and a gentle insult directed at
males, respectively. I had never considered the words
I grew up with for these items or people as merely a
collection of arbitrary communication signs. I was in
a different culture, where communication was subtly
and sometimes not-so-subtly different from the culture
1 
 o the best of the author’s knowledge, the term “bubbler” was coined by one Harlan Huckleby, whose idea for a drinking machine that shot
T
water upward toward the drinker’s mouth was patented in 1888 by the Kohler company of Kenosha, Wisconsin. The word may also be used
in parts of New England, Michigan, and Australia.
I knew, and was unaware of as being defined by the
four bullet points previously presented.
Dictionary of American
Regional English
The “Dictionary of American Regional English”
(DARE: http://dare.wisc.edu/, now in six
volumes) lists the many regional variants of
words and phrases that people in specific
geographical regions of the United States have
agreed to understand as having a specific
meaning, and that people in other regions of
the country are likely not to understand. This
dictionary is like a manual for the concept of the
arbitrary meanings of words.
The linkage between culture and communica-
tion has been studied for many years. The American
anthropologist Ruth Benedict, in her famous (and still
controversial) 1934 book Patterns of Culture, noted the
arbitrary nature of cultural customs and the error of
thinking, common among anthropologists who were
her contemporaries, that Western Society was a “ref-
erence” culture to which all others could and should
be compared (see Huntington, 1996, for an extended
consideration of this idea). For Benedict, and for many
subsequent scholars of linguistics and anthropology,
this idea of a “reference” culture extended to speech
and language. Benedict pointed out that the speech
sounds used by a specific language are a very small
subset of the total number of speech sounds that can
be produced by the human speech mechanism. The
speech sounds used in a specific language serve the
functional role of communication. These speech sounds
and the language forms (e.g., words) they create are a
critical component of a culture. There is nothing inher-
ently special or “correct” in the pronunciation of Eng-
lish spoken by Caucasians, in, say, Chicago, Illinois.
The pronunciation of speech sounds, the word choices,
the idioms, even the distance maintained by a talker
from his or her listener — these communication behav-
iors reflect culture, something shared among a group of
people that reflects their way of life.
The biological anthropologist Terrence Deacon
summed up this issue by saying, “If symbols ulti-

mately derive their representation power, not from the
individual, but from a particular society at a particular
time, then a person’s symbolic experience of conscious-
ness is to some extent society-dependent — it is bor-
rowed” (Deacon, 1997, p. 452). The “symbols” include
the arbitrary linguistic forms and usages as previously
mentioned. More importantly, Deacon claimed that an
individual’s language experience is really a cultural
experience of his or her society. Deacon says this expe-
rience is “borrowed” because the language/culture
matrix is constantly changing, even within the same
culture. An individual’s perspective on life is medi-
ated — some may even say dictated — by the language/
culture in which he or she is raised.
Many cultural factors influence communication.
A partial list is provided in Table 4–1.
Why It Matters
These introductory comments may seem far afield
from the topic of Communication Sciences and Disor-
ders, but in fact they are highly relevant to much of the
material in this text. As pointed out in several publica-
tions (e.g., Larroudé, 2004), the United States is becom-
ing increasingly diverse in its racial and ethnic identity.
Population growth in the United States is dispropor-
tionately accounted for by nonwhite persons, point-
ing to group diversity as a long-term characteristic of
American society. This diversity includes a multitude
of cultures. If language is a prominent feature of cul-
ture and not separable from it, a panorama of commu-
nication styles can be expected as part of everyday life
in the United States.
Table 4–1.  Selected Cultural Factors That Can
Influence Communication
Race and ethnicity
Social class, education, and occupation
Geographical region
Gender
Sexual orientation
Situation or context
Peer group association/identification
First language community/culture
Relationship between speaker and listener
Source:  Based in part on Giri, 2006.
4  Communication in a Multicultural Society 47
Everyday life includes health conditions, many of
which affect a person’s ability to communicate. Even
perfectly healthy persons who enter the United States
for family, work, or educational reasons, who speak
English as a second language, may feel as if their com-
munication skills are impaired. At some point in their
lives, many of these individuals may seek the services
of a speech-language pathologist (SLP) and/or audi-
ologist (AuD). Here is one good reason for special-
ists in Communication Disorders, whether clinicians
or college professors who help train clinicians and
researchers, to be well-versed in the influence of cul-
tural variation on speech and language behavior.
Clearly, an SLP or AuD cannot possess the entire
range of multicultural knowledge and skill required for
equal effectiveness among the many diverse groups in
the United States. It is unreasonable, for example, to
expect a professional in Communication Disorders and
Sciences to understand all aspects of African American,
Asian, Hispanic, and Native American cultures, includ-
ing their speech and language usage. The sheer variety
of cultures and their communication components form
an intimidating body of knowledge; for speech and
hearing professionals, “Becoming competent cross-
culturally is among the greatest of challenges” (Cheng,
2000, p. 40). Rather than trying to master this impos-
sibly large amount of information, a multiculturally
competent professional in speech and hearing should
master a “multicultural framework.” This framework
focuses on principles that are applicable across persons
from the many different cultural groups a speech and
hearing professional is likely to encounter in his or her
practice (see Cheng, 2001, p. 125). A few of these prin-
ciples are discussed later in this chapter. An important
“super principle” of this framework is discussed here
to illustrate why multicultural sensitivity and knowl-
edge are important to the SLP and audiologist. This
principle involves the distinction between a difference
and a disorder.
Difference Versus Disorder
Multicultural competence for a speech and hearing
professional is especially important when a patient has
communication behaviors that, in one or more environ-
ments (such as the classroom), call attention to them-
selves. A principle of multicultural competence is the
recognition of the distinction between a communication
difference and a communication delay or disorder. This dis-
tinction can be clarified with an example from the area
of typical language development in children.
Language scientists have studied in great depth
various aspects of typical language development,
48 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Ebonics
“Ebonics,” a term blending “ebony”
and “phonics,” is generally understood today to
be a largely historical term for African American
Vernacular English (AAVE), the dialect used
by many North American African American
people. Ebonics became a national issue in 1996
when the Oakland Public Schools, California,
passed a resolution recognizing it as a legitimate
language system. The resolution had the aim
of obtaining federal programs and support for
instruction in Ebonics. Learning of standard
English, it was argued, could be facilitated by
approaching instruction through the child’s
“home” language — Ebonics. This resolution, and
its educational implications, provoked spirited
controversy among public figures, politicians,
and linguists. Whatever the fine points of the
controversy might be, there is widespread
agreement among linguists that AAVE has
language forms, content, and use employed in a
rule-based system for effective communication.
Often these rules are not the same as the rules
we associate with “Standard American English”
(whatever that might be). McWhorter (2001) and
Kretzschmar (2008) have written histories of the
controversy, as well as differing opinions about
the legitimacy of Ebonics as a language system.
including the learning of grammatical rules. As dis-
cussed further in Chapter 6, during the course of typi-
cal language development, it is not unusual for children
aged 2 years (or a little older) to produce simple sen-
tences such as “He running.” Children communicate
the idea of a boy who is currently in the act of run-
ning with a sentence lacking the “to be” verb (in this
case, the word “is” or the contracted form, “He’s”). “He
running” is considered a “typical” sentence form for a
child in the early stages of language learning, but the
same sentence produced by a child aged 4 years may
create an impression of language delay. This is because
the “typical” course of language development involves
a fairly quick transition from “He running” to “He is
running” (or, “He’s running”).
This is all well and good, but this “typical” course
of verb development does not apply to all dialects spo-
ken in the United States. A relevant case is AAVE,2 in
which “He running” is a proper grammatical represen-
2 
 ome refer to this dialect as African American English (AAE), or Black English, but in this chapter AAVE is used. See the Box
S
on Ebonics.
tation to convey the meaning of a male in the act of
running (more precisely, it is “He runnin’”). When a
4-year-old African American child who is a speaker of
AAVE says, “He runnin’,” there is no language delay
(as evidenced by this particular utterance) because the
child uses the correct grammatical form for his cul-
tural/linguistic community (see Rickford, 1997). In
other words, the language community in which the
child is developing speech and language skills recog-
nizes “He runnin” as typical development, and as a
good match to fully developed language among adult
speakers of AAVE.
Standardized Tests and
Sample Size
In the discipline of Statistics, there is the concept
of a “population” and of a “sample.” When a
scientist chooses a sample of people to partici-
pate in an experiment, she hopes the sample
is sufficiently representative of the population
so that her results can be generalized (that
is, not restricted to the specific participants
she has studied in her experiment). There are
several approaches to creating a sample that
is representative of the population. Among
these is the selection of a sample consisting of
many participants (as compared to relatively
few participants). The thinking is, the larger
the sample, the more the results approach the
“true” population characteristics. Based on this
principle, most standardized tests are based on
data collected from relatively large numbers of
participants. Few people trust the results of an
age-normed, standardized test based on data
collected from, say, 10 children at each age. The
precise number required to make the sample
a good estimate of population characteristics
depends on many factors, but the larger the
sample, the more likely is the generalizability of
the results.
Standardized Testing
and Language Difference
Versus Disorder
The example in the Box above can be extended to for-
mal, standardized testing of speech and language skills. In

the case of speech and language development in chil-
dren, it is useful to have knowledge of age milestones
for specific events. For a typically developing child,
how many words are included in the spoken vocabu-
lary at age 2 years? At age 3 years? Or, at age 2 years,
which verbs are understood and/or spoken by a typi-
cally developing child? The answers to these questions
are clearly relevant to clinical diagnoses of delayed or
disordered language development. How are answers
to these questions determined, and how are they used
in clinical settings?
Age-normed, standardized tests provide one
way to answer these questions. The purpose of these
tests is to generate an accurate estimate of the age at
which most typically developing children master
a particular speech or language skill, and to express
the test scores in a way that permits direct compari-
sons across ages. The results of an age-normed, stan-
dardized test can be used to document the amount
of language delay, expressed as the number of years
behind performance expected based on the child’s
chronological age.
For example, a four-year-old child who has lan-
guage scores that are at the mean (average) of the
distribution of scores obtained from the three-year
old, normative sample, is said to be a year behind in
language development. And, these normative distri-
butions can be used to track a child’s progress during
speech-language therapy. In the example immediately
above, the desired outcome of the therapy is to move
the child’s standardized score in the direction of the
age-appropriate distribution (i.e., the four-year-old
distribution).
The standardized scores of typically developing
children at any age depend on the nature of the sample
used to construct the test. The nature of the sample is
critical to understanding the limitations of a standard-
ized test in making clinical decisions; the results of the
test, and their interpretation, depend entirely on how
the test was normed.
Consider the four-year-old, AAVE-speaking child,
described above, who produces verbs consistent with
adult use in AAVE (“He runnin”). Let’s assume we
have a standardized test of verb development, based
on samples of children living in the state of Wisconsin.
The sampling takes account of the proportions of Cau-
casian, African-American, Hispanic, Asian, and other
racial and ethnic groups in the state population. The
method used to develop this standardized test may fol-
low excellent principles of test development, includ-
ing the proportionate sampling of children within the
state population. However, the norms in the test are not
likely to reflect “typical” performance in other states
where the proportion of (for example) AAVE-speak-
4  Communication in a Multicultural Society 49
ing children is much greater than it is in Wisconsin.
For example, Illinois and Florida have a substantially
higher proportion of African-Americans than Wiscon-
sin, and a greater number of speakers of AAVE
The most obvious use of an aged-normed test is
clinical, in which a diagnosis can be made concerning
a possible delay in speech and/or language develop-
ment. The issue posed concerning an African American
child’s use of AAVE exposes one major, potential prob-
lem with age-normed tests: the results, and their inter-
pretation, depend entirely on how the test was normed.
Our hypothetical test of verb performance was devel-
oped from data collected in Wisconsin, a state with a
much lower proportion of African Americans than,
say, Illinois or Florida (http://www.wadsworth.com/
sociology_d/special_features/ext/census/african​
.html). If the test considers “standard English gram-
mar” as the requirement for correct verb performance,
the norms are likely to misrepresent “typical” language
development depending on the geographical location
of data collection. A “normative” test can reflect sub-
stantial cultural biases.
Here is a hypothetical example of cultural bias
in normative testing. An African American child who
uses AAVE in the home and with his friends is referred
by his preschool teacher to a speech-language clini-
cian for language evaluation. The teacher and the SLP
are not well informed about potential cultural bias in
standardized testing. These well-meaning individuals
were educated many years ago, before our discipline
had a clear sense of the professional implications of
cultural sensitivity. A 5-year-old child is given stan-
dardized tests based on samples from primarily white
populations, and his scores are like those of 3-year-old,
typically developing children who contributed to the
sample on which the test was based. In the absence of
cultural sensitivity and the strong link between culture
and language, the child’s score may be interpreted as
an indicator of developmental language delay. The
child is scheduled for sessions with the SLP to address
this clinical diagnosis. The child’s parents are confused
when informed of this diagnosis, because they have
not noticed a problem with the child’s ability to com-
municate. Their child’s language abilities seem age
appropriate, judging from their experience with other
children in their family, and in their community. For-
mal or informal testing of this child’s language skills
in AAVE would show, in fact, that the child’s language
development is age appropriate.
The SLP must have cultural competence, includ-
ing cultural sensitivity, to determine if a child’s speech
and language skills represent a difference from other
cultural expectations, or a true delay or disorder.
A speech/language difference is not something to be
50 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
treated (unless the patient or his parents request such
treatment: see later in chapter); a delay or disorder
should be treated.
This rather long example is the most obvious case
where unintentional cultural biases may influence the
interpretation of formal, standardized tests. In the eval-
uation of all aspects of language, including nonverbal
language, social use of language, and many other fac-
tors, SLPs and audiologists must have cultural compe-
tence to be most effective.
Cultural variations in all components of speech
and language are too numerous to document here, or to
be known by an individual SLP or AuD. The key is for
professionals in our field to be aware that differences
from their own ideas of communication normality may
be cultural, not clinical. This awareness should include
the knowledge and skills to identify sources — in the
clinical and research literature, or of the human vari-
ety — to assist in the evaluation of communication
behaviors as cultural differences versus communica-
tion delays/disorders.
A framework for knowledge and skills in cultural
sensitivity is now incorporated into the training of
SLPs and AuDs. More specifically, when an individual
SLP is working with many patients who identify with
a variety of cultures, whether it is African American,
Hispanic, Asian, Native American, Deaf, or any other
group, development of a solid understanding of com-
munication characteristics within the group is critical.
The SLP or AuD may not have a full range of
cultural knowledge for each group, but based on the
multicultural framework that is part of SLP and AuD
training, know how to identify and obtain the knowl-
edge relevant to any child or adult seeking diagnostic
or management (therapy) services.
The questions about speech-language and audiol-
ogy specialists and the possible intertwining of their
professional competencies and cultural identities can
be stated more broadly. Can Caucasian SLPs be effec-
tive in a school setting where the majority of students
use AAVE to communicate, or vice versa? Can an SLP
who is not familiar with Hispanic culture and language
usage diagnose and treat speech and language delays
or disorders in a school where the students are primar-
ily of Hispanic heritage (or vice versa)?
The steps taken by ASHA to ensure that all per-
sons being trained as SLPs and AuDs receive instruc-
tion in cultural competence are likely to address these
questions in a positive way. ASHA’s perspective on
cultural competence is summarized in an overview
statement on their Web page (http://www.asha.org/
Practice-Portal/Professional-Issues/Cultural-Compe​
tence/). Cultural competence is viewed by ASHA as an
issue much broader than the few examples provided in
this chapter. Cultural competence may involve cultural
issues associated with age, gender, and socioeconomic
status, to name a few.
Accent, Dialect, and Culture
Some aspects of cultural variation are plainly obvious.
For example, differences between Japanese and Ameri-
can culture, or between German and French culture, are
indisputable. A clear and dramatic difference between
these cultures, of course, is language. Even within the
same language, however, dramatic cultural differences
may exist. The “face” of these within-language dif-
ferences is often speech and language patterns, even
when the actual face does not suggest a difference.
Good examples are British versus American English,
the Chinese spoken in Taiwan versus Mainland China,
and Egyptian versus Jordanian Arabic. Accent and/or
dialect are often strong identifiers of geographic, ethnic,
and even cultural roots. Accent and dialect are some-
times used interchangeably, but as noted in the next sec-
tions, there is an important distinction between them.
Accent
In lay terms, accent refers to how a person “sounds”
when he or she speaks. More technically, accent refers to
how the sounds of speech and the melody and rhythm
of speech (prosody) are heard. The statement, “Bill has
a Boston accent,” refers to the way Bill says certain
sounds, and perhaps the melody and rhythm of his
speech. “Susan has a Southern accent” means the same
thing, and distinguishes the sound of her speech from
Bill’s. The way these two speakers sound allows almost
any speaker of American English to identify their
general geographic origin within the United States.
Accent is often thought to be conveyed primarily by
the way vowels are spoken, although consonants and
prosody can contribute in important ways to a regional
accent.
How many distinguishable accents exist in the
United States? This is a difficult question to answer,
but Dr. William Labov of the University of Pennsylva-
nia, who has studied regional accents in the lower 48
states, identifies six major accent regions (Labov, Ash,
& Boberg, 2006). These regions can also be thought of
as cultural regions. For example, among the six accent
regions are a Western accent and a Southern accent.
Most Americans would agree that Western culture
(as found in, say, California or Washington State) dif-
fers from Southern culture (as found in Louisiana or
Georgia, for example). These same Americans would
not expect much difficulty in identifying speakers with
Western versus Southern accents. The person with
an easily identifiable southern accent probably con­

siders himself a southerner, and not simply because of
his accent.
The six major accent regions identified by Labov
and his colleagues are almost certainly an oversimpli-
fication of accent variation in the United States. For
example, the “North” accent in this system includes
speakers in Minnesota, Wisconsin, Chicago, Michi-
gan, and western New York. Many people who have
grown up in Wisconsin can hear the difference between
a native Wisconsinite and a native Minnesotan, and the
Chicago accent is (to the author’s ear) different from
the typical Wisconsin accent. Labov and his colleagues
include 11 states and parts of two others in their “West-
ern” accent, but speakers from Colorado and Southern
California, included in the “Western” accent group do
not sound alike (at least to these ears).
The accent regions identified by Labov and his col-
leagues serve an important purpose even though each
of the categories contains accent variation. The aver-
age person walking on the street in Madison, Wiscon-
sin, who is introduced to someone from Mississippi,
Georgia, or South Carolina is likely to hear their accent
as “Southern.” The Georgian may hear the difference
between her accent and that of the South Carolinian or
Mississippian. But it is unlikely for a Georgian with-
out special training to detect the differences between
a Wisconsin, Minnesota, and Michigan accent; they all
sound “Northern.” So, the variation within any one of
the six accent groups is likely to be detected by some-
one within the accent group but not by someone from
a different accent group (see Clopper, Levi, & Pisoni,
2006, for experimental work on perceptual identifica-
tion and discrimination of regional accents).
Talker accents often highlight “us” and “them”
(Müller, Ball, & Guendouzi, 2000). Accents are an iden-
tifier of geographical/cultural allegiances and associa-
tions. Regional accents can contribute powerfully to
how we are perceived, and how we perceive ourselves.
When I first came to Madison, Wisconsin, it was not
only my initial inability to identify a “bubbler,” or to
understand what it meant when someone handed me a
hammer and said, “Hold this once,” that made me feel
different. I also sounded funny when I spoke. Within
10 minutes of driving into town and interacting with
several people as I signed a lease and got something to
eat at the (now defunct) Marc’s Big Boy, I was acutely
aware of my funny-sounding vowels.
Among all of these many accents, can one be
defined as “standard”? And what does it mean to
have a standard accent? This question and its possi-
ble answer have as much, if not more, social-political
meaning than linguistic importance. In Great Britain,
for example, there has been a long-standing debate
concerning the advantages of a standard accent. This
accent is defined as that heard in the speech produced
4  Communication in a Multicultural Society 51
by educated people who are likely to be from the Lon-
don area or have learned London-accented English
(Müller et al., 2000). In the United States, the debate
is not as public as it is in England, but the tendency
among some accent groups to regard other accents as
“substandard” or to associate certain accents with cer-
tain personality traits cannot be denied (see review in
Fridland, 2008). The issue of whether or not a standard
accent exists or should exist continues to be a matter
of debate among linguists and educators. In this text,
the position is taken that accent is such an important
part of regional identification and culture that any one
accent cannot be viewed as “better” or more desirable
than another. This is consistent with the acceptance
of all cultures, and specifically all the subcultures in
America, as equally worthy and equal partners in the
creation and shaping of the American social landscape.
Dialect
Labov and his colleagues actually called the six accent
regions described above “dialect” regions. As men-
tioned earlier, “accent” refers to an impression of the
sound of speech, which is what Labov meant when
he enumerated the six “dialect” regions. But the term
“dialect” is technically different from “accent” because
dialect includes aspects of language that go well past
the sound of speech. Dialect is defined as a language
variant, typically associated with a geographic region
or group of people. A dialect may include unique sound
and prosodic characteristics — that is, an accent — but
may also include unique vocabulary items, gram-
matical structure, and even rules for how people com-
municate. Accent is therefore a component of dialect.
The Wisconsin dialect, for example, not only includes
different-sounding vowels than the Philadelphia dia-
lect but as described earlier has vocabulary items such
as “bubbler,” “hoser” (probably borrowed from Can-
ada), and “pop” (as in, soda), which are typically not
part of the Philadelphian’s vocabulary.
A less subtle dialect difference in the United States
is between AAVE and the several accent and dialect
variants of American English spoken by white persons
around the country. In addition to the phonological
characteristics of AAVE which are different from most
white regional dialects, AAVE has vocabulary items not
heard in white American English, and may also have
different rules for social communication. AAVE is a
dialect of English, not simply an accent difference from
the several accent varieties of white American English.
What does it mean to say that a language such
as American English has several different dialects?
Dialects of a language are typically mutually intelli-
gible; speakers of different dialects can communicate
52 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

effectively, even if occasionally they are confused by
a word or grammatical usage, or if they find their
communication partner’s concept of personal body
space a little odd. This idea of mutual intelligibility,
even when accent, vocabulary, grammatical form, and
other aspects of language usage vary quite a bit, is the
usual standard for differentiating a dialect difference
from a language difference. When two people talk and
cannot understand each other, it is likely they are
speaking different languages, not different dialects of
the same language.
The mutual intelligibility criterion for distinguish-
ing a dialect difference from a language difference is
a technical distinction that does not always fit eas-
ily into real-world experience. Most Americans have
had the experience of listening to rapidly produced
British or Australian English — in a movie theater, for
example — and having great difficulty following the
dialogue. The languages spoken in various parts of the
United Kingdom, Canada, Australia, New Zealand,
and parts of India are surely English, technically are
dialects of English, but they are not always mutually
intelligible. If you travel to Manchester, England, and
ask someone on the street for directions and her reply
seems unintelligible, is she speaking a dialect of your
language? The answer seems to be “no” when “mutual
intelligibility” is the criterion for different speech pat-
terns/styles to qualify as dialects of the same language.
But the Manchester native is speaking English; how do
we resolve this?
Perhaps the resolution is to admit the uncertainty
of a dividing line between different dialects and differ-
ent languages (Backus, 1999). Languages evolve — they
are constantly changing — and over time a changing
dialect variation may be sufficient to make it unintel-
ligible to other users of the parent language. The dialect
difference then becomes a language difference.
The relationship between dialect and accent is
summarized in Figure 4–1. Accent is shown as a com-
ponent of dialect but as separate from other compo-
nents of language that contribute to dialect variation
(e.g., morphology, discussed in Chapter 3).
Code Switching
When dialect differences exist between two groups of
people who have extensive contact as a result of com-
mon neighborhood, common workplace, or friend-
ship (among other factors), speakers in one group may
develop the skill of switching to the dialect of the other
group. This skill is referred to as code switching. Lan-
guage is a code, and the ability to switch between dif-
ferent versions of the code is valuable. An SLP who can
code switch among children with different native dia-
lects or languages has a distinct advantage in the plan-
ning and execution of (for example) language therapy.
This advantage may enhance the language learning
process among the children.
Code switching takes place for all aspects of lan-
guage: for phonetics, phonemes, lexicon, morphology,
word order in sentences, and even pragmatics. The
role of code switching in American society is becom-
ing more important as multiple-language homes are
increasing, and parents are emphasizing among their
language-learning children mastery of the language
spoken in the home as well as that of the majority lan-
guage of the society in which they live.

The Angel’s Share

When whisky is aged in oak barrels, the fluid may fill the cask
nearly to the top. After aging, when the barrel is finally opened for bottling,
the volume of the whisky is less than it was when originally poured for
aging — the fill line has decreased. The evaporated whisky, lost during the
aging process, is called the “angel’s share” — people on earth will have
plenty to drink, they won’t miss this small tribute to those on a different
plane. The 2012 film The Angel’s Share is a story about a whisky heist by a
small group of Scottish men, looking to profit from the removal of a priceless
barrel of aged whisky from a famous distillery. The main actors are Scottish,
and the one British actor does a spot-on Scottish brogue; they all speak
English throughout the film. If you see the film (highly recommended), you
may be surprised to see subtitles. It is English, right? Why the subtitles?
After the first two or three minutes of the film, you understand the use
of subtitles perfectly: the dialogue is nearly unintelligible to the typical
American ear. Dialect or language difference? Watch the film; you decide.
 4  Communication in a Multicultural Society 53

Dialect

Accent Other Language Components

Grammar Morphology Vocabulary

Figure 4–1.  Dialect and accent.

they provide phoneticians (people who study the

Language Components sounds produced in different languages of the world)
and phonologists (people who study speech sound sys-
The language units referred to in
tems — the rules governing the use of speech sounds for
the text are described in Chapter 3 and appear
purposes of communication) with the opportunity to
frequently in subsequent chapters of this
ask, “How do the speech sounds of one language affect
textbook. By way of review, single-sentence
a person’s ability to produce the speech sounds of a
definitions of each component of language are
second language?” To illustrate, consider the Swed-
as follows: (a) phonetics designates the speech
ish, Greek, and American English languages. Swedish
sounds of a language; (b) phonemes designate
has a more complicated set of vowels as compared to
the speech sounds of a language that, when
English, which in turn has a more complicated set of
exchanged in the same position of a sequence
vowels than the relatively simple, five-vowel system
of sounds (e.g., the /k/ and /g/ of the words
in Greek. When a Swede and a Greek are attempting to
“coat” and “goat”) change the word meaning;
learn American English, does the relative complexity
(c) morphology designates the meaningful units
of their native vowel systems affect the way they learn
of speech that “inflect” words and change their
English vowels? The best answer we can give today
grammatical identity (e.g., making a word plural
for this question is: yes, the relationship between the
as in dog versus dogs, or indicating past tense
vowel systems of two languages influences the ability
as in “want” versus “wanted”; (d) vocabulary
to learn the nonnative system, but the specifics of this
(the lexicon) includes the word forms people
influence are complicated.
implicitly agree upon as having specific mean-
This scientific question, of how the sound sys-
ings; (e) syntax designates the grammatical rules
tems of two languages influence the ability to learn the
of language that permit certain word orders but
sounds of a second language, is relevant to the practi-
not others for the formation of sentences (e.g.,
cal issue of modifying a foreign accent. SLPs with rel-
in English, “Big dog” follows grammatical rules
evant training provide services to people who want to
but “Dog big” does not); and (f) pragmatics
modify a foreign accent. Modification of foreign accent
determine the social use of communication that
is also a rather controversial aspect of our field (see,
depend on factors such as age, gender, ethnic
e.g., Fitch, 2000; Müller, Ball, & Guendouzi, 2000; Pow-
group, and so forth)
ell, 2000; and Winkworth, 2000). One reason for the
controversy is found in the potential for independence
between accent severity and speech intelligibility.
Foreign Accent A speaker may have a substantial accent when speak-
ing a nonnative language — that is, the speaker can
Scientists and clinicians are interested in the character- clearly be identified as a nonnative speaker by a native
istics and possible modification of foreign accent. The speaker — yet be perfectly intelligible. If, for example, a
characteristics of foreign accent are interesting because native speaker of Mandarin Chinese produces accented
54 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
but perfectly intelligible English, why seek modifica-
tion of the accented English? Intelligibility is often the
main concern of people who seek to reduce their for-
eign accent; after all, being understood is the primary
goal of communication.
Some speakers may seek the help of an SLP, or a
specialist in English as a foreign language, to reduce
their foreign accent simply to make them sound less
“different.” Speakers may also recognize that their for-
eign accent does not compromise their intelligibility
but still causes their listeners to work harder to extract
the fully intelligible message (Floccia, Butler, Goslin,
& Ellis, 2009). Accent reduction therapy is most com-
monly initiated by the person seeking to reduce an
accent (rather than by a health care or education spe-
cialist). There may be certain situations, however, in
which a speaker’s accent is judged as a potential chal-
lenge to his or her professional success, and a recom-
mendation is made to seek accent reduction therapy.
For example, students enrolled in a master’s-level SLP
training program who are not native speakers of Eng-
lish may have accents that interfere with aspects of
therapy for articulation disorders in children or adults.
At least part of articulation therapy involves clinician-
produced models of the speech sounds being trained.
A clinician (the student with the accent) who produces
a sound model that is insufficiently native-like may be
recommended for accent reduction therapy.
Part of the controversy surrounding the idea
of accent (or even dialect) reduction therapy is who
decides what the “reference” accent or dialect is, and
even if there should be such a reference. The interplay
of accent, dialect, culture, and professional training is
complicated. A few years ago, the author had a chance
to visit a Communication Sciences and Disorders train-
ing program at a southern university, where the major-
ity of graduate students in clinical training had a strong
southern accent (to these northern ears, and I suspect
most northerners). I asked myself how these students,
having completed their clinical training program and
seeking jobs, might fare in an interview at a school
or hospital in a northern state. I reached a tentative
conclusion that two candidates for a job as an SLP in
a northern school or hospital with equivalent creden-
tials, graduate school success, and comparable letters
of recommendation, who both performed well at an
interview, but who differed by their regional accents,
would not be viewed as equally qualified for the job
because of the accent difference. (I suspect the same
situation would apply for the same hypothetical situ-
ation except with the regions reversed — native north-
erner and southerners applying for an SLP position in
a southern school or hospital.)
Bilingualism and
Multilingualism
The deep connection between language and culture is
a professional challenge when language development
takes place in two or more languages. A child who has
roughly equal exposure to multiple languages (and,
likely, cultures) as she learns language from birth is a
“simultaneous” bilingual (or, more rarely, trilingual,
or however many languages the child is immersed in).
Children who learn one language first and around the
age of 3 or 4 years are immersed in a second language,
and develop roughly equal competence in both lan-
guages, are called sequential bilinguals. Bilingualism
is not restricted to oral language. A person who is flu-
ent in both an oral and American Sign Language (ASL)
is considered bilingual.
Bi- or multilingual language development and
multilingualism in adults raise questions for the SLP
and audiologist. For example, in the early stages of lan-
guage learning, does equal exposure to two languages
affect language development, either in a positive or a
negative way (i.e., is typical bilingual language de-
velopment more or less the same as monolingual lan-
guage development)? If a child has language delay
in one of the languages but not the other, is speech-
language therapy appropriate for the language with
delay? When speech-language therapy is indicated for
developmental delay in both languages, does it make a
difference which language is used by the therapist for
language stimulation? Many other questions have been
asked about the role of multilingualism in language
development (see Goral & Conner, 2013, for a review of
these issues).
Scientists and clinicians have also been interested
in the effect of bilingualism on speech and language
perception and comprehension. For example, is a lis-
tener’s comprehension (or the cognitive processes that
support comprehension) affected when a speaker uses
the same language as the listener, but with a mild to
moderate accent? Let’s say that a monolingual, Eng-
lish-speaking child listens to a native speaker of Span-
ish who is speaking accented English; is the listener’s
comprehension affected by the accent, compared to lis-
tening to a native speaker of English?
At first glance, the role of accented speech in lan-
guage comprehension may seem no more than an aca-
demic, laboratory exercise. The implications for clinical
practice, however, are potentially substantial, as illus-
trated by the following two questions. First, when
language stimulation services are provided by an SLP
with accented English, for an English-speaking child
with language delay or an adult with a comprehension

deficit resulting from a stroke, does the accent result
in poorer comprehension as compared to speech with-
out an accent? Second, when an audiologist performs
speech perception tests as part of a diagnostic workup
for a possible hearing disorder, are the test results
affected by the accent of the speaker who produced
the words or sentences used in the testing (Shi, 2014)?
Based on research to date, the answer to both questions
seems to be “yes” even if all the details of accent influ-
ence have not been determined (Harte, Oliveira, Fri-
zelle, & Gibbon, 2016).
The study of the effect of accented speech on lan-
guage comprehension is worth the effort. It is a sig-
nificant aspect of consideration of multicultural and
multilinguistic influences in a speech and hearing
clinic. Accent and its potential relevance to speech and
language therapy may also apply to accent variation
within a language (e.g., the effect of New England–
accented English on comprehension in speakers who
hail from the Pacific Northwest, or of Irish-accented
English on American Southern–accented English).
Chapter Summary
Culture can be defined in many ways, but each defini-
tion mentions beliefs, behaviors, and symbol systems
that are shared and agreed upon by members of the
cultural community.
Language is intertwined with culture in the agree-
ment among members of the connection between sym-
bols and meaning; language is conventional.
The population change under way in the United
States, and in many other countries, requires SLPs and
audiologists to understand different cultures and the
influence of these cultures on speech and language
behaviors.
A major consideration in diagnosing and manag-
ing speech, language, and hearing disorders is recogni-
tion that there is no dominant language, meaning that
evaluation of a potential communication disorder must
account for cultural differences.
Standardized tests of speech, language, and hear-
ing disorders that are normed on a group of children
or adults from one culture are not likely to be valid as
assessment tools for children or adults from another
culture.
In the evaluation of a possible communication dis-
order, a cultural difference must not be confused with a
communication disorder.
Accent refers to the “way people sound” when
they talk; accent includes speech sounds and prosody,
4  Communication in a Multicultural Society 55
the latter including variations in the melody of speech
(intonation), loudness of speech, and rhythm of speech.
Accent may refer to regional accent (varying
accent among native-born speakers of one language) or
to foreign accent (accented speech of a speaker having
one native language who speaks a second language).
Dialect includes accent, but also word and phrase
choices, the order of words in sentences, and the use of
minimal units of meaning in language (morphemes).
Regional accent, dialect, and foreign accent may
affect speech, language, and hearing testing and manage-
ment, depending on the similarities between the thera-
pist or tester accent/dialect and the accent/dialect of the
person receiving management services or being tested.
References
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monolithic view of language. Topics in Language Disorders,
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ton Mifflin.
Cheng, L-R. L. (2000). Children of yesterday, today, and
tomorrow: Global implications for child language. Folia
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Cheng, L-R. L. (2001). Educating speech-language patholo-
gists for a multicultural world. Folia Phoniatrica et Logopae-
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Clopper, C. G., Levi, S. V., & Pisoni, D. B. (2006). Perceptual
similarity of regional dialects of American English. Journal
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Deacon, T. W. (1997). The symbolic species. New York, NY:
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Floccia, C., Butler, J., Goslin, J., & Ellis, L. (2009). Regional and
foreign accent processing in English: Can listeners adapt?
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Labov, W., Ash, S., & Boberg, C. (2006). Atlas of North Ameri-
can English. Berlin, Germany: Mouton de Gruyter.
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sions: Development of functional communication. Topics
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Müller, N., Ball, M. J., & Guendouzi, J. (2000). Accent reduc-
tion programmes: Not a role for speech-language patholo-
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Preverbal Foundations of Speech
and Language Development
Introduction
“Preverbal speech and language development” refers
to the set of communication skills developed by an
infant roughly between birth and the production of the
first word, typically around 1 year of age. This straight-
forward description does not do justice to the many
controversies surrounding exactly how and why chil-
dren move from producing no words and understand-
ing little at birth to uttering their first word around
12 months of age and at the same time understanding
many more words.
An understanding of preverbal speech and lan-
guage development requires knowledge of both
emerging production, perception, and comprehension
skills. Issues of motor maturity (production), auditory
perceptual skill (perception), and ability to represent
auditory percepts for the purposes of linguistic catego-
ries including those for meaning (e.g., words), are all
relevant to preverbal language development.
The issues in preverbal language development
are controversial. In the Chomsky view, speech and
language is not “learned” in the traditional sense but
rather triggered biologically at some point in develop-
5
ment. The alternative viewpoint regards speech and
language skills strictly as things to be learned, and the
first year of life as an intensive, immersion crash course
in language learning. Of course, biological maturity
plays a role in the efficiency and success of this learn-
ing, but the learning perspective typically rejects the
idea of a special speech-language device in the brain
that “turns on” the ability.
There is a substantial body of facts concerning the
development of speech and language skills during the
first year of life. Scientists have made many observa-
tions concerning preverbal speech and language skills
of babies, and written pages and pages of theory to
explain their results. In this chapter, the facts of preverbal
skills — those specifically relevant to speech and language
development, are presented chronologically, as they
evolve through the first year of life. This chronology is
supplemented by some ideas about how speech and lan-
guage development following the preverbal year — after
1 year of age — emerge from this preverbal skill develop-
ment. This is very important, because the way in which
the skills underlying speech and language develop dur-
ing the first year of life is not strictly logical — the way it
does happen is not the only way it could happen.
57
58 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Preparatory Notes on
Developmental Chronologies
Typical speech and language development in the first
year of life is chronicled in this chapter according to
three broad time periods: 0 to 3 months, 3 to 8 months,
and 8 to 12 months. These time periods are “loose”; they
represent average developmental sequences and are
by no means applicable to every typically developing
baby. Among children who are developing without dis-
ease or obvious delay resulting from an undiagnosed
problem, there is substantial variability in the chronol-
ogy of development. The notion of “typical” develop-
ment recognizes this variability by understanding the
emerging skills to fall within a fairly large range. An
understanding of this variability also explains the use
of rather broad time intervals for stages in the chro-
nology (for example, 3 to 8 months). In addition, the
discussion within each of the three time periods often
refers to developmental processes in one of the other
time periods. For example, preverbal skills in the 0- to
3-month period are presented along with the implica-
tions for preverbal skills in the 3- to 8-month and 8- to
12-month periods.
Throughout this chapter, keep in mind the vari-
ability in preverbal language skills across typically
developing children, as well as the links between ear-
lier and later preverbal skills. The chronologies are first
separated into production and comprehension skills,
followed by additional information on interactions
between the two.
Children in the first year of life must learn to use
their lungs, larynx, tongue, lips, and jaw (as well as
other structures of the head and neck) to perform the
motor skills required to make speech sounds; or they
reach an age where speech motor ability becomes
available to them for the purpose of producing speech
sounds (for this subtle distinction, see the section, “3 to
8 Months: Production,” on babbling). This is the pro-
duction part. Likewise, children must learn to make per-
ceptual distinctions relevant to their native language, to
associate specific sequences of sound distinctions (e.g.,
words) with meaning as a linguistic representation,
and to use their memory skills to access the link be-
tween the acoustic signals and their meanings. Or, from
the perspective of the Chomsky view of language devel-
opment, they must reach an age where the ability to per-
form the linguistic interactions between perception,
mental representation, and memory is “turned on”
by maturation of brain mechanisms dedicated to lan-
guage. This is the comprehension part. During the first
1
“ Sensorimotor,” as used here, denotes the brain mechanisms used to control movement. The inclusion of both “sensory” and “motor” in the
term reflects the role of sensory and motor capabilities, and the integration of the two, in movement control.
year of life, language comprehension skills are typically
more advanced than expressive (production) skills.
0 to 3 Months: Expression
(Production)
Babies cry a lot in the first few months of life; this is
hardly a surprise. Crying in very young infants is a
reflexive vocalization to hunger and other forms of
discomfort (e.g., being too cold or too hot, being in
pain because of gas, and so forth). Most experts do not
regard crying among very young babies to have propo-
sitional value, in the sense of the vocalization having
meaning. Infant cries and the variation of their qual-
ity clearly affect parent perception of a baby’s comfort
level and needs (Lagasse, Neal, & Lester, 2005).
At approximately 2 months of age, babies may
produce what Oller (1980) called quasi-resonant nuclei.
These are clearly not reflexive expressions of discomfort
and may occur as apparent “happy responses” when a
parent talks to the baby. Oller called them quasi-reso-
nant nuclei because they give the impression of slightly
muffled, nasalized vowels that often seem to be pro-
duced with the lips closed. If you have held a baby at
this age and heard these kinds of sounds, you will rec-
ognize them from this description, and may remember
thinking, “How is the baby making a sound that seems
vowel-like even though her mouth is closed?”
Toward the end of this period, the baby may pro-
duce vocalizations called “coos” and “goos.” The range
of speech sounds in these early, nonreflexive vocaliza-
tions is limited and often includes the vowels “ah” (as
in “hot”) and “oo” (as in “boot”), sometimes with a
consonant-like sound resembling a “k” or “g.” Most
likely, coos and goos are not intentional; the baby does
not intend to communicate some meaning with these
vocalizations.
An issue in the initial months of preverbal sound
development concerns the interaction between the
baby’s anatomical structures and sensorimotor capa­
bilities,1 and the sounds the baby produces. When a
gesture is produced, such as hand waving for “bye-
bye” or shaping the oral and throat cavities with a nar-
row oral constriction between the tongue and the front
of the hard palate (bony roof of the mouth) and a wide
throat passageway (as in the vowel “ee”), specific pat-
terns of muscle contraction must be produced. In addi-
tion, sensations from these contractions (such as the
feel of the sides of the tongue against the teeth when
the front constriction is made) are part of the package
 5  Preverbal Foundations of Speech and Language Development 59

of information used to verify the “correctness” of the
gesture. These sensorimotor skills mature in the first
year of life, but their relative immaturity in the first
several months is one limiting factor on the kinds of
sounds produced by a baby.
Of equal interest is the effect of vocal tract growth
on sound production during the first year of life. The
vocal tract is the air passageway between the lips and
the vocal folds (often called the vocal cords). The shap-
ing of this air passageway by movements of the lips,
tongue, jaw, and pharynx (the throat) determines which
speech sound is produced. Figure 5–1 shows an art-
ist’s rendition of two vocal tracts from a side view. The
drawing on the left shows a vocal tract for a newborn
and on the right for a young adult. The vocal tracts are
shaded light blue in these drawings, making it easy to
see not only the age-related difference in length but
also in shape. The shaded area is an air-filled, flexible
tube. Note the shortness of the newborn’s pharynx
(the distance from the posterior tip of the soft palate
to the vocal folds) in comparison to the adult’s. This
can be best appreciated by looking at the near-contact
of the posterior tip of the velum and upper edge of
the epiglottis in the newborn as compared to the clear
separation between these structures in the adult. The
shape differences are further highlighted by showing
the bend of the two vocal tracts, from the oral to throat
cavities, with simple straight lines. In the adult, the
pharynx (throat) cavity is oriented roughly at a right
angle to the mouth cavity. In the newborn, the two cav-
ities form a more open angle, and thus have a gentler
transition between them.
The close approximation of the epiglottis and soft
palate in the very young infant most certainly con-
tributes to the sound of the “quasi-resonant nuclei,”
as previously described. This is because the airway is
continuous from the vocal folds through the nasal cavi-
ties in the newborn — in the adult a clear airway path
from the vocal folds through the mouth is more avail-
able. Throughout the first year of life, a major growth
pattern of the infant vocal tract is a lengthening and
descent in the neck of the pharynx. As the pharynx
lengthens and the vocal folds at the bottom of this tube
move down and away from the velum, the pharynx
rotates relative to the mouth, creating the 90° bend seen
in adults (see Vorperian, Kent, Lindstrom, Kalina, Gen-
try, & Yandell, 2005, for measurements of patterns of
vocal tract growth from birth to nearly 7 years of age,
and in the adult years).
Why are the shape differences between the new-
born/early infancy and adult vocal tracts interesting
with respect to sound production? The vocal tract is an
air-filled tube with resonant frequencies that vary by
length and shape. “Resonant frequency” is an acous-
tic term that denotes a frequency (rate of vibration) at
which the amplitude of vibration is maximum. This
description may gain some clarity by considering pipes
in concert organs. The pipes of the instrument vary in
length. The longer the pipe, the lower is its resonant
frequency. In the human vocal tract, the tube not only
can be of a different length (e.g., the difference between
the short length of a baby and the long length of an adult
male), but because it is flexible, it can also change shape.
Changes in positions of the articulators create different
vocal tract shapes, which result in changes in resonant
frequencies of the vocal tract. The different resonant
frequencies for different vocal tract shapes are recog-
nized as different vowels. Chapter 11 provides more

Infant Adult

Figure 5–1.  An artist’s rendition of a newborn (left image) and adult

(right image) vocal tract, as seen from the side with one side of the head
removed. The blue lines on both vocal tracts show the angle of the mouth
(oral) and throat (pharyngeal) cavities.
60 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
information on how changes in vocal tract shape result
in changes in resonant frequencies of the vocal tract.
For many years, the gently curved vocal tract
shape of newborns was thought to limit the kinds of
vowels produced in cooing and gooing, and even in
babbling behaviors occurring later in the first year of
life. The frequent occurrence of vowels such as “ah”
and “oo” in coos, therefore, was thought to be as much,
if not primarily, a result of the baby’s anatomy as of the
baby’s limited sensorimotor control. Even if the baby’s
sensorimotor control was adult-like, the story went,
infant’s vocal tract size and shape prevented the cre-
ation of vocal tract shapes required for certain vowels.
Based on recent research, it seems this interpreta-
tion is only partly true. The infant vocal tract does not
actually prevent the occurrence of certain vowels, but
the nonadult anatomy may promote the production of
a limited type of vowel such as the “eh” in “bed” and
the “ah” in “hot” (Menard, Schwartz, & Boë, 2004).
Other vowels can, in theory, be produced by the baby
vocal tract, but during the first three months it is easier
to produce a limited set.
The ability to make certain speech sounds dur-
ing the first year of life, and especially the first three
months of life, is therefore related to a host of factors.
These include the child’s anatomical, sensorimotor, and
cognitive maturity. The development of speech sounds
also depends on the child’s ability to hear speech
sounds and distinguish them from each other.
0 to 3 Months:  Perception
and Comprehension
In this chapter, the term “perception” refers to the abil-
ity to detect an auditory feature in an acoustic signal or
to discriminate one acoustic signal from another. The
focus is on acoustic signals and the auditory abilities
required to hear and process them, because these are
most relevant to preverbal speech and language skills.
One can just as easily imagine cases in which percep-
tual skills for visual and tactile signals are important
for communication.
The combination of all perceptual skills plus cog-
nitive processes (such as memory) must be considered
in the meaning of “comprehension,” which is the abil-
ity to understand communicative intent and meaning.
2 
 he adult data on discrimination of phoneme contrasts were based on volitional responses (writing down the phoneme heard, or pushing a
T
button labeled with the phoneme heard). Infants obviously cannot make the same kinds of responses, so Peter Eimas and his research group
exploited a well-known baby skill — sucking on a nipple — to demonstrate the baby’s ability to discriminate between two sounds having just
slightly different acoustic characteristics.
3 
 he auditory system includes all auditory structures from the external ear (the part attached to the side of the head) to the cortex of the cerebral
T
hemispheres; see Chapter 22.
As an example, it is entirely possible for a baby to have
reasonable perceptual skills but poor comprehension,
or to be able to comprehend well even with nonoptimal
perceptual skills.
This distinction between perception and compre-
hension is illustrated by the baby’s skills in the 0- to
3-month period. It has been known for many years that
babies as young as 1 month of age can discriminate
between very similar sounds (such as “p” and “b,” or
“s” and “sh”) in much the same way as adults (Eimas,
Siqueland, Jusczyk, & Vigorito, 1971).2 Scientists agree,
however, that the ability of infants to comprehend
speech, to extract meaning from communicative situ-
ations, is extremely limited.
Babies’ abilities to discriminate subtle phonetic
differences in much the same way as adults may
reflect general auditory skills, rather than skills spe-
cific to speech perception. In other words, the baby’s
detection of “p” and “b” as different auditory events is
not relevant to “p” and “b” as linguistic events — that
is, as phonemes. Some scientists believe the newborn
auditory system3 is equipped for auditory distinctions
just like the adult auditory system. In fact, very young
babies can discriminate virtually all phonetic distinc-
tions that are used in languages of the world (Vihman,
2017). The auditory capability for any distinction is
available early in the first year of development. How
do babies begin the process of learning the distinctions
that are relevant to their native language?
There are theories that address this issue. A useful
theory must explain an additional phenomenon that
unfolds during the first year of life: the almost univer-
sal set of phonetic distinctions in the infant’s auditory
repertoire gets “pared down” to only the ones used in
the native language. Vihman (2017) said that progress
in phonetic perception is best defined as loss of the abil-
ity to discriminate contrasts that are not relevant in the
native language (Kuhl et al., 2006).
As the baby develops, auditory distinctions rel-
evant to phoneme distinctions in the baby’s language
are “tuned up” by exposure, whereas distinctions not
relevant to the native language weaken and then dis-
appear. The baby hears a huge amount of native con-
trasts, creating a special sensitivity for them. Over time,
the nonnative contrasts cannot compete for the baby’s
attention with native contrasts; the ability to discrimi-
nate the nonnative contrasts disappears.
 5  Preverbal Foundations of Speech and Language Development
We are a little bit ahead of the chronology that
organizes this chapter. The paring down to perceptual
sensitivity for acoustic contrasts used in the native lan-
guage and the disappearance of sensitivity to other
acoustic contrasts is complete by 10 to 12 months of
age. (The research by Segal, Hejli-Assi, and Kishon-
Rabin [2016] is an example of this kind.) The process
begins, however, in the first three months with a goal
at the end of the first year of life of maximal sensitiv-
ity to relevant phonetic contrasts — the establishment
of phonemic categories. As outlined later, these catego-
ries are essential to word learning and word produc-
tion as well.
One apparent skill possessed by infants as young
as 4 days of age that cannot be explained as part of gen-
eral auditory mechanisms is the ability to distinguish
utterances spoken in their native language from utter-
ances spoken in a foreign language. Jacques Mehler
and his colleagues (Mehler et al., 1988) demonstrated
this ability in 4-day-old French infants who appeared
to be sensitive to the difference between French and
Russian utterances, and in 2-month-old American
infants who gave evidence of hearing the difference
between Italian and English utterances. Mehler and
his colleagues believed the infants’ remarkable ability
to distinguish the languages was based on knowledge
of the prosodic characteristics of their own language,
as compared to other languages. This knowledge may
have been gained by native language exposure both in
the womb and after birth. Nonnative prosodic patterns
that do not match the native language may be detected
as a “new” event. No matter how recent the exposure,
babies appear to attend to and retain the melodic and
rhythmic characteristics of the language used in their
home. Scientists have argued that this ability to recog-
nize the rhythmic and melodic characteristics of their
native language is a foundation for infants’ developing
ability to recognize words (Werker, 2012). The ability
to detect the unique melody and rhythm of the native
language rhythm “bootstraps” the extraction of words
from the speech signal. Babies typically comprehend
their first words around 6 months of age, using their
knowledge of the rhythmic aspects of speech to isolate
a word (Werker, 2012).
Although babies between 0 and 3 months of age
almost certainly have very limited comprehension
of speech and language, other behaviors may lay the
groundwork for future communication skills. For
example, caregivers may interpret baby sounds and
mutual eye gaze as having communicative intent.
Based on this assumed communicative intent, the care-
giver may engage in turn-taking behavior, exchang-
ing vocalizations with the baby and using eye contact
according to the “typical” rules of conversation. Even
61
in the absence of true comprehension, turn-taking may
provide a model for the baby’s learning about commu-
nicative interaction.
3 to 8 Months:  Production
Most babies do not produce true babbling until 6 or
7 months of age. What does “babbling” mean? The
term is reserved for those vocalizations in which con-
sonants and vowels are clearly recognized but do not
form words. Early in the 3- to 8-month period, the coos
and goos have a few vowels, but as noted above, the
consonant-like sounds may have only a vague resem-
blance to the real thing. Prior to the onset of babbling,
there is an expansion of the baby’s vocal repertoire that
may be partially supported by an increasing ability to
mimic vocal behavior. As the baby moves toward the
first half-year of life, she is likely to produce squeals,
growls, yells, and Bronx cheers (“raspberries”), all of
which seem like vocal play, practice, and exploration.
When the baby starts producing consonants, they are
likely to be labials (p, b, m) and those made with the
front of the tongue (t, d, n). “Back” consonants such as
“g” and “k” typically come later as a regular feature
of babbling.
Babbling typically begins between 6 and 8 months
of age but in many cases of typical development may
not begin until 10 months or a bit later. Babbling has a
specific form. Its basic unit is a consonant-vowel (here-
after, CV) syllable, where the consonant is likely to be
a “b,” “m,” or “w,” and the vowel is an “eh” like in
the word “bet” and “uh” as in “but,” or an “ih” as in
“bit.” The syllable may be produced once or repeated
in a sequence (“buh-buh-buh-buh”). When the same
syllable is repeated in sequence, there is little varia-
tion in syllable-to-syllable duration, pitch, and loud-
ness. These syllable sequences are called reduplicative
babbling. Although the CV syllable is most frequently
observed in early babbling, other forms (such as vowel-
consonant [VC] syllables) may also be heard.
Why do most early babble syllables have a CV
form favoring bilabial consonants like “b” and only
a few of the possible vowels? Several proposals have
been set forth to account for this fact, but here we
briefly describe one perspective, chosen for its care-
fully developed background and theoretical simplicity.
Peter MacNeilage and Barbara Davis, in work done
at the University of Texas at Austin, view babbling as
the evolutionary product of the discovery by nonhu-
man primates, and ultimately early humans, of the
sound-producing capabilities of the moving articu-
lators (MacNeilage & Davis, 2000). Chewing is char-
acterized by rhythmic up-and-down motions of the
62 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
mandible as the tongue and teeth position and grind
food. At some point in early history, primates acciden-
tally or purposely phonated (created sound by vibrat-
ing their vocal folds) during this rhythmic mandible
movement and took notice of the modulation of the
sound (try it: generate a steady voice and move your
mandible up and down, see how the motion generates
a repeating “syllable-like” effect). According to Mac-
Neilage (1998), this is how the basic syllable was born.
Presumably speech evolved in humans from this basic
syllabic “frame.” In fact, MacNeilage and Davis refer
to the mandible opening-closing movement as a frame,
a vocal tract movement capable of holding the content
of a syllable. The closing of the vocal tract is conducive
to forming the kind of tight constriction that is charac-
teristic of consonants, and the opening permits the full
acoustic resonance typical of vowels. Content of the
basic syllable is the specific identity of the consonant
and vowel making up the syllable. From the simple
“buh-buh-buh” or “bih-bih-bih” resulting from rhyth-
mic motions of the mandible with the tongue resting
passively within the mouth, the tongue hitching a ride
on the jaw, so to speak, humans learned that different
content (different speech sounds) could be inserted
into the basic frame by changing the motion and posi-
tion of the tongue, lips, and jaw. This gave evolving
humans a wide range of sound combinations for the
labeling of different objects, actions, and people. When
the basic CV was expanded to include different syllable
shapes (e.g., VC, CCV) and different sequences of syl-
lable shapes (e.g., “baby,” an elaboration of “buh-buh”;
“ice cream” as an elaboration of “ay-ay”), the ability to
label objects, actions, and feelings became immensely
flexible. Together with advances in brain structure and
function, a vast collection of words was assembled, and
phrases to sequence those words allowed even wider
communication of meaning. The creation and evolu-
tion of sophisticated human language skills may pos-
sibly be traced back to the basic babble syllable.
The “Frames-then-Content” theory of MacNeilage
and Davis (2000) is appealing for several reasons. First,
it is a theory not only about the evolutionary basis of
speech sound development, but also about the develop-
mental course of speech sound development in the first
year of life. Prebabbling babies can often be observed
to wag their mandibles without sound, and it is not
unreasonable to imagine them adding sound to the
wags and discovering the syllable-like results, like their
early human predecessors. A “buh” or “bih” is a com-
mon first syllable in babbling, just as one might expect
from a simple mandible wag with sound added and a
relaxed tongue. Second, the theory derives the sound-
producing abilities of humans from very basic move-
ments of the lips, jaw, and tongue within the human
vocal tract. The motorically simple “frame” of rhyth-
mic mandibular movements can, as motor capabili-
ties of the articulators develop and mature, be “filled”
with increasingly complex content. This content will
include the motions, positions, and configurations of
the tongue, lips, jaw, and other parts of the vocal tract
required for the production of different consonants and
vowels. Third, the theory has universal implications: If
early babbling is indeed derived from simple motions
of the mandible, at least the early sound content of bab-
bling should be the same in all languages because all
babies are using the same mechanism.
This last point is important and invites the ques-
tion, “Do babies from different language environments
produce a uniform set of babbling sounds, or do they
also produce sounds showing the unique influence of
their native language?” For babies just beginning to
babble, a firm answer to this question is unavailable
because there are not enough relevant data from vari-
Phonetic Practice or
Random Sound Play?
Before scientists began careful, detailed studies
of babbling, it was thought to be no more than
sound play. Babies discovered the sound-making
capabilities of their little speech mechanisms:
adjustments to the respiratory system (e.g., loud-
ness change), larynx (e.g., pitch change), and
articulators (speech sound change) resulted in a
variety of speech sounds, some of them resem-
bling those produced by adults and therefore
very amenable to phonetic transcription. The
sound play perspective on babbling implied that
complete phonetic inventories for babies from
all over the world would be the same — even in
babbling from babies close to 1 year of age. In
these inventories, most if not all of the possible
phonetic events capable of being produced by
the human speech mechanism would be found.
There would be no language-sensitive influences
on babbling because the onset of true language
was initiated by the special language acquisition
described in Chapter 3. We now know babies
start this way, and as they progress to the end
of the first year of language learning, sharpen
and mold their phonetic inventories under the
influence of their native language phonetics.
Babbling is a well-practiced dress rehearsal for
the opening night of language performance — the
first words — rather than a cacophony of random
sounds from performers without a script.
 5  Preverbal Foundations of Speech and Language Development
ous languages. Some studies of early babbling suggest
a phonetic inventory that is essentially uniform across
several languages, with little evidence of the native-
language phonetic inventory. More data are available
on the preword, phonetic inventories of later babblers
whose native language is Swedish, Japanese, French,
and English. These data show an influence of the native
language on the phonetic inventory of babbling (Boys-
son-Bardies, Hallé, Sagart, & Durand, 1989; Boysson-
Bardies & Vihman, 1991; Lee, Davis, & MacNeilage,
2010). A conclusion from this work is that babbling
and its development is a kind of practice for the use of
native language speech sounds in first words.
Babbling with a “true” CV form in which the syl-
lable is repeated is called canonical babbling. D. Kim-
brough Oller of Memphis State University, Tennessee,
has been studying babbling for many years and believes
the CV form is a basic structure of human sound sys-
tems (Lee, Jhang, Relyea, Chen, & Oller, 2018). A CV
form, for example, is the most common syllable in
many languages, and its frequent appearance in early
(canonical) babbling is revealing of a basic structural
characteristic of speech sound systems. A baby is said
to produce canonical babbling when her previously
difficult-to-transcribe sounds become recognized as
“real” consonants and vowels in a CV form.
Later babbling clearly shows influences from the
phonetics of the parent language (as in a comparison
between Mandarin Chinese and American English:
see Lee et al., 2018). Other factors, such as parental
interaction style, may also affect babbling onset and
its content.
Canonical babbling is not just a cute characteris-
tic of infants taking their speech mechanism for a test
drive. There is evidence that the age at onset of bab-
bling predicts the age of onset of first words, and that
the specific phonetic content heard in babbling predicts
the phonetic content of first words (McGillion et al.,
2017). In other words, the practice of specific speech
sounds during babbling predicts early words hav-
ing the same speech sounds (“the consonants used
in babble are typically the ones used in first words”
[McGillion et al., 2017, pp. 157–158]). The age of onset
of babbling also seems to predict the development of
vocabulary at later childhood stages. Finally, canonical
babbling is delayed or absent in several developmental
speech disorders and may contribute to the diagnosis
of certain conditions (such as in autism, or in children
with intellectual disabilities [Lohmander, Holm, Eriks-
son, & Liberman, 2017]).
4 
 ecall from Chapter 3 that a minimal pair contrast is when one sound substitutes for another in the same position in a word (such as initial
R
consonants) and results in a change in word meaning.
63
3 to 8 Months:  Perception
and Comprehension
During the 3- to 8-month period, babies lose the abil-
ity to discriminate between selected sound pairs as
described previously. Phoneme contrasts that are not
used in the native language “drop out” of the infant’s
perceptual repertoire and the auditory system is grad-
ually tuned to those contrasts used in the native lan-
guage. A good example of this is the difficulty with the
“r”-“l” distinction experienced by native speakers of
Japanese when they are listening to (and producing)
English. The loss of the ability to discriminate /r/ from
/l/ does not affect the Japanese baby’s ability to master
her language, because the “r” and “l” sounds do not
create minimal pairs in Japanese.4 In English they do,
as evidenced by word pairs such as long-wrong, light-
right, hail-hair.
Toward the end of the 3- to 8-month period,
another remarkable, auditory-perceptual skill can be
observed among infants. Around 6 to 7 months of age,
infants show an ability to identify specific words within
the ongoing stream of speech. The speech acoustic
signal from connected speech does not show obvious
boundaries between words, and indeed the continuous
stream of sounds often makes the process of word iden-
tification difficult for digital speech recognition pro-
grams. Adults have little difficulty with this skill, but
at some point infants must (and do) learn to perform
segmentation of the speech signal to extract words from
the continuous sequence of auditory speech events.
An accumulation of evidence over the past 20
years suggests that even though infants may not com-
prehend the language being spoken around them,
they are paying attention to its structural properties.
Language exposure in the first half-dozen months of
life and beyond allows infants to build up a cognitive,
statistical model of these structural properties. Presum-
ably, a product of this cognitive model around 7 months
of age is knowledge of the likely forms of words. This
knowledge allows the baby to begin extracting words
from the stream of speech.
The learned skill of identifying words in the con-
tinuous stream of speech is probably the basis for an
increase in comprehension of language toward the
end of the 3- to 8-month period. Infants begin to show
comprehension of words as they approach 8 months of
age, but only within rich context. This means the word
is accompanied by supporting gestures and intona-
tion, and perhaps is spoken at a particular time of day
64 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

(e.g., waking up, or at meals), all of which contribute to
the infant’s comprehension. For example, a Mom who
leaves the house every morning with her baby may say
the word “out?” while pointing to the door; the baby
understands the word because of the rich context in
which it is spoken. The same word spoken at a different
time of day and without the supporting gesture may
not be understood by the 8-month-old baby.
Werker (2012) describes a more specific example,
relevant to the early comprehension of words, of how
the baby’s environment may shape the phonetic distinc-
tions that come to have phonemic status in the native
language. In her own words, “the cooccurrence of two
phones [she means, phonetic events] with two differ-
ent objects could help pull them apart, whereas the co-
occurrence of two phones with a single object could
help collapse the distinction” (Werker, 2012, p. 55).
What does Werker mean? Let’s imagine that a baby
who is learning American English hears the word “lap”
and “rap” in her environment. (“Come sit in Mommy’s
lap” as Mom lifts the baby into her lap, and, “Mommy
loves rap” as she turns up a tune in the car; Mommy
is old school.) Baby knows, of course, that Mommy’s
lap is a place she loves to be, and understands that
Mommy loves music with heavy beats and a steady
stream of human speech. The baby hears many ver-
sions of both words, because Mommy takes her in
her lap a lot, asking her if she wants to sit there, and
listens to a lot of rap in the car and is always telling
baby the name of the music style. Baby develops the
idea of the sounds, “l” and “r,” being associated with
different meanings because clearly, Mommy’s lap and
the music she calls “rap” are different things. This link-
age between sound differences on the one hand, and
meaning differences on the other hand, “hardens” the
“l” versus “r” sound contrast as a categorical differ-
ence — that is, the sound difference is phonemic, func-
tioning to distinguish words. A Japanese baby may
have a stuffed bunny rabbit, which her parents call
“rini” (Japanese word for “little bunny”). The Japa-
nese “r” is sometimes described as being articulated
between an English “r” and “l”, and Mom and Dad
may vary the way they say the “r” at the beginning of
“rini,” but the word is always spoken in the context of
the stuffed bunny. Baby hears the variations in the Jap-
anese “r” sound and in so doing learns to dismiss the
phonetic differences because the variation between “r”-
like and “l”-like phonetic sounds is not tied to mean-
ing differences (in this case, object differences). This is
what Werker means by a phonetic distinction being
“collapsed” — the variants of the sound are not critical
to signaling differences in meaning. In Japanese, they
are phonetic variations of the same phoneme category.
Werker’s (2012) idea about how phonetic differ-
ences may or may not become phonemic differences,
and how a child’s learning of the sound system of his
or her language is a pathway to word learning, is inter-
preted in Figure 5–2. The process of learning sound
distinctions and their relationship to word learning is
imagined in this figure as a circular, interactive pro-
cess. The left side of Figure 5–2 depicts the process of
learning the “l”-“r” distinction for babies whose native
language is English. Different speech sounds are heard
and paired with different objects or actions. The link-
age of the phonetic variation with different objects sug-
gests “l” and “r” as different categories, contributing

Words Established Words Established

Different Different
Different One
Speech Speech
Phonemes Phoneme
Sounds Sounds

Different Objects Same Object

or Actions or Action

Figure 5–2.  The learning of sounds as different phonemes (left circle) or variants of the same phoneme
(right circle). The learning of phonemes “primes” the baby to be sensitive to words with the same sounds, and
to develop early comprehension of words beginning with these sounds. Based on Werker, J. (2012). Perceptual
foundations of bilingual acquisition in infancy. Annals of the New York Academy of Sciences, 1251, 50–61.
 5  Preverbal Foundations of Speech and Language Development
to the learning of unique vocabulary items beginning
with these different sounds (“Words Established” in
Figure 5–2). The circular nature of the process repre-
sents the establishment of word items beginning with
“l” and “r” and identifies these sounds as good can-
didates for the learning of other word items begin-
ning with the same sounds. The newly learned “r”-“l”
contrast primes the baby to be on the lookout for new
words with these initial sounds. The process is inter-
active because it is not simply the accumulation of
massive amounts of speech acoustic data , as happens
when a baby is exposed to so much human speech, but
rather the organization for meaning of these sound data
by environmental data — people, objects, and actions.
The right side of Figure 5–2 shows the same pro-
cess for the baby learning Japanese. As in the case
of the English-learning baby, the Japanese baby is
exposed to phonetic variations that on close inspection
by a trained phonetician seem to be sometimes “r”-like,
sometimes “l”-like. In Japanese, these phonetic varia-
tions are applied to the same object or action, as if the
single object/thing can be represented by the “r”-like
or “l”-like variant. Unlike the case of English, the pho-
netic variants are not paired with different objects but
are “mapped” on to the same object. When the child is
exposed to multiple instances of the sound variations
applied to a single object, and many other objects,
names, and actions, she “collapses” the phonetic varia-
tions into a single phonemic category. New words can
be established within this category, but the phonetic
variants do not prime the child for “r”-like versus
“l”-like words.
8 to 12 Months:  Production
Canonical babbling may continue for several months
after its onset, certainly into the last part of the first
year of life. In some children, this most simple type of
babbling is followed by continued use of the repeated
frame, but with varied content across the syllables.
Now, along with (or instead of) “buh-buh-buh-buh”
the baby may produce “bah-dee-goo-gae,” or any num-
ber of other CV syllable combinations. This is called
variegated babbling in recognition of its varied content.
Variegated babbling retains certain features of
canonical babbling, namely, a “metered” syllable se-
quence, as if every syllable has the same duration and
“flat” melody, as if produced on a single pitch. If you
5 
I t could be part of the English lexicon, if users of the language would agree on its meaning. But at the current time, if you approached 50 people
on the street and asked them what “bahmp” means, most would probably shrug their shoulders and say they do not know. All of those people,
however, would recognize that the form of this protoword — a consonant-vowel-nasal-consonant (CVNC) form — is an allowable sequence of
sounds for the formation of English words (see discussion of phonotactics in Chapter 3).
65
listen to children or adults engaged in conversation,
you hear their voice pitch change frequently, rising
across certain groups of syllables and falling across oth-
ers. Pitch changes in speech are called intonation, and
most people can recognize “normal intonation” even
if they cannot define it explicitly. Unusual intonation,
whether the monotone speech of certain individuals
who are sad or depressed or the wild pitch changes of
a game-show host after too many cups of coffee, are
also easily recognized.
Adults are sensitive to small changes in intona-
tion — they recognize something momentous when a
baby begins to produce variegated babbling with into-
nation. It is as if the baby is trying to mimic the sound
of normal conversation but does not have the words to
convey meaning. This stage of babbling is called “jar-
gon” because the child’s utterances sound like “real”
speech even if consisting of strings of nonsense syl-
lables with varied sound content.
When children produce jargon, usually close to a
year of age, parents can expect a first, “real” word at
any time. Transitional forms between babbling and real
words, called protowords (also called phonetically con-
sistent forms), may also be heard. These are syllable-
sized utterances (usually more complex than canonical
syllables) produced by the child in a consistent way,
with a recognizable referent, apparently meant to con-
vey meaning. Protowords, however, are not part of the
adult lexicon — they are not real words. For example,
one of the author’s nephews consistently said “bahmp”
to refer to bread, either to identify it for the delight of
his easily delighted audience or to request a piece for
eating or shredding. The consistent use of “bahmp”
to refer to bread qualifies it as a protoword because
“bahmp” is not part of the English lexicon.5 Protowords
are often mixed in with jargon, and their use is another
signal that “real” words are just around the corner.
8 to 12 Months:  Perception
and Comprehension
In the 8- to 12-month period, infants continue to tune
their ability to discriminate speech sounds of their
native language. The corollary to this is the loss of
discrimination ability for nonnative sound contrasts.
Scientists believe this “sculpting” of speech percep-
tual skills is a result of continued exposure to the lan-
guage. The infant’s cognitive model of the structural
66 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
properties of the language is of prosodic form not only
for words (e.g., the relationship between stressed and
unstressed syllables) but also for the important seg-
mental (sound-level) properties.
As infants approach 1 year of age, they begin to
comprehend more language, including an increas-
ing number of words and, apparently, more complex
sentences. Before and after the first birthday, children
typically comprehend more words than they produce.
Around one year of age children also begin to com-
prehend more complex sentences. Comprehension of
complex sentences in this age period requires lots of
supporting context, as described previously for word
comprehension by children around 8 months of age.
As the first year of life is completed, infants begin
to show comprehension of some paralinguistic aspects
of communication. The term “paralinguistic” is used
here to denote nonsegmental (not associated with
speech sounds and their sequencing to form words)
aspects of voice and speech that nevertheless convey
meaning. Often, this meaning concerns the mood,
intent, or state of mind of the speaker. For example,
rising pitch across an utterance signals a question, as
in the difference between “He’s here?” versus “He’s
here” (for wh- questions, the rising pitch is not neces-
sary).6 Another example is loudness of the voice, which
can signal a range of speaker moods and intents. “Bed
time” means something very different spoken loudly
as compared to a soft, gentle version of the utterance.
Paralinguistic aspects of language are complex (ask
anyone who has aspired to be an actor), but by the end
of the first year, infants are beginning to comprehend
their meaning.
Gesture and Preverbal
Language Development
People gesture when they speak; this is hardly a sur-
prise. Perhaps a less obvious aspect of gesture is its
integral role in communication. Adults, and children
who are past their first words and on their way to two-
word utterances, coordinate gesture with oral speech.
Gestures play more than a supporting role in convey-
ing meaning. Indeed, gesture may accomplish com-
municative goals not easily conveyed by oral speech
such as (for example) representation of shape, size, and
orientation of an object that is being discussed (Brentari
& Goldin-Meadow, 2017; Goldin-Meadow, 2017).
6 
 he distinction between the intonation of statements (declarative utterances) and questions may be disappearing to some (or a large) degree.
T
In young people, there is a growing tendency to produce statements with a rising pitch. This is called “Uptalk” and seems to be more common
in young women compared with young men. Some writers trace this trend to the early 1990s. The author believes a catalyst for the widespread
use of this conversation style is the dialogue in the film “Clueless” (1995). For more on Uptalk, see Tyler (2015).
Gesture plays an important role in preverbal lan-
guage skills as well. Many gestures are initiated by par-
ents in their interactions with the baby. The gestures
accompany recurring actions (“where is it?”; “more”;
“all gone!”), emotional states (smiling, surprise, sad face),
and representation of object properties, as noted just
previously. As the baby enters the fourth month and is a
more active communication partner, pointing becomes an
important gestural component of communication interac-
tions. Parents connect spoken words to people, objects,
pictures, and actions by pointing at them. The baby hears
and sees a multitude of this coordinated communication
act, even for the same person, object, and so forth, and
learns the idea of a word (the spoken label) as well as the
potential utility of their own pointing gestures to request
a spoken label. Pointing therefore serves as a builder
of comprehension vocabulary in early babyhood and
throughout the first year of life and months after as well.
Pointing also serves to establish what is called joint
attention. Around 6 months of age, babies will follow
a point and look at the object or person to which (or
whom) the point is directed (Rohlfing, Grimminger, &
Lüke, 2017). The point joins the attention of both par-
ent and child to the object, or to the person, or in more
advanced cases to an action such as “running” (“Look,
the boy is running”). The emergence of pointing is a
landmark stage in preverbal language skills. Early
pointing may even predict the speed and sophistication
of language development in the first few years of life.
Conversely, some scientists believe delayed pointing
or its absence can be predictive of delay or disorder in
language development (Lüke, Ritterfeld, Grimminger,
Liszkowski, & Rohlfing, 2017).
Chapter Summary
Throughout the first year of life, babies learn a range
of linguistic and general knowledge skills that serve as
the foundation for language skills.
The skills include preparation for producing and
understanding language.
Three chronological age periods, 0 to 3 months, 3
to 8 months, and 8 to 12 months, are presented as age
ranges during which preverbal skills are developed;
the age ranges are somewhat arbitrary due to the large
chronological variability among children’s mastery of
these skills.
 5  Preverbal Foundations of Speech and Language Development
In the 0- to 3-month period, babies are able to dis-
tinguish closely related speech sounds but do not truly
comprehend language; during this period, their sound
production is dominated by vocalizations that do not
convey intention meaning.
In the 3- to 8-month period, babies begin to com-
prehend simple aspects of language, but a rich context
is needed to support comprehension.
Comprehension skills improve throughout the 3-
to 8-month period, but a rich context remains an impor-
tant component of language understanding
Early in the 3- to 8-month period, sound produc-
tion is characterized by coos and goos, and toward the
end of the period babbling emerges.
Canonical babbling, consisting of consonant-
vowel, repeated syllables, is the first syllable type
produced by babies, followed by variegated and then
jargon babbling.
In the 8- to 12-month period, children begin to
understand more complex utterances and have espe-
cially good comprehension skills with rich context.
Production skills in the 8- to 12-month period may
include protowords, also called phonetically consistent
forms, which are not “real” words but are used consis-
tently to refer to a specific toy, pet, parent, and other
objects/people.
First words are usually produced around 1 year
of age.
A good deal of theoretical controversy surrounds
how and why babies develop language skills through-
out the first year of life.
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gence. Annual Review of Linguistics, 3, 363–388.
Eimas, P. D., Siqueland, E. R., Jusczyk, P., & Vigorito, J. (1971).
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& Iverson, P. (2006). Infants show a facilitation effect for
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1251, 50–61.

Typical Language Development
Introduction
Typical (normal) language development is variable in
children. Some children develop language skills early,
some late, but most typically developing children
attain approximately equivalent levels of language
skill by the age of 5 or 6 years. Like preverbal lan-
guage skills, the sequence and milestones of normal
language development described in this chapter are
appropriate for the “average” child.
Some may argue that an “average” child does not
exist, and that variability in language development
among typically developing children can be tied to
environmental and cultural variables. For example, an
infant who has been spoken to a great deal by primary
caretakers may emerge as a child who develops lan-
guage very quickly. Substantial language stimulation,
however, may be culture specific. In some cultures,
adults do not direct much speech to children. For
example, a child reared in such an environment, or in
any environment with relatively infrequent language
stimulation, may have fewer words at 18 months com-
pared with an 18-month-old child who is spoken to a
lot, but the relatively small spoken vocabulary must
be evaluated relative to the prevailing environmental/
cultural influences. This child’s small vocabulary may
reflect a substantial influence of his culture. A good
summary of potential environmental/cultural influ-
ences on language development is given by Roseberry-
McKibben (2007, pp. 47–49).
6
The social setting in which a child matures, her
perceptual, cognitive, and conceptual skills, plus
linguistic factors, all have the potential to influence
language development (Johnston, 2006). These fac-
tors probably interact in different ways for different
children, accounting in part for the wide variability
in language development milestones observed across
children. The reader should keep in mind these poten-
tial influences on a child’s language development.
Table 6–1 presents a summary of language develop-
ment sequences and milestones for the typically devel-
oping child. This table includes information covered
in Chapter 5, summarizing how infants move through
coos, goos, and babbling stages as they approach the
end of the first year and the production of their first
word. Between 12 and 18 months, toddlers add 7 to
11 words per month to their vocabulary, for a total of
about 50 production words at age one and a half years.
These words are most often spoken as single-word
utterances, as if the child does not have the concept of
a sentence. At this point in development, the compre-
hension vocabulary is typically larger than the produc-
tion vocabulary.
Around 18 to 24 months, toddlers experience a
vocabulary “spurt,” adding a huge number of words to
their vocabulary and beginning to combine them into
simple two-word utterances. Between 2 and 3 years,
vocabulary continues to grow, utterances become lon-
ger, and children begin to use bound morphemes in an
appropriate way. During this period, children begin to
69
70 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Table 6–1.  Summary of Stages (by Age Range) of Typical Language Development

Age Range Language Skills

Newborn May be able to discriminate certain phonemes; may attend to
specific voices

1–3 months Coos, goos, probably not used intentionally for communication
purposes

3–6 months Onset of canonical babbling toward later end of age period

6–8 months Variegated babbling toward end of period, comprehension of

words in rich contexts

8–12 months Jargon, consistent phonetic forms (protowords), first word toward
end of first year, comprehension of sentences in context

12–18 months New words gained until a total of about 50 at the end of this period;
more words comprehended than produced

18–24 months Vocabulary “spurt” as a result of naming insight; two-word

utterances toward the end of the period, vocabulary of about
200–300 words, many more words comprehended and sentences
understood in rich context

2–3 years Usage of grammatical morphemes, longer utterances (three-word,

possibly four-word utterances), typical mean length of utterance
(MLU) around 1.5–2.5; comprehension excellent for simple
sentences, more complex sentences understood with context and
in familiar settings

3–4 years Vocabulary growth, continued mastery of grammatical morphology,

MLU ~3–4

4–5 years More complex sentences, developing pragmatic skills for

conversation and understanding of more complex sentences;
MLU ~3.5–4.7; relative clauses, coordination, passive forms;
metalinguistic skills begin to develop

5–6 years Mastery of grammatical morphemes complete, continued

development of conversational and narrative skills

7 years and Expanding vocabulary, production and comprehension of complex

beyond sentence forms, various metalinguistic skills improve into college-
age years

learn conversational and narrative skills as well, devel-
oping the pragmatic skills for effective communication
in real-life situations.
During the fourth year, vocabulary continues to
increase along with longer and more complex sen-
tences. By age 5 years, most typically developing chil-
dren are beginning to recognize that language has a
structure built from individual components (e.g., chil-
dren begin to recognize that words consist of individ-
ual sounds). Past age 5 years, language gains include
expanding vocabulary, comprehension, and production
of increasingly complex sentences, and language sub-
tleties such as understanding and telling jokes, social
use of language (“pragmatics,” such as turn-taking in
conversation, and understanding nonverbal cues to
communication such as facial expression and gesture).
The development of reading skills is likely to affect oral
language, both comprehension and expression (pro-
duction), and the development of oral language skills
is likely to affect reading skills. Mastery of high-level
vocabulary skills and sentence-level utterances con-
tinues into college-age years and beyond. Throughout
these developmental stages, language comprehension
including morphology, syntax, vocabulary, and prag-
matics is likely to be more sophisticated compared with
language expression (production).

12 to 18 Months
Between the ages of 12 and 18 months, a typical child
learns to produce about 50 words. These 50 words
are mostly nouns, including specific names for peo-
ple (“Mama,” “Dada,” “Muffy”), body part names,
food names, and names of other familiar objects (e.g.,
“book,” “cup”). The nouns included among the first
50 words tend to be very concrete — abstraction is
not prominent in the toddler vocabulary — and are
used frequently by both caretakers and the child.
A smaller number of the first 50 words are verbs such
as “run,” “walk,” and “play.” There may also be a few
adjectives such as “allgone,” “dirty,” and “cold,” and
a few greeting words (“bye-bye”) and function words
(e.g., “where,” “for”). Many of these observations
about the first fifty words are described by Nelson
(1973; 1981).
As in preverbal language development, compre-
hension outpaces production in the 12- to 18-month
period. If the relationship between comprehension
and production is measured in number of words recog-
nized versus spoken, an 18-month-old toddler under-
stands many more words than she produces. Children
in this age range may also appear to understand com-
plex sentences, but they are probably using context
and familiarity to comprehend these utterances. With
context eliminated, as in a laboratory experiment, sen-
tence understanding is probably limited to fairly sim-
ple utterances.
Much has been made of the phenomena of over-
extension and underextension in the child’s first fifty
words. When a toddler overextends the meaning of a
word, the semantic category is too broad. For exam-
ple, the toddler who refers to all four-legged animals
as “doggie” is generalizing from experience with the
family dog. Similarly, if Daddy has a beard, all men
with beards become worthy of the name. When over-
extension is viewed within the framework of linguistic
category formation, the establishment of different and
distinctive semantic categories is still at a very early
stage, as are the mental representations for different
four-legged animals. There is an ongoing process of
refinement of these categories as the child is exposed to
more linguistic data provided by parents, other adults,
and video.
The opposite phenomenon is underextension, in
which a single example of an object-word link becomes
sufficient to define an entire semantic category. Muffy,
the family dog, becomes the only dog in the world.
When Mom points out Spike the slobbering bulldog to
her 16-month-old and asks, “What’s that?,” the baby
does not respond because Spike, or any dog other than
Muffy, have not yet contributed a valid representative
6  Typical Language Development 71
to the doggie category. At this stage of language learn-
ing only Muffy qualifies as a doggie. For the child who
underextends a word such as this, the link between
object and meaning is entirely specific to the context
in which the object is named — the familiar four-legged
animal in the baby’s house, whom she has known for-
ever as a doggie.
18 to 24 Months
As the end of the second year is approached, some-
thing interesting happens to change the rate at which
toddlers add new words to their spoken vocabulary.
Up to this point, children have added roughly 7 to
11 new words per month, largely by constant repeti-
tion by caregivers of object-word links. Mom or Dad
has pointed to the dog many times and said the word
“doggie” before the toddler produces the word. Some-
time late in the second year, toddlers have a “nam-
ing insight,” which allows them to do fast mapping of
spoken words to objects, actions, descriptions, and so
forth. It is as if the child suddenly realizes, “I get it,
when something is pointed to and Mom uses a word
at the same time, that must be the name of the object!”
Now the child appears to need only a single instance
of object-name or action-name pairing, and the word
enters the spoken vocabulary. When the child has this
naming insight, he or she experiences a large spurt in
spoken vocabulary.
The child’s newly found skill of fast mapping is
likely to result in 20 to 40 new words per month. By
24 months, this vocabulary spurt results in a vocabu-
lary size of 200 to 300 words.
Toward the end of the second year, language skills
gain in sophistication, possibly as a result of the rapid
increase in vocabulary. To this point, children commu-
nicate by producing single words, but now two-word
utterances are heard for the first time. Some scientists
believe the vocabulary must reach a relatively large
size (for a toddler, at least), before the two-word utter-
ance stage is entered. In this view, a critical vocabulary
size “bootstraps” the grammatical step to two-word
utterances. Additional detail on multiword utterances
is provided later in the section entitled, “Multiword
Utterances, Grammatical Morphology.”
At 2 years of age, language comprehension skills
continue to improve, sharing a lot of the characteris-
tics of earlier stages of language development. Par-
ents often overestimate their toddler’s comprehension
abilities, when comprehension is defined as the abil-
ity to understand utterances in the absence of context.
Children use their growing fund of world knowledge,
however, to comprehend the meaning of relatively
72 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

complex utterances, and of course, comprehension Multiword Utterances,

always includes context.1 Grammatical Morphology

Beginning around 2 years of age, two notable and

Three Years (36 Months)
By 3 years of age, an average, typically developing
child has a vocabulary size between 600 and 2,000
words. The range of words is so large because “typical”
vocabulary size depends on so many factors, includ-
ing the toddler’s history and primary environment
(socioeconomic status, caregiver style of communica-
tion, and so forth), current toys (and the range of words
associated with them), exposure to television, day
care setting, and even the way in which it is decided
that the child “has” words (such as parent report, or
from specific experimental procedures). At 3 years
of age, the largest proportion of a toddler’s words is
still nouns.
There is another reason to be cautious about iden-
tifying a “typical” number of words in a toddler’s
vocabulary (lexicon) at a given age (the same cau-
tion applies to “typical” aspects of almost any aspect
of language development). Most of the information
we have concerning language development has come
from studies of English-speaking children. A recent but
growing body of knowledge is demonstrating how the
facts of language development differ across languages
and even across dialects within a language. Elin Thor-
dardottir, a multilingual language scientist from McGill
University in Quebec, Canada, showed that 3-year-old
children learning Quebec French have significantly
smaller vocabulary sizes than children learning Cana-
dian English (Thordardottir, 2005). Clearly, the French-
speaking children should not be regarded as having
delayed vocabulary development relative to English-
speaking children. Rather, the difference in vocabulary
size reflects differences between the structure of the
two languages, cultural differences, or some complex
combination of the two factors. Other examples of dif-
ferent vocabulary development in different languages
can also be found in the research literature. Throughout
the remainder of this chapter, the reader should keep
in mind the potential cross-linguistic differences in lan-
guage development.
related aspects of language development are the devel-
opment of grammatical morphology and the produc-
tion of multiword utterances.
Between the ages of 18 and 24 months, typically
developing children make first attempts at combin-
ing two words to enhance their communication skills.
Early attempts may not be two “real” words, but rather
an approximation to a multiword utterance supported
by combining words with gestures. For example, Bates
and her colleagues showed that toddlers often paired
gestures with words to create early, “two-word” propo-
sitions (Bates, 1980; Bates, Thal, Whitesell, & Fenson,
1989). For example, a child may say “Daddy” and point
to a chair, meaning “Daddy sit.” In this case, the com-
municative act is equivalent to two spoken words. Sim-
ilarly, some children may mix jargon (see Chapter 5)
with real words, creating a two-“word” utterance in
which only one of the words is recognizable to an adult.
In these examples, the child’s use of two units
of meaning suggests an awareness of the potential to
combine words for communicative purposes. Both
examples include one “unit” that is not a “real” word ​
— ​a gesture in one case, a spoken nonword in the
other. The transition from one- to two-word utterances
may therefore not be clear-cut. Children may produce
something in between, indicating they have the idea of
two-word utterances even if there are not actually two
well-formed words.
When children begin to produce two-word utter-
ances in which both words are “real,” the utterances
have certain “baby-ish” characteristics. The utterances
have only content words and lack articles, prepositions,
and grammatical morphemes. For example, the child
who wants to indicate to Daddy that the dog has pos-
session of a bone says “Muffy toy,” not “Muffy’s toy”;
the grammatical morpheme for possession is omitted
(see later in chapter).
A good deal of effort has been devoted to identi-
fying the regularities and rules of toddlers’ two-word
utterances. There are several different ways to review
this information; we have chosen to present Brown’s

1
 here are two points to be made here. First, an experimenter can estimate a child’s “pure” comprehension abilities by presenting utterances
T
isolated from any context to obtain responses that show the presence or absence of understanding. Results may not be particularly reveal-
ing of “typical” language usage but can contribute to models and theories of language competence across development. It is important to
understand that a child’s difficulty in comprehending a complex utterance in a laboratory study does not mean the child cannot understand
the same utterance when spoken in a familiar situation. Second, certain developmental language delays may involve an inability or deficit in
using world knowledge to comprehend utterances that are beyond current “pure” comprehension abilities. Scientists may want to separate
the two sources of comprehension ability (“pure” comprehension of language from use of world knowledge to assist comprehension) to better
estimate the relative effects in certain disorders.
 6  Typical Language Development 73

(1973) perspective on this stage of utterance develop-
ment. Brown interpreted two-word utterances as ex-
pressions of broader semantic relations. In other words,
toddlers organize these simple utterances in terms of
larger, relational categories that serve as “frames” for
many different possible utterances. Table 6–2 presents
some of the semantic relations proposed by Brown,
with examples of how different utterances “fit” the
frames. Also included are possible adult versions of
the toddler utterances.
“Agents” are people, animals, action figures, and
so forth — any individual who can cause something to
happen or stand in relation to an object. “Actions” are
typically verbs, indicating action (e.g., eat, cry), occur-
rences (e.g., shine, rain), or states of being (e.g., happy,
sad). “Objects” have an obvious definition. “Loca-
tives” are words that indicate locations and directions,
as in “Muffy down.” When children use locatives, it
suggests they know about objects or agents in differ-
ent locations (e.g., “Muffy bed” versus “Muffy out”).
Note how Muffy falls into different semantic relations
depending on her status. When she is doing something,
such as eating, she is an agent of the action; when she
is located on the bed (“Muffy bed”), she is an entity in
a specific location. Other semantic categories are also
used as frames for multiword utterances. For example,
“demonstratives” is a semantic category for specifying
something that may be ambiguous (“That one,” not the
one you’re pointing to, Dad, wake up!). “Possessor and
possession” are important categories for the toddler
who views connections between agents or objects and
their owners as critical to an orderly world (“Mommy
sock” is not so critical, of course, as “Daddy TV”; a sock
is a sock, but a big-screen TV . . . ).
The combinations of semantic categories, some of
which are listed as semantic relations Table 6–2, give
the toddler a great deal of flexibility in creating a vari-
ety of utterances. Words can be “slotted” into these
frames, providing the toddler a way to communicate
about important agency, actions, ownership, and loca-
tion in her environment. The semantic relations listed
in Table 6­–2 also provide the beginning of a grammar
for the toddler, amounting to a set of simple rules for
how words can be combined to produce meaningful,
effective utterances.
The semantic categories proposed by Brown can
be combined to create longer but still incomplete utter-
ances. Between 2 and 3 years of age, for example, the
toddler may generate utterances such as “Daddy watch
TV” and “Muffy eat shoes,” using the agent+action+​
object framework, or “Daddy watch TV den” or “Muffy
eat shoes den” (ruining Daddy’s expensive loafers

Table 6–2.  Brown’s Semantic Relations as “Frames” for Two-Word Utterances

Semantic Relation Examples How Would an Adult Say It?

Agent + Action Muffy eat Muffy is eating her food
Jenny cry Jenny is crying
Daddy yell Daddy is yelling at Bobby

Agent + Object Man hat The man is wearing a hat

Jenny dress Jenny has a dress
Mommy treat Mommy has a treat

Action + Object Kick ball I just kicked the ball

Eat popsicle I want to eat this popsicle
Drive car Mommy is driving the car

Action + Locative Go park We’re going to the park

Fly up The bird flew into the tree

Entity + Locative Muffy down Muffy is downstairs

Car there The car is over there

Demonstrative + Entity That car! That other car, not this one

Possessor + Possession Mommy sock This sock belongs to Mommy

Daddy TV Daddy has a big-screen TV
74 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
and therefore his big-screen TV experience) using the
agent+action+object+locative framework. None of
these utterances are adult-like, but they show increas-
ingly sophisticated language skills as more complex
relations are expressed by fitting words into the seman-
tic relations categories shown in Table 6–2.
Expanding Utterance
Length:  A Measure of
Linguistic Sophistication
After typically developing children master two-word
utterances, they extend utterance lengths in a system-
atic way. Utterance length has been a prime focus of
scientists interested in language development. As we
will see, consideration of how utterance length changes
as a child develops must include an account of gram-
matical morphology and how it is mastered.
In Roger Brown’s (1925–1997) 1973 book (Brown,
1973) he reported a detailed analysis of the early lan-
guage development of three children (Brown christened
them Adam, Sarah, and Eve). The observations were
longitudinal, meaning for each of the three children,
language samples were collected and analyzed over
time, as the children developed their skills. In addition,
the language samples analyzed for Adam, Sarah, and
Eve were taken from spontaneous utterances produced
in conversation with their mothers (and occasionally
other caretakers). Brown was interested in an account
of genuine, functional language development, rather
than the kind of data collected in a highly structured
experiment. Eve’s language was first sampled when she
was 18 months old, and Adam’s and Sarah’s when they
were 27 months old. Importantly, all three children had
roughly the same average length of utterance when the
longitudinal observations began. In this sense, at the
beginning of the longitudinal observations, the three
children were more or less at equivalent stages for the
complexity of their multiword utterances.
Mean Length of Utterance (MLU)
The idea of using the average (mean) typical length of
a child’s utterance as a measure of language sophistica-
tion was one of the conclusions of Brown’s study. In fact,
the measure he called mean length of utterance (MLU) has
become an “industry standard” as an index of language
sophistication. The computation of MLU is straightfor-
ward, even though the process of collecting and analyz-
ing usable data demands great care and patience.
2 
 hese morpheme counts demonstrate that there are cases in which the number of morphemes is not crystal clear: Is “Daddy’s” two or three
T
morphemes? (Dad + y (morpheme for diminutive) + possession morpheme, ’s). In the two examples, we count “Daddy” as one morpheme.
First, an adequate sample of spontaneous speech
must be obtained from a child, perhaps while the child
is playing with a parent. The utterances produced dur-
ing this interaction are recorded, along with Mom’s part
of the conversation, and the number of morphemes per
utterance is counted, and the sum of all morphemes
across the total number of utterances is divided by the
number of produced utterances.
Table 6–3 shows a simple example of the computa-
tion of MLU. Ten utterances from a 3-year-old child are
shown in the left column along with the Mom’s part
of the conversation; the number of morphemes for
each child utterance is given in the right column. Some
utterances are short (e.g., “Throw there,” “In street,”
both with two morphemes), and two are longer (“Dad-
dy’s big TV broked,” six morphemes; “Daddy don’t got
football,” five morphemes).2 This kind of variability in
utterance length for a given child at a given point in
language development is not unusual.
When utterance lengths are averaged across the
10 child utterances in Table 6­–3, the computed MLU is
3.3, which is representative for a typically developing
child of this age. Note especially utterances 6, 7, and 8,
where the number of morphemes exceeds the number of
words. The child is using grammatical morphology (see
later in this chapter), and the free and bound morphemes
are counted as separate “units” in the utterances, even
when the grammatical morphology is applied incor-
rectly (utterance 6, “broked” = two morphemes).
Brown’s MLU data for Adam, Sarah, and Eve are
shown in Figure 6–1. Age in months is shown on the
x-axis and MLU on the y-axis. Two general characteris-
tics of these data are clear: (a) MLU increases for each
child as he or she gets older, and (b) there are differ-
ences between the children. Most notably, Eve (blue
line) increases her MLU from about 1.5 to just under
4.5 over a younger age range (18 to 27 months) as com-
pared with Adam and Sarah (27 to 43 months). All
three children increase their MLU in the same way, but
Eve does so at a younger age.
Like vocabulary development, data on MLU may
vary across languages and cultures. In Elin Thordar-
dottir’s study of children’s language learning of Cana-
dian English and Quebec French, at comparable ages
French-speaking children had greater MLUs than
English-speaking children. Does this mean the French-
speaking children have more sophisticated language
development skills than the English-speaking children?
The answer is “no.” Rather, the difference between the
two groups of children can be explained by differ-
ences between the languages. French has a much more
 Table 6–3.  Example of Computation of Mean Length of Utterance for Ten
Utterances, with “Units” Being Morphemes (Shown Only for Child Utterance)

Utterance Morphemes
Mom:  What do you have?
1.  Child:  See I got ball. 4

Mom:  What are you going to do with the ball?

2.  Child:  Throw there. 2

Mom:  Be careful, you don’t want to break anything.

3.  Child:  This, break! 2

Mom:  Throw it over there (points), that’s safe.

4.  Child:  Break our house! 3

Mom:  Then where would we live?

5. Child: In tree! 2

Mom:  That wouldn’t be much fun.

6.  Child:  Daddy’s big TV broked. 6

Mom:  With the ball?

7. Child: I’m laughing! 4

Mom:  What’s funny?

8.  Child:  Daddy don’t got football. 5

Mom:  Not a bad idea!

9.  Child:  Throw at TV? 3

Mom:  Um, not a good idea . . .

10. Child: Not good. 2

Total Utterances: 10 Total Morphemes: 33

MLU = 33/10 = 3.3

4.5

4.0
MLU (morphemes)

3.5
Figure 6–1.  Plot of MLU data (y-axis)
as a function of age (x-axis) for the three
3.0
children studied by Brown (1973). Adapted
and modified from Brown, R. (1973). A first
2.5 language: The early stages. Cambridge, MA:
Harvard University Press.
Eve
Adam
2.0
Sarah

1.5
18 22 26 30 34 38 42
AGE (mos.)

75
76 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
extensive system of grammatical (bound) morphemes
as compared with English, which tends to make MLU
greater for French-speaking children. In other words,
French words are more likely than English words to be
inflected — that is, to have a bound morpheme (or mul-
tiple morphemes) attached. Interestingly, when Thor-
dardottir expressed length of utterance using words
as the unit within utterances, French- and English-
speaking children did not differ.
The lesson from this cross-linguistic comparison is
that a single measure such as MLU may reflect different
things in different languages. Because MLU is typically
computed by counting morphemes, the meaning of the
measure varies across languages with different types
of grammatical morphology. “Heavily inflected” lan-
guages — that is, languages with lots of frequently used
grammatical morphemes — may appear to have higher
MLUs at a given age as compared with languages with
fewer grammatical morphemes. What may be true for
English may not be true for other languages.
Grammatical Morphology
The child who combines the semantic categories previ-
ously described for two-, three-, and four-word utter-
Table 6–4.  Grammatical Morphemes of English
Morpheme
Present progressive (-ing)
Preposition “in”
Preposition “on”
Plural inflections (e.g., “s”, “es”)
Past inflections on irregular verbs
Possessive inflections
Uncontractible copula (is, am, and are)
Articles (the, a, an)
Past inflections on regular verbs (e.g., “ed”)
Regular third person forms (-s)
Irregular third person forms (has, does)
Uncontractible auxiliary forms
Contractible copula (e.g., ’s and ’re)
Contractible auxiliary forms (e.g., ’d)
Note. The order in which the morphemes are listed is roughly the order in which they are
acquired, starting at about age 2 years. Based on Brown, 1973.
ances still sounds “baby-ish” when the utterances do
not include grammatical morphemes. When children
enter the two-word stage, they begin to use some gram-
matical morphemes that make utterances sound “com-
plete.” English grammatical morphemes are listed in
Table 6­–4, in the order proposed by Brown for their
acquisition. Early grammatical morphemes such as
the present progressive (-ing, as in “She running”),
prepositions, and plurals are mastered by many chil-
dren sometime around the third birthday or a little
after. Other grammatical morphemes may not be used
accurately even in the fourth year. What is clear, how-
ever, is the degree to which the continued refinement
of the grammatical morpheme system — think of it as
the elegant window dressing of language — adds to the
adult-like sound of a child’s speech.
Grammatical Morphology and Rule Learning
Children’s learning of grammatical morphology reflects
rule learning. For example, the “-ed” grammatical mor-
pheme for past tense is applied as a rule to verbs when
the child wants to express something that has already
happened. The child does not need to learn the past
tense morpheme for every verb; rather, he learns the
following generalization (that is, rule): when express-
Example
She running
Muffy in bed
Spoon on floor
dogs, dresses
I went (go) home; I ate (eat) candy
Muffy’s ball
Here it is! They were naughty!
The dog; A man
He walked fast; The baby cried
She walks fast
He has some; She does
Is Daddy home? You were there
Muffy’s there; They’re gone
He’d play every day
 6  Typical Language Development 77

ing an action that has occurred, attach “-ed” to the verb.
Ironically, a proof of rule learning is that children attach
the morpheme to a verb that has an irregular past tense
form. In English, verbs such as “go,” “hit,” and “run”
all have irregular past tense forms (“went,” “hit,”
“ran”). Typically developing children often overgener-
alize the grammatical morpheme for past tense by say-
ing “goed,” “hitted,” and “runned.” This demonstrates
knowledge of the rule and the ability to combine free
and bound morphemes. Part of language development
is the elimination of these overgeneralized inflections
and the learning of irregular forms.
As with the other aspects of language develop-
ment, children vary in their order of development and
the rate at which they learn grammatical morphemes.
The order of mastery proposed by Brown is not fixed,
and in fact, varied somewhat for Adam, Eve, and Sarah.
The rate of mastery of grammatical morphemes also
varies among typically developing children. “Typical”
development may include the child who masters cor-
rect use of all grammatical morphemes by age 3 years
as well as the child who continues to have difficulty
with some grammatical morphemes at age 4.5 years.
Typical Language Development
in School Years
By age 5 or 6 years, about the time a child enters first
grade, typically developing children have a relatively
large and expanding vocabulary as well as mastery of
grammatical morphology. What else is there to learn
apart from new words, grammatical morphemes,
and multiword utterances? As it turns out, there is
still plenty to learn. Here we describe three aspects
of advanced language skills and their development
throughout the school-age years. These include meta-
linguistic, pragmatic (specifically discourse), and com-
plex grammar skills.
Metalinguistic Skills
Metalinguistic skills include the ability to reflect on lan-
guage and its components, to use language in a way
that demonstrates knowledge of these components and
the arbitrary way in which they are combined. Selected
examples of metalinguistic skills include the ability to
decompose words into their speech sound compo-
nents, to use (or understand) the same word with very
different meanings, to engage in linguistic wordplay,
to be able to judge the correctness (or incorrectness) of
word order in sentences, and to recognize ambiguity in
the meaning of a single sentence.
Words and Their Speech Sound Components
An adult who is asked the question, “What happens
to the word ‘about’ when the first sound ‘uh’ is taken
away?” will answer, “You have the word ‘bout.’ ” This
answer demonstrates the ability to break a word apart
into its speech sound components. This metalinguis-
tic skill is generally not part of the language capabil-
ity of toddlers. Ask a 4-year-old the same question,
and he or she will likely be baffled by it. This meta-
linguistic skill appears around the age of 5 or 6 years.
Before children develop this skill, they seem to treat
words as “unbreakable” units: break one part (take
away the “uh” from “about”), and you break the whole
word. Perhaps it is not a coincidence that the ability
to recognize words as being made up of individual
speech sounds appears around the same time as early
reading skills.
Same Word, Different Meanings
As children figure out that words can be broken down
into sound components, they begin to understand and
possibly use the same word with different meanings.
Preschool children tend to be rigid in their under-
standing of words and may have difficulty separat-
ing a particular word from its referent. “Cold” for a
4-year-old toddler is specific to temperature and does
not make sense as a description of someone’s person-
ality (“She is cold”) or as the effect of a particularly
vicious right hook in a prize fight (“Knocked him out
cold”). School-age children begin to understand how
one word may have multiple meanings and, in fact,
how certain words may function in metaphors and idi-
oms. This metalinguistic skill is developed throughout
the school-age years and into and through adolescence.
Some words can be used in very subtle, distant ways
from their most obvious meanings (as in the previ-
ous “cold” example, or “clam,” “clam up,” clammy”).
This language skill takes a good deal of time to reach
full maturity.3

3 
J ust how often words are used by native speakers in these multiple ways, with no sense of unusual language usage (i.e., recognition of frequent
use of idiomatic linguistic forms), becomes obvious when you communicate with people who are in a second language environment and
who have what appear to be pretty good skills in that language. The author has had a number of doctoral students from Taiwan and Korea,
and when meeting with them and speaking casually, he finds himself using phrases and expressions loaded with words having a variety of
metaphorical and idiomatic meanings. It is only after these expressions have produced a puzzled expression on the students’ faces that he
realizes how much our language is like an express train, avoiding all the local stops and getting to the final destination as fast as possible.
78 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Linguistic Wordplay
Preschool children may experiment with words by
changing sounds to make them funny, but real word-
play does not emerge until the school years. There are
many different types of wordplay; much of it is designed
to be humorous. Some forms involve simple changes in
sounds of words (“Captain Brunch” to describe some-
one who enjoys those Sunday trough feedings at the
local hotel chain) or mimic a foreign accent (“zome-
where” for French-accented “somewhere”). These lin-
guistic abilities depend on the earlier-acquired skill
of decomposing words into their component sounds.
Other types of wordplay may require the skill of under-
standing multiple meanings of different words and the
same meaning for different words, as in the following
silly exchange: “Question: How can you tell when a
bucket gets sick? Answer: It looks a little pale.” Still
others require much more sophisticated knowledge of
cultural slang, possibly combined with very low-level
humor: “You can tell if your doctor is a quack when
you see his large bill.”4
Pragmatic Skill:  Discourse
Pragmatics covers a wide range of behaviors that are
thought to be important to language use in social
contexts (see Chapter 3). The question of pragmatic
development as part of language development can be
stated simply as, “How do children learn the rules and
customs of social communication?” These rules and
customs may include something as straightforward as
politeness, to the more complex consideration of how
children figure out what someone means when what
they say is not what they really mean.
People who study this latter skill often refer to it as
the “presupposition” part of pragmatics, which means
placing a conversational experience within the speak-
er’s and listener’s world knowledge, and the child’s
ability to place a current communicative exchange
within the proper context.
For example, assume you have been attending
each lecture of a class, and it is the 13th week of a long,
hard, 15-week semester. In each lecture, the instruc-
tor has droned on without mercy, rarely making eye
contact with students or changing the melody of his
speech. He reads information from his slides, never
making impromptu remarks or elaborating on a point
in a natural, spontaneous way. The exams have been
as uninteresting and obtuse as the instructor. On this
day of the never-ending semester, you have brought
4 
 he word “quack” as a description of a doctor with questionable (or even fraudulent) skills is apparently derived from the 16th century Dutch
T
word “quacksalver,” meaning someone who boasts while they apply a salve to a wound, or who sells useless medicines on the street.
your 7-year-old brother to class; he is visiting and
wants to experience a real college class. As the instruc-
tor begins yet another long monologue, you turn to
a friend sitting on the other side of your brother and
say, “This class is awesome” without a surface trace of
sarcasm or irony — nothing in your facial expression,
your intonation, or your rhythm. Your statement sug-
gests nothing other than a straightforward declaration.
Hearing this, your friend knows you mean exactly the
opposite, but your little brother thinks, if this class is
awesome, maybe I want to reconsider college and instead
learn a useful trade.
This is an important part of pragmatics, and of
pragmatic development. The friend, hearing “This
is awesome” within the history and context of the
class, having had experiences with other, less immo-
bile instructors, knowing the big brother, and so
forth, used his presuppositions about the comment to
interpret it correctly: the class is clearly not awesome.
The little brother, however, does not have some of
the presuppositions available to his brother’s friend
(he had not been sitting in this mind-melting lecture
hall for 13 weeks), and even in the immediate context
of an obviously boring professor, with other students
in various stages of sleepiness, does not have the prag-
matic skill to understand the true meaning of his broth-
er’s comment.
Here we summarize the development of discourse
skills as an important part of pragmatic development.
Discourse is the broad term that includes conversation
skills and narrative (storytelling). According to Brinton
and Fujiki (1989), conversation skills include (a) turn-
taking, (b) topic management, and (c) conversational
repair.
Turn-Taking
Turn-taking during conversation is a skill, guided by
learned rules. In a conversation, you speak and when
you are finished with a thought, your conversation
partner replies, and so on and so on. People taking
part in this conversation typically know when to stop
speaking (if they have the floor), how to anticipate that
their turn to speak is near, and when to begin speaking
as the current speaker finishes. Turn-taking behaviors
seem obvious because we learn them relatively early
and so many people do take turns in a socially accept-
able way. But all of us have encountered people who
begin to speak long before their conversational partner
has finished speaking, who seem to miss those cues
that say, “I’m done with my turn in a second or two.”

The foundation for turn-taking skills is apparently
developed in infancy, when caregivers respond to
infant vocalizations as if they are participating in a true
communication exchange. Children as young as 1 year
of age seem to get the general idea of waiting until
someone speaking to them is finished before begin-
ning their own turn. By the preschool years — roughly
between the ages of 3 and 6 — children’s turn-taking
skills are fairly sophisticated.
Turn-taking in conversation becomes more sophis-
ticated throughout adolescence and into adulthood.
Speaking turns between members of a conversational
pair become more related, with the content of consecu-
tive utterances containing increasingly more agree-
ment in theme and factual basis (Nippold, 1998). As
turn taking becomes more sophisticated, there are
fewer off-topic turns, and people engaged in commu-
nication begin to value the perspectives of their com-
munication partners.
Topic Management
Topic management is what conversational partners do
to maintain a sensible spoken interaction. Conversa-
tion about a shared topic makes for sensible commu-
nication. If this sounds slightly ridiculous as an aspect
of language development, consider this: In a study of
conversations between toddlers aged 19 to 38 months
and their mothers, the youngest children shared top-
ics with their moms about 56% of the time, the old-
est about 76% of the time (Bloom, Rocissano, & Hood,
1976). Sometime between the ages of 2 and 3 years,
toddlers learn something about how to stay on topic
during a conversation.
The mastery of topic management as a compo-
nent of language development is difficult to pin down
because the definition of “topic” is loose and open to
different interpretations. Even with disagreements
concerning the fine points of what does and does not
constitute a conversational topic, the following two
examples make the point nicely, and easily, as 5-year-
old Bart tries to sample opinion from two of his friends
on his favorite football team:
Example 1
Bart:  What’s wrong with the Packers?
Milhouse:  Brett Favre is my favorite.
Bart:  He . . . he’s too old.
Milhouse:  He’s probably cold up there, he’s from
way down.
Bart:  Sacked again!
6  Typical Language Development 79
Example 2
Bart:  What’s wrong with the Packers?
Ralphie:  My doggie doesn’t know where to go to
the bathroom.
Bart:  Maybe they need a new quarterback . . .
Ralphie:  Watch my nose open and close all by itself!
Bart:  Do you care about the Packers?
Ralphie:  Okay, I’ll come back and play later.
These examples suggest that even if the nature of
the “topic” is hard to define, in many cases, it is easy
to tell when one member of a communication “dyad”
(two people in conversation) is off topic. Anyone who
has interacted with a small child knows that Example 2
is certainly possible. Throughout adolescence and into
adulthood, topic management is likely to change, with
fewer topic shifts per conversation and longer times
spent on a given topic (Nippold, 1998).
Conversational Repairs
One aspect of joint conversational efforts is the way in
which miscommunications are handled. In conversa-
tions between two adults, an adult and child, or two
children, there are instances of uncertain meanings,
unintelligible words, and ambiguous referents (e.g.,
when a speaker says “he,” who does he mean if the
person has not been identified previously?). The pro-
cess by which speakers or listeners “flag” a miscom-
munication and fix it is called conversational repair.
Here are two examples of conversational repair:
Example 3
Bart:  The Packers are huge!
Milhouse:  But I thought you said they’re no
good . . .
Bart:  No, they’re big guys, look at those linemen!
Example 4
Bart:  What is up with those CB’s?
Milhouse:  Huh, CB’s?
Bart:  You know, cornerbacks, the guys who can
intercept passes.
In the first case, Milhouse misinterprets Bart’s use
of the word “huge” to mean “good.” Milhouse is con-
fused because Bart had expressed his concern with the
Packers’ poor performance (Example 1). Bart repairs
80 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
the conversational breakdown by specifying his use of
the word in literal terms. The second example, referred
to as a clarification request, is a little more straightforward
as Milhouse simply does not know what “CB’s” means.
Bart repairs the conversation by defining the term.
Conversational repair skills develop throughout
childhood, although it is difficult to specify ages at
which particular kinds of repair (and there are many
more than the two examples given previously) are
learned. Clarification requests like the one in Example 4,
or simpler versions, as when a listener says “Huh,”
“What,” or responds to a statement with a quizzical
look, may be observed in children as young as 24 to 26
months. Other types of conversational repair, such as
a sequence of clarification requests that converge on
the intended meaning of the speaker (several requests
for clarification that become increasingly more spe-
cific) probably develop at a later age, perhaps around
36 months. More advanced conversational repair skills
continue to develop throughout the school-age years
and into adolescence.
Narrative
The term narrative means, in the simplest sense, story-
telling. A narrative can be an account of an event, a per-
suasive speech, or any extended sequence of utterances
(or paragraphs, in writing). A narrative can be elicited
from a child by asking a question such as, “Tell me
about your summer vacation” or “Tell me what hap-
pens in the movie Moana.” The child responds by pro-
ducing a series of utterances which are meant to “hang
together,” so that the result is a sensible narrative.
Utterances within the narrative can hang together
in a number of ways. They can have a consistent theme,
can be sequenced appropriately, can have explicit ref-
erents (can include all the information required by the
listener to understand the narrative), can use cohesive
devices such as pronouns and conjunctions to link
individual sentences with each other, and can be told
with a minimum of repetitions and alternate formula-
tions of the same statement. Here are two narratives
in response to the same question, produced by male
children around the age of 6 years; one hangs together,
and the other does not.
“Tell me what you did on your summer vacation”.
Well, we went to a mountain camp, which was at a
lake. They had guides who helped us and fed us lunch
every day, you know, hot dogs, chips, and pop and
stuff. They showed us how to, like, hike through the
forest around the lake, and sometimes there would be
animals, like bighorn sheep and these funny little guys
that looked like beavers. One time, one of those beaver
guys ran right across the trail and he like scared us,
even the guide. So he said we should keep our eyes
open for other animals on the trail, and then we were
really wide awake, man. Really. At night we would sit
around a, um, campfire and eat dinner and sing and
tell scary stories. Those were fun, lots of fun. Some-
times we wouldn’t go to bed until midnight, or maybe
even later. I think I’ll go back next summer.
“Tell me what you did on your summer vacation.”
This place had water and animals right in front of us.
He told us it was dangerous. The sheep and every-
thing. Those sheep, um, something else, too. I had a hot
dog and chips. We had some food, hot dogs. A bunch
of us went hiking. One time the guy told us to watch it.
The beaver animal. He said some scary stories; I cov-
ered my ears. The campfire was really hot; they gave us
paper plates for our food. I liked staying up late. I wish
the pop was a different flavor, I don’t like cola.
Some of you reading these examples are prob-
ably familiar with a slightly less obvious version of the
disorganized, second narrative — the ones you hear in
some lecture halls. The point is made by comparing
the two narratives: relating something in a coherent
way requires a consistent theme, a sensible sequence,
and grammatical devices to tie the different sentences
together. These cohesive devices are bolded in the first
narrative and nearly absent in the second one. Notice
especially the pronouns “he” in the fourth and fifth
sentences of the first narrative; these refer to different
entities (the first to the beaver-animal, the second to
the guide), but the listener has no problem knowing
who or what is being referred to. This is because the
narrative is well formed and therefore removes any
ambiguity that may arise as a result of the consecutive
use of the same pronoun. In contrast, the referents of
the two “he” pronouns in the second narrative (sec-
ond and tenth sentences) are not at all clear, because
the overall theme is unfocused, and the sentences are
oddly sequenced.
Narrative skills develop continuously, probably
well into adulthood, but it is not easy to attach ages
to the development of specific skills. Nippold (1998)
has said that from about age 5 years onward, narrative
skills are improved by increasing the length of stories,
including more details within them, incorporating sub-
themes within the major theme, and providing smooth
transitions between the various episodes of the story
(that is, not just jumping from episode to episode, as

might be the case for young children). The develop-
ment of narrative skills is important not only because
it serves an important social function, but because
adults — especially teachers — may make judgments
concerning a child’s intelligence and potential based
on the child’s ability to tell a coherent story.
Complex Sentences
When children begin school, their utterances are likely
to be relatively short and simple in grammatical form.
From about age 5 years, children begin to use more
compound and complex sentences, which increase the
length of their utterances (Nippold, 1998). A compound
sentence contains two independent clauses joined by
a conjunction (e.g., “I have a test today so I am going
to study”), and a complex sentence contains at least
one independent and one dependent clause (“I have
a test today if the instructor did his job”). These two
examples are a simplification of the many ways in
which sentences can have complex syntax. The impor-
tant point is, the use and understanding of these com-
plex forms develops through the school-age years and
adolescence.
Syntactically complex sentences  —  both their
production and their comprehension — are mastered
Table 6–5.  Transcripts of a Single Child’s Language Performance During Conversation With an Adult
Sample From 30 Months Old
C:  THIS BABY IS CRY/ING.
A: WHY?
A:  WHY IS HE CRY/ING?
C:  MOMMY AND DADDY GET HIM.
A:  OH, GOOD.
C:  THEY (ARE) GO(ING) UPSTAIRS.
C:  MOMMA GOT HIM.
C:  MOMMA GOT HIM OUT (OF) HIS CRIB.
A:  OH, GOOD.
C: YEAH.
A:  WHAT WAS THE MATTER?
C:  I DO/N’T KNOW.
C:  HE/’S SLEEPING WITH HIS DIAPER.
A:  SLEEPING WITH HIS DIAPER.
A:  THAT/’S PRETTY SILLY.
6  Typical Language Development 81
throughout the school years and beyond. Some con-
structions, such as passives with a conjunction (“The
dance number was turned down by the ballerina
because it was too difficult”) or the use of gerunds plus
past perfect voice (“Running through the woods was to
be her lifelong choice of exercise”) are clearly not heard
from children in the first few grades and perhaps even
through middle school. As a general rule, the greater
the syntactic complexity of an utterance, the later the
age at which it will be comprehended and mastered in
spoken language.
Sample Transcript
Table 6–5 contains a sequence of transcripts of con-
versations between an adult and a typically develop-
ing child at three ages — 30 months, 42 months, and
54 months. These longitudinal transcripts for a single
child allow direct comparison across age to demon-
strate developmental changes in language skills. The
transcripts are brief, but the child utterances show clear
developmental trends. Study the transcripts for the
changing language structures and usage, and compare
the changes to the discussion of language development
previously presented.
C:  DADDY (IS) TAKE/ING (A) SHOWER.
A:  HE/’S TAKE/ING
C:  {SHOWER NOISES}.
C:  (DO) (YOU) HEAR WATER COME/ING OUT (OF) HERE?
A:  I HEAR IT.
A:  I HEAR THE WATER.
C:  IT/’S IT/’S IT/’S IT/’S WATER RIGHT HERE.
C:  ME CLOSE/(ED) (THE) DOOR/S.
A:  YOU DID.
A:  THAT/’S A GOOD IDEA.
A:  THEN THE WATER STAY/3S INSIDE.
C:  {SHOWER NOISES}.
C:  HE/’S DONE TAKE/ING (A) SHOWER.
A:  HE/’S DONE [G]?
A: OKAY.
continues
Table 6–5.  continued

Sample From 42 Months Old

A:  WHAT HAPPEN/ED? C: HEY I WONDER IF THIS MIGHT BE SUPERMAN/Z
C:  SHE FELL RIGHT UP. DOG/S?
A:  SHE FELL UP HUH? A: OH.
C: {SCREECH}. C:  (SO) SO HE X HIM TO BE KRYPTO.
A: WELL WHO/’S GONNA WATCH THE BABY/S A: WHAT?
CHRISTOPHER? C: BECAUSE HIS NAME (COULD) COULD BE KRYPTO
C: THEY DON’T WANT TO HAVE GUY/S TO WATCH BECAUSE HIS HIS HIS NAME IS THAT/’S THAT/’S)
THEM. THAT/’S (WHAT) SUPERMAN/Z DOG IS NAMED.
C:  THEY DON’T WANT ANYONE WATCH/ING THEM. A:  SUPERMAN/Z DOG IS NAMED KRYPTO?
A: HEY, (CAN YOU) WHILE YOU/’RE OUT THERE, CAN C: MHM.
YOU CHECK THE MAILBOX AND SEE IF THERE/’S A: OH.
ANY MAIL? A: I THINK, IS/N’T THERE SOMETHING ABOUT
C:  THERE/’S NOTHING. SUPERMAN AND KRYPTONITE, IS/N’T THERE?
A:  NO MAIL TODAY? C: MHM.
C: NO. A: WHAT HAPPEN/3S IF SUPERMAN GO/3S BY
A:  OH THAT/’S TOO BAD. KRYPTONITE?
C:  HERE/’S THEIR DOGGY. C:  HE HE GET/3S HITTED BY IT.
A:  OH WHAT/’S HIS NAME? A: YEAH.
C:  HIS NAME IS GOODO. A:  IT/’S NOT GOOD FOR HIM, IS IT?
A:  GOODO [G]? C: UHUH.

Sample From 54 Months Old

C: WAIT. A: MHM.
C:  I THINK I KNOW WHAT THIS IS FOR. C: SEE?
A: OH. C: (THEN) AND THEN (IT) BRING/3S THE LITTLE BABY
A:  WHAT IS IT FOR? UP AND THEN IT BRING/S THE SOCCER PERSON UP.
C: I THINK THIS IS LIKE IF SOMEBODY IS TOO FAR AND C:  AND THEN IT BRING/3S THIS GUY UP.
THEY (ARE) TOO TIRED FROM DRIVE/ING THEY C: (AND THEN IT CLOSE/3S) AND IT CLOSE/3S (AND
HOOK THIS HOOK \ UP AND THEN THEY DRIVE BY. THEN DRIVE/ING) AND THEN EVERY SINGLE PEOPLE​
C: AND THERE/’S A FIRE ON THE HOOK AND (THEY) [EW:PERSON] GET/(S) HURT IN THE FIRETRUCK.
BRING IT UP HERE SO THEY CAN SPRAY IT. C:  SO THEY HAVE TO GO TO THE AMBULANCE.
A:  OH YEAH. A:  <OH MY GOODNESS>.
A:  THAT SOUND/3S LIKE A GOOD IDEA. C:  <YOU WANNA SEE>?
A:  I WONDER IF THEY NEED SOME HOSE/S. A: YEAH.
C:  THIS IS A HOSE. A:  I WANNA SEE THAT.
A:  IT IS A HOSE. C:  THEY TAKE THE THING OUT.
A:  YOU/’RE RIGHT. C:  THEN THEY TAKE OUT THE BED.
A:  THAT/’S A BIG ONE. C: THEN THE BABY GET/3S ON (AND THEN) AND THEN
C: LOOKIT. THE OTHER PERSON GET/3S ON.
C:  (THEY/’RE LAY/ING) THAT ONE FIT INTO THE BACK. C:  AND THE OTHER PERSON GET/3S ON AND THEN>
C: SEE? C:  (AH) THAT PERSON (IS/N’T) IS PRETTY SAFE.
A:  THEY ARE SO LUCKY. C:  SO THIS GUY ISN/’T GO/ING.
C:  AND THEN WATCH.
C: THE PEOPLE WITH SPECIAL LITTLE BED/S SO THEY
ALL LAY DOWN ON THE BED [EU].

Note.  The samples were taken at 30, 42, and 54 months. Child utterances are indicated by “C,” Adult utterances are indicated by “A.” Gram-
matical morphemes that were produced are preceded by a forward slash; grammatical morphemes and other words that were omitted
are enclosed in parentheses, so the complete utterances can be inferred from reading all the words. “3S” indicates third-person singular
(as in “GET/3S = “gets”).

