Understanding Voice Problems

A Physiological Perspective for Diagnosis and Treatment

FOURTH EDITION
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Understanding Voice Problems

A Physiological Perspective for Diagnosis and Treatment
FOURTH EDITION
Raymond H. Colton, Ph.D.
Professor Emeritus, Department of Communication Sciences and Disorders
Syracuse University, Syracuse, New York;
Professor Emeritus, Department of Otolaryngology and Communication Sciences
Upstate Medical University, Syracuse, New York

Janina K. Casper, Ph.D.

Professor Emeritus, Department of Otolaryngology and Communication Sciences
Upstate Medical University, Syracuse, New York

Rebecca Leonard, Ph.D.

Professor, Dept. Otolaryngology/HNS
University of California, Davis

With Contributions From:

Susan Thibeault, Ph.D.
Associate Professor
Departments of Surgery, Communicative Disorders and Biomedical Engineering
University of Wisconsin-Madison
Marie E. Jette, MS
Department of Communicative Disorders
University of Wisconsin-Madison
Madison, WI
Richard Kelley, M.D.
Assistant Professor, Department of Otolaryngology and Communication Sciences
Upstate Medical University, Syracuse, New York
Selected Color Photographs by Eijii Yanagisawa, M.D.
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Acquisitions Editor: Peter Sabatini

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Library of Congress Cataloging-in-Publication Data

Colton, Raymond H., author.
Understanding voice problems : a physiological perspective for diagnosis and treatment /
Raymond H. Colton, Rebecca Leonard. – Fourth edition.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-60913-874-5 (hardback : alkaline paper)
1. Voice disorders–Pathophysiology. I. Leonard, Rebecca, author. II. Title.
[DNLM: 1. Voice Disorders–physiopathology. 2. Voice Disorders–therapy.
3. Larynx–physiology. 4. Voice Disorders–diagnosis. WV 500]
RF510.C65 2011
616.85 5–dc22 2010045739

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CONTENTS

Preface vii

1. Introduction and Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

2. Differential Diagnosis of Voice Problems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
3. Morphology of Vocal Fold Mucosa: Histology to Genomics . . . . . . . . . . . . . 63
4. Phonotrauma: Its Effects on Phonatory Physiology . . . . . . . . . . . . . . . . . . . . . 75
5. Voice Problems Associated with Nervous System Involvement . . . . . . . . . . 113
6. Voice Problems Associated with Organic Disease, and Trauma . . . . . . . . . 165
7. Voice Problems Associated with the Pediatric and the Geriatric Voice . . . 187
8. The Voice History, Examination, and Testing . . . . . . . . . . . . . . . . . . . . . . . . . 213
9. Surgical and Medical Management of Voice Disorders . . . . . . . . . . . . . . . . . 273
10. Vocal Rehabilitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 313
11. Voice and Laryngectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 360
12. Anatomy of the Voice Production Mechanism. . . . . . . . . . . . . . . . . . . . . . . . . 372
13. Phonatory Physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 386
14. Neuroanatomy of the Vocal Mechanism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 397
15. Some Normative Data on the Voice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407

APPENDIX
Forms Used in Voice Evaluation: Clinic and Laboratory . . . . . . . . . . . . . . . . . . . 417

References 435
Figure and Table Credits 470
Index 475

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PREFACE

ithin the last 35 years or so, we have been witness to an explosion of interest in the voice by
W clinicians, scientists, physicians, and singers. This multidisciplinary interest in the voice has
led to a remarkable sharing of knowledge through the establishment of voice clinic teams, the
publication of dedicated scholarly journals, electronic communication, and an abundance of conferences
spanning not only a broad range of topics but also spanning the globe.
We are indebted to those who pioneered and pursued an interest in phonation, in how the larynx
works, and in how to alter or correct its function. They persevered despite criticism by some who found
these early efforts lacking in scientific stringency. We, our students, and our patients, are the beneficiaries
of their persistence. Nevertheless, much remains to be done. Although heartened and encouraged by
the increasing numbers of scientists and clinicians, teachers, and singers interested in study of the larynx
and voice production, we are dismayed by its continuing “stepchild” status in training programs for
speech–language pathologists and otolaryngologists and in singing pedagogy programs.
That, in large measure, is the reason for this book. We have been fortunate in being part of an inter-
disciplinary team that has studied normal and disordered phonation both clinically and experimentally
for many years. Through this experience, we have evolved a philosophy and framework for the examina-
tion of laryngeal function and for clinical management of the voice-disordered patient that differed from
others in its emphasis. Over the years, we have presented our ideas in many lectures and courses and, if
we are to judge by feedback received, have found our approach to be well received and helpful. Indeed,
the team approach to voice disorders has become the norm and is practiced in many hospitals, clinics,
and other facilities where the diagnosis and treatment of voice disorders occurs. That approach was our
guide, which led to the first edition of this book. We intended it to be used by students and practitioners
alike in all of the specialty areas involved in the management of the voice, including otolaryngology,
speech–language pathology, and coaching of the singing and dramatic voice. We intended this book to
be used as a reference text by other medical specialists, such as pediatricians, family practitioners, and
internists, who might be the first to come in contact with the patient with a voice disorder. Indeed, with
the burgeoning of managed care, this may be increasingly the case and the primary source of referral for
examination and treatment.
The first three editions of the book have been well received and are used in many of the training
programs in the United States and in parts of the rest of the world. In previous editions, we updated
and expanded many sections to reflect current practice and new knowledge. That same aim is reflected
in this edition. We believe that understanding voice disorders must begin with an understanding of
normal phonatory physiology and acoustics. Based on such knowledge, the student, speech–language
pathologist, or otolaryngologist can better understand the pathophysiology that results from misuse,
abuse, pathology, or neurological involvement. Because there is not a one-to-one relationship between
physiology and acoustics, it is not always possible to predict specific pathology or alterations in physiology
on the basis of acoustics or perception alone. Thus, neither acoustic nor perceptual data are sufficient
for the diagnosis and treatment of voice disorders. Knowledge of the pathophysiology together with
understanding the acoustic and perceptual factors and individual psychodynamics must all be added to
the equation in determining diagnosis and planning treatment.
We are firm advocates of the differential diagnosis model and have attempted to emphasize that
throughout the text. A differential diagnosis can only be carried out if it is based on knowledge. Indeed,
one of the fascinations of the area of voice is the amalgamation of knowledge from various fields that
must be brought to bear on the diagnostic process. The team approach is thus an ideal mechanism to
support this need. The approach to management has at its core the normalization of physiology, which

vii
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viii Preface

we believe will bring with it normalized phonation. When normalization is not a realistic goal due to
structural or neuromotor constraints, then the approach builds on making the most of what remains
functional. The choice of therapy technique is predicated upon a knowledge-based problem-solving
approach, rather than on an uninformed gunshot approach. The “if it works, use it” approach may be
occasionally successful but may be totally inappropriate at other times. It is important to know when
to use a technique and to be able to at least speculate about why it works or fails to do so. We firmly
believe that wherever possible, a technique used in voice treatment should be based on a firm theoretical
basis, have solid scientific evident, and work clinically. The clinician must understand the nature of
the altered physiology, must take into account the psychological dynamics that may be operative, and
must then be able to select an appropriate approach to rehabilitation that will address these issues. The
intertwined relationship between the voice and the person is an essential component in both diagnosis
and management. However, even in the patient with a psychologically based voice disorder, the deviations
in the manner of voice production and voice use must be understood.
In writing this book, we have presumed that the reader will have been exposed to the study of
laryngeal anatomy, physiology, neuroanatomy, and neurophysiology. Therefore, the chapters dealing
with these topics appear at the end of the book and are designed to be reviews of essential concepts
rather than extensive teaching chapters. Some have commented to us that these chapters would be
better placed at the beginning of the book. But we prefer to emphasize the essential clinical nature of
the book right from the beginning and firmly believe that the student should come to the study of
voice disorders thoroughly grounded in the basic anatomy and physiology of the larynx and related
structures.
There is much written about the voice that has yet to be substantiated by experimental data. We
have made note of such gaps in our knowledge base in many parts of the book. We have also chosen
to put ourselves out on a limb by raising questions about some long-held beliefs. In doing so, we have
brought to bear whatever data are available to support our positions, and, where data have been lacking,
we have had to rely on theoretical constructs. Although differences exist in the types of voice problems
that occur at various points along the lifespan, we have chosen to embed that information wherever
appropriate in the text, rather than to devote entire chapters to specific age groupings. Similarly, we have
not set aside a chapter specific to the problems of the professional voice user; there is liberal mention
made of matters specific to that group throughout the chapters.
Since the publication of the third edition, there have been numerous studies about the effectiveness
of various treatment options for a variety of voice disorders. Many of these studies have followed the
evidence-based protocol that has been used in other branches of medicine for many years. We are
gratified to see this development as it means we now have or are gathering the evidence to support our
therapeutic approaches or programs. Evidence that a program works has been in our work with voice
patients even before the first edition of this book. We have conducted many studies designed to test
whether or not a therapy protocol actually works or not. We have tried to bring all of the resources of
science to bear on testing our notions about diagnosis and therapy. We will continue to do so in the
future.
We have confined ourselves to those problems having laryngeal integrity and function at their core.
Thus, there is little discussion of the difficulties with voice experienced by the deaf and by those with
severe hearing impairment. Although we have come to learn that there may be physiological differences
in phonation between the hearing and the (congenitally) deaf, the problem usually lies primarily in
the absence of acoustic input, not in abnormality of the larynx. For the same reason, we have excluded
discussion of the resonance problems of hyper- and hyponasality. The velopharyngeal mechanism and the
anatomical structures involved in that mechanism are at the core of most resonance problems, rather than
the phonatory mechanism. One of the major criticism of our book has been the lack of any information
on laryngectomy. That omission was not an oversight on our part because we have written another book
that was devoted solely to this topic. However, that edition is now seriously out of date and the time has
come to update the material and to include it in this volume.
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Preface ix

The structure and philosophy of this revised edition retains much of the organization of the previous
editions. However, we have attempted to update material, to include more information in certain areas
and, to respond to some of the requests of those who have used this book as a primary text.
Chapter 1 introduces the study of the larynx, beginning with its important biological functions.
The uniqueness of human ability to speak is dependent in part on the ability of the larynx to produce the
acoustic signal we call voice. The changes in that signal that accompany lifespan changes are reviewed,
as is voice production. Various models of the team approach to the diagnosis and management of voice
disorders are introduced. Chapter 2 is key to the philosophy of this book. We have approached the process
of differential diagnosis in the manner usually experienced in the real world when the patient presents
with certain symptoms. We follow the process through the steps that the practitioner must pursue in
narrowing the possibilities until a diagnosis and etiology are assigned. Case studies are presented as an
aid to understanding the process. Our scheme rests on nine primary symptoms of disorders of voice
and expands from there to the various signs—perceptual, acoustic, and physiological—that would be
consistent with the symptom.
In Chapter 3, Dr. Susan Thiebolt with her student, Marie E. Jette, discusses current information and
concepts about the microstructure of the larynx. Chapter 4 addresses misuse and abuse of the larynx, with
a focus on the physiological effects related to specific behaviors. Expanded information on stroboscopic
findings is a feature of this revised text. One of the unique aspects of this book is a lengthy section in this
chapter devoted to the effects of drugs on the voice. The use of over-the-counter as well as prescription
drugs is extensive. Their effects on the laryngeal mucosa have been largely overlooked. There is still a
paucity of experimental evidence about these effects. Voice problems associated with nervous system
involvement are discussed in Chapter 5. Although voice problems in this population are extensive, the
available data on the acoustic parameters of the voice or the physiological parameters of airflow and
laryngeal muscle action potentials are exceedingly limited.
Chapter 6 is devoted to the discussion of voice problems associated with organic disease and trauma.
These are areas about which the speech–language pathologist must be knowledgeable. Chapter 7 traces
the development and occurrence of voice disorders in children and concludes with a more extensive
treatment than was in the first two editions about aging. The section on geriatric voice addresses some
of the current problems and concerns of this growing segment of our population. An extensive section
on taking the voice history introduces Chapter 8, and its length emphasizes our concern about the
relatively minimal training speech–language pathologists and otolaryngologists usually receive in this
critical area of communication between patient and practitioner. The remainder of the chapter is given
over to descriptions and discussion of methods of laryngeal examination and testing procedures, both
instrumental and noninstrumental. The information that has been generated about the larynx and
its function through the use of stroboscopy has been updated and expanded. Dr. Richard Kelley, the
otolaryngologist member of our team, discusses phonosurgery and the surgical management of voice
problems in Chapter 9.
The focus of Chapter 10 is vocal rehabilitation, the primary method used to alter phonatory behavior.
The chapter begins with a discussion of some general concepts, principles, and guidelines that we feel are
critical to the undertaking of a vocal rehabilitation program. The role of voice therapy in the treatment of
disorders associated with voice misuse or abuse, pathology, neuromotor involvement, and some unusual
problems is discussed. A variety of specific treatment techniques are offered. Each is described, and a
rationale for its usefulness is provided. This section contains updated information on various therapy
techniques as well as patient outcomes. The outcome of our treatment for all kinds of communication
disorders has received much more attention since the publication of the second edition of this book.
Much more information is available to assess the effect of our treatment on a patient’s everyday function
and on the quality of life. Some controversial areas related to voice therapy and some unresolved issues are
discussed, and the final sections of this chapter briefly address the issues of prevention and malpractice.
Chapter 11 focuses, in part, on laryngectomy and the care of patients who must use some form
of alaryngeal speech. The chapter also includes a discussion of various types of partial laryngectomy
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x Preface

and their potential effects on voice. “Conservation” surgeries that permit resections of pathology while
leaving as much healthy tissue as possible are increasingly utilized and create a new set of problems for
voice restoration or implementation in this patient population.
Chapters 12 to 14 were described earlier as reference chapters. They deal with the anatomy, phys-
iology, and neuroanatomy and neurophysiology of the vocal mechanism, respectively. It is our intent
that these chapters be referred to frequently as a differential diagnosis is pursued. Chapter 15, the final
reference chapter, provides normative data against which patient data can be compared. By placing this
material in a separate chapter, we have made it readily accessible for reference use. And finally, the Ap-
pendix offers a variety of forms and protocols that we have found to be useful in our assessment and
examination procedures and includes a copy of the rating form proposed by the Consensus Conference
on Voice Perception for rating patient voices.
This edition of the book has a companion Web site at http://thepoint.com/Colton4e. The site
contains all of the color images of vocal pathologies that appear in the book plus a variety of images of
other pathologies. The stroboscopic video recordings of the patients presented in Chapter 2 may also be
found here. Individual patient clips referenced in various chapters are also included. The original word
files of the material in the appendices may be found in another section of the site and we have added
material on laryngectomy and updated many of the photographs of laryngeal pathologies. Finally, a list
of all the Web sites referenced in the book can be found on this site.
As much as possible, we have attempted to construct our sentences so as to avoid the use of sex-
specific pronouns. When this attempt resulted in convoluted language structure that became an obstacle
to understanding, we have chosen to use gender pronouns (i.e., his or her) interchangeably. The reader
should be aware that despite the particular pronoun used, we are speaking of both sexes unless it is clearly
stated otherwise. Furthermore, because this book is intended for a broad audience, we have adopted the
use of the English alphabet rather than phonetic symbols to describe vowel sounds (such as /ee/ for the
sound in “see”).
We are indebted to Susan Theibolt, Ph.D., and Marie E. Jette, M.S., for their excellent treatment
of vocal fold histology (Chapter 3) and to Richard Kelley, M.D., for his superb chapter on surgical
intervention (Chapter 9). We also wish to thank again Dr. Hirano; he has been a leader and innovator
in the study of vocal fold physiology who contributed to the earlier editions of the book.
Many others have helped in diverse ways with the preparation of this book. Dr. David W. Brewer
has, throughout the years, been a source of constant support and encouragement, and he has been so
for this project as well. We thank him for that and for his insightful reading and critique of much
of the text. We acknowledge the help of the late Samuel Mallov, Ph.D., Professor Emeritus of Phar-
macology, SUNY Health Science Center at Syracuse, New York, who checked the accuracy of our
comments about the effects of drugs on the voice. Martha Hefner, medical illustrator at the SUNY
Health Science Center at Syracuse, New York, along with Elinor Griep, Brian Harris, and Craig Palmer,
provided splendid illustrative material, and always with a smile. We are grateful for the generosity of
Eijii Yanagisawa, M.D., in sharing with us his superb photographic skills. Others have read various
sections of the manuscript in preparation and have given us valuable direction. We wish to thank
Peak Woo, M.D., Fran Lowry, Carol Friedenberg, the late Herbert N. Wright, Joanne Chilton, and
Soren Lowell. Ashley Paseman has also been invaluable in contributing to the work described in this
book and now caries on the tradition of voice care in Syracuse, NY. And, for this revised edition, we
want to thank the many colleagues who have offered support and encouragement by adopting this
textbook for use with their students and by providing us with such useful and positively reinforcing
feedback.
Sadly, one of the authors of this book has passed away. Janina Casper was the consummate clinician
with a strong research background and ability. She was a dynamic therapist who could quickly establish
rapport with her patients and motivate them to get better and do what she told them to do. She routinely
got excellent results but was never satisfied with her current skills or knowledge. She always sought new
ways to understand the voice and to treat her patients. She thirsted for new knowledge and understanding
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Preface xi

from whoever impressed her with their abilities and knowledge. And she was, throughout her career,
forever generous in sharing her own knowledge and skills with colleagues and students. Janina is sadly
missed by us but will never be forgotten by us or by her profession.
We each have families who have been supportive and patient throughout this process. They have
been deprived of attention, of our presence, and of the availability of the computer, but not of our
gratitude and love.
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CHAPTER

1
Introduction and Overview

Keywords
biology, sensory, overlaid, larynx, voice, cry, adult, aged, professional, team,
otolaryngology

Biological Importance of the Larynx

The structures that make up the larynx play a role in support of an important life-sustaining function,
that of respiration. Both the true and false vocal folds, the aryepiglottic folds, and other structures within
the larynx were designed to maintain and protect the airway from foreign substances. The respiratory
system has multiple levels of protection from foreign substances, including the many harmful effects
of the environment. Therefore, there are numerous protective mechanisms in the respiratory tract, but
the most vigorous exist in the larynx. Some are mechanical and act to close off the airway; others are
expulsive and serve to force foreign substances out of the airway. All are reflexive and operate under
involuntary control.
Many sensory endings within the larynx collect information about the state of the larynx and transmit
this information via several reflex arcs, as well as directly, to the central nervous system. (See Chapter
12 for more detailed information.) These sensory systems exist to inform the brain about the state of
the environment within the respiratory tract. Wyke (1967, 1969) and others (Bradley, 2000; Lucier,
Daynes, & Sessie, 1978; Sant’Ambrogio, Mathew, Fisher, & Sant’Ambrogio, 1983; Warner, 1998) have
written extensively about these reflex control mechanisms. Various levels of these reflex mechanisms exist
within the larynx to provide an elaborate system of protection for the airway and to maintain life. For
example, sensory endings in the laryngeal lining respond to mechanical forces such as air pressure, and
these sensory endings signal information about the state of these forces to higher centers. The larynx
is also influenced by reflexive interactions with other structures, such as the esophagus. For example,
distention of the esophagus may produce closure of the vocal folds, likely in response the airway threat
posed by refluxate material (Shaker, 2006). Although reflex mechanisms speak primarily to the biological
importance of the larynx, they may also be very important to consider in understanding the physiology
of normal human phonation and its disorders.
Speech is an overlaid function; that is, the systems used to produce speech were developed long
before man learned to speak. These systems have evolved over eons and reflect the unique place of speech
in human existence. Clear evidence of this evolution is seen in the multiplicity of the protective laryngeal
reflex mechanisms. It is important to recognize that these protective “natural” acts may sometimes be
the cause of a voice disorder. For example, excessive coughing, a protective act, can result in trauma
to the vocal folds and cause edema, which in turn will interfere with the vibratory characteristics of
the vocal folds. By the same token, rapid, random movements of the vocal folds at rest or even during
phonation may interfere with normal vibratory motion. Central neurological dysfunction or disruption
in a reflex arc may create abnormal motions, which may interfere with phonation or, indeed, threaten
life.
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2 Understanding Voice Problems

The biological function of the larynx can never be ignored. The examiner who accidentally
touches the back wall of the pharynx when performing an indirect mirror examination or rigid
endoscopic or strobolaryngoscopic exam can attest to the rapid reflexive motions of the pharynx
and larynx that result from the “gag” reflex. But the reflex or biological functions of the larynx
can be subtle in their effects and may not be apparent to either the untrained observer or the
experienced eye. Many reflex endings are sensitive to small changes of movement or air pressure
that serve to inform the central nervous system about the normal operation of the airway. The
respiratory cycle itself and the activity of the nerve controlling the diaphragm may be affected
by these changes. They also affect the discharge pattern of the intrinsic laryngeal muscles. The
effects of these subtle changes are important to consider for an understanding of the physiology
of normal voice production.
We are still young in our understanding of the physiology of the human body. Our
fascination with modern instrumentation has produced a good deal of information about
human voice production (Baken & Orlikoff, 2000). Nevertheless, the fundamental mechanisms
of bodily function and regulation cannot be ignored. Reflexes are primitive neural control
subsystems. They operate at a very low level in the hierarchy of neural functioning and control
large muscle actions. But these mechanisms are always there, waiting in the wings, so to speak,
to alter body function. Our awareness and appreciation of their role should be apparent to us
and to our patients if we are truly to understand human voice function.

The Larynx and the Voice

The voice is an integral part of that uniquely human attribute known as speech. The larynx and
its capabilities are important in two broad areas: biological function and speech. The larynx
houses the major source of sound used during speaking. The vocal folds produce a tone that
becomes modified by the pharynx, palate, tongue, and lips to produce the individual sounds
of speech. Voice is present for most vowels and for many of the consonants. The point in time
at which the vocal folds begin to vibrate relative to the movement of the other articulators (i.e.,
lips, tongue, palate) is critical if the speaker is to produce the intended sound. The larynx must
operate in close synchrony with other parts of the speech production apparatus if intelligible
speech is to be produced. Although the voice is not visible to the eye during speech production,
its absence or malfunction is obvious.
In addition to its role as a carrier of words, the voice can also produce music and express
emotion—it acts as a mirror on the inner self. The singer with superb control of the vocal
instrument brings immense pleasure to the listener. Although the singer’s words may be con-
veying a verbal statement, the phrasing, control of pitch, and dynamic range may communicate
an even stronger message. In classical singing, for example, it is the rare listener who is not
enthralled by the sound of a clear and beautiful high C, sung with ease, power, and majesty.
The singing of a choir or the chanting of prayers can lead to a unique religious experience.
The actor’s voice, resonant and full of meaning, can add significantly to the message and
the intensity of emotion. Indeed, the actor’s delivery of the words can sometimes be more
engrossing to the listener than the words themselves.
The voice serves as an emotional outlet. Both laughter and crying release emotion and
frequently serve important cathartic functions. Shouts of joy and screams of rage or fear convey
meanings that are easily recognized.
The voice reveals the inner self. It is a reflection of the personality of the individual (Rosen
& Sataloff, 1997; Bruckert, Lienard, Lacroix, Kreutzer, & Leboucher, 2008). We recognize the
stereotypical driving, hard-hitting voice of the salesperson, the nasal singsong of the perpetual
whiner, and the monotonous, de-energized voice of the depressed. The voice of an outgoing
person may be characterized by variety in the pitch, loudness, or quality. On the other hand, a
monotone voice, one with little variety, may characterize the withdrawn individual or the loner
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CHAPTER 1 I Introduction and Overview 3

who wishes not to be disturbed. Markel and his colleagues (1964, 1973) have shown that the
pitch, loudness, and tempo of the voice can be used to reflect the personality of the individual
and correlate well with other standardized tests of personality measurement (Gawda, 2007).
The speaker’s voice is used to attract as well as to repel people. A soft, soothing voice is
more apt to calm an agitated person than a strident and loud voice. On the other hand, a
strident, loud voice may be used effectively to repel someone. We instantly use a loud, “firm”
voice to dispense with a pushy salesperson or avert a physically threatening situation.
The voice can reveal a person’s physical state, as well as the physical state of the larynx.
The weak or tremulous voice identified with illness is easily identified, and the voice altered by
laryngeal pathology is identified as abnormal.
Yes, the voice is a powerful tool that not only delivers the message but also adds to its
meaning. In learning to understand the voice, it is not enough to understand its mechanical
functioning. It is also necessary to recognize the important information the voice conveys about
the speaker.

Voice Changes in Life

The voice changes dynamically, minute by minute. But there are long-term changes that are
associated with growth and decline in life. At the major stages of life, the uses of the voice are
different, as are the demands placed upon it. The reasons for these differences are many and
include biological maturation and the emotional and social changes that occur in the individual’s
life.

The Voice in Infancy and Childhood

In the first few weeks of life, the infant voice is used to express pain, pleasure, displeasure,
and hunger. Crying, the major avenue of communication for the infant, is rich in its ability to
communicate (Lester, 1985).
Crying reflects the beginning ability of the infant to control his or her voice (Robb,
Goberman, & Cacace, 1997; Robb & Goberman, 1997; LaGasse, Neal, & Lester, 2005;
Manfredi, Tocchioni, & Brocchi, 2006; Branco, Fekete, Rugolo, & Rehder, 2007; Rautava,
Lempinen, Oiala, Perkkola, Rikalainen, & Lapinlairou, 2007; Varallyay & Benyo, 2007). It is
a gross physical act that can be described as ballistic in nature. In other words, crying, once
started, runs its course and stops. The infant (or parent) can do little to stop the crying once it
has begun. As the infant grows older, he is more responsive to the environment and also gains
more control of the physical apparatus used to produce the cry. Consequently, the quality of
crying is seen to reflect physical and psychological growth. As the infant gains finer and finer
motor control, the cry becomes increasingly controllable and much more purposeful in its use.
The next most obvious voice use change occurs as the child begins to use the voice in
the production of speech sounds. Concurrently, the child is learning the sounds of his specific
language. Then, the child can use the voice to express ideas and moods. At other times, the child
may use the voice merely as the expression of play in itself. As the child matures, increasingly
complex and sophisticated differentiations of acceptable modes of vocal behavior develop. This
differentiation begins in infancy. The infant’s vocal response to a caretaker’s familiar voice differs
from that given to an unfamiliar voice. In general, the child’s vocal response differs based on
the familiarity of the voice heard. Children learn that the voice of the playground is not the
voice of the classroom. Such differentiation continues through life in many subtle ways.
The voice reflects the physical development of the child. The infant possesses a larynx
that is pliable but exhibits a low level of neuromuscular coordination. It is also small, with
short vocal folds. The small structure means that the pitch of the infant’s voice will be high.
The infant’s ability to control the tension of the vocal folds is limited. Moreover, the limited
ability of the infant to control the air pressure required for speech results in short bursts of
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4 Understanding Voice Problems

sound, much of which is rather loud. As the infant grows, the ability to control vocal pitch and
loudness increases (Boone and McFarlane, 1988). This development is reflected in the longer
cries, which are lower in pitch and vary in loudness depending on the circumstances.
In summary, during infancy and childhood, the characteristics of the voice depend on the
physical, cognitive, and emotional maturation of the child. The physical size of the vocal folds
is a major determinant of the fundamental frequency of the child’s voice. The infant, with a
small larynx and short vocal folds, exhibits the highest vocal pitch, whereas the older child,
whose larynx has grown, possesses a lower vocal pitch. Adult vocal pitch is not attained until
puberty, when the larynx reaches its adult size.
Loudness variation is less affected by these growth changes and more affected by the level
of motor control exhibited by the child. Quality variation reflects physical growth changes of
the vocal folds, changes in the size and shape of the entire vocal tract, and finer control of
the neuromuscular system. Differentiation of appropriate voice use characteristics depends not
only on physical abilities but also on cognitive and social growth and awareness.

The Voice of the Adult

By the age of 18 years or perhaps younger, the voice reaches its mature or adult stage. The
fundamental frequency is where it will remain for several decades. The individual has full
control over the dynamic range (loudness) of the voice and can produce many variations of
pitch and voice quality. These vocal abilities reflect the maturation of the anatomical and
physiological systems for the support of speech (Kahane, 1982).
Although the adult voice has been attained by the age of 18 years, there is still much
refinement that can occur to expand vocal abilities. Indeed, vocal training for the singer or the
actor most appropriately begins when this level of maturation has been reached. Pitch range
can be extended, vocal control can be increased, and voice quality can be enriched.
The way the voice is used depends on the demands of the situation. These demands may
include the teacher’s need to instruct and maintain discipline, the minister’s need to deliver a
forceful sermon or to be consoling, or the salesperson’s need to sell a product.
It is easy to take the voice for granted. We can traumatize it with constant use and frequent
misuse. We can expose it to the harmful effects of smoke, drugs, and alcohol and expect it to
be unaffected. It is typically only when we experience difficulty talking that we cease taking
it for granted and seek help. Often we have difficulty recognizing potentially traumatic habits
and making the necessary changes, even when our lives are threatened.

The Aged Voice

After 65 years of age or so, the voice begins its decline, much the same way other body
functions begin to decline (Beasley & Davis, 1981; Kahane, 1981; Linville, 2001; Casper &
Colton, 2000). The voice, however, does not always mirror the extreme or rapid changes that
may occur in the physical functioning of the body. Aged individuals in good physical condition
possess voices that are similar in their characteristics to the voices of those of younger persons
(Ramig & Ringel, 1983). Some singers can maintain their artistic voices well into their 70s.
The voice may retain the essential elements of beauty, although it may not exhibit the range or
degree of vocal control that was present in younger years.
But for others, the voice readily betrays the effects of aging. Voices that show a decline or
increase in habitual vocal pitch, decreased control of loudness, or changes in voice quality may
be showing signs of diminished physical status. Acoustic changes such as upward or downward
frequency shifts, poorly controlled loudness, and quality changes reflect to some degree the
physiological changes that occur in the larynx with increasing age.
The vocal demands of the aged adult may also be different from those of the younger
adult. After retirement, the salesperson no longer must use that voice to sell a product. The
retired minister no longer has to deliver that forceful sermon. The decline of bodily function
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CHAPTER 1 I Introduction and Overview 5

is usually accompanied by reduced demand on the system. That is not to say that the voice is
no longer important to the elderly. On the contrary, the voice is important, but in a different
way. It retains its importance in the communication process. It is used to maintain contact
with friends and relatives. For some individuals, verbal communication becomes the only way
to maintain human contact and control of the environment.

Production of the Voice

To most lay people, the way in which the voice is produced is a mystery. The term “voice
box” is commonly used to refer to the larynx, the voice-generating mechanism. Most people
know they have one and that it is somewhere in the throat below the chin. From experience
they know that when they have laryngitis, they cannot talk, or that their voices sound “funny,”
but few understand why those changes occur. Some people may be aware that after strenuous
voice use, such as yelling at a sports event, their voices may sound hoarse. They surmise that
the hoarseness has to do with “straining” the voice. Some people may even realize they can
manipulate their voices in many ways, for example, raise or lower pitch, increase or decrease
loudness, and change their voice quality. This is such common knowledge that it is taken for
granted without thought about the workings of the mechanism that is capable of producing
such changes.
Understanding phonatory physiology goes beyond knowing laryngeal anatomy and recog-
nizing various laryngeal pathologies (Aronson, 1990; Kahane, 1982). Treatment of the voice-
disordered patient demands such a knowledge base. Disturbed physiology may be a by-product
of pathology and may persist after the pathological condition is resolved. On the other hand,
disturbed physiology may be the cause of tissue changes. Whatever the treatment modality,
restoration of normal function, or the closest possible approximation of it, is the goal.
The basic concepts of phonatory physiology have been understood for many years (Lieber-
man, 1968; Titze, 1994; van den Berg, 1958). Recent technological advances have, however,
significantly increased our knowledge base (Hirano, 1981a; Kahane, 1981; Khosla, Murugap-
pan, & Gutmark, 2008; Davis, Merati, Jaradeh, & Blumin, 2007; Kendall, 2009; Leydon,
Sivasankar, Falciglia, Atkins, & Fisher, 2009). The inaccessibility of the larynx, especially dur-
ing the phonatory act, has hindered our ability to understand its functioning more fully. In
1855, Garcia developed the laryngeal mirror (Moore, 1937) and made it possible to visualize
the larynx with the naked eye. Since then, greatly improved techniques of laryngeal visualiza-
tion as well as sophisticated analyses of laryngeal acoustics and improved methods of measuring
physiological events related to phonation have resulted in a greater understanding of phonatory
physiology (Fritzell & Fant, 1986).
Understanding the physiology of phonation is intimately bound up with an understand-
ing of laryngeal anatomy and neuroanatomy as well as respiratory function. Changes in the
structures, in the tissues, or in motor control, whether the result of neurological insult, trauma,
congenital anomaly, lesion, or disease process, will distort normal physiology in some fairly
predictable ways. This disturbed physiology will, in turn, have an effect on the acoustic char-
acteristics of the voice. Physiology can also be altered by changes in muscular and skeletal
tensions, with concomitant changes in the acoustics. Therefore, there is an interdependence
and interaction among anatomy, physiology, neurology, and acoustics. It is necessary to under-
stand this interaction to treat the voice problem effectively. It is imperative that teachers of the
professional voice increase their working knowledge of the complex phonatory process.
All users of voice, as well as those who treat or train it, can benefit from an understanding
of how the voice works. Simple knowledge of the effects of vocally traumatic behaviors and the
need for good vocal hygiene is important to the prevention of certain types of laryngeal pathol-
ogy and could be potent preventive measures for reducing the incidence of vocal nodules and
certain polyps. There are some people who, without the benefit of specific voice training,
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6 Understanding Voice Problems

are able to use their voices in strenuous ways without encountering any vocal problems.
They are the exceptions. Most people who use the voice in chronically strenuous ways are
at risk for developing vocal difficulty.
Many professional voice users may have had vocal training, although it is rare for such
training to include more than a cursory understanding of phonatory physiology. Typically,
voice coaches have been taught by other voice coaches, and techniques are passed on that are
believed to produce the desired results. There is little objective evidence that these techniques do
what they are purported to do. Although some techniques appear to be spectacularly successful,
others have done unwitting damage to voices.
Professional voice users need to understand the workings of their instrument to use it
most effectively and maintain its health. In addition to professional singers and actors, the
category of professional voice users should be expanded to include teachers, coaches, ministers,
salespersons, cheerleaders, and others who use their voices extensively and perhaps strenuously
in the performance of their occupations.
The growth of interest in the voice and the recognition of the need for multidisci-
plinary involvement in its care have resulted in increased understanding of the science un-
derlying voice physiology among vocal coaches and singers as well. The many multidisci-
plinary voice conferences throughout the world attest to this and continue to disseminate
information.

The Voice Team

There are many professionals representing numerous disciplines or fields of study who are
concerned with the voice. Some are concerned with basic studies of laryngeal function, others
are concerned with medical problems affecting the voice, and others are concerned with the
evaluation and treatment of voice problems. Still other disciplines are focused on developing
the voice to its pinnacle of performance ability. Each discipline brings its particular focus and
area of expertise to bear on diagnosis, treatment, or teaching.
The internist, the family practitioner, or the pediatrician may be the first specialist to
come in contact with a patient with a voice problem. These primary care physicians must be
aware of the voice as a sign of health or illness. For example, persistent hoarseness is recognized
among medical personnel and the public as one of the early warning signs of cancer. There
are other vocal symptoms that if recognized can be helpful in the early diagnosis of certain
disease processes. Recognition and identification of the existence of a problem is only the first
step. This must be followed by appropriate treatment or referral for further evaluation and/or
treatment.
The otolaryngologist is the most appropriate specialist for the diagnosis and treatment of
medical laryngeal problems. Although there are a growing number of otolaryngologists who
specialize in the treatment of voice problems, most will be expected to treat a variety of laryngeal
and other otolaryngologic problems. Laryngitis, vocal fold nodules, polyps, loss of voice, or
hoarseness of undetermined etiology are among the problems that affect the voice and are
typically seen identified by otolaryngologists.
As is true for otolaryngologists, there are many speech–language pathologists who work
with the voice disordered patients, but relatively few have made this an area of specialization.
The appropriately trained speech–language pathologist is the specialist who diagnoses and
treats problems of phonatory function or “vocal pathology.” The mode of treatment offered
by speech–language pathologists focuses on the modification of phonatory behavior. Indeed,
the speech–language pathologist’s broad-based understanding of behavior, whether it be the
result of inappropriate voice usage, disturbed physiology, or a manifestation of underlying
psychological problems, uniquely qualifies this professional to aid in the diagnostic process, as
well as to provide a primary resource for nonmedical treatment. Some speech pathologists have
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CHAPTER 1 I Introduction and Overview 7

had extensive training in singing, usually at the undergraduate level, that adds immeasurably
to their understanding of the professional voice.
Voice scientists have added to our knowledge and understanding of phonatory physiology
and acoustics through experimental verification of hypotheses. They are usually not directly
involved in either treating or teaching the voice user. However, the information available from
laboratory studies of the voice can be helpful in establishing a diagnosis, validating treatment
approaches (Verdolini & Titze, 1995), and in documenting change in vocal function as a result
of treatment. Furthermore, much can be learned about phonatory physiology from the study
of abnormal function.
Neurolaryngology, the specialized neurological approach to laryngeal function, is a fairly
new and developing area of knowledge, with far-reaching clinical implications. Many movement
disorders have laryngeal components that have not been well documented and are not well
understood. Indeed, it is not unusual for a phonatory problem to be the first symptom of a
motor disorder. A neurolaryngologist could be a valuable member of any team concerned with
voice disorders.
Imaging techniques are powerful tools assisting in the diagnosis of pathologic condi-
tions. Laryngologists whose special area of expertise focuses on head and neck problems
are frequently involved in initial and subsequent assessments of laryngeal abnormality. Ra-
diologists provide further information relative to the size, location, and extent of a lesion,
through a variety of imaging techniques. Such information is frequently critical to diagnos-
tic and management decisions, especially those that involve surgery. Imaging techniques such
as magnetic resonance imaging or computed tomography (Baer et al., 1987; Brooks, 1993;
Leboldus et al., 1986; Piekarski, 1992; Stark et al., 1984; Wippold, 2000) scan can provide
additional information about the state of the larynx and the vocal tract during speaking and
singing.
Patients whose voice problems are an expression of deep-rooted emotional problems may
require psychotherapy (Aronson, 1990; Aronson, Peterson, & Litin, 1966; Diehl, 1960). Re-
ferral to a psychotherapist is indicated when it has been determined that the vocal problem
exhibited by the patient may be an expression or symptom of significant psychiatric disabil-
ity. Our understanding of the bond between voice and personality has been enhanced by the
contributions of the fields of psychiatry and psychology.
Teachers and coaches of the singing and the speaking voice are interested in maximizing
the individual potential of each of their students while maintaining the health and structural
integrity of the vocal mechanism. Their unique knowledge of the professional voice and their
deep interest in its correct use necessitate a good knowledge of vocal anatomy and physiology.
This is especially true because the vocal demands on singers and actors are frequently much
greater than for the average speaker. Furthermore, even subtle changes in vocal production may
be critical to a performance.
The number and variety of disciplines involved in the understanding and management of
the voice give testimony to the complexity of the process of phonation. Our experience in the
“team approach” to understanding the voice and its disorders has led us to an appreciation of
the active involvement of a variety of disciplines working together in the assessment process.
The benefits of this interactive interdisciplinary team approach accrue not only to the patient
but also to the professionals involved. Each team member brings a particular perspective and
knowledge base to the diagnostic process, extending by far the single examiner expertise. For
example, the otolaryngologist is highly skilled in assessment of the health or disease state of the
larynx, the speech–language pathologist specializes in the phonatory function of the mechanism
and the manner in which that may be disturbed by various conditions, and the singing coach
recognizes problems in vocal technique that are specific to the singing voice.
The team approach may take various forms, each with its own set of advantages and
disadvantages. A description of several models follows.
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8 Understanding Voice Problems

Model A
The patient is seen individually during the course of a few hours by various specialists who
are located within the same facility or in close proximity. Typically, either the otolaryngolo-
gist or the speech–language pathologist will perform a videostroboscopic laryngeal examina-
tion. The team of specialists may subsequently meet to review the videotaped examination,
discuss their various findings, and agree on a treatment plan or individual reports may be
directed to the team leader who incorporates them into a complete report with recommenda-
tions for treatment.

Advantages
The patient is seen on a single day insuring that all specialists are seeing the patient at the
same point in the course of the problem. Each specialist has the necessary time to carry out a
complete evaluation. The opportunity for interaction among team members exists if the team
meets together to discuss the findings. Although it may take a few hours, this model nonetheless
can be a time saver for the patient.

Disadvantages
The process involves duplication of information that the patient must provide to each specialist.
Team members do not have the input from other findings until after they have made their own
assessments and arrived at their own plan. Even though the examinations take place within a
few hours, patients do fatigue, and the voice heard by one examiner may be quite different
from that heard by another. The patient is usually not present when the team meets precluding
further immediate assessment based on input from any individual specialist. For example, if the
stroboscopic examination is performed by the otolaryngologist, the voice clinician may not have
the opportunity to extend that examination into a phonoscopic (vocal behavior) examination,
or conversely, a voice clinician may fail to adequately examine the area for signs of disease. The
alternative here is for the patient to undergo two separate examinations, the ramifications of
which are obvious. Furthermore, if there is a time lag between the actual examinations and the
team meeting, much can be lost through dulling of memory. If individual findings are reported
to a single individual, the opportunity for invaluable interaction among specialists is lost.

Model B
The patient is seen individually by various specialists over the course of several weeks. In this
type of model, individual reports are typically sent to a single individual who is the manager
of the case. That individual blends all of the information and makes recommendations for
treatment.

Advantages
The only plus point for this model is the involvement of various disciplines rather than a single
specialist who functions without the benefit of additional information.

Disadvantages
This process may take some time to complete. Over that course of time, the patient’s problem
may undergo various changes in type, degree, and severity. Thus, each specialist may be seeing
quite a different picture. There is no opportunity for true interdisciplinary interaction. It is time
consuming for the patient and may prolong a problem by postponing appropriate intervention.
Most of the disadvantages cited for the first model also apply here.

Model C
The patient is seen either by the laryngologist or the speech–language pathologist and a vide-
olaryngostroboscopic examination is done. The history and tape may then be reviewed jointly
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CHAPTER 1 I Introduction and Overview 9

FIGURE 1.1. The team approach.

by these two specialists and a diagnosis and treatment plan agreed to, or, after the tape is re-
viewed individually, and a consensus is reached regarding diagnosis and treatment. Additional
specialists may be consulted as needed.

Advantages
This model may be a time saver for all concerned—the patient has one examination and
only one specialist’s time is involved in the examination. If specialists review the examination
together, a degree of interdisciplinary interaction is preserved.

Disadvantages
The patient is usually not present when the specialists meet thus precluding the possibility of
additional examination or data gathering at that time. Acoustic and other laboratory data may
not be obtained at the time of the initial examination. If the specialists do not jointly review
the examination tape, there is a lack of interaction. If further assessments are needed, the time
necessary to complete the examination becomes extended and interaction of all involved usually
becomes minimal.

Model D
The model which we find most satisfactory is one wherein a number of specialists are
present and interact with the patient and each other at the time of the videolaryngostro-
boscopic/phonoscopic examination with the opportunity for further individual assessments to
follow. In our model, laboratory data (acoustic and physiological) are obtained immediately
prior to or following (Fig. 1.1) the endoscopic examination. The team discusses the findings,
presents the diagnosis and treatment plan to the patient with full opportunity for questions
to be raised and answered. Patients have the opportunity to view the laryngeal imaging study
image and, with staff direction, they are able to observe laryngeal and/or vocal pathology or
other problems.

Advantages
An obvious advantage of this model is that all of those involved hear the same sample of voice
and observe the larynx at the same time. Each specialist has the opportunity to ask questions
during the history taking and to request that a specific phonatory task or nonphonatory gesture
be elicited during the examination. For example, the speech–language pathologist may wish
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10 Understanding Voice Problems

to assess laryngeal function through the use of both the rigid and the flexible endoscopes to
appreciate aspects of phonatory physiology, or to engage in preliminary treatment probing.
There is an opportunity for immediate discussion of the case and because the patient is still
present, further examination is possible if it seems warranted. Diagnosis and a treatment plan
are formulated by the team and discussed with the patient. The interdisciplinary interaction
is extremely valuable. The history and findings are clearly recalled by all without reliance on
memory over time.

Disadvantages
The number of people present (three or more) can sometimes be overwhelming to patients
if they have not been prepared to expect this. The history can only address major areas and
may not uncover more subtle or underlying problems which are not appropriately discussed
in the presence of the full team. Often such problems, if present, emerge when the patient
begins an individual treatment protocol. At that time, the individual practitioners attain a
better understanding of the patient and can more appropriately explore other issues.
Although we are committed to Model D of the team approach, we recognize that it is
not a universal mode of operation. Otolaryngologists often see patients with voice problems
in their offices and refer to a speech–language pathologist only those patients they feel are
appropriate candidates for voice therapy. Those referrals may frequently be based on indirect
mirror examinations with minimal information provided to the speech–language pathologist.
ASHA guidelines and Preferred Practice Patterns (American Speech-Language-Hearing Asso-
ciation, 1998) make it clear that all patients with voice disorders must have a laryngological
examination prior to the initiation of voice therapy.
When referrals for voice therapy fail to provide adequate information on which to base
a therapy approach, it is incumbent on the speech–language pathologist to request additional
information. That can be accomplished in a variety of ways. Professional protocol requires that
additional information be sought from the referring physician. If the speech–language pathol-
ogist is appropriately trained in phonatory function assessment and has access to videostrobo-
scopic equipment, such an examination is appropriately carried out. If neither of these avenues
provides the necessary information, patients can be directed to a voice laboratory or other
resource where additional information or a second opinion may be obtained. Referral infor-
mation of particular help to the voice clinician includes a thorough description of the type and
character of the pathology, its location on the vocal folds, whether it appears to be relatively
acute, that is, erythematous, edematous, compressible during vibration, or chronic, that is,
normal in color, well organized and incompressible on voicing. If the dysphonia is produced
largely by inappropriate use of the larynx, without clear evidence of organic pathology, then
a description of specific structures involved in voice production is helpful. In our experience,
once otolaryngologists understand the kind of information that might be of use to the voice
clinician, they are happy to provide it. Again, it is imperative that the clinician be equipped
with the best information possible prior to treating a patient.

Summary
The larynx serves essential reflexive biological functions that protect the airway and maintain
life. These basic functions determine the limits of voice and may occasionally affect its function.
The larynx also provides the acoustic signal for speech, that uniquely human capability. Singing,
dramatic exposition, laughing, and crying fulfill additional human needs through the voice.
The voice reflects individual identity, personality, and life stage. An understanding of phonatory
physiology, as well as of those factors that may disturb it, is necessary for all professionals involved
in the care of the voice and for all professional voice users. Assessment of the voice-disordered
patient is enhanced by input from various disciplines through a team approach.
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CHAPTER

2
Differential Diagnosis of
Voice Problems
Keywords
differential diagnosis, process, interview, symptom, sign, hoarseness, vocal fatigue,
breathy, pitch, range, aphonia, breaks, strain, struggle, tremor, pain, monopitch,
loudness, monoloudness, reduced loudness, quality, timbre, hoarse, rough, tension,
diplophonia, stridor, acoustic, fundamental frequency, perturbation, amplitude,
shimmer, signal-to-noise, air flow, air pressure, phonation threshold pressure,
stroboscopy, videokymography, high speed photography, case studies, evidence based
practice

In this chapter, and throughout this book, we will be using the term “diagnosis” in two distinct ways. In
the first sense, it will refer to the process involved when attempting to determine the nature of a problem.
That process involves examination and observation, a problem-solving approach. However, in the second
sense, the word “diagnosis” refers to the decision that is the end product of the diagnostic process.
The diagnostic process can be likened to solving a puzzle. Each piece of the puzzle must be examined
from many perspectives. Each piece is only a part of the total picture. As a piece is found, it is placed
into the puzzle, until the picture is complete. As often happens, one or more pieces may be missing.
In those instances, more time is required to search for the missing pieces. In the process of diagnosis
of voice disorders, there may also be missing pieces. The solution may not be apparent, and ongoing
examination of all relevant information must continue.
Analysis of voice problems involves the examination of many individual components. These com-
ponents include the statement of the problem, the symptoms, and the history or related information,
as well as a set of signs observed or measured by the examiners. The examination of these components
may involve a variety of procedures, including the following:
1. Interview.
2. Examination of medical records.
3. Rating of auditory perceptual characteristics.
4. Measurement of acoustic, aerodynamic, vibratory, and muscle action events.
5. Examination of the laryngeal structures and their function.
6. Evaluation of other bodily functions and systems as deemed appropriate.
7. Experimental therapy, sometimes referred to as treatment probing, in which attempts
are made to manipulate the patient’s vocal behavior.
Not all of these steps may be necessary depending on the findings from a previous step. The successful
completion of the diagnostic process requires a solid base of information. Diagnosis of voice disorders
requires a thorough understanding of laryngeal anatomy and physiology. A fundamental understanding of
phonatory physiology is essential so that rational hypotheses can be formulated about the voice problem
and the conditions accompanying it. Moreover, the clinician must be able to formulate hypotheses
concerning the expected changes in physiology based on analysis of perceptual and acoustic information.
11
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12 Understanding Voice Problems

The clinician must be aware of and sensitive to the relationship between personality and voice.
Knowledge about the various pathologies and how they affect phonation is, of course, essential.
The diagnostic process is differential. That is, it is necessary to consider all the possible
causes of a problem and to proceed through them all as if each is the real cause until proven
otherwise. The differential aspect of the diagnostic process involves consideration of the basic
question, what specific problem or problems might be composed of these component parts? The
available information relative to the patient is then matched against each of these hypotheses
in the search for a match, a good fit.
The process of differential diagnosis begins anew with each patient. In the clinical setting,
patients present with a complaint. The challenge for the diagnostician is to track down data
essential to an understanding of the physiology, to the making of a diagnosis, and, perhaps, to
determining etiology.

What Is an Etiology?
Etiology is defined by Webster’s Third New International Dictionary as “a science or doctrine of
causation or of the demonstration of causes.” Symptoms and signs describe various components
of the problem, providing part of the raw data necessary for determination of an etiology. The
first step in the treatment of any medical problem is determination of its cause or etiology.
Recognition of the correct etiology is essential for proper treatment. It is not only unwise but
also potentially dangerous to treat a problem for which a well-considered etiology has not been
established. An incorrect etiology may result in improper treatment, lack of needed treatment,
or, at the very worst, compromise of a patient’s life. For example, laryngitis is a common
cause of hoarseness and is treated not only by otolaryngologists but also by pediatricians,
family physicians, and internists. In many cases, laryngitis is caused by an upper respiratory
infection and is appropriately treated with medication. However, hoarseness may be a sign of
other laryngeal pathologies, including malignant lesions, and as such should be evaluated with
all possible etiologies in mind. In our experience, some patients have followed a protracted
and unsuccessful course of medical treatment only to have subsequent examination reveal the
presence of a vocal fold lesion as the etiology of the hoarseness.
Assigning an etiology is not always easy. It is possible for a condition that produces dyspho-
nia to be unobservable or to escape careful and thorough examination. It is also possible for a
condition to persist when the original cause of the problem is no longer present. For example,
an untrained singer may have developed vocal nodules while engaged in strenuous voice use
and abuse for a period of several months. The behaviors that led to the pathological condition
may no longer be present, but the resultant tissue changes persist. It is important to be aware
of antecedent conditions that may be responsible for the present problem.

Symptoms and Signs

The words “symptoms and signs” are used frequently in medical literature (Brewer, 1975).
What do they mean, and how can the distinction between them help the diagnostic process?

What Is a Symptom?
A symptom is a complaint. It is what the patient reports about the problem and its characteristics.
Symptoms may be described in various ways. The patient may complain of sensations associated
with phonation, such as pain along the side of the neck or soreness in the throat region after
prolonged conversation. Other complaints may refer to perceptual characteristics of the voice,
such as hoarseness, scratchiness, or perhaps a wobbly voice. Some symptoms can be verified;
some cannot. For example, you cannot “feel” the patient’s pain or record it. Sometimes, a patient
may be able to report the magnitude of the pain, but we have no way of interdependently
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CHAPTER 2 I Differential Diagnosis of Voice Problems 13

verifying the report. However, the report of pain is a very important symptom and can be
a potent factor in directing the clinician’s thinking about a problem. Other feelings (e.g.,
dry throat, scratchy throat, etc.) may also be difficult to verify. Symptoms, verifiable or not,
have reality for the patient and must be given serious consideration by the speech–language
pathologist (SLP) and the otolaryngologist.

What Is a Sign?
Signs are characteristics of the voice that can be observed or tested. For example, hoarseness may
be the patient’s complaint, but it is also a sign that can be observed and measured independently.
Signs represent an inventory of vocal characteristics based upon examination, observation, and
measurement.

Signs versus Symptoms: Why the Distinction?

Despite the fact that patients’ symptoms have reality for them, they do not tell the full story.
They can be misleading, are frequently underreported, and may not be the most salient and
significant vocal characteristics present in the voice. Thus, symptoms may not fully elucidate a
patient’s vocal difficulty.
Signs provide more objective information. Because a sign is not unique, there may be
redundancy in the data. For example, hoarseness may include the following acoustic signs:
low fundamental frequency, reduced variability of fundamental frequency, increased frequency
perturbation, increased spectral noise, and a large s/z ratio. (See “Acoustic Signs” later in this
chapter for a more complete discussion.) Which of these signs are significant in an individual
patient is sometimes difficult to determine. However, understanding how signs relate to each
other, and how they reflect underlying pathology, will assist the SLP and the otolaryngologist
in properly interpreting the sign and evaluating its significance.
This section will present the major symptoms and signs of voice problems. In the next
three sections, we will discuss perceptual, acoustic, and physiological signs. Finally, each of the
symptoms discussed in this section will be presented in greater detail, with listing of the major
perceptual, acoustic, and physiological signs as well as potential etiologies that might produce
the symptoms and signs. The emphasis throughout this chapter will be on the process of
discovering and interrelating the perceptual, acoustic, and physiological signs to the underlying
pathology or pathophysiology and to how this knowledge helps understand the etiology of the
problem.

Major Symptoms of Voice Problems

In our experience, patients with voice problems tend to present nine major symptoms. Not
included in this list are symptoms reflective of a problem with resonance due to incompe-
tent velopharyngeal closure. Resonance problems have been traditionally considered “voice”
problems, but they are not phonatory problems. The symptoms described typically occur in
combination rather than singly.
The nine symptoms presented in Table 2.1 are as follows:
1. Hoarseness: This symptom reflects aperiodic vibration of the vocal folds. Some patients
will use the term “hoarse” to refer to this symptom, whereas others might use terms
such as “raspy” or “rough” voice.
2. Vocal fatigue: Patients complain of feeling tired after prolonged talking and often state
that continued talking requires a great deal of effort. Moreover, they may report occa-
sional raspiness or hoarseness, which tends to be most apparent at the end of a working
day or with prolonged voice use.
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14 Understanding Voice Problems

TABLE 2.1 Nine primary symptoms of voice problems

Hoarseness
Vocal fatigue
Breathy voice
Reduced phonational range
Aphonia
Pitch breaks or inappropriately high pitch
Strain/struggle voice
Tremor
Pain and other physical sensations

3. Breathy voice: Patients sometimes complain that they are unable to say complete sen-
tences without running out of air and needing to replenish the air supply to continue
talking. They further report having difficulty being heard, especially in noisy situa-
tions. We usually label the voice as “breathy,” although patients will not always use this
term.
4. Reduced pitch range: This symptom is usually associated with singers who complain
that they are experiencing difficulty producing notes that had previously presented no
problem. Typically, these are the notes that occur at the upper end of their singing range
although some singers have difficulty in the transitional area of their frequency range.
They may also complain of tiredness and soreness in the throat area.
5. Aphonia: Aphonia means absence of voice. The patient speaks in a whisper and may
sometimes complain of a variety of symptoms, including dryness in the throat, soreness,
and a great deal of effort in attempting to speak.
6. Pitch breaks or inappropriately high pitch: A patient may complain of periodic squeakiness
and of voice cracks. The voice seems out of control, and the patient reports never
knowing what sound will come out. Therefore, we have labeled this symptom as pitch
breaks, although it is also possible to describe it as the inappropriate use of high pitch
or puberphonia. Often, this symptom is reported by a male adolescent who uses an
inappropriately high pitch as the habitual voice rather than the more typical lower
pitched male voice.
7. Strain/struggle voice: These patients report that it is difficult to talk. This may include
inability to get voicing started or to maintain voice. They report that it is a strain to
talk; they experience a great deal of tension while speaking and become fatigued due to
the effort involved.
8. Tremor: Patients may complain that the voice is wobbly or shaky. They are unable to
voluntarily produce a steady sustained sound. This “shakiness” or tremor is usually very
regular in rate and varies little.
9. Pain and other physical sensations: Pain described in association with voice production
varies considerably across patients and across location. Some report pain on both sides
of the neck lateral to the larynx, others localize the pain to a specific unilateral area or to
mid-larynx, and a few report pain radiating into the upper chest. In some patients, this
may be the only symptom, although this is very rare. Other physical sensations reported
by patients include feelings of a lump in the throat, feelings of strain or tension, or the
sensation of dryness. Sometimes, the patient’s main concern is a frequent cough.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 15

These nine symptoms are the most common in our experience. Patients may report several
symptoms, but usually the symptom mentioned first or emphasized should be considered the
primary symptom and is likely to relate most directly to the eventual etiology of the vocal
problem.

Major Signs of Voice Problems

Perceptual Signs
Perceptual signs of voice problems are the characteristics of an individual’s voice that are per-
ceived by the listener/observer. Although these impressions are subjective, they have psycho-
logical reality and may be assessed objectively and compared across listeners (see Chapter 8
for methods of scaling perceptions). Clinically, the perceptual signs—the clinician’s perception
of voice characteristics—paired with the history serve as initial guideposts in the process of
differential diagnosis.
Many adjectives have been used to describe voice qualities (Aronson, 1990; Colton &
Estill, 1981; Perkins, 1971). The list of perceptual signs presented in this chapter encompasses
a variety of perceptual characteristics that serve to focus our attention on clinically useful voice
characteristics. Some of these characteristics have reasonably clear, well-defined, measurable
acoustic correlates and others do not. For example, we may not be able to differentiate “hoarse-
ness” and “roughness” acoustically. Both hoarseness and roughness have increased perturbation
and a noisy spectrum. As another example, “tension” can be observed by a clinician, but its
measurement becomes problematic. Indeed, we would be hard put to specify the exact loci of
vocal tension, its acoustic parameters, and how to measure it.
Perceptions by their very nature are hard to describe. They are subjective and individual,
being influenced by personal preference, experience, and culture. In the following discussion,
perceptual signs of voice (Table 2.2) have been grouped within the broad areas of pitch, loudness,
quality, nonphonatory behavior, and aphonia (absence of phonation). The definitions of the
terms are intended to provide meaningful guidelines without undue restriction on individual
experience.

Pitch
Pitch is the perceptual correlate of fundamental frequency. However, it is possible that other
acoustic parameters may affect the listener’s perception of pitch.

Monopitch
This term refers to a voice that lacks normal variation of pitch during speech. There is a marked
absence of inflectional variation and in some instances an inability to voluntarily vary pitch.
Monopitch can be one of many signs characteristic of neurological impairments that may affect
the voice. It may also simply be a reflection of an individual’s personality or, more significantly,
of psychiatric disability.

Inappropriate Pitch
This refers to the voice that is judged to exceed the range of acceptable pitch for age and/or sex,
being either too low or too high. Norms for fundamental frequency (the acoustic correlate of
pitch) are available for age and sex (see “Acoustic Signs” later in this chapter). The high-pitched
voice of a young child is perceived to be inappropriate when produced by an adult and vice versa.
Similarly, the pitch range for an adult female voice does not generally extend as low as might be
acceptable in an adult male. The perception of voice pitch and the subsequent judgment of the
acceptability of that pitch can be fraught with danger. Research has shown (Plomp, 1976; Wolfe
& Ratusnik, 1988) that other characteristics of voice quality can affect our perception of pitch.
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16 Understanding Voice Problems

TABLE 2.2 Perceptual signs of voice problems

Pitch
Monopitch (reduced pitch variability)
Inappropriate pitch
Pitch breaks
Reduced pitch range
Loudness
Monoloudness (reduced loudness variability)
Loudness variation (soft, loud, or uncontrolled)
Reduced loudness range
Quality
Hoarse or rough
Breathy
Tension
Tremor
Strain/struggle
Sudden interruption of voicing
Diplophonia
Other behaviors
Stridor
Excessive throat clearing
Aphonia
Consistent
Episodic

Thus, although the hoarse voice of a person with a vocal lesion may be perceived to be lower
than acceptable, actual measurement of the fundamental frequency may fail to corroborate that
perception (Shipp & Huntington, 1965). The pitch of a voice is related to the size of the
larynx and its structures. A vocal pitch higher than expected may reflect underdevelopment or
immaturity of the larynx based on delayed development, endocrinological factors, or perhaps
a congenital anomaly. Vocal pitch may also be excessively low due to endocrinological factors
such as hypothyroidism or the use of male hormone by women. It is also possible for vocal
pitch to be too high or too low based on individual preferences or habit.

Pitch Breaks
Unexpected and uncontrolled sudden shifts of pitch in either an upward or downward direction
are readily perceived even by the untrained and unsophisticated listener. They are frequently
associated with the changing voice of the adolescent male and are usually a temporary stage
that resolves with time. Occasionally, pitch breaks persist beyond the expected laryngeal growth
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CHAPTER 2 I Differential Diagnosis of Voice Problems 17

period. Pitch breaks, however, may also occur as a result of laryngeal pathology or as an
accompaniment to conditions that involve some loss of neural control of phonation.

Reduced Pitch Range

Sometimes, a patient may complain about a reduction in pitch range, usually at the high end
of the range and an inability to produce these pitches without excessive strain or at all. Very
rarely do patients complain about loss of the low end of their range.

Loudness
Loudness is the perceptual correlate of intensity but may depend on several other factors such
as spectrum, vocal tract resonance, and the environment.

Monoloudness
This refers to voice that lacks variation in loudness level. The use of increased loudness for
emphasis is absent, and there may be an inability to voluntarily vary loudness. In this category,
the perception does not attend to the actual level of loudness being used but rather to the
variability of the level during speaking. Monoloudness may be (a) an indication of neurological
impairment in which the ability to voluntarily control and vary loudness may be lost, (b) a
reflection of psychiatric disability, or (c) a habit associated with personality.

Loudness Variation
When variations in loudness are extreme, either too soft to be heard easily in average conver-
sational settings or excessively loud for the setting, they are perceived as a sign of a problem.
Although norms are available for dynamic range (the softest to the loudest sound a person
is able to produce; see “Acoustic Signs” later in this chapter), appropriate loudness levels are
dependent upon the specific speaking situation. Unpredictable and uncontrolled variation of
loudness level, explosive to fading, constitutes another sign of loudness variability that is be-
yond accepted norms. Voices that are too soft or too loud may be a reflection of auditory
dysfunction, of personality, or of habit. A habitually loud speaker may have grown up in a large
and noisy family in which excessive loudness was the norm, or may have had to speak loudly
to be heard by a hearing-impaired relative. The inability to control vocal loudness may also
be due to the loss of neural control of the phonatory mechanism or to problems affecting the
respiratory mechanism. It is also possible that variations in vocal loudness, from explosive to
almost aphonic, may be a reflection of psychological problems.

Reduced Loudness Range

As was the case for reduced pitch range, this refers to the reduction in a patient’s loudness range,
usually a loss of the ability to produce loud sounds. Many times, reduced phonational range
and reduced loudness range occur in the same patient.

Quality
Hoarse or Rough
These words are descriptors of a voice quality that is noticeably aberrant in its lack of clarity, its
increased noisiness, and its discordance. Although hoarseness/roughness may be the primary
perceptual characteristic of an abnormal voice, its perception may be paired with other char-
acteristics such as breathiness, tension, or strain. The degree of hoarseness/roughness in the
voice is related to the acoustic correlates of perturbation (see later under section “Frequency
Perturbation”) and to the noisiness of the spectrum (see later under section “Signal-to-Noise
Ratio”). Pathologies that affect the vibratory behavior of the vocal folds will usually result in
some degree of perceived hoarseness/roughness.
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18 Understanding Voice Problems

Breathy
This designation refers to the perception of audible air escape during phonation. The voice
lacks clarity of tone and is usually reduced in loudness. A breathy voice quality is related to
the amount of airflow produced. Norms for airflow measures are available (see Chapter 15),
and its measurement can verify the perception of breathiness. Excessive airflow through the
glottis is usually a reflection of inadequate glottal closure. Inability to fully adduct the vocal folds
during phonation may be the result of peripheral neurological problems, of central neurological
impairment, of the presence of a lesion that interferes with closure, or of improper use.

Tension
Tension in the voice suggests to the listener a “hard edge” to the voice, combined with hard
glottal attacks and sometimes observable muscular tension in the external neck. Tension is a
perception that is difficult to verify through measurement. Assumptions can be made about
the dynamics of vocal tension, such as increased tension of certain muscle groups, but we
do not have adequate data to determine the most salient muscle groups, nor the amount of
tension, that is acceptable in the normal voice. In many instances, tension seems to be related
to “hyperfunctional” usage patterns. However, it may also be a reflection of compensatory
behavior in the presence of some laryngeal pathology or neurological disability.

Tremor
This sign may be described as regularly rhythmic variations in pitch and loudness of the
voice that are not under voluntary control. The voice is perceived as unsteady, “wobbly,” and
quavering. Tremor is a perception that can be verified through measurement. Indeed, the rate
of the tremor can be an important factor in determining the underlying pathology (see section
“Voice Tremor” later in this chapter). Tremor of any type is usually a reflection of a central
nervous system dysfunction that results in some loss of control of the phonatory mechanism.

Strain/Struggle
The voice perceived to reflect strain/struggle behavior suggests difficulty in initiating phonation
and struggle to maintain phonation. As speech is produced, there is the perception of inability
to control voicing as it fades in and out. Actual voice stoppages may occur. Physical correlates of
these perceptions, such as voice onset time, silence, and variations of fundamental frequency and
sound pressure level (SPL), are accessible to objective measurement. However, the perception
of the strain and struggle behavior is qualitatively unique and is not well expressed by the
various objective measurements. There continues to be some controversy (Aronson, 1990;
Dedo, Townsend, & Izdebski, 1978) regarding the etiology of this type of vocal behavior.
However, it would probably be fair to say that neurological dysfunction of some sort is implicated
in many cases, in particular, when there is no evidence of vocal fold pathology, such as a mass,
that may necessitate the speaker’s use of excessive effort to produce voice. Some experts continue
to believe that in a certain percentage of these patients, the etiology is psychological.

Sudden Interruption of Voicing

A sudden unexpected drop in loudness and an equally unexpected change in voice quality to
breathy voice is a very noticeable perceptual sign. The breathy voice may last only a fraction
of a second and may occur repeatedly within an utterance, alternating with essentially normal
voicing. This perceptual sign of an abnormal voice may be the result of sudden, unexpected,
and involuntary abduction of the vocal folds or delayed adduction when making the transition
from unvoiced to voiced phonemes (Ludlow, 1995), the etiology of which is usually neurolog-
ical dysfunction. Again, these perceived voice characteristics (e.g., loudness variability, airflow
changes) are accessible to objective measurement.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 19

Diplophonia
This word literally means “double voice.” It is said to be present when two distinct pitches
are perceived simultaneously during phonation. Theoretically, this occurs when the vocal folds
are under differing degrees of tension or mass and each vibrates at a different frequency. No
consistent pattern of the perception of diplophonia as a consequence of a given pathological
condition appears to exist.

Other Behaviors
Stridor
The term refers to noisy breathing, involuntary sound that accompanies inspiration, expiration,
or both and is indicative of a narrowing of the airway at a certain point. Although the pitch
or quality of the stridorous sound is taken by some to be diagnostic (Cotton & Richardson,
1981), the judgments of these factors appear to be based entirely on perception. There have
been a number of studies that have explored the acoustic characteristics of stridor as well as
other respiratory sounds such as coughing and snoring (Beck, Odeh, Oliver, et al., 1995; Brietze
& Mair, 2007, 2008; Chien, Wy, Chong, et al., 2007; Gavriely & Jensen, 1993; Hirschberg,
1980; Malone, Black, Lyndon, et al., 1993; Moeman, De, & Pevemagie, 2002). The presence
of stridor is always an abnormal finding and one with potentially serious implications because
it is a reflection of blockage of the airway.

Excessive Throat Clearing

A frequent accompaniment to a variety of voice disorders, excessive throat clearing may represent
an attempt by the patient to clear excess mucus or other secretions from the vocal folds or a
response to the sensation of “something in the throat.” It is a natural behavior but is considered
a perceptual sign of disordered voice when it occurs frequently and consistently.

Aphonia
Consistent
This is an absence of voicing, usually perceived as whispering, that is most or always present.
Aphonia may be the result of bilateral vocal fold paralysis in which the vocal folds are unable to
adduct or a result of central nervous system dysfunction, or it may be a psychogenic problem.

Episodic
Episodic aphonia may take a number of forms. A patient may exhibit unpredictable, involuntary
aphonic breaks in voice production that last for only a fraction of a second. Another patient
may experience aphonic periods lasting minutes, hours, or even days. Yet, another patient may
experience a gradual fading of voice to the aphonic state, particularly with increased physical
fatigue. Momentary involuntary aphonic breaks are not uncommon during the speech of
patients with laryngeal pathology. Episodic aphonia may be observed in patients with central
neurological dysfunction of the flaccid type, as noted in myasthenia gravis. However, episodic
aphonia may be psychologically based.

Acoustic Signs
Voice is produced by movements of the vocal folds interrupting the egressive airstream. The
movements of the folds are controlled by the biomechanical characteristics of the folds them-
selves, the magnitude of the air pressure beneath the folds, and their neural control. Pathology
may affect these movements by interfering with any of these variables.
Vocal fold movement results in periodic interruption of the airstream at rates appropriate
for the perception of sound. Acoustics is the study of sound, and voice acoustics can provide
important information about vocal fold movement. However, acoustics is one stage removed
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20 Understanding Voice Problems

TABLE 2.3 Acoustic signs of voice problems

Fundamental frequency
Mean or average speaking fundamental frequency
Frequency variability
Phonational range
Perturbation
Amplitude
Average overall sound pressure level
Amplitude variability
Dynamic range
Perturbation
Signal-to-noise ratio (harmonics-to-noise ratio)
Vocal rise or fall time
Voice tremor
Phonation time
Voice stoppages
Frequency breaks
Normal acoustics

from the movements of the vocal folds. Although acoustic signs are, at best, imperfect mirrors of
the underlying vocal fold physiology, there is a great deal of correspondence between the physi-
ology and acoustics, and much can be inferred about the physiology based on acoustic analysis.
Moreover, acoustic parameters are probably the easiest to record and to analyze objectively.
Many acoustic parameters of the speaking voice can be measured by various instruments, such
as the Visi-Pitch (Kay Elemetrics) or one of several computer programs such as Computerized
Speech Lab (CSL) (Kay Pentax, Lincoln Park, NJ), Dr Speech (Tiger DRS, Inc., Seattle, WA),
MacSpeech Lab (GW Instruments, Somerville, MA), or Praat (Boersma and Weenink, 2010).
Many acoustic signs may be associated with any given pathology (Table 2.3). Some are
unique and others redundant. For example, jitter (variations of period from one pitch period
to the next, also known as frequency perturbation) and noise spectrum may reflect the basic
aperiodicity of the vibrating vocal folds. Jitter may be easier to measure and therefore have greater
clinical utility. But all acoustic signs reflect some aspect of the underlying pathology of interest.

Fundamental Frequency
The vibrating frequency of the vocal folds is referred to as fundamental frequency. This acoustic
characteristic is usually defined as average fundamental frequency or, in the instance of sponta-
neous speech or reading, speaking fundamental frequency. Also of interest is the variability of
fundamental frequency usually expressed as the standard deviation of frequency and sometimes
labeled the pitch sigma (expressed in semitones). The range of frequencies that can be produced
by the voice may also be of interest and is called phonational range. Finally, there is considerable
interest in the short-term stability of the vocal folds. This stability (or lack thereof ) is reflected
in the measure termed frequency perturbation.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 21

Mean Fundamental Frequency

There are considerable normative data on fundamental frequency during speech for males
and females of all ages (Baken & Orlikoff, 2000). Males should produce average fundamental
frequencies during conversational speech between 100 and 150 Hz, whereas females should
produce fundamental frequencies between 180 and 250 Hz (Hollien, Dew, & Phillips, 1971).
Figure 2.1 presents an example of fundamental frequency as a function of time for a sentence
produced by a normal female speaker. The speaking fundamental frequency was 197.97 Hz.
Pathology may affect the vibrating frequency, with the result that males or females will produce
either too high a frequency or too low a frequency. By too high or too low, we mean frequencies
that lie outside the range expected for normal phonation.

FIGURE 2.1. Example of an analysis of fundamental frequency and SPLs in a sentence produced by a
normal female speaker. The upper panel shows the waveform of the sentence. The middle panel shows a
plot of fundamental frequency. The gaps in the plot indicate no measurable fundamental frequency. The
lower panel is a plot of the envelope of the waveform to show the variation of SPL. The analysis and the
plots were made with the Praat, Ver 3.9.34, written by Paul Boersma & David Weeninkn  c 1992–2001.
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22 Understanding Voice Problems

Pitch should not be confused with frequency. Pitch is the psychological feature of the voice,
whereas frequency is the physical feature. It is possible to perceive a voice as having excessively
low pitch without an excessively low fundamental frequency (Wolfe & Ratusnik, 1988).

Frequency Variability
The standard deviation of fundamental frequency (or pitch sigma) reflects frequency variability
for a reasonably large time segment or passage. During speech, both fundamental frequency
and intensity vary depending on the sounds, the words uttered, and the intent of the message.
Computing the standard deviation of frequency during a sentence or paragraph will provide an
estimate of this longer-term variability. In Figure 2.1, the standard deviation of fundamental
frequency for the sentence of the normal speaker was 27.97 Hz. In the literature, the standard
deviation of fundamental frequency is usually expressed in semitones and labeled the pitch
sigma. The pitch sigma of this production was 3.19 semitones FL. As a general guideline,
normal speakers should be expected to exhibit pitch sigmas between 2 and 4 semitones for both
males and females (Baken & Orlikoff, 2000; Linville & Fisher, 1985; Mysak & Hanley, 1959;
Stoicheff, 1981). Patients are sometimes unable to produce normal variability. This acoustic
measure would presumably be related to the perceptual features of monopitch, although little
research has been done on these relationships.