82

Chapter Summary
Typical language development occurs over a broad
range of ages at which milestones are reached. Age
benchmarks for major language-development accom-
plishments, such as 50 words at 18 months, initial use
of grammatical morphology around age 2 years, and
the metalinguistic skill of decomposing words into
component sounds around age 5 years, show substan-
tial variability across children for age of mastery.
Children’s lexicons — their vocabularies — begin to
grow rapidly when they have a naming insight and,
with a single trial of having an object labeled, “get” the
connection between words and objects and actions and
properties (such as colors or size).
The vocabulary spurt that begins with the naming
insight occurs around the same time as the appearance
of the two-word sentence.
Multiword utterances are typically combinations
of semantic categories, as originally discussed by Roger
Brown. The semantic categories are “frames” into
which children insert different words; the frames are
blueprints for acceptable sentence structures.
Two-word utterances are gradually expanded to
three- and four-word utterances. The mastery of gram-
matical morphology plays an important role in creating
longer sentences.
MLU, a measure of utterance length, is a good
index of the linguistic sophistication of a child; the
comparison of MLUs across different languages must
account for the different grammatical morphology
across languages.
Language development from the beginning of
grade school through adolescence and into young
adulthood involves expansion of the lexicon, increased
use and comprehension of sentences with complex syn-
tax, and development of pragmatic skills in conversa-
tion and narratives; although the focus of language
development is typically on the dramatic changes
6  Typical Language Development 83
occurring in the first several years of life, these later-
life language changes have a great deal of importance
for social and academic skills.
References
Bates, E. (1980). Vocal and gesture symbols at 13 months.
Merrill-Palmer Quarterly, 26, 407–423.
Bates, E., Thal, D., Whitesell, K., & Fenson, L. (1989). Integrat-
ing language and gesture in infancy. Developmental Psy-
chology, 25, 1004–1019.
Bloom, L. Rocissano, L., & Hood, L. (1976). Adult-child dis-
course: Developmental interaction between information
processing and linguistic knowledge. Cognitive Psychol-
ogy, 8, 521–552.
Brinton, B., & Fujiki, M. (1989). Conversational management
with language-impaired children. Rockville, MD: Aspen.
Brown, R. (1973). A first language: The early stages. Cambridge,
MA: Harvard University Press.
Johnston, J. (2006). Thinking about child language: Research to
practice. Eau Claire, WI: Thinking Publications
Leadholm, B. J., & Miller, J. F. (1992). Language sample analysis:
The Wisconsin guide. Madison, WI: Wisconsin Department
of Public Instruction.
Loban, W. (1976). Language development: Kindergarten through
grade twelve (Research Report No. 18). Urbana, IL: National
Council of Teachers of English.
Nelson, K. (1973). Structure and strategy in learning to talk.
Monographs of the Society for Research in Child Development,
38, 1–135.
Nelson, K. (1981). Acquisition of words by first-language
learners. Annals of the New York Academy of Sciences, 379,
148–159.
Nippold, M. A. (1998). Later language development: The school
age and adolescent years (2nd ed.). Austin, TX: Pro-Ed.
Roseberry-McKibben, C. (2007). Language disorders in children:
A multicultural and case perspective. Boston, MA: Pearson
Education.
Thordardottir, E. T. (2005). Early lexical and syntactic develop-
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Pediatric Language Disorders I
Introduction
There are many reasons why a child may have signifi-
cant difficulties in acquiring language. Hearing impair-
ment, intellectual disabilities associated with a variety
of conditions, acquired brain injury (resulting from a
traumatic brain injury, childhood stroke, seizure dis-
order, or tumor), or psychiatric problems can result
in a clinically significant language delay. The current
chapter covers language disorder of unknown cause,
language disorder associated with autism spectrum dis-
order (ASD), and language disorder associated with hear-
ing loss. As discussed later, language disorder without
an obvious cause or due to a related condition is re-
ferred to as either specific language impairment (SLI) or
developmental language disorder (DLD). The debate of
diagnostic terminology between SLI and DLD is ongo-
ing. In this chapter, the label “SLI/DLD” is used to re-
flect the usage of both terms even though clinicians and
researchers in different countries (including the U.S.)
use one or the other (see summary in Volkers, 2018).
These types of language disorder affect a large
number of children and continue into adulthood.
These disorders are not specific to race, ethnic group,
or country; they are observed and diagnosed around
the world.
7
Specific Language
Impairment/Developmental
Language Disorder
SLI is largely defined using exclusionary criteria — no
intellectual disability, hearing impairment, motor defi-
cits, autism, or other conditions that might account for
language difficulties (Leonard, 2014). Traditionally,
SLI has been defined in terms of normal range nonver-
bal IQ (score of 85 or better on standardized measure
of IQ, which is within 1 SD of the mean of 100). It
should be noted that at least in the United States the
term SLI has mostly been used by researchers, rather
than by clinicians.
A proposed alternative for the diagnostic category
of SLI is developmental language disorder (DLD). Chil-
dren diagnosed with DLD, like children with SLI, have
no obvious condition or disease that explains their lan-
guage delay. DLD may be preferred because it is a more
general term than SLI and does not exclude children
with nonverbal IQs of 70 to 85. In addition, the diag-
nostic term DLD may be more widely understood by
parents, educators, and administrators who approve
speech-language therapy for children evaluated for
language delay (Bishop, Snowling, Thompson, Green-
halgh, & CATALISE consortium, 2016, 2017).
85
86 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
SLI/DLD is the most frequent disability among
children. According to several estimates, SLI/DLD
occurs in around 7% of the population at school entry
(5 years of age) (Norbury et al., 2016; Tomblin, Records,
Buckwalter, Zhang, Smith, & O’Brien, 1997). Children
diagnosed with SLI/DLD are at increased risk for read-
ing problems as well as other academic problems. The
early language impairment and later reading problems
in school-aged children accumulate and lead to poor
school performance and a poor career outlook. Society
clearly benefits by an understanding of SLI/DLD, its
causes, characteristics, and treatment.
Even with the large variability in age milestones
and rates of learning in typical language development
(see Chapter 6), there are a surprisingly large number
of otherwise typically developing children whose lan-
guage skills are judged to be significantly impaired. In
these cases, deficits in language performance may be
primarily in the area of language production or in both
language comprehension and production.
Standardized Tests
A brief review of standardized tests
is as follows (Chapter 4). A large number of
typically developing children are tested on a
particular skill (such as vocabulary size), at a
particular age, resulting in a range of scores.
These scores are converted to standardized units
(z-scores), which are converted to a mean score
of 100 and a standard deviation of 15 points, on
either side of the mean. Sixty-eight percent of
the tested children have scores between 85 and
115 on the standardized test, and 95.5% of the
children have scores between 70 and 130.
There is a lot of variation in the language charac-
teristics of children diagnosed with SLI/DLD. A typi-
cal description of a child diagnosed with this disorder
is (a) the child did not produce his first word until 20
months of age, and at 3 years of age has an unusually
small vocabulary (e.g., less than 200 words) and is
just starting to combine words into short phrases; (b)
the child shows only minimal mastery of grammati-
cal morphemes; and (c) the child’s comprehension of
language is better than her production of language,
but both are delayed relative to typical development.
In addition, the child does not produce complex sen-
tences, may be hesitant to talk, and has problems with
social interactions.
When adults listen to a child diagnosed with SLI/
DLD, the language sounds “babyish,” as if the lan-
guage performance is mismatched with the child’s
age. Formal tests of hearing (Chapter 23) place these
children in the normal range for auditory sensitivity.
There are no obvious signs of neurological disease or
evidence of autism or psychiatric disturbance. There
is no evidence that the child has been raised in a
language-impoverished environment. Nonverbal tests
of intelligence (IQ tests), in which children do not have
to make responses requiring the use of language, reveal
IQ scores within the normal range.
SLI/DLD is a disorder with “fuzzy” boundaries.
The diagnosis is not always made with a high degree of
confidence because the delayed language may resem-
ble delayed language characteristics not only in other
disorders, but in language development in typically
developing children who are learning language more
slowly than most of their peers. Interested readers are
referred to the reviews published by Conti-Ramsden
and Durkin (2012), Kamhi and Clark (2013), Ellis Weis-
mer (2013), and Laasonen et al. (2018).
Language Characteristics
of Children with SLI/DLD
Children with SLI/DLD are like typically develop-
ing children in at least one important sense: they have
variable language skills at a specific age. Children
with SLI/DLD may have impairments in vocabulary
development, in phonology, in the use of grammatical
morphemes, in syntactic constructions, and in prag-
matics. Some children diagnosed with SLI/DLD seem
to have near-normal comprehension of language but
significant problems with the production (expression)
of language; others have marked problems in both
comprehension and production. A common thread in
children diagnosed with SLI/DLD is a marked impair-
ment in grammatical morphology, especially in pro-
ductive language.
Phonology
Children with SLI/DLD have more difficulty learn-
ing the sound structure of their language than typi-
cally developing children. At a given age, children
with SLI are likely to have more speech sound errors
than typically developing children. The problems with
speech sound development may be related to a deficit
in phonological memory, a kind of short-term memory
important for the encoding of speech sound character-
istics (Gathercole & Baddeley, 1990; Gathercole, 2006).
Children with SLI/DLD make many more errors than
typically developing children when asked to repeat
nonwords (“nonword repetition tasks”). Nonword

Phonology
This chapter and the next summarize
the language disorders of several groups of chil-
dren according to the components of language
summarized in Chapter 3. These components
are phonology, morphology, syntax, content,
and pragmatics. The first four are referred to as
“structural” components of language, the last
the social (usage) component. In this textbook,
pediatric phonological disorders are presented
in separate chapters. Why, then, are phonologi-
cal disorders presented as a potential component
of pediatric language disorders? Phonology, the
structure of speech sound systems and the rules
governing the use of those sounds, is not the
same as articulation. Articulation (phonetics) is
the physical act of producing a speech sounds;
it is a motor behavior that is not necessarily
unique to a specific language or dialect. Phonol-
ogy can be thought of as the bridge between
phonetics and language. Much as language is
organized and produced according to rules,
phonology is the organization of the phonetic
inventory into a rule-based sound system. This is
why we include phonology and its disorders as
a potential (and often-observed) component of
pediatric language disorders.
repetition errors are thought to reflect impairment of
phonological working memory. This is important
because impaired phonological memory may create
difficulty in learning new words. The smaller vocabu-
lary size in children with SLI/DLD may therefore be
due, in part, to impairments in phonological work-
ing memory (Cody & Evans, 2008; Jackson, Leitao, &
Claessen, 2016).
Grammatical Morphemes
Problems with grammatical morphemes are generally
viewed as the “signature” of SLI/DLD. Children diag-
nosed with SLI/DLD may have minimally delayed
vocabularies and even age-appropriate phonology but
significantly impaired production and/or comprehen-
sion of grammatical morphemes. The “babyish” char-
acteristic of expressive language in children with SLI/
DLD, mentioned earlier, is associated with this type
of difficulty. When a 4-year-old child produces sen-
tences such as, “That my doggie,” “Yesterday I play
with Bobby,” “Man in street,” and “My brother run to
Mommy,” the mismatch of age and grammar is notice-
7  Pediatric Language Disorders I 87
able. Children with SLI/DLD may have problems with
various grammatical morphemes (English grammatical
morphemes are listed in order of acquisition in Chapter
3). Some researchers propose that children with SLI/
DLD have particular difficulty with verb tense markers
(Rice, 2014).
Syntax
The delayed mastery of grammatical morphemes in
children with SLI/DLD may reflect a more general
problem of sentence comprehension. Children with
SLI/DLD who are diagnosed with a primarily expres-
sive language disorder still show comprehension skills
that lag those of their typically developing peers.
It is possible that the incorrect use of grammati-
cal morphemes is related to comprehension of sentence
structure. The difficulty with sentence processing (i.e.,
comprehension) is a poor model for the expression of
grammatical morphemes. This view is supported by
the finding of a relationship between sentence com-
prehension and grammatical morpheme expression
in children with SLI/DLD: better comprehension is
associated with better expression of grammatical mor-
phemes (Bishop, Adams, & Norbury, 2006).
Vocabulary
When children with SLI/DLD are given formal tests
for vocabulary size, their scores tend to be lower than
those of typically developing children of the same age
(Laws & Bishop, 2003). Vocabulary tests can be given
separately for expressive (productive) and receptive
(comprehension) abilities, and SLI/DLD children
often show a greater difference from typically devel-
oping children on the expressive test. This is consistent
with the idea that children with SLI/DLD tend to have
greater delays in expressive, as compared to recep-
tive, language skills. Besides early delays in acquiring
vocabulary during the preschool period, older chil-
dren with SLI/DLD display deficits in their breadth
(i.e., number of words they can define) and depth (i.e.,
amount of information for each word) of vocabulary
knowledge (McGregor, Oleson, Bahnsen, & Duff, 2013).
Older children and adolescents also have difficulties
with more abstract or less frequent meanings of words
(e.g., “cold” as a personality trait rather than a tem-
perature) and with nonliteral (figurative) expressions
(e.g., “feeling blue”).
Pragmatics
Helland and Helland (2017) review the evidence for
pragmatic difficulties among children diagnosed with
88 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
SLI/DLD. These children may have problems initi-
ating and maintaining conversations and may have
poor turn-taking skills. In addition, topic manage-
ment during conversations and narratives tends to be
poor, much like the examples given in Chapter 6. As
pointed out by Roseberry-McKibbin (2007) and Hel-
land and Helland, pragmatic problems lead to social
and academic difficulties; children with SLI/DLD are
often regarded as “different” by teachers and fellow
students. The perception by others as “different” may
be prompted by pragmatic difficulties such as normal
greetings (“Hi, what’s going on?”), being attentive to
the content and context of a conversation to become an
effective communication partner, and understanding
nonliteral aspects of language (“Let’s go” said as “Let’s
roll”). As discussed later in this chapter, pragmatic dif-
ficulties among some children with SLI/DLD are simi-
lar to those seen in ASD but are usually less severe.
Summary of the Language
Disorder in SLI/DLD
In the preceding profile of how language may be
delayed in children with SLI/DLD, each component
of language was presented separately. This approach
has some merit for instructional purposes, but in many
cases too much focus on the individual trees blinds
us to a proper view of the forest. Delays in particular
components of language almost certainly have conse-
quences for mastery of other components. As noted
previously, a child with significantly impaired mastery
of grammatical morphemes and who receive negative
social cues because of the “babyish” sound of their
speech is likely to initiate conversations less frequently.
This, in turn, may result in substantially less practice of
language skills, possibly resulting in lost opportunities
to develop vocabulary. A similar situation may occur
for children who have a substantial problem compre-
hending language. These children may have problems
following conversations; when they try to make con-
tributions to conversations their utterances may not be
consistent with the topic being discussed because they
have not understood it. Children with SLI/DLD may
also lose language practice opportunities when other
children or even adults do not choose them as conver-
sation partners because of their problems with topic
management.
Individual language components may, in fact, be
selectively disordered in children. This lends some
real-world validity to identification of the status of
separate language components in a child diagnosed
with SLI/DLD (or any pediatric language disorder).
The analysis of separate components of language may
also have use in guiding an intervention plan for the
child diagnosed with SLI/DLD. For example, separate
analyses of grammatical morphemes and vocabulary
may identify which component is most delayed and,
therefore, most in need of therapy. Whether the child’s
language disorder is viewed through the lens of sepa-
rate components of language, or as a disorder of mul-
tiple components of language development, the goal
is to understand how language is affected for use in
everyday life.
What Is The Cause of SLI/DLD?
The cause or causes of SLI are not well understood.
There are differing viewpoints among researchers
about possible factors underlying SLI/DLD. Process-
ing views suggest deficits in lower-level auditory
processing skills, higher-level memory abilities such
as working and phonological memory, and problems
with executive function — the ability to guide language
learning behavior, by focusing attention on important
stimuli (and by implication, to know how to ignore
other stimuli for the best learning outcomes).
An alternate view is that SLI/DLD can be explained
by language-learning problems that are specifically
related to grammatical morphology or sentence-level
syntactic constructions. More broadly, a genetic basis
for disordered learning of these specific language
components has been proposed to have a causal con-
nection with SLI/DLD (Dale, Rice, Rimfeld, & Hayiou-
Thomas, 2018).
The Role of Genetics in SLI/DLD
There is strong evidence of a genetic component in SLI/
DLD. SLI/DLD appears to be heritable, most likely as
a result of the interaction of several genes whose struc-
tures predispose an individual to have a developmen-
tal language disorder. In the case of SLI/DLD, these
several genes are likely to interact with environmental
conditions (Peterson, McGrath, Smith, & Pennington,
2007). The genetic predisposition to SLI/DVD means
that a language delay is not an inevitable outcome of
a child’s genetic profile. It is the predisposition that is
heritable; environmental influences such as extensive
versus minimal language input to the developing child
may work against or in favor of the predisposition.
Evidence for the heritability of SLI/DLD comes
from a range of studies, including twin and broader
familial studies. Twin studies reveal that SLI/DLD is
more likely to occur in both members of monozygotic
(identical) twins compared with both members of dizy-

gotic (fraternal) twins. Stated in a different way, if one
member of a twin pair has SLI/DLD, the probability
of the other member having SLI/DLD is significantly
higher in the identical versus fraternal twin pair. This
supports a genetic component in SLI/DLD because
identical twins have the same genetic profile, whereas
fraternal twins do not.
Other familial studies have uncovered evidence
of greater probability of language delay, or a history
of language delay, in relatives of a child with SLI/
DLD compared with relatives of typically developing
children (that is, a control group). The heritability of
a genetic predisposition for SL/DLD is supported by
these findings (Rice, 2013; Tomblin, 2009).
Language Delay and Autism
Spectrum Disorder
As defined by the Diagnostic and Statistical Manual of
Mental Disorders, fifth edition1 (DSM-5), (http://www​
.aappublications.org/content/early/2013/06/04/aap-
news.20130604-1), a diagnosis of Autism Spectrum Dis-
order (ASD) is made when a child has problems with
social communication/interactions and demonstrates
repetitive and restricted behaviors. Within these two
general categories of behavior, there are more specific
criteria for the diagnosis. Our focus is on the speech
and language characteristics of children diagnosed
with ASD according to the DSM-5 criteria.
Like SLI/DLD, the causes of ASD are unknown.
The Centers for Disease Control and Prevention (CDC)
estimated in 2018 that 1/59 children at 8 years of age in
the United States were diagnosed with autism (https://
www.cdc.gov/mmwr/volumes/67/ss/ss6706a1.htm​
?s_cid=ss6706a1_w). Between 2000 and 2014, there
was a dramatic increase in the prevalence of autism
(see review in Graf, Miller, Epstein, & Rapin, 2017).
Many children diagnosed with autism have some form
of language disorder in addition to the core deficit of
social communication (pragmatics), which are part of
the diagnostic criteria for this condition.
Language Characteristics in ASD
Chapter 3 described three major components of lan-
guage — form, content, and use. Form includes phonet-
ics, phonology, and morphology; content is meaning
1
The Diagnostics and Statistical Manual of Mental Disorders, version 5, is published by the American Psychiatric Association to specify diagnos-
tic criteria for disorders it classifies as “mental disorders.” ASD is included in this classification. The criteria for a diagnosis ASD have been
updated over the last 20 years and in some respects are controversial.
7  Pediatric Language Disorders I 89
(the lexicon); and use refers to pragmatics (social
communication).
At kindergarten age, 70% to 75% of children with
ASD are verbal. This group includes children with
well-developed language skills and varying degrees
of language disorders. Currently, there are not good
estimates of the proportion of children with ASD who
have language disorders in addition to difficulties with
social communication. Preschool children with ASD
who have limited language skills are referred to as
“preverbal,” and those without functional spoken lan-
guage after 5 years of age are referred to as “minimally
verbal.” Twenty-five to 30% of children diagnosed with
ASD are estimated to be minimally verbal at kinder-
garten age. Some nonverbal children may have a few
words or phrases but do not routinely use spoken lan-
guage to communicate.
Although the absence of multiple word utterances
at 5 years of age represents a significant language dis-
order (Chapter 6), these children are expected to make
gains in their language skills as they progress through
the school years (Tager-Flusberg & Kasari, 2013).
According to Boucher (2012). Even older children and
adults with autism who appear to have typically devel-
oping language skills may have subtle language differ-
ences from neurotypical children and adults (see Box,
“Neurotypical and Neurodiverse”).
Neurotypical and
Neurodiverse
“Neurotypical” is a term used primarily in the
autism community (autistic persons and their
allies) to indicate typical skills and behaviors;
the term is descriptive of what used to be
classified as “normal.” Many research publica-
tions on autism use the term “neurotypical” to
describe control groups of typically developing
(or developed) individuals. The term is not
used as the standard, but rather a point on a
continuum of brain types. A different point on
that continuum is “neurodiverse,” suggesting (in
the case of ASD) the brain type of persons with
autism. These two terms do not stand opposed
as “normal” versus “abnormal.” Rather, neurodi-
verse is regarded as different from neurotypical,
not disordered.
90 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Phonology
Phonological delays (speech sound delays/disorders:
see Chapters 13 and 15) have not been studied exten-
sively in children with autism. The lack of data may be
due partly to the clinical impression of normal or near-
normal phonetic/phonological skills among children
with autism.
Speech sound delays have been noted for a small
percentage of children with autism who have near-
typical speech and language development. The nature
of the speech sound errors is rarely reported, and the
resolution of the errors as the children mature has not
been addressed. This is important because typically
developing children have speech sound errors that
resolve during the course of phonetic/phonologi-
cal development. The speech sound errors reported
for children with autism may be similar to the errors
made by typically developing children and may
resolve without intervention (see Boucher, 2012, p. 224).
A review of speech sound disorders in children with
autism is available in Broome, McCabe, Docking, and
Doble (2017).
Morphology
Some children with ASD have deficits in morpho-
logical development. The delay may include mor-
phological markers such as tense (walk-walked) and
possessives (Bob-Bob’s) as well as other morphemes.
In children with speech and language skills that are
not severely impaired, the development of morphol-
ogy is often within age-level expectations or mildly
delayed. In fact, delayed morphological development
in some children with ASD has been described as simi-
lar to the profile of morphological errors observed in
SLI/DLD.
Syntax
The profile of syntactic development in ASD high-
lights the difference between expressive and receptive
(comprehension) language development. Syntactical
development in verbal children with ASD seems to be
near typical, and especially so for children with more
advanced language skills even when those skills are
delayed. Like morphology, expressive syntax may seem
near typical, but comprehension of syntax is not. This
split between expressive and comprehension develop-
ment becomes more obvious with more complicated
syntactical forms. An example of a difference between
a simple and more complicated syntactical form is the
sentence, “The boy came home” (simple) versus “The
boy who owns the bike came home” (more compli-
cated). It certainly is possible that children with ASD
may be less likely than typically developing children
to use (express) sentences with more complicated syn-
tax, but their comprehension of syntactical complexity
is clearly impaired.
Vocabulary
As with other language components, vocabulary skills
vary to a large degree among children with ASD. In
general, vocabulary skills in children with ASD are
delayed relative to those of typically developing chil-
dren. This is similar to the vocabulary profile of children
with SLI/DVD, as well as children with intellectual dis-
abilities (Chapter 8).
The relationship between receptive and expres-
sive vocabulary in ASD seems to be different com-
pared with typically developing children and groups
of children with delayed or disordered language
development. Larger receptive compared with expres-
sive vocabularies are the rule for these children — they
understand more words than they say. In contrast, a
significant number of children with ASD have receptive
vocabularies that are more impaired than their expres-
sive vocabularies, based on age expectations (Kover,
McDuffie, Hagerman, & Abbeduto, 2013; Kover & Ellis
Weismer, 2014).
Children with ASD may have delayed expressive
vocabularies because the new words they add tend to
be limited to word possibilities that sound alike (e.g.,
“house,” “mouse,” “ball,” “fall”; see Kover & Ellis
Weismer, 2014; McDaniel, Yoder, & Watson, 2017). Typ-
ically developing children add words from a broader
range of possibilities. It is not clear why this may be
the case, but if true, it points to a therapeutic strategy
to build expressive vocabulary in children with ASD:
extend vocabulary training items to words that do not
share sounds with words already in the expressive
vocabulary.
Why is receptive vocabulary affected to such a sig-
nificant degree in children with ASD? The answer is
not clear. One possibility is that nonverbal cognitive
abilities have a disproportionate effect on receptive, as
compared with expressive, vocabulary (Kover et al.,
2013).
An analysis of longitudinal expressive and recep-
tive vocabulary skill in McDaniel et al. (2017) was
done to evaluate the influence of receptive vocabulary
on expressive vocabulary. A large group of children
with ASD were studied over a 16-month period; the
investigators reasoned that change in receptive vocab-
ulary skill over this period would predict change in
 7  Pediatric Language Disorders I 91

expressive vocabulary skill. This is a very reasonable
expectation from the idea that the size of the receptive
vocabulary “drives” the size of the expressive vocab-
ulary. Surprisingly, the analysis did not support this
expectation (McDaniel et al., 2017).
The results of McDaniel et al. (2017) may have
important clinical implications. If the receptive vocab-
ulary does drive the expressive vocabulary, therapy
directed at improving the receptive vocabulary is a
sound idea for expanding the expressive vocabulary.
McDaniel et al.’s results, however, do not support this
approach. Perhaps therapeutic efforts to expand the
expressive vocabulary are best directed at expressive
tasks, or expressive plus receptive tasks.
Pragmatic Language
Recall that one of the two core deficits that must be
observed for a diagnosis of ASD is “problems with
social communication/interactions.” (The other core
deficit is “repetitive and restricted behaviors.”) In this
section, we focus on the core deficit of social communi-
cation/interactions.
A more precise understanding of the core impair-
ment of pragmatic language in ASD is its presence
across individuals despite a range of structural lan-
guage abilities. Structural language abilities include
phonological, morphological, syntactic, and semantic
components, which may range across individuals diag-
nosed with ASD from typically developing to severely
impaired skills. Whatever the range of structural lan-
guage skills may be, pragmatic language impairments
are always present in children diagnosed with ASD.
Many individual behaviors contribute to appropri-
ate pragmatic language. These behaviors are grouped
into five categories for observation of children 5 years
and older, listed in Table 7–1 (Cordier, Munro, Wilkes-
Gillan, Speyer, & Pearce, 2014). Several of the items
include behaviors that are not verbal but describe a
more abstract level of social communication (Baird &
Norbury, 2016). Observed impairments of the items in
Table 7–1 are not part of a formal checklist for diag-
nosis of ASD but serve as one way to appreciate the
wide range of pragmatic language behaviors and their
potential to contribute to a diagnosis of pragmatic lan-
guage impairment. Symptoms of pragmatic language
impairment in ASD may or may not appear until chil-
dren are old enough to engage in social situations in
which the impairments can be reliably observed (Baird
& Norbury, 2016).

Table 7–1.  Five General Categories, Each of Which Includes Several

Behaviors That May Be Observed in the Pragmatic Language Impairment in
Autism Spectrum Disorder

Category Examples
Introduction and Selects and introduces a range of conversational topics
responsiveness Initiates verbal information appropriate to the context

Nonverbal Uses and responds to identifiable, clear, intentional

communication body actions and movements
Uses and responds to a variety of facial expressions to
express consistent meanings

Social-emotional Considers/integrates another’s viewpoints/emotions

attunement Appropriate use of social language within context

Executive function Attends to communicative content; plans and initiates

appropriate responses
Versatile ways to interpret/connect/express ideas

Negotiation Uses appropriate methods for resolving disagreement

Expresses feelings appropriate to the context

Note.  Adapted from “Reliability and Validity of the Pragmatics Observational Measure
(POM): A New Observational Measure of Pragmatic Language for Children,” by R. Cordier,
N. Munro, S. Wilkes-Gillan, R. Speyer, and W. M. Pearce, 2014. Research in Developmental
Disabilities, 35, pp. 1588–1598.
92 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Social Communication Disorder
The DSM-5 includes specific criteria
for the diagnosis of Social (Pragmatic) Commu-
nication Disorder (SCD). This is a disorder of
social communication that does not include the
repetitive and rigid behaviors seen in ASD but
shares with it features of pragmatic disorder,
including nonverbal and verbal impairment.
In fact, some experts contend that SCD was
previously diagnosed as “Pragmatic Language
Impairment,” and others think these children were
labeled “Autism Spectrum Disorder Not Otherwise
Specified”— a category in the previous version of
Language Delay and
Hearing Impairment
Children born with hearing impairment have hear-
ing losses ranging from mild to profound. Degree of
hearing loss is defined on the basis of audiometric
findings. Audiometry, discussed fully in Chapter 23,
includes the quantification of sound energy (measured
in decibels) required for a listener to detect tones at a
series of different frequencies. According to the Ameri-
can Speech-Language-Hearing Association (ASHA),
mild hearing loss requires 21 to 40 decibels (dB) to
reach this “just detectable” criterion, moderate hear-
ing loss 40 to 55 dB, severe loss 71 to 90 dB, and pro-
found hearing loss 91 dB and greater (https://www.
asha.org/public/hearing/degree-of-hearing-loss/).
The “profound” category includes people who are
legally deaf, some of whom may be able to respond
to very high levels of sound energy with amplification
(e.g., a hearing aid). Some individuals do not respond
to any level of sound energy, even with amplification.
Epidemiology of Hearing Loss
The incidence of hearing loss is one to three per thou-
sand births (approximately 0.1% to 0.2%). Between the
ages of 5 and 9 years, the prevalence of hearing loss
increases to 2.7 to 3.5 per 1,000 children. Why is the
prevalence in school-age children higher than the inci-
dence in newborns? Possible reasons include the in-
clusion in prevalence estimates of children who were
not diagnosed with hearing loss at birth, the influ-
ence of certain medications on hearing, and the inclu-
sion of children who have acquired hearing loss
the DSM, meaning that a child had autistic-like
characteristics but did not fully meet the criteria
for a diagnosis of autism. SCD, diagnosed in
childhood, is likely to persist into adulthood.
SCD is not explained by low cognitive ability but
interferes substantially with social relationships
and academic and career performance. Children
diagnosed with SCD may also have impairments
of structural language (phonology, morphology,
syntax, and content). SCD, a controversial diag-
nosis, is discussed comprehensively by Norbury
(2014) and Baird and Norbury (2016).
due to various conditions/diseases or accidents (Kre-
mer, 2019).
It has been estimated that 54% to 68% of hear-
ing loss at age 4 has a genetic basis (Morton & Nance,
2006). Although there are many genes implicated in
congenital hearing loss, and especially hearing loss
in the severe and profound categories, a more limited
number of genes have been identified with direct influ-
ence on development of the cochlea, the sense organ
for hearing. These genes are often referred to as “deaf-
ness genes.”
Language Characteristics
in Hearing Impairment
All individuals with hearing loss are at risk for devel-
opmental speech and language impairment. The
degree of hearing loss predicts the risk of speech and
language delays in a general sense, but not absolutely.
There are children with severe hearing loss with speech
and language skills equivalent to those of children with
moderate hearing loss, and children with greater hear-
ing loss having better speech and language skills than
children with lesser loss (see Fitzpatrick, Crawford,
Ni, & Durieux-Smith, 2011, for examples of this). Led-
erberg, Schick, and Spencer (2013) have published an
excellent review of factors that may or may not contrib-
ute to speech and language development in children
with hearing loss.
Oral speech and language impairments in hearing-
impaired children make sense, because the input that
typically drives the development of speech and lan-
guage is degraded to varying degrees (mild, moderate,
severe) or unavailable (deaf). The input from parents,

siblings, and other people who speak to a baby, to a
toddler, and to older children, plays a huge role in the
development of both receptive and expressive skills for
oral language.
We use the term “oral language” to make clear that
other modalities for communication exist, and in fact
are critical to understanding language skills in persons
with congenital hearing loss, and especially children
who are born deaf. For example, deaf individuals who
are native users of American Sign Language (ASL) learn
language via a visual, rather than auditory medium.
Information is communicated as efficiently by ASL as
it is by speech, and the language has a structure of lin-
guistic rules, just like oral languages. In short, ASL is a
language like any other (Lederberg et al., 2013). ASL is
the native language of the Deaf community, the capital
“D” signifying the community whose members do not
view deafness as a disability. Roughly 10% of deaf chil-
dren are born to Deaf parents (Mitchell & Karchmer,
2004).
The discussion in the current section focuses
primarily on hearing impaired and deaf people who
choose to communicate orally, or have parents who
choose oral communication for their children. This choice
of oral communication may involve some support from
a manual language such as ASL or other manual com-
munication systems.
Speech and Language Development
and Hearing Impairment
As stated by Fitzpatrick et al. (2011, p. 605), “children
with hearing loss of all degrees of severity continue to
lag behind expectations for children with normal hear-
ing . . . in multiple communication domains.” Typically,
the issue is not so much if there is a delay, but the extent
of the delay. This is critical because delays in any or all
aspects of speech and language have significant poten-
tial to affect academic and social skills.
The following discussion of developmental speech
and language characteristics in children with hearing
loss is broad. The summaries do not necessarily apply
to every child with a hearing loss; just as in the typi-
cally developing population, different children have
different paths to speech and language learning. In
particular, and as previously noted, the pattern of
speech and language development varies broadly with
degree of hearing loss. Keep in mind, however, that the
influence of the degree of hearing loss on speech and
language development is often offset to some degree
by amplification (e.g., hearing aids) and/or cochlear
implants. Almost all of the research papers cited have
7  Pediatric Language Disorders I 93
excellent reviews of language development in children
with hearing loss, including deafness. A comprehen-
sive review of language development in deaf children
with cochlear implants is provided by Ganek, Robbins,
and Niparko (2012).
Phonology
Expressive phonological skills develop more slowly
in hearing impaired children compared with typically
developing children. In 4- and 5-year-old children with
moderate-to-severe hearing loss and either hearing aids
or cochlear implants, Fitzpatrick et al. (2011) found dra-
matically lower scores on the Goldman-Fristoe test of
articulation compared with scores of typically develop-
ing children of the same ages. The Goldman-Fristoe is
a standardized test that counts the number of correctly
articulated sounds and relates the score to expected
articulatory skills at a given age.
A significant deficit in speech intelligibility results
from the frequent occurrence of speech sound errors
among children with hearing loss. Listeners have dif-
ficulty understanding children with hearing loss partly
(and probably largely) due to speech sound errors; in
general, the greater the number of errors, the greater is
the speech intelligibility deficit.
Speech sound development in children with hear-
ing impairment depends on a number of receptive-lan-
guage factors. Hearing loss makes it difficult to learn
the acoustic properties required to develop a cognitive
representation of speech sounds. Some consonants
such as fricatives (e.g., “s,” “sh”) have less sound
energy than other consonants and are more susceptible
to the effects of hearing loss on forming phonological
representations. Phonological memory also seems to be
impaired in hearing impaired children (Halliday, Tuo-
mainen, & Rosen, 2017a). This is a short-term memory
specialized for speech sound information. Impairments
in phonological memory work against the establish-
ment of good cognitive representations of speech
sound categories.
Data on French-speaking children with mild-to-
moderate hearing loss and no other disabilities suggest
that phonological gains are made throughout child-
hood but do not “normalize” in adolescence. Halliday
et al. (2017b) and Nittrouer, Muir, Tietgens, Moberly,
& Lowenstein (2018) point to phonological skill as the
most impaired aspect of language skill in children at
all levels of hearing impairment. Phonological delays
that extend from grade school and into high school and
beyond have the potential to affect academic perfor-
mance, especially in the areas of reading and writing
(Deluge & Tuller, 2007).
94 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Morphology and Syntax
Morphological and syntactic skills are delayed in chil-
dren with hearing impairment. The degree and nature of
these delays depend on many factors, including sever-
ity of hearing loss, cognitive skills, and history of ampli-
fication (hearing aids) and/or cochlear implantation.
Delay in the mastery of grammatical morphemes
has been reported for children with mild, moderate,
and severe hearing loss. Syntax is also delayed, some-
times into the adolescent years (Deluge & Tuller, 2007).
The delays in mastery of grammatical morphemes and
syntax are observed for both receptive and expressive
language (reviewed in Halliday et al., 2017b).
Cochlear implants have a significant influence on
language learning among prelingually deaf children
(deaf before the age of 5 years). Cochlear implants
provide deaf individuals with auditory stimula-
tion that contributes to skills in all areas of language
development. In a study of deaf children aged 5 to
13 years who had received a cochlear implant (or
implants — both ears) prior to age 5 years, and had used
them for an average of approximately 6 years, children
with implants developed significant language skills,
but their expressive morphological and syntactic skills
continued to be delayed relative to a typically develop-
ing control group (Boons, De Raeve, Langereis, Peeraer,
Wouters, & van Wieringen, 2013). Within the group of
children with cochlear implants, some had morpho-
logical and syntactic skills equal to those of typically
developing children.
In general, even children who are implanted at
early ages (around 1 year old, or even younger) may
struggle with morphological and syntactic skills as
they grow older. This may be the case even when other
aspects of their language (e.g., vocabulary) are at typi-
cally developing levels (Ganek, Robbins, & Diparko,
2012). Chapter 24 presents additional information on
cochlear implants.
Vocabulary
Vocabulary is often regarded as a strength among chil-
dren with hearing impairment. Children between the
ages of 8 and 16 years with mild-to-moderate hearing
loss may have age-appropriate receptive and expres-
sive skills only slightly lower than age expectations
(Halliday et al., 2017b). When tested at age 5 years,
children who had cochlear implants before the age
of 2 years and at least 2 years of experience with the
implants, had significantly lower receptive vocabulary
skills than typically developing children. However,
when the same children were tested over two consecu-
tive years, their rate of vocabulary growth was greater
than that of typically developing children (Hayes,
Geers, Treiman, & Moog, 2009). In general, better lan-
guage outcomes can be expected with earlier age at
implantation (Ganek et al., 2012).
Pragmatic Language
As pointed out by Goberis, Beams, Dalpes, Abrisch,
Baca, and Yoshinaga-Itano (2012), very little research
has been done on social language use in hard of hear-
ing and deaf individuals. Goberis et al. developed a
questionnaire in which social language use items were
rated by parents of hard of hearing and deaf children;
these ratings were compared to ratings by parents of
children with typical (normal) hearing. The primary
findings were as follows: (a) children with hearing
loss had slower development of pragmatic language
skills compared with typically developing children,
and (b) the rate of social language learning from age 3
to 7 years depended on hearing loss category. Rate of
learning was relatively high in the mild hearing loss
group, and relatively low in the profoundly hearing
impaired group. Observation of children with hearing
loss in social language situations is needed to specify
characteristics of pragmatic language use suggested by
the parent questionnaire data. One reason that there
has not been much research on social language use in
this population is that it is not a primary area of dif-
ficulty as it is for children with ASD.
Chapter Summary
Specific language impairment (SLI) and developmental
language disorder (DLD) are two terms used to des-
ignate essentially the same disorder in children, that
of delayed language development in children who are
typically developing in every other way; in this chap-
ter, the disorder is labeled “SLI/DLD.”
SLI/DVD is the most frequent disability among
children between 3 and 5 years of age, occurring in
about 3% to 7% of the population.
SLI/DLD is typically diagnosed around the age of
3 years.
SLI/DLD is a diagnosis of language disorder in
the absence of known causes; hearing loss, autism and
other development disabilities, intellectual disability,
craniofacial anomalies, psychiatric disturbance, and
neurological disease must be ruled out as potential
causes for the language delay.
Children diagnosed with SLI/DLD may have
difficulties with all aspects of language development,

both expressive and receptive; expressive delay can
exist in the absence of receptive delay, but children
with a receptive delay are likely to have expressive
delays.
All components of language are likely to be
delayed in SLI/DVD, with especially prominent delays
in vocabulary and grammatical morphology.
SLI/DVD is a significant problem because many
of the preschool children who receive this diagnosis are
likely to experience substantial academic, social, and
career difficulties.
Strong evidence exists for a genetic component in
SLI/DLD, based on familial patterns of the disorder,
but the precise combination of genes that make a child
susceptible to SLI/DLD has not been identified.
Autism spectrum disorder (ASD) is diagnosed
when a child has a well-identified social communica-
tion disorder and repetitive and restricted behaviors.
Some children diagnosed with ASD are non-
verbal, but the great majority have language skills rang-
ing from significantly delayed to typical or even
advanc-ed; these skills are likely to improve as the child
matures.
Children with ASD have variable severity (and in
some cases, no delay) of structural language skills.
Like SLI/DLD, familial patterns of ASD have been
firmly established but the specific genes underlying the
disorder have not been identified.
All children with hearing loss, no matter the sever-
ity, are at risk for language impairment; the degree of
loss predicts the severity of the language impairment
to a substantial but not perfect degree.
A genetic, hereditable basis has been identified for
persons with deafness, although the precise combina-
tion of deafness genes has not been identified.
Expressive phonological skills develop more
slowly in hearing impaired children compared with
typically developing children; some researchers believe
that the most impaired language component in chil-
dren with hearing loss is phonological.
Impairments in speech intelligibility, resulting
from the phonological impairments, are a significant
problem in children with hearing loss.
Receptive and expressive morphological and
syntactical skills are delayed in hearing impaired
children.
Vocabulary is regarded as a relative strength in
children with hearing impairment.
Pragmatic language has not been fully studied in
children with hearing loss.
Language development in children with profound
hearing impairment seems to be optimal when a child
receives cochlear implants before the age of 2 years.
7  Pediatric Language Disorders I 95
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Pediatric Language Disorders II
Introduction
This chapter presents information on language charac-
teristics of children (and to some extent, adults) with
intellectual disability (ID). The focus is on ID and its
effect on speech and language in children with Down
syndrome (DS) and Fragile X syndrome (FXS), but the
information applies to other disorders in which ID is a
prominent characteristic.
The effects of hearing impairment on speech and
language development, discussed in Chapter 7, must
be factored into the effects of ID on speech and lan-
guage development. This is because children with
intellectual disabilities are much more likely to have
hearing impairment than children in the general popu-
lation (Carvill, 2001). The combination of an ID with a
hearing impairment makes the challenge of language
development more difficult than the effect of either dis-
ability alone. Although the combined effects of ID and
hearing impairment are not discussed in detail here,
the reader should keep in the mind the potential effect
of the combination of ID and hearing impairment on
speech and language development in DS and FXS.
DS and FXS account for the great majority of cases
of ID. Speech and language development are affected
by the intellectual disability, although not necessarily
in the same way for DS and FXS.
1
The wording of these requirements for a diagnosis of ID is a very close paraphrase of the wording in the DSM-5.
8
The term “syndrome,” common to DS and FXS,
deserves a formal definition: a syndrome is a group of
symptoms that occur together, and is seen in a series of
children (not just one child), and that represent a dis-
ease process. In DS and FXS, the grouping of symptoms
is an important part of the diagnosis; the diagnosis in
both syndromes can also be confirmed by genetic anal-
ysis as discussed below.
Criteria for a Diagnosis of ID
According to the Diagnostic and Statistical Manual
of Mental Disorders, Fifth edition (DSM-5) (American
Psychiatric Association, 2013), ID is diagnosed when
chronic impairments of general mental abilities have an
impact on adaptive functioning in three areas, includ-
ing (a) conceptual skills: language, reading, writing,
math, reasoning, knowledge, and memory; (b) social
behaviors: empathy, judgment, interpersonal communi-
cation skills, making and maintaining friendships; and
(c) practical behaviors: personal care, job responsibilities,
management of money, recreation, and organization of
tasks.1 These impairments must be observed during
childhood. Adults who acquire these impairments,
due to (for example) stroke, head trauma, or dementia
(Chapter 9), are not diagnosed with ID.
99
100 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
A 2011 analysis of the worldwide prevalence of
ID was estimated to be roughly 1% of the population
(Maulik, Mascarenhas, Mathers, Dua, & Saxena, 2011).
A follow-up analysis of a large number of international
studies, extending the work of Maulik et al. (2011),
found the intellectual disability prevalence in children/
adolescents and adults who as children met the criteria
for ID to range from 0.05% to 1.55% (McKenzie, Milton,
Smith, & Ouellette-Kuntz, 2016). The vast majority of
individuals with ID (roughly 85%) have mild, rather
than more severe, impairments.
Formal diagnosis of ID is based on standardized
scores obtained from an intelligence quotient (IQ) mea-
sure, as well as clinical observation of social and practi-
cal skills. A child diagnosed with ID typically has an IQ
score below 70. An IQ score of 70 is two standard devi-
ations below the average IQ score of 100 in the general
population. When “raw” IQ scores are standardized,
meaning they are transformed to form a normal distri-
bution with an average of 100, one standard deviation
equals 15 points; thus, an IQ score of 70 or below is at
least two standard deviations below the average of 100.
IQ scores typically reflect language skills, which
may underestimate the child’s intelligence. For exam-
ple, a child diagnosed with a language disorder may
have a relatively low IQ score due to the language-
based nature of the test. There are nonverbal IQ tests
that provide an estimate of intelligence that is indepen-
dent of language skills. It is not uncommon for chil-
dren to have nonverbal IQ scores that are higher than
IQ scores that are based in part on language skills. The
Human karyotype
Male
1 2 3 4 5 1
6 7 8 9 10 11 12
13 14 15 16 17 18
19 20 21 22 X Y
Figure 8–1.  Karyograms showing the karyotype for typically-developing (and developed) human
males (left ) and females (right ).
nonverbal IQ scores reflect the child’s cognitive ability,
which reflects skills such as reasoning, memory, and
processing speed.
ID is diagnosed based on IQ and deficits in adap-
tive behavior/functioning. Adaptive functioning refers
to the social and practical skills needed to get along in
the world. Clinical evaluation of adaptive functioning,
as well as scores on standardized tests of these skills,
are equally important as an IQ score in making a diag-
nosis of ID. IQ scores and scores on standardized tests
of social and practical behaviors are usually well below
the normal range for children who are evaluated for a
diagnosis of ID, and together support the diagnosis. In
some cases (probably very few), a child may have an IQ
score below 70 but have scores within the normal range
for both social and practical skills. Such a child is not
diagnosed with ID.
Down Syndrome (DS):
General Characteristics
The 23 pairs of chromosomes in the human genome can
be shown in an image called a karyogram, which shows
an individual’s genotype (see Box, “Genetic Terminol-
ogy,” for definitions of genetic terms). Figure 8–1 shows
karyograms for a typical human male (left) and female
(right). The chromosome pairs are numbered from 1 to
22; the 23rd pair is shown within the red circles. The
23rd chromosome pair in the male genotype has an X
and a Y chromosome, compared with the two X chro-
Female
2 3 4 5
6 7 8 9 10 11 12
13 14 15 16 17 18
19 20 21 22 X X

mosomes of the 23rd pair in the female genotype. An
individual’s sex is coded by the 23rd chromosome pair.
The genetic basis of DS is a de novo mutation (see
Box, “Genetic terminology”) of the 21st chromosome.
A de novo mutation is not inherited, but rather occurs
when the sperm joins the egg. The mutation is an addi-
tional chromosome — hence, the term “trisomy 21” to
designate a third chromosome added to the typical
pair at chromosome 21. The DS karyotype is shown in
Figure 8–2, where the added chromosome is indicated
by an arrow. There are other genotypes (genetic pro-
files) associated with Down syndrome, but Trisomy 21
is the most common and is the focus of the presentation
in this chapter. DS is the most common genetic cause
of ID. A photograph of a child with DS is shown in
Figure 8–3.
Epidemiology and the
DS Phenotype
Based on data from the years 2004 to 2006, the preva-
lence of DS is estimated to be 1 in 691 births, or 6,037
Genetic Terminology
Chromosomes:  Twenty-three pairs
of strands of DNA and proteins, each strand
carrying genes; the 23rd pair is often called the
sex chromosome because it is different for males
and females. The nuclei of most cells in the body
contain the genetic information carried by the
23 chromosomes.
Karyotype:  A description of a person’s chromo-
somes, such as, “The karyotype of a person with
Down syndrome is Trisomy 21 — a third chromo­
some added to the 21st pair of chromosomes”;
or, “The karyotype of a person with Fragile X
syndrome is damage to the X chromosome of
the 23rd pair.” A karyogram is an image of the
chromosomes arranged in the way shown in
Figure 8–1. The karyogram shows the karyotype
(https://www.quora.com/What-is-revealed-by-
a-karyotype).
Gene:  A unit of DNA, located on a chromosome,
that controls the development of anatomical
structures and traits. Genes are passed from one
generation to the next.
Genotype:  The complete set of genes in an organ-
ism, which varies across species; the human
genome is estimated to contain about 20,000 genes.
8  Pediatric Language Disorders II 101
Down Syndrome (Trisomy 21)
1 2 3 4 5
6 7 8 9 10 11 12
13 14 15 16 17 18
19 20 21 22 x y
Figure 8–2.  Karyogram of Down syndrome, showing
Trisomy 21. Arrow indicates the third chromosome at pair 21.
Phenotype:  The observable characteristics of an
individual, including traits, anatomical features,
biochemical characteristics, and so forth. A pheno-
type reflects the interaction of a genotype with
environmental factors. For a group of individuals
with the same genotype (e.g., a group of individu-
als with FXS, all of whom have the same genotype),
the phenotype is typically variable.
Mutation:  A gene mutation is a change in its
structure that differs from that gene’s structure in
most of the population. The change is not revers-
ible (that is, it is permanent) and may be inherited
(passed from generation to generation); a de novo
mutation is not hereditary but occurs when the
sperm and egg are joined and an error occurs
during cell division, resulting in a gene (or genes)
that differs (differ) from the corresponding genes
found in most of the population.
Monogenic:  A trait or condition, possibly with
many phenotype characteristics, associated with a
single gene (as in FXS).
Polygenic:  A trait or condition associated with
multiple genes (as in autism spectrum disor-
der [ASD]), typically with many phenotype
characteristics.
102 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Figure 8–3. Photo of a boy with Down syndrome.
Reproduced from https://en.wikipedia.org/wiki/Down_
syndrome. This file is licensed under the Creative Com-
mons Attribution-Share Alike 3.0 Unported license.
new cases annually (Kirby, 2017, adapting data from
Parker et al., 2010). DS is a complex condition. Like
FXS, there are many possible problems in DS, some
or all of which may be present in a given individual.
In other words, the genotype (trisomy 21) has a wide
range of phenotypes. Typically, individuals with DS
have some degree of intellectual disability and accom-
panying speech and language impairment. Additional
characteristics of a person with DS may include hearing
loss (often associated with middle ear disease), visual
impairment, congenital heart defects, sleep apnea due
to an obstructed airway, mental illness, and dementia.
Furthermore, the person with DS may be of small stat-
ure and have poor muscle tone and loose joints. The
presence or absence of these characteristics in a person
with DS may change over time. For example, demen-
tia, a chronic and usually progressive brain disease that
causes memory loss, impaired reasoning, and behav-
ioral changes, is likely to be observed in older indi-
viduals with DS. The phenotype variability includes
severity: any of the characteristics may be present in
mild, moderate, or severe form.
An individual with DS is also likely to have facial
differences, which may include a flattened face, eyes
that slant upward and have an almond shape, small
ears, a tongue that often sticks out of the mouth, and a
short neck.
Language Characteristics in DS
Speech and language impairments are common in
DS. The impairment may include deficits in phonol-
ogy, morphology, syntax, content, and social use of
language (pragmatics). Many of these deficits can be
attributed to ID, which is characteristic of DS (Wester
Oxelgren, Myrelid, Annerén, Westerlund, Gustafsson,
& Fernell, 2018). In addition, hearing loss may contrib-
ute to speech and language impairments in DS (Martin,
Klusek, Estagarribia, & Roberts, 2009).
Phonology
Acquisition of the sound system of the language is
delayed in most children with DS, with some errors
identified as disordered (i.e., not seen in typical speech
sound development; Kent & Vorperian, 2013). The pat-
tern of speech sound development often follows the
pattern seen in typically developing children, with a
variable age-of-acquisition delay and slower rate of
speech sound mastery (Chapter 13). Many adults with
DS also have speech sound errors that may be lifetime
impairments.
Some authors (e.g., Kadaverak, 2014) have stated
that the delay in speech sound acquisition in DS is a
result of anatomical differences in the speech mecha-
nism. These differences include a protruding tongue, a
small oral cavity (Xue, Caine, & Ng, 2010), and atypical
laryngeal structures as well as weakness of respiratory
muscles. Precisely how these anatomical differences
affect speech sound development is unknown. Another
factor likely to contribute to speech sound errors is dys-
arthria, or poor control of speech mechanism structures
(e.g., the articulators, and larynx) due to neurologic
deficits in speech motor control regions of the central
nervous system.
Disordered speech sound development in children
and adults with DS may involve errors for sounds that
are mastered early by typically developing children.
For example, sounds such as /t/, /d/, and /n/, typi-
cally mastered no later than age 3 years, may be pro-
duced incorrectly by children with DS, throughout
childhood and into adulthood. In addition, children
with DS make vowel errors as they learn their sound

system; as discussed in Chapter 13, vowel errors in
typically developing children are unusual past the age
of 3 years (see review in Kent & Vorperian, 2013).
Speech intelligibility is affected significantly by the
speech sound errors in DS. Wild, Vorperian, Kent, Bolt,
and Austin (2018) administered a single-word test of
speech intelligibility to typically developing individ-
uals and individuals with DS. In this kind of speech
intelligibility test, speakers record single words (such
as sheep, boot, bath, and hot), and listeners respond to
each of the recorded words by entering them via key-
board. Speech intelligibility is expressed as the percent-
age of total words presented that were heard correctly.
For example, 25 correctly heard words from a presenta-
tion of 50 words is expressed as 50% speech intelligibil-
ity. In Wild et al. typically developing children between
the ages of 4 and 5 years were close to 80% intelligi-
bility, on average; children with DS in this age range
had speech intelligibility ranging between 10% and
65%. Even at 20 years of age, individuals with DS had
speech intelligibility of only 60% to 70% (Wild et al.,
2018), well below adult speech intelligibilities which
are close to 100% in typically developing individuals.
For individuals with DS, poor speech intelligibility is a
significant problem in social interaction.
Finally, stuttering behaviors and other dysflu-
encies have been observed in approximately 30% of
children with DS; this compares with a prevalence
of stuttering among the typically developing popula-
tion of around 1% (Eggers & van Eedernbrugh, 2018).
Fluency disorders are covered in Chapter 17.
Morphology and Syntax
Morphology and syntax are both impaired in children
with DS. The impairment in these aspects of language
seems to be greater than expected from the children’s
cognitive skills. In contrast, vocabulary in children
with DS is often consistent with cognitive skill; thus,
the frequent statement in the research and clinical lit-
erature that in DS morphology and syntax are dispro-
portionately impaired, compared to other language
components (Martin et al., 2009). Language compre-
hension and expression for morphology and syntax
are both affected.
Bound morphemes (e.g., tense markers such as
-ed, third person singular such as he does [I do]) are
examples of morphological problems in DS. Syntac-
2 
I n other words, when typically developing children and children with DS are matched for cognitive skill using a nonverbal estimate of IQ, the
morphological and syntactic abilities of children with DS are significantly poorer than the abilities of the typically developing children. This
means that the poor morphological and syntactic abilities of children with DS are not accounted for by their cognitive level — the language
deficit is in excess of what would be predicted by cognition. Of course, when typically developing children and children with DS are matched
in this way, the children with DS are older than the typically developing children.
8  Pediatric Language Disorders II 103
tic impairments include difficulty with pronouns
(e.g., “Him pushed her” instead of “He pushed her”),
production of short, simple sentences unlike the more
complex sentences produced by typically developing
children with the same cognitive skill,2 and increas-
ed comprehension difficulties as utterances increase
in complexity (Martin et al., 2009). These problems
in language expression make individuals with DS
sound much younger than their chronological age.
Problems with language comprehension limit the
learning of more complex forms and therefore limit
the ability to incorporate these forms into expressive
language.
Vocabulary
Vocabulary has often been regarded as a relative
strength in individuals with DS. This applies to both
receptive and expressive vocabulary, with better skills
on the receptive side. When receptive vocabulary is
compared between children with DS and typically
developing children who are matched to children
with DS on cognitive skill (see footnote 2), perfor-
mance among children with DS is close to mental age
expectations.
Expressive vocabulary skill is not as much of a
strength as receptive skill. Delays in expressive vocab-
ulary relative to receptive vocabulary are common,
and the expressive vocabulary may be smaller than
expected based on nonverbal cognitive skills. Like typi-
cally developing children, children with DS continue
to add to their expressive vocabulary as they get older,
albeit at a slower rate compared with the former group
(Martin et al., 2009).
A recent study (Loveall, Moore Channell, Abbe­
duto, & Connors, 2019) demonstrates the potential
influence of one language component (verbs) on the
other (syntax) in language development. These authors
used a storytelling approach to obtain expressive lan-
guage samples from children with DS and from typi-
cally developing children. Children with DS produced
as many different verbs as typically developing children
but used those verbs less frequently.
Verbs, which are typically acquired after nouns in
both typically developing children and children with
DS (Loveall, Moore Channell, Philips, Abbeduto, &
Connors, 2016), require additional words to make their
meaning clear. This is unlike nouns, which can stand
104 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
alone and often do so in the early speech of children.
For example, “ball” does not need other words to make
its meaning clear, but “throw” is clarified when it is
joined to other words (“I throw the ball”). Verbs specify
the role of nouns in a sentence — that is, they require
syntax for support. Loveall et al. (2016, p. 83) explain
this interaction between verbs and syntax well: “verbs
are responsible for linking words within a sentence
together, and as such, they play a key foundational
role in syntax. If disrupted, then syntactic development
could also be impacted.”
Loveall et al. (2019) argue that the less frequent use
of verbs in the expressive language of children with
DS may have an important influence on the weak-
ness noted previously for expressive syntax. Expres-
sive syntax is disproportionately impaired in DS (see
earlier) — perhaps the less frequent verb usage of this
important “linking” vocabulary affects the develop-
ment of expressive syntactic skill.
This information, generated by carefully per-
formed research, has potentially important implica-
tions not only for diagnosis of language problems in
DS but also for therapy strategies. If expressive use of
a specific vocabulary category such as verbs stimulates
the growth of syntactic skills, a therapeutic focus on
increased use of verbs may be more than an exercise in
vocabulary building.
Language Use (Pragmatics)
Pragmatic language use is a complex skill with many
different aspects, as discussed in Chapters 3 and 7.
Examples of pragmatic language use include how
much talking is done in social situations, understanding
appropriate language use in different communication
settings, language redundancy (multiple repetitions
of the same sentences), patterns of eye contact during
conversations, and the ability (or willingness) to initi-
ate conversations (Klusek, Martin, & Losh, 2014).
Pragmatic language use in DS is widely viewed
as a weakness, in younger children, older children,
and adults (e.g., Klusek et al., 2014; Lee, Bush, Martin,
Barstein, Maltman, Klusek, & Losh, 2017; Smith, Næss,
& Jarrold, 2017). Not all aspects of pragmatic language
use are affected equally. For example, teenagers with
DS may have a deficit in indicating that they have
not understood a statement, but may have relatively
strong skills when they are asked to clarify something
they have said, or when they are narrating stories (see
review in Martin et al., 2009). Nonverbal skills in social
communication may also be a relative strength among
individuals with DS.
Pragmatic language skills in DS are typically
delayed relative to those of typically developing chil-
dren but not as affected as in FXS (especially FXS +
ASD) or ASD (see below). As with pragmatic deficits
in FXS and ASD, skills in pragmatic language among
children with DS are not only delayed but improve
at a slower rate when compared to typically develop-
ing children.
Fragile X Syndrome:
General Characteristics
FXS is diagnosed by genetic testing. In FXS, there is
a mutation of the X chromosome on the 23rd pair.
Figure 8–4 shows a karyogram with an arrow point-
ing to the area of mutation on the X chromosome of
the 23rd pair (enclosed within the red oval); there is a
slight break or discontinuity of the chromosome. The
mutation results in the group of characteristics (or a
subgroup of those characteristics) that make up the
phenotype of FXS (see Box, “Genetic Terminology”).
Both girls and boys are diagnosed with FXS (both have
X chromosomes), with boys usually having a more
severe version of the syndrome. This is because girls
have a second X chromosome that can compensate for
the single, mutated X chromosome in boys with FXS.
Much of the research literature in FXS is concerned
with boys.
The phenotype in FXS includes facial differences,
intellectual disabilities, cognitive and language disor-
ders, as well as other characteristics. These may include
anxiety, depression, visual, auditory, and psychiatric
problems. The facial differences are not necessarily
obvious at birth and may not be apparent for a while.
Figure 8–5 displays photographs of a male with FXS, as
a child (A) and as an adult (B). Note the long face with
the high forehead, the large jaw, and large ears charac-
teristic of the facial differences previously described.
The facial characteristics often gain greater prominence
with age.
Genetic testing may be done when ID is suspected
because of increasing developmental delays, perhaps
accompanied by facial and behavioral characteristics
that are increasingly like those observed in children
with FXS. The genetic testing confirms or disconfirms
the syndrome. The child may also show behaviors
consistent with ASD, such as poor eye contact, rock-
ing, and hand flapping. In fact, up to 90% of boys diag-
nosed with FXS have autistic-like behaviors, and 30%
to 50% meet the diagnostic criteria for ASD (Niu et al.,
2017). As reviewed in Chapter 7, ASD is diagnosed
with formal and semiformal tests of behavior; there is
no genetic test for the condition.
FXS is the leading heritable cause of ID. The muta-
tion on the X chromosome of the 23rd pair is passed
 Fragile X Syndrome

1 2 3 4 5

6 7 8 9 10 11 12

13 14 15 16 17 18

19 20 21 22 X Y

Figure 8–4.  Karyotype for a male with FXS. The arrow points to the
region of the chromosome in which there is a mutation. The chromosome
appears to be broken in this location.

A B
Figure 8–5.  A male with fragile X syndrome, as a young child (A) and young adult (B). Photos provided by permission
of Kelly Randels Coleman.

105
106 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
from parent to child. A child who receives the fragile X
mutation and is diagnosed with FXS may have a range
of the characteristic anatomical (e.g., the facial differ-
ences) and behavioral characteristics, and the severity
of those characteristics may range from very mild to
very severe. This is an example of a genotype being
associated with a wide range of phenotypes.
Epidemiology of FXS
The prevalence of FXS is approximately 1 in 5,000
males, and 1 in 4,000 to 8,000 females. Additional
details of prevalence and patterns of hereditary trans-
mission can be found in Niu et al. (2017) and Saldar-
riaga et al. (2014).
Children diagnosed with FXS are much more
likely to have intellectual disabilities compared with
children diagnosed with nonsyndromic ASD (e.g.,
children with ASD who are not diagnosed with FXS).
This has implications for the separate and combined
language disorders in FXS and ASD.
Language Characteristics in FXS
When relevant, the following description of the lan-
guage disorder in FXS includes discussion of the
language disorder in ASD. This is because of the over-
lap between the two disorders.
Language in all areas is typically delayed in boys
with FXS relative to typically developing agemates
because of the intellectual disability; therefore, most
investigations compare language profiles to typically-
developing children using mental-age matches. For
example, the language abilities of a 10-year-old with
FXS might be compared to a 5-year-old typically devel-
oping child because both children score similarly on a
nonverbal IQ measure. This allows us to answer the
question, “How is the language of children with FXS
similar/different from that of children at the same cog-
nitive level?”
A prominent language disorder in children (and
later, adults) with FXS is social communication impair-
ment (pragmatic language deficit). Other areas of
language deficit exist and contribute to the social com-
munication problems. Following the structure of the
previous chapter, language capabilities of children
with FXS in the areas of phonology, morphology, syn-
tax, content (lexicon), and pragmatics are presented.
Keep in mind variation across individuals in pheno-
type — children with FXS, even with a common genetic
source of the syndrome, do not have the same language
(or other) characteristics.
Phonology
Typically developing children learn the sound system
of their native language in a systematic way (Chap-
ter 13). Sounds such as stop consonants are mastered
before fricatives, /w/ before /r/ and /l/, single con-
sonants before consonant clusters, to name a few well-
known examples. Phonological processes also follow
a systematic trend. For example, the process of final
consonant deletion (“dah” for “dog”) is typically
eliminated earlier than the process of cluster reduction
(“pay” for “play” or “sop” for “stop”).
Barnes and colleagues (2009) reviewed previous
evidence for speech sound development in single-
word productions of children with FXS. This review
suggests that children with FXS have delayed, not dif-
ferent, speech sound development relative to typically
developing children. This means that the children with
FXS acquire the sound system of English with the same
error patterns as typically developing children but at a
slower rate.
The literature reviewed by Barnes et al. (2009)
included studies in which single-word productions
were analyzed. Barnes et al. wanted to know if the
same speech sound learning patterns were found in
children with FXS when the utterances were from
connected, “natural” speech. The participant groups
included children with FXS, children with FXS plus
ASD, and typically developing children. When the
data were analyzed for speech sound error patterns,
there was almost no difference between the two groups
of children with FXS (FXS alone and FXS plus ASD).
Children in both groups had more speech sound errors
compared with typically-developing children. Consis-
tent with these speech sound errors, speech intelligi-
bility was significantly lower for the connected speech
utterances of children with FXS, and FXS plus ASD,
when compared to speech intelligibility of typically
developing children. But when the children with FXS
and FXS plus ASD were matched to typically-devel-
oping children for the number of their speech sound
errors, the children with FXS were significantly less
intelligible than the typically-developing children. This
is somewhat surprising because speech intelligibility
is dependent to a large degree on the “goodness” of
consonants and vowels, and the matching across the
groups of sound errors might lead to the expectation
of equivalent intelligibility for the groups.
In summary, current research indicates that chil-
dren with FXS have speech delays with speech sound
error patterns very much like speech sound errors
observed in typically developing children during the
course of their speech sound development (Chapter 13).
The pattern of speech sound errors is similar to those

of typically-developing children, but the process of
speech sound mastery is delayed. This is similar to the
description in Chapter 15 of speech delay in otherwise
typically developing children. Even when children
with FXS are matched to typically developing children
for the stage of their speech sound development, chil-
dren with FXS are less intelligible than typically devel-
oping children. The severity of the speech intelligibility
problem in FXS is variable, ranging from essentially
normal speech intelligibility to severely unintelligible
speech. The variability of the phenotype is not well
understood. (See Box, “Embrace the Gray.”)
Morphology and Syntax
A fairly large research literature is available on the
language characteristics of children with FXS. Studies
of language deficits in FXS often report data for boys
because their language deficit, as well as the severity of
their ID, is typically worse than the deficits observed
in girls. The current review is based on information
found in several recent reviews and experiments (Fine-
stack, Sterling, & Abbeduto, 2013; Haebig & Sterling,
2017; Komesidou, Brady, Fleming, Esplund, & Warren,
Embrace the Gray
An introductory text for Communication
Sciences and Disorders must provide information
on the most current, research-generated knowledge
in a broad way. Coverage of the material must
be selective and avoid many of the research and
clinical details that are relevant to the conclusions
reached by authors. Higher-level courses build on
the general information presented in this textbook,
largely by adding details left out of an introductory
textbook. A good example is the coverage in this
chapter of the Barnes et al. study. Their conclusions
are that the phonological skills of children with
FXS, FXS + ASD, and typically developing children
are similar when matched for stage of speech-
sound development, but that speech intelligibility
is lower in the first two groups compared with
the typically developing group. This seems to be a
little odd. After all, it seems reasonable to expect a
strong relationship between the “goodness” of the
sound system and the goodness of speech intel-
ligibility. But the details of the study are revealing.
For example, Barnes et al.’s analysis is focused on
consonants and does not take account of vowels,
the articulatory “goodness” of which makes a
8  Pediatric Language Disorders II 107
2017; Martin, Losh, Estigarribia, Sideris, & Roberts, 2013;
Oakes, Kover, & Abbeduto, 2013; and Sterling, 2018).
Children with FXS, from toddlers to teenagers,
have language deficits that affect their ability to com-
municate and engage in social experiences. Deficits
in morphological and syntactical skills are frequent
among children with FXS. Morphological deficits
include (for example) tense marking (wait-waited),
proper form of the verb “is” (“he is”-“they are”), and
third person singular (“I do”-“he does”). Recall that
incorrect use of morphemes is characteristic of a brief
phase of typical language development; mastery of
most if not all morphemes is completed around age
4 years (Brown, 1973). Children with FXS take much
longer to master grammatical morphemes and may
maintain a deficit in morpheme use into adulthood.
Similarly, typically developing children master simple
sentence forms (“The boy fed the dog”) earlier than
more complex forms such as sentences with embed-
ded clauses or of greater length (“The boy who fed the
dog is Joe”). The severity of these deficits in language
form varies within the population of children with FXS.
These deficits do not necessarily involve the same mor-
phemes or syntactic forms for all children with FXS.
significant contribution to speech intelligibility.
Measures of other variables that are likely to
contribute to speech intelligibility are also left out
of the analysis. Another example is that children
in the FXS, FXS + ASD and typically-developing
groups were matched using a technique that makes
the language skills of children in the three groups
“equal.” The use of this matching technique means
that the children with FXS were much older than
the typically developing children when the conso-
nant “goodness” was compared across groups.
These strategies are controversial. Now, do not get
this author wrong: the study by Barnes et al. is a
fine study, and the results are relevant to both basic
science and clinical practice. But there is a lot of
gray area in the findings. This is the attraction of
science: embrace the gray area of current knowl-
edge and by careful analysis and experiment make
it less gray. This is the attraction of clinical practice:
embrace the gray area of an individual’s cognitive,
language, and social skills, apply clinical expertise
including familiarity with research findings, and
by a carefully structured therapeutic plan improve
the individual’s language and social skills.
108 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Not all morphemes are subject to incorrect use, and
children with FXS do not necessarily have difficulties
with the same morpheme(s) (Sterling, 2018).
Language researchers and clinicians who treat
developmental language disorders are interested in
both comprehension and production (expression) of
language forms. Comparison of comprehension with
expression skills may provide insight to the most pro-
ductive approach to language therapy. For example, a
child with relatively strong comprehension skills but
weaker expression skills may receive the greatest lan-
guage benefit from therapy focused on expression.
There are several ways to assess morphological
and syntactic skills for both comprehension and expres-
sion in children with FXS (as well as other children
with language disorders). These assessments include
formal, standardized tests, as well as analysis of lan-
guage patterns in more natural conversational settings.
A general measure of expressive language sophistica-
tion, taken from natural language samples, is mean
length of utterance (MLU), discussed in Chapter 6.
In general, children with FXS have impairments
in both comprehension and expression of morphology
and syntax, with expression more affected than com-
prehension. Children with FXS have shorter MLUs
compared to typically developing children and increase
their MLU throughout early language development
at a much slower rate than typically developing chil-
dren. As a general measure of language sophistication,
the difference in MLU between children with FXS and
typically developing children reflects a significant defi-
cit in the morphological and syntactic forms of expres-
sive language.
Vocabulary
Like other aspects of language development, both
receptive and expressive vocabulary of children with
FXS lag the vocabulary of typically developing children.
Even with this lag, the larger receptive as compared to
expressive vocabulary in typically developing children
is also found in FXS. The relative deficit of receptive
and expressive vocabulary in children with FXS, com-
pared with typically developing children, may be more
apparent in younger children (around 8 years of age).
Older children (around 12 years of age) may “catch up”
to vocabulary skills of typically developing, mental
age–matched children. This summary, and the one that
follows, is based on studies and reviews published by
Finestack, Sterling, and Abbeduto (2013), Haebig and
Sterling (2017), Kover and Abbeduto (2010), Lewis et al.
(2006), and Martin et al. (2013).
Expressive vocabulary development in children
with FXS is slower than vocabulary development in
typically developing children. In addition, a greater
deficit in expressive vocabulary may be observed in
children with FXS only compared with children with
FXS plus ASD. The increase in expressive vocabulary
over time is not predicted very strongly from a child’s
nonverbal, cognitive abilities.
The deficit in receptive vocabulary seems to be
different from the deficit in expressive vocabulary. An
important difference is that receptive vocabulary appears
to increase with development in a manner consistent
with increasing nonverbal cognitive ability. In other
words, unlike expressive vocabulary, receptive vocabu-
lary can be predicted from nonverbal cognitive abilities.
Language Use (Pragmatics)
Children with FXS have problems with language use
for social situations. As described by Klusek, Martin,
and Losh (2014), pragmatic language skills include,
“the selection of conversational topics fitting to the
situation, appropriate word choice, and the ability to
modify language in order to match the expectations
and knowledge base of the communication partner”
(p. 1692). Based on research to date, pragmatic lan-
guage skills are more affected in children (and adults)
with FXS who have also been diagnosed with ASD,
compared with children diagnosed with FXS “only”
(see review in Klusek et al., 2014). As discussed in
Chapter 7, social communication deficits (nonverbal
and verbal pragmatic abilities) are a hallmark of ASD.
An interesting issue is the possible difference in
the pragmatic language deficit in boys with FXS “only”
and boys with FXS plus ASD. Is the pragmatic language
deficit more severe in FXS plus ASD compared with
FXS “alone”? The answer seems to be “yes.” Niu et al.
(2017) have argued that research and clinical evidence
indicates that pragmatic language deficits in “nonsyn-
dromic” ASD are more severe than pragmatic language
deficits in FXS plus ASD. Notice the difference between
these group comparisons: FXS “only” compared to FXS
plus ASD, and “nonsyndromic ASD” compared to FXS
plus ASD. The determination of how ASD adds to or
changes FXS, or FXS adds to or changes nonsyndromic
ASD, is very complicated and awaits further research.
A specific example of a pragmatic language defi-
cit is difficulty with topic maintenance during a con-
versation. Conversing is a joint, socially reinforcing
pastime, in which the participants discuss a topic until
the conversation turns to a related or different topic. It
is as if the participants know the rules for supporting
productive and socially reinforcing talk. Individuals
who struggle with this skill may suddenly change the
topic under discussion, in effect not understanding the
rules of conversation. And within the same context,

the individual with a pragmatic language deficit may
continue to contribute this new, unrelated topic to the
discussion, even when the original topic continues to
be discussed by the other participants. Perseverative/
repetitious language is a prominent feature of language
use in individuals with FXS.
A pragmatic language deficit is potentially devas-
tating to an individual’s social development and life.
The deficit can partially or largely affect the ability to
make friends, share information, participate in sports,
and engage in many other aspects of life.
Chapter Summary
Intellectual disabilities, which have a prevalence world-
wide of approximately 1% of the population, are
defined as chronic impairments of mental abilities that
affect adaptive functioning in conceptual skills, social
behaviors, and practical behaviors. In most cases of ID,
the individual is mildly affected.
Diagnosis of ID is made in childhood and is not
used for adults who acquire mental deficits by (for
example) strokes, head injury, or degenerative neuro-
logical conditions.
Overall IQ scores, which are used as a component
of the diagnosis of intellectual disabilities, reflect ver-
bal skills in addition to nonverbal skills; IQ scores can
also be obtained by tests that include only nonverbal
test items for an estimate of cognitive ability indepen-
dent of language skills.
Down syndrome (DS) is the most common genetic
cause of ID.
DS occurs when there is a third chromosome at
pair 21, hence, the term “trisomy 21,” a description of
the genotype in DS.
As in other genetic disorders, there is wide vari-
ability in the phenotype in DS (i.e., across individuals),
which includes variability in language skills.
Phonological skills are primarily delayed in DS,
meaning that the learning of the speech sound system
follows the same progression as in typically develop-
ing children, but at a slower rate; some speech sound
errors in DS may be unusual, such as later learning of
sounds that are acquired early in typical speech sound
development.
An important outcome of the delay in speech
sound development in DS is that speech intelligibility
is affected, which may limit social interactions.
Morphology and syntax are thought to be particu-
lar areas of weakness for language skills in DS; both
receptive and expressive language are affected, with a
prominent weakness in expressive skills.
8  Pediatric Language Disorders II 109
Vocabulary in DS is characterized by better recep-
tive skills compared to expressive skills; the expres-
sive vocabulary may be less than expected based on a
child’s mental age.
Pragmatic language skills are generally impaired
in DS, but some components of pragmatics, such as
story narration and ability to respond to questions that
ask for clarification, are relative strengths.
FXS, which occurs in approximately 1 in 4,000
boys and 1 in 4,000 to 8,000 girls, is the leading heri-
table cause of ID, and many children diagnosed with
FXS are also diagnosed with autism.
The ID and other characteristics in FXS, including
impaired language skills, are more severe in boys, com-
pared with girls.
The phenotype in FXS is variable, both in the phys-
ical and behavioral characteristics; the language skills
component of the behavioral phenotype varies from
mildly to severely impaired.
A prominent characteristic of the language disor-
der in FXS is in the area of pragmatics.
Children with FXS acquire the sound system of
English with the same error patterns as typically devel-
oping children but at a slower rate; their phonological
development is delayed, not different.
The development of comprehension and produc-
tion (expression) of morphology and syntax is delayed
in children with FXS, although the specific morphemes
and syntactic structures that are affected vary across
children.
Both receptive and expressive vocabulary of chil-
dren with FXS lag the vocabulary of typically devel-
oping children; like typically developing children,
receptive skills for vocabulary are more advanced than
expressive skills.
Comparison of the language skills of children with
FXS “only” and children with FXS plus ASD do not
reveal a consistent difference, but children with FXS
plus ASD may have more severe language deficits,
especially in the area of pragmatic language.
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(2009). Language characteristics of individuals with Down
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Martin, G. E., Losh, M., Estigarribia, B., Sideris, J., & Roberts,
J. (2013). Longitudinal profiles of expressive vocabulary,
syntax, and pragmatic language in boys with fragile X
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& Saxena, S. (2011). Prevalence of intellectual disability:
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(2017). Autism symptoms in fragile X syndrome. Journal of
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Language Disorders in Adults
Introduction
Language disorders in adults are usually the result of
an acquired condition/disease that disrupts previously
normal language skills. An acquired, adult language
disorder contrasts with the chronic language impair-
ment that extends from early childhood into adulthood
due to conditions such as Down syndrome or Fragile X
syndrome. For the purposes of this chapter, a language
disorder is considered to be acquired if the condition/
disease responsible for the disorder occurs after the
mid-teenage years.
Many adult conditions/diseases can result in a
language disorder. Examples include stroke, traumatic
brain injury (TBI), adult-onset degenerative diseases
such as Parkinson’s disease, and dementia-related dis-
eases (such as Alzheimer’s disease).
The current chapter focuses on adult speech and
language disorders in stroke, TBI, and dementia-
related diseases. Speech impairments are included,
when relevant, because the conditions/diseases that
result in adult language disorders often include speech
disorders as well. We use the term “adult language dis-
orders” throughout the rest of this chapter to include
both speech and language.
A brief review of speech, hearing, and language
structures of the brain precedes the discussion of adult
9
language disorders. Chapter 2 provides more detailed
information on each of the review points.
Review of Concepts for the
Role of The Nervous System In
Speech, Language, and Hearing
Critical review concepts for the understanding of adult
language disorders are (a) the cerebral hemispheres;
(b) lateralization of language functions to the left cere-
bral hemisphere; (c) language expression and compre-
hension as represented in different regions of the left
hemisphere, called Broca’s area (expression) and Wer-
nicke’s area (comprehension), respectively; (d) the sig-
nificant role of connections between different regions
of the brain for language production and perception;
and (e) the perisylvian language areas.
Cerebral Hemispheres
The cerebral hemispheres include the left and right
hemispheres. Each hemisphere contains a frontal, pari-
etal, temporal, and occipital lobe. The frontal, parietal,
and temporal lobes play a major role in language pro-
duction and comprehension (reception). Figure 9–1
111
112 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Left Hemisphere
Frontal lobe
Temporal lobe
Figure 9–1.  The four lobes of the left hemisphere. Note the sylvian fissure, an important
landmark.
shows the four lobes in the left hemisphere as well as
the sylvian fissure (see Chapter 2).
Lateralization of Speech
and Language Functions
Both the left and right cerebral hemispheres contain
brain tissue associated with speech and language func-
tions. Tissue in the left hemisphere is specialized for
language production and comprehension. “Lateraliza-
tion of language functions” means that, even though the
two hemispheres have the same lobes, language func-
tions are represented most prominently in one hemi-
sphere — they are lateralized to the left hemisphere.
Language Expression and
Comprehension Are Represented
in Different Cortical Regions
of the Left Hemisphere
Language expression is primarily represented in the
frontal lobe of the left hemisphere, and language com-
prehension is primarily represented in the temporal
and parietal lobes of the left hemisphere. This does not
mean that language expression is represented exclu-
Parietal lobe
Occipital lobe
Sylvian fissure
sively in the frontal lobe, or that language comprehen-
sion is represented exclusively in the temporal/parietal
lobes. All three lobes play a role in language expression
and comprehension. The regions of Broca’s and Wer-
nicke’s area are shown in Figure 9–2. The blood supply
to the brain, shown in this figure, is discussed below.
Connections Between Different
Regions of the Brain
Different regions of the brain are connected by fiber
tracts, so the regions can exchange information. The
connecting tracts are not secondary to the cortical
regions but are equally important to brain function for
speech and language. Disruption of fiber tracts, even
when cortical regions are healthy, can result in speech
and language impairments.
Perisylvian Speech and
Language Areas of the Brain
A side view of the left hemisphere of the brain is shown
in Figure 9­–3. The front of the hemispheres (i.e., of the
head) is to the left. The lobes previously identified are
labeled, as is the sylvian fissure. The sylvian fissure is
 9  Language Disorders in Adults 113

Broca’s area
supply

Posterior

Middle cerebral
artery
Wernicke’s
area supply

Figure 9–2.  General regions of Broca’s and Wernicke’s area, shown by the shaded, oval
areas. Blood supply to the region of Broca’s and Wernicke’s area is also shown.

Left Hemisphere

Parietal lobe

Perisylvian
speech and
Frontal lobe language areas

Occipital lobe

Sylvian fissure
Temporal lobe

Figure 9–3.  View of the left hemisphere showing the region of cortical tissue, as well as the under-
lying white matter, called the perisylvian speech and language areas.

the deep groove in the cortical tissue that separates the tracts that are thought to be of critical functional impor-
temporal lobe from the frontal and parietal lobes. A red tance for speech and language. These brain regions are
oval encloses cortical tissue and the underlying fiber called the “perisylvian speech and language areas.”
114 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
The name implies that the enclosed regions are active
in speech and language functions and when damaged
are likely to cause speech and language impairments.
Adult Language
Disorders: Aphasia
Aphasia is an impairment of language expression and/
or comprehension, resulting from brain damage. Stroke,
the most common cause of aphasia, is a blockage or
rupture of the arteries that supply the brain with blood.
The blood supply of the cerebral hemispheres is
extensive and detailed. It is extensive because it reaches
all parts of the hemispheres, and it is detailed because
main arteries into the hemispheres branch into smaller
and smaller vessels that supply precise, local regions
of the brain.
A loss of blood supply to a region of the brain pre-
vents the affected neurons from sustaining their func-
tions; the neurons die. This compromises the ability of
that brain region to contribute to control of a behavior,
such as language.
Strokes occur for several reasons. Blood vessels
may be blocked completely by a tissue fragment that
travels through the bloodstream after breaking off
from an artery wall; the fragment may travel a long
way through the bloodstream before blocking an artery
and depriving blood to regions beyond the blockage.
An artery or vessel may have thickened walls due to
a buildup of plaque, which narrows the vessel, lim-
iting blood flow to regions beyond the point of nar-
rowing. The neurons beyond the narrowed vessel lose
functional ability either partially or completely. A third
possibility is a ruptured vessel, which spills blood into
the brain and does not allow sufficient blood to reach
regions beyond the rupture.
Figure 9–2 shows the blood supply to the surface
of the left hemisphere. Note the large artery (called the
middle cerebral artery) emerging between the tip of
the temporal lobe and the bottom of the frontal lobe.
The artery turns toward the back of the hemispheres
and gives off a branch to furnish blood to Broca’s area
(Figure 9–2, upward-pointing red arrow). As the main
artery continues in the direction of Wernicke’s area
(arrow pointing in the direction of the back of the hemi-
sphere), blood is supplied to Wernicke’s area.
Blood is supplied to other areas of language-
related tissue within the cerebral hemispheres, both
in the cortex and in subcortical structures. Figure 9–2
shows the potential for independent strokes in Broca’s
area and Wernicke’s area. For example, blockages can
occur in the branch to Broca’s area without affecting
blood flow to Wernicke’s area. If Broca’s area is the pri-
mary brain area for language expression, a stroke like
this is expected to affect language expression but not
language comprehension. The reverse is also possible: a
blockage after the main artery has passed the branch to
Broca’s area does not affect the frontal lobe (the location
of Broca’s area) but may affect Wernicke’s area. In this
case, language comprehension is likely to be affected
without any effect on language production. This simpli-
fied account of how blood loss affects language function
is not the whole story but makes the point of the rela-
tionship of blood supply to the brain and potential loss
of expressive versus receptive function.
Stroke is not a rare occurrence. There are approxi-
mately 800, 000 cases of stroke per year in the United
States (https://www.cdc.gov/stroke/facts.htm), and
many more worldwide. A significant number of strokes
have aphasia as a prominent deficit (Ellis & Urban,
2016). Many patients who have aphasia recover most,
if not all, of their language abilities in the days, weeks,
or months following a stroke. A smaller number of
patients have a chronic language impairment.
Classification of Aphasia
The history of aphasia, in both clinical and research
work, includes a substantial effort to classify differ-
ent types of the disorder. Six types of aphasia, linking
damage to specific brain structures with language com-
prehension and expression difficulties, are presented
here. They include Broca’s aphasia, Wernicke’s aphasia,
conduction aphasia, anomic aphasia, global aphasia,
and primary progressive aphasia. Primary progressive
aphasia is not the result of a stroke but is discussed here
because it is characterized by aphasic deficits (among
other deficits). A brief summary of apraxia of speech,
which in adults is typically the result of a stroke, is
also provided. There are other categories of aphasia
as well, but here we discuss the ones most relevant
to clinical practice and theories of brain function for
language.
Aphasia types can be classified in one of two ways
(and possibly other ways, not discussed here). One
way is to identify the location of brain damage with
an imaging technique such as CT (computed tomog-
raphy) or MR (magnetic resonance). Type of aphasia
is diagnosed based on the expectation of the language
disorder from brain-behavior relationships. For exam-
ple, damage to Broca’s area, confirmed by imaging, is
expected to result in Broca’s aphasia (see later in chap-
ter), which has certain characteristics that distinguish
it from other types of aphasia. Similarly, damage to
 9  Language Disorders in Adults 115

Wernicke’s area is expected to result in Wernicke’s
aphasia. This is referred to as a “localization” view of
aphasia type: specific areas of the brain are associated
with specific behaviors.
What does it mean to confirm a lesion (damage to
tissue) with an imaging technique? Figure 9–4 shows
two CAT (computerized axial tomography) scans, one
of a lesion in Broca’s area (top, left), the other in Wer-
nicke’s area (top, right). These images were taken from
slices through the brain in the horizontal plane. The
slice level is shown in the bottom photograph of a real
brain; note that the slice cuts through Broca’s and Wer-
nicke’s areas. The sides of the images are flipped: the
right side of the images is the left side of the brain. The
dark regions indicated by the pointers are lesions. As
expected, the lesion that includes Broca’s area is toward

Broca’s lesion Wernicke’s lesion

Central sulcus
Wernicke’s area

Broca’s area

Figure 9–4.  Two CAT (computerized axial tomography) scans, one of a lesion in Broca’s area
(top, left ), and the other in Wernicke’s area (top, right ). The labeled pointers show the lesions
as darkened areas of the scans. These images were taken from slices through the brain in the
horizontal plane, as shown in the lower image. The sides of the images are flipped: the right side
of the images is the left side of the brain.
116 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

the front of the left hemisphere, and the lesion that
includes Wernicke’s area is toward the back.1
A different way to classify aphasia is on the basis
of the speech and language impairments, regardless
of lesion location. For example, a patient who suffers
a stroke and has agrammatical, effortful speech, with
hesitations but close-to-normal comprehension skills,
is diagnosed with Broca’s aphasia, regardless of the
lesion location and its extent (how much of the brain
has been damaged). This chapter does not attempt to
resolve the classification controversy; the presenta-
tion is neutral, with both probable lesion location and
speech-language symptoms described.
Broca’s Aphasia
Much of the effort to classify aphasia according to the
location of damage within the brain was inspired by
the mid- to late-19th century work of Paul Broca (1824–
1880). Broca was a French physician who studied a
small group of patients who were able to produce only
a single syllable, or a few words but comprehended
language with little or no problem. When the patients
died, Broca performed autopsies of their brains and
found similars locations of brain damage in most of the
patients. The damage was in the lower part of the fron-
tal lobe, close to the motor cortex, just above the sylvian
fissure (see Figure 9–2). Broca suggested that the ability
to articulate syllables and words was localized to this
part of the frontal lobe. Damage to this area resulted
in a disorder of articulation, but not comprehension.
Broca published his results in 1865, and for more than
150 years the region he identified as the articulation
center of the brain has been called “Broca’s area.”
Broca’s aphasia is primarily an expressive lan-
guage problem, presumably associated with damage to
Broca’s area. The patients hesitate before speaking, and
when they do speak produce single words or utterances
of just a few words. Speaking seems to a listener to
require a great deal of effort; word finding is a problem.
The words that are spoken are usually content words;
function words are not used, or seldomly used. Patients
with Broca’s aphasia are also said to have agrammati-
cism, because of the lack of function words and the
resulting lack of grammatical completeness. Compre-
hension of language is good (perhaps not quite normal).
Broca’s aphasia is called a nonfluent aphasia
because of the hesitations and slow, effortful speech
patterns. Here is a transcript of a brief conversation
between a speech-language pathologist and a stroke
survivor who was diagnosed with Broca’s aphasia.2
SLP:  Can you tell us your name?
Patient:  John Doe (very carefully articulated).
SLP:  And John, when was your stroke?
P:  Seven years ago (each word carefully articulated,
with an even, robotic sequence of syllables).
SLP:  Okay . . .
P:  And . . . (nods, because he sees SLP wants to
continue a question).
SLP:  And what did you used to do?
P:  Um . . . well, um . . . worked (nodding head)
. . . um . . . on a desk (this phrase spoken rapidly,
does not sound impaired) . . . um . . . seven . . .
seven . . .
Spouse: Sales.
P:  Sales (nodding, confirming spouses assistance
and verifying the type of work). Sales . . . and . . .
worldwide, and . . . very good, yeah!
SLP:  Okay and who are you looking at over there?
When you turned your head over there?
P:  That’s my . . . wife.
SLP:  And why is she helping you . . . to talk?
P:  Um . . . she’s . . . a speech . . . (forms lip for a
“p”) . . . um . . . (again, tries to position articulators
but no sound comes out).
SLP:  So you have trouble with your speech?
P:  Yeah, yeah.
SLP:  And what’s that called?
P:  Um, phasia.
SLP:  Alright . . . and so why don’t you work now?
P:  Um . . . I . . . I . . . well I do (each word separated
by very brief pauses).

1
 s used here, the term “includes” means that the lesions are larger than would be expected for lesions confined strictly to the cortical regions
A
suggested by the aphasia type (i.e., Broca’s aphasia, Wernicke’s aphasia). In other words, brain lesions are typically larger than the anatomical
tissue identified as a specific area. Also, the other dark areas on the scans, such as the curved structures in the center and toward the front,
are not lesions but other structures where you would expect the scan to show dark. The curved structures are the lateral ventricles, through
which cerebrospinal fluid flows.
2 
 his conversation, and all subsequent transcripts, were transcribed from YouTube clips. “John Doe” substitutes for the patient’s name.
T
Comments are enclosed in parentheses, and long pauses are indicated by ellipses ( . . . ).

SLP:  What do you do now?
P:  Um . . . Voices ah home, aphasia (patient names
an organization).
In this 1-minute exchange between the SLP and
the patient, the frequent hesitations (“um”), pausing
( . . . ), word-finding problems, agrammaticism (“Sales
. . . and . . . worldwide, and . . . very good, yeah”), and
good comprehension (he clearly understands the ques-
tions) are clinical markers for a diagnosis of a mild-to-
moderate Broca’s aphasia.
Wernicke’s Aphasia
Carl Wernicke (1848–1905), a German physician, was
Broca’s equal in his influence on classification of apha-
sia types. Wernicke studied a series of patients who
had great difficulty in comprehending language but
gave no clinical evidence of a general (nonlanguage)
hearing loss. The comprehension problem seemed to
be specific to language. The patients had only slight
difficulty with articulation, but their expressive lan-
guage lacked meaning and often was not responsive
to questions even though they replied (but without rel-
evant content).
Autopsies of the patients’ brains showed damage
to the upper gyrus of the temporal lobe, toward the
back of the sylvian fissure and close to the lower edge
of the parietal lobe (see Figure 9–2). These patients had
no apparent damage in Broca’s area. Wernicke con-
cluded that the region of damage for these patients
represented the language comprehension part of the
brain. This region of the brain has since been known as
Wernicke’s area.
Here is a transcript of a brief conversation between
a speech-language pathologist and a stroke survivor
who was diagnosed with Wernicke’s aphasia.
SLP:  Hi John, how are you?
Patient:  I’m happy are you pretty? You look good.
(wants to speak more but SLP asks a question).
SLP:  What are you doing today?
P:  We stayed with the water over there at the
moment, talked with the people at the dam over
there, they’re diving for them at the moment, he
had a-water very soon . . . for him . . . with luck . . .
for him.
SLP:  So we’re on a cruise and we’re about to —  be seen on the hemisphere surfaces.
3 
Jane Doe.
9  Language Disorders in Adults 117
P:  We will sort right here and they’ll save their
hands right there (pointing).
SLP:  And what were we just doing with the iPad?
P:  Uh . . . right at the moment they don’t show
darn thing (laughs).
SLP:  Where’s the iPad that we were doing?
P:  (hesitates) I’d like my change for me and change
hands for me, it was happy, I would talk with Jane3
sometimes, we’re out with them, other people are
working with them with them, I’m very happy
with them — 
SLP:  Good! — 
P:  This girl was really (misarticulated) good. And
happy, and I played golf, and hit a trees, we play
out with the hands, we save a lot of hands on hold
for peoples for us, other hands, I don’t know what
you get but I talk with a lot of hand grands . . .
The 1-minute transcript shows the comprehension
problem — for the most part, the patient is not respond-
ing to the questions with relevant answers. The patient
does a lot of talking, with well-formed speech sounds,
a rapid speaking rate, and mostly grammatical utter-
ances, which nevertheless are nonsensical. There is
repetition (“hands” occurs half a dozen times in the
brief transcript) and one or two articulation errors (not
transcribed here). Wernicke’s aphasia is called a flu-
ent aphasia because utterances show little hesitation,
and articulatory sequences are smoothly produced
and even run on with excessive utterance length. The
diagnosis of Wernicke’s aphasia is consistent with
the transcript.
Conduction Aphasia
Fiber tracts in the cerebral hemisphere (“white mat-
ter”; see Chapter 2) connect one region of gray matter
to another. As demonstrated by Wernicke, and others
after him, a massive fiber tract called the arcuate fascic-
ulus connects Wernicke’s and Broca’s areas (Figure 9–5,
blue lines) (Smits, Jiskoot, & Papma, 2017). A tract con-
necting the same areas but lower (more ventral) in
the cerebral hemispheres is called the ventral stream.
These tracts run beneath the cortex — like all white
matter in the cerebral hemispheres, fiber tracts cannot
118 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Arcuate fasciculus

Parietal Lobe

Wernicke’s
Area

Frontal Lobe Occipital Lobe

Broca’s Area

Temporal Lobe
Ventral stream

Figure 9–5.  Two fiber tracts that connect receptive and expressive regions of the left hemisphere
(Wernicke’s region with Broca’s region). The fiber tract represented by the blue-line bundle is the arcuate
fasciculus, and the tract represented by the green-line bundle is the ventral stream. The color of the labels
matches the color of the areas (magenta, Broca’s area; blue, Wernicke’s area).

Conduction aphasia is believed to be the result of
a stroke that damages the arcuate fasciculus and func-
tionally disconnects Wernicke’s area from Broca’s area.
Wernicke’s area is not damaged, so the patient can hear
and understand a word or sentence. Broca’s area is not
damaged, so words and sentences can be produced in a
normal way. Damage to the arcuate fasciculus partially
or completely prevents the heard utterance from being
transferred to Broca’s area for repetition. It is possible
that the behavioral characteristics of conduction apha-
sia (i.e., expressive and receptive language; see below)
are related to damage to other areas of the brain in
addition to the arcuate fasciculus (Yourganov, Smith,
Fridriksson, & Rorden (2015).
The signature deficit in conduction aphasia is
difficulty repeating others’ utterances, even though
language comprehension is good. Expression is often
fluent and grammatically well formed. However,
expression may also have paraphasias, which are unin-
tended errors on speech sounds, syllables, and words
(Ardila, 2010; Pandey & Heilman, 2016).
A transcript of a patient with conduction aphasia
illustrates some of these characteristics.
SLP:  The producer asked us to count to 10, do you
remember that? Can you do that again?
P:  Yes. Why. (not a question). One, two, three, four,
five, (rapid intake of air), seven, nnn uh, boin, too
thuh, gehvry, beople, go I can’t oh I — 
SLP:  No, that’s hard, let me get you started — 
P:  I was ston — 
SLP:  Okay, one, two, three (SLP is counting with
the patient) — 
P:  One, two, four, five, ss-ff-sixth, better send
poined, um . . .
SLP:  Good enough, let’s stop — 
P:  Is that alright?
The patient clearly understands the questions,
requesting her to count. The patient begins counting
accurately but soon produces paraphasias (e.g., “boin”
and “gehvry”) and a fluent, short, well-formed sen-
tence (“Is that alright?”).

Anomic Aphasia
“Anomia” is from Greek, meaning “without name.” In
anomic aphasia, a patient is fluent but has great diffi-
culty with word-finding, especially for nouns, includ-
ing names and objects. Often, a patient with anomia
can describe the function of an object in great detail,
or a person’s appearance, but not be able to name the
object or person.
Anomia occurs in most types of aphasia — almost
all patients, regardless of the particular kind of apha-
sia, have some anomia. Aphasia in which anomia is the
dominant symptom is usually mild. Comprehension is
typically good in anomic aphasia.
The following transcript is an example of anomia
in a patient with aphasia. The patient is looking at pic-
tures of four tools, including a saw, a hammer, an axe,
and a screwdriver. The SLP is pointing to the saw and
asking the patient to name it.
P:  You knew what it is, I can’t tell you, maybe I
can . . . If I was to carry the wood and cut it in half
with that . . . you know . . . if I had to cut the wood
down to bring it in . . .
SLP: pointing to the saw:  Then you’d use one of
these . . .
P:  It’s called a . . . I have them in the garage . . .
they are yee-ar . . . you cut the wood with them . . .
it . . . sssaw!
SLP:  How is it? (asking patient to repeat the name
of the saw).
P:  Unnn . . . (sigh) . . . sss . . . sah (cuts off the end
of the vowel quickly) . . . sah (cuts off again) . . .
I can’t state it. I know what it is and I could cut the
word with it and it’s in my garage . . . and it’s . . .
a . . . and also when you go out and you want to
stay out in the woods with people you always take
those with you and you . . . um . . . it is a . . . it’s not
a knife, it’s not a . . . sssah (vowel quickly cut off),
I know what it is, I think.
SLP:  Well finish saying what you started to say.
P:  I’m not sure I’m stating I right.
SLP:  Try again.
P:  Ssssss. No, I’m incorrect.
The patient knows what the object is, what it does,
and why you use it. The patient recognizes his inability
to retrieve the name (“I can’t state it,” “I’m not sure I’m
stating it right,” “No, I’m incorrect”). Several times he
almost retrieves the word (“sssah” [cut off], “ssssss”).
9  Language Disorders in Adults 119
Global Aphasia
Global aphasia is a nonfluent aphasia in which both
expressive and receptive language are impaired. The
patient may be able to express short, automatic-type
phrases such as “Hello,” and “How are you?” but lon-
ger, less automatic utterances are not produced or are
very rare. The impairment of receptive language is sim-
ilar, with occasional understanding of short, familiar
utterances (e.g., “how are you?”) but poor understand-
ing of more complex language.
In global aphasia due to stroke, the blood supply to
both Broca’s area and Wernicke’s area is blocked. Other
areas of the brain, such as parts of the temporal lobe
that are important for word and sentence processing,
are also affected. In fact, the entire perisylvian language
region (see Figure 9–3) is affected, with widespread
effects on language expression and comprehension.
Global aphasia has been reported as the most com-
mon (Flamand-Roze, Flowers, Roze, & Denier, 2013) or
third most common (Hoffman & Chen, 2013) type of
aphasia. Global aphasia is often diagnosed shortly after
a stroke.
As a patient recovers from overall stroke symp-
toms, language recovery may also occur. Global apha-
sia may “evolve” to different types of aphasia as the
patient recovers (Klebic, Salihovic, Softic, & Salihoic,
2011). Global aphasia may continue to change to other
aphasia types along the pathway to language recov-
ery. A patient whose global aphasia evolves to func-
tional expressive and receptive skills is likely to have
residual anomia ranging in severity from mild to
severe. Patients with global aphasia who do not show
improvement within a month following a stroke have
a poor prognosis for future improvement of language
skills (Alexander & Loverso, 1992).
This transcript illustrates global aphasia in a
patient who had recently suffered a stroke.
{R1 = Relative 1} {R2 = Relative 2}
R1:  Alright, say hi!
P:  (Smiling) Hi!
R1:  What’s your name?
P:  What’s what?
R1:  What’s your name?
P:  Uh . . .
R1:  Do you know?
P:  . . . John?
R1: John.
P:  Yeah, John.
120 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
R1:  What’s my name?
P:  Wha- what’s whose name? (weakly).
R1:  My name (pointing to herself).
P:  Uh . . . hard to get ‘em all (weakly).
R1:  Yeah. Jane.
P: Yeah.
R1: Yeah.
R2:  Can you say Jane?
P:  Yeah (weakly).
R2:  Say it.
P:  Nndeer (unintelligible, weakly).
R2: Jaaane.
P:  I can’t say it . . . (weakly).
R1:  That’s okay.
P:  Takes me a little longer to say . . .
R1:  Do you know where you are?
P:  Do I know who it is?
R1:  Do you know where we are?
P:  Uh . . . no you live in uh . . . in the . . . park.
R1:  Close! We’re at the hospital.
P: Yeah.
R1: Yeah.
The patient’s anomia is apparent in his struggle to
retrieve his own name and his daughter’s name. The
content of this transcript suggests a mild-to-moderate
expressive component (R2: “Can you say Jane? P: Yeah
(weakly). R2: Say it. P: Nndeer (unintelligible, weakly)”
as well as a mild-to-moderate comprehension impair-
ment (e.g., R1: “What’s my name? P: Wha — What’s
whose name?”).
Primary Progressive Aphasia
Primary progressive aphasia (PPA) is a rare adult
language disorder in which a patient has an isolated
language problem that increases in severity over time
(Mesulam, 2018). PPA does not appear to be the result
of a stroke, but rather a separate disease in which
deterioration of brain tissue is specific to language
areas and networks. In the initial stages, the language
impairment is not accompanied by significant memory
or psychiatric problems and does not appear to be a
result of dementia (see section, “Language Disorders in
Dementia”). Throughout the course of PPA, dementia-
like symptoms appear, but the language impairment
remains a significant characteristic and barrier to daily
function (Montembeault, Brambati, Gorno-Tempini, &
Migliaccio, 2018).
A person with PPA may have speech and lan-
guage characteristics similar to those of Broca’s
aphasia, including dysarthria and apraxia of speech
(Gross-man, 2012; Chapter 14); or may have specific
difficulties with word retrieval and word comprehen-
sion, specifically for low-frequency (unusual) words; or
may have sentence repetition and comprehension
impairments together with reading and written-lan-
guage problems (Henry & Grasso, 2018). The specific
nature of the language impairment may suggest one
of three different types of PPA (Montembeault et al.,
2018).
Two different types of PPA are transcribed here.
Transcript 1
SLP:  We can speak about your concerns . . . .hi
Jane!
P:  How are you?
SLP:  I’m fine! So, tell me something . . . are you,
um, are you working on your speaking?
P: Yes.
SLP:  And what are you working on, specifically,
do you know?
P:  Uuh-tho (shakes head, means to say “I don’t
know”).
SLP:  Okay, so you don’t know, can you say “I,”
“don’t,” “know”? (slowly spoken, separating each
word with a short pause).
P:  I tho.
SLP:  Okay, now let’s go a little bit slower, because
you’ve got a little bit of a dysarthria.
P: Yeah.
SLP:  And a little bit of an apraxia (P shakes head
“yes”), for your speech to come out really nice,
we’ve got to slow it down and to put a nice space
between each word. Now watch me, see if you can
do this: “I.”
P: “I.”
SLP: “Don’t.”
P: Own’t.
SLP: Know.
 9  Language Disorders in Adults 121

P:  (Makes face as if saying this word is going to be P: Yep.

difficult) “Owe.”
R1: Rrrrrrrr.
SLP:  Good. Can you say that again? P: Rickford.
P:  I tho doh. R1:  Good. And, where did you meet your wife?
SLP:  Good. Very good. And where do you live? P:  My wife.
P:  Um . . . Iss? (answered as if uncertain, with R1:  Who’s your wife?
rising pitch).
P:  (Looks at his spouse).
SLP:  Do you know the name of the state where
you live? R1:  Is it that lady over there, is that your wife?

P: Yeah. P: Mmm-hmm.
R1:  And what’s her name?
SLP:  What state is it?
P: Jane.
P:  Biss? (again as if uncertain).
R1:  Good! And then you guys moved to Arkansas,
SLP:  Biss (very precisely, as if asking P if that’s
where did you live in Arkansas?
what he meant).
P:  (Looks around, doesn’t answer, looks to
P:  No (shaking head, meaning that’s not what he spouse).
meant).
R2:  We lived in . . .
SLP: No, Miss!
R1:  In Little Rockstar?
P: Yes.
P:  Little Rockstar.
SLP:  Oh, so you shorten it, don’t you, because it’s
got a lot of syllables in it. The patient in Transcript 1 has poor articulatory
P: Yes! skills (the sound errors in the transcript, e.g., “doh” for
“know”) and possibly poor ability to transform sounds
Transcript 2 as represented in the brain to sounds produced by the
speech mechanism. This latter problem is often referred
R1:  Okay. Hey Dad, can you look at me? to as an impairment of phonological coding, which can
P:  (unintelligible, does not turn to look). be independent of the ability to articulate sounds. It
is best illustrated by the patient’s labored attempts to
R1:  Can you tell me your name?
position the articulators to initiate an utterance, as if
P:  John Doe (spoken rapidly, with good articula- searching for the correct position. The patient’s com-
tion of sounds). prehension skills are good — she responds to questions
with no apparent problem.
R1:  And how old are you?
The patient in Transcript 2 has no problems with
P: Sixteen. articulatory skills — his speech is fluent and easy to
understand. But there are word-finding problems (the
R1:  When were you born?
several examples of not responding and searching for
P:  . . . . . . 19xx. a response, particularly of proper nouns such as the
name of towns or of his spouse), which are solved
R1:  Good! And where were you born? (P looking
when he is given a prompt (e.g., “In Little Rockstar”?
around the room as if he doesn’t understand the
and his immediate response, “Little Rockstar”). He
question; long pause). Do you know where you
may also have a comprehension impairment.
were born?
R2:  In the hospital (laughter from other family
members). Apraxia of Speech
R1:  Where-where did you grow up? Apraxia of speech is discussed in Chapter 15 as a child-
hood speech sound disorder. As noted there, the diag-
P:  (No response).
nosis of childhood apraxia of speech (CAS) is based in
R1:  Do you remember where you went to school? large part on speech characteristics in adults with brain
122 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
damage due to stroke and other brain injuries. These
characteristics include difficulty initiating speech, artic-
ulatory “groping,” in which the patient has difficulty
positioning articulators, such as the lips and tongue,
to produce a speech sound correctly, and speech sound
errors, especially for phonetically complex words. The
patients recognize their own speech sound errors and
make attempts to correct them. An example of this was
noted above in the transcript for the second patient
with PPA.
Apraxia of speech in adults (“AAS” to distinguish
it from “CAS”) is often observed in aphasic patients and
is considered by some to be a type of aphasia. Others,
perhaps most clinicians and scientists, consider AAS to
be strictly a motor speech disorder related to an impair-
ment of programming (planning) sound sequences. In
this view, correct speech sounds are represented in the
brain but are subject to errors in planning their articula-
tion and sequencing. . For example, phonemes for the
word “strategy,” /s/, /t/, /r/, /ae/ (as in “hat”), /d/,
/ə/ (a very short “uh”), /dg/ (as in “fudge”), and /i/,
are represented in the brains of people with AAS in
the same way as they are represented in the brains of
people without brain damage. The speech impairment
in AAS is an incorrect plan for how these sounds are
sequenced, the muscle contraction patterns to produce
the sequence, and other variables such as the timing of
different sounds. A word like “strategy,” which is pho-
netically complex with its word-initial, three-consonant
cluster /str/ and another complex sound, /dg/, is par-
ticularly challenging for people with AAS. Clinicians
and scientists who regard AAS as a speech motor dis-
order argue that phonetically complex words are more
susceptible than phonetically simple words (such as
“sag”) to speech motor planning disorders.
The view of AAS as an aphasia is not that pho-
neme sequencing is impaired, but rather that the pho-
neme representation and/or the ability to select the
correct phonemes is impaired. This view does not
regard AAS as a motor speech disorder. For example,
the /s/ in strategy may be incorrectly represented by a
/t/, resulting in a word production like “trategy.” The
patient could produce the /s/ well if the representation
of the sound in the brain was intact. Also, the process of
selecting the sounds — a stage of word production pre-
ceding the programming of sound sequences — may be
impaired. Eling (2016) provides a review of the debate
concerning the nature of AAS.
The following transcript of a patient with AAS fol-
lowing a stroke is taken from a monologue in which
she describes her speech and other impairments:
P:  The two areas that I have problems with, um
. . . is in my left hand (holds up her right hand),
I have that I’m gonna remember, I’m gonna . . .
have this meh, ber, my (syllable cut off quickly),
the word wrong. It’s struggity, wait my studiservist
. . . ssstext derity, and . . . that’s my hand, and . . .
that’s in my left hand (again, holding up right
hand) and I’m right-handed. So . . . if you notice
I really don’t have a lot of . . . uh . . . makeup,
I tried it fir-fir, th, the-fir first time today (syllable
repetitions in preceding phrase spoken very
rapidly), a lot of that I couldn’t I couldn’t write,
du-couldn’t write, I couldn’t write, I even tried
my hair spr- my . . . my . . . umm . . . my . . .
bandana . . . umm . . . but I had trouble with it,
so, . . . um . . . but that’s, that’s the little pit of the
problem, uh, my biggest problem is . . . with my
speech. Sooo, I started with, therapy, just last
week — this week. So, Monday I had . . . just,
um, an evaluation, and then, yesterday, Wednes-
day, . . . and then, hockey therapist, OT, I can’t
really pronounce it, opcheetherah . . . um, ah,
oxeetelabis, and then there’s, um, filicul, filucul,
therapis.
The individual recognizes her speech sound errors
(attempts to correct “struggity” and “studiservist,”
and the several attempts to produce “occupational”).
Simple words are well articulated, but multisyllabic,
phonetically complex words such as “struggle,” “dex-
terity,” and “occupational” are not. For the most part,
when the individual is not making speech sound errors,
her speech does not sound abnormal.
Aphasia Due to Stroke:  A Summary
Language disorders in adults are a common impair-
ment following stroke. The aphasia types summarized
in this chapter are in common use among SLPs and
aphasia researchers. However, aphasia types are not
always clearly defined — speech and language char-
acteristics of two or more types may be observed in a
single patient.
Indeed, “pure” aphasia types are unusual. For
example, patients diagnosed with Wernicke’s aphasia
are likely to have some language impairment expected
from other aphasia types; the same is true for other
diagnoses (e.g., Broca’s aphasics having some compre-
hension deficits). Perhaps a better way to think about
aphasia types is that any individual type reflects the
primary deficit, with recognition that other language
deficits are likely as well. Global aphasia may be the
endpoint of these multiple language deficits — all
aspects of language expression and comprehension
are affected by a stroke that damages most perisyl-
 9  Language Disorders in Adults 123

vian speech and language areas. With this in mind,

Table 9–1 provides a summary of speech and language
characteristics in the “classic” aphasia types, as previ-
ously discussed.
Figure 9–6 presents this idea in schematic (sim-
ple) form. One arrowhead is in Broca’s area, the other
arrowhead in Wernicke’s area. Localized lesions in the
far anterior region of the perisylvian language area are
likely to result in an aphasia with a primary impair-
ment in expression. Localized lesions in the far poste-
rior region of the perisylvian language area are likely
to result in an aphasia with a primary impairment
in comprehension. Lesions between these two end-
points, within the perisylvian language area, are likely
to produce a “mixed” aphasia, in which expressive
and receptive impairments are observed to varying
degrees. Aphasiologists often use the terms “anterior
lesion” and “posterior lesion” to indicate the general
location of damage because these terms are less restric-
tive than “Broca’s area” and “Wernicke’s area.”
It just so happens that the brains of
two of Broca’s patients have been
preserved. These brains, located in a
Paris museum until 2016 and now still in Paris
but at a different location, have been scanned by
researchers using modern imaging technology.
When Dronkers, Plaisant, Iba-Zizen, and Canabis
(2007) scanned these brains, the lesions were not
restricted to the classical, relatively small cortical
regions named Broca’s area. In fact, the lesions
were much larger, extending into middle struc-
tures including white matter and specifically
the arcuate fasciculus, the tract that connects
Wernicke’s and Broca’s areas. Research findings
like this suggest caution in linking expressive or
receptive speech and language deficits to damage
in the classical, cortical brain areas associated
with the work of Drs. Broca and Wernicke.

Table 9–1.  Summary of Speech and Language Characteristics in Aphasia Types

Aphasia Type Speech and Language Characteristics

Broca’s aphasia Expressive aphasia — nonfluent
Slow effortful speech
Agrammatism
Good comprehension
Anomia

Wernicke’s aphasia Receptive aphasia — fluent

Poor comprehension of language in the absence of hearing
loss
Articulation close to normal
Fluent, expressive speech lacks meaning
Not specifically responsive to questions

Conduction aphasia Good receptive and expressive skills

Impaired repetition
Paraphasias for speech sounds, syllables, and words
Anomia

Global aphasia Expressive and receptive aphasia — nonfluent

Short, automatic phrases may be preserved both in expression
and comprehension
Poor comprehension of complex language
Anomia

Primary progressive Like Broca’s aphasia (one type)

aphasia Poor word retrieval and comprehension (one type)
Sentence repetition and comprehension impairments
Problems with reading and written-language skills
124 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Frontal Lobe
Broca’s Area
Temporal Lobe
Figure 9–6.  The concept of anterior and posterior lesions. See text for details.
Traumatic Brain Injury and Aphasia
The definition of a traumatic brain injury (TBI) is “a
bump, blow or jolt to the head, or penetrating head
injury, that results in disruption of the normal function
of the brain” (Marr & Coronado, 2004). TBI is a major
health concern. According to a fact sheet published by
the Centers for Disease Control and Prevention (CDC),
in 2013 there were approximately 2.8 million emer-
gency room visits for head injuries in the United States
(https://www.cdc.gov/traumaticbraininjury/get_the_
facts.html). Both adults and children are included in
this estimate. Around 80% of people who are seen in an
emergency room for a TBI are diagnosed with a mild
injury (Douglas et al., 2019). In this section, the focus
is on closed head injuries, in which there is no pene­
tration of the skull and brain by a flying object such as
a bullet.
The evolution of TBI symptoms varies widely
across individuals and depends on factors such as age,
severity of the injury, and the consciousness status of
the patient immediately after the trauma. A TBI often
evolves as a sequence of events from the time of injury
to near or full recovery of function.
If the individual is unconscious after the head
injury, the time from the trauma to regaining conscious-
ness may vary from very short (e.g., a few minutes) to
very long (e.g., a week or more, or, in some cases, a
permanent comatose state). When consciousness is
Parietal Lobe
Wernicke’s
Area
Occipital Lobe
regained, a period of confusion is typical. During this
time, the individual may be confused about where he
is, how or even if an injury occurred, and personal
information. The individual’s language may reflect
this confusion. The person may not be able to speak for
a short period, may speak in disconnected sentences
with little content, and may have comprehension prob-
lems. After the period of confusion, most individuals
improve steadily; this includes significant improve-
ment in language abilities.
Nature of Brain Injury in TBI
Closed-head injuries are associated with brain dam-
age that is different from that observed in stroke. The
“bump or jolt” to the head causes the cerebral hemi-
spheres to slam into the bony casing of the skull. In the
case of a powerful blow to the head, the cerebrospinal
fluid in which the brain floats is not sufficient to protect
the soft tissues of the brain. The damage to brain tissue
is often in the frontal lobes where the impact may be
greatest due to the forward, high acceleration of the
cerebral hemispheres in response to the blow to the
head. Structures of the temporal lobe are also likely to
be damaged in a closed head injury.
The blow to the head may cause the cerebral hemi-
spheres to twist inside the skull at high accelerations.
This results in shearing injuries to neural tissue. Shear-

ing injuries occur in axons, which are stretched and
rotated so violently that they are torn. The injuries to
axons affect the integrity of white matter. Gray mat-
ter areas, such as in the cortex or in subcortical nuclei,
are partially disconnected by these shearing injuries,
which have profound consequences for the brain net-
works serving both cognitive and high-level language
functions (Douglas et al., 2019).
Language Impairment in TBI
Speech and language impairments are common in
TBI. The impairments are typically most severe imme-
diately after the trauma and improve over time. The
improvement often brings the patient back to “normal”
language skills.
Language skills in TBI are often assessed by formal
tests used to evaluate individuals who have suffered a
stroke and have aphasia. These tests evaluate language
skills such as word recall, naming of objects, and pro-
duction and comprehension of syntax. According to a
different perspective, as the patient recovers from the
injury formal tests of aphasia may suggest a return to
normal language skills but miss a continuing language
impairment of social language use. Language skills in
the area of phonology, morphology, syntax, and to a
large degree, content, are evaluated by these aphasia
tests as normal or near-normal (Steel, Ferguson, Spen-
cer, & Togher, 2015; Vas, Chapman, & Cook, 2015). The
remaining language impairment, potentially having
substantial functional consequences, is of higher-level
skills such as expressive discourse, comprehension of
the overall message of discourse, and social language
use (language pragmatics).
Structural Components of Language
Structural components of language include phonology,
morphology, syntax, and content (reviewed in Chapter
3). Dysarthria, a motor speech disorder caused by dam-
age to the speech motor control centers of the brain,
is not considered a phonological disorder, but may
affect speech sound production in persons with TBI.
Although dysarthria is not a language disorder, it is
important to mention because about 33% of individu-
als with TBI have dysarthria (Beukelman, Nordness, &
Yorkston, 2011). AAS following a head injury appears
to be rare (Cannito, 2014).
Morphology and syntax are often affected in the
initial phases of recovery from TBI. For all but the
most severe cases, morphological and syntactical skill
improve over time and are likely to return to normal
use. Anomia, an impairment of the content component
9  Language Disorders in Adults 125
of language, is a prominent characteristic of the early
phases of language recovery in TBI. Like morphology
and syntax, anomia improves over time but may per-
sist past the time when other structural language skills
have returned to normal.
Pragmatics (Social Use of Language)
Language use for social communication is a primary
area of concern in adults with TBI. Higher-level, dis-
course-type language skills may be impaired, even
when structural components of language are intact.
Comprehension of metaphors (“A veil of secrecy sur-
rounded the committee’s work”) and figurative lan-
guage (“He inhaled his lunch”) may be impaired.
Persons with TBI may not be able to narrate a story
in a coherent way. Individual utterances of the story
may not be sequenced correctly, and information that
is not relevant to the story may be included in the nar-
rative; story details may be repeated several times.
As summarized by Vas et al. (2015), there are
many other aspects of social language use: “we engage
in conversational discourse during speaker–listener
interactions and social exchanges, we use descriptive
discourse to explain attributes and features of an object,
we use narrative discourse to describe an event, we use
procedural discourse to explain a task procedure, and
we use expository discourse to inform a listener of a
topic through facts or interpretations” (p. 499). Narra-
tive language impairments have been demonstrated in
individuals with moderate TBIs whose structural lan-
guage skills are not impaired (Marini, Zettin, & Galleto,
2014). When words, individual sentences, and gram-
mar appear to be normal, and people are not aware that
the person they are interacting with has a TBI, it is easy
to understand how a social language impairment can
be a major challenge to everyday life.
Social language use requires a synthesis of cogni-
tive and linguistic skills (Steel, Ferguson, Spencer, &
Togher, 2017). Cognitive skills such as memory, pro-
cessing speed, flexibility in processing, attention, and
inhibition are joined with linguistic skills to make social
language use as effective as possible (Vas, Chapman, &
Cook, 2015). An example of the interaction and mutual
dependence of cognitive and linguistic skill is in turn
taking during conversation. Linguistic skills of follow-
ing content and knowing when an individual is about
to finish a contribution to a discussion are joined to
attention to the structure of the conversation, memory
of what has been said, and inhibition of interrupting
the speaker before he or she is finished.
Damage to the frontal lobes, and its connections
with almost all other area of the brain, is almost cer-
tainly the basis of impaired social communication in
126 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
individuals with TBI. A healthy frontal lobe is critical
to everyday functioning because of its central role in
executive function of the brain.
Executive function is important to many aspects
of behavior, among which are several of the cognitive
skills mentioned previously, such as memory, process-
ing speed, and attention. Executive function directs the
brain to pay attention to certain stimuli, and not oth-
ers, directs the brain to adjust its sensitivity to stimuli,
controls impulsive behavior, and is critical to organi-
zational and emotional skills (Wood & Worthington,
2017). Impaired executive function in TBI, due to dam-
age to the frontal lobes, affects an individual’s ability to
use language effectively in social situations.
Dementia
The CDC estimates that 5.7 million people in the
United States are living with Alzheimer’s disease (AD),
the leading cause of dementia (https://www.cdc.gov/
chronicdisease/resources/publications/aag/alzheim-
ers.htm). AD is most often diagnosed in people above
the age of 65 years. The growing number of elderly
people in the United States suggests a future with ever-
increasing diagnoses of AD (https://www.cdc.gov/
chronicdisease/resources/publications/aag/alzheim-
ers.htm).
In a 2011 to 2013 review of Medicare data,
Alzheimer’s disease accounted for roughly 45% of all
diagnosed dementias. The other subtypes of demen-
tia, such as vascular dementia, Lewy body dementia
(as well as Parkinson’s disease dementia), and fron-
totemporal dementia, had substantially lower preva-
lence compared with AD (Goodman et al., 2017) but
still accounted for slightly more than half of all diag-
nosed dementias. Thus, the total number of people
in the United States living with dementia is probably
in excess of 10 million. Worldwide the prevalence of
dementia and its impact on families is staggering.
Dementia has many different behavioral charac-
teristics which depend to some degree on the specific
type of the disease. Problems are observed in memory,
general cognition, executive function, psychiatric dis-
turbance, depression, and agitation. These all lead
to profound effects on everyday life functions. In all
cases of dementia, the underlying brain disease is pro-
gressive and irreversible. Death of neurons either in
specific regions of the brain or throughout the brain is
the cause of the dementia symptoms and their worsen-
ing over time.
For each of the dementias described later in this
chapter, a general statement of the underlying brain
pathology is provided. More detailed accounts of brain
pathologies in dementia are available in the scientific
literature.
Speech and language disorders are a prominent
characteristic of dementia. To some degree, the specific
characteristics of a speech and language impairment,
and the way they change throughout the course of the
disease, are different for the different types of dementia.
Brain Pathology in Dementia
The brain pathology in AD includes an extracellular (on
the outside of a brain cell) accumulation of a substance
called amyloid, and an intracellular (inside the cell)
accumulation of neurofibrillary tangles which are accu-
mulations of proteins that prevent normal function of
a neuron (Kumar, Kumar, Keegam, & Deshmuk, 2018).
These abnormal accumulations increase over time and
cause dysfunction and eventual death of neurons.
In vascular dementia, localized or general regions
of the brain are destroyed when blood flow to these
regions is limited or blocked completely (hence, the
term “vascular” dementia). The lesions created by the
loss of blood flow are the cause of many of the demen-
tia problems mentioned previously. Memory problems
are typically absent in this type of dementia, at least
at the beginning of the disease. O’Brien and Thomas
(2015) have published an excellent review of vascular
dementia and the debate surrounding the diagnosis.
Lewy body dementia is a broad category of differ-
ent dementias. Lewy bodies are pathological clusters of
proteins within nerve cells. Symptoms of Lewy body
dementia include cognitive impairment, visual diffi-
culties including hallucination, thinking and reasoning
impairments, and confusion that varies within a day
or from day to day (Walker, Possin, Boeve, & Aarsland,
2015). At the outset of Lewy body dementia, very few
patients have speech and/or language impairments,
but with progression of the disease, language impair-
ments are likely.
Frontotemporal dementia (FTD) is a complex
brain disease that takes one of several forms (Olney,
Spina, & Miller, 2017; Mesulam, 2018). Progressive pri-
mary aphasia, discussed previously, is considered to
be a form of FTD, or at least to progress over time to
FTD. Regardless of the form, the brain pathology com-
mon to a diagnosis of FTD is atrophy of the frontal and
temporal lobes (Bang, Spina, & Miller, 2015). The ini-
tial signs of an FTD that does not begin with language
deficits are primarily behavioral, including personality
changes, loss of inhibition, and impairment of execu-
tive function.
 9  Language Disorders in Adults 127

Language Disorders in Dementia “Classification of Aphasia.” Like the nonlanguage

symptoms of dementia, the speech-language symp-
Speech-language characteristics in several types of toms evolve during the progression of the disease and
dementia are listed in Table 9–2. Most of these char- may not be the same at two points in time. Speech and
acteristics have been discussed in the earlier section language impairments may be observed in the early

Table 9–2.  Selected Speech and Language Characteristics of Several Types of Dementia

Type of Dementia Speech and Language Characteristics

Alzheimer’s disease
Anomia
Semantic paraphasias (e.g., “toes” for “hand”)
Poor word comprehension
Reduced word fluency (poor ability to name as many animals as
possible)
Loss of narrative cohesion
Relatively preserved phonological and syntactical skills
Formulaic speech preserved (“Hi, how are you?”; “Excuse me”)

PPA (FTD):  Nonfluent Nonfluent speech (effortful, slow)

aphasia Agrammatism
Phonemic paraphasias
Impaired repetition
Late-stage mutism

PPA (FTD):  Semantic Fluent, empty speech

dementia Semantic paraphasias (e.g., “toes” for “hand”)
Severe anomia
Intact automatic speech (“Hi, how are you?”)
Loss of meaning in both expression and comprehension
Preservation of syntax

PPA (FTD):  Logopenic Poor word retrieval

Frequent pausing (presumably searching for words)
Impaired repetition

FTD: (Behavioral) Loss of narrative cohesion

Vascular Loss of phonemic fluency (poor ability to name things when

required to confine the names to a single beginning sound)
Reduction of expressive grammatical complexity

Lewy body dementia Early preservation of language skills

Later narrative incoherence
Anomia
Reductions in word fluency

Note.  Not all characteristics are seen in a specific type of dementia. FTD = frontotemporal dementia; PPA
= primary progressive aphasia. Based on information in “Cognition, Language, and Clinical Pathological
Features of Non-Alzheimer’s Dementias: An Overview,” by J. Reilly, A. Rodriguez, M. Lamy, and J. Neils-Strun-
jus, 2010, Journal of Communication Disorders, 43, pp. 438–452; “Connected Speech in Neurodegenerative
Language Disorders: A Review,” by V. Boschi, E. Catricalà, M. Consonni, C. Chesi, A. Moro, and S. F. Cappa,
2017, Frontiers in Psychology, 8, p. 269; Steel, Ferguson.
128 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
stages of dementia or become apparent with disease
progression. The possibility that type-specific impair-
ments of speech and language may contribute to a
differential diagnosis of dementia type is intriguing
(Reilly, Rodriguez, Lamy, & Neils-Strunjus, 2010). The
differential diagnosis of type of dementia is not always
agreed upon, even by experienced medical profession-
als. For example, the diagnostic distinction between
Alzheimer’s disease and vascular dementia may be
particularly challenging. Speech-language pathologists
can have an important role in sharpening diagnostic
distinctions in the dementias.
Chapter Summary
Stroke, TBI, and dementia are common causes of acquired,
adult language disorders.
Language disorders in adults may occur because
of damage to cortical and subcortical structures asso-
ciated with speech and language skills, or as a result
of connections between these structures, or both; these
structures are located (for most people) in the perisyl-
vian speech and language area, which includes parts of
the frontal, temporal, and parietal lobes.
Aphasia is an impairment of language expression
and/or comprehension, resulting from brain damage;
aphasia can be the result of a stroke, TBI, or dementia.
Stroke, which results from a loss of blood flow to
regions of the brain, may result in an expressive, recep-
tive, or mixed (both expressive and receptive) aphasia.
There are several types of aphasia, including Bro-
ca’s aphasia, Wernicke’s aphasia, conduction aphasia,
anomic aphasia, global aphasia, and primary progres-
sive aphasia.
Broca’s aphasia is a nonfluent, mostly expressive
aphasia likely due to anterior damage in the perisyl-
vian speech and language areas.
Wernicke’s aphasia is a fluent, mostly receptive
aphasia, likely due to posterior damage in the perisyl-
vian speech and language areas.
Conduction aphasia is a fluent aphasia in which
comprehension and expression are more or less intact
(Broca’s and Wernicke’s areas are unaffected by the
stroke), but repetition is impaired because of damage
to the arcuate fasciculus, the fiber tract that connects
Broca’s and Wernicke’s areas.
Global aphasia is a nonfluent aphasia in which
both expressive and receptive language is impaired; it
is usually the result of both anterior and posterior dam-
age in the perisylvian speech and language area.
Primary progressive aphasia is not due to stroke
but often begins as an isolated language problem that
increases in severity over time; the brain disease selec-
tively affects the frontal and temporal lobes, including
speech and language tissue in those lobes.
Apraxia of speech is thought by some to be a
motor speech disorder and by others to be an apha-
sia (or both); it is most commonly regarded as a motor
speech disorder in which the problem is poor speech
motor planning.
Aphasia is a frequent result of TBI, but the expres-
sive and receptive language deficits often do not easily
fit the aphasia types discussed in the chapter; as peo-
ple recover from TBI, their structural language deficits
resolve, but in many cases, a social language use dis-
order remains.
Dementia takes several different forms, including
Alzheimer’s disease, vascular dementia, Lewy body
disease, and frontotemporal dementia.
Language deficits in dementia are common and
vary depending on the type of dementia.
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Speech Science I
Introduction
The term “speech science” is used to designate the dis-
cipline in which normal (typical) processes of speech
production, acoustics, and perception are studied. An
underlying body of knowledge for these areas of study
includes the anatomy of the speech and hearing mech-
anism and an appreciation for the basic principles of
acoustics. The value of this knowledge is similar to the
requirement of full understanding of anatomy, biology,
chemistry, and physics for individuals preparing for a
career in clinical medicine, or the value of anatomy and
movement in the training of physical therapists. The
current chapter presents information on anatomy and
physiology of the speech mechanism. The acoustics of
speech are presented in Chapter 11, and the anatomy
and physiology of the hearing mechanism are pre-
sented in Chapter 22.
The Speech Mechanism:
A Three-Component Description
The speech mechanism is composed of three major
divisions, including the respiratory system, the larynx,
and the upper and nasal airways (Figure 10–1). Each
division has many anatomical components, including
bones, ligaments, cartilages, membranes, and muscles.
Each division can also be assigned a global function in
the production of speech. These global functions sim-
10
plify the actual workings of each part, but they pro-
vide a useful organizing perspective. The anatomical
structures and functions are as follows: (a) the respira-
tory system, which is the power supply for speech; (b) the
larynx, which by using airflow from the respiratory
system to vibrate the vocal folds is the primary sound
source for speech, and (c) the upper and nasal airways,
which by movements of structures modify the sound
source to form different speech sounds. Detailed presenta-
tions of speech anatomy and physiology are available
in Zemlin (1997) and Hixon, Weismer, and Hoit (2020).
Brain anatomy and physiology for speech production
and hearing, which is often included as part of speech
and hearing science, is covered in Chapter 2.
“Functional anatomy” is discussed for each com-
ponent of the speech mechanism. Functional anatomy
presents the anatomy of a component at a level that is
sufficient to understand the broad physiology (func-
tion) of the component. The functional anatomy pre-
sented in these sections is a much-simplified view of
the anatomy presented in courses such as the “Speech
Anatomy and Physiology” course listed in Table 1–3.
Respiratory System Component
(Power Supply for Speech)
It is useful to think of the respiratory system as con-
sisting of two major parts, one being the lungs and the
other being the chest wall. The lungs are composed of
131
132 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Upper and Nasal
Airways
Larynx
Respiratory
System
Figure 10–1. View of the three-part speech mechanism, including the respiratory
system, larynx, upper airways/nasal passages.
spongy, elastic tissues that inflate and deflate as air
passes into and out of them. Air in the atmosphere is
taken into the lungs via a series of tubes (called bron-
chioles and bronchi) that terminate in the alveoli, where
oxygen and carbon dioxide are exchanged between
the bloodstream and air. As air is expelled from the
lungs, it travels through the increasingly large tubes
and passes through the largest tube, the trachea, before
passing through the vocal folds and entering the air
spaces in the throat (pharynx), mouth, and nose.
The chest wall includes all structures of the respi-
ratory system that are outside the lungs but are capable
of compressing or expanding the air within the lungs.
The anatomical structures that can compress or expand
the lungs include a large set of muscles in the thorax
(often called the chest), abdomen, and diaphragm (a
large muscle that separates the thorax and abdomen).
Elastic properties of structures such as the ribs and the
sac-like membranes that enclose the lungs also contrib-
ute to compression or expansion of the lungs.
Compression or expansion of the lungs exerts a
force on the air within the lungs. When the lungs are
compressed, air molecules within them are compressed
(forced together more closely) which increases lung
pressure; when the lungs are expanded, air molecules
within them are expanded (pulled apart from each
other) which decreases lung pressure.
The Effect of Lung Pressure on Airflow
Changes in lung pressure are critical to moving air in
the expiratory (breathing out) and inspiratory (breath-
ing in) directions. When the lungs are open to the atmo-
sphere, which means there are no blockages along the
pathway from lungs to lips, or from lungs to the nares
(outlets of the nostrils), the pressure inside the lungs and
in the atmosphere are the same. In this circumstance,
air does not flow between the lungs and atmosphere,
in either direction. Air flows from one point to another
only when there is a pressure difference between the
points. Lung pressure is raised when the lungs are
compressed by muscular contraction and other forces
(such as elastic forces). When lung pressure is greater
than pressure outside the mouth, which we refer to as
atmospheric pressure, air flows from the lungs to the
atmosphere (as in exhalation). When lung pressure

is lowered relative to atmospheric pressure, air flows
from the atmosphere to the lungs (as in inhalation).
Speech is produced on exhaled air; inhaled air is used
to fill the lungs and make the air supply ready for the
next utterance.
The Respiratory System and
Vegetative Breathing
Vegetative breathing is the exchange of air between the
lungs and atmosphere that is required to sustain life.
Vegetative breathing, also called rest breathing, is what
you do when sitting at your desk and studying, sleep-
ing, watching television, or the many other activities
that involve quiet and seemingly effortless inhalation
and exhalation. The purpose of vegetative breathing is
simple. Air is inhaled to bring oxygen (O2) to millions
of alveoli, the tiny, sac-like structures that are the termi-
nal chambers within the lungs. The O2 is stored in the
alveoli and distributed to the bloodstream in a slow,
continuous process. As the O2 travels in the blood-
stream, it is picked up and used in the normal function-
ing of every cell within the body. The functioning of
these cells produces byproducts, one of which is carbon
dioxide (CO2). CO2 is a toxin that must be continuously
eliminated from the body. This is done by carrying
CO2 through the bloodstream to the alveoli — the same
100
Percent Vital Capacity
35
rest breaths VC
0 2
Time
Figure 10–2.  Spirogram showing lung volume events as a function of time. Three rest breaths
are followed by a vital capacity maneuver, and then by two more rest breaths. See text for addi-
tional detail.
10  Speech Science I 133
organ that stores O2 — where it is “leaked out” to the
airways and exhaled to the atmosphere. The alveoli
function as a two-way valve, storing O2 collected from
inhaled air for delivery to the bloodstream, and stor-
ing CO2 collected from the bloodstream’s uptake of
by-products of cellular activity for expulsion from the
body via exhalation.
Figure 10–2 is a breathing record called a spiro-
gram, generated with an instrument called a spirometer
or respirometer. The respirometer is an instrument that
measures the volume of air inhaled or exhaled to or
from the lungs. A participant breathes into the instru-
ment while wearing a face mask; the device records
the air volumes that have been displaced into or out
of the lungs. The spirogram shows inhalation going up
on the graph and exhalation going down. The x-axis of
the graph is time, and there are two y-axes: the one on
the left is labeled “Percent Vital Capacity” and the one
on the right is labeled “Volume in Liters.” These y-axes
are two different ways to express lung volume.
The spirogram shows three cycles of inhalation-
exhalation that begin and end at the same height on
the y-axis, indicated by the lower, horizontal dashed
line. These are rest breathing cycles, which have three
noteworthy characteristics. First, they repeat over time;
second, the inhalation and exhalation phases are sym-
metrical, both in time (it takes the same amount of time
to inhale as it does to exhale) and volume (the same
6
Volume in Liters
134 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
amount of volume is inhaled and exhaled); and third,
the volume exchanged is relatively small. In healthy
individuals, the volume exchanged during rest breath-
ing is no more than half a liter (500 milliliters), which is
about 1/8th the volume that can be exhaled after tak-
ing a maximally deep breath.. The volume inhaled and
exhaled during rest breathing is called tidal volume.
Now imagine that the person who has generated
these rest breathing cycles is asked to inhale as deeply
as possible and then exhale as much air as he can from
this maximum inhalation. The maximum inhalation is
shown on the spirogram as a large, upward trace fol-
lowing the rest breathing cycles. The subsequent long,
downward trace ending well below the volume of the
rest breathing cycles is the total volume of air that can
be exhaled from the maximum inhalation. The act of
inhaling maximally and then exhaling maximally is
called a vital capacity maneuver. Vital capacity (VC)
is defined as the volume of air that can be exhaled
from the lungs following a maximal inhalation. VC is
marked on Figure 10–2.1 The value of VC varies among
individuals, depending on sex, body size, age, health
history, and other factors.
The y-axis on the left of Figure 10–2 expresses the
volume of air within the lungs in a way that allows
comparisons across individuals, even though their
actual VC volumes may be quite different. This axis
expresses all lung volumes as percentages of an indi-
vidual’s VC.
Speech Breathing
The term “speech breathing” is used to differenti-
ate breathing for speech from vegetative breathing,
breathing during exercise, breathing to sing, and other
behaviors in which the respiratory system plays an
important role. Speech breathing depends on increas-
ing or decreasing lung pressure to cause air to flow out
of or into the lungs. Flow from the lungs to the atmo-
sphere is used to produce words, sentences, and para-
graphs; flow from the atmosphere is used to refill the
lungs between utterances.
What range of lung volumes do speakers use to
generate the airflows and pressures required to pro-
duce audible speech? In theory, speaking can take
place throughout the vital capacity — over the entire
lung volume range. As it turns out, most speakers
use only the lung volumes in the middle of the VC.
1
 ypical values of VC are 4.6 liters (L) for adult males and 4.0 for adult females; values will be lower for children. VC values vary with body
T
size, sex, and age, so the values given here are averages only. When a participant has exhaled all the air he or she possibly can, there is still a
volume of air remaining in the lungs, shown in Figure 10–2 as the shaded region at the bottom of the graph, but this is typically not measured
and is not included in the VC measures.
They begin speaking at around 60% of the VC, exhale
air during speaking to about 35% VC, refill the lungs
(without speaking) to about 60% VC, and continue
speaking. The pattern of lung volume usage for speech
is shown in Figure 10–4. Note the rest breathing cycles
immediately prior to the rapid inhalation, and the long,
slow decrease in lung volume for each phrase of the
utterances, “You wish to know all about my grandfa-
ther, well, he is ninety three years and he still thinks
as swiftly as ever.” The speech breathing inhalation-
exhalation pattern is different from the pattern for veg-
etative breathing.
The Goal of Speech Breathing
The goal of speech breathing is to maintain a roughly
constant lung pressure during an utterance. This is
illustrated in Figure 10–3, which shows lung pressure
measured before, during, and after the utterance, “This
is the best textbook on Introduction to Communica-
tion Disorders.” The word “best” is emphasized by the
speaker. Time is on the x-axis, and lung pressure is on
the y-axis, the latter measured in units of centimeters
of water (cm H2O, a unit of air pressure). The “zero”
value on the pressure scale, indicated by a horizontal
dashed line extending across the graph, corresponds to
atmospheric pressure. Positive pressures indicate lung
pressures greater than atmospheric pressure. Negative
lung pressures are less than atmospheric pressure.
The lung pressure during the entire utterance,
which has a duration slightly less than 2 s, is more or
less constant at a value of around +6.5 cm/H2O. There
is a small, temporary increase in pressure to about
7 cm/H2O (upward-pointing arrow) for the empha-
sized word “best.” Note the small, negative pressures
immediately before and after the utterance. These
negative pressures are the result of expansion of the
lungs to allow inhalations before and after the utter-
ance. The momentary pressure increase for the word
“best” makes it louder, consistent with the emphasis
on this specific word in the utterance.
Figure 10–4 shows percentage VC on the y-axis
and time on the x-axis for the first three utterances
of a famous reading passage in speech-language pa-
thology, the Grandfather Passage (Darley, Aronson, &
Brown, 1975). This lung-volume-by-time graph illus-
trates the small range of lung volumes used for each
of these three utterances. Two cycles of rest breathing
are shown before a rapid inhalation to about 60% VC.
 10

Lung pressure (cm H2O)

This is the best textbook on Communication disorders

breath breath
2 seconds
Time

Figure 10–3.  Graph showing lung pressure over time for the utterance, “This is the best textbook
on communication disorders,” with emphasis on the word “best.” Note how the positive pressure devel-
oped in the lungs is at a nearly constant value for the entire utterance, except for a brief and small
increase for the emphasized word “best.”

100
Percentage VC

60

35

You wish to know all about my grandfather well he is nearly ninety three years old and he still thinks as swifty as ever

Figure 10–4.  Graph showing lung volume, expressed as percent vital capacity (VC) over time, for
the three utterances, “You wish to know all about my grandfather/well he is nearly ninety-three years
old/and he still thinks as swiftly as ever.” For each utterance, the talker inhales to about 60% VC and
talks on exhalation down to a lung volume of about 35% VC. Speech is produced within a limited range
of lung volumes, even across three consecutive utterances.

135
136 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
The inhalation is followed by a slow, long decrease of
lung volume for the first phrase (“You wish to know
all about my grandfather”). When the lung volume
decreases to roughly 35% VC, there is another rapid
inhalation to approximately 60% followed by a similar
slow, decreasing lung volume for the second phrase
When Less Is More
That speech is produced using a small
range of lung volumes may seem uneconomical:
use of the entire VC for speech seems to suggest
the possibility of more message per unit time.
But, in fact, studies of speech breathing (Hixon,
Goldman, & Mead, 1973) have shown that
speech produced between about 60% and 35%
VC (about ¼ of all the air you can exhale follow-
ing a maximal inhalation) requires less muscular
activity in the thorax and abdomen, compared
with speech produced at very high lung volumes
(near 100%) or very low lung volumes (near
the point in lung volume where you cannot
exhale any more air). In the midrange of lung
volume — between 60% and 35% VC — the least
muscular activity is required to maintain a
constant lung pressure (see Figure 10–3). What
we have here is biological efficiency — minimal
exertion with more payoff.
Hands relaxed
Larynx
Thoracic
wall
Abdominal
wall
Figure 10–5.  Balloon model of how muscular effort in the respiratory system can be
applied under inefficient (middle) and efficient (right ) conditions to maintain the constant,
positive lung pressures required for speech production.
(“well, he is nearly ninety-three years old”). This se-
quence is repeated for the third phrase (“and he still
thinks as swiftly as ever”).
The breathing cycles for speech use much less air
volume than the VC. The breathing cycles for speech
also differ from the rest breathing cycles before the
first phrase in Figure 10–4. The lung volumes used for
rest breathing cycles are less than the volumes used
for speech. In addition, the relative durations of the
inhalation and exhalation phases of the two types of
breathing — rest breathing and speech breathing — are
different. The inhalation-exhalation phases are equiv-
alent for rest breathing, but in speech breathing, the
inhalation phase occurs very quickly, and the exhala-
tory phase is much longer. The long exhalatory phase
in speech breathing is largely a result of interruptions
of the outgoing airflow at the vocal folds and at loca-
tions in the airway between the vocal folds and the lips.
These interruptions are like valves opening and closing
as air flows through a tube.
Speech Breathing and Abdominal Muscles
Muscles of the thorax and abdomen contribute to lung
compression and therefore the raised lung pressures
that cause air to flow from lungs to atmosphere. Con-
traction of the abdominal muscles is especially impor-
tant for efficient speech breathing. A balloon model of
these muscular events is shown in Figure 10–5. The bal-
loon is inflated with the open end pinched closed. The
Thoracic wall Thoracic wall expiration
expiration and Abdominal wall
expiration

hands around the balloon represent the compressive
muscular effects of the thorax (top hand) and abdo-
men (bottom hand). In the left-hand image, the hands
are relaxed, as if the muscles of the thorax and abdo-
men are relaxed, exerting no force on the lungs. The
middle image shows a squeeze by the upper hand, as
if the muscles of the thorax exert compression of the
lungs; the bottom hand is relaxed. The upper squeeze
momentarily raises the pressure in the balloon, but the
incompressible nature of air in a closed volume results
in the bulge of the balloon’s bottom half. The pres-
sure increase of the air inside the balloon is “lost” in
the expansion of the bottom half — this is not what you
want to maintain a constant, positive pressure during
a speech utterance as shown in Figure 10–3.
How can the pressure be maintained at a con-
stant level when the expiratory muscles of the thorax
are contracted? The answer is in the contraction of the
abdominal muscles. A constant squeeze of the balloon
by the bottom hand (right image, Figure 10–5) allows
squeezes at the top of the balloon to maintain the con-
stant pressure required for speech utterances, with
relative ease. The thoracic squeezes do not have to be
excessive to maintain the pressure. In addition, small
squeezes of the top hand during speech can raise the
pressure with relative ease (e.g., emphasis on “best” in
Figure 10–4).
The Balloon Model
Provides a Clinical Hint
The balloon model of muscle activity of the
thorax and abdomen, and its effect on pres-
sure in the lungs, is more than a simple way
to explain speech breathing. Individuals who
have weak or paralyzed abdominal muscles
and normal or near-normal functioning of the
thoracic muscles can compress the lungs with
their thoracic muscles, but the increased lung
pressure is partially or completely reduced or
lost when weak or paralyzed muscles of the
abdomen cannot hold in the abdominal wall.
These speakers have to work much harder to
produce acceptable levels of lung pressure for
speech, which can have significant effects on
their ability to communicate. A low-tech clini-
cal approach to the speech breathing problem
of ineffective abdominal muscles is to use an
adaptive device (like a thick belt) to compress
the abdomen during speech. The belt takes over
the role of the abdominal muscles, holding in
the abdomen to prevent it from being pushed
outward.
10  Speech Science I 137
The muscular actions in the respiratory system for
the generation of utterance pressure are as shown in
the balloon model. The expiratory muscles of the tho-
rax do the primary job of lung compression, while the
abdominal muscles do the primary job of holding in
the abdominal wall, preventing it from bulging out and
causing the lungs to lose the pressure raised by con-
traction of thoracic muscles The constant contraction
of the abdominal muscles during speech is an efficient
solution to generating a constant lung pressure for
speech utterances.
Speech Breathing and Voice Loudness
The lung pressure value of 6.5 cm H2O in Figure 10–3
does not mean much to someone who has not worked
with air pressures in the speech mechanism, so a real-
world reference is offered here. If you are speaking
with someone in a quiet room and the two of you are
standing about 1 meter apart, speech with a lung pres-
sure of 6.5 cm H2O sounds comfortably loud — not too
loud, not too soft. It is a more or less typical value of
lung pressure used by people speaking to each other at
fairly close range. A lung pressure of 9 cm H2O makes
speech seem loud at this distance, and lung pressures
approaching 12 cm H2O produce a speech loudness
that seems like shouting.
Clinical Applications:  An Example
Lung pressure is the primary determinant of speech
loudness. Greater lung pressure typically results in
louder speech (assuming a constant distance between
a speaker and listener). Lung pressure is therefore an
important factor in the intelligibility of speech; softer
speech is more likely to suffer from intelligibility prob-
lems than louder speech. Speech-language clinics see
patients whose primary complaint is an inability to be
understood because they cannot generate an adequate
amount of lung pressure.
Speech intelligibility may not be the only problem
associated with a speech breathing problem. A person
who has speech breathing problems and difficulty
producing changes in lung pressure and therefore
speech loudness may experience a reduced ability to
convey emotional states. We use the loudness of our
voices to express a variety of emotions, and a patient
who does not have good control over lung pressures
may suffer in this area. This paralinguistic function of
speech breathing (“paralinguistic” meaning the use of
nonverbal cues such as loudness and pitch to convey
mood, emotion, and so forth) is an important aspect
of communication, especially in social situations (see
Chapter 3).
138 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

The Larynx (Sound
Source for Speech)
As shown in Figure 10–6, the larynx is a structure that
is composed of cartilage, muscle, ligaments, and mem-
branes. The vocal folds are the component of the larynx
that generates the sound source for all vocalic sounds
(vowels, semivowels, diphthongs, and nasals) as well as
a subset of consonants. This sound source comes from
the vibration of the vocal folds, as discussed below.
Laryngeal Cartilages
The laryngeal cartilages form a strong but flexible
framework to support a collection of soft tissues (mus-
cles, ligaments, and membranes). The major carti-
lages of the larynx, as well as the hyoid bone which is
attached to the larynx, are shown in Figure 10–6.
Figure 10–6 shows the position of the larynx
within the neck. Immediately above the larynx is the
bottom of the throat, and immediately below the lar-
ynx is the upper edge of the windpipe (trachea). The
two red bands between the arytenoid cartilages and
the front of the thyroid cartilage represent the vocal
folds — the tissue whose vibrations create the sound
source. The larynx is very small — from top to bot-
tom about 45 mm (1.75 inches) in men, 36 mm in
women (1.40 inches), and much smaller in children.
The length of the muscular part of the human vocal
folds is equally tiny — about 14 mm (0.58 inches)
in men, and 11.1 mm (0.44 inches) in women, and
smaller in children (for adults, see Su et al., 2002).

Hyoid bone
Thyroid cartilage
Epiglottis
Arytenoid cartilages

Cricoid cartilage

Figure 10–6.  The position of the larynx in the neck, with four
cartilages (cricoid, arytenoid [paired], thyroid, and epiglottis)
and one bone (hyoid bone) labeled. Note the top of the trachea
immediately below the cricoid cartilage.
 10  Speech Science I 139

Laryngeal Muscles and Membranes

Laryngeal muscles are classified broadly into one

of two categories according to their points of attach-
ment. Anatomists refer to muscle attachment points
as origins and insertions.2 Intrinsic muscles of the larynx
have both points of attachment within the larynx (e.g.,
from the arytenoid cartilages to the thyroid cartilage).
Extrinsic muscles have one point of attachment within
the larynx and one on a structure outside the larynx
(e.g., from the breastbone to the thyroid cartilage).
Extrinsic muscles are primarily responsible for posi-
tioning the larynx within the neck; they are the ones
that cause the Adam’s apple to bob up and down dur-
ing speech.
The intrinsic muscles of the larynx open and close
the vocal folds, stretch them, and adjust muscular ten-
sion to create different types of vocal fold vibration
and, therefore, different voice qualities.
Among the five intrinsic muscles of the larynx
three can close the vocal folds, one can open the vocal
folds, and one can stretch the vocal folds. Several (if Figure 10–7.  Insertion of a laryngeal mirror to the
not all) of these muscles serve double duty. For exam- throat to view the vocal folds (enclosed in the black oval ).
ple, one of the muscles can both close and tense the The tongue is gently pulled away from the mouth to move
vocal folds, another “closer” can also change the con- structures forward that are likely to prevent a clear view of
figuration of the vocal folds, which affects the quality the vocal folds.
of the voice.

folds, the target of the examiner’s view. A photograph

The Vocal Folds
The vocal folds are bands of muscular and nonmuscular
(e.g., membranes and ligaments) tissue that run from
their forward point of attachment on the inside of the
thyroid cartilage to the posterior point of attachment
on the vocal process of the arytenoid cartilage (red lines
in Figure 10–6). The muscular part of the vocal folds is
one of the five intrinsic muscles of the larynx.
Figure 10–7 illustrates how an examiner obtains
a “live” view of the vocal folds. A laryngeal mirror is
inserted into the mouth and positioned close to the
back of the throat, just under the flap of tissue called
the soft palate. The mirror is tilted at an angle relative
to the stem of the instrument. The tongue is pulled gen-
tly forward to move structures such as the tongue and
epiglottis forward and out of the way for a clear view of
the vocal folds. The vocal folds are reflected in the mir-
ror, which is illuminated by a bright light fastened to a
band around the examiner’s head, much like a miner’s
light. In Figure 10–7, a black oval surrounds the vocal
can be taken of the image in the mirror. Devices are also
available for recording successive images of the vocal
folds over time, during speech.
Two images of the vocal folds are shown in Fig-
ure 10–8. The image on the left shows open vocal folds.
The bands of vocal fold tissue, pearly gray with a touch
of pale pink, extend from the back to the front of the
larynx. One end of the bands of vocal fold tissue form
the point of a “V,” where the two vocal folds come
together at the front of the larynx, on the inner sur-
face of the thyroid cartilage. The arms of the “V”
diverge as they move to the back of the larynx. Follow
the bands from the front (at the point of the “V”) to
the back and along the edge of each vocal fold, and
you see a change of color from pearly gray/pinkish
white to pale white. The pale white is the posterior
attachment of the vocal folds. These posterior points
of attachment are to a part of the arytenoid cartilage
(called the vocal process) on the same side as the vocal
fold (see Figure 10–7).

2 
 raditionally in anatomical descriptions, when a muscle contracts, it pulls from the point of insertion toward its origin, and hence, the distinc-
T
tion between two points of attachment. Usually, the origin is thought of as the more “fixed” point of attachment, whereas the point of insertion
moves the structure to which it is attached. This is convenient anatomical terminology but, in reality (and especially for many muscles of the
speech mechanism), it is not quite so simple.
140 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Vocal folds open Vocal folds closed

(Anterior)
FRONT

Figure 10–8.  Two views of the vocal folds from above. In both images, the front of the neck is at the
bottom of the image, where the vocal folds come together on the inner surface of the thyroid cartilage.
The left image shows the vocal folds open; the glottis is wide. The vocal folds form the point of a “V”
where they meet at the thyroid cartilage. The right image shows the vocal folds closed. Technically, when
the vocal folds are closed there is no glottis. However, the term “glottis” is widely used to refer to the
vocal folds, whether closed or not.

The opening between the vocal folds is called the
glottis (see Figure 10-8). With the vocal folds open, air
can flow from the lungs and through the larynx to the
airways of the throat, nose, and oral cavities. Think of
the vocal folds shown in the left image of Figure 10–8
as an open valve between the lungs on the one hand
and the upper airways on the other hand.
The open vocal folds allow a view of rings of tissue
beneath the glottis. The structure containing these rings
is the tube-like windpipe (trachea). This is the large air
tube that gives off increasingly smaller tubes that reach
deep into the lungs where air can be absorbed by alve-
oli to carry oxygen to cells of the body, and that allows
CO2 to flow from the alveoli to the atmosphere.
The right side of Figure 10–8 shows a photograph
of closed vocal folds. Vocal fold closure in the absence
of phonation, the term used for the sound made by the
vibrating vocal folds, occurs during exertion (such as
lifting a heavy object, or going to the bathroom), and
importantly, as part of the swallowing process. Vocal
fold closure during swallowing is critical to protect-
ing the airway during the passage of fluids and solid
food from the mouth and pharynx into the esophagus
(Chapter 20).
The structure of the vocal folds is complex and
includes both muscular and nonmuscular tissues. The
nonmuscular parts include a membranous casing that
covers the main bulk, or muscular body of the vocal
fold. Very importantly, even though the membranous
cover and muscular body are part of the same structure ​
— ​the vocal fold — the two parts can move somewhat
independently of each other. Moreover, the degree of
their independent movement can be adjusted in fine
increments, depending on the contraction pattern of
laryngeal muscles.
The fine structure of vocal fold tissues, as viewed
under a microscope, has been studied in a fair amount
of detail with some surprising results. The eminent
Japanese physician Minoru Hirano (1932–2017) de-
voted much energy to histological study of vocal folds
in humans and various animals (“histology” is the
study of the microscopic characteristics of biological
tissue).
Hirano discovered that the adult, human vocal
fold has a complicated tissue structure unlike that of
any other species. This complicated tissue structure is
also not seen in human infants but develops as children
mature into adulthood. The difference between human
and animal vocal folds was surprising because the
primary function of the vocal folds is often regarded
as protection of the airway, as noted earlier. Because
protection of the airway is so important for health and
even life in humans and animals, the vibratory func-
tion of the vocal folds — their sound producing capa-
bilities — had sometimes been regarded as a secondary
capability of the mammalian larynx, as if the vocal

folds were adapted to a secondary purpose (phona-
tion) while maintaining its primary role of protecting
the lungs.
Hirano’s research suggested otherwise. His dis-
covery of the elaborate tissue structure of the human
vocal folds suggested strongly that they were special-
ized for human voice. This specialization explained
the remarkable range of voice qualities produced by
humans and the role played by phonation in the fine
nuances of human communication.
Phonation
Phonation is the production of sound by the nearly
periodic (repeating over time) vibration of the vocal
folds. The repetitive opening and closing of the vocal
folds during phonation is controlled by air pressures,
air flows, and elastic characteristics of vocal fold tis-
sue. While it is true that laryngeal muscles can open
and close the vocal folds, as described earlier, opening
and closing movements of vocal fold vibration are not
produced by repetitive muscle contractions.
To initiate phonation, a speaker brings her vocal
folds together through the action of laryngeal muscles.
Voice scientists refer to this action as adduction of the
vocal folds. At the same time, the speaker develops a
positive lung pressure, using the muscles and elastic
properties of the respiratory system. Because the tra-
chea contains air continuous with that of the lungs,
pressure in the lungs and in the trachea, immediately
below the closed vocal folds, is essentially the same.
The positive tracheal (lung) pressure acts as a force
against the closed vocal folds. This pressure overcomes
the force of the muscles that adducted them and blows
the vocal folds apart. Through a complex interaction
of mechanical (e.g., elasticity of vocal fold tissue) and
aeromechanic (e.g., air pressures and flows) forces, the
vocal folds are displaced outward and then return to
the midline, closing rapidly and firmly. With the vocal
folds again in the closed position, this cycle of events
is repeated, because the tracheal (lung) pressure is still
positive and blows the vocal folds apart, each time they
close. Recall from the first section of the chapter that
the goal of speech breathing is to maintain a constant
lung pressure during speech. In the present case, we
can say the constant lung pressure is maintained as
long as phonation is produced.
Figure 10–9 shows a series of images from a high-
speed digital recording of one cycle of vocal fold vibra-
tion. The instrument used to record these images is a
sophisticated digital camera that records sequences of
images in very rapid succession. The images are pho-
10  Speech Science I 141
tographed from the reflection of the vocal folds in a
laryngeal mirror, as previously described (see Fig-
ure 10–7). In each image, the front of the vocal folds
is at the bottom, and the back of the vocal folds is at
the top. The successive images are recorded so rapidly
because a cycle of vocal fold vibration lasts only a frac-
tion of second (e.g., in women about .005 seconds). One
cycle of vocal fold vibration is defined as movement
from the closed position (frame 1 in Figure 10–9) to the
most open position (frame 5), and back to the closed
position (frames 9 and 10).
When the series of still images in Figure 10–9 is
watched as a video, the highly complex motions of
the vocal fold tissues are revealed (Google “vocal fold
motion,” select “video,” and many options for view-
ing vocal fold motion are available (see Box, “Waving
in the Wind”). The membrane that encases the muscu-
lar bulk of the vocal fold vibrates somewhat indepen-
dently of the muscle, giving the motion of the vocal
folds during phonation a rippling appearance across
their top surface. In other words, during typical pho-
nation the vocal folds do not vibrate like rigid pistons
moving back and forth. Rather, the motions appear
complex, almost wavy. This complex motion is what
gives the human voice its unique sound. The pattern of
vocal fold movement varies depending on factors such
as the pitch of the voice and the smoothness or rough-
ness of the voice quality
Waving in the Wind
The opening and closing motions
of the vocal folds during vocal fold vibration
are controlled by aeromechanical forces. The
opening and closing motions are not produced
by rapid muscular “pulls and pushes”; in fact,
the muscles cannot respond quickly enough
to produce the extremely rapid motions of the
vocal folds. The fact that aeromechanical forces
control vocal fold vibration raises an interesting
question about the motions (or lack thereof)
of a paralyzed vocal fold. Vocal fold paralysis
usually occurs only on one side (one paralyzed
vocal fold, the other healthy). The paralyzed
vocal fold still moves during phonation, because
it is moved to the middle of the glottis and
away from the middle by aeromechanical forces.
However, the vibration is “floppy” and ineffec-
tive due to the loss of muscular control for vocal
fold tension. Vocal fold paralysis is discussed at
greater length in Chapter 18.
142 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

1 2 3 4 5

Bottom edge

Top edge
6 7 8 9 10

Figure 10–9.  Sequential photographs of one cycle of vocal fold vibration as imaged via a laryngeal mirror. The cycle
begins in the upper left-hand frame, continues along the top row of images from left to right, and then along the bottom row
of images, from left to right. The cycle is complete at the right-hand image in the bottom row. Frame 6 is labeled to show
the upper and lower edges of the vocal fold; this illustrates that the vocal folds do not vibrate like a “solid” piston but have
complex, wave-like motion. Adapted from Hixon, T. J., Weismer G., and Hoit, J. D. (2020). Preclinical Speech Science: Anatomy,
Physiology, Acoustics, Perception (3rd ed.). San Diego, CA: Plural Publishing.

Characteristics of Phonation The typical F0 for young adult females is roughly

Three variables are useful in a description of phona-
tion. The variables include fundamental frequency (F0),
voice intensity, and voice quality. The variables are not
necessarily independent from each other and are not
the only ways to describe phonation. They are conve-
nient for the purposes of this introductory discussion.
Fundamental Frequency (F0)
Fundamental frequency, abbreviated as F0 (spoken
as “F subzero” or “F-oh”), is the rate of vibration of
the vocal folds, expressed in cycles per second. One
complete cycle is defined as the motion of the vocal
folds from the closed position to the open position
and back to the closed position (see Figure 10–9). When
100 of these cycles occur in 1 s, then F0 = 100 cycles
per second.
190 to 200 Hz (Hz, short for hertz, is the abbreviation
for cycles per second, named after Heinrich Rudolf
Hertz, a 19th-century German physicist). Each of the
190 to 200 cycles per second is similar to every other
cycle, but every cycle is not exactly of the same duration.
The description of vocal fold vibration as nearly periodic
recognizes these slight differences (less than 1/1,000th of
a second) in the durations of successive cycles.
F0 varies with age and sex (as well as some other
factors) and is the primary determinant of the pitch
of a talker’s voice. Pitch is the perceptual correlate of
the physical measurement, F0. The higher the rate of
vibration of the vocal folds, the higher is the perceived
pitch of the voice. This can be illustrated by compar-
ing typical F0s and pitches of children’s, women’s, and
men’s voices. Five-year-old children typically have F0s
around 350 Hz (for either sex), young adult women
have F0s of 190 to 200 Hz, and young adult men have

F0s around 125 Hz. Thus, children at age 5 years typi-
cally have higher-pitched voices than adult women,
who have higher-pitched voices than adult men.
Why does the F0 differ so much across these three
speaker groups? What causes the vocal folds of a 5-year-
old child to vibrate at such a faster rate as compared to
adult women, or the faster rates of vibration for women
as compared to men? A simplified explanation to this
complicated question is that, across speakers, the length
of the vocal folds is a primary factor in the typical
F0 of the voice (Titze, 2011). For example, children have
shorter vocal folds than adult women, who in turn
have shorter vocal folds than adult men.3 Figure 10–10
illustrates the difference in length of the vocal folds
for adult males, adult females, and 5-year-old children
(Rogers, Setlur, Raol, Maurer, & Hartnick, 2014).
Notice that we have said that across speakers the
length of the vocal folds is a primary determinant of
F0. Within a given speaker, however, F0 is increased
by contraction of a paired muscle that stretches the
vocal fold. This is not a contradiction to the statement
of vocal fold length as the primary anatomical reason
for different F0s in children, women, and men. When
a given speaker stretches his or her vocal folds, the tis-
sue is not only longer but also thinner and more tense.
These factors cause the vocal folds to vibrate at a faster
rate (i.e., with a higher F0). The comparison across
View from above vocal folds
Front (toward thyroid cartilage)
13 mm
11 mm
Vocal fold
Adult Male
Figure 10–10.  Vocal folds viewed from above, showing the different lengths of the adult male, adult female, and child
(5 years old) vocal folds, as well as the sizes of laryngeal cartilages.
3 
 hese age- and sex-related differences in the length of the vocal folds follow differences in overall size of the larynx. Children have smaller
T
larynges (plural of larynx) than female adults, who have smaller larynges than male adults.
10  Speech Science I 143
children, women, and men assumes that the vocal
folds in the respective age and sex groups are in the
unstretched state.
F0 is more than a marker of a person’s age and sex.
A single individual uses a wide range of F0s for nor-
mal speech communication. The variation of F0 during
normal speech is an important component of prosody,
a term that refers to the melody and rhythm of speech.
When you listen to a speaker who seems particularly
expressive, you are probably reacting to (among other
factors) relatively large variations in F0 throughout
the speaker’s utterances. When you listen to the voice
of someone who is exceptionally sad, her voice may
sound as if it is produced on a single pitch, or nearly so.
Speakers use F0 to convey emotion, to subtly change
the meaning of the same words, to be sarcastic, and to
be playful.
Intensity
Intensity is a term used to describe the amount of
energy in a sound wave. Intensity is a physical measure
that reflects the amount of acoustic energy generated
by the vibrating vocal folds. Unlike F0, it is difficult
to offer “typical” values of voice intensity because
they depend so much on characteristics of the com-
munication situation, such as how much noise there is
7.5 mm
Adult Female 5-year old child
144 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

when speaking and the distance between the speaker
and listener.
The distance between a speaker and listener has
an effect on the voice intensity reaching the listener’s
ear. The sound waves produced by a speaker saying a
sustained “ahhhh” have a sound intensity that can be
measured at the lips. As shown in Figure 10–11, top
cartoon, the sound waves travel to the listener’s ear
where they also can be measured for intensity. These
measurements reveal that intensity measured at the
listener’s ear is less than the intensity measured at
the speaker’s lips. The decreasing intensities of sound
waves are shown as the decreasing sizes of the arcs
from the speaker to the listener. The fundamental prin-

Figure 10–11.  Cartoon illustrating the effect of distance on voice intensity. The person producing
the vowel “ahhh” does so with the same speech intensity measured at his lips, in both the top and bottom
cartoons. The intensity decreases steadily as the sound waves move away from him. At the listener’s ear,
the intensity is less when she is at a greater distance from the speaker.

ciple of acoustics that applies to the measurements is
that sound intensity decreases over distance, from the
source of the sound (in this case the speaker’s lips) to
the receiver of the sound energy (in this case the lis-
tener’s ear). Figure 10–11, bottom cartoon, shows what
happens when the distance between speaker and lis-
tener is doubled compared to the distance shown in
the top cartoon. The speaker in the lower cartoon pro-
duces the same sound intensity as in the top cartoon.
At this doubled distance, the sound intensity reaching
the listener’s ear is even less than in the top cartoon.
The greater the distance between speaker and listener,
the greater is the loss of sound energy from source to
receiver. Loudness is proportional to sound intensity,
so the listener hears the “ahhh” much less well in the
bottom cartoon than in the top cartoon, even though
the speaker’s sound intensity at the lips, in both cases,
is the same.
Commonsense Speech
and Listener Therapy
Parkinson’s disease (PD) is a degenerative disease
of the nervous system in which movement
functions, including articulatory and laryngeal
movements, are affected. A prominent charac-
teristic of the speech and voice disorder in PD is
reduced speech intensity. Persons with PD have
very stiff respiratory muscles and therefore cannot
generate the lung pressure to produce speech
with normal intensity. To compound the problem,
vocal fold vibration is inefficient. This results in
air leaking through the glottis, further affecting
the buildup of pressure below the vocal folds
that is so essential to generating adequate speech
intensity. Speech-language pathologists often
focus on training the person with PD to produce
greater intensity so that listeners will hear them
more easily. Especially with family members, SLPs
can also suggest reducing the distance between
the relative with PD and the listener. It sounds
obvious, but listeners do not always get it unless
they are told about distance and intensity. Plus,
this kind of speech therapy is simple to imple-
ment, very effective, and best of all, free.
Quality
Quality is a perceptual term, like pitch and loudness.
The terms breathy voice, harsh voice, rough, and metallic
voice, are some of the perceptual descriptions of voice
quality. The physical basis of differences in voice qual-
ity includes variations in frequency, intensity, and the
10  Speech Science I 145
presence of “noise” in the sound wave. “Noise” is an
acoustic term indicating energy that is not periodic but
has random frequency and intensity variations.
To demonstrate the difference between the tonal
quality of nearly periodic vibrations and the noisy
quality of nonperiodic vibrations, say “ah” for a few
seconds in a normal voice, followed by a long whis-
pered “ah” sound. The “ah” said with a normal voice
consists primarily of periodic energy — in fact, it is
the periodic nature of the energy that makes the “ah”
sound tonal. The whispered “ah,” conversely, does not
sound tonal but rather has a hissing quality of uncer-
tain pitch. The whispered “ah” sound is an example of
noise energy.
Clinical Applications:  An Example
When the vocal folds vibrate for phonation, they open
and close rapidly at a very fast rate, as discussed earlier.
Look again at Figure 10–9 and notice that at the begin-
ning (frame 1) and end (frame 10) of this single cycle,
the vocal folds are tightly closed. This is characteristic
of healthy phonation, although there are variations in
the population in which the closure is not so tight but
the phonation remains perceptually “normal.” There
are clinical cases, however, in which the voice is too
breathy on the one hand, or too “tight” on the other
hand. The underlying cause of these voices is often a
failure to close the vocal folds adequately on each cycle
of vibration (breathy), or a closure that is too fast and
forceful (“tight”).
An SLP who treats either one of these voice prob-
lems must know the structure and function of the vocal
folds and determine a way to modify vocal fold closure.
In the case of a chronically breathy voice, the SLP may
teach the client to exert more effort when phonating,
which often has the effect of a better approximation
of the vocal folds during vibration. The person who
closes the vocal folds too forcefully and has the “tight”
voice may be shown how to relax neck muscles, or
even be a candidate for an external (on the neck) laryn-
geal massage to reduce overall muscle tension that
may be contributing to the excessive phonatory effort.
Knowledge of the anatomy and physiology of the
larynx is essential to considering the best options for
voice therapy.
Upper Airway (Consonants
and Vowels)
Figure 10–12 shows an artist’s rendition of upper airway
and nasal cavity structures. The view is in the sagittal
plane, as if you are looking toward the side of the head.
146 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Nasal cavities
Tongue
Hard palate
Thyroid
cartilage
Figure 10–12.  Sagittal view of the upper and nasal airways,
with important landmarks labeled.
The upper airway can be thought of as two col-
umns of air, one with variable shape, the other with
relatively fixed shape. The air tube with variable shape
is called the vocal tract and extends from the vocal folds
to the lips. In Figure 10–12, this airway is filled with a
dark blue color. The boundaries of the vocal tract tube
include the walls of the throat, the soft and hard palates
(the latter typically called the roof of the mouth), the
lips, and the tongue. The length and shape of the vocal
tract can be changed by the action of most of these
movable structures (such as the throat, soft palate, lips,
and tongue; the hard palate is not movable) plus the
movements of the lower jaw (mandible) which is con-
nected anatomically to the lower lip and tongue. Thus
movements of the jaw can affect movements of the lips
and tongue.
The column of air with relatively fixed shape is
called the nasal tract (see Figure 10–12, light blue). The
shape of the nasal tract does not change much during
speech because the structures forming its boundaries
do not move, at least not to a significant degree. As
described in greater detail in section “Velopharyngeal
Mechanism,” during speech the nasal tract is intermit-
tently connected to and disconnected from the vocal
tract. Figure 10–12 shows the nasal tract connected
to the vocal tract airways by the lowered soft palate
(lighter red) and disconnected from the vocal tract air-
ways (darker red). The mechanism of this connection/
disconnection is of the utmost importance for under-
Soft palate
Pharynx
Vocal
folds
standing normal speech production and certain speech
pathologies.
Muscles of the Vocal Tract
Approximately 30 muscles contribute to movements of
the structures that change the length and shape of the
vocal tract (Hixon, Weismer, & Hoit, 2020). Muscles of
the vocal tract include about a half-dozen in the throat,
three or four in the soft palate, about eight that can
move and shape the tongue, and a dozen or so that can
open and close the lips and shape their configuration.
Combinations of these muscles, working at the same
time and with intricate timing, create many different
shapes of the vocal tract.
Several muscles control the outlet of the nasal pas-
sages. These outlets, called the nares, can be flared and
constricted during speech. The size of the nares may
also be adjusted during breathing for such behaviors
as singing and exercise.
Vocal Tract Shape and
Vocalic Production
The vocal tract can be considered as the “shaper of
speech sounds” because the shape of the column of air
between the vocal folds and lips determines the acous-
 10  Speech Science I 147

tic characteristics of a speech sound. Different vocal
tract shapes result in different acoustic sound waves
emerging from the lips, which in turn result in the dif-
ferent sounds we call speech sounds. In some cases, a
connection between the vocal tract and nasal cavities is
made for a class of sounds called nasals (such as /m/
and /n/ in English).
Recall that the source (phonation) for voiced
speech is the sound produced by the vibrating vocal
folds. This sound source is basically the same for all
voiced, vocalic speech sounds such as vowels, diph-
thongs, nasals, liquids, rhotics, and glides; the pho-
nated sound source is also used for voiced stops and
fricatives. Different shapes of the vocal tract, and con-
nections to the nasal cavities, modify the acoustic char-
acteristics of the vibrating vocal folds to form different
speech sounds. More specific information on individ-
ual speech sounds is provided in Chapter 12.
Figure 10–13 shows vocal tract shapes for five
vowels. These images were obtained from magnetic
resonance (MR) scans published by Zhou, Woo, Stone,
Prince, and Espy-Wilson (2013). The black parts in
each image are airways. The vocal tract airway is seen
extending from the level of the vocal folds (shown in
the left-most image) to the lips, and the nasal airways
are shown above the soft and hard palates. The airway
below the vocal folds is the windpipe (trachea).
Note the different shapes of the vocal tract among
these five vowels. For example, compare the vocal tract
shapes of /i/ and /u/. In the case of /i/, the front part
of the vocal tract, roughly from the middle of the hard
palate to the teeth, is tightly constricted by the tongue;
the slim black channel between the tongue and pal-
ate at the constriction shows the narrow, open airway.
Behind the constriction, in the back of the oral cavity
and in the pharynx, the large black area shows that the
vocal tract opens wide into a large airway.
The vowel /u/ has a tight constriction further
back in the vocal tract, in the region of the soft pal-
ate and the upper pharynx. In front of this constriction,
the vocal tract opens until a point at the lips where the
vocal tract is again narrowed down.
The difference between vocal tract shapes for /i/
and /u/ is easy to see, and consistent with the pho-
netic description of /i/ as a high-front vowel and /u/
as a high-back vowel (Chapter 12). Vocal tract shape
differences between other vowels may be more subtle
(compare /ɑ/ to /u/ in Figure 10–13) but are sufficient
to result in different speech sounds.
Velopharyngeal Mechanism
The velopharyngeal mechanism includes the soft pal-
ate and surrounding pharyngeal walls. The soft palate
is a soft-tissue, movable structure of the speech mecha-
nism with critical importance to speech production.
Figure 10–12 shows the soft palate in two positions,
one hanging down as it does at rest (lightly shaded,
solid line following the contour of the structure) and

Velopharyngeal port

Vocal folds /a/ /e/ /i/ /o/ /u/

“ah” “ay” “ee” “oh” “oo”

“hot” “hay” “heat” “hope” “hoop”

Figure 10–13.  Magnetic resonance images of an individual producing five different vowels. The black areas above
the vocal folds are airways. The varying shapes of the airways from vocal folds to lips — excluding the airways in the nasal
cavities — show how the vocal tract is shaped by the articulators for the different vowels. The openness of the velopharyn-
geal port also varies across the vowels. Adapted from Zhou, X., Woo, J., Stone, M., Prince, J. L., and Espy-Wilson, C. Y. (2013).
Improved vocal tract reconstruction and modeling using an image super-resolution technique. Journal of the Acoustical
Society of America, 133, EL439–445.
148 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

one raised and pushed against the back of the pharynx
(colored red). The hanging-down position allows air to
flow from the lower pharynx into the nasal cavity. The
lifted position in which the velum is pushed against
the back of the pharynx seals off the air in the pharynx
from the air in the nasal cavities. The region around the
soft palate and posterior pharynx is called the velopha-
ryngeal port. The velopharyngeal port is a valve that can
be opened or shut by action of a group of muscles that
control the movement of the soft palate and pharynx.
The velopharyngeal port is a critical component
of the speech mechanism because some sounds require
the port to be open (e.g., nasal sounds such as /m/
and /n/), some sounds require it to be completely
closed (e.g., stop and fricative consonants), and some
sounds are produced with the port partially open (e.g.,
certain vowels, see later in chapter). (Movements of
the soft palate, which are frequent and rapid during
speech production, can be seen at https://www.you-
tube.com/watch?v=T4KRbENmFDk; if that video is
not available, search on “MRI speech” for additional
relevant videos). The velopharyngeal port also plays
a role in rest breathing and swallowing. The velopha-
ryngeal port is typically open in rest breathing, dur-
ing which most people exchange air through the nasal
passageways. The velopharyngeal port must be closed
during swallowing to prevent movement of food and
liquid into the nasal passageways (see Chapter 20).
And, when you blow your birthday candles out, the
velopharyngeal port is closed to prevent the escape of
air through the nasal cavities which might reduce the
flow of air through your lips and therefore reduce the
likelihood of extinguishing all the candles (and having
your wish come true).
The closure of the velopharyngeal port for stops,
fricatives, and affricates (collectively called obstruents,
because in varying degrees they obstruct airflow) is
necessary to build up air pressure in the vocal tract.
The positive air pressure creates the conditions that are
unique to the sound of these consonants (see Chap-
ter 12). Stop consonants are produced when there is a
complete blockage of the airstream flowing in the vocal
tract. During this blockage, air pressure will build up,
but only if the vocal tract is sealed at the velopharyn-
geal port to prevent leaks of air through the nasal cav-
ity. This is illustrated in the left image of Figure 10–14,
which shows closed lips (red pointer) and a closed
velopharyngeal port (green pointer). This bilabial stop
consonant (/p/ or /b/ in English) has a closed volume
of air behind the blockage: one seal at the lips and the
other at the velopharyngeal port. Pressure can build
up behind the labial blockage for the unique sound

/b/ /ʃ/

Figure 10–14.  Left, closure of the vocal tract at the lips (red pointer) and velopharyngeal port (green
pointer) for the stop consonant /b/. Right, tight constriction of the vocal tract in the palatal-alveolar region (red
pointer) and closure of the velopharyngeal port for the fricative /ʃ/. Note the tight velopharyngeal port closure
for both sounds, necessary for the buildup of air pressure behind the constrictions.

characteristics of a stop consonant — a “popping” noise
when the block is broken (in this case when the lips
are separated).
The right image of Figure 10–14 shows a constric-
tion for the fricative /ʃ/ (as in the first sound of “shoe”).
Fricative constrictions, or blockages, are not complete
as in the case of stops but are sufficiently narrow to
allow pressure to build up behind them. The /ʃ/ con-
striction is shown at one location by the red pointer to
one part of the tongue, but as the image shows, the con-
striction is long and narrow. Pressure built up behind
this constriction pushes air through it and creates a
hissing noise (try producing a long “sh” and listen to
the hissing noise). As in the case of stop consonants,
a closed velopharyngeal port is required for efficient
pressure buildup. The closed velopharyngeal port is
shown clearly in the upper right of the /ʃ/ image. The
lips, however, are open to allow the passage of air that
emerges from the tight but not complete constriction.
Valving in the Vocal Tract and the
Formation of Speech Sounds
“Articulatory behavior for speech” refers to the posi-
tions and motions of the jaw, tongue, lips, pharynx,
and velum, as well the contacts between these movable
structures and the rigid boundaries of the vocal tract
(such as the hard palate). As might be imagined, obtain-
ing information on positions and motions of certain
articulators, especially the tongue, velum, and phar-
ynx, is exceedingly difficult because they are largely
hidden within the oral and pharyngeal cavities. Speech
scientists have developed several different techniques
over the years to study motions of these hidden artic-
ulators. Many of these techniques involve x-ray and
magnetic field technologies. In recent years, magnetic
resonance imaging (MRI) techniques have been used
to study speech movements. Regardless of the tech-
nique, one fact remains startlingly obvious: During
speech, each of the articulators is in constant motion,
making it nearly impossible to connect specific move-
ments with specific sounds. A speech scientist can-
not look at the motion of a particular articulator and
identify where it begins its contribution to a sound
(such as a vowel) and where it ends its contribution.
For example, when a speaker says the word, electric-
ity, we can represent its 11 component sounds — ee, l,
eh, k, t, r, ih, s, ih, t, ee — as a series of discrete sym-
bols (/əlEktrIsIɾi/, in phonetic transcription, Chapter
12), but the articulatory motions used to produce the
word appear as a rapid, sometimes jerky blur of undif-
ferentiated gestures. Good examples of speech move-
10  Speech Science I 149
ments are available at https://www.you​tube.com/
watch?v=Nvvn-ZVdeqQ and https://www​.youtube.
com/watch?v=ezOwCf835YA (enter “speech move-
ment” as a key phrase for more examples).
Knowledge of how articulatory movements relate
to speech sounds is likely to be beneficial when attempt-
ing to treat a speech disorder in which the underlying
problem is one of motor control (as in, for example,
Parkinson’s disease or cerebral palsy: see Chapter 14).
For the time being, our knowledge of the relationship
of articulatory movements to specific speech sounds is
very limited. It is a complex issue.
Coarticulation
Coarticulation is the term used to describe the influence
of one speech sound on another speech sound. For
example, even though the words “sad” (/sæd/) and
“sag” (/sæg/) share the vowel “ae” as in “hat,” tongue
movements throughout the vowel (i.e., across time)
differ because of the difference in the final stop con-
sonant. The “d” sound affects the “ae” in one way, the
“g” sound in another way. Now consider the word pair
“sheik” (/ʃik/) and “shock” (/ʃɑk/), in which the final
consonants are the same and the vowel is either “ee” or
“ah.” Here the different vowels affect the articulation of
the /k/; the movements and location of the complete
constriction for /k/ differ depending on the vowel. In
this case, the articulation of the consonant is affected by
the preceding vowel; in the first case, the articulation of
the vowel is affected by the following consonant.
Coarticulation is everywhere in speech produc-
tion. The articulation of any speech sound is simul-
taneously affected by the sounds preceding it and
the sounds following it. Notice the word “sounds”
in the preceding sentence. The influence of coarticu-
lation is present not only for adjacent sounds, as in
the examples of “sad” versus “sag” and “sheik” ver-
sus “shock,” but it can extend across multiple sounds.
A good example of this is the word combination “least
soon,” in which lip rounding for /u/ may be observed
on the “st” consonant sequence in “least.” When a sin-
gle sound — what is often called a sound segment — is
affected by so many variables, no wonder it is nearly
impossible to connect specific articulatory movements
with specific sound segments.
Clinical Applications:  An Example
Knowledge of the location and function of valves in the
speech mechanism is essential to accurately diagnose
150 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
The Weedy Garden of Speech
So . . . articulatory movements for any
specific speech sound, and their acoustic results,
depend on the sounds preceding and following
the specific speech sound. This is variability
of a specific speech sound due to its phonetic
context — the identity of the surrounding speech
sounds. But wait: phonetic context is hardly the
only variable that affects the movements and
acoustic characteristics of a speech sound. The list
of other variables that can cause variability of the
articulatory and acoustic characteristics of a speech
and properly treat speech disorders. A good example
is the case of a client who is perceived to speak with
excessive nasality. In many cases, excessive nasality
can be traced to a problem with control of the velo-
pharyngeal port. Structural problems, as in the case
of a repaired cleft palate, or muscle weakness in the
absence of an obvious structural issue, can prevent the
velopharyngeal port from closing sufficiently during
the production of vowels. This may result in hyper-
nasality. Specialized techniques for diagnosis and
therapy can be used by the person who understands
both the anatomical structure of the speech mechanism
valves — in the example, the velopharyngeal port — and
the physiology (function) of the valves.
Chapter Summary
The speech mechanism can be thought of as consisting
of three major components.
The respiratory system is the power supply, gener-
ating pressures and flows. These pressures and flows
initiate and maintain vibration of the vocal folds, which
generates the sound source for speech.
The acoustic signal generated by the vibrating
vocal folds is shaped into different speech sounds by the
moving structures and fixed boundaries of the upper
airway.
The respiratory system, larynx, and upper airways
are composed of many muscles, membranes, ligaments,
bones, and cartilages, all of which are covered in detail
in speech anatomy and physiology coursework taken
by students majoring in Communication Sciences and
Disorders.
sound includes speaking rate (how fast a person
talks), dialect, speaking style (e,g., casual versus
formal), and the level of emphasis placed on the
speech sound, age, and sex of the speaker. Speech
scientists have spent years researching coarticula-
tion and the variability that results from it, due to
all of these variables. This research has produced
many answers, but along the scientific way, new
questions have popped up like weeds in a well-
fertilized garden.
Knowledge of this basic anatomy and physiology
is important to understanding the many disorders and
diseases that affect the speech mechanism.
The respiratory system functions to support life,
exchanging O2 and CO2 at the alveoli; air is brought
into the lungs by expanding them (inhalation) and
transported out of the lungs by compressing them
(exhalation).
The respiratory system is composed of muscles
in the thorax and abdomen, plus a large muscle (the
diaphragm) that separates the thoracic and abdomi-
nal cavities; many nonmuscular tissues (membranes,
bone, cartilage) play an important role in the respira-
tory system.
Rest (vegetative) breathing involves inhalations
and exhalations of small volumes and roughly equal
durations.
Speech breathing involves very rapid inhalations
in preparation for an utterance and relatively long
exhalations during which speech is produced.
The main goal of the respiratory system is to main-
tain a constant, positive pressure in the lungs and tra-
chea during speech utterances; this pressure is critical
to vibrating the vocal folds for phonation.
The pressure generated in the lungs (and trachea)
for speech is related to the loudness of speech: the
higher the pressure, the greater is the loudness.
During speech, the lungs are compressed by the
muscular actions of both the thorax and abdomen;
abdominal muscles are critical to maintaining an
increased lung pressure for speech at a constant level.
The larynx is composed of a framework of carti-
lage, membranes, ligaments, and muscle; the bottom
part of the larynx sits on top of the trachea, and its top
part can be considered the lower end of the throat.

The vocal folds are two bands of tissue that run
from the front to the back of the larynx, between the
thyroid cartilage (front point of attachment) and aryte-
noid cartilages (back point of attachment).
There are five intrinsic muscles of the larynx. Three
of these muscles can close the vocal folds, one can open
the vocal folds, and one can stretch them. One of the
muscles that closes the vocal folds also tenses the main
muscular bulk of the vocal folds.
The vocal folds open and close. When they open,
the space between them is called the glottis, which is
the opening into the trachea. The vocal folds open to
allow air into and out of the lungs, via the trachea, for
breathing purposes.
The protective function of the larynx is to shut
down the airway (to close the vocal folds rapidly and
forcefully) when food, liquid, or other material enters
the top part of the larynx.
The vocal folds also open and close to vibrate for
the purposes of phonation; phonation provides the
sound source for speech, sometimes referred to more
specifically as voice production.
The opening and closing motions of the vocal folds
for phonation are controlled by aerodynamic (pres-
sures and flows) forces, rather than directly by muscle
contraction.
The rate at which the vocal folds vibrate depends
primarily on the length of the vocal fold.
The tissue of the human vocal fold is specialized
for purposes of phonation.
Important characteristics of vocal fold vibration
include the fundamental frequency (F0 = rate of vibra-
tion), intensity of the sound generated by the vibration,
and quality of the voice resulting from the vibration.
The upper airways include the vocal tract, which
is the tube of air between the vocal folds and the lips,
and the nasal tract, the airway between the velopha-
ryngeal port and the nostrils.
10  Speech Science I 151
The articulators shape the vocal tract for vocalic
sounds, in which the vocal tract is open and air can
flow freely to the atmosphere, and a class of consonants
called obstruents in which there is a constriction that
completely or partially blocks the airflow for a short
time interval.
An important valve between the vocal and nasal
tracts is the velopharyngeal port, where air coming
through the throat can be blocked from entering the
nasal cavities. The velopharyngeal port opens and
closes during speech production, according to the
requirements of the speech sound being produced.
References
Darley, F. L., Aronson, A. E., & Brown, J. R. (1975). Motor
speech disorders. Philadelphia, PA: Saunders.
Hixon, T. J., Goldman, M. D., & Mead, J. (1973). Kinematics
of the chest wall during speech production: Volume dis-
placements of the rib cage, abdomen, and lung. Journal of
Speech and Hearing Research, 16, 78–115.
Hixon, T. J., Weismer G., & Hoit, J. D. (2020). Preclinical speech
science: Anatomy, physiology, acoustics, perception (3rd ed.).
San Diego, CA: Plural Publishing.
Rogers, D. J., Setlur, J., Raol, N., Maurer, R., & Hartnick, C. J.
(2014). Evaluation of true vocal fold growth as a function
of age. Otolaryngology–Head and Neck Surgery, 10, 681–686.
Su, M. C., Yeh, T. H., Tan, C. T., Lin, C. D., Linne, O. C., &
Lee, S. Y. (2002). Measurement of adult vocal fold length.
Journal of Laryngology and Otology, 116, 447–449.
Titze, I. R. (2011). Vocal fold mass is not a useful quantity for
describing F0 in vocalization. Journal of Speech, Language,
and Hearing Research, 54, 520–522.
Zemlin, W.R. (1997). Speech and hearing science: Anatomy and
physiology (4th ed.). Boston, MA: Pearson
Zhou, X., Woo, J., Stone, M., Prince, J. L., & Espy-Wilson, C. Y.
(2013). Improved vocal tract reconstruction and modeling
using an image super-resolution technique. Journal of the
Acoustical Society of America, 133, EL439–445.
 11
Speech Science II

Introduction symbols are enclosed in forward slashes. For quick ref-

erence, the phonetic symbols used in this chapter are
In the previous chapter, reference was made to the listed in Table 11–1.
acoustic signal emerging from the vocal tract (or nasal
tract, or both at the same time). For the remainder of
this chapter, we refer to this as the speech acoustic signal. Table 11–1.  Phonetic Symbols Used in This Chapter
The speech acoustic signal is the product of respiratory,
laryngeal, and upper airway behaviors described in the /ɑ/ “ah” in “hot”
previous chapter.
The current chapter presents a brief introduction /i/ “ee” in “beat”
to the speech acoustic signal. Speech production can /u/ “oo” in “boot”
be thought of as the concerted action of all structures
of the speech mechanism to produce an acoustic signal /æ/ “ae” in “hat”
that can be recognized by a listener as an intelligible // “urr” in “bird”
message. The connection between the speech acoustic
signal and speech intelligibility suggests the impor- /2/ short “rr” in last syllable of “longer”
tance of knowing about speech perception as well. In /ɾ/ tapped “d” in “butter”
the absence of a listener who performs perceptual anal-
ysis of the speech acoustic signal, the signal is a little /dZ/ “j” as in “judge”
like the proverbial tree that falls in a forest empty of /z/ “zee” as in “zebra”
hearing organisms. The human forest is full of hearing
organisms, lots of them human, so speech perception is /ð/ “th” sound in “the”
also considered in the current chapter. /ɔ/ in “bought”*
To avoid confusions between orthographic and
phonetic representations of sounds, phonetic sym- *The vowel /ɔ/ is pronounced as /ɑ/ in many dialects of Ameri-
bols (discussed in Chapter 12) are used here, usually can English, such as the dialect heard in many parts of Califor-
nia. Words such as “caught” and “cot” are pronounced with the
following the orthographic and phonetic representa- same vowel (“caught” /kɑt/, “cot” /kɑt/). This is in contrast to the
tion: “beat” /bit/, “hat” /hæt/. Orthographic repre- “caught” /kɔt/ and “cot” /kɑt/ heard in eastern Pennsylvania and
sentations are enclosed by quotation marks; phonetic eastern Maryland, among other regions of the United States.

153
154 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
The Theory of Speech Acoustics
Theories are common in all academic disciplines. It is
relatively uncommon, however, for the majority of sci-
entists in one discipline to agree on a particular theory.
An exception to this is the acoustic theory of speech
production, developed in the 1940s and 1950s by Dr.
Gunnar Fant (1919–2009), an eminent speech scientist
who for many years was the director of a well-known
speech research laboratory in Stockholm, Sweden (the
Speech Transmission Laboratory).
In 1960, Fant published a textbook called (not
surprisingly), Acoustic Theory of Speech Production. The
book provided a detailed account of how the speech
mechanism generated the speech acoustic signal. In
most respects, this theory is accepted as correct by
speech scientists.. The theory has been refined and
elaborated by other speech scientists, most notably,
James Flanagan (1972) and Kenneth Stevens (1998).
Fant’s theory of speech acoustics can be summa-
rized in a single sentence: The output of the vocal tract
(that is, the speech acoustic signal) is the product of
the acoustic characteristics of a sound source combined
with a sound filter. Fant’s theory was developed using
elegant mathematics that were most precise for the case
of vowel production. Fortunately, explanation of the
theory does not require expertise in mathematics.
The Sound Source
The sound source in the acoustic theory of vowel pro-
duction is the signal generated by the vibrating vocal
folds. Vibration of the vocal folds generates an acous-
tic signal that has a fundamental frequency (F0) and a
series of harmonics (sometimes called “overtones”). F0
is defined in Chapter 10 as the number of full cycles of
vocal fold vibration per second. The speech acoustic
signal for vowels includes higher-frequency compo-
nents as well, called harmonics. The harmonic frequen-
cies of F0 are located at whole number multiples of the
F0, a fact best explained with a simple example. If an
adult male phonates the vowel “ah” with his vocal
folds vibrating with an F0 of 100 Hz, acoustic energy
is generated at the F0 as well as at frequencies that are
whole number multiples (2, 3, 4, 5, 6, . . . n) of the F0.
This acoustic signal has energy at 100 (F0), 200, 300, 400,
500, 600, . . . n × 100 Hz. A periodic signal with multiple
frequency components is called a complex periodic sig-
nal. Vocal fold vibration produces a complex periodic
signal, and it is this signal that serves as “input” to the
vocal tract — it is the source for the speech acoustic sig-
nal. It is also the signal that people refer to as “voice.”
The sound source is the same for all vowels; it is
not adjusted for different vowels. This is an important
aspect of the theory and is returned to following a
description of the sound filter.
The Sound Filter
In the acoustic theory of vowel production, the sound
filter is the vocal tract. Fant showed that the vocal tract
was like a resonating tube. Tube resonators have more
than one resonant frequency, or frequencies at which
they vibrate with maximal amplitudes. The air within
a tube is an example of a multiple-frequency resona-
tor. When the air within a tube is set into vibration, the
acoustic result is a signal with multiple resonant fre-
quencies. A good analogy to the acoustics of the vocal
tract filter is the acoustics of organ pipes.
Fant showed that the precise frequencies at which
these resonances occur depend on the shape of the
tube. Different shapes of the vocal tract tube, created by
different positions of the jaw, tongue, lips, and throat
(pharynx), result in different resonant frequencies.
This was illustrated in Chapter 10 by the MRI images
in Figure 10–13. Selected vocal tract shapes for three
different vowels are shown in Figure 11–1 in a more
schematic way. The shape of the vocal tract — the air
column between the vocal folds and the lips — is shown
in dark blue for the English vowels /ɑ/ “ah” (as in
“hot”), /i/, “ee” (as in “beat”), and /u/ “oo” (as in
“boot”). The shapes are different for the three vowels.
The different shapes change the resonant frequencies
of the vocal tract, even though the source signal remains
the same for all three vowels. The different shapes of
the vocal tract produce different sounds — they create
different vowels.
The acoustic result of different vocal tract shapes
is shown in Figure 11–1 by the three graphs in the right
column. These are vowel spectra, showing energy
peaks (the y-axis, labeled amplitude) as a function of
frequency (the x-axis, with frequency ranging between
0.0 and 5.0 kHz (0 Hz to 5000 Hz). The vowel spectra
are ordered from top to bottom just like the vocal tract
shapes: /ɑ/ at the top, /i/ in the middle, and /u/ at
the bottom. The peaks in each spectrum show the first
three resonant frequencies of each vowel; these peaks
are indicated by pointers from the labels “F1,” “F2,”
and “F3.” Notice how the peaks are at different fre-
quency locations for the three vowels. The frequency
of these peaks can be estimated by dropping a verti-
cal line from a peak to the x-axis and noting where the
line intersects the frequency scale. The use of the “F” to
identify the peaks is explained below.
 11  Speech Science II 155

F1
F2

F3
/ɑ/

F1
F3
F2

Amplitude (dB)
/i /

F1

F2

F3 /u /

1.0 2.0 3.0 4.0 5.0

Frequency (kHz)

Figure 11–1.  Vocal tract shapes (left ), shown in dark blue, for three vowels (/ɑ/, /i/,
/u/). On the right side are spectra associated with the vowels. F1, F2, F3 indicate peaks in
the spectrum, called “formants.” Note how the peaks in these spectra occur at different
frequencies. Those differences are related directly to the differences in vocal tract shapes
for the three vowels.

Vowel Sounds Result From
the Combination of Source
and Filter Acoustics
Now that the acoustic characteristic of the source and
filter have been identified, a more specific statement
of Fant’s theory can be made. The speech acoustic
signal results from a source whose frequencies and
amplitudes are “shaped” by the resonant frequencies
of the vocal tract filter (vocal tract tube). The source
has energy at a series of frequencies, and the different
shapes of the vocal tract “pick out” different frequen-
cies to emphasize or reject. The signal coming from the
vocal tract consists of frequencies in the source that are
emphasized by the resonant frequencies of the vocal
tract tube. This brings us back to the single-sentence
156 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

statement of Fant’s theory given previously: The out-
put of the vocal tract (that is, the speech acoustic signal)
is the product of the acoustic characteristics of a sound
source combined with a sound filter.
Form and Function
Students typically do not encounter
the word “formant” until they have lectures on
speech acoustics. The word is used to describe
speech spectra, and specifically, the peaks in
the spectrum (frequencies at which sound
intensity is the greatest). Resonators such as
organ pipes have spectra with multiple peaks
too, but these are not called “formants,” they
are called — well — peaks. “Formant” has a Latin
root that means “forming.” The idea behind the
word “formant” is something being formed, in
this case, a resonant frequency resulting from the
formation of a vocal tract shape. The word was
coined to designate a resonance that was formed
by the vocal tract — it is a speech-specific term.
Resonant Frequencies of Vowels Are
Called Formants:  Spectrograms
The difference in vowels is primarily a result of their
different resonant frequencies. This can be demon-
strated in a simple way. Figure 11–2 shows a spectro-
gram, a type of visual record of the speech signal. The
sentence, “The dude that dotted the deed was Dad”
was spoken by the author into a microphone connected
to a computer. A speech analysis program called TF32
(Milenkovic, 2001) generated the spectrogram and
was used to edit and analyze this speech signal. Spec-
trograms, which are related (but not identical) to the
voiceprints used in legal cases of speaker identification,
show time on the x-axis and frequency on the y-axis. In
Figure 11–2, frequency is marked in steps of 1.0 kilo-
hertz (1000 Hz) from 0 to 4.0 kHz (4000 Hz). On the
x-axis, time is marked by a series of hash marks, each
separated from the next by 1/10th s (100 ms).
The sentence shown in this spectrogram contains
examples of the “corner” vowels of English. Vowels are
classified by phoneticians according to three categories,
two of which describe the position of the tongue in the
vocal tract (Chapter 12). The vowels “oo” /u/, “ah”

/u / /ɑ/ /i / /æ /
“The dude that dotted the deed was Dad”

4.0

3.0
Frequency (Hz)

2.0 F3

F2

1.0
F1

baseline

100 ms

Time Beginning End

Measurement point

Figure 11–2.  Spectrogram showing the first three formant frequencies for the corner vowels of American English, in
the sentence, “The dude that dotted the deed was Dad.” The approximate formant frequencies for /æ/ are marked by a
short red horizontal bar halfway between the beginning and end of the vowel. Formant frequencies can be estimated for
the other vowels in the same way. Starting from the bottom of the frequency (y-axis) scale, the first dark band is F1, the next
one F2, and the next one F3 (see labeled formants for “oo” /u/). The red contours for F1, F2, and F3 of /ɑ/ show formant
movement (change of formant frequencies over time) throughout the vowel.

Speech Scientists Vow to Study Vowels
Many speech scientists have studied
the acoustic characteristics of vowels. Vowels are
fascinating for several reasons. Some languages use
just a few vowels, others use relatively many. For
example, Greek and Spanish are languages with
five vowels, in contrast to the 12-vowel system of
English. Differences between the vowel systems of
two languages have a significant influence on the
ability of a native speaker of one language (say,
Spanish) to produce “native-sounding” vowels of
a second language (English, for example). Spanish
has the vowel /i/ as in the English word “beat,”
but does not have the English vowel “ih” /I/ as
in the word “bit.” These two English vowels have
very similar vocal tract shapes and, as expected,
similar formant frequencies. The vowel /I/,
however, is quite rare in languages other than
English. So, when a native speaker of Spanish (or
of Greek, or Korean, or Japanese, as well as many
other languages) is learning English and attempts
to say a word such as “bit,” he or she is likely to
produce the vowel in an /i/-like way (i.e., to say
something closer to “beat” than “bit”). It is as if
/ɑ/, “ee” /i/, and “ae” (as in “hat”) /æ/, marked in
Figure 11–2, represent the extremes of English vowel
articulation — they define the “corners” of the space
within which all vowels are articulated. The highest
and most back vowel is /u/, the lowest and most back
vowel /ɑ/, the highest and most front vowel /i/, and
the lowest and most front vowel /æ/. Formant fre-
quencies distinguish different vowels, so the distinc-
tions should be obvious in an acoustic record of these
vowels.
In Figure 11–2, parts of the spectrographic dis-
play appear as dark bars. An example of these bars
is found above the vowel /u/ in the word “dude.”
Arrows labeled “F1,” “F2,” and “F3” point to the first,
second, and third dark bars above the baseline of the
spectrogram (bottom of the spectrogram). These bars
indicate the regions where there is maximum energy
in the signal — that is, they are the formant frequencies
of the vowel.
The first three formant frequencies for each vowel
can be estimated by making an eyeball measurement
halfway between the beginning and end of each vowel,
as marked for the formant frequencies of the vowel
/æ/ in “Dad.” The upward pointing arrows show the
beginning and end of the vowel. The red line is placed
11  Speech Science II 157
the second-language learner absorbs an unknown
vowel type like /I/ to a vowel type in her native
language (in this case, /i/). Another interesting
example of an English vowel that is unusual in
other languages is the /æ/ “ae” sound in words
such as “cat,” “bat,” and “and.” This English vowel
may not be as challenging for native speakers
learning English as a second language, possibly
because their native languages do not have vowels
close to /æ/, eliminating the competition, so to
speak. But /æ/ is also interesting in American
English because it is produced in so many different
ways depending on a talker’s dialect group. Some
talkers — such as in Wisconsin — produce this vowel
in a very distinctive way, almost as if they are
saying “kyat” for “cat.” Other talkers, especially
young adults from the east and west coasts (and in
parts of the country’s interior), produce this vowel
as something between the vowel of “cat” and of
“cot.” Vowel changes such as this are common in
languages of the world, adding yet another reason
why speech scientists tend to go ga-ga over vowels
and their acoustics.
in the middle of the vowel’s duration: halfway between
its beginning and end. To measure a formant frequency,
a single point in time must be chosen for the measure-
ment, because formant frequencies change through-
out a vowel (see later in text). The short horizontal
lines intersecting the vertical line show where the for-
mant measurements are made at the halfway point of
the vowel.
For example, the red cross for the F1 frequency of
/æ/ is below 1000 Hz (1.0 kHz) a little less than half of
the difference between 1000 Hz (1.0 kHz) and the base-
line. Referring to the frequency lines for the eyeball esti-
mate, this places the F1 around 600 Hz. The F2 frequency
is about one third of the way down from 2000 Hz to
1000 Hz; its frequency appears to be about 1700 Hz. The
F3 cross is halfway between 3000 Hz and 2000 Hz; its
frequency can be estimated by eye as 2500 Hz.
How accurate are the formant frequency esti-
mates for the vowel /æ/? Comparison data from Hil-
lenbrand, Getty, Clark, and Wheeler (1995) for a large
group of adult males who produced the vowel /æ/
show an average F1 = 588 Hz, F2 = 1952 Hz, and F3 =
2601 Hz — not bad for our eyeball estimates.
The first three formant frequencies for /æ/ can
be used as reference points for comparison with the
158 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
first three formant frequencies of the other corner
vowels. For example, compared to /æ/, /u/ clearly
has a lower F1 frequency, a lower F2, and a lower F3.
The vowel /i/ is even more different than /æ/, with
a very low frequency F1 and the highest F2 of all the
corner vowels.
The precise values of the formant frequencies are
not of concern to the present discussion. Rather, Figure
11–2 demonstrates that vowels are distinguished from
each other by the frequency values of their formants,
even by crude (eyeball) estimates of the frequencies.
The Tube Model of Human Vocal
Tract Makes Interesting Predictions
and Suggests Interesting Problems
The part of Fant’s theory that considers the vocal tract
a resonating tube, with multiple resonant frequencies,
makes an interesting prediction. Tubes that are exactly
the same in every way except for their length differ
in their resonant frequencies. Casual familiarity with
the construction of a pipe organ, with pipes (tubes) of
many different lengths, suggests that the shorter pipes
produce higher-pitched tones, the longer pipes lower-
pitched tones. The higher-pitched tones of short as
compared with long organ pipes result from the higher
resonant frequencies of shorter pipes.
The vocal tract tube is like a resonating pipe and
is subject to the same acoustical principles. A shorter
vocal tract has higher resonant frequencies than a lon-
ger vocal tract. Five-year-old children have shorter
vocal tracts than adult women, who in turn have
shorter vocal tracts than adult men. Fant’s theory pre-
dicts that when the same vowel is spoken by children,
women, and men, the formant frequencies are highest
for children, next highest for women, and lowest for
men. This prediction has been confirmed many times
in the research literature (Hillenbrand et al., 1995;
Peterson & Barney, 1952).
Earlier it was noted that perceptual differences
between vowel sounds can be explained by their differ-
ent formant frequencies. If vowel formant frequencies
for a given vowel depend on who is speaking, there is
the interesting problem of how listeners perceive the
same vowel spoken with such different acoustic char-
acteristics. For example, Table 11–2 shows the average
F1, F2, and F3 frequencies reported by Hillenbrand,
Getty, Clark, and Wheeler (1995) for the vowel “eh” (as
in “head”) spoken by relatively large groups of adult
males, adult females, and children aged 10 to 12 years.
The values of the first three resonances, or formants,
for this vowel are clearly different depending on the
speaker group. More specifically, as the vocal tract
Table 11–2.  Average Values of the First Three Formant
Frequencies (F1, F2, F3, in Hz) for the Vowel /E/ “eh” (as in
“head”) as Spoken by 45 Adult Males, 48 Adult Females,
and 46 Ten- to Twelve-Year-Olds
Decreasing Vocal Tract Length
Adult Men Adult Women Children
F1 580 731 749
F2 1799 2058 2267
F3 2605 2979 3310
Note. The data show how the formant frequencies for the same
vowel vary depending on who is producing the vowel. Values
reported by “Acoustic Characteristics of American English Vowels,”
by J. M. Hillenbrand, L. A. Getty, M. J. Clark, and K. Wheeler, 1995,
Journal of the Acoustical Society of America, 24, pp. 175–184.
shortens, formant frequencies increase, just as pre-
dicted from Fant’s theory. No one has quite figured
out how these differences are heard as the same vowel,
even though it is a central problem in speech percep-
tion research (see later in this chapter).
A Spectrogram Shows Formant
Frequencies and Much More
The continuous red lines in Figure 11–2 show contours
of the first three formant frequencies for the vowel
/ɑ/ from its beginning to end. The red contours show
that the formants move up and down the frequency
scale throughout the vowel. For example, F1 for /ɑ/
starts at a relatively low frequency, rises to its high-
est frequency close to the end of the vowel, and then
decreases. Similarly, the F2 contour falls in frequency
from its beginning and then rises a small amount.
As noted in Chapter 10, during speech the articula-
tors are in constant motion which create vocal tract
shapes — and therefore formant frequencies — that are
constantly changing over time. Formant transitions
are the acoustic result of the constantly changing vocal
tract shapes.
The speech acoustic signal reflects everything
taking place in the vocal tract as a speaker produces
speech. Courses in acoustic phonetics cover informa-
tion on the acoustic characteristics of different speech
sounds, voice qualities, and prosody (melody of voice).
This information is critical to understanding how lis-
teners perceive speech and its various meanings. It is
also critical to designing computers programs for the
synthesis and recognition of speech.

Letters and Sounds Are
Not the Same
Phonetic transcription symbols underscore the
difference between the speech sounds that are
actually produced compared with letters in an
orthographic representation of a word. The spell-
ing of “dotted” has a double “t” at the end of
the first syllable, which may lead to the expecta-
tion of the speech sound /t/. Most speakers of
American English (as compared with English
spoken in the United Kingdom) do not say
/dɑtəd/, however, or even /dɑdəd/. Instead,
they produce the middle consonant as a flap
(Chapter 12), which is a very short (~25 ms
or 0.025 sec) /d/-like sound, much like the
one in “butter” or “sitter.” This sound, whose
phonetic symbol is /ɾ/, is a good example of the
difference between a letter (orthographic) and
phonetic representation of words.
Speech Synthesis
Scientists have been trying to make machines talk for
many years, perhaps even centuries. Speech synthesis is
the term used to describe the production of speech-like
sounds, words, and sentences by machines. In the early,
modern days of speech synthesis, these machines were
large, awkward electronic devices. Computers now
generate high-quality synthetic speech using sophisti-
cated software. If you are interested in the history of
speech synthesis, a good place to start is the historical
account published by Dennis Klatt (1987), a pioneer in
the field. Enter the phrase, “history of speech synthe-
sis,” in a search engine to get a listing of many sites
devoted to the topic, some with audio examples of
synthesized speech from 1939 to the current time. Story
(2019) has published a more recent account of the his-
tory of speech synthesis.
The quality of speech synthesis improved dramati-
cally in the 1960s and 1970s. Much of this improvement
can be attributed to studies of the acoustic characteris-
tics of speech sounds, as produced by real talkers. These
studies were often completed using spectrographic
analysis, as in Figure 11–2, or with more sophisticated
acoustic analysis tools. As knowledge of the speech
acoustic characteristics of human speech became more
detailed, programs for the synthesis of speech were
improved, and a better “product” emerged from these
talking machines. Increases in computing power and
capacity allowed more complicated speech synthesis
programs to synthesize higher-quality speech. Modern
11  Speech Science II 159
speech synthesis is so good as to be nearly indistin-
guishable from genuine human speech. Acoustic pho-
netics research made this possible.
Relatively cheap, high-quality speech synthesis
is more than an academic exercise for geeks who like
speech research. Speech synthesizers are an impor-
tant communication option for persons who cannot
communicate orally because of neurological disease.
Speech synthesis by computer offers a wonderful
option for persons who, despite a neurological status
that prevents speech production, have sufficient con-
trol of their hands or another part of the body to issue
commands for the rapid synthesis of a message. For
example, some children with cerebral palsy cannot
speak intelligibly but can control a joystick or a head
pointer, which in turn can be used to control a speech
synthesizer. Speech synthesis is truly a case where basic
research has been translated to clinical application.
Speech Recognition
The flip side of speech synthesis is called automatic
speech recognition. This is the process of converting
human speech into text, or into an action (e.g., oper-
ating a door) based on speech commands. The use of
automatic speech recognition for simple decision-mak-
ing is familiar to everyone who has called a business
(such as an airline) and been led through a maze of
speech-guided options to achieve a goal (like talking to
a human, for example). These speech recognizers oper-
ate in a relatively simple way, storing a limited num-
ber of acoustic phonetic “templates” for words such as
“yes” and “no,” numbers from one to ten, or the letters
of the alphabet (“em,” “dee,” “ex”). Not surprisingly,
the greater the number of options to be distinguished,
the more complex the speech recognizer must be for
recognition success.
One component of modern speech recognition
devices is an acoustic analysis program that deter-
mines the sounds that make up words. This capability
is based on the speech acoustic work described above,
in which the acoustic characteristics are determined for
each speech sound. Although modern speech recogniz-
ers use much more information than just the acoustic
characteristics of speech sounds to “hear” speech accu-
rately, all recognizers must incorporate information on
these characteristics for successful performance.
Speech Acoustics and
Assistive Listening Devices
Speech acoustic characteristics are important because
they play a critical role in the design and programming
160 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
of assistive listening devices such as hearing aids and
cochlear implants. These devices, described in Chap-
ter 24, function as amplifiers and filters. They contain a
microphone to sense the speech signal, which is “pro-
cessed” by electronic components contained within the
device. The processing may include selection of certain
frequencies to be amplified, and suppression of other
frequencies. What is the rationale for amplification of
certain frequencies and suppression of others? The
most obvious answer is that the device is configured to
amplify frequencies most crucial to the understanding
of speech. Much of the acoustic phonetics research has
been devoted to determining the important frequency
characteristics of human speech sounds. Acoustic pho-
netics research informs the engineer who designs hear-
ing aids or cochlear implants about optimal processing
characteristics to achieve the best speech perception
performance.
Speech Perception
Many speech scientists, experimental psychologists,
and linguists throughout the world devote their
research careers to speech perception. As often hap-
pens when many scientists work on a single problem,
different camps have been developed to defend one of
several theories that seek to explain how humans per-
ceive speech.
All theories of speech perception require that the
acoustic characteristics of speech sounds and perhaps
of larger “units” (such as syllables, or perhaps even
whole words) be processed by the human auditory
system. Children presumably learn a great deal about
the acoustic characteristics of speech as they are devel-
oping language skills. At some point, children learn to
use their knowledge of the acoustic characteristics of
speech sounds and prosody (the melody and rhythm
of speech) to recognize words, emotional states of talk-
ers, and more subtle aspects of communication such as
anger or joking. Knowledge of speech acoustic infor-
mation is also likely to play a role in the development
of speech production skills. The best evidence for this
is the connection between “prelingual,” severe hear-
ing loss (loss suffered before the age of about 5 years)
and speech production that is significantly unintel-
ligible. Persons with severe hearing loss are likely to
produce speech that is difficult to understand. Clearly,
the speech acoustic signal plays an important role in
normal and disordered communication.
Many issues have been investigated to understand
the perception of speech. The question may seem triv-
ial: after all, as infants we are exposed to speech and
language and like many other skills we master, speech
perception is learned by connecting heard speech with
the people, characteristics, and actions to which the
speech refers. But this question is not an answer to
“how.” Rather, it is a statement of what happens, not
an explanation. A deeper question, the question of how
speech perception takes place, is what the listener’s
brain does with the acoustic signal to hear words and
determine the meaning of a speaker’s utterances
A brief consideration of some major issues in
speech perception research demonstrates that under-
standing the “how” of the process is challenging. In
the discussion that follows, the term “objects of speech
perception” is used. This refers to the possible goal of
the brain in perceiving speech. What is the final prod-
uct of the brain’s processing of the incoming speech
acoustic signal?
The Perception of Speech:
Special Mechanisms?
A very old but enduring theory of speech perception is
that part of the brain is devoted exclusively to speech
perception (Liberman, Cooper, Shankweiler, & Stud-
dert-Kennedy, 1967). This mechanism is thought to be
speech- and species-specific. The term speech-specific
means that the special brain mechanism is “turned on”
when a speech acoustic signal enters the ear. The special
mechanism is not used for general auditory perception,
such as music, the sound of breaking glass, or the rus-
tling of leaves that suggests the approach of a summer
storm. The term species-specific means that only humans
are endowed with this special mechanism, and that the
special part of the brain for speech perception evolved
over thousands of years to create a communication link
with speech production.
The theory is called the motor theory of speech percep-
tion. In its simplest form, the theory states that speech
is perceived by reference to articulation. The idea is
that speakers produce a speech acoustic signal that
encodes (like encryption) the articulator movements
that produced the signal. When the speech acoustic
signal enters the ear and the brain of the listener, the
code must be broken to perceive the sounds produced
by the speaker. The special mechanism in the brain
performs this decoding. In the motor theory, the role
of the speech acoustic signal is to carry the code that
allows the brain to unlock the underlying articulation
that produced the signal.
Why did the motor theorists reject the speech
acoustic signal as a reliable source of the perceptual
identification of speech sounds? In the view of the
motor theorists, the speech acoustic signal for any
given sound was too variable and therefore not reli-
able as a cue to the identity of the sound. The acoustic
characteristics of /b/, for example, vary depending on

such factors as the phonetic context in which the con-
sonant is produced (e.g., /bit/ “beat” versus /bæt/
“bat”), who is producing the sound (e.g., men, women,
children), how quickly the sound was produced (e.g.,
the speaking rate), as well as other variables (see the
earlier section, “The Theory of Speech Acoustics”).
The variable of the speaker is especially instruc-
tive. As discussed earlier, the vocal tract lengths of men,
women, and children are different, so the acoustic char-
acteristics of all sounds depend to a significant degree
on who is doing the speaking. The motor theorists
asked, “How does a human store all the many acous-
tic characteristics of a single sound? Their answer was,
“The speech acoustic signal for a speech sound may
be highly variable, but the articulatory movements
are not. All speakers — men, women, children — pro-
duce (for example) a /b/ by closing the lips and closed
velopharyngeal port so pressure can be built up in the
vocal tract.”
Hence, the idea was formed of focusing on the artic-
ulatory characteristics of speech sounds as the “objects”
of speech perception.
The coupling between speech production and
speech perception is critical to this theory. Over the
course of evolution, the special encoding/decod-
ing process served the needs of human communica-
tion, which depends equally on the performances
of a speaker and a listener. The specialized coupling
is relevant to the ability to produce and hear speech
Alex’s Magic Trick
The hypothesized match of the brain
mechanisms for speech perception and speech
production is complicated by talking parrots (as
well as other talking birds like mynahs and para-
keets [budgerigars]). Some of you may be familiar
with Alex (1977–2007), the African grey parrot
written about extensively by the MIT scientist
Irene Pepperberg and her colleagues (Patterson &
Pepperberg, 1998). Alex talked a lot, had a huge
vocabulary, and had a remarkable ability to imitate
a wide range of sounds, including speech. Alex
was not the only African grey to produce words
and sentence; in fact, they have the reputation of
being chatterboxes and of continuously learning
utterances over the course of their long lifetimes.
African greys and other parrots may “articulate”
speech, partially by moving their tongues, but
the evidence for this is scant or based on rather
artificial experiments (Becker, Nelson, & Suthers,
1994; Patterson & Pepperberg, 1994). Parrots do not
have a sound source (like the vibrating vocal folds)
11  Speech Science II 161
sounds. In other words, the theory did not have much to
say about how meaning is obtained from speech
perception.
The implications of the motor theory are inter-
esting. First, because the special brain mechanism for
speech perception is an outcome of human evolution,
it must be present in the brains of human infants. Of
course, even specialized mechanisms that are part of
the human brain endowment are likely to develop
throughout childhood, but nonetheless, the neural
hardware is there and presumably ready for operation.
In fact, there is a good deal of research (as reviewed
in Galle & McMurray, 2014) that shows infant speech
perception for sound category distinctions such as /p/
versus /b/ to be similar to the same distinctions per-
ceived by adults. This finding seems to be consistent
with the idea that the speech perception mechanism is
a special part of human brains, whether infant or adult.
Another implication is that animals should not be
able to make speech sound category distinctions simi-
lar to those observed in humans. Animals do not talk,
or at least they do not articulate sequences of speech
sounds in a human-like way. According to the motor
theory of speech perception, animals should not hear
phonetic distinctions because they do not produce pho-
netic distinctions. This makes sense from the evolu-
tionary perspective as previously discussed. Because
(according to the motor theory) speech production and
speech perception co-evolved in humans, the absence
modified by moving articulators to create different
acoustic signals. Watching an African grey’s beak
and tongue as he says a word or sentence, you
will not see much movement, certainly not the
kind required to produce consonants. You cannot
see their lips move because, well, they do not
have lips. Where, then, does the magic happen?
Like many birds, African greys have a syrinx, a
complex anatomical structure deep in their chests
(Figure 11–3). This is where the magic happens, but
exactly how it occurs is not clear. The anatomy of
the syrinx is understood well (Habib, 2019). It is
located in the chest and composed of muscularly
controlled valves that are “powered” by an air sac,
somewhat like the human lungs. African greys
present a problem to the motor theory of speech
perception because they do not have the speech
production mechanism that, over the course of
evolution, would evoke a special speech percep-
tion mechanism. Hmm. Learn more about Alex at
https://en.wikipedia.org/wiki/Alex_(parrot)
162 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Figure 11–3.  Photo of African grey parrot with an art-
ist’s image of the syrinx superimposed on the parrot’s chest.
The syrinx is located deep in the parrot’s chest. It consists
of muscles and membranes, as well as cartilage, that form
valves that can be opened and closed in complex ways to
produce human-sounding speech as well as a wide variety
of other sounds. This 29-year-old’s name is Friday, and he
lives with the author’s brother and his spouse. Friday says
a lot, even producing utterances that are not mimicked but
are contextually “correct.” These utterances include saying
“goodnight” when the lights go out, calling out the dog’s
name when the dog is present, and saying “hello” when the
phone rings. Friday also has lots of other sound productions ​
— ​he does a microwave beep, he whistles, he barks, he does
bodily noises really well, and, of course, does bird whistles
and bird chatters. All this with an open beak and no lips.
of speech production skills in animals predicts the
absence of human-like phonetic perception.
If only it were that simple. Experiments have
shown that animals such as Japanese quail (Kluender,
Diehl, & Killeen, 1987) and chinchillas (Kuhl & Miller,
1975; Kuhl & Miller, 1999) perceive phonetic distinc-
tions in much the same way as humans. This is a dif-
ficulty for the motor theory of speech perception, for
the reasons stated previously. Why should animals
perceive these distinctions in the same way as humans
if they, animals, do not have the special speech percep-
tion mechanism in the brain — how could they have
this mechanism when they lack speech production
capabilities?
These kinds of concern about the motor theory of
speech perception (and there are other concerns: see
Hixon, Weismer, & Hoit, 2020) convinced a group of
researchers to develop theory and data that support the
use of general auditory mechanisms in the perception
of speech. Auditory theories of speech perception are
built around the idea that the very sophisticated audi-
tory and general computing capabilities of the human
brain are well suited to make phonetic distinctions: no
special, species–mechanism is required.
The Perception of Speech:
Auditory Theories
Auditory theories of speech perception are based on
a simple idea. The auditory mechanisms used for the
perception of any acoustic event are used to perceive
speech. There is no special mechanism required. Audi-
tory regions of the brain, as well as areas associated
with these regions, are sufficiently sophisticated to pro-
cess and identify phonetic events.
Auditory theories are not free of problems. An
auditory theory is only as good as the speech acoustic
data presented for auditory processing. For example,
an auditory analysis that distinguishes between a /p/
and a /b/ must have some brain representation of the
acoustics of the two sounds, and especially how the
acoustics differ between the two. The only way the brain
can have such an acoustic representation is to learn
what makes a /p/ and what makes a /b/. This learn-
ing, presumably in the earliest stages of speech and
language acquisition, must be based on a consistent
speech acoustic characteristic that is always produced
when a person — any person — says a /p/ or /b/ (or
any speech sound). And, if the speech acoustic signal
demonstrates this consistency for each speech sound in
a language, where in the brain are these representations
stored, and what is the form of the stored data?
Speech scientists have entertained the idea that
the brain stores templates (also called prototypes) of the
acoustic characteristics of speech sounds (sometimes,
of the acoustic characteristics of syllables). Templates
can be thought of as “ideal” representations of these
speech sound acoustic characteristics. When a speaker
produces a /b/, for example, as the first sound in the
word “badgers” (/bæ2z/), the speech acoustic signal
entering the auditory system is compared with all the
stored templates to determine a match or mismatch.
A match to the /b/ template is equivalent to percep-
tion of the /b/ sound. In auditory theories of speech
perception, the “objects” of perception are the acoustic
characteristics of speech sounds, perhaps represented
in the brain as acoustic templates.

Matching Speech
Perception and Speech
Production Without a
Special Mechanism
An influence of speech perception skills on
speech production skills does not require a
special mechanism to match the two. But, speech
perception skills may still play a crucial role in
speech production skills. After all, the speech
acoustic signal you produce is heard not only
by a listener, but by the producer as well. The
speech perception mechanism is your monitor
for the quality of your speech production. This
idea has application in the speech and hearing
clinic, where children with delayed mastery of
speech sounds (see Chapter 15) are sometimes
thought to have poor auditory representations
(i.e., templates) of the speech sounds they
produce incorrectly. The clinical application is
called auditory training, or ear training, and is
implemented by stimulating the child’s auditory
system with multiple, correct repetitions of the
incorrectly-produced sounds. Improvement in
speech perception skills is assumed to result
in improved auditory representations of the
incorrectly-produced sounds, which become the
basis for improved speech production skills.
Is it true that each of the many speech sounds
within a language has unique and consistent speech
acoustic characteristics no matter who produces the
sounds? Some scientists say “yes” to this question (e.g.,
Diehl, Lotto, & Holt, 2004), and others say “no” (e.g.,
Liberman, Cooper, Shankweiler, & Studdert-Kennedy,
1967). Other scientists place themselves somewhere
between these two positions, arguing that speech per-
ception is based on articulatory gestures but assisted by
speech acoustic data (Fowler, Shankweiler, & Studdert-
Kennedy, 2016).
Motor Theory and Auditory
Theory:  A Summary
Figure 11–4 presents a schematic summary of the pri-
mary difference between the motor theory of speech
1
/eI/ is italicized to indicate that this diphthong (as in the word “take” /teI k/) is considered a single sound even though it is represented by
two symbols.
2 
“ Black box” is a term used to designate an unknown mechanism for a hypothesized or known process. In this case, the black box is the special
mechanism for perceiving speech.
11  Speech Science II 163
perception and an auditory theory of speech per-
ception. Part A shows the speech acoustic signal as
the input to the auditory system. The speech signal is
the sentence, “The blue dot is a normal dot.” There are
19 speech sounds in this sentence — in the phonetic tran-
scription of the sentence (/DɔbludɑtIzeI nɔrmldɑt/),1
each symbol is assumed to be a separate speech sound.
The middle image is a view of the surface of the left
hemisphere of the brain, widely considered as the
hemisphere that contains the tissue used to produce
and perceive speech. The oval encloses the perisylvian
speech and language areas, including Broca’s and Wer-
nicke’s areas as well as auditory cortex (see Chapter 2).
The right side of Figure 11–4A presents a “black box”2
containing the special mechanism that decodes the
encoded speech acoustic signal. The decoded signals
for each speech sound are the articulatory movements
that produced the speech sounds. The objects of speech
perception in the motor theory are these articulatory
movements.
A similar summary diagram is shown in Figure
11–4B for an auditory theory of speech perception. The
left and middle images are the same as in Figure 11–4A;
the input is the speech acoustic signal and the relevant
brain areas indicated by the tissue within the oval. On
the right side of the figure is a single sound segment,
the vowel /ɑ/ in “spot” (/spɑt/), which is analyzed
by auditory mechanisms that are not specialized for
speech perception. The auditory cortex analyzes each
sound, which it delivers to a long-term memory bank
of templates, each one representing a different sound
segment. Using /ɑ/ as an example, the auditory analy-
sis is delivered to a mechanism that compares the anal-
ysis to various vowel templates. The best match — in
this case the acoustic template for /ɑ/— is perceived.
In an auditory theory of speech perception, the objects
of perception are these best matches to acoustic tem-
plates that contain the ideal acoustic characteristics for
each sound segment.
Top-Down Influences:  It Is Not
All About Speech Sounds
Perhaps the most obvious way to imagine how we
perceive speech is to assume that each sound — what-
ever the object of speech perception may be — is ana-
lyzed as it comes into the auditory system. When these
sequential analyses (one analysis per speech sound)
164
Motor theory of speech perception
Speech acoustic input to auditory system Black box
Special brain
4.0
mechanism transforms
acoustic input to
3.0 articulatory
representations.
The articulatory
2.0 representations are
the objects of speech
perception.
1.0

Frequency (kHz)
Broca’s Wernicke’s
area Primary area
The blue spot is a normal dot auditory
A cortex

Auditory theory of speech perception

Speech acoustic input to auditory system

4.0

3.0

2.0

1.0

Frequency (kHz)
Broca’s Wernicke’s
area Primary area
The blue spot is a normal dot auditory
cortex ɑ
B Time (ms)

Figure 11–4.  Schematic summary of the primary difference between the motor theory of speech perception and an auditory theory of speech perception. A. Motor
theory, showing the speech signal input (left ), the left hemisphere speech and language areas (middle), and the “black box” special mechanism for converting the
acoustic signal into an articulatory representation (right ). The conversion is a speech- and species-specific mechanism. In the motor theory, the objects of speech per-
ception are the articulatory events that produced the acoustic input. B. Auditory theory, left and middle images same as in (A), right image showing a vowel identified
by its acoustic properties. General auditory mechanisms perform the analysis. The objects of speech perception are the acoustic characteristics of each speech sound.

are completed. the sounds are put together to iden-
tify the spoken word. For example, recognition of the
word “badgers,” which consists of the five sounds /b/,
/æ/, /dZ/, /2/, and /z/, takes place by analysis of the
sequence of sounds, followed by a process that groups
the sequenced sounds to determine if they form a word.
A process such as this requires very large storage in
long-term memory of all the acoustic sound sequences
that can form words. Each time an auditory (acoustic)
analysis is performed on a sequence of sounds, the
grouping of a specific sequence can be matched to a
word pattern in memory, if it exists.
There is good evidence that the process just des-
cribed is not the way word recognition happens. Listen-
ers are not passive perceptual beings — they are active
in the process of speech perception. Listeners use the
acoustic analysis of the first or second sound of a word
and then begin to search quickly all the words known to
them that may be good “word recognition candidates.”
This process is called “searching the lexicon.” When
this search produces a likely word match, the listener
moves on to the acoustic analysis of the next word and
another active word search as previously described. An
important aspect of this process is that listeners make
word identification choices before they have completed
the acoustic analyses of all the sounds in the word (an
excellent review of these findings is found in Gelfand,
Christie, & Gelfand, 2014). The word choices can be
made this way because other aspects of the communi-
cation setting, including the words already recognized,
the conversational setting, and even the very general
topic being discussed, help a listener to find the word
being analyzed — to predict it, in a sense — before all
the component sounds have been analyzed. When you
think about it, this is a much more efficient way to per-
ceive speech compared with an analysis of all sounds
in a word before a word decision can be made.
The use of various kinds of processes and knowl-
edge, such as searching a specific part of the lexicon
(e.g., all words beginning with /b/), using situational
context, the topic under discussion, and other sources
of information to guide word-choice decisions, is
called top-down processing. It is “smart” perceptual
processing, much more efficient than a passive process
of analyzing incoming data in steps and building up
a perception. This latter approach is called bottom-up
processing, and most scientists believe that as a pri-
mary psychological process it is a poor model for any
form of perception, including speech perception.
In the example previously given, in which the
acoustic analysis of the first one or two speech sounds
of a spoken word is used to initiate a focused, active
lexical search, both bottom-up and top-down processes
are used. The bottom-up part of the process is the initial
11  Speech Science II 165
acoustic analysis, and the top-down part is the lexical
search supplemented by other sources of knowledge
that contribute to word identification.
Speech Intelligibility
“Speech intelligibility” describes the degree to which
speech is understandable. The idea of a degree of intel-
ligibility is appropriate. Speech can be intelligible or
unintelligible by degrees; it is not an either-or phenom-
enon. Everyone has had the experience of not quite
understanding what someone has said or catching just
a few words of an utterance that is for the most part
unintelligible.
Speech intelligibility is an outcome of the pro-
cesses of speech perception regardless of the theory of
speech perception to which you pledge allegiance. The
degree to which an utterance is intelligible depends on
many variables. Let’s first assume that an utterance is
perfectly intelligible when spoken in a quiet environ-
ment. In a noisy room, the intelligibility of the same
utterance may decrease to a degree depending on the
level of the noise. Speak that same utterance over a
wireless transmission system (e.g., a cellphone) with
limited quality, and the intelligibility may be affected
(especially if the listener has a hearing loss — see later
in this chapter).
These examples are based on a hypothetical refer-
ence utterance with perfect intelligibility, heard in an
optimal listening environment. Other variables may
affect speech intelligibility as well, as is the case when
the person speaking the utterance has a speech impair-
ment or the listener has a hearing loss.
Speech intelligibility tests have been developed to
measure the degree of intelligibility loss among speak-
ers or listeners with communication impairments. For
example, the speech of individuals with cleft palate,
neurological disorders, and congenital hearing impair-
ment are unintelligible to various degrees. Speech
intelligibility tests, in which the listeners have normal
hearing, provide an index of the individual’s intelligi-
bility deficit. This index can provide objective data to
track progress due to surgery (as in the case of cleft
palate), speech therapy (as in the case of neurological
disease), and amplification (as in the case of speakers
with hearing loss who are fitted with hearing aids).
Speech intelligibility can be measured using scal-
ing techniques, word lists, and sentences. In addition,
intelligibility for specific speech sounds has been mea-
sured using phonetic or orthographic transcription.
Scaling techniques use a number scale, such as
a 7-point scale with 1 = least impaired and 7 = most
impaired. Another version of scaling, called Visual
166 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Analog Scaling, shows the listener a continuous line
with numbers ranging from 1 to 100. One end of the
scale is defined as completely unintelligible and the
other end as completely intelligible. The listener hears
an utterance and operates a slider to place a pointer on
the scale that corresponds to the perceived degree of
intelligibility.
Word and sentence tests are often-used mea-
sures to index speech intelligibility. Listeners hear a
list of words or sentences and write down (or enter
into a computer) what they heard. As one example,
when 50 words are presented and the listener writes
the correct word for 40 of them, speech intelligibility
is indexed as 80%. Sentence intelligibility works the
same way. In a sentence test having an overall num-
ber of 100 words, correct orthographic transcription
of 50 words is indexed as 50% speech intelligibility. In
some cases, an index of the percentage of speech sound
intelligibility is desired. Long passages of speech such
as reading or conversation are transcribed orthographi-
cally or using phonetic transcription to obtain a count
of the number of sounds that are heard correctly for
the entire passage. For example, a measure called Per-
centage of Consonants Correct (PCC) (Shriberg, Aus-
tin, Lewis, McSweeney, & Wilson, 1997) is a ratio of the
number of consonants heard correctly to the total num-
ber of consonants in the passage (PCC = percentage
of consonants correct/percentage of consonants in the
passage). PCC is used frequently to document phonetic
development and disorders in children.
Overall, speech intelligibility measures are use-
ful for indexing the degree to which a person’s speech
or hearing loss affects the transmission of information
between speaker and listener. Speech-language pathol-
ogists and audiologists value these measures due to
their straightforward clinical application.
Chapter Summary
The theory of speech acoustics, formulated by Gunnar
Fant, states that the output of the vocal tract (that is, the
speech acoustic signal) is the product of the acoustic
characteristics of a sound source (the vibrating vocal
folds) combined with a sound filter (the vocal tract).
The sound source consists of energy at the F0 (the
rate of vibration of the vocal folds) plus energy at har-
monic frequencies, which are whole-number multiples
of the F0.
The sound filter can be described as the resonant
frequencies of the vocal tract, which change depending
on the shape of the tract. The vocal tract, like any tube
(pipe) resonator, has multiple resonant frequencies.
The shape of the vocal tract is changed by motions
of the jaw, tongue, lips, and pharynx.
Vowels can be described acoustically by the first
three resonant frequencies of the vocal tract tube.
Speech scientists call these resonances formants. Differ-
ent vowels are heard because different shapes of the
vocal tract produce different formant frequencies.
Because the vocal tract resonates like a tube, or
pipe, shorter vocal tracts have higher formant frequen-
cies; longer vocal tracts have lower formant frequen-
cies. This explains why children have higher formant
frequencies than adult women, who have higher for-
mant frequencies than adult men.
Speech acoustics is important to assistive listening
devices, theories of speech perception, speech synthe-
sis and recognition, and language development.
The motor theory of speech perception states that
speech is perceived by a special, species-specific mech-
anism in the human brain; the objects of speech percep-
tion are the articulatory movements that generated the
acoustic signal.
Auditory theories of speech perception state that
the speech acoustic signal for any speech sound is suf-
ficiently stable to be analyzed reliably by general audi-
tory mechanisms; the objects of speech perception are
the acoustic characteristics of speech sounds.
Many speech perception theorists believe that the
sound-by-sound analysis of the speech acoustic signal
entering the auditory system is supplemented by top-
down processes.
Top-down processes are essential to an efficient
speech perception process; the listener’s knowledge
and expectations allow her to identify words before the
completion of the sound-by-sound analysis.
Speech intelligibility measures use scaling tech-
niques or word and sentence lists to estimate a person’s
ability to hear speech or the effect of a speech disorder
on the ability of others to perceive their speech. These
tests are applied frequently in clinical settings.
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Phonetics
Introduction
Speech sounds are the phonetic components of lan-
guage (Chapter 3). Speech sounds are often referred to
as speech sound segments to indicate that words can be
broken down into their individual, component sounds.
In American English, examples of speech sounds
include the vowels in words such as “bead” and “dot”
(“ee” and “ah,” respectively), the nasals in words such
as “Mom” and “never,” and the “f” sound in “rough.”
In these examples, the speech sounds do not always
match the orthographic representations of the words.
The “ah” in “dot” is represented orthographically by
an “o,” and the “f” in “rough” is represented by “gh.”
The mismatch between orthography and sound does
not apply to all languages; in languages such as Finnish
and Japanese, the match between the written and spo-
ken form of words is very good (but not always perfect).
Phonetic transcription is a tool for representing
speech sounds by means of a special set of symbols.
A trained transcriber uses the symbols, drawn from
the International Phonetic Alphabet (IPA), to record
the sounds of speech independently of the words they
form. High-quality phonetic transcription requires
extensive training. Speech-language clinicians and
researchers who have this training make extensive
use of phonetic transcription to generate a record of
produced or perceived speech sounds. For example,
a speech-language pathologist (SLP) who generates a
record of a child’s phonetic inventory — all the sounds
12
the child produces — uses phonetic transcription to gen-
erate the record. Or, a researcher who studies dialect
variation within a language uses phonetic transcription
to record all the sound variants in different dialects of a
specific language. A good example of this is the many
ways the “eh” sound in words such as “bed,” “head,”
and “lead” is spoken in American, British, Scottish,
and Irish English, as well as among dialect variations
within any of these languages.
The term “phonetics” is often broken down into
three subareas. These areas are articulatory phonetics,
acoustic phonetics, and perceptual phonetics. Articulatory
phonetics is the study of speech movements associated
with speech sounds. For example, a speech scientist
may be interested in documenting tongue movements
for the vowel /u/ in words (as in “boot”) and how the
movements are modified by variables such as speak-
ing rate, voice loudness, and speech style (casual or
formal). Acoustic phonetics is the study of the acous-
tic characteristics of a vowel like /u/ in words spoken
in different speaking conditions (Chapter 11). Articu-
latory and acoustic phonetics are not the same thing,
because knowledge of the articulatory characteristics
of a speech sound does not guarantee precise knowl-
edge of the acoustic characteristics of that same sound.
Finally, perceptual phonetics is the study of how lis-
teners hear articulatory and acoustic characteristics of
speech sounds. For example, a vowel such as /u/ may
be heard differently when spoken in a word at a fast
versus slow speaking rate.
169
170 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
This chapter deals with all three types of phonetics,
but its focus is on perceptual phonetics, because the IPA
is a tool for recording heard sounds. Nevertheless, an
IPA symbol that represents a heard sound implies some-
thing about the articulatory and acoustic phonetics of
the sound, as discussed in the material of this chapter.
The IPA is a universal tool for all people who study
languages and are interested in phonetic descriptions.
No matter the dialect, the language, the potential
speech and/or language disorder, even the sounds
produced by babbling infants, the IPA is meant to be
universally applicable and usable for the transcription
of speech sounds produced by any speaker.
The purpose of this chapter is not to make the
reader a transcription user. Rather, it presents the con-
cepts that support use of the IPA for transcription of
speech sounds and provides examples of transcrip-
tions. A “convention” (a rule we can all agree on) is
followed in this chapter when IPA symbols are used.
When the symbol is not the same as its English orthog-
raphy counterpart, the symbol is accompanied by a
word example that includes the sound. For example,
/ʃ/ “shave”, /E/ “bet”, /dZ/ “jazz.” Cases in which the
orthography and phonetic symbol match, such as the
/p/ in “pack,” are not followed by a word example.
International Phonetic
Alphabet
The history of the IPA extends back to the late 19th cen-
tury, when it was developed for precisely the reasons
noted before — to create a universal symbol system for
the speech sounds of the world’s languages. Over the
years, the IPA has been revised several times for bet-
ter accuracy as well as addition of sounds that were
not included in the original version. In the early 1990s,
the IPA was adapted by the International Clinical Lin-
guistics and Phonetics Association (ICPLA) for specific
use in clinical settings (see Shriberg, Kent, McAllister,
& Preston, 2019).
Vowels and Their Phonetic Symbols
An inventory of vowels in languages of the world is
shown in Figure 12–1.1 The four sides of this diagram
form a vowel quadrilateral. The vowel quadrilateral
shows (theoretically) where vowels can be articulated
using tongue heights and tongue forward-backward
positions within the oral cavity. This is illustrated in
1
 echnically, there are more vowels than those shown in Figure 12–1. Some languages like Japanese use differences in duration for the same
T
vowel sound as different phoneme categories. For example, Japanese has a short /i/ “ee” that contrasts with a long /i/.
Front Central Back
High i y ɨ ʉ ɯ u
ɪ ʏ ʊ
Mid-High
e ø ɘ ɵ ɤ o
Mid ə
ɛ œ ɜ ɞ ʌ ɔ
Low-Mid
æ ɐ
Low a ɶ ɑ ɒ
Figure 12–1.  The International Phonetics Association
vowel diagram. Vowels of American English are enclosed
by red circles. The tongue height dimension of the quadri-
lateral is shown on the vertical axis and the tongue advance-
ment dimension (front-back) on the horizontal axis.
Figure 12–2, where the quadrilateral is superimposed
on the oral cavity, and the “corner vowels” are indi-
cated by IPA symbols (see later in chapter). Different
vowels can also be made by adjusting the shape and
length of the lips.
In Figure 12–1, phonetic symbols for American
English vowels are circled in red. Table 12–1 lists these
phonetic symbols, each of which is paired with a word
containing the vowel sound. Vowels are typically cat-
egorized using three descriptors: tongue height, tongue
advancement, and lip rounding. The goal of the fol-
lowing discussion is not to promote learning of the IPA
symbol system, but rather to use the phonetic symbols
to make broader points about phonetics and its appli-
cation to language studies and speech disorders.
Tongue Height (High Versus Low Vowels)
Tongue height is a description of the height of the
tongue relative to the fixed boundary of the hard palate
(roof of the mouth). High vowels have a tongue posi-
tion very close to the hard palate, and low vowels have
a tongue position relatively far from the hard palate.
The upper left and right panels of Figure 12–3 show
the height of the tongue for two superimposed vowel
pairs — /i/ versus /æ/ (left) and /u/ versus /ɑ/ (right).
The tongue heights for /i/ and /u/ are very close to
the hard palate and are called high vowels; in fact, these
 12 Phonetics 171

Upward movements of the mandible carry the tongue

i u
to the hard palate, in the direction of high vowels. In
many cases, the movements of the tongue and man-
dible are in the same direction, and much of the differ-
ence in vowel height is due to mandible movements
with smaller contributions of tongue movement. The
IPA description of vowels is based on tongue positions,
so mandible positions are not considered further.

æ a
Vowel Phonetics Trivia
The sentence, “The vowel quadri-
lateral shows (theoretically) where vowels can
be articulated using tongue heights and tongue
forward-backward positions within the oral
cavity” is a simplification of vowel phonetics. It
is more accurate to say that the diagram shows
Figure 12–2.  The human vocal tract (the airway from the vowels of the world’s languages that are
the vocal folds to the lips) with the vowel quadrilateral currently known to function in a categorical
superimposed on the oral cavity. The quadrilateral shows fashion (hence, “theoretically”). “Categorical
the area in the oral cavity in which the tongue moves for fashion” means the vowels can function as
different vowels. phonemes, which are described in Chapter 3.
Certainly, vowel-like sounds may be produced
“between” some of the symbols shown in
Figure 12–1 but, to date, they have not been
Table 12–1.  List of Phonetic Symbols for Each
identified or confirmed as actual phonemes in a
American English Vowel, Together With a Word
language. In addition, the true vowel inventory
Containing the Vowel Sound
of the world’s languages includes lip articula-
tion, changes in the shape of the pharynx, and
Front Vowels Central Vowels Back Vowels
possible changes in voice (laryngeal behavior).
/i/ (beet) /ə/ (agree) /u/ (boot) Two famous phoneticians, Peter Ladefoged and
/I/ (bit) /2/ (brother)* /U/ (book) Ian Maddieson, estimated that a truly complete
inventory of vowels in languages of the world
/e/ (bait) // (bird)* /o/ (boat) may total 100 to 200 vowels (Ladefoged &
/E/ (bet) / / (buck) Maddieson, 1996). The vowel diagram in
Figure 12–1 reflects a 2018 update by the IPA;
/æ/ (bat) /ɔ / (bought)
the known phonetics of the world’s languages
/ɑ / (bog) are apparently always in transition and
accumulating.
Note. The “r” colored vowels (identified by asterisks) are not
included in Figure 12–1.