Phonational Range
Phonational range refers to the range of frequencies that a person can produce. Normal young
adults should be able to produce a phonational range of about three octaves, with singers slightly
higher than nonsingers (Colton & Hollien, 1972; Baken & Orlikoff, 2000). Phonational range
decreases with age (Linville, 1987).

Frequency Perturbation (Jitter)

Perturbation refers to the irregularity of vibration of the vocal folds and is often referred to a
vocal jitter or vocal shimmer. If the irregularity is in the time of vibration, it is called jitter. If
the irregularity is in the amplitude of vibration, it is called shimmer. Vocal jitter is a variation
of glottal period or frequency perturbation or the change of frequency from one successive
period to the next (Casper, 1983; Horii, 1979, 1980, 1982; Baken & Orlikoff, 2000). Normal
speakers have a small amount of perturbation, which may represent variation in vocal fold mass,
tension, muscle activity, or neural activity (Baer, 1979; Pinto & Titze, 1990). An example of
perturbation in a normal speaker’s sustained vowel production is shown in Figure 2.2. The
average jitter is expressed as a percentage of the average fundamental frequency and is 1.57%.
Chapter 15 summarizes some of the data on normal perturbation.
When pathological conditions affect the vocal folds, their vibrations will show increased
aperiodicity (Hecker & Kreul, 1971; Koike, 1967b; Lieberman, 1963). Many possible patho-
logical conditions can affect vibration, including but not limited to growths on the vocal folds,
changes in the mucosa, variations in the composition of the vocal folds, variations in muscle
function, and variations in the motor control of the muscles controlling the vibration. Thus,
perturbation may not be useful for differentiating among causes but may reflect the extent or
severity of a pathological condition (Colton, Reed, Sagerman, & Chung, 1982).

Amplitude
There are several acoustic variables that reflect the amplitude or strength of the tone produced
by the vocal folds. Many are expressed in decibels. Overall, SPL refers to the average sound
pressure level of an utterance (sustained vowel, spontaneous sentence, or paragraph). Amplitude
standard deviation is simply a measure of amplitude variability, whereas dynamic range reflects
the range of vocal amplitudes an individual can produce. Finally, amplitude perturbation
(shimmer) reflects the short-term variation of amplitude from one glottal period to the next.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 23

FIGURE 2.2. Fundamental Frequency of a short segment of a sustained vowel produced by a female
speaker.

Overall Sound Pressure Level

The average overall SPL in decibels provides an indication of the strength of the vocal fold
vibration. If a person speaks softly, the overall SPL will be low. Conversely, if a person speaks
loudly, the overall SPL will be high. Everyday conversational speech may exhibit SPLs between
70 and 80 dB (Baken & Orlikoff, 2000). SPLs as a function of time for a normal female
speaker’s production of a simple sentence are shown in Figure 2.1 (lower panel). The mean SPL
was 60.6 dB.

Amplitude Variability
During speech or a reading passage, the amplitude of speaking will vary depending on the
sounds spoken and the message. Variability of amplitude during speech would be expressed as
a standard deviation. The standard deviation of SPL for the normal speaker in Figure 2.1 is
18.33 dB.

Dynamic Range
This is the range of vocal intensities that a person can produce. Normal speakers should be
able to produce minimum intensities of around 50 dB and maximum intensities of around
115 dB; intensities for males are slightly higher than for females (Coleman, Mabis, & Hinson,
1977). Figure 2.3 presents the mean dynamic ranges as a function of fundamental frequency
for the normal subjects in the Coleman, Mabis, and Hinson study. Note how the SPLs at the
extremes of the fundamental frequency range are much smaller than the dynamic ranges at the
mid frequencies.

Amplitude Perturbation (Shimmer)

As was the case for fundamental frequency, it is possible that the amplitude of the vocal fold
tone will vary from one cycle to the next. This characteristic is called amplitude perturbation
or shimmer. Growths on the vocal folds or poor neural control of the vocal folds would be
expected to affect the stability of the vocal folds. Therefore, shimmer should reflect the kind
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24 Understanding Voice Problems

FIGURE 2.3. The left panel presents the average and range for 10 male subjects, whereas the right
panel presents the average and range for 12 female subjects. Each subject produced a sustained vowel
at 10% increments of their fundamental frequency ranges and at minimum and maximum SPL.

and degree of pathology that a speaker might exhibit. Chapter 15 summarizes some of the
available data on shimmer for normal speakers.

Signal-to-Noise Ratio
Noise is random, aperiodic energy in the voice. It may occur throughout the entire frequency
range of the voice, or it may be located in certain frequency bands. Normal voices have low levels
of noise, whereas abnormal voices show greater noise levels (Emanuel & Sansone, 1969; Fujiu,
Hibi, & Hirano, 1988; Hanson & Emanuel, 1979; Isshiki, Kitajima, Kojima, & Harita, 1978;
Kitajima, 1981; Newman & Emanuel, 1991; Wolfe & Steinfatt, 1987; Yanagihara, 1967a;
Yumoto, Gould, & Baer, 1982; Yumoto, Sasaki, & Okamura, 1984). Two general approaches
have been developed for the analysis of noise components in voice.
The first, reported by Yanagihara (1967b), uses spectrograms to classify voices, using the
level of noise near the second formants of several vowels. As such, the system is qualitative
although based on objective data. It may not provide data that might differentiate subtle
differences among patients, differences that might assist in diagnosis.
The second approach analyzes the level of noise directly. An example of this approach is
the harmonics-to-noise ratio, a variant of signal-to-noise ratio (Yumoto, 1987; Yumoto, Gould,
& Baer, 1982; Yumoto, Sasaki, & Okamura, 1984). Harmonics-to-noise ratios greater than
1.0 mean that the harmonic energy was greater than the noise energy. Normal speakers are
expected to have harmonics-to-noise ratios much greater than 1.
Noise may be generated in two ways. First, there may be a noise source at or near the vocal
folds (e.g., air rushing against the open vocal fold). Second, greater aperiodicity of vibration
may show up as greater noise in the spectrum (Klingholz & Martin, 1985). Most procedures
for the measurement of noise would not be able to distinguish between these two sources.
Nevertheless, increased noise levels would be associated with problems that affect the vibrating
frequency of the vocal folds or create additional, unwanted sources of sound at the level of the
vocal folds.

Vocal Rise or Fall Time

The ability of the vocal folds to start tone production quickly or to stop phonation quickly
may be impaired by pathology. The time it takes to produce a tone of full amplitude is referred
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CHAPTER 2 I Differential Diagnosis of Voice Problems 25

to as rise time. The time it takes for the vocal folds to stop producing a tone is called fall time.
Rise time is also associated with vocal attack. It has been shown that some pathologies will
affect the time it takes the vocal folds to attain their amplitude (Koike, 1967a). Pathological
conditions affecting the neural control of laryngeal muscles would theoretically be expected to
have a pronounced effect on the rise or fall time of glottal amplitude, although little work has
been reported on these relationships.

Voice Tremor
Tremor refers to a regular variation in the fundamental frequency or amplitude of the voice
(Aronson, Brown, Litin, & Pearson, 1968a; Izdebski & Dedo, 1979; Ludlow, Bassich, Connor,
& Coulter, 1986). As a patient attempts to sustain a tone at a constant frequency, there is a
slow variation of frequency around the desired constant frequency. Usually, this variation is
between 3 and 5 Hz about the mean fundamental frequency, although it could be higher or
lower than these limits. Tremor may also be exhibited by slow variation in the amplitude of
the voice signal. Tremor is associated with variations in muscle activity levels or the control
of the muscles used in phonation. As such it is usually associated with central nervous system
dysfunction and not impaired peripheral motor control or vocal fold pathology.
Figure 2.4 presents an example of tremor on a sustained vowel. Note the slow oscillations
of SPL during the production. Measuring the distance between the peaks of the SPL oscillations
would yield the tremor rate, which in this example was about 5 Hz.

Phonation Time
Maximum phonation time refers to the maximum time a subject can sustain a tone on one
breath. As a rule of thumb, one would expect normal adult male subjects to produce a vowel
for about 20 seconds, adult female subjects about 15 seconds, and children about 10 seconds
(Kent, Kent, & Rosenbek, 1987). However, these values may vary considerably between people
and among age groups. Phonation time may vary as a function of trials. With proper instruction
and practice, as few as three trials may be sufficient (Bless & Hirano, 1982; Sawashima, 1966).
Short maximum phonation times reflect inefficiency of the phonatory or respiratory system.
Another measure of phonation time is what is referred to as the s/z ratio (Boone &
McFarlane, 1988; Eckel & Boone, 1981), or the maximum sustained phonation time of /s/
divided by the maximum sustained phonation time of /z/. A normal speaker would be expected
to sustain both the voiceless /s/ and the voiced /z/ for approximately equal durations, resulting
in a ratio of 1. However, in the presence of a disturbance of vocal fold vibratory behavior
and/or ability to close the glottis, the duration of sustained voicing for /z/ would be expected to
suffer. The resulting s/z ratio becomes increasingly larger as the discrepancy between sustained
productions of these sounds (z shorter than s) becomes greater. For a group of normal subjects,
Eckel and Boone (1981) reported average s/z ratios between 0.4 and 2. Based on the results of
their statistical tests between normal and pathological speakers, they suggest that any s/z ratio
greater than 1.4 may indicate a vocal pathology. S/z ratios for children were similar (Shearer,
1983; Tait, Michel, & Carpenter, 1980; Weinberg, Bosma, Shanks, & DeMyer, 1968).

Voice Stoppages
Normal speech consists of phonation, noises, and silences. The latter are usually brief. When
silences become longer than normally expected or appear unexpectedly during phonation,
they call attention to themselves, disrupt intelligibility, and are considered abnormal. In some
disorders, the voice may suddenly stop for a brief period of time and then revert to its previous
level. These interruptions would be observable in the spectrum of the sound.
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26 Understanding Voice Problems

FIGURE 2.4. Example of tremor in a voice. The upper panel shows the amplitude variation of this sus-
tained vowel produced by a female with essential voice tremor. The lower panel shows the corresponding
trace of fundamental frequency.

Frequency Breaks
Frequency breaks refer to sudden shifts of fundamental frequency either upward or downward.
One would expect that these would be related to the perceptual pitch breaks often reported in
the literature in the speech of patients with certain vocal pathologies.

Normal Acoustics
Finally, it is possible that a patient with a phonatory problem will exhibit acoustic features
typical of a normal voice. In other cases, the differences between a normal and abnormal voice
may be so subtle that they are not manifested in these acoustic signs.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 27

TABLE 2.4 Measurable physiological signs of voice problems

Aerodynamics
Airflows (increased, decreased, variable)
Air pressures (increased, decreased, variable)
Vibratory behaviors
Aberrant glottal pulse shape
Slowed opening and closing phases of vocal folds
Inadequate or excessive closed times
Irregularity or asymmetry of vocal fold motion
Mucosal wave changes
Muscle activity
Absent, reduced, or excessive levels
Involuntary rhythmic variations of level
Sudden, unexpected bursts of activity
Slow rise or fall in amplitude
Diminution of level with sustained phonation
Imbalance of paired muscle activity

Measurable Physiological Signs

The physiological signs that may be affected by pathology include aerodynamic features (air-
flow and pressure), vibratory behavior (contact area, waveform shape), and muscle activity (as
recorded by electromyography [EMG]). These are summarized in Table 2.4.

Aerodynamic Measurements
Airflow
During normal speech, airflow may range between 50 and 200 mL/sec, with males producing
higher flows than females (Hirano, 1981b). Usually, the measurement of airflow represents
the average flow over several glottal cycles. It is possible to measure the peak flow that occurs
during a vibratory cycle. If possible, peak flow measures should be differentiated from the
steady airflow rates that occur during speech. The steady airflow rates for speakers with various
vocal fold pathologies are greater than those for normal speakers. Normal speakers exhibit a
small amount of airflow when the vocal folds adduct, whereas speakers with vocal pathology
may produce larger than normal airflows during the presumed closed phase of the vocal folds.
If closure of the vocal folds is compromised by a lesion or poor muscular or neural control,
airflow rates will be greater than normal.

Air Pressure
The magnitude of air pressure beneath the vocal folds is important in producing vibration and
determining the intensity of the sound. Typical pressures beneath the vocal folds (subglottal air
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28 Understanding Voice Problems

pressure, lung pressure, or alveolar pressure) range from about 0.3 to 2.0 kPa,1 depending on the
loudness of the sound. Pressures between 0.2 and 0.9 kPa would be expected for conversational
speech levels (Brodie, Colton, & Swisher, 1988; Holmberg, Hillman, & Perkell, 1988; Shipp
& McGlone, 1971). Higher than normal levels may indicate either excessive lung pressures or
inefficient valving of the vocal folds.
Variability of airflow or pressure may be important to measure in persons with vocal
pathology. Excessive variation could be associated with poor motor control of the vocal folds
or of the respiratory system.

Phonation Threshold Pressure

Phonation threshold pressure is the minimum pressure required to initiate vocal fold vibration
(Titze, 1992b). It is dependent on the pitch of the phonation and determined by the degree of
opening between the vocal folds, the thickness of the vocal folds, the velocity of the mucosal
wave, and the viscosity of the tissue (Titze, 1994). It may be a very important measurement to
obtain when describing the pathophysiology of phonation and appears to reflect the level of
hydration of the vocal folds (Verdolini-Marston, Titze, & Druker, 1990).

Vibratory Behavior Measurements

Vibratory characteristics of the vocal folds are important in determining the final acoustic output
of the vocal folds. Many of these characteristics have been studied using high-speed films.
Information about some of the vibratory characteristics can be obtained from stroboscopic
examinations or by using indirect techniques for assessing laryngeal function. Some of the
more popular systems include (a) electroglottography, (b) inverse filtering of the oral airflow
waveform (flow glottogram), and (c) photoglottography.
During normal voice function, the shape of the airflow pulse or the shape of the area
pulse is different depending on the mode of vibration2 (Colton & Estill, 1981; Timcke, von
Leden, & Moore, 1958). Similarly, the shape of the airflow pulse through the glottis is different
(Rothenberg, 1981; Sundberg, 1987). In pathology, the pattern of glottal opening becomes
irregular and distorted (von Leden, Moore, & Timcke, 1960), as does the airflow pulse (Colton
& Brewer, 1985). Thus, analysis of glottal area from high-speed films or airflow waveform shape
can help to describe the vibratory characteristics of voice-disordered patients.

Muscle Activity Measurements

Pathological conditions may affect the muscles that control vocal function directly by affecting
peripheral function or indirectly by affecting the central nervous system. Clinically, muscle
function can be assessed by observing the movements of the structures themselves (i.e., vibration
of the vocal folds) or by recording the electrical activity of the muscles (electromyography
or EMG). Faaborg-Andersen (1957, 1964; Faaborg-Andersen & Sonninen, 1960; Faaborg-
Andersen & Vennard, 1964) was among the first to use EMG in the analysis of muscle function
in the larynx. Many studies since that initial work have been concerned with various muscles
of the larynx in healthy subjects as well as subjects with voice disorders. EMG is an invasive
technique and should be performed only by those skilled in its application. EMG cannot and
should not be performed on every patient (Basmajian, 1979). But for a few patients, EMG
can be a valuable technique to assess laryngeal function (Faaborg-Andersen, 1957; Koufman
et al., 2001; Lindestad & Persson, 1994; Miller & Rosenfield, 1984; Parnes, 1988; Parnes &

1 kPa is kiloPascals, a unit of pressure measurement in the MKS (meter–kilogram–second) system. 1 kPa is approxi-
mately equal to 10 cm H2 O.
2 The vocal folds may produce different modes of phonation depending on the characteristics of the mucosa, tension
in the epithelium and muscle, and other inherent physical characteristics of the tissue. See Titze (1994), pp. 97–100,
for more information.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 29

Satya-Murti, 1985; Sataloff, 2000; Sataloff, Mandel, Mann, & Ludlow, 2003; Sataloff et al.,
2010).
When a muscle is activated for a task, an EMG recording will show a fairly rapid rise in
the amplitude of the signal, followed by a consistent level of activity. When muscle activity
ceases, the recording will show a fairly rapid fall in amplitude to a low level of baseline activity
adequate to maintain the tonus of the muscle (Basmajian, 1979; Kotby & Haugen, 1970).
Pathological conditions may severely reduce or increase the background levels as well as the
muscle levels during contraction (Kotby & Haugen, 1970; Sawashima, Sato, Funasaka, &
Totsuk, 1958). Muscles may be slow to become activated and slow to turn off, or a sudden
unexpected burst of muscle activity may be superimposed on steady activity during muscle
contraction, or muscles may show normal levels of activity when first contracted but with
continued contraction, diminishing levels. There may also be differences of activity between
pairs of muscles controlling the vocal folds (Hiroto, Hirano, & Tomita, 1968). Normal EMG
levels, onsets, and offsets will be found in those patients whose laryngeal pathology does not
affect muscles or their neural control.

Observable Physiological Signs

Stroboscopic Observations
The stroboscope has found increased usage in the diagnosis and treatment of voice problems.
Recent models are relatively easy to use and provide sharp imaging (Hirano, 1981b; Hirano,
Feder, & Bless, 1983; Kitzing, 1985).
The stroboscope flashes a light at a rate equal to or approximating the vibrating rate of the
vocal folds (Alberti, 1978; Kitzing, 1985). If the flash rate is equal to the vibrating rate of the
vocal folds, they appear to stand still because they are illuminated at the same phase of their
vibratory cycle. If the rate is slightly different from the vibration rate of the vocal folds, they are
illuminated at different phases of their vibratory cycle. The effect is a slowing of the vibratory
motion of the vocal folds, permitting observation of vibratory details.
The strobe must measure the fundamental frequency of the vocal folds to function. This
measure is available to determine the regularity of vocal fold vibration.
The stroboscopic signs of laryngeal pathology are obtained from the recordings of the
strobe images (Fex, 1970; Kallen, 1932). Their recognition, like many of the signs previously
discussed, depends on the knowledge and skill of the examiner. The signs listed in Table 2.5
are based on those presented by Bless (unpublished technical manual, B & K Stroboscope
Course), KayPentax Technical manual, Hirano (1981b; Hirano & Bless, 1993), and our own
experiences with stroboscopy.

TABLE 2.5 Observable physiological signs of voice problems—stroboscopic

Degree of glottal closure
Phase closure
Vertical level
Amplitude of vibration
Mucosal wave
Vibratory behavior
Phase symmetry
Periodicity
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30 Understanding Voice Problems

Glottal Closure
The extent and configuration of glottal closure can be described based on the stroboscopic
images. The terms most commonly used to describe glottal closure include complete closure,
posterior chink, anterior chink, bowed, hourglass configuration, irregular closure, incomplete
closure.

Phase Closure
This parameter refers to the relative amounts of time that vocal folds are open and closed
during a phonatory cycle. (Be aware that the stroboscopic image is not a representation of
cycle-by-cycle behavior, but rather a composite of a number of cycles; therefore, the use of the
term phonatory cycle in discussing stroboscopic observations is not entirely accurate. With
that understanding, however, it is convenient to use the term in a stroboscopic context.) In a
whisper or in aphonic speech, the vocal folds would be predominantly open, whereas in vocal
hyperfunction, the closed phase might predominate. The gauge for normal voice produced at
comfortable loudness levels is an equal distribution of open to closed time.

Vertical Level
The vocal folds should appear to be on the same vertical level so that as they approximate,
they appear horizontally level. In cases of trauma, paralysis, or other neurological involvement,
this may not always be true. One fold may appear to lie consistently at a level lower than the
other. Because the examiner is looking at the vocal folds from above, and the view is only
two-dimensional, it is not always possible to assess their vertical level.

Amplitude of Vibration
This parameter refers to the extent of horizontal excursion of the vocal folds as they open
and close during phonation. This parameter is greatly affected by the loudness of phonation,
becoming greater as loudness increases. The expected amount of movement from the midline
should approximate one third the visible width of the vocal fold. The movement of each vocal
fold is rated individually. Differences in movement between the two folds may be diagnostically
useful information.

Mucosal Wave
The mucosal wave is a rippling motion that can be observed as it travels mediolaterally across
the superior surface of the vocal folds. (Actually, the mucosal wave starts subglottally but
is only apparent in stroboscopic recordings as a lateral disturbance.) It is a reflection of the
complex structure and behavior of the vocal folds. It is most easily seen at low or middle pitches
and usually disappears at high pitch. Normally, the mucosal wave travels smoothly across the
visible width of the vocal fold but can be limited by pathology, scarring, or stiffness. In some
instances, the wave may appear to be larger than normal. This can occur in the presence of
highly fluid-filled polypoid degeneration. This parameter is rated separately for each vocal fold.

Vibratory Behavior
This refers to the presence or the absence of vibratory behavior in the entire vocal fold. The
extent of vibratory behavior may vary from normal to partially absent to totally absent. Once
again, each vocal fold is rated independently.

Phase Symmetry
During phonation, the vocal folds should appear to move as mirror images of each other. As
both folds open in phase, they separate in unison and then approach each other and close
in unison. That action is referred to as phase symmetry. Variations in this movement can be
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CHAPTER 2 I Differential Diagnosis of Voice Problems 31

observed when the voice is disordered. The vocal folds may appear to follow one another with
one fold closing (moving toward the midline) as the opposite fold opens (moves away from the
midline). This behavior may be constant or it may be intermittently present.

Periodicity
Periodicity is an estimate of the regularity of vibration of the vocal folds. Judgments of periodicity
may be made in a number of ways. Through observation, it is possible to subjectively judge
whether the movement of the two vocal folds appears to be regular and periodic. It is most
apparent when the strobe is placed in manual mode and the time at which the strobe light
flashes is adjusted to show what appears to be a stopped frame.
That is, the flashes are set to occur at the same point within each vibratory cycle. Normal
vibration filmed in this manner will show a stopped frame with some small amount of movement
because of the natural jitter in all voices. Fluctuation and variation of the fundamental frequency
often can be observed on screen in the readout of that measure, or it can be observed as slow
or rapid variations in the apparent motion of the vocal folds.
It is not always possible that all of these stroboscopic signs can be rated. In fact, there is
some evidence to suggest that it is not necessary to rate all of these signs to obtain the salient
information about the vibration of the vocal folds (Kelly, Colton, Casper, & Brewer, 2010).

Videokymography
The technique of videokymography uses a video signal to create a more detailed analysis of
a portion of vocal fold vibration (Schutte, Svec, & Sram, 1998). The technique is shown
in Figure 2.5. A black-and-white video image is shown in the left panel. This image is used
to select one of the lines in the video signal to perform the kymographic analysis shown in
the right panel. Only the variation over time for this line of the video is shown producing a
high-speed picture of the variation of the opening (or closing) of the glottis. This technique
allows a detailed examination of a portion of the glottis that the clinician wishes to examine in
greater detail. Several studies have been reported to support the value of this technique for the
examination of the normal and abnormal voice (Howard, 2009; Jiang, Zhang, Kelly, Bieging,

Standard High-speed
Selected line

Time 32 ms
Y

X X

FIGURE 2.5. Two modes of the videokymograph camera are shown. The standard mode (left panel) displays a
black-and-white video image for proper orientation. In high-speed mode (right panel), a single line selected from the
standard image is displayed approximately 8,000 times per second. (Images courtesy of KayPentax.)
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32 Understanding Voice Problems

& Hoffman, 2008; Pontes, Madazio, Behlau, & Cantoni, 2005; Popolo & Titze, 2008; Qiu
& Shutte, 2006; Svec, Horacek, Sram, & Vesely, 2000; Svec, Sundberg, & Hertegard, 2008;
Svec, Sram, & Schutte, 2007).

High-Speed Videography
There have been many studies in which high-speed photography has been used to record the
vibrations of the vocal folds. Most of these studies have used high-speed film and were reported
in the late 1930s, 1940s, and 1950s (Moore, 1938; Moore & von Leden, 1958; Timcke, von
Leden, & Moore, 1958, 1959; Moore, White, & von Leden, 1962). In the decade starting with
2000, there have been reports of studies of vocal fold vibration using high-speed videography,
a technique that allows for the rapid acquisition of the actual motion of the vocal folds in real
time (Honda, Kiritani, Imagawa, et al., 1986; Hirose, 1988; Imagewa, Kiritani, Honda, et al.,
1986; Hirose, Kiritani, & Imagawa, 1991; Deliyski, Petrushav, Bonilha, et al., 2008; Bonilha
& Deliyski, 2008; Shaw & Deliyski, 2008). This technique holds considerable promise for use
in the clinic and will permit a more detailed examination of vocal fold motion in voices with
disorders.

Laryngoscopic Signs
In this section, we will describe those physiological signs that can be observed using a variety
of visualization techniques other than stroboscopic imaging. These techniques include indirect
mirror examination, flexible nasendoscopy, examination with a rigid oral endoscope, direct
laryngoscopy under anesthesia, and ultrahigh-speed photography and videography. Table 2.6
summarizes the observations that can help to establish a diagnosis. The ability to make these
observations may vary with the visualization technique used.

Vocal Fold Approximation

Variations of vocal fold approximation may include (a) incomplete closure along the length of
the one or both vocal folds; (b) bowing of the vocal folds, seen as a central gap; and (c) lack of

TABLE 2.6 Observable physiological signs of voice problems—

laryngoscopic
Vocal fold approximation
Vocal fold movement
Tissue changes
Pyriform changes
Anteroposterior laryngeal dimensions
Ventricular folds
Anatomical malformations and congenital anomalies
Vocal fold lengthening
Vertical laryngeal position
Involuntary laryngeal activity
Phonatory apraxia
Normal appearing larynx
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CHAPTER 2 I Differential Diagnosis of Voice Problems 33

approximation of the vocal processes, resulting in a posterior chink. These behaviors may also
be seen in videolaryngostroboscopic recordings.

Vocal Fold Movement

Adductory or abductory movement of one or both vocal folds may be reduced or absent due
to a variety of conditions. The vocal folds may (a) not adduct (move to the midline), (b) not
abduct (move away from the midline), or (c) adduct excessively or abduct involuntarily and
at inappropriate times during phonation. It is, of course, not possible to see the vibratory
movements of the vocal folds with continuous light endoscopy.

Tissue Changes
A host of changes can affect the vocal fold mucosa or deeper layers of the true vocal folds.
These include edema, inflammation, and benign, malignant, or premalignant lesions. Each has
a characteristic appearance and/or site of occurrence (see Chapter 3).

Pyriform Changes
The pyriform sinuses usually increase with adductory movement of the vocal folds. Lack of
aperture variation of the pyriform sinus cavity is usually a sign of laryngeal paralysis and is
a significant sign to note when attempting to differentiate between paralysis and arytenoid
ankylosis or dislocation (Brewer & Gould, 1974).

Anteroposterior Laryngeal Dimensions

During phonation of the sustained /ee/ vowel, the distance between the epiglottis and arytenoids
(anteroposterior dimension) is sufficient to allow visualization of the full length of the vocal
folds in most normal speakers. However, in some persons, the epiglottis and arytenoids can
be seen to approach each other during phonation, thereby shortening this anteroposterior
dimension and obscuring visualization of the vocal folds. The extent of the visualization will
depend on the phonatory conditions produced by the patient (i.e., pitch, loudness, and vowel).
Marked compression of the arytenoids and epiglottis also can be observed in hyperfunctional
or MTD voice production.

Ventricular Folds
The ventricular folds are located superior and lateral to the true vocal folds, and there is variation
in the degree of their movement. During phonation, they are usually seen to maintain their
position relative to the edge of the true vocal folds. However, sometimes, they appear to move
toward the midline, obscuring all or part of the true vocal folds (Freud, 1962). They may even
approximate each other during phonation. Furthermore, their movements may not always be
symmetrical. Involvement of the ventricular, or “false,” vocal folds in phonation may reflect an
adaptive response to a circumstance that has interfered with normal voice production.

Anatomical Malformations and Congenital Anomalies

Structures may be malformed as the result of a congenital anatomical deformity (Ferguson,
1970; Ward, 1973; Cohen, 1985) or the result of abnormal growth and development. Laryn-
gomalacia, a softness or abnormal flaccidity of the laryngeal cartilages, is the most common
congenital laryngeal anomaly and may resolve by 1 to 2 years of age (Cotton & Richardson,
1981; Hollinger & Brown, 1967). This condition shows a characteristic movement pattern of
the larynx involving a downward and anterior displacement and a bowing of the aryepiglottic
folds during inspiration. Other congenital problems include (a) subglottal stenosis, a thickening
of subglottal tissues that may be sufficient to obstruct the airway; (b) vocal fold paralysis, often
a temporary condition lasting about 4 weeks (Hollinger & Brown, 1967); and (c) laryngeal
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34 Understanding Voice Problems

web, a band of tissue (which may vary in extent) joining the two vocal folds at the anterior
commissure.

Vocal Fold Lengthening

Vocal fold lengthening is usually observed as vocal pitch is raised. This is seen fiberoptically as
a lengthening of the distance between the arytenoid cartilages and the epiglottis as the vocal
folds elongate. In some persons, the elevation of pitch does not produce this effect.

Vertical Laryngeal Position

The larynx is able to move in the vertical dimension. This can be visualized in laryngoscopic
examination as a rising of the larynx as pitch is raised and a descent below resting level as pitch
is lowered. Degree of movement varies among individuals and between trained and untrained
singers (Shipp, 1975; Shipp & Izdebski, 1975). For a further discussion on vertical laryngeal
position, please see section “High Laryngeal Position” in Chapter 4.

Involuntary Laryngeal Activity

Rhythmic involuntary movement of laryngeal structures in the resting state, in the absence
of phonation, is often seen accompanying neurologically based disorders (Parnes, Lavarato, &
Myers, 1978). Another common observation is the movement of the arytenoids toward the
midline. In voluntary effort closure, a medial squeezing and “closing down” of the entire larynx
occurs. On occasion, such a movement occurs involuntarily and is described as hyperadduction.
The normal larynx, when viewed at rest, maintains a relatively static posture with a fully open
glottis, with subtle variations in opening and closing related to inhalation and exhalation,
respectively. In some individuals, random, arrhythmic movement of various structures may be
observed.

Phonatory Apraxia
Phonatory apraxia is an inability to produce phonation volitionally. Although seemingly normal
movement of the vocal folds and other laryngeal structures may be observed during swallow
and reflexive activities, it is absent when the person is asked to phonate voluntarily (Aronson,
1990).

Normal-Appearing Larynx
Despite the perception of a vocal abnormality, the larynx may appear to be normal in structure
and function.

Interrelationships of Perceptual, Acoustic, and Physiological Signs

The signs of voice problems are not independent of one another. That is, there are interrela-
tionships among the physiological, acoustic, and perceptual signs. Simply stated, movements of
the vocal folds (physiology) create pressure disturbances in the air (acoustics) that are received
by the ear and processed by the listener (perception).
A change in the structure of the vocal folds (e.g., a lesion, a tissue change) or a change
in their manner of use (e.g., excess tension, inadequate energy) will affect the acoustic signal
produced, which in turn will alter the perception of the voice. For example, a mass on the vocal
folds may interfere with their closure. Consequently, air will continue to flow during that part
of the vibratory cycle in which the vocal folds should be completely closed. This disturbed
physiology will create a weak acoustic disturbance. Furthermore, due to the constant flow of air
through a small glottal opening, there may be an increase of noise level. The weaker acoustic
signal in combination with noise from the air striking the vocal folds will create the perception
of breathiness.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 35

As another example, the fundamental vibrating rate of the vocal folds is determined by
their mass, length, and tension. If there is a mass on the vocal folds (e.g., a polyp or nodule), the
basic vibrating rate will be altered. Vocal folds with a large mass would vibrate at a lower rate,
producing a lower fundamental frequency and the perception of a lower pitch (Isshiki, Tanabe,
Ishizaka, & Board, 1977). Masses on both vocal folds that are asymmetrical in size will each
vibrate at a different rate, producing greater aperiodicity of vibration and increased frequency
and amplitude perturbation. Greater perturbation usually is associated with the perception of
greater roughness or hoarseness in the voice.
Many signs are redundant and provide the same kinds of information but perhaps in a
different way. For example, it is often the case that jitter, shimmer, and signal-to-noise ratios
are highly correlated because they reflect the instability of the vocal folds and any noise that
they may create. This redundancy is probably good for two reasons: (a) multiple similar but
not identical observations of the same effect (i.e., instability) help to confirm the effect and
(b) should it not be possible to measure one of the variables, another can be used to assess the
effect of interest.
Signs cannot be viewed in a vacuum. Signs interrelate within a domain (physiology, acous-
tics, or perception) and across these domains. Some are redundant and assist in the confirmation
of other signs. Patterns of signs accompany different voice problems and, when considered in
combination with laboratory tests, physical examination, and the patient’s history, assist in the
accurate diagnosis of the voice disorder.

Evidence-Based Practice
Evidence-based practice (EBP) is based on the general concept of evidence-based medicine that
stresses the need for objective, experimental evidence to support the practice of medicine. In
other words, diagnostic procedures and treatment should be based on the evidence that such a
procedure produces results and affects the outcome of the patient. EBP is not simply evidence
based but also includes the patient in the equation.

What are the Expectations and Wishes of the Patient?

ASHA advocates EBP for all SLPs and audiologists. In 2004, ASHA published a report on
Evidence-Based Practice in Communication Disorders: An Introduction (ASHA, 2004). In this
report, the authors reviewed the basic concepts involved in EBP, described the levels of evidence,
and explored other topics about EBP and research that should be reviewed by all clinicians.
The principles described in this report are applicable to all disciplines in the field, including
those treating persons with voice disorders.
ASHA defines EBP as “. . . the conscientious, explicit, and judicious use of current best
evidence in making decisions about the care of individual patients.” (Sackett et al., 1996, p. 71).
The report also emphasizes that the patient must be involved in the process. But what constitutes
“best evidence,” and how does one evaluate this evidence? In Table 2.7 are presented the levels of
evidence for studies of treatment efficacy as adapted from the Scottish Intercollegiate Guideline
Network (ASHA, 2004). At the bottom of the list are clinical case studies and expert opinions,
Proceeding up the list in Table 2.7 are objective, controlled studies that ask meaningful questions
about the topics to be addressed. Level IIb features a well-designed randomized controlled study
involving control groups, blind diagnostic or treatment procedures, and sufficient number of
patients to permit meaningful conclusions. We have too few of these types of studies in voice.
Figure 2.6 presents the basic aspects of a good clinical decision process, one that we have
advocated since the first edition of this book. All three of the top bubbles contribute to the
decision process and none should predominate over the other. We like the question posed in the
middle bubble; does the new treatment (or whatever procedure we contemplate using) work?
We are beginning to see more and more research articles published that try to answer that very
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36 Understanding Voice Problems

TABLE 2.7 Levels of evidence proceeding from the lowest levels of clinical
opinion and experience (bottom rung) that may have relevance to
the problem to systematic analysis of many good randomized
clinical trials (top rung)
Meta analysis of many randomized controlled studies
Randomized controlled studies
Well designed controlled study without randomization
Well-designed quasi-experimental study
Well designed nonexperimental studies
Reports and clinical experience
From ASHA Technical Report, Evidence-Based Practice in Communication Disorders: An Introduction, 2004.

questions for the multitude of problems in voice and the various treatment protocols that have
been advocated. The arrow points the way to search for evidence. That task may be daunting
to clinicians who may be hard pressed for time in view of their heavy caseloads. But we believe
that the search will, in the long run, save the clinician time and the patient time and money.
The search for evidence may produce many articles that bear on the topic at hand. But
the clinician must be able to evaluate that evidence and determine if it supports or does not
support the use of the diagnostic or treatment procedure being considered. Furthermore, the
clinician needs to evaluate the procedure’s appropriateness for a specific patient. In subse-
quent chapters, we will try to review evidence for some diagnostic and treatment procedures
that have been suggested for patients with voice problems. ASHA has compiled a nice list
of available reviews on some of these topics and these are available at the ASHA Web site
(http://www.asha.org/members/compendiumSearchResults.aspx?type = 1&searchtext = Voice)
or you can search for EBP on the ASHA Web site to find the pages relating for current infor-
mation about summaries of studies related to voice.

Clinical
What do we Patient and
Expertise &
know? family needs
Experience

Does the new treatment Evidence,

work? search data,
Can I make it work? articles

FIGURE 2.6. Model of the clinical decision process.

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CHAPTER 2 I Differential Diagnosis of Voice Problems 37

Differential Diagnosis of Voice Problems Demonstrated in Nine Case Studies

In previous sections of this chapter, we have defined the terminology used to describe the
symptoms and signs of voice disorders. In the following sections, each of the nine symptoms
will be explored in further detail in the manner of the differential diagnosis process, using case
studies. The first case will be presented and followed by a discussion of the process of differential
diagnosis as it applies to that case. For each of the other cases, we will present only the case
study, with questions designed to guide the reader’s thinking. Tables providing those signs that
are consistent with each major symptom are also provided throughout the text. Please keep
in mind that an individual patient would not necessarily present all of the signs listed in the
tables.

Hoarseness
G.N. is a 46-year-old female referred for a consultation because of hoarseness. The patient
reported that this voice quality had existed for about 2 years and she was concerned about the
possibility of cancer. Apparently, there was a family history of cancer including throat cancer.
She had previously seen an otolaryngologist who suggested a diagnosis of vocal fold nodules.

Q. Most ent physicians will perform an indirect mirror exam on voice patients.
what would you expect to see on an indirect exam of the vocal folds in a
patient with vocal fold nodules?

G.N. also reported soreness in the neck area after speaking and sometimes this pain began
in the neck region and spread down to her chest.

Q. Is such a complaint consistent with a diagnosis of nodules and if so, why?

Prior to her first visit with us, G.N. had been referred to an SLP and received voice therapy
with no beneficial results. She reported to us that when little progress was being noted, the SLP
had told her that if she were a more forgiving person she could expect more progress.

Q. Do you think personality characteristics affect progress in therapy, and if so,

what might those be?

G.N. works with handicapped children and uses her voice considerably during the day.
She denies throat clearing, is a smoker, and drinks three to four cups of coffee a day.

Q. Most people are familiar with the effects of smoking on the body but what is
the potential significance of drinking three to four cups of coffee during the
day?

G.N.’s general ENT exam of mouth, nose, and ears was negative; however, the strobo-
laryngoscopic examination (Fig. 2.7) showed bilateral midmembranous lesions with decreased
mucosal wave at the lesion sites and prominent blood vessels leading to both lesion masses.
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38 Understanding Voice Problems

FIGURE 2.7. Patient G.N. pretreatment.

Q. Is there any significance to the decreased mucosal wave around the

masses? does the presence of a prominent blood vessel leading to a le-
sion suggest any diagnosis?

Our examination led to a changed diagnosis. The visual image was inconsistent with the
initial diagnosis of nodules. The presence of the prominent blood vessels and reduced mucosal
wave specifically around the area of the masses was indicative of bilateral vocal fold cysts. Voice
therapy is not usually very effective with cysts. However, G.N. did participate in a preoperative
visit with our SLP for counseling about the surgery and education on vocal fold anatomy
and physiology. Numerous suggestions were given to facilitate a successful surgical outcome.
Needless to say, she was also counseled by our otolaryngologist to reduce or eliminate the
smoking.
About 3 months after this initial exam, G.N. underwent surgery for removal of the two
vocal fold masses. On follow-up examination about a week later, her voice was dysphonic,
strained, and breathy. She reported that it required considerable effort to phonate. About
2 weeks after surgery, G.N. was seen again and noted a problem initiating voice production.
During the exam, she produced a very severely dysphonic voice, essentially aphonic. The strobe
exam revealed that although both vocal folds were mobile, closure was incomplete. Mucosal
wave was significantly reduced and there was mild erythema of both folds. Both vocal folds
appeared to be stiff, probably as a consequence of surgery.
As part of each follow-up examination, G.N. was counseled about voice use. With erythema
still present, the amount and type of voice use recommended were specified.
G.N. was seen again about 2 months postsurgery. She had returned to work and was talking
about 6 hours a day. Her voice was still hoarse and soft. She reported some strain in her neck but
denied any significant vocal fatigue. The strobe exam revealed bilateral vocal fold scarring. She
was referred to our SLP for further voice therapy to help increase vocal fold vibratory behavior
and achieve a more flexible voice.

Q. Think about the kind of therapy that might help achieve these goals.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 39

The patient in this case was initially referred to an SLP with a stated diagnosis, vocal nodules,
made by an otolaryngologist. The primary symptom expressed by the patient, hoarseness, was
consistent with that diagnosis. An examination of Table 2.8 reveals the perceptual signs that
may accompany the symptom of hoarseness. A number of these signs were noted in this case
during the initial voice evaluation, for example, hoarse voice quality, increased breathiness,
episodic aphonia, excessive throat clearing, and increased tension.
Table 2.8 lists those acoustic signs that would be consistent with the symptom and the
perceptual signs. In other words, our ears hear certain vocal characteristics, some of which are
accessible to measurement, thereby providing an independent corroboration of our perception.
We would therefore expect to find a certain degree of match between the perceptual and the
acoustic signs. In this case, we find reduced phonational range, a significant s/z ratio, and
reduced phonation time.
Let us examine these factors a little more closely. Remember that hoarseness was given as
a perceptual sign. A lesion, such as a nodule, on the vibratory edge of the vocal fold mucosa
will disrupt vibratory behavior by adding mass at a specific location on the vocal fold. Addition
of the same amount of mass distributed along the entire length of the vocal fold would most
likely reduce fundamental frequency. In the case of a nodule, the extra mass loads down the
vocal fold and affects its periodicity. Stiffness of the vocal fold cover is also increased due
to the biomechanical characteristics of the nodule. This disruption results in a disturbance
of the periodicity of the signal, creating a noisy signal that is perceived as hoarseness. The
increased mass and stiffness of the folds will also interfere with their ability to stretch and
vibrate at a more rapid rate; therefore, pitch elevation is affected and phonational range is
decreased.
The s/z ratio is based on the theory that vocal fold vibration sufficient to produce phonation
(i.e., /z/) can be maintained for a time period equal to the time that airflow can be maintained
without vocal fold activity (i.e., /s/). When a lesion is present on the vocal folds, there is
incomplete glottal closure or very brief contact, resulting in a loss of air and a reduction in
the ability to sustain phonation. The resulting s/z ratio becomes significantly greater than 1.4,
which is reported to be the upper end of the normal range (Eckel & Boone, 1981). Similarly, the
maximum time that phonation can be sustained is reduced. When air leakage during phonation
is of a sufficient degree, there will be a perception of breathiness.
Excessive throat clearing is a common observation in patients who have vocal nodules or
other lesions. These patients report the sensation that something is in the way of their being
able to talk and that they must first attempt to dislodge it by clearing the throat, often quite
strenuously. Unfortunately, this leads in a cyclical fashion to increased vocal trauma, which
results in an exacerbation of the symptoms, which leads to an increased feeling of the need to
clear the throat, and so on.
When a vocal fold lesion is present and maximum phonation time is reduced, it is not
unexpected to find momentary episodes of absence of voicing. This occurs because the patient is
unaccustomed to the reduction in the ability to sustain phonation or because there is insufficient
effort, air pressure, or vocal fold approximation to compensate for the extra demands placed
on the system by the presence of the lesion.
We would expect that breathiness would be reflected in greater than expected airflow
during phonation. Indeed, when this patient was seen for further examination, one of the
physiological aerodynamic signs (see Table 2.8) was increased flow. The glottal pulse shape was
aberrant, revealing the poor glottal closure.
Stroboscopic examination, which was helpful in making the diagnosis of a vocal fold cyst,
revealed reduced mucosal wave in the area of the cyst (see Table 2.5) and prominent vessels
leading into the lesions. The laryngoscopic signs noted on fiberoptic laryngoscopic examination
revealed some tissue change, which appeared as a bilateral lesion on the superior surface of the
vocal fold mucosa at a midway point along their length (see Table 2.6).
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40 Understanding Voice Problems

TABLE 2.8 Signs that may be associated with the symptom of hoarse voice
Typical complaint: “My voice is hoarse or groggy. People think I have laryngitis.”
Perceptual signs
Hoarseness/roughness
Breathiness
Laryngeal tension
Inappropriate pitch
Excessive throat clearing
Episodic aphonia
Pitch breaks
Acoustic signs
Restricted phonational range
Restricted dynamic range
Excessive spectral noise
Greater jitter
Greater shimmer
Reduced maximum phonation time and high s/z ratios
Reduced fundamental frequency variability
Observable physiological signs—laryngoscopic
Anteroposterior shortening
Functional
Increased ventricular fold activity
Functional
Compensatory
Paralysis
Fixed cord
Inadequate closure
Tissue change
Nodules
Polyps
Carcinoma
Papilloma
Leukoplakia
Edema
Cyst
(continued )
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CHAPTER 2 I Differential Diagnosis of Voice Problems 41

TABLE 2.8 Signs that may be associated with the symptom of hoarse voice
(continued )
Color change
Burns
Heat
Chemical
Other vocal fold lesions
Variations of vocal fold approximation
Posterior chink
Functional
Bowing
Reduced muscle tonus
Keyhole
Aged voice
Incomplete anteroposterior approximation
Paralysis
Functional
Ankylosis
Dislocation
Anatomical malformation
Congenital
Malacia
Stenosis
Web
Trauma
Blunt
Penetrating
Surgery
Normal larynx
Functional
Psychogenic
Misuse
Neurological
Minor or hidden tissue change
(continued )
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42 Understanding Voice Problems

TABLE 2.8 Signs that may be associated with the symptom of hoarse voice
(continued )
Measurable physiological signs
Aerodynamics
Increased flow
Increased air pressure
Vibratory
Aberrant glottal pulse shape
Irregularity or asymmetry of vocal fold motion
Mucosal wave changes
Muscle activity
Higher than normal levels
Imbalance of paired muscle activity
Normal activity

During the differential diagnosis process, the pieces must fit together. The process can
work from a starting point of the patient’s complaint, or it can work backward, as it were, from
a previously arrived at diagnosis. It is typical for SLPs to be in the position of having patients
referred with a stated diagnosis. In certain cases, however, the observations and perceptions
of the SLP and information about the acoustic and physiological signs do not seem to be
consistent with the diagnosis. Further examination is often warranted in such cases. On other
occasions, as typified by the case of G.N., the symptoms and signs may be consistent with
the diagnosis, yet the patient’s treatment course suggests the need for further exploration of
the case. It is especially important to recognize that in the case of G.N., all the perceptual,
acoustic, and physiological signs could have been consistent with the original diagnosis. The
stroboscopic and laryngoscopic signs were the determining factors in making the diagnosis,
and the suspicion of the SLP, based on sudden and unexpected worsening of a condition, was
the catalyst for reexamination of the original diagnosis.
Although some case history material was provided in the description of G.N., that part
of the diagnostic process has been only briefly considered in this chapter. We do not mean to
suggest that it is not an essential part of the process. Indeed, a thorough case history is essential
and will be fully covered in Chapter 6.
We will explore the other primary symptoms of voice problems and the differential diag-
nosis process in the remainder of this chapter. Each symptom will be accompanied by a case
study that typifies the symptom. However, we will not explain each case in the same amount
of detail provided for G.N. Consult the tables for listings of all the various signs that we be-
lieve to be consistent with the symptom. Following the process should lead the reader to an
understanding of the interrelatedness of the various factors, that is, perception, acoustics, and
physiology and the need for complete evaluation. In turn, this understanding should help to
eliminate the cookbook approach to voice problems and replace it with the ability to follow
the process of differential diagnosis in a thoughtful and reasoned manner.

Vocal Fatigue
J.S. is a 55-year-old man who has sung professionally most of his adult life, primarily in clubs
and on cruise ships (Table 2.9). Several years ago, he began to experience difficulty with his
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CHAPTER 2 I Differential Diagnosis of Voice Problems 43

TABLE 2.9 Signs that may be associated with the symptom of vocal fatigue
Typical complaint: “My voice gives out at the end of the day.”
Perceptual signs
Monopitch
Tension
Breathiness
Hoarseness
Acoustic signs
Restricted phonational range
Reduced variability of fundamental frequency
Normal acoustics
Observable physiological signs—laryngoscopic
Variations of vocal fold approximation
Functional
Tissue change
Color
Nodule
Change of laryngeal position
Muscle tension
Normal appearing larynx
Neurological
Myasthenia gravis
Measurable physiological signs
Aerodynamic
Increased airflow
Vibratory
Inadequate closed time
Muscle activity
Muscle imbalance
Excessive levels
Variation of level
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44 Understanding Voice Problems

TABLE 2.10 Signs that may be associated with the symptom of breathy voice
Typical complaint: “My voice is weak. I run out of air. People can’t hear me.”
Perceptual signs
Breathiness
Little loudness variation
Hoarse/rough
Episodic aphonia
Acoustic signs
Restricted phonational range
Restricted dynamic range
Reduced sustained phonation time
Increased s/z ratio
Excessive spectral noise
Increased perturbation
Increased shimmer
Observable physiological signs—laryngoscopic
Variation of vocal fold approximation
Incomplete a-p approximation (most prevalent)
Paralysis (adductor)
Functional
Ankylosis
Dislocation
Neurological
ALS
Parkinson’s
Myasthenia gravis
Posterior chink
Functional
Bowing
Aging
Reduced muscle tonus
Lack of movement of one or both vocal folds
Paralysis
Ankylosis
(continued )
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CHAPTER 2 I Differential Diagnosis of Voice Problems 45

TABLE 2.10 Signs that may be associated with the symptom of breathy voice
(continued )
Dislocation
Carcinoma
Lack of change in appearance of pyriform sinuses
Paralysis
Anatomic malformation
Congenital
Laryngomalacia
Trauma
Blunt
Penetrating
Surgery
Tissue change
Burns
Heat
Chemical
Measurable physiological signs
Aerodynamic
Increased airflow
Increased air pressure
Vibratory
Aberrant glottal pulse shape
Inadequate closed time
Irregularity and asymmetry of vocal fold motion
Mucosal wave changes
Muscle activity
Absent or reduced levels
Imbalance of paired muscle activity

voice. He described his symptoms at that time as an inability to increase vocal intensity without
voice “breaks” and poor quality and control in the high part of his pitch range. Initially, he was
able to compensate for these problems by manipulating his material, for example, shifting to a
lower singing key and adjusting the amplitude of his accompaniment so that he did not have
to “force” his voice. However, over the last year, he began to experience vocal fatigue during
performances. The frequency and severity of these incidents eventually caused him to suspend
his singing career. In the interim, he has had other employment but continues to experience
symptoms of vocal fatigue and difficulty increasing vocal intensity. He is not a smoker. He
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46 Understanding Voice Problems

TABLE 2.11 Signs that may be associated with the symptom of reduced
phonational range
Typical complaint: “I am not able to produce the high notes of my range during singing.”
Perceptual signs
Tension
Pitch breaks
Normal-sounding voice
Acoustic signs
Restricted phonational range
Restricted dynamic range
Observable physiological signs—laryngoscopic
Tissue change of vocal folds
Nodule
Color
Normal appearing larynx
Functional
Misuse
Improper vocal technique
Minor or hidden tissue change
Measurable physiological signs
Muscle
Excessive levels
Normal physiology

described no injuries to his neck and no surgical procedures that required intubation or affected
the head or neck. At the time of this evaluation, he was taking medications for symptoms of
gastroesophageal reflux

Q. What types of vocal and laryngeal pathology might account for the specific
contexts of j.s.’s dysphonia, that is, difficulty with quality and control of high
pitches, and inability to generate increases in vocal intensity?

J.S.’s speaking voice at the time of this evaluation was pleasant and judged to be within
normal limits in quality. Phonatory function testing revealed a fundamental frequency range of
23 semitones and a fundamental frequency average of 102 Hz. Maximum phonation duration
on a vowel sustained at comfortable pitch and loudness levels was 20 seconds. Mean and peak
flows for a briefly sustained vowel were within normal limits but were elevated on a long
sustained vowel and on a rapid syllable repetition task. Glottal resistance estimates for the
same syllable repetition task were at the low end of normal for these measures. Measures of
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CHAPTER 2 I Differential Diagnosis of Voice Problems 47

TABLE 2.12 Signs that may be associated with the symptom of aphonia
Typical complaint: “I lost my voice” or “My voice is gone.”
Perceptual signs
Breathiness
Consistent aphonia
Acoustic signs
Excessive spectral noise
Observable physiological signs—laryngoscopic
Variations in vocal fold approximation
Incomplete vocal fold approximation
Bilateral adductor paralysis
Lack of movement of vocal folds
Phonatory apraxia
CNS lesion
Measurable physiological signs
Aerodynamics
Increased airflow
Increased air pressure
Vibratory
Not applicable
Muscle activity
Unknown

cycle-by-cycle variability in the voice, that is, jitter, shimmer, and harmonic-to-noise ratio were
within normal limits.
Laryngeal imaging with rigid endoscopy and stroboscopy revealed both true vocal folds
to be within normal limits in color. Mobility of both folds on abduction and adduction also
appeared within normal limits. At rest, the left fold appeared somewhat thinner than the right.
Under stroboscopic filming, a sulcus (or vergeture) was apparent on the left fold (Fig. 2.8). The
causes of these furrows, or grooves, along the vibratory edge of the fold, are not completely
understood but may be related to cysts that rupture and produce scarring. The affected portion
of the fold’s vibratory margin is typically thin and stiff. At comfortable fundamental frequencies
and intensities, glottal closure during phonation appeared complete (Fig. 2.9). However, glottal
closure during vibratory cycles produced at high fundamental frequencies and elevated vocal
intensities was incomplete (Figs. 2.8 and 2.9).

Q. Do the symptoms and phonatory function data appear consistent with each
other? do the observations from laryngeal imaging seem to account for both
the symptoms and the phonatory function findings?
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48 Understanding Voice Problems

TABLE 2.13 Signs that may be associated with the symptoms of pitch breaks
or inappropriately high pitch
Typical complaint: “My voice sounds squeaky.”
Perceptual signs
Inappropriate pitch level
Pitch breaks
Acoustic signs
Higher than expected speaking fundamental frequency
Rapid shifts of fundamental frequency
Restricted phonational range
Restricted dynamic range
Reduced maximum phonation time
Observable physiological signs—laryngoscopic
Normal-appearing larynx
Functional
Anatomical malformations
Hormone imbalance
Web
Measurable physiological signs
Aerodynamics
Decreased airflow
Vibratory
Inadequate closed times
Mucosal wave changes
Muscle activity
Excessive levels

The impression of the voice team was that the abnormality of the left fold could account
for the patient’s symptoms. That is, increases in vocal intensity require increases in subglot-
tal pressure and an accompanying increase in resistance in the true vocal folds. In J.S., the
apparent inability of the left fold to increase resistance and maintain closure during vibra-
tory cycles appeared consistent with his complaint of poor ability to increase vocal intensity
and could also explain the elevated airflows and reduced maximum phonation times noted
on phonatory function testing. Similarly, the patient’s description of poor quality and loss of
control at fundamental frequencies high in his range could be explained by the glottic incom-
petence (persistent glottal gap during vibratory cycles) noted on laryngeal imaging for elevated
fundamental frequencies. The team felt, further, that the pathology described, and its conse-
quences for voice production, were consistent with the patient’s complaint of vocal fatigue, in
particular, during vocal performances.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 49

TABLE 2.14 Signs that may be associated with the symptom of strain/struggle
Typical complaint: “My voice just stops. I can’t get anything out.”
Perceptual signs
Strain/struggle voice
Tension
Sudden interruption of voicing
Loudness variation (uncontrolled)
Tremor
Acoustic signs
Unexpected voice stoppages
Spectral interruptions
Reduced sustained phonation time
Observable physiological signs—laryngoscopic
Effort closure of the larynx
Spasmodic dysphonia
Myoclonus
Hyperkinetic dysarthria
Mixed dysarthria (ALS)
Functional
Anteroposterior shortening of the vocal folds
Spasmodic dysphonia
Functional
Rhythmic movement of laryngeal structures
Spasmodic dysphonia
ALS
Essential tremor
Myoclonus
Arrhythmic movements of laryngeal structures
Spasmodic dysphonia
Measurable physiological signs
Aerodynamic
Decreased airflow
Increased air pressure
Vibratory
Excessive closed times
(continued )
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50 Understanding Voice Problems

TABLE 2.14 Signs that may be associated with the symptom of strain/struggle
(continued )
Aberrant glottal pulse shape
Muscle activity
Excessive levels
Sudden, unexpected bursts of activity
Involuntary rhythmic variations of level
Slow rise or fall of signal amplitude

TABLE 2.15 Signs that may be associated with the symptom of tremor
Typical complaint: “My voice wobbles. My voice is unsteady.”
Perceptual signs
Tremor
Monopitch
Monoloudness
Loudness variations/uncontrolled
Acoustic signs
Voice tremor
Restricted phonational range
Restricted dynamic range
Less variability of
Fundamental frequency
Intensity
Slow rise or fall in signal amplitude
Observable physiological signs—laryngoscopic
Rhythmic movements of laryngeal structures
Essential voice tremor
Measurable physiological signs
Aerodynamics
Periodic variations of airflow
Vibratory
Aberrant glottal pulse shape
Muscle activity
Involuntary rhythmic variations of level
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CHAPTER 2 I Differential Diagnosis of Voice Problems 51

FIGURE 2.8. Patient

J.S., a 55-year-old man,
professional singer, co-
mplaining of poor qual-
ity at high F0’s, inability
to generate loud vocal
intensities and vocal fa-
tigue during performan-
ces. Note sulcus/verge-
ture on left true vocal
fold.

J.S. had previously undergone voice therapy, and although he reported learning a great deal
about voice production and vocal hygiene, the treatment had not resolved his dysphonia. When
symptoms necessitate, the treatment for this condition is typically surgical and may involve
an attempt to alter the tissue at the site of the pathology, or a medialization or augmentation
procedure of the involved fold to allow better contact between the true vocal folds during
phonation. These options are now being considered for J.S.

Breathy
M.T., a 58-year-old woman, was referred to the voice clinic with a diagnosis of bowing of
the true vocal folds and marked dysphonia. M.T. has been an elementary teacher for over

FIGURE 2.9. Opening, and maximum closing, during vibration at comfortable F0 and
I0. Note closure is complete (and voice quality good).
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52 Understanding Voice Problems

30 years. She reported episodes of hoarseness during this time, perhaps two to three times
per year, but never so severe that she had been unable to teach. Approximately 3 months ago,
she experienced symptoms of laryngitis and became extremely hoarse and breathy. The use
of amplification in her classroom reportedly did not help significantly and she described near
complete loss of her voice by midday. Although some improvement was noted with periods of
voice rest, her dysphonia did not resolve. For the last 10 weeks, she has been unable to teach
and is performing administrative duties. Her past medical history was not significant for factors
that may have produced her dysphonia. She did not smoke and denied symptoms associated
with gastroesophageal reflux.

Q. Why are smoking and reflux histories important to know in patients? what
are the possible effects of these conditions on vocal fold tissues, and voice?
what conditions might produce the symptoms m.t. describes?

Perceptual signs noted at the initial evaluation included moderate breathiness and vocal
strain. By the end of most breath groups, voice was aphonic. Phonatory function testing revealed
fundamental frequency range reduced and speaking fundamental frequency within normal
limits. Maximum phonation time on a vowel sustained at comfortable fundamental frequency
and intensity was 12 seconds. Mean airflow for a briefly sustained vowel produced at comfortable
fundamental frequency and intensity was within normal limits. However, on a syllable repetition
task produced at 80 dB, airflows were markedly elevated. Pitch perturbation, that is, jitter, was
consistently more than 3% on five repetitions of a vowel sustained at comfortable fundamental
frequency and intensity.
Laryngeal imaging with rigid endoscopy and stroboscopy revealed both true vocal folds
within normal limits in color and symmetrically mobile on abduction and adduction. On
phonation, a persistent glottic gap during vibratory cycles was observed. The impression was
that this was produced by granulation tissue, in particular, on the right posterior true vocal
fold (Fig. 2.10). Early contact at this site appeared to frequently preclude complete closure of
the folds. The situation was more marked with increasing vocal intensity. At soft voice, closure
was more complete. Under stroboscopic imaging, mucosal wave characteristics appeared within
normal limits in amplitude and symmetry.
The clinician may be wondering if “glottic incompetence” of the type described is synony-
mous with the term “bowing.” In our experience, bowing is more often used to characterize
thinness and atrophy of the vocal folds sometimes associated with aging, or perhaps to changes
in muscle tension associated with certain neurogenic conditions. The voice team did not feel
that M.T. demonstrated bowing of this type. Certainly, however, the effects of the early pos-
terior closure produced glottic incompetence and voicing similar to what can be observed in
patients who have bowing of the true vocal folds.

Q. What factors might have contributed to the granulation tissue noted?

Based on these findings, M.T. was placed on strict voice conservation and a reflux protocol.
She was advised to avoid vocal fatigue, loud talking, and talking other than in one-on-one
situations. It was also recommended that she return to the clinic for voice therapy. One goal
of therapy would be to attempt to change vocal, and vocal fold, behavior in a manner that
minimized contact pressures at the site of pathology.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 53

FIGURE 2.10. Fifty-eight-year-old woman, elementary teacher, with complaint of pro-

gressive hoarseness and vocal fatigue over last 2 years. Note apparent granulation tissue
at arrow that interferes with closure of true vocal folds during voicing. At right, folds
are shown at maximum closure during phonation at comfortable F0 and I0 levels. Voice
quality is breathy.

Q. What voice therapy strategies can you think of that might have this effect?

In Figure 2.11, M.T.’s vocal folds are shown 2 months following her initial evaluation. The
posterior granulation tissue has resolved to some extent and closed phases of vibration appear
appropriate. Interestingly, airflow values obtained at this time were substantially below normal,
which may have reflected the patient’s attempts to conserve air in the face of glottal gapping.
Thus, a second goal of therapy was to normalize airflow and achieve a better balance between
respiratory and phonatory behavior. These objectives were successfully achieved and a sample
of the patient’s voice posttreatment is presented in audio sample on the CD-ROM. In Figure
2.12, additional improvement in vocal fold closure is noted following voice therapy, although
a small amount of residual pathology is still present.

Q. What treatment strategies can you think of that might address the issue of
achieving balance between respiratory and phonatory components of voice
production?

Reduced Pitch Range

M.D. is a 46-year-old woman referred by another ENT physician because of a persistent voice
problem. She is a professional singer who has sung locally in the community for over 20 years.
She also does much of the scheduling for the band for which she sings and notes that this
activity requires considerable telephone work. M.D. reports that she has lost the top of her
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54 Understanding Voice Problems

FIGURE 2.11. Some improvement is noted 6 weeks later following reflux precautions
and strict voice conservation.

range in recent months and is hoarse when speaking. She also describes having reflux in the
past but does not believe she has any symptoms at the present time.

Q. What would be the effect of reflux on the larynx and vocal folds? why should
the ent physician carefully evaluate reflux symptoms?

FIGURE 2.12. Additional improvement is noted following voice therapy. Frame at right
reveals good closure between the vocal folds (and good voice quality) at comfortable F0
and I0.
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FIGURE 2.13. Patient M.D. initial visit.

Previous ENT exams have indicated a mild vocal fold edema and a right hemorrhagic
lesion. Topical steroids were tried with little positive result. She was treated for reflux with little
improvement of her voice. At this time, no behavioral modifications or changes in the voice
were instituted.
A rigid strobe exam was attempted but due to her gag reflex, it was abandoned in favor
of a flexible exam (Fig. 2.13). Bilateral vocal fold edema was found along with interarytenoid
erythema. The right vocal fold had a superior surface hemorrhagic lesion.
In addition to continuing M.D.’s antireflux medication, voice therapy was also recom-
mended. Surgery was considered but not recommended at this time due to concerns that the
patient would not follow prescribed vocal rest and proper postoperative rehabilitation. M.D.
was seen for one session of voice therapy and counseled about proper voice hygiene, including
water intake, and conservative voice use, that is, restrictions on amount and type of talking.
Vocal exercises were also recommended. A second therapy session focused on using soft glides
and a more relaxed mode of phonation.
M.D. was seen again after voice therapy and reported that she was unable to continue
treatment because it was not covered by insurance. At this time, she continued to have difficulty
with her speaking voice and described “pushing through” her singing performances. She stated
that she was doing considerable talking on the phone and although she had successfully managed
to sing over the past few months, a much more demanding schedule was forthcoming and she
was concerned about her voice.
The endoscopic strobe exam revealed a slight posterior chink, erythema, and slight stiffness
on the right vocal fold. Our ENT physician was concerned that when she started singing again,
the voice would worsen. He suggested that she continue voice therapy and start lessons with
a singing coach to improve her technique. She was offered exploratory microlaryngoscopy to
better determine the problem, but she declined. She has not followed through with any surgery
nor has she continued her voice therapy sessions.

Aphonia
J.F. is a 16-year-old girl who came to our voice clinic accompanied by her mother. J.F. is a junior
in high school and lives with her mother and two younger brothers. The parents have been
separated for 5 years and the father lives in another state. J.F. was essentially aphonic and the
mother reported that this has been the situation for the past 3 months. J.F. was able to whisper
and we obtained the history from her in that mode. She reported the onset of the problem
following a sinus infection when she was only able to produce sound only at a very high pitch.
Her voice continued to worsen until only the whisper was left. Although no strain was noted
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56 Understanding Voice Problems

during the whispering, J.F. claimed that her throat often hurt and that it was a strain to even
produce a whisper. She denied any prior episodes of voice difficulty although she has had sinus
infections previously. In addition to this problem, J.F. reports temporomandibular joint (TMJ)
problems and inability to fully open her mouth that began suddenly with facial spasms while
she was lifting weights. She has been treated for this problem for the past year and a half with
treatments including physical therapy; some surgical intervention, the details of which she was
unable to provide; and muscle relaxant drugs. She claims that these treatments have resulted in
minimal improvement.

Q. What are some possible etiologies of aphonia? which of those etiologies do

you think could explain this girl’s aphonia?

Throughout the history taking and the examination, J.F.’s mother appeared very anxious
and concerned although J.F.’s affect seemed quite unconcerned. Video fiberoptic laryngeal
examination was carried out using both rigid and flexible scopes.

Q. Given the aphonia, of what value do you think a stroboscopic exam would be
and why? what would you anticipate the position of the vocal folds would be
during phonation for the various possible etiologies you considered above?

The examination revealed normal laryngeal structure and function except during speech.
In carrying out nonvocal acts such as swallowing and whistling, the vocal folds were noted
to ab/adduct normally. During whispered phonation, the vocal folds remained apart. When
asked to produce sounds such as a cough, clearing the throat, producing a high pitch, etc., J.F.’s
response was always delayed and tentative at first but nothing more than the whisper was ever
produced.

Q. What diagnosis/diagnoses would you be considering at this time?

J.F. was referred for voice therapy and was subsequently seen for six sessions. We were using
a working diagnosis of aphonia of psychogenic etiology. The patient could best be described as
a very resistant patient and very guarded. Despite the use of a variety of techniques and gentle
but pointed probing, J.F. continued to deny any problems and stated that everything in her life
was fine. She remained totally aphonic for the first two sessions.

Q. What therapy techniques would you attempt with this patient?

During the third session, the clinician indicated to J.F. that this therapy approach seemed
not to be meeting with any success and might therefore need to be terminated. Quite suddenly
her voice began to improve, but in very gradual steps. By the sixth session, entirely normal
voice was restored, but J.F. had never provided any verbalized insight into any areas of concern.
The clinician strongly recommended to J.F., to the mother, and to the referring physician that
despite the return of voice, there were issues that had not been resolved for which counseling
should be sought.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 57

Pitch Breaks or Falsetto

V.P. is a 16-year-old boy with a history of voice problems beginning in the 7th grade. He was
initially treated for reflux by his family physician without any change in his voice. A CT scan of
the neck revealed no abnormalities. He was seen twice a week for 5 weeks by an SLP elsewhere
with no improvement in his voice.

Q. What was the purpose of the ct scan of the neck? what perceptual signs of
the voice would you want information on?

V.P. described his voice problem as consisting of pitch breaks and unsteadiness. He feels
that his voice is unpredictable. He admits to being a quiet and shy person. He does play tennis
and does well academically. During the interview, he was dysphonic with numerous pitch breaks
and difficulty sustaining a low modal pitch.
V.P. was examined stroboscopically using a flexible endoscope, and no abnormalities were
noted in the larynx or vocal folds. A diagnosis of puberphonia was made and V.P. was referred
to the SLP team member for voice therapy. Interestingly, his mother accompanied V.P. to the
diagnostic session and remarked that she was not concerned about his voice. Later in the session,
she stated that the new, deep voice that V.P. had demonstrated was not his voice.
During the first and only therapy session, an appropriate pitch and smooth phonation
could be elicited in a number of ways. The remainder of the session was spent in establishing
this lower pitch and smoothness of pitch, incorporating it into conversational speech. V.P.
seemed accepting of this new sound although he is a young man who reveals little emotion.
Discussion of the problem and of the “new” sound was pursued and again, V.P.’s responses,
although relatively minimal, demonstrated a willingness to use this new voice. He was willing
to use the voice when his father returned to the room.
The SLP did not believe that further therapy was necessary because V.P. seemed comfortable
with the new sound and was using it consistently for much of the session. V.P. was asked to
be in touch with us by phone so that we could ascertain that the change was adopted. He was
urged to contact us if there were any setbacks.

Strain/Struggle
M.V. is a 48-year-old obese woman who reported difficulty with her voice for many years. She
stated that her speech is very effortful and unpredictable and at times she cannot produce any
sound. She also complained of TMJ discomfort. She is a nonsmoker and denies use of alcohol
or recreational drugs. She claims to be in fairly good health with the exception of the above
complaints. Perceptually, her speech was marked by frequent voice stoppages, some of which
were prolonged. During these prolonged stoppages, facial grimacing was noted as she appeared
to be struggling to produce voice. She also demonstrated aphonic episodes especially at the end
of sentences. She was unable to sustain a vowel in a smooth, unbroken voice quality for more
than 2 seconds.

Q. Are these symptoms consistent with a diagnosis of spasmodic dysphonia

(sd)? what other diagnoses would be part of your differential diagnostic list?

Videolaryngoscopic examination was performed using a flexible fiberscope in the con-

tinuous light condition. The patient’s symptoms were more severe during this examination
than they had been during conversation. The image was marked by much strain with the
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vocal folds remaining in the closed vibratory phase most of the time. Once again, no smooth,
uninterrupted sustained phonations were elicited.

Q. Does this information confirm the diagnosis of sd? why was a flexible fiber-
scope used rather than the rigid scope? why was the continuous light
condition used? (you may wish to return to the last two questions when
you have learned more about various examination techniques.)

The examiners felt that more information was needed at this time to assist in making a di-
agnosis. Therefore, the patient was referred to a neurologist for electromyographic examination
to determine whether there was evidence of excessive muscle action potentials

Q. Which muscles do you think might show such excess activity in sd? the
neurologist’s report indicated that the patient’s examination was normal and
failed to show any excessive muscle action potentials. what does this infor-
mation mean to you regarding your diagnosis thus far?

Further diagnostic information seemed to be needed. Therefore, the patient was referred
for diagnostic voice therapy. She was seen for three sessions of such therapy over a 3-week period
of time. Her symptoms remained the same and at no time were we able to elicit significantly
smoother voice quality despite the trial of numerous techniques.

Q. What does the term “diagnostic voice therapy” suggest to you? (think about
some voice therapy techniques you might try with this patient.)

It was decided at this time to move forward with the diagnosis of adductor SD, despite
the fact that we continued to feel that there might be an overlaid component of muscle tension
dysphonia.. This was explained to the patient and treatment with botulinum toxin (BOTOX)
recommended. The patient subsequently received BOTOX injections into the thyroarytenoid
muscles bilaterally. Her posttreatment course was typical of patients with SD. Her voice quality
was markedly improved by this treatment and she has continued to receive these injections
every 3 to 4 months on average.

Tremor
M.L. is a 74-year-old woman referred because of problems with her voice for the past few years.
Her husband agreed that her voice was problematic and further stated that her head bobbed
occasionally. The patient reported that she had experienced some spasms in her voice, but she
does not believe that her speech is effortful.

Q. What could the observation made by her husband about the head bobbing
mean?

The ENT examination revealed an elderly but alert lady with no evidence of tremor in
the arms and hands. However, head oscillations were noted. All cranial nerves were tested and
were intact.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 59

FIGURE 2.14. Patient M.L. initial visit. This figure is a sequence of frames as the patient breathed quietly.
Note the changes of position of the vocal folds indicating movement of the vocal folds and arytenoids
during breathing when the vocal folds should remain open.

A flexible stroboscopic exam revealed rhythmic oscillations of the larynx especially on the
production of a sustained /ah/ and /ee/. In the pictures shown in Figure 2.14, note the variation
of position of the arytenoids and vocal folds from image to the next. These images were taken
from a segment of the exam where the patient was not phonating and was presumably at
rest. There was periodic movement of the arytenoids and vocal folds during this time. The
companion video clip on the DVD shows these rhythmic oscillations during the first part of
the exam. A diagnosis of vocal tremor was made. Options discussed with the patent included
referral to a neurologist, medications, botulinum toxin injection, or no treatment.

Q. What kinds of medications have been used to treat tremor and has such
treatment been successful? botox temporarily paralyzes the muscles of the
larynx. how might this be expected to help in the tremor that is a central
neurological problem?

M.L. decided to have the BOTOX injection. Two units of the drug were injected into the
thyroarytenoid on each side. She was then seen for voice therapy 5 days after the injection and
noted to have a breathy voice.

Q. Why would this patient be referred to a voice therapist with this diagnosis?

The severity of the tremor appeared to have been reduced compared with the preinjection
exam. The nature of the voice therapy was discussed with the patient, and techniques were
suggested to prolong the benefit of the injection. These techniques included (1) reduction of
loudness do not try to push the voice, (2) increase speaking rate, (3) speak in shorter phrases,
and (4) allow the natural breathiness that occurs because of the BOTOX to prevail and continue
a more breathy confidential voice.
About 4 months after her first injection, M.L. was seen again for another BOTOX injection.
She reported that she had prolonged breathiness for several weeks after the first injection. The
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effects of the tremor were becoming more marked over the last few weeks. Because of her
rather long period of breathiness after the last injection, it was decided to reduce the amount of
BOTOX from 2 to 1.5 units, again on both sides. Two weeks after the injection, M.L. reported
that she had been breathy for about a week and had a little trouble swallowing. The voice
sounded strong and much smoother than prior to the injection.