Tongue Advancement (Front

vowels are the highest of the American English vowels.
In contrast, tongue heights for /æ/ and /ɑ/ are rela-
tively far from the hard palate and are called low vow-
els; these two vowels are the lowest of the American
English vowels. Note in Figure 12–1 how other Ameri-
can English vowels fall between the highest and lowest
vowels along the vertical axis.
Vowel height differences are made not only by
the tongue, but also by the mandible (lower jaw). The
tongue is attached to the mandible, but not completely.
Versus Back Vowels)
Tongue advancement is a description of the extent to
which the tongue is forward or back in the vocal tract.
As shown in the two bottom panels of Figure 12–3, the
tongue blade and tongue dorsum — the parts of the
tongue extending approximately 20 to 25 mm behind
the tongue tip — can be placed as far forward as the
front of the hard palate. For the most back position, the
tongue blade/dorsum is pulled back about 15 mm from
the most front position. Vowels with a tongue blade/
172 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

[i] [u]

[ɑ]

[æ]

[ɑ]

[u] [æ]
[i]

Figure 12–3.  Tongue positions for /i/ versus /æ/ and /u/ versus /ɑ / (left and right upper
panels) showing differences in tongue height between front (/i/-/æ/) and back (/u/-/ɑ /) vowels.
Tongue positions for /i/ versus /u/ and /æ/ versus /ɑ / (left and right lower panels) showing dif-
ferences in tongue advancement between high (/i/-/u/) and low (/æ/-/ɑ /) vowels.

dorsum forward in the vocal tract are called front vow-
els; vowels with a tongue blade/dorsum pulled back
are called back vowels. These forward-backward posi-
tions of the tongue blade/dorsum are illustrated in
the lower two panels of Figure 12–3 for /i/ versus /u/
(left), and /ɑ/ versus /æ/ (right). The tongue position
for the vowel /i/ is more advanced (more front) than
the tongue position for /u/, as is the tongue position
for /æ/ compared with the tongue position for /ɑ/.
The difference for the latter pair of vowels is subtle.

Small Movements, Big Effects

Vowels are produced in a mini-world of
tongue position differences. The same point on the
tongue — such as on the tongue blade — may differ
in position by no more than 20 mm for the most
front high vowel (/i/) and most back vowel (/u/).
Measure 20 mm, and you will see what we mean;
these differences in position are surprisingly small
for the big effect of easily hearing the difference
between an /i/ and /u/, or between any other pair
of vowels in which the position differences are
even smaller. For readers more comfortable in the
world of inches, 20 mm is about 0.8 inch.

Lip Rounding
Lip rounding is a description of the configuration of the
lips for vowel production. In many languages, some
vowels are described as rounded, in contrast to other
vowels described as unrounded. Rounded vowels are
produced with a narrow opening between the lips, and
sometimes with the lips protruded, to create a narrow
air channel. For example, most (if not all) textbooks
on the phonetics of American English describe /u/ as
a rounded vowel. Ask a friend — preferably someone
in your grandparents’ generation — to say word pairs
like “boot”-“beat” or “food”-“feed.” Observe the con-
trast between the two vowels in the formation of the
speaker’s lips. Make the observations from the front (to
see the narrow opening between the lips for /u/) and
from the side (to see the protruded lips). Other vowels
in American English, most notably /U/ (“book”) and
/o/ (“boat”), are also described as rounded, although
not to the same degree as /u/. The remaining vowels
of American English are considered to be unrounded.
Vowels of American English Compared
With Vowels of Other Languages
Figure 12–1 shows a total of 28 vowel symbols, of which
12 are used to describe the vowels of American English.
America English has a relatively “dense” vowel system,
This Is Not Your
Grandparent’s Vowel
Why ask a grandparent to speak the words?
And why not include /æ/ in the corner vowels?
Let’s take the grandparent question first. Across
generations, there are always changes in the way
sounds are produced. Take /u/, for example.
College-age speakers especially, and even people
approaching age 40 years, have done two things
to this vowel. One, they have moved the tongue
forward to produce it, in the direction of /i/. Two,
they have stopped rounding their lips for the
vowel. So, if you ask a friend to do the “boot”-
“beet” “food”-“feed” thing, they may not show
much lip rounding for /u/. Second, let’s consider
/æ/. It may be a corner vowel in English, but it
is so odd — pronounced so differently in different
dialects, and absent from many vowel inventories
in languages of the world that it may be better
to leave open the question of the lowest, most
forward vowel position in American English. Take
a look at the /æ/-/ɑ/ contrast in Figure 12–3; it
is not easy to see much of a difference between
the tongue positions for these two vowels.
12 Phonetics 173
meaning it has a lot of vowel categories relative to many
other languages. Greek, for example, has only five vow-
els, as does Spanish. These languages, like many others,
have “sparse” vowel systems. The relative density or
sparseness of a vowel system has no effect on commu-
nication efficiency within a native language.
American English has several vowels that are
relatively rare among languages of the world. These
include /I/ “bit,” /E/ “bet,” /U/ “book,” and /æ/
“hat.” These vowels often present pronunciation prob-
lems for adult speakers learning English whose native
language (including such languages as Greek, Span-
ish, French, Korean, and Mandarin Chinese) does not
include at least one of these vowels.
Finally, in virtually all languages of the world,
the most extreme vowels — the highest and most front,
the highest and most back, and the lowest and most
back — define the limits of vowel articulation. These
vowels are /i/, /u/, and /ɑ/, respectively (see Fig-
ure 12–2). In theory, these vowels enclose the remain-
der of the vowels in any vowel system.
Tricky Vowels
Vowels are tricky. Uniform agreement
among phoneticians on the sound associated with
a particular phonetic symbol may be difficult to
obtain. However, whatever disagreements exist
are probably few in number. Organize a group of
50 phoneticians in a room, show them a vowel
symbol, and ask each phonetician to say the
sound. Your author believes 90% of the symbols
in Figure 12–1 will elicit the same vowel from
each phonetician. The trick is, what does “same”
mean in this context? Most American English
vowels are produced in many different dialects — ​
does the vowel /E/ (“bet”) sound the same in
Northern, Southern, and Western dialects?
Almost certainly not. But listeners can assign the
spoken vowel to the same category — they are all
examples of the /E/ in “bet” — even when
hearing the dialect-bound difference between
them. Vowels are tricky for additional reasons as
well. Take the vowels /ɑ/ and /ɔ/, for example.
These are separate vowel categories in dialects
spoken in places such as Philadelphia and
Baltimore (e.g., /dɑk/ “dock” versus /dɔg/
“dog”) but not so much in places such as South-
ern California /dɑk/ “dock” versus /dɑg/
“dog”). So, in SoCal, are the vowels in “cot” and
“caught” the same or different? And what about
the Bostonian or Pittsburgher who says /hɔt/
“hot” when almost everyone else in the country
says /hɑt/ “hot”? Vowels are tricky.
174 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Consonants and Their
Phonetic Symbols
An inventory of selected consonants in languages of the
world is shown in Figure 12–4. Some phonetic symbols
for consonant sounds in languages other than Ameri-
can English have been excluded from this image to
simplify the accompanying discussion. Selected non-
American English consonants are included to make a
specific point.
Consonants are categorized by the IPA using three
major descriptors: place of articulation, manner of
articulation, and voicing.
In Figure 12–4, American English consonant sym-
bols are shown in red. Selected consonants from other
languages, that are not found in American English, are
shown inside a green box.
American English consonants are made with con-
strictions at the lips (/p/, /b/, /m/, and /w/2); between
the upper teeth and lower lip (/f/, /v/); at the teeth or
between the tongue and the teeth, called dentals /ɵ/
“think,” /D/ “these”; just in back of the teeth, called
alveolars (/t/, /d/, /s/, /z/, /n/, /l/, and /ɹ/ [like the
“r” sound in “rose”])3; along the hard palate behind
the alveolars — hence postalveolars (/ʃ/ as in “shave,”
/Z/ as in “beige” or “azure”); in the velar region (/k/
and/g/, with the constriction close to the location
where the hard palate joins with the velum); and at the
level of the vocal folds (glottis) (/ʔ/, like the first sound
in “ever” with emphasis on the first syllable, and the
sound heard at the end of words such as “right” in
Cockney English; and /h/). American English conso-
nants are not produced at the retroflexed, uvular, or
pharyngeal places of articulation.

Place of Articulation Manner of Articulation

Consonants are made by forming a constriction some-
where in the vocal tract, between the lips and the vocal
folds. The location of the constriction is the consonant’s
place of articulation. Place of articulation is shown on the
horizontal axis, from left to right, with “bilabial” at the
left-most extreme, and “glottal” (at the vocal folds) at
the right-most extreme.
If place of articulation is the “where” of consonants,
manner of articulation is the “how.” Manners of artic-
ulation in American English include stops, fricatives,
affricates, nasals, approximants, and flaps (taps). Conso-
nants can have different manners of production, even
at the same place of articulation. Examples in American
English include the different manners of articulation

Place of Articulation
Bilabial Labiodental Dental Alveolar Postalveolar Retroflex Palatal Velar Uvular Pharyngeal Glottal

ʈ ɖ q ɢ ʔ
Manner of Articulation

Stop p b t d k g
Fricative ɸ β f v θ ð s z ʃ ʒ ʂ ʐ x ɣ χ ʁ h ɦ
Affricate tʃ dʒ
Nasal m n ɲ ŋ ɴ
Approximant w l ɹ j
Flap ɾ

Figure 12–4.  Chart showing selected phonetic symbols for consonants in languages of the world, adapted from the
most recent revision from the International Phonetics Association. Place of articulation is on the horizontal axis, from
the bilabial place (left-most column) to the glottal place (right-most column). Manner of articulation is shown on the vertical
axis, from top-to-bottom in the order stops, fricatives, affricates, nasals, and flaps (taps). Consonants in American English
are shown by red symbols. Selected consonants from other languages are enclosed by a green box. When two consonants
have the same place and manner of articulation (e.g., /t/ /d/), the first consonant is voiceless, and the second is voiced.

2
/w/ is a special case because it technically has two places of articulation, one at the lips and the other similar to the high-back vowel /u/.
3
/ɹ/ and /l/ are also special cases because they can have places of articulation different from “alveolar” yet be heard as correct versions of
these sounds.

produced at the alveolar place of articulation. Two stop
consonants (/t/, /d/) are alveolars. Stops, also called
plosives, are produced by a brief, complete constric-
tion, blocking the airstream from lungs to atmosphere
for a brief time interval. Brief, in this case, means about
0.06 to 0.1 s (60–100 ms). Because the velopharyngeal
port (the passageway between the throat and nasal cav-
ities, which can be open or shut) is completely closed
during this constriction, air pressure is built up and
released suddenly, creating the signature stop “pop”
when the constriction is released. Put your hand close
to your lips, say /ɑpɑ/ “ahpah,” and feel the puff of air
when the /p/ is released into the second /ɑ/.
Two fricatives (/s/, /z/) also have an alveolar
place of articulation. Fricatives have a tight constric-
tion, but not the airtight constriction characteristic of
stops. Air from the lungs flows to the fricative constric-
tion and results in a pressure buildup behind it, which
forces air to flow through the narrow constriction pas-
sageway. As air is forced through the constriction, it
makes a hissing noise. This hissing noise is a signature
characteristic of fricatives. Produce an /s/ for a few
seconds, and you will hear the hissing noise. Try the
same exercise with other American English fricatives
(e.g., /f/, /T/ “think,” /ʃ/ “shave”).
Affricates have a manner of articulation that is
like a stop followed by a fricative. Affricates are not
just stops followed by fricatives, but a unique manner
of articulation. In American English, /tʃ/ “chair” and
/dZ/ “judge” are made slightly posterior (in back of)
the alveolar place of articulation. In fact, these post-
alveolar affricates are the only affricates in American
English. Many other languages have affricates at dif-
ferent places of articulation.
There is one nasal consonant, /n/, produced at the
alveolar place of articulation. Nasals are produced by cre-
ating a complete constriction in the vocal tract but open-
ing the velopharyngeal port so air can flow through the
nasal passageways and to the atmosphere. Other nasals
include the bilabial /m/ and the velar /ŋ/ “running.”
Approximant is a manner of articulation in the
vicinity of the alveolar place — this type of speech
sound is categorized as an alveolar in Figure 12–4.
Approximants have a constriction that is not as tight
as in fricatives but tighter than in vowels. The hissing
noise associated with fricatives is not produced in most
approximants because their constriction is not suffi-
ciently narrow. Approximants produced at the alveolar
place of articulation include /l/ “long” and /ɹ/ “right.”
Note that /w/ is an approximant at the labial place of
articulation, and /j/ “yes” is an approximant at the
4 
 aps are much less frequent for words like “butter” and “letter” in British English, in which the consonant that separates the two syllables is
T
likely to be a full /t/ (btə).
12 Phonetics 175
palatal place of articulation. (“palatal place” is behind
the postalveolar place, see Figure 12-4).
Finally, flaps, also known as taps, are a type of stop
consonant but are usually given status as a separate
manner of articulation. One way to think of taps is as a
very brief /d/, produced not by placing the tongue tip
just behind the alveolar ridge and blocking the air-
stream for 100 ms, but rather by “flicking” the tongue
tip against the alveolar ridge in a quick touch-and-re-
lease gesture. A good way to describe taps is by exam-
ple. Words like /bɾ2/ “butter” and /lEɾ2/ “letter,” in
which the first syllable is stressed and the second sylla-
ble unstressed, are produced in American English with
a tap separating the two syllables. If the stress pattern
is reversed, the middle consonant sounds like a /t/.4
Consonant Voicing
The question, “What is the voicing status of a specific
consonant?” asks whether the consonant is voiceless or
voiced. Speech sounds categorized as “voiceless” are
produced without vibration of the vocal folds. Speech
sounds categorized as “voiced” are produced with
vibration of the vocal fold.
In American English, the speech sounds of seven
pairs of consonants are differentiated by their voicing
status. Stop consonants are in pairs at each of the three
places of articulation; one is voiced, and the other is
voiceless (bilabial, /p/ /b/; alveolar, /t/ /d/; velar,
/k/ /g/). Fricative pairs are differentiated by voicing
at four of the five places at which fricatives are pro-
duced (labiodental, /f/ /v/; dental, /T/ “think,” /D/
“then”; alveolar, /s/ /z/; postalveolar, /ʃ/ “shave,” /Z/
“beige”). The single affricate pair /tʃ/ “chair” and /dZ/
“judge” is differentiated by voicing (/tʃ/ voiceless, and
/dZ/ voiced). The fricative /h/, produced at the glottal
place of articulation, is voiceless but does not have a
voiced counterpart in American English.
In American English, all nasals and approximants
are voiced.
Consonants of American English Compared
With Consonants of Other Languages
Figure 12–4 shows 61 consonant symbols available to
represent consonants used in languages of the world.
American English uses 26 of these. The 26 consonants
used in American English are an average number among
languages of the world, similar to the number of con-
sonants in German, Italian, Norwegian, and Turkish.
Languages such as Estonian and Bulgarian have conso-
nants that number in the upper 30s to low 40s.
176 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
That’s a Lot of
Consonants
As with vowels, the 61 consonant symbols
underestimate the total number of consonants
used in languages of the world. There are two
reasons for this, one obvious and the other
less so. First, the consonant symbols shown in
Figure 12–4 are selected, as noted in the text. This
decision was made to simplify the discussion
of consonants; this is the obvious reason. The
less obvious reason is that there are certainly
consonant sounds in other languages that have
not yet been identified, and there are variants of
consonant symbols shown in Figure 12–4 that
are the same phoneme category but have slightly
different sounds. Such variants are called “allo-
phones” of the phonemic category. For example,
the stop consonant /t/, a phoneme category in
American English, is produced in (at least) two
ways. One is called aspirated (symbolized /t/,
see section, “Broad Phonetic Transcription”),
and the other unaspirated (usually symbolized
as /t/). The /t/ occurs when the /t/ begins a
word, as in “tough”; /t/ is usually found at the
end of words such as “cat.” These allophones
of the /t/ phoneme are all consonant sounds in
American English. If you are tallying up the total
number of consonant sounds in languages of the
world, the number is certainly greater than the
61 symbols shown in Figure 12–4. Peter Lade-
foged, the great British-American phonetician,
thought there may be as many as 800 consonant
sounds produced throughout languages of the
world.
The green boxes in Figure 12–4 enclose consonants
from other languages. Clearly, there are several places
of articulation that are not used in the phonetic inven-
tory of American English. Good examples are the uvu-
lar (at the back end of the soft palate) and pharyngeal
stops and fricatives that are prominent in Arabic lan-
guages. Also, places used in English but restricted to
one or two manners of articulation are used in other
languages for an additional manner of articulation.
German and Hebrew, for example, have velar frica-
tives; American English does not. Other examples are
found in Figure 12–4.
The shaded boxes in Figure 12–4 have an interest-
ing story. These are articulations that are considered
“impossible” for consonant production. For example,
a pharyngeal (place) nasal (manner) is considered
impossible. This is because the necessary physiologi-
cal condition for a nasal, which is airflow through the
velopharyngeal port to the nasal cavities cannot be met
if the place of articulation is in back of the velopharyn-
geal port. In this case, the airflow is blocked before it
can reach the velopharyngeal port; it is therefore not
possible to produce a pharyngeal nasal.
Clinical Implications of
Phonetic Transcription
The relative density or sparseness of a vowel system
may affect a speaker’s ability to master the vowel sys-
tem of a second language. American English, for exam-
ple, has a high-front vowel pair /i/-/I/ (“beat”-“bit”)
and a high-back vowel pair /u/-/U/ (“kook”-“cook”)
that are notoriously difficult to learn for speakers
whose native language does not have the vowels /I/
and /U/. American SLPs can offer services to people
who are not native speakers of English and who want
to improve their English pronunciation. Knowledge of
different vowel systems and the IPA symbol system for
vowel transcription is important for this “accent reduc-
tion” therapy. A component of the therapy is likely to
be improvement of the client’s ability to both perceive
and produce the difference between vowels, such as
the /i/-/I/ distinction, when only /i/ is part of the
vowel system of the client’s native language.
Let’s turn the issue around and consider a native
speaker of American English and her attempt to learn
Swedish. Swedish has a denser vowel system than
American English; there are between 15 and 17 vow-
els in Swedish. Swedish has four vowel pairs in which
the contrast between them is based primarily on lip
rounding versus no lip rounding. Figure 12–1 shows
the American English vowel symbol /i/ to be very
close to the symbol /y/, which is a rounded version
of /i/ (and, in many Swedish dialects, a little lower
and more forward than /i/). Similarly, Swedish /e/, a
vowel in American English, contrasts with its Swedish
rounded version /ø/. (Try prolonging the vowels /i/
and /e/, then round your lips without moving your
tongue — you will hear something like the Swedish /y/
and /ø/, respectively). A native speaker of American
English who is learning to speak Swedish might ben-
efit from a Swedish-speaking SLP who is well trained
in phonetic transcription and its application to vowels.
An understanding of the American vowel sys-
tem may also be useful to an SLP who records vowel
errors in children for the purpose of making a diag-
nosis between a speech delay of unknown origin and
a speech disorder called childhood apraxia of speech
(Chapter 15). Speech delay of unknown origin rarely
has vowel errors as a prominent problem; vowels are
mastered relatively early in the course of speech sound

development, even among children with delayed mas-
tery of consonants. In childhood apraxia of speech,
vowel errors may be a key diagnostic sign of the dis-
order. An accurate understanding and application of
IPA transcription for vowels are required to describe a
child’s vowel inventory and to compare that inventory
to age expectations for vowel development.
Knowledge of consonant phonetics is directly rele-
vant to the clinical practice of SLPs. SLPs must provide
a transcription record of the sound patterns produced
by children who are evaluated for possible speech
delay. “Speech delay” is a term used in the evaluation
of children’s speech to describe speech sound develop-
ment that significantly lags the expected sound skills
at a given age. For example, studies of typical speech
sound development have established the sounds that
should be mastered by age 5 years. The speech of a
5-year-old child who is evaluated for speech delay
requires an accurate phonetic transcription of his cor-
rectly and incorrectly produced consonants. The inven-
tory of correct and incorrect consonants can then be
compared to the speech sound mastery of a typically
developing child of the same age. Not only is a skilled
transcription of consonants required for this compari-
son, but the universal nature of the IPA symbols allows
the phonetic transcription of a child’s vowels and con-
sonants to be understood by any SLP.
Broad Phonetic Transcription
The phonetic transcription described to this point in the
chapter is called broad transcription. The phonetic sym-
bols represent catgeories of sounds that often function
as phonemes. Narrow phonetic transcription is a kind of
fine-tuned transcription of these broad symbols. Narrow
transcription can be especially useful in clinical settings.
For example, in broad transcription, a speech
sound is either an /s/ or an /ʃ/ “shave.” In clinical
phonetics, however, children and adults often produce
sounds that are neither /s/ nor /ʃ/ but something in
between the two; or, a sound may be recognized as an
/s/ or /ʃ/ but not as a “good” version. How does the
IPA handle such occurrences?
The basic symbol system of the IPA is supple-
mented by a series of symbols called diacritics, which
allow narrow transcription. These symbols are meant to
designate subtle changes in articulation that make a
speech sound “different” from a “good” version of the
sound, but not to the extent that the sound belongs to a
different category. Diacritic symbols are almost always
“attached” to the phonetic symbols described earlier,
to indicate the subtle articulatory changes heard by a
transcriber. The current chapter is a first introduction
to phonetic transcription and cannot delve into the
12 Phonetics 177
intricacies of diacritics. But one example can make the
transcription process clear.
Suppose you are a trained phonetician and you
hear a speech sound that seems like an /s/, but made
with the tongue tip placed very close to the upper teeth.
The speech sound is not interdental like /T/ “thin” but
seems close to it (see Figure 12–4). How do you tran-
scribe this sound? One way is to use a diacritic symbol.
Diacritics symbols are appended to an IPA vowel or
consonant symbol to indicate a subtle modification of
the speech sound. An /s/ that sounds too close to the
teeth is said to be dentalized, or more forward than the
expected alveolar place of articulation. The diacritic
symbol for “dentalized” is  and for the case described
here is transcribed as /s/ (dentalized /s/). The “den-
talized” diacritic can be used with (in theory) any
sound but is especially relevant to other alveolars such
as /t/, /d/, and /n/. A dentalized /d/, for example, is
transcribed as /d/. In-depth presentations of phonetic
transcription and diacritics are available in Bauman-
Waengler (2016) and Shriberg et al. (2019).
Chapter Summary
The IPA is a transcription tool that allows listeners
to use a universal set of symbols to represent heard
speech sounds. The tool is applicable to any language,
and it attempts to represent all the sounds known to
occur in languages of the world. Phonetic transcription
is a highly developed skill.
Vowels are described in phonetic terms along a
high-low dimension (the distance between the tongue
surface and the roof of the mouth (hard palate), a
front-back dimension (the advancement of the tongue
toward the front of the mouth versus the retraction
of the tongue toward the back of the mouth), and a lip
rounding dimension (rounded versus unrounded lips).
Vowels vary among different dialects in the United
States, and in the dialects of all other countries, as well.
Listeners can hear differences in the pronunciation of a
vowel even when they assign the different pronuncia-
tions to the same vowel category.
The vowel system of American English is differ-
ent from the vowel systems of many other languages,
including Greek, Spanish, and Swedish.
Consonants are represented by IPA symbols that
vary along the dimensions of place of articulation,
manner of articulation, and voicing status.
At a given place of articulation (such as alveolar),
consonants are produced with different manners of
articulation (such as stops, fricatives, affricates, nasals,
and approximants).
178 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
American English consonants represent only a
small proportion of consonants in the languages of the
world.
IPA transcription is a useful clinical tool for SLPs
so they can use a universal symbol system to document
correct and incorrect speech sounds in individuals with
speech and hearing disorders.
Diacritic symbols are used to show subtle modifi-
cations in the main phonetic symbols of the IPA.
References
Bauman-Waengler, J. (2016). Articulation and phonology in
speech sound disorders: A clinical focus (5th ed.). Boston, MA:
Pearson Education.
Ladefoged, P., & Maddieson, I. (1996). The sounds of the world’s
languages. Oxford, UK: Blackwell.
Shriberg, L. D., Kent, R. D., McAllister, T., & Preston, J. L.
(2019). Clinical phonetics (5th ed.). Boston, MA: Pearson
Education.

Typical Phonological
Development
Introduction
This chapter presents information on typical phonetic
and phonological development. As defined in Chap-
ter 3, phonology is the study of the sound systems of
languages. Casual observation of small children plus
years of scientific research point to a common con-
clusion — children do not master all speech sounds at
the same time. There is no mystery that some speech
sounds are easy for the developing child, and some are
very difficult. There is continuing mystery about why
this is so.
The continuum of speech sound difficulty in the
typically developing child is not the whole story of
speech sound development. Phonology is the study of
the sound system of a language. A speech sound in a
particular language is linguistically effective because
it plays a role relative to other speech sounds in the
language. The speech sound is part of a system.
A phoneme is defined as a speech sound that
changes the meaning of a word when it replaces
another speech sound in the same position in the word.
For example, in English, the speech sounds “b,” “p,”
and “f” are phonemes because word examples can
be identified in which meaning is changed when the
sounds replace each other at the beginning of the word
13
(“beer” versus “peer” versus “fear”). More precisely,
a phoneme includes a class of sounds, all of which are
treated as belonging to the same category (i.e., the same
phoneme). For example, in English, the “b” sound is
sometimes produced with the vocal folds vibrating
throughout the entire sound, but at other times, vocal
fold vibration may be delayed until just after the lip
contact is released. These two ways to produce a “b”
are phonetic variants or allophones of the phoneme “b.”
Other allophones of English “b” can be defined as
well. In saying the word “beer,” for example, a speaker
of American English may produce the “b” as if he or
she is swallowing the sound (the way some country-
western singers might produce the sound for extra
emphasis in a song, or to identify their dialect as “real
country”). No matter, in English, the swallowed “b” is
still an allophone of the “b” phoneme. All three of the
“b” allophones just described — the vocal folds vibrat-
ing throughout the entire sound, vocal fold vibration
delayed until just after the lip contact is released, and
country-western swallow — are members of the same
phoneme. It does not matter which one starts the word
“beer”; the meaning of the word will be clear to a native
speaker of American English.
Allophones are an important part of the “system”
of sounds in a language. The question of how children
179
180 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
learn this aspect of phonology is made more compli-
cated, and more interesting, by different languages hav-
ing very different phoneme/allophone relationships.
For example, in Uduk, a language spoken in parts of
Ethiopia and Sudan, the country-western-type “b”
and the “b” with continuous vocal fold vibration are
members of different phoneme categories (Ladefoged
& Maddieson, 1996). Swapping these sounds before the
same vowel will create different words in Uduk but not
in English. Somehow a child must learn not only the
phonemes of her language but also the various allo-
phones included within each phoneme category.
The child must also learn the phonotactics of
her language. Phonotactics concern the sequences
of sounds that form words. In a particular language,
some sequences are allowed to form words; others
are disallowed. These word-form rules are called pho-
notactic constraints. In English, a word can start with
an “l,” “r,” “s,” and so on, but cannot start with the
“ng” sound (the sound at the end of the word “rang”).
The “ng” sound can occur, however, at the beginning
of words in several languages (such as Swahili, a lan-
guage spoken in a good portion of East Africa, and
in Mandarin Chinese). The “ng” sound is a phoneme
category in both English and Swahili, but the phono-
tactic constraints on the sound are different in the two
languages.
Finally, the child must learn the prosodic charac-
teristics of the language, often considered as a compo-
nent of phonology. Prosody includes the melodic and
rhythmic features of spoken language. Of particular
interest for the present chapter is the role of prosody
in languages such as English, where multisyllabic
words — words with more than one syllable — have
a lexical stress pattern. The lexical stress pattern of a
word indicates which of the multiple syllables receive
linguistic stress and which are unstressed. In the Eng-
lish word “cinnamon,” for example, the first syllable
is stressed, and the next two are unstressed (diction-
ary entry: sin-uh-muhn, where bolding indicates the
stressed syllable). Say the word to yourself several
times, and you will see that the first syllable is more
“prominent” as compared to the second and third syl-
lables. Speakers stress syllables by producing them
with slightly longer duration, higher pitch, greater
loudness, and more precise articulation as compared to
unstressed syllables. These factors combine to make a
stressed syllable “stand out” for a listener — this is what
is meant by the syllable being “more prominent.” Now
say the word with stress on the second syllable — “sin-
nah-muhn.” Strange, isn’t it? Children must learn the
stress characteristics of multisyllabic words. Lexical
stress patterns vary across languages, and this cross-
linguistic variation often contributes heavily to what
we hear as an “accent” when a nonnative speaker of
English produces multisyllabic English words. Addi-
tional information on the development of lexical stress
is not included in this chapter.
The bulk of this chapter is devoted to the pattern of
sound learning in typically developing children. Some
material on the learning of phonotactic constraints and
phonological processes is also presented. It is important
to keep in mind that the “typical” pattern presented in
this chapter is an idealized description of normal pho-
nological development. Not every typically developing
child follows this pattern — there is a lot of individual
variation in “normal” phonological development (Vih-
man, 2004).
Finally, comments are made at the end of the chap-
ter on the interaction between vocabulary growth and
phonological development. Recent scientific develop-
ments suggest that development of the sound system is
not a foundation for the development of words. Rather,
word learning may be the foundation for the develop-
ment of phonology.
Phonetic and Phonological
Development: General
Considerations
The development of the speech sound system goes by
different names. It is variously called speech sound
development, articulatory (phonetic) development,
and phonological development. Two of the terms,
“speech sound development” and “articulatory (pho-
netic) development,” can be used interchangeably;
“phonetic development” is used in this chapter to refer
to these two terms. “Phonological development” refers
to something different from phonetic development, as
described below. The use of phonetic versus phono-
logical development is not an academic exercise — it
can have important implications for the diagnosis and
treatment of developmental speech sound disorders
(Chapter 15).
Phonetic and Phonological
Development
What is the difference between speech sound, articula-
tory (phonetic), and phonological development? The
terms “speech sound development” and “articulatory
(phonetic) development” share a similar meaning, as
discussed later. We use the term “phonetic develop-
ment” as the cover term for this aspect of speech sound
development. The primary distinction for this discussion
is between phonetic and phonological development.

Phonetic Development
Phonetic development is the sequence of mastering
the articulatory movements, positions, and shapes
required to produce speech sounds. Phonetic devel-
opment reflects the maturation of speech motor skills,
also called articulatory skills. Can a child position and
shape the tongue to produce an /s/? Can he move the
tongue sufficiently forward to produce an /i/? Ques-
tions like these can be asked about any speech sound
in a language.
Phonological Development
Phonological development refers to the role of speech
sounds in the sound system of a language. Rather than
asking if a child has the speech motor capability to
produce an /s/, the question is, does the child under-
stand the role of /s/ in the sound contrasts that can
distinguish words, the role of /s/ in the morphopho-
nemic aspects of a language, and the allowable sound
sequences for word formation?
Examples of the three aspects of phonological
development mentioned in the previous paragraph
and their differences from phonetic development are
as follows:
n A young child produces a good /s/ for words
such as “sip,” “Sue,” and “see,” but produces
the same /s/ for words such as “ship,” “shoe,”
and “she.” The use of /s/ for /ʃ/ may not
indicate an absence of speech motor control
skills (i.e., a phonetic issue) for /ʃ/, but rather the
absence of recognition of the /s/-/ʃ/ contrast as
phonemic. In this view, the /s/-/ʃ/ contrast has
not yet become one of the phonemic contrasts
in the phonological system of a child’s native
language.
n A young child produces a good /s/ and a good
/z/ at the end of words but does not use the
sounds appropriately when marking plurals
for words such as “tacks” and “tags.” The child
produces these words as /tæks/ and /tægs/,
when they should be /tæks/ and /tægz/. The
morphophonemic rule (that is, the interaction
between morphemes and phonemes) in the
phonological system of English is that plural -s
is phonetically /s/ when it follows a voiceless
stop (the “t” in “tack”) and z when it follows
a voiced stop (the “g” in “tag”). The error of
applying the /s/ for the plural in both words
is not due to a speech motor control problem,
as evidenced by the child’s ability to produce
13  Typical Phonological Development 181
words like “fuss” and “fuzz” with a good /s/
and /z/, respectively. The morphophonemic rule
is phonological, not phonetic.
n A child produces word forms with word-initial
“ng” /ŋ/. The word-forms are protowords
(phonetically consistent forms) discussed in
Chapter 5. These are phonetic sequences that are
used consistently to identify objects, people, or
possibly actions, but are not “real” words in the
child’s native language. The child’s use of word-
initial “ng” violates the phonotactic rules of
English. Word-initial “ng” cannot initiate a word
but can appear in word-medial and word-final
positions (as in “penguin” and “sing”).
Is it meaningful to consider a speech sound differ-
ence from the “correct” adult form as phonetic versus
phonological? Many clinicians and scientists believe
so. Typical speech development includes errors in indi-
vidual sounds as well as patterns of sound errors, an
example of the latter being the deletion of word-final
consonants. When a speech sound error is regarded
as phonetic in origin, there is a tendency to attribute
the error to immature speech motor skills. In this view,
speech motor skills for correctly produced speech
sounds are sufficiently developed for some sounds, but
not for others.
Patterns of speech sound errors in typical speech
development suggest an alternative view for the ori-
gin of the errors. Take the case of a typically devel-
oping child who says “da” for “dog,” “ka” for “cat,”
and “doh” for “those.” The phonetic view considers
the child’s errors as articulatory problems (immature
speech motor skills) in the production of the individual
sounds /g/, /t/, and /z/ in the word-final position. In
the phonological view of these errors, the sounds are
omitted as a result of the phonological process of dele-
tion of word-final stops. Phonological processes are
regarded as one of many cognitively based language
rules. The child probably has the speech motor skill to
produce the sounds but produces the intended conso-
nant-vowel-consonant (CVC) words as CV syllables
to simplify the task of learning to produce the words.
“Da” may not be correct phonetically, but the child’s
use of this CV form clearly means “dog.”
Typical Speech Sound
Development
Figure 13–1 is a representation of the ages at which
children learn the speech sounds of English. The pro-
cess of speech sound development in a typically devel-
oping child is not predictable in its details. From child
182 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

MONTHS
24 28 32 36 40 44 48 >48

vowels, diphthongs

nasals, glides

stops

lateral, rhotic (liquids)

fricatives, affricates

clusters

Figure 13–1.  A schematic summary of speech sound learning in typically

developing children. The left-hand edge of each bar indicates the age at which
about half of typically developing children produce the indicated sounds cor-
rectly, and the right-hand edge is the age at which most children have learned
correct production of the sound (90% to 95% of tested children). The right-hand
arrows extending past 48 months indicate that mastery of some sounds (laterals,
rhotics, fricatives, affricates, consonant clusters) may extend, on average, well
past 4 years of age.

to child, there is a fair degree of variation in the order
in which sounds are learned, and the ages at which the
sounds are “mastered.” For a large group of typically
developing children, however, general trends in speech
sound development can be identified. In fact, the steps
in speech sound mastery that are regarded as “typical”
enjoy broad agreement across studies (see summary
in Smit, Hand, Freilinger, Bernthal, & Bird, 1990; and
more recent summaries in Stein-Rubin & Fabus, 2012;
and Bauman-Waengler, 2015). Figure 13–1 shows these
trends. Studies on the developmental course of speech
sound learning have included as few as 90 children
(Bricker, 1967) and as many as 997 (Smit et al., 1990).
The ages shown in Figure 13–1 reflect the fact that
the bulk of speech sound learning takes place between
the ages of 2 and 4 years, even though learning begins
before age 2 years and continues past age 4 years. The
left-hand edge of each bar in Figure 13–1 indicates the
age at which about half of typically developing chil-
dren produce the indicated sounds correctly, and the
right-hand edge is the age at which most children have
learned correct production of the sound. For example,
roughly half of typically developing children produce
stop consonants correctly a little before 24 months, and
nearly all children produce all stops correctly just after
48 months.
Vowels, diphthongs, nasals, and glides are learned
early and probably mastered no later than shortly after
the third birthday (36 months). Stops are also learned
early but may have a lengthier period of development
than vowels, nasals, and glides. The mastery of liquids ​
— the “l” and “r” sounds — lags vowels, diphthongs,
nasals, glides, and stops in two ways. First, the age at
which half of typically developing children produce
liquids correctly is nearly a year later than the age for
the earlier-mastered sounds (compare in Figure 13–1
the starting age for liquids to that for the three sound
categories shown above the liquids). Second, the devel-
opment of liquids may extend well beyond 4 years of
age, as indicated in Figure 13–1 by the arrow pointing
past the 48-month landmark.
Mastery of fricatives and affricates lags that of liq-
uids slightly and extends well past 48 months. Finally,
correct production of consonant clusters, such as the
“sp” sounds in “spot,” the “skr” sounds in “scratch,”
the “pl” sounds in “play,” and the “rst” sounds in

“first,” begins to be mastered at around 3 years of age
and may not be fully mastered until well past 4 years
of age.
The last speech sounds acquired throughout the
course of sound development are often referred to as
“The Late Eight” (Bleile, 2018). These sounds include
voiceless and voiced “th” (/T/, /D/), voiceless “s” and
voiced “z” (/s/, /z/), “l” (/l/), “r” (/r/), “sh” (/ʃ/), and
“ch” (/tʃ/). As Bleile notes, the majority of children
with speech sound disorders have errors on one or
more of these sounds. Some of the late-eight errors may
be present past 8 or 9 years of age, the absolute upper
limit for typical development of the sound system.
Many children with these errors correct them sponta-
neously — the errors are “normalized” without therapy.
A small number of early and late-age teenagers and
even some adults continue to make these errors, most
likely on /s/, /z/, /l/, and /r/. Late-eight errors that
persist into the teenage and adult years are called per-
sistent or residual errors (Flipsen, 2016).
Determination of Speech
Sound Mastery in Typically
Developing Children
The arrangement of speech sounds in Figure 13–1, from
top to bottom, is from the earliest- to latest-appearing
sounds in the typical child’s development of English
speech sounds. This pattern of sound development
can be considered a kind of “average” developmental
pattern; as noted earlier, many departures from this
“average” pattern are normal and not cause for con-
cern. With this in mind, it is useful to consider how
these average patterns were determined, and why it
is important to be familiar with an average develop-
mental sequence, even if it does not represent every
typically developing child.
The basic research strategy for obtaining the infor-
mation summarized in Table 13–1 is to select a set of
words requiring a child to produce a target sound (e.g.,
the stop “b” or fricative “s”) in two or three positions-
in-word. The term “position-in-word” is typically
reserved for consonant production and refers to the
location of a consonant as word-initial, word-medial,
or word-final. For example, the word “baby” contains
the “b” sound in the word-initial and word-medial
positions, and the word “tub” has the “b” sound in the
word-final position. The decision to test the produc-
tion of a given sound in different positions-in-word
emerged from clinical experience. This experience sug-
gested that a child’s ability to produce a sound correctly
in any one position did not necessarily mean that he
could produce the sound correctly in other positions.
13  Typical Phonological Development 183
Table 13–1.  Example of a Transcription Analysis of a
Speech Sound Production Task
Word-Initial Word-Medial Word-Final
Target /b/
“baby” beIpi beIpi
“tub” tp
Target /s/
“sun” Tn
“whistle” wIf ə
“rice” wɑIf
Correct production of one allophone of a phoneme
category does not guarantee correct production of all
allophones of that category.
When a complete set of words has been devel-
oped and judged to be familiar to children as young
as 2 years of age, pictures or photographs of the object,
person, or action are created for each word. The child
is shown the picture or photograph and asked to say
what he or she sees. Ideally, the child produces the
word without hearing it spoken by the experimenter.
When a child cannot name a picture, the experimenter
provides a spoken model, and the child’s production of
the word is an imitation of the experimenter’s model.
Each child’s naming of a picture or photograph (or
word imitation) is transcribed by a skilled phonetician,
using the symbols of the International Phonetic Alpha-
bet (Chapter 12). This transcription shows the sounds
used by the child to produce the word. In some cases,
the transcription may include allophonic detail (nar-
row phonetic transcription).
Possible Explanations for
the Typical Sequence of
Speech Sound Mastery
Two major explanations for the sequence of sound
mastery shown in Figure 13–1 have been considered in
the research and clinical literature. These explanations
are not mutually exclusive; they may both explain, in
small or large ways, the early learning of sounds such
as vowels, stops, and nasals as compared to the later
learning of sounds such as liquids and fricatives and
of sound sequences such as consonant clusters. One
explanation concerns the maturation of speech motor
control capabilities. The other explanation concerns the
maturation of auditory mechanisms for speech sound
identification.
184 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Maturation of Speech Motor Control know them as demonstrated in comprehension tasks.

This knowledge is not yet useful for expressive (pro-
Children do not control their posture, the use of their duction) language.
hands, or any other aspect of movement or body posi- What is the assumed difference between early ver-
tioning in an adult-like way. The movements of an sus advanced speech motor control skill? Figure 13–2
18-month-old child are immature, becoming more shows the difference in tongue shape for a sound mas-
refined and accurate over many years. As noted many tered early (/t/, green surface) and one mastered late
years ago by the famous speech scientist R. H. Stet- (/s/, black surface). The view is from the front looking
son (1872–1950), speech production is a collection of back into the vocal tract, as if the mouth and teeth are
articulatory movements made audible (Stetson, 1951). transparent to reveal the contrasting tongue shapes,
Speech movements result in positions and shapes of both of which are made at the alveolar place of articu-
articulatory structures. For example, an adult-like /s/ ​ lation. Only the surface of the tongue at a specific loca-
— a “good” /s/— requires not only movement of the tion (a cross-section, along the width of the tongue) is
tongue to the correct location within the vocal tract, but shown. The shape for /t/ is more or less flat, with the
also an overall positioning and shaping of the tongue. tongue pressed against the alveolar ridge (the front of
For the remainder of this chapter, the term “speech the hard palate) to form a complete blockage of the
movement” is used to denote these aspects of motor airstream for about 1/10th of a second. The shape for
control. /s/ is more complex as shown by the groove in the
Like other movements of body structures, move- central part of the tongue width. The groove is narrow
ments of the speech mechanism develop and become and tight. When air flows from the lungs to the upper
increasingly adult-like as the child matures. The term airways, pressure builds up behind the groove and
“speech motor control” denotes the concept of ner- forces air through it, creating the hissing noise typical
vous system mechanisms (and the muscles they con- of fricative consonants. The grooved tongue shape for
trol) required for the execution of speech movements. fricatives is assumed to require more skilled speech
Maturation of speech motor control refers to the way
in which it changes over time from infant to adult-like
control capabilities. Maturation of speech motor con-
trol is necessary for an individual to transition from
infant- and toddler-like sound production to the fully
intelligible speech of the typical adult.
For the child with less mature speech motor con-
trol, some speech movements are likely to be challeng-
ing, whereas others may be less so and perhaps even
simple. Scientists have argued that fricatives and liq-
uids require rather precise and difficult movements
and positions and are therefore mastered later in devel-
opment, when the child’s speech motor control is “up
to the task.” Vowels, nasals, and stops are believed to
require relatively simple speech motor control capabili-
ties and can be produced accurately by younger chil-
dren. According to some studies, very young children
who are just beginning their speech sound develop-
ment may avoid producing words composed of “dif-
ficult” sounds such as fricatives and liquids (Vihman,
2004). For example, at 2 years of age, a child may pro-
duce words such as “dog,” “cat,” “poppa,” and “no,”
but not words such as “sun,” “shell,” and “rag.” Does
the child lack the latter three words in her lexicon (have Figure 13–2. Tongue shapes for /t/ (green) and /s/
they not yet been learned?), or does she have the words (black ). The view is from the front, looking into the mouth;
but avoid saying them because the component sounds the image is drawn as if the mouth and teeth are transpar-
(such as /s/, /ʃ/, and /r/) require speech motor control ent to show the side-to-side shape of the tongue behind the
abilities that are too advanced for her level of develop- teeth. The tongue is more or less flat for /t/ and grooved
ment? Many toddlers who do not say certain words for /s/.

motor control than the flat-tongued shape for stop con-
sonants. This may explain why /t/ is mastered earlier
in speech sound development than /s/ (and in general,
stop consonants are mastered earlier than fricatives).
Maturation of Perceptual Mechanisms
for Processing Speech
One of the great controversies in the field of speech
development concerns the relationship of what the
child hears to what the child produces. At a general
level, the ability to hear speech sounds, and more pre-
cisely to distinguish between different speech sounds,
must be related to how a child learns to produce speech.
An obvious example is the effect of significant hearing
loss on a child’s speech production abilities. Babbling
in babies with significant hearing loss at birth appears
much later than babbling in hearing babies (Eilers &
Oller, 1994). To the extent that auditory sensitivity pre-
dicts the complexity of babbling (von Hapsburgh &
Davis, 2006), the child’s auditory capability is one of
the foundations of speech sound development.
Speech-language pathologists are interested in a
more specific question concerning the role of hearing
in speech development: Is there a close match between
how the child perceives speech sounds and how he
produces them? For example, do children develop
the ability to produce the distinction between “w” and
“r” (as in words such as “right” versus “white”) only
when they can hear the difference between “r” and
“w”? More generally, do sounds such as liquids and
fricatives appear later in speech development because
children who are just beginning to learn speech have
difficulty hearing and distinguishing contrasts such
as /s/ versus /ʃ/ or /r/ versus /l/? Is the explanation
for early appearing sounds such as vowels, nasals, and
stops explained by an early ability to hear the differ-
ence between them?
Is there evidence that the perception of fricatives,
or liquids, is more challenging for younger, as com-
pared to older, children? In a more general sense, is
there evidence for the development of speech sound-
perception skills as children are learning language?
Or, is there evidence that little humans are endowed
at birth with the ability to hear all distinctions between
speech sounds?
The answer to the major question, of whether the
perception of speech sounds is a developmental pro-
cess (rather than being present in adult form, at birth),
1
 erker and Yeung (2005) have reviewed evidence that in the second half of the first year of life, babies’ evolving ability to associate words with
W
objects or actions is a “trigger” to organizing their greater sensitivity to the phonemes in their own language. In other words, early aspects of
word learning prepare the baby to perceive sound categories that have importance to making distinctions between words.
13  Typical Phonological Development 185
seems to be “yes.” The perception of speech sounds
becomes more skilled as a child matures. Infants begin
with the ability to discriminate between sounds not
only of their own language but of other languages as
well (see Chapter 5). At the end of the first year and
into the second year of life, children’s ability to hear the
difference between sounds that have a contrastive func-
tion in other languages, but not in English, diminishes
and eventually disappears. At the same time, babies
become especially sensitive to the important sound dis-
criminations in their own language (Werker & Yeung,
2005).1 This not only shows a developing speech per-
ception ability in childhood but also the influence on
perceptual skill of the specific language being spoken
in the child’s environment. As reviewed by Nittrouer
(2002), children’s speech perception abilities continue
to evolve past the first year of life. Humans at birth are
not endowed with a “fixed” set of speech-sound per-
ception abilities. Perceptual skills change and develop.
The more focused question of whether perceptual
skill for specific sounds must be in place for the correct
production of the sounds remains open. This is a com-
plex issue, and the answer (at this point in time) is no
more than a “maybe.” Late-developing speech sounds
such as liquids, fricatives, and affricates, are apparently
not difficult to perceive for the child who is early in
speech sound development, and who has not mastered
the production of these sounds (Vihman, 2004). Very
young children may have difficulty perceiving frica-
tives, or liquids, but this is not a general finding. But
the perception of sounds such as liquids and fricatives
may be fine even though the child has not mastered the
production of these sounds. This latter finding weak-
ens the case for a close relationship between a typically
developing child’s sound perception and sound pro-
duction capabilities. A study relevant to this issue is
provided by Dugan, Silbert, McAllister, Preston, Sotto,
and Boyce (2018), and an excellent review is provided
by Preston, Irwin, and Turcio (2015).
This question is not only relevant to the typical
development of speech but also has an important influ-
ence on explanations and treatment plans for develop-
mental speech sound disorders. Speech sound disorders
are conditions in which a child’s development of speech
sounds does not occur within a typically normal age
range. Children diagnosed with speech sound disor-
ders learn sounds in the typical order (see Figure 13–1)
but at a slower rate. As reviewed by Bankson and Ber-
nthal (2004a), there is a history of research attempting
186 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
to show a link between sounds misarticulated by chil-
dren with speech sound disorders, and their ability to
perceive those specific sounds. The practical, clinical
implication of this issue is that perceptual training may
be a significant aspect of speech therapy for accurate
production of a speech sound. Perceptual training may
even occur before training to produce the sounds cor-
rectly. Some clinical research has demonstrated, in fact,
that perceptual training of speech contributes to the
elimination of speech sound production errors (Bank-
son & Bernthal, 2004a).
The Jury Is Sometimes
Out and Sometimes In
Many speech-language pathologists and
audiologists use auditory training as an integral
part of speech therapy in children with speech
sound errors. Even though the relevant research
foundation for auditory training is not firm, we
do not have a completely hung jury on the issue.
As with the wide variability among children in
learning a sound system, some children with
speech sound disorders show improvement
in speech production skills following percep-
tual training. The training may be “auditory
bombardment” in which the child hears her
error sounds over and over. The theory is to
“shape up” the sound category in perception
so that it can be produced with reference to this
stabilized perceptual category. Alternatively,
therapy may consist of hearing perceptual
contrasts between closely related sounds, such as
the contrast between /s/ and /ʃ/, both voiceless
fricatives that differ only by place of articula-
tion. When a child is trained on the perception
of this contrast and shows improvement in /s/
versus /ʃ/ production, two explanations are
possible. One is that the auditory training has
a general influence on auditory skills, which
includes the skill required for the perception
of any phonetic contrast. In this case, improve-
ment in the /s/-/ʃ/ contrast and the resulting
influence on good /s/ and /ʃ/ production is a
consequence of an upgrade of overall auditory
skill. A second explanation is that the auditory
training is specific to the /s/-/ʃ/ contrast and
does not transfer to other problem contrasts such
as /w/-/r/. In either case (or maybe a little bit of
both), the possibility that auditory training may
contribute to improved articulation is worth the
therapeutic effort.
Phonological Processes and
Speech Sound Development
Phonological learning is not limited to the mastery of
individual speech sounds. Children must also learn
how words are formed from sequences of sounds (the
phonotactic characteristics of a language), and for some
languages, the proper prosodic pattern for words with
multiple syllables (i.e., lexical stress patterns). In the
course of learning these aspects of phonology, children
make errors when producing word forms that presum-
ably are intended to “match” the form produced by
adults. For example, a child around the age of 2 years
may say “da” when he sees the family pooch. The child
is attempting to produce the word “dog,” which has a
consonant-vowel-consonant (CVC) form. “Da” fails to
match the adult form as it lacks the word-final conso-
nant. Stated somewhat differently, the child uses a CV
word form for a “target” CVC word form. It is as if,
as mentioned earlier, the child simplifies the articula-
tory task of producing a CVC by eliminating one of the
component sounds.
Part of phonological development is learning the
correct matches to adult word forms by eliminating
these simplifying processes. Notice how the simpli-
fication of CVC to CV syllables introduces a phono-
tactic constraint on the child’s speech production: the
adult phonology allows words to be formed by CVC
sequences, but the child restricts his own word forms
to CV syllables.
The CV for CVC mismatch can be described as
a phonological error. Within certain age limits, such
errors are expected as a typical part of phonological
development. An interesting characteristic of phono-
logical development is found in the nature of these
errors: they are not random but are systematic. Some
examples make this clear.
For many children learning the phonology of their
language, an error such as “da” for “dog” is not an iso-
lated case of leaving off the final consonant of a specific
word. Many typically developing children go through
a phase of producing “target” CVC word forms by
always (or nearly always) deleting the final consonant.
“Dog” is produced as “da,” “cat” as “kah,” “bus” as
“buh,” and so forth.
Scientists who study normal and delayed/dis-
ordered speech in children acquisition of phonology
claim that groups of similar errors are the result of
phonological processes. A phonological process is a rule
that changes the expected word form (what an adult
produces) to a different, more simple form. In the cur-
rent example, the phonological process is one of final
consonant deletion, in which all (or nearly all) CVC
word forms are changed to CV forms. The rule is not

“delete the ‘g’ at the end of the word ‘dog,’” but applies
broadly across final consonants in any CVC word. Pre-
sumably, this phonological process simplifies the artic-
ulation of single-syllable, CVC word forms because CV
forms are easier to produce.
The phonological process of cluster reduction
changes words with a CCV(C) or CVCC form (where
“CC” = consonant cluster) to CVC forms. For exam-
ple, the CCVC form for the word “stop,” in which the
consonant cluster is the word initial “st,” is changed to
“top” (a CVC form). Or, the CVCC form for the word
“best” is changed to “bes” or “bet” (again, a CVC
form). In both cases, the child simplifies the articula-
tory requirements for the adult CCVC or CVCC forms
by “reducing” two successive consonants — a conso-
nant cluster — to a single consonant.
Another phonological process is called stopping of
fricatives. This process changes fricatives to stops, as
when “sip” is produced as “tip.” Stopping of fricatives
simplifies articulation by changing a sound thought to
require advanced speech motor skill (the fricative “s”)
to one of relatively simple speech motor skill (the stop
consonant “t”).
English words with multiple syllables have vary-
ing stress on the syllables. Some syllables are heard
as “prominent,” and others are heard as weak. In the
word “banana,” for example, the first syllable “ba” is
produced with very little stress and therefore does not
sound prominent. In contrast, the second syllable “na”
receives primary stress in the word and is heard as
prominent. The third syllable is also produced with lit-
tle stress and is not very prominent. The stress pattern
of this three-syllable word can be described as weak-
strong-weak. The phonological process of unstressed
syllable deletion reduces the number of syllables in a
multisyllabic word by eliminating an unstressed syl-
lable, typically the first “weak” syllable of the word.
“Banana” is produced as “nana” (strong-weak), “ele-
phant” as “elphant” (strong-strong), and “incredible” as
“creble” (“strong-weak”).2 Presumably, the articulation
of multisyllabic words can be simplified by eliminating
one (or more) of the syllables from the production.
Are phonological processes merely descriptions
of the way children modify word forms during typical
phonological acquisition, or are they the result of bio-
logical tendencies unique to the human ability to com-
municate by speech? The difference between these two
possibilities is important. Behavioral regularities can
always be described and stated as a formula or “rule”
2 
 hen my son Ben was learning the sound system of English, his multisyllabic word productions were changed by the phonological process of
W
unstressed syllable deletion. For a long time, he referred to “The Incredible Hulk,” one of his favorite destructive superheroes, as “creblhulk”
(three syllables). I combine “hulk” with the first part of the word because he obviously treated the two words as one. Ben had no idea, at this
point in his phonological development, that “incredible” was a word that could be separated from “hulk.”
13  Typical Phonological Development 187
such as “CVC becomes CV,” as in the phonological pro-
cess of final consonant deletion. This description does
not prove, however, the presence of a mechanism in
the heads of little humans that takes a CVC word form
and changes it to a CV form as a biologically directed
part of speech sound development. Nevertheless, some
scientists regard phonological processes as biologi-
cally based, cognitive mechanisms that guide, at least
in part, the natural course of phonological acquisition.
What kind of scientific evidence supports the bio-
logical view of phonological processes? One observa-
tion, that the same phonological processes are seen
among children learning very different languages
(Vihman, 2004), has been used to support the biologi-
cal perspective. Even when different languages have
different phonetic inventories and use them in different
ways (i.e., have different phonemes and allophones),
the same phonological processes tend to change adult
word forms to simpler forms. This suggests something
“universal” about phonological processes, something
applying to all languages even when other components
such as phonemes vary from language to language.
The concept of a “universal” language characteristic is
almost always an important piece of a belief in a bio-
logical basis of speech and language.
Like the mastery of individual speech sounds, dif-
ferent phonological processes seem to have a schedule
of appearance (and disappearance) during the course
of phonological acquisition. For example, the process of
final consonant deletion is typically seen in the early
stages of acquisition and disappears before the age of
3 years (Stoel-Gammon & Dunn, 1985). The concept of
disappearance of a phonological process is important:
the mastery of the phonological system of a language
is characterized not only by learning speech sounds
but also by the elimination of processes that create mis-
matches between child and adult word forms. There
are gains and losses along the child’s pathway to “cor-
rect” phonological behavior.
Based on available data, certain processes seem to
disappear early in typical speech sound development;
others persist to later ages. The process of final conso-
nant deletion has already been noted as disappearing
relatively early in the course of typical phonological
development. Cluster reduction may not disappear
until later in phonological development, around age 3
and a half years (Cohen & Anderson, 2011). Stated oth-
erwise, cluster reduction observed in a child’s speech
past the age of 3 years is not considered atypical, but
188 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
deletion of word-final consonants past the age of 3
years suggests a phonological delay. Bankson and Bern-
thal (2004b, pp. 245–249) have an excellent review
of phonological processes during the typical course of
phonological acquisition.
Phonological Development
and Word Learning
This chapter has focused on speech sound development.
Speech sounds have been treated as independent units
to be learned, such as the typical age of mastery of /g/ or
/s/. In addition, mastery of the sound system has been
shown to be part of word learning, as in the case of the
development of word forms with “allowable” sound
sequences (phonotactics) and simplification of word
forms (phonological processes). This description of pho-
nological development implies a directionality between
sound learning and word learning: sounds are learned,
and words are built from them. In different terms,
vocabulary growth is dependent on sound mastery.
In recent years, this logic has been reversed. The
results of several studies suggest that word learn-
ing leads sound learning. The growth of vocabu-
lary requires finer and finer articulatory distinctions
between sounds to distinguish the new lexical entries.
For example, the child may add words such as “sign”
and “shine” to the lexicon at about the same time,
perhaps before the child is making a sharp articula-
tory distinction between “s” /s/ and “sh” /ʃ/. The dis-
tinction between these two sounds is one of place of
articulation (alveolar for /s/, palato-alveolar for /ʃ/).
These late-mastered sounds may both be distortions,
with imprecise places of articulation. The acquisition
of these new words is thought to promote greater artic-
ulatory distinction between the sounds — to get their
places of articulation correct and thus match the adult
form of the words. In this sense, vocabulary growth
may “shape” sound system growth.
This idea has implications for speech-language
therapy, as described in Chapter 15. The way in which
phonological development is thought of — words built
from sounds versus sounds built from words — may
have important implications for treatment of develop-
mental speech sound disorders. Gierut (2016) has an
excellent review of the relationship between vocabu-
lary growth and mastery of the speech sound system.
Chapter Summary
Phonetic and phonological development in typically
developing children includes the development of both
speech motor skills (phonetic skills) and the sound sys-
tem (phonology) of a language.
Phonemic contrasts, allophones of the phoneme
categories, morpho-phonemic rules, phonotactic con-
straints, and prosody are components of phonological
development.
The development of speech motor control deter-
mines the development of phonetic skills, which are
sometimes referred to as articulatory skills.
Examples are provided of the potential indepen-
dence of speech motor and phonological development;
both of these contribute to development of speech
sounds.
The order in which speech sounds are mastered
is based on research using large numbers of typically
developing children; the age ranges over which specific
sounds are mastered is an average, and many typically
developing children do not follow a fixed pattern of
sound development.
Speech sound development begins around 1 year
of age and is often complete by 5 or 6 years of age; for
some children, speech sound development continues
until 8 or 9 years of age.
Speech sounds that are mastered early in devel-
opment include vowels, diphthongs, nasals, glides
and stops; lateral, rhotics, fricatives, and affricates are
learned later in speech sound development.
Consonant clusters are mastered later in the course
of speech sound development.
The order of mastery of specific sounds may be
explained by the development of speech motor skill,
perceptual skill, and cognitive skills.
Phonological processes are important in the devel-
opment of speech sounds; the processes often result in
mismatches between a child’s production of a word
and the “target” adult form.
Many phonological processes produce “errors”
early in speech sound development, but the pro-
cesses actually simplify the child’s task of producing
words; such processes are referred to as simplification
processes.
Throughout the course of speech sound develop-
ment, simplification processes disappear, which allows
the child to produce a word that is a good match to the
adult form of the word.
References
Bankson, N. W., & Bernthal, J. E. (2004a). Etiology/factors
related to phonologic disorders. In J. E. Bernthal & N. W.
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Articulation and phonological disorders (5th ed., pp. 201–267).
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Bauman-Waengler, J. (2015). Articulation and phonology in
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Pearson Education.
Bleile, K. M. (2018). The late eight (3rd ed.). San Diego, CA:
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Bricker, W. A. (1967). Errors in the echoic behavior of pre-
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519–527.

Motor Speech Disorders
in Adults
Introduction
Motor speech disorders are a group of speech disorders
resulting from damage to the central nervous system
(cerebral hemispheres and their contents, the cerebel-
lum, brainstem, and spinal cord) or peripheral nervous
system (nerves leading from the brainstem or spinal
cord to and from muscles). The causes of this dam-
age include a range of neurological diseases, includ-
ing degenerative diseases (like Parkinson’s disease, or
multiple sclerosis), strokes, tumors, inflammatory con-
ditions, and other conditions.
The clinical and research history of motor speech
disorders is unique in the field of communication sci-
ences and disorders. The history is unique because
there is a well-accepted classification system for dif-
ferent types of motor speech disorders. Many other
speech and language disorders do not enjoy the ben-
efit of agreement on their classification. The classifica-
tion of motor speech disorders assumes that damage
to different parts of the brain produces different — and
unique — speech symptoms.
Table 14–1 summarizes terms from Chapter 2
that are relevant to the classification of motor speech
disorders.
1
I n much of the clinical and research literature on apraxia of speech in adults, the acronym “AOS” (apraxia of speech) is used. However, “AAS”
is used in the textbook to be consistent with more recent literature in which the adult version of the disorder is compared and contrasted with
childhood apraxia of speech (CAS; see Chapter 15).
14
Classification of Motor
Speech Disorders
Figure 14–1 presents a simple classification scheme
for motor speech disorders in adults. Motor speech
disorders include two major subcategories, one being
dysarthria and the other apraxia of speech. Dysarthria
is a motor speech disorder in which neurological dis-
ease results in weakness, paralysis, or incoordination
among the muscles of the speech mechanism (Darley,
Aronson, & Brown, 1975; Duffy, 2013). These muscle
problems result in poor control of movements of the
lips, tongue, jaw, velum, larynx, and respiratory struc-
tures. The poor speech movement control results in
speech production problems.
SLPs are able to identify most cases of dysarthria
by listening to a short sample of speech. Occasion-
ally, speech of the hearing impaired or of adults with
apraxia of speech (see later in this chapter) may be con-
fused with dysarthria.
Apraxia of speech in adults (AAS, for “adult
apraxia of speech)1 is thought to be a planning (also
called programming) disorder resulting from neuro-
logical damage within the cortex and subcortical nuclei
such as the basal ganglia. Muscle paralysis, weakness,
191
 Table 14–1.  Terms From Chapter 2 That Are Relevant to the Current Chapter on
Motor Speech Disorders in Adults

Term Definition
Central nervous Cerebral hemispheres and their contents, cerebellum,
system brainstem, spinal cord.

Peripheral nervous Nerves attached to brainstem and spinal cord that carry
system information to and from the central nervous system; cranial
nerves serve structures of the head and neck, spinal nerves
serve structures of the limbs and torso.

Gray matter Clusters of neuron cell bodies. The cerebral cortex and
the cortex of the cerebellum are composed of cell bodies;
clusters of gray matter in the basal ganglia and thalamus,
the brainstem, below the cerebellar cortex, and spinal cord,
are called nuclei.

White matter Bundles of myelinated axons connecting one or more areas

of gray matter.

Substantia nigra A nucleus (group of cell neuron cell bodies) in the midbrain
(top part of brainstem) that manufactures dopamine, a
neurotransmitter critical to control of movement.

Motor neuron The cell body of a neuron whose axon carries information
to muscles to control their contraction time, force, and
coordination with other muscles. Groups of motor neurons
are found in the primary motor cortex and in other regions
of the central nervous system such as the basal ganglia and
brainstem, and spinal cord.

Upper motor neuron The pathways from the cortical motor neurons to motor
nuclei in the brainstem or spinal cord.

Lower motor neuron The pathways from the motor nuclei in the brainstem or
spinal cord to muscles of the head and neck (via cranial
nerves) and limbs and torso (via spinal nerves).

Motor Speech Disorders

Dysarthria Apraxia of Speech

Flaccid
Spastic
Ataxic
Hypokinetic
Hyperkinetic
Mixed
Unilateral upper motor neuron

Weakness, paralysis, Planning (no muscle deficit)

incoordination

Figure 14–1.  A simple classification scheme for motor speech disorders in adults.

192

and/or incoordination are not thought to be impaired
in AAS. Rather, the patient has difficulty with the plan
for production of the utterance. The planning deficit
may include problems with the order of consecutive
syllables in an utterance, and problems with instruc-
tions from the cortex for the correct timing of muscle
contractions throughout an utterance.
Dysarthria
The problem in dysarthria is thought to be limited to
neuromuscular execution. The speech disorder is not
thought to be a partial or significant result of problems
with the symbolic component of language, as in apha-
sia (see Chapter 9). In dysarthria the patient knows
what she wants to say, plans the utterance in a normal
way, but fails to produce it normally because of the
muscle problems noted earlier.
Subtypes of Dysarthria
The subtypes of dysarthria in Figure 14–1 constitute
the Mayo Clinic System for Classification of Dysarthria.
Darley, Aronson, and Brown (1975), clinician-scientists
who worked at the Mayo Clinic where they developed
the classification system, believed that each subtype
had a unique “sound” that could be related directly to
the location of damage within the nervous system. In
fact, Darley et al. (1975) claimed that in dysarthria, the
sound of a patient’s speech had a “localizing” value.
In this view, skilled clinicians can identify the loca-
tion of neurological damage by listening to a patient’s
speech. In the 1960s, when Darley et al. developed the
classification system, imaging techniques such as com-
puterized axial tomography (CAT) scans and magnetic
resonance imaging (MRI) were not available to identify
the location of brain damage. Localization of neurolog-
ical damage by listening to a patient’s speech was a
major contribution to medical diagnosis.
The Mayo Clinic Classification
System for Motor Speech Disorders
Throughout the 1960s, a monumental study of motor
speech disorders took place at the Mayo Clinic in Roch-
ester, Minnesota. Darley, Aronson, and Brown (1975)
listened to tapes of over 200 patients with different
2 
Note that many of these speech sound errors were not substitutions of one sound for another, such as a clear /ʃ/ (“shave”) for /s/ (“save”)
error. Documentation of these kinds of error requires narrow phonetic transcription (Chapter 12). Sound substitutions such as /ʃ/ for /s/ are
also heard in dysarthria.
14  Motor Speech Disorders in Adults 193
neurological diseases, and based on what they heard
made precise estimates of the severity of different
speech characteristics. For example, Darley, Aronson,
and Brown (hereafter, DAB) knew that a very com-
mon speech characteristic in motor speech disorders
was imprecise consonants. The term was meant to indi-
cate speech in which the consonant sounds appeared
to be articulated in a noncrisp, imperfect way.2 DAB
also knew, from listening to many patients with motor
speech disorders, that the loss of crisp consonant
articulation may range from a very subtle consonant
problem to an obvious loss of articulatory ability. They
therefore used a seven-point, equal-appearing interval
scale to record their impressions of the severity of each
patient’s consonant articulation ability.
The two ends of the scale are given labels — scien-
tists call this “anchoring” the scale — with the number 1
indicating normal consonant articulation and the num-
ber 7 a very severe deviation from normal consonant
articulation — severely imprecise consonants. The num-
bers in between these two extremes indicate different
degrees of imprecise consonants.
DAB made interval-scale estimates for a total of 38
characteristics of speech. The 38 perceptual dimensions
were selected to represent the different components
of the speech production process (speech breathing,
phonation, velopharyngeal function, articulation).
The selected dimensions were based on DAB’s exten-
sive experience with motor speech disorders and the
authors’ knowledge of aspects of speech most likely to
be impaired as a result of neurological disease. A few of
the dimensions scaled by DAB, along with their defini-
tions (as given by Darley, Aronson, & Brown, 1969) are
listed in Table 14–2.
The more than 200 patients studied by DAB were
not a random sample of people with motor speech
disorders seen at the Mayo Clinic but were selected
to represent six major disease types. These types were
brainstem disease, stroke, Parkinson disease, cerebellar
disease, Huntington’s disease, and amyotrophic lateral
sclerosis.
For each disease type, DAB summarized their per-
ceptual analysis of the 38 dimensions with a statistical
procedure designed to detect patterns among the per-
ceptual dimensions. According to DAB’s hypothesis,
each disease was expected to have unique patterns
among the 38 perceptual dimensions. Because each of
the diseases they studied has specific and unique loca-
tions of brain damage, DAB’s hypothesis of a unique
“sound” (in the broad sense, not in the sense of a
194 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Table 14–2.  Selected Perceptual Dimensions and Their Definitions

Dimension Definition
Imprecise consonants Consonant sounds lack precision. They show slurring,
inadequate sharpness, distortions, and lack of
crispness. There is clumsiness in going from one
consonant sound to another.

Strained-strangled Voice (phonation) sounds strained or strangled (an

voice apparently effortful squeezing of voice through the
glottis).

Harsh voice Voice is harsh, rough, and raspy.

Breathy voice Continuously breathy, weak, and thin

Distorted vowels Vowel sounds are distorted throughout their total

duration.

Prolonged intervals Prolongation of interword or intersyllabic intervals.

Hypernasality Voice sounds excessively nasal. Excessive amount of

air is resonated by nasal cavities.

Monopitch Voice is characterized by a monopitch or monotone.

Voice lacks normal pitch and inflectional changes. It
tends to stay at one pitch level.

Monoloudness Voice shows monotony of loudness. It lacks normal

variations in loudness.

Excess and equal Excess stress on usually unstressed parts of speech,

stress e.g., (a) monosyllabic words and (b) unstressed
syllables of polysyllabic words.

Note.  These perceptual dimensions were prominent in the Mayo Clinic analysis of patients
with motor speech disorders. The definitions are reproduced verbatim from Darley, Aronson,
and Brown (1969). Some dimension names have been reordered (e.g., “distorted vowels” was
“vowels distorted” in Darley et al. [1969]).

unique phoneme sound “problem”; see immediately Based on their analysis of the perceptual data,
above) for each of these diseases was equivalent to a DAB confirmed their hypothesis by identifying six
hypothesis of a unique-sounding speech for damage to unique dysarthrias. These include the first six listed
different parts of the brain. in Figure 14–1. The unique subtypes were flaccid,

The Nervous System Is More Complicated Than That

Darley, Aronson, and Brown stated their
hypothesis of a strong link between the location of
nervous system damage (neurologists call this “site
of lesion”) and speech symptoms, knowing that a
given neurological disease does not have a single
site of lesion. What Darley, Aronson, and Brown
meant was primary site of lesion. For example, in
Parkinson’s disease, the primary site of lesion is in
the midbrain (mesencephalon) where cells in the
substantia nigra deteriorate and die. The death of
these cells deprives the central nervous system of
dopamine, a neurotransmitter critical to control
of movement. Other lesion sites, however, have
also been identified in Parkinson’s disease, includ-
ing the cerebellum, basal ganglia, and brainstem
(Joutsa, Horn, Hsu, & Fox, 2018). The lack of simple
lesion-location/disease combinations applies to
other neurological diseases as well. Keep this in
mind when considering the idea that listening to
the speech of someone with a neurological disease
is a straightforward way to know where the
lesion is.
 14  Motor Speech Disorders in Adults 195

spastic, ataxic, hypokinetic, hyperkinetic, and mixed
dysarthria.
These six dysarthrias can be described by their
most severely affected perceptual dimensions, the
location of the relevant brain damage, and the muscle
control problems thought to produce the abnormal and
distinguishing speech symptoms. The reader should
refer back to Table 14–2 for explanations of the percep-
tual dimensions discussed later.
Flaccid Dysarthria
The distinguishing perceptual dimensions in flaccid
dysarthria included breathy voice, hypernasality, and
imprecise consonants. An overall impression of the
typical speaker with flaccid dysarthria is one of a weak,
somewhat nasal voice with weak (noncrisp) articulation.
The group of patients with flaccid dysarthria stud-
ied by DAB had damage in the brainstem (blue-shaded
areas in Figure 14–2) or in the cranial nerves exiting
the brainstem to innervate muscles of the speech
mechanism (yellow arrows pointing from the brain-
stem in direction of muscles). Damage to the brain-
stem motor neurons that innervate speech muscles
results in paralysis or weakness of the muscles, as well
as atrophy (often called “wasting”) of muscle tissue.
Similar problems occur with damage to the nerves that
carry the motor neuron commands to the muscles. For
example, weakness of the laryngeal muscles will pre-
vent firm closure of the vocal folds during each cycle of
phonation, producing the breathy voice noted earlier.
Similarly, weakness of muscles of the velopharyngeal
port will result in hypernasality; weakness of the jaw,
tongue, and lips will cause imprecise consonants.

To speech muscles

Spinal nerves to
muscles of respiratory system

Figure 14–2.  Sagittal (from the side) view of the inner wall of the right hemi-
sphere. The brainstem is shaded blue, yellow-orangish arrows directed away from
the pons and medulla represent cranial nerves that control the muscles of the speech
mechanism (muscles of the jaw, lips, tongue, soft palate, pharynx, and larynx). An
arrow below the brainstem represents spinal nerves that control muscles of the limbs
and torso. Corpus callosum, in red, is shown as a landmark.
196 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Flaccid dysarthria is the result of lower motor neuron
disease. “Lower motor neuron” refers to the motor nuclei
in the brainstem and the cranial nerves that carry informa-
tion from these nuclei to muscles. The term “lower motor
neuron” contrasts with “upper motor neuron” which is
discussed later in the section, “Spastic dysarthria.”
Spastic Dysarthria
Imprecise consonants, monopitch, and reduced stress
were the three most impaired perceptual dimensions
in spastic dysarthria. Many of these patients also had a
slow speaking rate and a strained-strangled voice qual-
ity. The extremely slow speaking rates of patients with
spastic dysarthria distinguished them from patients
with flaccid dysarthria (most patients with flaccid dys-
arthria had normal speaking rates), and the strangled,
harsh voice quality was very different from the breathy
voice quality of flaccid dysarthria.
Patients with spastic dysarthria typically had
damage somewhere along the fiber tracts connecting
motor cells in the cortex to motor neuron cells in the
brainstem. Recall from Chapter 2 that the cortex con-
sists of massive amounts of gray matter — clusters of
neuron cell bodies. These cell bodies are connected to
other groups of cell bodies in the brain by white mat-
ter, formed from bundles of axons (fiber tracts). In
Figure 14–3, cortical motor cells for muscles of the
speech mechanism such as the jaw, lips, tongue, velum,
and pharynx are represented by the two upper, brown
dots. The two brown dots located in the brainstem
represent the motor neurons for these muscles. The
yellow-orange arrows originating in the cortical cells
and ending on these brainstem motor neurons repre-
sent a fiber tract (white matter) called the corticobul-
bar tract. Part of this fiber tract terminates in motor
nuclei of the pons, another part of the tract terminates
in motor nuclei of the medulla.3 Patients with spastic

Corticobulbar
tract

Corpus
callosum

Pons
Medulla

Figure 14–3.  Sagittal (from the side) view of the inner wall of the right hemisphere. Two brown
circles in the cortex indicate motor cells controlling articulators such as the jaw and tongue, and two
brown circles in the pons and medulla indicate motor neurons that are connected directly via cranial
nerves to muscles of the speech mechanism. The yellow-orangish lines connecting the cortical motor
neurons and brainstem motor neurons represent the corticobulbar tract.

3 
Part of the corticobulbar tract also terminates in the midbrain where motor nuclei are located but are not associated with speech.

dysarthria studied by DAB had lesions on both sides
of the brain, that is, in the left and right corticobulbar
tracts.
The corticobulbar tract transmits motor commands
in the cortex to cells in the brainstem. Because the fiber
tract is above the motor neurons in the brainstem,
damage to it is referred to as upper motor neuron disease.
According to DAB, damage to this fiber tract — but not
to the motor neuron cells in the brainstem — results in
spastic dysarthria.4
Upper motor neuron disease usually results in
very specific changes to the affected muscles, such as
hypertonic (excessive) tone which makes them stiff.
The muscles also have overly sensitive reflexes (hyper-
reflexia), causing them to contract with unusual force
when stretched even a small amount. Hypertonic mus-
cles have difficulty causing movement of structures
(such as the jaw), and hyperreflexive muscles result
in unstable muscle contraction and movement. Thus,
movement is impaired in many muscles of the speech
mechanism, such as muscles of the tongue, lips, soft
palate, larynx, and muscles that control jaw opening
and closing.
DAB believed these excessively contracted, stiff
muscles were responsible for many of the primary
speech symptoms of spastic dysarthria. For example,
the “monopitch” characteristic of spastic dysarthria
was caused by excessive stiffness of the laryngeal
muscle responsible for voice pitch changes. Similarly,
the “strained-strangled” voice quality was caused by
excess tone of laryngeal muscles, resulting in overly-
tight vocal fold closure during phonation. Imprecise
consonants were the result of difficulty in moving
structures, such as the tongue, into the proper posi-
tions for the articulation of speech sounds. The percep-
tion of “weak stress” was due to the patient’s inability
to produce stress distinctions between unstressed and
stressed syllables, as in words like “about” in which the
first syllable is unstressed. This inability was thought
to be related to the difficulty of adjusting the aspects of
speech production (e.g., pitch, loudness, and duration)
that are used to create stress differences.
Ataxic Dysarthria
The primary perceptual features of ataxic dysarthria
were imprecise consonants, excess and equal stress,
and irregular articulatory breakdown. In English
speech production, syllables alternate between ones
with relatively long duration and ones with relatively
short duration. For example, in the sentence, “The
4 
 pper motor disease also refers to damage to the corticospinal tract connecting cortex to motor neurons in the spinal cord. The damaged
U
corticospinal tract and its possible relationship to dysarthria is not discussed further in this chapter.
14  Motor Speech Disorders in Adults 197
party is off the hook,” there are two relatively long
syllables (“par” and “hook”) and five relatively short
syllables (the two “the’s”; the “ee” in “party,” “is,” and
“off”). Long syllables are typically stressed and short
syllables unstressed. Speakers with ataxic dysarthria
tend to equalize all syllable durations in an utterance
by making each syllable long and fairly loud. This is
what is meant by “excess and equal stress.” “Irregular
articulatory breakdown” is a term coined by DAB to
capture the fluctuating nature of the speech problem
in ataxic dysarthria. Speakers with ataxic dysarthria
may sound fairly normal for short stretches of speech
and suddenly produce a clearly dysarthric string of
syllables.
Listeners often describe ataxic dysarthria as
drunk-sounding speech. This impression is due par-
tially to the excess and equal stress on the speaker’s
syllables, which sounds to listeners as if each syllable
is being “metered out” on a strict time schedule rather
than following the normal speech rhythm of alter-
nating long and short syllables. Speech-language
pathologists refer to this perceptual impression as
“scanning speech” (each syllable being “scanned”
carefully and then produced as if disconnected from
the next syllable). The impression of drunken-
sounding speech is probably also promoted by the ten-
dency of speakers with ataxic dysarthria to produce a
speech melody (intonation) with markedly exagger-
ated pitch changes, giving their speech an “out of con-
trol” quality.
Ataxic dysarthria results from damage to the cer-
ebellum or its connecting fiber tracts. In Figure 14–4,
cell bodies within the cerebellum are represented by
brown dots, and the connecting fiber tracts are shown
as yellow-orange lines ending in arrowheads. These
arrowheads point away from the cerebellum to other
parts of the brain or are directed from other parts of the
brain into the cerebellum.
Damage to the cerebellum causes a number of well-
known, general neurological symptoms. For example,
patients with cerebellar damage have difficulty main-
taining a steady rhythm, even when asked to open and
close their forefinger and thumb in a repetitive, simple
way. Patients also have difficulty controlling the force
of their muscle contractions, which results in actions
performed with either excessive or insufficient force.
It is as if the patient has difficulty scaling muscle con-
traction to the needs of the task. This may explain the
tendency of people with ataxic dysarthria to produce
sequences of syllables with excess and equal stress (see
Box, “Spanish and Ataxic Dysarthria”).
198 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Corpus
callosum

Cerebellum
Pons
Medulla

Figure 14–4.  Sagittal (from the side) view of the inner wall of the right hemisphere. The arrows
show the interconnections between the cerebellum and structures of the central nervous system. The
arrows show that the cerebellum is connected to the spinal cord, the brainstem, and the cortex, send-
ing and receiving information from all three major components of the CNS.

Spanish and Ataxic Dysarthria

Darley, Aronson, and Brown devel-
oped their classification system based on speech
production of American English speakers with
neurological disease. The reasoning for a promi-
nent “excess and equal stress” dimension in ataxic
dysarthria is solid, but only for languages (such
as English) with syllable sequences that vary in
a long-short-long-short pattern. Many languages
have syllable sequences in which each syllable
has roughly the same duration; syllables do not
vary in a long-short-long-short pattern. Spanish is
such a language, as are Finnish and several Asian
languages (Korean, Mandarin Chinese, Japanese).
Is “equal and excess stress” relevant to the
dysarthria classification of a Spanish speaker with
cerebellar disease? The same question can be asked
of many of the speech dimensions that contribute
to the Mayo classification system but do not apply
in the same way across different languages. The
answers to these questions are not known with any
certainty; cross-linguistic studies of dysarthria are
in their infancy (Kim & Choi, 2017; Liss, Utianski,
& Lansford, 2013).

Hypokinetic Dysarthria
Monopitch, reduced stress, and monoloudness were
the three prominent perceptual dimensions for patients
with hypokinetic dysarthria. In addition, many speak-
ers with Parkinson’s disease (PD) had imprecise con-
sonants and “short rushes of speech,” a tendency for
sudden, very rapid, and “mumbly” sequences of syl-
lables. Speakers with hypokinetic dysarthria are also
perceived as having an extremely weak, soft voice.
 14  Motor Speech Disorders in Adults 199

Hypokinetic dysarthria is associated almost exclu-
sively with Parkinson’s disease.5 Parkinson’s disease
involves cell death in a midbrain nucleus called the sub-
stantia nigra (see blue oval in Figure 14–5 for approxi-
mate location). Cells in the substantia nigra are of critical
importance because they manufacture the chemical dopa-
mine that is used as a neurotransmitter in parts of the brain
responsible for movement control (as well as other parts
of the brain involved in memory and the experience of
pleasure). Dopamine manufactured in the substantia nigra
is delivered to the basal ganglia, the group of cells above
the brainstem but deep within the cerebral hemispheres.
The dopamine pathway from the substantia nigra to the
basal ganglia is indicated in Figure 14–5 by the upward-
pointing arrows. The basal ganglia play an important role
in movement control; to perform that role, they need an
adequate supply of dopamine. Loss of dopamine due to
cell death in the substantia nigra is responsible for move-
ment problems in Parkinson’s disease.
The patient with Parkinson’s disease often has a
resting tremor, usually in the hand but sometimes in
other body structures. A resting tremor occurs when
the hand is not moving; the tremor is not seen when the
hand is moving to accomplish a goal such as twisting a
beer cap. Body structures such as the arms and legs, as
well as in the speech mechanism, have a rigid quality ​
— they are stiff and resist movement when displaced
(as when an examiner pulls or pushes on the arm or
leg). Movements, when produced, are slow and small.
At times, the patient has difficulty initiating move-
ment, as if he or she is “frozen” in place.
DAB thought that the top-ranked perceptual
dimensions in hypokinetic dysarthria of monopitch,
reduced stress, and monoloudness, as well as overall
reduced loudness and imprecise consonants, could be
explained by slow and small respiratory, laryngeal,
and articulatory movements resulting from the loss of
dopamine in the basal ganglia.

Corpus
callosum

Midbrain

Figure 14–5.  Sagittal (from the side) view of the inner wall of the right hemisphere. The blue
oval shows the location of the substantia nigra in the midbrain (mesencephalon) and the arrows the
direction of dopamine delivery to the basal ganglia where it is used as a critical neurotransmitter in
the control of movement.

5 
 ertain neurological diseases produce symptoms like those of Parkinson’s disease yet do not qualify for a specific diagnosis of the disease.
C
Patients with these diseases are often referred to as having “parkinsonism.” Patients with parkinsonism may also have hypokinetic dysarthria.
200 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Hyperkinetic Dysarthria ments give the patients the appearance of being in

Hyperkinetic dysarthria is a result of several different
diseases of the basal ganglia. DAB studied hyperkinetic
dysarthria in two of these diseases, Huntington’s dis-
ease and dystonia, both described later in this chapter.
The basal ganglia are a complex group of cells,
composed of several separate but interconnected
nuclei. Figure 14–6 shows a midsagittal view of the
right hemisphere in which an oval indicates the approx-
imate location of the nuclei of the basal ganglia. The
region outlined by the oval is deep within the cerebral
hemispheres, above the brainstem (Chapter 2, Figures
2–6 and 2–7). Damage to any one of these nuclei may
produce somewhat unique neurological symptoms,
far too many to cover in this chapter. Here the general
characteristics are presented for the two basal ganglia
diseases studied by DAB.
Huntington’s disease is a genetic disorder in which
movement difficulties are among the first symptoms.
Later in the course of the disease, patients experi-
ence severe cognitive and psychiatric disturbances.
The movement symptoms are dominated by chorea,
in which a series of twitches, jerks, and sudden move-
constant motion. Muscle tone may be continuously
variable in Huntington’s disease, sometimes being
normal but often ranging from excessively stiff (hyper-
tonic) to floppy (hypotonic) in a short period of time.
The movement symptoms are sometimes described as
having an ataxic component — inability to control the
range and force of movements, and difficulty in pro-
ducing a steady rhythm.
Dystonia is a basal ganglia disease in which muscle
contraction builds up and is sustained with excessive
force for unusually long intervals. Muscle contrac-
tions in dystonia are overly strong (hypercontraction)
for the task at hand, often resulting in an unintended,
sustained posture of the trunk, arm, hand, eyelids, or
jaw. Hypercontraction in dystonia often occurs as an
exaggeration of a purposeful movement to accomplish
a task, rather than occurring at random times or at rest.
For example, in oromandibular dystonia, a hypercontrac-
tion of the jaw muscles occurs when the patient begins
to speak, or perhaps when he chews, but typically does
not occur when the patient is not using the jaw for a
specific purpose. Similarly, spasmodic dysphonia is a
dystonia that affects the vocal folds by closing them

Corpus
callosum

Location of group
of nuclei called
the basal ganglia

Figure 14–6.  Sagittal (from the side) view of the inner wall of the right hemisphere. The large blue
oval encompasses the regions above the midbrain and below the cortex where the nuclei of the basal
ganglia are located. The basal ganglia include several interconnected nuclei.

forcefully when the patient attempts to produce voice
(i.e., to phonate). The forceful closing is the result of
overly strong and sustained contractions produced by
the muscles that close the vocal folds (see Chapter 10
and Chapter 18). This closing spasm of the vocal folds
interrupts vocal fold vibration, essentially preventing
the patient from producing voice. Like oromandibular
dystonia, the laryngeal spasms occur when a person
phonates, not at random times.
The most affected perceptual dimensions in these
two forms of hyperkinetic dysarthria were imprecise
consonants, prolonged intervals, and variable rate in
patients with Huntington’s disease, and imprecise con-
sonants, distorted vowels, and harsh voice quality in
dystonia. Both groups of patients had irregular articu-
latory breakdowns, as in ataxic dysarthria.
The hyperkinetic dysarthria in Huntington’s dis-
ease and dystonia is thought to be the result of overly
strong and sustained contractions of speech muscles,
which make it difficult to move from one speech sound
to the next. The sustained contractions in dystonia
“hold” articulators in one position when they should
be moving smoothly and quickly to the next speech
sound. The constant and variable movements in Hun-
tington’s disease are thought to affect the muscles of
the speech mechanism from making precise, consistent
movements. This loss of control causes speech to sound
inconsistent, with fluctuating voice and articulation
characteristics.
Mixed Dysarthria
In each of the five dysarthria types summarized previ-
ously, the lesion causing the problem was thought to be
in one major region of the brain. Flaccid dysarthria was
a result of brainstem or cranial nerve damage (lower
motor neuron disease), spastic dysarthria from damage
in the cortex or the tract that carries information from
the cortex to the brainstem motor nuclei (upper motor
neuron disease), ataxic dysarthria from cerebellar dis-
ease, hypokinetic dysarthria from substantia nigra lesions
(usually Parkinson’s disease), and hyperkinetic dysar-
thria from basal ganglia lesions (Huntington’s disease).
Some neurological diseases are known to have
damage to two or more of these major brain regions.
For example, patients with multiple sclerosis (MS) often
have upper motor neuron and cerebellar lesions. For
these patients, a dysarthria with both spastic (upper
motor neuron disease) and ataxic (cerebellar) character-
istics might be expected. DAB believed their perceptual
analyses of speakers with MS were consistent with a
mixed, spastic-ataxic dysarthria.
DAB regarded amyotrophic lateral sclerosis (ALS)
as another neurological disease associated with a
14  Motor Speech Disorders in Adults 201
mixed dysarthria. In ALS, death of motor neurons in
the brainstem (lower motor neuron disease) is com-
bined with lesions in the fiber tract connecting corti-
cal motor cells with brainstem motor neurons (upper
motor neuron disease). In this case, the mixed dysar-
thria is of the flaccid-spastic type.
In theory, a mixed dysarthria may consist of any
combination of the five major categories described pre-
viously. Whether or not patients with any combination
of a mixed dysarthria (such as a flaccid-hyperkinetic
dysarthria) have lesions consistent with these percep-
tual impressions is unknown. Surprisingly, there are
no brain imaging studies linking dysarthria categories
with documented site of lesion.
Unilateral Upper Motor Neuron Dysarthria
As described earlier, spastic dysarthria is thought to be
the result of bilateral (both sides) lesions to the corti-
cobulbar tract. Most of these lesions are the result of
stroke, where a loss of blood flow to the fibers connect-
ing cortical cells to brainstem motor neurons results in
damage to or destruction of the fibers. There are cases,
however, in which a stroke affects only one side of the
brain (unilateral damage), leaving the corticobulbar
tract on the other side intact and functional. In particu-
lar, some strokes may produce a loss of blood flow to
a very small part of the corticobulbar tract, resulting in
a typically mild and often transient motor speech dis-
order called unilateral upper motor neuron (UUMN)
dysarthria.
UUMN dysarthria was not part of the original
DAB classification system for motor speech disorders.
As pointed out by Duffy (2015), UUMN dysarthria was
probably left out of the classification system because
the speech characteristics were so mild. In addition,
the mild dysarthria often resolved over a short period
of time following a stroke. The mild characteristics of
UUMN dysarthria include imprecise consonants, irreg-
ular articulatory breakdowns, harsh voice, and slow
speaking rate (Duffy, 2015). The impression of impre-
cise consonants dominates the speech of persons with
UUMN dysarthria.
The Dysarthrias:  A Summary
Table 14–3 lists the categories of dysarthria in the Mayo
Clinic classification system, along with the prominent
perceptual dimensions heard by DAB for each type.
Some of the perceptual dimensions were prominent for
several dysarthria types (e.g., imprecise consonants)
and some were uniquely prominent in only one type
(e.g., distorted vowels). Table 14–3 also includes prom-
202 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Table 14–3.  Mayo Clinic Classification of Dysarthria With Prominent Perceptual

Impressions for Each Category

Classification Prominent Perceptual Impressions

Flaccid Breathy voice, imprecise consonants, hypernasality

Spastic Imprecise consonants, monopitch, reduced stress, slow rate

Ataxic Imprecise consonants, excess and equal stress, irregular

articulatory breakdowns

Hypokinetic Monopitch, reduced stress, breathy voice

Hyperkinetic Imprecise consonants, prolonged intervals, variable rate

(Huntingtons disease)
Imprecise consonants, distorted vowels, harsh voice
(Dystonia)

Mixed Any combination of above, e.g., spastic-flaccid dysarthria

(as in ALS), spastic-ataxic dysarthria (as in MS)

Unilateral upper motor Imprecise consonants, slow speaking rate, harsh voice,
neuron dysarthria irregular articulatory breakdowns (all mild)

inent perceptual characteristics of unilateral upper
motor neuron dysarthria.
When the speech of a person with dysarthria
is heard, listeners do not separate their perceptual
impressions into the individual perceptual dimensions
used by DAB to scale their prominence. Listeners hear
a “whole” (integrated) percept. The point made by
DAB, following analysis of all the perceptual dimen-
sions and how they clustered differently in each of the
dysarthrias listed in Figure 14–1 and Table 14–3, was
that listening to the speech of a person with dysarthria
provided a good clue to the location of damage within
the nervous system. This was the localizing value of
careful listening.
Some dysarthrias may have natural recovery,
such as the improvement of speech during recovery
from stroke. Some dysarthrias may become increas-
ingly worse, as in degenerative neurological diseases
such as multiple sclerosis, Parkinson’s disease, and
ALS. In most cases of dysarthria, SLPs are effective in

Identification of Dysarthria Type by Listening:

A Brief Natural History
In the mid- to late-1960s, when Darley, Aronson,
and Brown were developing their classification
system for dysarthria, the idea of identifying site
of lesion (location of damage) by listening to a
patient’s speech was a big deal. Brain imaging
techniques were in their infancy, making the
perceptual expertise of SLPs a significant
contribution to diagnosis of site of lesion. Two
developments have lessened the role of SLPs in
the medical diagnosis of site of lesion, and by
extension, the disease in persons with dysarthria.
First, in many cases, the contemporary use of
highly sophisticated imaging techniques (CAT,
MRI, positron-emission tomography [PET]) allows
for detailed visualization of brain structures and
accurate location of site of lesion. Second, identifi-
cation of disease type from listening to speech, and
the inference to site of lesion, are not very reliable.
Several studies have reported a relatively low level
of agreement among professionals for both individ-
ual perceptual dimensions and dysarthria type (see
review in Bunton, Kent, Duffy, Rosenbek, & Kent,
2007). Nevertheless, the Mayo Clinic classification
system is in contemporary use by both clinicians
and scientists.

finding treatment strategies to improve communica-
tion skills.
Apraxia of Speech
The other major subcategory of motor speech disorders
is AAS. AAS is a controversial disorder, mostly because
professionals have not agreed on its defining charac-
teristics (Ballard et al., 2016). AAS has been related to
lesions in various parts of the central nervous system,
most often in the left cerebral hemisphere (Graff-Red-
ford et al., 2013). It is possible that there are several
types of AAS, but in this chapter the possible subtypes
are not discussed.
In their original description of the Mayo Clinic
classification system, DAB claimed that AAS was dif-
ferent from dysarthria. Unlike dysarthria, the speech
characteristics of AAS were not the result of paralysis,
weakness, or incoordination of the speech muscles.
Despite the absence of muscle problems in AAS, the
patients had articulatory errors as well as other types
of speech abnormalities (Darley, Aronson, & Brown,
1975). These speech abnormalities typically appeared
following a stroke or surgery affecting the left hemi-
sphere of the brain. Because muscle problems did not
seem to explain AAS, the speech problems had to be
explained on a different basis.
The perceptual impressions of apraxia of speech
included very slow speaking rate (see earlier, descrip-
tion of spastic dysarthria), a tendency to produce
speech as if the component syllables were “pulled
apart” from each other (see earlier, description of ataxic
dysarthria), and imprecise consonants and vowels. In
addition, when asked to produce a word or sentence,
people diagnosed with AAS appeared to search for
the right articulatory configuration to begin the utter-
ance, as if they were unsure of the correct way to pro-
duce the initial speech sound(s). Patients configured
their lips and tongue in a certain position, hesitated,
and tried another configuration as if searching through
several attempts to “get it right” before beginning the
utterance. DAB described this searching as articulatory
groping. The patients also had greater articulatory dif-
ficulty when trying to produce a multisyllabic word
(such as “statistical”) as compared with the single syl-
lable at the beginning of the word (e.g., “statistical”
versus “stat”). The multisyllabic word was more likely
to elicit sound errors and articulatory groping (word
length effect).
DAB proposed AAS as a motor speech programming
problem. In this kind of disorder, the speech problems
are not the result of deficits in the direct control of the
14  Motor Speech Disorders in Adults 203
speech muscles but rather in the plan for their control.
Evidence in studies of speech motor control supports
the separation of neural planning (programming)
processes from execution of an act (Maas & Mailend,
2012). A programming problem is something like a
problem with computer code. A computer in which the
hardware is in perfectly good shape does not perform
its tasks correctly when the software code contains
errors (see Box, “The Code: Can It Be Fixed”). Apraxia
of speech is also diagnosed in children, as discussed in
Chapter 15.
The Code:  Can It
Be Fixed?
The analogy of a well-functioning computer
running defective software to the speech-motor
planning problem in AAS is based on the
meaning of the term “praxis.” Praxis, a word
from Old Greek, means the process of producing
a skill. DAB categorized the disorder as apraxia
of speech to represent the presumed deficits in
the process — that is, the plan for an articulatory
sequence, just as lines of computer code are
the process for the computer’s action. Other
kinds of apraxia occur in persons who have had
strokes and are recovering. For example, given
a toothbrush and asked to show how to use it,
a patient may raise the toothbrush to his face
and hesitate as if he is not sure how to continue
the act of brushing teeth. Then, the patient
may act but in the wrong way: he may use the
toothbrush to perform a hair-brushing gesture.
How does a clinician go about fixing (or reduc-
ing) the programming problem in AAS? A lot of
discussion surrounds this question (e.g., McNeil,
Ballard, Duffy, & Wambaugh, 2016), but at the
current time the evidence for effective clinical
approaches is not convincing.
Chapter Summary
Motor speech disorders in adults are a group of speech
disorders caused by damage to the central and/or
peripheral nervous system.
Many neurological diseases are associated with a
motor speech disorder.
Classification of motor speech disorders was
formalized by Mayo Clinic clinician-scientists in the
204 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
late 1960s and early 1970s; the classification system is
widely used and accepted by speech-language patholo-
gists and researchers.
The classification for motor speech disorders
was based primarily on perceptual impressions of the
patient’s speech.
The classification system for motor speech disor-
ders included a group of dysarthrias, associated with
problems in the control of speech muscles, and a plan-
ning disorder in which muscle control was more or less
intact, but the ability to plan (program) articulatory
sequences was impaired.
The classification categories for dysarthria included
flaccid, spastic, ataxic, hypokinetic, hyperkinetic, and
mixed types.
The classification category for the planning disor-
der was apraxia of speech.
The classification is based on groups of perceptual
impressions, called “perceptual dimensions,” which
were scaled from normal to most severe by the Mayo
Clinic clinician-scientists as they listened to audiotape
recordings of a paragraph-level passage.
The patients who read the passage included per-
sons with known neurological diseases, including
brainstem disease, damage to the corticobulbar and
corticospinal tracts, damage to the cerebellum, dam-
age to dopamine-producing cells in the midbrain, and
damage to the basal ganglia.
Patients with multiple sclerosis (damage to both
the corticobulbar/corticospinal tracts, and to the cer-
ebellum) and amyotrophic lateral sclerosis (damage to
both the corticobulbar/corticospinal tracts, and to the
brainstem) were also studied.
The general theory of the Mayo Clinic classifica-
tion system is based on the idea that by listening to a
patient’s speech, a trained clinician-scientist can make
a likely estimate of the location of neurological damage,
and by extension the patient’s neurological disease.
References
Ballard, K. J., Azizi, L., Duffy, J. R., McNeil, M. R., Halaki, M.,
O’Dwyer, N., . . . Robin, D. A. (2016). A predictive model
for diagnosing stroke-related apraxia of speech. Neuropsy-
chologia, 81, 129–139.
Bunton, K., Kent, R. D., Duffy, J. R., Rosenbek, J. C., & Kent, J.
F. (2007). Listener agreement for auditory-perceptual rat-
ings of dysarthria. Journal of Speech and Hearing Research,
50, 1481–1495.
Darley, F. L., Aronson, A. E., & Brown, J. R. (1969). Differen-
tial diagnostic patterns of dysarthria. Journal of Speech and
Hearing Research, 12, 246–269.
Darley, F., Aronson, A., & Brown, J. (1975). Motor speech disor-
ders. Philadelphia, PA: Saunders.
Duffy, J. D. (2015). Motor speech disorders: Substrates, differential
diagnosis, and management (4th ed.). St. Louis, MO: Mosby
Elsevier.
Graff-Redford, J., Jones, D. T., Strand, E. A., Rabinstein, A. A.,
Duffy, J. R., & Josephs, K. A. (2013). The neuroanatomy
of pure apraxia of speech. Brain and Language, 129, 43–46.
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kinsonism based on focal brain lesions. Brain, 141, 2445–2456.
Kim, Y., & Choi, Y. (2017). A cross-linguistic study of acoustic
predictors of speech intelligibility in individuals with Par-
kinson’s disease. Journal of Speech, Language, and Hearing
Research, 60, 2506–2518.
Liss, J. M., Utianski, R., & Lansford, K. (2013). Cross-linguistic
application of English-centric rhythm descriptors in motor
speech disorders. Folia Phoniatrica et Logopaedica, 65, 3–19.
Maas, E. L., & Mailend, M. L., (2012). Speech planning hap-
pens before speech execution: Online reaction time meth-
ods in the study of apraxia of speech. Journal of Speech,
Language, and Hearing Research, 55, S1523–S1534.
McNeil, M. R., Ballard, K. J., Duffy, J. R., & Wambaugh, J.
(2016). Apraxia of speech: Theory, assessment, differential
diagnosis, and treatment: Past, present, and future. In P. H.
H. M. Lieshout, B. Maassen, & H. Terband (Eds.), Speech
motor control in normal and disordered speech: Future develop-
ments in theory and methodology (pp. 195–221). Rockville,
MD: ASHA Press.

Pediatric Speech Disorders I
Introduction
Many writers have discussed the history of how the
field of Communication Sciences and Disorders has
viewed speech sound disorders in children (see Bank-
son, Bernthal, & Flipsen, 2017). The history is interest-
ing because the vast majority of children seen in speech
and hearing clinics for delayed or different speech
sound development do not present other symptoms
that clearly point to the cause of the problem. The
explanation for delayed or different speech sound
development in these children has therefore been the
cause of much speculation and debate; speculation and
spirited debate always make for an interesting scien-
tific and clinical history.
What kinds of conditions would clearly explain a
developmental speech sound disorder? Three condi-
tions are immediately suggested, including hearing
impairment, structural (anatomical) problems with the
speech mechanism, and neuromuscular problems asso-
ciated with a known form of disease of the central and/
or peripheral nervous system.
A significant hearing impairment has an effect on
a child’s speech sound development. The details of the
hearing impairment may not account for the details of
the speech sound problems, but in a general sense, the
child with hearing impairment has a strong likelihood
of delayed or different (as compared to the typically
developing child) development of the speech sounds
of her language.
15
Structural problems in the speech mechanism can
also result in developmental articulation disorders.
For example, a child born with a cleft palate may have
problems closing the velopharyngeal port even after
surgery is performed to close the palate and reattach
the relevant muscles in the correct configuration. This
child can be expected to have difficulty with obstru-
ents, the speech sounds requiring a positive oral pres-
sure for correct production. When the child attempts to
produce these sounds, air leaks through the ineffective
VP port and the resulting speech sounds are incorrect.
The same child may try to compensate for this struc-
tural problem in a way that introduces yet another
error into her developmental speech sound profile (see
Chapter 19).
Finally, a child born with a neurological disease
such as cerebral palsy or who suffers some other form
of brain insult (as a result of surgery, traumatic brain
injury, and other diseases) may have difficulty moving
the articulators, laryngeal muscles, and/or muscles of
the respiratory system, any or all of which may contrib-
ute to delayed or different speech sound development.
This chapter presents information on two pediatric
speech sound disorders. By definition, pediatric speech
sound disorders arise in childhood. The present chap-
ter considers two such disorders whose cause has yet to
be identified. These disorders are called speech delay
(SD), and childhood apraxia of speech (CAS).
Stuttering is also a developmental speech disorder
of currently unknown origin. There are well-founded
205
206 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
suspicions, however, that stuttering is best classified as
a developmental motor speech disorder — that a speech
motor control problem is the underlying basis of stut-
tering even if it is not the only factor that determines
stuttering behavior (Smith & Weber, 2017). We have
chosen to present material on stuttering in a separate
chapter (Chapter 17).
CAS is also considered a motor speech disorder
by many clinicians and scientists largely because some
of the speech symptoms are said to resemble those in
adults with known brain lesions and who have been
diagnosed with adult apraxia of speech (AAS) (Ad
Hoc Committee on Childhood Apraxia of Speech,
2007). There is some preliminary evidence for central
nervous system dysfunction in CAS (e.g., Fiori et al.,
2016). This evidence, however, requires extensive, spec-
ulative inferences from the tentative results of a few
brain imaging studies to the speech behavior in CAS.
Some scientists have argued that current evidence does
not support a brain basis for CAS (Liégeois & Morgan,
2012; Morgan & Webster, 2018).The evidence for a neu-
ral basis in CAS is also not nearly as strong as it is in
stuttering, and there is much uncertainty and contro-
versy about the diagnosis of CAS (Ad Hoc Committee
on Childhood Apraxia of Speech, 2007). In the current
chapter, CAS is considered as a speech sound disorder
of unknown origin.
Speech sound disorders with unknown causes
constitute the majority of all childhood speech disor-
ders. The term “speech delay” refers to speech sound
development that lags typical development (see
Chapter 13) without a clear explanation for the delay.
“Speech delay” is not the only term used to designate
this category of childhood speech sound disorders.
Some authors use the terms “phonological delay” or
“articulatory disorders” to refer to delayed mastery of
speech sounds with unknown cause (e.g., Eecen, Eadie,
Morgan, & Reilly, 2018). In this chapter, we use “speech
delay” to represent all of these terms. Some comments
are made, however, concerning potential implications
of the difference between the terms “speech delay,”
“articulatory delay,” and “phonological delay.”
CAS refers to delayed and disrupted speech sound
development that includes speech sound patterns,
prosodic characteristics, and continued (throughout
development) severity not seen in children with speech
delay. A child may have speech characteristics that do
not clearly suggest a diagnosis of either speech delay or
CAS. Clinicians and scientists do not always agree on
the specific speech characteristics that fit speech delay
versus CAS. As described in the section “Childhood
Apraxia of Speech,” the disorder may be due to a defi-
cit in planning speech sound sequences, in much the
same way as hypothesized for the adult version of the
disorder (AAS).
An understanding of pediatric speech sound dis-
orders can benefit from a classification system. The
classification system may include the cause of the
disorder, known or presumed, the severity of the dis-
order, the natural history of the disorder (if and how
it changes over time), and subtypes within a single
named disorder (e.g., subtypes of motor speech dis-
orders). A detailed classification system for pediatric
speech sound disorders, supported by some data as
well as reasonable speculation, has been published by
Shriberg and colleagues (2010). Some of the ideas from
this classification system are used in this chapter.
A final introductory point is the role of speech
intelligibility in a speech disorder. A basic question in
almost any speech disorder is, to what extent does it
affect a speaker’s intelligibility? How difficult is it to
understand what the speaker is saying? This is a cen-
tral concern in pediatric speech disorders, regardless of
the underlying cause.
Speech Delay
Estimates of the prevalence of speech delay are as high
as 15.6% in children aged 3 years. By age 6 years, many
of these children “catch up” to typical development
norms. Prevalence estimates of speech delay drop to
about 4% at age 6 years, reflecting a positive outcome
for many children who were diagnosed with speech
delay at age 3 years. This leaves a significant number
of children who enter first grade with speech charac-
teristics that are noticeably delayed relative to expec-
tations for their age. (See Vick, Campbell, Shriberg,
Green, Truemper, Rusiewicz, & Moore [2014] for a
review of the prevalence data and Flipsen [2016] for
a summary of data showing a decrease in the preva-
lence of speech sound disorders throughout grade,
middle, and high school.)
Speech sounds are mispronounced by typically
developing children who are partially or largely unin-
telligible at certain times during their speech develop-
ment. The expectation for children who have typically
developing sound systems is for a decreasing number
of speech sound errors and increasing speech intelli-
gibility as the child gets older. The child with speech
delay also mispronounces individual speech sounds
but at ages when these sounds are mastered by the
majority of children. Children with speech delay are
therefore more unintelligible than they should be at
a specific age. For example, a 4-year-old child who is
diagnosed with speech delay has more speech sound

errors and lower speech intelligibility than a typically
developing child of the same age. When a significant
degree of unintelligible speech seems to be unusual for
a child’s age, parents or teachers may refer the child to
an SLP for formal evaluation. A typical age of referral
is between 4 and 4½ years (Shriberg & Kwiatkowski,
1994). Of course, many children with speech delay cor-
rect their speech sound errors over time, without ther-
apy, and become fully intelligible.
Very generally, speech delay can be defined as a
childhood disorder in which speech sound errors and
phonological processes reflect immaturity of speech
development for a child of a given age. This impres-
sion of age-inappropriate speech skills by parents or
teachers is not very precise, especially in the absence of
an obvious cause for the delay as well as the significant
variability in speech development among typically
developing children. What seems to be excessively
unintelligible speech for a typically developing 5-year-
old may reflect nothing more than a different path to
full intelligibility; in a year or two, the child may have
no speech sound errors. This is one reason for a for-
mal evaluation of a child’s speech when a delay is sus-
pected. A decision to obtain a formal evaluation may
be prompted by parents, or by a teacher who has the
impression that a child is not learning speech sounds
in a typical way.
Diagnosis of Speech Delay
A speech-language pathologist is most likely to initiate
the evaluation by conducting a standardized articu-
lation test. Several formal articulation tests are avail-
able to speech-language pathologists. Most such tests
are based on the speech sound production of a large
sample of children whose ages range from 2 years 0
months (hereafter, 2;0) to as high as nearly 22 years.
These data are called “norms,” because they reflect
typical development as defined by the test. Most often,
the norms are in the form of ages at which a high per-
centage of tested children produce a sound correctly.
For example, one often-used test of articulation reports
the average age of mastery for /s/ in the word-initial
position as 5 years (Goldman & Fristoe, 2015). “Aver-
age age” means that a criterion percentage (e.g., 85%)
of all children tested produced the sound correctly.
Some children master /s/ by age 3 years, others may
not master it until age 8 years. But a percentage crite-
rion is a useful way to answer the question, “At what
age does the typically developing child master the /s/
sound?” The same question can be asked and answered
about any speech sound or combination of speech
15  Pediatric Speech Disorders I 207
sounds. Slightly different norms are given for males
and females to recognize the typically faster mastery
of the sound system by female children as compared
with male children.
The tested speech sounds are classified in one of
four ways, including correct, substitution, omission, or
distortion. A correct speech sound is self-explanatory
(e.g., a “g” in the word “dog”). A substitution is the
replacement of the correct sound with another pho-
neme (e.g., a “d” for “g” substitution, resulting in
“dod”). An omission is the absence of a sound that is
present in the correctly produced word (e.g., an omit-
ted “g” in “dog,” “da” (or “daw,” depending on dia-
lect) for “dog.” Finally, a distortion is a speech sound
having the characteristics of the target but produced
unclearly, like a poor version of the sound (e.g., a stop
consonant like a “g” produced slightly in front of the
place of articulation for “g”).
The results of formal articulation tests are com-
pared to the norms; the scores for a child are totaled
across all tested sounds. This total score is expressed
as a deviation from the average total score for the
typically developing norms. For example, a 4-year-old
child evaluated for speech delay may have a total
sound production score of 85, which is compared to
the total score norms for typically developing 4-year-
old children. In this example, we assume the 4-year-old
norm is 100. Depending on the score criterion recom-
mended in a specific test of articulation, the total score
of 85 may deviate sufficiently from the norm to merit a
diagnosis of speech delay.
Another approach to estimating a child’s articula-
tory mastery is to compute a measure of percentage of
consonants correct (PCC). Imagine a child engaged in a
conversation, a recording of which is made for analysis.
The recording of the child’s speech (the “speech sam-
ple”) is transcribed using the IPA (Chapter 12) to obtain
a count of all consonants within the sample includ-
ing correctly and incorrectly produced consonants.
The correctly produced consonants are expressed as
a percentage of the total number of consonants in the
sample. The PCC measure was originally described
by Shriberg and Kwiatkowski (1982) and has been
updated and refined several times (Shriberg, Austin,
Lewis, McSweeny, & Wilson, 1997).
At 5 years of age, typically developing children
have PCC scores of 90% to 95%. PCC varies with sev-
eral factors, including age and type of speech material
used to extract the measure. As described earlier, the
measure as originally developed was taken from con-
versational speech samples, but it has also been used
in the analysis of single words (e.g., Fabiano-Smith &
Hoffman, 2018).
208 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
PCC can also be used to diagnose speech delay.
Much like the score from a standardized articulation
test, there is no firm PCC cutoff to separate children
with typically developing speech sound mastery from
those with speech delay. The clinician who uses the
PCC score to confirm a diagnosis of speech delay must
adopt a criterion percentage to make the decision. For
example, original data reported by Shriberg and Kwi-
atkowski suggested a cutoff PCC of around 85%. Chil-
dren with a PCC score below 85% were candidates for
a diagnosis of speech delay.
Quantitative Measures of Speech
Delay and Speech Intelligibility
Articulation tests such as the Goldman-Fristoe Test of
Articulation (GFTA) and PCC are quantitative because
they use numbers to estimate the goodness of articula-
tory skills. This is in contrast to qualitative estimates of
a child’s speech such as “excellent,” “good,” “poor,”
and so forth. Earlier in the chapter, speech intelligibility
was cited as a primary issue for children with speech
delay. When quantitative measures of articulation (stan-
dardized articulation test or PCC) and speech intelligi-
bility (e.g., the number of words heard correctly) are
available for the same children, is there a relationship
between them that allows a reliable estimate of speech
intelligibility from the articulation score? This is a basic
It Just Doesn’t Add Up
Speech intelligibility tests were devel-
oped many years ago in the dark ages of landlines
to evaluate the quality of telephone transmission.
The idea was to have tests that “added up” the
quality of each speech sound in a list of words to
obtain a percentage of the words recognized by
a crew of listeners (Weismer, 2008). This seems to
make sense, but as it turns out it does not work very
well when speech intelligibility tests are used to
estimate the severity of a person’s speech disorder.
Speech intelligibility tests are used routinely
to estimate the severity of a speech problem in
persons with cleft palate, hearing impairment, and
motor speech disorders (dysarthria and apraxia
of speech), as well as in children with speech
sound disorders. Study after study has shown that
1
I f speech delay was the same for all speech sounds, it might seem reasonable to expect each sound to make an equal contribution to speech
intelligibility problems. This hypothesis is not correct, however, because the frequency of occurrence varies across the speech sounds of a
statistical question: can y (speech intelligibility score)
be predicted from x (articulation score)?
Among children diagnosed with speech delay,
there is, at best, a modest correlation between PCC
and a measure of speech intelligibility (Shriberg &
Kwiatkowski, 1982). More recent studies of children
with speech sound disorders fail to show a convincing
relationship between PCC and speech intelligibility:
“Improvements in severity (as measured by PCC) were
noted in some of the children, but these improvements
did not translate into improvements in intelligibility”
(Lousada, Jesus, Hall & Joffe, 2014, p. 593). Knowing
the PCC for an individual child may be a weak predic-
tor of speech intelligibility.
Speech Delay and Individual Speech Sounds
Children diagnosed with speech delay often have the
most pronounced delay for consonants mastered late in
the course of typical speech sound development (Shrib-
erg et al., 1997). In children with speech delay, the “late
eight” /s/, /z/, /r/, /l/, /T/ (“thin”), /D/ (“those”), /ʃ/
(“shine”), and /tʃ/ (“chop”) may show more delay
than sounds mastered early in development such as
/b/, /d/, /g/, /p/, /t/, /k/, /m/, /w/, and /n/. Speech
delay for the late eight, being more likely and lasting
a longer time than speech delay for early mastered
sounds, may have a disproportionate effect on speech
intelligibility.1 A therapy plan for a child with speech
counts of “phonemes correct” do not match overall
intelligibility scores (reviewed in Weismer, 2008).
This is consistent with the more recent findings of
Lousada et al. (2014) for children, and with results
of a study conducted by Ertmer (2010) on the
speech intelligibility of children with hearing loss.
Why doesn’t it add up? It is not yet entirely clear,
but a good guess is that the connections between
sounds — how you get from one sound to another
within a word — are just as important as the quality
of individual sounds. In addition, speech intel-
ligibility is not simply the “sum” of individual
sounds, but as discussed in Chapter 11 makes use
of top-down processes in which words are often
identified before all the sounds have
been analyzed.
 15  Pediatric Speech Disorders I 209

delay may include focused work on sounds thought to
have a large effect on speech intelligibility.
Speech Delay:  Phonetic,
Phonological, or Both?
Earlier, it was noted that some professionals use the
diagnostic term “phonological disorders” for develop-
mental speech sound disorders with no known cause.
The view of speech sound errors as phonetic (articula-
tory) or phonological may have important implications
for clinical practice.
A child diagnosed with multiple speech sound
errors may be treated with articulatory practice (also
called traditional articulation therapy: see Hegarty,
Titterington, McLeod, & Taggart, 2018) as part of his
speech therapy. A central component of this approach
is repetition of each error sound as a way to establish
and refine the speech motor control required for its cor-
rect production. An assumption of this approach is that
extensive movement and placement practice is likely
to result in mastery of an incorrectly produced speech
sound (Powell, Elbert, Miccio, Strike-Roussos, & Bras-
seur, 1998; Lousada et al., 2013). The effect of articu-
latory practice, in this view, is similar to the expected
effect of practice on any skill (e.g., throwing a football;
keyboarding).2
When speech sound errors are considered phono-
logical, the emphasis in therapy is on the sound sys-
tem, rather than on individual sounds and phonetic
practice (Brumbaugh & Smit, 2013). Children who
receive phonological therapy may be trained to recog-
nize and produce minimal pair contrasts. A minimal
pair is formed by words that differ by a single feature,
such as consonant voicing, place of articulation, and
manner of articulation. Examples of minimal pairs are
“pack-back” (word-initial voicing), “pack-tack” (word-
initial place of articulation), and “sack-tack” (word-
initial manner of articulation). Minimal pair therapy
addresses the component of the sound system that
makes phoneme contrasts — the sounds that change the
word meaning when exchanged in the same word posi-
tion. Treatment of phonological processes that have not
disappeared from the child’s sound system is another
example of phonological therapy. For example, when
a child deletes consonants from the word-final posi-
tion, the specific “missing” sounds are not treated one
by one. Rather, the child is exposed to groups of CVC
words in which the word-final C varies across several
consonant types (e.g., /t/, /g/, /s/, /n/). The object of
the therapy is the child’s mastery of the CVC word
form, which includes many different word-final con-
sonants. The assumption is that exposure to the CVC
words generalizes across consonant types, eliminating
the phonological process of final consonant deletion in
these word forms.
Residual and Persistent Speech Sound Errors
In the majority of typically developing children, mas-
tery of the speech sound system is complete around 8
years of age. A small number of children have speech
sound errors that extend past this age and into the
teenage years, and possibly into and beyond young
adulthood. The terms residual speech sound errors
and persistent speech sound errors have been used to
describe articulatory errors lasting past the age of com-
plete speech sound mastery.
As pointed out by Flipsen (2016), clinicians and
researchers have tended to use the terms, “residual”
and “persistent” speech sound errors interchangeably
to classify children who have these long-lasting errors.
Although the terms are now thought to classify chil-
dren with partially different histories of speech sound
errors, the two groups share a characteristic — the
speech sounds in error are transcribed as distortions,
rather than substitutions or omissions.
As discussed earlier, a distortion is recognizable
as the intended but poorly produced speech sound.
For example, the word-initial [s] in [sIn] “sin” is pro-
duced with the tongue too far forward in the mouth
(like a lisp) or in a “slushy” way. The perceived word
“sin” is recognized as such, not as “thin” or “shin.”
On the other hand, a substitution is heard as a differ-
ent sound than the one intended, as when the speaker
says “shin” for the intended “sin” (a /ʃ/ for /s/ substi-
tution). An omission is the absence of a sound in the
intended word. For example, omission of the /l/ in
“slow” results in a production transcribed as [soU], or
omission of the /ŋ/ in “sing” is spoken as [sI] (possibly
with a nasalized /I/, hence [sĨ ]).

language. For example /t/, /d/, and /n/ are frequently occurring sounds in American English, whereas /T/, /ʃ/, and /h/ occur relatively
infrequently (Mines, Hanson, & Shoup, 1978). /T/ and /ʃ/, two of the infrequently occurring sounds in this example, are also among the late-
eight sounds. Perhaps the late-eight difficulties are not so important to speech intelligibility problems in children with speech delay? Of course,
it is never that simple. /s/, a late-eight sound, is among the most frequently occurring speech sounds.
2 
 here are cognitive contributions to establishing and refining any motor skill. The analogy between articulatory practice and (for example)
T
throwing a football is not meant to eliminate cognitive skill, such as knowing the relationship between articulatory movement and placement
with acoustic results, or between arm motion and grip on the football with the location of the ball when it is thrown).
210 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
If speakers with residual errors are different from
speakers with persistent errors even though they both
produce distortions of speech sounds, how are they
distinguished?
Residual errors are usually distortions of /r/ and
/s/, with [w]-like for /r/ errors, and [T]-like for /s/
errors (or, slushy-like [s] for /s/ errors). The “-like”
part of these error patterns is important: casual listen-
ing to a distorted /r/ may at first seem like a [w] for
/r/ substitution, but closer listening reveals a [w]-like
sound with rhotic (/r/-like) qualities. The /r/ distor-
tion often sounds as if it is between an /r/ and a /w/.
/s/ distortions have the same “in-between” quality.
Many clinicians and researchers believe that /r/
and /s/ residual errors reflect an incomplete process
of speech motor learning and are usually unresolved
articulatory imperfections from a previously diagnosed
and treated speech delay (Flipsen, 2016). The diagno-
sis of speech delay earlier in the child’s developmental
history was made because of multiple speech sound
errors, not just /r/ and /s/ errors.
Persistent errors are thought to be /r/ and /s/
distortions that were present earlier in a child’s speech
sound development, but were not treated because
the remainder of the speech sounds were learned in
a typical way. In other words, the child was not diag-
nosed with speech delay because the errors were lim-
ited to only one or two speech sounds, both typically
mastered late in the speech-sound learning process.
There is, however, some evidence that children who
are thought to have persistent errors may have other
speech sound errors in addition to /r/ and/or /s/. This
may also distinguish these children from those who are
described as having residual errors.
Children with residual or persistent errors may
recover spontaneously to produce distortion-free /r/
and /s/. However, up to 25% of children who have
residual or persistent errors around 9 years of age may
not recover spontaneously, and may require services to
correct these errors. The distinction between residual
and persistent speech sound errors may be important
when therapy is undertaken to eliminate distortions of
these sounds.
Another potential explanation for residual and
persistent speech sound errors is that a child has subtle
perceptual problems specific to /r/-/w/ and /s/-/T/
(or /s/-/ʃ/) distinctions. In a recent study, children
aged 9 to 14 years with residual /r/ errors were able to
hear the difference between /r/ and /w/ with the same
proficiency as children without residual errors (Pres-
ton, Irwin, & Turcios, 2015). Other studies, reviewed
by Preston et al., have found some evidence of subtle
perceptual problems in children with speech sound
disorders.
The possibility of perceptual difficulties in chil-
dren with residual errors is relevant to treatment
options. If residual /r/ and /s/ errors have a basis in
poor perception of phoneme-specific contrasts (e.g., the
/r/-/w/ contrast), “ear training” makes sense as part
of a therapy program to correct the production errors.
Ear training — listening to many examples of /r/-/w/
pairs — may establish a better representation of the
sounds as different phoneme categories. Once the cat-
egories are established by improvements in perceptual
skill for specific contrasts, the child uses the categories
to produce the sounds correctly.
Additional Considerations in
Speech Delay and Residual and
Persistent Speech Sound Errors
Speech sound disorders, including both speech delay
and residual errors, have been associated with causes
and effects other than those presented. For example,
some authors (review in Eaton, 2015) have suggested
that subtle deficits in cognitive abilities may be a fac-
tor in residual errors. “Cognitive abilities” include the
ability to process, represent, store, and represent infor-
mation and to focus on relevant stimuli and exclude
irrelevant stimuli. Of special interest to the presence of
residual speech sound errors, these cognitive abilities
must be employed to compare speech sound output,
such as a residual error, to stored representations of
the sound. This is called self-monitoring. The success
of self-monitoring depends on the ability to focus on
the speech output, to use memory to access the rep-
resentation of the sounds in the brain, and to make a
proper comparison between the output and the stored
representation. In theory this makes sense, but research
to date has not produced clear results on deficiencies in
cognitive abilities in children with residual errors, or
the effectiveness of therapy techniques to correct resid-
ual errors based on training of self-monitoring skills.
Still, cognitive skills as a partial explanation of residual
errors and as a potential target in therapy deserve fur-
ther research effort.
Children with residual errors may also experi-
ence challenges in social settings and academic perfor-
mance. Hitchcock, Harel, and Byun (2015) conducted
a survey filled out by parents whose children had
/r/ errors. The survey focused on the effect of the /r/
errors on the child’s social and academic life. The rat-
ings suggested that the greatest impact of the residual
errors was on social interactions, especially for chil-
dren over 8 years of age. The findings of this survey
are consistent with research suggesting that children
with residual errors are judged more negatively than

children with typically developing articulation (Crowe
Hall, 1991). In another survey, adults who as children
had a history of speech sound disorders received lower
grades in high school and had fewer years of post–high
school education as compared to children who had typ-
ically developing speech sounds (Felsenfeld, Broen, &
McGue, 1994). Children diagnosed with speech delay
as they enter grade school may also have delayed lit-
eracy skills (literacy skills include reading, writing, and
spelling) relative to children with typically developing
speech sound skills (Haylou-Thomas, Carroll, Leavett,
Hulme, & Snowling, 2017). Delayed literary skills can
have profound effects on academic success.
These studies, taken together, suggest a connection
between childhood speech sound disorders and the
quality of social and academic aspects of life. A clear
cause-and-effect relationship cannot be established
from these studies, and certainly not all children with
speech sound disorders have, or as adults will have,
social and academic problems. The trends in these
studies, however, point to the potential value of speech
therapy to correct speech sound disorders and mini-
mize their effect on the quality of life.
Speech Delay and Genetics
Finally, there is interest in the possibility of a genetic
basis for speech delay. A simplified explanation for this
interest is the possibility of inheritance of a predispo-
sition for speech delay. Researchers acknowledge the
unlikely case of a single gene “explaining” speech delay,
Rather, a larger group of genes under the influence of
variables in the environment is thought to contribute
to speech and language development (Lewis, Shriberg,
Freebairn, Hansen, Stein, Taylor, & Iyengar, 2006; Peter-
son, McGrath, Smith, & Pennington, 2007); a disruption
in these speech/language genes may result in speech
delay. Variation in the environment (e.g., extensive lan-
guage stimulation versus minimal language stimula-
tion) almost certainly modifies if, and how, the speech/
language genes affect speech sound development. An
interaction between multiple genes with an environ-
mental basis for speech/language development makes
the identification of specific speech-language genes
very challenging.
Given the complexity of human genetic material
and its interaction with environmental factors, why do
researchers explore a genetic predisposition for speech
delay? As reviewed by Felsenfeld (2002), children with
speech sound disorders (including speech delay) are
more likely to have family members with a history of
speech sound disorders when compared to children
whose speech sound development is typical. The rea-
15  Pediatric Speech Disorders I 211
soning is that the likelihood of children with speech
delay having family members with speech sound dis-
orders should be the same as children with typically
developing speech sounds, if there is no hereditable
(genetic) susceptibility to speech sound disorders.
This line of reasoning is complicated by the effect
of environment on speech sound development. As
previously noted, the familial pattern of speech sound
disorders may reflect a language stimulation environ-
ment that is similar in multiple generations of a family.
Perhaps parents in a family do not direct a good deal
of spoken language to their babies, much in the same
way that the parents’ parents did with them. Across
generations, this style of language stimulation may
be an environmental influence on speech-language
genes that results in a high probability of speech sound
disorders.
Evidence in support of a hereditable component
for speech sound disorders has also been gathered
from studies in which the tendency for speech sound
disorders among adopted children was tied to a his-
tory of speech sound disorders in a biological parent,
as compared with an adoptive parent (Felsenfeld &
Plomin, 1997). This finding is consistent with a genetic
component in childhood speech sound disorders, but
does not rule out an environmental effect as well.
Childhood Apraxia of Speech
CAS is a diagnostic term for children with a speech
sound disorder that shares some characteristics with
speech delay and has unique characteristics as well.
“Praxis” is a Greek word meaning “doing,” or “action.”
“Apraxia” is “not doing.” Most patients diagnosed
with CAS are able to “do” speech behaviors, albeit with
difficulty. This is why some clinicians and researchers
prefer the term “dyspraxia” to categorize the disorder.
In this chapter we use the acronym CAS to designate
childhood apraxia of speech.
Apraxia is a diagnostic term that has been in use
for many years to describe an inability to perform cer-
tain motor behaviors in the absence of muscle weak-
ness, or other muscle problems.
Praxis is defined as the ability to perform . . . skilled
or learned movements. Apraxia refers to the inability
to carry out . . . praxis movements in the absence of
elementary motor, sensory, or coordination deficits that
could serve as the primary cause. (Park, 2017, p. 317)
A nearly identical definition for apraxia is provided
by Zadikoff and Lang (2005, p. 1480), who also point
out that apraxia may coexist with “elementary” (e.g.,
212 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
weakness, loss of sensation) muscle disorders. For
example, a limb may be weak but capable of produc-
ing an appropriate gesture, even if slow and reduced in
magnitude. A patient with apraxia and limb weakness
is likely not to produce the appropriate gesture, even if
slow and small.
The 2007 American Speech-Language-Hearing
Association (ASHA) Committee report on CAS pro-
posed the following definition of the disorder:
Childhood apraxia of speech (CAS) is a neurological
childhood (pediatric) speech sound disorder in which
the precision and consistency of movements underly-
ing speech are impaired in the absence of neuromus-
cular deficits (e.g., abnormal reflexes, abnormal tone).
CAS may occur as a result of known neurological
impairment, in association with complex neurobehav-
ioral disorders of known or unknown origin, or as an
idiopathic neurogenic speech sound disorder. The core
impairment in planning and/or programming spatio-
temporal parameters of movement sequences results in
errors in speech sound production and prosody.
Apraxia as a sign of neurological disease has
been recognized for many years. Long before the
term “apraxia” was used to describe speech deficits,
it referred to a neurologically based disorder of limb
and orofacial movement in which patients are unable
to produce voluntary actions that may nevertheless be
produced spontaneously. The apraxic patient, asked
to demonstrate how to brush his hair (either miming
the action or asked to use a brush), may have difficulty
initiating the proper gestures (or use an actual brush
properly), make stop-and-go movements around his
head that are not hair-brushing movements, and show
a good deal of frustration with his inability to respond
appropriately to the request. Similar difficulties may
be observed when asking the patient to open and close
the jaw, stick out his tongue, or purse his lips. These lat-
ter movement problems are called orofacial nonverbal
apraxias, or simply oral apraxias. Another example of
orofacial nonverbal apraxia is the patient who, when
asked to “Show me how you whistle,” hesitates before
attempting to respond to the request, and once move-
ment begins may have difficulty narrowing the lips,
forming them into the shape required for a whistle. The
patient seems to “grope” for the required lip configura-
tion and make several attempts to get it right.
Interestingly, the diagnosis of oral nonverbal
apraxia does not mean the patient is also diagnosed
with apraxia of speech, and vice versa: a patient diag-
nosed with apraxia of speech does not necessarily have
oral nonverbal apraxia (Whiteside, Dyson, Cowell, &
Varley, 2015).
In adults, oral nonverbal apraxia, and/or apraxia
of speech, are almost always the result of a known brain
lesion or known neurological disease. Studies such as
that by Whiteside et al. (2015) included 50 patients
who had suffered a stroke and had documented brain
lesions. Adult stroke survivors are the most frequent
participants in studies of apraxia of speech.
CAS Compared With Adult
Apraxia of Speech (AAS)
AAS is covered in greater detail in Chapters 9 and
14, but a sketch of the speech problem is required to
introduce the speech characteristics in CAS. The char-
acteristics of AAS include hesitation in the initiation of
speech, groping for articulatory postures as if search-
ing for the correct articulatory position and shape for a
specific sound, production of multisyllabic words as if
each syllable is “pulled apart” with a robotic-sounding
effect due to equal stress on each syllable, vowels and
consonants that have unusually long durations, and
inconsistent sound errors such as substitutions and
distortions. Many clinicians and scientists have com-
mented on the inconsistency of these sound errors:
when asked to repeat the same word many times, the
sound errors are not the same on each repetition, and
a sound error on one repetition may be produced cor-
rectly on the next repetition (Bislick, McNeil, Spencer,
Yorkston, & Kendall, 2017).
Adults with apraxia of speech are also likely to
make more sound errors and to show more initiation
problems and articulatory groping, as a sound sequence
increases in complexity. For example, the three words,
“please,” “pleasing,” “pleasingly” increase in complex-
ity by virtue of the number of syllables in the words:
“pleasing” is more complex than “please,” and “pleas-
ingly” is more complex than “pleasing.” The key to
understanding this phenomenon is to focus on errors
made, or increased hesitation before, the initial sounds
(/p/ and /l/) of each word. Adults with apraxia of
speech tend to make more word-initial errors with an
increasing number of syllables following the word-
initial syllable. Articulation of the word-initial /p/
and /l/ in “please-pleasing-pleasingly” is affected by
the number of syllables following it, suggesting that the
beginning of multisyllabic words is not produced inde-
pendently of the middle and end of the word. Another
example of a difference in phonetic complexity is the
word pair “sit” and “split.” The /spl/ consonant clus-
ter is considered more complex than the singleton /s/;
otherwise, the two words share the same phonetic seg-
ments (/s/ as the word-initial sound, /I/ and /t/ as
the final two sounds). Adults with apraxia of speech
 15  Pediatric Speech Disorders I 213

typically have greater difficulty with the word-initial
/s/ for words such as “split” as compared with “sit.”
Selected speech characteristics in AAS are listed in
Table 15–1 (a complete review of these characteristics is
found in McNeil, Robin, & Schmidt, 2009). These char-
acteristics are not observed in every patient diagnosed
with apraxia of speech and may even appear and dis-
appear in the speech of a single patient.
Speech Motor Programs
One explanation for the phonetic complexity effect
depends on the concept of a motor program. Motor
programs are thought to be the organizational pro-
cesses in the brain that prepare execution of an action.
The speech motor program is assumed to contain plans
for placement and configuration of the articulators as
well as the timing of muscle contractions to produce
these articulatory goals. A program is not the same as
the action; the program (sometimes called the “plan”)
is the representation in the brain of the action and may
exist without its execution. The idea of speech motor
programs is controversial, and even the nature of what
is programmed (phonemes? syllables? Whole, multi-
syllabic words?) is debated.
Even with controversy, the concept of speech
motor programs enjoys widespread acceptance among
clinicians and scientists who study apraxia of speech.
Motor programs are thought to take time to assemble,
even if the scale of the time is in micro- or milliseconds
(typical for brain-time processes to be fast). The pro-
gramming time is assumed to be longer for complex
actions compared with simpler actions. For example,
the motor program for the production of “pleasingly”

Table 15–1.  Selected Speech Characteristics of AAS

Characteristic Brief Description

Initiation difficulties Patient hesitates before the onset of speech, as if he
cannot get started; he appears to “grope” for the
correct articulatory configuration for the first sound.