Pain and Other Physical Sensations

As noted in the initial discussion of this section, symptoms are reported by patients in a variety
of ways. Thus, rather than a single case presentation representative of a single symptom category,
we will present a number of patients who complain of specific types of pain or sensations and
relate that sensory information to the underlying pathophysiology.
J.F. reports having a severe cough for several weeks. Following resolution of the cough,
he noted residual slight hoarseness that did not abate. He also complained of slight sore-
ness and burning in a localized area on the left neck near the posterior aspect of the larynx.
He was found to have a contact granuloma over the left vocal process slightly superior to
the vocal fold. This lesion was surgically removed but recurred and required two additional
surgeries. The granuloma recurred yet again. Each time the soreness recurred and was always
localized to the same spot. According to the patient’s report, the pain was exacerbated by
phonation.

Q. Why would pain be present and what could be happening during phonation
to increase that pain?

A 24-hour Ph probe study had ruled out gastroesophageal reflux as a contributing factor.
J.F. was referred for a course of voice therapy when a videolaryngostroboscopic study revealed
a consistent pattern of approximation of the arytenoids occurring prior to closure of the vocal
folds. This pattern could be described as a “toeing in” of the arytenoid cartilages.
Voice therapy was directed at changing this closure pattern and reducing the force of the
contact. The granuloma reduced in size and the symptom of pain was eliminated.

Q. What could account for the resistance of this granuloma to treatment?

A CT scan revealed the probable answer. The left arytenoid was found to be entirely
calcified. Thus, the thin mucosal cover overlying a hard and “nongiving” calcified cartilage was
unable to absorb the impact forces of arytenoid closure. Although this is not a typical case, it
again focuses attention on the need for thorough and ongoing assessment.
L.D. is a 26-year-old woman who has been singing with various local rock groups for
approximately 10 years. Until this past year, she had never experienced more than fleeting
hoarseness that never lasted more than 2 days and rarely occurred. This year she has noticed
increasingly frequent episodes of hoarseness that have now culminated in a constant degree of
hoarseness that does not go away. Although her singing voice was affected, others seemed not
to be aware of it. She was aware that she had to work harder to produce voice, that she was
changing musical arrangements to avoid the upper range (which was especially difficult), and
that she was exhausted by the end of a set. She finally sought medical attention because she
began to experience pain and soreness that radiated from the neck down to her upper chest. It
was the pain that frightened her into recognizing that she had a problem.
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CHAPTER 2 I Differential Diagnosis of Voice Problems 61

Q. In this case, what specifically do you think could be creating pain or sore-
ness? why would that soreness be in the areas described?

L.D. was found to have vocal fold nodules and a course of voice therapy was prescribed.
After two sessions of voice therapy directed at eliminating abusive vocal behavior, restricting
the amount of talking, and using very soft breathy voice when it was necessary to talk, L.D.
reported that the pain was gone. Voice therapy was continued for another six sessions with
eventual resolution of the nodules. L.D. had no further complaint of pain.

Q. Would this be consistent with your responses to the question above?

A 35-year-old minister, R.S., complained of vocal fatigue and of soreness on both sides of
the neck lateral to the larynx. This soreness was especially intense as he was giving sermons.
Laryngovideostroboscopy with a rigid oral endoscope was performed and revealed on sustained
vowel productions healthy vocal folds with good vibratory behavior, normal mucosal wave,
normal amplitude, good closure, and good phase symmetry. Very slight inflammation of the
larynx was observed.

Q. What other type of examination might you want and why?

We felt that use of the flexible nasendoscope might allow the patient to provide a sample of
the speech he uses when he gives a sermon, thereby allowing us to visualize phonatory behavior
in that mode. What we observed did not come as a total surprise. Marked anteroposterior
squeezing was noted and the entire larynx moved superiorly as he began phonation.

Q. Do these observations help to explain the nature and location of the pain
and vocal fatigue of which the patient complained? how and why?

Summary
In this chapter, a basic approach to the diagnosis of voice problems is presented. The approach,
based on the medical model of differential diagnosis, carefully considers the patient’s symptoms
(complaints) and relates them to the signs of the patient’s voice problem. There are four
categories of signs: perceptual, acoustic, measurable physiological, and observable physiological.
Nine primary symptoms are presented: hoarseness, vocal fatigue, breathiness, loss of range,
aphonia, pitch breaks, strain/struggle, tremor, and pain. These are defined and discussed within
the context of case studies of individual patients.
Signs can be observed and tested independently of the patient’s report. The major percep-
tual signs associated with voice problems include those related to pitch, loudness, and quality
as well as aphonia and nonphonatory signs. Acoustic signs include reduced phonation and
dynamic range, higher or lower fundamental frequency, perturbation, low or high intensity,
and spectral noise. Measurable physiological signs include reduced or excessive airflow and
pressure, aberrant airflow or electroglottographic waveform, reduced or excessive muscle ac-
tivity, and unusual muscle activity. Observable physiological signs are those stroboscopic signs
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62 Understanding Voice Problems

that include mucosal wave, level of folds, symmetry of vocal folds, and amplitude of vocal fold
motion. Laryngoscopic signs include tissue change, vocal fold approximation, anteroposterior
approximation, movement of the vocal folds, and anatomic malformations. Table 2.16 presents
a summary of the relationships between symptoms and signs discussed in this chapter.
Case studies have been presented to illustrate the symptoms of a voice problem and the signs
associated with each symptom. The process by which the symptoms and signs are considered
in the making of the diagnosis of a voice problem is emphasized in this chapter. The diagnosis
of a voice problem is an ongoing, dynamic process. It is incumbent on those who work with
patients with voice disorders to continue to ask questions about the nature of the problem and
the treatment approach.
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CHAPTER

3
Morphology of Vocal Fold Mucosa:
Histology to Genomics
Key Terms
morphology, mucosa, genomics, ECM, lamina propria, proteins, fibrils fibronectin,
epithelium, nodules, polyps, cyst, edema, granuloma, scar, sulcus vocalis,

Voice is created as a consequence of vocal fold vibration. The quality of voice production is dependent
upon the uniquely layered ultrastructure of the vocal folds, which is defined by its cellular and extracellular
matrices (ECMs). Pathological changes of the vocal fold ECM alter vocal quality secondary to loss of
normal vibratory function and alteration of tissue viscosity and thereby create mild to debilitating
levels of dysphonia. Select characteristics of the layered structure have been documented for normal
and pathological states, but methodologies have been limited to histological and immunohistological
analyses. Little has been completed using cellular, molecular, or genetic techniques such as gene expression
analysis (i.e., polymerase chain reaction or northern analysis) and protein synthesis analysis (i.e., Western
blot or enzyme-linked immunosorbent assay [ELISA]). Significant unanswered questions concerning the
ECM and its effect on vocal fold vibration remain. However, recent advances in protein and genetic
engineering have allowed for expansion of our knowledge of the ECM, particularly regarding its role in
providing homeostasis between the cellular elements and the surrounding stromal matrix.
This chapter begins with an introduction to ECM biology, followed by a section on characteristics
of the ECM specific to the vocal fold lamina propria. The final section contains descriptions of benign
vocal fold lesions detailed by characteristics of their ECM.

The Extracellular Matrix

The ECM is formed of connective tissue, which is composed of cells and an organized meshwork of
macromolecules. There are various kinds of connective tissue, which differ in the types and amounts
of cells and macromolecules present in their ECM. Variations in the relative amounts of the different
types of matrix macromolecules and the way they are organized in the ECM give rise to a variety of
structures. At one time, the ECM was thought to solely provide structure and support for tissue. Today’s
conventional wisdom suggests that the ECM not only provides support but also provides homeostasis
between the cell and its surroundings.
The ECM is a molecular complex composed mainly of fibrillar proteins (fibrous and interstitial),
proteoglycans, and glycosaminoglycans (GAGs). The fibrous matrix macromolecules are secreted largely
by fibroblasts (Martins-Green, 1997). Molecules and amount present vary with tissue type and at different
stages of development in a single tissue type. Hanson et al. (2010) found that vocal fold fibroblasts are
mesenchymal stem cells as defined by cell surface markers and differentiation potential. Mesenchymal
stem cells possess the ability to differentiate along multiple tissue lineages, participate in the tissue
repair and regeneration process through a variety of paracrine mechanisms, and suppress activation and
proliferation of immune and inflammatory cells.

63
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64 Understanding Voice Problems

Fibrillar proteins are frequently broken down into two functional types: structural (collagen
and elastin) and mainly adhesive (fibronectin and laminin). Collagens account for 25% of total
mammalian protein mass; there are currently 19 known subtypes of collagen (Ehrlich, 2000).
After being secreted into the ECM, the collagen molecules assemble collagen fibrils, which
can aggregate into large bundles referred to as collagen fibers. Collagen provides strength to
tissue. Elastin is made of a highly hydrophobic (water fearing) protein which, when secreted
into the ECM, becomes highly linked with other elastin proteins. Elastin is responsible for the
tissue’s ability to recoil after stretch. Fibronectin, a glycoprotein (sugar molecular with a protein
attached), has multiple forms. It is secreted into the blood by the liver. Fibronectin contains
multiple binding sites for collagen, heparin, fibrillin, integrins, and cell surface receptors.
It participates in such varied biologic activities as inflammation, malignant metastasis, and
thrombosis. Laminin is known to bind to collagen type IV, heparin, and cell surface receptors
(Alberts, 1999). Laminin and fibronectin are responsible for organization of the ECM and cell
binding in the ECM in differing tissue types.
GAGs are unbranched chains composed of repeating sugar units (Alberts, 1999). GAGs are
negatively charged and strongly hydrophilic or “water loving.” They tend to adopt an expansive
conformation and attract large amounts of sodium, which causes large amounts of water to be
absorbed by the tissue. This allows the tissue to be able to withstand large compressive forces.
Hyaluronan is the simplest of GAGs; it consists of a regular repeating sequence of sugar units.
It has been suggested that hyaluronan functions in resisting compressive forces, wound repair,
and lubrication (Alberts, 1999; Balazs & Larsen, 2000; Chan & Titze, 1999).
Proteoglycans are composed of GAGs that are also attached to a protein. They are a diverse
group. Proteoglycans are believed to play a major role in signaling between cells and serve to
regulate the activity of other proteins. Versican is a large aggregating proteoglycan that binds to
hyaluronic acid (HA). There is a family of small proteoglycans that include decorin, biglycan,
fibromodulin, and lumican. Decorin has been found to inhibit collagen formation and modify
the structure of collagen. Fibromodulin has also been shown to regulate the formation of
collagen. Lumican has a structure that is homologous to fibromodulin and has been shown to
compete with fibromodulin for collagen binding in vitro. Biglycan’s specific role is unknown.
ECM regulation is the process by which old proteins are broken down and new proteins
are made. Under normal physiological conditions, the maintenance of the proteins is tightly
controlled through a balance between synthesis and degradation. Any changes in this balance can
alter normal tissue architecture, impair tissue function, and change the mechanical support for
tissues. Net degradation or net synthesis of the ECM is most often associated with pathologic
conditions. For example, benign vocal fold lesions are thought to be a result of either net
degradation or net synthesis of the ECM.
Matrix metalloproteinases (MMPs) are a family of molecules that breakdown specific
ECM components. MMPs are made and secreted by the connective tissue and are known to
be important in both normal remodeling and in the early destruction on the ECM occurring
in many diseases (Murphy & Docherty, 1992). Twenty-four MMPs have been identified to
date, each acting against a specific protein. The major natural inhibitors of MMPs are the tissue
inhibitors of MMPs (TIMPs) (Alberts, 1999). TIMPs are complex glycoproteins that work
to prevent matrix degradation by the MMPs. There are four types of TIMPs in vertebrates,
TIMP-1, TIMP-2, TIMP-3, and TIMP-4. We know that ECM regulation is a tightly controlled
process. It is dependent not only upon total amount of secreted proteins but also upon activation
and inhibition of MMPs by TIMPs.

Vocal Fold Extracellular Matrix Biology

The lamina propria of the vocal folds is connective tissue made up of ECM. All of the com-
ponents and characteristics of the ECM described in the previous section are pertinent to the
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CHAPTER 3 I Morphology of Vocal Fold Mucosa: Histology to Genomics 65

TABLE 3.1 Vocal fold lamina propria extracellular matrix fibrous and
interstitial proteins function and location in the lamina propria
ECM Constituent Function Localization in Normal Lamina Propria

Collagen Provide strength to lamina Density increases across superficial layer of

propria (Gray, Titze, Alipour, lamina propria to deep layer of lamina propria
& Hammond, 2000) (Gray et al., 2000)
Elastin Provide stretch and recoil of Highest density in middle layer of lamina
the lamina propria (Gray propria (Gray et al., 2000)
et al., 2000)
Hyaluronic acid Effects tissue viscosity, Found throughout the vocal fold with the
tissue flow, tissue osmosis, highest density in the ILLP (Butler et al., 2001)
tissue dampening (Laurent,
Laurent, & Fraser, 1995)
Attracts water
Decorin Promote lateral association Found throughout lamina propria. Highest
of collagen fibrils to form density is in the superficial layer of the
fibers and fiber bundles in lamina propria (Gray et al., 1999)
the ECM. Binds to fibronectin
(Iozzo, 1997)
Fibronectin Induces cell migration and Found throughout the lamina propria
ECM synthesis. May be including the BMZ (Gray et al., 1999)
involved in the development
of fibrosis (Ehrlich, 2000)
Fibromodulin Plays role in collagen Found in the intermediate and deep layers of
fibrillogenesis (Ignotz, 1986) the lamina propria (Gray et al., 1999)

vocal fold lamina propria. Table 3.1 summarizes ECM components known to be in the vocal
folds. The dynamic interactions between proteins, proteoglycans, and glycoproteins provide a
balanced environment for normal vocal fold development. In general, fibrous proteins provide
structural maintenance, whereas the interstitial proteins may affect the mechanical properties
of the vocal fold through changes in tissue viscosity, fluid content thickness of lamina propria
layers, and even collagen fiber population density and size. If disequilibrium occurs in the levels
of components of the lamina propria, pathological vocal fold conditions arise.
Hirano (Hirano, 1974; Hirano & Kakita, 1985) was the first to provide a detailed descrip-
tion of the morphological structure of the human vocal folds. Histologically, the human vocal
fold has been divided into three distinct layers: epithelium, lamina propria, and muscle. The
more superficial tissue was termed the cover and the deeper tissue named the body. The cover-
body theory of phonation (Hirano & Kakita, 1985) suggests that superficial and medial tissues
slide and move over the more rigid body tissue. This theory necessitates that histologically the
superficial and medial tissues allow freedom of movement, while the deeper tissues are more
tightly bound. This is indeed what occurs ultrastructurally.

Epithelium
The epithelium of the vocal fold (medial edge) is composed of stratified squamous cells. This
is adjacent to ciliated pseudostratified epithelium of the posterior glottis, ventricular folds and
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66 Understanding Voice Problems

trachea, and stratified columnar epithelium of the epiglottis. Work by Fisher, Telser, Phillips,
and Yeates (2001) has demonstrated the presence of sodium potassium adenosine triphos-
phatase channels in the vocal fold epithelium. Additional research has revealed an epithelial
sodium channel, a cystic fibrosis transmembrane regulator chloride channel, and two aquaporin
water channels (Lodewyck, Menco, & Fisher, 2007) localized to the cell membrane of the vocal
fold epithelium (see Leydon et al., 2009, for a review). These channels are important for ion
and water movement in and out of the vocal fold, providing an intrinsic mechanism for vocal
fold hydration. As an additional protective mechanism, a mucociliary blanket, that is, a layer of
mucous, which serves to prevent dehydration of the underlying epidermis, covers the epider-
mis. Mucoserous secretions covering the vocal fold must travel from glands located superior,
anterior, posterior, and inferior to the edge of the vocal fold, as there are no mucous glands
within the vocal fold epithelium itself.

Lamina Propria
The lamina propria has been categorized into three layers based upon histological composition.
The three middle vocal fold layers are superficial layer of the lamina propria (SLLP), interme-
diate layer of the lamina propria (ILLP), and deep layer of the lamina propria (DLLP). This
is illustrated in Figure 3.1. ECM is the major constituent of superficial, intermediate, and
deep layers of the lamina propria. The innermost vocal fold layer is the thyroarytenoid
muscle.
The basement membrane zone (BMZ), a specialized ECM, divides and secures the epithe-
lium to the SLLP. This zone can be broken down into the lamina lucida and the lamina densa.
Anchoring filaments (made of collagen type IV and fibronectin) secure the lamina lucida to
the lamina densa. Anchoring fibers (collagen VII) loop between the lamina densa and SLLP.
Figure 3.2 demonstrates the electron microscopic photo of the BMZ of normal vocal folds.
The number of anchoring fibers in the BMZ appears to vary depending upon the location
in the vocal fold with the density appearing greatest in the midmembranous fold area. Gray
et al. (Gray, Pignatari, & Harding, 1994) have speculated that these anchor fibers may pro-
vide increased structural integrity for this delicate tissue transition and interface particularly

FIGURE 3.1. A schematic of the five layers of

the vocal fold—the epithelium, the three layers of
the lamina propria (superficial, intermediate, and
deep), and the thyroarytenoid muscle.
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CHAPTER 3 I Morphology of Vocal Fold Mucosa: Histology to Genomics 67

FIGURE 3.2. A normal vocal fold basement membrane zone (specialized ECM) taken with transmission
electron microscopy. The arrows demonstrate the thickened region separating the superficial lamina propria
from the epithelial cells.

in regions of high shear and stress. In addition, the population density of anchoring fibers
may be genetically determined. Briggaman and Wheeler (1975) determined that the average
person may have between 80 and 120 anchoring fibers per unit area of BMZ (in skin), whereas
someone who has the recessive gene which does not create as many anchoring fibers may
have only 40 to 60 anchoring fibers per unit area. Persons who are homozygous for the recessive
gene will have few or no anchoring fibers. Given Gray et al.’s (1994) speculation above, there
may be a specific genetic predisposition for vocal lesions in areas of high shear and stress. To
date, this speculation has not been tested.
The SLLP is a pliable, flexible region also known as Reinke’s space. In general, the SLLP
is made up of loose fibrous elements and it is the loose nature of the fibrous elements that
gives this layer the ability to move liberally during voicing. Hammond et al. (1997) found
relatively small amounts of mature elastin and collagen (type I, II, and III) and HA in the SLLP.
They report that the elastin in the SLLP is present in nonfibrillar forms, elaunin and oxytalan,
which are not verified using the common EVG elastin stain. Hahn, Kobler, Starcher, Zeitels,
and Langer (2006) stained for fibrillin-1, a primary microfibril associated with all forms of
elastic fibers and interpreted their results in conjunction with elastin staining to indicate the
spatial arrangements of oxytalan, elaunin, and mature elastic fibers. They found more superficial
localization of fibrillin-1 relative to elastin, suggesting that the superficial portion of the SLLP
contains relatively high levels of oxytalan. Decorin, fibronectin, macrophages, and myofibrils
were described by Pawlak et al. (1996) and Catten et al. (1998) using immunocytochemical
techniques in the SLLP. Macrophages and myofibrils are cells that are present when there is
inflammation and cell repair occurring. Their presence suggests constant tissue injury and
repair in the SLLP. Interestingly, minimal macrophages and myofibrils are found elsewhere
in the lamina propria. Decorin’s role in reducing fibrosis and scarring after injury is well
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documented in the dermal literature (Sayani, Dodd, Nedelec, Shen, Ghahary, et al., 2000). Its
high concentration in the SLLP may be a reason surgical procedures limited to this area rarely
involve scar formation. Fibronectin has many roles including structural, adhesive, and reparative
indicating that it may be necessary for the assembly and maintenance of other proteins and
cells of the lamina propria ECM (Hirschi, Gray, & Thibeault, 2002).
The ECM constituents observed in the SLLP differ from those seen in the ILLP and DLLP.
Overall, there is a concomitant increase in the presence of fibrous and interstitial proteins in
the ILLP and DLLP. The ILLP and DLLP make up the vocal ligament. The increased presence
of fibrous and interstitial proteins in this area of the lamina propria is suggestive of the body’s
requirements to enhance tissue ligament performance for specific vocal needs. The ILLP is
marked with a distinct elevation in the relative amount of elastin (Hirano, 1981) and collagen
and this continues through the DLLP (Hammond, Gray, & Butler, 2000; Hahn, Kobler, Zeitels,
& Langer, 2006). Hahn et al. (2006) found strong elastin staining and relatively weak fibrillin-1
staining in the ILLP, suggesting that the ILLP is made up of mature elastic fibers. Fibromodulin
and fibronectin are present in both layers. The GAG HA is present at its highest concentration
in the ILLP (Gray, Titze, Chan, & Hammond, 1999; Hahn, Kobler, Starcher, Zeitels, & Langer,
2006), particularly in the infrafold area of the ILLP. Speculatively, the presence of HA in the
ILLP may provide bulk and thickness to the vocal folds, indirectly affecting vocal fold pliability
(Ward, Thibeault, & Gray, 2002). There is a direct relationship between pliability and thickness
in vocal fold vibration (Yumoto, Katata, & Kurokawa, 1993). It has also been hypothesized that
given its influence on growth factor activity, HA in the ILLP may contribute to the maintenance
of normal lamina propria cellular physiology (Hahn et al., 2006). A schematic representation
of the major ECM constituents is represented in Figure 3.3.

Age and Gender Differences in the Lamina Propria

Little has been published assessing age and gender differences in the ECM constituents of the
lamina propria. In newborns, the entire lamina propria is uniform in structure, resembling the
SLLP (Hirano, 1981). Fibroblast density is highest in newborns, with a decrease as one ages
(Hirano, 1981).
Gender-related differences and age differences have been reported for collagen (Hammond
et al., 2000). Infants have significantly less collagen than adults and males have greater amounts
of collagen than females. The difference in the amount of collagen across the layers of the lamina
propria was minimal across ages and gender with more collagen present in the DLLP.
No gender differences have been reported for elastin, but there are age-related differences.
Sato and Hirano (1997) and Hirano, Kurita, and Sakaguchi (1989) found less elastin with
age, whereas Hammond et al. (1998) found increases in elastin with age, with a subsequent
thinning of the SLLP secondary to infiltration from the middle layer protein or atrophy. The
disparate findings between these two research groups may be explained by the methodology
used. Hammond et al. (1998) utilized a quantitative image analysis system and fewer samples.
Sato and Hirano (1997) and Hirano, Kurita, and Sakaguchi (1989) utilized a qualitative visual
assessment on more vocal fold specimens. Gray et al. (2000) suggest that the dissimilar elastin
findings may be explained by possible racial variations in the specimens.
Gender differences have been found in regard to HA (Butler, Hammond, & Gray, 2001).
Men have significantly more HA than women (3:1 men:women). When controlling for age, a
gender difference was found in the concentration of HA across the depth of the lamina propria.
Females have less HA in the SLLP and more HA in the DLLP than males. Because HA is
known to influence the biomechanics of voice production and voice quality by affecting tissue
viscosity, thickness, and hydration, it has been theorized that less HA in the SLLP implies less
protection from vibratory trauma and overuse. This may explain in part why more females
than males suffer from phonotrauma (Butler et al., 2001).
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CHAPTER 3 I Morphology of Vocal Fold Mucosa: Histology to Genomics 69

FIGURE 3.3. A schematic representation of the major ECM constituents and their
relative proportion distribution across the three layers of the lamina propria. Relative
amounts should not be compared across constituents, only across layers for each
individual constituent.

Lamina Propria in Animals

Hahn, Kobler, Starcher, Zeitels, and Langer (2006) found that mean HA levels in animal
model LPs were approximately three to four times higher than that in human lamina propria.
Histologic evaluation of elastin staining has revealed that the porcine LP elastin distribution is
most similar to that of the human (Hahn et al., 2006); however, HA staining in pig vocal folds
was most intense along the epithelial border and in the inferior ILLP. Hahn, Kobler, Zeitels,
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and Langer (2006) determined that porcine collagen distribution is also most similar to that of
humans.

Biology of Benign Vocal Fold Lesions

The increasing density of the layers of the vocal fold dissects it into two functional biomechanical
layers—the body and the cover. The body is composed primarily of muscle, whereas the cover
is the LP. The shape (determined by the ECM) and tension of the cover determine the vibratory
characteristics of the folds and subsequent vocal quality. The shape and tension may be modified
by benign lesions, which arise from the cover and change the biomechanics and thus the voice
source. The composition of the ECM of the LP is altered in benign lesions. This change
in ECM composition directly influences tissue viscosity that can lead to higher phonation
threshold pressure necessary for voice production (Titze, 1992). As technology progresses,
more details regarding the genetic and molecular cellular activity responsible for causing these
changes are revealed. As the molecular ultrastructure is defined for pathological states, a better
understanding of how these alterations subsequently affect the vibratory characteristics of the
vocal folds can be determined. To date, there is limited published information about the various
vocal fold benign lesions. Table 3.2 summarizes the molecular ultrastructure of common benign
laryngeal lesions.

Vocal Fold Nodules

It is generally agreed that vocal nodules result from trauma to the vocal folds. Changes in the
BMZ appear to reflect that trauma. Thickening of the BMZ (Gray et al., 1994) and increased
fibronectin (Courey, Shohet, Scott, & Ossoff, 1996), which may represent tearing forces and
subsequent wound repair in the subepithelium, have been reported. Figure 3.4 compares a
normal vocal fold BMZ with the BMZ of a vocal fold with nodules. It is easy to see the
increased thickening of the BMZ in the presence of vocal fold nodules.
Kotby et al. (1988) further report nodular lesions with gaps at the intercellular junctions,
disruption and duplication of the BMZ, and collagen fiber dispositions. It has been proposed by
Gray et al. (1995) that the disorganized BMZ (particularly injury to the anchoring fibers) may
leave the vocal fold in a predisposed state for repetitious injury, and the fibronectin deposition
may lead to increased stiffening of that part of the membranous fold.

Vocal Fold Polyps

Histological analyses of vocal fold polyps and comparison with normal vocal fold lamina propria
structure have found less fibronectin deposition, more vascular injury (thrombosis), fibrin and
iron deposition (Dikkers & Nikkels, 1995; Courey et al., 1996) in the presence of vocal fold
polyps. Karahan, Baspinar, Yariktas, and Kapucuoglu (2007) found that vocal fold polyps
showed high levels of MMPs (MMP-2 and MMP-9) and cyclooxygenase-2. Analysis of protein
levels with Western blot demonstrated decreased collagen levels and increased fibronectin levels
in five polyps (Thibeault, Gray, Li, Ford, Smith, et al., 2002). Increased fibronectin may be
responsible for the decreased mucosal wave observed with videostroboscopy preoperatively in
these five patients. Analysis of genomic messenger RNA levels in these same samples revealed
increased transcription levels for decorin and downregulation of transcription factors necessary
for HA and fibromodulin synthesis.
The state of the BMZ in vocal fold polyps is presently unknown. Thibeault et al.
(Thibeault, Hirschi, & Gray, 2003) using microarray genetic analysis to measure gene ex-
pression levels in one vocal fold polyp report abnormal levels for genes that are involved in
epithelial differentiation and BMZ formation. In a study of 11 Reinke’s edema specimens and
17 polyps using microarray analysis, 65 genes were found to differentiate polyps from Reinke’s
edema (Duflo, Thibeault, Li, Smith, Schade, et al., 2006). Polyps expressed genes related to
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CHAPTER 3 I Morphology of Vocal Fold Mucosa: Histology to Genomics 71

TABLE 3.2 Extracellular matrix characterizations of benign vocal fold

lesions
Vocal Fold
Lesion Histopathology Genomic Pathology

Nodules Abnormal BMZ with altered anchoring Not reported to date

fibers
Increased fibronectin
Increased collagen
Polyps Fibrin Altered gene levels for
Iron deposition epithelial genes involved in
Decreased fibronectin BMZ organization
Thin BMZ Increased fibronectin protein
Decreased collagen protein
Cysts Lined with columnar or squamous Not reported to date
epithelium
Thickened BMZ
Reinke’s Edema Hemorrhage Decreased messenger RNA
Fibrin levels for fibronectin
Edematous lakes Increased messenger RNA
Thickened BMZ levels for decorin
Granuloma Focal ulceration Altered gene levels for genes
Desquamating epithelium involved in wound healing and
Edematous lamina propria inflammation
Inflammatory cells Neutrophils
Scar Conflicting reports of collagen levels Not reported to date
depending on age of scar
Conflicting reports of procollagen levels
depending on age of scar
Increased fibronectin
Decreased elastin
Decreased HA
Decreased decorin
Decreased fibromodulin
Sulcus Vocalis Epithelial thinning Not reported to date
Loss of layered lamina propria,
Inflammation

inflammatory processes and fibroblast growth. Loire et al. (1988); Kotby, Nassar, Seif, Helal, and
Saleh (1988); and Courey, Shohet, Scott, and Ossoff (1996) report atrophy of the epithelium
of VP with a thin BMZ and an intact BMZ, respectively, in their histological samples.

Vocal Fold Cysts

Vocal fold cysts can be lined with columnar or squamous epithelium (Shvero, Koren, Hadar,
Yaniv, Sandbank, et al., 2000), with a BMZ thickness that is between that of polyps and nodules
indicating some degree of BMZ injury (Courey et al., 1996).
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72 Understanding Voice Problems

B
FIGURE 3.4. A. A light microscope image of a normal vocal fold with a normal basement membrane
zone. B. A light microscope image of a vocal fold polyp with thickened basement membrane zone.

Reinke’s Edema
Reinke’s edema is manifested by edema of the SLLP and collagen fiber disruption (Sakae,
Imamura, Sennes, Mauad, Saldiva, et al., 2008). Dikker and Nikkels (1995) have described
hemorrhage, fibrin, edematous lakes, and thickening of the BMZ. Using transmission electron
microscopy to examine the morphology of 54 Reinke’s lesions, Garcia-Martins et al. (2009)
found abundant blood vessel proliferation with inflammatory cells and fibroblasts in the SLLP.
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CHAPTER 3 I Morphology of Vocal Fold Mucosa: Histology to Genomics 73

7
8
1
2
2
3
3
4 1
5
4

A B 6

1 2
1
3 3
4
4
C D
FIGURE 3.5. Schematics of repeatedly observed microstructural subdivisions within vocal
fold lamina propria by species. A. Humans. B. Dogs. C. Pigs. D. Ferrets. Numbers correspond
to the following regions: (1) basement membrane zone (BMZ), (2) superficial layer of the
lamina propria (SLLP), (3) intermediate layer of the lamina propria (ILLP), (4) deep layer of the
lamina propria (DLLP). (From Hahn, M. S., Kobler, J. B. Zeitels, S. M., & Langer, R. (2005).
Midmembranous vocal fold lamina propria proteoglycans across selected species. Annals
of Otology, Rhinology, and Laryngology, 114, 451–462. Copyright 2005, Annals Publishing
Company.)

Genomic messenger RNA levels were measured in four Reinke’s edema samples; decreased gene
expression levels for fibronectin and increased decorin levels were reported (Thibeault et al.,
2002). Increased decorin levels in the SLLP may be present as an active reparative process.
Duflo et al. (2006) reported differential oxidative gene expression in tissue specimens collected
from patients with Reinke’s edema compared with benign vocal fold polyps; this suggests a
protective response against cigarette-smoke–mediated oxidative stress and cell death. Branski
et al. (2009) found elevated gene expression for a microsomal enzyme with anti-inflammatory,
antiproliferative, and antiapoptotic characteristics.

Vocal Fold Granuloma

Histological structural analysis of granulomas reveal defined ulceration, with desquamating
epithelium and lamina propria that is swollen and marked with infiltration by chronic in-
flammatory cells and neutrophils (Shin, Watanabe, Oda, Umezaki, & Nahm, 1994). Genomic
microarray analysis for messenger RNA levels (Thibeault et al., 2003) report altered gene levels
for inflammatory and wound healing genes. This indicates that granulomas are an injury. This
would be consistent with the literature that suggests that granulomas are a result of vocal abuse
and/or gastroesophageal reflux. Both cause injury to the larynx.
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Vocal Fold Scarring

Vocal fold scarring causes significant changes in the physical properties of vocal fold tissue,
altering the body–cover relationship and inhibiting propagation of normal mucosal wave.
Histological characterization of fibrous and interstitial proteins of the lamina propria in vocal
fold scarring has been utilized in animal models at different points postinjury (see Hansen
& Thibeault, 2006, for review). Differing results have been reported depending upon animal
model and healing time. In the rabbit model, there is a maximum increase in HA 5 days
postinjury, which is similar to levels found in uninjured vocal folds and skin. Scar tissue at
2 months (Rousseau, Hirano, Welham, Thibeault, Bless, et al., 2002; Thibeault, Gray, Bless,
Chan, & Ford, 2002), ultrastructurally, has been defined by no change or decrease in collagen
levels, with markedly increased procollagen levels (precursor to collagen) and fibronectin with
decreased HA, elastin levels, decorin, and fibromodulin (Thibeault, Bless, & Gray, 2003). More
chronic scar formation (6 months) is characterized by increased collagen, decreased procollagen,
and decreased elastin (Rousseau et al., 2002). The canine model of wound healing shows similar
results to the rabbit model with elevated procollagen at 2 months, increased collagen deposition
at 6 months, and reduced elastin and elevated fibronectin in the SLLP at both 2 and 6 months,
respectively (Rousseau, Hirano, Scheidt, Welham, Thibeault, et al., 2003). In the pig, there
was reduced HA and increased collagen deposition by day 15 postinjury (Rousseau, Sohn,
Montequin, Tateya, & Bless, 2004). The rat model shows an increase in HA and collagen
by day 3 postinjury, peaking at day 5, and then decreasing again, as well as an increase in
fibronectin up to 4 weeks postinjury (Tateya, Tateya, Sohn, & Bless, 2006). It is theorized
that elevated fibronectin in young scar is gradually replaced by collagen sometime between 2
and 6 months postinjury. Similarly, procollagen synthesis is thought to be related to decreased
levels of fibromodulin. The relationship between the tissue stiffness observed in vocal fold scar
and fibrous and interstitial proteins does not seem to be straightforward and requires further
investigation. Advances in regenerative medicine for treatment of vocal fold scar have included
administration of HA into injured or scarred vocal folds, growth factor therapy, and cell therapy
using stem cells or mature fibroblasts.

Sulcus Vocalis
Sulcus vocalis has been described as an indentation, groove, or furrow along the medial edge of
the vocal fold with varying thickness involving differing layers of the lamina propria depending
on the severity of the sulcus. The lesion may only involve the epithelium, or it may involve
several or all of the layers of the lamina propria up to and including the thyroarytenoid muscle.
Histopathological findings include epithelial thinning and loss of the lamina propria cellular
layered structure with minimal inflammatory response (Ford, Inagi, Khidr, Bless, & Gilchrist,
1996).

Summary
Vocal fold biology is intricate. Normal vibratory function is dependent upon the complex
interactions within the ECM. An understanding of the normal layered structure of the vocal
folds is necessary for all clinicians. Knowledge of the pathological changes that occur with
the presence of a vocal fold lesion provides a better understanding of changes that are seen
concomitantly in vocal fold vibratory patterns and perceived in voice quality. At this time, we
have a basic understanding of the vocal fold structure. This is an exciting and rich area for
research. With the use of more advanced molecular and genetic techniques, our knowledge of
vocal fold biology and genetic implications for voice disorders is expected to expand rapidly
over the next decade.
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CHAPTER

4
Phonotrauma: Its Effects on
Phonatory Physiology
Key Terms
phonotrauma, attack, squeezing, puberphonia, glottal fry, ventricular, aphonia, abuse,
misuse, coughing, screaming, drugs, nodules. polyps, cysts, edema, laryngitis, sulcus
vocalis,

The term “phonotrauma” was proposed by Verdolini (Verdolini, Hess, Titze, Bierhals, & Gross, 1999) as
a more appropriate and less punitive term than the traditionally used “vocal abuse” terminology. Although
we agree with Verdolini’s arguments in this matter and accept the use of the term phonotrauma as an
umbrella term, there are still times, it seems to us, when the nature of phonatory behavior is best described
by the word “abusive,” that is, the behavior abuses (or traumatizes, if you prefer) the tissues of the vocal
folds sufficiently to cause a change in the voice. We caution voice clinicians, however, to explain their use
of terminology to patients in ways that do not “blame the victim.” Other useful terms include “misuse”
or “inappropriate use” of the voice, which will be described later in this chapter.
Phonotrauma refers to vocal behaviors that are thought to contribute to the cause or development of
voice problems. Some of these behaviors are considered sufficiently abusive to damage vocal fold tissues.
Others simply represent the misuse, or inappropriate use, of the voice. The behaviors are thought to con-
tribute to the laryngeal tissue changes that result in the formation of such benign lesions such as nodules,
polyps, and cysts contact ulcers. Other behaviors, or the extent to which they are present, may be thought
of as mechanisms of misuse. Such behaviors may or may not result in laryngeal tissue changes. What
behaviors actually damage tissues? How much trauma can laryngeal tissues tolerate? How do patterns of
phonotrauma evolve, and what maintains them? How does phonotrauma create voice problems? These
questions must be asked, and surprisingly few answers are available. In this chapter, we will discuss the
current state of knowledge about phonotrauma, including both abuse and misuse categories.

Misuse, Inappropriate Use

Misuse suggests voice production behaviors that distort the normal propensity of the phonatory mech-
anism to work effectively and efficiently. An efficient system produces its best results with a minimum
effort. A car engine whose various components are in top working condition so that its operation is
smooth and uses the least energy to perform its work is said to be operating efficiently. Similarly, a
phonatory system in which the individual components are healthy and in tune with the coordination
and interaction of its supporting parts and systems produces voice in an efficient manner.
There are a number of ways in which smooth operation of the voice may be altered. Each of us
can voluntarily produce voice in a variety of different ways, some of them efficient and some inefficient.
Those who work with disordered voices should be able to produce inefficient as well as efficient voice
to better understand how various changes in voice production can be made. For example, take a breath,
and as you begin to speak, tighten your chest to the point of almost holding your breath. Without taking
another breath, try to count to 10. How does it feel to talk like that? Where do you feel the tensions?
75
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TABLE 4.1 Characteristics of vocal behaviors categorized as misuse

A. Increased tension or strain
1. Hard glottal attack
2. High laryngeal position
3. Anteroposterior laryngeal squeezing
B. Inappropriate pitch level
1. Puberphonia
2. Persistent glottal fry
3. Lack of pitch variability
C. Excessive talking
D. Ventricular phonation
E. Aphonia and dysphonia of psychological origin

How did it change the sound of your voice? As another example, try to squeeze your larynx
tightly and speak in a hoarse voice. Think about how that feels and what you have done to
change the sound of your voice. As a final experiment, pick a pitch about two tones above
your present pitch level and try to converse, and then do this at a pitch about two tones
lower than your comfort level. Has your larynx height changed? What does it feel like to try
to do this? What does it do to your breathing, your degree of tension, and your inflection
patterns?
All of these activities could be categorized as vocal misuse, yet all are within the ability of
each of us to produce. In Table 4.1, we have identified some of the behaviors that, when used
habitually, constitute misuse. Each of these will be discussed in the following sections.

Increased Tension or Strain

Descriptions of what is meant by increased vocal tension abound but frequently lack speci-
ficity. The judgment of vocal tension is most frequently made on a subjective basis. The
subjectivity may be the reporting by the patient of the sensation of tension, or sometimes
even pain, accompanying speaking, or it may be the judgment of the voice clinician based
on auditory and/or visual observations. There are few objective methods of documenting ten-
sion, and there are none that can be put to routine clinical use to provide measurement of
specific muscle tensions. Biofeedback using externally placed electrodes has been attempted,
but it is not at all clear what specific muscles are being tapped, nor is there sufficient in-
formation available to identify which muscles are the most significant in assessment of vocal
tension.
In cases of vocal misuse, the laryngological examination may be negative for the presence
of lesions, though with, perhaps, a suggestion of increased redness or slight swelling of the vocal
folds. In some cases, it is noted that a strand of mucus forms and reforms between the vocal
folds at the nodal point, a sign thought by some to be an early indication of, or tendency toward,
nodule formation. The phonoscopic exam (described in Chapter 10), which pairs visualization
of the larynx endoscopically with a voice evaluation, can be of great help in identifying patterns
of excessive laryngeal tension in some patients. The specific, observable signs of that tension
include glottal attack, high laryngeal position, and excessive medial compression of laryngeal
and supralaryngeal structures.
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CHAPTER 4 I Phonotrauma: Its Effects on Phonatory Physiology 77

In any discussion of behaviors thought to comprise vocal or laryngal “misuse,” it is impor-

tant to note that the normal larynx is capable of a wide range of behaviors. For example, when
the larynx is protecting vocal folds, with or without medial movement of the airway, it is usual to
see ventricular fold medialization; approximation of the arytenoid cartilages with the epiglottis
by the arytenoids, or medial compression; and squeezing of the false supraglottal structures
so as to obscure visualization of the laryngeal inlet and true vocal folds. In fact, these gestures
are necessary and critical to safe swallowing. Similarly, such behaviors may sometimes reflect a
strategy for achieving a certain vocal output, for example, when we see anteroposterior approx-
imation of the arytenoids and epiglottis during loud voice production. Our understanding of
normal laryngeal behavior is in fact not complete, and we need to be careful in characterizing
any isolated behavior as hyperfunctional or abusive. However, when we observe behaviors that
appear to require excessive effort or more work to produce voice, and when these behaviors
appear to contribute to our perception of the speaker’s voice as dysphonic, then it is reasonable
to think of them as comprising “misuse.” A number of authors have discussed behaviors that
may fall into this category (Koufman & Blalock, 1991; Morrison & Rammage, 1993; Rosen
& Murry, 2000).

Hard Glottal Attack

The hard glottal attack or glottal coup is a term that describes a manner of initiating vowels,
usually characterized by rapid and complete adduction of the vocal folds prior to the initiation of
phonation. This adducted state, which may be accompanied by considerable muscle tension,
requires that subglottal pressure be increased to overcome vocal fold resistance and initiate
phonation. The characteristic sound of a hard glottal attack is an abrupt, explosive, and hard-
edged onset of phonation. This form of voice initiation is often visible fiberoptically, especially
when subjects are asked to produce isolated vowel sounds (Casper, Colton, Brewer, & Woo,
1989). It appears to be produced in at least two ways. In one method, medial compression
of the vocal folds is observed almost simultaneously with the onset of phonation. The second
variation is characterized by prephonatory laryngeal constriction in which the ventricular folds
approach each other, as do the arytenoids and the epiglottis, obscuring visualization of the true
vocal folds. As phonation is initiated, there is a reduction in the forced adduction and a sudden
springing open of the larynx as the true vocal folds become visible. Again, it is important to
interpret such behaviors with caution. We have observed occasional evidence of this hard glottal
attack in speakers who were judged to have normal voices and who were not experiencing voice
problems. It is a behavior that may occur on occasion in most speakers. In some instances, the
behavior may be a reaction to the examination procedure and the tensions associated with it.
Whether or not this particular behavior is identified, as evidence of misuse must depend in
part on the degree of its presence and the circumstances under which it is observed. In general,
when the hard glottal attack is present to a significant degree, it is but one of several behaviors
that give evidence of increased tension and strain.

High Laryngeal Position

Vertical laryngeal height has been the subject of some study and controversy. It has been
reported that untrained singers show greater laryngeal elevation with increased pitch level
than do trained singers (Shipp & Izdebski, 1975; Shipp, 1987). There are different schools
of thought among singers, singing coaches, and voice scientists relative to the benefits of
maintaining a low laryngeal position. Many believe that raising laryngeal height with elevation
of pitch is improper singing technique and detrimental to the voice (Sundberg & Askenfelt,
1983). However, Sundberg reported that an X-ray study of two well-trained female singers
revealed an increase in vertical laryngeal height with an increase in pitch, in what he described
as a “very elegant” and “well-trained” behavior (Shipp, Guinn, Sundberg, & Titze, 1987). It
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was suggested that varying laryngeal position may be useful and that raising the larynx during
singing may not be abusive.
There are many differences between singing and speaking that make it difficult to suggest
that a particular behavior in one activity is the same or has the same effect in the other activity.
Raising the larynx results in (a) a shortening of the vocal tract, with a subsequent raising of all
formant frequencies; (b) a stiffening of vocal fold tissues that alters the vibratory pattern and
increases fundamental frequency; and (c) an increased tendency for tight vocal fold closure.
This tight adduction is a desirable and essential part of the swallowing process wherein the
larynx elevates and a tight valving maneuver ensues, thereby protecting the lower airway. In
speaking, it is not variability of laryngeal height that is suggestive of excessive tension but rather
a speaker’s tendency to consistently speak with the larynx in an elevated position. Titze believes
(Shipp et al., 1987) that the human body seems naturally to do that is easiest to do, and it seems
to optimize itself for a given task. Furthermore, he suggests that the speaker who constantly
maintains a low laryngeal posture may be using more energy in doing so than the speaker who
allows the mechanism to move freely.
Vocal tension is characterized by increased tension in both the intrinsic and extrinsic
laryngeal muscles. However, we are not yet able to isolate the contributions of each muscle
group to voice problems associated with misuse. Indeed, the system as a whole is so interactive
that when excessive tensions exist in one muscle, they will probably occur also in some other
muscles. Thus, although laryngeal height is primarily controlled by extrinsic laryngeal muscle
activity, we cannot attribute a voice disorder to that condition alone and must recognize the
total physiological disturbance. A high laryngeal position may be related to excessive tension
in both extrinsic and intrinsic muscle groups. Sundberg and Askenfelt (1983) stated that “the
muscles used for raising the larynx also may affect the way in which the vocal folds vibrate”
(p. 307), which underscores the relationship between larynx height and the voice source. Shipp
(1987) addressed this relationship and reported that increased stiffening of the vocal fold margin
results from the upward stretch of tissues created by laryngeal height elevation.
It is not unusual for patients with this particular pattern of hyperfunction to report sen-
sations of pain or soreness in the neck lateral to the larynx, sometimes radiating upward or
downward. These patients also report that their voices tend to become worse with increased
use and that by the end of the workday, they feel it takes too much effort to talk.

Anteroposterior Laryngeal Squeezing

In the endoscopic laryngeal examination of voice-disordered patients, we have often observed
(usually in the absence of observable pathology) a “squeezing” of the larynx in which the
epiglottis and the arytenoids approach each other during phonation. A similar but not iden-
tical movement is typical in the production of the low back vowels (e.g., /ah/), when the
tongue position dictates a posterior movement of the epiglottis. That movement is a natural
one in which none of the “squeezing” elements is present. During production of the vowels
/ee/ and /oo/, the epiglottis is normally expected to be pulled somewhat anteriorly and supe-
riorly, making the vocal folds fully visible. This does not occur in patients with a “squeezed”
larynx. These patients, even in the production of the /ee/ and /oo/ vowels, as well as other
stimulus materials heavily loaded with these vowels, demonstrate anteroposterior “squeezing”
behavior to the extent that visualization of the true vocal folds along their full length is often
obscured.
Another vocal maneuver that is normally expected to “open” the larynx when it is being
viewed endoscopically is pitch elevation. However, persons who tend to habitually use very
tight laryngeal posture with anteroposterior shortening maintain this closed posture even as
they raise pitch. In fact, they often encounter difficulty in raising pitch and may exhibit a
reduced phonational range. We believe that this vocal behavior is an indication of disturbed
phonatory physiology, probably due to excess strain and tension.
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Inappropriate Pitch Level

A common concept in the voice literature is that of optimum pitch. Clinicians are instructed
that the use of a too high or a too low habitual pitch level is a frequent cause of voice disorders.
Much therapy time is spent in identifying what is purported to be an individual’s optimum
pitch, and therapy is then directed toward teaching the patient to use that pitch. We have
difficulty with this approach for a number of reasons.
If the fundamental frequency of a person’s voice is altered by pathology, for example, it
seems to us that attempts to “measure” an optimum pitch are immediately flawed. The most
common methodology espoused for obtaining the so-called optimum pitch was first described
by Fairbanks (1960) and involves obtaining a measure of phonational range. Recall, however,
that phonational range is often reduced in the presence of certain laryngeal pathologies and
voice disorders. It is important to recognize that despite the apparently widespread use of the
concept of optimum pitch, there are no data to demonstrate or document its validity nor its
therapeutic efficacy. (See Chapter 10 for further discussion of this topic.)
The physiological approach to voice disorders, based on an understanding of vocal fold
physiology and acoustics, suggests that a disturbance of physiology due to mass lesions, manner
of use, or abnormal motor control will result in acoustic changes. Thus, an inappropriate pitch
level, if indeed it is present, may well be a sign of a problem rather than the cause of the problem.
Attention needs to be paid to the underlying cause of the problem, and when the physiology
is normalized or improved, then the pitch level of the voice will also improve or normalize.
Indeed, it is quite possible for a person to speak at a totally appropriate pitch level and yet do
so in an abusive way.
Judgments of the pitch of a voice can be made subjectively but those perceptions should
always be checked against objective measurement of fundamental frequency. Perception of pitch
levels can be quite erroneous, especially in the presence of hoarseness or excess noise energy in
the voice. Objective measurement of fundamental frequency rather than casual judgments of
pitch may be made easily using methods described in Chapter 8 and should always be done
before any judgments about the acceptability of this parameter are considered. However, in a
very rough voice, even measurements of fundamental frequency should be suspect because of
the difficulty in obtaining reliable and accurate estimates of the period of vibration.
Inappropriate pitch is typically the hallmark of puberphonia, persistent glottal fry, and
lack of pitch variability. It is necessary to recognize, however, that inappropriate pitch may be
only one sign of an underlying problem.

Puberphonia
This category is referred to in the literature by a number of names: adolescent falsetto, pubescent
falsetto, incomplete mutation, and mutational falsetto, to name a few. We have chosen to use
the term puberphonia (not as the most desirable, but as the least objectionable) because it
suggests the developmental stage at which this problem is encountered (puberty) and tells us
that it involves the voice (phone). Rather than add yet another term, we prefer to describe the
nature of the problem.
Puberphonia refers most simply to the persistence of a high-pitched voice beyond the age
at which voice change is expected to have occurred. This is primarily a problem in males.
Although some women continue to have very high pitched and childlike voices into their
adult years, there is little stigma attached to this situation for two reasons: first, the lowering
of the fundamental frequency in women (3–4 semitones) as a result of laryngeal growth is
not as marked as for men (one octave); second, women are expected to have higher pitched
voices. Thus, the presence of a high-pitched voice in a woman is not always perceived to be as
unusual or inappropriate as in a man. That is not to deny, however, that a childlike voice can
be inappropriate, can jeopardize a woman’s employment status, and can negatively affect how
she is perceived.
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In cases of puberphonia, it is important that a determination be made first as to whether

an organic abnormality is present. The adequacy of laryngeal growth must be assessed, and
potential endocrinological problems must be ruled out. The laryngeal examination and the
history may provide sufficient information regarding these concerns. The vocal symptoms
include not only the inappropriately high-pitched voice but also often hoarseness and some
degree of breathiness. The voice tends to sound unstable and uncertain, and the patient’s
reporting often confirms that perception: “It sounds funny, and I never know what it is going
to sound like” is a commonly heard self-description of the voice problem. Pitch breaks may also
be heard. Although the onset of the problem is, by definition, during the adolescent growth
spurt and the emergence of secondary sex characteristics, it may persist for a considerable length
of time before any treatment is sought.
Psychosocial factors, such as difficulty with male identification or with the acceptance of
emerging adulthood are most often cited as the primary etiological factors. Our experience,
however, suggests that, if present, these factors are not overwhelming in their expression. It
seems quite logical to us that a certain percentage of young boys may have fairly traumatic
voice change experiences not only in the psychological sense but also in the physical sense.
Pitch breaks may be frequent and extreme, and the lack of control over the voice may be
pronounced. Feelings of embarrassment result and are aggravated by a lack of understanding
of what is happening. An understandable reaction to such feelings might be an attempt to
hold on to the voice that is known (the child voice) and to attain control of what otherwise
seems to be an uncontrollable behavior. In many cases, when asked if they have another voice,
young men with this problem will answer in the affirmative. In some, we have observed a
profound sense of relief when this admission has been made and reassurance has been provided
about the normalcy of the “hidden” voice. Indeed, for many, little additional treatment has
been necessary beyond providing a period of practice in using the new voice, coupled with
encouragement and guidance. In others, the process of “releasing” the adult voice (see Chapter
10) is usually very effective in producing a more typical adult voice within a short time period.
Interestingly, getting the patient to use the “new” voice, that is, return to school or home with
a voice that is now substantially different from before, can be problematic. We have sometimes
paired this with a school break or even summer vacation, to make the adjustment easier. We
are not aware, either through personal experience or perusal of the literature, of posttherapy
failures wherein there is a regression to the high-pitched voice. We also have not been impressed
that the young men who have presented with this problem in our clinic have had difficulty
with male identification. Indeed, we would not describe the sound of their voices as ever having
been effeminate. The characteristics of an effeminate voice are composed of speech mannerisms
and suprasegmental differences that go well beyond just the presence of a higher than expected
pitch level. We believe that the theory of the domineering mother figure and the weak father
figure as the primary underlying cause for the maintenance of the inappropriately high pitch
level has not been validated and we do not believe it to be true.
We have recently become aware of several cases of “falsetto-like” voice in the female. These
voices exhibit instability similar to that described for the puberphonic male with frequent pitch
breaks and elevated fundamental frequency. The underlying etiology and the pathophysiology
in these cases has not been well explored, but they appear to differ from other psychogenically
based voice problems in that the voice has not undergone a recent change. It has been consistently
present for many years with no recall of it ever having sounded different. In the cases we have
encountered, eliciting and establishing a more appropriate pitch level and vocal stability has
been accomplished fairly readily through voice therapy.

Persistent Glottal Fry

Glottal fry, vocal fry, or pulse register, is described as one of the three normal voice registers,
the other two being loft (falsetto) and modal. These registers are characterized by a change
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in the mechanical mode of vibration (Fairbanks, 1960), and there is usually overlap in the
frequency of phonation between adjacent registers. Daniloff, Shuckers, and Feth (1980) state
that the physiologically complex larynx “can vibrate in three (or more) relatively different ways,
giving rise to airflow modulation that yields acoustically and perceptually distinct vocal quality”
(p. 209). Glottal fry is the register lowest in fundamental frequency and the least flexible. The
vocal folds close quickly, and the closed phase of the vibratory cycle is very long relative to
the length of the entire period (Hollien, Moore, Wendahl, & Michel, 1966). Moore and von
Leden (1958) described the occasional occurrence of two open phases during one vibratory
cycle. Zemlin (1988) reported that the closed phase occupies about 90% of the cycle. In
describing the characteristics of glottal fry as seen in high-speed motion pictures, he observed
tightly approximated vocal folds with flaccid free edges. Zemlin further noted that air seemed
to “bubble up” between the folds near the junction of the anterior two thirds of the glottis.
Glottal fry is produced with much lower airflows than the other registers (Murry, 1971), and
air is released in irregularly timed bursts. Pulsated voice, according to Perkins (1983), allows the
production of only very low fundamental frequencies, with a decay of energy in every glottal
cycle.
Glottal fry has a very characteristic sound, which has been described variously as similar to
the popping of corn, the imitated sound of a motor boat engine, or a creaky voice. The vibratory
pattern is so slow that individual vibrations of the vocal folds are heard. The amplitude of vocal
fry sound is very low.
Although glottal fry is a normal mode of vibration, its consistent and habitual use is
atypical and may be considered misuse of the voice. It is difficult to produce glottal fry with
adequate volume for many speaking situations. A person using this mode of phonation will
show increased tension when attempting to increase vocal loudness. The lack of flexibility
of pulse register makes it difficult to achieve variation of fundamental frequency and results
in monotonic voice. Complaint of a sense of vocal fatigue and a constant awareness of vi-
bration even below the larynx are typically heard from speakers who habitually use glottal
fry.

Lack of Pitch Variability

There are some individuals who speak in a monotone with barely perceptible variations in
fundamental frequency, as corroborated by acoustic analysis. A monotonic voice may be a sign
of neurological dysfunction affecting the ability to control pitch, a reflection of psychological
depression, or it may be a habitual pattern that is a sign of misuse. We have been impressed
with the presence of this problem in untrained speakers who lecture or frequently address large
groups. They do not know how to modulate their pitch level for maximum communication
effectiveness. In this type of pattern, the phonatory mechanism establishes a “set” that rarely
varies. This set includes a certain configuration of the vocal folds, with the adductory and
contact forces occurring with the same strength and in the same area over and over again. This
behavior fails to take advantage of the flexibility of the phonatory mechanism and tends to
become fatiguing. It is not unusual to find that persons with this pattern allow their voices
to drift into vocal fry at the end of utterances. The delivery usually is perceived as lacking in
energy, vitality, and interest.

Excessive Talking
Each larynx has a physiological limit that varies not only from person to person but also intra
individually, as influenced by numerous factors. A healthy, well-rested, well-nourished, emo-
tionally stable individual may encounter no vocal difficulties despite heavy voice use demands.
However, should that same person be physically exhausted, eating poorly, and perhaps tak-
ing some medication, the same amount of demand on the larynx, or even less, may result in
phonatory problems. Factors of individual selectivity are involved in determining the physical
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tolerance limits of body structures and systems. Therefore, it is not possible to predict whether
excessive talking per se will result in a problem or, if a problem does result, how severe the
impairment will be.
Excessive talking may result in vocal fatigue. The voice quality may be reported to become
slightly rough or hoarse, the voice may sound weak, and the person may report that talking
requires effort. Frequently, those who have such complaints in the presence of a chronic pattern
of excessive voice use report that a night’s rest or a weekend with fewer vocal demands may
temporarily restore the voice to normal but that the symptoms recur with the next period of
excessive voice use. It is also important not to lose sight of the fact that patterns of misuse do
not always occur as single, isolated behaviors. It is, of course, quite possible that the excessive
talker is also engaging in other patterns of vocal misuse or abuse. Thus, a distinction should be
made between amount of talking and manner of talking (i.e., is it just a lot of talking or is it a
lot of talking in an excessively loud or tense voice).

Ventricular Phonation
The diagnosis of ventricular phonation is usually made when laryngological examination reveals
greater than expected movement of the ventricular folds toward the midline. Visualization of
the true vocal folds is often largely obscured by the compression of the ventricular folds,
particularly in indirect mirror examination. Use of the flexible fiberoptic laryngoscope often
permits visualization of some part of the true vocal folds or of their adductory and abductory
movements. Stroboscopic examination can document whether or not there is actual ventricular
fold vibration present.
Ventricular fold phonation is typically low in pitch and has been described as very hoarse
in quality, rattling, rumbling, cracking, reduced in intensity, and diplophonic (Aronson, 1990;
Case, 1984). However, acoustic data to support these perceptual descriptors are not available.
The pathophysiology of ventricular phonation is not well understood (see Chapter 10 for
further discussion). We have observed it as a manifestation of a psychogenic dysphonia (Brewer
& McCall, 1974), as a compensatory behavior in the absence of adequate vocal fold movement
(Woo, Casper, Brewer, & Colton, 1995) as one component in a pattern of hyperfunction, and
as an unexplained phenomenon. Other studies have reported use of the false folds related to
a variety of conditions affecting the true vocal folds (Von Doersten, Izdebski, Ross, & Cruz,
1992). Furthermore, in a study of normal nonsymptomatic speakers, Casper, Brewer, and
Colton (1987) observed much variability in the degree of medial movement of the ventricular
folds accompanying adduction of the true vocal folds in normal speakers.
Therapeutically, we have found ventricular phonation to be reversible when its etiology is
psychological or when it is a manifestation of hyperfunction. Its use as compensatory behavior
may well be very functional allowing the individual to produce the best voice of which he is
capable. In such instances, it is an appropriate behavior requiring neither change nor elimination
unless improved function of the vocal folds can be restored. When the etiology is unclear, or
when it is a true compensatory behavior, we have found this increased ventricular fold activity
to be very resistant to change through behavioral therapy.
When excess medial compression of the ventricular folds is present in the absence of
laryngeal pathology, and when a voice problem seemingly related to this ventricular fold activity
is present, ventricular phonation may be considered vocal misuse.

Aphonia and Dysphonia of Psychological Origin

There is no single way to characterize the patterns of misuse of the phonatory mechanism
exhibited by persons whose voice problems are psychogenically based (Roy, 2003). In our
experience, we have encountered a wide diversity of patterns, including (a) total aphonia in
which even the voiceless consonants were inaudible and the vocal folds were maintained in an
abducted posture; (b) dysphonia in which the laryngeal mechanism was held in a tension equal
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to that of very forceful effort closure, with episodic bursts of explosive vocalization alternating
with extreme hoarseness; (c) dysphonia in which the ventricular folds appeared to adduct;
and (d) dysphonia so variable that it encompassed normal voicing, aphonia, hoarseness, and
very strained phonation, all within two or three sentences. In all of these instances, when the
physiology was normalized, so too was the voice. Therapeutic approaches to achieve normal-
ization are discussed in Chapter 10.

Adaptive Dysphonias (Muscle Tension Dysphonia, “Functional” Voice Disorders)

“Muscle tension dysphonia, “or “MTD,” first described by Aronson (1990), and “functional”
dysphonias are terms often used to refer to voice disorders of supposed psychological origin,
with no actual tissue pathology. Some have suggested a deep-seated psychological problem
as a cause of the disorder, implied by such terms as hysterical aphonia; hysterical dysphonia;
and psychiatric dysphonia. However, we have found that the vast majority of these kinds of
patients do not manifest a psychiatric problem. Rather, the voice problem reflects the manner
in which the patient is coping with psychological stress, a true pathological problem or simply
the continuance of a way to cope with a transient or other kind of physical problem. Thus, it
is the way in which the patient is using the voice that defines the voice problem. This could
manifest itself as hoarseness, breathiness, aphonia, dysphonia, excessive muscle tension, or in a
variety of other ways.
This position is consistent with other authors who appear to have altered or expanded
the earlier definitions, in particular, of MTD. Morrison, in the 1980s and 1990s, included
patients with muscle weakness, reflux, and some kinds of benign lesions in the category of
MTD, supporting the idea that “muscle tension” can be a consequence of existing pathology.
More recently, Altman, Atkinson, and Lazarus (2005) reviewed 150 patients that had been
seen in their voice clinic over a 30-month period. These authors also described patients with
a variety of benign pathologies as demonstrating MTD. Of interest, they reported that of the
150 patients, 94 (63%) were female with a median age of 41.7 years. The males were slight
older (44.7 years). These results agree with other reports that show that MTD tends to occur
in middle age females. The most common complaints of the patients are shown in Table 4.3.
Hoarseness was the most frequent complaint (83%) with vocal fatigue a distant second (26%).
In the other category (all less then 10%) were voice loss, inability to project the voice, globus,
and loss of pitch range. The assessment of the laryngoscopic and stroboscopic characteristics
(Fig. 4.1) included reflux (35%), polyps (23%), nodules (13%), and other lesions and a small
number of patients with paralysis or paresis of the vocal folds (3%).
If there is confusion about “MTD” or “functional dysphonia,” it is likely related to the
difficulty in differentiating causes and consequences of dysphonias. That is, some behaviors
certainly lead to the development of organic pathology. Others may develop in response to
pathology, either that induced by vocal practices, or by other causes, that is, vocal fold paralysis,
temporary edema. At a given point in time, the clinician is seeing, and hearing, a patient
who represents the composite of perhaps multiple etiological factors. Some may reflect the
original etiology; others response to the original pathology, and some, residual maladaptive
behaviors that appear to persist after the original problem has resolved. Sorting individual
components is not always easy. Our preferred term for these types of dysphonias is “adaptive
dysphonias,” suggesting that in response to some provocation or stressor, either psychological
or physiological, the speaker makes adaptations to his usual vocal practices. In the primary form
of adaptive dysphonia, the implication is that the original problem has resolved or is sufficiently
subtle that it has not yet been identified, or, perhaps, is the consequence of a psychological
stressor. A secondary adaptive dysphonia is one in which at least some of the maladaptive
behaviors observed are a consequence of tissue pathology that persists. Rarely, in our experience,
does a thorough case history fail to reveal details of the likely stressors, or causes, of the
dysphonia.
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A further problem with the term “muscle tension dysphonia” is the inference that excessive
tension is always a feature of the dysphonia. Muscles tense, of course, so what’s implied in
“MTD” is that excessive tension is utilized in voice production. Though this is apparent in
many cases, there are also patients whose vocal practices, though inappropriate or ineffective,
cannot be characterized as involving excessive tension. The term, “functional,” does not specify
excessive tension as a feature of the dysphonia, but it does suggest no physiological basis
for the dysphonia. Again, though this may apply to some patients, our experience suggests
that many patients characterized as having a “functional” dysphonia have experienced some
physiological provocation that triggers the adaptive behavior. Possibly, as noted, the original
cause may have resolved by the time the patient presents to the clinician. It is also possible
that an organic cause is sufficiently subtle that it was missed on routine laryngological exam.
And this leads us to a further reason for preferring the term “adaptive,” to either “MTD” or
“functional.” It encourages the clinician to continue to consider all possible etiological factors
while attempting to modify maladaptive behaviors. In fact, through this process, the original
etiological factors, resolved, subtle, or still apparent with careful examination, are sometimes
revealed.
The specific task of the clinician treating phonotrauma is to identify and modify behaviors
associated with adaptive dysphonias, whatever their etiologies, that can damage vocal fold
tissues. As noted earlier, patients may present with a wide range of vocal signs and symptoms,
including hoarseness, huskiness, loss of pitch range, and/or tightness. Other symptoms patients
may report are pain and vocal fatigue.
Reports of acoustic characteristics in patients described as having MTD with no apparent
tissue pathology offer additional insights. The fundamental frequency of patients may be
similar to normal (Roy et al., 1997; Roy & Hendarto, 2005) or if aphonic there would be no
fundamental frequency. Jitter and shimmer may be high, whereas signal to noise (SNR) is low
(Roy et al., 1997).
Rees et al. (2007) reported some of the spectral characteristics of patients with MTD as
compared with adductor spasmodic dysphonia (ADSD), a condition that shares some of the
same perceptual and acoustic features of MTD. Using spectrograms, they found that patients
with MTD rarely exhibited any voice breaks, had occasional irregular vertical striations, ill-
defined formant structure, and excessive high-frequency noise.
Houtz et al. (2010) analyzed the spectral moments of the LTAS in 59 (10 males, 49
females) patients with MTD and 41 patients (19 males, 22 females) with ADSD. The four
moments (mean, standard deviation, skewness, and kurtosis) were calculated from the LTAS
spectra of an all-voiced sentence. There were no statistically significant differences between the
male MTD and ADSD patients, but the standard deviation (moment 2) did separate out the
female MTD from the female ADSD. Patients with MTD tended to have greater standard
deviations, suggesting greater frequency spread in the spectrum.
Higgins, Chait, and Schutte (1999) investigated airflows in nine female patients with
ADSD and nine female patients with MTD. The patients with ADSD had lower airflows (mean
= 130 ml/s) than the patients with MTD (mean = 195.4 ml/s). However, the difference was
not statistically significant. Neither group differed significantly from a normal control group
of 18 females. The authors commented on the large variability of airflow for the two groups
contributing to the difficulty in differentiating between them.
In summary, there are dysphonic patients who present with some form of excess tension
in the larynx or head and neck region. This excessive tension could be the cause of the voice
disorder, or the result of the attempt to cope with the problem. Another group of patients may
persist in using inappropriate vocal behaviors after the original problem has resolved, or when
subtle pathology persists. There are other patients whose dysphonia develops in response to a
nonorganic stressor. We would, as noted, describe all inappropriate vocal practices that appear
to represent the patient’s attempt to deal with one or a set of original provocative stressors,
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whatever these may be, as “adaptive dysphonias.” This will promote careful and continuing
efforts to identify the stressors as well as to induce more appropriate vocal behaviors. Specific
therapeutic approaches will be discussed in detail in Chapter 10.

Differentiating Misuse from Abuse

Prior to discussing vocal abuse, it is appropriate to return to some of the questions posed in the
first paragraph of this chapter. We have thus far discussed the vocal behaviors that we believe
constitute misuse. However, the line between misuse and abuse is a very thin one, and perhaps
rather than there being a division between the two, the behaviors might be thought of as existing
along a continuum. Bear in mind, however, that a continuum is only a scale. It is usually thought
to represent lesser or greater degrees of a behavior (in this case), but it does not necessarily imply
progression of a behavior or disorder along the continuum. Thus, a pattern of misuse such as
puberphonia can remain misuse and may not necessarily develop into a problem of greater
severity. We are unable to predict if or when misuse may become abuse and lead to tissue
change. It is logical to assume that excessive talking, for example, might at some point result
in actual tissue changes. Indeed, many patients with lesions such as nodules or polyps admit
to being incessant talkers. However, we all know nonstop talkers who never develop a voice
problem. Certainly there are individual selectivity factors operating about which we know little.
How patterns of misuse evolve is often difficult to determine. One of the most frequently
asked questions we have encountered clinically, and often a difficult one to answer, is the
patient’s incredulous wonderment about how it is possible, after several decades of presumably
talking correctly, to no longer be doing so. We have no prospective information about this and
can therefore only theorize retrospectively, using the information provided by patient recall.
There are inherent dangers in doing this because most people are usually unaware of their
speaking patterns until they encounter difficulty. To speak, to produce voice, is so innately
human that very little conscious effort or thought is involved. Furthermore, memory is often
flawed. The tendency to date the onset of a problem to a coincident event or one closely related
in time is sometimes very useful, but it may also be totally misleading.
The most common antecedents to vocal misuse that seem to have validity include periods
of increased personal tension or of greater than usual demands on the voice. A change in
employment that requires new demands, including greater vocal demands, is one such example.
Patients frequently report an episode of what they describe as laryngitis as the precipitating
event. This laryngitis is reported to have been but one symptom of a more extensive upper
respiratory infection, or it may have been an isolated symptom. While other symptoms resolve,
the altered voice persists. Some patients recall periods of voice difficulty in the past that they
ascribed to laryngitis and that had always resolved spontaneously within a short period of time.
On occasion, they may report that these episodes had become increasingly frequent and that
each one had taken longer to resolve. Because producing voice is such a “natural” phenomenon,
and because sensory feedback from the larynx is so limited, it is possible to change phonatory
behavior with little awareness of having done so. In the presence of laryngitis, whether due
to infection or to vocal fold edema resulting from misuse, adjustments in phonatory behavior
need to be made to produce any voice. It is conceivable that these changes may go unrecognized
and persist after the precipitating condition has resolved or may contribute to maintaining the
condition. One other factor that is often neglected must be considered. That is, we are not
the same person from moment to moment or day to day. Our bodies are constantly changing
and reacting to nutritional status, to drug intake, to effects of age, to environmental factors,
to emotional state. A behavior that may have been present for many years and tolerated by the
body may, due to some of the above factors, become intolerable and create what appears to
be a sudden change in body function. It is also possible that the body reaches a threshold of
tolerance for a certain behavior, the effects of which may have been minimal but cumulative.
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The changes may have been so gradual as to have gone unnoticed until the cumulative effect
surpassed threshold level.

Abuse
Recognizing the fine distinction between misuse and abuse and the possibility of misuse be-
coming abuse, behaviors that we categorize as abuse tend to be harsher than those previously
described, with a greater likelihood of causing trauma to the laryngeal mucosa. Table 4.2
presents vocal behaviors that we categorize as outright being abusive of the mechanism.

Excessive, Prolonged Loudness

In this category of speakers who abuse voice, we would include persons who have habituated
patterns of excessively loud voice use, those who spend much time talking above high levels of
environmental noise, teachers who have come to depend on loudness as a means of capturing
and maintaining attention and discipline, cheerleaders, aerobics instructors, some ministers,
sports coaches, and untrained or poorly trained singers, speakers, or actors whose activity
requires loud voice usage, often in environments not conducive to good voice production.
The mechanism for loudness requires the creation of increased resistance of the laryngeal
valve until an appropriate level of air pressure is produced and released. The vocal folds must
be adducted strongly to create the increased medial compression required for this valving
capability. Awareness of this mechanism results in an understanding of the abusive nature of
excessive or prolonged loudness. The laryngeal mucosa, especially along the glottal edge, may
become irritated, inflamed, and swollen. This may result in altered mass and affect the stiffness
of the cover of the vocal folds. Vibratory behavior is changed and reflected in the sound of the
voice. Continued use of the voice in this abusive manner may lead to further tissue changes,
resulting in organized local lesions at the point of the greatest force of contact of the vocal
folds, that is, the midpoint of the vibratory portion of the vocal folds. (In more generalized
pathology, a greater extent of the vocal folds may be affected.) The ability to fully adduct the
vocal folds may be altered by mass lesions, and this will change the sound of the voice. Leakage
of air through an incompletely closed glottis is heard as noise and adds a breathy component
to the voice. As changes in phonatory function occur, there is a natural tendency on the part
of the speaker to make compensatory adjustments. However, these attempts often constitute
further abuse and can result in greater tissue damage.
Daniloff et al. (1980) have pointed out that untrained speakers and singers have difficulty
changing vocal parameters (e.g., pitch, loudness) independently of one another. Thus, as loud-
ness is increased, the increased air pressure produces faster vocal fold vibration, resulting in an
elevation of pitch. This may put additional strain on the mechanism.

TABLE 4.2 Abusive behaviors

A. Excessive, prolonged loudness
B. Strained and excessive use during period of swelling, inflammation, or other tissue changes
C. Excessive coughing and throat clearing
D. The screamer and noise maker
E. Sports and exercise enthusiast
1. Observer
2. Participant
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Strained and Excessive Use During Periods of Swelling, Inflammation,

or Other Tissue Changes
In the previous section, we mentioned the negative effect of continued use of excessive and
prolonged loudness after such behavior had already resulted in irritation of the vocal fold
mucosa. There are other times when similar caveats must be recognized. Edema of the vocal
folds may result from infection, allergic reaction, or noxious environmental agents. Other
conditions, such as chronic sinusitis with purulent drainage and gastroesophageal reflux, may
serve to irritate, swell, and inflame the mucosa. Excessive drying of the tissues, resulting from
the use of certain drugs (discussed later in this chapter), extreme dryness of heated buildings
(due to inadequate humidification or the use of wood burning stoves for heating), excessive
use of alcohol, or reduced function of mucus glands can also increase the vulnerability of the
mucosa. The chances of creating further damage to the vocal folds are increased if abusive
vocal behaviors occur in the presence of any of these conditions. Tissues that are not in their
healthiest and strongest condition are unable to withstand added stress.
It is not at all unusual for a patient to report that a voice problem seemed to begin with
an episode of laryngitis, but that normal voice did not return after the infection had cleared.
Persons who rely heavily on voice use are often the most likely to engage in abusive behavior
by continuing to use their voices during periods of laryngeal irritation. They tend to strain and
exert greater than usual effort to produce as much voice as possible, and in so doing increase the
abuse. They may also produce other tissue changes that persist after the infection has cleared.

Excessive Coughing and Throat Clearing

It is a normal occurrence for all of us to cough and clear our throats. Coughing may be in
response to a local irritation or to infection and serves a life-sustaining purpose in guarding
the airway against the entry of foreign objects. The cough reflex evokes a blast of air at high
pressure as a mechanism for expelling anything that has attempted to pass through the larynx. It
is also the reaction to irritation of the mucosa of the vocal fold edge. The sensation of needing
to clear the throat may result from momentary collection of mucus on the vocal folds that
interferes with phonation. For some people, certain foods may create a reaction of increased
mucus secretions (dairy foods seem to be the most common culprits) and an increased need to
clear the throat. An allergic reaction of irritation and swelling of the vocal fold mucosa can also
result in the need to cough or clear the throat. During upper respiratory infections or other
illnesses, or as a reaction to drugs or treatment such as radiation therapy, the mucus tends to
thicken and become tenacious. The sensation aroused seems to make clearing the throat nec-
essary. Inadequate laryngeal lubrication may result from drug effects, from emotional reactions
such as stage fright, from excessive smoking or drinking, or from poorly functioning mucus
glands.
A chronic cough is one that persists for more than 3 weeks in duration. From 14% to
23% of adults who do not smoke are reported to have a persistent cough (Wynder, Lemon,
Mantel, 1965). Smokers have a greater incidence of coughing. Chronic cough, usually dry and
unproductive, can result from irritation of the mucosa due to smoking, secondary to reflux of
stomach contents in patients with gastroesophageal reflux disease (GERD) (Deveney, Benner,
& Cohen, 1993; Gaynor, 1991; Koufman, 1991; Olson, 1991; Wilson, Pryde, Cecilia, &
Macintyre, 1989), postnasal drip, asthma, chronic bronchitis, and some medicines (See Chapter
6 for more complete discussion of this topic).
Occasional coughing and throat clearing are not of concern. It is when these behaviors
become excessive or habitual that they can be abusive. The entire larynx and supraglottal
structures are involved in a cough. High-speed films of coughing behavior reveal wide glottal
opening first, followed by firm and protracted glottal closure during which large lung pressures
build up, and ending in a complex expulsive phase (von Leden & Isshiki, 1965). The vocal
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folds and supraglottal structures, including the posterior pharyngeal wall, are all involved in that
final vibratory phase and show periodic undulations of a violent nature. Very vigorous laryngeal
activity has also been described during throat clearing (Timcke, von Leden, & Moore, 1959).
An understanding of the “violent” nature of these behaviors makes it clear that both excessive
coughing and habitual throat clearing can be damaging to the sensitive laryngeal mucosa.
An inventory of abusive behaviors frequently reveals habitual throat clearing as one such
behavior. It is not uncommon to find the pattern so habituated that it is almost at an involuntary
level and the patient’s general level of awareness of it is limited. Most patients who exhibit this
behavior report sensations of something in the throat that they feel they must dislodge to begin
to speak. A habitual, hacking cough and frequent throat clearing are recognized hallmarks of
the cigarette smoker and occur in response to the mucosal irritation caused by the noxious
agents and the heat of the inhaled substances. They may also be symptomatic of an allergic
reaction or other laryngeal irritation.

The Screamer and Noise Maker

Some young children are the prime exhibitors of these behaviors. They tend to be aggressive
youngsters who talk a lot, habitually using loud voice in most situations and engaging in much
yelling and screaming in interactions with family and friends, be it in anger or in play (Barker &
Wilson, 1967; Toohill, 1975; Wilson & Lamb, 1973). Parents frequently report that a child has
been a “screamer” since infancy, being perhaps the only one in the family to be so categorized.
On other occasions, the report implicates other family members who also tend to be “loud”
in their vocal behavior. Because of factors of individual selectivity coupled with amount and
degree of excessive screaming, a child may begin to exhibit a voice problem. Vocal nodules
are often referred to as “screamer’s nodes” due to their frequent occurrence in association with
excessive screaming and yelling behavior.
Another manifestation of abuse of the voice most frequently noted in young children is
that of using the voice to make a variety of sound effects. Not all such behavior need be abusive;
however, many of the sounds typically produced by these children tend to involve strained
vocalizations. Some children take special delight in producing the most unusual sounds they
can devise. Others tend to supply all of the sound effects during play, not only for themselves
but also for their friends.
There are many more boys implicated in screaming and noise making than girls. The
incidence of vocal nodules is similarly greater for boys than girls (Coyle, Weinrich, & Stemple,
2001; Moore, 1986; Senturia & Wilson, 1968). Aronson (1990) assigns the “abnormal speaking
behavior” of these youngsters to personality or emotional factors. Barker and Wilson (1967)
studied the amount and type of voice use in the classroom of children with hoarse voices and
compared them with a group of children with normal voices. They noted that those with
hoarseness produced almost three times as many vocalizations within a 2-hour period than did
those with normal voices. These dysphonic children were also observed to be more behaviorally
active during unstructured classroom time than the control group of children. A further finding
of interest was that 65% of the hoarse children came from families in which there was much intra
family conflict, while only 35% of the nondysphonic children had such a family background.

Sports and Exercise Enthusiast

Observer
Prime demonstrations of vocal abuse may be seen at many sporting or political events. The
roar of the crowd is made up of many individual roars. In concert with the crowd noise, it
becomes difficult to monitor the loudness of an individual voice. In the heat of the moment,
and in keeping with socially accepted behavior, the louder the scream or yell, the better. These
loud yells are usually produced with great tension and with elevated pitch, which adds to the
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degree of tension under which the laryngeal mechanism is held. This behavior and its results
are so commonly known that lay people talk about screaming till the voice is gone. Indeed,
even Shakespeare commented on this phenomenon in Henry IV with the exclamation, “For
my voice, I have lost it with halloing and singing of anthems.”
The delicate vocal fold mucosa becomes edematous and irritated in response to this abuse,
thereby increasing the mass of the folds and interfering with their vibratory behavior. The
severity of the vocal symptoms will be related to the extent of this irritation and the tissue reaction
to it. However, return to normal or slightly reduced vocal use plus a good night’s rest will usually
suffice to restore the vocal folds to their normal condition. But should the person continue to
use the voice abusively, or place greater demands on it than the weakened mucosa can withstand,
further deterioration of both the condition of the mucosa and the dysphonia may occur.

Participant
A number of sports or fitness exercises by their very nature may set the stage for vocal abuse.
Whenever it becomes necessary to build intra-thoracic pressure, the laryngeal valve is involved,
and effort closure of the glottis often results. Producing voice under this condition is very
stressful. When lifting weights, for example, it is necessary for the person to build and maintain
lung pressure as ballast against which the weight may be lifted. This is a reflexive behavior
when attempting to lift any heavy weight. Weightlifters often produce grunting sounds during
the actual lift. It is not difficult to recognize the abusive nature of phonation produced with
the larynx and vocal folds in tight adduction and with increased subglottal pressure present.
Similar effort closure of the glottis occurs accompanying a tennis serve or a golf drive.
In other types of sports, it is often necessary for team members to yell to one another above
the noise of the spectators. Aerobics instructors who not only participate in the routine but also
verbally cue the class above the sound level of the music are a new group of voice abusers to
encounter problems. Persons who use motorized sports equipment such as snowmobiles and talk
above the noise of the engines may also find themselves having repeated episodes of dysphonia.
When dealing with vocal misuse or phonotrauma, it is essential to pursue an exhaustive
history of voice use. Patients do not readily identify behaviors other than the obvious ones,
such as screaming, excessive talking, and loud singing. It is necessary for the clinician to explore
the full range of potentially abusive traumatic vocal behaviors. Although we have attempted
to highlight many such behaviors, our listing is probably not all inclusive. Each voice clinician
will be able to add to it from personal experience.

Damaging Effects of Drugs on the Voice

This section of the chapter will deal with the known and potential effects of drugs on the voice.
Although the taking of drugs does not come under the category of a vocal behavior, the effects
of drugs can be potentially damaging to the mucosa and disruptive to phonation. For these
reasons, we have chosen to place this material in this chapter.
Research on the effects of various drugs on the laryngeal mucosa and laryngeal physiology is
almost nonexistent. New drugs are developed and marketed annually, making the process even
more problematic. And, in fact, the unintended, aversive effects of drugs may not be realized
until they have been in use some time. Therefore, in discussing the effects of drugs on voice,
we are talking about expected effects based on an understanding of drug action and laryngeal
anatomy and physiology. The following summary is based on the work of pharmacologist
F. Gene Martin (1988; 1983; 1984), who presents five basic pharmacological principles to keep
in mind when discussing the general effects of drugs:
1. Biological response variability: There is wide biological variability in individual re-
sponse to drugs, based on a large variety of factors including age, body composition,
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kidney function, genetic inheritance, biochemistry, stress level, disease, drug/drug in-
teraction, and nutritional status. Responses may differ both quantitatively and qualita-
tively.
2. The placebo effect: The expectation of an effect may influence the type and degree of
effect obtained. This is a poorly understood but generally accepted phenomenon.
3. Dose–response relationship: The intensity of the effect of a drug is usually expected to
be proportional to the dose administered or taken; that is, the larger the dose, the greater
the effect, proportionally. However, the dose–response relationships of most drugs form
sigmoid-shaped curves rather than straight lines when their effects are plotted against
dosage. Such curves indicate that the intensity of a drug increases gradually at first, then
rapidly, and then gradually again, eventually reaching a ceiling or plateau level as the
dose is increased incrementally (step-wise). Increasing the dose after the ceiling effect
has been obtained produces no further enhancement of effect and may only produce
undesirable toxic side effects. Allergic reactions to drugs may appear with any dose, no
matter how small, and the intensity of allergic effects is not related to the magnitude of
the dose.
4. Multiple effects of a single drug: Drugs may have a multiplicity of effects. Those that
are not the specifically intended effect are usually referred to as side effects. These are
the effects that most frequently have ramifications for voice production.
5. Drug efficacy versus drug dosage: The efficacy of a drug is of more concern than its
potency. Thus, if drug A produces a desired level of response at a lower dose than drug
B does, it does not necessarily mean that drug A is better than B. Drug A may, in fact,
be worse, if even at its lower dose it produces more undesirable side effects than drug B.
It matters little to the patient whether the pill swallowed contains 5 mg or 200 mg of a
drug. What matters is the production of an adequate therapeutic effect and the absence
of unacceptable side effects with a given reasonable dose.
To those basic principles, an additional caution should be included concerning the geri-
atric population. Elderly people may respond differently, quantitatively or qualitatively, than
younger persons do to the same dose of the same drug. This difference in response is due to
the loss, reduction, or alteration of certain body structures and functions with aging, as, for
example, a reduced ability to metabolize or absorb certain drugs. Furthermore, many drugs are
combinations of several agents, each of which may have an effect on the voice. It is important
for the consumer to be aware of these combinations and their possible effects.
The voice-related effects of drugs may be classified in the following seven categories:
(a) coordination and proprioception, (b) airflow, (c) fluid balance, (d) secretions of the up-
per respiratory tract, (e) structure of the vocal folds, (f ) irritation of vocal fold mucosa, and
(i) miscellaneous. The various classes of drugs and their effects are shown in Tables 4.3 and 4.4.

Coordination and Proprioception

Any agent that is stimulating or depressing to the central nervous system has the potential to
affect coordination, including the fine motor control of phonatory behavior. Central nervous
system stimulants include amphetamines, dextroamphetamine sulfate (Dexedrine), cocaine,
caffeine, and phenylpropanolamine, the active agent in over-the-counter diet aids. Stimulants
are used primarily as recreational drugs and appetite depressants. Their adverse effects may
include nervousness and tremor and difficulty in performing acts requiring well-controlled
coordination. For example, the shaky or tremorous voice of a person who is highly agitated
results from a breakdown of the ability to control fine aspects of voice production.
Central nervous system depressants include alcohol, barbiturates, tranquilizers such as
diazepam (Valium) and chlordiazepoxide hydrochloride (Librium), and chloral hydrate. They
are used primarily as antianxiety agents and produce a sedating effect that in high enough
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CHAPTER 4 I Phonotrauma: Its Effects on Phonatory Physiology 91

TABLE 4.3 Complaints of patients with MTD

Complaint N Percent

Hoarseness 125 83
Vocal fatigue 39 26
Vocal strain 35 23
Pain on or after phonation 26 17
“Tightness” in throat 17 11
Voice loss 13 9
Unable to project voice 7 5
Globus 7 5
Loss of pitch range 3 2

MTD, muscle tension dysphonia.

Adapted from Table 2 in Altman, Atkinson, and Lazarus, 2005, pp. 263.

doses may have a negative influence on muscle coordination. For example, slurred and slowed
speeches are well-recognized hallmarks of the person who has had too much to drink.
Diazepam (Valium) is often prescribed for patients with a variety of voice disorders. How-
ever, administration of diazepam is usually unproductive of any beneficial change in voice
production or in the alleviation of voice symptoms. In a study of the effect of diazepam on
respiratory and laryngeal muscle activation, Ludlow, Schulz, and Naunton (1988) reported

TABLE 4.4 Drug classes and their laryngeal effects

Coordination Secretions of Structure Irritation
Drug and Fluid the Upper of the of the Vocal
Type Proprioception Airflow Balance Tract Vocal Folds Fold Mucosa
CNS stimulants X
CNS depressants X
Anesthetics X
Bronchial dilators X
and constrictors
Diuretics and X
decongestants
Corticosteroids X
Drying agents X
Wetting agents X
Androgens X
Lower esophageal X
sphincter effects
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92 Understanding Voice Problems

strong inter-individual respiratory and phonatory effects, which may be age related. Laryngeal
activation (as at the onset of phonation?) decreased in their older subjects, while it increased in
their younger subjects. The authors cautioned that use of diazepam as a treatment for spastic
dysphonia or other movement disorders affecting the voice may, in some individuals, result in
a worsening of symptoms. Furthermore, they called attention to the not uncommon adminis-
tration of diazepam or other such medications to subjects in studies of laryngeal muscle activity
during speech, suggesting that this practice may significantly alter the results of such studies.
Another group of drugs that affect the central nervous system are those that produce
an anesthetic effect. Local anesthetics such as benzocaine (Americaine), lidocaine (Xylocaine),
procaine hydrochloride (Novocain), or phenol may be the primary ingredients in over-the-
counter lozenges and sprays used to treat a sore throat. These agents are capable of blocking nerve
impulse conduction and reducing pain sensation. Pain serves as an alarm system, indicating the
presence of a problem somewhere in the body. The usual response to throat or laryngeal pain is
to reduce voice usage. Reduction of pain by the use of these analgesic agents masks the presence
of the problem, and the individual may then be prone to overstressing voice use. Leonard and
Ringel (Leonard & Ringel, 1979) reported some changes in laryngeal behavior following the
dripping of a local anesthetic onto the vocal folds.

Airflow
Drugs that either dilate or constrict the bronchioles will affect the movement of pulmonary air
through the larynx. Bronchodilators, such as albuterol (Proventil, Ventolin), metaproterenol
sulfate (Alupent), and others are used primarily as antiasthma agents. Negative side effects may
be nervousness and tremor. Bronchoconstrictors potentially have a more adverse effect on voice
production. The mechanism most often used to cause bronchoconstriction pharmacologically
is an allergic reaction. The effects may vary from very mild discomfort and wheezing to a
significant, even life-threatening effect on respiratory function. Many environmental irritants,
such as dust, pollen, and molds, produce similar effects in individuals with sensitivity to these
environmental factors. One of the newer asthma medications, marketed as Advair, can irritate
laryngeal tissues sufficiently in some patients to produce a fungal infection. There is also some
concern that medications delivered under rapid flow may traumatize laryngeal tissues.

Fluid Balance
Fluid balance in the mucosa of the vocal folds may have a very significant and direct effect on
voice production. There are many drugs that, either as a consequence of their primary intended
effect or as their side effect, work in such a way as to reduce edema either systemically or in a
more localized manner. Diuretics, which reduce the formation of edema, are commonly used
in the treatment of high blood pressure and heart or kidney failure. Perhaps, the most widely
used group of agents with the effect of reducing edema are the decongestants, many of which
are sold as over-the-counter preparations in tablet, capsule, or liquid form or as topical sprays
(e.g., oxymetazoline hydrochloride [Afrin], pseudoephedrine hydrochloride [Sudafed]). These
are used in the treatment of the symptoms of cold, cough, allergy, or sinus problems.
Vocal fold edema, under most circumstances, is the result of protein-bound water
(Lawrence, 1987; Sataloff, 1987) and will not be responsive to diuretic agents. Corticosteroids,
often used as drying agents in the treatment of vocal fold edema in performers following vocally
abusive episodes, affect protein-bound water directly. Although they are often effective, they
offer only a palliative, not a curative, effect. A patient may be using a diuretic agent for a number
of reasons not directly related to vocal fold edema. In such instances, the danger of reducing
the normally desirable fluid level in the laryngeal mucosa must be kept in mind. Long-term use
of decongestants may cause a rebound effect wherein, as the vasoconstrictive effects of the drug
wear off, there is a return of the edema and congestion to a greater degree than was previously
present. As a result, a vicious cycle may be established in which the patient must continue to
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CHAPTER 4 I Phonotrauma: Its Effects on Phonatory Physiology 93

take the decongestant in an attempt to counteract the side effect that is being caused by the
drug itself. The long-term effects of vasoconstriction and the adverse effects from the loss of
adequate fluid balance include a reduction in blood flow to the mucosa; loss of electrolytes with
concomitant decrease of potassium level, leading to a decrease in energy and a sedating effect;
increased nervousness and tremor; and potential damage to the mucous membranes. Edema
formation in reaction to drugs occurs primarily in the form of an allergic response. Agents
that cause an allergic reaction in a patient may have more than a single effect. Although bron-
choconstriction may be one effect, edema of the mucosa may occur simultaneously. Edema
of the laryngeal mucosa may also occur in response to vocal abuse, trauma, infection, and
environmental allergens.
Corticosteroid inhalants are used in the treatment of asthma. Their effect on voice is not
entirely clear. Williams, Baghat, DeStableforth, Shenoi, and Skinner (1983) reported dysphonia
and bilateral vocal fold bowing in patients using an inhaled corticosteroid. The vocal fold bowing
appeared to be related to the dose and potency of the drug used and was believed to represent
a local steroid myopathy. The bowing and concomitant dysphonia were reversed in all patients
after cessation of use of the steroid inhalant. Watkin and Ewanowski (1979) reported that
prolonged administration of aerosol-delivered triamcinolone acetonide (Kenalog), a drug used
by chronic asthmatics, results in significantly altered vocal tract functioning and an elevation
of fundamental frequency of approximately 20 Hz. They reported that changes were evident
after 1 year of use, with a cumulative effect described after 2 years.

Secretions of the Upper Respiratory Tract

According to Martin (1988; 1983; 1984), exposure to agents that affect upper respiratory tract
secretions occurs with great frequency. Many drugs act as drying agents by causing a reduction
in secretions of the salivary and mucus glands. Furthermore, Martin states, a major portion of
our lives “is spent in buildings with very low humidity, and we are continuously breathing air
with moisture levels similar to that of the Sahara” (Martin, 1988; McClean, 1987; Stoicheff,
Giampi, Passi, & Fredrickson, 1983). A vicious cycle ensues in which breathing dry air results
in dryness and irritation of the mucosa, which leads to coughing, which serves to further irritate
and dry the mucosa.
Among the drugs creating a drying effect, the most common are the antihistamines used in
the treatment of allergy, cold, cough, sinus, motion sickness, and insomnia. Drugs functioning
as antispasmodic agents (e.g., atropine, scopolamine, diphenoxylate hydrochloride [Lomotil])
used in the treatment of diarrhea also create a reduction in glandular secretions. The action
of antitussive drugs such as codeine and dextromethorphan hydrobromide (Benylin DM),
used in cough remedies, is drying, and a side effect is sedation. Antipsychotic agents such as
chlorpromazine hydrochloride (Thorazine) and haloperidol (Haldol) and antidepressant agents
such as amitriptyline (Elavil) and lithium carbonate (Lithane, Lithobid) cause drying and
sedation. The last group of drying agents is the antihypertensive drugs used in the treatment of
high blood pressure, such as methyldopa (Aldomet), reserpine (Sandril, Serpasil), and captopril
(Capoten).
The most effective wetting agent is water, abundantly available and easily consumed.
Ambient humidity may be voluntarily controlled, as may the amount of water consumed.
Expectorants, used in the treatment of cough, are agents that increase secretions. However,
many of these products contain other drugs that have the opposite effect. Guaifenesin (Robi-
tussin, Glycotuss) is the most commonly used expectorant drug and can be obtained as the
only drug in a product. Saliva substitutes (e.g., dibasic sodium phosphate [Moi-stir], sodium
carboxymethylcellulose [Salivart]) have recently become available and appear to be very helpful
as wetting agents. They are used primarily by persons who have salivary gland pathology but
can be effectively used to combat the dry mouth caused by the use of drying agents and also
by preperformance anxiety. Thompson (1995) has suggested that the efficacy of wetting agents
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94 Understanding Voice Problems

has not been proved and perhaps the most beneficial effect may be the increased water intake
required while taking this medication.

Changes in Structure of the Vocal Folds

The androgens, which are structurally related to the male hormone testosterone, change the
actual structure of the vocal folds. They are used in the treatment of hormonal imbalance
(frequently in postmenopausal women), in sexual reassignment from female to male, and by
body builders seeking to increase muscle mass. Androgens cause an increase in the mass of the
vocal folds, which, of course, results in a change in the voice, referred to as the virilization of the
voice. Once this change has occurred, it is irreversible (Damste, 1967). A synthetic androgen,
danazol androgen (Danocrine), is commonly used in the treatment of benign fibrocystic breast
disease, although a side effect of voice change occurs in about 10% of the patients treated. It is
not yet clear whether these voice changes are reversible (Martin, 1988). These agents can be used
effectively to lower fundamental frequency of the voice in individuals who have undertaken
sexual reassignment from female to male.

Irritation of Vocal Fold Mucosa

Laryngeal tissue (as well as esophageal and pharyngeal) is susceptible to irritation and damage
caused by the acidic contents of gastric juices that reflux into the hypopharynx in GERD. Lower
esophageal sphincter (LES) pressure has been reported to be decreased by the following drugs:
atropine, dopamine, smoking, calcium blockers, sedatives/tranquilizers, nitrates, theophylline,
and adrenergic (Gaynor, 1991). Because decrease in the tightness of the LES is implicated in the
pathophysiology of GERD, it is logical to assume that use of any of these drugs may predispose
an individual to GERD. Caffeine, fat, alcohol, and highly spiced foods are also believed to
reduce LES pressures. (See Chapter 6 for more information on GERD.)

Miscellaneous
Martin (1988; 1983; 1984) notes additional agents that are thought by some to have an effect on
voice production and on performance, although they do not specifically fit any of the previous
categories. These include ototoxic drugs, herbal teas, aspirin, beta-blockers, and tobacco and
other smoked or inhaled drugs.

Hearing
A number of drug groups are known to be potentially ototoxic. Some of these are aminoglycoside
antibiotics, such as amikacin sulfate (Amikin) and tobramycin sulfate (Nebcin), which are used
intravenously in life-threatening disease states. Certain diuretics, referred to as “loop” or “high
ceiling” diuretics, such as furosemide (Lasix) or bumetanide (Bumex), used in the treatment
of heart failure and high blood pressure, also have the potential to create hearing loss. Some
drugs used in chemotherapy for cancer are also suspected to have ototoxic side effects, and their
use should be monitored closely. Obviously, the loss of hearing will not have a direct effect on
laryngeal anatomy. However, laryngeal physiology may be indirectly affected in the profoundly
and congenitally hearing impaired. In those who have acquired hearing impairment of a severe
degree, and perhaps not an immediate effect on laryngeal physiology. Indirectly, however, this
loss of hearing may affect vocal production, and it is likely that vocal physiology may be altered
over time. When vocal loudness considerations are a component of a voice disorder, auditory
acuity must be taken into account.

Herbs and Alternative Therapies

It has been estimated that between 42% and 57% of the population of the United States
have used some form of alternative medical therapies including the ingestion of various herbs
and other organic material (Fisher Jr. & Veronneau, 2000). Furthermore, about one in five
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CHAPTER 4 I Phonotrauma: Its Effects on Phonatory Physiology 95

individuals who take a prescribed medication also use herbal substances. The problem is that
many individuals do not inform their physicians that they are taking the herbal supplements.
In fact, it is routine practice today for physicians to specifically inquire about a patient’s use of
herbal substances. Serious negative interactions have been known to occur between prescribed
medications and herbal materials. Moreover, herbs may have an undesirable side effect and
some have been reported to produce serious health problems and even death. For many herbal
preparations, the claimed benefit has not yet been substantiated.
The lay person’s view of herbs is that they are natural substances and cannot, therefore, cause
any harm. That may be true when taken in moderation and recommended by a reliable source.
Unfortunately, herbal preparations are not regulated by the Food and Drug Administration
and are considered food supplements. Thus, there are no regulations regarding the purity or
even the accurate labeling of these substances.
Herbal substances may have adverse effects. Some documented adverse effects include (or
reported cases of ) hallucinogenic actions effects, sedative effects, or cardiovascular reactions
(Fisher Jr. et al., 2000). Surow and Lovetri (2000) have described most of the adverse reactions
to alternative medical therapies. These possible reactions commonly used herbal preparations
are shown in Table 4.5. Some of these adverse reactions are dose related or could be due
to impure or undocumented additional substances in the herbal preparation. How does one
know which herbs are good and which are not? How does one know where to purchases these
herbs with a reasonable assurance about their purity and content? The Web site of B & K
Prescription shop, a seller of herbs and supplements, has some good tips for the wary consumer
(www.bkrx.com/tips.htm). Check this page for a complete list of tips. The best advice is to be
wary of any advertising claims of the efficacy of herbal supplements, buy from a reputable (and
large) manufacturer, look for standardized products, consult with your physician especially if
you are taking any medications and be wary of fad products. Singers should be even more
careful about these preparations, as they may have subtle effects on the body and perhaps voice.
However, there have been few, if any, scientific studies that reported the effects of taking herbal
substances on the voice (see Tables 4.5 and 4.6).

Aspirin
Aspirin (nonsteroidal anti-inflammatory drugs) has anticoagulant properties that are not usually
of consequence to the average voice user unless that individual has a bleeding disorder or is
taking other anticoagulant medication. Because the professional voice user is called upon to use
the voice strenuously, the risk of vocal fold hemorrhage may be somewhat greater than for the
average speaker. Such risk may be further increased, and particularly so if that person is taking
aspirin or any preparations containing acetylsalicylic acid.

Beta-Blockers
During times of stress and fear, the adrenal glands release the chemicals epinephrine and
norepinephrine. It is the increased level of these chemicals that results in rapid heartbeat,
tremor, elevated blood pressure, sweaty palms, dry mouth, respiratory tension, nausea, and
an urge to urinate. These are also the well-known symptoms of the phenomenon known as
stage fright. Beta-blockers, of which propranolol (Inderal) is the most common, act to block the
effect of epinephrine on glands, smooth muscles, and the heart, thereby reducing the symptoms
described above. Whether or not the reduction of symptoms produces enhanced performance
has not been determined. Instrument musicians have been reported to demonstrate improved
performance and a lessening of subjective stage fright symptoms with the use of beta-blockers
(Brantigan, Brantigam, & Joseph, 1982; James, Pearson, Griffith, & Newburg, 1977; Liden
& Gottfries, 1974). Evidence of their effectiveness in singers is less conclusive. Gates and
Montalbo (1987) suggest that low-dose (20 mg) beta blockade had no significant effect on
singers’ performance. In an earlier study, Gates et al. (1985) reported a deleterious effect on
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TABLE 4.5 Some common drugs and their possible voice side effects

96
Drug Group Brand Name Manufacturer Generic Name Effect on Voice

Antiasthmatic Azmacort Rhn-Plnc Rr Triamcinolone Patients using inhaled steroids sometimes experience significant voice changes (including
P2: OSO/OVY

complete loss of voice). The onset of symptoms and severity of symptoms are highly variable
among patients. Studies show that discontinuation of inhaled steroids rest
LWBK726-Colton-v1

Anticoagulant Coumadin Wafarin Dupont Barr Warfarin Vocal performers, particularly, should be cautious about using medications that decrease
platelet function during periods of strenuous voicing demands, due to an increased
possibility of vocal fold hemorrhage
QC: OSO/OVY

Antidepressant Paxil Zoloft Glaxo-SmithKline Paroxetine Sertraline Paxil and Zoloft may have a drying effect on the body, including vocal fold tissues, which can
Beecham Pfizer lead to hoarseness, soreness, voice changes, or laryngitis. In addition, dry vocal tissues may
be more prone to injuries such as nodules
Antihistamine Allegra Zyrtec Hoech Mar R Fexofenadine Cetirizine Antihistamines have a drying effect on mucous membranes that may cause hoarseness, sore
T1: OSO

Zantac Pfizer Glaxo Ranitidine throat, voice changes, or laryngitis. In addition to irritation, dry vocal folds may be more
Wellcome prone to injuries, such as nodules
Antihyperlipidemic Mevacor Zocor Merck Lovastatin Simvastatin No effects on voice or speech mechanisms have been reported
Cardiovascular Zestoretic Zeneca Lisinopril/HCTZ Two adverse reactions are possible: (1) excessive coughing has been associated with the use
of ACE inhibitors, which in turn, may lead to hoarseness and possible vocal tissue damage
and (2) the diuretic component may have a drying effect on mucous membrane
Hormone Necon 1/35 Watson Lab Norethindrone The use of oral contraceptives has not been shown to significantly affect female voices
Diuretic Lasix Bumex Hoech Mar R Furosemide Bumetanide Diuretics have a drying effect on mucous membranes, including those used for speaking and
Demadex Torsemide singing. Hoarseness, sore throat, voice changes, or laryngitis are possible symptoms. In
addition to irritation effects, dry vocal folds may be more prone to injuries
Nonsteroidal Naproxen Ibuprofen Various Naproxen Ibuprofen Vocal performers, particularly, should be cautious about using medications that decrease
anti-inflammatory platelet function during periods of strenuous voicing demands, due to an increased
possibility of vocal fold hemorrhage
Steroid Flonase Flovent Glaxo Wellcome Fluticasone Mometasone Throat irritation and dryness, cough, hoarseness, and voice changes are all possible adverse
decongestant Nasonex Rhinocort Schering Astra Budesonide reactions

Note: Material excerpted from http://www.ncvs.org/vocol/rx.html.

November 15, 2010
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CHAPTER 4 I Phonotrauma: Its Effects on Phonatory Physiology 97

TABLE 4.6 Commonly used herbs, their claimed benefit and possible
adverse effects
Product Claimed Use(s) Adverse Effects

Echinacea (E. Purpurea) Immune stimulant generally used Possible allergies

for colds, sore throat, and flu. Used
for treatment and prophylaxis
Garlic (Allium sativum) Lowers cholesterol and blood May cause GI irritation.
pressure
Ginger (Zingiber officinale) Helps prevent motion sickness, GI upset in large doses
morning sickness
Ginkgo (Ginkgo biloba) Improves memory, circulation, Minor GI disturbances
helps treat depression, impotence
Ginseng (Panax ginseng) Reduces stress, improves stamina, Nervousness and excitation first
adaptogen few days of taking
Saw Palmetto (Serenoa repens) Benign prostatic hyperplasia Very few. Headache reported
St. John’s wort (Hypericim Mild-to-moderate depression Avoid use with other
perforatum) antidepressants. May cause
photosensitivity

Note: Based on material presented at www.bkrx.com.

singing quality with the administration of beta-blocker in high doses (40–80 mg). There does
not appear to be strong evidence that beta-blockers significantly enhance performance. Indeed,
it has been suggested by some that heightened preperformance anxiety serves a useful purpose
in that it lends a degree of intensity and excitement to the performance that might be lost if
beta-blockers were used. Data to support this contention or its corollary are not yet available.

Tobacco and Other Smoked or Inhaled Drugs

We should not leave this section on the effect of drugs on the voice without some direct
mention of tobacco, marijuana, and other drugs that are smoked or inhaled. There is very
convincing evidence (Burch, 1981; Hammond, 1966; Kahn, 1966; Wynder, Covey, Mabuchi,
& Muchinski, 1976; Wynder & Stellman, 1977) that cigarette smoking is closely related to
laryngeal cancer. The vast majority of individuals who present with laryngeal carcinoma have a
history of heavy smoking. Precancerous conditions such as leukoplakia and hyperkeratosis are
also closely linked to smoking. Some smokers present with very boggy, polypoid vocal folds
(Reinke’s edema), a condition that is benign but usually results in significant dysphonia and can
be severe enough to compromise the airway. Redness and generalized irritation of the mucosa
of the upper respiratory tract and the larynx are often present in persons who use tobacco,
marijuana, and other inhaled substances. The harmful effects of inhaling environmental smoke
have been documented (U.S. Department of Health and Human Services, 1986). Lung cancer
and emphysema are also known to be directly related to smoking. When the respiratory system
is compromised, there is a direct effect on voice production. Thus, even in the absence of actual
laryngeal pathology, the effects of smoking on lung function are sufficient to produce a broad
effect on phonation.
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98 Understanding Voice Problems

Vocal Pathologies Secondary to Phonotrauma

In this section, we will discuss pathologies that are thought to be caused by or contributed to
by vocally traumatic behaviors. These pathologies are nodules, polyps, cysts, edema, chronic
laryngitis, and sulcus vocalis. However, as noted above, phonotrauma may not be the only cause
of some of these pathologies. Indeed, in some cases, the exact etiology is still in question. All of
the pathologies do appear to have an abusive component even if it may not be the primary cause.
Throughout this section, we will report some of the data that we have collected on a large
patient sample of patients with benign lesions (Colton et al., 1997). In this project, we analyzed
various acoustic and aerodynamic variables prior to treatment and at selected intervals after
treatment. We also studied the patient’s own perceptions of their disability and rated the degree
of dysphonia. These patients were treated with medical, surgical, or voice therapy depending
on the specific diagnosis and presenting symptoms. Specific results will be presented in the
appropriate sections that follow.

Nodules
Primary Voice Symptom: Hoarseness
Description and Etiology
Nodules are localized benign growths on the vocal folds that are usually thought to be the result
of vocal abuse. They are a reaction of the tissue to the constant stress induced by frequent, hard
oppositional movement of the vocal folds. In the initial stages of the formation of a nodule,
the trauma causes localized edema on the vocal fold edge. Early or acute nodules are fairly
soft and pliable; they may be reddish in appearance and are mostly vascular and edematous.
The remainder of the vocal fold may also be edematous, and the entire larynx may be slightly
inflamed. In this early stage, the nodule may be evident only on one side and may easily be
mistaken for a polyp. With continued trauma, the tissue undergoes hyalinization and fibrosis
and becomes firm. Chronic or “older” nodules are usually hard, white, thick, and fibrosed.
Arnold (1962; 1980) reported that at this chronic stage of nodule development, the epithelium
may show hypertrophy, horny or very rough surfaces, and a change in the type of cells present.
Chronic nodules are usually bilateral and not always entirely symmetrical in size. Figure 4.1 is
an illustration of a pair of vocal nodules.
There is some controversy about the distinction between nodules and polyps. A polyp
is a projecting mass with a central core of fibrous tissue of greater density than the lamina
propria and covered by a normal or slightly hyperplastic epithelium (in contrast to nodules).
Clinically, there are times when the distinction between the two lesion types is very clear and

FIGURE 4.1. Vocal fold nodules. Note

the small hematoma on the right fold.
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CHAPTER 4 I Phonotrauma: Its Effects on Phonatory Physiology 99

other times when the difference is minimal. Histologically, the distinction between nodules and
polyps is often overlooked. Fitz-Hugh, Smith, and Chiong (1958) reviewed the histological
findings of 300 consecutive cases of benign tumors of the vocal folds. They commented on the
difficulty of distinguishing among nodules, polyps, and polypoid degeneration. Many nodules
were classified as polyps and vice versa, on review. They eventually concluded that a nodule was
a trauma-related lesion consisting of a local nodular or polypoid degeneration of the lamina
propria. They state that a polyp has its origin in the subepithelial (or Reinke’s) space. From the
perspective of the voice clinician, both types of pathology frequently respond to conservative
treatment, particularly in their acute or early stages.
Gray and his colleagues (Gray, Titze, & Lusk, 1987) have described some of the histological
changes that co-occur as a result of extended phonation, and the changes that co-occur in
nodules. Hyperphonation results in several changes to the vocal fold epidermis including (1)
damage to the microvilli, (2) creation of a cobblestone appearance along the surface, and
(3) damage to the surface and underlying cells (Gray et al., 1987). Nodules appear to result
from damage to the basement membrane zone (BMZ), an area connecting the outer epidermis
to the lamina propria. Trauma produces a disorganization of the BMZ that reduces the strength
of the attachment of the epidermis to the lamina propria.
Nodules occur more frequently in adult women and young, prepubescent male children.
In their retrospective study of 1158 patients with voice disorders seen in two ENT offices in
Ohio over 3 years, Coyle, Weinrich, and Stemple (2001) reported that about 10% of patients
had vocal fold nodules. Of the total number of patients reviewed, the percentage of women
with vocal nodules was 12.5, whereas 6.6% of men had vocal nodules. Most of the patients
with nodules were between the ages of 25 and 44 years. Although this study had a large number
of patients, one should interpret its results with caution for two reasons. One, the study only
reports the prevalence of voice problems for two medical practices in one mid western state.
Second, the study is retrospective with the lack of controls one might wish in a study such as this.
Luchsinger and Arnold (1965) considered general physical constitution, personality, and
local laryngeal signs to be important predisposing conditions for nodules (or polyps). Allergies
or thyroid imbalances may contribute to precipitating factors; tobacco and alcohol use may be
aggravating factors.
In adults, nodules occur most frequently in women between the ages of 20 and 50 years.
In children, nodules occur predominantly in boys from 3 to 6 years. The children are typically
reported to be prone to excessive loud talking and screaming. However, increasingly in our
practice, it is not unusual to see children whose parents describe them as having “always
sounded this way.
Nodules may be found in children who are prone to excessive loud talking or screaming.
They usually occur in children who have a history of loud, constant voice usage in conversation
use, in at school, at home, and at play. In this age group, the nodules occur most frequently in
boys.

Perceptual Signs and Symptoms

Hoarseness and breathiness are the major perceptual signs of nodules. Some individuals com-
plain of soreness or pain in the neck lateral to the larynx that may radiate upward to the ear
or downward to the upper chest. Some have the sensation of something in the “throat” that
they need to try to clear. Difficulty in producing pitches in the upper third of the range is a
complaint especially true for singers. The degree of hoarseness or breathiness present may be
related to the size and firmness of the nodules and may vary from slight to moderately severe.

Acoustic Signs
The acoustic characteristics of a patient with vocal fold nodules will depend on a number of
factors, including the severity of the dysphonia. Depending on the size of the nodule, a patient
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may have a mild, moderate degree of dysphonia. In some cases, a patient may be perceived
to have a normal voice even though a vocal nodule can be seen on videostroboscopy. In our
study of 35 adult female patients with vocal fold nodules (Colton et al., 1997), we found that a
majority of our patients were perceived as only mildly dysphonic, a factor that should be kept
in mind when evaluating the results from our acoustic studies.
Acoustically, a patient with nodules will exhibit increased frequency and amplitude per-
turbation (jitter and shimmer) with a fundamental frequency within the normal range. Davis
(1981) reported pitch perturbation quotient (PPQ) values of 2.61% and 1.87% for two patients
with nodules, compared with a PPQ of 0.42% for normal speakers. Others have reported sim-
ilar greater than normal frequency perturbation measurements in the presence of nodules. Our
group of 35 female patients with nodules had an average jitter of 0.32% and average shimmer
of 2.72%. Takahashi and Koike (1975) reported a mean relative average perturbation (RAP;
see section in Chapter 2 on frequency perturbation) of 0.0084, whereas Ludlow, Coulter, and
Gentges (1983) reported a mean jitter of 9.26 microseconds, compared with a normal value of
5 microseconds. Davis also reported an amplitude perturbation quotient (APQ) of 9.07% and
15.33% for the nodule cases, compared with a normal APQ of 6.14%.
Phonational range may be markedly reduced in these patients, especially at the upper end.
Our group of 35 patients had a mean phonational range of 24 semitones F, a value slightly
less than would be expected for normal female speakers. The magnitude of the reduction in
phonational range appeared to depend on the severity of the dysphonia. For example, patients
perceived to be normal or only slightly dysphonic had an average phonational range of about 28
semitones, whereas patients perceived to be moderately dysphonic had an average phonational
range of 21 semitones. The single patient perceived to as “be very dysphonic” had a phonational
range of slightly more than 7 semitones.
The patient may also show a reduced dynamic range, with marked inability to produce
high sound pressure levels. Our patients showed about a 27 dB range at a single comfortable
pitch, a value somewhat lower than others have reported (Coleman, Mabis, & Hinson, 1977).
Again, patients with more severe dysphonia tended to have smaller dynamic ranges.
Eckel and Boone (1981) reported an average s/z ratio of 1.65 for their group of 28 patients
with nodules and polyps. Normal subjects produced an s/z ratio of 0.99. Spectrum analysis of
a patient’s phonation typically reveals evidence of noise in the spectrum (Arnold & Emanuel,
1979; Yanagihara, 1967), the degree of which depends on lesion size and accompanying the
severity of hoarseness and lesion size. Interestingly, nodules seem to produce little effect on
fundamental frequency of phonation (Murry, 1978).

Measurable Physiological Signs

Airflows in a patient with nodules may be equal to or slightly higher than normal (Iwata,
Esaki, Iwami, & Mimura, 1976; Iwata, von Leden, & Williams, 1972). Tanaka and Gould
(1985) reported a mean value of 275 ml/sec in their two patients with nodules. Normal male
subjects produce flows of about 125 ml/sec. Woo, Colton, and Shangold (1987) reported a
mean flow rate of 265 ml/sec for their combined polyp and nodule group, collapsed across 14
male and 18 female subjects. In their study, normal speakers in the study produced a mean
flow rate of 144 ml/sec. The magnitude of the increase of airflow rates appears to depend on
the severity of the lesion (Shigemori, 1977). Lung pressures may also be high because of the
tendency for an individual to increase the driving force to overcome incomplete glottal closure
(Tanaka & Gould, 1985). However, in our sample of 35 females with nodules, we found some
elevation of pressure (6.41 cm H2O) versus as compared with normal (Colton et al., 1997).
Our patient group showed some elevation of leakage airflow and slightly elevated peak airflows,
the magnitude of which depended on the severity of dysphonia. Electroglottograms will show
decreased closing times of the vocal folds and an irregular pattern. Normal electromyogram
levels would be expected, although it is possible for these to be elevated if the patient shows
excessive laryngeal tension.
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Observable Physiological Signs

Laryngoscopy Nodules have typically been described as benign lesions located at the junc-
tion of the anterior third and posterior two thirds of the vocal folds. It is there that the forces
encountered during vibration are the largest (Luchsinger et al., 1965). It must be remembered
that the posterior one third of the vocal fold (i.e., the vocal process) is composed of stiff cartilage
that does not vibrate. The remaining two thirds of the vocal folds vibrate, and it is at the mid-
point of this vibrating portion that the contact forces will be the greatest. However, in a study
of 24 patients with vocal nodules, Casper et al. (1995) reported that one third of those patients
were found to have nodules located at mid-cord. Laryngoscopically, there may be evidence of
incomplete closure of the vocal folds, especially in the area surrounding the nodules or a large
posterior chink. Some edema of the folds is not uncommon, and there is increased vascularity.
Stroboscopy According to Kitzing (1985), the vocal folds will show normal symmetry and
periodicity but reduced amplitudes and mucosal waves at the nodule site and reduced glottal
closure. In view of the greater frequency perturbation found in patients with vocal nodules (as
reported in “Acoustic Signs,” above), Kitzing’s finding of normal periodicity is questionable. It
is possible that a small nodule may have a minimal effect on the vibratory frequency of the vocal
folds. Hirano and Bless (1993) report absence of the mucosal wave in the nodule area when the
mass is firm, but find it present and unchanged when the nodule is edematous and soft. In our
study of stroboscopic signs in a group of 30 female patients with nodules (Colton et al., 1997),
the amplitude of the vocal fold movement was slightly reduced. Glottal closure had traditionally
been described as having an hourglass appearance. Using frame-by-frame analysis procedures
in which even a single frame of vocal fold closure results in a “complete closure” rating (Colton
et al., 1997), about 47% of our patients with nodules exhibited a posterior chink closure pattern,
whereas 32% showed an hourglass closure pattern. Eighteen percent of the patients showed
complete closure. When viewed as a gestalt (rather than frame-by-frame), the “appearance” of
both hourglass closure and posterior chink ratings would be more predominant. In another
study (Casper et al., 1995), we found that about half of the nodules identified could be described
as being pinpoint in shape with the remainder described as broad based.

Pathophysiology
A nodule will increase the mass of the cover of the vocal fold. The stiffness of the cover will
be increased by a hard and firm nodule and decreased or unchanged by a soft and pliable one
(Hirano, 1981; Hirano & Bless, 1993). It has been theorized that the mechanical properties of
the transition layers and the muscle will not be affected by the nodule. However, Gray’s recent
work on the BMZ (Gray, 1991; Gray, Hirano, & Sato, 1993; Gray, Pignatari, & Harding,
1994) suggests that the BMZ area as the possible site of some damage. Because the mechanical
properties of the cover are very important in determining the vibratory characteristics of the
vocal folds, a nodule may have a pronounced effect on the mechanics of vibration. The extra
mass along the medial edge of the vibrating vocal folds results in increased aperiodicity of
vibration, greater frequency perturbation, and greater hoarseness. Depending on the size of the
nodule, glottal closure will also be affected. Incomplete closure (such as occurs in the hourglass
configuration) will permit increased air escape, resulting in the perception of breathiness.

Polyps
Primary Voice Symptom: Hoarseness
Description and Etiology
There are a number of forms a polyp may take that may affect voice differentially and require
different interventions, and the subsequent effects and treatment may also vary. If the polyp is
localized, it may show up as pedunculated (attached to the vocal fold only by a slim stalk of
tissue) or it may be sessile (closely adhering to mucosa). Another variant is that of hemorrhagic
polyp, which has the appearance of a blood blister. Finally, some polyp-like lesions are diffuse,
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FIGURE 4.2. A single vocal fold polyp.

and may cover one-half to two thirds of the entire length of the one or both vocals. These
lesions are folds and are usually referred to as polypoid degeneration or Reinke’s edema and will
be discussed in a separate section. The distinction between polyp and polypoid degeneration is
sometimes confusing. According to Lowenthal (1958), the pathologies are very similar in that
they are localized or diffuse inflammatory tumors involving the space of Reinke. Histologically,
both types are also very similar.
Polyps are thought to result from a period of vocal abuse, although they can occur as the
result of a single traumatic incident, as for example, yelling at a basketball game. The latter
tend to be hemorrhagic polyps with sudden onset of hoarseness. Luchsinger and Arnold (1965)
considered that polyps and nodules have the same etiology and differ only in degree. According
to Jackson (1941), a polyp is larger and more vascular, edematous, and inflammatory than a
nodule, which is described as an organized mass of tissue (Fig. 4.2).
Polyps are usually predominantly unilateral, although sometimes a small polyp can be
found on the contralateral side. This apparent contralateral polyp may, in reality, be a lesion
created by the contact with the unilateral polyp during phonation. Although polyps usually
occur on the free margin of the vocal folds, they may also be found on the superior surface of
the folds as well as subglottically and in the subglottis. In the latter case, there may be little
or no alteration in the voice. The polyps may also involve a large portion of the vocal fold
(Fig. 4.3).

FIGURE 4.3. Large sessile polyp, involv-

ing the entire length of the vocal fold.
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It is easy to see how acute nodules can be mistaken for polyps. Polyps usually occur in
Reinke’s space (the superficial layer of the lamina propria) and may consist of dilated blood
vessels, fibrotic tissue, and small hemorrhages.
Polyps comprised about 7.7% of the patients seen in the ENT practices reported by Coyle
et al. (2001). A little more than 5% of these patients were female and a little slightly less than
2.5% were male. We studied 25 patients with vocal fold polyps (Colton et al., 1997). Eighteen
of these patients were female with a mean age of 48 years. The remainders were males with a
mean age of 44 years. Due to missing data, the reports about the acoustic, aerodynamic, and
stroboscopic data that follow in the appropriate sections are based on 23 subjects (15 females,
7 males).

Perceptual Signs and Symptoms

Typical perceptual signs of a polyp include hoarseness, roughness, or breathiness. In addition,
the patient may report the sensation of something in the throat.
In our polyp patient group, 35% of the females and 17% of males exhibited a “moderate”
severity of dysphonia, whereas the 17% of males exhibited this level of severity. The next
most frequent category was “very severe” (22% females, 4.35% males). Thus, the polyp group
exhibited a greater severity of dysphonia than did the nodule group discussed previously in the
last section.

Acoustic Signs
The acoustic features created by a polyp are very similar to those of a nodule. Increased jitter
and shimmer would be expected depending on the location of the polyp. Davis (1981) reported
a PPQ of 0.60% and an APQ of 11.68% for his one patient with a polyp. Normal PPQ is
0.42% and APQ is 6.14%. We found jitter scores ranged from 0.27% to 1.83%, the latter for a
group of female subjects with a “moderate” severity rating. Reduced phonational and dynamic
ranges, as well as increased spectral noise, would also be anticipated acoustic characteristics.
We found a significant reduction in phonational range for both male and female patients with
vocal fold polyps. Please note that the “slight” dysphonia category for both sexes and the “very”
dysphonic category for males had each included only one patient. Our data for dynamic ranges
showed little difference between patients with polyps and normal speakers.

Measurable Physiological Signs

Increased airflow may be present if the polyp interferes with complete glottal closure, but
available data regarding this matter are somewhat variable. In one report, 18 patients with
polyps had an average airflow rate of 162 ml/sec (Iwata et al., 1972), whereas in another report,
Iwata et al. (1976) reported an average airflow rates of 253 ml/sec for 29 male patients and
247 ml/sec for 19 female patients with unilateral polyps. In the same study, patients with
bilateral polyps had airflow rates of 256 ml/sec (8 males) and 359 ml/sec (8 females). For their
seven patients with polyps, Tanaka and Gould (Tanaka et al., 1985) reported a mean flow rate
of 223.71 ml/sec. Woo, Colton, and Shangold (1987) reported a mean flow rate of 265 ml/sec
for their combined polyp and nodule group, collapsed across 14 male and 18 female subjects.
In the Woo et al. study, normal speakers produced a mean flow rate of 144 ml/sec. We found
significantly greater vibratory airflow rates for our group of 23 patients but no differences in
leakage airflow. Subglottal or lung pressure also appears to increase due to attempts to produce
phonation in the presence of a leaky glottis (Tanaka et al., 1985). Our patient group had
subglottal air pressures within normal limits, but the average open quotients were markedly
reduced as compared with the normal group. Electroglottography tends to suggest decreased
closing times of the vocal folds and irregular patterns. Muscle action potentials would again be
expected to be normal, unless the patient showed excessive laryngeal tension.
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Observable Physiological Signs

Laryngoscopy Polyps often can typically be visualized with standard continuous light laryn-
goscopy using a mirror or flexible endoscope. They typically appear as rather large a masses on
one vocal fold, sometimes with a very broad base, sometimes attached to a stalk. Most of the
times, they appear somewhat translucent, although on occasion they may be red and apparently
filled with blood and therefore appear reddish in appearance.
Stroboscopy Stroboscopically, asymmetry of motion of the vocal folds and increased aperi-
odicity are noted. Polyps tend to show distinct phase differences between the two folds, especially
if the lesions are grossly different in size or if the lesion is unilateral. The vibratory amplitude
of the vocal folds is reduced, but the effect of the polyp on mucosal waves, especially in the
vicinity of the polyp, may vary from being decreased or absent (as in the case of a hemorrhagic
polyp) to being increased (as in large sessile polyps) to being normal (as in a pedunculated
polyp). Glottal closure may also be affected (Hirano, Feder, & Bless, 1983; Kitzing, 1985). In
our study of 24 patients with polyps (Colton, Woo, Brewer, Griffin, & Casper, 1995), the most
common closure pattern was irregular. Aperiodicity of vocal fold movement may be increased
although in our study (Colton & Woo, 1995), the most frequent periodicity category rating
was regular. In some instances, the movement of the polyp lagged behind the vocal fold proper
and thus appears as a “coupled” movement. The results of our study further revealed that the
amplitude of vocal fold movement in patients with polyps was moderately decreased, especially
for the affected fold. Vibration of the affected vocal fold was also altered by the presence of the
lesion (Colton et al., 1995); that is, there was little or no mucosal wave, especially over the site
of the lesion.

Pathophysiology
A polyp will increase the mass of the cover of the vocal folds. If the polyp is soft, edematous,
and pliable, the stiffness of the cover will be decreased (Hirano, 1981). However, if bleeding,
hyaline degeneration, or other histological changes are present, stiffness of the cover may be
increased (see Chapter 3). The mechanical properties of the transition layers and the muscle
should not be affected. As described in the case of nodules, the mechanical properties of
the cover will determine the vibratory characteristics of the vocal folds. An extra mass at the
midpoint of the vibrating vocal folds results in increased aperiodicity of vibration, greater
frequency perturbation, and greater hoarseness. However, if the polyp is pedunculated, there
will probably be little effects on vibration because the mass of the polyp does not affect the
cover directly. Depending on the size of the polyp, glottal closure may be affected. If excessive
air can escape through the closed glottis, breathiness will be perceived.

Intracordal Cysts
Primary Voice Symptom: Hoarseness
Description and Etiology
Intracordal cysts appear as small spheres on the margins of the vocal folds (Fig. 4.4) and
sometimes or on the superior surface. They may be mistaken for early nodules because small
nodule-like growths may appear on one cord but not the other. Cysts are predominantly
unilateral and can often be mistaken for early nodules or polyps. Cysts may also occur in
association with vocal nodules (Monday, 1983).
Intracordal or retention cysts may be caused by blockage of a glandular duct in which
there is retention of mucus (Cornut & Bouchayer, 1989; Monday, 1983). Typically, the cyst
is lined with glandular epithelium, may appear to have a slightly yellowish color, and does not
drain spontaneously. Because there is no way for the mucus to escape, a cyst may, with time,
grow larger. Another type of cyst, usually smaller than a retention cyst, is the epidermoid cyst.
These types of cysts of the vocal folds have a strong similarity to epidermal cysts of the skin.
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FIGURE 4.4. Intracordal cyst.

Cornut & Bouchayer (1989) make a clear distinction between epidermoid and a retention
cyst. Pseudocysts are yet another variant. They are easily mistaken for polyps or nodules as they
appear in the same area. They tend to be unilateral and have a translucent appearance. They
occur most frequently in young adult women (Bouchayer et al., 1985; Monday, 1983). Cysts
often occur in professional voice users. The etiology of cysts is not entirely clear, but it is thought
that vocal trauma may be a contributory factor that starts the process of cyst development.

Perceptual Signs and Symptoms

Typical signs of a cyst include hoarseness and a lowered pitch. The patient may report a “tired”
voice.
Our sample of cyst patients consisted of three males and nine females. The most frequent
dysphonia severity rating was “moderate.” One patient had missing data; therefore, the data
presented in the following sections were pooled across severity ratings from 11 patients.

Acoustic Signs
The female patients in our sample of patients with vocal fold intracordal retention cysts exhib-
ited a significantly lower than normal value for phonational range. No other differences were
statistically significant. This was the only acoustic measure that reached significance.
It is also possible that different types of cysts may produce differing acoustic signs.

Measurable Physiological Signs

Again, there are few physiological data available on patients with cysts. However, higher than
normal average airflows might be expected if glottal closure is incomplete as a result of elevated
offset flows and higher than normal peak flows. The closing phase of the vocal folds, as seen in
an electroglottogram, may also be slower than normal.

Observable Physiological Signs

Laryngoscopy Identification of a cyst can be very difficult. Bouchayer et al. (1985) reported
that in only 10% of their cases was a cyst obvious on initial examination. However, the appear-
ance of fullness of the vocal fold and dilated capillaries raised the suspicion of a cyst in 55% of
cases. Endoscopically, cysts are sometimes highlighted by a persistent light reflection from the
slightly raised area of the cyst. The telltale sign noted above, of a dilated and prominent blood
vessel, can further be described as a vessel that flows laterally or irregularly across the fold and
appears to terminate at the site of the cyst.
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Stroboscopy Stroboscopy has been found to be very helpful in the diagnosis of a cyst because
there is an absence of mucosal wave in the area over the cyst and the typically round shape of
the lesion is very visible. Other signs include greater aperiodicity and reduced glottal closure
(Kitzing, 1985). In our sample of 12 patients with cysts, 42% had an hourglass closure pattern,
33% a posterior chink pattern, and 25% had complete closure. We have also found that the
vibration of the two folds was often asymmetric, especially over the area of the cyst (Colton
et al., 1995). Amplitude of the affected side, in particular, was decreased in our patient sample.

Pathophysiology
A cyst originates in the superficial layer of the lamina propria (Hirano, 1981). As the encap-
sulated lesion grows, it increases the distance between the cover and the lamina propria but
usually does not extend into the layers. A cyst increases the mass and stiffness of the cover,
whereas the transition layers and the body are unaffected.

Edema
Primary Voice Symptom: Hoarseness
Description and Etiology
Although edema refers to the buildup of fluid that occurs primarily in the superficial of the vocal
folds, all edema does not have the same appearance or etiology layers of the lamina propria.
The outermost layer includes Reinke’s space, which is composed of loose, pliable fibers. When
it occurs in the first layer of the lamina propria, fluid collects at this site; it is referred to as
Reinke’s edema because Reinke’s space occurs in this layer (Fig. 4.5). Other names used to
refer to this problem condition are diffuse polyposis or polypoid degeneration. Some apparent
swelling of the vocal folds, especially when localized, may also be a sign of a cyst. The lesions
are seen bilaterally but are usually asymmetric in size. Reinke’s edema is highly associated with
heavy and long-term smoking. It appears to occur more frequently in females than in males
(Bastian, 1986; Nielsen, Hojslet, & Karlsmose, 1986).
Edema is a natural reaction of tissue to trauma and misuse. It may result from misuse or
excessive use of the voice or as a concomitant of infection or inflammation. Person’s taking
certain drugs may have edema as a side effect. Edema is often a component of an allergic
reaction. When the vocal folds are involved, they appear edematous but tend to be pale in color.
In addition to vocal abuse, chronic Reinke’s edema is most often associated with smoking. It
appears to occur more frequently in females, especially if they are long-term smokers (Bastian,
1986; Nielsen et al., 1986).

FIGURE 4.5. Reinke’s edema.

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CHAPTER 4 I Phonotrauma: Its Effects on Phonatory Physiology 107

Perceptual Signs and Symptoms

Typical symptoms of edema include a lower than normal pitch level and hoarseness. If the
Reinke’s edema is particularly severe, the patient may complain of shortness of breath because
the edematous vocal folds may partially block the airway. In some other instances, cases of
edema patients complain of loss of pitch range and increased effort required to produce voice.
There were 13 patients in our group of patients with edema. Twelve of the 13 were female,
and therefore, we will only report our data for the female patients.

Acoustic Signs
The fundamental frequency of phonation is lower than that expected for the sex and age of
the patient. Bennett, Bishop, and Lumpkin (1987) reported a mean fundamental frequency
of 108 Hz for their group of 29 females with Reinke’s edema and 91 Hz for their 6 male
patients. In our sample of 12 patients, the fundamental frequency was lower than normal, but
the difference failed to reach significance. Jitter and shimmer on the vowel /ah/ were also within
normal limits but significantly greater on the vowel /oo/. The only acoustic variable that was
significantly lower than normal was dynamic range.

Measurable Physiological Signs

Electromyographic recordings may also show no abnormalities. Our patients showed a signif-
icantly greater mean and AC flow rate than normal. Pressures and vocal efficiency measures
were within normal limits.

Observable Physiological Signs

Laryngoscopy In Reinke’s edema, the vocal folds have the appearance of enlarged fluid-filled
boggy structures. They do not appear firm or solid. The edema usually involves most of the full
length of the vocal folds bilaterally. In some respects, Reinke’s edema gives the appearance of a
mild-to-moderate stage and often has the appearance of broad-based polyps occupying the full
length of the vocal fold. Vocal folds may also be seen to be E vocal folds edematous but without
the boggy appearance of Reinke’s. In such cases, they have a firmer, rounded appearance, rather
than a flat with a rounded, superior surface along the full length of the folds.
Stroboscopy Stroboscopic features of Reinke’s edema are expected to show greater than
normal excursion of the mucosal wave and complete glottal closure. In our published study of
four patients with Reinke’s edema (Colton et al., 1995), the mucosal wave was slightly decreased
but glottal closure was complete. In our larger sample of 12 patients, a complete closure
pattern was again most frequent, but there were more ratings of moderately decreased and
severely decreased mucosal wave. Amplitude of vibration of the vocal folds was also moderately
decreased. We have found that the vibration of the two folds was often symmetrical. In superior
surface edema, the stroboscopic appearance may be quite different. The vocal folds may appear
to be stiffened with reduction of both amplitude of vibration and mucosal wave.

Pathophysiology
Edema affects the superficial layer of the lamina propria. The mass of the cover is increased.
However, stiffness of the cover may depend on the specific nature of the lesion. Bennett,
Bishop, and Lumpkin (1987) suggested that Reinke’s edema disturbs the elasticity of the cover,
resulting in decreased stiffness. Such a reduction in stiffness would allow for greater amplitudes
of vibration. The transition layers and body are not affected in Reinke’s edema. The increase
in bulk and reduction in stiffness would contribute to a lowered fundamental frequency of
vibration.
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FIGURE 4.6. Acute laryngitis, with poly-

poid change.

Laryngitis
There are several kinds of inflammatory conditions that are referred to as laryngitis. One is
reflux laryngitis thought to be caused by reflux from the stomach contents. This condition
will be discussed in a later chapter. The second kind of laryngitis, acute laryngitis, is due to
an upper respiratory infection, either bacterial or viral in nature. The third form is caused by
phonotrauma and can be either acute or chronic. The following discussion will focus on this
last type of noninfectious laryngitis.
In their study of 1158 patients, Coyle et al. (2001) reported that laryngitis was one of the
fifth most frequently occurring pathologies in their population. Patients with laryngitis of any
form were not included in our study of benign lesions.

Primary Voice Symptom: Hoarseness

Description and Etiology
Laryngitis is an inflammation of the vocal folds and larynx. It may result from exposure to nox-
ious agents (tobacco, alcohol, drugs), acidic gastric contents (GERD), environmental agents
(allergens, dust), or phonotrauma. Laryngitis may also be the result of upper respiratory in-
fections, which have a generalized effect on the mucosa of the respiratory tract, including the
larynx (Fig. 4.6). The problem may be acute or chronic. Acute laryngitis resulting from bac-
terial or viral infection requires medical attention and is not directly related to phonotrauma
vocal abuse. However, it does affect voice production and indirectly may be aggravated by vocal
excesses, as will be described later. Chronic abuse can lead to chronic laryngitis with persistent
inflammation and perhaps a thickening and drying of the vocal folds. Laryngitis may lead to
tissue changes, such as nodules, polyps, or hypertrophy of the laryngeal epithelium.

Perceptual Signs and Symptoms

The symptoms of laryngitis include marked roughness or hoarseness of the voice with accom-
panying sensations of discomfort and dryness in the throat. When secondary to infection, the
hoarseness may persist for some time after the infection has been controlled. Continued heavy
use of the voice during this time may contribute to exacerbate the laryngitis and contribute to
the continued hoarseness. The pitch level of the voice may appear to be either higher or lower
than normal, and it will be difficult to speak in a loud voice.

Acoustic Signs
Greater than normal frequency and amplitude perturbation would be expected. Takahashi and
Koike (1975) found a mean RAP of 0.0069 and 0.0078 in their two female patients with
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CHAPTER 4 I Phonotrauma: Its Effects on Phonatory Physiology 109

chronic laryngitis. Their nine normal subjects had a mean RAP of 0.00582. Takahashi and
Koike (1975) reported a mean fundamental frequency level of 103 Hz for one of their female
patients with chronic laryngitis and 284 Hz for the other. Thus, it appears that fundamental
frequency may be either elevated or reduced. Fundamental frequency may be related to the
severity of the cordal involvement and may be either elevated or reduced. One would also
expect that phonational range would be reduced (Shipp & Huntington, 1965). Maximum
sustainable intensities may be much lower than normal. Finally, there should be greater than
normal spectral noise in the voice.

Measurable Physiological Signs

When laryngitis is present, airflow and air pressures may be elevated, especially if there is in-
complete glottal closure. However, average airflows appear to be within normal limits (Hirano,
1981; McGlone, Richmond, & Bosma, 1966). Based on our experience, vibratory airflows
show increased variability from one cycle to the next, and there may be greater than normal
offset and peak airflows. Woo et al. (1987) reported a mean flow rate of 222 ml/sec for their
combined acute, chronic, and postradiation laryngitis group, collapsed across 7 male and 11
female subjects. (Normal speakers produced a mean flow rate of 144 ml/sec.) The electroglot-
tographic signal may show marked variability from one cycle to the next, although closure
times may be normal. Electromyographic levels would be expected to be normal or slightly
elevated.

Observable Physiological Signs

Laryngoscopy Laryngitic larynges in the acute stages will show a marked redness, and small,
dilated blood vessels may be visible on the inflamed folds. Chronic laryngitis may not be marked
by inflammation, but rather by thickened and dry epithelium.
Stroboscopy The vocal folds may show increased asymmetry and aperiodicity, with reduced
mucosal waves and reduced amplitude. We have noted a jerk-like movement of the mucosal
wave, in which the wave appears to travel along part of the surface at one speed, then changes
its speed for the remainder of its travel. The movement may also be called biphasic (Woo, P.,
personal oral communication, 1988). There is a stiff, jerky quality to this movement.

Pathophysiology
Laryngitis affects the cover of the vocal folds by increasing its stiffness, but may have little effect
on the mass of the vocal folds.

Other Comments
Chronic laryngitis, if allowed to continue untreated, may result in serious complications, in-
cluding laryngitis sicca, which is characterized by marked atrophy of the mucosa of the larynx.
The major abnormality is the lack of vocal fold lubrication due to the reduction or absence
of glandular secretions. The vocal folds will become dry and sticky, and a chronic cough
may be present as the system attempts to remove the thick secretions that gather on adher-
ent to the vocal folds tissues. On occasion, laryngeal crusting may result, requiring surgical
removal.
Other forms of laryngitis result from diphtheria, tuberculosis, and syphilis, all of which are
extremely rare. Another special form of laryngitis is acute epiglottitis, in which the inflammatory
changes affect the mucosa of the epiglottis. Epiglottitis may be life threatening if the epiglottis
becomes sufficiently enlarged to result in airway obstruction. Emergency treatment may be
required. Antibiotics may be used to control the infection, or steroids may be used to reduce
the inflammation (Sataloff, 1987).
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110 Understanding Voice Problems

FIGURE 4.7. Vergeture (sulcus). See

Color Plate.

Sulcus Vocalis
Sulcus vocalis did not appear in the list of pathologies seen in the two ENT practices in Ohio
reported by Coyle et al. (2001). We only had four patients with sulcus vocalis in our study of
patients with benign lesions of the vocal folds.

Primary Voice Symptom: Hoarseness

Description and Etiology
Sulcus vocalis refers to a condition in which a furrow along the upper medial edge of the vocal
folds is observed. Bastian (1986) described it as an “epithelial-lined furrow or pocket whose lips
parallel the free edge of the cords” (p. 1974). In a cross-section of the vocal folds, the furrow
appears as a pocketed ledge on the medial surface of the vocal folds (Fig. 4.7). The longitudinal
extent of the furrow is variable, as is its depth. If very deep, it seems to divide the cord vocal fold
in half. According to Arnold (1980), sulcus vocalis may be associated with other laryngeal or
oral asymmetries. Ford et al. (1996) described three different types of sulci and their differential
effects on the lamina propria.
The etiology of sulcus vocalis is uncertain, although Bastian (1986) attributes it to vocal
misuse and abuse. Luchsinger and Arnold (1965) in their review of the literature summarized
the possible etiological factors as being congenital, developmental, or traumatic. Bouchayer et
al. (1985) argued for a congenital etiology. The disorder is rather rare, at least in Europe and
in the United States (Luchsinger et al., 1965); it may be more prevalent in Japan (Hirano,
1981). According to Hirano and Bless (1993), sulcus vocalis is either congenital or the result
of repeated chronic inflammatory processes.

Perceptual Signs and Symptoms

Symptoms include a breathy, hoarse voice quality that apparently is due to incomplete closure
of the vocal folds and disturbed vibratory behavior. Hirano et al. (1990) reported that 64% of
their patient sample of 126 with sulcus vocalis had a mild breathiness. Lindestad and Hertegard
(1994) estimated that the pitch was higher than normal in 72% of their sulcus patients.

Acoustic Signs
Hirano et al. (1990) reported Jitter (PPQ) and Shimmer (APQ) within normal limits for their
samples of 126 patients. Normalized noise energy was also within normal limits. Maximum
phonation time was only slightly shorter (18.1 seconds) than normal. Phonational ranges were
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CHAPTER 4 I Phonotrauma: Its Effects on Phonatory Physiology 111

22.7 semitones for unilateral sulci and 19.4 semitones for bilateral sulci, values lower than
would be expected.

Measurable Physiological Signs

Airflows may be slightly elevated (Shigemori, 1977), although Hirano et al. (1990) reported a
mean flow rate of 148 ml/s for patients with unilateral lesions and 195 ml/s for patients with
bilateral lesions. These values are slightly higher than the mean flow rates for normal speakers
(see Chapter 14) but are probably within normal limits. We found that in our four patients,
mean flows and peak flows of our patients were greater than would be expected. Leakage flow
was within normal limits.
Electroglottographic recordings may show increased perturbation with the possibility of
short closed times.

Observable Physiological Signs

Laryngoscopy Laryngoscopically, a sulcus will be seen as a depression or line along the upper
medial edge of the vocal fold. The depression may be variable in length from partial to full
extend the entire length of the vocal fold and may vary in depth from shallow to very deep.
Sulci may be either unilateral or bilateral.
Stroboscopy Hirano at al. (1990) reported an incomplete glottal closure pattern in 69 of their
126 patients with sulcus vocalis in combination with a slightly decreased amplitude of vibration
and a slightly decreased mucosal wave. Lindestad and Hertegard (1994) reported a spindle-
shaped glottal closure pattern as most frequent in their sample of 47 patients with a sulcus.
Seventy-nine percent of these patients also had a diminished mucosal wave. Forty-nine percent
of the patients with a bilateral lesion had a slightly decreased amplitude of vibration, whereas
only 21% of the patients with a unilateral lesion showed a decrease. In cases of unilateral sulcus,
a mucosal wave can usually be seen across the uninvolved superior surface of the uninvolved
vocal fold, but it may be diminished in amplitude.

Pathophysiology
The sulcus is located in the superficial layer of the lamina propria, which decreases the mass of
the cover but may increase its stiffness. The body and the transition layers are normal.
Bouchayer and Cornut (1984) have described a variant of a sulcus that they term vergeture.
Lindestard and Hertegard (1994) described a vergeture as an adhesive type of lesion wherein
the epithelium attaches directly to the underlying muscle through the division produced by
the sulcus. They use the term sulcus vocalis to refer to a pocket-like appearance of the mucosa.
Distinguishing these two forms of a sulcus may be difficult, especially without the use of a
stroboscope and may only become clear during microscopic laryngeal surgery.

Summary
Phonotrauma is a recently proposed term that is meant to cover the broad category of vocal
behaviors that may cause phonatory and/or laryngeal tissue changes. Such behaviors may include
what we describe as results from a variety of causes including voice misuse, or inappropriate
use, and those that are abusive to the vocal fold tissues. The goal of this chapter is to sensitize
the practitioner to the many forms that misuse and abuse of the phonatory mechanism may
take. As defined here, the primary misuses of the voice include hard glottal attack, elevated
laryngeal posture, anteroposterior squeezing, and inappropriate pitch level. Abusive behaviors
include excessive coughing and throat clearing, yelling, shouting, cheerleading-type activities,
and prolonged loud talking. Abusive behaviors may result in mechanical trauma to the vocal
folds or vocal processes. Continued trauma may result in the production of tissue change that
will alter the vibratory characteristics of the vocal folds, which in turn results in hoarseness or/and
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112 Understanding Voice Problems

FIGURE 4.8. Vocal abuse.

produce roughness in the voice perceived as rough or hoarse. In some cases, the tissue alteration
will prevent complete glottal closure and result in the production of breathy phonation. An
understanding of these behaviors will allow the clinician to help patients make a thorough
inventory of their own behaviors.
The goal of this chapter’s section on drugs is to increase awareness of the potential phonatory
effect of a vast array of pharmaceuticals, many of which are frequently considered to be quite
benign, especially if they are of the over-the-counter variety. There are certainly many overriding
reasons why drugs must be used in the treatment of various conditions, even if some degree of
voice change may occur. However, the practitioner who works with the voice patient must be
aware of the effects various drugs may have on voice and/or on mucosal tissues. This can be
particularly critical for the professional voice user.
In the last section, a variety of specific tissue changes associated with vocal misuse and
phonotrauma have been reviewed, including vocal nodules, polyps, cysts, edema, laryngitis,
and sulcus vocalis. Although some of these conditions may be caused by infection, viral agents,
external trauma, congenital disposition, or disease, vocal phonotrauma is often considered to
be directly or indirectly involved as either a precipitating or exacerbating factor. Recognition
of the contribution of phonotrauma to these conditions is necessary to arrive at a treatment
protocol that will be effective in reducing and/or eliminating these vocal behaviors restoring
the voice to the best quality attainable, with the least trauma and expense to the patient
(Fig. 4.8).
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CHAPTER

5
Voice Problems Associated with
Nervous System Involvement
Keywords
nervous system, organization, myasthenia gravis, parkinsonism, Shy–Drager, peripheral
nerve, spasmodic dysphonia, Huntingtons chorea, suprabulbar palsy, ALS, essential
tremor, cerebellar ataxia, multiple sclerosis, Arnold–Chiari malformation, Tourette
syndrome

Role of Nervous System

The nervous system is that portion of the body concerned with the control of body functions. Viewed
as a unit, it is responsible for the total control of all systems in the body, even self-regulating systems that
are capable of carrying out their own functions. The smaller units of the body’s organizational system
(cells, tissues, and organs) function only within their own little world and in an environment that must
be controlled. It is the responsibility of the nervous system to create this environment by regulating
systems that provide for the proper nourishment, temperature regulation, gas exchange, and byproduct
disposal necessary for all the component parts to work effectively.
Coordination of function is another aspect of the control exerted by the nervous system. One system
must work at the proper time if another system is to function properly. Within a system, the various
parts must perform their tasks at the proper times for the final output of the system to be meaningful
and productive. The necessity for coordination is even more apparent in the production of skilled motor
acts involving the various striated muscles of the body. Simple walking is an example of a highly skilled
motor act involving the properly timed contraction and relaxation of various muscles for its smooth
action.
The nervous system is divided into two major parts: the central nervous system and the peripheral
nervous system. The central nervous system (CNS) is that portion residing within the cranial cavity or
skull and vertebral column. The peripheral nervous system (PNS) resides throughout the body outside
of the cranium. The central nervous system is responsible for the initiation and coordination of function,
whereas the peripheral nervous system carries the instructions of the central nervous system to the various
organs and muscles of the body.
The nervous system may also be divided into two components, according to whether information is
conducted to the central nervous system (afferent) or from the central nervous system (efferent). Indeed,
information from muscles, organs, and tissues is needed by the central nervous system for proper control
to be maintained. Information from the outside world via the several senses is also used by the central
nervous system to make it possible for the body to exist in the hostile world. Without the nervous
system, the body cannot live. With a damaged nervous system, the body cannot function “normally” in
its environment.