Loss of stress contrasts* Syllables in multisyllabic words have roughly equal

duration and seem “pulled apart” from surrounding
syllables, making speech sound robotic.

Vowels and consonants have Adults with apraxia of speech have slow speaking rates,
long durations which means that the durations of speech sounds are
longer than normal.

Sound errors are substitutions Speech sound errors are replacements of one sound
and distortions with another (like phonemic errors) or poorly produced
sounds (phonetic errors).

Sound errors are inconsistent
Multiple repetitions of one word by a patient do not
always have sound errors that are the same. The sound
errors are variable in type. A word such as “save” may
have a substitution for /s/ in one repetition (“shave” for
“save”) and a distortion in another repetition (a sound
between an “s” and “sh” for “save”). Another repetition
may have a correct “s.”

Increased hesitation, groping, Multisyllabic words “bring out” apraxic errors more
and articulatory errors with than single-syllable words; more complex syllables
increased phonetic complexity (“spl” versus single-consonant “s”) also bring out more
apraxic errors.

*This speech characteristic in adult apraxia of speech is specific to languages such as English (and, e.g.,
Dutch, French, and Russian) in which there are “long” and “short” syllables within multisyllabic words. In
the English word “elephant,” the first syllable is stressed, the second and third are unstressed (the first
syllable is longer than the following two syllables). Try saying “elephant” with equal duration for each syl-
lable to get an idea of the “robotic speech” characteristic of adult apraxia of speech. There are languages
(e.g., Spanish, Korean, Mandarin Chinese), however, in which successive syllables are not long or short
but have roughly equal duration. The characteristics of apraxia of speech have not been defined well (or
at all) in these languages.
214 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
takes more time to assemble than the programming for
“please,” as does the programming of “split” compared
with “sit.” One hypothesized proof of motor program-
ming and the complexity effect is that reaction times to
say the word “split” are greater than reaction times to
say “sit.” Similarly, reaction times are longer for “pleas-
ingly” versus “please.” Ballard, Tourville, and Robin
(2014) provide a review of the programming hypoth-
esis in adult apraxia of speech.
CAS:  Prevalence and
General Characteristics
In a 2007 report posted at the ASHA website (https://
www.asha.org/practice-portal/clinical-topics/child​
hood-apraxia-of-speech/), CAS was estimated to have
a prevalence of between 0.1% and 0.2%, or between 1
and 2 per 1,000 children with the disorder. Boys are
diagnosed with CAS more often than are girls. The
prevalence estimate is an educated guess, because fixed
criteria for the diagnosis have not been determined, or
at least have not been widely agreed upon in clinical
and research settings. Excessive diagnosis of CAS has
been discussed in the literature, although it is hard to
know how to identify an incorrect diagnosis (a “false-
positive” diagnosis) when the criteria for diagnosing
the disorder have not been firmly established.
CAS is thought to occur as part of the develop­
mental delays and disorders in several genetic condi-
tions. CAS can be said to have a known origin when it
is part of a known disease or syndrome (such as frag-
ile X syndrome, discussed in Chapter 8). Because the
majority of diagnosed CAS cases are not associated
with known genetic disorders, this chapter includes
CAS as a developmental speech sound disorder of
unknown origin.
CAS:  Speech Characteristics
Children diagnosed with CAS often have a severe
articulatory disorder. These children are likely to have
many speech sound errors, possibly including frequent
vowel errors. The vowel errors are notable because
vowels are mastered early in the course of speech
sound learning and are typically not observed as errors
in children diagnosed with speech delay.
3
 n example of the poor speech intelligibility of children diagnosed with CAS is found in Namasivayam et al. (2015, Figure 2, p. 539). Speech
A
intelligibility scores for word or sentence lists (number of correctly heard words/sentences by a group of listeners) that are less than 50% are
typically considered to indicate a severe intelligibility deficit. In Namasivayam et al., the average intelligibility scores for children with CAS
are no greater than 30% and as low as 7%.
As in AAS, speech sound errors are inconsistent
in CAS. A specific sound segment may be misarticu-
lated in different ways as a child repeats the same
word multiple times. The inconsistent errors may be
omissions, substitutions, or distortions; for some rep-
etitions of a word, the speech sound may be produced
correctly. Children diagnosed with CAS are likely to be
quite unintelligible as a result of the severe articulatory
disorder.3
Additional speech characteristics in CAS include
lengthened connections between speech sounds (that
is, longer transitioning movements between successive
sounds, similar to the “pulled apart” syllables in AAS),
disturbed prosody, articulatory groping, increased
articulatory errors with increased phonetic complexity,
and “unusual” phonetic errors such as the omission of
word-initial consonants (/æt/ for “cat”). Table 15–2
lists selected speech characteristics in CAS.
This list of speech characteristics in children with
CAS is in many cases similar or identical to the list of
characteristics described earlier for AAS. This seems
to validate the use of the term “apraxia” for both the
adult and child versions of this speech sound disorder.
In fact, the speech sound disorder in CAS is thought to
be the result of a motor programming disorder, as it is
in the adult form of apraxia of speech (ASHA, 2007).
There are interesting differences between the adult
and child versions of apraxia of speech. With very few
exceptions, the adult version is associated with known
neurological diseases such as stroke, Parkinson’s dis-
ease (review in Presotto, Rosenfeld Olchik, Schumacher
Shuh, & Reider, 2015), and dementia (e.g., Alzheimer’s
disease; review in Cera, Ortiz, Bertolucci, & Minett,
2013). In most cases of stroke, a region of damaged
brain tissue (a lesion) is seen in brain images. In Par-
kinson’s disease, lesion locations in the midbrain and
frontal lobe have been demonstrated at autopsy. Lesion
locations throughout the central nervous system have
also been demonstrated in Alzheimer’s disease and
other types of dementia.
Brain lesions in CAS have been difficult or impos-
sible to locate. Imaging studies have suggested size dif-
ferences in certain locations of the cerebral hemispheres
of children with CAS as compared with typically devel-
oping brain areas (ASHA, 2007). In at least one study,
children with CAS appear to have different connections
between brain areas compared with children who do
not have speech sound errors (Fiori et al., 2016).
 15  Pediatric Speech Disorders I 215

Table 15–2.  Selected Speech Characteristics in Childhood Apraxia of Speech

Characteristic Brief Description

Severe articulatory disorder
Sound errors are inconsistent
Lengthened durations between
adjacent syllables or individual
sounds
Disturbed prosody
Increased hesitation, groping,
and speech sound errors with
increased phonetic complexity
Unusual speech sound errors
(unusual in the process of normal
speech sound development)
Many speech sounds in error, including vowels;
children often have severe intelligibility deficits.
Multiple repetitions of one word by a child do not
always have sound errors that are the same. The sound
errors are variable in type.
Speech perceived as slow and lacking smoothness.
Speech characteristics that distinguish stressed from
unstressed syllables, which include pitch, loudness, and
duration, are atypical; melody of whole utterances may
seem atypical.
Multisyllabic words “bring out” apraxic errors more
than single syllable words; more complex syllables
(“spl” versus “sit”) also bring out more errors than
phonetically simple syllables.
Vowel errors may be common; word-initial consonants
may be omitted.

CAS and Overlap With Other
Developmental Delays
Some children with speech delay, as discussed previ-
ously, also have language and reading delays. In chil-
dren with CAS, language learning delays tend to be
more common and more severe than in children with
speech delay. Problems in language comprehension
and language expression, as well as literacy skills, have
been linked with CAS. The clinical opinion of many
SLPs is that the speech and language deficits associated
with CAS are likely to persist into the teenage years
and even into adulthood. The implications of these co-
occurring speech and language disorders for academic
and work-life success are clear and point to the need
for effective speech and language therapies for children
with CAS. Reviews of the co-occurring speech and lan-
guage deficits in CAS are available in ASHA (2007),
Peterson et al. (2007), Gillon and Moriarty (2007), and
Zaretsky, Velleman, and Curro (2010).
There are many treatments available for the child
who is diagnosed with CAS. Almost all treatment strat-
egies include a focus on the reduction of articulatory
errors for individual sound segments, in the same way
as treatment for speech delay. The focus on correction
of articulatory errors does not seem to reflect the view
of CAS as a programming disorder — that is, there is no
attempt to modify or correct the program for an articu-
latory sequence. It is not clear how a motor program
can be modified or corrected, although an argument
can be made that practice of multisyllabic words can
achieve this goal. A therapy like this for children with
CAS has been developed by Murray, McCabe, and Bal-
lard (2012) and has shown some preliminary, promising
results. Morgan, Murray, and Liégeois (2018) provide a
comprehensive review of therapies for CAS.
CAS and Genetics
As in speech delay, children with CAS have family
members with a higher probability of a history of CAS (or
other speech sound disorders) compared with typically
developing children. The interest in the genetic basis of
CAS was significantly motivated by study of a multi-
generational family in Great Britain (Lai, Fisher, Hurst,
Vargha-Khadem, & Monaco, 2001). Severe speech prob-
lems with characteristics resembling apraxia of speech
were identified in roughly 50% of the family members,
across generations and in both children and adults.
Many of the family members with apraxia of speech
also had intellectual disability (Chapter 8). Study of the
genetic profile of each of the family members revealed
that those with apraxia of speech shared an abnormality
216 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
of a single gene, on the seventh chromosome. The com-
mon gene abnormality among the family members with
apraxia of speech suggested the presence of a “speech
and language gene.” During embryonic development,
this gene abnormality was hypothesized to disturb
the regulation of other genes that are important to the
proper development of brain structures thought to be
active in speech and language development.
Since the original publication of the Lai et al. (2001)
report, several other gene abnormalities have been pro-
posed to be important in developmental speech and
language disorders. Some of these speech and language
disorders are characteristic of other diseases in which
there are many other problems. In these diseases, the
speech and language problems in CAS do not stand
alone, as in a “pure” version of CAS. At this point in
time, it seems clear that multiple genes play a role in
“pure” cases of CAS (see Box, “What Is ‘Pure’ CAS?”).
A review of genetic factors in CAS is found in Worthey
et al. (2013).
What Is “Pure” CAS?
In theory, “pure” CAS is a speech
sound disorder with a neurological basis. Pure
CAS, if it exists, is a speech motor control
disorder. The control of the nervous system
over movements of the articulators, larynx, and
respiratory system are compromised, resulting
in the selected speech characteristics listed in
Table 15–2. Other speech characteristics may
also be observed in pure CAS, but they are all
the result of a speech motor control problem.
More often, as described in the text, children
with CAS have other developmental delays
and problems including language and literacy
delays. If most children with CAS have these
additional problems that cannot be explained by
a pure disorder of speech motor control, why are
scientists interested in the identification of the
small number of children with the pure variety?
The reason is that pure cases may allow the iden-
tification of the genetic basis of the speech motor
control component of CAS. Stated in a different
way, perhaps the pure cases have a more focused
genetic basis — one or two gene abnormalities.
The genetic basis of the more frequent “CAS
plus language disorders” may be harder to pin
down because of the presumed larger set of
genes at work in the disorder (Morgan, Fisher,
Scheffer, & Hilde­brand, 2017).
Chapter Summary
Speech delay and CAS are presented in this chapter
as two speech sound disorders of unknown origin,
meaning that factors such as abnormal structural char-
acteristics of the speech mechanism, documented neu-
rological disease, intellectual disability, and/or hearing
loss are ruled out and therefore do not explain the
speech disorder.
Speech delay is a childhood speech sound disorder
with high prevalence and unknown origin; the charac-
teristics of the disorder include speech sound mastery
that is delayed relative to age and sex norms that are
documented as a part of standardized tests of articula-
tion, or by other measures.
Children with speech delay are most likely to have
speech sound errors for later-learned, as compared to
earlier-learned sounds, which presumably reflects the
more complex speech motor control skills required for
the later-mastered sounds.
Possible explanations for speech delay include
(but may not be limited to) immature speech motor
control, delayed learning of phonological rules, and
delayed speech perception skills, or some combination
of the three.
The speech intelligibility problem in speech delay
is partly, but not completely, a result of speech sound
errors. The speech intelligibility deficit that is due to
the speech sound errors is greater than expected for a
child’s age.
Speech delay may be associated with problems
in socialization and academic performance in grade
school and possibly into middle and high school.
Some children have /r/ and/or /s/ errors, called
residual errors, past the age (around 8 or 9 years) at
which speech sound mastery is typically completed.
A smaller number of children have persistent
speech sound errors for several speech sounds in addi-
tion to /r/ and /s/ errors.
Speech delay is frequently a communication com-
ponent of a more general language delay, which may
include language comprehension and/or expression
delay.
Children with speech delay are more likely to have
delays in reading ability compared with children who
have typically developing sound production.
Research evidence points to a genetic component
in speech sound disorders, including speech delay; the
genetic component is likely to involve multiple genes
that interact with the environment to make a child
more susceptible to speech delay, compared with chil-
dren who do not have these genes.

CAS is a relatively rare, severe speech sound dis-
order in which inconsistent, multiple speech sound
errors and prosodic disturbances are thought to be core
features.
Vowel errors, hesitation before initiating speech,
and groping for articulatory positions and shapes are
also speech characteristics observed in CAS.
The speech characteristics of CAS are similar
(but not identical) to the speech characteristics seen in
AAS.
As in AAS, the core and other speech characteris-
tics in CAS are hypothesized to be the result of a plan-
ning/programming problem in the brain mechanisms
that control speech production.
CAS is a disorder in which the diagnosis does
not have good-to-excellent reliability; there is dis-
agreement about the precise characteristics that point
to a diagnosis of CAS, and apparently many diagno-
ses of the disorder that turn out to be incorrect (“false
positives”).
Children with CAS are frequently diagnosed with
expressive and/or receptive language delay and with
poor literacy skills.
Children with CAS and language and liter-
acy delays are at risk for poor academic and career
achievement.
Like speech delay, there is interest in a possible
genetic basis for CAS.
Research publications over the last 20 years have
demonstrated the likelihood of a group of genes that
are associated with typical speech and language devel-
opment, and when mutated (when a gene is changed
from its typical properties) predispose a child to CAS
and language and literacy delays as well.
Speech-language treatments for CAS show prom-
ise and are still in the early stages of development and
evaluation.
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Pediatric Speech Disorders II
Introduction
Motor speech disorders in children are often discussed
separately from motor speech disorders in adults. Sev-
eral educated guesses for the separate discussion can
be offered. First, motor speech disorders in adults, as
discussed in the professional literature and reviewed
in Chapter 14, are almost always the result of acquired
neurological disease. In these cases, a previously healthy
adult has a stroke or other acute condition affecting the
brain. Dysarthria and apraxia of speech may also result
from neurological deficits resulting from degenerative
diseases such as Parkinson’s disease, amyotrophic
lateral sclerosis, and multiple sclerosis. Dysarthria in
adults may also be an outcome of a traumatic brain
injury; traumatic brain injury and motor speech disor-
ders in children are discussed later in the chapter.
When these conditions, and other neurological
diseases in adults, affect the neurological substrate of
the speech mechanism, the damage is to a fully mature
system, one in which speech motor control has been
established. Presumably, the speech motor control
skills developed and maintained over a lifetime may
be used by adults, to some degree, to compensate for
the loss of control associated with the acquired neuro-
logical damage.
In contrast, motor speech disorders in children
are associated with known or suspected neurological
16
damage present at birth or throughout childhood. The
neurological damage may be acquired in early child-
hood, as in the case of a child who has a brain tumor
removed surgically or experiences a penetrating or
closed head injury. It is safe to say that in the case of
childhood neurological disease, the development of
speech motor control is within the context of brain
mechanisms different from those of either healthy
adults, or in adults who acquire a neurological disease
after typical development of speech motor control. We
therefore expect speech behavior, developed within the
context of atypical brain mechanisms, to look different
from speech behavior of someone whose mechanisms
are mature and then damaged by an acquired disease
process. “Expect” is an important word in the previous
sentence: the difference between speech motor control
in children born with neurological disease (or acquir-
ing it very early in life) versus speech motor control
in previously healthy adults who acquire neurologi-
cal disease is a hypothesis. Firm data to support this
hypothesis are not yet available.
This chapter describes motor speech disorders in
children with cerebral palsy, traumatic brain injury, and
who have had surgical removal of tumors. The reader
is encouraged to review Table 14–1 in Chapter 14 as
preparation for the current chapter. Speech disorders in
hearing impairment, many cases of which are the result
of neurological disease, are discussed in Chapter 23.
219
220 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Childhood Motor Speech
Disorders:  Cerebral Palsy
Cerebral palsy is the most common motor disability
in childhood, with an estimated prevalence of 1.5 to
4 cases per 1,000 live births (Stavsky, Mor, Mastrolia,
Greenbaum, Than, & Erez, 2017). The estimated preva-
lence varies by race, country, and other factors beyond
the scope of this chapter; the range of 1.5 to 4 is thought
to encompass all of these varying estimates (see Stavsky
et al., 2017). Motor speech disorders are found in a
minimum of 20% and possibly as many as 50% of chil-
dren born with cerebral palsy (Nordberg, Miniscalco,
Lohmander, & Himmelmann, 2013). The motor speech
disorder in cerebral palsy is almost always dysarthria,
which results in speech intelligibility deficits. In a small
number of cases, apraxia of speech may co-occur with
dysarthria.
Cerebral palsy is a childhood disorder resulting
from brain damage incurred before, during, or shortly
following birth. The term “cerebral palsy” includes
several different types. A unifying feature of cerebral
palsy across types is the impairment of posture and
movement. When the impairment of movement is also
observed in the speech mechanism, dysarthria is a
likely result.
Roughly 40% to 45% of children with cerebral palsy
have intellectual impairment, which may range from
mild to severe (Reid, Meehan, Arnup, & Reddihough,
2018). In addition, about 40% of children with cerebral
palsy have some degree of hearing loss (Foo, Guppy,
& Johnston, 2013; Weir, Hatch, McRackan, Wallace, &
Meyer, 2018). Intellectual disability and hearing loss
are both associated with speech production problems.
Speech breathing, voice, prosodic, and sound errors in
cerebral palsy may therefore have more complicated
causes than a purely speech motor control problem.
Subtypes of Cerebral Palsy
The types of cerebral palsy have been classified in many
different ways since the disease was first described in
the mid-19th century (Morris, 2007). In this chapter, we
adopt a classification system in common clinical use
and that fits with a discussion of speech disorders in
cerebral palsy. The main types of cerebral palsy are
1
 ome scientists and clinicians add to this classification the number of limbs involved. For example, “spastic diplegia” indicates the spastic
S
type with symptoms observed in two limbs, “spastic quadriplegia” symptoms observed in all four limbs, and “spastic hemiplegia” symptoms
observed on just one side of the body (usually in both limbs).
2 
 ercentages vary in different surveys published in the literature. In all surveys, however, the spastic type of cerebral palsy clearly occurs with
P
the greatest frequency. As reviewed by Bugler, Gaston, and Robb (2019), the occurrence of the spastic type of cerebral palsy among all cases in
six major studies (including their own) ranged from 81% to 100% (average across all six studies = 91% spastic type, based on a total of 4,385
children diagnosed with cerebral palsy).
spastic, athetoid/dyskinetic, ataxic, and mixed.1 Recent
estimates of the occurrence of these types are 85% to
90% for the spastic type, 7% for the dyskinetic type,
and 4% for the ataxic type (Wimalasundera & Steven-
son, 2016).2 The most common mixed type is a com-
bination of spasticity and dyskinesia. Other subtypes
have been discussed in the literature, but they are rare
and not discussed here.
A brief review of neuroanatomical structures pro-
vides a framework for the following description of
cerebral palsy types. The corticobulbar and corticospi-
nal tracts (fiber bundles) connect cells in the primary
motor cortex to motor cells in the brainstem (corti-
cobulbar) and spinal cord (corticospinal). The basal
ganglia, a group of subcortical nuclei with connections
to cortical cells, play a major role in the planning, ini-
tiation, and execution of movements; the basal ganglia
also inhibit movement when it is not appropriate for
an action. Finally, the cerebellum is located beneath the
cerebral hemispheres, just behind the brainstem. The
cerebellum plays an important role in the coordination
of movements, and the smoothness with which the
movements are executed.
The Spastic Type of Cerebral Palsy
Spastic cerebral palsy is the outcome of damage to the
corticobulbar and/or corticospinal tracts. The damage
is likely to occur early in fetal development. Damage to
these tracts results in excessive muscle tone that results
in stiffness and weakness in affected structures (such
as a limb or the jaw). The excessive muscle tone may
be chronic. The constant contraction of wrist, arm, and
leg muscles may result in distorted postures of these
structures, even when they are not being used. Damage
to the corticobulbar and corticospinal tracts also results
in hypersensitive reflexes, which may be triggered by
a purposeful movement. These reflexes can interfere
with the movement and its goal.
The Dyskinetic Type of Cerebral Palsy
Dyskinetic cerebral palsy is the result of damage to
the basal ganglia. Dyskinesias are uncontrolled body
movements, either at rest or during purposeful move-
ments. Dyskinesias are sometimes described as writh-
ing, uncontrolled movements and have the potential

to interfere with proper movement control to achieve
a goal. A simple example of a disturbance in achieving
such a goal is the involuntary, uncontrolled movement
of the arm that interferes with the act of raising a fork
to the mouth.
The Ataxic Type of Cerebral Palsy
This relatively rare type of cerebral palsy results from
damage to the cerebellum. The function of the cerebel-
lum is to control posture and balance, coordination
of muscle contraction during voluntary movement,
and control of the force of muscle contraction to guar-
antee accuracy and scale of movement (how big or
small the movement is depends on the goal of a move-
ment). Cerebellar damage often results in disturbance
of these functions.
A child may be diagnosed with the ataxic type of
cerebral palsy when his feet are widely planted when
walking and he is unsteady. The diagnosis is rein-
forced if accuracy and force of movement are poorly
controlled. Walking may be delayed in babies with
suspected ataxia, and other milestones (e.g., sitting up)
may also be delayed.
The Mixed Type of Cerebral Palsy
Children diagnosed with the mixed type of cerebral
palsy are assumed (or known, as revealed by imag-
ing studies) to have damage in multiple parts of the
brain. As reviewed earlier, the mixed type of cerebral
palsy is infrequent, the most likely type being a spastic-
dyskinetic form of the disease.
Dysarthria in Cerebral Palsy
The dysarthria in cerebral palsy is often described by
the Mayo Clinic classification system, described in
Chapter 14. Children diagnosed with the spastic type
of cerebral palsy are typically judged to have spastic
dysarthria, the dyskinetic type of cerebral palsy have
hyperkinetic dysarthria (dysarthria resulting from
involuntary movements during attempts to move
articulators), and so forth. As in adult dysarthria, the
diagnosis of dysarthria type is made by perceptual
analysis. Also as in adults, the dysarthria diagnosis is
not necessarily matched to the diagnosis of cerebral
palsy type. Thus, a child diagnosed with the spastic
type of cerebral palsy may be perceived with hyperki-
netic dysarthria (or vice versa).
An important question is the extent to which the
dysarthria of a specific type in children has the same
speech characteristics as the adult dysarthria of the
same type. For example, does spastic dysarthria in
16  Pediatric Speech Disorders II 221
children with cerebral palsy sound the same, and on
careful analysis have the same characteristics, as spas-
tic dysarthria in adults who have suffered a stroke?
Keep in mind an important caution throughout
the description of speech characteristics in different
types of childhood dysarthria. For a particular type
of dysarthria, not every characteristic applies to each
child diagnosed with the type. There is a good deal of
variation from child to child in speech characteristics
of any single dysarthria type. This is similar to the case
of adult dysarthrias.
Spastic Dysarthria
According to Workinger (2005), children with the spas-
tic type of cerebral palsy have speech breathing and
phonation problems, with less-affected articulation.
The speech breathing and laryngeal problems result in
a weak voice and a strained voice quality (Solomon &
Charron, 1998). The strained voice quality, the result
of unusually strong muscle force in the larynx during
phonation, may be a compensation for the muscular
problems in the respiratory system and larynx. If the
natural result of spasticity in the larynx — excessive
muscle tone, for example — prevents the larynx from
closing during phonation, laryngeal muscles may
work too forcefully to overcome excessive “leaks” of
airflow through the vibrating vocal folds. Similarly, the
stiff muscles of the respiratory system that compress
the lungs may have difficulty generating the pressures
required for phonation. The low lung pressures and
consequently low airflows are tightly metered through
the larynx to conserve the limited air supply, resulting
in the strained voice quality.
More recent research (Lee, Hustad, & Weis-
mer, 2014; Levy, Chang, Ancelle, & McAuliffe, 2017;
Schölderle, Staiger, Lampe, Strecker, & Ziegler, 2016)
points to a more prominent role of disordered articu-
lation in children with the spastic type of cerebral
palsy and dysarthria. The outcome measure of inter-
est in these studies is speech intelligibility; increases
in the articulatory deficit result in decreases in speech
intelligibility. Another aspect of articulatory problems
noted by Lee et al. and Levy et al. is an abnormally
slow speaking rate in children with spastic dysarthria.
Slow speaking rates stretch out the duration of speech
sounds, which may contribute to problems with speech
intelligibility.
The results of Lee et al. (2014) and Levy et al.
(2017) are consistent with results reported by Platt,
Andrews, Young, and Quinn (1980), who performed
detailed analysis of sound errors and speech intelligi-
bility in young and older adults with the spastic type
of cerebral palsy. On average, approximately 20% of all
sounds in the words, including consonants and vowels,
222 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
were misarticulated. The average speech intelligibility
for these speakers was 59%. Platt et al.’s results sug-
gest a substantial role for speech sound errors in speech
intelligibility.
Are the data on speech sound errors reported for
adults with the spastic type of cerebral palsy applica-
ble to children with spastic dysarthria? A convincing
answer is not available. No one has done a study of
children with spastic dysarthria, similar to the study of
Platt et al. (1980), in which detailed phonetic transcrip-
tion was performed to identify speech sound errors.
However, Platt et al. compared the types of phonetic
errors they obtained to the same kind of analysis
reported by Byrne (1959) many years ago for children
with cerebral palsy. The pattern of errors in both stud-
ies was the same, suggesting (tentatively) that the adult
data may provide a partial model for speech sound
errors in children with cerebral palsy. The reason for
the exaggerated caution in the previous sentence is the
strong possibility of change in a child’s dysarthria char-
acteristics as he grows older, which may change the
similarity between the adult and child forms of spastic
dysarthria in cerebral palsy (Schölderle et al., 2016).
Prosody is also affected in spastic dysarthria. The
effect is a reduced ability to change the pitch of the
voice to produce the melody (intonation) of speech, and
Intelligibility Is More
Than Understanding
Words
Prosody is tricky. Melodies of statements
versus questions are different, but not always.
In general, “Who,” “what,” “where,” “when,”
and “why” questions have falling pitch at the
end of an utterance. Exceptions to this for “wh-”
questions occur when a speaker does not quite
get the question, or is in disbelief at the question:
“When do I get my allowance?” (typical falling
pitch) versus “When do I get my allowance?”
(rising pitch at the end, parent response in disbe-
lief that the question was asked). The inability
to control the melody of utterances can interfere
with a listener’s understanding of subtle shades
of meaning between these utterances that
share the same speech sounds. This potential for
communication failure extends to mood, which
is conveyed both subtly and in dramatic ways by
pitch change across utterances. Happy, sad, bored,
angry, hopeful, are all communicated by varia-
tions in the melody of utterances. The lesson is:
Intelligibility is more than understanding words.
the pitch contrasts for syllables in multisyllabic words.
Pitch contrasts at the sentence level are used to convey
meaning (as in the difference between statements and
questions) and emotion. Pitch contrasts for syllables in
multisyllabic words are an important component of lis-
tener word recognition. A word such as “copycat” has
two stressed syllables “cop” and “cat” surrounding an
unstressed syllable. The unstressed “ee” in “copy” is
very short, with a lower pitch compared with the two
stressed syllables. The pitch differences are part of lexi-
cal stress as indicated in dictionaries.
Compensation in the
Speech Mechanism
Like limb motor control strategies, adjustment of
the speech mechanism for changing or changed
conditions is not unusual. For example, when
speakers are asked to increase speaking rate,
they make articulatory movements that are
smaller than movements at “habitual” (normal)
speaking rates. This strategy allows the produc-
tion of more syllables per unit time — smaller
movements require less time. Speech therapy
that utilizes variations in speaking rate are based
on the idea that movements at a slowed rate are
larger than at habitual rates. A slowed rate gives
clients a better chance to produce the articula-
tory movements required to position articulatory
structures (the tongue, lips, soft palate) for
a correct speech sound. Another example of
compensation in persons with speech motor
control problems is a tightening of the larynx
to restrict the limited airflow coming from the
lungs. Individuals adjust one part of the speech
mechanism — in this case, the tightness of closure
during vocal fold vibration — to compensate for
another part (the respiratory system) that is not
functioning well. In some cases, the adjustment
can be excessive — like the strain-strangled voice
in spastic dysarthria that attempts to compensate
for weak airflow from the lungs.
Dyskinetic Dysarthria
Damage to the basal ganglia occurs in 10% to 20% of
children with cerebral palsy. The damage occurs later
in fetal development as compared with the earlier dam-
age thought to occur in the corticobulbar and cortico-
spinal tracts.
As reviewed earlier, damage to the basal ganglia
results in loss of control of speech structures. Articula-
 16  Pediatric Speech Disorders II 223

tory movements are directed to unintentional locations
within the vocal tract, and sudden, unintentional move-
ments disrupt these movements. Also, slow, unplanned
changes occur in structures that are intended to main-
tain articulatory and phonatory positions and shapes
for a limited amount of time. The writhing, changing
configuration of the lips for vowel sounds is one exam-
ple of this motor control problem. Another example is
the background muscular tone in the larynx that allows
the vocal folds to vibrate for phonation with controlled
pitch, loudness, and quality. The inability to stabilize
these background forces results in a lack of phona-
tory control. These motor control problems — really,
a group of motor control problems — are called dys-
kinesias (impairments of voluntary movement). The
older literature on types of cerebral palsy uses the term
“athetoid cerebral palsy” to describe these movement
problems. Currently, dyskinetic cerebral palsy is the
preferred term.
The involuntary, often constant movements in
the dyskinetic form of cerebral palsy are frequently
observed in structures of the head and neck. Many
children with dyskinetic cerebral palsy have random,
involuntary movements of the mouth and tongue. The
involuntary movements of the head and neck, and
especially of speech mechanism structures such as the
lips and tongue, are thought by many scientists and cli-
nicians to play a major role in the dysarthria observed
among many children with the dyskinetic type of cere-
bral palsy.
Dysarthria in the dyskinetic type of cerebral palsy
shares many characteristics with spastic dysarthria.
Both types have many speech sound errors and similar
patterns of errors across different speech sounds (Platt
et al., 1980). The lack of voice stability in dyskinetic
dysarthric is different from the strain-strangled voiced
quality in spastic dysarthria. Dyskinetic dysarthria
may have a more intermittent hypernasality (some-
times too nasal, other times not) compared with spastic
dysarthria in which the hypernasality may be more or
less constant.
Selected characteristics of spastic and dyskinetic
dysarthria in children observed directly or expected
from analyses of adult data are summarized in
Table 16–1. As stated above, not all characteristics are
seen in each child, and the severity of the characteris-
tics varies across children even when they share a com-
mon speech diagnosis such as spastic dysarthria.

Table 16–1.  Summary of Speech Characteristics of Children With the Spastic

and Dyskinetic Types of Cerebral Palsy and Dysarthria

Spastic type Speech breathing problems (difficulty generating positive

lung pressure and adequate airflows)
Weak voice; strain-strangled quality
Speech sound errors (consonants and vowels) contribute
heavily to speech intelligibility deficits
Slow speaking rate (lengthened sound durations)
Chronic hypernasality
Pauses (dysfluency)

Dyskinetic type Instability of phonatory (voice) pitch, loudness, and quality

Speech sound errors (consonants and vowels)
Intermittent hypernasality
Speech breathing problems
Pauses (dysfluency)
Prosody problems

Note.  Data from adults with the spastic type of cerebral palsy and dysarthria contribute to this
summary, mostly for the component of speech sound errors. Data from “Dysarthria of Adult
Cerebral Palsy: I. Intelligibility and Articulatory Impairment,” by L. G. Platt, G. Andrews, M.
Young, and P. T. Quinn, 1980, Journal of Speech and Hearing Research, 23, pp. 28–40; “Dysarthria
In Adults With Cerebral Palsy: Clinical Presentation and Impacts on Communication,” by T.
Schölderle, A. Staiger, R. Lampe, K. Strecker, and W. Ziegler, 2016, Journal of Speech, Language,
and Hearing Research, 59, pp. 216–229; Platt, Andrews, & Howie, 1980; and review of the adult
literature in “Acoustic-Phonetic Contrasts and Intelligibility in the Dysarthria Associated with
Mixed Cerebral Palsy,” by B. M. Ansel and R. D. Kent, 1992, Journal of Speech and Hearing
Research, 35, pp. 296–308.
224 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Ataxic Dysarthria This is an important consideration in the likelihood

of dysarthria in TBI. Morgan, Mageandran, and Mei
The ataxic type of cerebral palsy reflects damage to the
(2009) reported on an 8-year series of 1,895 children
cerebellum, or to the fiber tracts that connect the cer-
with a recent TBI and identified only 22 diagnosed with
ebellum with other parts of the central nervous system.
dysarthria. However, Morgan et al. point out that chil-
Although ataxic disorders in children who have a vari-
dren with more severe head injuries — the ones likely
ety of diseases are not exceedingly rare, the ataxic type
to have significant lifelong deficits — were also more
of cerebral palsy is. An estimate of the prevalence of the
likely to have dysarthria.
disorder is 0.1 cases per 1,000 live births (Musselman
TBI occurs as a result of motor vehicle accidents,
et al., 2014).
falls, sports-related accidents, and other mishaps. Most
The data on the dysarthria of the ataxic type of
children with a TBI show improvement following the
cerebral palsy are limited, largely due to the rareness
accident, and many show great gains over time and
of the disorder. In the small number of ataxic chil-
regain nearly normal function. This recovery includes
dren studied by Workinger (2005), the dysarthria was
speech and language function, and nearly full speech
judged to be mild. However, among dysarthric chil-
function may be recovered even when a child is mute
dren with the spastic, dyskinetic, and ataxic types of
shortly after the accident (Campbell & Dollaghan, 1995).
cerebral palsy, Nordberg, Miniscalco, and Lohmander
The brain damage in TBI is often diffuse, meaning
(2014) reported that the most severe speech symptoms
it includes widespread parts of the brain. Recall that
were observed for the ataxic children. The ataxic chil-
the brain is protected from the bony casing of the skull
dren had more severe consonant errors compared with
by the fluid surrounding it and a thick, hide-like cov-
the spastic and dyskinetic children.
ering which is the outer layer of the meninges. In TBI,
The number of children in the Workinger (2005)
the brain may be twisted and rotated at high accelera-
and Nordberg et al. (2014) studies is too small to draw
tions within this protective environment, resulting in
firm conclusions concerning the typical characteristics
injury to the fiber tracts connecting various cell groups
of the dysarthria in the ataxic type of cerebral palsy. It is
(nuclei). The axons — the parts of brain tissue that make
possible that these match speech characteristics that are
up the fiber tracts — are stretched and in some cases
well-documented in the adult literature on ataxic dys-
“sheared” by the twisting and rotating motion. There
arthria (Chapter 14). It is also possible that descriptions
also can be focused regions of damage in the brain, as
of ataxic dysarthria in children with cerebral palsy can
when the brain tissue beneath the point of impact on
be estimated from ataxic dysarthria in children who
the skull is damaged.
have had tumors removed from their brainstem or cer-
Children who suffer TBI are likely to have speech,
ebellum. These cases are reviewed in the next sections.
language, and cognitive symptoms that interfere with
their academic and social lives. One clinic’s experience
over a 5-year period suggests that approximately 15%
Childhood Motor Speech of the children seen for TBI-related services will have
Disorders: Traumatic some form of dysarthria (Hodge & Wellman, 1999).
Brain Injury and Tumors

Traumatic Brain Injury Prevalence and

The diagnostic category traumatic brain injury (TBI) is
separated into closed-head injuries and penetrating
head injuries. Closed-head injuries include blows to the
head that leave the skull more or less intact but result
in brain damage. In penetrating head injuries, an object
(such as a bullet or bomb fragment) pierces the skull
and enters the brain. Here we limit our discussion to
closed head injuries.
In the United States, the prevalence of childhood
TBI has been estimated at 2.5%; approximately 18%
of children with lifelong effects from a TBI have dys-
arthria and language deficits (Haarbauer-Krupa, Lee,
Bitsko, Zhang, & Kresnow-Seddaca, 2018). Note the
phrase, “lifelong effects,” in the preceding sentence.
Incidence — Part I
The term “prevalence” refers to the existing
number of cases of a disorder or condition at a
given time; “incidence” refers to the number of
“new” cases over some time period, such as at
birth, or over the course of a year. Analysis of
prevalence and incidence are ways to estimate
the “true” numbers in the whole popula-
tion — think, for example, of doing a study that
sampled the entire population in the United
States for prevalence of fourth ventricle tumors.
Thus, percentages vary across investigators
because they are estimates, not true values.

Dysarthria in TBI
Speech breathing, voice, velopharyngeal function, and
articulation are likely to be affected in children with TBI
and dysarthria (Morgan et al., 2009). The Mayo Clinic
system categories (Flaccid, Spastic, Ataxic, Hyperki-
netic, Hypokinetic, Mixed) have been used to describe
the speech of these children, but in all likelihood, the
“mixed” type is the most frequent. This reflects the dif-
fuse brain injury in TBI. Chronic hypernasality, slow
speaking rate, voice quality abnormalities, prosodic
abnormalities (including inappropriate pauses), and
imprecise consonants and vowels are heard frequently
in this clinical group.
Results of a brain imaging study suggest that the
corticobulbar tract is frequently damaged in children
with TBI and dysarthria (Liégeois, Tournier, Pigdon,
Connelly, & Morgan, 2013). As discussed earlier, the
spastic type of cerebral palsy is associated with dam-
Prevalence and
Incidence — Part II
In the series of children analyzed by Morgan
et al., 1.2% were diagnosed with dysarthria. This
series of children was a consecutive one — the
children were not selected for the study based
on a characteristic other than being diagnosed
with a TBI. This means that the sample of 1,895
children included mild, moderate, and severe
cases. When cases are chosen only for severe TBI,
a greater percentage of children are diagnosed
with dysarthria. A different series of patients
with TBI, over a 5-year period, estimated a 15%
occurrence of dysarthria (Hodge & Wellman,
1999). Children in Hodge and Wellman came to a
speech-language clinic seeking services, whereas
children in the Morgan et al. (2009) study were taken
from a social medicine registry in Australia,
and no doubt included many cases in which
services were not pursued. Thus, the Moran
et al. sample probably included many more mild
cases (hence, not seeking services for speech and
language problems) compared with Hodge and
Wellman. When Morgan et al. extracted from
the total sample only those children who had
been referred for services to a speech-language
pathologist, 14% of the children were diagnosed
with dysarthria, a number very similar to the
one reported by Hodge and Wellman. These
percentages are estimates of prevalence, not inci-
dence, and many variables affect the estimates.
16  Pediatric Speech Disorders II 225
age to the corticobulbar and corticospinal tracts. Based
on the imaging data of Liégeois et al., spastic dysar-
thria alone or in combination with another dysarthria
type might be expected to occur frequently among
children with TBI and dysarthria. When diffuse injury
affects both cerebral hemispheres or the tracts between
cortical motor cells and motor cells in the brainstem
and/or spinal cord, the dysarthria is severe. In these
cases, there is a poor outlook for improvement of the
dysarthria.
Brain Tumors
Tumors in the region of the fourth ventricle are called
posterior fossa tumors; they are relatively rare. The
posterior fossa is a cradle within the skull base in
which the posterior structures of the brain — the brain-
stem, fourth ventricle, and cerebellum — are contained.
These structures are immediately below the occipital
lobes of the cerebral hemisphere. The occipital lobes
are the most posterior of the four lobes of the cerebral
hemispheres.
Posterior fossa tumors are typically cancerous and
are removed surgically. Often the surgery is followed
by radiation and/or chemotherapy.
Dysarthria in Brain Tumors
Approximately 50% of childhood brain tumors are
located in and around the fourth ventricle. The fourth
ventricle is the diamond-shaped cavity located between
the posterior wall of the brainstem and the anterior
wall of the cerebellum (see Chapter 2, Figure 2–8).
The fourth ventricle is one of the cavities in the brain
through which cerebrospinal fluid flows. A tumor in
this area exerts pressure on brainstem and cerebel-
lar structures and causes disruptions of the functions
served by those structures. Two of those important
functions are speech and swallowing.
The cerebellum plays a major role in the coordina-
tion of muscles of the respiratory system, the larynx,
and the articulators to produce speech smoothly and
with syllable sequences that sound “seamless.” A dis-
ease process that interferes with cerebellar function dis-
rupts coordination and makes speech sound choppy,
as if consecutive syllables, and even sounds within a
syllable, are pulled apart.
The cranial nerves are connected directly to mus-
cles of the larynx and articulators and issue the final
commands to control contraction characteristics such as
force and timing. Muscle contraction strength is weak
and ineffective when cranial nerves that serve head and
neck muscles are affected by a disease process.
226 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Many children with posterior fossa tumors have
dysarthria. Shortly after surgical removal of the tumor,
approximately 10% to 33% of the children have a con-
dition called cerebellar mutism (compare Morgan et
al., 2011, to Tamburrini, Frassanito, Chieffo, Massimi,
Caldarelli, & Di Rocco, 2015). In this stage of postsurgi-
cal recovery, children are mute (unable to speak) for a
variable period of time. The duration of mutism can be
2 weeks or more, although some children with cerebel-
lar mutism begin to speak within hours or a few days
after the surgery.
Children who are mute and then regain an abil-
ity to speak usually have dysarthria, which typically
improves but not necessarily to the point of normal
speech. The disruption of cerebellar and cranial nerve
speech functions by a posterior fossa tumor may be
expected to result in a flaccid dysarthria, or a cerebellar
(ataxic) dysarthria, or a mixed flaccid-ataxic dysarthria
(Chapter 14). Some authors endorse this expectation,
based on their data (Morgan et al., 2011), whereas oth-
ers do not (De Smet et al., 2012). Children who are not
mute following surgery often regain normal speech
abilities even when dysarthria is present during the
early days of their recovery.
Treatment Options and
Considerations
The end-goal of speech-language pathologists when
treating children with neurologically based speech dis-
orders is to improve speech intelligibility. Publications
in the speech-language pathology literature provide
preliminary evidence that speech-language therapy
can result in positive gains in the outcome goal of
improved intelligibility.
In one approach, speech-language pathologists
focus initially on simple strength and coordination of
structures of the speech mechanism. The idea behind
this first step is to provide a foundation for the more
complex motor control requirements of speech produc-
tion. These therapy activities are called oro-motor non-
speech exercises, because they are done in the absence
of phonation (voice) or articulatory movements.
For example, the lips and tongue can be exercised
by having a child compress his lips together as force-
fully as possible or push his tongue against a resistance
(e.g., using tongue protrusion to move a barrier placed
in front of the lips). The analogy to increasing strength
in an arm or leg by exerting high limb force and press-
ing against resistances is direct. Nonspeech exercise is
also extended to muscles of the respiratory system that
support speech breathing (Chapter 10). These muscles
can be strengthened by a program of forceful exhala-
tion through an airflow resistance. The airflow resis-
tance is provided by a tube containing a float that is
displaced by incoming air, or a wire mesh screen held
in place by a face mask. Forceful exhalation exercises
rib cage muscles used to raise lung pressures required
to vibrate the vocal folds and achieve an effective voice
loudness.
When a child succeeds in completing multiple tri-
als of the nonspeech exercises, a layer of motor com-
plexity is added to the task. One version of this is to
train the child to coordinate the initial part of expi-
ratory airflow with phonation of a sustained “ah.”
Although this seems to be a very simple task, many
children with either cerebral palsy or a TBI are chal-
lenged by it. When the training of coordinating speech
breathing with phonation results in good performance,
a child may be trained to open her jaw wide during
phonation to produce a louder sound.
These exercises are hierarchical, in the sense that
separate training tasks are sequenced to build on sim-
ple skills and make them increasingly complex. In the
sequence just described, there is no mention of direct
training of articulatory skills. Some therapeutic pro-
grams may, in fact, not have a major goal of training
articulatory skills. Rather, the foundation of stronger
speech muscles, coordination of speech breathing,
and increased vocal loudness are thought to have a
“spreading effect” to articulatory skill. Even in the
absence of training to produce (for example), good fric-
ative, vowel, rhotic and lateral sounds, the improved
foundation of speech motor skills leads to improved
articulatory behavior. The overall effect of the therapy
is better speech intelligibility — the long-term outcome
goal of speech therapy.
A small amount of research evidence is available to
support the connection between a stronger foundation
of speech motor skills and improved speech intelligibil-
ity. In both young (5 to 11 years old) and older children
(12 to 18 years) with cerebral palsy, speech intelligibil-
ity for single words improved between 9% and 14% fol-
lowing the therapy previously described (Pennington,
Miller, Robson, & Steen, 2010; Pennington, Roelant,
Thompson, Robson, Steen, & Miller, 2013). Not every
child in these studies had improved intelligibility fol-
lowing the therapy, but the overall improvement for
the groups of children is encouraging.
Whether or not the examples of speech therapy in
children with cerebral palsy can be generalized to chil-
dren with tumors of the fourth ventricle or with a TBI
is unknown; the appropriate studies are not available.
Clark (2003) provides a review of treatment in neuro-
logical speech disorders.
When a child has severe dysarthria, and is either
completely unintelligible or barely intelligible, therapy

approaches exist to provide the child with communi-
cation options. Augmentative and alternative com-
munication (AAC) technology can supplement (aug-
mentative) or substitute (alternative) for the severely
impaired speech skills. AAC can be low-tech, such as
an alphabet board that allows users to spell words or
a picture board to convey simple ideas, or high-tech,
such as speech synthesizers, controlled by hand, a light
pointer, or eye movements, like the one used by the
famous physicist Stephen Hawking. AAC options are
adapted to each user’s needs and capabilities, under
the guidance of a specialist, to make communication
available to those children who cannot speak.
Chapter Summary
Motor speech disorders in children are discussed sepa-
rately from motor speech disorders in adults because
the effects of neurological disease on a child’s speech
are in the context of a developing brain, while in adults
the effects are in the context of a previously developed
and mature brain.
Cerebral palsy is the most common motor disabil-
ity in childhood, and it has been estimated that dysar-
thria is present in 20% to 50% of the diagnosed cases.
The major types of cerebral palsy are spastic, dys-
kinetic, and ataxic, with the majority of children with
cerebral palsy having the spastic type.
The spastic type of cerebral palsy results from
damage to the corticobulbar and corticospinal tracts,
the dyskinetic type from damage to the basal ganglia,
and the ataxic type from damage to the cerebellum and
its tracts connecting it to other parts of the central ner-
vous system.
The types of dysarthria in children with cerebral
palsy are often matched to those in adults with dys-
arthria: spastic dysarthria in the spastic type, hyper-
kinetic dysarthria in the dyskinetic type, and ataxic
dysarthria in the ataxic type.
The perceptual analysis used to diagnose the dys-
arthria type may not match the diagnosed type of cere-
bral palsy (e.g., spastic dysarthria may be diagnosed in
a child diagnosed with the dyskinetic type of cerebral
palsy).
Spastic dysarthria in cerebral palsy is thought to
result from stiff muscles which are the result of exces-
sive tone in speech structures such as the larynx and
tongue.
The speech characteristics in spastic dysarthria
include sound errors (consonants and vowels) and
problems with prosody; these characteristics result in
speech intelligibility deficits.
16  Pediatric Speech Disorders II 227
Hyperkinetic dysarthria in cerebral palsy is
thought to result from uncontrolled movements of the
speech structures, and muscle tone that is constantly
changing.
The speech characteristics in dyskinetic dysarthria
are similar to those in spastic dysarthria, including
problems with speech intelligibility.
Ataxic dysarthria in cerebral palsy is thought to
result from coordination problems among the articula-
tors, larynx, and respiratory system.
The speech characteristics in ataxic dysarthria are
not well understood because of the small occurrence of
the ataxic type of cerebral palsy, and a lack of relevant
studies.
Traumatic brain injury (TBI) associated with a
closed head injury results in diffuse damage to brain
tissue, as well as focal (one part of the brain) injuries.
Children with TBI often have cognitive, social,
and speech and language problems, many of which
improve over time; approximately 15% of children
with TBI have dysarthria.
The dysarthria in TBI is likely to be a mix of the
Mayo categories and to include slow speaking rate,
hypernasality, abnormal voice quality and prosodic
deficits, and speech sound errors.
Posterior fossa tumors are located in and around
the fourth ventricle and may result in muteness imme-
diately after surgery, followed by a period of recovery
of speech skills; many children regain nearly normal
speech following surgery, but some children have dys-
arthria as a long-term communication disorder.
In preliminary studies, speech therapy has been
shown to be effective in children with dysarthria, espe-
cially when the focus of the therapy is improvement of
speech intelligibility by working on basic strength and
coordination skills as the foundation for more complex
speech motor tasks.
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Fluency Disorders
Introduction
A diagnosis of stuttering is made when a child or adult
cannot maintain the normal flow of speech even when
there is no firm evidence of a disease process or struc-
tural problem affecting the peripheral speech mecha-
nism (respiratory system, larynx, upper articulators) or
the brain. Typically, the diagnosis is made by listening
to the child (or adult) and counting dysfluencies.
Historically, stuttering has been mysterious and
intriguing because it is a speech problem of unknown
cause. In keeping with contemporary scientific and
clinical literature on fluency disorders, we use the term
“people who stutter” (PWS), among whom are chil-
dren who stutter (CWS) and adults who stutter (AWS).
Stuttering behavior is variable. PWS may have
severe episodes of stuttering in some situations but
not others. PWS may enjoy extended periods of appar-
ent fluency, preceded and followed by long periods of
severe stuttering behavior. Within a matter of minutes,
certain types of speech may be produced with severe
stuttering, whereas other types (e.g., singing, perhaps
talking to a pet) may be completely fluent. Stuttering is
therefore not a fixed set of symptoms, but rather a vari-
able set of behaviors. For children who are diagnosed
with stuttering around age 3 years and who continue
to stutter past the age of 5 or 6 years and into the teen-
age years and adulthood, nonspeech behaviors may be
associated with stuttering (Table 17–1, discussed later).
17
Incidence and Prevalence
of Stuttering
A great deal of research has been devoted to the inci-
dence and prevalence of “childhood-onset fluency
disorder” (Yairi & Ambrose, 2013). Childhood-onset
fluency disorder (hereafter, developmental stutter-
ing), classified in the Diagnostic and Statistical Manual
of Mental Disorders (American Psychiatric Associa-
tion [APA], 2013) as a neurodevelopmental disorder,
begins in very early childhood, perhaps as early as
2 years of age. “Incidence” is the percentage of new
diagnoses of a disorder within the population, over a
given time period (such as a year). “Prevalence” is an
estimate of the percentage of the population who stut-
ter at a particular point in time. The contrast between
incidence and prevalence of all cases of stuttering
(including CWS and AWS) is particularly important
to understanding the developmental nature of the
disorder.
The focus in this chapter is on developmental stut-
tering because the great majority of cases are diagnosed
well before the age of 6 years. One estimate of the aver-
age onset age of stuttering is 33 months.
A conservative estimate of the incidence of stut-
tering is 5% to 8% of the population (Yairi & Ambrose,
2013). As previously noted, this estimate includes all
children and adults newly diagnosed within a fixed
period of time. In contrast, the prevalence of stuttering ​
229
230 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Table 17–1.  A Brief, Natural History of Stuttering

Age Range
Stage (years) Core Behaviors Secondary Behaviors
Typical dysfluencies 1.5–6 • Low number of dysfluencies None
• Part-word or single syllable
repetitions
• Possible sound prolongations
and “tense” pauses
• Revisions more frequent
over time

Borderline stuttering 1.5–6 • High number of dysfluencies Rare

• Multiple syllable repetitions

Beginning stuttering 2–8 • Rapid, multiple repetitions • Escape behaviors (e.g.,

with tension eyeblinks, “um’s”)
• Blocks • Frustration (awareness)
• Difficulty initiating words

Intermediate stuttering 6–13 • Blocks • Escape behaviors to

• Repetitions, prolongations terminate blocks
• Avoidance behaviors
(sounds, words, situations)

Advanced stuttering >14 • Long, tense blocks • Sophisticated escape and

• Repetitions, prolongations avoidance behaviors

• Lip, jaw tremors

Note. It has been argued that a group of children, perhaps about one-third of all children who are diagnosed with child-
hood stuttering, do not begin stuttering behavior with easy repetitions, as summarized in text and this table. Rather, these
children show initial symptoms that look more like intermediate or advanced stuttering, with tense blocks and struggle
behavior. This sudden onset of more severe symptoms, rather than the gradual onset and progression summarized in
this table, does not seem to predict which children will have persistent stuttering and which children will have natural
recovery. See Guitar (2005) and Yairi & Ambrose (2005) for more details. Adapted from Stuttering: An Integrated Approach
to Its Nature and Treatment, by T. J. Peters and B. Guitar, 1991, Baltimore, MD: Williams & Wilkins; Stuttering: An Integrated
Approach to Its Nature and Treatment (3rd ed), by B. Guitar, 2005, Baltimore, MD: Lippincott Williams & Wilkins.

— all CWS and AWS — is 1% of the population, or even
a bit lower (Yairi & Ambrose, 2013).
The lower prevalence, compared with the inci-
dence, reveals a critical characteristic of stuttering:
roughly 80% of children who are diagnosed with stut-
tering as toddlers recover without therapy. This “natu-
ral recovery,” which currently is not well understood,
results in a higher incidence than prevalence. Many
children included in the incidence estimate do not con-
tribute to the prevalence estimate — they become flu-
ent and are not included in the estimate of “percentage
of people who currently have the disorder.” Children
who do not recover fluency in childhood are said to
have persistent stuttering.
Diagnoses of stuttering in toddlerhood are made
about equally for boys and girls. Girls, however, are
much more likely than boys to recover naturally.
Roughly 80% of children who recover fluency after
the early diagnosis are girls. Because of the difference
in recovery rates between girls and boys, the ratio of
males to females who stutter in teenage years and
adulthood is about 4:1.
There is little evidence that the incidence and prev-
alence of stuttering varies in a significant way across
countries, cultures, races, and socioeconomic groups.
Thus, the population of any of these groups (countries,
cultures, and so forth) can be multiplied by1% to arrive
at the number of people who currently stutter in that
group (see http://www.nsastutter.org/ and https://
www.stutteringhelp.org/).

Genetic Studies
Research since the 1960s and extending to the present
time leaves little doubt that stuttering or a predisposition
to stuttering is transmitted from parent to child (Etch-
ell, Civier, Ballard, & Sowman, 2018; Smith & Weber,
2017). As reviewed by Peters and Guitar (1991), “family
tree” studies from the 1960s and 1970s showed that PWS
were far more likely to have a first-degree relative who
stuttered, when compared with a control group of flu-
ent speakers. Twin studies (see Andrews, Morris-Yates,
Howie, & Martin, 1991; Felsenfeld et al., 2000) added to
the evidence for a genetic component in stuttering. The
results of these studies were striking. If one member of
an identical twin pair stuttered, the likelihood of stutter-
ing in the other member of the pair was about 70%. In
contrast, if one member of a fraternal (nonidentical twin
pair) stuttered, there was only a 25% to 30% likelihood of
stuttering in the other member of the pair. Identical twins
are genetically the same; fraternal twins are genetically
no more similar than any siblings from the same family.
The much higher likelihood of stuttering in both mem-
bers of identical twins, as compared to fraternal twins,
provides strong evidence of a genetic component in stut-
tering. Frigerio-Domingues and Drayna (2017) provide
an up-to-date review of twin studies and stuttering.
The specific nature of the genetic component in
developmental stuttering remains unknown. Candi-
date genes for stuttering have been suggested but for
the time being are best regarded as hypotheses rather
than settled fact (Frigerio-Domingues & Drayna, 2017;
Yairi & Ambrose, 2013). Whatever genetic component
exists in developmental stuttering is probably more a
predisposition for stuttering, rather than a guarantee of
stuttering (see Chapters 7 and 15 for similar observa-
tions on a genetic component in pediatric language
disorders, and speech sound disorders, respectively).
This is consistent with the high but not perfect occur-
rence of stuttering in identical twins. As noted by Smith
and Weber (2017), the “expression” of genes is shaped
by the environment. If there is a stuttering gene (or
genes), it does not guarantee stuttering in a child who
has received the gene(s) from a parent.
Diagnosis of Developmental
Stuttering
Dysfluencies are a normal part of speech and language
learning in toddlers. How, then, is stuttering diagnosed
in a young child? How are normal dysfluencies distin-
guished from dysfluencies that suggest a diagnosis of
developmental stuttering?
17  Fluency Disorders 231
Ambrose and Yairi (1999) used the term “stuttering-
like dysfluencies” (SLDs) to identify instances of dysflu-
ency that are typically not seen in children who develop
fluent speech. More specifically, children perceived to be
stuttering, by parents or other caretakers, made multiple
repetitions of single syllables (in multisyllabic words) or
of single-syllable words. “Multiple repetitions” means
at least three to five syllable repetitions (e.g., “buh-buh-
buh-buh . . . ”). These repetitions were produced easily,
with no apparent struggle, and rapidly. Children devel-
oping fluent speech often produced only a single repeti-
tion of a single syllable or a single-syllable word.
Ambrose and Yairi (1999) computed the number of
SLDs per 100 syllables spoken by fluent children and
by children with suspected stuttering. Children with
typically developing fluency produced, on average,
less than one SLD per 100 syllables spoken. Children
with suspected stuttering onset produced at least three
such dysfluencies per 100 syllables. Although there
were other types of SLDs, multiple syllable repetitions
were the dominant sign of the onset of developmental
stuttering. Types of SLDs are listed in Table 17–2.
The Natural History of
Developmental Stuttering
Developmental stuttering can have a sudden onset in
toddlers, with symptoms that develop slowly or rapidly.
Because the development of stuttering occurs through-
out the same time period as speech-sound and language
development, a potential interaction between fluency
and speech and language skills has been discussed in
the literature (see Smith & Weber, 2017, for a summary).
These interactions are discussed later in this chapter.
Table 17–2.  Types of Stuttering-Like Dysfluencies
(SLDs) Observed in Children Who Stutter (CWS)
SLD Example
Sound, syllable and/ “b-b-b-but . . . ”
or single-syllable “buh-buh-buh . . . ” (for “but”)
repetition
Whole-word repetition “but, but, but . . . ”
Sound prolongations “Ffffffffffffine”
Blocks Inaudible stoppage of speech
with mouth open or closed;
inability to initiate sounds
Note.  Adapted from https://www.asha.org/practice-portal/clinical-
topics/childhood-fluency-disorders/
232 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Early symptoms of developmental stuttering, such
as the easy repetitions described earlier, to advanced
stuttering behavior can be described as a sequence of
behaviors. We call this the natural history of persis-
tent stuttering. The abbreviated description given here
owes much to information published by Peters and
Guitar (1991), Guitar (2005), Yairi and Ambrose (1999),
and Yairi and Seery (2015).
Table 17–1 provides a summary of this history. As
in all cases of normal and disordered speech and lan-
guage development, child-to-child variability is to be
expected. The age ranges and characteristic symptoms
listed in Table 17–1 are general guidelines to the devel-
opment of stuttering, rather than fixed milestones.
Table 17–1 contains columns labeled Core and
Secondary Behaviors. The distinction is important in
the natural history of developmental stuttering. Core
behaviors are actual speech behaviors produced by a
person who stutters. These include syllable and word
repetitions, “blocks” (stoppages) in the stream of
speech, and prolongations of speech sounds.
Secondary behaviors are learned behaviors in
PWS. These are reactions to the difficulty of producing
a fluent stream of speech. Secondary behaviors include
almost anything with the purpose of avoiding or escap-
ing an ongoing or anticipated SLD (Peters & Guitar,
1991; Guitar, 2005). Secondary behaviors include
“um”s, hesitations, and body part movements such as
blinking or turning the head (as well as others).
Stage I: Typical Dysfluencies
As noted earlier, toddlers have dysfluencies that are
typically single repetitions of syllables or words. Exam-
ples of these typical dysfluencies are part-word (“mi-
milk”) or whole-word (“milk-milk”) repetitions and
single repetitions of syllables in multisyllabic words (as
in “do-doggie eat”). Sound prolongation (“sssssssee”)
is another type of typical dysfluency. Many scholars
interested in the development of stuttering have sug-
gested that these early dysfluencies make sense because
children are learning complex aspects of language such
as syntax, vocabulary, and grammatical morphology. In
addition, children are trying to output this complicated
new stuff of language through a system — the speech
mechanism — that is undergoing growth and matura-
tion of motor control. Some hesitations, repetitions, and
movement prolongations should be expected, as with
the initial learning of any complicated skill.
The distinction between typical dysfluencies and
SLDs is important — children who are diagnosed with
developmental stuttering are best served when they
receive clinical services at the earliest possible age
(Conture, 2001).
Table 17–1 contrasts “typical” dysfluencies like the
“mi-milk” or “do-doggie” examples given, with SLDs
such as “Mi-mi-mi-milk” or “Do-do-do-doggie.”
Even when a young (preschool) child produces
multiple repetitions and is considered for a diagnosis
of developmental stuttering, the repetitions are likely
to sound relaxed and without struggle. As the fluency
problem develops, frequent signs of struggle with the
flow of speech are important in the diagnosis of stutter-
ing as a potentially persistent problem.
Research suggests that typical dysfluencies are
fairly rare when actually counted. In Table 17–1, the
entry “low number of dysfluencies” for Stage I indi-
cates the relative rareness of dysfluent events in typical
speech-language development.1
Note in Table 17–1 the fairly wide age range for
typical dysfluencies during speech and language devel-
opment. Peters and Guitar (1991) summarize research
suggesting that, as typically developing children mas-
ter speech production skills, part-word and whole-
word repetitions become less frequent, and revisions of
the repetitions more frequent. Children age 2 years and
5½ years may both have “normal” dysfluencies, but the
younger child repeats more, whereas the older child
has few repetitions but more revisions (e.g., “I was
going . . . when I left I went . . . and before I left . . . ”).
Stage II:  Borderline Stuttering
Borderline stuttering covers the same age range as the
period of “typical” dysfluencies (Table 17-1). Border-
line stuttering is distinguished from typical dysfluency
in the following two ways: (a) dysfluency becomes
more frequent in children with borderline stuttering,
compared with typically developing children, and
(b) part- or whole-word repetitions include three or

1
 he actual number of dysfluencies per 100 words that distinguishes typically dysfluent children from those who are diagnosed later with
T
stuttering varies somewhat in different studies. Peters and Guitar (1991) summarized research to the date of publication of their text and sug-
gested that typically developing children had fewer than 10 dysfluencies per 100 words spoken, whereas children who stutter (or who would
eventually be diagnosed with stuttering) had 16 to 20 dysfluencies per 100 words. Yairi and Ambrose (1991) used a much more stringent cri-
terion, separating beginning stutterers from those with “typical” dysfluencies with a criterion of 3 dysfluencies per 100 words spoken — more
than 3/100, and the child was considered to be atypically dysfluent.

more consecutive repetitions in borderline stuttering.
For the most part, the child who meets criteria for bor-
derline stuttering shows no secondary behaviors. Occa-
sionally, the child with borderline stuttering may begin
to show some frustration with the repetitions.
As noted by Guitar (2005), there is substantial
gray area between the stages of typical dysfluency and
borderline stuttering. The behaviors outlined here for
the two stages may blend together and even shift over
time. Sometimes the child may seem to have typical
dysfluencies; other times, SLDs suggest borderline
stuttering. The child who fits criteria for borderline
stuttering may, in fact, become fluent in the near future;
a smaller number of children in this category continue
to show stuttering behavior.
Stage III:  Beginning Stuttering
Beginning stuttering, which may be diagnosed across
a wide age range of 2 to 8 years but rarely after about
6 years of age, differs from borderline stuttering in
several ways. First, the multiple, part-, or whole-word
repetitions are produced very rapidly. These repeti-
tions sound less controlled than the easy, relaxed rep-
etitions heard in borderline stuttering. The repetitions
of beginning stuttering also appear to be produced
with tension, indicating signs of struggle with the flow
of speech.
Another sign of tension in beginning stuttering
is the presence of blocks — the complete stoppage of
speech. The child seems to get “stuck” on a speech
sound. Blocks may occur with the child’s mouth open,
or closed, but it is clear that he or she is trying to pro-
duce speech but cannot release the air required to
maintain the flow of syllables. Blocks may last for a
second or two, or much longer.2
Beginning stuttering is often accompanied by
the onset of secondary behaviors. Now the child who
stutters incorporates escape behaviors into his or her
attempt to speak. These behaviors are meant to assist
the child in reestablishing the flow of speech when it is
interrupted by a series of repetitions or blocks or sound
prolongations (Peters & Guitar, 1991). Eye blinks, head
nods, or even slapping a hand against the body, are
used to “release” a stuttering episode, to trigger the
resumption of the smooth flow of speech. The child
who meets the criteria for the beginning stage of stut-
tering shows awareness of his or her fluency problems
2 
 hen I was an undergraduate student, I had a clinical assignment in a summer residential program for AWS. The day I was introduced to
W
one of the young men assigned to work with me, the client began to introduce himself and when he came to his name, he had an open-mouth
block that lasted well over 30 seconds.
17  Fluency Disorders 233
and may feel a good deal of frustration with the inabil-
ity to produce fluent speech.
Stage IV:  Intermediate Stuttering
Intermediate stuttering is an elaboration of behaviors
seen in beginning stuttering. Blocks, repetitions, and
sound prolongations are heard in the child’s speech
with increasing frequency and severity. In the interme-
diate stage of stuttering, the child uses escape behav-
iors to release blocks and other dysfluencies, and
begins to use and refine avoidance behaviors. Avoid-
ance behaviors may be associated with specific speech
sounds and/or words, communication partners, and
communication situations. For example, the child in
the intermediate stage of developmental stuttering
may have sufficient experience with dysfluency to
know that the “m” sound is particularly difficult and
may begin to avoid words beginning with this sound.
Or, the child may have a history of dysfluency with a
person’s name, and avoid saying it.
Avoidance of specific sounds and words reflects
anticipation of upcoming dysfluencies, and often
leads to a search for a different way to communicate
the same thought. Such behavior may involve revi-
sions, hesitations, and insertions of “um’s” to give the
child time to find an “easier” way to produce the mes-
sage. Children in the intermediate stage of stuttering
begin to connect their stuttering with negative conse-
quences, and, like all of us, look for ways to avoid the
negative feelings.
Stage V:  Advanced Stuttering
The age range of 14 years and older for advanced
stuttering (see Table 17–1) includes individuals who
have been dysfluent for many years and have sub-
stantial experience with the entire spectrum of stutter-
ing behaviors. The core behaviors include long, tense
blocks, part- and whole-word repetitions, and visible
lip and jaw tremors (Smith & Weber, 2017). A distin-
guishing characteristic of advanced stuttering is the
sophistication of learned and practiced escape and
avoidance behaviors. For example, one of the authors
of the Peters and Guitar (1991) textbook recounts a
behavior he used, as a young man, to avoid placing
food orders in restaurants. He knew that the pressure to
234 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
speak his order quickly would cause him to be dysflu-
ent. He waited until he saw the server approaching the
table, let his friends know what he wanted to order, and
then excused himself to go to the rest room. Personal
accounts from adults who stutter reveal many of these
types of avoidance behaviors (https://www.mnsu.edu/
comdis/kuster/PWSspeak/PWSspeak.html).
Recovery of Fluency
An important component of the natural history of
stuttering is the trajectory of the stages outlined in
Table 17–2. For example, when a child appears to be
in Stage III of this natural history, with multiple repeti-
tions, blocks, and evidence of frustration in attempts to
deal with dysfluency, does he necessarily move through
the final two stages and into advanced stuttering?
This question has occupied a good number of sci-
entists whose findings agree in a general sense, but
perhaps not specifically. Yairi and Ambrose (1999)
concluded that many children diagnosed with stutter-
ing around the age of 3 years stop stuttering within a
year or two (or even sooner) and become fluent speak-
ers. This recovery from the diagnosis of stuttering in
young children seems to be a natural process, one that
does not require (although may be helped by) clinical
treatment.
Recall that about four of five children who are
diagnosed with stuttering recover, and become fluent
speakers (Yairi & Ambrose, 1999). The question con-
cerning the natural, or spontaneous, recovery of stut-
tering has focused on the factors that may explain why
children recover fluency after an initial diagnosis of
developmental stuttering. One factor is clearly the sex
of the child: females are much more likely to recover
fluency compared with males (see sections “Incidence
and Prevalence of Stuttering”).
Recovery of fluency may also be predicted by
family history (Walsh et al., 2018; Yairi, 2007). Children
with a documented family history of persistent stut-
tering are less likely to recover fluency than children
whose family history of persistent stuttering is less cer-
tain. These facts suggest that persistent stuttering has a
genetic component (see sections, “Genetic Studies” and
“Possible Causes of Stuttering”).
Recovery of fluency may also be linked to lan-
guage skills and temperament at the time of diagno-
sis, but the research findings on these factors are much
less convincing than the sex and family history fac-
tors. Other factors, such as age at onset of stuttering
symptoms, type of dysfluency (e.g., repetitions versus
tense blocks), the child’s phonological development
(development of the sound system), and a child’s
speech motor skills may also be important factors in
persistent stuttering versus recovery from stuttering.
Factors that appear to contribute to recovery of flu-
ency versus persistence of stuttering are summarized
in Figure 17–1 (see Ambrose & Yairi, 1999; Conture,
1999; Nippold, 2001, 2002; Walsh et al., 2018; Watkins,
Yairi, & Ambrose, 1999; and Yairi & Ambrose, 2005 for
additional information on the controversy surround-
ing factors that account for persistence versus recovery
from stuttering).
Possible Causes of Stuttering
Three theories of stuttering are considered here. These
include psychogenic, learning, and biological linguistic
theories. The theories are labeled this way for conve-
nience of presentation; they are not necessarily mutu-
ally exclusive in their proposed explanations. The first
two theories are presented only briefly. These theories
provide historical perspective but among contempo-
rary researchers and clinicians are not widely accepted.
Psychogenic Theories
Psychogenic theories explain stuttering as a neurosis.
The neurotic basis of stuttering may include hostility,
repression of unwanted feelings, phobias, as well as
other psychological constructs often associated with
Freudian psychopathology (see summaries of psycho-
genic theories of stuttering in Owens, Metz, & Haas,
2003, and Ramig & Shames, 2006). In contemporary
thinking about stuttering, a psychogenic basis for the
disorder is largely discounted because evidence of
common personality traits among PWS is not compel-
ling, and psychotherapy does not seem to lessen stut-
tering symptoms. PWS seem to be just like everyone
else, except that they stutter.
This conclusion may need to be qualified by con-
sidering the differences between underlying causes
of a disorder, and psychological outcomes of hav-
ing a disorder. Tran, Blumgart, and Craig (2011), in a
review of the literature on psychological issues among
PWS, failed to find a persuasive case for psychologi-
cal problems as the cause of stuttering. Results of their
own study, however, in which AWS filled out a ques-
tionnaire concerning their levels of anxiety, mood, and
other psychological states, suggested differences from
a control group. PWS were more likely (by self-report)
than control participants to have anxiety and negative
mood states. Tran et al. regarded these findings as indi-
cators of the potential effect of stuttering on psycho-
logical well-being, rather than the cause of stuttering.

BEGINNING STUTTERING
%)
20
(~
nt
ste
rsi
Pe
Male
Family members with history
Age at onset?
Type of SLDs?
Developmental speech sound
and/or language disorders?
Temperament?
Figure 17–1.  Variables likely to be associated with persistent versus recovered stut-
tering in children.
Learning Theories
Learning theories of stuttering propose that some chil-
dren learn to be dysfluent during a period of typical
dysfluencies. A child develops an association between
normal dysfluencies and fear of speaking; when the
dysfluencies are “released,” an immediate reduction
of fear reinforces dysfluency, making it more likely to
occur in the future. Over time, this pattern of dysflu-
ency, fear, release of the dysfluency with its reduction
in anxiety and fear, leads to chronic stuttering as a
learned habit.
Learning theories of stuttering are controversial.
There is little doubt that as stuttering develops, emo-
tions such as fear, anxiety, and shame increase as the
child finds it more difficult to produce fluent speech
and be an effective communicator. Moreover, it makes
sense that chronic, speaking-related emotions compli-
cate and possibly undermine the child’s attempts to
produce fluent speech.
As a child who stutters matures through adoles-
cence and young adulthood, and has lengthy expe-
rience with advanced stuttering, a deeply rooted
association of frustration, anxiety, fear, and shame
with the act of speaking may be established. It is easy
to see how this association, together with the reduction
17  Fluency Disorders 235
Re
co
ve
re
d(
~8
0%
)
Female
Lack of family history
Age at onset?
Type of SLDs?
Typical speech and language
development?
or elimination of the negative emotions when fluency
follows repetitions or blocks, is viewed as a likely set-
ting for stuttering as learned behavior. To add to this
logic, reviews of the efficacy (effectiveness) of speech
therapy in CWS and AWS indicate that therapies using
rather simple principles of learning can reduce stutter-
ing to a significant degree (Bothe, Davidow, Bramlett,
& Ingham, 2006). If we follow the logic used earlier to
discount neurotic theories of stuttering, the relative
success of many of these “learning” therapies could be
taken as “proof” for stuttering as learned behavior.
Biological Theories
A biological theory of stuttering implies a physical or
physiological basis for the disorder (or both). Biological
explanations for stuttering focus on brain differences
between PWS and fluent speakers, because there is
no evidence that articulators such as the tongue, lips,
and jaw are different in PWS than in fluent speakers.
In most cases, these hypothesized brain differences are
thought to be present at birth.
Over the past several decades, three types of
evidence have been used to support a brain basis for
childhood-onset fluency disorder. Differences in brain
236 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
anatomy and brain physiology between CWS and
children who are fluent constitute two of the three
types of evidence. The third type of evidence, which
may be the basis for the first two, suggests that stutter-
ing is a genetic disorder. The three types of evidence
are not independent. A genetic basis for stuttering
may include a difference in the development of speech
motor control mechanisms in the central nervous
system.
Anatomical Differences
Sophisticated brain imaging techniques are available to
address the question of anatomical differences between
PWS and fluent speakers. Studies have examined the
relative size of gray matter in brain locations known
to be part of the speech production network, as well as
the connections (white matter) between these locations.
A related question has been the possibility of different
patterns of anatomical asymmetry in the cerebral hemi-
spheres of PWS compared with fluent speakers. Sum-
maries of this work are found in Etchell, Civier, Ballard,
and Sowman (2018) and Ingham, Ingham, Euler, and
Neumann (2018).
Recall from Chapter 2 the size differences between
structures in the left and right hemispheres: in a fluent
speaker, left-side structures that are part of the speech
and language network are often larger than corre-
sponding right-side structures, apparently consistent
with the left-side dominance for speech and language
structure.
The findings of several relevant studies of AWS are
not always consistent, but Etchell et al. (2018) conclude
that compared to fluent adults, two structures in the
right hemisphere of AWS have more gray matter. These
structures are the right-hemisphere areas in the fron-
tal lobe corresponding more or less with Broca’s area
in the left hemisphere, and the planum temporale, an
auditory area important for speech perception. In other
words, the asymmetries observed in fluent speakers
may be reduced or not observed in PWS.
At first glance, these claims for the brain structures
in PWS contradict the typical lateralization of speech
structures to the left hemisphere. As argued by Etch-
ell et al. (2018), though, the conclusion makes sense if
poorly functioning speech motor control structures in
the left hemisphere, which presumably are one cause of
stuttering, are compensated for by activity in the analo-
gous structures of the right hemisphere. It is as if the
right hemisphere structures take over part or all of the
job of fluent speech production, and the assumption of
greater speech activity requires more gray matter (see
Foundas, Bollich, Corey, Hurley, & Heilman, 2001; and
Foundas et al., 2003).
In another example, the size difference in many
humans between the left- and right-hemisphere pla-
num temporale — larger in the left hemisphere, con-
sistent with left lateralization of speech and language ​
— ​has been shown to be eliminated or even reversed in
AWS, but not in CWS. This makes it unclear if the loss
of asymmetry in AWS is due to the origin of stuttering
(e.g., is part of “programmed brain growth” in PWS) or
is the result of chronic stuttering into adulthood which
results in changes in brain anatomy (Chang, Erickson,
Ambrose, Hasegawa-Johnson, & Ludlow, 2008).
White matter differences between PWS and fluent
adults (or the comparison of CWS and fluent children)
include differences in the corpus callosum (the fiber
tract that connects the two hemispheres). Specifically,
the corpus callosum has been reported to have greater
volume in CWS compared with fluent children (Etch-
ell et al., 2018). This may be consistent with increased
gray matter on the right side of the brain of PWS. Com-
pensation by the right side of the brain for dysfunc-
tional left-side speech structures may require that more
information be transferred to the right hemisphere
during speech. To accommodate this increased flow of
information, a larger interhemispheric (between hemi-
spheres) fiber tract may be needed.
There is also evidence that white matter connec-
tions between brain structures for speech and lan-
guage, such as between Wernicke’s and Broca’s areas or
between cortical and subcortical areas for speech motor
control, are less well developed in CWS compared with
fluent children (Chang, Zhu, Choo, & Angstadt, 2015).
Poor development of white matter tracts that are essen-
tial to the speech motor control brain network may
play a role in childhood stuttering.
Physiological (Functional) Differences
Functional neuroimaging studies (using, for example,
the functional magnetic resonance imaging [fMRI]
technique described in Chapter 2) have revealed dif-
ferences in brain activity patterns for speech produc-
tion in PWS, compared with fluent people. Brown,
Ingham, Ingham, Laird, & Fox (2005) examined brain
regions for fluent speakers as they produced speech
and observed a small “core” set of active regions. These
regions included Wernicke’s and Broca’s areas, among
others known to be involved in the motor control of
structures such as the lips, tongue, and larynx. PWS
showed activation during speech of the same “core”
regions but had either stronger- or weaker-than-normal
activity in those areas. In addition, regions of the brain
associated with auditory processing, typically active
in fluent speakers, showed little activity in PWS. This
last finding is provocative in light of the planum tempo-

rale asymmetries discussed previously. Both the ana-
tomical and physiological findings therefore suggest a
role of the brain’s auditory processing centers in stut-
tering, and perhaps specifically for the perception of
speech and language and its integration with speech
motor control.
Speech Motor Control and Stuttering
The possibility of developmental stuttering as a con-
sequence of immature or dysfunctional speech motor
control has been gaining traction over the past few
decades. Execution of speech movements, such as
tongue speed and coordination of two or more articula-
tors, is believed to be affected in toddlers who begin to
stutter. As stated by Smith and Weber (2017), “Disflu-
encies arise when the motor commands to the muscles
are disrupted, and normal patterns of muscle activity
required for fluent speech are not generated” (p. 2487).
Deficits in the planning of speech sound sequences
are also thought to be a component of the speech motor
control deficit. As discussed previously for apraxia of
speech in adults (Chapter 14) and in children (Chap-
ter 15), the distinction between the planning and execu-
tion components of speech motor control is important.
Execution is the direct control over movements of the
speech mechanism (such as the tongue) by cells in the
primary motor cortex. Planning is the preparation of
a program for the execution of movements, which
includes (at least) the selection of speech sounds, their
ordering, and the commands for intended movements.
A speech motor control plan can be assembled without
executing the plan — it is like a mental representation
of what is intended. In contrast, execution of the plan
is the result of the commands from the primary motor
cortex that have direct control over the muscles. Smith
and Weber (2017) say, “It has been hypothesized that
the underlying speech motor deficit in adults with per-
sistent stuttering is a failure to form stable underlying
motor programs for speech” (p. 2487). Smith and Weber
support the idea of immature speech motor programs
by citing their own work on articulatory stability (vari-
ability of articulator movements over multiple repeti-
tions of a short phrase). Fluent adults did not improve
their stability over many trials of the repetitions
because their speech was already planned at a mature
level. Conversely, AWS and fluent children showed
improvement over trials, presumably in the stabil-
ity of the program. When the planned speech sound
sequence is stable, so are the executed movements.
AWS improved because they had immature speech
motor programs and therefore had room to improve.
Fluent children improved because their speech motor
control is still maturing; they too had room to improve.
17  Fluency Disorders 237
A speech motor control perspective on develop-
mental stuttering is compelling for several reasons.
First, it explains why articulatory movements of PWS
are different from the articulatory movements of a flu-
ent speaker — even during fluent utterances. (Zimmer-
man, 1980).
Second, it is consistent with different types of stut-
tering, most notably clonic versus tonic SLDs. “Clonic”
is a term that describes rhythmic, repetitive movements
of a body part. Multiple, consecutive sound or syllable
repetitions can be considered a type of speech clonus
(noun form of “clonic”). Similarly, “tonic” is a term that
describes a muscle contraction that is sustained for a
relatively long period of time. The long “blocks” seen
in advanced stuttering can be regarded as a form of
speech tonus.
The terms “clonus” and “tonus” are, in fact, used
to describe signs of certain neurological diseases, but a
caution is in order: although the terms have been used
to describe the SLDs of multiple repetitions and blocks,
respectively, they are not used to link stuttering with
specific neurological diseases (Schwartz & Conture,
1988). However, these two SLD types fit with unin-
tended and uncontrolled aspects of speech production
that seem explained better by a speech motor control
deficit than by (for example) a learning theory.
A third piece of evidence concerns the hypothe-
sized speech motor planning component of a speech
motor control deficit. Stuttering is not a linguistic, equal-
opportunity speech disorder. As reviewed by Anderson,
Pellowski, and Conture (2005), stuttering is most likely
to occur on low-frequency words, one of the first three
words of an utterance, function words in young CWS
versus content words in older CWS and AWS, and lon-
ger, grammatically complex utterances (for grammati-
cal complexity, see Melnick & Conture, 2000).
An argument can be made that each of these four
linguistic conditions requires more speech motor plan-
ning skills than its opposite. For example, lipstick and
rabbit are low- and high-frequency words, respectively,
likely to be known by a 4-year-old. Frequently used
words such as rabbit are produced so many times by
children, and therefore planned so many times, that
the plan becomes more or less automatic. In contrast, a
low-frequency word like lipstick that is said fewer times
may require more active planning, and thus be sub-
ject to programming demands that challenge speech
motor control maturity in CWS. Similarly, longer and
more grammatically complex utterances such as Where
does he go when he is hungry? are likely to require more
sophisticated planning skills than the shorter and less
complex, Where does he go?
Finally, an explanation of developmental stut-
tering as a speech motor control deficit may seem
238 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
incompatible with the possibility that CWS and AWS
are more likely to stutter when they are anxious (e.g.,
Davis, Shisca, & Howell, 2007). How does a speech
motor control perspective on stuttering accommodate
the effect of anxiety on either speech motor planning
and/or execution? Although this question has no cur-
rent answers, two observations from the research litera-
ture are relevant to an increased understanding of why
motor planning and execution might be expected to be
sensitive to fluctuating states of anxiety.
The quality of any motor control task, including
speech production, is likely to be sensitive to a person’s
anxiety level at the time the task is performed. For
example, fine motor control and precise coordination
required for finger movements during skilled piano
performance deteriorates to various degrees when the
person playing the piano is anxious (Kotani & Furuya,
2018). The cognitive resources associated with plan-
ning and execution of finger movements may be com-
promised by anxiety. This suggestion has been made
directly for the case of speech motor planning and
execution by Hennessy, Dourado, and Beilby (2014),
who showed in an experimental task that severity of
stuttering in a verbal task was related to the current
anxiety state in the person who stutters. Nonverbal
responses (pressing a button to indicate an answer to
the same question posed in a verbal-response task)
did not show this relationship between anxiety and
button-press errors. Hennessy et al. concluded that the
relationship between variations in stuttering severity
and variations in anxiety was specific to speech, and
probably was due to anxiety competing for response
resources with speech motor planning and execution.
Speech Motor Control and Developmental
Stuttering:  A Summary
Smith and Weber (2017) suggest the idea that the
onset and progression of stuttering in children can be
explained by the brain anatomy and physiology dif-
ferences previously described, and (importantly) by
the child’s ability to find a compensation for these dif-
ferences. Two young children who are diagnosed with
stuttering at age 3 years, for example, may have equal
levels of immaturity in brain structures and physiol-
ogy for speech. One child may not recover fluency and
have persistent stuttering into adulthood; the other
may become fluent within months. This hypothetical
comparison illustrates how genetic predispositions for
stuttering do not guarantee persistent stuttering. Both
children may have the same, genetically determined,
immature brain structures and physiology for speech.
The child who becomes fluent does so because an
environmental influence “shapes” the genetic predis-
position away from persistent stuttering and toward
recovery of fluency (Smith & Weber, 2017).
Acquired (Neurogenic)
Stuttering
Adults who have been fluent throughout their lives
(with some exceptions) and who acquire brain dam-
age from (for example) a stroke (Theys, van Wierin-
gen, Sunaert, Thijs, & De Nil, 2011) or traumatic brain
injury (Penttilä, Korpijaakko-Huuhka, & Kent, 2019)
may have stuttering as a speech-language problem. It
is called “neurogenic” stuttering to recognize its cause
from a documented brain injury/damage. Neurogenic
stuttering is rare and is not well understood.
Two questions are often asked about neurogenic
stuttering. First, are the symptoms of neurogenic stut-
tering like those seen in developmental stuttering?
Second, which neurological diseases have neurogenic
stuttering as a possible symptom, and when neuro-
genic stuttering occurs in one of these diseases, which
parts of the brain are likely to be damaged? The sum-
mary that follows is based on the reviews cited previ-
ously, as well as articles cited in those reviews.
Symptoms of Neurogenic
Stuttering Compared With
Developmental Stuttering
A significant amount of attention has been devoted to
the similarity (or dissimilarity) of stuttering symptoms
in acquired (neurogenic) as compared to developmental
stuttering. The reason for making this comparison is, in
a broad sense, to determine if the two kinds of stutter-
ing are the “same” thing. Think of the comparison as an
experimental hypothesis: If symptoms in acquired and
developmental stuttering are clearly different, the dis-
orders may share a name (stuttering) but are different
types of communication disorders. This has implications
for both the clinical management of the disorders and
their underlying theories. But if the symptoms in the
two disorders are the same, stuttering may be viewed
as the same phenomenon in both children and adults.
This potential outcome, in which stuttering behavior is
essentially the same in developmental and acquired ver-
sions of the disorder, may be regarded as consistent with
a biological view of all stuttering behavior.
As noted earlier, stuttering episodes in devel-
opmental stuttering are not found equally at word
beginnings and endings, or on content versus function
words. Early case reports of acquired (neurogenic) stut-
tering suggested that patients may not follow this pat-

tern, but rather stutter frequently at word endings and
on function words. More recent data, however, suggest
as much similarity as difference for the actual types and
locations of dysfluencies observed for developmental
and acquired stuttering (Theys, van Wieringen, & De
Nil, 2008). Types and locations of dysfluencies do not
seem to reveal a clear-cut distinction between develop-
mental and acquired stuttering.
Another well-known feature of developmental
stuttering, at least in the intermediate and advanced
stages (see Table 17–1), is the presence of secondary
characteristics that include struggle and release behav-
iors associated with repetitions, prolongations, and
blocks. Some case reports (articles written to describe
a single patient’s behavior, common in the medical lit-
erature) indicated that secondary characteristics did
not occur in acquired stuttering. Other cases show
struggle, avoidance, and release behaviors similar to
those seen in the later stages of developmental stut-
tering and in AWS. Theys et al. (2008) concluded that
the presence versus the absence of secondary behaviors
does not seem to provide a reliable distinction between
acquired and developmental stuttering.
In summary, evidence collected so far has not
shown a clear distinction between the core or second-
ary characteristics of acquired and developmental stut-
tering. A future analysis may reveal a clear distinction,
but for the present it seems best to regard the symp-
toms of the two forms of the disorder as overlapping.
Treatment Considerations
Many different behavioral techniques exist for the treat-
ment of stuttering, in both children and adults. In chil-
dren past the age of 9 or 10 years, and in adults, several
of these techniques seem to work for many, as evalu-
ated by very strict scientific criteria (Baxter et al., 2016;
Bothe, Davidow, Bramlett, & Ingham, 2006). The tech-
niques work not only in the therapy session, where a
person who stutters can reduce or eliminate stuttering
episodes under controlled circumstances and with the
help of a clinician, but also in real-world talking situ-
ations. PWS who have been treated by an SLP have a
real hope that stuttering, and the various feelings and
behaviors associated with it, can be brought under
some degree of control.
Evaluation of treatment effectiveness in preschool
children is complicated by the 80% spontaneous recov-
ery rate of children who have an initial diagnosis of
beginning stuttering. Treatment may be the reason for
recovery of fluency, or may be due to natural recovery
(Salturklaroglu & Kalinowski, 2005). Of course, treat-
ment may hasten recovery in children who at a later
17  Fluency Disorders 239
date have spontaneous recovery. A review of tech-
niques used to treat developmental stuttering in pre-
school children is by Shenker and Santayana (2018).
Chapter Summary
Stuttering is a speech-language disorder in which the
smooth, fluent stream of speech is interrupted by rep-
etitions, blocks, complete stoppages of speech, and
revisions; its cause is unknown.
Developmental stuttering begins in early child-
hood and usually involves a slow progression of
symptoms in which the “typical” dysfluencies of early
speech and language development increase in fre-
quency and severity as the child matures.
A “natural history” of developmental stuttering
describes how these symptoms change from the early,
typical dysfluencies to the later blocks, repetitions, and
especially struggle behaviors that are characteristic of
advanced stuttering.
As many as 80% of children suspected of having
a stuttering disorder recover with or without therapy.
The likelihood of recovery from childhood stuttering is
greater for girls, as compared to boys, and for children
who do not have a first-degree relative who has or had
a stuttering problem.
There are several different theories of stuttering.
Psychological theories, which regard stuttering as
an expression of a neurosis, were popular at one time
but do not have much scientific support.
Learning theories are based on the assumption
that the normal dysfluencies of early childhood become
a chronic pattern as the child learns to associate stutter-
ing episodes with negative outcomes, and the “release”
of the stuttering episodes with positive outcomes; in
these theories, the child becomes conditioned to stutter.
Biological theories hold that there is some brain
difference or dysfunction that explains stuttering; in
contemporary scientific discussions, biological theories
are very much intertwined with the idea of a genetic
basis for stuttering.
The genetic basis for stuttering is supported by
(a) the greater likelihood of stuttering among relatives
of PWS, as compared to relatives of fluent speakers;
and (b) the greater occurrence of stuttering in monozy-
gotic as compared to dizygotic twins.
Dysfluencies are sensitive to the linguistic struc-
ture of an utterance; these linguistic factors can be inte-
grated with biological theories of stuttering.
Neurogenic stuttering is the term used to describe
the onset of stuttering in adulthood, usually as a result
of neurological disease such as stroke or head injury.
240 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
The symptoms of neurogenic stuttering are in
some ways like those of developmental stuttering, but
in some cases, there may be differences (such as the
absence of struggle behaviors in neurogenic stuttering,
at least according to some reports).
Evidence exists in the scientific literature that
developmental stuttering can be treated successfully.
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Voice Disorders
Introduction
Chapter 10 describes the role of the vibrating vocal
folds as the primary sound source for speech. The vocal
folds, contained within the cartilage framework of the
larynx, vibrate periodically and generate a tone whose
pitch is proportional to the rate of vibration. The pro-
duction of tone by the vibrating vocal folds is called
phonation.
Perceptual impressions of voice production include
pitch, loudness, and quality. The physical (acoustic)
bases of these perceptual impressions are fundamen-
tal frequency (F0), intensity (amount of sound energy),
and spectrum (mix of periodic and noise characteristics
produced by the vibrating vocal folds).
The first sign of a voice disorder is often a percep-
tion of voice abnormality, either by the person produc-
ing the voice or by listeners. The pitch may seem too
low for the speaker’s gender and/or age, the loudness
too soft, or the quality too rough or breathy. Alterna-
tively, a first sign of a voice disorder may be a sense
of pain, unusual effort, or tightness in the neck when
producing phonation.
Voice disorders are not only a concern for their
social implications  —  listeners often do not “like”
abnormal-sounding voices — but also for their potential
to affect careers. Teachers with serious voice problems
cannot teach, or can teach but with reduced effective-
ness. Actors, tour guides, singers, athletic coaches, and
other professionals are greatly affected by a voice dis-
18
order. These effects include lost workdays; voice disor-
ders have an economic impact.
Voice disorders have many different causes.
A selected group of voice disorders are presented in
this chapter. The term dysphonia is used to indicate voice
characteristics that sound abnormal. More specifically,
dysphonia is the auditory impression of abnormality in
the pitch, loudness, and/or quality of the voice. Dys-
phonia may also be used to describe a voice perceived
as being produced with unusual effort.
Dysphonia may or may not have an obvious cause.
The present chapter focuses on adult voice disorders;
pediatric voice disorders are discussed briefly at the end
of the chapter. (See https://www.asha.org/PRPSpecific​
Topic.aspx?folderid=8589942600&section​=Overview
for a comprehensive overview of voice disorders.)
Epidemiology of
Voice Disorders
How prevalent are voice disorders in the general popu-
lation, and are there specific factors that make people
more or less likely to have had (or have) a voice disor-
der? Among people who have been diagnosed with a
voice disorder, which voice disorders are most common?
Roy, Merrill, Gray, and Smith (2005) conducted
a survey in which approximately 6.5% of the respon-
dents claimed they were experiencing a voice disorder.
In a survey of 14,794 young adults, Bainbridge, Roy,
243
244 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Losonczy, Hoffman, and Cohen (2017) found that 6%
reported having a voice problem over the previous
12 months.
A prevalence estimate of 6% to 7% for voice dis-
orders among the general population is startling. In
a state such as Wisconsin, which has a population
of approximately 5,800,000 people, Roy et al.’s work
(2005) suggests that 350,000 people have had a voice
problem over a 12-month period. Voice disorders can
be short term (such as laryngitis), or longer term, as
described later in this chapter.
The prevalence of voice disorders reported by sur-
veyed individuals increases with age, is greater with a
family history of voice disorders, is greater for females
compared with men, and is higher among professional
voice users (e.g., teachers; Roy et al., 2005) than in the
general population
Initial Steps in the Diagnosis
of Voice Disorders
Patients are referred by primary physicians, or refer
themselves, to a voice clinic because of a perceived
change in voice production and/or a sense of extreme
effort during phonation. The voice therapist goes
through a series of steps to diagnose the presence and
type of voice disorder. These steps include a case his-
tory, perceptual evaluation of the client’s voice, viewing
of the vocal folds via a laryngeal mirror (Chapter 10),
recording of vocal fold motion during phonation by
videostroboscopy, and measurement of basic voice
parameters. Information gathered in these assessments
contributes to a diagnosis, which in turn is the basis
of a treatment plan. The treatment plan may include
behavioral therapy which involves direct modification
of voice, and/or indirect therapy such as counseling
which addresses psychological aspects of the voice
disorder. The treatment plan may also include sur-
gery to correct a structural problem of the vocal folds.
Behavioral and surgical treatments are combined for
certain diagnoses.
Case History
As in any type of medical setting, a case history is
critical to accurate differential diagnosis of a disease or
condition. Differential diagnosis is the systematic iden-
tification of the cause or causes of a symptom (or symp-
toms) by ruling out likely candidates. For example,
when a patient reports hoarseness for 2 weeks, many
possible causes may explain the voice disorder. A care-
ful case history can rule out some or most of these can-
didates prior to more in-depth testing.
The voice therapist wants to know if a patient is a
professional voice user or has a recent or chronic his-
tory of unusual voice usage, such as overuse of the
voice (e.g., shouting, screaming), if there is extended
use of the voice every day, as in teachers (Martins,
Pereira, Hidalgo, & Tavares, 2014), and if there is use
of the voice in a unusual way for long periods of time.
Professional voice users may develop inflammation
of the vocal folds or vocal fold fatigue from excessive,
high-effort phonation. Excessive, high-effort phonation
can also occur when the voice is pushed to its operat-
ing limits, as in the parent who screams at a child, or a
child who screams when he or she plays.
The voice therapist also wants to know about the
patient’s history of tobacco and alcohol use, current or
previous use of therapeutic and/or recreational drugs,
and if there is a history of frequent laryngopharyngeal
reflux (LPR, a technical name for acid indigestion).
Smoking and drinking alcohol (especially in combina-
tion), certain drugs, and LPR are all known to be causes
of inflammation and in some cases permanent tissue
change in the vocal folds.
Perceptual Evaluation of the Voice
Voice therapists are trained to listen carefully for
perceptual signs (voice characteristics) associated
with specific disorders. The terms used most often to
describe disordered voice characteristics include, but
are not limited to, rough, breathy, weak, strain, hoarse,
spasm, pitch, and loudness; overall severity is also an
important perceptual evaluation of a voice disorder
(Kempster, Gerratt, Verdolini Abbott, Barkmeier-Krae-
mer, & Hillman, 2009).
Perceptual impressions, even those of carefully
trained voice therapists, do not provide specific infor-
mation concerning the underlying cause of a voice dis-
order. For example, the impression of a breathy voice
may be the result of vocal fold paralysis, the aging pro-
cess, or vocal nodules. Or, a breathy voice quality may
not be associated with an underlying disease — it may
be simply one of the variants of voice quality heard in
the population. Perceptual impressions of voice quality
are an important step in the diagnostic process, espe-
cially when they serve the purpose of narrowing down
hypotheses of the underlying cause of a voice disorder.
Viewing the Vocal Folds
Indirect laryngoscopy is a technique used to view the
vocal folds (Chapter 10, Figure 10–1). The examiner
places the mirror close to the back of the throat while
holding the tongue with a gauze pad. A strong light
 18  Voice Disorders 245

is aimed at the mirror and reflected to illuminate the Measurement of Basic

vocal folds. The laryngeal mirror examination is per-
formed first as the patient is breathing normally, rather
than during phonation. This allows the examiner to
see obvious lesions on the vocal folds, such as nodules,
polyps, or other growths, and may also provide evi-
dence of vocal fold paralysis, if it exists.
The patient is then asked to phonate while the
examiner views the vocal folds. The individual cycles
of vocal fold vibration are not visible to the examiner
because they are faster than the time-resolving ability
of the human eye. If there is a lesion on one or both
vocal folds, however, the examiner may be able to see
whether or not it interferes with vocal fold closure
during phonation. Videostroboscopy provides a slow-
motion view of the vibrating vocal folds that allows an
examiner a more detailed evaluation of possible causes
of voice disorders. (See Google “laryngeal videostro-
boscopy” for video clips of vibrating vocal folds.)
Voice Parameters
The present discussion focuses on three acoustic mea-
surements that are used often to describe voice char-
acteristics: F0 (perceptual correlate = pitch), intensity
(perceptual correlate = loudness), and spectrum (per-
ceptual correlate = voice quality).
F0 (Pitch)
F0 is the number of cycles of vocal fold vibration com-
pleted in 1 second. The perceptual correlate of F0 is
pitch. All other things being equal, as F0 increases so
does voice pitch.
F0 has been widely studied in the normal popula-
tion. A graphic summary of F0 data by age, for both
males (curve with blue points) and females (curve with
pink points), is shown in Figure 18–1. Age is shown on

300

260
Fundamental frequency (Hz)

220

Female
180

140

Male
100
0 10 20 30 40 50 60 70 80 90 100

Age (years)

Figure 18–1.  Plot of fundamental frequency (F0) across age for males (blue points) and females (red
points). Age is on the x-axis, and F0 is on the y-axis. Adapted from Hixon, T. J.,Weismer, G., and Hoit, J. D. (2020).
Preclinical speech science: Anatomy, physiology, acoustics, perception (3rd ed.). San Diego, CA: Plural Publishing.
246 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

the x-axis, F0 in Hz on the y-axis. The curves reflect data
from many sources in the literature, including Baken
and Orlikoff (2000), Kent (1976), Nishio and Niimi
(2008), and Lee, Potamainos, & Narayanan (1999).
F0 is related to the size of a person’s larynx — in
general, the larger the larynx, the lower is the F0.
Prior to puberty, the F0 values of males and females
are similar, because sex-specific anatomical charac-
teristics of the larynx do not appear before puberty.1
Around puberty, the size of both the male and female
larynx grow, with more dramatic growth in males.
This is reflected in Figure 18–1 in which male F0 low-
ers substantially around puberty relative to female F0.
Postpuberty F0 values are close to adult values, which
remain relatively constant until old age. Female adults
between ages 20 and 70 years have F0 values between
190 and 210 Hz. Over this same age range, F0 for males
ranges between 115 and 135 Hz. This sex-related differ-
ence in F0 explains why males are typically perceived
to have lower-pitched voices than females.
In old age, the F0 of females decreases (probably
as a result of hormone changes), and the F0 of males
increases (probably as a result of increased stiffness of
the vocal folds and the cartilages of the larynx).
Diagnosis of a voice disorder in which pitch seems
abnormal can make use of the average data shown in
Figure 18–1. These data are a rough guide to “normal.”
However, people with heathy voices, at any given age,
have a range of F0 values. The F0 values in voice prob-
lems with unusual pitch are usually very different from
average F0 values such as those shown in Figure 18–1.
Intensity (Loudness)
Voice intensity is not precisely the same as voice loud-
ness. Voice intensity refers to the amount of acoustic
energy generated by the vibrating vocal folds and
modified as the energy passes through the vocal tract
and exits the lips. Voice loudness refers to a listener’s
perception of the voice. Greater voice intensity typi-
cally results in greater voice loudness.
Voice intensity is likely to change with the loud-
ness of background noise, as well as with the distance
between the speaker and the listener. For example, at
a party where many people are talking, voice intensity
must be greater than usual to be heard above the loud-
ness of the background noise. Voice intensity is also
likely to change with the distance between a speaker
and the listener. To maintain a constant loudness for
the listener as the distance between speaker and lis-
tener increases, voice intensity must increase as well.
This is because sound energy decreases as it travels
over distance. An increased intensity of the voice is a
normal adjustment when speaking to someone located
at a distance.2
How do SLPs judge a person’s voice loudness
as typical or atypical? Like F0, there is a great deal of
speaker-to-speaker variation in voice intensity (and
hence, perceived voice loudness) that is accepted by lis-
teners as “normal.” In most cases, however, voice loud-
ness that calls attention to itself is not subtle. The case
of an unusually soft voice, or the less-frequent case of a
chronically loud voice, is sufficiently noticeable to elim-
inate the need for precise measures of voice intensity as
a requirement to perform further diagnostic tests.
The diagnostic evaluation of voice intensity is
further complicated by factors that are internal to the
speaker. An individual may speak with what appears
to be normal loudness but complain about the effort
required to make herself heard, even when the com-
munication setting is quiet. Or, a speaker may feel as if
he is exerting a normal effort for voice intensity but in
fact sound too soft. The case history includes questions
to determine the individual’s judgment of effort for the
production of loudness appropriate for the communi-
cation situation.
Voice Spectrum (Voice Quality)
An acoustic spectrum is defined as the relative ampli-
tudes of the many frequency components that make up
a sound. In the sound generated by the vibrating vocal
folds, the voice spectrum has energy at the F0, as well
as a series of harmonics (sometimes called overtones).
These harmonic components are found at frequencies
2 times, 3 times, 4 times, . . . n times the F0.3
The precise details of the voice spectrum are
related to voice quality. For example, breathy voices
have fewer frequency components (harmonics) com-
pared with normal voices, as well as a substantial
degree of noise (aperiodic energy), which is not typi-
cal of the normal voice. Strained voice qualities (often

1
 ubtle signs of sexual dimorphism in the human larynx may begin to appear several years before puberty, and these may account for the
S
slightly lower F0 values seen for males, as compared to females, around 8 to 9 years of age.
2 
 he relationship between sound intensity and distance from the sound source is described by the inverse square law. This law states that
T
sound intensity decreases from its source at a rate proportional to the inverse of the square of the distance from that source (in formulese,
Sound intensity ~ 1/d2, where d = distance from the source). Also, the relationship between sound intensity and loudness, like that between
frequency and pitch, is not one-to-one.
3 
 or example, a voice spectrum for a speaker whose F0 = 100 Hz has harmonics at 200, 300, 400, 500, . . . n × F0. The amplitude of the harmonics
F
decrease with increasing frequency.
 18  Voice Disorders 247

called “pressed” qualities) have many harmonics with Classification/Types of

excessive intensity. Voice spectra are obtained with
speech analysis computer programs and are used clini-
cally as an objective, acoustic measure of voice quality.
What is the value of objective measures of voice
production? Scientists and clinicians may prefer acous-
tic measures of voice production, compared with per-
ceptual measures which are notoriously unreliable
(Kreiman, Gerratt, Kempster, Erman, & Berke, 1993).
Acoustic measures of voice production may be better
suited than perceptual measures as metrics of the effec-
tiveness of voice therapy.
Voice Disorders
Voice disorders can be classified in several different
ways but do not always fit neatly into one classifica-
tion or another. The classifications presented here are
not mutually exclusive, as explained later. Specific
examples of voice conditions and pathology are pre-
sented and discussed within the framework of different
classification systems. Table 18–1 provides a summary
of ways to classify voice disorders; each of these clas-
sification approaches is discussed in the next sections.

Table 18–1.  A Summary of Alternative Classifications of Voice Production and Voice Disorders

Classification Description
Hypo-hyperfunctional A description of voice types based on the levels of contraction of laryngeal
muscles and how those levels affect the closing phase and closed phase of vocal
fold vibration. The hypo-hyperfunctional continuum includes many normal voice
types; voice types that are chronically close to or at the ends of the continuum are
often diagnosed as dysphonia.

Phonotrauma A classification based on voice disorders resulting from excessive phonatory

behaviors such as constant and effortful talking (e.g., teachers, actors), singing
(e.g., professional vocalists), and overdriving the phonatory mechanism
(e.g., yelling, screaming). Such phonatory behaviors may result in benign
mass lesions on the vocal folds, such as nodules and polyps. The dysphonia
resulting from phonotrauma may be of the hypo- or hyperfunction type. Chronic
hyperfunction (e.g., excessive screaming) may lead to nodules, which can result
in a hypofunctional-sounding voice, which makes the individual exert excessive
muscular force (hyperfunction) to overcome the difficulty in closing the vocal
folds due to the benign, bilateral masses.

Organic voice Organic voice disorders is a classification of voice disorders that are the result of
disorders benign vocal fold masses. These include (but are not limited to) nodules, polyps,
cysts, and granulomas. These benign masses have the potential to interfere with
vocal fold vibration by preventing adequate closure and stiffening the cover of the
vocal folds. The classification of organic voice disorders may include disorders
classified as resulting from phonotrauma.

Functional voice Dysphonia in the absence of observable pathology in the larynx, or known
disorders neurological disease. Functional voice disorders are in some cases called
psychogenic voice disorders, meaning that psychological issues are partly or
largely responsible for the voice disorders. Muscular tension dysphonia (MTD) is
an example of a functional voice disorder in which some of the cases are regarded
as psychogenic voice disorders. Puberphonia is another functional disorder that is
considered to be psychogenic.

Neurological voice Neurological voice disorders are those in which a known or suspected disease/
disorders condition of the peripheral or central nervous system is the cause of dysphonia.
A neurological voice disorder may be found in diseases of the central nervous
system (e.g., stroke, and degenerative diseases such as Parkinson’s disease and
multiple sclerosis) or damage to a peripheral nerve that supplies the muscles of
the larynx, as in unilateral vocal fold paralysis. Spasmodic dysphonia is a voice
disorder that has a suspected neurological cause.

Cancer of the larynx Cancer of the larynx, in which malignant tumors grow within the larynx, often on
or in the vocal folds, causes dysphonia that worsens as the cancer spreads.
248 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

The Hypo-Hyperfunctional
Continuum
The hypo-hyperfunctional continuum of vocal fold
vibration is best understood by a simple illustration of
how the opening, closing, and closed phases of vocal
fold cycles can be changed by muscular activity within
the larynx.
Figure 18–2 is a schematic drawing of three consec-
utive cycles of vocal fold vibration. The trace shows the
space between the two vocal folds (that is, the glottis)
as they vibrate over time. The glottal space increases as
the vocal folds move apart and decreases as they come
together. As the trace moves up on the graph, the vocal
folds are separating (opening); as it moves down, they
are coming together (closing). The horizontal line at the
bottom of the trace shows the portion of the cycle dur-
ing which the vocal folds are closed. One cycle of vocal
fold vibration is marked.
Two parts of a single vocal fold cycle, the closing
phase and the closed phase, are critical to understanding
the functional variations of vocal fold vibration. The
closing phase is the time between the maximum open-
ing of the glottis (at the top of the trace for each cycle)
to the instant of vocal closure (the left-hand edge of the
horizontal lines at the bottom; Figure 18–2). The closed
phase is the portion of the cycle during which the vocal
folds are completely closed, as described earlier.
The closing phase and closed phase intervals are
the basis of the hypo-hyperfunctional continuum (Fig-
ure 18–3). During normal vocal fold vibration, the clos-
ing phase occurs quickly. Once the vocal folds close, they
remain so for a significant portion of the cycle — nearly
40% to 50% of the entire cycle time, which is called

One cycle
Close
Open

Time (sec)

Figure 18–2.  A schematic drawing of three cycles of vocal fold vibra-

tion, drawn as the opening and closing of the vocal folds over time. The
horizontal lines show the portion of each cycle during which the vocal
folds are closed.