113
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114 Understanding Voice Problems

General Characteristics of Nervous System Dysfunction

The nervous system may malfunction due to disease, abnormal growths, accidents, or trauma.
The nature of the malfunction will depend on where the problem occurs. In some cases, there
will be difficulty in initiating an action or activity, whereas in others the activity will begin
without difficulty but control of it may be impaired. In still other cases, incoming information
will be distorted or nonexistent, so that the nervous system will not have the proper information
for the control of motor or organ activity appropriate for the task at hand.
The central nervous system is responsible for initiating skilled motor acts that involve the
starting and stopping of motor activity. Walking is a good example of an activity that must be
initiated and terminated. Most internal body functions are ongoing; that is, once started, they
continue or else the body will to cease to function (e.g., blood flow, respiration, temperature
regulation). Other internal body functions are episodic and may be stopped and started (e.g.,
digestion, hormone production). Speech itself is a very good example of an act that is constantly
started and stopped even during its execution. There are centers and cells within the central
nervous system that have this function of starting an act. If damaged, the initiation of the act
may not take place or will be delayed, uncertain, or otherwise impaired.
The central nervous system also coordinates function. There are many examples of the
need for coordination of body systems, the act of walking being just one. Speech is also a highly
coordinated event involving coordination within bodily systems (e.g., phonation, respiration,
articulation) and among these systems. Damage to the central nervous system may affect control
of coordinated function.
Lower brain centers, including the spinal cord, maintain a measure of control, albeit local,
on muscles and systems. For example, muscles must be maintained in a state of readiness for
action. Muscle tone reflects this state of readiness. Muscles show steady levels of electrical activity
even when they are not being used for a motor act. This state of readiness is often regulated
and maintained by lower neuron systems. The central nervous system exerts its control by
inhibiting the activity of the lower centers, so that they do not get out of control. Damage to
the central nervous system can result in the disruption of this inhibition and the production of
unnecessary or unwanted movements.
Finally, incoming sensory information is critical for the control process. The central nervous
system must know when the right foot has touched the floor in order to command the left leg to
rise and move the left foot forward. Otherwise, the walker will fall flat on his face or cease moving.
The central nervous system relies on visual information in order to properly control the hand
and arm in reaching for the glass of water on the kitchen table. Deprived of sensory information,
the organism will not know about the environment and its potential effects. Incoming sensory
information need not be entirely external. Internal sensory information is also critical for neural
control. Examples of internal sensory information include joint kinesthetics, position sense,
pain, pressure, and temperature. Kinesthetic feedback from joints and muscles must be available
if skilled movements are to be possible. The job of the central nervous system is to receive and
integrate information and prepare a proper plan for dealing with it.

Role of the Nervous System in Phonation and Speech

Speech is a complex, fine motor act that involves several diverse systems or parts of systems
for its execution. The respiratory system, basically designed for the exchange of gases for
use by the tissues of the body, is also used for speech, with contributions from the digestive
system, primarily the mouth, jaw, and teeth. Speech requires the use of the respiratory system
mechanically, that is, for the generation and control of the airflows and pressures needed
for speaking. Thus, the control of the respiratory system for life support and the control of
the respiratory system for speaking are quite different. The nervous system must provide the
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 115

control appropriate to the task at hand. Furthermore, during speech, there must be a high
level of coordination among the chest wall, the abdominal mechanical system, the larynx and
pharynx, and the lips, tongue, teeth, and mandible so that all function at the proper time and
for the length of time necessary for the production of the individual sounds. During the act of
speaking, the system receives information about the state of its structures and muscles via both
kinesthetic and acoustic feedback. Thus, the auditory system is yet another important system
that must enter into the control exercised by the nervous system.
Disease, malformation, or injury will affect the control capabilities of the nervous system.
The manifestation of nervous system damage will vary depending on where the lesion occurs.
If the lesion occurs at the cortex, many components of speech may be affected, including the
ability to use language, to initiate speech, to produce muscle movements necessary to produce
intelligible speech or control muscle movements, or to receive information from the body
systems about where they are and what they have done. The symptoms and signs that the
patient presents are critical to the proper diagnosis of the problem and identification of the
source of the problem.
In this book, we are interested in the effects of nervous system damage on the control
of phonation. Although the system remains complex, there is a finite set of brain sites and
pathways that have been shown to be important for the control of phonation. Lesions will
produce specific symptoms that will help the diagnostician identify the site of lesion. Some of
the possible problems affecting phonation and their possible locations in the nervous system
are discussed by Barlow, Netsell, and Hunker (1986). They note that in the lateral precentral
cortex, there appears to be a convergence of pathways from other parts of the brain that may
be the site of the final common pathway through the brain to the periphery. Lesions at this
site would be expected to result in complete loss of phonation because input from the higher
control centers will have been lost. Furthermore, lesions in this area and other adjacent areas
would also be expected to produce loss of function in other muscles concerned with speech.
Consequently, such lesions will be expected to produce aphonia or dysphonia, dysarthria, and
perhaps even aphasia. Lesions in the anterior cingulate cortex are also reported to produce
akinetic mutism in humans (Barlow et al., 1986). In monkeys, this area seems to be critical for
the control of conditional, learned vocalization. Lesions in other areas of the brain (e.g., basal
ganglia, periaqueductal gray) produce a disruption in phonation characterized by breathiness,
roughness, tremor, or complete disruption of vocalization. Lesions in the cerebellum result in
ataxic dysarthria and changes in the velocity of lip and jaw movements and would presumably
affect the speed of movements of structures in the larynx. Larson, Sutton, and Lindeman
(1978) concluded that the cerebellum is very important in the control of pitch and loudness
of phonation but is not required for the initiation of phonation.
One way to consider the neurological problems that affect phonation would be to recognize
the levels of organization within the nervous system, as discussed previously. The following is
such a scheme, proposed by Ward, Hanson, and Berci (1981). It is both simple and effective
as an aid in understanding how a specific lesion or syndrome may affect phonation.

1. Afferent sensory, autonomic

Sympathetic nervous system: prepares body for stressful situations, producing a fight or
flight type of response
Parasympathetic Nervous System: restores body to normal after excitement and acts to
calm the system
2. Efferent motor
Upper-motor neuron (cortex and pyramidal tracts)
Extrapyramidal (reticular substance)
Cerebellar
Nuclear (lower-motor neurons)
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116 Understanding Voice Problems

Organization of the Nervous System and Voice Pathology

The following section is a brief review of the major systems involved in phonation. More
complete information about the nervous system can be found in Chapter 14. Ward et al.
(1981) discuss the role of the afferent or sensory system in the control of phonation. Our
discussion here will concentrate on the efferent or motor system involved in the control of
phonation.
In the cortex, area 4 of the precentral gyrus is very important in the control of vocalization.
Neurons from this and other areas of the cortex converge to form the corticobulbar tracts. These
tracts pass through the internal capsule and cerebral peduncle and eventually comprise what is
known as the pyramidal tracts (Fig. 5.1). At the upper part of the medulla, many fibers cross over
(decussate) to the opposite side and continue down to the nucleus ambiguus in the brainstem.
As discussed in Chapter 14, the nucleus ambiguus houses the motor nuclei for the 9th, 10th,
and 11th cranial nerves. Thus, lesions anywhere along this pathway may involve the precentral
cortex, the corticobulbar tracts, the internal capsule, or the cerebral peduncles, the medulla,
the brainstem, or the nucleus ambiguus itself, causing differential effects on phonation.
The extrapyramidal system (Fig. 5.2) consists of the reticular substance, corpus striatum
(with the caudate and lenticular nuclei), and the basal ganglia (specifically the globus pallidus
and the substantia nigra; Ward et al., 1981). Lesions here will affect the coordination of

FIGURE 5.1. Schematic of the direct (pyramidal)

motor pathway. (From Gardner, E. (1963). Fundamen-
tals of neurology. Philadelphia: W. B. Saunders Co.)
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 117

FIGURE 5.2. Schematic of the indirect (extrapyrami-

dal) motor pathway. (From Gardner, E. (1963). Fundamen-
tals of neurology. Philadelphia: W. B. Saunders Co.)

laryngeal function. Athetoid movements are characteristic of patients with lesions in these
areas. Degeneration of the basal ganglia and the reticular substance produce the symptoms
typical of parkinsonism (see later section on parkinsonism for a more complete discussion of
this disease). The Shy–Drager syndrome, in which there is progressive abductor paralysis of
the larynx, is thought to be a disease affecting the extrapyramidal system as well as the motor
nuclei of the vagus (see later section on Shy–Drager syndrome for a more complete discussion
of this disease).
Lesions in the cerebellum affect the coordination of motor function and result in slurred
speech and problems with coordination of the various speech systems, as well as nonspeech
symptoms, such as ataxia, nystagmus, and gait problems. The voice may exhibit a breathy
quality, or it may exhibit spastic behavior. In the Arnold–Chiari Malformation, for example,
the vocal folds may typically demonstrate involuntary abduction (see later section on Arnold–
Chiari malformation for a more complete discussion).
Lower-motor neuron problems occur in the brainstem and medulla. There are many
syndromes that result from lesions in the medulla and in which voice will be affected, as will
the functioning of the palate, pharynx, tongue, face, and other body parts. Lesions in the
nucleus ambiguus may produce classic symptoms of a combined paralysis of the superior and
recurrent laryngeal nerves, resulting in flaccid vocal folds. Such lesions, depending on their
extent, may also affect the palate and pharynx.
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118 Understanding Voice Problems

Finally, there can be an interruption of control in the peripheral nerves supplying the
larynx itself. Such disturbance can result from lesions or injury to the superior laryngeal nerve,
the recurrent laryngeal nerve, or both. Furthermore, the lesions may be either unilateral or
bilateral. Again, the specific symptoms presented by the patient will help to determine the
proper diagnosis and locus of the problem.
There are voice problems in which neurological involvement is suspected but cannot be
determined with certainty. Some of these problems may involve diffuse areas of the brain, and
no specific single site of lesion can be determined. In other instances, the etiology is unknown
or described as idiopathic in nature. However, “unknown” or “idiopathic” is not a diagnosis. It
should signify a temporary condition during which further data are gathered in the search for
the diagnosis. A more precise diagnosis may result from additional testing, but occasionally the
simple passage of time reveals additional symptoms that help to refine the diagnosis. In some
cases, a more specific diagnosis may remain undetermined or unknown.
In the following discussion about specific neurological problems that affect the voice, a
primary vocal symptom will be stated. In most cases, this refers to the most frequently reported
symptom for that disease, as reported by Aronson, Brown, Litin, and Pearson (1968b). In some
cases, other studies were used to identify the primary vocal symptom. There will usually be
additional voice symptoms associated with each neurological problem. These will be discussed
for each disease in the section entitled “Perceptual Voice Signs and Symptoms.”

Classification of Neurological Voice Disorders Based on Phonatory Dysfunction

Ramig and Scherer (1992) have proposed an organizational scheme that focuses on the phona-
tory dysfunction affected by the disorder and emphasizes the general form of treatment for
it. In this way, the SLP is provided an overall framework within which to direct treatment.
There are three general categories of phonatory dysfunction that may be affected by neuro-
logical disorders. These are (1) adduction or abduction problems, (2) stability problems, and
(3) coordination problems (Ramig & Scherer, 1992; Smith & Ramig, 1995). The authors
recognize that a given neurological problem may affect one or more of the three areas. The
overall organizational framework is shown in Table 5.1.

Adduction or Abduction Problems

Hypoadduction
Myasthenia Gravis (MG)
Primary Voice Symptom: Breathiness
Description and Etiology “Myasthenia Gravis is a chronic autoimmune neuromuscu-
lar disease characterized by degrees of weakness of the skeletal (voluntary) muscles of the
body.” (NINDS Myasthenia Gravis Information Page, http://www.ninds.nih.gov/disorders/
myasthenia gravis/myasthenia gravis.htm) Patients with MG show a characteristic weakening
of the striated muscles and a prolonged return of function after activation. Muscles innervated
by cranial nerves seem most susceptible to this disease. The disease is relatively rare, with a
prevalence of 20 per 100,000 (Garfinkle & Kimmelman, 1982; Howard, 2008). It tends to
affect the sexes differentially in terms of incidence and age of onset. It occurs twice as often in
women and much earlier than in men. Onset for women is reported in the third decade of life,
whereas in men it is during the sixth decade (Garfinkle & Kimmelman, 1982).
Patients with MG tend to show bulbar symptoms, with the earliest and most common
being ptosis or drooping of the eyelids (Grob, 1961). Other symptoms include diplopia, weak-
ness of the legs, fatigue, dysphagia, dysphonia, and blurred vision. All patients will not exhibit
all symptoms. Furthermore, these symptoms are not unique to myasthenia gravis but are
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TABLE 5.1 Classification of neurological disorders of voice based on

phonatory dysfunction (Adapted from Smith and Ramig, 1995,
Table 14-2)
Classification Neurological disorder
I. Adduction or abduction problems
A. Hypoadduction Myasthenia gravis
Parkinsonism
Peripheral nerve paresis/paralysis
Shy–Drager
Supranuclear palsy
B. Hyperadduction Adductor spasmodic dysphonia
Huntington’s disease
Pseudobulbar palsy
C. Malabduction
II. Phonatory stability
A. Short-term (jitter and shimmer) Most neurological disorders
B. Long-term (tremor) Essential tremor
Parkinsonism
ALS
III. Phonatory incoordination/voiced–voiceless distinction abductor spasmodic dysphonia
IV. Mixed disorders
Cerebellar ataxia
Multiple sclerosis
V. Miscellaneous disorders
Tourette syndrome
Other miscellaneous disorders (see Table 5).

encountered in other disease states. The symptom of diplopia, for example, can be associated
with infection, glioma of the brainstem, multiple sclerosis, toxicity, aneurysms, tumors, and
trauma (Baker, 1958). Paralysis or muscle weakness can also be a sign of poliomyelitis or brain-
stem glioma in children. In adults, paralysis can be a sign of poliomyelitis, Guillain–Barré
syndrome, brainstem glioma, cerebellopontine angle tumor, cerebral artery occlusion, amy-
otrophic lateral sclerosis, and pseudobulbar palsy or tumor (Stuart, 1965; Tucker & Lavertu,
1992). Carpenter, McDonald, and Howard (1979) emphasized the need for differential diagno-
sis among myasthenia gravis, amyotrophic lateral sclerosis, and multiple sclerosis. The unique
features of MG are fatigability, fluctuation of function, and restoration of function after rest.
These features do not occur in amyotrophic lateral sclerosis or multiple sclerosis. The voice
symptoms of MG, because of their variability, have been mistaken for aphonia of psychological
origin (Ball & Lloyd, 1971).
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Some MG patients may present with voice or speech dysfunction as their initial symptom.
Wolski (1967) reported a case of myasthenia gravis in which nasality was the initial presenting
symptom. Colton and Brewer (1985) and Levine, Hatlali, and Zaggy (1985) each reported
cases diagnosed as MG that presented unusual fiberoptic laryngoscopic findings.
In MG, the body’s autoimmune system produces antibodies that block, alter, or destroy
receptors for acetylcholine. Several tests are used in the diagnosis of myasthenia gravis. A special
blood test detects immune molecules or acetylcholine receptor antibodies. Edrophonium chlo-
ride (Tensilon, Enlon, and Reversol) may be used to test for this disease. A positive response
to injection results in temporary improved muscle strength and tone. Slight to moderate im-
provements should be interpreted with caution because similar improvement has been noted in
patients with brain stem lesions, oculomotor palsy, diabetic abducens paresis, and even in some
normal individuals. Repetitive nerve stimulation may be also used to diagnose MG (Howard,
2008). The treatment of MG is primarily pharmacological with occasional necessity for excision
of the thymus gland.
Perceptual Voice Signs and Symptoms The primary symptom of MG is the general fatiga-
bility of muscle function in the head, neck, tongue, pharynx, and larynx. Voice signs include
hoarseness, breathy voice, and vocal weakness (Carpenter et al., 1979). In one study, 60% of
myasthenia gravis patients presented voice symptoms (Rontal, Rontal, Leuchter, & Rolnick,
1978). The following voice characteristics were reported in ratings of 11 patients with myas-
thenia gravis: hypernasality, nasal emission, inspiratory voice, dysphonia, intermittent aphonia,
and aspirate voice (Maxwell & Locke, 1969). Interestingly, these symptoms were completely
eliminated with pharmacological treatment.
A more recent study (Mao et al., 2001) of 40 patients reported that 65% of the group
exhibited hoarseness, 52.5% exhibited vocal fatigue, 30% difficulty with pitch variation, and
20% had a breathy voice; 5 or fewer patents had other symptoms.
Acoustic Signs Few studies have been reported about the acoustic characteristics of voice
in patients with myasthenia gravis. In a study of 11 women and 1 man with myasthenia gravis,
average fundamental frequency of speech was found to be very similar to normal expectations
in both medicated and unmedicated states (Maxwell & Locke, 1969).
Rontal et al. (1978) presented spectrographic evidence of aperiodicity and high-frequency
noise in the speech of patients with myasthenia gravis.
Walker (1997) described a case of a patient whose major acoustic characteristics of the
disease was a slow, steady reduction of fundamental frequency during a sustained vowel. He
referred to this characteristic as the “sinking pitch sign.”
Mao et al. (2001) reported lower-than-normal values of speaking fundamental frequency
compared to age- and sex-matched controls (154.3 Hz vs. 172 Hz). Maximum phonation time
was also reduced (16.8s vs. 27.4s). Shimmer, however, appeared to be within normal limits.
Measurable Physiological Signs Electromyographic studies have shown a characteristic
decrement of activity with repetitive stimulation (Warren, Gutmann, & Cody, 1977). We
have studied the airflow and electroglottogram characteristics of a patient with myasthenia
gravis. The data are shown in Figure 5.3. Note the extremely long opening phase of the air-
flow waveform cycles, with a rather slow (but faster than the opening phase) closing phase.
The electroglottogram waveform seems to mirror these slow opening and closing phases of the
vocal folds. The airflow/slope ratio (ratio of the closing slope to the opening slope) and the
electroglottogram closing time were significantly greater than for normal individuals.
Mao et al. (2001) reported a significantly greater mean airflow rate for their sample of
40 patients (294.5 mL/s vs. 111.5 mL/s for normal control group).
Observable Physiological Signs The characteristic sign seen in laryngoscopic evaluations is
sluggishness of vocal fold abduction. Continued phonation by a patient with myasthenia gravis
over a period of time may show increasing weakness of arytenoid and vocal fold motion. Normal
movement will return, however, with sufficient rest.
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 121

FIGURE 5.3. Inverse filtered airflow and electroglot-

togram (EGG) waveforms for a 65-year-old woman with
myasthenia gravis. Note the extremely long opening
phase of the vocal folds and the slow closing phase.
The electroglottogram waveform mirrors these slow vari-
ations of vibration. Lung pressure was within normal
limits.

There is one report of the stroboscopic signs associated with myasthenia gravis (Maeo et al.,
2001) where 92.5% of the patents exhibited what is termed mobility deficits either unilateral
or bilateral. These deficits included mucosal wave decrements and asymmetries in phase closure
and amplitude.
Pathophysiology Muscle weakness will be expected to affect the patient’s ability to raise
the vocal pitch and produce loud voice. However, these changes may occur only when the
mechanism has fatigued following phonation over a period of time. The inability to maintain
the proper tension in the vocal folds will result in increased aperiodicity and the inability to
maintain good glottal closure. These conditions will produce roughness or hoarseness and
breathiness in the voice. Drugs can help relieve some of the symptoms of myasthenia gravis.
Neostigmine bromide (Prostigmin Bromide) and pyridostigmine bromide (Mestinon, Regonol)
are often prescribed. Immunosuppressive drugs are often used. In some cases a thymectomy is
performed. Plasma pheresis may also bring improvement (Sanders & Scopetta, 1994).

Parkinsonism
Primary Voice Symptoms: Monopitch and Reduced Loudness
Description and Etiology Parkinson’s disease (PD) is a progressive, degenerative disease of
the central nervous system affecting the basal ganglia, specifically the substantia nigra resulting
in depletion of dopamine. There is also a decrease of dopamine in the caudate nucleus and
the putamen. The disease results in rigidity, resting tremor, and reduced range of movement
in the limbs, neck, and head. The general characteristic of PD is a slowness of movement
and loss of automatic movements, referred to as bradykinesia (Brin et al., 1992). Bradykinesia
also encompasses the masked facies or absence of facial expression, decreased dye blinking,
decreased spontaneous swallowing, and difficulty in initiating movement on command that
are features of PD. The amplitude of voluntary movement and impaired postural and righting
reflexes are impaired (Hoehn & Yahr, 1967). All movements may be affected. It is important
to realize that the muscles are not paralyzed but rather are hypokinetic and lack the dynamic
aspects of movement. Respiratory movements are also affected, producing a shallow and ir-
regular respiratory cycle sometimes at twice the normal frequency (Ramig & Gould, 1986).
Patients may have a limited vital capacity and inspiratory capacity. These respiratory deficits
may contribute to the patient’s ability to produce speech of normal loudness and utterance
length. Laryngeal muscle involvement also contributes to the difficulty in initiating phonation,
producing adequate loudness, and varying pitch.
Although the etiology of any particular case of PD is usually unknown, there are sev-
eral causes that have been hypothesized or been directly linked to the disease. Some cases
of PD have been traced to a disease called encephalitis lethargica that occurred in small
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TABLE 5.2 Stages of degree of severity for patients with Parkinson’s disease
(after Hoehn & Yahr, 1967)
Stage Description
I Unilateral involvement only
II Bilateral or midline involvement
III Impaired righting reflexes (unsteadiness in turning or sudden change from a standing
position)
IV Severely disabling disease; patient can walk or stand but is otherwise incapacitated
V Patient confined to bed or wheelchair

epidemics in the 1920s. The last reported cases of this disease were in the 1940s (Duvoisin,
1976). With the recognition of postencephalitic parkinsonism, the concept of multiple eti-
ologies for the disease became understood. Other possible etiologies include an undetermined
slow-growing virus, head trauma, toxic buildup, drugs, vascular trauma, or carbon monoxide
poisoning (Darley, Aronson, & Brown, 1975). Iatrogenic PD is caused by antipsychotic phe-
nothiazine drugs. It is usually reversible by withdrawal of the drug or sometimes by reduction in
dosage.
Patients with Parkinson’s disease may be classified into several distinct groups. The first,
often referred to as idiopathic Parkinson’s disease (IPD), displays the classic symptoms of
this disease. Parkinson Plus Syndrome (PPS) involves multiple symptom atrophy. One of
these syndromes is called Shy–Drager and will be discussed separately. The speech and voice
deficits in PPS are usually more severe, and they deteriorate faster than in patients with IPD.
Other possible groups include postencephalic parkinsonism, Iatrogenic parkinsonism, juvenile
parkinsonism, and secondary or symptomatic parkinsonism (Duvoisin, 1976).
Parkinson’s patients can be staged according to the severity of the symptoms as discussed
by Hoehn and Yahr (1967). The scale used is arbitrary but is based on the level of clinical
disability observed. The stages and their definition are displayed in Table 5.2. According to the
data presented by Hoehn and Yahr, there is a tendency for staging to be correlated with the
duration of the illness (r = 0.97). Other rating systems have also been proposed to assess the
physical status and limitations and daily living problems that might be encountered (Martı́nez-
Martı́n & Bermejo-Pareja, 1988). Speech and voice disorders are present in 75% of persons
with PD, and virtually 100% will develop problems in these areas as the disease progresses into
the more debilitating stages (Oxtoby, 1982; Streifler & Hofman, 1984).
Perceptual Voice Signs and Symptoms The most frequently rated voice dimensions, as re-
ported by Aronson et al. (1968b; Fig. 5.4), were monopitch, excessively low pitch, and harshness.
According to Aronson et al. (1968b), variability of loudness is reduced, but rate of speech is
highly variable, sometimes with fast bursts and at other times a slow rate. The reduced vari-
ability of vocal loudness, pitch, and rate are thought to be the consequence of muscle rigidity
and hypokinesia. Speech production is also affected by slurring and phoneme misarticulations,
again associated directly with the physical symptoms described.
In a study of 200 patients with Parkinson’s disease, Logemann, Fisher, Boches, and Blonsky
(1978) found that 87% showed some laryngeal dysfunction and that 45% had laryngeal dys-
function as the only symptom. The specific voice signs these authors reported were breathiness
(15%), roughness (29%), hoarseness (45%), and tremulousness (13.5%). Ramig (1995) reports
that reduced vocal loudness is a classic speech symptom along with those noted previously. This
vocal loudness reduction may be one of the first signs of PD (Aronson, 1985).
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 123

FIGURE 5.4. Percentage of 32 patients with Parkinson’s disease showing deviant voice signs. Voice
tremor was rated during contextual speech.

Acoustic Signs Numerous acoustic characteristics of the voices of individuals with PD have
been studied with mixed results (Aronson et al., 1968a; Canter, 1963, 1965; Kent et al., 1994;
King et al., 1994; Logemann et al., 1978; Ludlow et al., 1983; Ramig et al., 1988, 1990;
Zwirner et al., 1991). The conflicting results of many of these studies probably had to do
with the nature of the participant pool, differences in methodology, and analysis procedures
(Table 5.3).
Available acoustic data suggest that in patients with Parkinson’s disease, the mean funda-
mental frequency is similar to normal speakers, but the variability of fundamental frequency
within a speech segment is increased, probably reflecting loss of control of the motor act. Jitter
and shimmer are also increased, whereas signal-to-noise ratio is slightly decreased.
Measurable Physiological Signs
Aerodynamic Jiang et al. (1999) reported some aerodynamic measurements made on
24 patients with stage 4 severity of Parkinson disease and 17 normal speakers of equivalent age.
Mean subglottal air pressures were significantly higher in the Parkinson group compared to the
normal control group. Airflow rates were not significantly different between the two groups.
Laryngeal resistance was also significantly higher in the parkinsonism group.
Lin, Jiang, Hone, and Hanson (1998) found that the Parkinson group (n = 15) had
significantly greater speed quotients (SQ) than their control group (n = 15) as obtained from
photoglottographic recordings. They observed that the opening time of the vocal folds was
longer in the patient group, which they interpreted to reflect increased rigidity of laryngeal
muscles. It would appear that speed quotient may be a good measurement to make in patients
suspected of Parkinson’s disease.
Patients with PD appear to produce higher resting and background activity in the interary-
tenoid and posterior cricoarytenoid muscles (Guidi, Bannister, & Gibson, 1981). Lip muscles
also show greater resting and background activity levels, and the degree of activity seems to
be related to the side of the body most affected by the disease (Leanderson, Meyerson, &
Persson, 1972). Luschei et al. (1999) reported significantly lower firing rates of the thyroary-
tenoid muscle in their Parkinson groups compared to a young control group. However, the
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TABLE 5.3 Some acoustic characteristics of patients with Parkinson’s

disease
Ludlow et al., Ramig et al., Zwirner et al., Kent et al.,
Measure 1983 1989 1991 1994
Average fundamental 163.9 128 120 140.7
frequency (Hz)
SD FF 34.5 16 21 22
N 7a 8 12 22
Jitter (%)
Average 1.26
SD 1.05
Jitter (ms)
Mean 0.1 0.17
SD 0.17
Jitter ratio
Mean 7.21
SD 2.97
Shimmer
Mean 5.18 6 5.42
SD 3.43 6.6 3.2
Signal-to-noise ratios
Mean 14.75 17.5 18.85
SD 2.97 4.5 4.64
a Includes four men and three women.

firing rates were not much different for their elderly male group suggesting that any change of
firing rate of this muscle may be more due to aging than to the effects of the disease.
Observable Physiological Signs
Laryngoscopy Cisler (1927) reported diminished vocal fold movement, and Schilling
(1925) described a rigor of the vocal folds. Darley et al. (1969b) reported no abnormal laryn-
goscopic signs.
The most extensive description of laryngoscopic signs in PD patients was reported by
Hanson, Gerratt, and Ward (1984). They studied 32 patients, of whom 30 had abnormal
laryngoscopic signs. The most prominent sign was bowed vocal folds, and the vocal folds ap-
peared to vibrate with greater amplitude. In 26 patients, varying degrees of laryngeal asymmetry
were observed. Many patients showed a characteristic pattern consisting of a more posterior
position of the vocal process, a more posterior and lateral position of the apex of the arytenoid,
and a more contracted ventricular fold than seen in normal speakers. These signs were associ-
ated with the side of the body affected by the disease. Many patients also showed overclosure
of the vocal folds, and 5 of the 32 exhibited an extreme degree of supraglottal constriction.
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FIGURE 5.5. Glottal closure patterns of patients with Parkinson’s disease as rated from
stroboscopic video images. Open bars show data collected from flexible scope recordings,
whereas filled bars show data collected from rigid scope recordings.

Stroboscopy There have been two reports on the stroboscopic signs of Parkinson’s dis-
ease (Perez, Ramig, Smith, & Dromey, 1994; Smith, Ramig, Dromey, Perez, & Samandari,
1994). Smith et al. (1994) studied 22 patients with the idiopathic form of Parkinson’s disease
(IPD). Both flexible and rigid endoscopes were used to view and record the laryngeal images
as the patients produced a sustained /ee/. The images were visually rated by four experienced
raters on glottal closure configuration, degree of glottal incompetence, and laryngeal hyper-
function. The results of the glottal closure configuration ratings are shown in Figure 5.5. The
severity of glottal incompetence was in the mild range. As a group, the patients showed mild
false fold and anterior-posterior approximation. Interestingly, although Hanson et al. (1984)
found that the overwhelming majority of their patients had a bowed vocal fold configuration,
Smith et al. reported that about 50% of their patients exhibited such a pattern. The exact
percentage depended on the type of scope used to make the recording, that is, flexible or
rigid.
Perez et al. (1994) rated tremor, phase closure, symmetry, amplitude of vocal fold lateral
excursion, and excursion of the mucosal wave in 22 patients with IPD. A majority of the patients
(53%) exhibited tremor on at least one of the three experimental conditions. The incidence of
tremor in each experimental condition is shown in Figure 5.6.
The incidence of abnormal strobe findings is shown in Figure 5.7. Many patients showed
abnormal phase closure and phase symmetry, probably due to the hypotonic characteristics of
Parkinson’s patients.
In spite of tremor, the stroboscopic signs of patients with Parkinson’s disease can be rated
successfully. These patients may show a variety of closure configurations, including bowing,
anterior chinks, posterior chinks, and incomplete. Some may show a normal closure pattern.
The severity of closure probably depends on the degree of severity of the disease, but, in the
early stages, one might expect mild symptoms, symptoms that might be correlated with the
weak-intensity voice often heard in these patients.
Pathophysiology Muscle rigidity and squeezing of structures within the larynx may produce
a symptom of strain/struggle in the voice. Unequal tensions in the vocal folds, as noted by
Hanson et al. (1984), would be expected to produce aperiodicity, resulting in hoarseness or
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FIGURE 5.6. Incidence of tremor in structures of the larynx at rest and during phonation
at conditions of normal loudness and normal pitch (NPNL) and loud voice among 22 patients
with Parkinson’s disease.

roughness in the voice. In more advanced stages of the disease process, patients often have
much difficulty with chewing and swallowing. Management of saliva and drooling also are
problematic. The typical characteristics of PD are mirrored in speech and voice production.
Difficulty in initiating movement is seen in initiating speech attempts as it is in initiating
walking. Muscle rigidity and hypokinesia are seen in the reduced range of motion of the
speech mechanism, which results in reduced loudness (rigidity of respiratory and laryngeal
muscles), monotone (rigidity of laryngeal muscles), and imprecise articulation (rigidity of all
oral articulators). Tremor may be heard in the voice as well as seen in the extremities.

FIGURE 5.7. Percentage of 22 patients with Parkinson’s disease showing abnormal strobe
signs during phonation at normal loudness and normal pitch.
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Shy–Drager Syndrome
Primary Voice Symptom: Hoarseness
Description and Etiology Shy–Drager syndrome is a variant of Parkinson’s disease, some-
times referred to as Parkinson’s Plus. It is a disease of later middle age and affects men more often
than women. The major characteristic of Shy–Drager is generalized autonomic nervous system
failure. It is considered one of the degenerative neurological disorders that is characterized by
multiple system atrophy, not all of which include autonomic nervous system dysfunction. The
initial symptoms are postural hypotension (decrease of blood pressure when the patient stands),
impotence, and sphincter problems. In their study of 12 patients with Shy–Drager syndrome,
Hanson, Ludlow, and Bassich (1983) reported symptoms of weakness of the accessory muscles
of respiration, respiratory obstruction, limited movement of the soft palate, and dysphagia.
They suggest that these symptoms are indicative of extrapyramidal, pyramidal, and bulbar
involvement.
Shy–Drager syndrome was first described in two cases by Shy and Drager (1960). In one
case, they were able to examine the brain after the patient’s death and reported changes in the
spinal cord, autonomic ganglia, and medulla (i.e., marked changes in the inferior olives) and a
reduced number of Purkinje cells in the cerebellum as well as extensive changes in the substantia
nigra and the caudate nucleus of the basal ganglia.
Williams, Hanson, and Calne (1979) reported on 12 cases of Shy–Drager syndrome in
which 8 had moderate to severe bilateral abductor paresis or paralysis of the vocal folds. Two
patients, upon initial examination, showed a unilateral paresis, but these patients eventually
developed bilateral paralysis as the disease progressed. They concluded that the combination
of vocal fold paralysis and respiratory difficulties in some of their patients may be consistent
with a lesion in the nucleus ambiguus and the retrofacial nucleus. Denervation of the posterior
cricoarytenoid muscle, the muscle primarily responsible for vocal fold abduction, has been
reported in Shy–Drager patients who had bilateral abductor vocal fold paralysis (Guidi et al.,
1981).
Linebaugh (1979) reviewed 35 patients with Shy–Drager syndrome who presented with a
dysarthria. He identified three major types of dysarthria: ataxic, hypokinetic, and mixed. A total
of 15 of the 35 presented with ataxic dysarthria, which involves the cerebellum and affects the
accuracy, force, range, and timing of speech movements; 11 exhibited a hypokinetic dysarthria
in which the extrapyramidal system was affected, resulting in muscular rigidity; and 9 showed
a mixed dysarthria involving combinations of the extrapyramidal, cerebellar, and pyramidal
systems. Linebaugh presented examples of patients with these various types and commented
on how careful listening can help to distinguish among them.1
Perceptual Voice Signs and Symptoms The most complete description and study of the
speech signs and symptoms of Shy–Drager syndrome was presented by Hanson et al. (1983).
They rated the speech of 12 Shy–Drager syndrome patients, using scales reported previously
by Darley et al. (1969a). Shy–Drager syndrome patients were rated most severe on scales of
rate of speaking (variable rate and rate 1). The mean ratings on 5 voice scales are shown in
Figure 5.8. The format of this figure is different from that of Figures 5.4 and 5.5. Hanson et
al. (1983) did not report the proportion of patients with aberrant ratings on the scales used,
probably because of the small number of patients. Rather, the mean ratings were reported using
a 7-point scale on which 1 means normal and 7 means very severe. Other speech scales on
which these patients were rated as severe included intensity (this scale may relate to the over-
all level of voice), imprecise consonants, reduced stress, monopitch, and monoloudness. These
authors performed a discriminant analysis of these ratings to determine whether they could sep-
arate groups of Shy–Drager syndrome patients from idiopathic Parkinson patients who exhibit
some of the same symptoms and from a group of normal participants. Three scales did a very
good job of distinguishing among these groups, that is, strain/struggle, glottal fry (a low pitch,
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FIGURE 5.8. Rated severity of voice signs in seven patients with Shy–Drager
syndrome.

popping sound), and monopitch. Shy–Drager patients were rated higher on impaired function
on the scales of strain/struggle and glottal fry than the PD patients but lower (less impaired) on
monopitch. Perceptual speech scales may be useful in distinguishing the Shy–Drager syndrome
from IPD and normal speakers.
Acoustic Signs Various indices of perturbation were reported by Ludlow and her colleagues
(1983) for a group of seven patients with Shy–Drager, four men and three women. Mea-
surements included perturbation (in msec), DLT (perturbation after removal of fundamental
frequency due to linear trend), a diplophonia ratio, fundamental frequency, and duration of
phonation. As a group, the Shy–Drager patients had a mean f0 of 160.3 Hz compared to a
f0 of 127.6 Hz for age- and sex-matched controls; the difference was statistically significant
suggesting perhaps greater vocal fold tension and/or muscle rigidity.2 There were no statis-
tically significant differences between the Shy–Drager and normal controls on any measure
of frequency perturbation. The data provided some evidence of diplophonia, at least for two
of the participants. Although not statistically significant, the patients’ diplophonia ratio was
somewhat higher (1.418) than the normal controls’ (1.046).
Measurable Physiological Signs In a study of activity in the laryngeal muscles, Guidi et al.
(1981) reported that all five of their Shy–Drager patients showed denervation of the posterior
cricoarytenoid muscle, and two of the five showed fibrillation potentials in the interarytenoid
muscle. Histological studies have shown marked atrophy of the posterior cricoarytenoid muscle
(Bannister, Gibson, Michaels, & Oppenheimer, 1981). Interestingly, there was little evidence
of cell losses in the nucleus ambiguus, suggesting a possible biochemical abnormality (Ludlow,
Coulter, & Gentges, 1983). These electromyographic characteristics were very different from
the muscle activity recorded in patients with IPD.
Observable Physiological Signs The primary laryngoscopic sign seen in Shy–Drager syn-
drome is bilateral abductor vocal fold paresis. Hanson et al. (1983) reported that 11 of their
12 patients presented moderate to severe abductor paresis (also reported by Williams, Hanson,
& Calne, 1979). Longridge (1987) reported a case of Shy–Drager with bilateral vocal fold
paralysis but did not specify whether it was of the adductor or abductor type.
We know of no studies in which the stroboscopic signs of patients with Shy–Drager
syndrome have been reported.
Pathophysiology Shy–Drager syndrome is a disease involving the pyramidal, extrapyrami-
dal, and cerebellar systems. It may also involve atrophy of neurons in the brainstem and part of
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the spinal cord (Bannister & Oppenheimer, 1972). It affects the control and coordination of
speech and voice. Lesions that affect the upper-motor neurons will result in the loss of muscle
coordination. Lesions in the cerebellum will also affect muscle coordination, whereas lesions
in the medulla and brainstem will affect the motor nuclei of the muscles serving the larynx,
producing problems of muscle tone and function. Interestingly, the disease affects the neurons
that control abductory function and not adductory function. The hyperadduction that results
in strain/struggle in speech is produced by lesions higher in the brain. In many respects the
disease is similar to IPD, but with its own unique features. The outlook for patients with Shy–
Drager syndrome is bleak, with few surviving more than 5 or 10 years (Thomas & Schirger,
1970). The course of the disease is a steady increase in neuromuscular impairment that will
eventually affect the respiratory muscles and compromise respiratory function.

Lesions of the Peripheral Nerves

Primary Voice Symptom: Breathiness
Description and Etiology Lesions that affect the vagus nerve somewhere along its course
from the base of the skull to the larynx will result in a paresis (weakness) or paralysis of muscles
in the larynx. These peripheral lesions of the vagus are the most common cause of vocal fold
paralysis. The intrinsic laryngeal muscles affected will depend on the exact location of the lesion.
Recall that a branch of the superior laryngeal nerve (SLN) of the vagus controls the cricothyroid
muscles, whereas the recurrent laryngeal nerve (RLN) controls the remaining muscles of the
larynx. The SLN branches off from the vagus high in the neck. The RLN branches off somewhat
below the SLN. A paralysis of all the muscles suggests that the lesion is high in the neck or in
the brainstem itself. Lesions affecting only the RLN will be much lower in the neck or as far
down as the thorax.
Lesions of the SLN or RLN may affect the position of the vocal folds. In RLN paralysis, the
lesion may be unilateral or bilateral and may be of the adductor or abductor type, depending
on the muscles affected. In the instance of a unilateral adductor paralysis, the affected vocal
fold will not be actively moved toward the midline when phonation commences. When the
glottis cannot be completely closed, the voice produced will be weak and breathy. In bilateral
adductor paralysis, neither vocal fold will be capable of moving to the midline, thus making
phonation impossible. Furthermore, the ability to swallow will be severely compromised with
aspiration being a life-threatening sequelae. The position of the paralyzed vocal folds, that is,
how far apart they are, will depend partly on whether or not the SLN is affected. The SLN
innervates the cricothyroid muscle, which when contracted tends to contribute to adduction of
the vocal folds, in addition to tensing them to create a rise of vocal pitch. Some of the symptoms
associated with SLN paralysis are vocal fatigue, hoarseness, and loss of vocal range (Dursun et
al., 1996) Paralysis of this muscle in addition to muscles controlled by the RLN will further
reduce the adductory forces of the vocal folds, thereby increasing their distance from each other
over what it might be with an RLN lesion alone. Other factors, such as degree of fibrosis of the
affected fold, tension of the conus elasticus, and freedom of joint movement may also affect
the final position of the vocal folds after paralysis of the RLN or SLN (Ballenger, 1985).
Lesions may also affect the abductory function of the vocal folds, which opens the airway
for inspiration. Such lesions affect the recurrent laryngeal nerve and specifically the posterior
cricoarytenoid muscle, which may produce unilateral or bilateral abductory paralysis. Bilateral
abductor paralysis in which the vocal folds remain in an adducted posture causes serious
respiratory problems (dyspnea), for which most patients will require a tracheotomy or excision
of some portion of one or both vocal folds, thereby sacrificing phonation.
Unilateral vocal fold paralysis is much more common than bilateral paralysis. Benninger,
Gillen, and Altman (1998) reported that 79.8% of their cases were unilateral whereas the
remainder were bilateral. In their cases of unilateral paralysis, the left vocal fold was involved
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TABLE 5.4 Miscellaneous medulla syndromes affecting the vocal folds

Name Effect Etiology
Wallenberg’s Paralysis of half of larynx, pharynx, Infarction of posterior inferior
palate, loss of sensation to the face, cerebellar artery
vestibular dysfunction, ataxia,
Horner’s syndrome
Babinski–Nageotte Similar to Wallenberg’s, including Similar to Wallenberg’s, plus
paralysis of tongue, loss of position, involvement of medial bulbar area
and vibratory sense
Cestan–Chenais Similar to Babinski–Nageotte, except Infarction of vertebral artery below
little or no involvement proximal to the posterior inferior cerebellar
nucleus ambiguus artery
Avellis’ Causes laryngeal, pharyngeal, and Vascular or inflammatory lesion in
palatal paralysis with dysphonia and medulla; lesion in nucleus
dysphagia ambiguus of vagus, plus cranial
part of spinal accessory
Hughlings–Jackson Results in ipsilateral paralysis of the Intramedullary lesion or a lesion
soft palate, pharynx, larynx, tongue, high in the lateral pharyngeal
and sternocleidomastoid muscles space; affects vagus, spinal
accessory, and hypoglossal nerves
Schmidt’s Ipsilateral paralysis of soft palate, Vascular lesion in caudal part of
pharynx, larynx, sternomastoid, and medulla
trapezius muscles
Mackenzie Unilateral paralysis of soft palate, Vascular lesion in medulla
pharynx, larynx, and tongue
Bonnier’s General weakness Lesion in Deiters’ nucleus or
associated vestibular tracts

much more than the right side (62.5% vs. 37.5%). The more extended and circuitous route
followed by the left recurrent laryngeal nerve is thought to be a factor in its vulnerability.
The etiology of vocal fold paralysis is varied and, as mentioned previously, can include
lesions in the brainstem itself. These high vagal lesions (from the nodose ganglion up) will affect
all laryngeal muscles, as well as muscles supplied by other cranial nerves. The lesions include
tumors at the base of the skull, carcinoma of the nasopharynx, or trauma. A listing of some of
the lesions in this area that could affect the larynx is shown in Table 5.4.
The possible etiologies of low vagal lesions are even more numerous. Neuritis is a frequent
cause and occurs with upper respiratory infection, infectious mononucleosis, sarcoidosis, and
infections of the parapharyngeal spaces (Ballenger, 1985). Neoplasms in the neck, bronchi, and
chest may invade and affect the nerve. Mechanical stretching or compression of the nerve may
also result in paralysis of the laryngeal musculature. Among the most common etiologies are
nonlaryngeal malignancies (primarily pulmonary), acute external trauma to the neck, surgery,
and idiopathic etiologies (Ballenger, 1985; Tucker, 1980). The percentages for etiologies for
both unilateral and bilateral paralysis as presented by Benninger et al. (1988) are shown in
Figure 5.9. Thus far the discussion has centered on acquired paralyses. However, it has been
reported that 10% of all congenital lesions are laryngeal paralysis (Gereau, LeBlanc, & Rubin,
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 131

A B

FIGURE 5.9. Etiology of vocal fold paralysis in adults. A. Unilateral paralysis. B. Bilateral paralysis.

1995). The diagnosis may not be made immediately as the symptoms are often nonspecific.
Indeed, most congenital unilateral paralyses recover spontaneously although the percentage is
smaller in bilateral paralyses (deGaudemar, Roudaire, Francois, & Marcy, 1996). Congenital
bilateral paralysis occurs more frequently than unilateral and is usually secondary to central
nervous system problems or other congenital abnormalities (Gereau et al., 1995) Daya et al.
(2000) reported on their analysis of 102 cases of children with vocal fold paralysis. The group
was divided about equally between unilateral and bilateral paralysis. Presenting symptoms of
paralysis in children include stridor, abnormal cry, feeding difficulty, and cyanosis (Fig. 5.10).

FIGURE 5.10. Etiology and symptoms of peripheral nerve paralysis in a study of

children (N = 53) with unilateral paralysis and 49 with bilateral paralysis.
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Iatrogenic etiologies were found more often in the unilateral paralysis group, whereas idiopathic
etiologies were found more often in the bilateral group (see Fig. 5.10).
Some of the causes of SLN paralysis are neuritis, trauma, and iatrogenic. Dursun et al.
(1996) reported that 93.6% of their cases with SLN paralysis were causes by a viral infection
prior to the onset of the paralysis.
Perceptual Voice Signs and Symptoms The most common perceptual symptoms of acquired
unilateral paralysis are breathiness and hoarseness. Occasionally diplophonia may be present.
Bilateral paralysis of the adductor type will cause severe breathiness or aphonia, but near-normal
voice may be present in the abductor type. An additional perceptual sign of bilateral abductor
paralysis is inspiratory stridor that results from the passage of ingressive air over approximated
vocal folds that are incapable of opening. The most common perceptual sign of congenital
unilateral paralysis is a weak cry. In bilateral paralysis, stridor may be present in addition to
weak cry. Vocal fatigue, hoarseness, and loss of vocal range are the most common symptoms of
SLN paralysis (Dursun et al., 1996).
Acoustic Signs We know of no data on acoustic signs in congenital paralysis, or in either
abductor or adductor bilateral paralysis. Thus, the following comments apply only to acquired
unilateral adductor vocal fold paralyses. We would theorize that the aphonia or severe aperi-
odicity of voice in the presence of bilateral adductor paralysis would make acoustic analysis
invalid.
Acoustically, increased aperiodicity (jitter and shimmer), a reduced pitch range, reduced
variability of pitch, higher noise levels, and a reduced vocal intensity range are found. Murry
(1978) reported the fundamental frequency characteristics of 20 patients with unilateral paral-
ysis of the vocal folds as they read a standard reading passage. The patient group had a mean
fundamental frequency of 127 Hz, whereas a group of 20 normal speakers had a mean funda-
mental frequency of 121.9 Hz. This difference was not statistically significant. The variability
of fundamental frequency (pitch sigma) between the two groups of participants was also not
significant.
Davis (1981) reported pitch perturbation quotient (PPQ), or jitter, and amplitude pertur-
bation quotient (APQ), or shimmer, values for two patients with unilateral paralysis of the vocal
folds. The average PPQ was 9.165% for the patients versus 0.42% for a group of 10 normal
speakers. The APQ was 12.96% for the patient group and 6.14% for the 10 normal speakers.
It is difficult to generalize about these findings based on only two participants, but they appear
to be in the direction hypothesized. That is, patients with unilateral paralysis will show greater
frequency and amplitude perturbation than can speakers with normally functioning vocal folds.
We have found that persons with a unilateral vocal fold paralysis exhibit greater-than-
normal jitter, shimmer, and signal-to-noise ratios (S/N). Our sample consisted of 22 women
and 23 men who had been referred to our clinic. As part of our routine clinical examination,
we record the patients as they produce the sustained vowels /ah/ and /oo/, two sentences, and
a reading passage. Jitter, shimmer, and S/N ratios are computed only on the sustained vowels.
Men and women produced greater than normal jitter, shimmer, and S/N ratios with men
producing values much greater than women did. The results show that patients with unilateral
vocal fold paralysis produce greater aperiodicity and greater noise levels than normal speakers.
Kim, Kakita, and Hirano (1982) carried out spectrographic analysis of some acoustic
characteristics of the voices of 10 persons with unilateral RLN paralysis. They were unable
to obtain accurate measures of fundamental frequency, probably due to the large amount of
aperiodicity in the voice. The only difference between the patient and the normal group on
amplitude variation and extent (a rough analog of shimmer) occurred between men. Other
differences measured in these spectrograms included higher harmonic energy in the patient
group as well as greater noise energy. These latter features may correlate with the greater
breathiness and noise levels that are present in many patients with unilateral recurrent nerve
paralysis.
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 133

FIGURE 5.11. Open quotient measurements of four forms of unilateral vocal fold paralysis
compared to a group of normal control participants.

Measurable Physiological Signs There have been several investigations concerned with the
measurement of average airflow during the speech of patients with acquired unilateral vocal
fold paralysis. Hirano (1981a) summarized several of these studies, noting that the mean flow
rates in paralysis are much higher than normal, although they range from a low of 35 ml/sec
to a high of 1150 ml/sec (Hirano, 1981a, Table 3.3, p. 30). Normal-speaking men produce
rates of about 110 ml/sec, and women of the same category produce about 94 ml/sec (Koike &
Hirano, 1968). Yanagihara and von Leden (1967) reported a mean flow rate of 442.2 ml/sec
for their 10 patients with unilateral paralysis, whereas Iwata et al. reported a mean flow of
353 ml/sec for their group of 19 unilateral paralysis patients. Hirano, Koike, and von Leden
(1968) reported a mean flow rate of 312.8 ml/sec for their 10 patients with bilateral paralysis.
Thus, it would appear that higher mean flow rates occur in unilateral paralysis than in bilateral
paralysis.
Based on their analysis of EGG waveforms of paralysis patients, Hanson, Gerrat, Karin,
and Berke (1988) were able to differentiate among four etiologies of unilateral vocal fold
paralysis. Vagal lesions produced an open quotient that was much smaller than the other
etiologies studied (Fig. 5.11). Measures of speed quotient showed greater variation among the
four etiologies studied (Fig. 5.12). Perhaps, measurements such as these and others yet to be
tried could be used to differentiate the type of etiology responsible for paralysis of a vocal fold.
We have recorded the inverse filtered airflow characteristics and electroglottograms of
several patients with unilateral paralysis. One patient is shown in Figure 5.13. Note the high
levels of offset flow (from baseline to lowest point on the airflow waveform), which were much
greater than for the normal participants. The airflow waveform is variable, perhaps indicative
of the greater aperiodicity of the vocal folds. This increased aperiodicity is also evident in the
electroglottographic trace shown below the airflow trace.
Kuroki (1969) studied the subglottal pressures produced by patients with unilateral and
bilateral recurrent nerve paralysis. Most patients with unilateral paralysis produced higher-than-
normal subglottal pressures (normal, about 6–8 cm/H2 O), and two bilateral paralysis patients
showed much-higher-than-normal subglottal pressures. This might be expected in view of the
air loss during phonation and the natural tendency for the speaker to attempt to compensate
for this loss with greater driving pressures below the vocal folds. On the other hand, patients
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FIGURE 5.12. Speed quotient measurements of different forms of unilateral vocal fold
paralysis compared to a group of normal control participants.

with vocal fold paralysis may produce greater pressures (therefore greater flows) because of their
inability to achieve glottal closure during the vibratory cycle.
Electromyography is a valuable tool for the evaluation of vocal fold immobility (Koufman
et al., 2000; Sataloff et al., 2000; Woo & Arandia, 1992). It is used to determine whether a
laryngeal muscle is truly paralyzed and may help to differentiate the causes of the paralysis
(Sataloff et al., 2000). The EMG interference pattern represents the sum of many motor units
and shows a typical triphasic pattern in normal muscle. Little to no electrical activity may be

FIGURE 5.13. Inverse filtered airflow and electroglottogram (EGG) waveforms

for patient K. B., a woman with a congenital unilateral vocal fold paralysis. Note
the large airflow offset, indicative of a large leak through the vocal folds. The
electroglottogram also exhibits unusual waveforms with marked change from
one cycle to the next. Due to technical problems, we were unable to record the
lung pressure used with this phonation.
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 135

TABLE 5.5 Miscellaneous peripheral syndromes resulting in laryngeal

paralysis
Name Effect Etiology
Collet–Sicard Last four cranial nerves Tumor, meningitis, or trauma to
posterior cranial fossa
Vernet’s Nerves 9, 10, 11; dysphagia and dystonia Lesion in jugular fossa
Villarets Like Vernet’s, including sympathetic Lesion in retroparotid or lateral
paralysis and Horner’s syndrome pharyngeal space
Tapia’s Ipsilateral paralysis of tongue and Neoplasm where hypoglossal
neoplasm where hypoglossal larynx crosses vagus and internal carotid
Gard– Paralysis of vocal folds, weakness of 11th and vagus below nodose
Gignoux trapezius and sternomastoid muscles ganglion
Klinkert Paralysis of recurrent and phrenic nerves Lesion in root of neck or
mediastinum

seen in paralyzed muscles or activity that shows abnormal patterns, fibrillation, or decreases
recruitment of the motor fibers. In SLN paralysis, EMG will show decreases recruitment and
fibrillation potentials (Dursun et al., 1996)
Observable Physiological Signs
Laryngoscopy The typical laryngoscopic view in unilateral paralysis is that of one vocal
fold that does not fully adduct during phonation, while the unaffected fold moves to the midline.
There may be some apparent movement of the affected vocal fold caused by movements of other
structures or by contraction of the cricothyroid (assuming an intact SLN), which will tend to
exert some adductory force on the vocal folds (as described earlier), or perhaps the affected fold
is driven by air pressure. Movement in the pyriform sinus on the affected side may be reduced
or absent (Brewer & Gould, 1974) in patients with unilateral vocal fold paralysis. Differences
in the horizontal level of the two vocal folds have been reported by Isshiki and Ishikawa (1976).
About one-half of their 56 patients showed a higher level of the paralyzed vocal fold. Reasons
for this level difference may include (a) the position of the arytenoid on the paralyzed side,
(b) effects of the extrinsic muscles, and (c) the possibility of a paralyzed cricothyroid muscle that
would affect the tension that can be placed on the affected fold. It should be noted, however,
that others have failed to find a consistent level of difference (Adran, Demp, & Marland, 1954;
Ballantyne & Groves, 1978; Casper, Colton, & Brewer, 1985; Lee, 1973).
Stroboscopy Hirano, Feder, and Bless (1983) discussed some of the stroboscopic signs
seen in patients with peripheral nerve paralysis. These signs will vary depending on the severity
of involvement and the type of problem, that is, superior or recurrent nerve involvement, or
both. A summary of the important signs they report for unilateral adductor paralysis is presented
in Table 5.5.
Kitzing (1985) reported that stroboscopic signs in vocal fold paresis include vocal fold
asymmetry and aperiodicity, greater-than-normal vibratory amplitudes, absence of a mucosal
wave, and incomplete glottal closure. These signs are consistent with the nature of the disease
and the perceptual, acoustic, physiological, and laryngoscopic signs discussed earlier.
We have observed many of these same signs (Table 5.6). The paralyzed fold vibrates
occasionally but not at the same rate or in the same way as the unaffected fold. There is an
anteroposterior (or the reverse) ripple-like motion on the affected side. We have observed a
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TABLE 5.6 Stroboscopic signs in laryngeal paralysis

Abnormal vibration with predominant vertical movements
Large irregular amplitudes
Poor vocal fold closure
Affected fold seems to flutter
Absence of edge deflections (upward on affected fold)

mucosal wave on the affected fold, although it is usually not as regular as the unaffected side.
Amplitude of vibration of the affected fold sometimes appears to be increased. Most often, the
paralyzed fold and the nonparalyzed fold produce an aperiodic motion. There are a variety of
glottal closure patterns observed, but most often, we have observed incomplete closure (22/39
patients).
The location of the pathology in vocal fold paralysis is in the muscle; that is, the thyroary-
tenoid muscle has little or no neural control (Hirano & Bless, 1993). There may be glottal
incompetence with a bowed fold sometimes seen. The stiffness of the cover and the transition
layers are normal. The stiffness of the body is decreased.
Sercarz and his colleagues (Sercarz, Berke, Ming, Gerratt, & Natividad, 1992) reported on
stroboscopic findings in 3 normal speakers whose recurrent and/or superior laryngeal nerves
were paralyzed with drugs and 20 patients with unilateral paralysis. Their most significant find-
ing was the asymmetry of traveling-wave motion in the paralyzed larynx. The normal fold has the
fastest traveling wave; the difference of wave velocity produced a phase asymmetry of vibration.
In SLN paralysis, Dursun et al. (1996) reported increases amplitude asymmetry, phase
asymmetry, incomplete glottal closure, decreased amplitude of vibration, and decreased mucosal
wave in most of their patients. They also reported a decrease in the ability of their patients to
produce a glissando pitch glide.
Pathophysiology A paralyzed vocal fold may affect adduction or abduction of the vocal
folds. Voice problems are most commonly associated with unilateral adductor paralysis. In
bilateral adductor paralysis, the patient may be aphonic, but the patient’s primary and potentially
life-threatening problem in need of urgent attention will be loss of protection of the airway and
the attendant risk of aspiration. The incidence of unilateral vocal fold paralysis is much greater
than that of bilateral paralysis.
One problem encountered in the diagnosis of vocal fold paralysis is whether or not there
is a true paralysis of the fold or whether the immobility of the vocal fold is due to fixation of
the arytenoid joint or a dislocated arytenoid (Rontal & Rontal, 1986). The diagnostician must
carefully explore these other possibilities either indirectly by observing other structures in the
larynx (e.g., the pyriform sinus) or by directly manipulating the arytenoid to test its mobility.
EMG evaluation of muscle electrical activity may also assist in making the correct diagnosis.
Most important of all is a complete and careful case history (Woo, Colton, Brewer, & Casper,
1991).
In unilateral paralysis, the affected fold cannot move to the midline and assist in closure of
the glottis. Because of this incomplete closure, greater-than-normal airflows and a weak voice
will be produced. The affected fold may also exhibit muscle tensions vastly different from the
unaffected cord, resulting in asymmetrical tension and increased aperiodicity in the voice. This
will be perceived as roughness or hoarseness. A difference in level between the two folds may
also contribute to the increased aperiodicity and excessive airflow, although its precise effect
remains unknown. If the superior laryngeal nerve is involved, additional problems with pitch
control may be noted.
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 137

An Unusual Case of Unilateral Vocal Fold Paralysis

R. C. is a 52-year-old man who awoke one morning with pain and pronounced weakness
in both arms, slightly more pronounced on the right with impaired manual dexterity in the
right hand that prevented simple acts such as eating, writing, and so on. After visiting his
general practitioner, he was referred to a neurologist who performed routine neurological tests
and conduction velocity tests on nerves in the right arm. The diagnosis was Guillain–Barré
syndrome (acute inflammatory demyelinating polyneuropathy), and R. C. was hospitalized
immediately. On the day after hospitalization, R. C. developed a breathy and hoarse voice
quality consistent with a unilateral vocal fold paralysis. Also, he developed mild dysphagia. A
flexible fiberoptic laryngeal examination was conducted 2 days later and revealed a left vocal
fold paralysis.
Guillain–Barré is a neuropathy (Dowling, Blumberg, & Cook, 1987) that affects some-
where between 0.6 to 2 individuals per 100,000 population. It is the body’s reaction to a virus
that the person may have had up to 8 weeks prior to the onset of symptoms. (R. C. reported
a mild upper respiratory infection about 2 months previous to onset and a very mild, 1-day
illness about 5 days previous to onset.) The affected individual’s immune system develops an-
tibodies in reaction to the virus that begin to attack the myelin sheaths of nerves, primarily
peripheral nerves. It is probably an autoimmune T cell–mediated disease (Taft, 1988). No
nerve is safe, including those that control respiration, the heart, and other vital functions. The
classic symptoms of Guillain–Barré begin with weakness in the legs and ascend to the trunk,
arms, head, and neck. However, other variants of the disease exist as evinced by R. C. How far
the demyelinating extends and what systems are affected is unpredictable. Until quite recently,
persons with this diagnosis were hospitalized so that the progression of the disease could be
monitored and appropriate life-saving intervention, such as respiratory assistance, could be
introduced as necessary.
R. C. was hospitalized not only to monitor the progress of the disease but also to start him
on a treatment program of plasmapheresis (Guillain–Barré Syndrome Study Group, 1985).
This treatment has been found to be an effective method of interrupting the course of the
disease in some patients. During the plasmapheresis treatments, each of which can take several
hours, blood is continuously extracted from the body; the white and red blood cells are separated
from the plasma; the plasma is discarded; and the red and white cells are mixed with human
albumen and pumped back into the patient. The theory is that the antibody causing the
problem attaches itself to a protein in the plasma. Removing the plasma removes the offending
antibody. R. C. remained in the hospital for 8 days and completed 4 plasmapheresis treatments.
He did not develop any additional symptoms; indeed, the dysphagia and the acute arm pain had
resolved. He still had arm weakness, vocal fold paralysis, and fatigue. He was then discharged to
recuperate at home for another 2 weeks. During this time, he received two additional pheresis
treatments as an outpatient. He returned to work about 22 days after the onset of the first
symptom. The vocal fold paralysis persisted for about 6 weeks after its onset. R. C. recovered
full use of his voice and at 3 months postonset had only mild soreness in his arms, especially
his right, secondary to remyelination. Twelve years postdiagnosis, R. C. is doing fine with very
few residual effects.
Vocal fold paralysis is a rare complication of Guillain–Barré syndrome. It appears to respond
to the treatment for the disease itself, that is, plasmapheresis. Early diagnosis and immediate
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treatment appear to be critical, and patients can often experience full recovery of function
with time. The presentation of vocal fold paralysis must be viewed as potentially one sign
of an underlying problem that may have life-threatening implications. A thorough history is
critical to alert the examiner to areas that need further exploration. It is essential to rule out the
presence of more diffuse disease; the presence of a neck, thoracic, or lung lesion, which might
be impinging on the nerve (RLN); the possibility of joint ankylosis or dislocation; and possible
psychogenicity.

Hyperadduction
Spasmodic Dysphonia
Primary Voice Symptom: Strain/Struggle
Description and Etiology
Spasmodic dysphonia, according to Ludlow (1995), is a “focal dystonia affecting laryngeal
muscle control during speech” (p. 436). It has received much attention over the past 25 years,
perhaps out of proportion to its incidence. It is a relatively rare voice disorder with an estimated
prevalence of 1 per 100,000 persons (Konkiewiewitz et al., 2002), although judging from the
many reports in the literature it appears that its numbers have increased. Perhaps this is due to
the availability of methods of providing some form of symptom relief or to increased awareness
of and knowledge about the disorder. Spasmodic dysphonia seems to occur somewhat more
often in women (60%–85%; Ludlow et al., 2008), with onset most frequently in middle age,
although we have seen patients as young as 20 years of age with a history of onset in the teens.
The nature of the onset of spasmodic dysphonia is variable. In some patients, onset is
associated with a major upper respiratory infection (Aronson et al., 1968b), in others a traumatic
emotional event is identified (Aronson, 1990; Brodnitz, 1976), and in still other patients the
onset is insidious, beginning as a mild hoarseness and progressing to interrupted, strained
phonation. The progression of symptoms may be rapid or may take place over a number of years.
In the past, the thinking about the etiology of spasmodic dysphonia had taken two major
forms (Aronson, 1990; Salamy & Sessions, 1980). Some authors advocated a psychologi-
cal origin (Arnold, 1959; Block, 1965; Brodnitz, 1976; Heaver, 1959; Henschen & Burton,
1978), whereas others have implicated a neurological origin (Aminoff, Dedo, & Izdebski, 1978;
Aronson et al., 1968a, 1968b; Blitzer & Brin, 1992; Rabuzzi & McCall, 1972; Robe, Brumlik,
& Moore, 1960; Shaefer, 1983). Current thinking considers spasmodic dysphonia as a form of
focal dystonias (Ludlow et al., 2008).
One rationale for the psychological etiology is that patients often report a traumatic
emotional event closely associated with the awareness of the onset of symptoms. Another reason
may be the difficulty in differentiating the symptoms and signs of spasmodic dysphonia from
those found in certain manifestations of psychogenic or muscle tension dysphonias. Advocates
of the psychological etiology theory point to some success in therapy (voice or psychiatric) or
to relief of symptoms with the use of tranquilizing or neuroleptic drugs (Brodnitz, 1976) as
positive evidence of the correctness of the theory. Advocates of a neurological etiology would
suggest that these patients had perhaps been incorrectly diagnosed.
Advocates of the neurological etiology of spasmodic dysphonia point to the sizable body
of evidence of associated neurological signs in these patients (Aronson et al., 1968b) and to
the documented existence of abnormal findings in various tests of brain function (Aminoff et
al., 1978; Dordain & Dordain, 1972; Finitzo-Hieber, Freeman, Gerling, Dobson, & Schaeffer,
1982; Robe et al., 1960; Shaefer, 1983). Many of these authors also point out that there has
been little actual documentation of symptom relief as a result of voice therapy or in response
to psychiatric treatment. Reports of successful treatment have been anecdotal (Cooper &
Cooper, 1977), and, moreover, the lack of success of these treatment protocols for patients with
spasmodic dysphonia has been extensively noted (Aronson, 1990).
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In the late 1970s the unilateral severing of the recurrent laryngeal nerve was introduced
by Dedo (1976), who reported lasting symptom relief in these patients. Others have also
reported results of this procedure (Dedo & Izdebski, 1981, 1983; Izdebski, Dedo, & Shipp,
1981). Reports of recurrence of symptoms of SD despite the permanence of the paralysis of
the severed side reduced the popularity of the procedure. Simultaneously, the use of BOTOX
(botulinum toxin) injection in the treatment of SD began to receive attention (Benninger,
Gardner, & Grywalski, 2001; Blitzer, Brin, Stewart, Aviv, & Fahn, 1992; Blitzer & Sulica,
2001; Boutsen et al., 2002; Brin, Blitzer, & Stewart, 1998; Courey et al., 2000; Ford, Bless, &
Patel, 1992; Inagi et al., 1996; Ludlow, 1990; Ludlow et al., 2008; Shaefer et al., 1992; Whurr,
Nye, & Lorch, 1998; Woo, Colton, Casper, & Brewer, 1992; Zwirner, Murry, Swenson, &
Woodson, 1991).
Most scientists and practitioners have come to accept that spasmodic dysphonia is a prob-
lem with a neurological substrate, one of the family of dystonias. The exact locus of the
dysfunction is not clear, although many point to the basal ganglia or associated structures as
the most likely location (Blitzer & Brin, 1992; Izdebski, 1992; Swenson, Zwirner, Murry, &
Woodson, 1992). The problem probably has many causes (Izdebski, 1992) and may be linked
to other neurological disorders (Swenson et al., 1992). Izdebski (1992) presented a model of
spasmodic dysphonia in which sudden or sustained increases of muscle activity occur, probably
in response to faulty processing of afferent information about various events within the larynx
such as the variation of air pressures during phonation. The symptoms are absent in vegeta-
tive tasks and in speech tasks that do not involve phonation. Thus, in a whisper, symptoms
are absent or minimal because there is no variation of air pressures or vocal fold movement.
Effective treatment should focus on reducing the afferent information to the central processing
unit (e.g., basal ganglia) or by reducing the motor response because of faulty input processing.
Section or crush of the recurrent laryngeal nerve would potentially remove sensory input as
well as motor control. Injection of BOTOX reduces the motor response to any faulty input.
The focal nature of spasmodic dysphonia (i.e., involvement of only a few muscles) suggests that
specific therapeutic techniques should be most effective in obtaining symptom relief. Perhaps,
this explains why the use of drugs systemically has been reported to have little lasting effect on
the amelioration of the symptoms in spasmodic dysphonia.
There are two forms of spasmodic dysphonia, adductor type that will be discussed in this
section and abductor type that will be discussed in its own section. It is also possible that
an individual may have a mixed form of the problem involving both adductor and abductor
musculature.
Another common name for spasmodic dysphonia is spastic dysphonia. Many believe that
the use of the term “spastic” is inappropriate. “Spastic” implies lesions in the corticobulbar or
corticospinal (pyramidal) systems. That does not seem to be the case in this disorder. Current
evidence suggests that the underlying disease state in spasmodic dysphonia affects structures in
the extrapyramidal system. Aronson et al. (1968b) suggested that the term “spasmodic” would
be more appropriate.
There are other voice problems whose signs and symptoms may cause a clinician to suspect
spasmodic dysphonia, and the problem becomes one of differential diagnosis. One common
problem that may be considered SD is muscle tension dysphonia (MTD). Ludlow et al. (2008)
discussed the speech examination findings in SD and MTD that would help in the correct
diagnosis of SD. (See section “Differentiating Spasmodic Dysphonia from Other Dysphonias”
later in this chapter for more information.)
Perceptual Voice Signs and Symptoms The most characteristic symptom (and sign) is the
struggle and strain to talk, in association with intermittent stoppages of voice (Aronson, 1990;
Aronson et al., 1968b; Brodnitz, 1976). Associated symptoms may include hoarseness, harsh-
ness, and tremor (Fig. 5.14). Other patients present with a creaking, choked, tense, or squeezed
voice with extreme tension noted in the entire speech production system. Perceptual signs
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140 Understanding Voice Problems

FIGURE 5.14. Percentage of 31 patients with spasmodic dysphonia showing voice devia-
tions. Voice tremor was rated during contextual speech.

include strain/struggle, sudden interruption of voicing, tension, loudness, and pitch variations,
pitch breaks, and stoppages of phonation. According to Ludlow (1995), voice stoppages occur
primarily in vowel productions.
Acoustic Signs There have been considerable data reported in the literature about the various
acoustic signs accompanying spasmodic dysphonia.
Fundamental Frequency Davis, Boone, Carroll, Davenzia, and Harrison (1988) re-
ported the average fundamental frequencies during a reading passage for 16 female and 7 male
patients with adductor spasmodic dysphonia and compared these data to those of a set of
control participants. The female patients had a mean fundamental frequency of 162 Hz com-
pared to a mean fundamental frequency of 175 Hz for the 17 female control participants. The
male patients had a mean fundamental frequency of 134 Hz compared to a mean fundamen-
tal frequency of 106 Hz for 7 male controls. These authors also reported that the spasmodic
dysphonia patients had a much greater variation of fundamental frequency during the passage
than the controls (21.89 semitones [ST] for women and 14.79 ST for men compared to 12.29
ST for normal women and 11.89 ST for normal men).
Fritzell, Feuer, Haglund, Knutsson, and Schiratski (1982) analyzed the distribution of
fundamental frequency in the voices of four patients (three men and one women) reading a
short passage. Mean fundamental frequency ranged from 111 to 238 Hz. The distribution of
fundamental frequency was bimodal, with a major peak centered above 200 Hz and a minor peak
centered around 150 Hz. These patients underwent section of the recurrent laryngeal nerve for
relief of symptoms (see Chapter 8). Postsurgically, the fundamental frequency distribution was
much lower (mean fundamental frequencies ranged from 125 to 171 Hz) and the distribution
was unimodal.
Long-Term Average Spectrum Izdebski (1984) measured the long-term average spec-
trum (LTAS, a spectrum computed over a sentence or paragraph) in 23 patients with adductor
spasmodic dysphonia. Figure 5.15 illustrates his results. The solid line shows the spectrum of
a female speaker before surgery (recurrent nerve section), and the dotted line shows the same
patient after surgery. Note the high levels of high-frequency energy in the speech before surgery,
but the dramatic decrease of high-frequency energy after surgery.
Fritzell et al. (1982) analyzed the LTAS in the voices of four patients reading a short passage.
They reported only a slight difference of spectral shape and levels after surgery. Because there
was no control group, it is not known whether the levels of energy at the higher frequencies were
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 141

FIGURE 5.15. Long-time average spectra

of a female patient with spasmodic dyspho-
nia before and after recurrent nerve section.

greater than normal. Informal comparisons of the data presented by Fritzell et al. (1982) to those
presented by Hammarberg, Fritzell, Gauffin, and Sundberg (1986) for normal speakers suggest
that the patient group exhibited greater-than-normal energy levels in the high frequencies.
Hartman, Abbs, and Vishwanat (1988) observed pronounced peaks between 4 and 7 Hz
in the spectrum of sustained /ah/s produced by 4 patients with adductor spasmodic dysphonia.
These peaks may be indicative of vocal tremor. The finding of low-frequency tremor in the
frequency spectrum of these patients is of interest. Wolfe and Bacon (1976), using spectro-
graphic analysis of a patient with adductor spasmodic dysphonia, showed a breakdown in the
harmonic structure of vowels, dark areas on the spectrogram (indicating greater loudness), and
sudden changes of gray levels on the spectrogram, indicating the irregular variation of voicing
present in adductor spasmodic dysphonia (Fig. 5.16).