Average “normal” phonation

HYPOFUNCTION HYPERFUNCTION

Range of “normal” voice qualities

Insufficient muscular tension Excessive muscular tension

Slow closing phase Overly fast closing phase
Short closed phase Too-long closed phase
“Breathy” (weak) voice quality “Pressed” voice quality

Figure 18–3.  The hypo-hyperfunctional voice continuum. See text for additional detail.

the period of vocal fold vibration. In certain voice dis-
orders, an excess of muscular tension in the larynx
may result in an excessively fast closing phase and an
overly long closed phase. The excess muscular tension
is called hyperfunction and results in a voice quality that
sounds overly effortful and strained. A hyperfunctional
voice quality is often called “pressed,” as if the speaker
is pressing the vocal folds together too tightly.
In contrast, insufficient muscular tension during
vocal fold vibration results in a very slow closing phase
and overly short closed phase. This is called laryngeal
hypofunction and is associated with a breathy, weak
voice quality.
The hypo-hyperfunctional continuum shown in
Figure 18–3 reflects the concept of continuous varia-
tion in voice qualities between two extreme endpoints.
One endpoint (hypo) reflects too little muscular ten-
sion in the larynx, the other endpoint (hyper) too much
muscular effort. Any combination of closing phase
speed and closed duration may occur due to different
amounts of muscular effort, resulting in many different
voice qualities between breathy/weak and strained/
pressed. Because the hypo-hyperfunctional voice con-
tinuum includes normal voice production, it is not so
much a classification of voice disorders as a range of
phonation styles. The more extreme parts of the range
are often associated with voice disorders.
Direct Control of the
Closing and Closed
Durations?
When you change voice quality from breathy
to pressed, the adjustments do not reflect
conscious control of specific laryngeal muscles.
If you make the strange decision to approach
someone on the street and ask, “Can you slow
up the closing phase of your vocal fold vibra-
tion so we can see how it affects your voice?”
in all likelihood a puzzled look will follow. But
ask someone to gradually change voice quality
between breathy, through “normal,” and then
with increasing tension (the layperson will not
understand the term “pressed”) — most people
understand, and they can do it. How do they
do it? Most likely, they imitate a series of voice
images, from auditory memories, connected
with the terms “breathy,” “normal,” and “tense.”
Like a continuous movement between smiling
and frowning, people can do it easily but cannot
state conscious muscular strategies for how it
is done.
18  Voice Disorders 249
As shown in Figure 18–3, the hypo-hyperfunc-
tional continuum of voice qualities includes a wide
range of “normal” voices. An ideal voice does not exist,
either for the person producing voice or for the person
listening to voice. A range of acceptable voice qualities
is produced among different people.
An individual uses different voice qualities for
different circumstances. Many of these voice qualities
vary within the normal range, but some may be out-
side the normal range, temporarily, to fit a situation, to
make a point, to convey a message that supplements
words. For example, speakers may use extreme hypo-
function to produce a breathy voice outside the normal
range to comfort someone or express tender emotion.
Anger may be expressed with pressed voiced resulting
from extreme hyperfunction.
Extremely breathy or pressed voice is therefore
not unusual in certain situations. These voice qualities
become a clinical issue when they are used chronically ​
— when they are a person’s typical voice quality.
Phonotrauma
The vocal folds consist of delicate tissues that may be
damaged by certain phonation and lifestyle behaviors.
Damaged vocal fold tissues interfere with the vibratory
motions that produce normal voice qualities. The term
“phonotrauma” is used to describe damaged vocal
fold tissues (lesions) and the resulting dysphonia due
to excessive phonatory behaviors and/or other causes.
The lesions caused by phonotrauma are referred to as
benign vocal fold lesions, to differentiate them from
precancerous or cancerous lesions.
Phonotrauma results from behaviors such as over-
use of high-intensity voice (as in some kinds of singing
or acting), chronic screaming (or sometimes a single
episode of very intense screaming), chronic throat
clearing, and chronic use of a hyperfunctional voice
quality. Vocal fold tissues may also be damaged when
they are chronically exposed to environmental agents
such as tobacco and alcohol, in individuals who experi-
ence chronic reflux, and in persons who have chronic
cough and/or throat clearing. The phonation behaviors
that result in phonotrauma are usually associated with
hyperfunctional voice disorders — far to the right in the
continuum of voice use (see Figure 18–3).
For the discussion that follows, Figure 18–4 can be
used as a reference for the appearance of healthy vocal
folds. The photo on the left shows the vocal folds open,
during inhalation. The point of the “V” at the bottom
of the frame is the most anterior part of the vocal folds,
where they are attached to the inside of the thyroid
cartilage. The posterior attachment of the vocal folds
250 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Arytenoid cartilage Vocal folds making contact

for closure during phonation
Anterior (Front)

Normal vocal folds Normal vocal folds

Open for inhalation Closed during phonation

Figure 18–4.  Normal vocal folds as seen through an endoscope; the point of the “V” is the front
attachment of the vocal folds to the inside of the thyroid cartilage. Left, vocal folds open for inhalation,
note straight edge of both vocal folds at their medial boundary (next to the glottis). The space between
the vocal folds is the glottis; right, vocal fold closure for the closed phase during phonation, the incom-
plete rectangle shows firm closure front to back, with just a small opening at the back. Photos courtesy
of Professor Susan Thibeault, Department of Surgery, University of Wisconsin Clinical Sciences Center.

is to the arytenoid cartilages. The glottis is the space
between the vocal folds.
Notice the smooth, straight edge of each vocal fold
as it extends from anterior to posterior along its border
with the glottis. Each vocal fold is a mirror image of
the other — they give the appearance of symmetry. The
photo on the right shows the vocal folds during the
closed phase of phonation. The vocal folds are pressed
together firmly, from front to back, with only a slight
opening at the very back of the glottis.
Vocal Nodules
Chronic overuse of the voice, whether in singing,
screaming, or cheerleading, may result in growths on
the vocal folds called vocal nodules (sometimes called
singers’ nodules). Vocal nodules are callous-like lesions
resulting from chronic slamming together of the vocal
folds during phonation. The nodules develop in much
the same way as callouses develop on a gymnast’s or
baseball player’s hands, or a guitarist’s fingertips. In
the early stages, the growths are soft and blister-like.
As phonotrauma continues, the growths develop the
hard, fibrous texture of a callous.
The location and appearance of vocal nodules
are shown in Figure 18–5. The photo on the left shows
bilateral nodules on the open vocal folds. The nodules
are the small “bumps” along the edge of each vocal
fold, about one third of the distance between the front
and back of the glottis. The bumps interrupt the smooth
edges of the vocal folds, and are located at the same
location on the two folds — they are symmetrical.
Nodules occur one-third of the distance between
the front and back of the vocal folds because the
highest collision forces occur at this location when
the vocal folds come together for each cycle of vibra-
tion. When these forces are chronically excessive, as
in behaviors such as yelling, screaming, and constant
talking, nodules may develop and interfere with nor-
mal phonation.
Vocal nodules are likely to change voice quality
due to incomplete closure during vocal fold vibration.
In Figure 18–5, the folds appear to be closed at the loca-
tion of the nodules, but not in front (forward toward
the thyroid cartilage) or back (toward the arytenoid
cartilages). Voice quality may be breathy and noisy due
to the escape of air through these openings in the vocal
folds. Attempts to overcome the effect of vocal nodules

Bilateral
Anterior (Front) nodules
Figure 18–5. Vocal fold nodules: Two endoscopic views of the vocal folds. Left, vocal folds open
for inhalation, with bilateral nodules indicated by pointers; right, vocal folds during the closed phase of
vocal fold vibration; nodules interfere with complete closure as seen in front of and in back of the point
of contact between the nodules. Photos courtesy of Professor Susan Thibeault, Department of Surgery,
University of Wisconsin Clinical Sciences Center.
on vocal fold closure with additional, excessive muscu-
lar effort may add strain to the voice quality (Leonard,
2009). The phonotrauma that resulted in the nodules
induces more phonotrauma in an attempt to overcome
the poor closure due to the presence of the nodules.
This may become a viscious cycle of voice behavior
which increases the size of the nodules and their effect
on vocal fold vibration.
The nodules also stiffen the outer layers of the
vocal folds, interfering with their motion and affect-
ing voice quality. Nodules grow in the outer layer of
the vocal folds, restricting the independent motion of
the different tissue layers. Partial loss of the wave-like
motion of the outer layer of vocal fold tissue relative
to inner layers has a significant effect on voice quality.
Vocal Fold Polyps
Vocal fold polyps are the result of phonotrauma but
have a tissue structure unlike the callous-like nodules.
Polyps are softer and often larger than nodules, and
may occur as a result of long-term phonotrauma or
even from a single instance of extreme vocal use, such
as a particularly intense scream or cheer. Polyps are
often unilateral, unlike the typically bilateral nodules.
Polyps interfere with phonation in much the same way
as nodules, preventing firm vocal fold closure and inter-
fering with the wave-like motion of the vocal fold cover.
18  Voice Disorders 251
Nodules prevent full
closure for phonation
Other Benign Vocal Fold Lesions
Benign vocal fold lesions are not limited to nodules and
polyps. Other phonotrauma-related damage to vocal
fold tissue, including the temporary inflammation of
viral laryngitis or the long-term inflammation due to
chronic LPR, can result in dysphonia. Cysts (fluid-
filled sacs) may also occur on or in the vocal fold. These
benign lesions may interfere with vocal fold closure
and/or stiffen the top layer of the vocal folds. Excellent
sources for information on benign vocal fold lesions
are Altman, (2007), Naunheim and Carroll, (2017), and
Sapienza and Ruddy (2017).
Treatment of Phonotrauma
Vocal nodules are often treated with vocal rest — if the
patient does not talk for a period of time, nodules may
disappear, much as callouses disappear when the irri-
tating cause is removed. Polyps are more likely to be
treated surgically, although they may also be treated
with behavioral voice therapy.
Even when a benign vocal fold lesion is treated
surgically, usually by removal of the mass as in the case
of polyps, voice therapists play an important role after
the surgery. Information on vocal hygiene — using the
voice properly, avoiding overuse, restricting talking
time, maintaining proper hydration — can be structured
252 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
for the patient to achieve voice recovery. Vocal hygiene
programs are relevant to the behavioral treatment of
vocal fold nodules and are often successful (Hosoya
et al., 2018).
Organic Voice Disorders
Dysphonias that are classified as organic voice disor-
ders are often the result of phonotrauma that leads to
benign mass lesions — growths on the vocal folds such
as nodules, polyps, and cysts (Carding et al., 2017). The
presence of a benign mass lesion is a reason to clas-
sify a voice disorder as organic; a misuse of the voice
is a reason to classify the cause of a voice disorder as
phonotrauma. This is an example of overlap between
classification categories for voice disorders.
Functional Voice Disorders
Dysphonia can exist in the absence of observable
pathology on or around the vocal folds. The phonation
problem may include an inability to produce voice, an
extremely weak, whispery voice, or a voice interrupted
by apparent spasms. When neurological disease and
mass lesions are ruled out as explanations for dyspho-
nia, a functional voice disorder may be diagnosed — one
not explained by organic pathology.
Individuals diagnosed with functional dysphonia
are often professional voice users. This includes, but
is not limited to, teachers, actors, clergy, singers, and
tour guides. Extremely talkative and unusually loud
individuals may also be at risk for a functional voice
disorder (Bastian & Thomas, 2016).
The term “psychogenic voice disorder” may be
used to classify a functional voice disorder with roots
in a psychiatric disorder. As such, psychogenic voice
disorders may be considered as a subtype of functional
voice disorders. According to the famous speech-lan-
guage pathologist Arnold Aronson (1990), a psycho-
genic voice disorder “is a manifestation of one or more
types of psychological disequilibrium, such as anxiety,
depression, conversion reaction, or personality disor-
der, that interferes with normal volitional control over
phonation” (p. 131).4
The diagnosis of a functional versus psychogenic
voice disorder may have important implications for
treatment. A patient diagnosed with a functional voice
disorder may be treated by a voice therapist who has
experience in training patients to regain a normal voice;
psychiatric concerns are not significant, and the thera-
4 
Dr. Aronson lived from 1928 to 2018.
peutic focus is on voice behaviors. A patient diagnosed
with a psychogenic voice disorder may be best treated
with combined psychiatric and voice therapy.
There is no clear-cut distinction between func-
tional and psychogenic voice disorders. Patients with
functional voice disorders are likely to have varying
psychological issues such as anxiety and depression
(Andrea, Dias, Andrea, & Fugeira, 2017; Rosen, Heuer,
Levy, & Sataloff, 2003). A voice disorder called muscu-
lar tension dysphonia (MTD) illustrates the potential
role of psychological issues in a well-known functional
voice disorder.
Muscular Tension Dysphonia
MTD is a voice disorder in which vocal fold vibration
is disturbed by excessive tension in head and neck
muscles. Many of these muscles attach to laryngeal
cartilages. Hypercontraction of the muscles during
phonation may distort the position and shape of the
cartilages, the effect of which is to squeeze the vocal
folds front to back and side to side, preventing normal
vibration.
Figure 18–6 shows the closed phase of vocal fold
vibration for phonation in a speaker with healthy vocal
folds (left) and in a speaker with MTD (right). This
view shows how the laryngeal cartilages and the vocal
folds are squeezed together in MTD (the incomplete
rectangle shows the comparative lengths of the vocal
folds during phonation by the two individuals). Indi-
viduals with MTD often experience voice fatigue and
neck pain when phonating.
Although a large-scale study of the prevalence
and demographics of MTD has not been published, an
estimate of gender and age distribution can be made
from various publications. da Cun Pereira, de Oliveira
Lemos, Gadenz, and Cassol (2018), in a review of treat-
ment success in MTD, found that 68% of 252 individu-
als diagnosed with MTD were female. The age range of
these individuals was 18 to 84 years. Dietrich, Verdolini
Abbott, Gartner-Schmidt, and Rosen (2008) reported
similar results among 68 individuals with MTD: 82%
were female within an age range of 18 to 68 years. Simi-
lar gender and age data were reported by Eastwood,
Madill, and McCabe (2014). Taken together, MTD
seems to be diagnosed largely in women and from
people in young to elderly adulthood.
Voice disorders are due to a wide variety of
causes, ranging from the clearly organic, where there
is a known lesion on the vocal folds, and neurological
disease, to functional disorders in which no underly-

Anterior (Front)
Healthy phonation
Vocal folds together for phonation
No excessive contraction
Figure 18–6.  Left, closed phase during normal vocal fold vibration. Right, closed phase during vocal
fold vibration in an individual with muscular tension dysphonia. Photos courtesy of Professor Susan Thi-
beault, Department of Surgery, University of Wisconsin Clinical Sciences Center.
ing physical cause is present and the disorder is likely
to respond to behavioral voice therapy. MTD seems
to have characteristics of both organic and functional
voice disorders. Hypercontraction of neck muscles
may be the result of a speaker trying to compensate for
an organic problem in the larynx (e.g., a mass lesion
resulting from phonotrauma), and/or a symptom of
underlying psychological issues (such as anxiety and
depression, all of which may be associated with per-
sonality traits). As stated by Van Houtte, Van Lierde,
and Claeys (2011), MTD is “the bridge between the
purely functional voice disorders . . . and prominent
organic disorders” (p. 205).
Speakers with MTD have strained voiced qualities
that are perceived to be produced with excessive effort.
Hoarseness and breathiness may also be heard. In some
cases, individuals with MTD may be aphonic — unable
to produce phonation even when attempting to use
the voice.
There is controversy surrounding the diagnosis
of MTD. Most often, MTD is confused with a disorder
called spasmodic dysphonia, even when experienced
voice therapists, voice scientists, and otolaryngologists
make the diagnoses (Ludlow et al., 2018). Spasmodic
18  Voice Disorders 253
Muscular tension dysphonia
Vocal folds together for phonation
Hypercontraction, vocal folds compressed
side-to-side, front to back
dysphonia is described later in the section, “Neurologi-
cal Voice Disorders.”
Treatment of MTD
The following information on treatment of MTD is
based on Andreassen, Litts, and Randall (2017), da
Cun Pereira et al. (2018), Ramig and Verdolini (1998),
and the ASHA website on voice therapy (https://www​
.asha.org/PRPSpecificTopic.aspx?folderid=8589942600
&section=Treatment).
Voice therapy for MTD can be direct or indirect.
In a direct approach, the therapist works on the indi-
vidual’s ability to produce a better voice. Indirect
approaches may involve education about voice produc-
tion and vocal hygiene (taking good care of the voice
mechanism), and counseling when anxiety and depres-
sion are believed to play a significant role in MTD.
The general consensus is that voice therapy for
MTD is often successful, but that a specific technique
among several available has not emerged as a clear
choice for maximally effective treatment (Andreassen
et al., 2017). Psychological counseling may be a com­
ponent of MTD, if the health care team believes there
254 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
is a mental health issue as one of the causes of the dis-
order (Dietrich, Verdolini Abbott, Gartner-Schmidt, &
Rosen, 2008).
Voice Therapy by Straw
A therapy technique called “semi-
occluded vocal tract” has shown promise in the
treatment of MTD. Recall from Chapter 10 that
phonation is initiated when the vocal folds are
brought together and then blown apart when
the air pressure below them (in the trachea) is
sufficiently greater than the air pressure above
them (in the vocal tract). As long as this pressure
difference is maintained, the vocal folds vibrate,
each cycle of vibration defined by an opening,
closing, and closed phase. To a large degree, the
force with which the vocal folds close against
each other increases as the pressure difference
across the vocal folds increases. In MTD, part
of the phonation problem is that the exces-
sive tension in head and neck muscles results
in overly forceful closure of the vocal folds.
Using the semi-occluded vocal tract technique,
individuals learn to reduce the excessive closing
force by phonating into a straw. Phonation into
the straw (usually submerged in water) creates
a partial “block” of the air coming through the
vocal tract, which raises the vocal tract pressure
to a value closer to the pressure below the vocal
folds. This reduces the pressure across the vocal
folds and therefore reduces the force of vocal fold
closing. The reduced force is thought to lead to
a less-tense voice, which helps the patient learn
a more relaxed voice quality. Straw phonation
is gradually eliminated during therapy, with a
goal of transferring the reduced-force vocal fold
closing to more natural speech.
Puberphonia
Another functional voice disorder that responds well
to treatment is puberphonia (sometimes called muta-
tional falsetto). This is a disorder of voice pitch in which
a postpubescent male with a normal-sized larynx pro-
duces phonation with very high F0, well outside the
range typical for adult males. Examination of the lar-
ynx fails to show any abnormality or underdevelop-
ment of laryngeal structures that would be consistent
with the high-pitched voice.
5 
 he description of the specific nerve paralysis responsible for the vocal fold appearance applies to one branch of the nerves that supply the
T
larynx. There is a nerve that supplies a single muscle of the larynx — the muscle that stretches the vocal fold. This nerve can also be paralyzed,
but it is not considered further in this chapter.
Treatment of Puberphonia
Puberphonia, a functional voice disorder considered
to have psychogenic origins, is treatable. Once patients
are shown the ability to generate a male-appropriate
voice pitch, there seems to be little problem in main-
taining a gender-appropriate pitch (Roy, Peterson,
Pierce, Smith, & Houtz, 2017).
Neurological Voice Disorders
Neurologic disorders that affect phonation are seen fre-
quently in voice clinics (De Bodt et al., 2015). Degenera-
tive neurologic diseases, such as Parkinson’s disease,
multiple sclerosis, and amyotrophic lateral sclerosis
often have a voice problem as a prominent symptom.
The same can be said of strokes in adults, head injuries
in children and adults, and congenital neurologic dis-
eases such as cerebral palsy. The focus in this chapter is
on dysphonia in two neurological diseases: vocal fold
paralysis and spasmodic dysphonia.
Unilateral Vocal Fold Paralysis
Vocal fold paralysis has many causes, including inflam-
matory conditions, neck or chest trauma, neck or chest
tumors, and surgical procedures. A diagnosis of vocal
fold paralysis implies an absence of innervation by the
nervous system to one or both folds. There are also
cases of vocal fold paresis (“paresis” means “weak”),
in which the affected fold is not completely paralyzed
but is weakened to varying degrees by dysfunction of
the nerves supplying the larynx (Syamal & Benninger,
2016). Many of the symptoms of vocal fold paralysis
and vocal fold paresis are similar; therefore, the follow-
ing discussion focuses on paralysis.
The nerves that control contraction of laryngeal
muscles exit the brainstem and run down the neck and
chest where they are susceptible to compression trauma
(e.g., from upper chest injuries) and accidental surgi-
cal damage (e.g., removal of part or all of the thyroid
gland). Nerves supplying the larynx are on both sides of
the neck; surgical or traumatic injuries may affect only
one side, resulting in unilateral vocal fold paralysis.
Figure 18–7 shows two images of unilateral vocal
fold paralysis, one during inhalation (left), and the other
when the speaker was attempting to phonate (right).
The paralysis of the left vocal fold (right, in the image)
is due to injury to the nerve that innervates the main
muscle of the vocal folds as well as muscles that open,
close, and compress them.5
 18  Voice Disorders 255

Paralyzed vocal fold

Anterior (Front)

Unilateral paralysis of left Unilateral paralysis of left vocal fold

vocal fold attempt to bring vocal folds together
inhalation

Figure 18–7.  Unilateral vocal fold paralysis. Left, paralysis of left vocal fold during inhalation; right,
paralyzed vocal fold during closed phase of phonation. Note the inability of the paralyzed vocal fold to
reach the midline for closure. Photos courtesy of Professor Susan Thibeault, Department of Surgery, Uni-
versity of Wisconsin Clinical Sciences Center.

The image on the left shows the vocal folds open
for inhalation. Compared with the healthy, right vocal
fold, the paralyzed fold is shorter; in many cases, a par-
alyzed vocal fold appears to have less mass compared
with a healthy fold.
The image on the right shows the position of the
paralyzed vocal fold during the closed interval of
vocal fold vibration. Note the lack of contact between
the two vocal folds and the slightly curved appearance
(“bowed”) of the paralyzed fold.
A paralyzed vocal fold can vibrate for phonation.
This is because the rapid opening-and-closing motions
of the vocal folds for phonation are controlled by air
pressures and air flows, not by direct muscular contrac-
tions (see Chapter 10 and earlier discussion). However,
the loss of muscular control of the paralyzed vocal fold
makes it difficult to achieve adequate vocal fold closure
for each cycle of vibration. The paralyzed vocal fold
vibrates, but weakly.
The loss of muscular control of the paralyzed
vocal fold affects voice quality. As reviewed by Sam-
lan and Story (2017), a paralyzed vocal fold is likely
to result in a breathy, weak, and strained voice quality.
The strained component of the voice quality reflects
an individual’s attempt to overcome the inability to
achieve good closure of the folds by means of excessive
effort. People with a paralyzed vocal fold may experi-
ence fatigue when phonating for extended periods of
time; it is hard work to produce voice when the vocal
folds cannot close effectively.
Treatment of Unilateral Vocal Fold Paralysis
Treatment of unilateral vocal fold paralysis combines
direct voice treatment with surgical techniques. Direct
voice therapy focuses on improving speech breathing
to manage the airflow problems of a “leaky” glottis,
and voice exercises to achieve better vocal fold clo-
sure for the closed phase of vibration. Effort exercises,
such as pushing against a fixed-position surface (e.g., a
wall) or pulling up on the underside of a chair while
sitting in it, may be used to evoke closure of the glottis
during phonation.
Surgical techniques to improve phonation in uni-
lateral vocal fold paralysis may or may not include
the injection of biomaterials into the paralyzed fold
to “plump it up.” This provides a larger mass against
which the healthy fold can make contact for phonation.
Another popular surgical technique is to reposition
the paralyzed fold closer to the midline, so it is easier
256 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
for the healthy fold to contact it during vibration. The
measure of success of these surgical techniques is an
improved voice quality, as well as better swallowing
function (see Chapter 20).
Bilateral vocal fold paralysis, a rare disorder in
which the nerves serving the muscles of the larynx are
damaged on both sides of the neck, is a life-threatening
condition. Because the nerves control the single muscle
of the larynx that separates (abducts) the vocal folds,
paralysis on both sides prevents separation of the folds
for inhalation. A tracheostomy (opening in the neck,
below the vocal folds) is a common way to provide a
patient with an alternate airway to sustain life. Another
surgical approach is a permanent repositioning of one
or both vocal folds away from the midline to restore
the natural airway (Naunheim, Song, Franco, Alkire,
& Shrime, 2017).
Spasmodic Dysphonia
Spasmodic dysphonia (SD) is a rare voice disorder
regarded by a majority of voice specialists as a neu-
rological disease. The estimated prevalence of SD is 1
in every 100,000 people. This estimate is complicated
by disagreement among professionals as to the nature
and even existence of the disorder as a neurologically
based voice disorder (Hintze, Ludlow, Bansberg, Adler,
& Lott, 2017).
Patients diagnosed with SD typically have inter-
mittent, irregularly occurring voice spasms when they
attempt to phonate; they may also have voice tremors
(shaking voice). The spasms are related to massive and
sustained hypercontraction of laryngeal muscles. In
some cases, hypercontraction is observed in muscles
above the larynx, such as the tongue. Patients with SD
appear to be exerting tremendous effort to initiate and
maintain phonation.
SD is a controversial disorder. The reader may
notice a similarity between symptoms of SD and those of
MTD. The two diagnoses — SD, implying a neurologic
cause, MTD a psychological cause, are often in dispute.
Voice specialists who are asked to make a diagnosis of
one or the other disorder, based on audio recordings of
speech or views of the vocal folds during phonation,
often disagree. Even the case histories and other charac-
teristics of the individuals with the two disorders can be
very similar. For example, in both disorders, a large per-
centage of patients are women, typically professional
and/or frequent voice users in the middle years of life.
Many patients with either of the two diagnoses report a
traumatic event preceding the onset of voice symptoms.
Botox  injections in laryngeal muscles are effective for about 3 to 4 months. Patients return for periodic injections to maintain the ability to
6 
phonate without spasms.
Differences between SD and MTD include the fol-
lowing: (a) SD does not seem to respond to voice ther-
apy in the way described previously for MTD; (b) the
symptoms of SD seem to be sensitive to specific speech
sounds, whereas the symptoms of MTD are more con-
stant regardless of which speech sounds are produced;
and (c) a significant number of patients with SD have a
voice tremor, and patients with MTD do not.
Treatment of Spasmodic Dysphonia
SD, as mentioned earlier, does not respond well to
behavioral voice treatment. SD is treated by injection
into the vocal folds or other muscles of the larynx of
the neurotoxin botulinum toxin. Botulinum toxin inhib-
its the release of the neurotransmitter acetylcholine at
the junction of motor nerves and muscle fibers. Acetyl-
choline is required for the contraction of muscles. By
inhibiting the release of acetylcholine to laryngeal mus-
cles, laryngeal spasms are less likely to occur, allow-
ing patients to phonate more or less normally until the
effect of the drug wears off.6
Cancer of the Larynx
The vocal folds are affected in about 50% of laryngeal
cancers, but cancer can occur at any site in the larynx.
Cancer of the larynx is almost always a disease of
adulthood and is substantially more frequent in males
compared with females. At age 60 years, the 2005 inci-
dence in males and female was approximately 35 in
100,000 and 5 in 100,000, respectively (Schultz, 2011).
In most cases, cancer of the larynx is a result of
long-term tobacco and/or alcohol use. Other environ-
mental factors (such as exposure to certain chemicals)
also contribute to the risk of laryngeal cancer.
Often, the initial symptoms of laryngeal cancer
are voice changes that become increasingly severe
over time. The dysphonia in laryngeal cancer has been
described as hoarse, rough, and irregular. Cancerous
lesions on the vocal folds interfere with the motions
essential to normal phonation. The dysphonia worsens
as the lesions increase in size.
Treatment of Cancer of the Larynx
An initial bout of dysphonia may not be regarded as
unusual by an individual. Voice changes such as lar-
yngitis may interfere with phonation for several days
or even longer but may not seem to warrant a visit to
an otolaryngologist. Even persistent voice changes

coupled with swallowing problems may not seem like
compelling reasons to see a physician.
Laryngeal cancers in early stages may be treated
by surgeries to remove the lesion while preserving
sufficient tissue for voice production and swallowing.
More advanced stages of laryngeal cancer require more
extensive surgeries, ranging from removal of large
parts of the larynx to removal of the entire larynx. This
latter procedure, called a laryngectomy, requires the
creation of a new airway because the path through the
larynx is eliminated. The trachea is attached via a small
opening in the front of the neck, providing the ability
to breathe for life.
Surgeries for the removal of laryngeal cancers are
performed with an objective of restoring the ability
to produce speech with a sound source. Most often,
a valve connecting the trachea with the esophagus is
inserted during surgery. Air within the trachea is con-
nected to the esophagus; when tracheal pressure is
raised in the respiratory system, the increased pressure
is forced through into the esophagus. The esophageal
pressure causes sound-producing vibration of the ring
of muscles at the top of the esophageal tube, resulting
in a sound source for the articulation of speech sounds.
The sound source does not have the quality of vibrat-
ing vocal folds, but it is sufficient for intelligible speech.
Other techniques for a substitute sound source follow-
ing removal of the larynx are also available (Sapienza
& Ruddy, 2017).
Pediatric Voice Disorders
Many vocal fold conditions/diseases that result in dys-
phonia are similar to those described previously for
adults. The summary that follows is based on a selected
group of relevant publications (Lee, Roy, & Dietrich,
2018; Possamai & Hartley, 2013; Smillie, McManus,
Cohen, Lawson, & Wynne, 2014; Smith, 2013; Verdo-
lini Abbott, 2013). A comprehensive textbook on voice
disorders in children has been written by Kelchner,
Brehm, and Weinrich (2014).
Prevalence of Childhood
Voice Disorders
The prevalence of voice disorders in children has been
estimated to be 4% to 6%. Some authors believe the
prevalence may be even greater because a childhood
dysphonia may not be regarded as a health concern.
The prevalence estimate of 4% to 6% is similar to the
prevalence estimate of voice disorders in the adult pop-
ulation (Bainbridge et al., 2017).
18  Voice Disorders 257
The child larynx is not simply a scaled-down ver-
sion of the adult larynx (Chapter 10). Most importantly,
the layer structure of adult vocal folds is not fully
developed in children. Benign vocal fold masses are, in
adults, typically located within the cover of the vocal
folds ​— the outer two layers. In adults, it is relatively
easy to remove a mass such as a polyp and reattach the
cover to preserve near-normal phonation. In children,
the absence of well-defined outer layers increases the
difficulty of a surgeon’s task to remove a mass without
damaging the developing layers.
Types of Childhood Voice Disorders
Vocal nodules are the most frequent cause of dyspho-
nia in childhood. The cause of vocal nodules in chil-
dren is similar to their cause in adults — phonotrauma,
resulting from excessive closing forces during vocal fold
vibration, and subsequent damage to the outer edges of
vocal fold tissue. The dysphonia heard in cases of child-
hood vocal nodules is often described as hoarseness.
Other benign vocal fold masses such as polyps and
cysts are found in children. Like nodules, these masses
have the potential to interfere with adequate vocal fold
closure. Also like nodules, polyps, and cysts in adults,
the interference with closure may result in the compen-
sation of excessive muscular effort to achieve closure.
The original problem — poor closure of the vocal folds
due to a phonotrauma-related mass — is magnified by
attempts to overcome the dysphonia with increased
phonotraumatic behaviors.
For children under the age of about 12 years, vocal
nodules are more common among boys compared
with girls. There is evidence that children — and per-
haps especially boys — with extraverted, talkative, and
immature behavior styles are more likely to develop
vocal nodules. Similar evidence of a link between per-
sonality type and vocal nodules exists for adults (Roy,
Bless, & Heisy, 2000).
Treatment of Childhood
Voice Disorders
The treatments described earlier for adult voice dis-
orders are, in many cases, applied in childhood voice
disorders. Vocal fold nodules are first treated with
behavioral therapy to minimize talking for a period of
time, and to teach and practice the use of a “normal”
voice. When nodules do not respond to voice therapy,
the masses may be removed surgically. Polyps and
cysts are more likely than nodules to be treated surgi-
cally and followed up with voice therapy.
258 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Chapter Summary
There are many different types of voice disorders, with
many different causes.
Dysphonia is the term used to describe a voice that
seems abnormal in pitch, loudness, and/or quality.
Based on survey data, it is estimated that approxi-
mately 6% to 7% of the adult population experiences
dysphonia over any 12-month period.
Dysphonia is more common among professional
voice users (teachers, singers, actors) than in the gen-
eral population and can have profound effects on
social, emotional, and employment aspects of life.
A case history, perceptual evaluation, laryngo-
scopic study of the vocal folds, and measurement of
acoustic and aerodynamic parameters are important to
the accurate diagnosis of a voice disorder.
Important acoustic measures of the voice include
fundamental frequency (F0), intensity, and a voice
spectrum; the perceptual correlates of these measures
are pitch, loudness, and quality, respectively.
Voice disorders are classified in several ways
that overlap; the different classifications are not
independent.
Voice disorders can be classified along a hypo-
hyperfunctional continuum that ranges from very
weak to overly forceful closure of the vocal folds dur-
ing their vibration.
Phonotrauma is a classification for a group of voice
disorders resulting from excessive use of the voice that
results in damage to vocal fold tissue, which in some
cases may lead to nodules, polyps, and other lesions on
the vocal folds.
Organic voice disorders are classifications of dys-
phonias caused by benign mass lesions on the vocal
folds such as nodules and polyps, which typically are
the result of phonotrauma.
Functional voice disorders are dysphonias in
which there is no laryngeal pathology that explains the
disorder, as in MTD; a subset of functional voice disor-
ders, called psychogenic voice disorders, are thought to
have their roots in psychological disorders.
Neurological voice disorders are those in which
damage to peripheral nerves or structures of the central
nervous system affects vocal fold vibration as a result
of weakness, paralysis, or dyscoordination of laryngeal
muscles; laryngeal spasms during phonation may also
reflect a central nervous system disorder.
Laryngeal cancer may occur anywhere within the
larynx; lesions of the vocal folds occur in nearly half
of all laryngeal cancers and interfere with vocal fold
vibration and therefore result in dysphonia.
Treatment for voice disorders ranges from direct
therapy to reduce or eliminate dysphonia, includ-
ing voice exercise and laryngeal manipulation, indi-
rect therapy to counsel patients on issues that may be
associated with dysphonia, and surgical techniques to
remove benign masses and cancerous lesions.
Pediatric voice disorders such as benign vocal fold
masses result in a dysphonia often called “hoarseness”
and may not be recognized by parents or teachers as
a disorder requiring professional attention; a combi-
nation of voice and/or surgical therapy may be used
for pediatric voice disorders, depending on the type of
pathology causing the dysphonia.
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Craniofacial Anomalies
Introduction
Craniofacial anomalies include a wide range of dis-
orders with effects on speech production that are, in
a general sense, predictable from the structural (ana-
tomical) problems in the head and neck area. This
chapter describes the origin and nature of craniofa-
cial anomalies and relates the structural problems to
speech production problems. In addition, the concept
of syndromes is introduced. A craniofacial anomaly is
often one component of a syndrome, in which there
are multiple anomalies. The knowledge that cranio-
facial anomalies are often a syndrome component is
important in health care settings where the totality of a
child’s needs must be considered and integrated across
various specialists who treat the different problems.
Definition and Origins of
Craniofacial Anomalies
A craniofacial anomaly is defined as any deviation from
normal structure, form, or function in the head and
neck area of an individual. The craniofacial anomalies
that receive the most attention in this chapter are cleft
lip and cleft palate. Cleft lip and cleft palate can occur
independently of each other but often occur together. To
appreciate the potential independence of cleft lip and
cleft palate, basic aspects of embryological development
of head and neck structures must be considered. For a
19
more in-depth presentation of general embryology and
with excellent chapters on head and neck embryology
see, Schoenwolf, Bleyl, Brauer, and Francis-West (2014)
and Moore, Persaud, and Torchia (2019).
Most cases of cleft lip and/or cleft palate result
from errors in embryological development that result
in incomplete or incorrectly formed structures. People
who study such embryological errors are called dys-
morphologists; dysmorphogenesis is the process of
abnormal tissue development during embryological
development.
Embryological Development
of the Upper Lip and
Associated Structures
Figure 19–1 shows a photo of an embryo, 26 to 28 days
after fertilization; an artist’s drawing of the embryo
is at the right. The view is from the side. The struc-
tures labeled “Pharyngeal arches” are duplicated on
the other side of the embryo (that is, the structures of
the embryo are bilaterally symmetrical). Each of the
pharyngeal arches, the four ridges in sequence along
the side of the embryo, are separated from the adjacent
arch by a deep groove. The pharyngeal arches are num-
bered from one (closest to the head) to four as labeled
in Figure 19–1. A fifth and sixth pharyngeal arch are
located behind the fourth, but they lack the prominent
ridge-like bulge of the first four and are not easily seen.
261
262 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Figure 19–1.  Left, photo of embryo 26 to 28 days after fertilization; right, artist’s drawing of the
embryo with first four arches labeled.
The pharyngeal arches are the source of embryo-
logical tissue for the development of the majority of
head and neck structures. The first pharyngeal arch is
the source of tissue for the development of the lower
lip, jaw, upper lip, and hard palate, as well as many
structures of the ear.
A frontal view of the embryonic head tissue that de-
velops into head and neck structures is shown at 5,
6, 8, and 10 weeks post-fertilization in Figure 19–2.
The structures labeled “mandibular prominence” and
“maxillary prominence” are generated from the first
pharyngeal arch. In the center of the embryo, the small
space just above the mandibular prominence (hence-
forth, “mandibular arch”) is the primitive mouth which
is called the “stomodeum.” Embryological develop-
ment of the mandibular arch results in the lower jaw
(the mandible). The development of the maxillary
prominence results in the fully formed upper lip, parts
of the nose, a small wedge of bone that will eventually
contain the upper four front teeth, and the bones that
form the roof of the mouth. Most of the muscular soft
palate (velum) is formed from the 4th and 6th pharyn-
geal arch.
The formation of the upper lip and its associated
structures proceeds as follows. Roughly 6 weeks after
fertilization, the two maxillary prominences begin to
“push” toward the center of the face. The nearly circular
Pharyngeal arches
12 3 4
structures right next to the maxillary prominences (Fig-
ure 19–2, upper right panel), which could be mistaken
for the primitive eyes but are actually the early version
of the nose, are moved toward the center of the face by
this push.
As the maxillary prominences and circular struc-
tures move toward the center of the face, they begin
to fuse, meaning that tissues of the two structures knit
together. Figure 19–2 shows this process as a sequence
of drawings over time. The fusion is complete around
10 weeks, and when successful creates an upper lip that
is continuous from the right to left corner of the mouth,
a well-formed nose, and a small wedge of bone in the
front of the mouth. Figure 19–3 (discussed further in
the next paragraphs) shows on the right another view,
looking up at the roof of the mouth at the completed
upper lip and wedge of bone. Keep in mind that the
wedge of bone that will contain the upper four teeth is
formed with the upper lip and soft tissue of the nose. It
is not considered part of the hard palate, even though
it becomes bone.
Figure 19–3 shows the formation of the hard pal-
ate in two views, one looking directly into the mouth
(left column of images), and the other looking up at the
roof of the mouth (right column of images). At 7 weeks,
the two shelves of embryological tissue (called the
palatine shelves, see Figure 19–3) that become the

5 weeks
Maxillary
prominence
Mandibular
prominence
8 weeks
Maxillary
prominence
Mandibular
prominence
Figure 19–2.  Embryological development of upper lip and associated structures, nose, philtrum, inter-
maxillary segment (wedge of bone with upper four front teeth, see Figure 19–3), at 5, 6, 8, and 10 weeks
post-gestation).
bony hard palate are widely separated; there is an
open space between them. The top image in the left
column shows why this is so. The palatine shelves are
oriented at a downward angle and, in fact, are beneath
the tongue tissue that is high in the mouth because the
mandible (lower jaw) is still very small. The embryologi-
cal tongue prevents the palatine shelves from “snapping
up” into the horizontal position, which is required for
the shelves to meet and fuse, thus forming the hard
palate. As indicated by the downward-pointing arrow
(left column, top image), the tongue must be low-
ered to get out of the way of the palatine shelves. The
right-hand image at 7 weeks, this view from above the
tongue and looking directly up at what becomes the roof
of the mouth, shows the wide separation between the
palatine shelves.
19  Craniofacial Anomalies 263
6 weeks
Eye
Stomodeum
10 weeks
Eye
Philtrum
At 9 weeks, the tongue has lowered, and the pala-
tine shelves have snapped up into the horizontal posi-
tion (seen in both the left and right images of the middle
row). The lowering of the tongue is made possible by
growth of the mandible, which allows the tongue to
drop down in the mouth and free the palatine shelves
to move. The shelves are not yet touching each other
as shown in both of these middle row images, but the
opening between the shelves is smaller at 9 weeks than
it was at 7 weeks.
The tissue of both shelves grows toward the
midline to fuse and form a continuous hard palate that
separates the oral cavity from the nasal cavity. This
growth is indicated in the image in the right column
by the short horizontal arrows pointing toward each
other.
264 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

7 weeks

Primary
Nasal palate
chamber Nasal
Septum

Palatine
Tongue shelf

9 weeks

Primary
Nasal Nasal palate
chamber Septum
Palatine
shelf

Tongue

12 weeks

Nasal Incisive
chamber foramen
Nasal
Septum

Fused
palatal shelves
Oral
cavity
Tongue
Uvula

Figure 19–3.  Embryological development of hard and soft palates at 7, 9, and 12 weeks post-
gestation. Note at 7 weeks palatine shelves trapped under tongue; at 9 weeks mandible has grown
substantially, allowing tongue to drop in oral cavity so palatine shelves can snap up into horizontal
position and grow to midline where they fuse together, front to back. Left column of images, look-
ing directly into the mouth; right column of images, looking upward to the roof of the mouth.

The bottom images show the fused palatine shelves
forming a continuous hard palate. The closure of the
hard palate is seen looking up to the roof of the mouth
(left image) and in the frontal view (right image).
The images at the bottom show the development
of the structures at 12 weeks post-gestation. The image
in the right column contains a vertical arrow point-
ing from the front of the mouth to the back. This is the
direction of fusion of the hard and soft palates. Fusion
occurs first at the front, immediately behind the yellow
wedge of bone described previously. Fusion continues
systematically from front to back, like a closing zipper.
This fusion pattern is important for understanding par-
tial clefts of the palates, which are discussed later.
Embryological Errors and
Clefting:  Clefts of the Lip
Cleft lips are the result of an error (dysmorphogenesis)
in the embryological process of upper lip develop-
ment. The errors are failures of tissue moving from the

two sides of the developing lip to meet each other and
“knit” tissue together to form a continuous lip. These
embryological errors occur in varying degrees, and on
one or both sides of the lip midline. A cleft on one side
only is a unilateral cleft lip; a cleft on both sides is a
bilateral cleft lip. Unilateral cleft lips are more common
than bilateral cleft lips.
Unilateral cleft lips may be partial, sometimes no
more than a “notch” in the upper lip, or a cleft that is
halfway between the upper lip and floor of the nostrils.
A complete unilateral cleft lip extends into the base of
the nasal cavity (Figure 19–4, left). Note how the cleft
is to the left of the center of the mouth (see Box, “More
Embryology”).
More Embryology
Two questions that are often asked
by students about orofacial embryology are as
follows: (a) why are clefts of the lip off the midline
(to the left or right of the center of the mouth),
and (b) what is the meaning of a unilateral versus
bilateral cleft of the palate? Both questions can be
answered with reference to Figure 19–3. First, note
in the right-hand column of images the boundar-
ies between the yellow wedge of bone (called the
intermaxillary segment) and the front part of the
maxillary arch (the pink part). Remember that
the embryological formation of the intermaxillary
segment is part of the formation of the upper
lip. The boundaries between the intermaxillary
segment and the maxillary arches are off center;
Unilateral, complete cleft lip
Figure 19–4.  Left, complete, unilateral cleft of the lip; right, complete bilateral clefts of the lip.
19  Craniofacial Anomalies 265
Figure 19–4, right, shows bilateral (both sides),
complete clefts of the upper lip. The mass of tissue
in the center of the lip is the intermaxillary segment
(wedge of bone in Figure 19–3, in yellow), which like
the lip is cleft on both sides and therefore not attached
to the maxillary arch (pink in Figure 19–3).
Embryological Errors and
Clefting:  Clefts of the Palate
Clefts of the palate are the result of an error in develop-
ment of the palatal shelves, or of the mandible, or both.
Like clefts of the upper lip, clefts of the palate occur in
they are also the location of fusion of embryo-
logical tissue to make a complete upper lip. An
embryological error of failure to fuse tissue occurs
at these boundary points ​— ​hence, the lip clefts
are to the side of the center of the mouth. Second,
note in the left-hand column of images the nasal
septum, which during embryological development
of the palate descends and fuses with the nasal
surface of the palate. What happens to the nasal
septum when there is a cleft palate? Either the
nasal septum is attached to one maxillary (palatine)
shelf, or it is attached to neither. A unilateral cleft
palate is when the septum is attached to one
shelf; a bilateral cleft palate is when the septum is
attached to neither shelf.
Bilateral, complete cleft lip
266 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

varying degrees, from a minimal, notch-like split at the
back of the soft palate to a full split from the back of the
soft palate to the bone wedge formed with the develop-
ment of the upper lip. Figure 19–5 shows drawings of
three degrees of cleft palate severity, ranging from the
notch-like defect in the back of the soft palate (left), to
a partial cleft of the soft and hard palates (middle), and
to a complete defect of the hard palate, extending to the
wedge of bone formed with the upper lip. The middle
image shows a partial cleft of the soft and hard palates;
the dashed line is the approximate boundary between
the hard and soft palates.
Clefts of the palate also result when the mandible
fails to grow sufficiently to allow the tongue to lower
in the oral cavity so that the palatine shelves are free
to snap up in the horizontal position. As previously
described, early in the embryological development
of the hard palate, the palatine shelves are trapped
beneath the developing tongue tissue. When the man-
dible fails to grow at a specific time during the embry-
ological schedule of development, the two shelves
remain trapped and lose their ability to fuse together.
The cleft palate is a result not of a primary embryo-
logical error of palatal development, but of a primary
error of mandible development that prevents the pala-
tine shelves from lifting and fusing. The mandible may
eventual grow sufficiently to allow the tongue to drop
in the oral cavity, and the palatine shelves may elevate
to the horizontal position. The problem is that the tis-
sue growth required of the two palatine shelves to
extend to the midline for fusion is, like much of the rest
of embryological development, on a schedule. When
the schedule is not met or prevented, as when the high
tongue prevents the shelves from meeting their time
for growth, the schedule for the growth is cancelled.
Photos of partial and complete clefts of the palate
are shown in Figure 19–6. A partial cleft is on the left
and a complete cleft is on the right. The partial cleft
on the left is called a submucous cleft. The mucous
membrane that covers the muscles of the soft palate
is intact, but the underlying muscle is cleft. Note the
small “notch” (arrow) in the soft palate. A complete
cleft of the hard and soft palates is seen on the right of
Figure 19–6. Both photographs show clefts of the palate
in the absence of clefts of the lips.
Cleft Lip With or Without a
Cleft Palate; Cleft Palate Only
(Isolated Cleft Palate)
As noted, cleft lips and palates occur as independent
dysmorphologies. Children are born with cleft lips but
a fully formed palate, or isolated cleft palates with a
fully formed upper lip. Some scientists and clinicians
believe, however, that a cleft lip with a cleft palate is
a more severe form of cleft lip alone. In other words,
clefting of the lip and palate together is viewed as one
category of clefting, with cleft lip alone being a less
severe form of the defect. This category is referred to
as cleft lip with or without a cleft palate (abbreviated
as CL/P).
Isolated cleft palate (abbreviated as CPO) is
regarded as a category separate from CL/P. The dis-
tinction between the two categories is made because
(a) sex ratios computed for babies born with clefts favor
boys for CL/P but favor girls for isolated cleft palate;
(b) the incidence (frequency of occurrence) of the two
categories is different — approximately 1 in 700 babies
are born with CL/P, but the incidence for isolated cleft

Figure 19–5.  Left, a partial cleft of the soft palate; center, partial cleft of soft and hard palates, extending from
the back of the soft palate to the middle of the hard palate; right, complete cleft of the soft and hard palates. The
dashed, horizontal line is the approximate boundary between the hard and soft palates.

Submucous cleft palate
Figure 19–6.  Left, partial cleft of the soft palate, submucous cleft with a small notch indi-
cated by arrow; right, complete cleft of hard and soft palates.
palate is about 1 in 2,000; and (c) CL/P occurs more fre-
quently in certain racial groups as compared to others
(e.g., more frequently in Asian as compared to African
American populations), but isolated cleft palate does
not seem to vary with racial group (Shkoukani, Law-
rence, Liebertz, & Svider, 2014).
Epidemiology of Clefting
The epidemiology of clefting is complicated because it
depends on where the data were collected. Prevalence
of clefting at birth varies by country. European birth
registries for the years 1993 to 1998 showed a substan-
tially higher rate of CL/P in Sweden and Norway com-
pared with Spain. Even within a single country, such as
France, the rate of CPO for the same years was higher
than the rate of CL/P.
An average global estimate of the prevalence of
orofacial clefting (both CL/P and CPO) is about 1 in
every 700 live births (Mossey, Little, Monger, Dixon,
& Shaw, 2009). In the United States, the prevalence
of live-birth clefting is lower, estimated at 1 in every
940 live births for Cl/P, and 1 in every 1,574 for CPO
(Parker et al., 2010).
In a Norwegian study covering nearly 2,700 live
births of children with clefting between the years 1967
and 1998, CL/P was roughly 1.5 times more likely than
CPO. The same study reported that 42% of these chil-
19  Craniofacial Anomalies 267
Complete cleft palate
dren had clift lip only, and 58% had a cleft lip and cleft
palate (Harville, Wilcox, Lie, Vindenes, & Abyholm, 2005).
Prevalence of CL/P in different countries should
be kept in mind when thinking about the place of cleft-
ing in the big picture of medical care. In the United
States, CL/P is among the most common birth defects.
For more information, see: https://www.asha​
.org/PRPSpecificTopic.aspx?folderid=8589942918&​
section=Incidence_and_Prevalence
Speech Production
in CL/P and CPO
As presented in Chapter 10, the velopharyngeal port
(hereafter, VP port) is the passageway between the oral
and nasal cavities. The VP port is opened and closed
by muscular forces. These forces lift the soft palate to
the posterior pharyngeal wall, as shown in Figure 19–7.
The salmon-colored soft palate is shown in the open
position, which allows airflow coming from the lungs
and through the larynx to pass through the pharynx,
into the nasal cavities, and through the nostrils to the
atmosphere. In contrast, when the soft palate is lifted by
muscular forces, it is pushed against the posterior pha-
ryngeal wall (soft palate shown as red structure with
dashed outline). The muscular lift of the soft palate is
accompanied by muscular activity of the pharyngeal
walls. Pharyngeal muscles squeeze the sides of the soft
268 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Nasal cavities

Soft palate
Lips
Tongue Pharynx

Vocal
folds

Figure 19–7.  Vocal tract with lips closed for bilabial stop con-
sonant /b/. With the VP port open (salmon-colored soft palate) the
airflow leak into the nasal cavities prevents the pressure buildup in
the vocal tract required for correct production of /b/. With the VP
port closed (red soft palate) the vocal tract is completely sealed and
pressure can be developed for /b/.

palate. These muscular actions — lifting the soft palate
and squeezing its sides when it makes contact with the
back (posterior) wall of the pharynx — close off commu-
nication between the nasal cavities and oropharyngeal
cavities. The effect of squeezing the sides of the soft
palate with contraction of the pharyngeal muscles is as
relevant to VP closure as the contact of the soft palate
with the posterior pharyngeal wall.
Opening of the velopharyngeal port from the
closed position is largely due to relaxation of the lifting
and squeezing muscles which allows gravity to pull
down on the soft palate. A small degree of muscular
contraction may also contribute to opening the VP port.
Overall, the VP port is closed and opened like the tight-
ening and loosening of a sphincter.
The VP port is constantly opening and closing
during speech production, opening for nasal sounds
such as “m,” “n,” and the “ng” sound in words like
“ring,” and closing for vowels and obstruent conso-
nants. In English, the VP port closes for vowels and
other vocalic-like sounds (such as “r,” “l,” “w,” and
diphthongs like the sounds in “eye,” “ay,” and “oy”)
to prevent them from sounding too nasal. These vowel
and vowel-like sounds can be produced with an open
VP port, but they will sound displeasing because of
excessive nasality resulting from the transmission of
sound through the nasal cavities.
Closure of the VP port for obstruent consonants — ​
stops, fricatives, and affricates — is required for the
buildup of oral pressure in the vocal tract. Obstruents
are speech sounds that have a tight or complete con-
striction in the vocal tract. When airflow encounters
these constrictions, pressure behind them rises above
atmospheric pressure provided there is no leak to the
atmosphere. These positive pressures are necessary for
the correct production of obstruents, as discussed in
Chapters 10 and 12. A potential leak through the VP
port is prevented by its closure, so that the effort of
increasing air pressure behind the obstruent constric-
tion is not compromised by the escape of air through
the nasal passageways.
The requirement that the VP port be closed for
production of obstruents is illustrated in Figure 19–7
by closure of the lips for the bilabial stop consonant
/b/. The lip closure seals the vocal tract at its front end
and closure of the VP port seals the vocal tract toward

the back. As air flows into the closed volume of the
vocal tract, pressure builds up, just as it should for a
stop consonant. A completely sealed vocal tract cavity
is necessary for all stops, fricatives, and affricates.
This review suggests two major problems when an
individual does not have good control over the open-
ing and closing of the VP port during speech produc-
tion. First, the individual is likely to have intermittent
or chronic hypernasality. Hypernasality denotes exces-
sive nasality during speech, and especially during
vowels. Hypernasality is regarded by most listeners as
aesthetically displeasing and has the potential to pro-
duce a muffled-sounding sequence of sounds, mak-
ing speech relatively difficult to understand. Second,
a speaker who has difficulty closing the VP port can-
not produce obstruents correctly because of a partial
or complete inability to develop a positive pressure in
the vocal tract. An open VP port during an attempt to
produce a stop consonant results in air leaking through
the nasal cavities and into the atmosphere. This makes
it nearly impossible to build up and maintain an oral
pressure for the time interval during which the oral
cavity is sealed by either the lips (as in “b” and “p”) or
by contact between the tongue and part of the palate
(“t,” “d,” “k,” “g”). Failure to develop a positive oral
pressure and produce obstruents correctly is likely to
have a major effect on speech intelligibility.
Patients who have problems with control of the VP
port have velopharyngeal insufficiency (typically abbre-
viated VPI). VPI is a matter of degree; patients may
have no control over the opening and closing of the VP
port, whereas others may have some, but not complete
control. It is not unusual for a person with a repaired
cleft palate to have some remaining VPI, and therefore
hints of hypernasality and perhaps audible escape
of air through the nose when he produces obstruent
consonants.
An individual with an unrepaired cleft palate (an
almost nonexistent circumstance in developed coun-
tries for children who are old enough to have speech
and language skills) has VPI of the most severe kind,
because the structural basis for closing the VP port
does not exist. The concept of VPI is more applicable
to those patients born with a craniofacial anomaly and
who have had surgery to restore the structural basis
for opening and closing the VP port. The surgeries are
not only designed to close the palate, thus eliminating
the “hole” in the roof of the mouth, but also to reat-
tach muscles in their proper orientation so the VP port
can be closed for speech production (and, it should
be added, efficient swallowing: see Chapter 20). As
noted previously, surgery does not always eliminate
VPI completely.
19  Craniofacial Anomalies 269
Diagnosis of VPI
Perceptual analysis is one approach to the diagnosis
of VPI. Hypernasality may be judged by listening and
making a qualitative judgment (e.g., mild hyperna-
sality versus severe hypernasality) or using simple
scales, such as a 5-point scale with one end of the scale
defined as “no hypernasality,” and the other end of
the scale defined as “severe hypernasality.” In addi-
tion, listening for consonant errors made by a child
or adult under evaluation for a speech disorder can
be a valuable source of diagnostic information. Most
speech-language pathologists, including those who do
not regularly provide services for children or adults
with cleft palate, are able to listen to a speech sample
from an individual and, with a high degree of certainty,
identify the presence of VPI due to cleft palate.
Perceptual analysis, however, cannot give reliable
information on the magnitude of, or specific reasons
for, the VPI problem. For example, two patients may
have the same-sounding hypernasality and consonant
errors due to VPI but have different underlying reasons
for the VPI. Recall the sphincter-like closure of the VP
port, produced by several different muscles. Different
muscles may be responsible for VPI in different speak-
ers. Precise knowledge of which muscles are contrib-
uting to VPI may have direct implications for surgical
and behavioral treatment of the problem.
Fortunately, speech-language pathologists and
surgeons have techniques for direct visualization of
the VP port. Two of these techniques are described
briefly here; the interested reader can consult Peterson-
Falzone, Trost-Cardamone, Karnell, and Hardin-Jones
(2017), and Kummer (2018, 2020) for further informa-
tion on these and other techniques.
Most patients with craniofacial anomalies and
VPI have x-ray studies performed to gain knowledge
on the function of the VP port. These studies focus the
x-rays at the VP port, from several different angles.
A technique called videofluoroscopy generates x-ray
motion pictures to evaluate movement of VP port
structures during speech. An example of the benefit of
these studies is the ability to determine whether VPI
is due to inadequate movement of the soft palate, the
pharyngeal walls (due to contraction of the pharyn-
geal muscles, as previously described), or both. This
information, which cannot be derived from perceptual
evaluation, is very informative for the combined efforts
of an SLP and craniofacial surgeon to determine future
management of an ongoing problem with VPI.
Another way to visualize the VP port is by means
of a nasoendoscope inserted through the nose and
positioned just above the port. Advantages of this kind
270 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
of examination are the ability to see the entire, circu-
lar perimeter of the port, and to see which parts of the
circle are not moving in cases of VPI. Nasoendoscopy
is usually performed using a topical anesthetic applied
within the nasal cavities. This lessens the discomfort of
the procedure. A skilled endoscoper can collect valu-
able information from this procedure without exposing
the patient to radiation.
VPI and Hypernasality
As previously noted, the VP port opens and closes dur-
ing speech. The three sounds of English called nasals
(“m,” “n, “ng”) are produced with an open VP port
because they are meant to sound nasal. An open VP
port during the production of vowels and other vocalic
sounds, however, causes speech to sound hypernasal.
This is because sound waves move through the nasal
cavities where they produce characteristic nasal reso-
nances. The vowels of the person with VPI therefore
have the characteristic resonances of the vocal tract — ​
those usually associated with vowels and vocalic sounds ​
— mixed with the nasal resonances. It is as if the vowels
are “colored” by nasal acoustic energy, a coloring not
present when the VP port is closed for vowel production.
The idea of closure of the VP port for obstru-
ents and opening for nasals is a simplification of the
behavior of the port during connected speech such as
occurs during conversation. The size of the VP port is
constantly changing during connected speech, from
completely closed to completely open, as well as many
sizes in between these two extremes. The complexity of
VP port behavior during speech produced by a healthy
adult can be observed at https://www.youtube.com/
watch?v=-kHtGlhPs3Y .
Children who are born with a cleft palate and
who have had surgery to repair the cleft around 12
months of age may still, in later childhood, be per-
ceived with excessive hypernasality. Among recently
studied 10-year-olds with repaired clefts and variable
severity of hypernasality, children with greater severity
had other developmental difficulties (such as delayed
language or reading difficulties). Most children with
repaired clefts and “normal” nasality did not have such
problems (Feragen, Auckner, Særvold, & Hide, 2017).
When compared to children who are not hyperna-
sal, children who have a surgically repaired hard palate
but remain hypernasal are perceived as less intelligent,
less likely to make friends, and more likely to be teased
(Watterson, Mancini, Brancamp, & Lewis, 2013). These
are negative social consequences of hypernasality in
cleft palate speech.
VPI, Consonant Articulation,
and Speech Intelligibility
Speech-language pathologists are interested in the kinds
of consonant errors made by individuals who seek ther-
apeutic services for speech intelligibility problems. The
thought is that if a set of errors is identified by means of
careful testing, the nature of specific consonant errors,
or a pattern revealed by several different consonant
errors, can guide a therapy plan (Kummer, 2011).
Clinical observation and formal research stud-
ies have established the kinds of consonant obstruent
errors made by individuals with clefts and VPI. These
errors fall into one of two categories: obligatory errors
and compensatory errors (Kummer, 2011).
Obligatory Errors
Obligatory obstruent errors are produced in the cor-
rect way except for the required closure of the VP port.
For example, a child with a repaired cleft palate and
VPI may produce the correct articulatory placement
for a “d,” with the tongue tip properly placed at the
front of the palate, immediately behind the upper front
teeth. However, the VPI results in air leakage through
the VP port, which prevents the proper buildup of oral
pressure within the vocal tract. The resulting obstruent
speech sound is weak, possibly sounding somewhat
like a nasal of the same place of articulation (e.g., an
“n” instead of the intended “d”). The sound may also
be perceived as a more complex error because there
is audible nasal emission of air during the attempt to
produce the stop. In this case, the sound has stop-like
characteristics but is not heard as correct due to the
nasal emission. Audible nasal emission is the result of
air rushing through the nasal cavities as a result of VPI.
Speech sound errors such as these are called
obligatory because even with correct positioning of the
articulators, other than the soft palate and pharyngeal
walls, the sound is obligated to be produced as an error
because of the VPI.
Compensatory Errors
Unlike obligatory errors, compensatory errors are not
produced with correct placement of the articulators.
Compensatory errors, as the category label suggests,
are a response to VPI, specifically as a way speakers
“solve” the problem of air leakage through the VP port.
The lips are the front end of the vocal tract tube
and the larynx is the back end; the VP port is like a
valve midway between these two locations. The valve,
when open, allows air coming through the glottis to
 19  Craniofacial Anomalies 271

flow through the VP port and into the nasal cavities.
Some speakers with VPI compensate for the leak at
the VP port by forming an articulatory constriction for
an obstruent consonant before (i.e., in back of) the leak.
This is shown in Figure 19–8, where a compensatory
articulation error (right) is contrasted with an obliga-
tory articulation error (left). In both cases, the “target”
sound is /d/, a voiced stop consonant. The left image
shows the constriction in the vocal tract made by the
tongue tip pressing against the palate just in back of
the upper teeth; this is the correct place of articulation
for this sound. The VP port is open, however, which
prevents the required buildup of pressure inside the
vocal tract. The image on the right shows a compensa-
tory solution to this problem. The constriction for the
stop is made in the pharynx, before the airflow reaches
the open VP port.
The place of articulation for all English obstruents
is in front of the VP port. Attempts to produce any of
these sounds with tongue placement in the “correct”
way (obligatory errors) cannot avoid a leak caused
by VPI. Production of obstruents behind the VP port
avoids a leak, allowing a buildup of air pressure behind
the constriction to generate the desired popping noise
of stop consonants and hissing noise of fricatives (see
Chapters 10 and 12).
The compensatory errors produced by children (or
adults) with VPI due to cleft palate are errors of place
of articulation; manner of articulation is retained. The
compensatory stop consonant shown in Figure 19–8 is
produced with the characteristics of a stop (complete
blockage of airflow in the vocal tract for a brief interval,
released suddenly to make the popping noise), but at
the wrong place of articulation.
Many children with repaired cleft palates who
continue to have VPI make these kinds of errors. The
error sounds are called pharyngeal stops, pharyngeal
fricatives, and glottal stops. In pharyngeal stops, the
airstream is completely blocked by placing the back of
the tongue against the posterior pharyngeal wall and
then releasing it suddenly. The articulation of pharyn-
geal fricatives is similar, except that the constriction
formed between the back of the tongue and the pos-
terior pharyngeal wall is not quite complete, allow-
ing air to be forced through the narrow passageway
to generate a hissing noise. Pharyngeal stops are used
to replace the “correct” stops of English (most often
“k” and “g”) and pharyngeal fricatives the “correct”

Nasal
cavities
Nasal
cavities

Outer
nose Outer nose
Velopharyngeal
port

Airflow
Airflow

Figure 19–8.  Left, an obligatory error for /d/, tongue makes the required constriction at the front of the hard palate to
block airflow at the alveolar place of articulation (immediately behind the teeth) but VP port is open due to VPI, preventing
the buildup of pressure within the vocal tract; right, a compensatory error for /d/, tongue blocks air at a place of articulation
behind the leak, in the pharynx, with the resulting speech sound retaining the manner of articulation (stop) but produced
at the wrong place of articulation.
272 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
fricatives (“f,” “v,” “th,” “s,” “z,” “sh,” and “zh”). Note
that the manner of articulation is preserved in these
error patterns.1
Glottal stops are frequent compensatory errors
in speakers with VPI. They are made by bringing the
vocal folds together forcefully and after a short inter-
val blowing them apart with a high tracheal pressure.
The two vocal folds are like two articulators that form
a complete constriction, and the pressure immediately
below them, in the trachea, is like the positive oral
pressure typical of stop consonants. Speakers with VPI
typically substitute glottal stops for the “correct” stops
of English, especially voiceless stops /p/, /t/, and /k/
in words such as “puppy” and “light.”
Many speakers with VPI produce a mixture of
obligatory and compensatory errors. When children
begin producing compensatory errors early in their
developmental history, the errors may become habit-
ual and resistant to therapeutic modification. This
is an argument for early surgery to correct a cleft pal-
ate, to establish a normal or near-normal VP mecha-
nism, and to prevent compensatory errors before they
begin and over time become fixed as part of the child’s
sound system.
Obligatory and compensatory speech sound errors,
or a mixture of both kinds, affects a speaker’s intelligi-
bility. When there is substantial hypernasality in addi-
tion to these errors, the child’s ability to be intelligible,
and thus to communicate, is further impaired (Kum-
mer, 2011).
Palatoplasty and Speech Sound Errors
Palatoplasty is the surgery performed
to close a cleft palate. It is more than simply
closing the hole, however. Muscles that lift and
shape the soft palate for contact with the posterior
pharynx are not attached correctly in a cleft palate;
a critical part of the surgery for speech outcomes
is the reconfiguration and correct attachment
of these muscles to the tissue of the soft palate.
Obligatory speech sound errors are likely to be
eliminated by successful surgery. This is because
the problem in obligatory errors is the inability
to close the VP port — the rest of the articulatory
characteristics are correct for the target sound.
Compensatory errors are not “fixed” by successful
1
 haryngeal stops and fricatives are not part of the sound inventory of English but are present in the sound inventory of Arabic and Hebrew.
P
It may be the case that these sounds are not made with a constriction between the tongue and pharynx, but rather between the epiglottis and
pharynx (Ladefoged & Maddieson, 1996). It is equally possible that an epiglottal-pharyngeal articulation is the basis for some of the compen-
satory errors heard in speakers with VPI.
Clefting and Syndromes
A syndrome is a group of anomalies, including ana-
tomical, physiological, and/or behavioral components,
that are observed in an individual and have been
observed previously in other individuals. Some of the
components of a syndrome may seem unrelated, such
as heart and specific psychiatric problems, but their
presence in a group of individuals suggests that they
are part of a pattern, perhaps with a single, underlying
cause (Shprintzen & Bardach, 1995). Syndromes may
also be defined as a collection of anomalies that occur
together in individuals but without a single, underly-
ing known cause.
The syndromes discussed here are all conditions
present at birth or known to be present at birth. Many
syndromes have a genetic cause, such as velocardio-
facial syndrome and Treacher Collins syndrome (see
later discussion in this chapter). Environmental factors
may also result in syndromes present at birth, such as
fetal alcohol syndrome and syndromes associated with
vitamin deficiencies.
More than 275 syndromes include some form of
craniofacial anomaly (Leslie & Marazita, 2013). Many
of these syndromes are rare; the following summa-
ries are of more frequently occurring syndromes with
CL/P or CPO as a component. The reader is encour-
aged to search the Internet for photographs of indi-
viduals with the syndromes described in the following
sections.
palatoplasty, because the errors are due to more
than the functioning of the VP port. The child with
compensatory errors has, in a sense, learned a new
system for producing obstruents — move the place
of articulation behind the leak. It is almost as if
the child has invented a new sound system to deal
with the available speech structures. This is why
palatoplasty is usually recommended as early as
possible — perhaps 9 to 12 months of age, before
the child is developing the speech sound system
in the context of first words. Compensatory errors
are less likely when VPI is significantly reduced or
eliminated by surgery prior to first words.

22q11.2 Deletion Syndrome
(Velocardiofacial Syndrome)
Children with velocardiofacial syndrome (VCFS), also
known as 22q11.2 deletion syndrome, often have clefts
of the palate. The anomalies appearing most often in
VCFS include an isolated cleft palate (hence, the “velo”
part of the syndrome name), heart defects (hence,
“cardio”), and a characteristic appearance of the face
(“facial”), which has been described as pear shaped
with a long nose having a broad root, a small jaw, and
small ears. Many children with VCFS have learning dis-
abilities, and approximately 10% may develop severe
psychiatric disturbance around the time of puberty.
VCFS is a genetic disorder, involving a deletion of
genetic material on the 22nd chromosome pair. VCFS
occurs in 1/4,000 births, and usually involves speech
and language disorders (McDonald-McGinn & Sul-
livan, 2011). Like many of the genetic disorders dis-
cussed in previous chapters, the phenotype of VCFS
varies widely, even with the same genotype. People
with VCFS have characteristics of the syndrome that
range from very mild to very severe.
Treacher-Collins Syndrome
(Mandibulofacial Dysostosis or First
Pharyngeal Arch Syndrome)
Treacher-Collins syndrome is also called first pha-
ryngeal arch syndrome because its main characteris-
tics reflect problems in the development of structures
originating from this arch. As described earlier, the first
pharyngeal arch generates all structures of the face,
as well as the hard palate, the external ear, and parts
of the middle ear. Typical facial differences in children
born with Treacher-Collins syndrome include down-
ward-slanting eyes, underdeveloped or missing cheek
bones, a small jaw, underdeveloped or malformed
ears, and an unusually shaped mouth. An individual
with Treacher-Collins syndrome may have an unusu-
ally shaped palate or a cleft palate. In addition, the
small bones in the middle ear that conduct sound
(see Chapter 22) may be affected, producing some hear-
ing loss.
Treacher-Collins syndrome is believed to result
from a problem with chromosome 5, which is respon-
sible for the embryological development of the first
pharyngeal arch. The syndrome is fairly rare, being
found in roughly one in every 10,000 births. Treacher-
Collins syndrome is distinctive, however, for having
its symptom set confined to the structural malforma-
tions described previously. In most cases, persons with
Treacher-Collins have normal cognitive abilities and no
other anomalies in distant structures or functions.
19  Craniofacial Anomalies 273
Stickler Syndrome
Stickler syndrome includes a range of anomalies, all of
which — including cleft palate — can be traced to prob-
lems with genes that control the production of colla-
gen. Collagen is a protein important for the creation of
cartilage, connective tissue, and some bony structures
that have cartilaginous origins during embryological
development. Specifically, an individual with Stickler
syndrome is likely to have a round, flattened face, a
variety of eye problems including detachment of the
retina and degeneration of the fluid inside the eyeball,
problems with joints, poor growth of long bones result-
ing in short stature, hearing loss resulting from struc-
tural problems in the end organ of hearing (called the
cochlea, analogous to the retina in the eye: see Chap-
ter 22), an underdeveloped mandible, and cleft pal-
ate. When a cleft palate occurs in Stickler syndrome,
it is probably a result of the underdeveloped jaw that
prevented the palatine shelves from moving into the
proper position for fusion (see earlier). Like VCFS and
Treacher-Collins syndrome, Stickler syndrome has a
genetic basis. The genes that fail to produce a normal
pattern of collagen production are apparently located
on the 1st, 6th, and 12th chromosomes. An estimate of
the prevalence of Stickler syndrome is 1 in 7,500 to 1 in
9,000 births (Printzlau & Andersen, 2004).
Craniosynostosis (Apert and
Crouzon Syndromes)
Craniosynostosis is a syndrome in which the bones
of the skull do not fuse together at the proper time.
Craniosynostosis includes Apert and Crouzon syn-
dromes (as well as other nonsyndromic variants),
which have slightly different characteristsics (not
discussed here). In a study conducted in Atlanta. cra-
niosynostosis occurred in 4.3 in every 10,000 births
between the years 1989 and 2003 (Boulet, Rasmussen,
& Honein, 2008). A frequent consequence of the early
fusion of skull bones is cleft palate. Craniosynostosis
has a genetic basis, often associated with anomalies of
the 10th chromosome.
Cleft Palate: Other Considerations
CL/P and CPO are complex health care problems. The
focus in this chapter has been on speech production in
children with these craniofacial anomalies, but many
children with CL/P or CPO have additional issues that
must be dealt with by a health care team. Children with
CL/P and CPO have problems with dentition, multiple
surgeries, socialization, language development, hear-
ing, and nutrition (especially as young children). The
274 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
health care team is therefore likely to include dentists,
maxillofacial and plastic surgeons, psychologists/
social workers, speech-language pathologists, audiolo-
gists, and nutritionists.
Of particular interest are the possibilities of delayed
language development and hearing loss in children with
CL/P and CPO. In a review of language development
in CL/P and CPO, Morgan and colleagues (2017) note
that language disorders are not unusual in this group
of children and are likely to be more severe in children
with CPO. The greater severity of language disorders in
children with CPO may be related to the greater likeli-
hood of CPO being associated with a syndrome, com-
pared with CL/P. Many syndromes such as VCFS in
which CPO is a component may be characterized by
language learning and cognitive delays (Hardin-Jones
& Chapman, 2011). This may explain why children with
CPO have more severe language disorders compared
with children who have CL/P.
Hearing problems in children with CL/P and
CPO are largely due to frequent middle ear infec-
tions (technically, otitis media with effusion [OME]:
see Chapter 23). Frequent OMEs are a problem with
nearly all children with clefts. The hearing loss is con-
ductive, meaning that it is caused by interference with
the middle ear mechanism, not the sensory organs of
the inner ear. The mild-to-moderate hearing loss asso-
ciated with OME is present during the infection but
not when it resolves. The high percentage occurrence
and recurrence of OME in children with clefts (75% or
greater), compared to children with normal head and
neck structures (around 20%), is not well understood
but is thought to be related to the orofacial defects that
are part of clefting (Flynn, Möller, Jönsson, & Lohman-
der, 2009). Not all children with recurrent OMEs have
hearing loss when the middle ear is infected. As in the
general population, the frequency of OMEs in children
with clefts decreases with age.
OMEs are a health problem for children regard-
less of their other concerns. A specific concern with the
high rate of OMEs in children with clefts is that the fre-
quent conductive hearing loss, even though not severe,
may interfere with language development and have last-
ing effects on children’s literacy skills. Happily, there is
little evidence that this is the case (Roberts et al., 2004).
Chapter Summary
A craniofacial anomaly is defined as any deviation
from normal structure, form, or function in the head
and neck area of an individual; this chapter focuses on
cleft lip and cleft palate.
Knowledge of embryological development of the
head and neck is important to understanding how and
where clefts of the upper lip and palate occur.
The embryological errors that result in cleft lip and
cleft palate are independent; a child can be born with
a cleft lip and cleft palate, a cleft lip only, or a cleft pal-
ate only.
Clefts of the upper lip almost always occur to the
side of the center of the mouth; the clefts may be uni-
lateral (one side only) or bilateral (both sides) and vary
in severity from a very small notch in the lower lip to a
complete cleft lip from the lower lip through the floor
of the nasal cavity.
Clefts of the palate may arise from two types of
embryological error: one in which the palatine shelves
snap up into a horizontal position but fail to generate
sufficient tissue to meet in the middle and fuse, the
other in which the palatine shelves cannot snap up
into the horizontal position because they are trapped
beneath the tongue, which has not been lowered due
to incomplete growth of the mandible.
Clefts of the palate may be minor ranging from a
small notch at the back of the soft palate, to a complete
cleft, splitting the palate from back to front.
Two general categories of clefts are recognized:
cleft lip with or without a cleft palate (CL/P) and cleft
palate only (CPO).
The incidence of clefting varies depending on
country/region and other factors; worldwide the inci-
dence is about 1 in every 700 births.
The velopharyngeal port (VP port), the passage-
way between the pharyngeal and nasal cavities, is
opened by gravity and perhaps some muscular forces,
and closed by complex muscular forces of the soft pal-
ate and pharynx.
When the VP port is open, air can flow from the
pharyngeal cavity to the nasal cavities; during speech,
an open VP port is consistent with the production of
nasal sounds (such as /m/, /n/, /ŋ/ [final sound in
“ring”]).
When the VP port is closed, air is prevented from
flowing into the nasal cavities; if there is another “seal”
in the vocal tract, such as the closure of the lips for a
/b/, the vocal tract is a closed volume and the flow
of air into it from the lungs and through the vibrating
vocal folds causes the pressure in the vocal tract to rise
above atmospheric pressure.
Children or adults who have difficulty producing
closure of the VP port even after surgical repair of pala-
tal clefts have some degree of velopharyngeal insuf-
ficiency (VPI) which is likely to result in hypernasality
and obstruent errors (stops, fricatives, and affricates,
speech sounds that require a buildup of pressure inside
the vocal tract).

Obstruent speech sound errors that result from
VPI are categorized as obligatory errors and compen-
satory errors.
Obligatory errors are those in which the speaker
has the correct articulatory placement for the sound, but
the leak through the VP port prevents the buildup of air
pressure required for correct production of the sound.
Compensatory errors are those in which the
speaker changes the place of articulation for the “tar-
get” sound to avoid the leak, and thus produces the
correct manner of articulation (e.g., a stop manner or a
fricative manner); compensatory errors are often made
with a pharyngeal or glottal place of articulation.
Many syndromes (a collection of symptoms and/
or anomalies that occur together and are seen repeat-
edly in a number of children) have cleft palate as one of
their characteristics; it is more typical for these clefts to
be isolated clefts of the palate, rather than cleft lip with
or without a cleft palate.
Diagnosis of VPI is done by perceptual and instru-
mental methods, the latter including x-ray and endo-
scopic techniques that provide direct visualization of
the VP port to determine why it is not closing correctly.
Clefting is a complex health care problem, requiring
a team that may include speech-language pathologists,
audiologists, surgeons, nutritionists, and psychologists.
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P. F. (2014). Cleft palate: A clinical review. Birth Defects
Research (Part C), 102, 333–342.
Shprintzen, R. J., & Bardach, J. (1995). Cleft palate speech man-
agement. St. Louis, MO: Mosby.
Watterson, T., Mancini, M., Brancamp, T. U., & Lewis, K. E.
(2013). Relationship between the perception of hyperna-
sality and social judgments in school-aged children. Cleft
Palate-Craniofacial Journal, 50, 498–502.

Swallowing
Introduction
The ease of eating and drinking is deceptive. These
are complicated activities that require coordinated
actions of the lips, mandible, tongue, velum, pharynx,
larynx, esophagus, and other structures. Because eat-
ing and drinking engage many of the same structures
and much of the same airway as those used for speak-
ing and breathing, it is not uncommon for there to be
competition between these activities or for tradeoffs
to occur when trying to do them simultaneously. For
example, chewing must stop to be able to speak clearly,
and breathing must stop to be able to swallow safely.
The entire act of placing liquid or solid substance
in the oral cavity, moving it backward to the phar-
ynx, propelling it into the esophagus, and allowing
it to make its way to the stomach is called deglutition.
Although the word swallowing is sometimes used as a
synonym for deglutition, swallowing actually includes
only certain phases of deglutition. Nevertheless, to
simplify the explanations that follow, the term “swal-
lowing” is used in place of deglutition and is meant to
include all phases of deglutition.
Swallowing disorders are common in hospital set-
tings, and in fact account for a significant number of
hospital deaths. The deaths are usually a result of pneu-
monia due to food and/or drink going into the lungs
instead of the stomach. Food and drink in the lungs
cause bacterial infections — serious cases of pneumonia.
20
Anatomy of Swallowing
Figure 20–1 shows the structures that participate in
swallowing. These structures extend from the lips
to the stomach. Structures such as lips, jaw, tongue,
soft palate, pharynx, and larynx are used in speech
production as well as swallowing (see Chapter 10).
The esophagus and stomach, critical structures for the
process of swallowing, are not used in the speech pro-
duction process.
Esophagus
The esophagus is a flexible tube, about 20 to 25 cm
long in adults, which extends from the lower part of
the pharynx to the stomach. The esophagus begins
below the base of the larynx and runs behind the tra-
chea and lungs. It runs through the diaphragm (see
Figure 20–1) and enters the abdominal cavity where
it connects to the stomach. It is composed of a combi-
nation of skeletal (voluntary) muscle (the top part of
the tube) and smooth muscle (the bottom part of the
tube). Smooth muscle is not under “willful” control
(like, e.g., muscles of the arm), but contracts in reaction
to various stimuli.
The upper end of the esophagus is normally closed.
During swallows, it is opened by muscular action (see
later in this chapter).
277
278 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Oral cavity
Pharyngeal cavity

Vocal folds
Esophagus

Lower
esophageal
sphincter Diaphragm

Pyloric Stomach
sphincter

Small
intestine

Figure 20–1.  Structures of the swallowing mechanism.

Stomach The Act of Swallowing

The stomach is a large, saclike structure made up of
smooth muscle, mucosa, and other tissue. It is on the
left side of the abdominal cavity, against the undersur-
face of the diaphragm. The stomach is connected to the
lower esophagus on one end, and to the small intestine
at the other end. After a typical meal, the stomach holds
about a liter of solid and/or liquid substance. Gastric
juices in the stomach break up ingested substances so
that they can be absorbed into the body through the
stomach lining.
Although many of the structures that participate in
swallowing are the same as those that are used for
speaking, the forces and movements for the two activi-
ties are very different. In general, the forces are greater
and many of the movements are slower during swal-
lowing than during speech production.
There are four phases of swallowing. These
phases, illustrated in Figure 20–2, are the oral prepa-
ratory phase, oral transport phase, pharyngeal phase,
and esophageal phase. The phases are used to describe
 20 Swallowing 279

the movement of a bolus through the oral, pharyngeal, being swallowed. The physiological events associated
and esophageal regions of the anatomical structures of with each of these phases are described in the follow-
the swallowing process. Bolus is the word used to refer ing text and summarized in Table 20–1. In Figure 20–2,
to the volume of liquid or the mass of solid substance the green areas show the location and shape of the

Oral Oral Pharyngeal Esophageal

preparatory transport

Figure 20–2.  Images of the oral preparatory, oral transport, pharyngeal, and esophageal phases of swallowing. Table
20–1 provides a summary of these phases.

Table 20–1.  Summary of the Actions Associated With the Four Phases of Swallowing

Swallowing Phase Actions

Oral preparatory This phase begins as the liquid or solid substance comes in contact with the oral opening and
ends with the bolus held in the oral cavity with the back of the tongue elevated to contact the
velum and create an impenetrable wall. This phase can be as short as 1 second when ingesting
liquid and as long as 20 seconds when chewing (preparing) a solid food.

Oral transport During this phase the bolus is transported back through the oral cavity to the pharynx. To do so,
the tongue elevates in progressively more posterior regions to push the bolus back toward the
pharynx, the velum begins to elevate, and the upper esophageal sphincter begins to relax. This
phase lasts less than 1 second.

Pharyngeal During this phase, the bolus usually divides to run through the right and left sides of the bottom
of the tongue and is transported through the pharynx to the upper esophageal sphincter. This
phase is “triggered” automatically once the bolus passes the back of the oral cavity and is
associated with numerous and rapid events: the velopharynx closes, the tongue pushes the bolus
backward, the pharynx constricts segmentally, the hyoid bone and larynx move upward and
forward, the larynx is closed, and the upper esophageal sphincter opens. This phase lasts less
than 1 second.

Esophageal This phase begins when the bolus enters the upper esophageal sphincter. At the same time, the
lower esophageal sphincter relaxes. The bolus is moved through the esophagus by peristaltic
contractions. This phase ends when the bolus enters the stomach and can last from 8 to 20
seconds.
280 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
bolus for each phase; the time sequence of the phases
is from left to right.
Oral Preparatory Phase
The oral preparatory phase is depicted in the first panel
of Figure 20–2. This phase begins as a solid or liquid
substance makes contact with the structures at the front
of the oral cavity. The jaw is lowered and the lips part
in anticipation of the swallow (Shune, Moon, & Good-
man, 2016). What happens next depends on the nature
of the substance to be swallowed.
Liquid Swallows
If the substance is liquid, the jaw elevates and the lips
close. This creates a tight closure at the front of the
mouth to contain the bolus. The bolus is contained in the
front region of the oral cavity by actions of the tongue
and other structures, and held there momentarily (for
about 1 second). The front of the tongue depresses and
the sides of the tongue elevate to form a cup for the
bolus (Dodds et al., 1989). The back of the tongue ele-
vates to make contact with the soft palate to form a back
wall that separates the oral from the pharyngeal cavities
and helps ensure that no substance leaks through into
the throat, and possibly into the pulmonary airways.
During the oral preparatory phase, the velopha-
ryngeal port is open so that breathing can continue
with air flowing to and from the lungs through the
nasal passageways. Many people stop breathing
momentarily at this point in the swallow (this is called
the apneic interval) or even before the glass or straw
reaches the lips (Martin, Logemann, Shaker, & Dodds,
1994; Martin-Harris, Brodsky, Price, Michel, & Walters,
2003; Martin-Harris, Michel, & Castell, 2005). The stop-
page of breathing reduces the risk of aspiration, which
is the invasion of food or drink below the vocal folds
and into the lungs.
Solid Swallows
The events of the oral preparatory phase are different
when the substance to be swallowed is solid rather
than liquid, primarily because solid substances need
to be chewed into smaller pieces and mixed with saliva
before being transported toward the esophagus. Saliva
is an important ingredient in this process because it
moistens the solid substance to facilitate its transport.
Saliva also introduces enzymes that begin to break
down the substance for digestion.
Actions of the mandible (and teeth), lips, tongue,
and cheeks grind and manipulate the solid substance
into a well-formed bolus and position it on the front
surface of the tongue. The lips may close (though this
is not necessary) while the mandible moves to grind
the bolus. During chewing, the mandible moves up
and down, forward and backward, and side to side.
The soft palate makes contact with the back part of the
tongue to seal off the oral from the pharyngeal cavity
and prevent the bolus from moving into the pharynx
and larynx. The velopharyngeal port is open during
preparation of the bolus, and breathing may either con-
tinue or may stop momentarily (McFarland & Lund,
1995; Palmer & Hiiemae, 2003). The duration of the oral
preparatory phase may last from as short as 3 seconds,
when chewing a soft cookie, to as long as 20 seconds,
when chewing a tough piece of steak.
At the end of the oral preparatory phase, the sub-
stance in the oral cavity is ready to be consumed. Usu-
ally the bolus is immediately transported back toward
the pharynx (oral transport phase, see the next section).
Oral Transport Phase
The oral transport phase is shown in the second panel
of Figure 20–2. From the ready position (the oral pre-
paratory phase), the bolus is transported back through
the oral cavity. This is done by using the tongue tip to
squeeze the bolus against the hard palate; then pro-
gressively more posterior regions of the tongue elevate
and squeeze the bolus against the palate, moving the
bolus back toward the pharynx. At the same time as
the bolus is being moved in the direction of the palate,
the velopharyngeal port begins to close as the top of the
esophagus begins to open. The oral transport phase is
short, lasting less than a second (Cook et al., 1994; Tracy
et al., 1989).
Pharyngeal Phase
The pharyngeal phase of the swallow is “triggered”
when the bolus approaches the boundary between the
back of the oral cavity and the pharynx. During this
phase, depicted in the third panel of Figure 20–2, sev-
eral events occur rapidly and nearly simultaneously
to move the bolus quickly through the pharynx while
protecting the airway. “Protecting the airway” means
not allowing any part of the bolus to travel through the
vocal folds and into the trachea, and then deeper into
the lungs.
This pharyngeal phase is under “automatic” neu-
ral control, so that once triggered, it proceeds as a
relatively fixed set of events that cannot be altered vol-
untarily (except in certain respects that are not covered

here). These events occur within about half a second
(Cook et al., 1994; Tracy et al., 1989) and include velo-
pharyngeal closure, elevation of the hyoid bone and
larynx, laryngeal closure, pharyngeal constriction, and
opening of the upper entrance to the esophagus.
During the pharyngeal phase, the velopharynx
closes like a sphincter valve by elevation of the velum
and constriction of the pharyngeal walls. This closure
is forceful (more forceful than for speech production)
so as to prohibit substances from passing through the
nasopharynx into the nose.
The hyoid bone and larynx (Figure 20–3) move
upward and forward as a result of contraction of
muscles that attach to the hyoid bone. These muscles
have their origins on the jaw, and in the floor of the
mouth. As the hyoid bone is pulled upward and for-
ward, the larynx is pulled along with it by its mus-
cular and nonmuscular connections to the hyoid
Epiglottis
Figure 20–3.  Skeletal framework of the larynx and associated
structures; note especially the hyoid bone and cartilages of the
larynx.
20 Swallowing 281
bone. Elevation of the larynx also causes the pharynx
to shorten.
Closure of the larynx for swallowing forms a seal
to the entrance of the trachea to protect the pulmo-
nary airways. Closure occurs at multiple levels, which
include the vocal folds, the false vocal folds (locat-
ed immediately above the true vocal folds), and the
epiglottis. Upward and forward movement of the lar-
ynx contribute to airway protection by tucking the
larynx against the root of the tongue and moving the
trachea away from the pathway of the bolus to the
esophagus.
As the tongue propels the bolus into the pharynx,
the muscles of the pharynx contract from top to bot-
tom. The tongue root moves backward and the pha-
ryngeal walls constrict to squeeze the bolus toward the
esophagus. The top-to-bottom contraction of pharyn-
geal muscles is like a directional “squeeze” toward the
Hyoid bone
Thyroid cartilage
Arytenoid cartilages
Cricoid cartilage
282 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

esophagus. This is conceptually similar to the front-to-

back squeezing by the tongue against the palate in the
oral transport phase, described previously.
As all of these events are taking place, the upper
border of the esophagus is opening to allow the bolus
“in.” Two sets of actions appear to contribute to its
opening: (a) stretching of the upper esophageal sphinc-
ter by forward and upward movement of the hyoid
bone and larynx, respectively, and (b) relaxing of a
muscle that forms a ring around the top of the esopha-
gus (Omari et al., 2016).1 As suggested by the concept
of a muscle relaxing to accomplish a task (in this case,
swallowing), this muscle is usually in a state of contrac-
tion, holding the top of the esophagus closed.

Esophageal Phase

The esophageal phase, the initial part of which is illus-

trated in the right-most panel of Figure 20–2, begins
when the bolus enters the upper esophagus and ends
when it passes into the stomach through the lower
opening of the esophagus (seen in Figure 20–1). This
phase may last anywhere from 8 to 20 seconds (Dodds,
Hogan, Reid, Stewart, & Arndorfer, 1973). The bolus is
propelled through the esophagus by peristaltic actions
(alternating waves of contraction and relaxation) of the
esophageal walls. Peristaltic contraction raises pressure
behind the bolus and relaxation lowers pressure in front
Figure 20–4.  Eating, in which one part of the bolus has
of the bolus, creating the pressure differential needed to
been moved into the lower pharynx, while another part is
propel it toward the stomach. The esophageal phase of
still in the oral preparatory phase of swallowing.
swallowing, like the pharyngeal phase, is “automatic”
in the sense of not being under voluntary control.

Breathing and Swallowing

Overlap of Phases
Although the phases of swallowing are described as
though they are discrete and occur one after the other,
in fact, they overlap substantially. When a person is
eating a solid substance, for example, preparation of
part of the bolus in the oral cavity may continue while
another part of the bolus moves into the pharyngeal
area, as illustrated in Figure 20–4. The two boluses,
originally a single bolus, are shown in Figure 20–4 as
the brown-speckled material. The partial bolus in the
lower pharynx may remain above the esophagus as
long as 10 seconds before it merges with the rest of the
bolus and the pharyngeal transport phase of the swal-
low is triggered (Hiiemae & Palmer, 1999).
Protection of the pulmonary airways during swal-
lowing depends, in large part, on the coordination of
breathing and swallowing. Without such coordination,
inspiration might occur at the same time a substance
is being transported through the pharynx, and that
substance might be “sucked” through the larynx into
the pulmonary airways (aspiration). This is avoided, as
reviewed earlier, by closing the larynx, an action that
stops breathing for a brief period during the swallow.
The risk of aspiration appears to be further reduced
by timing the swallow to occur during the expiratory
phase of the breathing cycle. During single swallows
(swallowing a single bolus), the most common pat-
tern is expiration-swallow-expiration; that is, expi-

1
 his ring of muscle is the same tissue that can be used as an alternate sound source when a patient has had his larynx removed because of
T
cancer, as described in Chapter 18.

ration begins, the swallow occurs (accompanied by
breath-holding), and then expiration continues (Martin
et al., 1994; Martin-Harris, 2006; Nishino, Yonezawa,
& Honda, 1985; Perlman, Ettema, & Barkmeier, 2000;
Selley, Flack, Ellis, & Brooks, 1989; Smith, Wolkove,
Colacone, & Kreisman, 1989).
Nervous System Control
of Swallowing
A person with swallowing problems is said to have
dysphagia. Dysphagia has many causes, including neu-
rological disease. People with Parkinson’s disease,
multiple sclerosis, and amyotrophic lateral sclerosis
(ALS), as well as people recovering from stroke, may
have dysphagia as a prominent component of their
challenges. Thus, it is important to have some idea
of how the nervous system controls the swallowing
process.
The neural control of swallowing is complex and
not completely understood. Nevertheless, studies of
humans and animals have offered important insights
into how swallowing is controlled by the nervous sys-
tem. Some of the important features of that control are
discussed in the next sections.
Role of the Peripheral
Nervous System
Nearly all the structures involved in swallowing are the
same as those involved in speech production (the most
notable exceptions being the esophagus and stomach).
Those structures that participate in both swallowing
and speech production are innervated by the spinal
nerves and cranial nerves as described in Chapter 2.
The cranial nerves are involved in swallowing through
their innervation of the lips, mandible, tongue, velum,
pharynx, and larynx; spinal nerves are primarily
involved in breathing and its cessation as they relate to
swallowing. Disease or trauma problems that affect the
cranial nerves that serve these structures, such as dam-
age to a laryngeal nerve that results in unilateral vocal
fold paralysis (Chapter 18) or damage to the nerves
that control the contraction of pharyngeal muscles, are
likely to affect swallowing ability.
The voluntary and smooth muscles of the esopha-
gus are also innervated by nerve branches that arise
from a single cranial nerve. This nerve is called cranial
nerve X, or the vagus nerve. It is noteworthy that the
vagus nerve and its branches also innervate muscles
of the larynx. Because the larynx plays a critical role
20 Swallowing 283
in protection of the airway in swallowing, and the
esophagus has a muscle that relaxes to open its top
to allow entry of food and drink, and the muscles of
the esophagus push the bolus down into the stomach,
damage to this one nerve has the potential to create
major swallowing problems. The coordinated phases
of swallowing, described previously, can be signifi-
cantly disrupted by damage to this single cranial nerve
(Corbin-Lewis & Liss, 2015).
Role of the Central Nervous System
Although swallowing and speech production are
executed using many of the same peripheral nerves,
central nervous system control of these two activities
is quite different. This means that a given structure,
such as the tongue, is under one form of neural control
during swallowing and under another form of neural
control during speech production. Because of this, it is
possible to have central nervous system damage that
impairs the function of a neural structure for speech
production but not swallowing, and vice versa. There
are two major regions within the central nervous sys-
tem that are responsible for the control of swallowing.
One is in the brainstem, and the other is in cortical and
subcortical areas.
The brainstem center is located primarily in the
medulla, the part of the brainstem that is contigu-
ous with the uppermost part of the spinal cord. The
brainstem center has primary control over the more
automatic phases of swallowing (pharyngeal and
esophageal phases).
Many cortical and subcortical regions contribute
to the generation and shaping of swallowing behav-
iors. Activity in cortical and subcortical areas of the
cerebral hemispheres has a strong influence over the
control of the more voluntary phases of swallowing
(oral preparatory phase, including chewing, and oral
transport phase). Cortical damage due to stroke (and
possibly other diseases that affect structures in the cere-
bral hemisphere), however, may also affect the auto-
matic phases of swallowing (pharyngeal phase and
esophageal phase).
Sensory input that travels from structures of the
head and neck to the central nervous system, via cranial
nerves, is also an important component of swallowing.
Many forms of sensory input play a role in swallow-
ing, including (among others) bolus size, texture, tem-
perature, taste, and unpleasant stimuli (e.g., something
that tastes bad, has a texture that is sufficiently dif­-
ferent from the range of familiar bolus textures, and
so forth).
284 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Sphenopalatineganglio­
neuralgia
This sounds like something you wouldn’t want
to meet in the dark. But it comes from something
really good. As a child (or even as an adult)
you may have said the phrase, “I scream, you
scream, we all scream for ice cream.” Scream
has a meaning of anticipation in this context,
but it can also have a meaning of hurting. You
know the feeling. You take a bite of ice cream
and momentarily hold it against the roof of your
mouth before you swallow it. Then suddenly
you get an intense, stabbing pain in your fore-
head. What’s up? The pain is caused as your
hard palate warms up after you made it cold.
Cold causes vasoconstriction (reduction in blood
vessel diameter) in the region, which is followed
by rapid vasodilation (increase in blood vessel
diameter). It is the rapid vasodilation that hurts
and gets your attention. The technical term for
this pain is “sphenopalatineganglioneuralgia.”
The common term (and the one more easily
pronounced) is “brain freeze.” Fortunately, the
pain lasts only a few seconds.
Variables That Influence
Swallowing
A number of variables influence swallowing, including
characteristics of the bolus, the swallowing mode, and
developmental and aging effects. The sections below
discuss each of these.
Bolus Characteristics
Although the act of swallowing occurs generally as
described near the beginning of this chapter, the pre-
cise nature of the swallow is determined, in part, by
what exactly is being swallowed. Bolus consistency
and texture, volume, and taste are variables that have
been found to influence the act of swallowing.
Consistency and Texture
One of the most important contrasts that determines
swallowing behavior is the difference between liquids
and solids. Whereas a liquid bolus is usually held briefly
in the front of the oral cavity before being propelled to
the pharynx, a solid bolus may be moved to the phar-
ynx and left there for several seconds while the remain-
der of the bolus continues to be chewed (Hiiemae &
Palmer, 1999; Palmer, Rudin, Lara, & Crompton, 1992;
see Figure 20–5, later in the chapter). Although some-
thing similar can also happen with liquids (Linden,
Tippett, Johnston, Siebens, & French, 1989), it is much
less common, except in cases where a combined liquid-
and-solid bolus is chewed and swallowed (Saitoh et al.,
2007), such as what might occur during mealtime eat-
ing (Dua, Ren, Bardan, Xie, & Shaker, 1997). Even when
not combined, the consistency of liquids and the tex-
tures of solid food influence swallowing behavior.
Liquid substances can be characterized accord-
ing to consistency, ranging from as thin as water to
as thick as pudding. Differences in consistency have
been shown to influence swallowing. Thick liquids
or puree consistencies tend to take longer to swal-
low than thin liquids (Chi-Fishman & Sonies, 2002;
Im, Kim, Oommen, Kim, & Ko, 2012). Tongue forces
in the oral preparatory and oral transport phases are
higher when swallowing thick substances compared
to thin liquids (Chi-Fishman & Sonies, 2002; Steele &
van Lieshout, 2004). As might be predicted, it is more
difficult to maintain a cohesive (single) bolus when
swallowing thinner liquids as compared to thicker
liquids. As a result, laryngeal penetration (where part
of the bolus moves into the opening to the larynx but
remains above the vocal folds; Robbins, Hamilton, Lof,
& Kempster, 1992) is more common when swallowing
thin liquids than when swallowing thicker substances
(Daggett, Logemann, Rademaker, & Pauloski, 2006;
Steele et al., 2015).
The textures of solid substances can also influ-
ence the swallow (Steele et al., 2015). For example, the
harder and drier the substance, the greater the num-
ber of chewing cycles (Engelen, Fontijn-Tekamp, &
van der Bilt, 2005), the longer the duration of the ini-
tial transport of the bolus from the anterior oral cavity
to the region where the oral cavity meets the pharynx
(Mikushi, Seki, Brodsky, Matsuo, & Palmer, 2014), and
the greater number of times the tongue squeezes the
bolus back toward the pharynx (Hiraoka et al., 2017).
Volume
It seems intuitive that the volume (size) of the bolus
might affect the swallow, and most studies indicate
that, in fact, it does (Chi-Fishman & Sonies, 2002;
Cook et al., 1989; Kahrilas & Logemann, 1993; Loge-
mann et al., 2000; Logemann, Pauloski, Rademaker, &
Kahrilas, 2002; Perlman, Palmer, McCulloch, & Van-
Daele, 1999; Perlman, Schultz, & VanDaele, 1993; Tasko,
Kent, & Westbury, 2002). When a person is swallow-
ing a larger bolus compared to a smaller bolus, tongue

movements are generally larger and faster, hyoid bone
movements begin earlier and are more extensive, pha-
ryngeal wall movements and laryngeal movements
are larger, and the upper esophageal sphincter relaxes
and opens earlier and stays open longer (Cock, Jones,
Hammer, Omari, & McCulloch, 2017; Kahrilas & Loge-
mann, 1993).
Despite the success of the adjustments made
to accommodate a larger bolus, there tends to be a
greater frequency of laryngeal penetration as bolus
size increases, at least for liquid boluses. For example,
part of the bolus penetrates the opening into the larynx
more than twice as often when swallowing a 10-mL
bolus than when swallowing a 1-mL bolus (Daggett
et al., 2006). Nevertheless, when laryngeal penetration
occurs in healthy individuals, the substance is almost
always pushed away from the larynx and transported
to the esophagus without being aspirated (going below
the vocal folds).
Sword Throats
Sword swallowing is an ancient art
that continues to be practiced. There is even a
Sword Swallowers Association International
with both professional and amateur members
from all over the world. The practice and ill
effects of sword swallowing were discussed
in an article in the prestigious British Medical
Journal (Witcombe & Meyer, 2006). Major
complications from sword swallowing are more
likely when the swallower is distracted or when
swallowing unusual swords. Complications
can include — little wonder — perforation of the
pharynx or esophagus, gastrointestinal bleeding,
pneumothorax (collapsed lung), and chest pain.
Novice sword swallowers must learn to desen-
sitize the gag reflex, align the upper esophageal
sphincter with the neck hyperextended, open the
upper esophageal sphincter, and control retching
as the blade is moved down the pipe. All in all, it
does not sound like fun; it also makes for a very
long bolus.
Development
Many important anatomical changes influence swal-
lowing during the period from infancy through
childhood. Among these changes are the following
(Arvedson & Brodsky, 2002): (a) the infant’s tongue
goes from nearly filling the oral cavity to filling only
20 Swallowing 285
the floor of the oral cavity; (b) the infant’s oral cavity
goes from being edentulous (lacking teeth) to having a
full set of “baby” teeth; (c) the cheeks of the infant have
fatty pads (sometimes called sucking pads) that even-
tually disappear, to be replaced with muscle; (d) the
infant goes from having essentially no oropharynx
to having a distinct one as the larynx descends; and
(e) the infant’s larynx goes from being one-third adult
size, with relatively large arytenoid cartilages and a
high position within the neck, to the adult configura-
tion and position.
Swallowing (of amniotic fluid) begins well before
birth, as early as 12.5 weeks’ gestation (Humphrey,
1970). Interestingly, although many of the components
of swallowing are in place before birth, velopharyn-
geal closure during swallowing is not (Miller, Sonies,
& Macedonia, 2003). Immediately after birth, the velo-
pharynx closes for swallowing and the infant exhibits
a suckling pattern characterized by forward and back-
ward (horizontal) movements of the tongue (Bosma,
1986; Bosma, Truby, & Lind, 1965). These tongue move-
ments are accompanied by large vertical movements
of the mandible and serve to draw liquid into the oral
cavity. Around the age of 6 months, this suckling pat-
tern converts to a sucking pattern that is characterized
by raising and lowering (vertical) movements of the
tongue, firm approximation of the lips, and less pro-
nounced vertical movements of the mandible. Sucking
is stronger than suckling and allows the infant to pull
in thicker substances into the oral cavity and to begin
the ingestion of soft food (Arvedson & Brodsky, 2002).
During the first few months of life, the infant relies
on breastfeeding (or nipple feeding from a bottle) for
all nutritional intake. This form of feeding consists
of suck-swallow or suck-swallow-breathe sequences,
typically repeated several times (8 to 12 times) and fol-
lowed by a rest period (several seconds). During this
period, several oral reflexes that aid in early feeding
are active. These disappear around 6 months of age,
with the exception of the gag reflex, which remains
active throughout childhood and adulthood. Knowl-
edge of the neural interactions among feeding, swal-
lowing, and airway protection is essential for providing
quality care for infants with impairments in any of
these functions (Jadcherla, 2017).
By about 6 months of age, infants are ready to
begin eating solid foods and being fed by spoon. Foods
such as crackers and soft fruits and vegetables are intro-
duced during the next few months. The basic patterns
for chewing are in place by 9 months and continue to
develop over the next few years of life (Green et al.,
1997; Steeve, Moore, Green, Reilly, & Ruark McMur-
trey, 2008). By 2 to 3 years of age, the child is able to eat
regular table food.
286 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Age
As with most physiological functions, swallowing
changes with age across adulthood. The most promi-
nent age-related change is that swallowing becomes
slower, particularly after age 60 years (Leonard & Mc-
Kenzie, 2006; Logemann et al., 2002; Robbins et al.,
1992; Sonies, Parent, Morrish, & Baum, 1988).
An outcome of the age-related slowing of the
swallow (combined with age-related reductions in
sensory function; for example, see Malandraki, Perl-
man, Karampinos, & Sutton, 2011) is that the fre-
quency of laryngeal penetration increases with age
(Daniels et al., 2004; Robbins et al., 1992). Laryngeal
penetration occurs in people over 50 years about twice
as often as it occurs in adults under 50 years, and
more frequently when swallowing liquids than when
swallowing solids (Daggett et al., 2006). Although
this appears to be a dangerous situation and a pos-
sible precursor to aspiration, in healthy individuals
the substance is moved out of the space immediately
above the vocal folds to be rejoined with the rest of the
bolus (Daggett et al., 2006). Nevertheless, the risk of
aspiration may be higher in older adults, compared
to younger adults, because of their greater tendency to
inspire immediately after swallowing (Martin-Harris,
Brodsky, et al., 2005).
Measurement and Analysis
of Swallowing
Measurement and analysis of swallowing are not only
critical to research endeavors but have also become
essential to clinical practice and to the diagnosis and
management of dysphagia (meaning swallowing dis-
orders and pronounced dis-FAY-juh). Measurement of
swallowing using instruments is especially important
when considering that as many as half of the clients
who aspirate do so “silently” without any signs of
coughing or other signs of visible or audible struggle
(Logemann, 1998). In such cases, aspiration can only
be detected through instrumental examination (as pre-
viously defined, aspiration is the invasion of food or
drink below the vocal folds and into the lungs).
There are many approaches to measuring and ana-
lyzing swallowing. Two are highlighted here — video-
fluoroscopy and endoscopy.
Videofluoroscopy
Videofluoroscopy is an x-ray technique used to image
the movements of speech production. Videofluoros-
copy can also be used to image movements associated
with the opening and closing of the velopharyngeal
port (Chapter 18). Videofluoroscopy is also used rou-
tinely in clinical settings to evaluate swallowing in
clients with suspected dysphagia. When used for this
purpose, the substance to be swallowed is mixed with
barium sulfate. Barium is a contrast material that allows
the bolus to be tracked visually as it travels through the
oral, pharyngeal, and esophageal regions.
The videofluoroscopic swallow examination, some-
times called a modified barium swallow (MBS) study,
was first described by Logemann, Boshes, Blonsky,
and Fisher (1977). The adjective “modified” is used to
differentiate this study from a barium swallow study,
which is conducted by a gastroenterologist to evaluate
esophageal structure and function.
A videofluoroscopic examination is usually con-
ducted with the client seated in a specially designed
chair. The examination is performed in a radiology
laboratory, with a radiologist (or radiology technician)
running the x-ray equipment and a speech-language
pathologist directing the swallowing protocol. The
examination protocol typically consists of the swallow-
ing of a series of liquid and solid substances (mixed
with barium or accompanied by ingestion of a barium
capsule to provide contrast) that vary in volume and
consistency or texture.
Figure 20–5 is an example of a videofluoroscopic
image of the oral preparatory phase of swallowing. The
single frame was extracted from a moving image (i.e., a
movie) recorded during a swallow.
Both timing and spatial measurements can be
made from the videofluoroscopic images. Temporal
(timing) measurements can be made to determine the
time from the beginning of bolus movement from the
oral cavity to its arrival at the upper esophageal sphinc-
ter. Spatial measurements may be used to determine
the extent of velar elevation or extent of the upward
and forward movement of the hyoid bone. There are
also measures of the amount of penetration (entry of
food or liquid to the laryngeal area) and/or aspiration
(Rosenbek, Robbins, Roecker, Coyle, & Wood, 1996).
It is generally agreed that videofluoroscopy pro-
vides the most comprehensive evaluation of swallow-
ing, and for many it is considered the “gold standard”
of measurement. It has several advantages over other
measurement approaches, including the following:
(a) it provides relatively clear views of nearly all the
important structures involved in swallowing and their
movements, with the exception of the vocal folds;
(b) it is possible to visualize barium-laced substances
through the oral preparatory, oral transport, pharyn-
geal, and esophageal phases; (c) it is possible to view
swallowing events from at least two different perspec-
tives (from the side, and from the front); and (d) it is

Figure 20–5. Videofluoroscopic image showing the
oral preparatory phase of a swallow. The large, dark area
in the oral region is the bolus. The thin, dark line that runs
along the tongue to the epiglottis indicates that there may
be some trace bolus residue from a previous swallow or
that there has been some premature spillage during the
oral preparatory phase. Modified and reproduced with
permission from “Dynamic swallow studies: measurement
techniques,” by R. Leonard and S. McKenzie in Dysphagia
assessment and treatment planning: A team approach (2nd
ed., p. 273). Edited by R. Leonard and K. Kendall, 2008, San
Diego, CA: Plural Publishing, Inc. Copyright 2008 by Plural
Publishing, Inc.
possible to identify penetration and aspiration events.
The major disadvantages of videofluoroscopy are that
it requires exposure to radiation, it must be coordinated
with radiology, and it cannot be conducted at bedside.
Endoscopy
Another way to visualize swallowing is with endoscopy
(Langmore, Schatz, & Olson, 1988), also mentioned in
Chapter 19. This approach requires the use of a flexible
fiberoptic endoscope, like the one used for visualizing
the larynx and velopharynx. To view the swallowing
apparatus, the endoscope is inserted through one of
the nares (following the administration of topical anes-
thesia and decongestant), routed through the velopha-
ryngeal port, and guided until its tip is positioned in
the laryngopharynx (the bottom part of the pharynx,
just above the opening into the larynx). This approach
20 Swallowing 287
is called flexible endoscopic evaluation of swallowing
(FEES). No x-rays are used in endoscopy, and therefore
no barium-infused boluses are required for evaluation
of swallowing disorders. A FEES station is shown in
Figure 20–6.
The examination usually includes a preliminary
viewing of the structures included in the process of
swallowing, such as (among others) the velopharyn-
geal region, pharyngeal walls, back part of the tongue,
entrance to the larynx, and the vocal folds. Abnormali-
ties in structure or color are noted and are used to help
interpret abnormal swallow behaviors. The evaluation
protocol is similar to that used for videofluoroscopic
examination, using liquid and solid substances of dif-
ferent consistencies, textures, and volumes.
Endoscopy offers certain advantages over other
approaches to evaluating swallowing. For example,
the equipment is portable so that the examination can
be done at bedside in a hospital; there is no exposure
to x-rays and no need to use barium products; and it
is possible to see structural and color abnormalities.
In addition, the procedure can often be performed
by a speech-language pathologist without the direct
oversight of a physician or the aid of other health care
professionals. The speech-language pathologist can
also observe the client eat an entire meal at the client’s
usual pace.
A disadvantage of endoscopy for evaluation of
swallowing is that there are some clients who cannot
tolerate the procedure, including those with structural
abnormalities such as a deviated nasal septum, certain
movement disorders, bleeding disorders, and certain
cardiac conditions. Furthermore, it is sometimes diffi-
cult to detect penetration and aspiration with endos-
copy, although there are techniques to get around this.
Client Self-Report
An important form of measurement, especially in
clinical settings, is the client self-report. The client self-
report can reveal symptoms (e.g., pain during swallow-
ing, lump in the throat, difficulty swallowing certain
foods) that indicate the need to perform instrumental
evaluation of swallowing using measurement proce-
dures such as those just described. One way to glean
information about the client’s perspective of the swal-
lowing problem is by using an unstructured interview.
An alternative or complementary approach is to use a
more formal, symptom-specific assessment tool. There
are several to choose from, one of which is called the
Eating Assessment Tool-10 (EAT-10; Belafsky et al.,
2008). The EAT-10 contains several statements, such
as “My swallowing problem has caused me to lose
288 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Figure 20–6.  Fiberoptic endoscope used for evaluation of swallowing. Reproduced

with permission provided courtesy of KayPENTAX, Montvale, NJ.

weight” and “I become short of breath when I eat,”
that the client rates on a scale ranging from “No prob-
lem” to “Severe problem.” Research has shown a good
correspondence between the symptoms reported on
the EAT-10 and the identification of dysphagia-related
signs obtained from measures in patients with head
and neck cancer (Arrese, Carrau, & Plowman, 2017)
and in amyotrophic lateral sclerosis (Plowman et al.,
2015).
Health Care Team
for Individuals With
Swallowing Disorders
Evaluation and management of dysphagia (swallow-
ing disorder) are a large part of the clinical practice of
speech-language pathology. Although there are cases
of functional dysphagia (wherein there is no known
physical reason for the dysphagia) (Baumann & Katz,
2016), dysphagia usually has an identifiable structural,
neurogenic, and/or systemic cause. Structural causes
include (among others) tumors, diverticula (abnormal
pouches in the wall of a structure), deformation caused
by surgical removal of tissue or trauma (e.g., as in sur-
gical removal of tissue in treatment of head and neck
cancers), congenital malformations, and tracheostomy
(a surgically created opening at the front of the neck).
Dysphagia can also have neurogenic causes such as
stroke, degenerative diseases (such as Parkinson’s dis-
ease), and traumatic brain injury.
Evaluation and management of swallowing disor-
ders often require a team of health care professionals
including a speech-language pathologist, radiologist,
gastroenterologist, otolaryngologist, dietitian, occupa-
tional therapist, and others, depending on the nature of
the swallowing disorder.
The speech-language pathologist is responsible for
the evaluation and behavioral management of oropha-
ryngeal dysphagia (swallowing disorders involving
the oral preparatory, oral transport, and pharyngeal
phases). Usually the speech-language pathologist is
asked by a physician to evaluate a client with a poten-
tial swallowing disorder. The speech-language pathol-

GERD and LPR
Your stomach is rich with chemicals
that have about the same acidity as the battery
acid in your car. That’s right, that’s the same
battery acid that will burn a hole in your clothes
if you splash some of it on you. GERD, an
acronym for gastroesophageal reflux disease,
is a chronic condition in which acid from the
stomach backs up into the esophagus when
the lower esophageal sphincter (the valve that
separates the esophagus and stomach) fails to
do its job properly. Although a certain amount
of reflux (backflow) from the stomach into the
esophagus is considered normal, too much can
cause heartburn and the need to see a gastro-
enterologist (GI doctor). When stomach acid
travels all the way through the esophagus and
spills onto the larynx it is called laryngopharyn-
geal reflux, or LPR. LPR can irritate and erode
laryngeal tissue. LPR can cause a hoarse voice,
chronic cough, frequent throat clearing, and
other problems that may lead to the need to seek
help from an otolaryngologist (ENT doctor).
Some helpful hints for avoiding GERD and LPR:
do not stuff yourself before you go to bed, lay off
foods that make it worse, and sleep with your
body inclined so that your head is higher than
your feet.
ogist may begin by performing a bedside swallowing
evaluation, which includes a case history interview, a
physical examination of the swallowing structures, and
visual, auditory, and tactile observation of the client
during swallowing of water and possibly other sub-
stances. If a problem is suspected, the speech-language
pathologist will perform a videofluoroscopic swal-
lowing examination in collaboration with a radiolo-
gist. During the swallow study, the speech-language
pathologist may screen for esophageal problems, and if
any are noted, a gastroenterologist is notified. Alterna-
tively, a fiberoptic endoscopic evaluation of swallow-
ing may be conducted, a procedure that can usually
be performed by the speech-language pathologist inde-
pendently. Behavioral management might include the
teaching of postural strategies to improve swallowing,
diet (consistency) recommendations, therapeutic exer-
cises (to improve strength and coordination of swal-
low-related structures), and counseling regarding the
swallowing disorder.
The radiologist has a limited, but critical, role in
the evaluation of swallowing. Specifically, the radi-
20 Swallowing 289
ologist is responsible for the instrumental aspects of
videofluoroscopic swallow (modified barium swal-
low) studies and barium swallow studies and, in some
instances, may help in their interpretation.
Chapter Summary
Eating and drinking involve intricately coordinated
actions of the lips, mandible, tongue, velum, pharynx,
larynx, esophagus, and other structures.
The term swallowing is as a synonym for degluti-
tion and is used as such in this chapter, although swal-
lowing technically involves only part of the deglutition
process.
Many of the important anatomical and physiologi-
cal components of the speech production apparatus,
discussed in Chapter 10 of this text, are also important
anatomical and physiological components of the swal-
lowing apparatus.
The stomach is a liter-sized sac whose upper end
connects to the esophagus and whose lower end con-
nects to the small intestine through the pyloric sphincter.
The forces and movements associated with the
act of swallowing can be categorized in four phases
that include an oral preparatory phase, oral transport
phase, pharyngeal phase, and esophageal phase.
The oral preparatory phase involves taking liquid
or solid substances in through the oral vestibule and
manipulating them within the oral cavity to prepare
the bolus (liquid volume or lump of solid) for passage.
The oral transport phase involves moving the
bolus (or a part of it) through the oral cavity toward
the pharynx by rearward propulsion due largely to a
squeezing action of the tongue, against the palate, that
moves from front to back of the oral cavity.
The pharyngeal phase is usually “triggered” when
the bolus passes the junction of the oral cavity and
pharynx, and consists of a combination of compres-
sive actions that force the bolus downward toward the
esophagus while at the same time protecting the lower
airways.
The esophageal phase begins when the bolus
enters the esophagus and continues as the bolus is
moved toward the stomach by a series of peristaltic
waves of muscular contraction and relaxation that
progress down the muscular tube.
Although it is convenient to describe swallowing
as four discrete phases, the reality is that there is sub-
stantial overlap among the phases.
Structures within the brainstem exert neural con-
trol over the automatic aspects of swallowing (i.e., the
pharyngeal and esophageal phase), and structures
290 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
within the cerebral hemispheres exert neural control
over the voluntary aspects of swallowing (i.e., the oral
preparatory and oral transport phases).
Characteristics of the bolus can influence the swal-
lowing pattern, including bolus consistency and tex-
ture, volume, and taste.
The development of swallowing from infancy is
rapid and complex and moves through different suck-
ing and chewing patterns toward adult-like eating
and drinking behaviors, and carries with it important
developmental processes related to social and emo-
tional development.
The effect of aging on the swallow is an overall
slowing and a subtle deterioration in the spatial and
temporal coordination among certain structures of the
swallowing apparatus.
Several ways to measure and analyze swallowing
are available and include videofluoroscopy (which uses
x-ray to image all phases of swallowing), and endos-
copy (which uses a flexible endoscope to image the
pharyngeal and laryngeal regions); client self-report
(which provides insight into the client’s experiences
with swallowing) is also a useful measure that helps
determine if further instrumental testing is warranted.
Some of the more important health care profession-
als who work with clients with dysphagia (impaired
swallowing) include speech-language pathologists,
radiologists, gastroenterologists, otolaryngologists,
dieticians, and occupational therapists.
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Hearing Science I:
Acoustics and Psychoacoustics
Introduction
Acoustics is the science of sound. The study of sound
is relevant to Communication Sciences and Disor-
ders because speech is produced as an acoustic signal,
and hearing uses acoustic signals as “data.” The term
“acoustic signal” in this text refers to a disturbance in
air pressure, created by a vibrating source. We are spe-
cifically interested in acoustic signals that fall within
the frequency range of human hearing. Hixon, Weis-
mer, and Hoit (2020) and Kramer and Brown (2019)
present more detailed information on basic acoustics,
and the Internet is an endless source of outstanding
websites on acoustics, many of which include anima-
tions of sound wave events.
This chapter covers the transmission of sound in
air. Sound is a disturbance in air pressures but can also
be a disturbance in the molecules of fluid or of solids.
This disturbance is the bunching up and spreading
apart of molecules in response to an external source.
The changing density of air molecules results in pres-
sure variations. Sounds, in fact, are pressure waves.
When the author was a child, his family made
regular summer trips to a lake in New Jersey, where
21
he and his brothers would amuse themselves by each
taking two rocks, submerging underwater at opposite
ends of the lake, and sending Morse code signals by
banging the rocks together. The impact of the rocks
created a pressure disturbance in the water — a sound
wave — that was transmitted rapidly and heard clearly
underwater, at a substantial distance across the lake.
A more dramatic example is putting an ear to a railroad
track and hearing an approaching train even though it
is more than a mile away. The train wheels vibrate the
steel track, setting up a pressure disturbance in steel
track molecules. This disturbance, or pressure wave, is
transmitted down the rails to the person whose ear in
on the track.
The difference in speed of sound wave trans-
mission is determined by the relative densities of the
molecules in the different media. All other things
being equal, the denser (more highly packed) the mol-
ecules, the faster is the speed of sound transmission.
Air has less dense molecules than water, which has
less dense molecules than steel. Among these three
sound-conducting media, therefore, steel conducts
sound waves at the greatest speed and over the great-
est distances.
293
294 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Inherent Forces, Constant Motion

Air molecules can, in theory, sustain
indefinitely an oscillation like the one shown in
Figure 21–1. Air molecules, like springs, are elastic.
They have a rest position (Figure 21–1, time 1), and
when they are stretched away from that position
(Figure 21–1, time 2), they generate a recoil force
to get back to the rest position. Air molecules
also have mass, which means they demonstrate
the force of inertia. When after being stretched
the molecule recoils back to the rest position, it
is moving quickly and cannot “stop on a dime”
at the rest position (“A body in motion tends to
stay in motion,” courtesy of Sir Isaac Newton);
the molecule moves through the rest position
(Figure 21–1, time 3, same as the initial rest posi-
tion) and is again stretched away from it (Figure
21–1, time 4), building up recoil force to spring
back to the rest position (Figure 21–1, time 5). The
forces of elasticity and inertia are intrinsic to the
air molecule, meaning the molecule itself, or more
precisely its motions, produce the forces and keep
the molecule moving without the assistance of any
“external” forces other than the initial stretch. Start
the molecule moving, and in theory, it will oscillate
forever under its own power. In the real world,
motions of air molecules are opposed by external
forces, the most common one being friction.
Friction is a force that opposes the movement of
molecules and generates heat as a product of this
opposition. When molecules in motion rub against
each other or against surfaces of containers, walls,
or human tissue, they generate heat. The intrinsic
forces of elasticity and inertia are degraded, or run
down, by the generation of heat; when the forces
of friction overcome the forces of elasticity and
inertia, the motion stops.

Oscillation referred to as periodic vibrations because of their repeti-

The motion depicted in Figure 21–1 is called an oscil-
lation. The back-and-forth motion repeats itself over
time. The repetition of this motion over time allows it
to be described according to its period (and its inverse,
frequency) and amplitude. In fact, such oscillations are
tive nature.
Imagine that we timed the motion of the mol-
ecule in 21–1 from the original position shown at time
1 through one complete back-and-forth oscillation to
the position shown at time 5. The time taken for one
complete cycle of this back-and-forth motion is called

Time 1

Time 2

Time 3

Time 4

Time 5

Figure 21–1.  Motions of a single air molecule at five consecutive

instants in time after the molecule is “bumped” by some unknown
force. The arrow at time 1 indicates the force moving the molecule to
the right, and all subsequent arrows indicate the direction of the
resulting motion of the molecule. The motions at different times are
shown on separate rows for clarity, but the path of the motion really
occurs in a single dimension, back and forth along the same path.

the period of vibration and is symbolized by the letter
T. T is expressed in seconds (sec) or milliseconds (msec;
1 msec = 0.001 sec). An oscillation with T = 0.001 sec
means that the motion from time 1 to time 5 is com-
pleted in 1/1,000th of a second.
Periodic motion can also be described in terms of
frequency. Frequency (symbolized as F) is the number
of complete cycles of oscillation that occur in 1 sec. Fre-
quency and period are the inverse of each other — if you
know one, you know the other. For example, if the com-
plete cycle of molecule movement shown in Figure 21–1
has a duration of 0.001 sec (T = 1 msec), then F = 1/0.001
= 1,000 cycles per second (cps), or 1000 hertz (Hz).
The human ear responds to a large range of frequen-
cies, from a low frequency of about 20 Hz (T = 1/F, =
1/20 = 0.050 sec, or 50 msec) to a high frequency of about
20,000 Hz (T = 1/20,000 = 0.00005 sec or 0.05 msec). Even
in the case of the lowest frequency, the time taken for
one complete cycle, 0.05 sec, is merely a fraction of a full
second. Acoustic oscillations occur very rapidly.
Waveform
A waveform is the amplitude of vibration as a function
of time, as shown on the left side of Figure 21–2; ampli-
tude is on the y-axis, and time is on the x-axis.
Time Domain
Relative Amplitude
T = 0.008 sec
0 2 4 6
Time (msec)
Figure 21–2.  Left, molecule motion from Figure 21–1 replotted as a sine wave. The
graph is a waveform, with amplitude (displacement) on the y-axis and time on the x-axis;
right, spectrum of the waveform in the left side of the figure. In the spectrum, amplitude is
on the y-axis, and frequency is on the x-axis.
21  Hearing Science I:  Acoustics and Psychoacoustics 295
The waveform in Figure 21–2 is called a sine wave.
A sine wave is a sound composed of a single period,
and, therefore, only a single frequency. In Figure 21–2,
left, the period is marked as T, and the value of the
period is 0.008 sec, or 8 msec. T is the inverse of fre-
quency, so the frequency of this sine wave can be cal-
culated: F = 1/0.008 = 125 Hz.
Spectrum
The spectrum is the amplitude of vibration plotted as
a function of frequency; amplitude is on the y-axis,
and frequency is on the x-axis (Figure 21–2, right). This
spectrum has a single frequency component at 125 Hz,
as expected from a sine wave with a period of 0.008 sec.
Waveform and Spectrum
The waveform and spectrum are two different ways to
represent the same event. A waveform is the time rep-
resentation (“time domain” in Figure 21–2) of an acous-
tic event; a spectrum is the frequency representation
(“frequency domain” in Figure 21–2) of the event. The
difference between the two is conveyed by the x-axis
of the two representations: time for the waveform, and
Frequency Domain
Relative Amplitude (dB)
8 125 250 375 500
Frequency (Hz)
296 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

frequency for the spectrum. Both representations have
amplitude on the y-axis.
Complex Periodic Acoustic Events
A spectrum with a single frequency event is called a
pure tone. Chapter 23 describes how pure tones are
used as one way to evaluate hearing.
Most sounds in nature, however, including speech,
consist of many different frequencies having many
different amplitudes. Sound waves that are made
up of many different frequencies are called complex
acoustic events. They are like a collection of single
frequencies that are all added together. Even when
an acoustic event consists of many different frequen-
cies, its waveform can still repeat itself over time. That
is to say, complex acoustic events, like sine waves,
can be periodic. Figure 21–3, left, shows a waveform
(top) and spectrum (bottom) for the vowel “ah”. The
frequency scale for this spectrum is marked off in kilo-
hertz (kHz), meaning “1” is 1000 Hz, “2” is 2000 Hz,
and so forth.
Note first the shape of the waveform: it is much
more complicated compared with the shape of the sine
wave in Figure 21–2. That is because this is a complex
periodic waveform, reflecting a sound with many dif-
ferent frequencies and amplitudes. Second, the wave-
form has a clearly repeating pattern — it is periodic.
The period (T) for one of the cycles is marked on the
waveform. Third, the spectrum contains many sharply
defined frequency components (the series of closely
spaced amplitude peaks along the frequency scale
(x-axis). These multiple-frequency components vary
greatly in their amplitude (the height of the peaks on
the y-axis).
Complex Aperiodic Acoustic Events
Complex acoustic signals can also be aperiodic. Like
complex, periodic acoustic events, complex aperiodic
signals contain more than one frequency. Unlike com-
plex periodic events, the waveforms of complex peri-
odic events do not repeat over time. That is why they
are called aperiodic acoustic events.

7.99 ms

Time Time

10dB 10dB
Relative amplitude (dB)

Relative amplitude (dB)

1 2 3 4 5 6 7 8 9 10 1 2 3 4 5 6 7 8 9 10

Frequency (kHz) Frequency (kHz)

Figure 21–3.  Left, a waveform (top) of an “ah” vowel and its’ spectrum (bottom). Note the repeating pattern in the wave-
form, which allows measurement of a period, as marked; note also the difference between the appearance of this waveform
and the appearance of the sine wave waveform in Figure 21–2; the more complicated looking waveform in this figure
indicates that it reflects multiple frequency components, as shown in the spectrum. This waveform and spectrum reflect a
complex, periodic acoustic event. Right, a waveform of a noise like the sound of the ocean; there is no repeating pattern in
this waveform, thus no period can be measured. The spectrum shows energy as a function of frequency, but not at specific
“peaks” of frequency as in the spectrum on the left side of this figure. The right-hand waveform and spectrum reflect a
complex, aperiodic acoustic event.
 21  Hearing Science I:  Acoustics and Psychoacoustics
The right side of Figure 21–3 shows a waveform
and spectrum for a sound like the ocean. The wave-
form does not contain a repeating pattern; therefore,
a period cannot be measured. The spectrum does not
contain sharply defined peaks at specific frequencies.
The spectrum appears to be made up of continuous
energy, rather than a series of frequency components
as seen in the spectrum of the complex periodic event.
Resonance
Every vibrating object has a natural frequency of vibra-
tion, also called a resonant frequency. In some cases, an
object will have multiple resonant frequencies. A reso-
nant, or natural, frequency is the frequency at which an
object vibrates with maximal amplitude.
The phenomenon of resonance has central impor-
tance to an understanding of both speech (see Chap-
ter 11) and hearing (Chapter 22). For example, the
resonant frequencies of the vocal tract are changed
when the shape of the vocal tract is changed; this is the
basis for the acoustic difference between different vow-
els (Chapter 11). As described later, in Chapter 22, the
resonant frequency of the external ear canal, which car-
ries sound energy from the external world to the ear-
drum, contributes to the sensitivity of hearing for certain
important frequencies in the understanding of speech.
Resonance has interesting applications to other
events which may be more familiar in the popular
imagination. For example, when a glass shatters in
response to a singer’s high-pitched, strong note, you
are seeing a particularly dramatic example of reso-
nance. Physiological events in the singer’s speech
mechanism (see Chapter 10) produce powerful sound
waves, some of which have air molecule oscillations at
the resonant frequency of the glass. These oscillating
air molecules apply force to the glass, which responds
with forceful vibration of its own because its resonant
frequency has been “excited” by the same frequency
of the air vibrations. The forceful vibration of the glass
eventually exceeds the elastic limit1 of the material, and
the glass shatters.
Bridges can also be “excited” at their resonant
frequency by marching soldiers. Marching is a peri-
odic event, and if the marching frequency matches
a bridge’s resonant frequency, the bridge may be set
into forceful vibration and eventually collapse. This
explains why marching soldiers (at least in the past)
break ranks when crossing a bridge.
1
“ Elastic limit” means the degree to which an object can be stretched before there are permanent changes in the object’s shape. In the current
example, the shape of the glass material that makes up the wine glass is “changed” permanently — the glass shatters — when the vibration
amplitude exceeds the elastic limit of the glass. Excessive stretch of a rubber band is another good example.
297
Tacoma Narrows Bridge
In 1940, the Tacoma Narrows bridge
collapsed as a response to the forces of nature.
This suspension bridge, a mile-long span over
the Puget Sound, connected Tacoma, Washing-
ton, with Gig Harbor, Washington. The bridge
was set into motion by strong winds. (It had a
previous history of vibrating before it collapsed;
travelers likened crossing the bridge in a car to
a roller coaster ride.) Eventually, on the fateful
day, the bridge began to twist rhythmically,
reaching such violent, periodic amplitudes that
it eventually fell apart completely. Fortunately,
no one was injured, as the rhythmic twisting
grew over a period of hours, allowing people to
get off the bridge. Some have claimed that the
collapse occurred because the wind “excited” the
bridge at its resonant frequency; the explanation
is probably more complicated than that, but the
resonant frequency of the bridge played a role
in the collapse. Google “Tacoma Narrows” and
enjoy the still photos and film clips of the bridge
rolling and twisting in the wind like a child’s toy.
Note the periodic twisting motions of the bridge.
The ability to “excite” objects at their resonant fre-
quencies and cause them to shatter or disintegrate also
has positive applications. A therapy for kidney stones,
a condition in which a hard mass is formed somewhere
in the urinary tract (which includes the kidneys), pul-
verizes the stones with very high-frequency sound
waves which match the resonant frequencies of the
stones. The stones shatter because they vibrate vio-
lently, much like the wine glass shatters when set into
vibration at its resonant frequency.
Psychoacoustics
Psychoacoustics is the science of the psychological
response to sound. Important psychological terms
for an understanding of speech and hearing are pitch,
loudness, and quality. Localization, another psycho-
acoustic phenomenon, is not discussed in this chapter.
The following discussion simplifies the relation-
ships between physical characteristics of sound (fre-
quency, amplitude, and complex acoustic events) and
298 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

the psychological responses to them more. Detailed the struck strings have higher frequencies of vibration.
information on psychoacoustics is presented in Hixon, Look inside a piano and note how the strings become
Weismer, and Hoit (2020) and Kramer and Brown (2019). increasingly thinner and shorter as you move from left
to right. Thicker, longer strings have a lower frequency
of vibration as compared to thinner, shorter strings.
Pitch Thus, a relationship exists between frequency of vibra-
tion and perceived pitch.
Pitch is a term generally understood as the per- A general statement of the relationship between
ceived “height” of a tone. In lay conversation, pitch frequency of vibration and pitch perception is that
often refers to musical notes. The left-hand keys of a pitch increases with frequency. The relationship is not
piano or organ produce lower pitches than the right- simple, because equal changes in frequency do not
hand keys. Striking keys from left to right on a key- result in equal changes in pitch.
board produces increasingly higher-pitched notes. This relationship is illustrated in Figure 21–4,
Not surprisingly, piano strings struck when the keys where a piano keyboard standing on its side with the
to the left of the keyboard are depressed have lower low notes at the bottom is pictured next to a graph
frequencies of vibration; to the right of the keyboard, showing the relationship between changes in fre-
A BCDE FGA BCDE FGA BCDE FGA BCDE FGA BCDE FGA BCDE FGA BCDE FGA BC
1 1 1 1 1 1 1 2 2 2 2 2 2 2 3 3 3 3 3 3 3 4 4 4 4 4 4 4 5 5 5 5 5 5 5 6 6 6 6 6 6 6 7 7 7 7 7 7 7 8

High
A7

A6
Pitch (musical note)

A5

A4

A3

A2

A1

A0
220 440 880 1760 3520
Low 110
55 Frequency (Hz)
27.5

Figure 21–4.  Relationship between the perceptual variable pitch (y-axis) and the physical variable frequency (x-axis).
The pitch axis is represented as a sequence of “A” notes from the lowest to highest on the piano keyboard. The graph shows
that the perception of the pitch of adjacent octaves (e.g., A4–A5 and A5–A6), or of more separated octaves (e.g., A2–A3, and
A6–A7), which sound like equivalent pitch ranges, is not matched by equivalent frequency ranges. The frequency range for
octaves increases with increasingly higher octaves on the piano keyboard.
 21  Hearing Science I:  Acoustics and Psychoacoustics
quency and changes in perceived pitch. All “A” notes
on the piano keyboard are highlighted, ranging from
the lowest-pitched A0 (frequency = 27.5 Hz) to the
highest-pitched A7 (frequency = 3520 Hz). The fre-
quency of each “A” note can be verified by the vertical,
dashed lines dropped from each note to the x-axis.
Most people, musicians and nonmusicians alike,
know that consecutive “A”s (or any other consecutive
notes such as “B”s, “C”s, and so forth) cover a range
called an octave. Octaves are frequency and perceptual
ranges: for a listener, the perceptual distance between
A3 and A4 is the same as between A4 and A5. These
two pitch distances are psychologically equivalent. The
less-than-simple relationship between frequency and
pitch is well illustrated by this example of consecu-
tive musical notes of the same letter (i.e., consecutive
pitches) and the frequencies of those consecutive notes.
In Figure 21–4, the frequency difference between
A3 and A4 is 220 Hz (A3 = 220 Hz, A4 = 440 Hz), and
the frequency difference between A4 and A5 is 440 Hz
(A4 = 440 Hz, A5 = 880 Hz). The frequency ranges of
these consecutive A’s are different, but the pitch change
associated with these two ranges is the same. Even in a
comparison of the small frequency difference between
A2 and A3 (110 Hz) and the large frequency difference
between A6 and A7 (1760 Hz)the pitch change for the
two frequency differences is the same (the two differ-
ences are associated with equivalent pitch changes).
Frequency and pitch do not change in a one-to-one
relationship.
Sine waves (pure tones), complex periodic events
(like the acoustic result of piano string vibration),
and complex aperiodic events all have pitches, even
if pitches of the aperiodic events may be fuzzy. The
pitch of complex acoustic events is much more compli-
cated compared with the pitch of sinusoids. The pitch
of complex acoustic events is not pursued further in
this chapter.
Loudness
“Loudness” refers to the perceived volume of a sound.
Sounds can be perceived as very soft, comfortably
loud, and uncomfortably loud, as well as all degrees of
loudness between these three examples.
The perceptual phenomenon of loudness has a
very complex relationship to the physical intensity
of the sound. The measure of sound intensity can be
obtained using a device called a sound level meter,
2 
 o be precise, a sound level meter measures a quantity of sound pressure level (SPL), which varies in response to sound energy much like the term
T
we are using, sound intensity. The difference between the two measures is not relevant to the point being made in the text. Almost any textbook
on hearing science and audiology describes the difference between sound intensity and SPL and how one measure can be derived from the other.
299
which gives the user a decibel (dB) value for the sound’s
intensity. This is a measure of the physical energy of a
sound. For the purposes of this chapter, the dB scale is
considered the standard measurement scale for sound
intensity, and higher values are associated with greater
perceived loudness. As in the case of pitch, there is not
a one-to-one relationship between decibel values and
perceived loudness.2
The following decibel values provide general stan-
dards for the meaning of numbers on the decibel scale.
A sound intensity of roughly 30 dB is measured when,
in the dead of night, you place a sound level meter in
the middle of a desert, far from any city. Thirty dB is
obviously very quiet. When speaking in a normal voice
to a friend separated from you by 1 m, the intensity of
your voice measured at your listener’s head is some-
where between 60 and 70 dB. Sound intensity at a con-
cert involving a band with gigantic amplifiers — the
kind of concert where you cannot hear what your
friend is saying, even though she is standing next to
you — is anywhere from 100 to 120 dB, measured in the
middle of the room.
A simple example of the lack of a one-to-one rela-
tionship between a physical measure of sound energy
and a perceptual measure of loudness is as follows.
Assume you were doing an experiment in which a par-
ticipant turns a dial to adjust the loudness of a sound
presented at 50 dB. The dial controls the intensity (the
physical measure) of the sound, and the participant
has access only to the dial — there is no access to num-
bers labeled on the dial with decibel values. You, as the
experimenter, have that access. You ask the participant
to turn the dial to double the loudness of the sound.
Most participants turn the dial for a doubling of loud-
ness to about 60 dB; they do not turn the dial to 100 dB.
The loudness of a sound presented at 100 dB is many
times the loudness of a 50-dB sound. As with frequency
and pitch, the physical quantities (the decibel values)
are not related directly to the perceptual values.
Sound Quality
When someone says, “That’s an interesting sound, lis-
ten to it and tell me what you think,” they are asking
for a subjective description. Psychoacousticians and
speech scientists often refer to the subjective impres-
sion of an acoustic event as the quality of the sound.
Quality, like pitch and loudness, can be scaled percep-
tually with numbers. The nature of the scaling task,
300 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
however, must be specified more precisely than simply,
“Scale the quality of this sound.” A sound may have
any number of different quality terms, such as rough,
weak, shrill, boomy, piercing, thin, fat, slappy, light,
and smooth, to name a few of the many, many terms
people use to describe how an acoustic event “sounds.”
Perceptual scaling of sound quality may involve
assigning numbers to just one of these descriptions — for
example, “Scale the boominess of the sounds you will
hear.” Perceptual scaling of sound qualities tends to
be less reliable than scaling of pitch or loudness, but
it can be done and has been the object of a great deal
of research in communication sciences and disorders.
In the earlier discussion of pitch and loudness,
these perceptual terms were connected to the physi-
cal acoustical characteristics of frequency and inten-
sity, respectively. What is the physical basis of quality
judgments? What causes a person to label one acous-
tic event “shrill,” another “smooth”? This is a compli-
cated question, but we can offer a general answer as
well as some more specific hints about the relationship
between sound quality and physical acoustics.
The general answer is that quality perception
depends to a large degree on the frequency composi-
tion of an acoustic event — that is, the frequency com-
ponents of the sound and their amplitudes. Sounds
with a highly tonal quality, such as a piano note or a
sung note by a trained singer, have mostly periodic fre-
quency components, and little aperiodic energy. Sound
with a noisy quality, like the hissing sound of a boil-
ing tea kettle or a sustained “sh” sound as in the word
“shop,” are composed mostly or completely of aperi-
odic energy. An extensive, probably unlimited number
of sound qualities are possible, depending on the fre-
quency components, their amplitudes, and the mix of
periodic and aperiodic energy in the sound. And, the
physical aspects of sound — frequency, amplitude, peri-
odic and aperiodic energy — can vary over time, lend-
ing another dimension to sound quality.
Take another look at the two spectra in Figure 21–3.
They have obvious differences in frequency compo-
nents and the mix of periodic and aperiodic energy,
and these differences account for the vowel quality
of the left-hand spectrum and the ocean-noise qual-
ity of the right-hand spectrum. A fascinating aspect of
the relationship between the physical and perceptual
aspects of complex sounds like the ones in Figure 21–3
is that a frequency component, or its amplitude, can be
changed in very small amounts for listeners to detect a
quality change. Humans are very sensitive to shades of
sound quality differences.
Chapter Summary
Acoustics is the science of sound; sound waves are
pressure waves, initiated by a vibrating source.
The periodic motion of air molecules can be used
as a model for sine waves, in which the molecules oscil-
late back and forth.
Sine waves are the most basic type of sound wave;
sine waves have a single frequency.
Periodic motions of sine waves can be quantified
(measured) in terms of the period of vibration (the time
taken to complete one complete cycle of vibration), the
inverse of which is frequency (number of complete
cycles per second); and in terms of amplitude, or the
extent of displacement of the molecule during the
vibratory motion.
Acoustic events can be represented by a wave-
form, which is a plot of amplitude (sound energy) as
a function of time, or by a spectrum, which is a plot
of amplitude as a function of frequency; a waveform
and a spectrum are two ways to represent the same
acoustic event.
Complex acoustic events are composed of many
sine waves having different frequencies; complex
acoustic events can be periodic or aperiodic, or a mix
of periodic and aperiodic energy.
Resonance is the phenomenon where an object
vibrates with maximal amplitude at a specific fre-
quency, or at multiple frequencies.
Psychoacoustics is the science of the psychological
reaction to acoustic events. Terms such as pitch, loud-
ness, and quality are perceptual terms.
Frequency is the primary physical (acoustic) mea-
sure related to pitch, and intensity the primary acoustic
measure related to loudness.
The relationships between the physical event (e.g.,
frequency) and its perceptual correlate (e.g., pitch) are
not one-to-one; equal changes in frequency are not asso-
ciated with equal changes in pitch, and equal changes
in intensity are not associated with equal changes in
loudness.
References
Hixon, T. J., Weismer, G., & Hoit, J. D. (2020). Preclinical speech
science: Anatomy, physiology, acoustics, perception (3rd ed.).
San Diego, CA: Plural Publishing.
Kramer, S., & Brown, D. K. (2019). Audiology: Science to practice
(3rd ed.). San Diego, CA: Plural Publishing.

Hearing Science II:
Anatomy and Physiology
Introduction
This chapter presents the anatomy and physiology of
the auditory mechanism. Structures covered include
the external ear canal, eardrum (tympanic membrane),
ossicles (middle ear bones), cochlea (end organ of hear-
ing), auditory nerve, and central auditory pathways.
Abele and Wiggins (2015); Barin (2009); Goutman,
Elgoyhen, and Gomez-Casati (2015); Hudpseth (2014);
Lemmerling, Stambuk, Mancuso, Antonelli, and Kubi-
lis (1997); Luers and Hüttenbrink (2016); and Olsen,
Duifhuis and Steele (2012) have been used as sources
for the information presented in this chapter.
A solid understanding of the auditory mechanism
is critical to anyone interested in pursuing a career
in audiology, speech-language pathology, hearing or
speech science, or any other career related to communi-
cation. Selected reasons for gaining this knowledge are
the following: (a) The great majority of children learn
speech and language via the auditory system, (b) an
understanding of the normal structures and functions
of the auditory mechanism allows an appreciation of
the ways in which various diseases and conditions
affect hearing, and (c) knowledge of the anatomy and
physiology of the auditory mechanism is essential to
understanding the design and purpose of formal tests
22
of hearing. The knowledge is also essential to under-
standing devices such as cochlear implants and hearing
aids which are used to treat hearing loss. Information on
diseases of the auditory system, the audiological tests to
evaluate their effect on hearing, and auditory devices to
treat hearing loss is presented in Chapters 23 and 24).
Structures of peripheral auditory anatomy can be
classified as belonging to one of three major divisions:
the outer ear, the middle ear (tympanic cavity), and the
inner ear. Anatomical structures of the auditory system
are the same for both ears; descriptions of the struc-
tures of one ear apply equally to the structures of the
other ear. “Peripheral auditory system” refers to those
structures outside the central nervous system.
Temporal Bone
Much of the peripheral auditory mechanism is encased
in the temporal bone of the skull. Figure 22–1 shows
the complex shape of the temporal bone. Figure 22–1,
top, is a view of the skull from the left side of the head.
The perimeter of the temporal bone is outlined in
red. The temporal bone includes the bony part of the ear
canal — the opening inside the pinna (the structure often
referred to in lay terms as “the ear”; see below).
301
302 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

External
ear canal
Temporal
bone

Temporal bone
(petrous portion)

Figure 22–1.  Top, view of temporal bone of the skull from the left side,
outlined in red; bottom, view of temporal from above, as part of the base of
the skull, shaded pinkish.

Figure 22–1, bottom, shows the interior base of of the skull. The three major structures of the periph-
the skull as if the top half has been removed, with eral auditory system — the bony ear canal, the middle
the view from above. The temporal bone extends ear, and the inner ear — are encased within the tempo-
toward the middle of the skull, forming part of the base ral bone.
 22  Hearing Science II:  Anatomy and Physiology 303

Peripheral Anatomy of the Ear
Figure 22–2 is an artist’s rendition of the peripheral
anatomy of the ear. The structures are shown as if the
head has been cut into front and back halves, with the
front half removed. The peripheral auditory mecha-
nism is separated into three major parts: the outer ear,
the middle ear, and the inner ear. The outer ear plus
middle ear are components of the conductive part of
the auditory mechanism. The inner ear is the sensori-
neural part of the mechanism. Figure 22–3 is a sche-
matic chart of the divisions of auditory anatomy. Both
Figures 22–2 and 22–3 should be referred to frequently
throughout the following sections.
Outer Ear (Conductive Mechanism)
The outer ear includes the pinna (auricle) and the exter-
nal auditory canal, also called the external auditory
meatus. Part of the tympanic membrane (eardrum) ​
— the sheet of tissue that terminates the external audi-
tory meatus — is also considered a structure of the outer
ear. The tympanic membrane is the boundary between
the outer and middle ear.
Pinna (Auricle)
The pinna is composed of cartilage and fat tissue. In
humans, the pinna collects and directs sound energy
into the external auditory meatus and toward the ear-
drum. Careful examination of a human’s pinna shows
many creases, folds, and cavities. Anatomical character-
istics of the pinna vary a good deal among individuals.
External Auditory Meatus (EAM; also
called External Auditory Canal)
The entrance to the external auditory meatus is a small
opening easily seen inside the pinna. The external
auditory meatus (external ear canal) is a tube extending
from this opening to the tympanic membrane; meatus is

Temporal bone
Middle Ear
Semicircular
canals
Ossicles
Incus
Stapes
Malleus

Internal
auditory
meatus
Pinna Auditory
(Auricle) nerve

Cochlea

Tympanic
cavity
Tympanic Auditory
membrane (Eustachian) tube
External
ear canal (eardrum) Inner Ear

Outer Ear

Figure 22–2.  Coronal-plane view (head cut in front and back halves, view from the front) showing structures of the
peripheral auditory system.
304 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Outer Ear
• Pinna
• EAM
Conductive
Middle Ear
mechanism
• Eardrum
• Ossicles
- malleus
- incus
- stapes
Inner Ear
• Vestibular Apparatus
• Cochlea
- basilar membrane Sensorineural
mechanism
- organ of Corti
• Auditory nerve
Figure 22–3.  The anatomical components of the outer,
middle, and inner ear, and their relationship to the func-
tional distinction between conductive versus sensorineural
auditory components.
a Latin term meaning “opening” or “canal.” In adults,
the external auditory meatus is roughly 2.5 cm in
length and 0.7 cm in diameter. These dimensions vary
quite a bit across individuals.
The external auditory meatus is not a straight,
level tube. Rather it runs slightly “uphill” (see Fig-
ure 22–2) and between the opening to the canal and
the tympanic membrane has a small bend or kink in the
direction of the back of the head. (The bend cannot be
seen in Figure 22–2 because the frontal view does not
provide depth perception.) You may have noticed that
your medical practitioner, when inserting an otoscope
(ear scope) into your ear canal to examine the canal and
view your tympanic membrane, gently pulls the pinna
up and toward the back of the head. The practitioner
does this to straighten out the natural “kink” in the
tube for a more direct view of the tympanic membrane.
The outer part of the external auditory meatus is
surrounded by cartilage. Near the bend in the external
auditory meatus, the surrounding walls change from
cartilage to bone. The remaining length of the ear canal,
from bend to eardrum, is encased by part of the tempo-
ral bone. The external auditory meatus ends as a closed
tube at the tympanic membrane.
The primary auditory role of the external auditory
meatus is to conduct sound energy through the ear
canal to the tympanic membrane. The sound energy is
in the form of molecule-sized pressure waves (Hixon,
Weismer, & Hoit, 2020). As it conducts sound energy,
the external auditory meatus acts like a resonator, caus-
ing energy at certain frequencies to vibrate with greater
amplitude as compared to energy at other frequencies.
Getting a Boost
The resonant frequency of the exter-
nal auditory meatus is approximately 3300 Hz.
What does this mean? When sound waves travel
through the canal, sound energy at 3300 Hz and
nearby frequencies are amplified by the canal’s
resonant frequency. Frequencies much lower
or higher than 3300 Hz are amplified less. The
resonant frequency of the ear canal contributes
in a significant way to hearing in humans. For
example, the human ear is most sensitive to
sound energy at and near 3300 Hz. Second,
human speech contains important sound energy
over a range of frequencies around 3300 Hz,
making the resonant frequency of the ear canal
particularly useful for accurate perception of
speech sounds.
The external auditory meatus also serves a protec-
tive function. Glands in the cartilaginous walls of the
external auditory meatus secrete cerumen (earwax)
which presents a barrier to foreign objects (insects, for
example) and may also block the movement of bacteria
or fungal agents toward the tympanic membrane. The
kinked tube of the external auditory meatus is also a
barrier to foreign objects moving easily from the outer
ear to the delicate tissues of the tympanic membrane.
Tympanic Membrane (Eardrum)
The tympanic membrane, or eardrum (Figure 22–4),
is the boundary between the outer and middle ear.
The circular perimeter of the tympanic membrane is
linked to a bony foundation via a cartilage-ligamentous
ring called the annulus. The annulus fits into a small
circular, bony depression at the boundary between the
outer and middle ear to fix the tympanic membrane
in place.
Figure 22–4 is a photograph of the right tympanic
membrane as seen through an otoscope. The otoscope
has a viewing lens and a light source to illuminate the
ear canal and the tympanic membrane. As a result of
the shallow conical shape of the tympanic membrane
and its tilt with the lower half further from the scope

Pars
flaccida
Incus of eardrum
Stapes
Malleus
(handle)
Umbo
Light
reflex
Annulus
Figure 22–4.  View of the right tympanic membrane as
seen through an otoscope.
than the upper half, a “light reflex” (also called a “cone
of light”) reflects off the normal tympanic membrane.
The light reflex is directed forward, downward, and to
the right. The light reflex is directed to the left when
viewing the left tympanic membrane. Middle ear
bones (ossicles) can be seen through the translucent
membrane.
In the otoscopic view, the tympanic membrane
looks more or less flat — not conical, not tilted along its
top-to-bottom axis relative to the observer. The cone
shape and tilt are seen in the artist’s cross-sectional
rendition of the tympanic membrane in Figure 22–2.
The tympanic membrane has the shape of a flattened
bowl with a conical base that points into the middle
ear cavity.
The tympanic membrane is tiny but tough. The
membrane has a diameter of roughly 8 to 10 mm and
a surface area of about 55 mm2. The thickness of the
membrane is little more than one-tenth of a millimeter
(0.0001 meters). The tympanic membrane is composed
of three tissue layers. The middle layer is the one most
sensitive to sound waves, and because of its tissue
makeup, which is different from the two layers that
sandwich it, is exceptionally strong.
Middle Ear
The middle ear is an air-filled cavity surrounded by
bone. Its complexly shaped volume contains tiny, mov-
22  Hearing Science II:  Anatomy and Physiology 305
able bones (ossicles), ligaments, two muscles, nerves,
and a bony opening to a tube that leads to the top part
of the throat.
Ossicles
The ossicles are the three smallest bones in the human
body. They extend across the middle ear cavity from
the tympanic membrane to the oval window of the
cochlea. These bones are so tiny they can be placed on
a penny and occupy no more than the bottom half of
the coin.
The malleus (hammer) is the ossicle attached to the
tympanic membrane; the stapes (stirrup) is the ossicle
attached to the cochlea (part of the inner ear); and the
incus (anvil) is the middle bone, linking the malleus to
the stapes. The three connected ossicles are together
called the ossicular chain.
The malleus has a handle-like part called the
manubrium, which is attached at its lower end to the
tympanic membrane. The lowest attachment point of
the manubrium to the tympanic membrane is called
the umbo and can be seen through the translucent tis-
sue of the tympanic membrane when viewed through
an otoscope (see Figure 22–4).
The top of the malleus has a knobby bump that
fits into a cup-like depression at the top of the incus.
This is where the connection between the two bones is
made. A long, bony limb descends from the top of the
incus and forms a hook at its bottom. This hook fits into
the neck of the stapes (see Figure 22–2, pointer to the
stapes, at its neck), connecting the two bones.
The stapes, the smallest of the ossicles, has a neck
(mentioned in the previous paragraph) and two arches
that project from it. The base of each arch is attached to
the footplate of the stapes, which is oval shaped. The
footplate of the stapes fits into an oval window cut into
the bony casing of the inner ear. The footplate is held in
that window by a fibrous ligament.
The ossicles function to transmit sound energy
from the tympanic membrane to the footplate of the
stapes, and eventually to the fluid-filled cochlea. This
function can be explained as a series of events begin-
ning with sound wave energy in the air (pressure
wave), conversion of the pressure wave to mechanical
energy in the form of vibration of the eardrum and ossi-
cles with the final mechanical energy taking the form
of vibratory movement of the footplate of the stapes,
in and out of the oval window. The vibratory move-
ment of the stapes displaces fluid in the cochlea, thus
the mechanical energy is converted to fluid energy.
1. Sound vibrations in the air enter the ear canal and
initiate vibration of the tympanic membrane.
306 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
2. Vibration of the tympanic membrane is trans-
ferred to the malleus, to which it is attached.
3. The sound vibration is transmitted via the
connected ossicles to the footplate of the stapes.
4. The footplate of the stapes moves in and out of
the oval window; behind the oval window is the
fluid-filled cochlea, so the vibratory movement of
the footplate of the stapes displaces cochlear fluid
(see later in this chapter).
Ligaments and Muscles of the Middle Ear
The ossicles are anchored to the walls of the middle
ear cavity by several ligaments and two muscles.
Figure 22–5, a “zoom” view of the middle ear cavity,
shows three of the ligaments (short, pinkish bands
of tissue), each attached to an ossicle with their other
ends attached to one of the middle ear walls. In this
chapter, we note the importance of these attachments
as anchors for the ossicles, and their role in limiting
ossicular movement when they vibrate in response to
sound energy. Additional details about the middle ear
ligaments are available in the publications cited in the
first paragraph of the chapter.
Superior incudal
ligament
Superior malleolar
ligament
Lateral malleolar
ligament
Anterior
malleolar ligament
(point of attachment)
Stapedius tendon
Figure 22–5.  Close-up (“zoom”) view of middle ear cavity, showing ossicles, muscles, and ligaments.
The two muscles of the middle ear cavity are the
tensor tympani muscle and the stapedius muscle (Fig-
ure 22–5). The tensor tympani muscle enters the mid-
dle ear canal and attaches to the malleus by means of a
short tendon. The stapedius muscle is buried in a small
bony canal in the back wall of the middle ear. It issues
a tendon that enters the middle ear cavity and attaches
to the neck of the stapes (Figure 22–5).
Contraction of the tensor tympani muscle pulls
on the malleus, retracting the tympanic membrane
into the middle ear cavity. Contraction of the stapedius
muscle pulls on the footplate of the stapes (by means
of the stapedius tendon), away from (but not out of)
its “fit” into the oval window. Contraction of either
muscle stiffens the ossicles, which as discussed later,
reduces the efficiency of sound energy transfer from
the tympanic membrane to the footplate of the stapes.
There is some debate about the role of the tensor
tympani muscle in hearing, which is not presented
here. The stapedius muscle, however, is known to
be a key component of the acoustic reflex. The acous-
tic reflex is the contraction of the stapedius muscle
in response to very high levels (intensities) of sound
energy (see Chapter 23 for diagnostic testing for the
Posterior incudal
ligament
Annular ligament
Tensor
tympani muscle

acoustic reflex). High-intensity sound vibration has the
potential to drive the footplate of the stapes too force-
fully into the cochlear fluid, leading to excessive fluid
displacements that can damage the delicate sensory
organs of hearing. Recall that contraction of the sta-
pedius muscle pulls the footplate of the stapes away
from the oval window and in so doing stiffens the
ossicular chain. A stiffer ossicular chain reduces sound
transmission and prevents the footplate of the stapes
from too-forceful displacement into the cochlear fluid.
The acoustic reflex therefore protects the cochlea from
extremely high sound levels.
The acoustic reflex is “wired” by a loop made up
by the auditory nerve, structures in the brainstem, the
facial nerve (cranial nerve VII, see Chapter 2) and the
stapedius muscle. The reflex is fast: about a tenth of a
second (0.1 sec) passes between the introduction into
the ear of extremely high sound levels, transmission
of the sound energy (in mechanical, fluid, and elec-
trochemical forms) through the cochlea and auditory
nerve to the brainstem, and a signal from the brainstem
via the facial nerve to contract the stapedius muscle
and exert its pull on the stapes.
Auditory (Eustachian) Tube
The auditory tube (also called the Eustachian tube,
after the 16th-century Italian anatomist Bartolomeo
Eustachi) is shown in Figure 22–2 as a bone-encased,
open tube in the lower part of the middle ear cav-
ity; The bony tube opening near the bottom of the
middle ear cavity is also seen in the “zoom” image
No Ossicles??
What would happen if we did not
have ossicles? We would not be able to hear
as well. Your ossicle-less ear would have an
eardrum and a cochlea, separated by an air-filled
middle ear cavity. Vibrations of air molecules in
your outer ear would be transmitted to the air
in your middle ear and strike the membrane of
the oval window behind which resides the fluid
(liquid) in your cochlea. Would the fluid in your
cochlea be displaced by these sound waves? The
answer is “yes,” but very ineffectively because
sound energy in air does not push against fluid
very effectively. In fact, in addition to transmit-
ting sound energy from the tympanic membrane
to the oval window, the ossicles amplify the
energy by means of their anatomy. We all need
our ossicles.
22  Hearing Science II:  Anatomy and Physiology 307
of Figure 22–5. The tube becomes cartilaginous as it
extends downward and terminates in the upper part
of the pharynx (throat). The auditory tube is normally
closed at its pharyngeal ending; the tube is opened
briefly during swallowing, chewing, and yawning.
When the tube opens, it connects air in the middle ear
cavity to air in the nasopharynx. Thus, intermittent
opening of the pharyngeal part of the auditory tube
serves to maintain middle ear pressure at normal val-
ues (i.e., at atmospheric pressure, the same pressure in
the pharynx when the mouth and/or nostrils are open
to atmosphere). Normal values of air pressure within
the middle ear cavity are important to the health of
middle-ear structures.
Inner Ear (Sensorineural
Mechanism)
The inner ear is encased in a complex, bony struc-
ture that is itself encased in the temporal bone. This
structure is called the bony labyrinth, shown for the
right ear in Figure 22–6. In this view, the semicircular
canals are to the left, the vestibule in the middle, and
the cochlea at the front. The vestibule joins the semicir-
cular canals and cochlea and has the oval window as a
notable landmark. All structures of the bony labyrinth
are filled with fluid. The bony labyrinth is identical in
the left ear.
There are two openings into the bony labyrinth.
The upper opening is called the oval window where the
footplate of the stapes is attached. The lower opening
is the round window, which is covered by a membrane
similar in structure (although not identical) to the tym-
panic membrane. As described earlier, inward move-
ment of the footplate of the stapes displaces fluid in the
cochlea. The fluid travels like a wave through cochlear
channels to the round window, which bulges when the
wave arrives. The displacement of the cochlear fluid
and its importance to auditory sensation are described
later in this chapter.
Semicircular Canals
Three fluid-filled semicircular canals comprise the left-
most structure of the bony labyrinth in the right ear
(see Figure 22–6). One canal is oriented vertically, one
horizontally, and one from front to back. Any one of
the canals is oriented at right angles to the other two.
The semicircular canals control balance. The fluid
within them contains sensory organs called hair cells.
Movement of the head displaces the fluid, which bends
the hair cells and initiates a signal to the nervous sys-
tem. The fluid displacement in the semicircular canals
308 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Superior
Semi-circular
canals
Lateral
Posterior
Ampullae
Round window
Figure 22–6.  The bony labyrinth (otic capsule), as if viewed from the middle ear cav-
ity of the right ear. The semicircular canals are to the left, the vestibule in the middle, and
the cochlea is to the right.
and the resulting bending of the hair cells sends signals
to the brain regarding the precise location of the head in
space. Balance is an important outcome of these signals.
Vestibule
The vestibule contains the oval window in which the
footplate of the stapes is fixed. Two structures within
the vestibule, also fluid filled and with hair cells, detect
motion of the head, which supplements the position
detection signaled by the semicircular canals.
Cochlea
The cochlea (meaning snail) is made up of many smaller
structures. Among the most important of these are the
scalae (plural for scala, another name for duct), the bas-
ilar membrane, and the organ of Corti, which sits atop
the membrane and includes hair cells. These structures
are the basis for the transformation of sound waves
into neural signals. The neural signals code proper-
ties of the sound and deliver this information from the
cochlea via the auditory nerve (cranial nerve VIII) to
the central nervous system.
The cochlea consists of three membranous, fluid-
filled ducts that are coiled in a snail-shell spiral. The
spiral of the membranes, like its bony casing, includes
two-and-one-half turns from its base to its tip (apex).
At the tip of the cochlea, the two outside ducts are con-
nected by a small opening. This connection explains
Cochlea
Vestibule
Oval
window
Apex
Base
why the fluid displacement at the oval window (push-
ing into the scala vestibuli) is transmitted to the scala
tympani and results after a very brief delay in a bulg-
ing of the round window (the termination of the scala
tympani).
Figure 22–7 shows the coiled cochlea cut in several
cross sections; the three ducts are visible at each cut.
The footplate of the stapes fits into the oval window
at the duct called the scala vestibuli. Movement of the
footplate pushes into the fluid in the scala vestibuli,
displacing it in the direction of the tip of the spiral.
The direction of this fluid displacement is indicated
by the blue arrow in Figure 22–7. The fluid displace-
ment travels through the opening at the tip of the
cochlea, from the scala vestibuli to the scala tympani
(red arrow, Figure 22-7). The fluid wave travels through
the scala tympani to its termination at the round win-
dow, which bulges when it is pushed by the arriving
fluid wave.
Each of the cross-sectional cuts in Figure 22–7
show a membrane separating the scala tympani from
the third duct, called the cochlear duct (also called the
scala media). The membrane is called the basilar mem-
brane; sitting on top of the membrane is the organ of
Corti. The organ of Corti contains hair cells similar to
those in the semicircular canals of the vestibular sys-
tem. The hair cells in the organ of Corti are bent when
the fluid displacement in the scala vestibuli and scala
tympani creates a sound-induced, fluid wave pattern
that displaces the basilar membrane in precise ways.

Cochlea duct
Scala vestibuli
Cochlea
Figure 22–7.  The cochlear spiral cut in several cross-sections. The cross-section cuts through
multiple turns of the cochlea. Each section of the cochlea contains three scalae, the scala vestibuli,
the scala media (cochlear duct), and scala tympani.
Basilar Membrane and Organ of
Corti (Sensory Mechanism)
An artist’s rendition of the basilar membrane and
Organ of Corti, at one “slice” through a turn in the
cochlea, is shown in Figure 22–8. The organ of Corti
sits atop the basilar membrane. The basilar membrane,
organ of Corti, and a membrane above the hair cells
(labeled “tectorial membrane”) form the sensory end
organ of hearing.
To get an idea of how much this image has been
magnified relative to the size of the actual organs,
consider that the nearly vertical structures labeled
“inner hair cells” and “outer hair cells” are roughly 30
micrometers (0.000030 meters, around 1/1000th of an
inch) in length and 10 micrometers in diameter.
Note the single hair cell (inner hair cell) to the left
of the image and the row of three hair cells (outer hair
cells) to the right. These hair cells run the length of the
cochlea, from base to tip. Note also the nerve fibers
(shown in yellow) connected to the inner and outer
22  Hearing Science II:  Anatomy and Physiology 309
Scala tympani
Auditory nerve
Away from the tip,
toward the round window
Away from the oval
window, toward the tip
Basilar membrane
Organ of Corti
hair cells. Each hair cell in the organ of Corti, from base
to tip of the basilar membrane, is attached to a nerve
fiber that becomes part of the auditory nerve. The audi-
tory nerve carries information from the cochlea to the
brain, and in some cases from the brain to the cochlea
(see discussion later in this chapter).
Coding of Frequency Along the Basilar Mem-
brane.  The hair cells within the organ of Corti are
critical to auditory sensation, much like the rods and
cones of the retina, the end organ of vision, are critical
to visual sensation. Here we focus on the role of the
basilar membrane and inner hair cells in coding fre-
quency of incoming sound waves. The outer hair cells
are critical to hearing as well. They control the sensitiv-
ity of the inner hair cells, allowing the detection of very
soft sounds and increasing the precision of frequency
analysis by the inner hair cells. The outer hair cells are
not discussed further in this chapter.
The basilar membrane is displaced (“deformed”) by
the fluid wave within the cochlea. The precise location
310 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Tectorial membrane
Inner Hair Cell
Nerve fibers
Figure 22–8.  The basilar membrane and the organ of Corti, at one cut along the cochlear spiral.
of maximum displacement along the basilar mem-
brane depends on the frequency (or frequencies) of
the incoming sound wave. This is because frequency
analysis is arranged systematically along the basilar
membrane and the hair cells in the organ of Corti. The
systematic arrangement of frequency along the basilar
membrane is called tonotopic representation.
Tonotopic representation is illustrated in Figures
22–9 and 22–10. In Figure 22–9, the snail shell–like
cochlea (top) is “unrolled” (bottom) to better explain
tonotopic representation.
The basilar membrane is shown in Figure 22–9,
bottom, by the flat pink strip running from the base to
tip of the cochlea. The arrows show the path of fluid
displacement from the scala vestibuli, through the nar-
row opening at the tip, and then through the scale tym-
pani in the direction of the round window.
The basilar membrane is narrow at its base (the
left end of the membrane in Figure 22–9) and becomes
increasingly wider as it extends to the tip of the
cochlea. The narrow base of the basilar membrane is
very stiff, and the wide tip end of the membrane is rela-
tively floppy. The hair cells at the base (narrow part)
of the membrane are sensitive to the highest frequen-
cies humans can hear (about 20,000 Hz). Moving from
Outer Hair Cells
Basilar
Membrane
the base toward the tip of the basilar membrane, the
hair cells are sensitive to increasingly lower frequencies
until at the tip they are sensitive to the lowest frequen-
cies human can hear (about 20 Hz).
Now we can make a more precise statement about
tonotopic representation: frequency is represented
tonotopically along the basilar membrane such that the
location of a hair cell along the membrane determines
its frequency sensitivity. Hair cells at the base of the
basilar membrane are sensitive to the highest frequen-
cies, and hair cells at the tip of the basilar membrane
are sensitive to the lowest frequencies.
Displacement of the Basilar Membrane and Fre-
quency Analysis.  Tonotopic arrangement of the hair
cells along the basilar membrane raises the question of
how different locations along the membrane are stimu-
lated when vibratory motions of the conductive mecha-
nism are transferred to the cochlear fluid.
We owe the understanding of frequency analysis
in the cochlea to experiments performed by Georg von
Békésy (1899–1972), a Hungarian physicist and engi-
neer who in 1961 won the Nobel Prize for this work.
Von Békésy observed that when the footplate of the
stapes vibrated in response to sound energy, it pushed

Basilar
membrane
Highest
frequencies
Oval
window
Round
window
Base
Figure 22–9.  Top, the cochlea as if rolled out to form a straight structure (bottom). In the bottom image,
the scala vestibuli is the top duct, the scala tympani the bottom duct, and the basilar membrane is shown as
the pinkish partition in the middle, narrow and stiff at the base and wide and floppy at the apex.
into the cochlea and created a fluid wave that traveled
through the scala vestibuli and scala tympani. The fluid
wave displaced the basilar membrane, and the location
of its maximum displacement depended on the fre-
quency of the incoming sound wave. Low frequencies
resulted in a basilar membrane displacement that built
up gradually and reached its peak near the tip of the
membrane. In contrast, high-frequency sound energy
produced displacement of the basilar membrane that
built to a peak at a short distance from the oval win-
dow (that is, near the base). In his world-famous 1928
paper, von Békésy described this fluid movement in
the cochlea as a traveling wave.
Figure 22–10 is a schematic summary of how dif-
ferent frequencies of incoming sound waves result in
different locations of maximum displacement along the
22  Hearing Science II:  Anatomy and Physiology 311
Apex
Lowest
frequencies
basilar membrane. Three unrolled cochleae (plural of
cochlea) are shown, with three schematic “blips” rep-
resenting maximum displacement of the basilar mem-
brane for high (top), mid (middle), and low (bottom)
frequencies. These are the wave patterns expected for
single frequencies. Traveling wave patterns for sound
waves made up of many different frequencies result
in more complex patterns of displacement along the
basilar membrane.
How does displacement of the basilar membrane
result in a frequency signal that is sent to the brain? The
traveling wave that has maximum displacement of the
basilar membrane at a specific location causes bending
of the hair cells at the same location. When bent, the
membranes of the hair cells change their sensitivity to
certain molecules, which in turn cause their attached
312 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

High Mid Low

Highest
frequencies
Apex

Oval
window

Round
window

Lowest
Base frequencies

High Mid Low

Highest
frequencies
Apex

Oval
window

Round
window

Lowest
Base frequencies

High Mid Low

Highest
frequencies
Apex

Oval
window

Round
window

Lowest
Base frequencies

Figure 22–10.  Three unrolled cochleae, showing the location of maximum displacement along
the basilar membrane for high (top), mid (middle), and low (bottom) frequencies.

nerve fibers (see Figure 22–8) to “fire” and send a sig-
nal to the brain via the auditory nerve (see Figure 22–2
for the auditory nerve emerging from the cochlea). The
nerve fibers attached to the individual hair cells have
the same tonotopic arrangement as the basilar mem-
brane: The fluid displacement that causes a traveling
to wave to crest at a specific location, which depends
on the frequency of the incoming sound wave, results in
the firing of a nerve fiber that is maximally sensitive
to that frequency.
 22  Hearing Science II:  Anatomy and Physiology 313

Auditory Nerve and Auditory problems and facial weakness may have diagnostic
Pathways (Neural Mechanism) significance.

The auditory nerve in the peripheral auditory system,
and the auditory pathways within the central nervous
system, comprise the neural component of the hearing
mechanism.
Auditory Nerve. Individual nerve fibers emerg-
ing from the base of the inner hair cells are gathered
together and form a significant part of the auditory
nerve, which is part of cranial nerve VIII. The auditory
nerve travels through the internal auditory meatus, a
narrow, short tunnel in the temporal bone. The nerve
emerges from the tunnel and enters the central nervous
system at the lower levels of the brainstem.
The internal auditory meatus also contains the
fibers of the other part of cranial nerve VIII — the ves-
tibular nerve — as well as fibers of cranial nerve VII
(the facial nerve). Figure 22–2 shows the cochlear
and vestibular components of cranial nerve VIII and
the fibers of cranial nerve VII. The close proximity of
the facial nerve to the auditory nerve is significant
because the facial nerve may be affected by a disease
of the auditory nerve, and the combination of auditory
Auditory Pathways. The auditory pathways are struc-
tures in the nervous system that carry auditory impulses
from the auditory nerve to the cortex, the highest level
of the central nervous system. The auditory nerve also
includes fibers carrying information from the central
nervous system to the cochlea; these fibers innervate
the outer hair cells. The focus in this section is on the
pathways from the auditory nerve to the cortex of
the cerebral hemispheres
When electrical impulses are transmitted in the
auditory nervous system, they travel along nerves (or
tracts, as they are called in the central nervous system)
and make connections (synapses) in clusters of cell
bodies. These cell bodies issue another tract aimed at
a different cluster of cell bodies along the pathway to
the auditory cortex. The auditory pathways are more
or less dedicated to transmitting information from the
auditory nerve all the way to the auditory cortex. The
pathway terminates in the primary auditory cortex,
located on the upper lip of the temporal lobe. Like the
hair cells and auditory nerve, cells within the auditory
cortex are tonotopically arranged.

Tests of Hearing and Auditory

Anatomy and Physiology
Tests of hearing are designed based on knowledge of the auditory system.
For example, in pure-tone audiometry, tones of a single frequency are
used to estimate the response of the hair cells at different locations along
the basilar membrane. Because of the tonotopic arrangement of the hair
cells from base to apex of the cochlea, single-frequency tones allow a tester
to assess the health of the hair cells very precisely at different locations
throughout the cochlea. There are also techniques for assessing the stiff-
ness of the conductive mechanism (outer and middle ear). These stiffness
evaluations, all performed at the entrance to the ear canal with minimal
discomfort to the person being tested, are used to diagnose many auditory
disorders ranging from middle ear infections, which are very common
in childhood, to possible diseases of the auditory nerve which may be
reflected in poorly functioning acoustic reflexes. One more example is
the use of electrodes placed on the scalp to measure the amplitudes and
timing of electrical activity of cell groups within the auditory pathways of
the central nervous system, as brain analysis of an acoustic signal makes
its way from the auditory nerve to the auditory cortex. Clearly, audiologi-
cal tests reflect an intimate knowledge of the structure and function of
the auditory system. Chapter 23 presents details of these tests and their
interpretation.
314 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Chapter Summary
Knowledge of the structure and function of the audi-
tory mechanism is critical to those who plan a career
in communication sciences and disorders, whether the
career goal is to understand (a) how children learn lan-
guage, (b) how diseases affect the normal mechanism,
and (c) how formal evaluations of hearing are designed
and interpreted.
Most of the auditory mechanism is housed within
the temporal bone, a complex bone of the skull.
The peripheral auditory mechanism can be subdi-
vided into the conductive mechanism, comprising the
outer and middle ear, and the sensorineural mecha-
nism, comprising the inner ear and auditory nerve.
The external auditory meatus (or external audi-
tory canal) is a canal approximately 2.5 cm long and
0.7 cm in diameter that extends from an opening in the
auricle to the tympanic membrane, in which cerumen
(earwax) is produced and through which sound waves
are directed to the tympanic membrane.
The external auditory meatus has a resonant fre-
quency of roughly 3300 Hz, which explains in part the
very acute sensitivity of the human auditory mecha-
nism in this frequency region.
The tympanic membrane (or eardrum) is a small
(about 55 mm2 area), three-layered structure located at
the internal end of the outer ear; the middle tissue layer
is sensitive to the very small pressure variations associ-
ated with sound waves.
The middle ear is an air-filled cavity located between
the outer ear and inner ear, and contains three small ossi-
cles (bones), several ligaments, and two muscles.
The ossicles are stabilized by ligaments that attach
to the walls of the middle ear, and the tissue of two
muscles, the tensor tympani muscle that attaches to
the malleus and the stapedius muscle that attaches
to the stapes; contraction of both muscles stuffen the
ossicular chain when they contract.
The stapedius muscle is an important component
of the acoustic reflex; the muscle contracts in response
to high-level sound energy, and in so doing prevents
the footplate of the stapes from excessive displacement
force into the cochlear fluid.
The auditory tube (or Eustachian tube), a 3.8-cm
(1.5-inch) tube that runs from the middle ear to the
nasopharynx, is bony and open at the middle ear and
cartilaginous and flexible toward the top part of the
pharynx (the nasopharynx) where it is usually closed,
but opens occasionally to equalize the pressure in the
middle ear.
The inner ear is housed within the bony labyrinth
of the temporal bone and contains the semicircular
canals, vestibule, and cochlea, all structures that com-
municate with the central nervous system via cranial
nerve VIII (auditory-vestibular nerve).
Three semicircular canals, each oriented at right
angles to the other two, contain hair cells that bend
when the head moves and cause the vestibular part of
cranial nerve VIII to fire and send information about
head position and orientation to the brain.
The vestibule contains the oval window as well as
structures that contain hair cells that send signals to
the brain about the relative position and acceleration
of the head.
The cochlea is the spiral-shaped end organ of
hearing that converts sound into neural signals and
contains many important structures including the
scalae, basilar membrane and organ of Corti, and hair
cells.
Within the cochlea are three membranous, fluid-
filled ducts called the scala vestibuli, scala media (or
cochlear duct) and scala tympani, the first and last of
which are connected at the top of the cochlear spiral.
The scala media is separated from the scala tym-
pani by the basilar membrane.
On top of the basilar membrane sits the organ of
Corti, which contains a row of inner hair cells and three
rows of outer hair cells.
Movement of fluid in the cochlea (caused by sound
waves transmitted through the outer and middle ear,
and the movement of the stapes into the oval window)
deforms inner hair cells and causes them to send a sig-
nal to an attached nerve fiber, which makes the nerve
fiber “fire.”
Hair cells are arranged tonotopically along the bas-
ilar membrane, ranging from those that respond best to
the highest frequency at its narrow base (20,000 Hz) to
those that respond best to the lowest frequency at its
wide apex (20 Hz).
As discovered by Georg von Békésy, hair cells are
stimulated by traveling waves transmitted through
the cochlear fluid, the highest amplitude of which is
frequency dependent, with high-frequency sounds
creating waves that peak near the base of the basilar
membrane and low-frequency sounds creating waves
that peak near the apex of the basilar membrane.
The auditory pathways consist of the audi-
tory nerve, and the tracts and clusters of cell bodies
that carry auditory signals from the brainstem to the
cortex.
References
Abele, T. A., & Wiggins, III, R. H. (2015). Imaging of the tem-
poral bone. Radiological Clinics of North America, 53, 15–36.

Barin, K. (2009). Clinical neurophysiology of the vestibular
system. In J. Katz, L. Medwetzky, R. Burkard, & L. Hood
(Eds.), Handbook of clinical audiology (6th ed., pp. 431–466).
Baltimore, MD: Lippincott, Williams, & Wilkins.
Békésy, G. (1928). Zur Theorie des Hörens; die Schwingungs-
form der Basilarmembran. Physik. Zeits. 29, 793–810.
Goutman, J. D., Elgoyhen, A. B., & Gomez-Casati, M. E.
(2015). Cochlear hair cells: The sound-sensing machines.
FEBS Letters, 589, 3354–3361.
Hixon, T. J., Weismer, G., & Hoit, J. D. (2020). Preclinical speech
science: Anatomy, physiology, acoustics, perception (3rd ed.).
San Diego, CA: Plural Publishing.
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Hudpseth, A. J. (2014). Integrating the active process of hair
cells with cochlear function. Nature Reviews Neuroscience,
15, 600–614.
Lemmerling, M. J., Stambuk, H. E., Mancuso, A. A., Antonelli,
P. J., & Kubilis, P. S. (1997). CT of the normal suspensory
ligaments of the ossicles in the middle ear. AJNR American
Journal of Neuroradiology, 18, 471–477.
Luers, J. C., & Hüttenbrink, K.-B. (2016). Surgical anatomy
and pathology of the middle ear. Journal of Anatomy, 228,
338–353.
Olsen, E. S., Duifhuis, H., & Steele, C. R. (2012). Von Békésy
and cochlear mechanics. Hearing Research, 293, 31–43.

Diseases of the Auditory System
and Diagnostic Audiology
Introduction
This chapter presents an overview of the diseases of
the auditory and vestibular systems, and how they are
diagnosed. The chapter has been written specifically to
discuss the various tests used to evaluate hearing and
balance disorders. Subsequent chapters discuss what
can be done to rehabilitate auditory disorders. With
your new knowledge of the anatomy and physiology
of the auditory and vestibular system from the last
chapter, we can start to understand the tests needed to
determine which parts of the auditory system are func-
tional. Further information about the senses of hearing
and balance can be gathered from the outstanding texts
by Kramer and Brown (2019) and Jacobson and Shepard
(2016). Then we evaluate the different tests and their
outcomes for each of the main types of hearing disor-
ders — conductive, sensorineural, and mixed losses.
With a current population in the United States of
approximately 327 million people, the National Insti-
tute of Deafness and Other Communication Disorders
(NIDCD) reports that approximately 15% or 37.5 mil-
lion American adults over the age of 18 have some
trouble hearing, which is about the same as the total
population in the state of California. It is estimated
that 90% to 95% of these individuals can be helped
23
with hearing aids, which indicates that there are just
under 30 million people for whom hearing aids would
be of some benefit (NIDCD, 2016). As you can see in
Table 23–1, hearing loss is a problem in the general
population. We should know that individuals with
hearing loss will also have problems understanding
speech. But in addition to this obvious problem, we also
know that hearing loss is associated with other serious
negative consequences such as academic difficulties,
problems in the workplace, and psychosocial issues
such as social isolation, depression, anxiety, loneliness,
and lessened self-efficacy (Mueller, Ricketts, & Bentler,
2014). However, as audiologists we need to identify
these individuals and determine the type, degree, and
configuration of their hearing loss so that we can assist
them in developing effective communication.
Hearing Evaluation
According to the American Academy of Audiology, an
audiologist provides services in the audiologic identifi-
cation, assessment, diagnosis, and treatment of persons
with impairment of auditory and vestibular function
while in their roles as clinician, therapist, teacher, con-
sultant, researcher, and administrator. They identify,
317
318 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Table 23–1.  Quick Statistics About Hearing
Children • Two to three out of every 1,000 children
are born with a hearing loss in one or
both ears
• More than 90% of deaf children are
born to hearing parents
• Five out of six children have an ear
infection by the time they are 3 years old
• At least 1.4 million children (18 or
younger) have hearing problems
Adults • Three in 10 people over age 60 years
have hearing loss
• One in six baby boomers (ages 41–59
years), or 14.6%, have a hearing
problem
• One in 14 Generation Xers (ages 29–40
years), or 7.4%, already have hearing
loss
• 10% of adults (about 25 million) have
experienced tinnitus
Treatment • Only about 16% of adults with hearing
loss use hearing aids
• 58,000 cochlear implants have been
implanted in adults and 38,000 in
children
Source:  From “Quick Statistics About Hearing,” National Institute
on Deafness and Other Communication Disorders (NIDCD), 2016.
Retrieved from https://www.nidcd.nih.gov
assess, diagnose, and treat individuals with impair-
ment of either peripheral or central auditory and/or
vestibular function (AAA, 2004). Audiologists (or cli-
nicians as they are often referred) are trained as both
diagnosticians and habilitation/rehabilitation experts
for the auditory system. They spend much of their
time determining the type, degree, and configuration
of any hearing loss they detect and determining what
can be done to rehabilitate communication problems
associated with the loss. In most cases, this makes
audiologists heavily reliant on technology. Therefore,
audiologists need to be technologically savvy to be
competent in their job.
The assessment of an individual’s hearing includes
the administration and interpretation of behavioral,
psychoacoustic, and electrophysiologic measures of the
peripheral and central auditory systems. The assess-
ment of an individual’s vestibular system includes the
administration and interpretation of behavioral and
electrophysiologic tests of equilibrium. Both of these
types of assessments are accomplished using standard-
ized testing procedures and instrumentation in order
to diagnose any abnormality in their hearing and/or
vestibular systems (AAA, 2004).
Case History
It is important that before you start your assess-
ment, you obtain some information about the patient.
Referred to as a case history, you can learn important
information and gain great clinical insight about the
patient’s primary complaints and symptoms. Through
the case history, you will obtain answers to your ques-
tions about the extent of any hearing and communi-
cation problems, when the problem began, whether
it has worsened, if it came on suddenly or gradually,
and if the patient has associated dizziness and/or tin-
nitus (ringing in the ears). Additional topics you may
explore in the case history include how family mem-
bers perceive the patient’s problem, any associated cir-
cumstances or activities that brought on the conditions,
what medications they are taking, a family history of
hearing problems, results of previous hearing tests, and
any previous use of hearing aids. Based on the patient’s
answers to these questions and/or information from
other sources, additional questions may be appropri-
ate. With this information, you can begin to develop a
clinical impression of the patient and his or her prob-
lem, which will help guide you to the next steps.
Otoscopy
After completing a case history, it is important to visu-
ally inspect the ear canal and tympanic membrane
before attempting any audiologic assessment, espe-
cially ones that require placing an ear insert or ear
probe into the canal. This technique is called otoscopy
and requires you to place the speculum of the otoscope
into the patient’s ear canal. Figure 23–1 shows a photo
of a standard otoscope with its handle, neck, head, and
specula. The otoscope has a light source and magni-
fies the view down the ear canal. This ability to peer
into a patient’s ear canal can determine the status of
the outer and middle ear by assessing the color, shape,
and general appearance of the structures to see if they
are normal.
As shown in Figure 23–2, the clinician holds the
otoscope with a pencil grip and uses proper bracing
technique (i.e., other fingers are placed against the head)
to support the insertion of the specula into the patient’s
ear. The opposite hand is used to grip the auricle
(pinna), gently but firmly pulling up and back, which
will straighten out the canal and provide better visual-
ization. Using this bracing technique to hold the oto-
 23  Diseases of the Auditory System and Diagnostic Audiology
Head
Specula
Neck
Handle
Figure 23–1.  A standard otoscope used in visualizing
the ear canal and tympanic membrane. Disposable specula
are used to prevent the spread of germs from one patient
to another.
scope will avoid injury to the patient’s ear canal, as it
will move with the patient should he or she suddenly
move the head. As you insert the speculum (plural,
specula) into the ear canal, you can look through the
otoscope to view the tympanic membrane at the far end
of the canal (Figure 23–3). As you examine the ear canal
and tympanic membrane, not only are you looking for
excess cerumen (earwax) and foreign objects but also
for diseases and disorders of the outer and middle ear.
Immittance
Immittance audiometry describes the sound energy
that is transferred through the outer and middle ear
1
Immittance is the overall term that includes both admittance and impedance. Admittance is the amount of energy that moves through the
middle ear system while impedance is the reciprocal of admittance. In other words Admittance values (Y) and impedance values (Z) are
related, Y = 1/Z or Z = 1/Y. Audiologists commonly use admittance when measuring middle ear function (Kramer & Brown, 2019).
319
Figure 23–2.  When viewing the tympanic membrane
through a standard otoscope, it is important to use proper
bracing technique where one hand pulls up and back on
the auricle and the other holds the otoscope pencil-style
using the other fingers to brace the otoscope against the
patient. Courtesy of AudProf.com.
systems.1 If we apply a known sound (Chapter 21) to
the ear, the acoustic and mechanical properties of the
outer and middle ears (Chapter 22) provide opposition
to the energy flow, which is referred to as impedance.
A high impedance system (i.e. a middle ear that is filled
with fluid or an ear infection) will have a greater oppo-
sition to the flow of energy than a low impedance sys-
tem (i.e., a normal, healthy middle ear). The reciprocal
of impedance is called admittance, which is the measure
of how much of the applied energy flows through the
middle ear system, so that a high admittance system
(i.e., a normal, healthy middle ear) has a greater flow
of energy. These concepts can be applied to the evalu-
ation of the conductive part of the hearing mechanism
(Chapter 22) by making different types of measure-
ments including tympanometry and acoustic equiva-
lent volume of the ear canal.
Figure 23–4 shows the basic components of an
admittance instrument. To obtain a measure of admit-
tance, the probe must include an air pressure pump,
which allows the system to vary the pressure within
the ear canal. The system also has a speaker, which pro-
duces an 85 dB sound pressure level (SPL) pure tone
(usually at 226 Hz), called the probe tone. The tone is
320 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

presented to the ear through a probe assembly placed 226 Hz probe tone is not a valid measure, and a higher
at the entrance to the ear canal. A microphone, also a probe-tone frequency (1000 Hz) is recommended.
part of the probe assembly, is used to monitor the level
of the probe tone in the ear canal. For infants younger Tympanometry
than 6 months, conventional tympanometry with a
Tympanometry is one of the most commonly used tests
in the basic audiometric test battery. This test is used to
measure how the admittance changes as a function of
applied air pressure and how this function is affected
Pars by different conditions of the middle ear. The results of
flaccida this test are displayed on a graph (Figure 23–5) called
Incus of eardrum a tympanogram, where the admittance is on the y-axis
(mmhos, a unit of admittance), and the pressure range
is displayed on the x-axis (decaPascals or daPa, units
Stapes of pressure).
In conducting this test, the first step is to place
Malleus
(handle) the probe in the ear and obtain an airtight seal with an
appropriate-sized rubber probe tip. This allows the air
Umbo
pressure to be manipulated by the air pressure pump.
The canal is pressurized to +200 daPa, while the probe
Cone of tone is presented to the ear as shown in Figure 23–4.
light The pressurization of the ear canal forces the tympanic
Annulus membrane in the direction of the middle ear cavity
(positive pressure), reducing the tympanic membrane’s
ability to vibrate (low admittance). The admittance is
recorded at +200 daPa and plotted on the graph (see
Figure 23-5). The pressure is then swept continuously
Figure 23–3. The view of a normal tympanic mem- from +200 to −200, and the admittance is recorded
brane through an otoscope. along the way. In a normal ear, maximum admittance

Probe
Air pressure

Tone generator

Ear drum

Microphone

EAM

Figure 23–4.  The key components of an admittance instrument or tympanometer. The air pressure
pump is used to apply air pressure during tympanometry, the speaker sends the probe tone down the
ear canal toward the tympanic membrane, and the microphone measures the intensity of the tone as it
is reflected back from the tympanic membrane.
 23  Diseases of the Auditory System and Diagnostic Audiology 321

EAM Side Middle Ear Side

Negative
pressure (–)

Admittance
Positive
pressure (+)

– 0 +
Pressure in Ear Canal

Figure 23–5.  A tympanogram where the admittance is plotted across ear canal pressure.
Note the effect of pressure on the tympanic membrane, where the positive pressure is drawn in
red and the negative pressure in blue. Compare the position of the TM (on the left side) with the
movement of the TM on the tympanogram (on the right side). In this example, the TPP is 0 daPa.

is found at 0 daPa, where the air pressure is equal on
either side of the tympanic membrane allowing it to
vibrate most effectively (high admittance). As the
applied air pressure becomes negative, the admittance
again decreases because the tympanic membrane does
not vibrate as efficiently when the eardrum is pulled
out with negative pressure. The pressure at which
admittance is maximum corresponds to a specific
amount of pressure; this is referred to as the tympano-
metric peak pressure (TPP).
Acoustic Equivalent Volume of the Ear Canal
Ear canal volume is an important measure, as it will
provide information about the outer and middle ear.
The acoustic equivalent volume (Vea) is a measure of
the physical volume of the ear canal, as estimated from
the admittance obtained at +200 daPa. It can provide
diagnostic information about the condition of the tym-
panic membrane and/or ear canal. For a normal ear
canal and tympanic membrane, the admittance at +200
should be within the normal range of ear canal vol-
umes. If the tympanic membrane has a perforation or
pressure equalization (PE) tube inserted, then the Vea
will be larger than the normal range. This is because
the volume estimate includes not only the volume of
the ear canal but also the volume of the middle ear
(and potentially eustachian tube). If the Vea is smaller
than the expected normal range, it may be an indica-
tion that the external ear canal is obstructed. For either
of these abnormal Vea conditions, the tympanogram
will not show any changes in admittance as the applied
air pressure is varied and appears as a flat line.
Types of Tympanograms.  Tympanograms can be
categorized based on the five types described by Jerger
(1970). Although Jerger’s classification scheme is
widely used, it is a more useful approach to describe
the actual characteristics of the tympanogram such
as a “flat tympanogram” or a “normal-shaped tym-
panogram with the peak admittance occurring at
−150 daPa.” The description of a normal tympanogram
varies with a number of factors including age. The dif-
ferent types of tympanograms and their descriptions
are briefly described next.
An abnormal tympanogram is a good indication
of some middle ear involvement that affects the admit-
tance characteristics of the middle ear. However, the
tympanogram is not a predictor of the amount (if any)
of conductive hearing loss.
Normal admittance (Type A) tympanogram has a
characteristic peak shape with normal compliance and
322 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

the tympanic peak pressure within the normal range
(Figure 23–6). A normal Type A tympanogram occurs
in normal functioning middle ears, and this patient will
not have a conductive hearing loss.
Flat (Type B) tympanogram does not have the char-
acteristic peak shape (i.e. no TPP) seen for Type A, but
instead appears to be relatively flat across the pressure
Admittance
range (Figure 23–7B). A flat tympanogram occurs with
either an ear infection (fluid in the middle ear), a hole
(perforation) in the tympanic membrane (i.e.,larger
than normal Vea), impacted cerumen, or when the
probe is pushed against the ear canal wall (reduced
Vea). Patients with a flat tympanogram will most likely
have a conductive hearing loss.

-400 -200 0 +200

Pressure at which peak compliance occurs,
measured in decaPascals.

Figure 23–6.  Type A or normal admittance tympanogram.

Retracted eardrum No Mobility

(Type C Tympanogram) (Type B Tympanogram)
1.5 cm3 1.5 cm3
Admittance

Admittance

-400 -200 0 +200 -400 -200 0 +200

Pressure (daPa) Pressure (daPa)

A B

Figure 23–7.  A. Type C negative pressure tympanogram. B. Type B or flat tympanogram.

 23  Diseases of the Auditory System and Diagnostic Audiology
Negative pressure (Type C) tympanogram has a char-
acteristic peak with the same shape as a Type A; how-
ever, the TPP is shifted to a more negative pressure
(Figure 23–7A). A negative pressure tympanogram
indicates that the pressure in the middle ear space is
not equal to the atmospheric pressure. However, when
the TPP is outside the normal range and a negative
pressure tympanogram persists for an extended period
of time, then fluid can build up in the ear, at which
point it will change to flat (Type B). A patient with a
negative pressure tympanogram usually does not have
a conductive hearing loss.
Reduced admittance (Type As) tympanogram has a
characteristic peak shape with the TPP in the normal
range as for Type A; however, the admittance is lower
than the lower end of the normal range (Figure 23–8).
This type of tympanogram is sometimes referred to as
“shallow.” A reduced tympanogram suggests reduced
movement of the tympanic membrane. A patient with
a reduced tympanogram will have a conductive loss on
the audiogram.
High admittance (Type Ad) tympanograms have a
characteristic peak shape with the TPP in the normal
range as for Type A; however, the admittance is higher
than the upper end of the normal range (Figure 23–8).
A high admittance tympanogram suggests a highly
mobile tympanic membrane, which may be seen in
some cases of disarticulation of the ossicular chain or
cases of thinned tympanic membranes resulting from
previous middle ear infections. These high admittance
tympanograms (Type Ad) are suggestive of a disartic-
Admittance
-400 -200
Pressure (daPa)
Figure 23–8.  Type Ad or hypermobile tympanograms.
323
ulation (break) of the ossicular chain, and the patient
will usually have a conductive hearing loss.
Acoustic Reflex Threshold
In this section, we will discuss the contraction of the
stapedius muscles (Chapter 22) by the ear’s involun-
tary middle ear reflex in response to a loud sound. The
acoustic reflex threshold (ART) test, as it is known, uses
the same immittance instrument and is usually per-
formed immediately after obtaining a tympanogram.
This acoustic reflex is a bilateral response that occurs
when a loud tone is delivered to one ear resulting in
a contraction of the stapedius muscle due to firing of
the seventh cranial (facial) nerve in both ears. This con-
traction of the stapedius muscle changes the transmis-
sion efficiency of the sound energy as it travels through
the ossicular chain, decreasing the admittance of the
probe tone. Figure 23–9 provides a simplified diagram
of the acoustic reflex pathway, illustrating the main
ART pathways and key structures. The ART is defined
as the lowest intensity level (in 5 dB steps) of a reflex
eliciting tone that produces a repeatable acoustic reflex.
This test takes into account pathologies that occur in
the outer and middle ear as well as abnormalities of the
cochlea, eighth cranial nerve, lower brainstem, and/or
the seventh cranial nerve, as they can also influence the
ability to record an acoustic reflex.
The goal is to monitor any change in the admit-
tance of the probe tone that occurs when the stapedius
muscle contracts in response to a loud tone presented
Hyperflaccid
(Type Ad)
Normal Ear
(Type A)
Stiff Ear
(Type As)
0 +200
324 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

SOC & SOC &

VII Nucleus VII Nucleus VI
IN
e e
rv

rv
e
IN

e
VI
CN CN

ve

VI
II
er

Ne
II N

rv
VI

e
Inner ear Inner ear
Middle ear Middle ear
Right ear Right ear

Figure 23–9.  A simplified diagram of the acoustic reflex pathway showing the ipsilateral reflex arcs
for the right ear in red and for the left ear in blue.

to the ear. The probe tone is a hum-like sound (226 Hz)
that is constantly playing in the ear; the clinician then
presents a tone to elicit the reflex. If the acoustic reflex
is triggered, the stapedius muscle fires, and there is an
abrupt reduction in admittance of the probe tone. In
an individual with normal hearing, the ART should
fire between 75 and 95 decibels hearing level (dB HL)
(Wiley, Oviatt, & Block, 1987) as shown in Figure 23–10.
In this example, you can see that at the beginning, the
level of the reflex eliciting tone is below the stapedius
reflex threshold, and there is no measurable change in
admittance. As the reflex eliciting tone is increased in
intensity (level), it will eventually become loud enough
causing the stapedius to contract and the admittance
to decrease. As the intensity of the reflex eliciting tone
increases above the ART, there is a range in which the
stapedius contraction strengthens and the size (ampli-
tude) of the downward deflection of the acoustic reflex
increases with increasing dB HL.
Audiometric Testing
Audiometric testing has been the mainstay in the audi-
ologist’s armament of diagnostic tests since audiology’s
modern beginnings in the mid-1900s (Jerger, 2009). The
standard battery of audiometric testing includes both
pure-tone audiometry and speech audiometry. When

Higher
80 dB 85 dB 90 dB 95 dB 90 dB
Admittance
mitta

At TPP
.00
.01
.04 .03
Lower
.08

Figure 23–10.  An acoustic reflex measure illustrating different levels

of the reflex eliciting tone. The acoustic reflex threshold is defined as the
lowest level of the reflex eliciting tone that produces a downward deflection
(reduced admittance) ≥0.02 mL. In this example, the acoustic reflex threshold
is 90 dB HL. Reproduced with permission from Audiology: Science to practice
(3rd ed., p. 232) by S. Kramer and D. K. Brown, 2019, San Diego, CA: Plural
Publishing, Inc. Copyright 2019 by Plural Publishing, Inc.
 23  Diseases of the Auditory System and Diagnostic Audiology
assessing a cooperative patient for a hearing concern,
pure-tone audiometry is a part of the basic audiologic
assessment. It should be pointed out that audiologists
use a test battery approach, not counting on one single
test to determine a person’s ability to hear because the
auditory system is complex, and we have the ability
to assess many of its parts independently. Using the
cross-check principle2 along with the battery of tests,
we are able assess a person’s hearing to determine
type, degree, and configuration of the hearing loss with
confidence.
Pure-Tone Audiometry
Pure-tone audiometry is the heart of the standard test
battery and involves finding the lowest intensity across
the frequency range that a person is just able to hear.
The lowest intensity for a particular tone that a person
can reliably respond to at least 50% of the time is called
his or her threshold for that frequency. In pure-tone
audiometry, thresholds are obtained in a quiet envi-
ronment for a range of frequencies between 250 and
8000 Hz. This range is important because it contains the
frequencies that are most relevant for speech sounds.
The pattern of hearing loss according to the thresh-
old across the frequency spectrum is often characteris-
tic of certain types of hearing loss. For example, high
frequencies are more affected than low frequencies
for persons with hearing loss due to noise exposure.
Pure-tone thresholds can be used to describe why a
patient’s hearing loss might relate to their inability to
hear different speech sounds. Speech sounds such as
the consonants “f”, “s”, or “th” have higher-frequency
components than vowels “a” or “o”, which suggests
that the person with a high frequency hearing loss
will have more trouble hearing these consonants (and
others as well) compared with hearing the vowels.
This simple test of determining a person’s threshold
may be quite easy to accomplish with a cooperative
adult but may require considerable skill and expe-
rience to be able to recognize and adapt to different
patient response abilities and patterns when testing an
8-month-old child or an elderly patient with dementia.
It is the audiologist’s responsibility to incorporate and
integrate the pure-tone results with other test findings
and make appropriate interpretations, impressions, and
recommendations for management of the hearing loss.
Pure-tone audiometric thresholds are used by
audiologists to (a) describe the amount of the patient’s
2 
 he cross-check principle, first suggested by Dr. James Jerger (1976), is the checking of results of a single test by the results of another inde-
T
pendent test. With this principle, we can compare results from a number of tests to determine if the outcome is supported. For example, we
can compare the results of the pure-tone audiogram with the results of tympanometry.
3 
dB hearing level (HL) is a scale used on the audiogram where 0 dB HL at any frequency represents the lowest level for normal hearing.
325
hearing loss, (b) determine which parts of the auditory
system are involved, (c) determine if a medical referral
is needed, and (d) predict how the patient’s hearing loss
may relate to his or her ability to listen and communi-
cate. To be able to measure a pure-tone threshold, the
audiologist uses an instrument called an audiometer to
produce the variety of stimuli needed for the test. The
audiometer is used to create pure tones (Chapter 21)
from 125 to 8000 Hz (in octave or half-octave steps) at
a variety of intensities through a variety of transduc-
ers such as an earphone, an ear insert, a bone vibrator,
or speakers. It can also produce different noises such
as speech noise or narrow-band noise, which are used as
maskers to keep the nontest ear busy while determin-
ing the threshold for the test ear. Pure-tone audiom-
etry is first completed using earphones or ear inserts,
this means that the sound is transmitted down the
ear canal and through the middle ear. This pathway
is referred to as air conduction, as the initial sound is
traveling through air before it is converted to mechani-
cal energy by the tympanic membrane and passed
along to the cochlea. The other pathway is referred to
as bone conduction and requires the use of a bone oscil-
lator, which vibrates the skull in order to transmit the
sound directly to the cochlea, bypassing the outer and
middle ear. Differences in thresholds between air and
bone conduction results in an air-bone gap, and gaps
greater than 20 dB are considered to be a conductive
hearing loss (discussed later in this chapter).
The next step is to take the threshold and plot it on
an audiogram to record the results. However, we must
first understand the audiogram or graphical record
on which we record a patient’s thresholds. When try-
ing to understand how well a patient hears, we must
place these thresholds on the audiogram, according to
the frequency and intensity. The audiogram, as shown
in Figure 23–11, is a description of a person’s hearing
with frequency (in Hz) on the x-axis and their thresh-
old (in hearing level, dB HL)3 on the y-axis. The legend
or audiogram key indicates the various symbols that
can be used to describe the results. Once the thresh-
olds are plotted on the audiogram, we can calculate
the pure-tone average (PTA), which is simply the
average of the thresholds for 500, 1000, and 2000 Hz.
The degree or amount of loss is based on the person’s
threshold. Once you have determined the patient’s
threshold for a particular frequency, you will plot it
on the audiogram according to the frequency and
intensity of the stimulus.
326 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Frequency (Hz)
250
2 500 1000 2000 4000 8000
-10 Audiogram Right Left
0 Key Ear Ear
10 AC unmasked O X
Decibels Hearing Level (dB HL) 20 AC masked
<
BC unmasked <
30
BC masked [ ]
40 No response
50 Sound-field S
60
70
AC transducer:
80 Patient:
90
De

100
110
120

Figure 23–11.  An audiogram for plotting a person’s thresholds. The sym-

bols as shown in the legend are the key to comparing the air and bone conduc-
tion thresholds. Reproduced with permission from Audiology: Science to practice
(3rd ed., p. 130) by S. Kramer and D. K. Brown, 2019, San Diego, CA: Plural Pub-
lishing, Inc. Copyright 2019 by Plural Publishing, Inc.

Speech Audiometry completed using recorded speech so that there can be

Speech audiometry is a method used in the clinic to
evaluate how well a patient can hear and understand
specific types of speech stimuli. Speech tests provide
a formal way to determine the patient’s ability to rec-
ognize speech. Speech audiometry can also contribute
to the diagnosis of different hearing disorders. For
example, if a patient has a cochlear problem, he or she
can have a predictable relation between the shape of
the audiogram and his or her understanding of speech;
however, an eighth cranial nerve problem can result in
significantly poorer speech recognition than would be
suggested by the audiogram.
Results of speech tests are used to compare and
validate pure-tone thresholds (i.e., cross-check), com-
pare speech recognition ability between the two ears,
and/or monitor changes across time. Speech audiom-
etry can also help determine whether a patient is an
appropriate candidate for a hearing aid or cochlear
implant, or to compare a patient’s performance with
different amplification devices. Speech audiometry
includes two basic types of speech tests: (a) the estab-
lishment of a speech threshold and (b) a measure of
speech recognition ability performed at a level above
his or her threshold (suprathreshold). These tests are
consistency across visits and across clinics.
Speech Reception Threshold.  One of the goals of
speech audiometry is to determine a person’s speech
reception threshold and find the lowest intensity at
which that person can produce a response to speech
stimuli. Speech stimuli are generally more familiar
than pure tones. Speech reception thresholds are mea-
sured using the same dB HL scale as the pure-tone
thresholds. The degrees of hearing loss for speech can
be described by the same categories used for degree
of hearing loss for pure-tone audiometry. The SRT is
conducted using spondee words, which are two-syl-
lable compound words (i.e., baseball). The first step
when conducting an SRT is to familiarize the patient
with the list of words, and any words that are not cor-
rectly identified are omitted from the test (Tillman &
Jerger, 1959).
The SRT level is recorded on the audiogram, where
it is compared with the pure-tone average (PTA), this
is used as a cross-check with the pure-tone thresholds.
The speech threshold is usually equal to or slightly
better than the PTA, but it should be within 10 dB
HL of the PTA. If there is more than a 10 dB differ-
 23  Diseases of the Auditory System and Diagnostic Audiology
ence between the speech threshold and the PTA, then
a determination of why there is a difference should be
explored.
Word Recognition Score.  Speech audiometry also
includes an evaluation of how well a patient can rec-
ognize speech, at one or more levels above his or her
SRT or PTA. This test is performed using single-syllable
words, which are phonetically or phonemically bal-
anced lists of single-syllable words (consonant-vowel-
consonant), called PB (phonetically balanced) words. The
PB word lists were constructed to approximate the
frequency of occurrence for different speech sounds
or phonemes based on their occurrence in the English
language. For example, the sounds “t,” “n,” and “d”
occur in English more frequently than the sounds “k,”
“f,” and “z”; the phonetic composition of the PB words
reflects these differences.
One example of these lists is the set of NU-6 (pho-
nemically balanced) word lists developed by research-
ers at Northwestern University (Tillman & Carhart,
1966). These words are used to acquire a word recog-
nition score for a patient’s right and left ears in quiet.
The words are presented to the patient at a comfortable
listening level, approximately 30 or 40 dB above the
patient’s PTA.
The word recognition score (WRS) is obtained by
having the patient repeat back the words from the list.
The WRS is simply calculated as a ratio of the number
of words the patient was able to correctly repeat back
to the tester over the number of words given; the ratio
is expressed as a percentage correct. After calculating
the percentage score for both ears, they are recorded
on the audiogram. Additionally, the audiologist will
interpret the score based on the categories in Table 23–2
for use in describing the result in the report. WRS can
be used as an estimate of how a patient’s hearing loss
Table 23–2.  Categories Used to Describe Results From Word
Recognition Score (WRS) Testing
WRS (% Correct) Degree of Impairment
100–90 None
89–75 Slight
74–60 Moderate
59–50 Poor
<50 Very poor
Source:  Reproduced with permission from Audiology: Science to Practice (3rd ed.,
p. 168) by S. Kramer and D. K. Brown, 2019, San Diego, CA: Plural Publishing, Inc.
Copyright 2019 by Plural Publishing, Inc.
327
will affect his or her speech understanding at normal
conversational level. It can also be used for differential
diagnosis or to suggest the need for further evaluation
of an eighth cranial nerve disorder.
Speech in Noise. A primary complaint of many
people with hearing loss is that they have difficulty
understanding what is being said in the presence of
background noise (Beck et al., 2018). However, the
speech measures described earlier are usually pre-
sented in quiet. There are speech tests, however, that
are designed to assess how well a patient can recognize
speech in the presence of different levels of background
noise. These measures of speech recognition are more
representative of real-world listening situations. The
tests present speech materials for different levels of
noise, referred to as a speech-to-noise ratio (SNR) in the
same ear as the noise. For example, if the speech mate-
rial is presented at 50 dB HL and the noise is presented
in the same ear at 45 dB HL, this would be considered a
+5 SNR. There are a number of commonly used speech-
in-noise tests including the Speech Perception in Noise
(SPIN) test, the Quick Sentence in Noise (QuickSIN)
test, and the Bamford-Kowal-Bench Speech in Noise
(BKB-SIN). Each test has its own administration pro-
cedure and method of scoring. The results can then be
compared to the Speech in Quiet test results and the
pure-tone audiogram.
Physiological Responses
Otoacoustic Emissions
It is difficult to think that your ear produces a sound
when it hears a sound, but that is just what happens
with an otoacoustic emission. In 1978, Kemp first
Word Recognition Ability
Excellent/normal
Good
Fair
Poor
Very poor
328 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
described the phenomenon of the otoacoustic emis-
sion (OAE) after measuring low-intensity acoustic sig-
nals in the ear canal with a sensitive microphone. The
emissions originate in a normal functioning cochlea.
Specifically, the emissions have their origin in the move-
ment of the outer hair cells (OHCs) that enhance the
vibrations on the basilar membrane. These emissions
travel outward along the basilar membrane, through
the middle ear, and finally produce an OAE in the
ear canal. OAEs are soft signals that can only be
recorded with a very sensitive microphone placed in
the ear canal and coupled to a computer that uses sig-
nal averaging to enhance these low-level OAEs and re-
duce any unwanted background noise (Glattke &
Robinette, 2007; Lonsbury-Martin, Martin, & White-
head, 2007).
The inner ear uses an active mechanism delivered
through the OHC to generate the OAE. This process is
operational only at low intensity levels (≤65 dB SPL),
and a mild cochlear hearing loss due to a loss of OHC
function is sufficient to eliminate them. Therefore, the
presence of an OAE suggests normal cochlear function
in that ear. It also provides evidence of normal middle
ear function. OAEs have two main clinical purposes:
newborn hearing screening and diagnostically as a test
of cochlear function (Dhar & Hall, 2018).
OAEs are a very popular test not only because
they are easy to measure and can be performed quickly,
but also because they are objective and can be a pow-
erful source of information. The function of the OHCs
can be determined in just seconds by simply placing a
small probe in the ear canal. Audiologists include OAE
testing as part of the basic audiologic evaluation of all
patients but especially for young children (Blanken-
ship et al., 2018). One of the main reasons is that they
are easily administered and can provide an excellent
cross-check to verify audiometric information. Diag-
nostically, the presence of robust OAEs can provide
strong evidence of normal cochlear (OHC) function
(see Chapter 22). They can be used to determine if a
sensorineural hearing loss is due to a problem in the
cochlea or in the neural pathway. If the sensorineural
hearing loss identified with behavioral audiometry has
normal OAEs, this suggests that the cochlea is func-
tioning normally, and the problem lies in the eighth
cranial nerve or central auditory pathway. However,
it is important to remember that OAEs are not a test
of hearing (i.e., a patient’s degree of hearing loss) but
that they can only determine whether the OHCs are
functioning normally or not.
In the presence of normal middle ear function,
the absence of an OAE can mean that the OHC are
not functioning. However, a problem with the outer
or middle ear can interfere with both the inward and
outward transmission of the cochlear-generated OAEs
and cause a decrease in the emission. Think about “gar-
bage in–garbage out” — if the inward transmission of
the stimuli travels through an abnormal middle ear
system, it will reduce the sound energy that reaches the
cochlea. This will then effectively reduce any energy
created by the OHC, and the energy will be further
reduced as it transmits back out through the middle ear
resulting in an absent OAE (Hof, Anteunis, Chenault,
& van Dijk, 2005). Therefore, if OAEs are present, the
OHC are functioning, but if they are absent, there is
either a transmission problem (conductive loss) or
there is a cochlear problem (OHC), and further testing
is needed.
There are two main types of OAEs commonly used
in clinical settings: distortion product otoacoustic emis-
sions (DPOAE), and transient evoked otoacoustic emissions
(TEOAE). Fundamentally they are very similar; how-
ever, the main difference is the type of stimulus used to
evoke them. DPOAEs use two-tones (f1 and f2 where
f2 > f1) to produce an additional tone or harmonic in
the cochlea, and TEOAEs use a series of broad-band
clicks to stimulate most of the basilar membrane and
evoke the emission. For both types of OAEs, after the
stimuli are sent into the ear, the emission that it gen-
erates and the background noise measured in the ear
canal are displayed on a graph where a signal-to-noise
(SNR) comparsion can be made. An emission can only
be considered present if the SNR ratio is greater than
6 dB, otherwise the emission is absent. Failure to have
an OAE that is at least 6 dB above the noise for any of
the frequency regions would indicate that the OHCs
from those frequency regions are not functioning nor-
mally or are contaminated by a high noise level (Dhar
& Hall, 2018; Kimberley, Brown, & Allen, 1997). Results
from two patients are presented: one with a present
DPOAE at all frequencies in one ear and absent in the
other ear (Figure 23–12) and the other patient who
has a present TEOAE at all frequencies in one ear and
absent results in the other ear (Figure 23–13).
Auditory Brainstem Response
The Auditory Brainstem Response (ABR) is a neuro-
electric response to an auditory stimulus sent into
the ear. The stimulus is a broadband click that excites
the entire cochlea to send the neural activity along the
auditory (eighth cranial) nerve toward the brainstem.
This is a very quick phenomena and typically happens
within 10 ms after the initial stimulation. The electrical
activity is recorded through electrodes attached to the
scalp. This response is very small (<1 μV) in relation
 23  Diseases of the Auditory System and Diagnostic Audiology 329

B
Figure 23–12.  DPOAE responses. A. Results from an ear with nor-
mal hearing; amplitudes of the DPOAEs are larger (>6 dB) than the noise
floor across the frequency range. B. Results from an ear with hearing
loss; amplitudes of both the response and noise floor are low (<6 dB)
indicating no emissions from the cochlea. Courtesy of AudProf.com.

to other electrical activity in the brain, but it is possible
to remove the other activity and focus on this small
auditory response. By repeating the stimulus and
averaging the responses, we can decrease the random
background electrical activity and enhance the neural
response. To further enhance this small ABR signal
or reduce the background noise, the patient needs to
be very still or asleep (natural or sedated) in order to
detect the response from the background noise. Fortu-
nately, the ABR is unaffected by level of attention, sleep
state, or drugs, and can be reliably recorded across all
ages, including premature infants.
The ABR is characterized by a series of five posi-
tive peaks as shown in Figure 23–14. The first peak,
Wave I, is a reflection of the synchronous discharge
of neurons in the distal (more peripheral) portion of
the auditory portion of the eighth cranial nerve as it is
leaving the cochlea. Subsequent waves are generated
by the synchronous neural activity in the proximal part
of the eighth cranial nerve (Wave II), cochlear nucleus
330 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

20 20

10 10
dB SPL

dB SPL
0 0
TE TE
-10 NF -10 NF
-20 -20
0 1 2 3 4 5 6 0 1 2 3 4 5 6
Frequency (Hz) Frequency (Hz)

Figure 23–13.  TEOAE responses. Results from an ear with normal hearing on the left; amplitudes of the
TEOAEs are larger (>6 dB) than the noise floor across the frequency range. Results from an ear with hearing
loss on the right; amplitudes of both the response and noise floor are low (<6 dB) indicating no emissions
from the cochlea. Background noise is usually larger in the low frequencies. Courtesy of AudProf.com.

I-IV interwave latency

Absolute latency of wave V

IV V
III
0.20 µv

I
II

0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Latency (ms)

Figure 23–14.  A normal auditory brainstem response (ABR) waveform to a

click at a relatively high intensity level showing the waves (positive peaks) labeled
I–V. The latency (time) of each wave is called the absolute latency, which is relative
to the onset of the stimulus (at 0 ms). An example of absolute latency is shown for
wave V, which is usually the most prominent wave. The latency difference between
any two waves is called the interpeak latency difference. Reproduced with per-
mission from Audiology: Science to practice (3rd ed., p. 253) by S. Kramer and D. K.
Brown, 2019, San Diego, CA: Plural Publishing, Inc. Copyright 2019 by Plural Pub-
lishing, Inc.

(Wave III), superior olivary complex (Wave IV), lateral
lemniscus, and input to the inferior colliculus (Wave V)
(Møller, 1994). Although the generators for the differ-
ent ABR waves are found in the eighth cranial nerve
and brainstem, the response latencies and thresholds
are affected by peripheral (cochlear) hearing loss.
Neurodiagnostic ABR. Soon after the ABR was
developed in the 1970s, clinicians saw its utility in
identifying possible eighth cranial nerve pathologies.
The ABR was seen as a less costly and noninvasive
method when compared to a computed tomography
(CT) scan. Any patient who had an asymmetric senso-
 23  Diseases of the Auditory System and Diagnostic Audiology 331

rineural hearing loss (a hearing loss that is greater in
one ear that the other) was routinely referred for a neu-
rodiagnostic ABR. When using the ABR to evaluate the
eighth cranial nerve or brainstem function, measure-
ments are made at a relatively high stimulus level to
maximize the likelihood of measuring the absolute and
interpeak latencies for Waves I, III, and V as described
in Figure 23–14. Resulting waveforms for a patient
with an acoustic neuroma (tumor on the eighth cranial
nerve) may show a different pattern than one with nor-
mal hearing (compare Figures 23–14 and 23–15). Fig-
ure 23–15 shows the ABR from three different patients
illustrating the types of abnormal responses that can
occur with an eighth cranial nerve pathology.
Threshold ABR.  ABR can be used as a screening test
at a single preset intensity. Often a stimulus level of
30 or 35 dB nHL is used to determine a pass or fail.
Those who fail the ABR screening are referred for fol-
low-up evaluations that will include a threshold ABR
if the child is younger than 6 months. As with OAEs,
the ABR is not a test of hearing, and only inferences
can be made about any potential degree of hearing loss.
However, because ABR is a relatively quick, objective
measure of hearing sensitivity, especially in newborns,
young infants, or other difficult-to-test populations,
ABR for threshold estimates has far surpassed the neu-
rodiagnostic applications of ABR.
Currently, the greatest use of ABR is for determin-
ing thresholds in infants who did not pass their new-
born hearing screening. Similar to determining hearing
thresholds in an adult, we can estimate a child’s hear-
ing by determining the lowest level where a repeatable
Wave V response can be obtained at a number of fre-
quencies. Figure 23–16 shows characteristic changes in
the ABR waveform, specifically Wave V, for different
frequencies presented at relatively low intensity lev-
els within the range of normal hearing for neonates.
Frequency-specific ABRs can be obtained down to lev-
els of 10 to 20 dB for the frequencies 500, 1000, 2000,
and 4000 Hz (Elsayed, Hunter, Keefe, Feeney, Brown,
Meinzen-Derr, Baroch, Sullivan-Mahoney, Francis,
& Schaid, 2015). Since this technique is not the same
as determining thresholds through audiometry, there
is an additional step. Once you have determined the
lowest level at which Wave V can be identified, then

Figure 23–15.  Three different auditory brainstem response (ABR) waveforms

illustrating different abnormal recordings associated with eighth nerve disorders.
In the top waveform, the tumor only affects the proximal (more central) part of the
eighth cranial nerve, the ABR on the affected side may show a normal Wave I and
abnormalities in the later waves. In the middle waveform, the results for a patient
with an eighth cranial nerve pathology show abnormal interpeak latency inter-
vals (I–III and/or I–V) that are delayed from normal interpeak latency intervals.
The bottom waveform shows the results from a patient with no discernible waves.
Reproduced with permission from Audiology: Science to practice (3rd ed., p. 256)
by S. Kramer and D. K. Brown, 2019, San Diego, CA: Plural Publishing, Inc. Copyright
2019 by Plural Publishing, Inc.
332 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

V
4000 Hz
30 dB
V

10 dB
V
2000 Hz
30 dB
V
10 dB

1000 Hz V
30 dB
V
20 dB

500 Hz V 0.0.1 V
30 dB
V
20 dB

0 2 4 6 8 10 12 14 16 18 20 22 24
Latency (ms)

Figure 23–16.  Results from a threshold ABR on a newborn, the tone-

burst ABR waveforms are recorded near threshold (“threshold ABR”).
Results show wave V at each frequency from 500 to 4000 Hz at 30 dB and
at either 10 or 20 dB nHL, which are considered normal thresholds for
this neonate, indicating that they have normal auditory function at least
through the brainstem (and most likely has normal hearing). Reproduced
with permission from Audiology: Science to practice (3rd ed., p. 257) by S.
Kramer and D. K. Brown, 2019, San Diego, CA: Plural Publishing, Inc. Copy-
right 2019 by Plural Publishing, Inc.

specific correction values need to be added for each fre-
quency (Small & Stapells, 2017). These new estimated
thresholds can then be compared to behavioral thresh-
olds for determination of hearing loss and fitting of
amplification if needed.
Vestibular Assessment
A component of an audiologist’s scope of practice is
to deal with the identification and rehabilitation of the
vestibular or balance system. Anatomically, the ves-
tibular system is a part of the inner ear and is impor-
tant for maintaining one’s balance (see Chapter 22).
The integration of neural activity from the vestibular,
visual, somatosensory, and cerebellar systems allows
you to maintain an upright posture, perform coordi-
nated complex movements, and maintain a visual tar-
get while moving (Semaan, Wick & Megerian, 2015).
A problem with one or more of these systems results
in a patient feeling dizzy (i.e., unsteady, lightheaded),
and/or a spinning sensation, called vertigo. Vertigo is a
symptom of a peripheral vestibular disorder, whereas
other dizziness or balance problems may be related
to central nervous system involvement, other medi-
cal conditions, and/or psychological factors. It is esti-
mated that 35% of adults (Agrawal, Ward, & Minor,
2013) and 5.3% of children (Li, Hoffman, Ward, Cohen,
& Rine, 2016) in the United States have some dizziness
and/or balance problems.
Audiologists are involved in both screening and/
or diagnostic assessment and management of vestibu-
lar problems. As with hearing assessments, audiolo-
gists utilize a test battery approach to assess a patient’s
vestibular system. There are two main vestibular
pathways: the vestibulo-ocular reflex (VOR) and the
 23  Diseases of the Auditory System and Diagnostic Audiology 333

vestibulospinal reflex (VSR). In the VOR, the system oscillations at different frequencies like an amusement
connects the vestibular neural pathway in the brain- ride. As shown in Figure 23–18, the patient is seated in
stem to neurons that reflexively control the muscles of the chair, which spins him or her around at different
the eyes to automatically maintain a clear visual image
during head movement (Wright & Schwade, 2000).
The VSR has direct connections from the vestibular
nuclei in the brainstem to motor neurons that will
reflexively control the relevant skeletal muscles, which
is important in controlling the body when unexpected
changes in position occur relative to gravity. Tests have
been developed to assess the various components of
the balance system, the most common of which are
described next.
There are four main tests that the audiologist
uses to assess a patient’s vestibular system. They
include videonystagmography (VNG), rotary chair
testing, posturography, and vestibular-evoked myo-
genic potentials (VEMPs). VNG is a balance test that
uses an infrared video system with cameras built into
goggles that track eye movements in response to vari-
ous subtests. The VNG objectively evaluates a person’s
nystagmus (i.e., rapid eye movement), watching and Figure 23–17.  Conducting videonystagmography as-
measuring their eye movement as illustrated in Fig- sessment utilizing goggles with a small infrared camera
ure 23–17. Rotary chair testing uses a motorized chair built in to the lenses to track the person’s eye movements.
in a darkened room; the chair revolves in calibrated Courtesy of AudProf.com.

Figure 23–18.  A rotary chair system used to determine if the vestibu-

lar or the neurological system is involved in the balance disorder. Image
courtesy of Interacoustics A/S © 2019.
334 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

speeds and with rapid accelerations and decelerations
while measuring eye movements with the same type of
goggles as in VNG. The results of these tests are com-
pared to individuals with a normal functioning system
to evaluate differences in eye movement (VOR) gain,
phase, and symmetry.
Posturography assesses a patient’s functional bal-
ance while changing vestibular, visual, and somato-
sensory inputs. As shown in Figure 23–19, the patient
stands on a platform and tries to stay stable while the
platform is moving. During the test, the patient’s pos-
tural stability/control and ability to correct for any
change is monitored and evaluated. Finally, there are
VEMPs, which measure myogenic (muscle) poten-
tials elicited by a high-intensity low-frequency tone
recorded from around the area of the neck (cervical)
or ocular muscles (Figure 23–20). Similar to ABR, the
electrical activity is recorded and averaged to reveal
a waveform with a negative and positive peak. The
VEMP waveforms from the right and left sides are com-
pared to assess a patient’s vestibulocollic reflex (VCR)
and vestibuloocular reflex (VOR) (Jacobson et al., 2011).
Together these tests provide a wealth of information to
assess a patient’s balance system and create a plan for
treatment or rehabilitation.
Audiometric Results
Audiologic test results provide the clinician with infor-
mation about a patient’s hearing acuity and sense of
balance. This information will help provide a differ-
ential diagnosis of any pathologies in either hearing
or balance. Determining if there is a hearing loss and,
if so, whether it is conductive, mixed, sensorineural,
unilateral, or bilateral will all assist this quest. In addi-
tion to the audiogram, information from speech tests,
immittance tests, otoacoustic emissions, auditory-
evoked potentials, and/or vestibular testing may also
be useful in reaching a proper diagnosis and course
of treatment. For example, audiologic test results may
help localize the disorder to a possible perforation of

Figure 23–19.  A computerized dynamic posturography system with

an immersive virtual environment for testing a person’s balance. Image
courtesy of Bertec Corporation © 2019.
 23  Diseases of the Auditory System and Diagnostic Audiology
Figure 23–20.  Electrode placement used to record a
VEMP on a patient with an electrode placed on the fore-
head and on the sternocleidomastoid muscle in the neck.
Courtesy of AudProf.com.
the tympanic membrane or suggest that there may be
pathology of the eighth cranial nerve. It is important
to keep in mind that a medical diagnosis can only be
determined by a physician, who conducts a thorough
medical examination and may order lab work, imaging
studies, or other diagnostic tests. All medically related
auditory disorders must be referred by hearing health
care professionals to a physician for evaluation and
ongoing care. In cases where an adult has a sensori-
neural hearing loss, with no apparent medical or neural
involvement, the audiologist may provide appropriate
services without the need for medical evaluation; how-
ever, any hearing loss in a child should be referred to a
physician for evaluation.
Type, Degree, and
Configuration of Loss
Since we know that there are a significant number of
people in the country with a hearing loss and each
335
individual’s hearing loss will be different, how can we
describe each individual’s loss? The easiest method is
to describe their hearing loss based on their pure-tone
audiometric thresholds. Specifically, we need to iden-
tify the type of hearing loss, the degree (or amount) of
hearing loss, and the configuration (or shape) of the
loss. After you have determined a patient’s thresholds
and placed them on the audiogram, you can establish
their type of hearing loss. To describe the type of hear-
ing loss from the audiogram means you need to deter-
mine whether the hearing loss involves the conductive
and/or sensorineural portions of the auditory path-
ways. The conductive portion of the auditory system
refers to the outer and middle ear, and the sensorineu-
ral portion of the auditory system refers to the cochlea,
eighth cranial nerve, and central pathways. The degree
of loss refers to the amount of hearing loss that a per-
son has. Table 23–3 examines the categories used to
describe the degree of a person’s hearing loss. The
configuration of a person’s hearing loss refers to the
shape of the audiogram, showing how the thresholds
compare across the frequency range. For example, a
hearing loss where the thresholds are consistent across
the frequency range would be described as flat. If the
thresholds are better in the low frequencies and gradu-
ally become poorer, we would call that a sloping hear-
ing loss; if it was flat across the frequency range except
for a decrease in hearing at a particular frequency
(usually 4000 Hz), we would call that a notch. Ears that
have a bilateral hearing loss are said to have a loss in
both ears, and a unilateral loss is a loss in only one ear.
Normal Hearing
If a patient has air conduction thresholds across the fre-
quency range at 20 dB HL or less, he or she is said to
Table 23–3.  Categories Used When Describing the
Degree of Loss in Adults
dB HL Range Descriptive Category
−10 to 20 dB HL Normal
21 to 40 dB HL Mild
41 to 55 dB HL Moderate
56 to 70 dB HL Moderately severe
71 to 90 dB HL Severe
91+ dB HL Profound
Source:  Adapted with permission from Audiology: Science to Prac-
tice (3rd ed., p. 139) by S. Kramer and D. K. Brown, 2019, San Diego,
CA: Plural Publishing, Inc. Copyright 2019 by Plural Publishing, Inc.
336 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Frequency (Hz) Frequency (Hz)

250
2 500 1000 2000 4000 8000 250
2 500 1000 2000 4000 8000
-10 < < -10
<
0 <O <O X <O <<O
X O O
X 0 [ ] [ ] [ ] [ ]
X <O
< <
X X <O X X [ ] [ ]
10 10
Decibels Hearing Level (dB HL)

Decibels Hearing Level (dB HL)

20 20
30 30
O
X O O X O
X O
40 40 X X X O O
X X
O
50 50
60 60
70 70
80 80
90 90

De
100 100
110 110
120 120

Figure 23–21. A normal audiogram. Note that the
unmasked air and bone scores are less than 20 dB HL at all
frequencies for both the right and left ears.
Figure 23–22.  Conductive hearing loss for a patient’s
right and left ears as noted by the air-bone gap. This is
an example of a patient with a conductive loss from otitis
media with effusion as discussed in Chapter 19 for children
with craniofacial abnormalities.

have normal hearing as shown in Figure 23–21. How-
ever, normal is not always normal, and since there are
a significant number of components that make up the
auditory system, it is possible that there can be some
issues that do not affect thresholds but cause hearing
difficulties. It is estimated that 26 million American
adults have hearing within normal limits but report
difficulty hearing and/or have problems with hearing
speech in noise (Beck et al., 2018).
Conductive Hearing Loss
The conductive portion of the system is in the outer
and middle ear. A hearing problem in the conductive
parts of the ear would show an air-bone gap, that is,
normal hearing by bone conduction and poorer hear-
ing by air conduction. An example of an audiogram
from a patient with a conductive hearing loss from oti-
tis media with effusion can be seen in Figure 23–22,
which shows that the patient has abnormal air conduc-
tion thresholds but normal bone conduction thresh-
old with an air-bone gap of approximately 30 dB. The
air-bone gap (or difference between the air conduction
threshold and bone conduction threshold) is consid-
ered significant if it is greater than 10 dB.
Sensorineural Hearing Loss
A hearing problem in the sensorineural portions of the
auditory pathway (see Chapter 22) would have essen-
tially the same hearing loss when tested by air conduc-
tion as when tested by bone conduction. An example
of a patient with a sensorineural hearing loss can be
seen in Figure 23–23. This type of hearing loss indicates
that there is a disorder of the cochlea or neural disorder
(eighth cranial nerve or central pathway).
Mixed Hearing Loss
A hearing loss that occurs in both the sensorineural
and conductive parts of the auditory system (see Chap-
ter 22) is called a mixed hearing loss. In this type of
loss, you would have a hearing loss by air conduction
and by bone conduction; however, there would also be
an abnormal air-bone gap of greater than 10 dB. An
example of an audiogram from a patient with a mixed
hearing loss can be seen in Figure 23–24.
 23  Diseases of the Auditory System and Diagnostic Audiology 337

Frequency (Hz) Frequency (Hz)

250
2 500 1000 2000 4000 8000 250
2 500 1000 2000 4000 8000
-10 -10
0 0
10 10
Decibels Hearing Level (dB HL)

Decibels Hearing Level (dB HL)

20 20
30 30 [ ] [ ]
[ ] [ ] [ ] [ ]
40 < 40
<O < <O < X
<O <O
< <
50 X X X < X O
X O 50 O
X O O X O
X O
<O
X <O X X X X O O
X X
60 60 O
70 70
80 80
90 90
De

Dec
100 100

D
110 110
120 120

Figure 23–23.  Sensorineural hearing loss. Note the Figure 23–24.  Mixed hearing loss. Note that the air
moderate degree of loss and that there is no difference conduction scores are poorer than the bone conduction
between the air conduction and bone conduction thresh- thresholds but that they both show a hearing loss.
olds (no air-bone gap).

Hearing and Balance Disorders Case 1

Now that we have gone through all of the steps in Test Results
assessing a patient’s hearing and balance system from
the case history, otoscopy, pure-tone audiometry, Case history A 6-year-old female came to your
speech audiometry, immittance, otoacoustic emis- clinic because she did not pass
sions, auditory brainstem response, and vestibular her hearing screening at school.
assessment, we can turn our thoughts to putting it Her parents reported no history of
together and determining the disorder. The first part hearing problems in the family, and
is to determine the location of the problem; remember they felt that she had no hearing
that this plays a large part in the type of hearing loss, concerns.
since conductive losses occur in the outer and middle Otoscopy Ear canals appeared normal
ear and sensorineural losses occur in the cochlea or bilaterally
eighth nerve. Table 23–4 lists a number of disorders
and describes their condition and location. Audiometric Using Figure 23–25, calculate
results the PTA, determine the type and
degree of loss, and confirm using
Patient Examples the cross-check principle.

The following are a few examples of patient outcomes.
Try and work your way through them from the case
history to the audiometric results. Identify the tests and
their results and see how they all fit together (cross-
check principle), then compare your outcome to the
outcomes at the end of the case.
Outcome:  Pure-tone thresholds indicate hearing within
normal limits for both the right and left ears. Speech
reception thresholds are in good agreement with pure-
tone averages. Word recognition scores are excellent
for both the right and left ears. Tympanometry results
showed normal middle ear function bilaterally. Acoustic
 Table 23–4.  Hearing and Vestibular Disorders for Different Locations

Location Disorders Condition

Outer ear Atresia Congenital absence of an external auditory canal,
conductive hearing loss
Exostosis Bony outgrowths in the external auditory canal caused by
repetitive irritation from cold water, normal hearing
Impacted cerumen Abnormal buildup of earwax (cerumen) that completely
blocks off the ear canal, conductive hearing loss
Stenosis Abnormal narrowing of the external auditory canal, normal
hearing

Middle ear Disarticulation Separation of the ossicular chain or break in one of the
ossicles, conductive hearing loss
Otitis media Inflammation or accumulation of fluid in the middle ear, can
- acute be fluid free of bacteria or infected with bacteria, conductive
- effusion hearing loss
- chronic
Otosclerosis Caused by outgrowth of bony wall (otospongiosis)
around the stapes footplate; commonly causes middle ear
conductive hearing loss when stapes is immobilized; less
commonly, toxins may invade the cochlea and cause a
sensorineural hearing loss
Perforation Hole in the tympanic membrane, depending on size and
location may cause conductive hearing loss

Inner ear Ototoxicity Sensorineural hearing loss due to poisonous side effects
from some therapeutic drugs or environmental toxins
Meningitis Inflammation of the meninges (membranous sheets covering
the brain), may cause sensorineural hearing loss
Noise-induced hearing loss Sensorineural hearing loss resulting from excessive
exposure to loud sounds
Presbycusis Sensorineural hearing loss related to aging

Neural Acoustic neuroma Benign tumor involving the eighth cranial nerve,
disorders sensorineural hearing loss
Auditory neuropathy Congenital hearing disorder in which the eighth nerve
spectrum disorder (ANSD) neurons do not fire with normal synchrony; characterized by
the absence of ABR and the presence of normal OAE, normal
hearing to sensorineural hearing loss

Vestibular Benign paroxysmal Caused when some calcium carbonate crystals of the
positional vertigo (BPPV) otoconia within the macula of a utricle become dislodged
and fall into one or more of the semicircular canals; most
commonly found in the elderly, no hearing loss
Labyrinthitis Infection (viral) of the inner ear labyrinth and/or vestibular
nerve that may cause temporary disruption of vestibular
function producing dizziness/vertigo, balance problems,
nausea, and/or hearing and vision problems
Superior canal dehiscence A small opening in the bony labyrinth of the superior
semicircular canal that acts as a third window of the inner
ear that allows the membranous portion of the superior
semicircular canal to be displaced during sound or
increased pressure, vestibular disorder
Vestibular schwannoma Benign tumor involving the vestibular portion of the eighth
cranial nerve; vestibular disorder

338
 23  Diseases of the Auditory System and Diagnostic Audiology 339

Frequency (Hz)
250
2 500 1000 2000 4000 8000
-10 <
<O
<
0 <O < O <O
<
X< X X O
X
X
X
< <O Speech Audiometry
10
Decibels Hearing Level (dB HL)
Ear PTA SRT WRS dBHL
20 Right 5 100% 50 dBHL
Left 5 100% 50 dBHL
30
40 Ipsilateral Acoustic Reflex Thresholds
Ear 500 Hz 1000 Hz 2000 Hz
50 Right 85 dB 85 dB 85 dB
60 Left 85 dB 85 dB 85 dB

70
80
90
De

100
110
120

Figure 23–25.  Audiometric results for Case 1.

reflex thresholds were present for both the right and left ears. Tympanometry results showed normal mid-
left ears. As expected, all tests suggest that this young dle ear function in the left ear but abnormal middle
girl has hearing within normal limits bilaterally. ear function in the right ear. Acoustic reflex thresholds
were present in the left ear but absent in the right ear.
As expected, all tests suggest that this boy has hearing
Case 2
within normal limits in the left ear and a mild conduc-
tive loss in the right ear.
Test Results
Case history An 8-year-old male was brought
to your clinic complaining about Case 3
a sore ear and that he was having
a hard time hearing his teacher in Test Results
school. His parents reported that
Case history A 59-year-old male came to your
prior to 2 weeks ago, he had not
clinic complaining about not
had any problems hearing.
hearing as well as he used to and
Otoscopy Right ear was red and inflamed; left that his children complain that the
ear canal appeared normal TV is too loud at his house. He
reported that he was in the artillery
Audiometric Using Figure 23–26, calculate during the war and that he worked
results the PTA, determine the type and in a factory most of his adult life.
degree of loss, and confirm using
the cross-check principle. Otoscopy Ear canals appeared normal
bilaterally
Outcome: Pure-tone thresholds indicate hearing
Audiometric Using Figure 23–27, calculate
within normal limits for the left ear and a mild conduc-
results the PTA, determine the type and
tive loss in the right ear. Speech reception thresholds
degree of loss, and confirm using
are in good agreement with pure-tone averages. Word
the cross-check principle.
recognition scores are excellent for both the right and
340 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Frequency (Hz)
250
2 500 1000 2000 4000 8000
-10 <
0< [
<

X
<
[X [ < [X <
Speech Audiometry
10 X X X
Decibels Hearing Level (dB HL)
Ear PTA SRT WRS dBHL
20 Right 45 100% 80 dBHL
Left 10 100% 50 dBHL
30
O
40 O O Ipsilateral Acoustic Reflex Thresholds
O O Ear 500 Hz 1000 Hz 2000 Hz
50 O Right NR NR NR
60 Left 85 dB 80 dB 90 dB

70
80
90
De

100
110
120

Figure 23­–26.  Audiometric results for Case 2.

Frequency (Hz)
250
2 500 1000 2000 4000 8000
-10
0
< Speech Audiometry
10 <O
X
Decibels Hearing Level (dB HL)

Ear PTA SRT WRS dBHL

O
X
<O
<
20 X Right 20 72% 80 dBHL
< Left 20 76% 80 dBHL
30 <O
X
<
40 <O
X Ipsilateral Acoustic Reflex Thresholds
Ear 500 Hz 1000 Hz 2000 Hz
50 Right 95 dB 100 dB NR
60 O
X Left 95 dB 100 dB NR

70
80
90
De

100
110
120

Figure 23–27.  Audiometric results for Case 3.

Outcome:  Pure-tone thresholds indicate hearing within with pure-tone averages. Word recognition scores are
normal limits to 1000 Hz sloping to a moderately good for both the right and left ears. Otoscopic results
severe sensorineural hearing loss at 8000 Hz bilaterally. were unremarkable bilaterally. Tympanometry results
Speech reception thresholds are in good agreement showed normal middle ear function bilaterally. Acous-
 23  Diseases of the Auditory System and Diagnostic Audiology
tic reflex thresholds were present ipsilaterally for 500
and 1000 Hz but absent at 2000 Hz in both ears. These
test results suggest that this gentleman has a high-fre-
quency sensorineural hearing loss bilaterally.
Chapter Summary
Assessment of an individual’s hearing includes the
administration and interpretation of behavioral, psy-
choacoustic, and electrophysiologic measures of the
peripheral and central auditory systems.
Assessment of an individual’s vestibular sys-
tem includes the administration and interpretation of
behavioral and electrophysiologic tests of equilibrium.
Use of a case history allows the clinician to collect
information about a patient’s primary complaints and
medical history to help develop a clinical impression
about the patient’s problem.
Prior to inserting anything into the ear, the clinician
needs to visually inspect the ear canal using otoscopy.
Immittance audiometry assesses the function of
the middle ear through a battery of tests. Tympanom-
etry measures how the admittance changes as a func-
tion of applied air pressure and how that is affected
by different conditions of the middle ear. Jerger types
(A, B, C, As, Ad) are used to describe the results of the
tympanometry measurement.
The acoustic equivalent volume (Vea) test allows
for an estimation of the ear canal volume to determine
if it is larger or smaller than normal.
Acoustic reflex thresholds measure the lowest-
intensity tone that can elicit a reflex where the stape-
dius muscle is contracted to reduce the vibration of
the stapes.
Pure-tone audiometry allows for development of
an audiogram, which shows air and bone conduction
thresholds for both ears. Pure-tone audiometric thresh-
olds are used by audiologists to describe a patient’s
hearing loss, determine the parts of the auditory sys-
tem that are involved, and predict how the patient’s
hearing loss may relate to his or her ability to listen and
communicate.
Speech audiometry evaluates how well a patient
can hear and understand speech by formalizing a way
to determine the patient’s ability to recognize speech.
One test called the speech reception threshold (SRT) is
used as a cross-check principle with the patient’s pure-
tone average. Word recognition score testing evaluates
how well a patient can recognize speech at a supra-
threshold level. These tests are performed in quiet, but
there are some tests (i.e., BKB-SIN test) that can assess
their ability in the presence of background noise.
341
Otoacoustic emissions assess the function of the
cochlea by measuring sounds produced by the outer
hair cells.
The evoked electroencephalography (EEG) is used
to generate the auditory brainstem response (ABR)
and measure the neurodiagnostic ABR response. This
technique is used to measure the neural activity in
the auditory nerve and brainstem. The ABR test can
also be used to estimate thresholds, especially in very
young children.
Not only do audiologists assess a person’s hearing,
but they are also involved in evaluating their balance
system. This can be accomplished using videonystag-
mography (VNG), rotary chair testing, posturography,
and vestibular-evoked myogenic potential (VEMP).
Each of these tests assesses a different part of the ves-
tibular system.
The results of all of these evaluations can assist
the audiologist in determining the type, degree, and
configuration of hearing loss such as conductive, sen-
sorineural, or mixed hearing loss and provide differ-
ential diagnosis of the patient’s hearing and balance
problems.
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Mueller, H. G., Ricketts, T. A., & Bentler, R. (2014). Modern
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spondee threshold in normal hearing subjects. Journal of
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immittance measures in normal ears. Journal of Speech and
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Assistive Listening Devices
Introduction
This chapter presents an overview of the different types
of listening devices available to maximize an individ-
ual’s residual hearing for daily functioning. Students
interested in detailed information about hearing aids
and other implantable devices are encouraged to con-
sult the outstanding text by Ricketts, Bentler, and Muel-
ler (2019). In the current chapter, we review three kinds
of listening devices: hearing aids, cochlear implants,
and hearing assistive technology systems.
As we indicated in the previous chapter, there are
approximately 37.5 million adults in the United States
with hearing loss. It is estimated that just under 30 mil-
lion people could be helped with hearing aids but only
about a third will have a need for them (National Insti-
tute on Deafness and Other Communication Disorders
[NIDCD], 2016). The audiologist is responsible for eval-
uating, fitting, and verifying these individuals’ ampli-
fication or assistive listening devices. The audiologist
also determines whether the device is appropriate for
their hearing problem and evaluates any benefit they
might receive from the device. The audiologist is also
a member of the auditory implant team (i.e., cochlear
implants, middle ear implantable hearing aids, fully
implantable hearing aids, bone-anchored hearing aids,
and all other amplification devices) who determines
audiologic candidacy based on hearing and communi-
cation information. The audiologist provides pre- and
postsurgical assessment, counseling, and all aspects
24
of audiologic treatment, including auditory training,
rehabilitation, implant programming, and maintenance
of the devices.
Hearing Aids
Steps in Selecting and
Fitting a Hearing Aid
The key component in the treatment and rehabilitative
process for a patient with a hearing loss is the providing
of amplification or the fitting of a hearing aid. Unlike
providing the patient with glasses, it is not simply the
provision of the device that allows the patient to have
better communication. The audiologist has an impor-
tant role in the comprehensive selection and fitting pro-
cedure, coupled with appropriate counseling before,
during, and after the fitting of hearing aids. Patients
will also require various types of auditory and acclima-
tization training in order for them to achieve maximal
benefit. To make this happen, there is a general work-
flow to the treatment process that the audiologist will
follow to assist the patient in making maximal gains
in his or her rehabilitation. In this six-step procedure
(Table 24–1) for the fitting of a hearing aid, the audi-
ologist will guide the patient through the assessment,
treatment planning, selection, verification, orientation,
and validation for selecting and fitting a hearing aid
(Mueller & Hall, 1998).
343
344 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Table 24–1.  Typical Workflow for the Selection and Fitting of Hearing Aids

• Step 1.  Assessment:  Determine the extent and cause of hearing loss. Determine candidacy for
hearing aids based on pure-tone hearing loss, self-assessment inventories, and patient history.