FIGURE 5.16. Broadband spectrogram of a patient with abductor-type spasmodic dysphonia (left panel)
and adductor-type spasmodic dysphonia (right panel). The utterance was the word “colors.”
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142 Understanding Voice Problems

Measurable Physiological Signs Several studies have reported airflows and air pressures for
spasmodic dysphonia patients. Hirano, Koike, and von Leden (1968) reported flows within the
normal range for their eight spasmodic dysphonia patients, whereas other studies have reported
low (Casper et al., 1985; Davis et al., 1988; Farmakides & Boone, 1960; Hirano, 1974, 1981b;
Hollien, Dew, & Phillips, 1971; Javkin, Antonanzas-Barros, & Maddieson, 1987) to very
low flows (Briant, Blair, Cole, & Singer, 1983; Garrett & Healey, 1987; Hill, 1938; Hollien,
1975). In adductor spasmodic dysphonia, patients may exhibit strain during voicing, which
may produce small glottal apertures through which air can flow. Low flows would be expected in
this situation. We have shown very low average flow rates in patients with adductor spasmodic
dysphonia (72 ml/sec; Woo et al., 1992). Airflow rates increased after nerve section (232 ml/sec)
or BOTOX (138 ml/sec).
Shipp, Izdebski, Schutte, and Morrissey (1988) studied subglottal air pressure magnitudes
in two patients with adductor spasmodic dysphonia. They reported much higher pressures (13–
14 cm/H2 O) than normal (about 6 cm/H2 O). These very high pressures are consistent with
patients’ reports of the increased effort required to speak. The elevated pressures in combination
with the low flows suggest increased glottal resistance during voicing for patients with adductor
spasmodic dysphonia.
Observable Physiological Signs
Laryngoscopy Anatomically, the larynx appears essentially normal. However, during
phonation it is possible to observe the hyperadduction of the adductor type of spasmodic
dysphonia. Hartman and Aronson (1981) reported the appearance of bowed vocal folds in
2 of 17 patients with otherwise normal-looking vocal folds. Hartman et al. (1988) reported
the observations of quick adductory movements of the true vocal folds, the ventricular folds,
and much of the supraglottal structures in one patient; small, irregular movements of the true
vocal folds in another patient; and, in a third patient, periodic laryngospasms. In the study
reported by Davis et al. (1988), most patients had normal laryngoscopic exams, but interrup-
tion of voicing was reported to occur in seven patients due to action of the true vocal folds,
in two patients tremor seemed to cause the interruption, and in four other patients the ven-
tricular folds appeared to cause the voice stoppage. Blitzer and Brin (1992) advocate the use
of flexible fiberoptic laryngoscopy to study the hyperadduction characteristics of spasmodic
dysphonia.
Stroboscopy Few data have been reported on the vibratory characteristics of patients
with spasmodic dysphonia as seen via stroboscopy. Fritzell et al. (1982) report that stroboscopy
was carried out prior to recurrent nerve section, but no data were presented. Postsurgically,
two patients showed symmetrical vocal fold vibrations, indicating a return of function to the
muscle. Because patients with spasmodic dysphonia have difficulty in sustaining phonation,
stroboscopic visualization of the vocal folds might be unproductive.
Pathophysiology The pathophysiology of adductor spasmodic dysphonia is not well under-
stood. High levels of muscle activity are seen in the thyroarytenoid muscles of some, but not
all, patients with adductor spasmodic dysphonia. Muscle hypertonia or hypotonia for various
groups of speakers (i.e., adductor spasmodic dysphonia, abductor spasmodic dysphonia, and
normal speakers) has not been well studied or compared. The mechanism for spasmodic bursts
of increased activity in specific muscles is not clear.
The spasm activity of the vocal folds will have a pronounced effect on the production of
sound. Excessive adductory forces will require greater-than-normal pressures to force the vocal
folds apart during phonation. Greater air pressures will be associated with greater sound pressure
levels and a more rapid opening and closing phase of the vocal folds. Rapid closing phases are
associated with the production of greater energy in the higher frequencies and high-energy,
high-frequency spectra. The intermittent nature of the problem will produce wide variations
of spectrum and fundamental frequency unless some compensatory mechanism is used in the
attempt to maintain a steady, smooth flow of speech.
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 143

Other Considerations In many patients with spasmodic dysphonia, other neurological signs
will appear, including vocal tremor, jaw or facial jerks or tremor, hand or limb tremor, hyper-
reflexia, sucking reflex, torticollis, or asymmetries in the face or palate (Aronson et al., 1968b;
Davis et al., 1988). Many patients with spasmodic dysphonia also show tremor suggesting that
a proportion of some patients diagnosed with spasmodic dysphonia are in fact patients with
essential tremor (Aronson et al., 1968a). On the other hand, it is possible that in some cases
spasmodic dysphonia is another manifestation of essential tremor (Aronson & Hartman, 1981;
Davis et al., 1988). At the very least, the frequency of occurrence of additional neurological
signs suggests that spasmodic dysphonia probably has a neurological substrate somewhere in
the brain, most likely in the extrapyramidal system (Charcot, 1881).
Sharbrough, Stockard, and Aronson (1975) reported brainstem abnormalities in 7 of their
18 spasmodic dysphonia patients. They concluded that spasmodic dysphonia is “a symptom
due to organic CNS disease which, in some cases, incidentally produces asymptomatic slowing
of conduction within the brainstem auditory pathway” (p. 200).
Patients with spasmodic dysphonia may show abnormal auditory brainstem responses
(Finitzo-Hieber et al., 1982); that is, the capacity of the brainstem to conduct impulses is
impaired. Furthermore, spasmodic dysphonia may be a disease involving multiple cranial nerves
that, when stressed, break down and disrupt the speech system (Shaefer, 1983). Such a notion
may explain why patients with spasmodic dysphonia present such variable symptoms.
Blitzer and his colleagues (Blitzer & Brin, 1991, 1992; Blitzer, Brin, Fahn, & Lovelace,
1988; Blitzer, Lovelace, Brin, Fahn, & Fink, 1985; Brin et al., 1992) placed spasmodic dysphonia
as a member of the family of dystonias. Dystonias are characterized by uncontrolled spasmodic
muscle contractions. Dystonias may begin at any age, but many patients show either an early
onset (before age 26) or late onset. They may be focal (restricted to a few muscles), segmental
(involving a group of muscles), or general (involving larger areas of the body). Examples of
focal dystonias are blepharospasm (involuntary eye closures), torticollis (neck twisting), and
writer’s cramp. Focal dystonias are apparent during the execution of a task and are not usually
seen when the affected structure is at rest. Blitzer and his colleagues believe that spasmodic
dysphonia is an action-induced dystonia involving the larynx. They found tremor in only 25%
of their patients and question the hypothesis proposed by Aronson (Aronson & Hartman,
1981) that some spasmodic dysphonias are a manifestation of essential tremor. The tremor is
irregular and can sometimes be reduced through compensatory maneuvers (Brin et al., 1992;
Folkins, 1978; Kinney, Kado, & Royner, 1972). Brin states:

Adductor spasmodic dysphonia is characterized by abnormal involuntary co-

contraction of the vocalis muscle complex muscles [sic] resulting in inappropriate
adduction of the vocal folds. As an action-induced, “task specific,” or “functional”
movement disorder, the muscles and anatomical structures are normal at rest but
move inappropriately with action

Dystonias can be induced by trauma, may have a genetic link, and show a variety of
midbrain, brainstem abnormalities. Often, there is a psychological component that may have
developed in response to the dystonia and the patient’s efforts to deal with the problem.
Spasmodic dysphonia has been very resistant to treatment. Drugs do not alleviate the
symptoms in most patients; surgery of the recurrent laryngeal nerve has been shown to have
limited success; speech therapy and/or psychotherapy do little to relieve the symptoms. BOTOX
injection offers some relief but is not a true long-term solution to the problem.
Differentiating Spasmodic Dysphonia from Other Dysphonias Although a number of fea-
tures of spasmodic dysphonia, psychogenic dysphonia, and musculoskeletal tension (hyper-
functional) dysphonia may be similar in some respects, careful history taking, examination,
and analysis of characteristics of speech production will reveal unique features of each. Patients
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144 Understanding Voice Problems

with psychogenic problems will frequently reveal a long history marked by the presence of
stress, those with hyperfunctional dysphonia may report a clearly defined period of increased
stresses and tensions, and the patient with spasmodic dysphonia will more frequently report
increased stress since the onset of the symptoms.
The voice symptoms in the patient with psychogenic problems may be variable with
return of normal voice for hours, days, or even weeks at a time, may be slightly bizarre in their
presentations, show no pattern of phonemic variability, are not present in reflexive acts with
associated phonation, show a consistent “phonatory set” during flexible endoscopic laryngeal
examination, and often respond well to voice therapy. In contrast, patients with spasmodic
dysphonia present with minimal variability and no instances of normal voice since the onset of
the symptoms. The symptoms are usually in keeping with the underlying nature of the problem
(not bizarre); are spasmodic, not constant, in presentation and can be visualized to be so on
laryngoscopic examination; show a pattern of phonemic variability (hyperadduction on voiced
segments or difficulty in voiceless to voiced transition); have voice arrests as a very characteristic
feature; and do not respond well to voice therapy.
Persons with hyperfunctional dysphonia usually present with symptoms that tend to be
fairly consistent; do not vary phonemically; are characterized by consistent rather than episodic
vocal tension, which is visible on examination but is responsive to alteration through guided
probes and suggestions; and respond well to voice therapy.

Huntington’s Chorea (HC)

Primary Voice Symptom: Hoarseness
Description and Etiology Chorea refers to a hyperkinetic disorder in which there are abrupt,
jerky, and purposeless movements of the head, neck, or limbs. There are several variants, in-
cluding Sydenham’s chorea (which is often associated with children) and Huntington’s chorea
(more often associated with adulthood). There are many causes of chorea, including trauma,
neoplasms, cerebrovascular disorders, infection, compromised immune system, metabolic dis-
turbances, intoxications, and drugs (Padberg & Bruyn, 1986). Some forms are linked to hered-
itary causes.
Huntington’s chorea is a disease of the basal ganglia with an incidence of 4 to 7 per
100,000 (Merritt, 1979). It has a genetic basis; the child of an affected person has a 50%
chance of developing the disease. It usually appears in the third through fifth decades of life
(average age of 38 years; Brin et al., 1992), although it has been reported to appear as early
as age 5 and as late as age 70 (Merritt, 1979). The basic signs are choreiform movements and
progressive mental deterioration. The abnormal movements appear to increase with heightened
emotional levels, are dramatically reduced during sleep, and affect any voluntary movements.
Mentally, a patient with Huntington’s chorea experiences a progressive loss of memory and
intellectual capacity.
Ramig (1986) reasoned that generalized instability of muscle contraction (involuntary
contractions, variable tone, or tremor) would be expected to affect the muscles of the larynx.
Therefore, disorders of phonation associated with Huntington’s chorea would be likely.
Perceptual Voice Signs and Symptoms The most prominent perceptual voice sign is harshness,
followed by monopitch and strain/struggle voice quality (Aronson, 1990; Aronson et al., 1968a).
Figure 5.17 presents the percentage of patients exhibiting the various voice signs rated by Darley
et al. (1969a).
Acoustic Signs Jarema, Kennedy, and Shoulson (1985) studied some acoustic characteristics
in 12 adults with Huntington’s chorea. There were 7 women with a mean age of 44 years and
5 men with a mean age of 42 years. The authors also collected these data for a normal-speaking
group. They measured habitual (mean) fundamental frequency and intensity during sustained
vowel production and obtained estimates of phonational range and maximum phonation time.
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 145

FIGURE 5.17. Percentage of 30 patients with Huntington’s chorea showing voice devia-
tions. Voice tremor was rated during contextual speech.

Their data on fundamental frequency and vocal intensity are summarized in Table 5.7. There
is no statistically significant difference between the patient and normal-speaking groups on
habitual fundamental frequency. Although there were some restrictions at both ends of the
patients’ phonational and dynamic ranges, the differences compared to the normal control
group were not statistically significant. The male patients in the study were found to produce
shorter maximum phonation times (15 seconds) than the normal male speakers (23 seconds),
but this difference was not statistically significant. However, the female patient phonation times
(14 seconds vs. 23 seconds) were significantly shorter than those for the normal group.
Ramig (1986) also measured some acoustic features in the speech of eight patients (four
men and four women). She noted frequent, abrupt, low-frequency segments during a sustained
vowel (sudden drop of fundamental frequency, then a return to almost the same fundamental
frequency), voice arrests, and reduced duration of the sustained vowels /ah/, /ee/, and /oo/.

TABLE 5.7 Fundamental frequency and intensity characteristics of the

speech of patients with Huntington’s chorea
Female Male
Patient Normal Patient Normal
Fundamental frequency (Hz)
Habitual 166 182 106 103
Low 155 143 92 83
High 592 716 390 422
Intensity (dB SPL)
Habitual 71 71 74 72
Soft 68 66 71 66
Loud 100 108 104 106
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146 Understanding Voice Problems

Voice arrests (370–510 msec in mean duration) occurred in six of the eight patients. Mean
vowel durations for the patients ranged from 0.50 to 9.75 seconds, whereas mean normal vowel
durations on the same task were 14.61 seconds.
A later report by Ramig et al. (1988) reported further acoustic data on these eight patients.
The patient group did not show large cycle-to-cycle variation but rather abrupt drops of
fundamental frequency. Low-frequency segments occurred 102 times in the 27 vowel segments
produced by these patients. Furthermore, another group of patients at risk for Huntington’s
chorea showed 34 instances of low-frequency drops in 90 vowel segments. These abrupt low-
frequency segments support the hypothesis of increased phonatory instability in these patients.
Another study (Zwirner, Murry, & Woodson, 1991) compared measurements of funda-
mental frequency, standard deviation of fundamental frequency, jitter, shimmer, and SNR of
13 patients with Huntington’s chorea. There was no statistically significant difference between
the patients and normal controls on fundamental frequency. Frequency variability was much
greater for the patient group as was jitter. Shimmer and SNR were different from the normal
group, but the difference was not statistically significant. Another interesting finding was the
lack of a significant correlation between perceptual ratings of voice severity and any measure
of perturbation or variability (standard deviation of fundamental frequency, jitter, shimmer,
SNR).
We have observed in a recording of a patient producing a sustained vowels /ah/ (Fig. 5.18)
an abrupt change in phonation about in the middle of the vowel and a loss of the ability of the
analysis program to track the pitch. Note the gap in the pitch trace (dark line just below the
dotted line in the figure). There was a noticeable quality change during the brief segment.

FIGURE 5.18. Spectrogram of a patient with Huntington’s chorea. Note the break during the sustained
vowel.
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 147

Measurable Physiological Signs Little measurable physiological data have been reported on
voice in chorea. Jarema et al. (1985) measured airflow rates during sustained vowel production
for their 12 adults with Huntington’s chorea and found much higher flow rates (220 ml/sec
for women, 320 ml/sec for men) than for their normal control participants (178 ml/sec for
women, 254 ml/sec for men). These data would suggest increased breathiness in patients with
Huntington’s chorea.
Ramig (1986) suggested that the previously noted voice arrests had to be associated with
sudden adductory or abductory movements of the vocal folds, as they occurred much too fast
to be produced by articulatory movements. This could be seen as indirect evidence of either
hyper- or hypo-tense vocal folds.
Observable Physiological Signs Usually, the larynges of patients with Huntington’s chorea
appear normal (Aronson, 1990). However, close observation may reveal short periods of ad-
ductory or abductory movement, especially in patients exhibiting voice arrests. Sudden shifts
of fundamental frequency (usually downward) may be accompanied by jerky movements of
the vocal folds. Further research is needed on the laryngoscopic signs of Huntington’s chorea.
No data have been reported on the stroboscopic signs in Huntington’s chorea. Because the
movements in Huntington’s chorea are very jerky and irregular, visualization of the larynx with
stroboscopy might be difficult in some patients.
Pathophysiology The jerky, sudden, and abrupt movements of Huntington’s chorea would
seriously interfere with the production of smooth, controlled sound. Patients have decreased
phonatory stability. Sudden adduction of the vocal folds may result in intensity bursts or voice
arrests. Sudden abductory bursts would be accompanied by excessive airflow and breathiness
or aphonic episodes. It is possible for a patient to exhibit both conditions, although one or the
other characteristic will probably be the most prominent.

Supra- or Pseudobulbar Palsy

Primary Voice Symptom: Hoarseness or Harshness
Description and Etiology Two major pathway systems converge on the lower-motor neurons
for control of muscles that affect voice and speech. These are the pyramidal and extrapyramidal
tracts. Selected damage to the extrapyramidal or indirect pathway1 usually results in spasticity
and increased muscle reflexes. Selected damage to the direct or pyramidal pathway results in a
loss of function, especially for skilled movements. The pyramidal system is said to be the newer
system phylogenetically. Both pathways are located very close to each other anatomically, and
lesions in these pathways would most likely affect both pathways and voluntary movement in
four ways: spasticity, weakness, limitation of range, and a slowing of movement. The disease
known as pseudobulbar palsy results when lesions affect these two systems.
Pseudobulbar palsy is actually a misnomer. The symptoms of the problem are in some
instances very similar to those of bulbar disease (muscle weakness), and yet the evidence for
bulbar lesions is equivocal. Langworthy and Hesser (1940) recommended the term “supranu-
clear bulbar paralysis.” Aring (1965) agreed, believing that the term had an anatomical basis,
locating the lesions rostral to the appropriate cranial motor nerve nuclei. However, the term
“pseudobulbar palsy” has remained in use.
Pseudobulbar palsy results from progressive lesions that occur bilaterally in the corticobul-
bar tracts. These lesions occur most frequently in the internal capsules (Aring, 1965; Langworthy
& Hesser, 1940), although there may be pontine or midbrain lesions. These lesions are usually
the result of a stroke, although other reported causes have been cerebral palsy, brain injuries,
multiple sclerosis, and arteriosclerosis (Darley et al., 1975; Langworthy & Hesser, 1940). The

1 Indirect refers to the fact that information traveling along this pathway encounters many synapses or connection
points along its way to the final destination. The direct pathway or pyramidal system has a single, continuous
pathway from the motor cortex to the lower motor neurons in the spinal cord or nuclei in the brainstem.
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148 Understanding Voice Problems

chief symptoms are difficulties with speech and swallowing, plus emotional lability. The latter
presents a unique feature of this problem. Patients may show bursts of laughter or crying in
the presence of very mild stimuli or no stimuli at all. It is as if the patient’s higher centers
have released their control of these responses, and they appear uncontrolled. Kreindler and
Pruskauer-Apostol (1971) documented these unusual behaviors, and Aronson (1990) empha-
sized that reduced thresholds for crying and laughter are critical cues in the diagnosis of this
disorder.
Perceptual Voice Signs and Symptoms A major sign of pseudobulbar palsy is dysarthria of
speech, as documented by Darley and his colleagues (Darley et al., 1969a, 1969b, 1975).
They grouped perceptual signs into clusters of the dysarthric symptoms that best characterize
a particular type of neurological dysfunction. The important perceptual signs in pseudobulbar
palsy are reported to be (using Darley et al.’s terminology) (a) prosodic excess (relates to rate
and stress characteristics of speech), (b) prosodic insufficiency (monopitch, monoloudness,
reduced stress, short phrases), (c) articulatory-resonatory incompetence (imprecise consonants,
distorted vowels, hypernasality), and (d) phonatory stenosis (harsh voice, strain/struggle, pitch
breaks).
Aronson et al. (1968a) rated the voice characteristics of 30 patients with pseudobulbar
palsy (Darley et al., 1969a, 1969b) and found that 97% of the patients were considered to have
monopitch and harsh voices, 87% had a too low pitch level, 67% demonstrated considerable
strain and struggle in phonation, and 30% exhibited pitch breaks and voice tremor. (These
voice signs of pseudobulbar palsy are shown in Fig. 5.19.) Aring (1965) commented that the
speech of a patient with pseudobulbar palsy is nasal, monotonic, with soft intensity and rapid
rate, making it difficult to understand.
Acoustic Signs There have been few data reported on the acoustic characteristics of patients
with pseudobulbar palsy other than a study by Kammermeier (1969), who reported a mean
fundamental frequency of 124.1 Hz in male participants with a mean age of 61.7 years. When
compared to the mean fundamental frequency (F0 ) values reported for normal adult male
speakers by Mysak (1959; n = 5, mean frequency = 124.3 Hz, mean age = 73.3 years) and
Hollien and Shipp (1972; n = 5, mean frequency = 112 Hz, mean age = 64.6 years), the
pseudobulbar participants produced fundamental frequencies that were equal to or slightly

FIGURE 5.19. Percentage of 30 patients with pseudobulbar palsy showing deviant voice
signs. Voice tremor was rated during contextual speech.
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 149

higher than that of normal speakers. Kammermeier (1969) reported reduced variability of
fundamental frequency in pseudobulbar patients, as well as reduced intensity variation. These
findings may be related to the perception of monopitch and monoloudness.
It appears that patients with pseudobulbar palsy exhibit normal or near-normal average
fundamental frequency, reduced fundamental frequency variation, and reduced intensity vari-
ation.
Measurable Physiological Signs We know of no data on the measurable physiological char-
acteristics of the speech of patients with pseudobulbar palsy. Higher-than-normal subglottal
pressures might be expected because of the hypertonicity and strain/struggle characteristics of
the voice. If breathy, the patient would probably exhibit greater-than-normal airflows. If the
range and force of movement of the vocal folds are affected, this might be reflected in slow
opening and closing times of the vocal folds and perhaps a short closed phase due to the inability
to maintain sufficient muscle forces.
Observable Physiological Signs
Laryngoscopy According to Darley et al. (1975), no laryngeal abnormalities have been
reported. However, it is possible that vocal fold hyperadduction as well as hypofunction of
other laryngeal structures might be observable, utilizing the improved instruments available
today for laryngoscopic examination. Further study of these characteristics is needed.
Stroboscopy Again, there appear to be no reports on stroboscopic signs in patients with
pseudobulbar palsy. When vocal fold hypertonicity is present, typical findings, according to
Kitzing (1985), would include reduced vocal fold amplitudes, diminished mucosal waves, and
excessive glottal closure. However, if the muscles have reduced force and movement, glottal
closure may not be complete, and there may be asymmetry and aperiodicity of vocal fold
movement.
Pathophysiology Pseudobulbar palsy results in a loss of muscle coordination and a re-
lease of inhibition of the lower centers. The latter condition results in hyperactivity of the
muscle reflexes and spasticity. In speech, pseudobulbar palsy patients will show a reduction in
the force and range of the muscle movement (Darley et al., 1969b). In addition, the release of
the lower-motor centers results in hypertonicity of the vocal folds. Pseudobulbar palsy seems
to be a condition in which both muscle weakness and muscle hyperactivity coexist, with differ-
ential effects on the motor act being performed. Hypertonicity would be consistent with the
perception of harshness in the voice as well as the strain and struggle to speak. It is not neces-
sarily consistent with the perception of a low pitch level or the findings that the fundamental
frequency of these patients is within the normal range. These findings might be understood by
hypothesizing that the cricothyroid is minimally affected in pseudobulbar palsy but that the
other adductors or abductors of the larynx are affected differentially. Breathiness (noted in 14
out of 30 patients with pseudobulbar palsy studied by Darley et al., 1969b) would be produced
by excessive opening of the vocal folds or perhaps by hypertonicity of the abductor muscle
of the larynx (posterior cricothyroid). Hyperactivity in the adductors would have an effect
similar to hypertonicity and would be consistent with strain/struggle quality as well as excessive
hoarseness or harshness. The specific voice signs (perceptual, acoustic, or physiological) noted
in a patient with pseudobulbar palsy may reflect lesions at different locations along the long
pathway from the brain to the ultimate motor neurons controlling the muscles of the larynx.

Phonatory Stability
Short Term
Most patients with a neurological problem affecting the voice may show increased jitter and
shimmer, especially if they exhibit hoarseness.
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Long Term (Tremor)

Amyotrophic Lateral Sclerosis (ALS)
Primary Voice Symptom: Hoarseness or Strain/Struggle
Description and Etiology Amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) is a
progressive, degenerative disease of the central nervous system that involves both upper and
lower-motor neurons. As a result, the patient with amyotrophic lateral sclerosis may have
symptoms such as spasticity (upper-motor neuron symptom) along with muscle weakness (a
symptom of lower-motor neuron lesions). The lower-motor neuron lesions usually affect the
ventral horn cells. The incidence of amyotrophic lateral sclerosis is about 0.4 to 1.8 per 100,000
people (Janzen, Rae, & Hudson, 1988). The initial manifestation is muscle weakness, cramps,
and fasciculation. The disease usually affects people later in life, although reports of early onset
are known. The rate of progression of the disease may vary.
In the study by Carpenter et al. (1988), 28% of 123 patients with amyotrophic lateral
sclerosis presented symptoms in the head, neck, larynx, or voice. The mean age of these patients
was 61, and the ratio between men and women was about equal. Of the patients presenting
head/neck symptoms, 68% exhibited slurred speech, 14% had hoarseness, and 13% presented
with dysphagia. On physical exam, the patients presented muscle weakness and fasciculation
in various areas, as shown in Table 5.8. In many patients, excessive drooling may exist and
presents unique problems for management. In the latter stages of the disease, it is likely that
100% of patients exhibit severe respiratory, speech, voice, and swallowing difficulties. Most
require respiratory assistance and augmentative speech systems.
Speech signs in ALS include flaccid dysarthria or spastic dysarthria or both. A more detailed
list of speech signs is presented in Table 5.9. Tjaden and Turner (1997) reported articulatory
differences between the /s/ and /sh/ for his group of patients with ALS. Weismer, Martin,
Kent, and Kent (1992) reported shallower formant frequency characteristics of ALS patients
suggesting a reduced articulatory space in their speech.
There are many possible etiologies for this condition. Aronson (1990) listed infection,
malignancy, and genetic defects. Janzen et al. (1988) added toxins, autoimmunity problems,
and metabolic deficiencies. There is no effective treatment, although certain drugs have been
used to ease the symptoms. For example, Mayo clinic may use Riluzole to the slow the progress
of the disease and other drugs to control muscle spasms, stiffness, or secretions. (Mayo Clinic
Web site: www.mayoclinic.org/lou-gehrigs-disease/treatment.html)
Perceptual Voice Signs and Symptoms The early primary symptom is hoarseness or harsh-
ness, with slurred speech as an additional symptom. In their classic study of the perceptual
characteristics of dysarthria, Darley et al. (1969a) listed imprecise consonants, hypernasality,

TABLE 5.8 Percent of patients with ALS presenting physical abnormalities

in the head and neck region
Area Weakness Fasciculations
Tongue 66 54
Extremities 66 30
Neck 412 10
Face 2 38
Palate and pharynx 2 32
Masseter muscle 8 2
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TABLE 5.9 Frequency of speech deviations in patients with ALS

Speech deviation Percent
Harsh voice 79.75
Hypernasality 74.68
Breathy voice 64.56
Voice tremor 63.29
Strain/struggle voice 59.49
Imprecise consonants 56.96
Reduced intelligibility 46.84
Slow rate 46.84
Phonemes prolonged 45.57
Audible inspiration 40.51
Continuous phonation 37.97
High pitch 37.97
Phrases short 36.71
Inappropriate silences 32.91
Nasal emission 30.28
Vowels distorted 24.05
Low pitch 7.59
Fast rate 2.53

harsh voice, slow rate, and monopitch as the prominent speech characteristics in their group of
30 participants with amyotrophic lateral sclerosis. Figure 5.20 presents a summary of the voice
signs and symptoms found in a group of patients with amyotrophic lateral sclerosis patients,
as reported by Aronson et al. (1968b). Similar speech and voice symptoms were reported by
Carrow, Mauldin, and Shamblin (1974). One limitation of these early studies is the lack of
information about the stage of the disease in the participant groups. Since this is a progressively
deteriorating disease, all symptoms become increasingly severe and debilitating with the passage
of time.
Acoustic Signs Caruso and Burton (1987) reported that the stop gaps in stop consonant
syllables and vowel duration were much longer in the speech of patients with amyotrophic
lateral sclerosis than in normal speakers. Voice-onset time in the two groups was very sim-
ilar. These authors suggest that laryngeal structures may move more slowly in amyotrophic
lateral sclerosis than in normal speakers. They point out that because the nucleus ambiguus
is often affected, the neural control of adduction and abduction by the vocal folds may be
impaired.
In a study primarily concerned with patients with other neurologic problems, Ramig et al.
(1988) reported on the changes of f0, jitter, shimmer, and harmonics-to-noise ratio (HNR) of
a 69-year-old man recorded 4 times over a period of 6 months. Shimmer and HNR were most
sensitive to the changes that occurred over the 6-month period. At the end of the recording
sessions, the patient displayed greater acoustic instability. Additional data on this patient were
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152 Understanding Voice Problems

FIGURE 5.20. Percentage of 30 patients with amyotrophic lateral sclerosis showing voice
deviations. Voice tremor was rated during contextual speech.

reported by Ramig et al. (1990). The coefficient of amplitude and the coefficient of frequency,
measures that reflect the long-term stability of phonation, were also greater for the patient than
for his control. These data are consistent with the notion that ALS patients exhibit decreased
phonatory control that is exacerbated by the progression of the disease.
Kent et al. (1991) reported abnormalities of fundamental frequency and perturbation in
their group of 10 female patients with ALS. Kent et al. (1991) found that the fundamental
frequency of their male patients with ALS (N = 32) was somewhat higher than the normal
controls (127.4 Hz vs. 112.8 Hz; Table 5.10).
Strand, Buder, Yorkston, and Ramig (1993) also reported on fundamental frequency,
intensity, jitter, shimmer, and SNR of four women with ALS. Although the patient data were
different from the normal controls, the patients did show considerable variation of fundamental
frequency both in sustained phonation and in phrase samples. All four patients exhibited greater
jitter and shimmer than the control participant. One interesting facet of this study is the report
of the perceptual voice characteristics of the four patients that should be considered when
interpreting the acoustic data. One patient was characterized as having a strained/struggle
voice quality, whereas another exhibited breathy phonation with low volume. The other two
participants exhibited harsh voice quality with fluctuations of intensity and frequency. The
group was heterogeneous, and one should expect variation in the acoustic data. Such was
the case in this report. ALS speech is characterized as a mixed dysarthria; some patients can

TABLE 5.10 Acoustic measures in ALS

Males Females
ALS Control ALS Control
Fundamental frequency 127.4 112.8 179 194.5
Jitter (msec) 0.11 0.12 0.24 0.07
Shimmer (%) 5.3 7 18.53 2.61
SNR (dB) 19.32 16.87 13.08 21.38
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exhibit symptoms characteristic of spasticity, whereas others can exhibit a flaccid dysarthria.
The acoustic features of each type of dysarthria are very different.
Measurable Physiological Signs There have been no data reported on the physiological
characteristics of the speech of ALS patients. However, electromyographic studies have been re-
ported on nonlaryngeal muscles and reveal sporadic action potentials, a reduction in the number
of potentials, and fibrillation. Similar findings might be expected in the laryngeal muscles.
Observable Physiological Signs The larynx in amyotrophic lateral sclerosis usually presents
a normal appearance (Aronson, 1990). However, it is possible to observe hyperadduction if the
major component in the disease is spasticity. If the major component is flaccidity, one might
expect incomplete closure, bowing, and/or slower speed of vocal fold movement.
There have been no data reported on stroboscopic signs specifically in amyotrophic lateral
sclerosis patients. However, signs typical of flaccid paralysis (reduced mucosal wave, incom-
plete closure) or those associated with problems affecting the upper-motor neurons (spastic
characteristics such as hyperadduction) would be consistent with the nature of the effects of
the disease.
Pathophysiology Amyotrophic lateral sclerosis impairs central nervous system control of
the muscles of the larynx (as well as most muscles in the body). Furthermore, if the lower-
motor neurons are affected, muscle tone and strength are affected. Patients may exhibit spastic
phases or flaccid phases depending on the precise areas affected. Spastic effects might result
in a strain/struggle type of voice, whereas flaccid effects might reduce the efficiency of glottal
valving.

Essential Tremor
Primary Voice Symptom: Tremor
Classification of Tremor There are various types of tremor that may have differing etiolo-
gies (central, peripheral, or both), characteristic timing features, and unique characteristics of
presentation. Tremor may be present as an isolated symptom or it may be one characteristic of
a more generalized neurological disorder.
Tremor is characterized by relatively regular, involuntary movements of the distal or prox-
imal muscles. Everyone has some degree of normal tremor, which ranges in frequency from 6
to 12 Hz. Abnormal tremor has a lower frequency range, larger amplitudes, and may interfere
with purposeful movements. Tremor may occur while a structure is at rest (resting tremor)
or in action (action tremor). Action tremor may consist of postural tremor (when holding a
structure in position), contraction tremor, and/or intention tremor (Brin et al., 1992). It may
be focal or more generalized.
Essential tremor is a disorder of the central nervous system that may result in tremor in the
head, limbs, tongue, palate, and larynx. It tends to start in the hands and then progresses to the
arms, head, neck, face, and so on (Brown & Simonson, 1963). “Essential tremor is typically
absent at rest, maximal during maintenance of a posture, attenuated during movement and
often accentuated at the termination of movement” (Brin et al., 1992; Emanuel & Sansone,
1969). Typically, the frequency of tremor in patients with essential tremor is between 3 and 7
Hz (Brin et al., 1992).
Description and Etiology In some patients voice tremor may be the primary or sole char-
acteristic. In the Brown and Simonson study (1963), only 6 of 31 essential tremor patients
exhibited isolated voice tremor, whereas the remaining 25 had tremor in the head, tremor
of the extremities, or both, in addition to voice tremor. Some have reported voice tremor in
10% to 20% of their patients (Brin et al., 1992). Lou and Jankovic (1991), reporting on 350
patients with essential tremor, found only one case of voice tremor as the sole symptom, grad-
ual onset of tremor, and frequent occurrence of family members with some kind of tremor.
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154 Understanding Voice Problems

Seventeen patients had associated neurological signs, including a positive sucking reflex, spas-
modic torticollis, bilateral facial spasms, incoordination, and diadochokinesis.
Larsson and Sjogren (1960) reported that essential tremor occurred more frequently in
men than in women, with a mean age of onset of 48 years. Aronson and Hartman (1981)
reported the mean age of onset at 57 years. They also found extralaryngeal tremor in 93%
of their patients. In their study of 678 patients with essential tremor, Koller, Busenbark, and
Miner (1994) found that about 49% were women and 51% were men. The average age of onset
was 45.3 years. About 90% of the patients had tremor affecting either hand; about 20% had
head tremor with smaller numbers of patients with tremors of the leg, chin, trunk, and tongue.
Thus, essential tremor seems to be associated with aging, although the reasons for this
are unclear. The highest prevalence is in the seventh decade of life. Heredity may affect the
development of the tremor. About one-half of patients with essential tremor have a history of
an affected family member (Young, 1986). In sudden-onset cases, Brown and Simonson (1963)
suggested that some kind of arterial disease may have been responsible.
It is difficult to determine the locus of the central nervous system lesion that causes essential
tremor. Critchley (1949) suggested that the extrapyramidal system is involved, but it is possible
that other structures might be affected. Brin et al. (1992) suggest that tremor may be the result
of oscillation in the olivocerebellar tracts. Young (1986) noted that a ventrolateral thalamotomy
reduced or eliminated the tremor. There may be a possibility of dysfunction in the cerebellum
as a cause of the tremor (Young, 1986).
Perceptual Voice Signs and Symptoms The most prominent voice symptom and sign is
tremor, as well as a regular modulation of frequency or intensity, which is most noticeable
during prolonged production of a vowel but is also apparent during contextual speech. In 100%
of their patients with essential tremor, Aronson et al. (1968b) reported tremor on a sustained
/ah/ vowel (only tremor in contextual speech is shown in Fig. 5.21) as well as harshness and
strain/struggle. Figure 5.21 presents a summary of the voice symptoms in essential tremor as
reported in the Aronson et al. (1968b) study.
In general, the voice of essential tremor patients may be described as sounding quavery and
tremulous. Some patients will have a relatively constant and noticeable tremor during speech.
Some may have such severe tremor that stoppage of voice occurs, as reported by Ardran,
Kinsbourne, and Rushworth (1966).

FIGURE 5.21. Percentage of 26 patients with essential tremor showing voice deviations.
Voice tremor was rated during contextual speech.
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FIGURE 5.22. Spectrogram of a patient with essential tremor producing a sustained vowel.

Acoustic Signs There are little data on many of the acoustic signs in essential tremor. Most
studies have concentrated on the variation of amplitude during sustained vowel production.
Brown and Simonson (1963) measured the rate of tremor from oscillograms of 23 patients.
Tremor frequencies of 5 to 6 Hz were measured in most patients. Ardran et al. (1966) reported
spectrographic evidence of low-amplitude noise during the production of monosyllabic words
by a single patient. This noise, they suggested, gave evidence of breathiness in the patients’
speech. Aronson and Hartman (1981) analyzed the tremor in oscillograms of 14 patients with
essential tremor and reported a mean tremor frequency of 5.7 Hz. Lebrun, Devreux, Rousseau,
and Darimont (1982) reported a tremor frequency of 4 Hz in the voice of their 84-year-old
patient. They also observed erratic voice breaks and arrests.
Figure 5.22 shows a spectrogram of a male patient producing a sustained vowel /ah/.
Note the rhythmic variations of intensity in the waveform along the top of the figure and the
variations of fundamental frequency (shown by the gray line in the spectrogram).
Measurable Physiological Signs There have been few data reported on the measurable phys-
iological characteristics of patients with essential tremor. Ardran et al. (1966) performed elec-
tromyograms on the cricothyroid and hyoglossus muscles of a 72-year-old female patient. They
showed that at rest, both muscles had regular variation in activity at about a rate of 5 to 6 Hz.
They comment that this was low-level activity that did not result in movement of the struc-
tures. This variation in muscle activity was not entirely regular and disappeared occasionally.
Furthermore, the variation of activity between the hyoglossus and the cricothyroid muscle was
not synchronized. There was also resting tremor in the electromyogram of the pectoralis major
and external intercostal muscles in this patient. However, these disappeared when the patient
contracted these muscles.
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Observable Physiological Signs By and large, the larynges of patients with essential tremor
will show normal structure and movement. Rhythmic movement of one or more laryngeal
structures may sometimes be observed during phonation and/or at rest. Brown and Simonson
(1963) reported normal-appearing larynges in 13 of their essential tremor patients and vocal
fold bowing in 1 patient. However, 17 of their patients were not examined laryngoscopically.
We know of no data on the stroboscopic signs in essential tremor. It has been our experience
that obtaining stroboscopic imaging of sufficiently acceptable quality from which to make
reliable interpretation of stroboscopic signs has not been possible. The tremor makes tracking
of the fundamental frequency difficult. Current stroboscopic equipment appears to be able to
track vibration in the presence of tremor.
Pathophysiology The rhythmically changing activity in the muscles of the larynx create vary-
ing degrees of tension in the vocal folds and lead to a rhythmic change in fundamental frequency.
Furthermore, the degree of adduction varies systematically in synchrony with the variation of
muscle activity, creating a rhythmic change in the force of adduction. This results in variations
of subglottal air pressure and, thus, of vocal intensity. If the tremor is severe, the adductory
force could become large enough to completely stop voice production. Voice stoppages are also
characteristic of spasmodic dysphonia. As discussed earlier (see “Spasmodic Dysphonia, Other
Considerations”), Aronson and Hartman (1981) and others have suggested that some forms
of spasmodic dysphonia may have essential tremor as their etiology. Medication has been used
to treat essential tremor with mixed results. Propranolol (sometimes in conjunction with di-
azepam), primidone, and clonazepam have been used. Brin et al. (1992), however, report limited
success in using these drugs to treat essential tremor. The voice tremor characteristics of patients
with spasmodic dysphonia and those with essential tremor are different (Brin et al., 1992).

Phonatory Incoordination/Voiced–Voiceless Distinction

Abductor Spasmodic Dysphonia
Abductor spasmodic dysphonia involves the muscle of abduction of the vocal folds and results
in an intermittently breathy voice quality. Some authors (Hartman & Aronson, 1981; Shipp,
Mueller, & Zwitman, 1980) have suggested that abductor spasmodic dysphonia is so dissimilar
to the adductor type that it should be given a name more indicative of its pathophysiology.
Hartman and Aronson (1981) have suggested the term “intermittent breathy dysphonia,”
whereas Shipp et al. (1980) advocate the term “intermittent abductory dysphonia.” Ludlow
(1995) believing the cause of the symptoms to be a failure in the execution of smooth transition
from abductory to adductory posture during speech has argued that this form of spasmodic
dysphonia represents a problem of coordination.
Perceptual Voice Signs and Symptoms Descriptions of the abductor type of spasmodic dys-
phonia vary. Some authors describe intermittent episodes of breathy dysphonia, drops in pitch,
and vowel prolongations (Hartman & Aronson, 1981; Merson & Ginsberg, 1979; Zwitman,
1979). Aronson (1973, 1990) states that in many respects it is the mirror image of adductor
spasmodic dysphonia. Ludlow (1995) describes the perceptual attribute characteristic of the
abductor type of spasmodic dysphonia as a delay in voice onset following production of voice-
less consonants. Pitch breaks may occur in some patients. Close attention to the episodes of
voice interruption in these patients confirms the preponderance of difficulty associated with
the transition from voiceless (i.e., /h/, /s/,/f/, /p/,/t/) to voiced phonemes.
Acoustic Signs
Fundamental Frequency Merson and Ginsberg (1979) reported mean fundamental
frequencies of 161.3 Hz and 203.8 Hz for two female patients with abductor spasmodic
dysphonia reading a sentence.
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Vocal Intensity Hartman and Aronson (1981) reported the amplitude variations ob-
served in the speech of 17 abductor spasmodic dysphonia patients. They found a steady but
random variation of amplitude in some patients, rhythmic variation in other patients, and evi-
dence of moments of breathiness in still other patients. We know of no data on vocal intensity
in the abductor type of spasmodic dysphonia. It has been our experience, however, that some of
these patients use much-reduced intensity levels in conversation, even to the point of aphonic
whisper. This is perhaps a compensatory behavior adopted in order to avoid voice stoppages.
Little other data have appeared in the literature about the acoustic characteristics of ab-
ductor spasmodic dysphonia. Wolfe and Bacon (1976) reported some spectrographic findings
for a patient with what appears to be abductor spasmodic dysphonia, in which there is evidence
of interruptions of voicing, as well as irregularly spaced vertical striations indicating a variation
of voicing associated with the strain and struggle to speak. Zwitman (1979) reported similar
findings for two patients with abductor spasmodic dysphonia. He also reported that voiceless
stops seem to be distinguished from voiced stops by a sustained frication during the voiceless
stops. Some of the spectrographic features of abductor spasmodic dysphonia can be seen in
Figure 5.16.
Ludlow and her colleagues reported the most extensive analysis of the acoustic features.
An illustration of the delay in the onset of phonation often observed in patients with abductor
spasmodic dysphonia is shown in Figure 5.23. The upper panel is the waveform of the sentence,
“Do queens eat honey?” The lower panel shows the spectrogram of the same sentence along

FIGURE 5.23. Spectrogram of a patient with abductor spasmodic dysphonia producing the sentence,
“Do queens eat honey?” The upper panel is the acoustic waveform, whereas the lower panel shows the
spectrogram and the fundamental frequency trace (dark broken line). The light-colored rectangle at the end
of the sentence shows the acoustic changes that occurred when the patient produced the word “honey.”
Note the long noise duration followed by a very brief voiced segment.
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158 Understanding Voice Problems

with the trace of fundamental frequency (the dark line running about in the center of the
spectrogram). The lightly colored rectangle at the end of the sentence brackets the word “honey.”
Note the initial period of silence/breathiness corresponding to the /h/ in honey, followed by a
very brief voiced segment followed by breathiness for the remainder of the word.
Measurable Physiological Signs One would expect large airflows to be associated with ab-
ductory spasmodic dysphonia. Indeed, Merson and Ginsberg (1979) reported such large flows
in two patients (e.g., 321 ml/sec on a sustained /ah/ vowel, 400 ml/sec, and 435 ml/sec) during
sentence production.
Observable Physiological Signs
Laryngoscopy and Stroboscopy There are little data on the laryngoscopic and strobo-
scopic characteristics unique to abductor spasmodic dysphonia.
Pathophysiology In abductor spasmodic dysphonia, the spasm results in a sudden increase
of airflow and relatively short closed times. The combination of rapid airflows and short closed
time would be expected to produce much less energy in the higher frequencies of the spectrum.
The voice will be perceived as intermittently breathy and weak. Again, there are periods of
normal vocal fold vibration, but it is the sudden, unexpected stoppages that create havoc in the
production of voice and speech.

Mixed Disorders
Cerebellar Ataxia
Primary Voice Symptom: Hoarseness
Description and Etiology Cerebellar ataxia is a disorder of the cerebellum. Its accompanying
speech disorder is called ataxic dysphonia or, more generally, ataxic dysarthria. A lesion in the
cerebellum results in a loss of muscle coordination and movement. Fulton and Dow (1937)
considered two kinds of speech defects in cerebellar lesions: (a) errors in the rate, range, direction,
and force of movements, and (b) hypotonia. Kent, Netsell, and Abbs (1979) presented some
acoustic evidence for “scanning speech” and suggested that it may be the result of the inability of
the cerebellum to properly integrate movements or it may be due to an alteration in the motor
programming plan of the cerebellum. In their study of ataxic dysarthria, Brown, Darley, and
Aronson (1970) concluded that excess and equal stress plus irregular articulatory breakdown
were the speech scales most suggestive of this condition.
The etiology of dysphonia in ataxic dysarthria is varied. In their study, Brown et al. (1970)
reported that 3 patients had a neoplasm, 1 had experienced trauma, 1 had an infarct, 1 was
thought to have multiple sclerosis, and 24 were diagnosed with cerebellar degeneration. They
suggested that the important areas of the cerebellum serving speech were the vermis and the
adjacent paravermis. Lechtenberg and Gilman (1978) implicate the left cerebellar hemisphere as
important for the control of speech. Based on that implication, Kent et al. (1979) hypothesized
that the right cerebral hemisphere must send its information to the left cerebellar hemisphere,
making both hemispheres responsible for the control of speech prosody. If true, one might expect
patients with ataxic dysarthria to have greater difficulty in the control of the suprasegmental
features of speech (i.e., stress and intonation), both of which involve the vocal folds.
Perceptual Voice Signs and Symptoms In their rating study of the speech of patients with
various kinds of neuromuscular diseases, Aronson et al. (1968a) noted the voice features of
harshness, monopitch, too low pitch, strain/struggle, and pitch breaks as prevalent in ataxic
dysarthria. The percentage of patients showing these perceptual signs of the voice is shown in
Figure 5.24.
Aronson (1990) noted that some ataxics may exhibit normal voice quality but that many
will show harshness, monopitch, and monoloudness as characteristic perceptual features.
Acoustic Signs Kent et al. (1979) reported a study on the acoustic characteristics of the
speech of five ataxic patients. They found abnormally long vowel and segment durations and
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FIGURE 5.24. Percentage of 30 patients with ataxic dysarthria showing voice deviations.
Voice tremor was rated during contextual speech.

strongly suggested that there were aberrations in the control of fundamental frequency. In an
earlier study, Kent and Netsell (1975) reported on the speech characteristics of a female ataxic
patient. Among other variables, they examined fundamental frequency contours during the
production of words and sentences. They noted that many fundamental frequency contours
had a monotone appearance, whereas others had marked variability of fundamental frequency.
They suggested that ataxics may have more difficulty controlling fundamental frequency during
speech than they have in articulating the phonemes. They also noted spectrographic evidence
of harshness and/or vocal fry.
The fundamental frequency of ataxic dysphonics is very similar to normal speakers (Zwirner
et al., 1991); however, the standard deviation of fundamental frequency of these patients was
more than 3 times as large as normal speakers (1.3 Hz vs. 6.1 Hz). Jitter was also much larger
than normal. Patients also showed a difference of shimmer and SNR compared to the normal
controls, but the differences were not statistically significant.
These data support the notion of Kent and Netsell (1975) that persons with cerebellar ataxia
have difficulty controlling fundamental frequency. Both the standard deviation of fundamental
frequency and jitter reflect frequency variability, and both are much larger than normal. Patients
with cerebellar ataxia can produce the desired fundamental frequency, but they have difficulty
controlling it.
Measurable Physiological Signs There appear to be no data available in the literature con-
cerning the measurable physiological characteristics of the voice of ataxic patients. In their
single-participant analysis, Kent and Netsell (1975) reported that cineradiographic analysis of
the oral cavity during speech revealed abnormal but small anteroposterior lingual adjustments.
Furthermore, they found that the patient’s articulatory movements were longer in duration
than normal movements. Thus, valving movements of the vocal folds might show abnormally
long durations.
Brown et al. (1970) reported that electromyographic recordings were made on 6 of their
30 patients with ataxic dysarthria but failed to specify which muscles were studied. They
reported normal electromyographic patterns in two patients, evidence of a motor lesion in one
patient, and evidence of a peripheral neuropathy in three patients. Similar abnormalities might
be found in the laryngeal muscles, although not in all patients.
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Observable Physiological Signs Aronson (1990) expects to find a normal-appearing larynx

in patients with ataxic dysphonia. Evidence of reduced speed of adduction or abduction during
valving and movements of the vocal folds might be observed on careful study. We know of no
reported data on the stroboscopic signs in patients with ataxic dysphonia.
Pathophysiology Ataxic dysphonia or dysarthria seems to be characterized by hypotonia
and an incoordination of muscles. Hypotonia manifests itself as a delay in the generation of a
force, a reduced rate of muscular contraction, and a reduced range of movement (Brown et al.,
1970; Kent & Netsell, 1975; Kent et al. 1979). Reduced muscle activity may account for the
reduced fundamental frequency range during conversational speech, since in order to increase
vocal pitch, cricothyroid muscle activity must be increased. Reduced muscle tone may also
account for hoarseness in ataxic voices because of tension differences between the two vocal
folds. Hypotonicity will have a similar effect on the control of intensity, although few data
have been reported on this acoustic variable. Incoordination of phonation may be manifested
by difficulty in controlling the magnitude and extent of laryngeal movements as well as the
control of the magnitude and extent of articulatory movements.

Multiple Sclerosis
Primary Voice Symptoms: Impaired Loudness Control and Hoarseness
Description and Etiology Multiple sclerosis was first described by Charcot (1881), who
referred to it as disseminated sclerosis. It is a disease characterized by multiple scarring (sclerosis)
of the white matter in the brain, brainstem, and spinal cord. The initial symptoms of the
disease may be very mild. As it progresses, the severity of the symptoms may increase; however,
intermittently there may be long periods of remission or latency during which the person
may seem well. It is very likely an autoimmune disorder, but the evidence is not clear on this
(Corboy, Goodin, & Frohman, 2003). In the United States, the incidence of multiple sclerosis
is about 50 per 100,000. It is much more common in the temperate regions of the Northern
and Southern hemispheres, with the incidence dropping markedly close to the equator. The
male–female ratio is unclear. Recent evidence suggests that it occurs more often in women. One
study from Canada found a 3:1 female/ male ratio (Orton et al., 2007). The disease frequently
develops in young adulthood, although it has been suggested that the onset of the very slowly
progressing symptoms occurs in childhood but only becomes apparent in the adult (Millar,
1971).
Approximately 50% of patients with multiple sclerosis initially seek medical attention be-
cause of ENT symptoms, including vertigo (25%), nystagmus (40%–70%), dysarthria (20%),
or dysphagia (10%–15%; Garfinkle & Kimmelman, 1982; Ward, Cannon, & Lindsay, 1965).
Bilateral abductor paralysis of the vocal folds may also occur. Noffsinger, Olsen, Carhart, Hart,
and Sahgal (1972) documented many of the auditory and vestibular system dysfunctions in
patients with multiple sclerosis. Of course, a patient may present with multiple symptoms.
Most patients present a relapsing–remitting form of multiple sclerosis (RRMS) that most
often develops into a progressive deterioration of various brain functions. About 10% present a
progressive disease from the start with little or no evidence of remission (Corboy et al., 2003).
The reported loci of central nervous system involvement are not consistent. In a study of
234 multiple-sclerosis patients, 85% were reported to have pyramidal involvement, followed
by cerebellar (77%) and brainstem (73%) involvement (Kurtzke, Beebe, Nagler, Auth, &
Kurland, 1972). Multiple system involvement was also noted by Garfinkle and Kimmelman
(1982). Patients with multiple sclerosis present a variety of neurological signs. Some of these are
summarized in Table 5.11, based on the data presented by Darley, Brown, and Goldstein (1972).
It has been stated that the cardinal signs of multiple sclerosis are scanning speech, nys-
tagmus, and intention tremor (Ivers & Goldstein, 1963). However, available data suggest that
speech/voice problems, although sometimes present, are not pervasive. Darley et al. (1972)
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CHAPTER 5 I Voice Problems Associated with Nervous System Involvement 161

TABLE 5.11 Neurological signs in multiple sclerosis

Neurological sign Percent
Finger to finger/toe to finger tests 82
Dysdiadochokinesis 71
Impairment of posterior column sense 60
Pyramidal signs (sucking reflex, Hoffman’s sign, Babinski’s sign, increased muscle 92
stretch reflexes
Muscular weakness 9

found that 59% of their 168 patients presented normal speech patterns, and another 29% had
minimal speech impairment. Table 5.12 presents a summary of the speech and voice symp-
toms in their patients. These authors also noted that the severity of speech difficulty increased
with an increase in the severity of the neurological deficit. They concluded that dysarthria was
not characteristic of multiple sclerosis speech, nor was scanning speech. Kurtzke et al. (1972)
reported that scanning speech was present in only 18.9% of their 525 male patients with
multiple sclerosis.
Treatment of MS may involve a variety of drugs that have shown promise for the relief
of some of the symptoms of MS including interferon-beta-1a and interfon-beta-1b as well as
other drugs (Corboy et al., 2003). Some have suggested the use of alternative medicines for the
relief of some symptoms although the use of such drugs have shown only slight improvement
of some symptoms (Bowling & Stewart, 2003). Others (Bever, 1999; Bielekova & Martin,
1999) have discussed additional treatment options for patients with MS, including traditional
therapy for the relief of pain, fatigue, and mood changes.
Perceptual Voice Signs and Symptoms The primary voice symptoms associated with multiple
sclerosis are impaired loudness control and harshness (Darley et al., 1972; Farmakides &
Boone, 1960; Hartelius, Buder, & Strand, 1997). Hypernasality is also prominent (Farmakides
& Boone, 1960), whereas impaired pitch control, inappropriate pitch level, and breathiness

TABLE 5.12 Speech deviations in multiple sclerosis

Speech deviation Percent
Normal speech performance 59
Defective speech performance 41
Impaired loudness control 77
Harshness 72
Defective articulation 46
Impaired emphasis 39
Impaired pitch control 37
Hypernasality 24
Inappropriate pitch level 24
Breathiness 22
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can occur less frequently. Speech characteristics include a slowing of speech rate, defective
articulation (Darley et al., 1972; Jensen, 1960), impaired emphasis (scanning speech), and
occasionally poor respiratory control (Table 5.13).
Acoustic Signs The range of fundamental frequencies produced by patients with multiple
sclerosis appears to be very similar to that of normal speakers, with the possible exception of a
slightly greater fundamental frequency range and larger variability of fundamental frequency
(Zemlin, 1962). In their study of five MS speakers, Hartelius, Nord, and Buder (1995) found
little difference in the fundamental frequency between their study participants, their normal
controls, and already published data. These authors also noted that their MS speakers exhibited
considerable variability in the various measurements they made.
Hartelius et al. (1997) analyzed the sustained vowel productions of 20 individuals with
MS and compared the results to 20 age- and gender-matched controls. Their method of
analysis focused on the stability (i.e., variation) of both fundamental frequency and intensity.
One unique acoustic analysis involved analyzing the sustained phonations for fundamental
frequency and intensity contours and then analyzing the results of those analyses for low-
frequency spectral components. One measure they derived involved looking at the magnitude
of the frequencies present in three low-frequency bands, 0 to 4 Hz, 4 to 6 Hz, and 16 to
19 Hz. They demonstrated distinct differences between the MS patients and their controls for
the low- and high-frequency bands. These authors concluded that this type of fine analysis of
variability and stability could be useful in helping to differentiate MS patients from normal
controls before any evidence of dysarthria was discernible.
Measurable Physiological Signs We know of no data on the measurable phonatory physio-
logical characteristics of patients with multiple sclerosis. If harshness is present, suggestive of
vocal fold hypertonicity, low flows and high subglottal pressures might be expected. The vibra-
tory cycle of the vocal folds is probably highly variable because of the harshness and impaired
muscle control.
Observable Physiological Signs In most patients, the larynx would be expected to appear
normal. In patients with abductor paralysis, vocal fold opening should be impaired, and the
patient may present problems related to air intake. There may be reduced range of motion of
the vocal folds and momentary stoppages of vocal fold motion.
We know of no data on the stroboscopic signs in multiple sclerosis. We might expect to
find good closure of the vocal folds (unless the patient is very breathy), but there may be a
reduction of the amplitude of vibration and perhaps poor phase symmetry.
Pathophysiology Multiple sclerosis is characterized by increasing incoordination, spasticity,
and weakness of the muscles in the body. When the laryngeal musculature is affected, these
same characteristics might be evidenced by impaired phonatory coordination and control
and by reduced range and force of movement. Spasticity and muscle weakness will affect the
ability of the vocal folds to adduct smoothly and to maintain the proper adductory forces
needed for phonation. Weakness of vocal fold adduction may mean an inability to produce
the proper subglottal pressures needed for speech. This will manifest itself in reduced vocal
loudness. The spastic characteristic of multiple sclerosis may impair the ability to maintain
control over vocal fold adduction and, therefore, may result in uneven vocal loudness. Poor
coordination of the vocal folds may produce aperiodicity of vibration and lead to greater
perceived hoarseness/harshness. The rate of movement of the vocal folds may also be impaired
similarly to the impaired rate of speaking (Jensen, 1960).
Treatment may involve various drugs to produce relief of symptoms such as spastic-
ity, fatigue, neurobehavioral disorders, paroxysmal disorders, pain, bladder dysfunction, and
cerebellar dysfunction (Mitchell, 1993). Immunotherapies may also provide benefits (Rolak,
2001).
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Miscellaneous Disorders
Arnold–Chiari Malformation (Chiari II Malformation)
The Arnold–Chiari malformation is a congenital anomaly of the hindbrain where the brainstem
and cerebellum are squeezed into the cervical portion of the spinal column, causing injury to the
cerebellum, medulla, and lower cranial nerves (Bralley, Bull, Gore, & Edgerton, 1978; Merritt,
1979). It was first described by Arnold (1894) and more extensively by Chiari (1896). There
are actually four types of malformations originally discussed by Chiari. Types I and II are often
referred to as the Arnold–Chiari type (Bamberger-Bozo, 1987; Salam & Adams, 1978). Type I is
one in which only the cerebellar tonsils are displaced. Types III and IV are much more severe and
in some cases incompatible with life. In type II, malformation of the medulla, cerebellum, and
mesencephalon are encountered usually with a lumbar meningomyelocele. Interestingly, many
of the clinical manifestations of type II occur after birth (Bamberger-Bozo, 1987). Infants will
usually have difficulty swallowing, apneic episodes, laryngeal paralysis, stridor, and occasionally
arm weakness. Most laryngeal paralysis is the abductor type.
In some cases, this malformation can result in vocal fold paralysis (Rullan, 1991) in which
voice symptoms will appear that are similar to cerebellar ataxia (discussed earlier) or to lesions
affecting the medulla or the peripheral nerves as they leave the cranium and causing flaccid
paralysis. In the latter case, perceptual, acoustic, and physiological signs as seen in recurrent nerve
paralysis would be expected (see “Peripheral Nerve Lesions” for a more complete discussion.)

Gilles de la Tourette Syndrome

Gilles de la Tourette syndrome develops in early childhood, usually between the ages of 2
and 13 years. It is characterized by twitching and grimacing, with tics of the face and eyes
being the most common symptom (Golden, 1977; Merritt, 1975). The tics may later spread
to the limbs. The speech of these individuals is characterized by unusual noises, explosive
outbursts, and the unexpected utterance of profanities. Contrary to most belief, coprolalia
(foul explicatives) and echolalia are not frequently heard in childhood. The disease increases
in severity during childhood, but the symptoms may diminish in adulthood. The disease can
usually be controlled by the use of the drug haloperidol, although there have been reports of
unwanted side effects in some patients. Lang and Marsden (1983) reported a case in which
spasmodic dysphonia developed during the use of haloperidol and persisted after removal of
the drug.
Gilles de la Tourette syndrome, although interesting and unusual, does not present any
unique challenges for the speech pathologist insofar as the voice is concerned. The symptoms are
not under voluntary control and cannot be altered or controlled through a behavioral approach.
It would appear that pharmacological treatment can be effective in reducing or eliminating the
symptoms.

Summary
Vocal fold vibration depends on an intact neurological system in order to maintain the proper
tension in the vocal folds, produce the proper airflow and air pressures needed for voicing,
and adduct or abduct the vocal folds in accord with the requirements of the speaking act.
Disruption of this control will affect the normal vibration of the vocal folds. This disruption
may occur either in the central or the peripheral nervous system. When lesions occur in the
peripheral nervous system, the phonatory system will show signs of denervation and flaccidity.
The muscles controlled by the nerves will fail to receive the proper innervation and will not
contract.
When lesions occur within the central nervous system, the phonatory system may show
signs of flaccidity or hyperfunction depending on the site of the lesion(s). Lesions high in the
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central nervous system but not in the cortex affecting the pyramidal or extrapyramidal systems
will produce hypertonia and exaggerated reflexes. Lesions in the cerebellum will produce deficits
in the control of muscles, especially groups of muscles needed for the complex motor act of
speech. The signs and symptoms of phonatory difficulty that develop will depend on the site
of lesion. A good working knowledge of the appropriate physical signs and symptoms as well
as the voice signs and symptoms is needed before the clinician can properly diagnose and/or
understand the nature of the difficulty presented by a patient. In this chapter we have presented
an overview of many different neurological problems in which voice may be affected, including
Parkinson’s disease, myasthenia gravis, amyotrophic lateral sclerosis, Shy–Drager syndrome,
multiple sclerosis, cerebellar ataxia, spasmodic dysphonia, essential tremor, and many of the
problems that may affect the recurrent and superior laryngeal nerves when they exit the central
nervous system or as they travel in the neck and thorax to their ultimate destinations.
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CHAPTER

6
Voice Problems Associated with
Organic Disease, and Trauma
Keywords
trauma, keratosis, granuloma, contact ulcer, pachydermia, papilloma, ankylosis, varix,
ectasia, carcinoma

The conditions discussed in this chapter represent organic disease states that have an effect on phonation.
The etiology of these conditions is unrelated to ways in which the voice has been used, and their treatment
is primarily medical and/or surgical. It is important for clinicians to be familiar with these conditions and
their effect on phonatory physiology and to be prepared to offer the appropriate level of service as the
need for it becomes timely. It is often the case that the speech-language pathologist provides presurgical
treatment counseling and, secondarily, is called upon to provide voice therapy along with or subsequent
to medical or surgical intervention. The conditions include keratosis, granulomas, pachydermia laryngis,
ankylosis of the cricoarytenoid joint, papillomas, carcinoma and other malignancies, blunt or penetrating
trauma, and chemical or heat trauma.

Benign Lesions
Keratosis
Primary Voice Symptom: Hoarseness
Description and Etiology
Keratosis refers to epithelial lesions in which there is abnormal tissue growth on the vocal folds (Fig. 6.1).
This usually originates in epithelium but may enter the superficial layer of the lamina propria. Other
terms may be used to describe this condition, including leukoplakia, hyperkeratosis, keratosis with
cellular atypia, and dyskeratosis. According to Frangez, Gale, and Luzar (1997), leukoplakia is a clinical
term that describes a whitish patch on the laryngeal mucosal, whereas keratosis is a histological term
indicating a pathological condition and the accumulation of keratin on the epithelial surface. Two kinds
of lesions may be seen: flat, white, plaque-like lesions (leukoplakia) or irregular growth of epithelium
that results in a warty lesion (papillary keratosis). There is a full spectrum of premalignant laryngeal
tissue changes observed in smokers that are not seen in nonsmokers (U.S. Dept. of Health and Human
Services, 1985). These lesions must be carefully monitored.
Smoking, environmental pollutants, and other factors have been implicated in the development of
keratotic epithelium on the vocal folds. These lesions tend to occur more often in men than in women.
Gastroesophageal reflux disease (GERD) has also been implicated as an etiology of these tissue changes
(Cohen, Bach, Postma, & Koufman, 2002; Koufman, 1991). The lesions may be unilateral or bilateral
but are usually asymmetric in appearance. The glottal edge is often rough.

Perceptual Signs and Symptoms

The primary symptom is hoarseness or roughness in the voice.
165
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FIGURE 6.1. Hyperkeratosis of the

vocal folds. See color plate.

Acoustic Signs
There are few data available on the acoustic characteristics of patients with keratosis of the vocal
folds. Due to the growths on the vocal folds, greater-than-normal frequency and amplitude
perturbation as well as greater-than-normal spectral noise would be expected.

Measurable Physiological Signs

Minimal measurable physiological data exist on patients with keratosis of the vocal folds. Iwata,
von Leden, and Williams (1972) reported a mean airflow rate of 227 ml/sec for patients with
leukoplakia of the vocal folds. Lesions that might have a similar effect (papilloma, epithelial
hyperplasia) also show greater-than-normal airflows (see Table 3.6 in Hirano, 1981b).

Observable Physiological Signs

In patients with leukoplakia, there will be whitish plaque-like lesions on the mucosal surface
of the vocal folds. These may be limited in extent or may cover almost the entire vocal fold.
Ballenger (1985) reports that another form of this lesion, papillary keratosis, may show a piling
up of small, reddish epithelium or an irregular mucosa covered by keratin.
Because these lesions can be so variable in extent and in location on the folds, their
stroboscopic appearance will vary. Vocal fold edges may be rough and result in an irregularly
shaped glottic chink on vocal fold closure. There will be asymmetric behavior and aperiodicity.
In extensive lesions, diminished amplitude of lateral vocal fold excursion and limited mucosal
wave, especially over the sites occupied by the lesion, are seen. Colden et al. (2001) studied the
amplitude of vocal vibration and the mucosal wave in 62 patients with a diagnosis of keratotic
lesion. The lesions of 45 of these patients were subsequently identified as intraepithelial keratosis
and 17 as cancer. Four judges blind to the diagnoses rated the amplitude of vibration and lateral
extent of the mucosal wave. Only two of the intraepithelial lesions were rated as normal with
respect to both amplitude of vibration and lateral extent of the mucosal wave. According to the
authors, neither reduced amplitude of vibration and/or reduced mucosal wave were predictive
of the presence of cancer. They conclude that the presence of a mucosal wave probably indicates
that the vocal ligament is not extensively involved.

Pathophysiology
Keratotic-type lesions, for the most part, affect the cover, increasing its mass and stiffness.
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CHAPTER 6 I Voice Problems Associated with Organic Disease, and Trauma 167

FIGURE 6.2. Contact granuloma involv-

ing the posterior part of the glottis.

Laryngeal Granulomas
Primary Voice Symptom: Hoarseness
Description and Etiology
Laryngeal granulomas most commonly are a complication of intubation (Fig. 6.2). Their
development may be an early complication occurring at some point between intubation and
extubation, or a late complication, the morbid sequelae of extubation (Balestrieri & Watson,
1982). The passing of an intubation tube between the vocal processes may be necessary in
order to provide access to the airway for purposes of delivering anesthesia and maintaining
appropriate oxygenation during a surgical procedure. Intubation may also be necessary in
nonsurgical situations to maintain adequate oxygen supply for persons in need of respiratory
assistance. Contact between the tube and the vocal processes may occur at the time of intubation
or with the tube in situ. During such contact, the mucosal perichondrium of the vocal processes
may be traumatized, causing a small ulcer to appear on the vocal process. The bare process will
eventually be covered by granulation tissue, which will become epithelialized and present as
a granuloma. The condition is surprisingly uncommon in light of the frequency with which
intubation is required, and spontaneous resolution occurs within a few weeks in most cases. The
incidence of granuloma is dependent on factors such as duration of intubation, the method of
intubation, the patient’s age and general condition, nursing techniques, and other factors. All
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reported cases have occurred in patients aged 15 years or older, and women are more prone to
develop an intubation granuloma because of small laryngeal size and a thinner mucosal layer
covering the vocal processes (Snow, Hirano, & Balogh, 1966).
Endotracheal intubation is being accepted for longer and longer periods of time. Although
it is not a benign procedure, mortality and morbidity rates, when compared to the option of
tracheotomy, are much lower. Weymuller (1988) presents a thorough review of the pertinent
factors relating to endotracheal injury, its nature, the biomechanical factors of the tube itself,
and the efforts made to prevent injury from the procedure.

Perceptual Signs and Symptoms

The symptoms of granuloma are breathiness and hoarseness. Some may not affect phonation
due to their location.

Acoustic Signs
There are no data on the acoustic characteristics of patients with granulomas. Greater-than-
normal frequency and amplitude perturbation would be expected, and depending on the severity
of the hoarseness, greater-than-normal spectral noise could be present.

Measurable Physiological Signs

Normal airflow rates have been reported in patients with contact granulomas (see Table 3.7 in
Hirano, 1981b). Very little other physiological data are available on the physiological charac-
teristics associated with granulomas of the vocal folds.

Observable Physiological Signs

Granulomas manifest themselves laryngoscopically as irregularly shaped masses of tissue either
at the site of the vocal processes of the arytenoids (if an intubation granuloma) or elsewhere on
the vocal folds or larynx.
The vocal folds will show normal stroboscopic signs unless the granuloma appears on the
vocal fold margins. In that case, glottic closure may be incomplete and we would expect to
see reduced amplitude of lateral excursion of the affected vocal fold(s) and some degree of
disturbance of the mucosal wave.

Pathophysiology
Intubation granulomas primarily affect the mucosa of the vocal processes of the arytenoids.

Vocal Process Granuloma (Contact Ulcer)

Primary Voice Symptom: Hoarseness
Description and Etiology
Vocal process granuloma is a benign lesion affecting the vocal process of the arytenoid cartilage.
These lesions have been given a variety of names in the literature, including contact ulcer, contact
granuloma, arytenoid granuloma, and vocal process granuloma. We prefer the term vocal process
granuloma to refer to all of these type lesions as suggested by Hoffman et al. (2001). Usually, a
small ulceration develops on the medial surface of the vocal processes of the arytenoid cartilages.
The ulceration may be unilateral or bilateral and may present a “cup and saucer” appearance,
with a protuberance on one side and a crater or concavity on the other. Continued irritation
results in an ulceration on one side and the production of granulation tissue on the other.
The thinking about the etiology of vocal process granulomas has undergone major change
within the recent past. The traditional view had been that they occurred predominantly in
adult males with an average age of 50 years (Peacher, 1947) who engaged in a great deal of
forceful, aggressive speaking, the so-called type A personality.
In support of that view, von Leden and Moore (1960) described some of the anatomical
and physiological variations of phonation that could contribute to the formation of a vocal
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process granuloma. They pointed out that at low pitches the arytenoids oscillate vigorously,
in a rocking-type motion. Thus, at low pitches it is more likely that the arytenoids would be
subjected to greater trauma. They also observed that at low pitches, there is greater vocal fold
approximation, the approximation is prolonged, and it tends to persist beyond the vibratory
phase of the vocal folds. Greater loudness will also increase the degree of approximation as well
as its duration. Harsh, guttural sounds will increase the force of approximation of the vocal
folds, as will other nonphonatory acts (throat clearing, etc.). Voice therapy was a treatment
course often followed but with little documentation of its efficacy. Vocal process granulomas
were often surgically excised, but they showed a propensity to recur.
In a study relating gastric reflux to vocal process granulomas, Cherry and Margulies (1968)
studied three patients who showed evidence of peptic ulcer. All were treated with antacids,
reduced food intake at night, and elevation of the head during sleep, and all experienced
resolution of the ulcer. Delahunty and Cherry (1968) demonstrated that continued exposure
of the arytenoid vocal processes to stomach acids would create ulcers and granulation tissue
in dogs in about a month’s time. Histologically, these lesions exhibited epithelial necrosis with
an organized fibrous exudate beneath. Submucosal edema and nonspecific inflammation were
also described. In a control condition, saliva was applied to the arytenoids over the same time
period, with no development of granulation tissue. Ward, Zwitman, Hanson, and Berci (1980)
reported that vocal process granulomas result from constant throat clearing that is secondary to
irritation of the mucosa due to gastroesophageal reflux (regurgitation of peptic acids, especially
at night), and with less frequency to irritation from nasal secretions (postnasal drip). They
further reported that of 28 cases, only 2 failed to respond to medical treatment. Feder and
Michell (1984) divided ulcers into two groups: hyperfunctional and hyperacidic. Watterson,
Hensen-Magorian, and McFarlane (1988) reported that 51% of their patients with a vocal
process granuloma also exhibited a hiatal hernia. It had been thought that hiatal hernia and
GERD were two parts of the same problem. According to Bozymski (1993), most hiatal hernias
are now thought to be normal variants of the anatomy. Thus, it would appear that the etiology
of vocal process granulomas may be primarily related to reflux with hyperfunctional vocal abuse
being a contributory factor.
Benjamin and Croxson (1985) reported clinical and histological similarities between vocal
process granulomas and other laryngeal granulomas. They studied 16 patients, of whom 7 had
postintubation granulomas and the remainder contact ulcers. The most common symptom of
all patients was hoarseness. They concluded that vocal process granuloma was not a precursor
to granulomas since the history of the problems was different and the patient with a granuloma
did not present the profile of a patient with a vocal process granuloma. There is considerable
literature to implicate GERD as the primary etiology of vocal process granuloma, and, further,
postnasal drip is also thought to be related to the same process of mucosal irritation resulting
from the reflux of gastric juices (Bozymski, 1993; Deveney, Benner, & Cohen, 1993; Gaynor,
1991; Koufman, 1991; Wilson, Pryde, Cecilia, & MacIntyre, 1989).

Perceptual Signs and Symptoms

The primary perceptual symptoms of a vocal process granuloma are low pitch, throat clearing,
and vocal fatigue. There may be a breathy voice with some hoarseness, accompanied by dis-
comfort, or even severe, stabbing pain. The pain is usually unilateral and located in the area of
the greater horn of the thyroid. The pain may radiate to the ear. There is usually the constant
feeling of something in the throat, which accounts for the continual throat clearing.

Acoustic Signs
Depending on the severity of the voice symptoms, some increased frequency perturbation
and spectral noise may be present in the voice. Several investigators have reported lower-than-
normal fundamental frequency of vibration (Hillman et al., 1989; Ylitalo & Hammarberg,
2000). If the voice is hoarse, greater-than-normal frequency and amplitude perturbation would
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be expected, but Ylitalo and Hammarberg (2000) reported no significant changes of frequency
perturbation in the group of 19 male patients. It is also possible that little or no abnormal acoustic
characteristics may be present. Verdolini, Hoffman, and McCoy (1994) reported on one patient
whose only abnormal finding was higher-than-normal phonatory effort during singing.

Measurable Physiological Signs

Isshiki and von Leden (1964) reported a mean flow of 144 ml/sec for their group of patients
with contact ulcers. This value is not much higher than would be expected in normal speakers.
However, Hillman et al. (1989) found significantly higher airflows in their two patients with
a contact ulcer. Both patients also had higher-than-normal open quotients when phonating at
normal loudness. Hillman et al. (1989) also reported that subglottal air pressures were within
normal limits for their two patients. Muscle activity levels should be within normal limits.

Observable Physiological Signs

Laryngoscopically, a vocal process granuloma will be visible as a buildup of pink or pinkish-
white tissue on one of the vocal processes of the arytenoids. This usually occurs at the tip of the
process, but it is possible to find such an outgrowth elsewhere on the vocal process or on the
lower base of the arytenoid. On the contralateral process, there may be injection of the mucosa
or a depression. This has been described as the “cup and saucer” appearance because the two
processes fit together in that way. Inflammation of the arytenoids and the posterior pharyngeal
wall may be seen. In the early stages of vocal process granuloma development, even prior to
tissue outgrowth, a strand of mucus may be seen between the two processes. This is referred to
as a vocal process granuloma diathesis.
Unless there are abnormal voice symptoms, normal stroboscopic features would be anti-
cipated.

Pathophysiology
Since the vocal process granuloma does not involve the membranous vocal fold, there will be
little change in the mass or stiffness of the cover, transition layers, or body.

Pachydermia Laryngis
Primary Vocal Symptom: Hoarseness
Description and Etiology
This is a relatively rare problem whose etiology is unknown. Some suspect smoking to be
the major cause and others suspect irritation caused by GERD. Pachydermia laryngis is char-
acterized by a thickening of the epithelium with acanthosis and keratosis (Ballenger, 1985).
Clinically it appears as a whitish mass of tissue in the interarytenoid space. The membranous
vocal folds may also be injected and thickened. Conservative treatment usually consists of
cessation of smoking and alcohol use and treatment (behavioral and pharmacological) of the
GERD. Surgical removal may be necessary.

Perceptual Signs and Symptoms

Hoarseness will be a primary perceptual sign of this disease.

Acoustic Signs
Little data exist on the acoustic signs for this vocal problem. A lower fundamental frequency
may be expected if the vocal folds are thickened sufficiently.

Measurable Physiological Signs

We have no knowledge of physiological data on this vocal problem. One might expect that if
the lesion interfered with glottal closure, excessive airflows would result.
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Observable Physiological Signs

On direct or indirect laryngoscopy, the vocal folds may look thickened and rough, and there is
an excess of rough, uneven tissue present in the interarytenoid space.
We know of no data concerning the stroboscopic signs associated with pachydermia laryn-
gis. However, we would expect that glottal closure might be compromised, and mucosal wave
and amplitude may be reduced due to the thickened mucosa.

Papilloma
Primary Voice Symptom: Hoarseness
Description and Etiology
Papilloma is a rather common benign tumor that starts in the epithelium and is thought to
be caused by a virus, usually the human papilloma virus types 6 and 11. It occurs in both
children and adults. In children, it is referred to as juvenile papilloma; there are an estimated
4.3 cases/100,000 population, and it is very resistant to eradication. Surgical excision is required,
as papillomas tend to proliferate and can obstruct the airway. It is not uncommon for children
with this problem to require multiple surgical excisions before the condition runs its course. If
juvenile papilloma persists or begins in adulthood, it continues to be a condition that is highly
resistant to treatment. Adult papilloma occurs about 1.8 cases per 100,000 population.
The papilloma may occur in various parts of the larynx: subglottally, at the level of the vocal
folds, and supraglottally. It is sometimes necessary for children with aggressive papilloma growth
to undergo tracheotomy. When the papillomas have ceased recurring, or perhaps between
episodes of recurrence, voice therapy may be appropriate in order to maintain or restore the
best possible voice production. The prognosis will depend largely on the state of the vocal fold
mucosa.

Perceptual Signs and Symptoms

Hoarseness is the primary symptom and sign of the voice disorder caused by this condition.
Other symptoms include low pitch, breathiness, and a strained voice in the adult patient. In
the child, there may be a weak cry, chronic cough, swallowing difficulties and stridor.

Measurable Physiological Signs

We know of no measurable physiological data reported for individuals with papillomas of the
vocal folds. However, because of the increased stiffness of the cords we might expect greater
expiratory air pressures.

Observable Physiological Signs

Laryngoscopy A papilloma will typically present as a whitish cluster of tissue, somewhat
comparable in texture to a raspberry. An example of the laryngoscopic appearance of a papilloma
is shown in Figure 6.3. In Figure 6.4, multiple papillomas are evident, illustrating the potentially
extensive nature of the disease.
Stroboscopy Papillomas will often interfere with glottal closure. To what extent this is true
will depend on the extent of the lesion. The increased stiffness created by the lesion will impede
horizontal excursion of the folds, and mucosal wave will be absent in the area of the lesions.
When multiple surgical excisions have been required for vocal fold papilloma, the membranous
cover of the vocal folds may have been sufficiently damaged to interfere with amplitude and
vibratory behavior.

Pathophysiology
Papillomas affect vocal fold vibration by increasing the mass and the stiffness of the vocal folds
and altering the biomechanical characteristics of the mucosa. Although they can be removed
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172 Understanding Voice Problems

FIGURE 6.3. Papilloma of the

vocal folds. See color plate.

surgically, the lesions tend to recur, especially in children (Bastian, 1986). Surgery is usually
the treatment of choice and includes traditional knife surgery as well as CO2 laser (Simpson
& Strong, 1983). Various other treatments have been tried, including interferon (Benjamin
et al., 1988; Leventhal, Kashima, & Mounts, 1991; Sessions, Dichtel, & Goepfert, 1984;
Sessions, Goepfert, & Donovan, 1983), photodynamic therapy (Abramson, Shikowitz, Mul-
looly, Steinberg, & Hyman, 1994), and various drugs (Indole-3-carbinol, Ribavirin, Acyclovir,
and others; Avidano & Singleton, 1995).

FIGURE 6.4. Multiple papillomas of the vocal folds.

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Ankylosis of the Cricoarytenoid Joint

Primary Voice Symptom: Hoarseness
Description and Etiology
Fixation of the cricoarytenoid joint may be due to several causes, including arthritis, trauma,
or joint disease. Ankylosis of the cricoarytenoid joint is sometimes difficult to distinguish from
paralysis of the vocal folds. Clinically they appear very similar (Cummings, 1986). However,
pain may be a symptom of ankylosis due to arthritis and would usually not be a symptom
of paralysis. An attempt to manipulate the joint under direct laryngoscopy may be necessary
in order to distinguish between the two conditions. Treatment of ankylosis requires surgical
arytenoidectomy or arytenoidopexy (Ballenger, 1985). Voice therapy is usually not helpful.

Perceptual Signs and Symptoms

The primary perceptual symptoms of unilateral arytenoid fixation are hoarseness and breathiness
secondary to the anticipated inadequacy of posterior vocal fold closure. In the event that the
condition is bilateral, stridor may be present, and the patient may display symptoms of dyspnea.

Acoustic Signs
We know of no experimental data concerning the acoustic characteristics of voice in the presence
of cricoarytenoid ankylosis. In unilateral ankylosis, these might include increased frequency
and amplitude perturbation (jitter and shimmer), reduced phonational and dynamic ranges,
increased spectral noise, and reduced phonation time. Acoustic signs in bilateral ankylosis may
be minimal.

Measurable Physiological Signs

Physiological signs of ankylosis are not documented. As with unilateral vocal fold paralysis, if
the glottis is not fully adducted during phonation, we would expect increased airflows and a
glottogram that would reveal the incomplete closure and reduced closed time. On the other
hand, in the bilateral condition, airflows might be expected to be reduced, and the glottogram
should reveal minimal vocal fold opening phase.
One would also expect normal electrical activity of the muscles of the larynx.

Observable Physiological Signs

As noted previously, the laryngeal appearance of ankylosis might be difficult to distinguish from
vocal fold paralysis. If unilateral, we would expect to observe lack of movement of the arytenoid
and incomplete glottal closure. In bilateral ankylosis, the position of both arytenoids would
be fixed and unmoving, resulting also in lack of either adduction or abduction of the folds.
We have observed that, in paralysis, movement in the opening of the pyriform sinuses may be
absent, whereas in ankylosis such movement continues to be present. If the cause of ankylosis
is an arthritic condition (usually rheumatoid arthritis), mucosal edema, inflammation, or both
may be seen in the area of the cricoarytenoid joint.
We know of no data on the stroboscopic signs of a fixed arytenoid. One might expect to
see incomplete glottal closure, but minimal aberrations in the vibratory motion of the vocal
folds.

Pathophysiology
The movement of the ankylosed arytenoid cartilage(s) is reduced or absent. The glottis may be
incompletely adducted, or, in the case of bilateral ankylosis, it may be neither fully adducted
nor abducted.
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Vascular Disorders
Hemorrhage
Primary Voice Symptom: Hoarseness, Occasional or Intermittent Aphonia,
and Loss of Pitch Range
Description and Etiology
Hemorrhage into the vocal fold is usually unilateral, although it may be bilateral. It can involve
the full length of the vocal fold or portions of the fold. The hemorrhagic area appears reddish
in color with significant swelling. Hemorrhage is most frequently the result of a single episode
of traumatic voice use or laryngeal trauma, or it can result from the combination of heavy
voice use and use of anticoagulants and salicylates (such as aspirin), or extended use of inhaled
steroids. Neely and Rosen (2000) reported on the case of an opera singer on Coumadin who
developed a hemorrhage that seriously restricted her ability to sing.

Perceptual Signs and Symptoms

Patients may complain of pain particularly at the time of the precipitating event. Dryness,
vocal fatigue, and loss of upper range are among the perceptual symptoms that accompany the
primary symptom and sign of hoarseness. Depending on the severity of the bleed, the voice
may be intermittently aphonic, and it may require added effort for voicing to be produced.
Vocal fold hemorrhage occurs more frequently in women than in men and usually in adults
(Lin, Stern, & Gould, 1991).

Acoustic Signs
Although there are no data for this population, we would anticipate increased shimmer and
jitter related to the hoarseness that is perceptible. We would also expect decreased signal-to-noise
ratio, restricted pitch, and dynamic ranges.

Measurable Physiological Signs

We would expect subglottic air pressures to be increased as the patient must exert greater effort
to produce phonation. Increased air flows may also be noted as a result of the limitations in
laryngeal valving due to stiffness of the hemorrhagic cord.

Observable Physiological Signs

As noted in the description, hemorrhage is visible when the vocal folds are visualized by the
apparent redness of the area of the fold involved, the significant swelling present, and the
stiffness of the cord. A prominent blood vessel may be seen.
Under stroboscopic observation, stiffness of the hemorrhagic vocal fold or part thereof
is apparent with reduced amplitude of the involved fold and absence of mucosal wave in the
area of the hemorrhage. Glottal closure may vary in degree, depending on the amount of
stiffness and swelling. The vocal fold edge usually remains straight as long as the hemorrhage
has not organized into a specific lesion such as a hemorrhagic polyp. Because the lesion is
usually unilateral, asymmetry of movement between the vocal folds would be apparent as
would aperiodicity.

Pathophysiology
Rupture of blood vessels results in bleeding into the submucosal layer. This produces extreme
swelling of that area decreasing the efficiency of the vibratory behavior of the vocal folds. The
mass and stiffness of the cover are increased.
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Varix and Ectasia

Primary Voice Symptom: Hoarseness
Description and Etiology
A varix is seen as a prominent, distended, lengthened, and tortuous blood vessel on the surface
of the vocal fold. The location of a varix may be either on the superior surface of the fold or
on the free edge of the fold. A varix is often visualized following resorption of a hemorrhage
or in conjunction with a hemorrhagic polyp. We have also observed varices in the absence of
a known previous hemorrhage. The etiology seems to be related to vocal abuse or trauma and
usually results from a single or focused short-term episode of abuse.
Ectasia is defined as a dilation of a small vessel. Occasionally, vascular microectasias are
seen on the surface of the vocal folds, which may affect vibration in that location.

Acoustic Signs
These signs will vary depending on the size and location of the varix or ectasia. When hoarseness
is present we would anticipate increased shimmer and jitter magnitudes.

Measurable Physiological Signs

Airflow should not necessarily show any change from normal unless the varix is large or ectasias
are extensive enough to create vocal fold stiffness and interfere with glottal closure.

Observable Physiological Signs

Laryngoscopy Varices and ectasias may be seen on the surface of the vocal folds as increased
vascularity not normally present (Fig. 6.5). When a hemorrhagic polyp is present, it is often
possible to visualize a prominent blood vessel leading directly to the polyp, suggesting that the
vessel is “feeding” the polyp and is a factor in its presence.
Stroboscopy The area of the varix or the ectasia may appear stiffened with reduced mucosal
wave. The effect on vibratory behavior of the fold will be in direct relation to the location and
the extent of the varix or the ectasia. A small varix on the superior surface of the fold may have
minimal effect on the vibratory characteristics of that fold, whereas a large vessel along the edge
or even on the superior surface of the fold will limit mucosal wave and perhaps amplitude of
lateral excursion of the fold. Glottal closure pattern will also vary depending on the size and
location of the lesion.

FIGURE 6.5. Vocal fold ectasia.

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FIGURE 6.6. Laryngeal web.

Pathophysiology
The varix is usually in the submucosal layer and the amount of distortion of that layer will
depend on its size. A large varix or large cluster of small vessels will increase stiffness and mass
of the cover. If a varix is the residual effect of a hemorrhage, full resorption of the hemorrhage
may not have occurred and the behavior of the fold will be affected by that as well.

Laryngeal Web
Primary Voice Symptom: Hoarseness
Description and Etiology
Laryngeal webs (Fig. 6.6) are often congenital and are a result of incomplete maturation of the
developing larynx. Webs are often manifested as a sheet of tissue between the vocal folds, usually
at the anterior end. Typical symptoms in the child include a weak cry, difficulty breathing, and
stridor. In the adult, the complaint is hoarseness, high pitch, and, perhaps, shortness of breath.
Small webs at the anterior commissure may present few problems, whereas extensive webs could
necessitate a tracheotomy. Treatment typically consists of surgery to split the web, but, unless
the surgery is carefully performed, the possibility of a refusion of the web is very possible.

Perceptual Signs and Symptoms

Typically, the major signs are hoarseness and a high pitch. In a child, there may be a weak cry.
The high pitch may be due to the shortening of the effective vibrating length of the vocal fold
due to the attachment of the web between the two vocal folds. The web also will interfere with
the normal vibratory movements resulting in the hoarseness.

Acoustic Signs
Little data exist on the acoustic signs of a laryngeal web. One would expect acoustic features
consistent with increased frequency and amplitude perturbation. If the patient has a higher-
than-normal pitch level, a higher-than-normal fundamental frequency of phonation would be
expected.

Measurable Physiological Signs

We know of no data concerning the airflow or air pressure characteristics of children or adults
with a laryngeal web. Since the web would restrict the vibratory amplitude of the vocal folds,
a decreased airflow might be expected. Air pressure could be elevated if the patient is trying to
force vibration.
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CHAPTER 6 I Voice Problems Associated with Organic Disease, and Trauma 177

Observable Physiological Signs

Stroboscopically, the patient with a web would show decreased amplitude of vibration and no
mucosal wave in the area of the web. If the voice is hoarse, the periodicity of vocal fold vibration
would be affected.
Pathophysiology
The attachment of tissue to the margins of the vocal folds would limit their vibratory motions
and produce instability. Moreover, the attachment of the web would limit the effective vibrating
length of the vocal folds producing a higher-than-normal pitch. Often, voice symptoms take a
back seat to establishing an airway, thus making it easier for the patient to breath.

Blunt or Penetrating Trauma

A variety of traumatic injuries may affect the larynx. These may include attempted strangulation,
a penetrating neck wound, blunt trauma resulting from a blow to the neck or from the body’s
being hurled with force, and the neck’s striking an object. In severe trauma, the structures of
the larynx may be fractured or severely damaged, compromising the airway and resulting in
vocal difficulty. An example of the effects of trauma to the vocal folds is shown in Figure 6.7.
Most cases of blunt or penetrating trauma require medical/surgical treatment. The most
urgent concern is management of the airway. Subsequently, there will be an attempt to repair or
reconstruct the damaged structures. Voice restoration, following the completion of the repair,
may be very difficult. A speech-language pathologist may be asked to help the patient achieve
the best-possible voice. In these cases, the speech-language pathologist should ask for, and expect

FIGURE 6.7. Trauma of the vocal folds.

Note the obliteration of clear definition of ei-
ther vocal fold due to the formation of a web
that has grown after trauma. There is also ex-
cessive vascularization of the folds. See color
plate.
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178 Understanding Voice Problems

to receive, detailed information about the altered laryngeal anatomy, in order to understand
the constraints on the system and to be able to plan the treatment approach accordingly.

Inhalation and Thermal Trauma

There is a paucity of information in the literature about the long-term laryngeal and phonatory
sequelae of the inhalation of gases, smoke, or steam. Inhalation injuries are usually referred
to as chemical tracheobronchitis, a term that seems to exclude laryngeal and supraglottal effects
of such injury even though they occur as frequently and almost always with greater severity
(Hunt, Agee, & Pruitt, 1975; Miller, Gray, Cotton, & Myer, 1988). Hot fumes cause reflex
closure of the glottis, which, in combination with the cooling capacity of the upper respiratory
tract, protects the trachea and lower tract (Miller et al., 1988). Acute airway obstruction can
result from either supraglottal or laryngeal edema, or both. Hunt et al. (1975) point out that
laryngeal and supraglottal structures tend to show massive amounts of edema in a short period
of time due to the loose attachment of the surface mucosa to the underlying basal layers.
During the acute stage, those who suffer inhalation injury are frequently at risk for survival,
making their medical condition and treatment of the utmost urgency. The severe edema of
the respiratory tract may appear immediately or may develop within a matter of hours and
can quickly lead to airway obstruction and to death (Crapo, 1981; Cudmore & Vivori, 1981).
Intubation or tracheotomy may be required. A risk of intubation is the possibility of damage
to the already compromised mucosal tissue. Symptoms of inhalation trauma include swelling,
inflammation, burns, or soot around the nose and mouth and in the oropharynx (even with
minimal body surface injury), respiratory distress, stridor, wheezing, and hoarseness (Crapo,
1981). The symptoms will depend on the severity of the trauma, the type of fumes or gases
inhaled, and the stage of the body’s response to the trauma. The trauma may result not only
from heat but also from the particles and toxic chemicals released as the burning material breaks
down and from the reduction in oxygen. The heat capacity of steam is 4000 times greater than
that of air; thus, steam inhalation can quickly produce thermal burns of the respiratory tract.
Steam inhalation burns may occur with a scald injury in young children. According to Cudmore
and Vivori (1981), inhalation of hot, dry gases causes damage primarily to the upper airway
(including the larynx) because there is a rapid decrease in temperature of the gases as soon as
they enter the airway. Chemical damage to the entire airway results from inhalation of smoke.
Smoke from the combustion of polyurethane foams is reported to be especially damaging (Dyer
& Esch, 1976). This fact is all the more disturbing in view of the increased numbers of house
fires resulting in more inhalation burns in children (Chisnall, 1977) and the increased use of
plastics and polyurethane foam in homes.
Voice can only become a concern after the patient has survived the acute stage of trauma
and has completed the major portion of treatment for the injuries sustained. If there has been
extensive body-surface burn in addition to the inhalation injuries, treatment may be quite
lengthy. Only when the patient is sufficiently recovered is it appropriate to focus on aspects
of vocal recovery. However, during the recovery period, consultation by the speech-language
pathologist may be helpful in establishing the most efficacious means of communication for
patients whose ability to communicate has been significantly compromised.
As noted previously, there is little documentation of the long-term effects of laryngeal
trauma on the voice. Close, Catlin, and Cohn (1980), reporting on the chronic effects of
ammonia inhalation burns, cite one case in which breathy phonation was present and showed
some improvement with voice therapy. In another instance, severe and progressive hoarseness
noted in the early posttrauma stage apparently resolved spontaneously. 22 patients who had
been treated in the regional burn unit at the SUNY Health Science Center over a 10-year period
were examined for voice problems (Casper, Clark, Kelly, & Colton, 2002). Of these, 11 (50%)
were judged by an experienced voice clinician to show some degree of voice abnormality that,
according to patient reports, was not present prior to the trauma. Although most of the patients
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so identified had been either intubated or tracheotomized, or both, some patients had not
experienced either of these procedures. Thus, injury resulting from intubation or tracheotomy
cannot fully account for the resulting voice abnormality.
In view of these findings, we would suspect that there are more residual voice problems in
inhalation-burn survivors than have previously been recognized. The pathophysiology is not
well understood and may differ from patient to patient. There are many unanswered questions
relative to phonatory function in this population, such as whether problems result from changes
in laryngeal mucosa, peripheral nerve damage from the burn or from subsequent surgery, or
central nervous system damage due to hypoxia.
Our experience in voice therapy with this population is very limited. Nevertheless, the
case study of C. H. is instructive.

Case Study
C.H. was a 17-year-old young man who had suffered extensive burns of the head, neck, face,
hands, and upper body following the crash of an ultralight plane that he had been flying alone.
He also suffered inhalation injury. His treatment course included two periods of intubation,
the first for a week and the second for 4 days, with a 2-day intervening period. He survived
a long and painful course of treatment and surgeries. Although now he was being followed as
an outpatient, he faced further surgery in the future. He was in constant physical pain and
discomfort, and his emotional pain due to his grotesquely deformed appearance was perhaps
even greater. He was essentially aphonic, as he had been throughout the entire posttrauma
course. Ear, nose, and throat examination was reported to be negative, with no observable
reason for the aphonia. The vocal folds were reported to show good movement, although they
did not adduct completely during speaking.
C.H. responded minimally to questions, offered no information spontaneously, and did
not make eye contact with the clinician. He generally kept his eyes downcast or looked out of
the window. Several sessions were required to work through this resistance and to establish a
relationship. As he began to open up, C.H. talked more about the crash, and also about his
parents, who were divorced. He was living with his mother; he would have preferred to have
been with his father, but the accident had occurred during a time spent with the father, who
was apparently finding the guilt related to the event overwhelming. C. H. was supposed to be
returning to school but had thus far been resisting that because he saw himself as a “monster”
whom others saw as disgusting. As therapy progressed, C.H. was increasingly willing to attempt
voicing. Indeed, he was able to produce voice, but with a hoarse and somewhat breathy quality.
The sound of this voice was just one more abnormality that he could not deal with, and his
response had been to be aphonic. Work with C.H. continued for a period of time, during which
he began to use voice routinely and with some improvement in quality. He was clearly in need
of psychological counseling but had previously refused to consider such referral. Leading him
to an acceptance of such counseling had been one of the goals of therapy, and, indeed, after his
experience with us, he was able to accept the support that had been offered and to recognize
his need for continuation of such support. Although his voice quality was not “normal,” C.H.
was using voice routinely and finding that communication was easier.
The reason for C.H.’s hoarse voice quality was never fully understood. However, more test-
ing, given his initial level of resistance and the subsequent determination of his very vulnerable
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180 Understanding Voice Problems

psychological state, was not entirely necessary and might have resulted in his withdrawal from
further therapy. He made sufficient progress so that his voice was entirely usable and, although
still hoarse, was not severely so. The reason for his aphonic presentation appeared to be pri-
marily psychological. This case highlights the need to be alert to more than a single problem
being present at one time, especially when there may be an obvious cause that might explain
the problem.

Carcinoma and Other Tumors

Carcinoma
Primary Voice Symptom
The primary voice symptom of laryngeal cancer is hoarseness. Indeed, this is recognized as one
of the seven warning signs of cancer.

Description and Etiology

Cancer is one of the diseases that may affect the structures of the oral cavity, pharynx, and
larynx. If allowed to proceed unchecked, it is life threatening. The incidence of laryngeal
cancer is reported to be between 2% and 5% of all malignancies. Persistent hoarseness is well
known as one of the primary symptoms of cancer. If a malignant lesion affects one or both
vocal folds directly, hoarseness will result. Figure 6.8 shows a cancer involving both vocal folds.
Laryngeal lesions that do not affect the vibratory characteristics of the vocal folds will not
necessarily result in a change in the voice.
There are many possible etiologies for cancer, including smoking, environmental irritants,
chemicals and other contaminants, metabolic disturbances, and unknown causes. According
to the Surgeon General’s report (U.S. Department of Health and Human Services, 1985),
“Cigarette smoking is a major cause of cancers of the lung, larynx, oral cavity and esophagus”
(p. vi). Furthermore, 50% to 70% of oral and laryngeal cancer deaths are associated with
smoking. The report also states that a synergistic effect is created by the use of alcohol in
conjunction with smoking that greatly increases the risk of oral and laryngeal cancers. The
ratio of men to women who develop these cancers was reported to be 5 to 1 in 1985 (Ballenger,
1985), but that ratio has been narrowing steadily for the past 20 years. The carcinogenic effects
of cigar and pipe smoke are similar to those of cigarette smoke.
The severity of the malignancy is evaluated using the “TNM” system or its variants
(American Joint Committee for Cancer Staging and End Results Reporting, 1983). The T
refers to the site of the primary tumor, the N indicates the involvement of lymph nodes, and
the M signifies spread of the lesion to other parts of the body (metastasis). Low numbers as-
sociated with each code indicate a lesser involvement, and the numbers increase as severity or
extent increase (Table 6.1). Thus, a patient described to have a T1N0M0 lesion has a locally
confined tumor with neither node involvement nor any distant metastasis. Where the values
of N and M are zero, the description is often truncated (e.g., T1 or T2 carcinoma) (Fig. 6.9).

Perceptual Signs and Symptoms

Hoarseness is the primary sign and symptom (Stoicheff, Giampi, Passi, & Frederickson, 1983).
Other signs of cancer of the larynx may include (a) a lump in the neck; (b) a broadening of the
larynx, detected on palpation; and (c) tenderness in the neck. Other symptoms may include
dysphagia, odynophagia (pain on swallowing), and dyspnea.

Acoustic Signs
Cancer will affect the vibration of the vocal folds and, therefore, will affect the acoustic charac-
teristics of the voice. The magnitude of the effect will depend on the extent of the carcinoma.
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FIGURE 6.8. Carcinoma of the vocal

folds.

Frequency and amplitude perturbation will be increased. For their sample of 5 cancer patients,
Hecker and Kruel (1971) reported pitch perturbation quotients similar to normal (patients
[n = 5] 13.6 vs. normal [n = 5] 13.0) but much greater directional perturbation quotients
(patients [n = 5] 48.9 vs. normal [n = 5] 33.3). Lieberman (1963) had reported large perturba-
tion values in an earlier study. Murry, Bone, and von Essen (1974) reported lower-than-normal
phonational ranges for their one male participant with T1 carcinoma of the vocal folds. Colton,
Reed, Sagerman, and Chung (1982) reported slightly higher fundamental frequencies for the
vowels /ah/ and /ee/ for male patients with T1 or T2 carcinoma and much larger fundamental
frequencies for both vowels produced by female patients with T1 cancer of the vocal folds
(Fig. 6.10). Pitch perturbation quotients were increased in both vowels for both male T1 and
T2 cancer classification groups. However, female patients tended to show lower PPQs for the
vowel /ah/ and similar PPQs for the vowel /ee/ when compared to the control group (Fig. 6.11).
Spectral noise levels are also increased. Colton, Sagerman, Chung, Young, and Reed (1978)
reported elevated spectrum levels, especially in the higher frequencies, for their sample of
5 cancer patients. Similar findings were reported for a much larger group of patients with can-
cer (Colton et al., 1982). In the same study, both phonational and dynamic ranges were found
to be lower in patients with laryngeal cancer than in control-group participants (Fig. 6.12).
Measurement of the noise energy in the voices of patients with laryngeal cancer may be
predictive of the severity of the cancer (Kasuya, Ogawa, Mashima, & Ebihara, 1986). Noise
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TABLE 6.1 Classification of glottal cancers

T: Location of Primary Tumor
Tx Cannot be staged
T0 No evidence of tumor
Tis Carcinoma in situ
T1 Confined to vocal folds
T2 Supraglottal or subglottal extension, normal or impaired mobility
T3 Confined to larynx but with fixed cord
T4 Massive tumor
N: Involvement of Regional Lymph Nodes
Nx Cannot be assessed
N0 No involvement
N1 A single small node on one side
N2 A single large or multiple small nodes on one side
N3 Massive nodes on one or both sides
M: Distant Metastasis
Mx Cannot be assessed
M0 No known metastasis
M1 Metastasis present

levels were measured in sustained vowels and a measure called normalized noise energy (NNE)
was calculated for 64 samples of normal voice and 57 samples of patients with carcinoma of the
vocal folds. NNE was effective in detecting 91% of the normal voices. In voices with carcinoma,
NNE was effective in detecting T1 cancer about 77% of the time and always detected T2, T3,
or T4 cancer. Thus, measurement of noise levels may be a very useful clinical technique for
documenting the magnitude of the voice change of cancer patients and for following effects of
treatment.
Leeper et al. (2002) also studied some acoustic characteristics of patients receiving irra-
diation for their T1 cancer. Their recorded their voices over five sessions during and after the
treatment and found greater harmonics-to-noise ratios (HNR), and lower normalized-noise-
energy levels across the five recording sessions. Perceptual judgments of hoarseness systemically
decreased over the same period. Dworkin et al. (1999) found many of their patients receiving
irradiation showed values of jitter, shimmer, and HNR within normal limits.

Measurable Physiological Signs

There are very little data on the measurable physiological characteristics of patients with cancer.
Airflows are generally increased with large leakage flows associated with large tumors that
prevent complete vocal fold closure. Mean airflow rates are increased (Murry et al., 1974).
EGG recordings will reflect reduced time of closure. Subglottal air pressures may be increased
because of the increased stiffness of the vocal folds.
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FIGURE 6.9. Extensive carcinoma in-

volving both folds.

FIGURE 6.10. Fundamental frequencies of the vowels /ah/ and /ee/ for 38 men and 5 women with T1
cancer classification and 13 men and 7 women with T2 cancer classification compared to a control group
of 35 men and 27 women.
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184 Understanding Voice Problems

FIGURE 6.11. Pitch perturbation quotients for the vowels /ah/ and /ee/ for 38 men and 5 women with
T1 cancer classification and 13 men and 7 women with T2 cancer classification compared to a control
group of 35 men and 27 women.

Observable Physiological Signs

Laryngoscopy Laryngoscopic examination may reveal anything from a small, well-defined
tumor to a large and diffuse one involving any part of the larynx or vocal folds. Precise diagnosis
of carcinoma usually requires biopsy and histological analysis. Most carcinomas of the larynx
arise from the epithelium and are of the squamous cell variety. As the severity of the lesion
increases it becomes more invasive in nature as well as more extensive in size.

FIGURE 6.12. Phonational and dynamic ranges of 38 men and 5 women with T1 cancer classification
and 13 men and 7 women with T2 cancer classification compared to a control group of 35 men and 27
women.
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CHAPTER 6 I Voice Problems Associated with Organic Disease, and Trauma 185

Stroboscopy Early carcinoma in situ can be more readily diagnosed using stroboscopy than
other methods of examination. The distinguishing feature is the presence of a small lesion that
has a markedly negative effect on vibratory vocal fold behavior (Sessions et al., 1989). It has
been suggested that stroboscopy can be used to detect cancer by its effect on the mucosal wave
or amplitude of vibration. Colden et al. (2001) tested that hypothesis by rating the extent of
mucosal wave and the amplitude of vibration in 52 participants with premalignant-appearing
lesions and then related the strobe results to the actual extent of the lesion found after surgery.
They concluded that stroboscopy was not a reliable method for determining the presence of
cancer or the depth of the lesion. A variety of benign as well as precancerous lesions would affect
the vibratory characteristics in a similar manner. Stiffness of any kind would affect the mucosal
wave and the amplitude of vibration. Thus, stroboscopy may not be a viable technique to help
differentiate a cancer from a noncancerous lesion. However, stroboscopy may be used to detect
the return of a mucosal wave after the suspected lesion has been treated with radiotherapy
(Tsunoda et al., 1997).

Pathophysiology
Cancerous lesions invade the tissue and destroy the normally behaving cells. Depending on
its location and size, the tumor may affect vocal fold closure. Invasion of the tumor into the
various levels of the lamina propria and muscle results in greater stiffness of the tissue resulting
in reduced horizontal excursion of the affected fold and often of the contralateral fold and
restricted or absent mucosal wave.

Treatment
There are several approaches to cancer treatment. These include surgery, radiation therapy,
and chemotherapy. Their use depends on many factors and is determined on a case-by-case
basis. Spector and Ogura (1985) have discussed some of the considerations in the diagnosis
and treatment of carcinoma. Patients who undergo radiation therapy as the primary treatment
mode may experience some alterations in voice during the course of the treatment (Colton
et al., 1978; Finizia et al., 1999; Fung et al., 2001; Leeper et al., 2002). Depending on the
extent of the lesion, a patient may still have a normal-sounding voice after radiation therapy.
Voice therapy is usually not necessary or indicated.
There are a variety of surgical approaches in the treatment of laryngeal cancer, which may
involve excision of the lesion, of up to half of the larynx, of supraglottal structures only, or of
the entire larynx (Cassisi, Sapienza, & Vinson, 1996; Franco & Zeitels, 2003). The effect on
voice production capability will depend on the extent and the nature of the surgery performed.
In addition to concerns about voice, patients who have had extensive surgery may also have
difficulty with swallowing. A full discussion of the problems of dysphagia and those associated
with the total absence of the larynx is beyond the scope of this chapter.
The voice problems associated with partial laryngeal excisions will vary a great deal. Both
voice problems and dysphagia will require the assistance of a speech-language pathologist. The
role of the speech-language pathologist is to assist the patient in producing the best-possible
voice. In order to do so, the speech-language pathologist must be completely informed about
the specifics of the surgical procedure. It is important to know what structures remain intact,
how the anatomy is altered, and what functional skills remain relative to phonation.
Some patients with laryngeal cancer have extremely extensive disease that requires excision
of not only the larynx but also of other structures essential to the production of speech, such
as the tongue. The speech-language pathologist should also be involved with these patients in
an effort to provide a means of communication.
Chapter 11 presents a more complete discussion of one of the major treatment options for
persons with laryngeal cancer, laryngectomy.
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Other Tumors
A variety of benign and malignant tumors may be found in the laryngeal or neck area in both
children and adults. Such tumors may obstruct the airway directly, or they may occupy space and
place pressure on the trachea or larynx, thereby creating airway problems indirectly. The effect on
the voice will depend on the position of the tumor. These lesions require medical and/or surgical
treatment. In many cases of small or benign tumors, surgery is a viable treatment option. In cases
of extensive malignant tumors, radiation therapy or chemotherapy or a combined protocol may
be possible treatment choices. Rarely is there need for speech therapy services unless the tumor
(or surgery) has compromised vocal or speech function. Tumors that are frequent in children
include cysts, hemangiomas, and lymphangiomas; malignant neuroblastomas and lymphomas
also occur. Many of these same tumors may also be found in adults.

Summary
In this chapter, some organic problems that may affect the voice have been reviewed. The
etiology of these problems is not related to voice use. However, their effects can drastically
alter voice production. A variety of medical and surgical approaches are the primary treatment
modalities. Vocal rehabilitation may be helpful in establishing the best voice the patient is
capable of producing. A section on geriatric voice discusses physical changes attributable to
aging that may affect phonation and stresses the need to distinguish between age-related changes
and those attributable to associated disease states.
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CHAPTER

7
Voice Problems Associated with the
Pediatric and the Geriatric Voice
Keywords
aging, aging theories, anomalies, children, congenital, cysts, development, EGG,
frequency, geriatric, histology, injury, intubation, laryngomalacia, MPD, MPT,
neuromuscular, nodules, obsolescence papilloma, paralysis, pediatric perturbation,
reflux, stenosis, VRP, webs

The Pediatric Voice

Dysphonia in children deserves careful consideration by the speech–language pathologist. Many con-
genital conditions, including difficulty breathing, stridor, or abnormal cry that affect the larynx, are
diagnosed at birth. But conditions that have more subtle effects may go unrecognized until later. In our
own practice, for example, identification of school-age children with webs, and even laryngeal paralyses
that appear congenital or related to a birth injury, occasionally occurs. Parents may become aware of an
unusual voice as the child experiences greater vocal and speech development. Interestingly, however, it
may also be a teacher, or speech–language pathologist, who initially questions the child’s voice quality.
Parents of these children sometimes report that the child’s voice has “always sounded this way” and,
consequently, has not been a source of concern. It is also important to note that children can experi-
ence many of the same laryngeal pathologies more frequently diagnosed in adults, including nodules,
papilloma, cysts, polyps, and, possibly increasingly, ulcerative lesions likely related to laryngopharyngeal
reflux (Benjamin, 1990; Block & Brodsky, 2007; Dejonckere & Lebacq, 1984; Michaels, 1984; Morrison
& Rammage, 1994; Tucker, 1987). Pathology that produces dysphonia requires accurate diagnosis as
well as assessment in terms of its impact on the child’s speech–language and social development. Thus,
hoarseness in children warrants appropriate attention by the speech–language pathologist and other care
providers. Pertinent to this objective is an understanding of the unique characteristics of the pediatric
larynx and voice. The intent of this section is to review laryngeal and vocal development in children as
well as both congenital and acquired conditions that may produce voice disorders in this population.

Laryngeal and Vocal Development in Children

Normative data for various measures of phonatory function in children are few. Their collection is beset
by a number of problems, including a need for data that account for respiratory and phonatory structures
and processes that are continually changing. Not only is the pediatric larynx different from the adult
larynx but it also is in a continual state of change throughout childhood. These changes are particularly
rapid in the first 2 to 3 years, then decelerate until puberty.

Larynx Position
In a newborn, for example, the larynx is high in the neck, with the lower border of the cricoid cartilage
approximately at the level of the 3rd or 4th cervical vertebrae (C3–C4; Hirano, Kurita, & Nakashima,
187
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1983; Magriples & Laitman, 1987; Roche & Barkla, 1965; Symington, 1881). It will descend
to about C5 by the age of 2 years and to C6 to C7 by the age of 15 years. This descent is
associated with increasing separation between the hyoid bone and the thyroid cartilage, which
are contiguous at birth. The higher position of the larynx in the child’s neck prior to the age of
2 years suggests that vertical adjustments of the larynx are limited. In addition, cartilages are
more elastic in children, becoming more osseous with aging. If either or both of these factors
are associated with less stability in the laryngeal framework they may have implications for
adjustments of structures that lie within it, such as the intrinsic laryngeal muscles. From a
clinical perspective, the higher, more anterior position of the pediatric larynx makes it more
difficult to intubate when required for any surgical procedure.
Investigating laryngotracheal structures in a large number of autopsy specimens of fetuses
and infants who had no malformations and who had not been intubated, Fayoux, Marciniak,
Devisme, and Storme (2008) reported gender differences for thyroid cartilage measurements
and interarytenoid distance, with measures for females smaller in both cases. Linear relationships
between laryngotracheal measurements and body weight and height were noted except for glottis
length, interarytenoid distance, and anterior cricoid height. Of perhaps particular interest
clinically, diameter of the cricoid lumen was significantly less than that of the trachea and
glottis lumen. In other studies, however, the glottal diameter has been reported to be smaller
than the cricoid lumen. Understanding these relationships, and how they may change with age,
has implications for intubation, and selection of intubation tube size, in this population.

Vocal Fold Histology

The pediatric larynx is less complex structurally than the adult larynx. Tissues of the vocal fold
cover are loose and elastic and not comprised of the multiple layers characteristic of the adult.
The cover is also thicker, relative to the length of the membranous vocal fold, than in adults.
Hirano, Kurita, and Nakashima (1983) have suggested that the three connective tissue layers
of the lamina propria are apparent at puberty but continue to become more differentiated until
at least 16 years. According to Hirano et al., the vocal ligament, comprised of the intermediate
and deep layers of the cover, may appear by the age of 4 years but again continues to develop
through puberty. Boseley and Hartnick (2006) reported that the superficial layer of the lamina
propria comprised 22% of the total lamina propria by the age of 7 years and that this percentage
approximates the typical adult lamina propria. Other authors (Ishii, Yamashita, Akita, & Hirose,
2000) have described a lamina propria distinguished by superficial and deep layers in children
older than 10 years of age, with differentiation of superficial, intermediate, and deep layers
complete by the age of 17 years. This evidence is supported by Hammond, Gray, Butler,
Zhou, and Hammond (1998). These authors investigated the presence of elastin, which is
characteristic of the intermediate layer of the lamina propria, in larynges representing the age
span from infant to geriatric. Elastin content between the epithelium and vocalis muscle was
significantly less in infant specimens, consistent with the lack of a well-defined intermediate
layer.
The differentiated layers of the lamina propria are a hallmark of the adult larynx, and the
relatively undifferentiated cover of the pediatric larynx may affect the child’s ability to make fine
adjustments necessary for certain vocal behaviors, for example, to produce voice in different
registers or phonatory modes, or to generate a mucosal wave. Clinically, the denser and more
vascular character of the pediatric cover makes it more susceptible to inflammatory or post-
traumatic edema. Interestingly, Schweinfurth and Thibeault (2008) have reported differences
in both the distribution and tissue concentration of hyaluronic acid in the neonate, as com-
pared to the adult. A more compact organization of collagen with less intercellular space may,
according to the authors, contribute to the newborn’s capacity for greater loudness per mass
output, a feature that may be critical to the infant’s greater dependency on vocalization, that is,
crying, for communication. Interestingly, Rosenberg and Schweinfurth (2009) have described
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CHAPTER 7 I Voice Problems Associated with the Pediatric and the Geriatric Voice 189

the hypercellular and monolayered character of the lamina propria as demonstrating change
consistent with development, that is, decreasing cell density, as early as 27 weeks gestational
age.
Other differences in vocal fold mucosa between newborns and adults have been described
by Allah, Dkhil, and Farhoud (2009). These investigators examined fibroblasts in the mac-
ula flava and Reinke’s space, respectively, in newborn, adult, and geriatric autopsy specimens.
Macula flava fibroblasts were predominantly stellate in shape and otherwise similar in both
newborns and adults. However, fibroblasts from Reinke’s space tended to be more oval in new-
borns, spindle-shaped in adults, and stellate-shaped in the geriatric specimens. In addition,
newborn fibroblasts demonstrated a small nucleus to cytoplasm ratio and less developed en-
doplasmic reticulum and Golgi apparatus, as compared to adults. Sato and Nakashima (2009)
reported that dense stellate cells in the infant macula flava act to synthesize extracellular matrices
necessary to growth and development of the viscoelastic properties of the lamina propria. Sato,
Umeno, Nakashima, Nonaka, and Harabuchi (2009) further note that vibration of the vocal
folds stimulates the stellate cells of the maculae flavae and suggest that this behavior contributes
to the differentiation of layers in the lamina propria.

Neuromuscular Development
Neuromuscular differences between the pediatric and adult larynx have also been described. In
young children, there is a higher proportion of type II muscle fibers in the vocal fold, which
are fast acting, consistent with airway protection, and not as capable of prolonged contraction,
which is likely critical to the development of phonation. By puberty, a preponderance of type
I fibers, capable of slow, prolonged contraction, is noted (Kersing, 1986). There are also fewer
muscle fibers in the child’s vocal folds, and some muscles share attachments. Konig and Von
Leden (1961) have reported that the development of the vocalis muscle continues to at least
the third year of life.
Changes in neural structures and neural control with growth also have an impact on
laryngeal and vocal behavior. It appears that both the superior and recurrent laryngeal nerves
demonstrate an adult pattern of distribution even at the end of the embryonic period (Muller,
O’Rahilly, & Tucker, 1985). But nerve fibers continue to increase in size, in myelination, and in
the number and extent of both dendritic and axonal endings, until about the age of 3 years. One
study has described motor end plates in the intrinsic laryngeal muscles of infants innervated
by either single or multiple axons. In adults, only single axon innervation was identified (Perie,
St. Guily, & Sebille, 1999). These authors further noted that both the size and axonal complexity
of motor end plates were increased in the adult specimens they investigated, as compared to
fetal and infant larynges.
Central laryngeal mechanisms also demonstrate developmental effects. For example, in the
fetus and newborn infant, chemical stimuli that pose a threat to the airway induce laryngeal
constriction, apnea (cessation of breathing), and swallowing, among other responses. The
laryngeal chemoreflex (LCR) that mediates these behaviors develops in an environment of
amniotic fluid, which poses an aspiration risk to the airway. Swallowing is thus a primary
means of airway protection at this stage of development. With maturation, infants appear to
transition from apnea and swallowing responses to cough, reflecting the change in environment
(Thach, 2001). It is reasonable to speculate that laryngeal control, manifest in the speed, range,
and accuracy of various laryngeal adjustments required for vocal behavior, is directly related to
neural maturity and that this is not complete in the child.

Anatomical Changes
Exactly how such changes influence the child’s emerging vocal skill are not clear, but we might
expect that mass/length/tension adjustments, and particularly the fine coordination among
them, undergo similar development. The voice source at birth is shorter and thicker and
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more circular in shape and, with growth, becomes longer, thinner, and more ovoid in shape.
The overall length of the vocal folds, including both cartilaginous and membranous portions
measured from the anterior commissure to the posterior laryngeal ventricle, may change from
about 3 mm at birth to 13 to 16 mm at the age of 10 years and increase to, perhaps, 20 to 30 mm
for adult women and men, respectively. Hirano, Kurita, and Nakashima (1983) have postulated
that, in general, vocal control improves as the ratio of membranous vocal fold to cartilaginous
vocal fold increases (from 1–1.8 in newborns to 3–6 in adults) and as the proportion of cover
thickness to membranous vocal fold length decreases (from about .4–.5 in newborns to .1 or less
in adults). As the membranous portion of the vocal fold increases in length, the vibratory source
becomes a better, more stable oscillator. It has been further suggested (Dejonckere, Wieneke,
Bloemenkamp, & Lebacq, 1996) that these changes may account for decreased perturbation
in the voice associated with development. In short, the larynx at birth serves respiratory and
airway protection purposes particularly well, whereas more complex vocal behaviors associated
with speech and singing may not be fully mature until adulthood.

Voice Physiology
Given the complexity of the issue, it is not surprising that the relationship between laryn-
geal development and vocal development has not been thoroughly elaborated. Longitudinal
studies involving large numbers of participants, dependent variables that adequately reflect the
maturing larynx, and the use of measures beyond central tendencies, are few. Most available
data are cross-sectional, describing children in particular age groups, and often involve a lim-
ited number of participants. In studies that have been performed, large intra-and inter-subject
variability is typical. A major problem with these types of studies, in fact, is that intersubject
variability is often larger than the age-related changes being investigated (Bennett, 1983). These
cautionary statements notwithstanding, there is some evidence available that may be useful for
documenting phonatory function in children.

Fundamental Frequency Characteristics

Change in fundamental frequency associated with growth and development is the variable most
often investigated in developmental studies (Baken & Orlikoff, 2000; Kent, 1976). In general,
the data available suggest a rapid lowering of frequency in the first 2 to 3 years of life and then
a more gradual drop until puberty. At birth, the fundamental frequency (F0 ) of cry is about
500 Hz. Between 5 and 8 years, we would expect F0 to be in the mid- to high-200s. From 8
years to puberty, F0 is likely to drop to the lower 200s. At puberty, gender differences begin and
are much more pronounced in boys than in girls. In particular, the angle of the thyroid cartilage
becomes more acute (from approximately 120◦ to 90◦ ) in boys, and this is accompanied by
a marked increase in vocal fold length and pharynx size. Adult F0 s measure approximately
200 to 220 Hz for women, an octave lower for men. Other studies have described fundamental
frequency ranges in children aged between 9 and 10 years to be on the order of 21 to 25
semitones (Flatau & Gutzman, 1908; McAllister, Sederholm, Sundberg, & Gramming, 1994).
Further evidence suggests that children’s voices may demonstrate slightly greater frequency
perturbation than adult voices (Cheyne, Nuss, & Hillman, 1999; Dejonckere et al., 1996).
It is well known that Fo in adult speakers (nonsingers) tends to increase with increases
in intensity. Titze (1996) has postulated that these changes may be greater in children, due to
the shorter length of the vocal folds. In excised larynges, the author found that folds with a
membranous portion of 5 mm in length produced a 40-Hz increase in fundamental frequency
with a doubling of subglottal pressure. In larynges of 10 mm in length, a doubling of subglottal
pressure produced only a 5-Hz increase in Fo . To our knowledge, the model has not been tested
in children.
Baker, Weinrich, Bevington, Schroth, and Schroeder (2008) reported on fundamental
frequency changes in children according to task. F0 measures were taken from a sentence
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repetition, sustained vowel /a/, vowel embedded in a phrase, and from counting 1 to 10.
According to the authors, F0 values were significantly higher for the counting task than in
the phrase or sentence tasks. Hunter (2009) used the same tasks described by Baker et al.
(2008), as well as voice samples taken from unstructured speaking activities, to investigate F0
task variability in a single child. Structured samples produced in a clinical environment were
similar and typical for values reported for children of comparable age. However, the child’s
mean fundamental frequency during unstructured activities, recorded in natural speaking tasks
over the course of a day, was substantially higher than that noted for the structured tasks
(257 Hz compared to 376 Hz). These studies illustrate both the effect of task on F0 and the
need for uniformity in task selection if voice is to be monitored over time or with treatment.

Aerodynamic Characteristics
Other studies have reported age-related differences in aeromechanical properties of voicing.
For example, mean airflow rates for maximally sustained vowel sounds (Beckett, Thoelke,
& Cowan, 1971) and oral flow rates for consonant productions (Stathopoulos & Weismer,
1985) have been reported to be less in children than in adults. Interestingly, differences in
phonation threshold pressure, defined as the minimal subglottal pressure required to produce
the softest possible phonation at a particular fundamental frequency, have also been reported
(Stathopoulos & Sapienza, 1997). At both conversational and loudest levels of phonation in
the lowest part of their Fo ranges, children’s threshold pressures were found by these authors to
be 2 to 4 times and 4 to 8 times greater, respectively, than values predicted for a mean speaking
Fo of 250 Hz. At higher Fos, children’s threshold pressures were similar to those predicted for
adult female voices. The authors suggested that the structure of the vocal folds in children 8
to 11 years of age may demand relatively higher subglottal pressures to vibrate. Other data
indicate that mean subglottal pressures at normal conversational loudness levels may also be
somewhat higher in children than in adults (Stathopoulos et al., 1985). In an investigation of
children aged between 4 years and 14 years, Keilmann and Bader (1995) reported that higher
subglottal pressures in the younger children diminish to some extent with age. These authors
also noted increasing flow rates with age and glottal resistances that remained stable across the
age range considered.
Changes in subglottal pressure may also affect vocal intensity somewhat differently in
children, as compared to adults. Stathopoulos and Sapienza (1997) reported that doubling
subglottal pressure yielded a 16-dB-SPL (sound pressure level) increase in intensity in a group
of 8-year-old children, but only a 11-dB gain in adults. In a second study, these authors found
that doubling subglottal pressure produced a 10-dB-SPL gain in 10-year-old children, results
that are quite similar to data reported for 8- to 11-year-old children by McAllister and Sundberg
(1998). These differences are reasonable if the smaller vocal folds of children, in particular, under
10 years of age, undergo greater vibratory displacement, and hence greater closing speeds, than
the longer vocal folds of adults.

Maximum Phonation Times/Durations (MPT, MPD)

The appropriateness of tests of maximum performance in clinical evaluations has been ques-
tioned (Kent, Kent, & Rosenbek, 1987). Nevertheless, some of these measures continue to be
widely used, in particular, to assess treatment effects in individual patients. Maximum phona-
tion duration (or time), for example, is frequently included in tests of vocal function for this
purpose. Harden and Looney (1984) examined maximum duration of sustained vowels /i/,
/a/, and /u/ in 160 children with an average age of 6.2 years. No differences according to
gender were identified, and children with voice disorders achieved significantly shorter dura-
tions than those in the control group. The authors also identified a significant vowel effect,
with /i/ sustained for longer times than either /a/ or /u/. Finnegan (1985) reported maximum
phonation times in children in the age range of 3 to 17 years. Each participant performed 14
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trials of sustained /a/ and was provided with visual feedback and encouragement in an attempt
to maximize performance. Data were based on the three longest times obtained for each par-
ticipant. In contrast to Harden and Looney (1984), Fninegan identified gender differences at
several age levels. The range of maximum times from the youngest to oldest participants was
7.92 seconds to 28.7 seconds in men, and from 6.28 seconds to 21.99 seconds in women. Our
own experience suggests that the use of repeated trials, and careful attention to producing the
same vowel at the same fundamental frequency and intensity levels, contributes to the utility
of MPT in assessing treatment effects in both children and adults. Cielo and Cappellari (2008)
investigated MPT in children between 4 and 6 years of age and found significant increases
in duration for the older children. Of interest, the authors began with a population sample
of 78 children but, after exclusion due to perceived abnormalities in the voices, only 23 were
included in the final report. Variability in children’s voices, as noted previously, may represent
a confounding factor in identifying “normal” in this population.
Another duration measure frequently used clinically is the s/z ratio. To determine the ratio,
the participant first sustains /s/ for as long as possible and then repeats the task sustaining /z/.
The assumption, which to our knowledge has not been validated, is that the amount of air
expelled during phonation should be equal for each phoneme in normal participants, so that
the resulting ratio is “1.” In the event of a mass on one or both vocal folds, however, excessive
airflow on the /z/ might be expected to reduce its duration, with a resulting ratio larger than
“1.” One study has investigated the maximum duration of /s/ and /z/ in children aged 5, 7,
and 9 years (Tait, Michel, & Carpenter, 1980). The authors reported no significant differences
in the s/z ratio by age or gender. However, they did find a significant increase in the maximum
duration of both /s/ and /z/ with increased age. Carefully obtained, the s/z ratio may be useful in
assessing treatment effects in an individual patient. However, the measure does not differentiate
laryngeal from respiratory components of voicing.

Voice Range Profile Characteristics

Also referred to as phonetograms, voice range profiles (VRPs) have been investigated for some
age groups of children. Having the participant produce a sustained vowel sound at the softest
and loudest intensities possible at selected intervals within his or her Fo range generates these
profiles. In a study of 10-year-old children, McAllister, Sederholm, Sundberg, and Gramming
(1994) found that both pitch range, in semitones, and maximum dynamic range, defined as
the difference between SPL at a given fundamental frequency, were generally compressed in
children. According to the authors, differences in the higher contour of the profile, which
was reduced in children, may reflect a restricted ability of the vocalis muscle to resist the
high subglottal pressures required to produce loud voice at a high pitch. Differences in the
lower contour, which was elevated in the children investigated, were attributed to a need for
greater subglottal pressure to initiate vibration in children’s vocal folds. The authors recommend
the VRP as a useful means not only of differentiating adult and pediatric voices but also of
differentiating normal and dysphonic voices in the pediatric population.
Heylen et al. (1998) have described VRPs obtained for a large number of children with
and without vocal fold pathologies. Participants were between 6 and 11 years of age. Based on a
discriminant analysis that identified VRP characteristics most sensitive to vocal pathology, the
authors constructed a Voice Range Profile Index for Children (VRPIc). Calculation of the index
utilizes a combination of the child’s age, the highest vocal fundamental frequency produced, the
softest intensity produced, and the slope of the upper VRP contour. According to the authors,
the VRPIc may be used as a screening tool for voice disorders or to assess the effects of time or
treatment on a child’s vocal performance.
In a comparison of a large number of vocally trained and untrained children, Schneider,
Zumtobel, Prettenhofer, Aichstill, and Jocher (2009), children with some vocal training were
found to have greater ranges on the VRP than untrained children. Across children, F0 ranged
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from 22 to 26 semitones. Approximately 25% of children were able to produce voice at inten-
sities greater than 90 dB.

EGG Characteristics
Another measure with potential for documenting vocal function in children has been described
by Cheyne, Nuss, and Hillman (1999). These authors investigated 164 children between the
ages of 3 and 16 years, using electroglottography (EGG). The authors reported no significant
differences for age or gender for the variables of open quotient, closing quotient, opening
quotient, and jitter. Jitter values, or relative average perturbation for frequency, were somewhat
larger than those reported for adults, and open quotient values were more similar to those
reported for adult males than for adult females. Fundamental frequency data, which can also
be obtained from EGG, were reportedly similar to other literature reports. The apparent lack
of gender or age effects suggest that some elements of vibratory timing are maintained across
growth of the larynx, and the authors speculate this may be critical to the perception of normal
vocal quality in children.

Conditions Affecting the Larynx and Voice in Children

Congenital Anomalies
Some congenital conditions affecting the larynx may be resolved with time or intervention,
while others may have long-term effects on voice. Furthermore, some conditions can be either
congenital or acquired. The treatment may differ depending on the age of emergence.
Laryngomalacia, which is the most common congenital laryngeal disorder (Morrison
et al., 1994; Tucker, 1987), involves immature development of cartilaginous structures that
allows soft tissues to collapse and obstruct the airway, particularly during inspiration. Since a
primary clinical sign is stridor, this condition is typically identified at birth or shortly thereafter.
Though surgery to protect the airway may be required, the condition often resolves with growth
and development and does not generally come to the attention of the speech pathologist.
Subglottic stenosis identified at birth is usually associated with respiratory difficulty
(Benjamin, 1990; Dejonckere, 1984; Tucker, 1987). The condition may represent a failure in
the development of vestibulotracheal tract that becomes the airway and can involve soft tissues
only or cartilage. Other stenoses may be the consequence of an inflammatory process (Benjamin,
1990). If respiration is significantly affected, surgical reconstruction is likely to be required,
and there can be long-term consequences for voice (Macarthur, Kearns, & Healy, 1994; Smith,
Marsh, Cotton, & Myer, 1993). Stenosis involving soft tissues may resolve spontaneously
during childhood (Schultz-Coulon, 1984).
Laryngeal paralyses present at birth can occur as a consequence of birth trauma; ab-
normalities in cardiac, pulmonary, or other structures that affect laryngeal innervation; or
in association with central nervous system damage. Bilateral paralyses are typically related to
central nervous system conditions and, thus, more likely to be permanent (Michaels, 1984).
Effects on respiration and voice will, of course, be dependent on the specific type of paralysis.
If the paralysis is bilateral and the folds are fixed in an adducted position, respiratory difficulty
and stridor would be expected. If one or both folds are fixed in an abducted position, weak
and breathy or aphonic cry, and aspiration, may result. Bilateral vocal fold paralysis frequently
accompanies Arnold Chiari malformation, which involves displacement of the cerebellum and
brainstem into the cervical spinal canal through the foramen magnum with subsequent injury
to the medullary respiratory center and cranial nerves 1X and X.
Congenital webs involving the true vocal folds may produce respiratory difficulty or
stridor that leads to their subsequent identification. Webs are a consequence of anomalous em-
bryological development and recently have been related to specific chromosomal abnormalities
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(Milczuk, Smith, & Everts, 2000). In the embryological development of the larynx, the vestibule
and laryngeal lumen are at one time comprised of an epithelial lamina that fuses the primordial
epiglottis and arytenoid cartilages. Reestablishment of the supra- and infra-glottic airways in-
volves the eventual regression of this epithelial tissue. A failure of this process can lead to webs at
various sites. When the true vocal folds and glottis are significantly involved, early identification
is more likely. If the web is thin and membranous, surgical correction may result in good voice
quality (Benjamin, 1983). However, surgical excision of thicker, more fibrous webs is likely to
have serious implications for voice quality. As noted previously, webs and paralyses may not be
recognized until much later, particularly if their functional consequences are subtle.
Congenital cysts of the vocal folds are apparently rare. In a series of 657 congenital
anomalies of the larynx, Holinger and Brown (1967) reported only 3 cases of cysts. However, it
is possible that some congenital cysts may not be identified at birth but become apparent later.
In other series of benign laryngeal pathologies, cysts have been reported in young children,
though again, infrequently (Kawasaki, Kuratomi, & Mitsumasu, 1983). In a description of an
intracordal cyst identified in an infant, Smith, Callanan, Harcourt, and Albert (2000) described
episodic stridor, respiratory distress, and feeding difficulties. The symptoms were resolved by
excision of the cyst. It has been reported that congenital cysts are most often epidermoid
(Milutinovic & Vasiljevic, 1992) and may represent remnants of the fourth and sixth branchial
arches that become trapped in the vocal fold cover (Bouchayer et al., 1985). Tucker (1987)
notes that simple cysts are likely a consequence of obstruction of ducts associated with mucus,
serous, or minor salivary glands. Entrapment of air or secretions in the anterior portion of the
laryngeal ventricles, or saccule, can produce laryngoceles that may become enlarged during
pneumatizing activities, such as crying or straining at stool. Cysts that interfere with respiration
or voicing are more likely to be identified at birth or shortly thereafter.
Papilloma in the larynx is of viral origin, often recurring, and requiring surgical, medical,
or a combination of surgical and medical management strategies. When papilloma directly
affects the vocal folds and requires excision, dysphonia may be marked, and therapy directed at
optimizing functional oral communication may be of value. This is also true for children who
have sustained laryngeal injuries from frequent or prolonged intubations.
Intubation Injury: The child who requires a long-term tracheotomy from birth to main-
tain the airway presents unique challenges to the speech–language pathologist. With a tra-
cheostomy tube in place, air enters and exits the airway below the level of the vocal folds. In
perforated tubes, occlusion of the tube with a finger during exhalation will divert air across the
vocal folds to produce voice, assuming the true vocal folds are capable of this function. Passy–
Muir valves respond to increases in pressure (consistent with voicing) to close the tracheostomy
tube and divert air with no external manipulation and have been used in pediatric patients with
good pulmonary function (Morrison et al., 1994). In children with a long-term, compromised
ability to vocalize, for whatever reason, a key role of the speech–language pathologist is to max-
imize both the child’s functional communication skills and his or her development of speech
and language.

Signs and Symptoms of Congenital Laryngeal Disorders in Children

In general, the primary signs of a congenital laryngeal abnormality include dysphonia, difficulty
breathing, and stridor during respiration. Feeding difficulty may also be noted, indicated by
coughing, choking, and cyanosis (bluish discoloration of skin and mucous membranes due
to reduced hemoglobin in the blood). Observation of the larynx endoscopically, and perhaps
with radiographic studies, is likely to produce at least a preliminary diagnosis of the specific
pathology. To our knowledge, there is little experimental evidence that specifically addresses
the differentiation of dysphonias associated with congenital laryngeal anomalies according to
acoustic or perceptual characteristics of voice or cry (Manfredi, Tocchioni, & Bocchi, 2006).
Nor are we aware of measurable physiologic variables that are used to differentiate congenital
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anomalies of the larynx. Tucker (1987) noted that careful attention to voice, however, may be
helpful in directing diagnostic efforts. For example, the presence of inspiratory and expiratory
stridor, as well as weak or muffled cry, suggests a web, whereas the presence of stridor with a
normal voice points to stenosis.

Acquired Pathologies
Vocal Nodules
The most common laryngeal pathology associated with voice disorders in children is vocal nod-
ules, possibly accounting for 50% of voice disorders in this population (Morrison et al., 1994).
Most often, these lesions are attributed to excessive voice use or habitual vocal hyperfunction.
However, there are reports in the literature of nodules even in infants, and it has been suggested
that these may be related to laryngopharyngeal reflux, that is, acidic material that is refluxed
from the esophagus onto the structures of the larynx (Halstead, 1999). Typically, nodules are
bilateral and occur at the midmembranous point of the true vocal folds, which is the site likely
to experience the greatest contact forces during voicing. As noted previously, the composition
and position of the larynx differs markedly in newborns and infants as compared to adults and
older children. At birth, the cartilaginous portion of the vocal folds comprise about half of their
length from the anterior to posterior commissure, with the membranous portion responsible
for the remainder (Hirano et al., 1983). This is in contrast to adults, in whom the posterior
cartilaginous processes comprise approximately 40% of the anterior-posterior length of the
true vocal folds. Nodules may, therefore, be more anteriorly located in children than in adults.
Histologically, they appear as fibrotic thickenings or swellings of the mucosa. They may be
soft or firm, depending, in part, on how long they have been present. With greater chronicity,
thickened epithelium contributes to the fibrotic character of the nodule.
Vocal nodules rarely require surgical excision. Most contemporary otolaryngologists writ-
ing about nodules in children (Morrison et al., 1994; Tucker, 1987; von Leden, 1985) suggest
that only in rare cases, for example, when oral communication or social development is signif-
icantly affected, and when conservative measures, including voice therapy, have failed, would
surgery be considered. One reason for this is that, at puberty, growth of the larynx typically
changes the point of maximum compressive forces of the vocal folds. With a reduction in the
collision forces acting on them, the nodules may improve or resolve spontaneously. In addition,
vocal behaviors that produced the nodules are likely to attenuate with increasing maturity of
the individual.
Conservative management is the recommended treatment for vocal nodules in children.
In our experience, focus is directed to the identification and modification of those behaviors
considered most excessive or hyperfunctional, that is, screaming and yelling, imitating machine
or animal noises. In all cases, a team approach directed to achieving stable voice quality (no vocal
fatigue) and reinforcing appropriate voice use by parents, teachers, and other care providers
appears to have the best chance of being effective. The intent is not to criticize communicative
behavior, but to minimize excessive or inappropriate vocal behaviors. The older the child, the
more possible it is to discuss directly the need for modification of vocal behaviors and strategies
for achieving this objective.
DeBodt et al. (2007) followed 91 postmutational adolescents (mean age = 16 years) who
had been diagnosed with vocal nodules as children. Clinical voice and laryngological exams
and questionnaires were used to determine persistent voice complaints. The authors noted
that 21% of the adolescents had voice complaints that had persisted and that more girls were
included in this group than boys. Of individuals with persistent complaints who also underwent
postpubescent laryngological exams, 47% of girls and 7% of boys, respectively, had nodules.
Gender, severity of dysphonia, and presence of allergies were considered predictors for persistent
voice complaints.
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In our clinical experience, adults who present with vocal nodules or other voice use–
related pathologies sometimes report frequent episodes of dysphonia when they were children
or teenagers. On reflection, they may acknowledge to us that they have consistently engaged in
excessive or hyperfunctional vocal behaviors throughout their lives. These patients often note
that they were not treated for dysphonia at an earlier age, possibly because of the intermittent
nature of the hoarseness. Based on these experiences, we believe it may always be worthwhile to
engage in at least some counseling of parents, and of older children, regarding the nature and
cause of the child’s vocal nodules. Our hope, of course, is that these early educational efforts
may prevent the individual from having difficulty as an adult.

Vocal Fold Paralysis

Noncongenital unilateral vocal fold paralysis may be seen in children, perhaps most often as
a consequence of trauma (Daya, Hosni, Bejar-Solar, Evans, & Bailey, 2000; King & Blumin,
2009). In some cases, trauma may be related to surgery, for example, as in the repair of a
congenital heart anomaly that damages a recurrent laryngeal nerve. Depending on the likelihood
that a unilateral vocal fold paralysis may be permanent, and on the severity of symptoms
produced, surgical intervention may be required. If so, careful consideration must be given to
treatment choices, and the same options available to adults may not be applicable to children.
For example, augmentation procedures used to medialize a fixed vocal fold may reduce the
size of the airway, particularly if the augmentation material is overinjected to compensate for
anticipated resorption. Though the added mass usually doesn’t present a problem for adults, it
could produce respiratory difficulty in the smaller pediatric airway. Treatment alternatives that
could interfere with the continuing growth and development of the larynx are also avoided, if
at all possible. Voice therapy in such cases may be of value in maximizing optimal vocal fold
function, and in preventing hyperfunctional compensatory behaviors that could develop in
response to the paralysis. Acquired bilateral vocal fold paralyses resulting from trauma would
be expected to produce immediate consequences for respiration or airway protection and to
require immediate intervention.

Tissue Changes Related to Laryngopharyngeal Reflux

Reflux of material from the esophagus into the pharynx and larynx has become increasingly
recognized as a source of laryngeal tissue change and subsequent chronic dysphonia in children
(Block & Brodsky, 2007; Halstead, 1999; Kalach, Gumpert, Contencin, & Dupont, 2000).
Block and Brodsky (2007) reviewed test results and endoscopic evaluations for a series of
337 children who presented with hoarseness. The authors found that 36% of the children
(mean age = 7.2 years) had laryngopharyngeal reflux only. Another 20% were diagnosed with
both laryngopharyngeal reflux and vocal nodules. In a study of 17 chronically hoarse children
between 2 and 12 years of age, laryngeal findings included interarytenoid erythema and/or
edema with vocal fold granuloma or nodules in 13 cases and isolated granuloma or nodules in
3 cases (Kalach et al., 2000). Only one participant had a normal appearing larynx. A 24-hour
dual-probe pH monitoring was performed in all children and revealed abnormal findings in 15
of the 17 participants. The possible role of gastroesophageal reflux in the development of a wide
range of pediatric upper-airway disorders has also been investigated (Halstead, 1999). Results
of pH probe testing, laryngeal examination, and bronchoalveolar lavage suggested reflux as a
causative factor in subglottic stenosis, recurrent croup, apnea and chronic cough, and as an
inflammatory cofactor in chronic sinusitis/otitis/bronchitis, laryngomalacia, and possibly true
vocal fold nodules (Halstead, 1999). Otolaryngologists and voice clinicians routinely consider
reflux as a causative or exacerbating influence on laryngeal pathology in adults; it would appear
that similar attention should extend to dysphonic children as well.
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Pharmaceutical Causes
It should also be remembered that children, as well as adults, may take medications that affect
the vocal folds in ways that may contribute to voice change. In our own clinic, for example, the
number of children who are using corticosteroid inhalants for asthma appears to be on the rise.
The effects of these drugs in adults have been frequently described and include mucosal changes
of the vocal folds, fungal infections, and adductor myasthenia (Lavy, Wood, Rubin, & Harries,
2000). We would, therefore, urge clinicians to be as thorough in reviewing pharmacological
regimens in their pediatric patients as they are in evaluating adults.

Signs and Symptoms of Acquired Laryngeal Disorders in Children

The acquired laryngeal disorder that has been most investigated in children is vocal nodules,
and consequently, most of the available experimental evidence regarding signs and symptoms,
as related to voice, pertains to this population. This information will be reviewed here.

Perceptual Signs and Symptoms

McAllister, Sederholm, Sundberg, and Gramming (2000) described perceptual characteristics
in a group of 60 normal children who underwent laryngeal examinations. Though 10% of
the group was found to have vocal nodules, 14% were perceived as demonstrating hoarseness
on 2 separate occasions. At least one participant with vocal nodules was perceived as having a
normal voice. The authors note that, in particular, the perception of breathiness, which is often
associated with laryngeal pathology in adults, may not be perceived as unusual in children.
In a much earlier study, Silverman (1975) found that listeners perceived 23% of 162
school-age children screened for speech and voice abnormalities as hoarse. Again, of the hoarse
children who underwent laryngeal exams, not all were identified with laryngeal pathology. It
would seem, thus, that not all children with vocal nodules experience significant voice change;
similarly, some children perceived to have normal voice quality may also have vocal nodules.
It is, of course, those children with perceived hoarseness, or abnormal voice quality, which
come to the attention of the voice clinician. In our opinion, children who demonstrate chronic
hoarseness are candidates for laryngeal exam. Though factors other than serious laryngeal
pathology may contribute to perceived hoarseness in children, for example, tissue changes
related to asthma medications, or to allergies, the only means of ruling out pathology is by
laryngeal examination.
The relationship between perceived voice quality and laryngeal pathology is but one issue
in the perceptual evaluation of voices. Another is the reliability, both within and between raters,
of listeners attempting to evaluate the same voice. In recent years, a number of investigators
have considered ways to expand and improve perceptual assessments in the pediatric popula-
tion. For example, Kelchner et al. (2009) used the CAPE-V (Consensus Auditory Perceptual
Evaluation) to assess voice in 50 children and young adults being followed for laryngotracheal
reconstruction. Interrater reliability tests across 3 experienced listeners demonstrated intraclass
correlation coefficients of 71% for breathiness, 68% for pitch and roughness, and 67% for
overall severity. Reliability for loudness and strain, the other parameters of the CAPE-V, was
poorer.