• Step 2.  Treatment Planning:  Review the assessment results with the patient and/or family
members. Identify areas of difficulty and explore different amplification options.

• Step 3.  Selection:  Determine the type of fitting (style, etc.). Decide on electroacoustic
parameters and what special features are needed.

• Step 4.  Verification:  Determine that the hearing aids meet a set of standardized measures,
including electroacoustic performance and patient’s real-ear match to desired levels
(presumably based on validated prescriptive targets). The hearing aids also should have good
sound quality, be comfortable to wear, and have acceptable cosmetics.

• Step 5.  Orientation:  Counsel the patient on the use and care of the hearing aids. Discuss
hearing aid adjustments and realistic expectations. Determine the need for a more
comprehensive audiologic rehabilitation program.

• Step 6.  Validation:  Assess the effectiveness of the use of hearing aids in the patient’s everyday
environment, through the use of patient interview and/or formal self-assessment inventories of
benefit and satisfaction. Readdressf areas of need regarding the fitting.

Source:   Reproduced with permission from Audiologists’ Desk Reference by H. G. Mueller and J. W. Hall, 1998, San
Diego, CA: Singular.

The first step is to assess the patient’s hearing to
determine the type, degree, and configuration of loss as
we discussed in the previous chapter. Using the pure-
tone audiogram, speech audiometry, tympanometry,
and other tests as needed, we can determine patients’
hearing loss and how it is affecting their communica-
tion ability. Patients must also believe that their hearing
loss is causing a problem and that they are motivated
and have the appropriate expectations for hearing aid
use. Once this is complete and the patient is determined
to be an appropriate candidate, the audiologist needs to
develop a treatment plan. In this plan, we will review
the results with the patient, identify any areas in which
the patient is having difficulty such as in noisy restau-
rants, on the phone, or at work and explore the differ-
ent amplification options available to him or her.
The third step is the selection of the hearing aid
style, the electroacoustic parameters for the hearing aid
based on the patient’s hearing loss, and the ear or ears
to be fit. In the United States, approximately 80% of
patients are fit with two hearing aids; however, many
will become unilateral hearing aid users (Mueller, Rick-
etts, & Bentler, 2014). Working with the patient, the
audiologist determines the style of hearing aid and the
features required. In addition to the standard features,
some instruments will have optional features such as
digital noise reduction, wireless Bluetooth connectivity,
or directional microphones that the patient may desire.
The hearing aid settings or electroacoustic parame-
ters are programmed into the digital hearing aid circuit
through an interface with a computer. The audiologist
uses a computer program or validated prescriptive fit-
ting method (Mueller, Ricketts, & Bentler, 2017) to set
the hearing aid to the desired gain and output targets
based on the patient’s hearing loss. There are two fit-
ting methods that are commonly used, the National
Acoustic Laboratories’ (NAL) NonLinear method v.2
(NAL-NL2) and the Desired Sensation Level method
v.5 (DSLv5.0). Most audiologists use the NAL method
with adults and the DSL method with children. The
goal of these fitting methods is to determine the
optimal frequency-specific gain and output for soft,
average, and loud speech inputs and to calculate the
maximum power output so that the hearing aid cannot
exceed the patient’s loudness discomfort level.
Once the hearing aid selection has been made,
the audiologist’s focus can turn toward verification of
the hearing aids, which is the fourth step. Verification
is the determination by the audiologist that the hear-
ing aids are comfortable to wear and have acceptable
cosmetic appeal, have good sound quality, and meet a
set of standardized measures including electroacous-
tic performance and that a patient’s real-ear measures
match their desired levels. After a hearing aid has been
programmed for the patient’s hearing loss using a pre-
scriptive fitting method, it is important to verify that
the output as measured in the ear canal, when actually
being worn by the patient, is appropriate. Verification
of prescriptive targets is accomplished using probe-
microphone real-ear measures, where a thin silicone

tube is placed in the ear canal and is attached to a mea-
surement microphone, which measures the aided ear
canal levels for an external speech signal. This method,
referred to as speech mapping, records the real-ear
aided response (REAR), thus allowing the audiologist to
reference the ear canal sound pressure level (SPL) so
that he or she can visualize the portion of the speech
signal that is audible for individual patients in their
own ear and determine if it is equal to the patient’s
prescriptive targets.
As a part of Step 5, the audiologist provides an
extensive hearing aid orientation. During this orienta-
tion, the patient receives hands-on instruction about
the care and use of the new hearing aids. This portion
of the fitting process cannot be underestimated, as the
first few weeks of ownership are critical regarding
hearing aid use and acceptance. It has been estimated
that as high as 10% of people who own hearing aids
do not use them, and many times they are not used
simply because the patient becomes frustrated with the
basic operation and handling of the instruments during
those first few days (Mueller, 2019). The best hearing
aid circuitry in the world does not help if the patient
cannot properly fit the hearing aid in his or her ear or
if they are uncomfortable to wear. Extensive counseling
about anticipated benefits of the hearing aids is also
required. Patients often believe (incorrectly) that sim-
ply putting on the hearing aid will immediately allow
them to hear. However, providing them with more
realistic expectations will assist in their acclimatization
to the new hearing aids. This counselling can take the
form of frequent clinic visits, follow-up phone calls,
and group classes for new hearing aid users.
Following the verification of hearing aid perfor-
mance and orientation to the new devices, the next step
in the fitting process is to conduct some measure of val-
idation. Hearing aid validation is the process of ensuring
that the goals set forth in the treatment plan or in the
communication needs assessment are met. This type of
validation includes different measurements, which can
be used to determine if the fitting was successful during
real-world use by the patient, if the hearing aids have
improved their social and emotional well-being, and
if this process improved their quality of life. This can
be accomplished through the use of post-fitting self-
assessment inventories. These self-assessment invento-
ries consist of questionnaires completed by the patient
and the patient’s communication partners (i.e., spouse,
significant other, or family member). Many different
types of questionnaires are available, from informal
questionnaires to standardized assessment tools. There
are a large number of questionnaires because there are
a variety of ways to measure success with hearing aids.
Some examples of questionnaires are the International
24  Assistive Listening Devices 345
Outcome Inventory for Hearing Aids (IOI-HA), the
Client Oriented Scale of Improvement (COSI), and the
Abbreviated Profile of Hearing Aid Benefit (APHAB).
These measures usually compare a pretest/pre-fitting
or unaided measure to an aided or post-fitting measure
of success and evaluate a difference score or benefit
measurement. These questionnaires are easy to admin-
ister and score and address many of the different areas
of hearing aid success. Since the purpose of the valida-
tion process is to assess the effectiveness of the hearing
aids and the patient’s subjective satisfaction with them,
a low score would indicate the patient may need the
hearing aids adjusted and/or require more counseling.
Thus, a properly fitted hearing aid has the ability to
change a person’s life for the better, and the audiolo-
gist is the professional who is able to make it happen.
These six steps, summarized in Table 24–1, will allow
the audiologist to assess, fit, verify, and validate the
patient’s hearing loss and the patient’s rehabilitation
of his or her hearing problem.
Types of Hearing Aids
There are different types of hearing aids for different
kinds of people and their problems. As summarized
in Table 24–2, there are basically two types of hearing
aids, either a behind-the-ear (BTE) or a custom hearing
aid. Fundamentally, these hearing aids differ in size,
application, and features. It is important not to confuse
hearing aid type with the technology contained within
the aid. Many manufacturers have different hearing aid
models with the same digital processing chip across
the various types they offer; therefore, different types
of the same product model will tend to sound similar
to the patient.
The BTE type of hearing aid is worn behind the
ear with an earhook, which rests on top of the auricle
and helps keep it in place behind the ear. The amplified
sound is delivered through the earhook and custom-
made earmold that fits into the concha and ear canal.
The earmold, which is shown in Figure 24–1, is used
to secure the hearing aid to the ear. This type contin-
ues to be used for fitting individuals with severe to
profound hearing losses, individuals with visual or
dexterity issues, and young infants and children with
hearing loss. Alternatively, the BTE can be connected
to the ear with a one-piece thin tubing, or a wire that
has the receiver at the end (see Figure 24–1). This com-
bination allows for a smaller size, which has made it
very popular.
Custom hearing aids require an impression of the
ear, which the manufacturer uses to create a case fit for
the user’s ear in which they place all of the components
346 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Table 24-2.  Hearing Aid Types. Hearing aids become smaller and have less gain as you move from left to
right side of the table.

Behind-the-Ear Custom Hearing Aid

Connection to the Ear

Standard Receiver-in-the- Receiver-in-the In-the-Ear In-the-Canal Completely-in-

canal (RIC) aid (RITA) the-Canal

Custom Thin electrical Thin/small Hearing aid Only fills the Resides
earmold wire connected diameter (nearly housed in a lower one completely in
to a receiver invisible) tube custom Half or quarter of the the ear canal
with a non- with a non- Full Shell concha
custom eartip custom eartip

AB
Earhook
Thin wire

Tubing

Non-custom
open eartip

Earmold Slim tube

Figure 24–1.  Behind-the-ear (BTE) hearing aid style. A. Standard BTE with custom earmold. B. Mini-
BTE hearing aids in a receiver-in-the-canal (RIC) and receiver-in-the-aids (RITA) configuration.

of the hearing aid. Within the custom line of hearing
aids, there are a number of different styles from which
the patient can choose. The largest custom style is the
in-the-ear (ITE) hearing aid, which uses a custom case
that fills the concha and a portion of the ear canal.
The development of the digital integrated circuit has
allowed hearing aid sizes to be reduced to the point
where all the hearing aid components can be fit into a
customized case that fits into the ear canal. Examples of
different custom styles are shown in Figure 24–2. The
ITE or in-the-canal (ITC) hearing aid has all the hearing
aid components built inside of a small customized cas-
ing (Figure 24–3). The ITC hearing aid only partially
fills the lower approximate one quarter of the concha;
 24  Assistive Listening Devices 347

a. b. c. d.

Figure 24–2.  Examples of different styles of custom hearing aids. a. Mini Canal, b. ITC, c. Half Shell, and d. Full Shell.
Images courtesy of Sonova AG © 2019.

Microphone ports

User toggle switch

Battery door

Volume control

Figure 24–3.  External features of a full-shell ITE. Image courtesy of Sonova

AG © 2019.

thus, the ITC is even smaller than the half-shell ITE but ate for those with some cosmetic concerns regarding
with the smaller size comes less amplifier gain. For this hearing aids, and who have less severe hearing loss
reason, the selection of an ITC may be most appropri- and relatively good manual dexterity to operate and
348 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Earshell

Microphone

Battery door

cm inch Removal string

Vent

Figure 24–4.  A CIC hearing aid that fits completely in the ear
canal and has a removal string to allow the user to remove it. Image
courtesy of Starkey Hearing Technologies © 2019.

insert/remove the aid. The last style is the completely-
in-the-canal (CIC) hearing aid (Figure 24–4). It is the
smallest of the custom-style hearing aids and is often
selected by the patient who is looking for the “invis-
ible” hearing aid. CICs typically do not offer enough
amplification for patients with moderate or greater
hearing losses.
Hearing Aid Components
The basic components of a digital hearing aid include
a microphone, amplifier, receiver, battery, and volume
control. As shown in Figure 24–5, these components
work together to detect the incoming signal, amplify
it, and then deliver it to the ear. The microphone or
microphones are used to pick up the acoustic signal
from the sound source and convert it to an electrical
signal that is then sent to the amplifier. Most current
hearing aids have two microphones, which allows for
special directional processing. The electrical signal is
then converted into digital information by the digital
processer, through which the incoming signal can be
manipulated and different processing algorithms can
be applied.
The main component of the hearing aid circuitry is
the amplifier, a computer chip that is used to increase
the level and alter the frequency of the input signal.
This chip also includes algorithms for all special signal
processing features that the hearing aid may have. The
digital signal is subsequently reconverted to an electri-
cal signal that is sent to the receiver. The receiver is in
actual fact a speaker that converts the amplified signal
from the hearing aid into an acoustical signal that is
delivered to the patient’s ear. This is all powered by a
battery, which comes in different sizes to match the size
and power requirements of the hearing aid. The level of
the output can be adjusted by the user through the vol-
ume control. Many hearing aids have a volume control
that is either a wheel or button on the aid itself; how-
ever, on some aids, it may be a function on a remote-
control device or controlled with a smartphone app.
An additional component is the telecoil, an alternative
input source for electrical signals. The telecoil converts
 24  Assistive Listening Devices 349

Microphones

BTE

Switch

Earhook Receiver

Processor

Battery

RIC Microphone
Switch

Processor

Receiver

Battery

Dome

Figure 24–5.  Main components found in both standard BTE and RIC hearing aids. Adapted
with permission from Audiology: Science to Practice (3rd ed., p. 327) by S. Kramer and D. K.
Brown, 2019, San Diego, CA: Plural Publishing, Inc. Copyright 2019 by Plural Publishing, Inc.

an electromagnetic signal from a telephone, an assistive
listening device, or a wide-area loop system to a signal
that can be delivered directly to the amplifier.
Auditory Implantable Devices
Depending on the type of hearing loss, some patients
will perform better with the use of a different type of
hearing device. Rather than being fit with a conven-
tional hearing aid, sometimes a patient needs to have a
different treatment option depending on the individual
patient characteristics. In these types of patients, the
audiologist will work with an otologist (ear, nose, and
throat surgeon) to manage the patient’s case. There
are three such specialized auditory devices: the bone-
anchored implant (BAI), the middle ear implant (MEI),
and the cochlear implant (CI). Each of these devices fits
a specific type of hearing loss or meets the need of a
certain type of patient.
The BAI can be used with patients who have a con-
ductive or mixed hearing loss or for those with single-
sided deafness (unilateral hearing loss). The MEI is
typically used with patients who have an intact middle
ear system but have a mild to severe sensorineural hear-
ing loss. A CI is a different type of hearing device, where
the acoustic signals are converted to electrical impulses
and delivered to electrodes that are implanted into the
cochlea. The CI is inserted into the cochlea and requires
an intact eighth cranial nerve to be able to function.
350 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Bone-Anchored Implant
A BAI consists of a hearing device that is surgically
implanted into the mastoid area behind the ear. Candi-
dates for this technology usually have a bilateral con-
ductive or mixed hearing loss, but some patients with
a unilateral hearing loss also receive benefit. The BAI is
similar to a bone conduction oscillator used in testing a
patient’s hearing (see Chapter 23) because it can trans-
mit a signal to the cochlea and bypass the outer and
middle ears. By missing the conductive parts of the ear,
the acoustic signals are picked up by the BAI’s micro-
phone and transduced into vibrations that stimulate
the skull, thus creating the normal vibratory energy in
the normal hearing cochlea.
In order for the BAI to function, it must transmit
the auditory signal to the cochlea via bone conduc-
tion. The device is permanently attached to the skull
through a process called osseointegration. Osseointegra-
tion is the connection between living bone and the sur-
face of a load-carrying implant, or in other words, it is
the method by which the implant adheres to the bone.
The implant is made of titanium, which allows for a
strong and stable implant-to-tissue interaction giving it
a structural and functional contact between the implant
and the bone (Kuhn & Perez, 2015). As shown in Fig-
Bone conduction
Air conduction
Figure 24–6.  A percutaneous bone-anchored implant. Note the device’s penetration through
the skin where it makes direct connection to the bone, allowing for sound to be transferred to the
cochlea via bone conduction.
ure 24–6, the surgeon implants an abutment or magnet
made with a titanium screw into the skull behind the
pinna. First, a hole is drilled into the skull, and then the
surgeon threads the screw into the bone. Over a period
of time, usually 4 to 6 weeks, the bone creates a fibrous
layer around the screw, and the bone begins to weave
itself into the implant creating a solid integration of the
implant with the bone.
BAIs can be either percutaneous or transcutane-
ous. A percutaneous device, as shown in Figure 24–6,
has an abutment with a screw attached that is osseoin-
tegrated into the skull and a post attached to the abut-
ment that penetrates through the skin. The fixture or
abutment that penetrates the skin is used to connect
to the hearing device and acts as a breakaway point
if something happens to hit the device. The hearing
device is attached to the abutment and contains the
microphone, battery, and other components similar to
a regular hearing aid. The advantages of percutane-
ous devices include a threshold improvement in the
mid to high frequencies and a lower force level when
compared to transcutaneous BAIs. Disadvantages are
that patients must be diligent about cleaning around
the abutment or risk causing skin infections because of
poor hygiene, for this is an open wound that they will
have for life (Hodgetts, 2017).
 24  Assistive Listening Devices 351

Transcutaneous BAIs have a magnet that is surgi-
cally attached to the skull under the skin and a reten-
tion magnet on the outside of the skin; therefore, they
do not penetrate through the skin. The transcutane-
ous magnet is osseointegrated to the skull under the
skin, and the hearing device attaches to it magnetically
because the magnets are attracted to each other across
the skin (Reinfeldt, Hakansson, Taghavi, & Feg-Olofs-
son, 2015). An example of a transcutaneous device is
shown in Figure 24–7. The sound processor is located
outside the skin and contains the microphone, battery,
and vibrating source to transmit the signal to the mag-
net under the skin. Similar to the percutaneous devices,
the device will detach from the scalp without trauma
or injury to the user. An advantage of transcutane-
ous devices includes an improvement in thresholds,
especially in the low frequencies. However, the disad-
vantages are that as the vibrations travel through the
skin, they lose energy when compared to percutaneous
devices, and patients may experience minor complica-
tions because of the pressure on the skin between the
two magnets (Hodgetts, 2017; Kohan, 2015).
Candidates for a BAI must be over 5 years of age
(Kuhn & Perez, 2015) and fall into one of two catego-
ries (Table 24–3): (a) have a conductive or mixed hear-
ing loss or (b) have a unilateral hearing loss. Specific
requirements are set by each manufacturer based on
the audiometric criteria reported to the U.S. Food and
Drug Administration (FDA). However, candidacy
requirements are similar for both those patients with
conductive/mixed hearing loss and those with single-
sided deafness. Patients with a conductive hearing loss
must have at least a 30 dB HL conductive component,
and those with a mixed hearing loss must have at least
a 30 dB HL conductive component and a mild to mod-
erate sensorineural component. Currently, patients
with single-sided deafness (SSD) must have normal
hearing in the better hearing ear (a PTA <20 dB HL by
air conduction) and a profound sensorineural hearing
loss (a PTA >90 dB HL) in the poor ear (Zeitler, Snapp,
Telischi, & Angeli, 2012).
Middle Ear Implant
A MEI is a type of hearing aid that differs from a con-
ventional hearing aid because it is surgically placed into
the middle ear space by an ear, nose, and throat (ENT)
surgeon. This specialized type of hearing device is used
with patients who are considered unsuccessful hear-
ing aid users or whose lifestyle would be hampered by
the use of a regular hearing aid. In some cases, these
patients are medically unable to wear conventional
hearing aids; therefore, a MEI may become an option.

Figure 24–7.  An example of a transcutaneous device with an implanted mag-

net and an external hearing device — the Sophono Alpha 2 MPO. Note the four holes
in the implant portion through which the titanium screws are placed to attach the
implant to the skull. Courtesy of Medtronix, Jacksonville, FL.
352 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Table 24–3.  Candidacy Considerations for a Bone-Anchored Implant
Conductive/Mixed Loss
Atresia — bilateral
Abnormal ear canal structure
Chronic ear drainage
Stapedectomy
Failed middle ear surgery
Unable to use air conduction hearing aid
Hypersensitivity to earmolds
Severe dermatitis of the ear canal
Severe otitis externa
Source:  Reproduced with permission from Audiology: Science to Practice (3rd ed., p. 349) by
S. Kramer and D. K. Brown, 2019, San Diego, CA: Plural Publishing, Inc. Copyright 2019 by Plural
Publishing, Inc.
These devices are implanted in the middle ear and cou-
pled to the ossicles, essentially bypassing the ear canal.
This leaves the ear canal unoccluded, which is poten-
tially more cosmetically appealing to patients (Achar,
2013). Although MEIs are a viable option for patients,
they have only a small share of the U.S. market.
The MEI is a device that is categorized either by
its implant status (partially or fully implanted) or on
the type of transducer used in the device (Channer,
Eshraghi, & Lui, 2011). MEIs are surgically implanted
in the middle ear and depending on the device can be
attached to the ossicular chain, oval window, or round
window (see Chapter 22) and used as a method of
treating SNHL (Bassim & Fayad, 2010; Gifford, 2017).
Most transducers used in MEIs are piezoelectric or
electromagnetic transduction mechanisms (Kuhn &
Perez, 2015). The piezoelectric implementation uses
an external microphone placed by the ear or under the
skin in the ear canal to detect sounds around the lis-
tener. From this, an electrically encoded signal is sent
to an implanted middle ear crystal placed on the ossic-
ular chain. The crystal moves in response to stimula-
tion from the sound transduction and propagates this
electrical activity into the cochlea, where it is processed
by the remaining hair cells and eighth cranial nerve
fibers. Piezoelectric devices are smaller and use less
power than electromagnetic devices. The electromag-
netic implementation is larger than the piezoelectric
version; therefore, it is only partially implantable. Most
of the electromagnetic implants have an external coil
that is connected to a microphone and an amplifier. The
amplified signal is sent to an implanted magnet located
at or near the incus–stapedial joint of the ossicular chain
Unilateral Hearing Loss
Atresia — unilateral
Acquired unilateral conductive/mixed
hearing loss
Congenital or acquired profound
unilateral loss
Tumors of the conductive pathway
Autoimmune inner ear disease
Ménière’s disease
and oscillates as electromagnetic waves move past the
magnet; thus, the electromagnetic energy is converted
to mechanical energy (ossicular movement). The elec-
tromagnetic devices have greater gain and output, but
they are offset by a greater power consumption and
larger size compared to the piezoelectric transducers
(Channer et al., 2011).
Candidacy for a MEI is set by each manufacturer
according to the audiometric criteria they reported
to the FDA during their clinical trial. Typically, MEIs
are designed for patients with a stable SNHL in the
moderate to severe range (≤65 to 70 dB HL), and word
recognition scores greater than 40% to 60% (Achar,
2013; Kuhn & Perez, 2015). Candidates must also be
medically stable and not have any preexisting medical
conditions.
Examples of currently available devices include
the Esteem, Maxum, and Vibrant Soundbridge. The
Esteem is a two-channel analog device, which uses a
different approach because it does not have an external
processor or microphone. As shown in Figure 24–8, the
Esteem device is totally implanted within the temporal
bone and the middle ear space. This device including
the battery is housed in the ear, including a piezoelec-
tric transducer or sensor, which connects to the incus
and moves with the motion of the tympanic mem-
brane. It functions by receiving the mechanical vibra-
tions from the incus and converts them to electrical
signals, which are sent to a sound processor implanted
in the temporal bone. The sound processor filters and
amplifies the signal and sends the processed signal to
the driver (another piezoelectric transducer) coupled
to the stapes footplate. The electrical signal is converted
 24  Assistive Listening Devices 353

Figure 24–8.  An example of a middle ear implant — the Esteem. (1) An electronic micro-
phone is not used, instead the external ear funnels the sound waves down the ear canal to the
tympanic membrane causing it to vibrate and act as the microphone. (2) The sensor is con-
nected to the incus and receives the mechanical vibrations, converting them to an electrical
signal and forwarding them to the processor. (3) The processor implanted in the temporal
bone amplifies the signal. (4) The driver is coupled to the stapes footplate and converts the
enhanced signal back to mechanical energy for transfer into the cochlea. Courtesy of Envoy
Medical Corporation, White Bear Lake, MN.

back to mechanical energy at the driver, which moves
the stapes in and out of the oval window, transmitting
the signal to the cochlea.
MEIs have slightly better pure-tone thresholds,
word recognition scores in quiet, and speech-in-noise
performances when compared to conventional hear-
ing aids (McRackan, Clinkscales, Ahlstrom, Nguyen, &
Dubno, 2018; Truy, Philibert, Vesson, Labaassi, & Collet,
2008). Results have also shown an overall improvement
in patient satisfaction. However, more importantly,
354 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
patients have reported additional benefits with MEI
including reduced problems with feedback and other
distortions of the sound (Kuhn & Perez, 2015). For this
select group of patients, MEI serves a useful purpose
and allows many who would otherwise not be success-
ful with amplification, gain auditory benefit.
Cochlear Implant
A CI is a biomedical device that bypasses the middle
ear and most of the cochlea, and electrically stimu-
lates neurons of the eighth cranial nerve. The stimula-
tion from a CI provides an input that is different from
normal hearing. Therefore, it can provide benefit for
individuals with severe to profound hearing loss, who
have some functional auditory nerve fibers but mini-
mal or absent hair cells in the cochlea (see Chapter 22),
meaning that a conventional hearing aid would not
help. Much like a hearing aid, a CI can provide reason-
ably good detection and correct identification of envi-
ronmental and speech sounds.
The actual success and the functional level obtained
with a CI depend on many factors, including the time
of onset of the hearing loss, length of deafness prior
to implantation, residual function of auditory neurons,
appropriate programming of the implant, and consis-
tent use of the implant. Some limitations to CIs include
the risk of undergoing the surgery, the loss of remain-
ing functional hair cells from implanting the electrode
array, the expense of undergoing the surgery, and the
need to travel to and from a CI center for remapping
A. Volume control
Microphone
Processor
Headpiece
Battery
Figure 24–9.  Components of a cochlear implant. A. External device with the processor and coil that
attaches to the internal magnet. B. Implant with the electrode array which is inserted into the cochlea.
Images courtesy of Advanced Bionics LLC, © 2017.
and/or programming and checks. Fortunately, the cost
associated with cochlear implants, including the sur-
gery, device, and programming visits, is covered by
most medical insurances.
A CI can be divided into external and internal
components as illustrated in Figure 24–9. The external
components consist of a microphone, speech processor,
and external transmitter (headpiece). As with all ampli-
fication devices, the microphone changes the acoustic
energy into electrical energy. The signal is sent to the
speech processor for processing and analyzing, and
then bandpass filtered, creating frequency bands of
electric stimulation. The external transmitter receives
these signals and sends them to the internal implant
via radio frequency. The implant consists of a magnet,
receiving coil, and an electrode array. As illustrated,
the external transmitter is attached to the implant via
a magnet. The signal from the external transmitter is
sent to the receiving coil and then to the electrode array,
thus bypassing the ear canal, middle ear, and cochlear
hair cells, where the electrical impulses stimulate the
eighth cranial nerve.
After the sound is converted to an electrical sig-
nal, it is changed via a speech coding strategy. These
strategies convert the sounds into patterns of electri-
cal signals and deliver them to the cochlea in order to
convey frequency, intensity, and duration information.
The internal receiver coil picks up the carrier signal
from the transmitter and sends the electrical code to
the various channels of the electrode array. As shown
in Figure 24–10, the electrode array is attached to the
implant and surgically inserted into the cochlea where
B.
Electrode array
Coil
Magnet

Figure 24–10.  Cochlear implant with placement of
external and internal CI components. (1) The microphone
on the sound processor picks up and converts the sound
into digital information. (2) This information is transferred
through the coil to the implant located under the skin.
(3) The implant sends electrical signals down the elec-
trode into the cochlea. (4) The auditory nerve fibers in the
cochlea pick up the electrical signals and conduct them up
the auditory pathway to the auditory cortex. Image cour-
tesy of Cochlear Americas, © 2017.
the nerve fibers are activated by the electrical signals
from the internal component.
The candidacy requirements for a CI are as fol-
lows: (a) the patient must have a severe to profound
bilateral sensorineural hearing loss and (b) receive little
or no benefit from hearing aids. Additionally, an evalu-
ation of the patient is required by a team of medical
professionals for consideration of a cochlear implant.
The CI team consists of the ENT surgeon, audiologist,
a speech-language pathologist, psychologist, social
worker, and educator of the deaf. The entire CI team
participates in the evaluation and makes a final deci-
sion on whether a patient is appropriate to receive a
cochlear implant. A medical evaluation includes a com-
puted tomography (CT) scan to determine the presence
of a cochlea and auditory nerve, as well as an assess-
1
 ostlingually acquired hearing loss is where a person’s hearing loss is acquired after they have developed language at age 5 or greater. Refer
P
to Chapter 7 for further details.
24  Assistive Listening Devices 355
ment of the patient’s ability to cope physically with
surgery. The audiology evaluation includes air and
bone conduction thresholds, tympanometry, acoustic
reflex thresholds, and word recognition scores.
The CI is programmed by the audiologist through
a process called CI mapping 3 to 6 weeks following the
surgery. During this process, the electrical thresholds
for soft inputs and the upper limits of comfort thresh-
olds are established. It is common for the audiologist
to turn off any electrodes where the stimulation causes
pain, facial twitches, and/or no improvement in hear-
ing sensitivity. The patient will return multiple times
within the first year for additional sessions to fine-tune
the CI. Most adults with postlingually acquired hearing
loss1 show significant improvements in speech recogni-
tion abilities after implantation. The speech recognition
abilities appear to improve and plateau for most indi-
viduals within the first 3 months but may continue to
improve up to 1 year postimplant. Their outcome per-
formance is negatively correlated with their duration
of deafness and age (Sharma, Dorman, & Kral, 2005).
After implantation, children will require significant
rehabilitation to obtain maximum outcomes; however,
they can develop spoken language skills (Fitzpatrick,
Crawford, Ni, & Durieux-Smith, 2011). Individuals and
their families will need counseling regarding realistic
expectations, additional training with communication
strategies, speech-language therapy, academic support,
continued instruction, and additional fine-tuning of the
cochlear implant.
Chapter Summary
Hearing Aids
A main component of the treatment and rehabilita-
tive process that we know as audiology is the fitting
of hearing aids. Audiologists have an important role in
the comprehensive selection and fitting of the device.
Six steps in selecting and fitting a hearing aid
include the following:
1. Assessment — determine the type and degree of
loss
2. Treatment Planning — review results, identify
areas of difficulty, and explore amplification
options
3. Selection — determine type of fitting and decide
on electroacoustic parameters
356 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
4. Verification — determine that aids meet electro-
acoustic performance and that real-ear results
match desired levels
5. Orientation — counsel patient on hearing aid use
and care and give realistic expectations
6. Validation — assess effectiveness of hearing aids
and patient’s subjective satisfaction
Types of hearing aids include BTE, RIC, ITE, ITC,
and CIC.
Hearing aid components include a microphone,
amplifier, receiver, battery, and telecoil.
Fitting strategies are used to program a hearing
aid to the desired gain and output for the patient. The
NAL-NL2 program is used mostly for adults and the
DSLv5.0 is used mainly with children.
After a hearing aid has been programmed using
a prescriptive fitting method, it is important to verify
that the ear canal output is appropriate for the patient.
Probe-microphone real-ear measures (REAR) are used
to verify prescriptive targets.
Validation of hearing aid benefit is accomplished
using a self-assessment inventory or questionnaire
(i.e., International Outcome Inventory for Hearing
Aids [IOI-HA], Client Oriented Scale of Improvement
[COSI], and Abbreviated Profile of Hearing Aid Benefit
[APHAB]) completed by the patient.
Auditory Implantable Devices
Depending on the type of hearing loss, some patients
will perform better with the use of a different type of a
hearing device.
Three specialized auditory devices include the
BAI, the MEI, and the CI.
BAIs are used with patients who have a conduc-
tive or mixed hearing loss or for those with single-
sided deafness (unilateral hearing loss). There are two
types: percutaneous (penetrate through the skin) or
transcutaneous (across the skin).
MEIs are a specialized type of hearing device
because they are surgically placed in the middle ear.
They are used with patients who have an intact mid-
dle ear system but have a mild to severe-to-profound
SNHL. They usually have a lifestyle that would ham-
per the use of conventional hearing aids. MEIs have
slightly better thresholds, word recognition scores in
quiet, and speech-in-noise performance compared to
conventional hearing aids, and patients reported ben-
efits such as reduced problems with feedback.
CIs are used with individuals with a severe to
profound SNHL and receive limited benefit from con-
ventional hearing aids. They bypass the middle ear
and the sensory hair cells and electrically stimulates
the eighth nerve.
The processor transduces acoustic signals into
electrical signals along the electrode array to stimulate
the auditory nerve. After implantation, individuals
will need to undergo cochlear implant mapping. This
process allows the audiologist to identify the patient’s
electrical thresholds for soft inputs and establish the
upper limit of comfort thresholds.
Adults with postlingually acquired hearing loss
show significant improvement in speech recognition
abilities, and children will require significant rehabili-
tation to obtain maximum outcomes; however, they
can develop spoken language skills.
References
Achar, P. (2013). Hearing rehabilitation with middle ear
implants: An overview. Surgeon, 11(3), 165–168. https://
doi.org/10.1016/j.surge.2013.02.002
Bassim, M. K., & Fayad, J. N. (2010). Implantable middle
ear hearing devices: A review. Seminars in Hearing, 31(1),
28–36.
Channer, G. A., Eshraghi, A. A., & Lui, X. Z. (2011). Middle
ear implant: Historical and futuristic perspective. Journal
of Otology, 6(2), 10–18.
Fitzpatrick, E. M., Crawford, L., Ni, A., & Durieux-Smith,
A. (2011). A descriptive analysis of language and speech
skills in 4- to 5-year-old children with hearing loss. Ear and
Hearing, 32(5), 605–616.
Gifford, R. H. (2017). The future of auditory implants. In A.
M. Tharpe & R. Seewald, Comprehensive handbook of pediat-
ric audiology (2nd ed., pp. 793–812). San Diego, CA: Plural
Publishing.
Hodgetts, B. (2017). Other hearing devices: Bone conduction.
In A. M. Tharpe & R. Seewald (Eds.), Comprehensive hand-
book of pediatric audiology (2nd ed., pp. 781–792). San Diego,
CA: Plural Publishing.
Kohan, D. (2015, February). Implantable auditory devices. Paper
presented at the Ultimate Colorado Midwinter Meeting,
Vail, CO.
Kuhn, J. J., & Perez, A. J. (2015). Implantable hearing devices.
In M. L. Pensak & D. I. Choo, Clinical otology (4th ed., pp.
402–420). New York, NY: Thieme.
McRackan, T. R., Clinkscales, W. B., Ahlstrom, J. B., Nguyen,
S. A., & Dubno, J. R. (2018). Factors associated with benefit
of active middle ear implants compared to conventional
hearing aids. Laryngoscope, 128, 2133–2138.
Mueller, H. G. (2019). Hearing aids. In S. Kramer & D. K.
Brown. Audiology: Science to practice (3rd ed, pp. 319–346).
San Diego, CA: Plural Publishing.
Mueller, H. G., & Hall, J. W. III (1998). Audiologists’ desk refer-
ence (Vol. II). San Diego, CA: Singular Publishing Group.
Mueller, H. G., Ricketts, T. A., & Bentler R. (2014). Modern
hearing aids: Pre-fitting testing and selection considerations.
San Diego, CA: Plural Publishing.

Mueller, H. G., Ricketts, T. A., & Bentler, R. (2017). Speech map-
ping and probe microphone measurements. San Diego, CA:
Plural Publishing.
National Institute on Deafness and Other Communication
Disorders (NIDCD). (2016). Quick statistics about hearing.
Retrieved from https://www.nidcd.nih.gov
Reinfeldt, S., Hakansson, B., Taghavi, H., & Eeg-Olofsson, M.
(2015). New developments in bone-conduction hearing
implants: A review. Medical Devices (Auckl), 8, 79–93.
Ricketts, T. A., Bentler, R., & Mueller, H. G. (2019). Essentials
of modern hearing aids: Selection, fitting, and verification. San
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24  Assistive Listening Devices 357
Sharma, A., Dorman, M. F., & Kral, A. (2005). The influence
of a sensitive period on central auditory development in
children with unilateral and bilateral cochlear implants.
Hearing Research, 203(1–2), 133–143.
Truy, E., Philibert, B., Vesson, J. F., Labaassi, S., & Collet, L.
(2008). Vibrant Soundbridge versus conventional hearing
aid in sensorineural high-frequency hearing loss: A pro-
spective study. Otology and Neurotology 29, 684–687.
Zeitler, D. M., Snapp, H. A., Telischi, F. F., & Angeli, S. I.
(2012). Bone-anchored implantation for single-sided deaf-
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Otolaryngology-Head and Neck Surgery, 147, 105–111.

Aural Habilitation and
Rehabilitation
Introduction
This chapter presents an overview of what can be done
to habilitate or rehabilitate individuals with hearing
loss. Now that you have learned about the anatomy
and physiology of the auditory and vestibular systems
(Chapter 22), the clinical tests used to identify and diag-
nose hearing loss (Chapter 23), how to improve an indi-
vidual’s auditory function with the use of hearing aids
or auditory implants (Chapter 24), and the information
relevant to the development of speech and language
Chapters 5, 6, and 13), we move forward and provide
information on the audiologic treatment services for
individuals with hearing loss and their family unit
according to their needs. Individuals (mainly adults)
who have had hearing and lost it will require different
interventions than those (mainly children) who have
not been able to hear. Infants and children with hear-
ing loss and their families will require services that can
include clinical treatment, home intervention, family
support, and case management.
Audiologists not only provide treatment to indi-
viduals (children or adults) with hearing loss but they
also counsel patients and their families concerning
hearing loss, the use of amplification, and strategies for
improving speech recognition. Additionally, audiolo-
25
gists counsel patients regarding the effect hearing loss
has on the communication process and on their psycho-
social status in personal and social situations.
When working on the communication skills of
individuals with hearing loss, we must utilize an inter-
vention that is aimed at minimizing and alleviating the
communication difficulties associated with the hearing
loss (Tye-Murray, 2020). The first step in this process
is to assess their hearing acuity and communication
ability; in doing so, we can assess their communication
skills and determine the level of intervention they will
require. The depth of the problem is associated with
his or her ability at the time of the loss. Infants and
young children who are born with or acquire hearing
loss soon after birth have not learned to listen or com-
municate. Older children and adults who have had
hearing and then subsequently lost it will require dif-
ferent strategies and techniques.
Children who have not learned communication
skills will need to undergo aural habilitation, which
is an intervention for children who have not devel-
oped listening, speech, and language skills (American
Speech-Language-Hearing Association [ASHA], 2019).
Whereas, aural rehabilitation focuses on restoring a
skill that is lost. Although aural rehabilitation has been
around since the beginning of audiology, it has evolved
359
360 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
over time to keep pace with our knowledge and technol-
ogy, but continues to be an integral part of what we do
as audiologists. Aural rehabilitation is the intervention
for individuals who have had a reduction in function,
activity, participation, and quality of life caused by their
hearing loss, but whose difficulties can be overcome by
sensory management, perceptual training, and counsel-
ing (Boothroyd, 2007). In sensory management, we use
hearing aids, cochlear implants, or other hearing assis-
tive technology systems (e.g., frequency-modulated
[FM] system) to make sounds as audible as possible.
Perceptual training is the enhancement of auditory or
auditory-visual perceptual skills (e.g., our ability to
perceive spoken language) through auditory training
(e.g., retraining our listening ability). Counseling is the
discussion both informally and formally of the practi-
cal, social, and emotional consequences of hearing loss.
Aural Habilitation
It is very fortunate that newborn hearing screening is
being completed in every state in the nation.1 Through
this endeavor, over 6000 infants (1.7 per 1000 live
births) are identified with hearing loss annually (Cen-
ters for Disease Control and Prevention [CDC], 2016).
Using the 1, 3, 6 rule, infants must have their hearing
screened by 1 month, the diagnosis must be completed
and amplification fitted by 3 months, and they must be
enrolled in intervention by 6 months (Joint Committee
on Infant Hearing [JCIH], 2007). This early identifica-
tion and intervention has a significant positive impact
on the child’s development, leading to a normal range
of language (comprehension and expression) and social
development between 1 and 3 years of age (Yoshinaga-
Itano, Sedey, Coulter, & Mehl, 1998). Through the use
of aural habilitation, whose goal is to develop normal
listening skills, a child with hearing loss can acquire
language as naturally as possible. The habilitation pro-
cess emphasizes the child’s usable hearing through
an appropriate amplification device, whether hearing
aids or a cochlear implant (CI). Note that children can
receive a CI as early as 1 year of age if they are found
not to benefit from a hearing aid.
Assessment of Communication
Needs in Children
The first step in the aural habilitation process is to
determine the child’s type and degree of hearing loss
1
 he CDC (2016) indicates that 98% of all babies born in the US are screened, 1.7% of those infants do not pass their screening but most go on
T
to have normal hearing as identified through the diagnostic process. The end result is 1.7 per 1000 (n = 6,337) live births will have a hearing
loss diagnosed by 3 months of age.
(see Chapter 23) in each ear and to fit the child with a
hearing aid (see Chapter 24). In this way, we can estab-
lish exactly what the child hears. The audiologist will
need to encourage the child’s use of his or her hearing
aids by helping the parent/caregiver become famil-
iar with the child’s hearing loss and hearing aids and
guide the parent/caregiver in achieving full-time use
of the amplification device by the child.
Since these children are very young, they may not
be able to be assessed easily. Audiologists can use sub-
jective information provided by parents about auditory
behaviors in everyday life to assess how the child is
performing and complement it with some objective test
results from a battery of assessments (Bagatto, Moodie,
Seewald, Bartlett, & Scollie, 2011). There have been a
number of questionnaires or scales developed to col-
lect parent feedback. These questionnaires have been
standardized, and some even provide normative data
so that the results can be compared to those of their
peers. Examples of these questionnaires include the
Infant-Toddler Meaningful Auditory Integration Scale
(IT-MAIS), the LittlEARS questionnaire, and the Par-
ents’ Evaluation of Aural/Oral Performance of Chil-
dren (PEACH).
The Infant-Toddler Meaningful Auditory Integra-
tion Scale (IT-MAIS) (Zimmerman-Phillips, Robbins,
& Osberger, 2000) is a structured interview designed
to assess the child’s spontaneous responses to sound
in his or her everyday environment. The assessment is
based on information provided by the child’s parent(s)
in response to 10 probes (Figure 25–1). These probes
assess three main areas: (a) vocalization behavior,
(b) alerting to sounds, and (c) deriving meaning from
sound. Through this scale, the clinician can determine
how a child is accessing and using sound in his or her
everyday environment, determine potential issues for
the child regarding his or her hearing in everyday situ-
ations, and determine goals for intervention.
The LittlEARS® Auditory Questionnaire (LEAQ) is
a parental questionnaire that assesses auditory behavior
in children up to 24 months of age (Coninx, Weichbold,
Tsiakpini, Autrique, Bescond, Tamas, et al., 2009). This
language-independent tool can be used to document a
child’s progress with his or her current amplification,
provide evidence of the need for a cochlear implant, or
demonstrate the need for follow-up in other develop-
mental areas. This brief questionnaire uses a series of
35 yes/no questions that can be compared to a set of
expected values based on parent-observed reactions that
the child has to acoustic stimuli. Results from the child
can be compared to data for normal hearing children
 IT-MAIS
Infant-Toddler Meaningful Auditory Integration Scale

1
Is the child’s vocal behavior affected while wearing his/her sensory aid (hearing
aid or cochlear implant)?
The benefits of auditory input are often apparent first in the speech production skills of very young children. The
frequency and quality of vocalizations may change when the device is put on, turned off, or not working properly.

1. Ask the parent: Describe _____’s vocalizations when you first put his/her device on each day. Have the parent
explain how and if the child’s vocalizations change when the sensory aid is first turned on and auditory input is
experienced at the start of each day.

2. Ask the parent: If you forget to put the device on ____, or if the device is not working properly, do you and/or
others notice that ____’s vocalizations are different in any way (e.g., quality, frequency of occurrence)?

3. Or ask: Does the child test the device by vocalizing when the device is first turned on?

_____ 0 = Never
No difference in the child’s vocalizations with the device turned on versus the device turned off.

_____ 1 = Rarely
Slight increase in the frequency of the child’s vocalizations (approximately 25%) with the device on (or
similar decrease with the device off).

_____ 2 = Occasionally
Child vocalizes throughout the day, and there are increases in vocalizations (approximately 50%) with the
device turned on (or similar decrease with the device turned off).

_____ 3 = Frequently
Child vocalizes throughout the day, and there are noticeable increases in vocalizations (approximately
75%) with the device on (or a similar decrease with the device off). Parents may report that individuals
outside the home notice a change in the frequency of child’s vocalizations with or without the device.

_____ 4 = Always
Child’s vocalizations increase 100% with the device on compared to the frequency of occurrence with the
device turned off.

Parent Report:

Figure 25–1.  An example of a question from the Infant-Toddler Meaningful Auditory Integration Scale (IT-MAIS) (Zim-
merman-Phillips,
3 Robbins, & Osberger, 2000). This is one of the 10 probe questions from the parent-report scale that is
administered in an interview format. The questions are designed to elicit a dialogue between the examiner and parent
about their child’s spontaneous responses to sound in his or her everyday environment. Utilization of this question format
discourages the clinician from leading the parent to provide desired responses and from only providing yes/no answers.
It is often used with children who have a severe to profound loss, in order to compare ability both pre- and post-cochlear
implantation. Source: © 2013 Advanced Bionics AG and affiliates. All rights reserved.

361
362 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
and used to develop his or her aural habilitation plan
or to assess improvement by evaluating change on the
LEAQ scale after intervention.
The Parents’ Evaluation of Aural/Oral Perfor-
mance of Children (PEACH) scale is used to assess
functional performance of children under 5 years of
age with hearing loss ranging from mild to profound
(Ching & Hill, 2007). The PEACH is a validated ques-
tionnaire that asks parents to reflect on their child’s lis-
tening behavior and rate each of the 12 items, which
correspond to different hearing and communication
scenarios. The child’s results can be compared to nor-
mal hearing children and provide information about
his or her performance in everyday situations. They
can also be used to monitor the child’s progress, evalu-
ate the effectiveness of the child’s hearing aid and/or
cochlear implant, or assist in tailoring an intervention
plan by identifying a child’s specific area of difficulty.
Along with the objective information gleaned
from the audiological evaluation (i.e. audiogram, tym-
panogram, hearing aid evaluation) and the subjective
information gathered directly from the parents, the
audiologist can synthesize this data and form a pic-
ture of the child’s auditory ability. The audiologist is
then able to compare the child’s functional outcomes to
that of their peers with normal hearing and develop
a set of treatment goals and monitor progress toward
those goals.
Pediatric Intervention
The main objective of aural habilitation is to enhance
the listening skills of children with hearing loss by hav-
ing them progress through an auditory skills hierarchy.
Obtaining this objective will enable the child to func-
tion to his or her maximum auditory potential. How-
ever, there are factors that can affect the outcomes of a
child’s auditory development (Fitzpatrick, 2010). These
factors include issues involving the child, his or her
family and the environment.
Environmental factors are related to the family’s
access to care, the knowledge of providers, and the
type of intervention available in the child’s location.
Geography can play a role in the type of services that
are available; not every service is available in every
state, and even within states, there are often disparities
between services provided in urban and rural commu-
nities. These disparities can create delays in identifica-
tion, amplification, and intervention.
Family factors, which revolve around the char-
acteristics and functioning of the family can also con-
tribute to poorer outcomes. These factors include the
makeup of the family, cultural and linguistic practices
(i.e. languages spoken in the home), religious beliefs,
education level of the parents, previous experiences
with hearing loss, engagement with the process, and
socioeconomic status.
The factor that has the greatest impact on a child’s
auditory development is the child himself or herself,
including the child’s age of diagnosis, hearing age,
type and degree of hearing loss, developmental level
and additional disabilities. The age of diagnosis is an
important factor, as there is a large difference in terms
of language development between a child who has
lost his or her hearing prelingually and a child who
has lost his or her hearing postlingually. Children who
have developed language and then lost their hearing
only require rehabilitation of their auditory skills, as
their language development has already been com-
pleted. Whereas a prelingual child needs habilitation to
develop not only his or her auditory skills but also lan-
guage skills. Hearing age is the amount of time that the
child has spent hearing, which can be different from
the child’s chronological age. For example, a child with
a profound hearing loss who was not identified until
1 year of age has a hearing age of zero because he or
she has yet to develop auditory skills. Furthermore, the
type and degree of hearing loss (see Chapter 23) will
also affect the child’s auditory skill development, as a
child with a conductive loss (i.e. a child with a CL/P,
see Chapter 19) will have more auditory awareness as
long as the sound is loud enough to reach the cochlea.
In contrast, a child with a sensorineural loss (see Chap-
ter 7) will have less auditory awareness because even
if the sound is loud enough, the system is still not fully
functional, so sound may not make it from the periph-
eral system to the auditory cortex.
Approximately 30% to 40% of children with hear-
ing loss have one or more additional disabilities (i.e.,
blindness, cerebral palsy) (Gallaudet Research Insti-
tute, 2009). Further studies have shown that as many
as 32% of children with hearing loss also have a devel-
opmental disability (Fitzpatrick & Doucet, 2013). This
suggests that in addition to the child having a hearing
loss, a substantial number will also have a develop-
mental disability. This will further add to the difficulty
of learning auditory skills. Others will show limited or
no ability to acquire spoken language as their primary
mode of communication.
Although there are factors that can affect the devel-
opment of a child’s auditory skills, there are some com-
ponents that when present should lead to a successful
intervention program. According to the Joint Com-
mittee on Infant Hearing (JCIH), these should include
(a) using a family-centered approach, (b) providing
every family with unbiased information on all options
regarding approaches to communication, (c) monitor-
 25  Aural Habilitation and Rehabilitation 363

ing development at 6-month intervals using norm-ref-
erenced instruments, (d) providing services in a natural
environment such as in their home, and (e) being sensi-
tive to cultural and language differences and (f) provid-
ing accommodations (JCIH, 2007).
In the early stages of intervention, the goal is to
enable the child to function at his or her maximum
auditory potential. However, at this stage the primary
focus is on parent support and education, rather than
on “therapy” with the child. Figure 25–2 illustrates that
parents are at the center of family-centered interven-
tion. The parents need to receive support and coaching
from the clinician so that they, in turn, can implement
the program with their child.
Coaching Model of Intervention
There are two main approaches used with early inter-
vention programs, one emphasizes a direct therapy
model of intervention, and the other utilizes a coaching
model. A direct therapy approach is where the profes-
sional interacts with the child while the parent observes
and receives guidance from the clinician (Tye-Murray,
2020). Direct intervention focuses on the child and the
professional-child interaction is, whereas the coaching
model requires that the parent implement the program
while the clinician observes the parent–child interac-
tions and provides the parent with support. Coaching
is a family-centered approach, where the parent is sup-
ported and given hands-on practice through which the
parent develops a sense of self-efficacy. The coaching
approach is usually completed in the child’s home dur-
ing a home visit. Due to the ongoing interactions that
occur between family members and the child, training
the family will have substantially more of an effect in
the long term. In this model, the professional’s goal is
to help turn everyday activities in the home environ-
ment into rich learning experiences for the child.

Developing
auditory skills

Support
Creating
optimal Information
listening
and learning
Parent about hearing
and technology
environments

Coaching
Developing
consistent
hearing device
use in their
child

Figure 25–2.  Components of a family-centered intervention model.

The role of the audiologist is to provide information to support parents and
to train them through coaching. When parents feel empowered, children
have better outcomes.
364 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
Tye-Murray’s Coaching Principles
Dr. Tye-Murray, a noted expert in Aural
Rehabilitation, has developed a set of principles for
use in coaching parents of children with hearing loss
(Tye-Murray, 2020). Remember that the emphasis of
habilitation process is on the function of communi-
cation and on linking learning within routine inter-
actions between the parent and child. These routines
provide families with a naturally occurring and sup-
portive framework to promote language and con-
versational abilities. These principles can be used to
guide the interaction between the professional and
the parent, and they include:
n When it comes to the child, the parents are the
experts because it is the parents, not the profes-
sional, who understand the child’s personality,
preferences, and routines, and the emphasis
must be placed on the parent–child relation-
ship not the professional–child relationship.
n Both the parents and the professional
must work together as members of a team,
giving them a balanced partnership in any
decision-making.
Components of a
Family-Centered Intervention
The role of the audiologist is to provide parents with
the information necessary to make informed deci-
sions for their child and to support the decision made
by the family. A family-centered approach reflects the
entire family unit, as it is not just the child who is being
treated but the family unit with all of its individual
members, some of whom may have unique needs and
challenges (Head & Abbeduto, 2007). When parents
feel empowered, children have better outcomes.
Figure 25–2 shows that in the early stage of aural
habilitation, the parents are the center of the family-
centered intervention and that it is the role of the
audiologist to support and coach them. In this model,
there are four components in which the audiologist
must support the parent. These components include:
providing information about hearing and technol-
ogy; developing consistent hearing device use in their
child; providing the parents with information on the
development of auditory skills; and, creating optimal
listening and learning environments. The audiologist
will educate the parents about hearing and their child’s
hearing loss. They will provide information on hearing
n The intervention program must be
driven by the family’s needs and desires.
The professional must learn to adapt to
the family’s values, culture, ethnicity,
socioeconomic status, and background
information.
n The professional must learn to utilize the
child’s toys and the family’s resources rather
than what they would bring so that learn-
ing strategies can be incorporated into the
families everyday activities.
n Parents must learn to attend to their child’s
attentional lead and to stimulate conversation
based on the child’s focus.
Having conversational strategies embedded
into play and caregiving routines by the parent
individualizes the intervention to the family where
it uniquely combines their personal and cultural
values, ecological constraints, and resources. These
principles can be used to strengthen the intervention
for the parent, child and professional in order for the
child to have the best outcome.
testing, amplification, and cochlear implant technol-
ogy. Another component is the development of consis-
tent hearing device use in the child. It is anticipated
that through the hearing aid evaluation, the amplifi-
cation device they choose will allow the child to hear
optimally. The next step is to keep the technology on
the child, consistent use is important to ensuring access
to sound but it is difficult to accomplish without sup-
port from the audiologist (Moeller, Hoover, Peterson, &
Stelmachowicz, 2009).
Information on auditory development will also be
provided by the audiologist. Parents need to under-
stand the auditory developmental milestones and how
to develop auditory skills in their child. Table 25–1 lists
some typical auditory development milestones and
provides an example of information that parents need
to acquire.
Parents will need to participate in creating the
optimum listening and learning environments for
their child. To do so, parents need to be taught spe-
cific listening and language facilitation techniques by
the audiologist. In turn, parents can use this informa-
tion to stimulate audition and language in the home
and become aware of listening and language learn-
ing opportunities in everyday activities. Therefore, by
 25  Aural Habilitation and Rehabilitation 365

Table 25–1.  Auditory Behaviors Exhibited by Children With Normal Hearing in the
First Year of Life

Child’s Age
Auditory Behavior (months) Auditory Example of Behavior
Quiets to sound 1 Baby will stop or quiet when he or she hears a
sound (i.e., while sucking on a bottle, baby will
stop sucking when he or she hears a sound)

Turns head to sound 3–6 Baby will stop and turn head when he or she
hears a novel sound (i.e., baby playing on floor
will stop and turn head when mother starts the
blender on the counter)

Localizes sound 6–9 Baby turns head to visualize where the sound is
coming from (i.e., baby sitting in highchair, turns
toward sibling as sibling walks up to right side)

Turns to locate a 9–12 When facing away, baby will turn around and
sound from behind acknowledge the sound (i.e., baby playing on
floor, and dog barks behind him or her, baby will
stop and turn around to locate the dog)

Note.  Parents of children with a hearing loss will need to acquire this as a part of their general knowl-
edge about auditory development.
Source:  Adapted from Pediatric Audiologic Rehabilitation: From Infancy to Adolescence, by E. Fitzpatrick
and S. P. Doucet, 2013, New York, NY: Thieme Medical Publishers.

using these four components, the audiologist can sup- Table 25–2.  Erber’s Hierarchy of Auditory Awareness
port and coach the parents to develop the child’s listen-
ing skills and spoken language in an enhanced family, Detection Knowledge of presence/absence
play and learning environment. of sound (may be turning, smiling,
stilling, searching, or vocalizing)

Auditory Training in Discrimination Tell that two sounds are different

Aural Habilitation quiet/loud, short/long
(not only detects, but also shows
Auditory training is the development of listening skills awareness through searching,
using auditory information; through which children smiling, head turning)
learn to listen and to make use of any residual hearing Identification Say it/repeat it (begins to understand
they may have. Children who use hearing aids benefit and add meaning to sounds)
from auditory training because they learn to use the
input from their devices to understand their auditory Comprehension Understand it (child begins to
understand connected speech)
world. Similarly, children who use cochlear implants
can learn through auditory training to interpret the
electrical signal and associate them with a particular
speech sound. Auditory training can be conceptual- Communication Options
ized in terms of the hierarchy of auditory development.
This hierarchy was first developed by Erber (1982) One decision that parents will need to make is that of
who described the building blocks for auditory skills communication mode,2 as described previously, the
development (described in Table 25–2). Table 25–3 role of the audiologist is to provide parents with suf-
shows an example of how the hierarchy is utilized with ficient information to make an informed decision and
young children. to support the decision they make. This decision can be

2 
 ommunication mode is the method by which a sender shares information with a receiver. The method can include speech, writing, symbols,
C
or hand gestures.
366 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Table 25–3.  Auditory Training Activities Appropriate for Each Stage of Auditory Skill Development

Auditory Skill Activity

Sound awareness Play peek-a-boo.
(Detection) Play musical chairs.
March to the beat of a drum.
Push the toy car whenever the clinician says “vrrrrm.”

Discrimination Play a game with toy animals (“The cow says ‘moo’ ”; “The sheep says ‘baaa’ ”).
Respond to commands (“Clap your hands”; “Jump!”).
Play a Same or Different game (“car car”; “car star”) using pairs of picture cards
where the child has to point to the correct illustration.
Repeat what you hear (“Mama”; “Papa”).

Identification Play the game Candy Land and listen for the names of the colors.
Play with sets of postcards or stickers (“Show me the cat”).
Play Go Fish with cards (“Give me your sevens”; “Give me your twos”).

Comprehension Listen to a read-aloud story and then answer questions about the plot and characters.
Play I Spy (“I spy a red sweater”; “I spy some blue jeans”).
Play 20 Questions (“Is it bigger than a chair?”; “Is it alive?”).

Source:  Reproduced with permission from Foundations of Aural Rehabilitation: Children, Adults, and Their Family Members
(5th ed., p. 400) by N. Tye-Murray, 2020, San Diego, CA: Plural Publishing, Inc. Copyright 2020 by Plural Publishing, Inc.

very difficult for parents and brings with it much emo-
tion and distress because of personal biases brought
forth by the many people/professions that the par-
ents come in contact with. Choices for communication
mode vary across a continuum from auditory to visual
as shown in Figure 25­–3. Families have to decide if they
want their child to be auditory or manual. Someone
who is auditory will rely on his or her auditory skills
to understand what is being said and his or her verbal
skills to communicate to others, whereas someone who
is manual will utilize a sign system.
American Sign Language (ASL) is a manual system
of communication used by many in the Deaf commu-
nity. ASL is its own language with its own vocabulary,
grammar, and social rules for use that are different from
English. Handshapes, palm orientation, location of the
hands, and facial expression are important components
of ASL. An individual who uses ASL is a fully visual
communicator (see Figure 25-3). Total communica-
tion is a visual system that incorporates more English-
based systems of signing (i.e., Signing Exact English)
with spoken English, mime, facial expression, and ges-
tures. This system has the intention of providing any
and all strategies necessary to bridge ASL and Eng-
lish, and supports the development of communication
and language. Cued speech is a visual communication
system in which phonemically based hand gestures
supplement speechreading. The mouth movements of
speech are combined with “cues” to make the sounds
(phonemes) of spoken language appear different. The
“cues” consist of eight handshapes which are used to
distinguish the consonant phonemes and four locations
near the mouth used to distinguish vowel phonemes,
when combined, a handshape and a location form a
syllable.
Auditory-oral and auditory-verbal systems are
similar to one another in that both use spoken lan-
guage. The auditory-oral approach encourages the use
of speechreading (i.e., watching the movement of the
mouth, face, and body to assist in the understanding
of what the speaker is saying). Auditory-verbal focuses
on using the child’s listening ability to learn spoken
language. These listening skills require consistent use
of amplification to access conversational speech and
utilize a systematic approach to increasing focused,
sustained auditory attention. As shown in Figure 25–3,
auditory-verbal communicators are fully auditory
communicators. The method of communication is a
personal/familial decision. Families will evaluate the
different methods across the continuum and make
their own decision, and the clinician is there to provide
information and to support their decision.

Fully
Auditory Auditory Auditory- Cued
Communicator Verbal Oral Speech
Auditory
Figure 25–3.  Families will need to choose a communication mode for their child, these modes are
shown as they extend across a continuum from auditory to visual. The more auditory the communication
mode, the further to the left; the more visual the mode, the further to the right.
Outcome Measures for Children
The final stage in the aural habilitation process is to
look at the outcomes of the intervention; at this stage, it
is important to assess the amount of improvement over
preintervention levels and to determine if the child is
on track with his or her normal-hearing peers. This
assessment of a child’s ability and comparison of results
with their peers is important not only for measuring
progress but also for determining further intervention
goals. To measure outcomes, the same tools from the
original assessment will be used. As the intervention
has emphasized the child’s usable hearing through an
appropriate amplification device, the outcome should
reflect this improvement. Most children who are identi-
fied early and receive optimal auditory and language
stimulation can develop spoken language skills com-
mensurate with age-matched peers. However, children
with hearing loss continue to benefit from intervention
during the preschool years.
Aural Rehabilitation
Aural rehabilitation (AR) is an intervention aimed
at restoring or optimizing a person’s participation in
activities and with others whom they have removed
themselves from because of their hearing loss (Tye-
Murray, 2020). It focuses on restoring a skill that is
lost, unlike habilitation as we discussed in the previ-
ous section. The objectives of AR are to alleviate the
difficulties related to the hearing loss and minimize
its consequences. It also seeks to work with and assist
families or communication partners of those with hear-
ing loss in adjusting to the impact of hearing loss. The
outcome of AR is to enhance the conversational fluency
and reduce the hearing-related disability of an individ-
25  Aural Habilitation and Rehabilitation 367
Fully
Total Visual
Communication ASL Communicator
Visual
ual with hearing loss (Tye-Murray, 2020). Unlike aural
habilitation that uses a family-centered approach, AR
uses a patient-centered approach in which the patient
is seen as an individual who is involved in his or her
own care and the decisions about the appropriate
intervention (Grenness, Hickson, Laplante-Lévesque,
& Davidson, 2014).
Assessment of Communication
Needs in Adults
As with children, the first step in an AR program is
to evaluate the individual’s overall hearing health.
This will require an audiological assessment includ-
ing a case history, and an audiometric evaluation (see
Chapter 23), and a hearing aid evaluation, including
self-assessment inventories (see Chapter 24). However,
other factors can influence an individual’s communi-
cation ability and should be evaluated, especially in
older adults. They include the individual’s social cir-
cumstances, emotional variables, living arrangements,
physical variables, reduced vision, arthritis, dementia,
and other cognitive variables. As a part of this assess-
ment, we also need to evaluate their activity limita-
tions, participation restrictions, and other contextual
factors. These assess how smoothly conversations
unfold, the time spent repairing conversational break-
downs, the amount of shared speaking time, and the
conversational time spent in silence.
Assessment Methods
Most of the testing performed by audiologists involve
measuring the patient’s response to a sound in some
fashion. However, some information can only be col-
lected directly from the patient. This is most often
368 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
accomplished through an interview, usually in the form
of a case history, where the clinician utilizes patient-
centered tools to determine personal characteristics of
the patient. The audiologist will utilize self-assessment
tools with both the patient and their communication
partners (usually their spouse). These tools take the
form of questionnaires, many which have been clini-
cally validated. Others are subjective impressions,
where the patient self-reports information about their
hearing and communication. These questionnaires use
either open-ended or closed-ended questions, both of
which have advantages and disadvantages. Examples
of highly respected questionnaires include: the Hear-
ing Handicap Inventory for Adults and Elderly (HHIA
and HHIE), International Outcome Inventory of Hear-
ing Aids (IOI-HA), Satisfaction with Amplification in
Daily Life (SADL), Self-Assessment of Communication
(SAC), and Significant Other Assessment of Communi-
cation (SOAC).
Another method of obtaining information from
the patient is through the use of daily logs; a procedure
where the patient monitors his or her behavior and self-
reports the outcome. A log is to be completed by the
patient over several consecutive days. Once completed,
these responses provide a general index of the patient’s
daily use of communication strategies, conversational
fluency, and communication difficulties.
Adult Intervention
The main component in any AR program is to make
sure that the patient is receiving optimal auditory input
and maximizing his or her residual hearing for daily
functioning. Following the audiological evaluation,
the audiologist will perform a hearing aid evaluation
using the steps laid out in Chapter 24. Depending on
the type and degree of hearing loss, the patient will be
fit with an appropriate style of hearing aid or a cochlear
implant. There are times, however, when hearing aids
or cochlear implants are not sufficient. Usually these are
the result of the distance between the sound source and
the listener, the background noise around the listener,
or the reverberant nature of the area. In these cases, the
listener may need to utilize additional assistance from
a hearing assistive technology system (HATS).
HATS is a general term for listening, alerting,
and/or signaling devices that facilitate patients’ com-
munication with other people and the environment or
enhance personal safety through the use of auditory,
visual, or tactile modalities. There are two types of
HATS: assistive listening devices (ALDs) and assistive
alerting devices (AADs). ALDs are designed to facili-
tate the reception of speech, to improve signal-to-noise
ratios or enhance communication with others usually
via amplification. An example of this technology is an
amplified telephone or FM system that allows a teach-
er’s voice to have a constant level no matter where the
student is in the room. The FM system also assists with
reducing background noise by amplifying the teacher’s
voice over the other noise in the room.
AADs are designed to react to alarm situations
and notify users that a situation is occurring. An exam-
ple is a light that flashes when the telephone rings or
a strobe light that flashes when the smoke detector is
activated. You may find it easy to get up for class in the
morning but how would you do it if you had a hear-
ing loss? This could be a difficult situation if you had a
hearing loss since you do not wear your hearing aids or
cochlear implant to bed. However there are ADDs that
can assist with this potential problem. One method to
wake a person is with the use of an alarm clock capa-
ble of shaking the bed, or vibrating under a pillow, or
flashing a strobe light.
Auditory Training in
Aural Rehabilitation
Auditory training is another major component of AR.
It is a process designed to maximally utilize an indi-
vidual’s residual hearing by enhancing their ability
to interpret auditory experiences (Sweetow & Sabes,
2009). In auditory training, the focus is on rehabilitat-
ing (retraining) skills that were previously in place and
providing training on “new” skills to accommodate for
an individual’s hearing loss. Through this process, the
clinician must teach the individual to take full advan-
tage of all of the auditory cues available. Like in aural
habilitation, the objectives for an auditory training pro-
gram in AR include: teaching the person to use his or
her amplification and take advantage of its features, to
maximize the perception of speech through the use of
auditory and other available cues, and to develop an
individual’s ability to recognize speech using the audi-
tory signal and to interpret his or her auditory experi-
ences (Tye-Murray, 2020).
There are two main methods used in auditory
training: analytic and synthetic. The analytic approach
breaks down speech into the smallest components
or features of the acoustic cue. Using this bottom-up
process with small speech segments (phonemes or syl-
lables), this method focuses on how hearing influences
communication. This method follows the four levels
from Erber’s hierarchy (see Table 25–2). In compari-
son, the synthetic approach uses a top-down process
to focus on the overall meaning of the discourse. With
an emphasis on auditory comprehension, it uses the

segments of speech (i.e., words, phrases, sentences),
as well as syntactic and contextual cues to allow the
user to fill in the missing gaps of information in a real-
world situation.
Auditory training programs using home-based
computer-delivered programs have increased in the
past few years (Lawrence et al., 2018). Results suggest
that there is a positive effect from these programs on
the speech perception and cognition in people with
hearing loss. This improvement is due to the targeted
auditory training on working memory, attention, and
communication (Pizarek, Shafiro, & McCarthy, 2013).
Computer programs such as Angel Sound, the Com-
puter-Assisted Speech Training (CAST), and the Lis-
tening and Communication Enhancement Training
(LACE) are widely used. The most well-known pro-
gram is LACE, a home-based, self-paced adaptive audi-
tory training program designed to improve listening
and communication skills. This training is composed
of 10 to 20 half-hour sessions taken over the course of
a 1-month period. LACE provides exercises for dif-
ficult listening situations and can adapt for cognitive
characteristics of the aging process that interfere with
effective communication. It combines listening training
(analytic) with repair strategies (synthetic) and gives
patient feedback regarding his or her performance.
Communication Strategies
When working with individuals with hearing loss, we
can train them to use strategies to enhance communi-
cation. A breakdown in communication can be caused
by a number of factors; however, there are two broad
Table 25–4.  Common Communication Problems and Recommended Repair Strategies
Communication Partner
Common Communication Problems
Listener only understood part of the message
Listener is unable to see the communication
partner’s mouth when he or she is speaking
Communication partner is speaking too quickly
Communication partner’s speech was too soft
Communication partner’s sentence was too long
Communication partner’s speech was not clear
The sentence was too complicated
25  Aural Habilitation and Rehabilitation 369
strategies that can be used to facilitate communication.
These strategies include anticipatory strategies and
repair strategies. Anticipatory strategies focus on good
communication habits and control of the environment.
These are things the listener can do to better prepare
for a successful communication encounter. In this strat-
egy, the listener tries to anticipate any difficulty and
prevent it from occurring. For example, after walking
into a room, the listener notices a band playing on the
left side and bright sunshine streaming through large
windows on the right side. For an optimum communi-
cation setting, the listener will want to have any con-
versations on the right side of the room with his or her
back toward the window so that he or she can minimize
background noise and optimize the speechreading
environment (see section on “Speechreading,” next).
In contrast, repair strategies are tactics used by
a listener with hearing loss when the message pre-
sented by a communication partner is not understood.
In other words, it is a way to fix the communication
breakdown after it has occurred. Repair strategies use
specific and effective tactics to help repair the com-
munication breakdown while reducing the stress from
any miscommunication. Table 25–4 shows a number of
common communication problems and their recom-
mended repair strategies.
Speechreading
Humans use both auditory and visual information
to understand communication. We combine auditory
signals with visual cues, including facial expressions
and gestures, and other available cues (i.e., setting and
Listener
Recommended Repair Strategies
1. Repeat the part you understood (e.g., “you flew to Paris?”)
2.  Ask for the part you did not understand to be repeated
Ask the partner to please put his or her hand down away
from the mouth when he or she is speaking
Ask the partner to please speak a little more slowly
Ask the partner to please speak a little more loudly
Ask the partner to please make the sentence shorter
Ask the partner to please speak a little more clearly
Ask the partner to please rephrase that in a different way
370 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
context) to interpret the meaning of communication.
In using this additional information (visual and con-
textual), we can enhance understanding communica-
tion in noisy situations (i.e., noisy airplane or subway)
when a message cannot be understood without seeing
the speaker’s face. The development of speechreading
skills can augment communication when an individual
has hearing loss. In other words, if a normal-hearing
individual uses speechreading in normal conversa-
tion, we can expect that individuals with a hearing loss
will also need to speechread to have effective commu-
nication. The hearing aid does not eliminate the need
to speechread but rather requires the user to com-
bine listening and speechreading to have optimum
communication.
Speechreading sounds like a simple thing, just
watch what a person is saying as if you are reading the
movement of his or her lips. However, in reality, it is
not that easy as 60% of sounds (e.g. /g, k, n/) are not
visible or easily seen. In addition, the rate of conversa-
tional speech is 150 to 250 words per minute or four to
seven syllables per second, which would be difficult
and taxing to follow in a long conversation. The level
of difficulty is also increased because sounds belong to
viseme groups and words are homophonous. Visemes
are groups of speech sounds that look the same on the
lips such as /b, m, p/, and homophones are words that
look the same on the lips (without sound) such as bat
and pat (Tye-Murray, 2020).
There are four factors that can affect the speechread-
ing situation: the talker, the message, the speechread-
ing environment/communication situation, and the
Table 25–5.  Individual Components for Each of the Four Factors That Can Influence Speechreading
Talker Message
Facial expressions Length
Diction Syntactic complexity
Body language Frequency of word
usage
Speech rate
Shared homophenes
Familiarity to the speechreader
Context
Accent
Facial characteristics
Speech prosody (intonation,
stress, and rhythm)
Objects in or over the mouth
Source:  Reproduced with permission from Foundations of Aural Rehabilitation: Children, Adults, and Their Family Members (5th ed., p. 132)
by N. Tye-Murray, 2020, San Diego, CA: Plural Publishing, Inc. Copyright 2020 by Plural Publishing, Inc.
speechreader. As shown in Table 25–5, each factor has a
number of components that can affect communication.
However, there are methods that can be employed to
help improve or at least minimize the problem. Within
speechreading, it is not sufficient to simply watch the
visemes and repeat them, but, rather, speechreaders
must also learn what will assist them in gathering addi-
tion information and how to make that change happen.
For example, if the talker is speaking rapidly and this
is hampering good communication, the speechreader
can learn that it is appropriate to ask the speaker to
slow down. Also, if the talker is obscuring his or her
mouth with a paper, the speechreader can learn to self-
advocate and ask the speaker to keep his or her mouth
visible. Issues with the speechreader and the environ-
ment are easily repaired because the speechreader can
manipulate them (i.e., move closer to the speaker).
Outcome Measures for Adults
The assessment of outcome measures in AR includes
four key domains: performance, benefit, usage, and
satisfaction of the device. These domains are mea-
sured by a variety of tests both on the amplification
device itself and in combination with the user. Verifi-
cation techniques are primarily used to determine if
the hearing aids meet a particular standard and are
performing appropriately. The use of electroacoustic
analysis including measures of the sound (e.g., inten-
sity) output and frequency response will determine if
the sound produced by the hearing aids is appropriate
Environment Speechreader
Viewing angle Lipreading skill
Distance Residual hearing
Background noise Use of appropriate amplification
Room acoustics Stress profile
Distractions Attentiveness
Fatigue
Motivation to understand
Language skills
Uncorrected vision impairment

for the hearing loss. As you may recall from Chapter 24,
performing only verification measures provides infor-
mation regarding how much gain the individual is
receiving but does not provide information about
whether this amount of gain is actually benefiting
them. After setting the prescriptive target for the ampli-
fication, we need to verify that the prescriptive targets
have been met and that the fitting is appropriate for
the user. This will determine whether the hearing aid
is working as desired on the user’s ear. The next step is
validation — through the use of functional gain, speech
perception, questionnaires, or interviewing, we can
determine how much benefit the user is receiving from
the hearing aids. Both verification and validation of the
fitting and function of the hearing aids are a part of
the AR process. These measures are described in Chap-
ter 24, and the reader is referred to those sections for
further information about the procedures.
Outcomes can also be determined for an individ-
ual’s speechreading ability and use of communication
strategies. A number of speechreading tests are avail-
able such as the Craig Speechreading Test and the NTID
Speechreading Test. These tests can be used pre and
post-evaluation of speechreading instruction to deter-
mine if sufficient improvement is being obtained. Com-
munication strategies can also be assessed through the
use of questionnaires and log books, which will assist
with determining if his or her goals have been reached.
Group Aural Rehabilitation
AR can take place individually, but it may also be
offered as a group activity. AR can also be provided to
individuals in a group setting, since adults are postlin-
gually deafened and thus require retraining of skills
that were lost. This is less complicated and requires less
individualization than facilitating the acquisition of
language. There are many benefits to individuals being
a part of a group AR program; these benefits impact
both the user and the clinician. Individuals, especially
adults, will benefit from the group interaction, the peer
support, and the improved self-sufficiency and emo-
tional well-being gained in an AR program. The clini-
cian benefits from being able to counsel multiple users
at a time thus increasing the number of people who can
be assisted. Furthermore, group AR allows the clinician
can help his or her patients use their new hearing aids,
which will lead to a reduction in the number of hear-
ing aids being returned. However, probably the biggest
benefit is in quality of life; people who have partici-
pated in group AR report an improvement in quality of
life indicators compared with those who do not attend
25  Aural Habilitation and Rehabilitation 371
group programs (Abrams, Chisolm, & McArdle, 2002).
Group AR has also been shown to improve a user’s
hearing aid satisfaction, help a user be more adept at
employing communication strategies, reduce the user’s
self-perceived hearing handicap, help a user be more
relaxed but also more assertive in communicative situ-
ations, and improve their emotional well-being and
coping behaviors. These improvements lead to a user’s
increased self-sufficiency and self-efficacy, improved
ability to address psychosocial influences on behavior,
improved socialization (the user knows he or she is not
the only one with a hearing loss), and will improve the
relationship with the clinic and audiologist.
When developing a group AR program you need
to consider the group, the number of sessions, and the
content. In determining the group composition, con-
sider the age and experience of the users and their com-
munication partners. It is important to include his or
her daily communicative partners (i.e., spouses, chil-
dren, or caregivers) as they will also benefit from the
program (Preminger, 2003). The size of the group is
also important, it should not be larger than 10 or 12, or
it will be too large to accomplish any meaningful work
or interaction. The number of sessions can be as few as
two or as many as 8 or 10. Different participants may
only be able to attend a few sessions, so different types
of programs may be required.
Not only do we need to consider the content and
the group makeup, but the facility is important as well.
For a successful program, you need to ensure that the
group members can hear and understand the content.
The meeting should be a held in a quiet room with
good lighting and a single table that participants can
sit around. It should also have ALDs with microphones
so all participants can hear and be heard by the other
members. Other assistive services such as closed cap-
tioning may be required depending on the content
delivery. The moderator needs to provide ground rules
for communication and address emotional reactions
(i.e., anxiety, frustration, fear, or shame). In some cir-
cumstances, it will be beneficial if the group members
determine the content for the sessions.
The content of an AR program should provide
information on problem management and managing
the emotional response to hearing difficulties (Oestreich,
2018). Problem management will focus on communica-
tion strategies; training, identifying and solving prob-
lems with communication (i.e., speechreading or other
strategies); self-advocacy; and, providing informational
lectures. These lectures can include information on
hearing aids, ALDs, and such obscure topics as travel-
ing with a hearing loss (i.e., communicating in a car or
your Americans with Disabilities Act [ADA] rights in a
372 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice
hotel). To target management of the emotional response
to hearing difficulties, participants can work on psy-
chosocial exercises and/or stress reduction training.
Chapter Summary
Aural Habilitation
The 1, 3, 6 rule is where infants must have their hearing
screened by 1 month, the diagnosis must be completed
and amplification fitted by 3 months, and the child
must be enrolled in intervention by 6 months.
Aural habilitation is an intervention for persons
who have not developed listening, speech, and lan-
guage skills. Activities are designed to teach the par-
ent how to help their child develop auditory skills and
create an optimal listening environment for their child.
After determining type and degree of hearing loss
in each ear, fitting the hearing aid, and establishing
exactly what the child hears, audiologists can gather
additional information about auditory behaviors in
everyday life from parents through the use of question-
naires that will complement other objective test results.
Examples: Parents’ Evaluation of Aural/Oral Perfor-
mance of Children (PEACH), Meaningful Auditory
Integration Scale (MAIS), and LittlEARS questionnaire.
Factors that affect the outcomes of a child’s audi-
tory development in a negative way include environ-
ment, family, and child. Factors that positively affect
the development of a child’s auditory skills include the
use of a family-centered approach, providing unbiased
information on all options, monitoring auditory devel-
opment at 6-month intervals, providing services in a
natural environment, and being sensitive to cultural
and language differences. In the early stages, the focus
is on parent support and education rather than on
“therapy” with the child.
Auditory training is the development of listen-
ing skills using auditory information. Children learn
to use the information from their amplification device
to understand the auditory input. This occurs as they
work through a hierarchy of auditory development
that includes detection, discrimination, identification,
and comprehension.
Parents will need to make a choice about the com-
munication mode their child will use. Audiologists
provide parents with information to make an informed
decision and supports the parent’s decision. Choices
for communication mode vary across a continuum
from auditory to visual and include auditory-verbal,
auditory-oral, cued speech, total communication, or
American Sign Language.
Children identified early and who receive optimal
auditory and language stimulation develop spoken
language skills commensurate with age-matched peers.
Aural Rehabilitation
AR is a patient-centered care intervention aimed at
restoring a hearing-impaired individual’s participa-
tion in activities. It also strives to alleviate difficulties
related to hearing loss; works with families or com-
munication partners to adjust its impact; enhances the
conversational fluency and reduces the hearing-related
disability of an individual with hearing loss.
Hearing aids or cochlear implants may not be
sufficient for communication; the listener may need
additional assistance from HATS. Either an ALD (to
facilitate the reception of speech, to improve signal-
to-noise ratios and communication with others) or an
AAD (to react to alarm situations and notify users that a
situation is occurring) can assist with various situations.
Home-based computer-delivered programs can
be used to improve working memory, attention, and
communication. Examples include Angel Sound, the
Computer-Assisted Speech Training (CAST), and the
Listening and Communication Enhancement Training
(LACE).
Strategies that help facilitate communication
include anticipatory strategies (focus on good com-
munication habits and on controlling the environment
to prepare for the communication encounter) or repair
strategies (fixing the communication breakdown after
it has occurred).
Speechreading involves use of visual information,
auditory information, facial expressions, gestures, and
any other available cues to interpret communication.
It is difficult because most sounds are not visible, and
conversation speech is rapid. Four factors that affect
the speechreading situation include the talker, the mes-
sage, the speechreading environment/communication
situation, and the speechreader.
Group AR benefits both the user and the clinician.
Individuals benefit through peer support as well as by
and improved self-sufficiency, emotional well-being,
and improved quality of life. Clinicians benefit from
being able to counsel multiple users at a time.
Group AR programs should include the par-
ticipants and their communication partners, have
fewer than 12 participants, and consist of no more
than 10 sessions. The programs need to occur in an
appropriate room with appropriate HATS. The con-
tent needs to include information on problem manage-
ment and managing the emotional response to hearing
difficulties.

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Index
Note:  Page numbers in bold reference non-text material.

22q11.2 Deletion syndrome, 273 AD (Alzheimer’s disease), 33, 126

Adduction, of vocal folds, 141
Admittance, 319
A Adults
AAA (American Academy of Audiology), 2, apraxia of speech, 23, 191, 193, 203–204
317 childhood compared with, 212–214
AAS (Adult apraxia of Speech), 121–122, terms, 192
203–204 language disorders
in adults, 121–122, 191, 193 aphasia, 114–125
compared with childhood apraxia of cerebral hemispheres and, 111–114
speech, 212–214 motor speech disorders
AAVE (African American Vernacular English), classification system, 191–203
48 described, 191
Abbreviated Profile of Hearing Aid Benefit dysarthria, 193
(APHAB), 345 Advanced stuttering, 233–234
ABR (Auditory Brainstem Response), Affricatives, 182, 185
328–332 development of, 188
Accent African American Vernacular English (AAVE),
described, 50 48
dialect and, 53 Age, swallowing and, 286
foreign, 53–54 Agents, defined, 73
language, 50–51 Air conduction, pure tone audiometry and,
Acoustic Theory of Speech Production, 154 325
Acoustics Air molecules, 293
described, 293 Airflow, lung pressure and, 132–133
events Allophones, 179–180
aperiodic, 296 Alpert syndrome, 273
periodic, 296 ALS (Amyotrophic lateral sclerosis), 201
phonetics, 169 Alzheimer’s disease (AD), 33, 126
reflex, 307 American Academy of Audiology (AAA), 2,
threshold, 323–324 317
signal American Academy of Speech Correction, 1
described, 293 American English
from talker, 3 consonants, compared to other languages,
speech, 154–158 175–176
assistive listening devices and, 159–160 vowels, compared to other languages, 172
sound filter/source, 154 American Sign Language (ASL), 93
Acquired stuttering, 238–239 American Society for the Study of Disorders
Actions, defined, 73 of Speech, 1

375
376 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

American Speech and Hearing Association (ASHA), 2 Audiologist, preparation for, 12–13
American Speech Correction Association, 2 Audiometric testing, 324–327
Amyotrophic lateral sclerosis (ALS), 201 pure tone, 325
The Angel’s Share, 52 results of, 334–335
Anomic aphasia, 119 Auditory
Anvil, 305 anatomy
Aperiodic, acoustic events, 296 temporal bone, 301–302
APHAB (Abbreviated Profile of Hearing Aid Benefit), tests of, 313
345 cortex, primary, 24
Aphasia, 114–125 implantable devices, 349–355
classification of, 114–125 nerve, 313
anomic, 119 pathways, 27–28, 313
apraxia of speech, 121–122 theories, of speech perception, 162–166
Broca’s, 116–117 training, aural habilitation, 365, 368–369
conduction, 117–118 tube, 307
global, 119–120 Aural habilitation, 360–367
primary progressive, 120–121 auditory training in, 365
Wernicke’s, 115–116, 117 communication needs
described, 114 of adults, 367–368
stroke and, 122–123 of children, 360–362
traumatic brain injury and, 124 communication options, 365–366
Applied science, described, 5 intervention
Apraxia, defined, 211 coaching model of, 363
Apraxia of speech, 23, 203–204 family-centered, 364–365
in adults, 121–122, 191, 193 pediatric, 362–363
childhood, 211–216 outcome measures, for children, 367
Arcuate fasciculus, 30–31 Aural rehabilitation, 367–372
Articulation adult intervention, 368
manner of, 174–175 auditory training in, 368–369
place of, 174 communication strategies, 369
Articulatory phonetics, 169 group, 371–372
ASD (Autism Spectrum Disorder) outcome measures, for adults, 370–371
defined, 89 speechreading, 369–370
language characteristics of, 89–91 Auricle, 303
morphology of, 90 Autism, incidence of, 89
phonology, 90 Autism Spectrum Disorder (ASD)
pragmatics and, 91 defined, 89
syntax and, 90 language characteristics of, 89–91
vocabulary and, 90–91 phonology, 90
ASHA (American Speech and Hearing Association), 2 pragmatics and, 91
ASL (American Sign Language), 93 syntax and, 90
Aspiration, 282 vocabulary and, 90–91
Assistive listening devices Automatic speech recognition, 159
auditory implantable devices, 349–355 Axon, 18
bone-anchored implant, 350–351
cochlear implant, 354–355
hearing aids, 343–349
B
rear-ear measures, 344–345 Babbling, 62
selecting/fitting, 343–349 described, 61–63
validation of, 345 BAI (Bone anchored implant), 349
middle ear implant, 351–354 Balance, disorders, 337
speech acoustics and, 159–160 Basal ganglia, 24
Ataxic described, 200
cerebral palsy, 221 lesions, 201
dysarthria, 197, 201, 224 neurological diseases and, 25
Spanish and, 198 Parkinson’s disease and, 145
 Index 377

Basal nuclei, 24 Cartilages, laryngeal, 138

Basilar membrane, 308–312 CAS (Childhood apraxia of speech), 121–122, 211–216
Beginning stuttering, 233 characteristics of
Behind-the-ear (BTE) hearing aid, 345 general, 214
Bench-to-bedside, 5 speech, 214, 215
Benedict, Ruth, 46 compared with adult apraxia of speech, 212–214
Bilateral cleft lips, 265 developmental delays and, 215
Bilingualism, 54–55 genetics and, 215–216
Biological theories prevalence of, 214
of stuttering, 235–238 CCC-A (Certificate of Clinical Competence in
anatomical differences, 235 Audiology), 2, 12–13
physiological (functional) differences, 236–237 CCC-SLP (Clinical Competence in Speech Language
Bolus, swallowing and, 284–286 Pathology), 12–13
Bone-anchored implant (BAI), 350–351 CDC (Centers for Disease Control and Prevention), 124
Bone conduction, pure tone audiometry and, 325 on autism, 89
Bony labyrinth, 307 Cell body, 18
Borderline stuttering, 232–233 Centers for Disease Control and Prevention (CDC), 124
Botulinum toxin, 256 on autism, 89
Bound morphemes, 40 Central nervous system (CNS)
Brain described, 17–18
adult language disorders and, 111–114 swallowing and, 283
connections between regions of, 112 Central sulcus, 22
dominant hemisphere, 29 Cerebellum, 27
frontal lobe, 22–23 Cerebral
hemispheres, 22 hemispheres
left, 23 adult language disorders and, 111–112
language and, 38 pediatric speech disorders and, 220–224
MRI of, 31–32 palsy
occipital lobe, 23 ataxic type of, 221
parietal lobe, 24 childhood speech disorders and, 220–224
pathology in dementia, 126–127 dyskinetic type of, 220–221
perisylvian speech and, 112–114 mixed type of, 221
structures of, 26 spastic type of, 220
temporal lobe, 23–24 Certificate of Clinical Competence in Audiology
tissues of, 18 (CCC-A), 2, 12–13
traumatic injury to, 124–125 Childhood apraxia of speech (CAS), 121–122, 211–216
language impairment in, 125–126 characteristics of, 215
tumors, dysarthria in, 225–226 compared with adult apraxia of speech, 212–214
view of developmental delays and, 215
from above, 22 genetics and, 215–216
left hemisphere, 23 prevalence of, 214
Brainstem, 26–27 Childhood speech disorders
Breathing, swallowing and, 282–283 apraxia of speech, 211–216
Broad phonetic transcription, 177 brain tumors and, 225–226
Broca’s aphasia, 116–117 cerebral palsy and, 220–224
Broca’s area, 23, 28–30 speech delay
adult language disorders and, 111 phonetic/phonological, 209–210
Bronx cheers, 61 quantitative measures of, 208–209
Brown, Roger, semantic categories, 73–74 speech sounds and, 208–209
BTE (Behind-the-ear) hearing aid, 345 traumatic brain injury and, 224–225
treatment options/considerations, 226–227
Childhood voice disorders, prevalence/treatment of,
C 257
Camp, Pauline, 2, 6, 13 Children, communication needs of, 360–362
Cancer, of larynx, 256–257 Children who stutter (CWS), 229
Canonical babbling, 63, 65 Children with velocardiofacial syndrome (VCFS), 273
378 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Chomsky, Noam, 57–58 phonetic symbols and, 174–176

language acquisition device (LAD) and, 43 manner of articulation, 174–175
Chromosomes, defined, 101 place of articulation, 174
CI (Cochlear implant), 349, 354–355 voicing, 175
CIC (Completely in-the-canal hearing aid), 348 Constraints, phonotactic, 180
Cleft Conversation
lip/palate (CL/P), 266–269 conversational repairs, 79–80
speech production in, 267–269 pragmatics and, 78
lips, 264–265 topic management, 79
palate turn-taking in, 79
isolated, 266–267 Conversational repairs, 79–80
with/without cleft lips, 266–267 Corpus callosum, 22
Clefting Cortex
epidemiology of, 267 hidden, 24
syndromes and, 272–273 insular, 24
Client Oriented Scale of Improvement (COSI), 345 perisylvian, 31
Clinical Competence in Speech Language Pathology primary
(CCC-SLP), 12–13 auditory, 24
Clinical Competence in Speech of Audiology (CCC-A), motor, 22
12–13 sensory, 24
Clinical work, review of, 7 Corticobulbar tract, 197
CL/P (Cleft lip/palate), 266–269, 272, 273–274 COSI (Client Oriented Scale of Improvement), 345
speech production in, 267–269 CPO (Isolated cleft palate), 266–267, 272, 273–274
Cluster reduction, 187 Cranial nerves, 27
CNS (Central nervous system), described, 17–18 Craniofacial anomalies
Coaching model of intervention, 363 defined, 261
Tye-Murray principles, 364 described, 261
Coarticulation, 149–150 upper lip/associated structures, embryological
Cochlea, 24, 305, 308 development of, 261–267
Cochlear implant (CI), 349, 354–355 Craniosynostosis syndrome, 273
Code switching, 52 Crouzone syndrome, 273
Cognitive-linguistic, described, 3 CT (Computed tomography), 32
Cognitive processes, language and, 42–44 Culture, defined, 45
Communication Curriculum, undergraduate, 10, 11
cultural factors influencing, 47 CWS (Children who stutter), 229
difference versus disorder, 47–48
Communication Sciences and Disorders
activities of, 2
D
as interdisciplinary field, 3–4 Davis, Barbara, 61–63
levels of evidence, 8–10 DBS (Deep brain stimulation), 25
required areas of knowledge, 4 Deacon, Terrence, 46–47
Compensatory errors, 270–272 Deafness genes, 92
Completely in-the-canal (CIC) hearing aid, 348 Deep brain stimulation (DBS), 25
Comprehension Deglutition, 277
language and Dementia, 33, 126–128
0 to 3 months, 60–61 language disorders in, 127–128
8 to 12 months, 65–66 Dendrites, 20
left hemisphere and, 112 Developmental chronologies, language, 58–66
Computed tomography (CT), 32 Developmental stuttering
Conduction aphasia, 117–118 diagnosis of, 231
Conductive hearing loss, 336 natural history of, 231–232
Consonants Diacritic symbols, 176, 178
American English compared to other languages, Diagnostic and Statistical Manual of Mental Disorders
175–176 on Autism Spectrum Disorder, 89
articulation, 270–272 on childhood-onset disorder, 229
imprecise, 193 criteria for, intellectual disability, 99
 Index 379

Dialect auditory nerve/pathways, 312

accent and, 53 basilar membrane, 308–312
code switching, 52 cochlea, 308
defined, 51 semicircular canals, 307–308
language and, 51–52 vestibule, 308
Dictionary of American Regional English, 46 middle, 305–307
Diffusion tensor imaging, 32–33 ligaments/muscles of, 306–307
Digital hearing aids, components of, 348 Eardrum, 304–305
Diphthongs, 147 Earmolds, hearing aids, 345
development of, 182, 188 Ebonics, 48
Discourse EBP (Evidence-based practice), 7–10
pragmatics and, 78 Embryological development, craniofacial anomalies,
turn-taking in, 79 261–267
Dominant hemisphere, brain, 29 Endoscopy, swallowing and, 287
Dopamine English, American, vowels compared to other languages,
basal ganglia and, 25 172
substantia nigra and, 199 Epidemiology
Dorsal stream, 30–31 clefting, 267
Down syndrome (DS), 100–104 Down syndrome, 101
epidemiology, 101 fragile X syndrome, 106
language and, 102–104 hearing impairment, 92
Dysarthria, 125, 193 voice disorders, 243–244
ataxic, 197, 201, 224 Equal-appearing interval scale, 193
Spanish and, 198 Erber’s hierarchy, 368
in brain tumors, 225–226 Esophageal phase, of swallowing, 282
dyskinetic, 222–223 Esophagus, swallowing and, 277
flaccid, 195–196, 201 Eustachian tube, 307
hyperkinetic, 200–201 Evaluation, hearing, 317–337
hypokinetic, 198, 201 acoustic reflex threshold, 323–324
mixed, 201 audiometric testing, 324–327
spastic, 196–197, 201, 221–222 case history, 318
subtypes, 193 immittance audiometer, 319–320
unilateral upper motor neuron, 201 otoscopy, 318–319
Dysfluencies patient examples, 337–341
stuttering, 232 physiological responses, 327–332
described, 232 speech audiometry, 326–327
Dyskinetic speech in noise, 327
cerebral palsy, 220–221 speech reception threshold, 326–327
dysarthria, 222–223 tympanometry, 320–323
Dysmorphogenesis, 264 word recognition score, 327
Dysphonia Evidence-based practice (EBP), 7–10
muscle tension, 252–254 Evidence, levels of, 8–10
treatment of, 253–254 Executive function, brain, 22
spasmodic, 200–201 Expression, language and, 0 to 3 months, 58–60
Dystonia External auditory
hyperkinetic dysarthria and, 200 canal, 303–304
oromandibular, 200 meatus, 303–304
Extrinsic muscles, 139
E
EAM (External auditory meatus), 303–304
F
Ear F (Frequency), 295
anatomy of, 303–313 F0 (Fundamental frequency), 245
outer, 303–305 intonation and, 245
canal, acoustic equivalent volume of the, 321 phonation and, 142–143
inner, 307–313 Face validity, 7–8
380 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Family-centered intervention, 364–365 Genotype, defined, 101

Fant, Gunner, 154 GERT (Gastroesophageal reflux disease), 289
Fast mapping, of spoken words, 71 Gesture, 66
FEES (flexible endoscopic evaluation of swallowing), 287 language and, 66
First pharyngeal arch syndrome, 273 GFTA (Goldman-Fristoe Test of Articulation), 208
Flaccid dysarthria, 201 Glia, 18
Imprecise, 195–196 defined, 18
Flanagan, James, 154 Glial cells, 18
Flat (Type B) tympanogram, 322 Glides, 147
Flexible endoscopic evaluation of swallowing (FEES), development of, 182
287 Global aphasia, 119–120
Fluency, recovering of, 234 Glottal stops, 272
Fluency stuttering disorders, 229–239 Glottis, 140
acquired, 238–239 Goldman-Fristoe Test of Articulation (GFTA), 208
advanced, 233–234 Grammatical
beginning, 233 morphemes, SLI/DLD and, 87
borderline, 232–233 morphology, 76–77
causes of, 234–238 development of, 72–74
developmental, 231–232 Gray matter, 18
dysfluencies, 231–232 Gross anatomy, described, 21–22
genetic studies, 231 Group aural rehabilitation, 371–372
incidence of, 229–230 Gyri, 22
natural history of, 230 Gyrus, 24
prevalence of, 229–230
treatment considerations, 239
fMRI (Functional magnetic imaging), 32–33
H
Foreign accent, 53–54 Habilitation, aural, 360–367
Formants, 156–158 Hammer, 305
Fragile X syndrome (FXS), 104–109 Hard palate, 264
Frame movement, 62 cleft, 266
Frame-then-content theory, 62 HATS (Hearing assistive technology systems), 368
Free morphemes, 40 Hearing
Frequency (F), 295 aids, 343–349
Fricatives, 147, 182, 185 components of, 348–349
development of, 188 in-the-canal (ITC), 346–348
stopping, 187 in-the-ear (ITE), 346
Friction, defined, 293 rear-ear measures, 344–345
Frontal lobe, 22–23 selecting/fitting, 343–345
Frontotemporal dementia (FTD), 126 types of, 345–348
FTD (Frontotemporal dementia), 126 validation of, 345
Functional magnetic imaging (fMRI ), 32–33 disorders, 337
Functional theory, of stuttering, 236–237 evaluation, 317–337
Functional voice disorders, 252–254 acoustic reflex threshold, 323–324
Fundamental frequency (F0), 245 audiometric testing, 324–327
intonation and, 245 case history, 318
phonation and, 142–143 immittance audiometer, 319–320
FXS (Fragile X syndrome), 104–109 otoscopy, 318–319
patient examples, 337–341
physiological responses, 327–332
G speech audiometry, 326–327
Gastroesophageal reflux disease (GERT), 289 speech in noise, 327
Genetics speech reception threshold, 326–327
childhood apraxia of speech and, 215–216 tympanometry, 320–323
defined, 101 word recognition score, 327
SLI/DLD and, 88 impairment
speech delay and, 211 adult language disorders and, 111–114
 Index 381

epidemiology of, 92 semicircular canals, 307–308

language characteristics in, 92–93 vestibule, 308
language delay and, 92–94 Insertions, muscle attachments, 139
speech/language development and, 93 Insula, 24
loss, 335–337 Insular cortex, 24
conductive, 336 Intellectual disability (ID), 99–100
mixed, 336 Intensity
sensorineural, 336 phonation and, 143–145
normal, 335–336 voice disorders and, 246
tests of, 313 International Clinical Linguistics and Phonetics
Hearing assistive technology system (HATS), 368 Association (ICPLA), 170
Hearing Handicap Inventory for Adults and Elderly International Outcome Inventory of Hearing Aids
(HHIA and HHIE), 368 (IOI-HA), 345, 368
HHIA (Hearing Handicap Inventory for Adults and International Phonetic Alphabet (IPA), 169–170
Elderly), 368 Intonation, pitch and, 65
HHIE (Hearing Handicap Inventory for Adults and Intrinsic muscles, 139
Elderly), 368 IOI-HA (International Outcome Inventory of Hearing
Hidden cortex, 24 Aids), 345, 368
Hierarchical, defined, 42 IPA (International Phonetic Alphabet), 169–170
High admittance (Type Ad) tympanograms, 323 Isolated cleft palate (CPO), 266–267
Hirano, Minoru, 140–141 ITC (In-the-canal) hearing aid, 346–348
Huntington’s disease ITE (In-the-ear) hearing aid, 346
basal ganglia and, 25
hyperkinetic dysarthria and, 200, 201
Hypercontraction, dystonia and, 200
J
Hyperkinetic dysarthria, 200–201 Jargon, 65
Huntington’s disease and, 200, 201
Hypernasality, 269
velopharyngeal insufficiency and, 270
K
Hyperreflexia, 197 Karyotype, defined, 101
Hypofunction, 249
Hypokinetic dysarthria, 198, 201
L
Labov, William, 50–51
I LAD (Language acquisition device), 43
ICPLA (International Clinical Linguistics and Phonetics Language
Association), 170 accent, 50–51
ID (Intellectual disability), 99–100 bilingualism and, 54–55
IDEA (Individuals with Disabilities Education ACT), 13 brain and, 38
Impairment code switching, 52
hearing cognitive processes and, 42–44
adult language disorders and, 111–114 components of, 38–42, 53
epidemiology of, 92 content, 40–42
language characteristics in, 92–93 morphology, 40
language delay and, 92–94 phonology, 38–40
speech/language development and, 93 syntax, 40
Impedance, 319 as a conventional system, 36
Imprecise consonants, 193 delay, hearing impairment and, 92–94
In-the-canal (ITC) hearing aid, 346–348 described, 35–36
In-the-ear (ITE) hearing aid, 346 developmental chronologies, 58–66
Incus, 305 dialect, 51–52
Individuals with Disabilities Education ACT (IDEA), 13 difference versus disorder, 48–50
Inner ear, 307–313 as a dynamic system, 36–37
auditory nerve/pathways, 312 expression, left hemisphere and, 112
basilar membrane, 308–312 form, 38
cochlea, 308 functions, lateralization of, 112
382 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Language  (continued) Laryngeal

as a generative system, 37 cartilages, 138
impairment, traumatic brain injury and, 125–126 hyperfunction, 249
mental representations and, 37–38 hypofunction, 249
multilingualism and, 54–55 Laryngopharyngeal reflux (LPR), 289
preverbal development of, 66 Larynx
semantics and, 40 cancer of, 256–257
social use of, 42, 125–126 laryngeal
structural components of, 125 muscles/membranes, 139
Language acquisition device (LAD), 43 cartilages, cartilages, 138
Language development, 69–70 phonation and, 141–145
0 to 3 months speech and, 138–145
expression (production), 58–60 upper airway and, 145–150
perception/comprehension, 60–61 velopharyngeal mechanism, 147–150
3 to 8 months vocal tract and, 146–147
perception/comprehension, 63–65 vocal folds and, 139–141
production, 61–63 Lateral sulcus, 22
8 to 12 months Lateralization of function, 28–29
perception/comprehension, 65–66 Learning theories, of stuttering, 235
production, 65 Left hemisphere, 113
gesture and, 66 language expression/comprehension and, 112
grammatical morphology, 72–74, 76–77 view of, 23
hearing impairment and, 93 Lesions, vocal fold, benign, 251
linguistic sophistication, 74 Levels of evidence, 8–10
mean length of utterance, 74–76 Lewy body dementia, 126
multiword utterances, 72–74 Lexical stress pattern, 180
school years, 77–81 Linguistic
complex sentences, 81 sophistication, 74
conversation repairs, 79–80 wordplay, 78
linguistic wordplay, 78 Lips
metalinguistic skills, 77–78 cleft, 264–265
narrative, 80–81 with/without cleft palate, 266–267
pragmatics, 78 palate, 265–266
sample transcript, 81–82 upper airway and, embryological development of,
topic management, 79 261–267
turn-taking, 78–79 roundings, vowels and, 172
stages of, 70 Liquids, 147, 182–184
12 to 18 months, 71 development of, 185
18 to 24 months, 71–72 swallowing, 280
36 months, 72 Locatives, defined, 73
Language disorders Loudness
adult, cerebral hemispheres and, 111–114 psychoacoustics and, 299
adult language disorders and, aphasia, 114–125 voice disorders and, 246
dementia and, 33, 126–128 LPR (Laryngopharyngeal reflux), 289
pediatric Lung pressure
autism spectrum disorder, 89–92 airflow and, 132–133
Down syndrome, 100–104 voice loudness and, 137
fragile X syndrome, 104–109
hearing impairment and, 92–94
SLI/DLD, 85–89
M
speech delay, 206–211 MacNeilage, Peter, 61–63
Language use, 42, 78 Magnetic resonance imaging (MRI), brain activity, 31–32
Down syndrome, 104 functional (fMRI), 32–33
fragile X syndrome, 108–109 Malleus, 305
hearing impairment and, 94 Mandibular arch, 262
 Index 383

Mandibulofacial dysostosis, 273 vocal tract, 146

Mayo Clinic System for Classification of Dysarthria, Mutation, defined, 101
193–195 Myelin, 21
Mean length of utterance (MLU), 74–76 described, 18
Medulla, 26
Mehler, Jacques, 61
MEI (Middle ear implant), 349, 351–354
N
Membranes Narrative, 80–81
basilar, 308–312 phonetic transcription, 177
laryngeal, 139 Nasals, 147
tympanic, 304–305 development of, 182, 188
Metalinguistic skills, 77–78 National Acoustic Laboratories, 344
Midbrain, 26 National Institute of Deafness and Other
Middle ear, 305–307 Communication Disorders (NIDCD), 317
implant (MEI), 349, 351–354 National Institutes of Health (NIH), 5
ligaments/muscles of, 306–307 Natural frequency of vibration, 297
Mixed Negative pressure (Type C) tympanogram, 323
dysarthria, 201 Nervous system
hearing loss, 336 adult language disorders and, 111–114
type of cerebral palsy, 221 cells, 18
MLU (Mean length of utterance), 74–76 described, 17–18
Molecules, air, 293 gross anatomy of, 21–22
Monogenic, defined, 101 swallowing and, 283
Morphemes, 40 Neural mechanism, 313
SLI/DLD and, 87 Neuroanatomy, described, 21–22
Morphology Neurodiagnostic ABR, 330–331
ASD and, 90 Neurodiverse, 89
Down syndrome, 103 Neurogenic stuttering, 238–239
fragile X syndrome, 107–108 Neuron, described, 18–21
hearing impairment and, 94 Neurotransmitter, 20
Motor cortex, primary, 22 Neurotypical, 89
Motor speech disorders in adults NIDCD (National Institute of Deafness and Other
apraxia of speech, 191, 193 Communication Disorders), 5, 317
classification system for, 191–203 NIH (National Institutes of Health), 5
described, 191 Nodules, vocal tract, 250–251
dysarthria, 193 Noise, defined, 145
terms, 192 Nonsignaling cells, 18
Motor theory of speech perception, 160–166 Normal admittance (Type A) tympanogram, 321–322
MRI (Magnetic resonance imaging), brain activity, 31–32 Normal hearing, 335–336
functional (fMRI), 32–33 Nuclei, subcortical, 24–26
MS (Multiple sclerosis), 201
myelin and, 18
MTD (Muscle tension dysphonia), 252–254
O
treatment of, 253–254 OAE (Otoacoustic emissions), 327–328
Multilingualism, 54–55 Objects, defined, 73
Multiple repetitions, stuttering, 231 Obligatory errors, 270
Multiple sclerosis (MS), 201 Occipital lobe, 23
myelin and, 18 Oller, D. Kimbrough, 58, 63
Multiword utterances, 72–74 Oral
Muscle tension dysphonia (MTD), 252–254 preparatory phase, of swallowing, 280
treatment of, 253–254 transport phase, of swallowing, 280
Muscles Organ of Corti, 308–312
extrinsic, 139 Organic voice disorders, 252
intrinsic, 139 Origins, muscle attachments, 139
laryngeal, 139 Oromandibular dystonia, 200
384 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Oscillation, 294–295 Pharyngeal

Ossicles, 305–306 arches, 262
Otoacoustic emissions (OAE), 327–328 phase of swallowing, 280–282
Otoscopy, 318–319 Phenotype, defined, 101
Outer ear, anatomy of, 303–305 Phonation
Overextension, language and, 71 characteristics of, 142–145
intensity and, 143–145
Phonemes, 38–39
P defined, 179
Palate, cleft, with/without cleft palate, 266–267 Phonetic
Palatine shelves, 263 development, 181
Palatoplasty, 272 inventory, 38–39
Paralinguistic, 66 speech delay, 209–210
described, 66 symbols, 153
function, 137 consonants and, 174–176
Parietal lobe, 24 vowels and, 170–173
Parkinson’s disease (PD), 145 transcription, 69, 159, 166, 169, 176
basal ganglia and, 25 broad, 176, 177
Pathways, auditory, 27–28 clinical implications of, 176–177
Patterns of Culture, 46 Phonetically balanced (PB) words, 327
PB (phonetically balanced) words, 327 Phonological
PCC (Percentage of consonants correct), 207–208 development, 181, 186–188
PD (Parkinson’s disease), 145 work learning and, 188
basal ganglia and, 25 learning, 186
Pediatric speech delay, 209–210
intervention, 362–363 Phonology, 38–40
language disorders ASD and, 90
autism spectrum disorder, 89–92 defined, 141
Down syndrome, 100–104 Down syndrome, 102–103
fragile X syndrome, 104–109 fragile X syndrome, 106–107
hearing impairment, 92–94 hearing impairment and, 93
SLI/DLD, 85–89 larynx and, 141–145
speech delay, 203–211 SLI/DLD and, 86–87
voice disorders, 257 Phonotactic
Penfield, Wilder, 30 constraints, 180
People who stutter (PWS), 229 rules, 39–40
Percentage of consonants correct (PCC), 207–208 Phonotrauma, 249–252
Perception treatment of, 251–252
language and Physiological differences theory, of stuttering, 236–237
0 to 3 months, 60–61 Pinna, 303
3 to 8 months, 63–65 Pitch, 245
8 to 12 months, 65–66 intonation and, 65
speech, 160–166 phonation and, 142–143
auditory theories of, 162–166 psychoacoustics and, 298–299
Perceptual phonetics, 169 PNS (Peripheral nervous system), described, 17–18
Periodic Polygenic, defined, 101
acoustic events, 296 Polyps, vocal fold, 251
motion, 295 Pons, 26
vibrations, 294 Pragmatics, 42, 78
Peripheral nervous system (PNS) Down syndrome, 104
described, 17–18 fragile X syndrome, 108–109
swallowing and, 283 hearing impairment and, 94
Perisylvian traumatic brain injury and, 125–126
cortex, 31 Praxis, defined, 211
speech, brain and, 112–114 Preverbal
Persistent speech sound errors, 209–211 language development, 66, 71
 Index 385

speech and language development, 57 Semicircular canals, 307–308

Primary Sensorimotor skills, 60–61
auditory cortex, 24 Sensorineural hearing loss, 336
motor cortex, 22 Sensory cortex, primary motor, 24
progressive aphasia, 120–121 Sentences, complex, 81
sensory cortex, 24 Significant Other Assessment of Communication
Production, language and (SOAC), 368
3 to 8 months, 61–63 SLDs (Stuttering-like dysfluencies), 231
8 to 12 months, 65–66 SLI/DLD (Specific language impairment/developmental
Protowords, 65 language disorder), 85–89
Psychoacoustics, 297–298 cause of, 88
loudness and, 299 genetics and, 88
pitch, 298–299 language characteristics of children with, 86–88
sound quality and, 299–300 grammatical morphemes, 87
Psychogenic theories, of stuttering, 234 phonology, 86–87
Puberphonia, 254–255 syntax, 87
Public Law 94-142, 13 vocabulary, 87–88
Pure tone audiometry, 325 summary of, 88
PWS (People who stutter), 229 SLP (Speech-language pathologist), 10, 145, 185
consonant errors and, 270
end goal of, 226
Q preparation for, 10–12
Quality, voice, 145 swallowing disorders and, 288–289
Quasi-resonant nuclei, 58 SOAC (Significant Other Assessment of
Communication), 368
Social communication disorder, 92
R Soft palate, 264
Randomized control trials (RCTs), 8–9 cleft, 266
RCTs (Randomized control trials), 8–9 Solids, swallowing and, 280
REAR (Rear-ear aided response), 345 Somatotropic representation, 23
Rear-ear aided response (REAR), 345 Sound
Rear-ear measures, 344–345 filter, 154
Reduced admittance (Type As) tympanogram, 323 production, vocal tract growth and, 59–60
Reduplicative babbling, 61 quality, psychoacoustics and, 299–300
Research Grants for Translating Basic Research into Clinical source of, 154
Tools, 5–6 vowel, 155–156
Residual speech sound errors, 209–210 Spanish, ataxic dysarthria and, 198
Resonance, 297 Spasmodic dysphonia (SD), 200–201, 256
Resonant frequency, 59, 297 Spastic
vowels and, 156–158 cerebral palsy, 220
Respiratory system dysarthria, 196–197, 201, 221–222
speech and, 131–137 Specialization of function, 28
vegetative breathing and, 133–134 Species-specific, defined, 160
Respirometer, 133 Specific language impairment/developmental language
Rest breathing, 133–134 disorder (SLI/DLD), 85–89
Rhotics, 147 cause of, 88
genetics and, 88
language characteristics of children with, 86–88
S grammatical morphemes, 87
SAC (Self-Assessment of Communication), 368 syntax, 87
SADL (Satisfaction with Amplification in Daily Life), 368 vocabulary, 87–88
Sample size, 48 obtaining a Clinical Competence in Speech-Language
Satisfaction with Amplification in Daily Life (SADL), 368 Pathology, 12
SD (Spasmodic dysphonia), 200–201, 256 phonology, 86–87
Self-Assessment of Communication (SAC), 368 preparation for, 10–12
Semantics, 40 summary of, 88
386 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Spectrograms, of formant frequencies, 156–158 end goal of, 226

Spectrum, waveform and, 295–297 preparation for, 10–12
Speech swallowing disorders and, 288–289
acoustics, 154–158 Speechreading, 369–370
assistive listening devices and, 159–160 Sphenopalatineganglioneuralgia, 284
sound filter/source, 154 Spinal cord, 27
acts, 42 Spirogram, 133
audiometry, 326–327 Spirometer, 133
breathing, 134–137 Standardized tests, 48, 86
abdominal muscles and, 136–137 language difference versus disorder, 48–50
goal of, 134, 136 Stapedius muscle, 306–307
intelligibility and, 137 Stapes, 305
voice loudness and, 137 Stevens, Kenneth, 154
delay, 206–211 Stickler syndrome, 273
disorders in childhood, 208–210, 224–227 Stinchfield, Sara Mae, 1
apraxia of speech, 211–216 Stirrup, 305
brain tumors and, 225–226 Stomach, swallowing and, 278
cerebral palsy and, 220–224 Stopping the fricatives, 187
diagnosis of, 207–208 Stops, 147
genetics and, 211 development of, 182, 188
phonetic/phonological, 209–210 Stuttering, 229–239
quantitative measures of, 208–209 acquired, 238–239
sounds and, 208–209 advanced, 233–234
traumatic brain injury and, 224–225 beginning, 233
treatment options/considerations, 226–227 biological theories of, 235–238
development, hearing impairment and, 93 anatomical differences, 235
in noise, 327 physiological (functional) differences, 236–237
intelligibility, 165–166 borderline, 232–233
speech breathing and, 137 children, 229
lateralization of, 112 causes of, 234–238
mechanism developmental
larynx, 138–145 diagnosis of, 231
respiratory system, 131–137 natural history of, 231–232
upper airway, 145–150 dysfluencies
motor control described, 231
maturation of, 184–185 typical, 232
stuttering and, 237–238 functional theory of, 236–237
MRI and, 31–32 genetic studies, 231
perception, 160–166 incidence of, 229–230
auditory theories of, 162–166 learning theories, 235
motor theory of, 160–166 natural history of, 230
processing, maturation of, 185–186 prevalence of, 229–230
reception threshold, 326–327 psychogenic theories of, causes of, 234
recognition, 159 speech motor control and, 237–238
science, described, 131 treatment considerations, 239
sounds, 206–207 Stuttering-like dysfluencies (SLDs), 231
development of, 181–183, 186–188 Subcortical nuclei, 24–26
errors, residual/Persistent, 209–210 Substantia nigra
explanations for mastery 183–186 dopamine and, 199
influences, 163, 165 hypokinetic dysarthria and, 201
top-down Sulci, 22
vocal tract valving and, 149 Swallowing
synthesis, 159 act of, 278–282
teachers, 1 esophageal phase, 282
Speech-language pathologist (SLP), 10, 145, 185 oral preparatory phase, 280
consonant errors and, 270 pharyngeal phase, 280–282
 Index 387

analysis of, 286–289 language impairment in, 125–126

anatomy of, 277–278 nature of brain injury in, 124–125
esophagus, 277 Treacher-Collins syndrome, 273
stomach and, 278 Tube model, vocal tract, 158
breathing and, 282–283 Turn-taking, 78–79
client self-report, 287–288 Tympanic membrane, 304–305
expiration-swallow-expiration, 282–283 Tympanograms, types of, 321–323
health care team for, 288–289 Tympanometry, 320–323
measurement of, 286–289 Type A tympanogram, 321–322
nervous system control of, 283 Type Ad tympanograms, 323
variables influencing, 284–286 Type As tympanogram, 323
bolus, 284–286 Type B tympanogram, 322
Sword throats, 285 Type C tympanogram, 323
Sylvian fissure, 22, 112–113
Synapse, 21
Syndromes, clefting, 272–273
U
Syntax Underextension, language and, 71
ASD and, 90 Undergraduate curriculum, 10, 11
Down syndrome, 103 Unilateral
fragile X syndrome, 107–108 cleft lips, 265
hearing impairment and, 94 upper motor neuron dysarthria, 201
SLI/DLD and, 87 vocal fold paralysis, 254–255
Synthesis, speech, 159 Unstressed syllable deletion, 187
Upper airway
larynx and, 145–150
T velopharyngeal mechanism, 147–150
Tacoma Narrows Bridge, 297 vocal tract and, 146–147
TBI (Traumatic brain injury) Upper lip, embryological development of, 261–267
aphasia and, 124 Upper motor neuron disease (UUMN), dysarthria, 197,
childhood speech disorders and, 224–225 201
dysarthria in, 225 UUMN (Upper motor neuron disease), dysarthria, 197,
language impairment in, 125–126 201
nature of brain injury in, 124–125
Temporal
bone, 301–302
V
lobe, 23–24 Van Riper, Charles, 1, 2
Tensor tympani muscle, 306 Variegated babbling, 65
Terminal buttons, 20 VC (Vital capacity), 134
Thalamus, 24 VCFS (Children with velocardiofacial syndrome), 273
Thordardottir, Elin, 72, 74 Vegetative breathing, 133–134
Threshold ABR, 331–332 Velocardiofacial syndrome, 273
Tongue Velopharyngeal insufficiency (VPI), 269–270
advancement, tongue advancement and, 171–172 consonant articulation and, 270–272
embryological, 263 hypernasality and, 270
Top-down influences of speech sounds, 165 Velopharyngeal mechanism, 147–149
Tourette’s syndrome, basal ganglia and, 25 Velopharyngeal port (VP), 148, 268–269
Transcription VEMPs (Vestibular-evoked myogenic potentials),
phonetic, 69, 159, 166, 169, 176, 177 333–334
broad, 176 Ventral stream, 30–31
clinical implications of, 176–177 Vestibular assessment, 332–334
narrow, 177 Vestibular-evoked myogenic potentials (VEMPs),
Translational research, 5, 6 333–334
Traumatic brain injury (TBI) Vestibule, inner ear, 308
aphasia and, 124 Vestibulo-ocular reflex (VOR), 332
childhood speech disorders and, 224–225 Vestibulospinal reflex (VSR), 333
dysarthria in, 225 Vibration, natural frequency of, 297
388 Introduction to Communication Sciences and Disorders:  The Scientific Basis of Clinical Practice

Videofluoroscopy, swallowing and, 286–287 loudness and, 246

Videonystagmography (VNG), 333 muscle tension dysphonia, 252–254
Vihman, M.M., 59–60 neurological, 254–256
Visual Analog Scale, 165–166 organic, 252
Vital capacity (VC), 134 parameter measurement, 245
VNG (Videonystagmography), 333 phonotrauma, 249–252
Vocabulary quality and, 246–247
12 to 18 months, 71 spasmodic dysphonia, 256
18 to 24 months, 71–72 spectrum and, 246–247
36 months, 72 vocal folds and, unilateral paralysis of, 254–255
ASD and, 90–91 Voice loudness
Down syndrome, 103–104 lung pressure and, 137
fragile X syndrome, 108 speech breathing and, 137
SLI/DLD and, 87 Voicing, consonants, 175
Vocal VOR (Vestibulo-ocular reflex), 332
folds, 139–141 Vowels, 147
adduction of, 141 American English compared to other languages, 172
benign lesions, 251 development of, 182, 188
polyps, 251 lip rounding and, 172
unilateral paralysis of, 254–255 phonetic symbols and, 170–173
viewing, 244–245 tongue height and, 170–171
nodules, 250–251 resonant frequencies of, 156–158
tract sounds of, 155–156
muscles of, 146 tongue advancement and, 171–172
shape of, 146–147 VP (Velopharyngeal port), 148, 268–269
sound production and, 59–60 VPI (Velopharyngeal insufficiency), 269–270
tube model of, 158 consonant articulation and, 270–272
valving, 149 hypernasality and, 269–270
Vocalic production, 146–147 VSR (Vestibulospinal reflex), 333
Voice
perceptual evaluation of, 244
quality of, 145
W
Voice disorders Waveform, 295
childhood, 257 spectrum and, 295–297
classification of, 247–257 Wernicke, Carl, 29, 117
functional, 252–254 Wernicke’s aphasia, 115–116, 117
hypo-hyperfunction continuum, 247–252 Wernicke’s area, 28–30
neurological, 254–257 adult language disorders and, 111
described, 243 White matter, 18
diagnosis of, 244–247 Word recognition score, 327
case history, 244 Wordplay, linguistic, 78
epidemiology of, 243–244 Words
functional, 252–254 fast mapping, 71
hypo-hyperfunction continuum, 248–249 speech sound components, 77
intensity and, 246 Work learning, phonological development and, 188