Acoustic Signs
Hufnagle (1982) reported an increase in the habitual fundamental frequency of boys with vocal
nodules, as compared to a group of boys without laryngeal pathology. The groups were matched
for age and size, and fundamental frequency measurements were obtained from narrowband
spectrograms magnified to expand the spectrum from 0 to 1300 Hz. The group with vocal
nodules had significantly higher fundamental frequencies (mean of 301 Hz) than did the normal
group (246 Hz). Using the VRP described previously, McAllister, Sederholm, Sundberg, and
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Gramming (1994) reported a decrease in fundamental frequency range in 10-year-old children

with vocal nodules (19 semitones), as compared to a control group (25 semitones). These
authors did not find a difference in the two groups for maximum dynamic range (lowest to
highest intensity at a given fundamental frequency), however.
Heylen et al. (1998) investigated 94 normal children and 130 children with laryngeal
pathology, primarily vocal nodules (118/130), using a number of variables derived from the
VRP. The authors found that the two groups, matched for age, differed significantly on all
measures considered, with the exception of the lowest fundamental frequency produced. Both
fundamental frequency range and maximum dynamic range were significantly reduced in
children with pathology. Interestingly, in contrast to the Hufnagle study, modal fundamental
frequency was found to be lower in the pathology group. The authors suggest that the presence
of mass-adding lesions is likely to interfere with more rapid vibratory rates of the vocal folds,
thus limiting the high end of the fundamental frequency range. In addition, nodules or other
mass-adding lesions affecting the vocal folds are likely to require greater driving pressures
to initiate and maintain phonation, affecting, in particular, the generation of intensities at
the lower end of the maximum dynamic range. As noted previously, from their preliminary
testing, the authors constructed for each participant a voice range profile (VRPIc) using a
combination of age, highest fundamental frequency produced, lowest intensity produced, and
the slope of the upper VRP contour. The measure was found to demonstrate good sensitivity
(90%) and specificity (83%) in differentiating the normal group from the group with laryngeal
pathology.11∗
Campisi, Tewfik, Pelland-Blais, Hussein, and Sadeghi (2000) examined a number of mea-
sures from the MultiDimensional Voice Program (MDVP; Kay Elemetrics, Lincoln Park, NJ)
in boys with and without vocal nodules. The 2 groups were matched in age and participants
were in the age range of 7 to 12 years. Boys with vocal nodules were found to have statisti-
cally significant elevations in absolute jitter, jitter percent, relative average perturbation, pitch
period perturbation quotient, smoothed amplitude perturbation quotient, and fundamental
frequency variation. These findings suggest, not surprisingly, that cycle-by-cycle variability in
vocal fold vibration is increased by the presence of nodules.
One other acoustic measure that has been considered in children with vocal nodules is the
noise-to-harmonics ratio (NHR). Pereira, Cervantes, Abrahao, Parente Settanni, and Carrara
de Angelis (2002) described higher NHR values in a group of boys with laryngeal pathology,
including vocal nodules, as compared to a group of boys without laryngeal pathology. The
NHR does not differentiate sources of noise in the voice, which may be related to turbulence,
increased cycle-to-cycle amplitude, and/or frequency variability, voice breaks, or possibly to
other factors. However, in the case of vocal nodules (or other mass-adding lesions), we might
reasonably expect that any one or all of these factors may account for the finding of greater
noise in the acoustic signal produced. Meredith, Theis, McMurray, Zhang, and Jiang (2008)
have described nonlinear dynamic analysis methods for both adults and children that may serve
to complement traditional acoustic assessments and, possibly, provide improved reliability and
objectivity in characterizing dysphonia.

Measurable Physiologic Signs

Sapienza and Stathopoulos (1994) examined respiratory and laryngeal measures in children and
women with vocal nodules and in control-group participants without pathology. Higher peak
and minimum airflows were found in the nodule participants as well as larger lung-volume
excursions. We have found, clinically, that airflows may be particularly elevated in children

∗ Sensitivity refers to the proportion of dysphonic children correctly identified by the test, specifically, to the propor-
tion of normal children correctly identified.
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with vocal nodules during syllable repetition tasks and may be accompanied by elevations in
subglottal pressure estimates as well. Interestingly, this has not always been our experience in
adults with laryngeal pathology. Though some adults with lesions demonstrate similar elevations
in airflow and subglottal pressure, others appear able to manipulate respiratory behavior, that
is, to significantly reduce expiratory airflow, possibly in an attempt to preserve durational
characteristics of speech (as number of syllables per exhalation).
Characteristics of different types of vocal initiation in children with vocal nodules were
investigated by Leeper (1976), using both acoustic and aerodynamic measures. Results revealed
consistently longer voice initiation times and greater air-volume expenditure during the initial
few hundred milliseconds of phonation in the children with vocal nodules, as compared to
the control group. This was true for three types of vocal initiation, including hard, soft, and
breathy.

Observable Physiologic Signs

Laryngoscopy
As noted previously, nodules are more anteriorly located in young children than in adults.
However, as in adults, they are typically bilateral. Closure of the vocal folds on phonation
may be incomplete, particularly on either side of the pathology. If the nodules are of recent
origin, there may be accompanying edema and erythema. In our experience, nodules are often
broad-based in children, appearing as a fibrous thickening or swelling of the mucosa. They
may be soft or firm, depending, in part, on how long they have been present. With greater
chronicity, thickened epithelium contributes to the fibrotic character of the nodule.

Stroboscopy
In our experience, stroboscopic examination of the larynx in children with a rigid endoscope
can be somewhat compromised by the small size of structures and the child’s ability to undergo
the task. The task may be easier when stroboscopy is used with flexible endoscopy. But even
when the child’s true vocal folds can be visualized easily, it may be difficult to elicit sustained
sounds of the several seconds duration required for good stroboscopic imaging. This appears
to be true in children, in general, regardless of whether they have laryngeal pathology or not.
Extent and/or duration of the closed phase, and symmetry from right to left, may be difficult
to judge. Our impression, however, is that stroboscopic findings in children with nodules are
generally comparable to those in adults. That is, the mucosal wave is likely to be affected by the
size and character of the pathology, being unaffected or minimally affected with soft lesions,
and reduced significantly with firmer lesions. Similarly, degree of closure will vary depending
on size and compressibility characteristics of the pathology.

Case Study: Dysphonia of Unclear Origin in a 7-Year-Old Child

A 7-year-old girl (N. S.) was referred to the Voice Clinic by an outside otolaryngologist. He
indicated that the child’s parents had consulted him on the advice of the speech–language
pathologist at N. S.’s school. The SLP had noted hoarseness on a screening exam and was
concerned that it may be related to underlying laryngeal pathology. The otolaryngologist had
performed an indirect laryngeal exam on the child and found the true vocal folds to be normal
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in appearance and function. However, he noted that N. S. was using her false vocal folds on
phonation and felt that her marked dysphonia was functional in origin. The remainder of the
HEENT (Head Eyes Ears Nose Throat) exam was normal. The otolaryngologist referred N. S.
to the Voice Clinic for voice therapy.
N. S. presented to the Voice Clinic as a happy child who enjoyed friends, family, and
many activities. She appeared small for her age. Voice quality was soft, low in pitch, and judged
as severely hoarse. Her history was significant, given her 3 months premature birth requiring
respiratory assistance for 1 month. The parents did not recall if this involved intubation. N. S.
required frequent hospitalizations for pneumonia during her infancy and, at the age of 3 years,
underwent an adenotonsillectomy. At 5 years, a tympanoplasty was performed. She had been
diagnosed with attention-deficit disorder for which she was currently taking medication. She
was enrolled in a special education classroom at her school and was making good progress. Her
parents reported that N. S. had sounded the same since she began talking, and they were not
particularly concerned about her voice quality until recently. They also described their daughter
as active, but generally quiet. They felt she in no way fit the profile of a child whose voice use
is excessive or hyperfunctional. Her teachers described N. S. in a similar manner.
Phonatory function testing revealed an average speaking fundamental frequency of 233 Hz,
and a range of 11 semitones (215–405 Hz). Maximum phonation time on a sustained vowel was
12 seconds. Perturbation measures for both frequency and amplitude were mildly elevated, and
the noise-to-harmonics ratio was .32. Laryngeal function testing revealed reduced airflow for a
sustained sound (<25 cc/sec). On a syllable repetition task, however, airflow was extremely high
(>400 cc/sec), with a subglottal pressure estimate of 4.52 dyne/cm2 . The estimate of glottal
resistance was so high as to be invalid. Though maximum dynamic range was not tested, N. S.
appeared unable to produce voice at loud intensities. A pulmonary screening exam suggested
a moderate restriction, although neither the parents nor N. S. reported respiratory difficulties.
On laryngeal exam with rigid endoscopy, our initial impression was that the larynx was
within normal limits. However, on phonation, the impression was that the false folds medialized,
almost completely obscuring the underlying true folds. In exploring this behavior further, we
continued to observe the larynx over a wide range of vocal and vegetative tasks—evaluation
strategy we refer to as a phonoscopic exam (see Chapter 10). N. S. was compliant with the
laryngeal examination, and the prolonged observation was productive. During this testing, it
became clear that N. S. had a laryngeal web. The web was above the level of the true folds and
appeared to originate from the anterior commissure and to extend into the laryngeal ventricles,
between the false and true vocal folds (Fig. 7.1). When her true vocal folds were abducted
(Fig. 7.1A), the web retracted and was not apparent; however, as the vocal folds moved to an
adducted state (Fig. 7.1B), the web moved posteriorly until it formed a cover over the true
vocal folds (Fig. 7.1C and 7.1D). By observing the vocal folds carefully, and on slow-motion
replay of the videotaped exam, we were eventually able to make this determination.
Whether the visualized web was congenital, or came about as a consequence of intubation
or other trauma, was not clear. But it did explain N. S.’s marked dysphonia and probably most
of the unusual findings on phonatory and pulmonary function testing. For example, during the
production of a sustained sound, the web covered the true vocal folds to the extent of markedly
reducing any airflow. On a syllable repetition task, requiring rapid abduction and adduction
gestures of the true vocal folds, airflows were greatly elevated, possibly reflecting a tethering
effect of the web.
The case of N. S. reminds us that not all laryngeal pathology in children is related to vocal
nodules and that long-standing hoarseness in children needs to be explained. In this instance,
a number of clues in her case history suggested the possibility of a congenital pathology, or
early trauma to the larynx. Similarly, N. S. did not appear to fit the profile of a child we
might suspect of developing vocal nodules related to excessive or hyperfunctional voice use.
Both the phonatory function and pulmonary screening results were unusual, and the careful,
phonoscopic examination of the larynx over a broad range of tasks was critical to the eventual
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A B
FIGURE 7.1. Seven-year-old girl
with supraglottic web. (A) True vo-
cal folds appear within normal lim-
its when fully abducted. (B) As folds
begin to adduct, web can be seen to
move posteriorly. Coverage of true
vocal folds becomes more exten-
sive in (C) and is nearly complete in
(D).
C D

diagnosis. Excision of the web required surgery, and both N. S.’s parents and the voice team
felt that, if performed, it should be carefully timed to optimize results. Factors such as N.S.’s
small size for her age, her apparent lack of respiratory signs and symptoms related to the web,
and her own awareness of the unusual quality of her voice were given careful consideration in
the decision-making process.

Case Study 2: Dysphonia of Unclear Origin in a 14-Year-Old

Aspiring Singer
M. P. was a 14-year-old girl referred to the Voice Clinic by an outside otolaryngologist. His
report indicated that M.P.’s voice teacher felt that there was a marked change in her vocal quality
as M.P. ascended in her fundamental frequency range. The otolaryngologist had performed a
laryngological exam and thought nodules were present bilaterally. Referral to our clinic was for
additional evaluation and therapy.
According to her parents, M.P.’s voice had never been a concern to them. They reported
no recent change in her voice and in fact were surprised that the voice teacher had noted some
possible difficulty. M.P. was home-schooled and described as a typical, but not excessively vocal,
young lady. M.P. noted that she had always enjoyed singing and had never noted any particular
difficulties with her voice. However, during her voice lessons, the instructor had asked her to
engage in scales and other activities that required using the higher portion of her pitch range.
Both she and the instructor felt there was a marked difference in the quality of her voice as she
moved from lower to higher frequencies. In particular, M.P. described her voice as “very airy”
at these levels. She also reported difficulty sustaining tones when at higher pitch levels, even
though she was trying to regulate expiratory flow.
Perceptually, the quality of M.P.’s speaking voice was judged as within normal limits.
Phonatory function testing revealed a moderately reduced fundamental frequency range (13
semitones) and normal average F0 (228–232 Hz) for reading and speaking. Maximum phona-
tion duration was 17 seconds at comfortable pitch. Mean airflow during sustained vowel pro-
duction at comfortable pitch and loudness was 210 cc, and 170 cc during a syllable repetition
task. Produced one octave higher than her comfortable pitch level, airflows for sustained vowels
increased to 400 to 500 cc/sec. Estimates of glottal resistance and subglottal pressure, again, for
syllable repetition at comfortable pitch and loudness levels, were within normal limits as well.
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Laryngeal imaging was performed with rigid endoscopy and stroboscopy; a clip of this exam
is included here. Both true vocal folds appeared within normal limits in color and size. Both
moved on abduction and adduction. On phonation, both true vocal folds moved to the midline.
At comfortable frequencies, there was closure between the folds anteriorly, with a larger-than-
usual posterior chink. Asked to produce tones higher in her range, adduction was incomplete,
with little contact between the folds. Consistent with these observations, voice quality at
the higher pitches was quite breathy. In voice produced at comfortable pitch and loudness,
mucosal and vibratory displacements appeared symmetric from right to left, and appropriate
in amplitude. These characteristics were difficult to accurately assess at higher pitches. The
diagnosis was bilateral vocal fold paresis. Neither fold appeared to adduct completely, and this
was particularly evident at higher pitches. Possible involvement of the cricothyroid muscles
could not be ruled out.
Further interview with M.P.’s mother revealed that M.P. had undergone 2 surgeries (un-
related to structures of the head and neck) at the age of 3 years. Reportedly, M.P. had been
intubated for both these, and both had been fairly long surgeries. The mother remembered the
surgeon noting after one procedure that intubation had been very difficult. She described M.P.
as having wakened once during the surgery, requiring extubation and subsequent reintubation.
M.P. also had very negative memories of this experience. However, the parents had apparently
not noted a change in her voice after either of the procedures. No other surgical experiences,
serious illnesses, or trauma were reported. Questioned more carefully, the impression was that
M.P. had learned to be guarded during swallowing, in particular, of liquids. Whether the paresis
described was related to surgery, was congenital, or related to other circumstances, was not clear.
However, trauma to the larynx at the time of surgery was considered a strong possibility, in
particular, given the history of traumatic intubation.
Treatment options were felt to be somewhat limited for M.P. She was in fact managing most
functions of voicing, breathing, and swallowing with little difficulty, and had only noted the
voicing difficulty during singing. A follow-up session is planned to “map” her vocal space both
acoustically (using the VRP), and then, with flexible endoscopy. Possibly, additional strategies
for expanding and optimizing her available vocal space in a manner that does not elicit excessive
or inappropriate behaviors may be forthcoming.

The Geriatric Voice

In this section, the biologic and voice characteristics of the geriatric voice will be discussed.
Here, geriatric will refer to individuals aged 65 years or older. Aging is a process that results
in a progressive decline of the multiple control mechanisms needed for daily life (Barry &
Eathorne, 1994). All organs are affected, although the change may be prevented or minimized
by physical activity, diet, and lifestyle. There may be a large difference between the chronological
age of an individual and his or her biological age. We do not all age at the same biologic rate.
Individuals with identical chronological ages can be very different in their biological abilities.
In his preface to the book Geriatric Otolaryngology, Dr. Jerome Goldstein (1989) reported on
several geriatric individuals to demonstrate that even at 72, 76, or 81 years of age, an individual
can be very active and biologically fit. One of his examples was an 81-year-old female power
lifter who dead-lifts 245 pounds, squat-lifts 148 pounds, and works out daily with running,
swimming, and lifting (Goldstein & Salmon, 1978). Clearly, we do not all age at the same
rate; we merely count the number of years from birth in the same way. A very good review of
the effects of aging on communication may be found in Linville (2001). A brief review of the
current understanding and treatment of the voice of the older adults can be found in Current
Opinions in Otolaryngology (Casper & Colton, 2000).
The term “presbyphonia” has been coined to describe characteristic voice changes that occur
with some frequency in the geriatric population. Increasingly, changes in voice are recognized
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as a significant factor in affected individuals’ quality of life. Clinically, we are often presented
with one older adult spouse who has a marked hearing loss, and the other who complains
that “no one can hear me.” Other symptoms commonly encountered include vocal fatigue,
that is, a change in quality or increase in effort required to produce voice from a.m. to p.m.,
difficulty coughing or clearing the throat, and an inability to enjoy social activities, or more
vocally demanding activities, such as singing.

Theories of Aging
The following is a brief discussion of some of the major theories of aging. Some of these theories
share similar concepts and information suggesting that we are still awaiting the development of
a theory that will account for all of the processes involved in aging and will help us understand
what aging is and how we might control it.

Planned Obsolescence Theories

The focus of these theories is DNA and the effect genetics has on the aging process. We all have
our own unique DNA code, a code that determines all of our physical characteristics and may
even determine how long we will live (and what kinds of diseases we may experience). DNA
can be easily damaged by outside influences such as diet, lifestyle, environmental pollutants,
and many other factors. Gene damage appears to occur when the gene repairs itself after being
damaged. The gene duplicates itself incorrectly, eventually leading to dysfunction of the cell.
Other factors that may damage the DNA molecules include the lack of important enzymes
used in DNA repair and the presence of free radicals produced as a byproduct of process used
to extract oxygen from the air we breathe.
A variant of this type of theory is the Telomerase Theory of Aging (Ahmed & Tollefsbol,
2001; Boukamp, 2001; Djojosubroto, Choi, Lee, & Rudolph, 2003; Kipling & Faragher, 1999).
Telomeres are repeating sequences of nucleic acids extending from the end of a chromosome.
When a cell divides, the length of the telomere is shortened. When the length reaches a critical
value, the cell can no longer replicate, and ultimately it dies. In a way, the telomere is a biological
clock that eventually winds down to cause death. However, there is some skepticism about this
theory because some animals have rather long telomeres but have relatively short life spans.

Free Radical Theory

This theory was developed by Denham Harman (Harman, 1992, 1998, 2001) and later pop-
ularized by others. Normal cell metabolism produces a byproduct, generally known as free
radicals. Free radicals are molecules with an extra electron. These free radicals cause damage
to the cell’s DNA structure, other proteins, and mitochondria. The extra electron causes the
molecule to try to bind with other balanced molecules. Thus, a free radical attacks other cells
in the attempt to become balanced. This attack in turn creates waste products that interfere
with normal cell function. Antioxidants are scavengers that bind to free radicals and reduce
their effects. They help to remove these free radicals and have been part of the popular herbal
medicine culture. Some researchers have suggested that antioxidants actually work to suppress
appetite. Reduced caloric intake has been shown to increase the life span of animals.

Neuroendocrine Theory
This theory focuses on the endocrine system and the role hormones may play in the aging
process. As we grow older, the hypothalamus loses its ability to precisely regulate the hormones
circulating through our bodies. This results in the receptors for the hormones becoming less
sensitive, which in turn results in less of the hormones being manufactured. The theory was first
introduced by Vladimir Dilman (Dilman & Dean, 1992) and has been advanced by Ward Dean
(Dean, 1999, 2003). Dean claims that more than 85% of deaths of the middle-aged and older
adults may be attributed to this faulty neuroendocrine regulation. He believes that replacement
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204 Understanding Voice Problems

of essential hormones and other substances involved in the regulatory process could extend life.
Dean recommends drugs that can reestablish some degree of regulatory ability to the various
structures involved in this regulatory control.

Membrane Theory
This theory was introduced by Imre Zs-Nagy who postulated that age-related changes in cell
membranes interfere with the ability of the cell to interchange chemicals, heat, and oxygen
with the external environment (Zs-Nagy, 1997). Cell membranes become less watery thereby
impeding the efficiency of membrane transfer. Waste products and toxins may accumulate
within the cell, resulting in cell death. Substances exist that improve the ability of the membrane
to transfer waste products, needed chemicals, and other substances.

Mitochondrial Decline Theory

Mitochondria are the energy-producing structures of the cells (Beckman & Ames, 1998;
Cadenas & Davies, 2000; Kowald, 2001). They are responsible for the production of ATP
(Adenosine Triphosphate) needed for everyday function. ATP cannot be stored in the body
and must be continually replenished by mitochondria. Mitochondria produce free radicals and
are also susceptible to free radicals, against which they have few defenses. As the production
of ATP declines because of mitochondrial damage, there is less energy for organ function.
Each organ has its own set of mitochondria and when these are damaged, the organ itself may
become damaged and fail. Antioxidants can be used to minimize the free radical damage of the
mitochondria.
There are other theories of aging, many of which are variants on the basic themes presented
previously. A single unified theory will no doubt emerge in time as more is learned about the
process of aging. That single theory will need to account for all of the effects described earlier
and generate methods to control the aging process and extend life.

Anatomical and Physiological Changes in the Larynx

Aging in the larynx affects cartilages, connective tissue, blood supply, glandular secretions, and
muscle. Changes in the lamina propria include loss of collagenous and elastic fibers, atrophy
of submucous glands, disorganization of collagen fibers, increased fibrosis, and atrophy of
the muscles (Gracco & Kahane, 1989; Kahane, 1987, 1981a, 1981b). Other authors have
reported an increase in the proportion of type I collagen fibers, diminished extracellular spaces,
disorganization and increased density of collagen layers, and a decrease in hyaluronic acid,
possibly related to a decrease in fibroblast growth factor (Butler, Hammond, & Gray, 2001).
Collectively, such changes could contribute to an increased stiffness in the lamina propria.
This observation, in fact, has led to investigation of growth factors as a potential injectable
material in aging vocal folds. As noted earlier (Allah et al., 2009), fibroblasts from Reinke’s
space were typically more stellate-shaped in geriatric specimens than in other age groups. Ding
and Gray (2001), investigating the extracellular matrix of rat vocal folds, found differences in
gene expression across young, old, and denervated muscle, with changes in the older specimens
more consistent with denervated muscles.
Structural changes may include ossification of the thyroid cartilage and changes in the
articular cartilages, including degenerative changes in the cricoarytenoid joints. Degenerative
changes in cartilaginous tendon attachments are also likely, with related effects on the viscoelastic
properties of vibratory structures. Blood supply decreases, and the types of cells present and
their proportional quantities are altered. Again, increased stiffness and decreased flexibility may
occur as a consequence. Decreased or altered production of secreting glands has been reported,
with implications for hydration of laryngeal tissues. Some or all of these alterations may affect
the vibratory characteristics of the vocal folds, thereby altering the perceptual, acoustic, and
physiological voice signs. Table 7.1 presents a summary of the age-related changes in various
parts of the body for men and women.
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CHAPTER 7 I Voice Problems Associated with the Pediatric and the Geriatric Voice 205

TABLE 7.1 Summary of significant changes due to aging (From Casper & Colton,
2001)
Morphologic Changes in Connective Tissue Male Female
Edema within superficial layer of lamina X X
Fiber density decreases leading to thinning of muscle and vocal ligament X X
Loose connective tissue replaces myofibrils X X
Decrease in number of fibroblasts that control synthesis of elastin and collagen, leading X X
to decreased synthesis of fibrous components in lamina propria
Elastic fibers in lamina propria no longer smooth or uniform in size; become rough and X X
variable in size
Elastic fibers no longer aligned parallel to free edge; run in various directions as a branched X X
network
Elastic fibers in superficial layer degenerate and atrophy affecting stiffness of vocal fold X X
Increase in density of collagen fibers More Less
Slow turnover and repair rates of elastic fibers More Less
Mucosal Changes
Mucous membrane becomes thinner and atrophic X
Mucous membrane thickens in postmenopausal women (edema, polypoid) X
Underlying tissue becomes infiltrated with fatty tissue X X
Underlying tissue becomes infiltrated with fatty tissue X X
Fatty tissue and keratosis lead to graying and yellow discoloration X X
Cartilaginous Changes
Ossification of cartilages More Less
Arthritic changes of cricoarytenoid joint X X
Thinning of articular joint surfaces, irregularities, breakdown in collagen fiber X X
organization
Muscle Changes
Atrophy More Less
Stiffening More Less
Apoptosis, programmed cell death occurs in TA muscle X X
Proportion of regenerating fibers increases with age, but the properties of those fibers X X
are not known
Decrease in surface density of certain muscle fibers X X
Increase in atrophy factor of certain muscle fibers X X
Decrease in ratio of satellite cells to myonuclei X X
(continued )
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206 Understanding Voice Problems

TABLE 7.1 Summary of significant changes due to aging (From Casper & Colton,
2001) (continued )
Morphologic Changes in Connective Tissue Male Female
Vascular Changes (Animal Studies)
Mucosal blood flow probably decreased as result of atrophy and increasing fibrous X X
characteristic of aging vocal folds
Decreased flow in PCA, TA, and CT X X
Sensory Changes
Decrease in number of small myelinated fibers in the superior laryngeal nerve
(animal)
Peripheral neuropathy (human)
Respiratory Changes
Decreased elasticity of respiratory tissues X X
Decreased vital capacity of lungs X X
Changes in chest-wall structure X X
Irregular respirations X X
Phonation initiated at higher lung and ribcage volumes X X
Higher lung and ribcage excursions X X
Trachea softens and widens; peribronchial muscle atrophy X X
Neuromuscular Control Changes
Vocal instability X X
General slowing of CNS functions X X
Increase in muscle fiber–type grouping X X
Glandular Changes
Decreased number of mucous glands due to atrophy X X
Decreased number of lymphatic channels X X
Hormonal Changes
Decrease in thyroid hormone X
Decrease in sex hormones X
Systemic Changes
Increased incidence of gastroesophageal reflux X X
Decreased auditory acuity X X
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Anatomical changes that may occur in the brain and spinal cord may have an impact
on the neurological control of the vocal muscles. Luschei et al. (1999) studied the electrical
activity of cricothyroid, thyroarytenoid, and lateral cricoarytenoid muscles in aged men and
women (>65 years). They reported lower firing frequencies of the thyroarytenoid in aged
men and suggested that a change in the morphology of motor units may account for these
differences. Similar findings were reported for a nonlaryngeal muscle (first dorsal interosseous)
by Erim, Beg, Burke, and De Luca (1999), who reported a decrease in firing rates, decreases in
fluctuations of firing rates, increased delays between motor unit firing rates, and a lower starting
firing rates for their geriatric subjects. In a rat model, Connor, Suzuki, Lee, Sewall, and Heisey
(2002) described significant changes in the neuromuscular junction of the thyroarytenoid
muscle with aging, including reduced axon terminal areas, and both increased variability in
unoccupied nerve terminals. The authors further noted (Connor et al., 2002) a decrease in
type IIB myosin heavy chain and increase in type IIX myosin (slower-contracting isoform of
the heavy chain) in both the thyroarytenoid and lateral cricoarytenoid muscles, but not in
the posterior cricoarytenoid muscle. McMullen and Andrade (2009), also investigating rats,
found that neuromuscular junctions were both smaller and less abundant in thyroarytenoid and
posterior cricoarytenoid muscles in the aged specimens, as compared to the younger animals.
The possible influence of these changes on laryngeal tissues and biomechanics is speculative.

Perceptual Signs
Extensive reviews of acoustic and perceptual features of the geriatric voice have appeared in the
literature (Casper et al., 2000; Colton, 1989; Linville, 1987a, 2001, 2002; Linville & Fisher,
1985a; Linville & Rens, 2001; Shindo & Hanson, 1990), and only a brief review will be pre-
sented here. Perceptually, listeners can identify a geriatric voice and can do so from a recorded
sample with surprising accuracy. Hoarseness, low pitch, imprecise articulation, breathiness, and
long pauses were found to be characteristic of geriatric voices by Hartman and Danhauer (1976).
In another study (Ryan & Capadano, 1978), the important perceptual features of the geriatric
voice included pitch, volume, speed, clarity, and authority. According to this study, geriatric
voices sounded less clear and less flexible. In a novel investigation, Harnsberger, Brown, Shri-
vastav, and Rothman (2009a,b) compared natural and manipulated voice samples to determine
perceptual characteristics associated with geriatric voice in men. Voice samples from young
men were resynthesized to reflect changes in fundamental frequency, speaking rate, tremor,
and presence of noise. The samples were added to unmanipulated samples representing young,
middle-aged, and older male voices and presented to listeners asked to estimate the speaker’s age
from each sample. Increases in speaking rate, tremor, and noise were all associated with increases
in perceived age; increased fundamental frequency did not show a similar effect, however.

Acoustic Signs
A number of acoustic features appear to change as a result of aging, though there is not universal
agreement about the type and extent of changes (see Table 7.2). Fundamental frequency has
been reported to rise as a function of age in men (Benjamin, 1981; Hollien & Shipp, 1972) and
fall in women (Brown, Morris, & Michel, 1989; Makiyama, Yoshihashi, Park Shimazaki, &
Nakai, 2006; Linville et al., 1985a). Nishio and Niimi (2008) reported decreased fundamental
frequencies in women, but did not find increases in speaking fundamental frequency in men
until the seventh decade, and this trend was reportedly not significant. Hollien (1987) postulated
the male–female coalescence model of voice change in which, with aging, men and women
become more vocally similar. The model predicts that the fundamental frequency of a male
voice will increase substantially as it ages, whereas the female voice will show a slight downward
change of fundamental frequency or no change at all. These predicted changes are thought to
be the consequence of the pronounced changes with the larynx of a male voice but with fewer
or less pronounced changes in the female larynx.
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208 Understanding Voice Problems

TABLE 7.2 Summary of physiological changes due to aging (From Casper &
Colton, 2001)
Perceptual Male Female
Determine age from voice sample X X
Classify into age groups X X
Pitch changes X X
Hoarseness X X
Breathy X X
Slow rate X X
Acoustic
Average fundamental frequency changes? Higher Lower
Variability of fundamental frequency Greater Greater
Frequency perturbation Greater Greater
Fundamental frequency range Smaller Smaller
Average intensity level Greater ?
Variability of intensity Smaller Smaller
Intensity range Smaller Smaller
Speaking rate Slower Slower
Spectral changes Yes ?
Physiological
Vital capacities Smaller Smaller
Lung pressure Lower Lower
Peak airflow rates Greater
Leakage airflow rates Greater
Open quotient Greater
MFDR Less
Muscle Electrical Activity
Thyroarytenoid—firing frequency or ISI Reduced Reduced
Cricothyroid—firing Frequency or ISI Same Same
Lateral cricoarytenoid—firing frequency or ISI ? ?

Fundamental frequency variability is also affected by aging. Mysak (1959) reported larger
values for men, whereas Stoicheff (1981), Linville and Fisher (1985b), and Morris and Brown
(1994) reported larger values for women. Fundamental frequency range is also reduced both
in men (McGlone & Hollien, 1963; Ptacek, Sander, Maloney, & Jackson, 1966) and women
(Linville, 1987b).
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Fundamental frequency perturbation also appears to be affected in aging. Orlikoff (1990)

reported much higher jitter values for his group of older participants (0.728) versus the young
group (0.461). On the other hand, others (Brown et al., 1989; Casper, 1983; Linville, 1987a,
1987b; Ramig & Ringel, 1983) reported no difference in jitter between young and geriatric
subjects. Baken (2005) relates a number of anatomical changes in aged larynges to a nonlinearity
model of laryngeal biomechanics and suggests that understanding causes of increased nonlin-
earity may provide novel ways to explain and perhaps treat voice disorders in this population.
Some investigators have suggested that the intensity of a geriatric voice may be slightly
greater than a young voice (Brown et al., 1989; Ryan, 1972) although the differences are
small. On the other hand, Hodge, Colton, and Kelley (2001) found that their older adult
speakers produced slightly lower SPLs at percentage points of their total intensity range. Morris
and Brown (1994) reported smaller variability of intensity for their group older adults (mean
age = 79.4 years) versus their young group (mean age = 27.5 years). Amplitude perturbation
or shimmer may be generally higher in the geriatric speaker (Biever & Bless, 1989; Ramig et al.,
1983; Ringel & Chodzko-Zajko, 1987). Huber (2008) and Huber and Spruill (2008) have also
described respiratory changes associated with aging, in particular, with louder voicing and longer
utterances, as compared to younger adults. Changes noted for the older adults reflected reduced
chest-wall compliance and elastic recoil forces, as compared to younger individuals. Consistent
with these data, Awan (2006) reported decreases in both vital capacity and maximum phonation
duration in aged female speakers, as compared to younger females. Collectively, these studies
suggest that both changes in stiffness and elasticity of the vocal folds and changes consistent
with sarcopenia and other alterations in respiratory tissues affect voice in older adults.

Observable Physiological Signs

Laryngoscopic changes reported in the geriatric population include bowed vocal folds, atrophy,
or apparent thinning of the vocal folds, edema, and a posterior glottal gap (1980). Segre (1971)
noted a yellowish discoloration of the vocal folds, atrophy of the ventricular folds, loss of normal
tension, and a fissure in the middle or anterior one-third of the glottis. A vocal fold sulcus has
been noted in some older individuals (Honjo & Isshiki, 1980; Mueller, Sweeney, & Baribeau,
1984).
Stroboscopic signs studied in the geriatric voice have been concerned with glottal closure
configuration (Biever & Bless, 1988; Biever et al., 1989; Linville, 1992; Södersten & Lindestad,
1990). Most young men exhibit complete closure of the vocal folds during the closed phase of
the vocal fold vibratory cycle (Linville, 1992). In contrast, and based on a small number of par-
ticipants investigated, geriatric men have been reported to demonstrate a greater incidence of
incomplete vocal fold closure (Honjo et al., 1980). In the female voice, Biever and Bless (1989)
reported that 90% of their 20 geriatric participants exhibited some kind of glottal gap. However,
80% of their group of 20 young men also exhibited some form of a glottal gap. Most of the young
women with glottal gaps had a posterior chink, whereas the older participants had midmem-
branous or anterior gaps in addition to a posterior chink. Pontes, Yamasaki, and Behlau (2006),
in a comparison of 50 geriatric and 50 younger adult participants, found increased instances of
vocal process prominence, vocal fold bowing, glottic closure, tremor, and phase and amplitude
symmetry in the geriatric participants. Observations were from endoscopic and stroboscopic
imaging studies, and no participant in the study had a vocal complaint. Linville (1992) also
reported a high incidence of glottal gaps in her sample of 10 patients (79%). Most common was
an anterior chink (27%), but she also described configurations such as posterior chink (13%),
spindle (11%), and incomplete closure (5%). Linville further reported that 86% of her group
of 10 young participants had some form of a glottal gap. It would appear that the presence of
a glottal gap, at least in women, is not a significant feature of aging. However, the precise form
of the gap may help to differentiate the older adults from the young ones, at least in women.
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210 Understanding Voice Problems

Other stroboscopic features studied in older individuals include mucosal wave, amplitude
of vibration, asymmetry, and stiffness. In their study of 20 geriatric women, Biever and Bless
(1989) reported that 85% showed aperiodicity of vocal fold vibration, 45% to 55% had some
mucosal wave changes on either vocal fold, 50% to 55% showed decreased amplitude of
vibration for either vocal fold, and between 5% and 10% of the patients showed some apparent
increase of stiffness of either vocal fold. Their young female participants showed much smaller
percentages of these signs. Thus, it would appear that aging may result in physical changes that
produce changes in the vibratory characteristics of the vocal folds.

Pathophysiology of the Geriatric Voice

Aging affects the structures of the larynx in varied ways and at varied times during the aging
process (see Table 7.2). Although there is a general trend toward age-related decline of function
in many body systems, the decline may be ameliorated or exacerbated by other factors such as
lifestyle, diet, and amount of physical activity. Similar comments may be said about the voice
itself. Singers who continue singing as they age can produce wonderful tones well into their
70s and, if infrequently, even into the 80s. Concomitant with increased age is the likelihood
that an individual will contract some kind of disease or experience some kind of accident.
Herrington-Hall et al. (1988) reported the prevalence of voice problems in their sample of
285 participants aged 65 and older (see Fig. 7.2). Of the men in their sample, cancer affecting
the voice constituted the largest group, followed by those with laryngeal paralysis and then
edema. Prevalent findings in women were paralysis, followed by polyps, and then nodules.
Cancer was present much more often in men (about 32%) than in women (about 10%).

FIGURE 7.2. Prevalence of voice problems in children 0–14 years. (Data are from Herrington-Hall, B. L.,
Lee, L., Stemple, J. C., Niemi, K. R., & McHone, M. M. (1988). Description of laryngeal pathologies by age,
sex, and occupation in a treatment-seeking sample. Journal of Speech and Hearing Disorders, 53, 57–64.)
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CHAPTER 7 I Voice Problems Associated with the Pediatric and the Geriatric Voice 211

FIGURE 7.3. Prevalence of voice problems in geriatric patients. (Data are from Herrington-Hall, B.L.,
Lee, L., Stemple, J. C., Niemi, K. R., & McHone, M. M. (1988). Description of laryngeal pathologies by age,
sex, and occupation in a treatment-seeking sample. Journal of Speech and Hearing Disorders, 53, 57–64.)

Kendall (2008) reported that benign lesions such as polyps account for most voice problems
in individuals over the age of 60, followed by malignant lesions and paralysis.
In our clinic, the vast majority of geriatric patients with a voice disorder have had a
physical or neurological problem associated with their voice disorder (1992). The most common
diagnosis among our group of 151 geriatric patients was vocal fold paralysis followed by cancer
(see Fig. 7.3) Voice disorders thought to be caused by the aging process itself accounted for only
about 4% of the patients. It is well known that many progressively deteriorating neurological
conditions typically affect people between the sixth and seventh decades of life. Many of these
have serious implications for voice production and communication problems. Manifestation
of the disease, as well as medications and other treatments for the condition, may be implicated
in voice changes noted.
Aging per se may not result in voice problems. However, geriatric individuals in poor
physical condition may experience more communication problems than those of the same age
who are in good physical condition. Quality of life in a group of older adults was also found to
be significantly related to perceptions of voice quality (Costa & Matias, 2005). We believe that
voice problems that might be attributable to aging can be minimized and improved by proper
attention to lifestyle, diet, and physical condition. Exercise is known to maintain or improve
heart rate, blood pressure, muscle strength, bone mass, as well as many other bodily functions
(Lowenthal, Kirschner, Scarpace, Pollock, & Graves, 1994). Preliminary evidence suggests
some benefit of voice therapy and of exercises designed to strengthen suprahyoid muscles, in
individuals with age-related dysphonia (Berg, Hapner, Klein, & Johns, 2008; Easterling, 2008).
Prevention of communication problems in the geriatric population may be the best course of
action. Vocal rehabilitation techniques for this population will be discussed in Chapter 10.
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212 Understanding Voice Problems

Summary
The chapter began with a review of the anatomical changes that occur during a child’s develop-
ment and how these characteristics compare with adults. Some of the anatomical changes may
help to explain some of the physiological characteristics of children’s voices. Congenital and
acquired conditions that affect the larynx and the voice are presented. Vocal nodules represent
the most frequently seen laryngeal pathology in children. Fortunately, nodules, or midmem-
branous thickenings, tend to resolve or improve with maturation. If needed, voice therapy and
counseling regarding likely causes, and strategies for minimizing them, may be quite helpful.
The pediatric section concludes with the presentation of a 7-year-old child with a laryngeal
web, and a 14-year-old aspiring singer with likely bilateral adductor paresis.
The section on the geriatric voice in this chapter begins with a brief discussion of a number
of theories on the aging process. No single theory has yet been found to be adequate. Tissue
changes implicated in all of them could have consequences for the larynx and voice. Organic
problems that may affect the voice of the geriatric population were also reviewed. The etiology
of these problems is not typically related to voice misuse but rather to illness. The effects of
these problems can drastically alter voice production, and the importance of differentiating
these effects from those related to aging is of paramount importance in assessing and treating
geriatric voice disorders. A variety of medical and surgical approaches available to address these
problems are presented in Chapter 9.
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CHAPTER

8
The Voice History, Examination,
and Testing
Keywords
history, interview, listening, examination endoscopes, laryngoscopy, disinfection,
flexible fiberoptic scopes, stroboscopy, high-speed film and video, videokymography,
fundamental frequency, phonetogram, perturbation, jitter, shimmer, spectrum, LTAS,
spectrogram, electroglottography (EGG), photoglottography, inverse filtering,
subglottal air pressure, electromyography (EMG), kymography, magnetometers,
respiration, CAPE-V, vocal effort, noninstrumental testing, special tests

Voice History
The clinical skills of the practitioner are critical when working with a patient with a voice problem.
The interview with the patient, the search for information, and the elicitation of the history require a
combination of art and science. The art is the skill of the clinician with the interview process and in
fitting together the various pieces of information. The science is the knowledge base that guides the
selection of questions and informs the interpretation of responses. The two are inseparable, and there is a
constant interplay between them throughout the interview and the treatment. It is not enough to know
what questions to ask, if there is no skill in the asking. It is not enough to know what questions to ask, if
there is no understanding of their implications or of why it is important to ask. It is not enough to know
what questions to ask, and to have skill in the asking, without adequate knowledge and understanding
for interpretation of the responses.
Another way to distinguish between what we have referred to as art and science is to think of
them as process and content (Reiser & Schroder, 1980). All communication between people involves a
process level. It is at this level of communication that many associations, silent questions, and feelings
are expressed by both the patient and the professional through both verbal and nonverbal means. The
content level of the interview refers to information specific to the problem.

The Interview Process

Teaching the skill of interviewing and the art of communication with patients is woefully neglected in
the training of most speech-language pathologists and physicians. Aronson (1985) states:

Any in-depth study of voice disorders forces us to conclude that so long as clin-
icians obtain privileged information from patients; so long as people have voice
problems because of life stress and interpersonal conflict; so long as voice disor-
ders produce anxiety, depression, embarrassment and self-consciousness; so long
as patients need a sympathetic person with whom they can discuss their distress,
will speech pathologists [and physicians (author’s addition)] need to consider their
training incomplete until they have learned the basic skills of psychological inter-
viewing and counseling. (p. 271)
213
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214 Understanding Voice Problems

Aronson presents further rationale for the need for good interviewing and counseling skills
and also discusses the personal characteristics clinicians must bring to the process. Although
Aronson targets his discussion on the interaction of the clinician with patients whose voice
problems are largely of psychological etiology, we feel the concepts are pertinent to interactions
with all voice patients.
During the past decade, the field of medicine has shown an increasing awareness of the emo-
tional components of disease processes. Furthermore, it has been recognized that effective treat-
ment of these components occurs when there is a positive relationship between the patient and
the health professional (Bernstein & Bernstein, 1985). The initial interview, usually the history-
taking session, establishes the patient–clinician relationship. It is the foundation on which the
success of treatment may depend (Bernstein & Bernstein, 1985; Hersen & Turner, 1985).
An interpersonal relationship by definition involves the dynamic interaction of at least
two people, each of whom brings emotions, expectations, experience, and knowledge to the
process. How these two sets of “baggage” match up, or fail to do so, will determine how well the
process unfolds. Indeed, some studies have indicated that the breakdown in this relationship
may be a major cause of malpractice suits (Blum, 1960; Rosenthal, 1978).
The clinical interview is an interaction of a particular type. Its specific purpose is to explore
the nature and history of the patient’s presenting symptoms. Unfortunately, it occurs within
set time limits and a busy office environment. Despite these limitations, the interaction need
not and must not be allowed to become rigid with preset boundaries.
Before we become clinicians, we are people who have been socialized into avoiding certain
topics of conversation, not asking overly personal questions of relative strangers and not probing
when a topic appears to make our conversational partner uncomfortable. As clinicians, we must
recognize that clinical interviews are different from social conversations. The professional has
not only the right but indeed the obligation to ask personal questions and to probe gently when
areas require further exploration. A patient’s indication of discomfort or avoidance may be a
very important sign to the skilled clinician who knows how to probe without shutting off the
flow of information. A clinician can only do this successfully by reaching a level of self-comfort
in discussing sensitive areas.

What the Patient Brings to the Process

The patient comes to an evaluation or examination with a heightened sense of anxiety. The
patient brings a personal history not only of the current problem but also of previous problems,
previous contacts with members of the health professions, relationships, education, social ease,
personal needs, and culture. The patient’s ethnic background may shape attitudes toward illness
and affect interaction with professionals (Bernstein & Bernstein, 1985). The patient may also
have need for support and guidance in understanding the current problem. All of these factors
will fashion the patient’s behavior and responses.

What the Professional Brings to the Process

The most obvious contribution of the professional is expertise with a body of knowledge
concerned with voice production. But the professional also brings a history of encounters with
many patients, relationships with peers as well as with family and friends, personal needs, and
the pressures of time. In the current climate of frequent litigation, the practitioner may also
bring a sense of anxiety or wariness to the process, perhaps generating a defensive posture
toward the patient.
Bernstein and Bernstein (1985) identify the following as the responsibilities of the profes-
sional in the interview process:
1. Assume responsibility for the conduct of the interview.
2. Avoid control and rigidity that inhibits or intimidates the patient.
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CHAPTER 8 I The Voice History, Examination, and Testing 215

3. Keep the interview in focus.

4. Maintain flexibility.
5. Remain sensitive to the patient’s feelings expressed both verbally and nonverbally.
6. Do not permit expression of subjective, personal feelings.
7. Remain open and accepting of the patient even when the patient is hostile or uncoop-
erative.
To that list we would add that the professional must be able to speak in language tailored
to the individual patient language that the patient can understand and that is neither insulting
to the patient’s intelligence nor patronizing in manner.

Listening
Although we cannot fully explore all of the crucial aspects of interview skills in a single chapter,
the art and skill of listening demands more discussion. A frequent request of beginning clinicians
or of those who have not developed a level of understanding of a particular area sufficient to
allow them to be comfortable with it is for a checklist of questions to ask. Indeed, forms
providing such questions are readily available (Boone, 1983; Darley & Spriesterbach, 1978;
Wilson, 1987; Wilson & Rice, 1977). They will, however, prove to be of little help to the
inadequately trained clinician. For the trained and skilled practitioner, a form is a convenient
way to organize the interview, but is not cast in stone. The value of a form is directly dependent
on the skill of the clinician in conducting the interview and extracting the relevant information.
Attentive and sensitive listening on the part of the professional, rather than extensive
talking, is the key. Some argue that engaging in note taking during an interview is disruptive to
the process of attentive listening. Furthermore, patients may be influenced to focus on specific
areas if the clinician’s note taking appears to indicate those as areas of importance. Others,
however, feel that patients are made to feel confident about the importance of their reporting
when they observe the practitioner taking notes. Whichever system a given clinician uses, it
is important that the taking of notes be done in such a way as to minimize interference with
active and attentive listening.
Listening is more than hearing the spoken words. It involves observation of facial expres-
sions, both as one’s questions are heard and during the response. It involves observation of
body language. It involves attention to the sound of the voice, the suprasegmentals of stress and
inflection and prosody. And it involves hearing messages sometimes hidden behind the words,
the well-known “listening with the third ear” (Reik, 1948), and utilizing the sixth sense of
feelings or intuitions (Browne & Freeling, 1976). If the clinician is focused on self or the next
question to be asked, all of this will be missed. Indeed, much information will never be elicited.
As a component of developing good listening skills, it is necessary to develop a tolerance
for moments of silence. The beginning or insecure clinician tends to abhor silence, and the very
busy and rushed clinician has no time for it. Moments of reflection, of allowing the patient to
provide additional information or sometimes to raise a new point, can be exceedingly valuable.
The silence must be a comfortable one, however, in which the clinician must nonverbally
project a sense of ease and of understanding.
Listening well need not be a lengthy process. Good listening skills enable the clinician to
shape and control the interview. A balance must be maintained between the patient’s need to
talk and the clinician’s need to elicit pertinent information. The clinician learns to pick up the
important cues, to follow them while always targeting the problem, to ask directed questions
when indicated, and to refocus responses when necessary. Patients will usually provide all the
information needed by the professional, if they can be helped to express it in their own way in
an environment of understanding and acceptance.
It is difficult to learn the skill of interviewing by reading about it. Our intent here is
not to exhaust the topic but rather to raise it and recognize its importance. It is so extremely
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216 Understanding Voice Problems

important when dealing with voice patients because of the very close linkage between voice
and personality and emotional states. There are readily available resources that provide skills
training in listening and in interview skills. We would strongly urge that all academic courses
in voice disorders incorporate such skills training as part of the curriculum. Suggested readings
on interviewing may be found at the end of this chapter.
Before leaving this topic, we must not ignore the use of history questionnaires that can
be completed by patients prior to their appointments. There is some value in the use of such
questionnaires because they make it possible for patients to review personal medical records,
to validate their impressions against those of other family members or friends, and to think
about the issues raised by their answers. However, if questionnaires are taken at face value, they
clearly eliminate the immensely important interview process and abort the establishment of
a relationship between the patient and the clinician. If such forms are to be used, it is very
important for their contents to be reviewed verbally, allowing the patient to elaborate and
clarify, and opening the door for further probing by the clinician.

Content of the Interview: The Case History

The Problem
After initial introductions and review of identifying and demographic data, it is usually ap-
propriate to begin the interview by asking the nature of the problem that has brought the
patient for the examination. Not only is this a natural place to begin the interview, but the
patient’s response may hold a vast amount of information. The clinician will begin to get an
impression of how aware the patient is of the problem, how articulate the person is in providing
descriptive information, and what the patient’s level of concern or motivation is relative to the
problem. It is important to recognize that these early impressions should be recognized as just
that—impressions—which need to be verified or altered as the interview progresses. Indeed,
what eventually results from the interview and subsequent examination may be quite different
from the concerns voiced initially. Nevertheless, it is important to have this starting point.
Some patients will provide an almost nonstop narrative in response to the very first question,
whereas others will have to be prodded and asked many questions. Either type of patient will
require that the clinician manage the questioning skillfully so as to obtain all the important
information without being either drowned by trivia or blinded by an absence of response. It
is important to ask many open-ended questions in an attempt to elicit information without
putting words into the patient’s mouth. For example, the open-ended request, “Tell me about
the problem that brought you to see me today,” may bring a more complete response than, “I
understand you are here because you have a polyp on your vocal folds.”
In response to the question concerning the nature of the problem, it is helpful to obtain
the patient’s description of the sound of his or her voice and how it differs from other voices
or from his or her own premorbid voice. We have found that patients often are accurate in
describing the problem and that their statement of the primary symptom is an important one.
It is instructive to ask what patients believe may have caused the problem or what they
have been told about the problem by others they have consulted. Patients frequently indicate
a lack of understanding, or perhaps a misunderstanding, of information received from the
physician. It is not unusual for a patient to say, “My doctor said I have polyps or something
growing in my throat, but I don’t know what that means or what it has to do with my
being sent to you.” Other patients, of course, can quote the dates of office visits, procedures
that were done, and their outcome. Despite what they have been told, or in the absence of
having been given any information, patients often have their own ideas about the cause of
the problem. Frequently heard comments include “It’s this postnasal drip,” “It’s probably my
sinus condition,” and “I think I’m allergic.” It is important for the clinician to recognize that
patients frequently have difficulty giving up such ideas, even when they are unsubstantiated,
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and that the inability to do so may compromise the treatment program. Therefore, it will
be important for these issues to be raised at the appropriate time in the process, and for the
patient to be provided with information that is understandable and acceptable. The nature of
the clinician–patient relationship established during the initial contact will have an important
impact on this subsequent interaction and the patient’s acceptance of new ideas.

Effect of the Voice Problem

If the patient has not spontaneously commented on the effect of the voice problem on his life,
it is important to ask about this as a follow-up question. Once again, this information will help
the clinician understand the degree of importance the patient attaches to the problem. Voice
problems may exert profound effects on people, including depression, anxiety, withdrawal,
embarrassment, and self-consciousness. Indeed, a voice problem may have a profound effect
on the individual’s total being. On the other hand, for some the voice problem may be a
minor embarrassment or have little effect on lifestyle. The severity of this reaction is not always
directly proportional to the severity of the voice problem. Equally important is the information
as to what effect the problem has had on family members, on work-related activities, and on
coworkers or superiors, that is, on all aspects of the person’s life. Some patients may express
denial of a problem and a lack of personal concern. Such statements must be fully explored
before they are accepted as valid. Feelings expressed by the patient in this discussion must be
listened to carefully. The clinician must use skill in helping the patient to discuss feelings openly
without fear of being judged or humiliated.

Developmental History of the Problem

Very valuable information may be obtained from this section of the case history. It is important
to learn as much as possible not only about the onset of the current episode but also about
how it has developed. Information relative to previous episodes of voice difficulty and any
prior treatment and outcome must be known. When patients suggest dissatisfaction with the
outcome of previous treatment, it is necessary to inquire whether there is any litigation in
progress or in planning. This information may sometimes be obtained in an oblique or indirect
manner rather than by a direct, confrontational question. In some instances, patients may have
been referred by a lawyer specifically for a second opinion. This knowledge may have little
impact on your assessment of the patient, but it is helpful to know it in advance, and it may
have some impact on the degree to which the entire interaction is documented.

Onset
The onset of a voice problem may be gradual or precipitous. Why is this a critical piece of
information? In understanding the natural history of the development of laryngeal pathologies,
we know that it is most likely that certain problems will develop over a period of time, whereas
others may have a very sudden onset. Although some patients can provide only rather vague
information about the onset of the problem, others will provide the date, time, and exactly what
they were doing at the very moment that the problem began. Clues to the diagnosis may be
contained in each of these types of responses as well as in the host of responses that lie between
these two extremes. Patients frequently date the onset of the symptoms of a problem to another
stressful occurrence in their lives. This is a natural tendency that can sometimes be misleading
if accepted without full and careful exploration. Another common report is the association of
an episode of laryngitis or upper respiratory infection with the onset of the current problem.
This event may indeed have some bearing on the problem, but it requires verification.
Most laryngeal lesions develop over time. An exception to that would be the apparently
rapid development of a polyp or vocal fold hemorrhage coinciding with a specific episode
of excessively strenuous voice use. Patients have reported the sensation of a sudden, sharp
pain during shouting or loud, stressful singing, with the subsequent finding of a hemorrhage
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218 Understanding Voice Problems

or hemorrhagic polyp. We know that professional singers may show evidence of beginning
nodules immediately after a performance; these usually resolve spontaneously if the voice is
allowed to rest in a state of less strenuous use.
The majority of patients with laryngeal growths that affect the vibratory behavior of the
vocal folds (and thus the sound of the voice) report a gradual onset of voice symptoms over a
period of weeks, months, or even years. Often they describe early episodes of voice change lasting
only brief periods of time, with return to what they describe as normal voice. The episodes
increase in frequency and in duration over time, and the normal voice does not return. By the
time they seek medical attention, the problem may have become chronic and be worsening.
Voice changes that result from vocal misuse, including increased musculoskeletal tension,
also tend to run a gradual course even though observable laryngeal pathology may not be
present. Indeed, it is not uncommon for patients to be totally unaware of when or how a
problem developed. Small, gradual changes tend not to be noticed, and persons unaware of
these minor changes show little or no concern until a more obvious change is noticed either by
themselves, a friend, or a family member.
Neurologically based voice problems may have either a sudden or a gradual onset. Progres-
sive deteriorating neurological diseases that affect the voice tend to do so in a gradual manner,
whereas the precipitous nature of a stroke or a head injury may have an equally precipitous
effect on voice production. Recurrent laryngeal nerve paralysis is not an uncommon result of
severing the nerve during thyroid surgery (Johns & Rood, 1987). Obviously, the resulting voice
problem will be immediately noted postoperatively. However, the history provided by patients
with idiopathic recurrent laryngeal nerve paralysis is not so clear. Some patients report a slight
voice change at first, with worsening of the voice symptoms over a relatively short period of
time. Others report a very sudden change that neither worsens nor improves.
The voice of the adolescent male that fails to lower in pitch despite normal laryngeal growth
no longer sounds exactly like it did prior to laryngeal growth, but it usually takes months, or
more likely years, for it to be recognized as unusual.
Sudden, marked vocal change that can be pinpointed as to date and time, in the absence
of other symptoms suggestive of an organic etiology, is often the first clue of a psychogenic
dysphonia. It is important to caution, once again, that the process of differential diagnosis
involves the exploration of all facets of a problem and does not allow for premature conclusions.
Clues such as this must be viewed as only one piece of a puzzle, and the clinician must be careful
to maintain an open mind so as not to overlook important information that might not fit a
preconceived notion.

Duration
When a voice problem has occurred in a sudden manner, its effect on the person is usually more
disturbing than a gradual change, and, as a result, consultation may be sought more quickly.
Nevertheless, it has been our experience that a period of months has usually elapsed from the
onset of the problem to the time the person is referred for a voice evaluation. The pattern
usually involves a period of consultation and treatment with the family physician, pediatrician,
or other practitioner, followed by referral to an otolaryngologist. Another period of treatment
may ensue, and if the problem persists, referral is made to a voice management team, to an
otolaryngologist who specializes in laryngeal problems, or to a speech-language pathologist.
As noted previously, many problems have a gradual onset or may have been tolerated at
a low level of dysfunction for lengthy periods of time. It is often not possible to determine
how long a condition has been present. The germane question, then, is, “Does it matter?” The
answer is, “yes,” and “maybe.” Obviously, if the patient’s problem involves a malignant lesion,
time is of the essence. The earlier a malignancy is identified, the more positive the prognosis
and the less traumatic the treatment. Early identification of any organic condition is, of course,
a desired goal. It is easier to obtain resolution of a small, soft, new nodule than one that has
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CHAPTER 8 I The Voice History, Examination, and Testing 219

become increasingly fibrotic over time. It is also easier to change abusive habits that have not
had a lengthy period to develop. Early identification of certain neurological disease processes
may allow early treatment of symptoms, if possible, although such treatment may not change
the course of the disease. Early diagnosis and treatment of psychogenic dysphonias may shorten
the period of time during which the patient must be dysfunctional. In some cases, the longer
maladaptive behaviors persist, the more difficult it can be to modify them.
The clinician needs to obtain the best estimate possible of the duration of the problem.
This information, put into context, will help the clinician plan a treatment protocol.

Variability Versus Consistency

The reporting of the variability or the consistency of a voice problem is very important. It
is unlikely, for example, for a person with paralysis of the recurrent laryngeal nerve to report
much variability in voice production from hour to hour or day to day. Some minor worsening
of symptoms might occur with extensive or strenuous voice usage. (It is important to recognize,
however, that return of nerve function and thus return of normal voice may occur in cases of
idiopathic paralysis. This would not constitute variability of symptoms so much as a change
or improvement of voice.) We would not expect a person with a mass lesion to experience
periods of normal voice. Such a patient may report improved voice for periods of time, but if
questioned carefully it will become apparent that improved does not mean a return to normal
voice. However, that same patient may experience worsening of symptoms associated with voice
use. Another caution here is that patients who have experienced months or years of disordered
or changed voice may no longer have a very clear auditory memory of how they used to sound,
or be sensitive to minor variability.
Variability in voice production can be understood in the light of certain neurological dis-
orders. For example, patients with myasthenia gravis may experience periods of entirely normal
voice production but will report a gradual worsening of voice with prolonged speaking and
increased fatigue. Patients with voice disorders of psychological origin frequently report much
variability in voice production. This variability, usually unpredictable, may occur throughout
the day, from day to day, or for other time intervals.
Some patients report that their voices are at their worst in the morning, for the first
hour or two after arising. Such report should raise the suspicion of gastroesophageal reflux
disease. Reflux frequently occurs while the person is sleeping in the prone position, allowing
acidic stomach contents to actually wash up over the posterior laryngeal areas, including the
arytenoids.
Variability of voice production may be situation related, use related, or related to general
physical well-being. Voice-disordered patients frequently report a worsening of vocal function
when under stress and when physically fatigued. Both of those states have a tendency to
exacerbate any existing condition, but the clinician must not assume psychological causation
based on such reports. When patients report variability in symptoms, they should routinely be
asked to describe those things that seem to make the problem better and those that make it worse.
Once again, it is important to emphasize that in order to understand the implications
of information received, the clinician’s knowledge base must include awareness of the ways in
which phonation can be affected by pathology and use factors.

Associated Symptoms and Sensations

It is always important to ask patients about any other symptoms they may have experienced
that they associate with the voice problem. These may include difficulty in swallowing, slurring
of speech, loss of fluids through the nose, weight loss, excessive coughing, increased fatigue,
heartburn, and the like. In addition, it is important to inquire about sensations in the neck,
throat, and larynx, either accompanying phonation or at other times. Patients with patterns
of vocal abuse and increased musculoskeletal tension frequently report the sensation of pain
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localized lateral to the larynx and a feeling of fatigue. It is not uncommon for a patient to say, “I
just feel my throat is too tired to talk.” Some patients with mass lesions or laryngeal irritation
report the sensation of a constant lump in the throat and a need to strain to produce voice loud
enough to be heard. A feeling of dryness in the mouth and throat is often reported. Reporting
of many other sensations may be provided by the patient. Such reports may be helpful not only
in the diagnostic process but also as useful indicators of change in response to treatment.

Patient History
Voice Use
Exploration of how much a person talks and of where and how the voice is used constitutes
a crucial part of the total history. An individual’s job and lifestyle may not give indication of
excessive or abusive voice use until it is discovered that she is or was a cheerleader, or he is the
soloist in a church choir, or she performs with an amateur theater group.
There are specific concerns relative to voice use and, indeed, the entire voice history, if the
patient is a professional voice user, a person whose profession is dependent upon use of a “good”
voice (e.g., a singer, actor, teacher, lawyer, minister, or public speaker). Of major importance is
whether or not the person has had professional voice training. It has been our experience that
among the most difficult patients to treat are singers who have had no vocal training but who
have had a few years of success in singing with a small group or choir, or in amateur theatrical
productions. They have not recognized their abusive vocal behavior, which now has “caught
up with them,” often resulting in laryngeal tissue changes. It is difficult for these patients to
understand or accept that what they have been doing constitutes the problem.
Vocal performers work in a variety of settings and environments and engage in many styles
of performance. Some must sing above the sound of amplified music, some perform in large
areas without adequate amplification; some use a belting style, some sing rock, some perform
in smoke-filled rooms, and some may be performing at night after rehearsing all day. The vocal
demands of actors’ scripts vary from job to job. All of these factors must be explored. Not to
be forgotten, however, are the nonperformance vocal demands and voice habits of professional
voice users. It is not at all uncommon for well-trained performers who have learned their art to
use their voices well when singing or on stage but show little transfer of those habits to everyday
speaking behavior. In addition, professional voice users are not immune to vocal abuse when
engaging in noisy postperformance parties, loud talking backstage, teaching, and during other
strenuous uses of the speaking voice. Sataloff (1981, 1986, 1987a, 1987b, 1987c) presents a
thorough discussion of the voice history to be used with professional singers as well as samples
of case history forms.
As noted earlier, any individual whose livelihood depends on the use of voice can be
considered a professional voice user. Lawyers who must effectively argue cases before juries
present with their own particular sets of phonatory demands and issues. These must be explored
along with the individual’s total patterns of voice use in and outside of a court room. Clergy often
present unique problems due to the constant demands on voice use, for example, preaching,
teaching, community meetings, and person-to-person interactions, and all to be done without
the benefit of voice training. It is imperative that preaching style be explored thoroughly by
reviewing recordings of actual preaching or obtaining a truly representative sample. The vocal
demands placed on teachers are often heavy and compounded by lunchroom and recess duty,
extracurricular activities, parent–teacher meetings, dusty environment (from chalk) with poor
ventilation, difficult room acoustics, and the added demands on voice outside of school. All of
these factors must be thoroughly explored during the initial information gathering session.
Children constitute another group for whom the voice use history must be carefully inves-
tigated. Some children may use their voices at appropriate levels and in acceptable ways much
of the time, but the voice of the playground may be excessively loud, or making “weird sounds”
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may be a hobby. There are, of course, children who use their voices loudly and aggressively
much of the time.
The voice and the manner of voice usage demonstrated in the office situation during the
initial visit may not be an accurate reflection of potentially abusive voice use on the job, at the
playground, or in the home. It is necessary to explore all these areas thoroughly during the
interview and perhaps pursue them further during the voice evaluation.

Health
Because the voice is such an integral part of the whole person, it serves to reflect not only
emotional states and personality but also physical states. We recognize the weak voice of the
very ill, the lifeless voice of the pharmacologically subdued, or the tired voice of the physically
exhausted. It has been said that the whole person “is considered to be greater than the sum of
its parts; each part can only be understood in the context of the whole; a change in any one
part will affect every other part” (Papp, 1983). It is for these reasons that the voice history must
explore a patient’s health history. The vital importance of the proper functioning of all body
systems for the professional singer has been described by Sataloff (1981, 1986, 1987a, 1987b,
1987c), who provides as one example the effect a broken leg may have in altering the singer’s
posture, thereby affecting abdominal support for singing.
It is most appropriate to inquire first about the patient’s present health status. We are
most interested in whether the patient has any neurological problems, respiratory problems,
problems affecting the gastrointestinal tract, allergy-related problems, or psychiatric problems;
suffers from any chronic conditions such as arthritis; has any congenital anomalies or hearing
loss; or has any other current health problem. The past health history, which may be relevant
to the present vocal difficulty, is also important, as is the patient’s history of surgeries and
hospitalizations. It is important to know the nature of surgical procedures that the patient has
undergone, particularly those that may have some connection to the present difficulty, such as
laryngeal, head and neck, thoracic, or cardiac surgery. For example, a history of appendectomy
at 4 years of age may not be pertinent in the case of a 35-year-old patient. However, the history
of cardiac surgery in that same patient should be explored to determine whether any sequelae
of that surgery were directly related in time to the onset of the voice problem. What kind
of sequelae may accompany such surgery? The most obvious might be hoarseness following
intubation. However, recalling the course of the left recurrent laryngeal nerve, injury to that
nerve might also be a possible sequela of cardiac surgery.
When exploring the surgical and hospitalization histories of a patient, it is important
to learn either from the patient or from medical records whether the patient was intubated
and, if so, whether it was a difficult or traumatic intubation, whether extubation and repeated
intubation were required, the duration of the intubation, and whether there is a time relationship
between the procedure and the present voice problem.
Another related area to be explored is whether or not the patient has experienced any
trauma, the effects of which might have an impact on the structure of the larynx or the mucosa.
Some possible categories of such trauma would be blows to the neck, knife or gun wounds,
automobile or other vehicular accidents, chemical ingestion or inhalation, and body burns or
smoke inhalation.
A thorough history of substance use is important and takes some skill to elicit truthfully and
completely. Substance abuse, that is, excessive use of alcohol or illegal drugs, is often not readily
admitted. Questions about these areas must be asked in the same manner as inquiries into all
other areas. The clinician must, however, be prepared to pursue vague responses or to probe
further whether there is reason to believe that the patient may be withholding information. It
is often necessary for patients to be reassured about the confidential nature of the interaction.
But patients do not seem to be reticent in divulging a history of tobacco use even when it is
quite excessive.
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There is widespread use of over-the-counter and prescription drugs in the treatment of

illness or various physical discomforts. Because drugs work systemically, they often have an
effect on all mucosa or tissues, not just that which is being targeted. For example, diuretics are
used in many conditions in which release of fluids from body tissues is desired. However, it
must be recognized that the laryngeal mucosa is not exempt from the diuretic action. Whereas
release of excess body fluid may be very helpful to a person with certain medical conditions,
the associated drying of laryngeal mucosa may have a negative effect on phonation.
Because the effect of various drugs on the laryngeal mucosa and laryngeal motor control
is such an important yet relatively unreported area, additional information on it was presented
in Chapter 4.

Vocational
It is not sufficient to simply obtain a person’s occupation. It is necessary to discuss the nature
of the work done, the environment in which it is done, the need for an adequate voice to
carry out the job requirements, interactions with coworkers and superiors, and the level of job
satisfaction. In this area, as well as throughout the history taking, open-ended questions, such
as “Tell me about your job and the people with whom you work,” may elicit more complete
information than closed questions, such as “Do you need to talk as part of your work?”

Social
The focus of questioning in this area is designed to obtain information about the patient’s
lifestyle, family constellation, and even living arrangements. Environmental factors such as lack
of adequate humidification or the use of a wood stove may have adverse effects on laryngeal
tissues. People often do not recognize vocally abusive behavior that may occur in the home when
yelling to the children or pets who are out in a large backyard or upstairs in another part of a
house. Perhaps a hard-of-hearing person is a member of the family, requiring louder-than-usual
voice usage. Home life is replete with examples of the need to raise the intensity level of the
voice: talking above the television or music, talking above the level of others’ speech in order to
gain their attention, and arguments. If the lifestyle includes much entertaining of large groups
or frequenting of bars where extremely loud music is a constant background noise, vocal abuse
may well be involved in the voice problem. Relationships with family members or “significant
others” may be a source of stress or anxiety, which may be reflected in a problem with the voice.

Recreational
Certain recreational activities may have implications for the voice. For example, the weightlifter
who strains mightily while lifting, simultaneously producing harsh, grunting phonation, is
placing considerable stress on the laryngeal tissues, and so, too, the golfer or tennis player who
phonates with each swing of the club or racket. Forceful phonation accompanying strenuous
exercise of any type may constitute abusive behavior.

Psychological
Placing this information at the end of this section should not suggest that it has the least im-
portance. Indeed, psychological factors may be of utmost etiological importance. Furthermore,
as stated previously, all disease processes carry components of emotional stress.
Throughout this chapter, and elsewhere in this book, frequent reference is made to the
close link between voice and personality, between voice and self-identity, and between voice
and emotions. After our physical appearance, it is the voice that sets us apart from others
and serves to identify us to others. It reports about our physical condition as well as our
emotional state and well-being. How often during a phone conversation have you commented
to a friend that she sounds tired or depressed or, perhaps, really happy? Because of this close
linkage, the voice may also be the primary reflector of inner turmoil. The importance of
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recognizing stress-related voice usage and the need to explore the patient’s social interactions
and interpersonal relationships cannot be overstated. The skilled clinician will be alert to
indications, both verbal and nonverbal, of psychological stress factors. A patient’s history of
previous or current involvement in counseling or psychotherapy is valuable information.

Examination of the Voice

Examination of the larynx and testing of its performance can be carried out through a variety of
techniques. It is our bias that no one or two procedures are enough to provide the best and most
complete information about a person’s vocal functioning. Furthermore, each procedure adds to
our understanding of normal voice production and of the deviations that alter the normal state.
We are well aware that many assessment techniques are not immediately available to many
speech-language pathologists or voice coaches, or to all practicing otolaryngologists (Feder,
1986). However, within the past decade there has been an explosion of interest in the voice and
a concomitant development of voice laboratories. These laboratories can often provide testing,
examination, and diagnosis by an interdisciplinary team of voice specialists. It is, therefore,
highly likely that full information is obtainable from sources within the community or in close
geographic proximity, if it is sought. It is no longer acceptable to make diagnoses of voice
disorders without adequate data. Claiming lack of immediate availability of equipment is akin
to a physician failing to obtain an x-ray because he does not own radiology equipment.

Examination Procedures
There are many procedures that can be used to examine the larynx and vocal folds. Some
involve direct visualization of the vocal folds, whereas others record some of the aerodynamic,
vibratory, or acoustic events in the larynx. Direct examination of the larynx usually requires
the insertion of a device to transmit light to the folds and receive the image back. This involves
invasion of the airway of the patient with potential risks to both the patient and the examiner.
It is important that anyone who examines patients be aware of the potential risk of infection
or injury and follow universal precautions during the examination. Gloves should be worn by
the examiner when manipulating any part of the patient’s anatomy, particularly those areas
where the examiner could come into contact with body fluids, that is, saliva, blood or blood
products, or other fluids. Any instrument that is inserted into the patient’s oral cavity or nasal
cavity should be properly cleaned and disinfected after use. If the instrument touches any blood
product, it must be sterilized.
Oral or nasal endoscopes used for continuous or stroboscopic light examinations need
to be disinfected (Rutala, Clontz, Weber, & Hoffmann, 1991). A solution of glutaraldehyde
such as found in Cidex is often used to disinfect endoscopes. This solution will not harm the
components of the endoscope (unless allowed to soak for very long periods of time) and can
be effective in eliminating most bacteria and viruses. Read and follow the directions on the
product to determine the effective concentration and length of time the endoscope should be
immersed. It is essential to be knowledgeable about guidelines for infection control that may be
in use within your employment setting. Private practitioners should also have such guidelines
in place and ensure adherence to them by all employees.
Face masks are often used to collect information about the airflows during speech. Although
these do not usually come into contact with blood or even mucus, they should be disinfected.
Although glutaraldehyde solutions could be used, we are not certain about their effects on the
individual components of face masks, especially the rubber seals that surround the circumference
of the mask. We routinely use a diluted solution of common household bleach to disinfect all
parts of our face masks. A 25:1 dilution is recommended (Rutala, 1990) and should be effective
for about 30 days. However, since bleach is so inexpensive, we mix fresh solutions every week
or so. Thoroughly clean all parts of the mask with a water/soap solution (Hibiclens, Stuart
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224 Understanding Voice Problems

Pharmaceuticals) to remove any foreign matter on the mask. Immerse the masks and its parts
for at least 20 minutes in the bleach solution. Rinse off and allow to dry before use. (For more
information on disinfecting face masks, see Colton, 1994) If spirometry is routinely used in
your clinic, you should be aware of the potential risks of transmission of airborne pathogens
via the instruments used (Rutala, Rutala, Weber, & Thomann, 1991).

Indirect Laryngoscopy
Indirect laryngoscopy is the traditional means of examining the larynx using a laryngeal mirror.
This technique requires that the tongue be pulled forward as the mirror is introduced into the
oropharynx and positioned in such a way as to reflect the image of the vocal folds. Pulling the
tongue forward has the effect of moving the epiglottis forward, thereby allowing visualization
of the laryngeal structures. The patient is then asked to produce a high-pitched /ee/ sound.
The choice of the /ee/ vowel enhances visualization of the larynx during phonation because its
production is usually characterized by superior and anterior movement of the dorsum of the
tongue and the epiglottis. The reasons for the use of a high pitch are (a) the vocal folds are
expected to lengthen in the phonation of a high pitch, and this lengthening maneuver tends to
“open” the larynx to view, and (b) there is usually some degree of upward vertical movement
of the larynx in the production of a high pitch, which brings the structures closer for viewing.
Indirect laryngoscopy is thought of as a fairly noninvasive procedure because it does not
require anesthesia or surgery, nor does it cause any pain or other trauma to the patient. It does,
however, have some limitations. There are patients who have very active gag reflexes and are
unable to tolerate the presence of the mirror deep in the oropharynx. Anatomical variations
not infrequently make it difficult to visualize the larynx adequately with the mirror exam. It is
especially difficult to visualize the larynx of a young child through indirect laryngoscopy due
to the anatomical relationships of the structures, which are different from and smaller than
those of the mature adult. Another limitation is the inability of the patient to speak in a normal
manner in the position required for this examination, thus limiting the information available
relative to laryngeal physiology. Indeed, it is possible that the unnatural positioning required
and the tension created in the patient may actually alter the typical laryngeal behavior of an
individual, thereby rendering a less-than-accurate impression of phonatory behavior.
Despite these limitations, indirect laryngoscopy continues to be a useful means of exam-
ining the larynx, especially in conjunction with other visualization techniques.

Direct Laryngoscopy
Direct laryngoscopy is perhaps the most invasive of the laryngeal examination procedures. It
is usually a hospital-based procedure requiring that the person be anesthetized. Direct laryn-
goscopy permits more detailed examination of laryngeal structures, including their actual ma-
nipulation. It is required when it becomes necessary to obtain a biopsy of a lesion and in
attempts to determine the extent of a lesion. Manipulation of the arytenoid cartilages may be
helpful in making the distinction between a diagnosis of arytenoid ankylosis versus vocal fold
paralysis related to a nerve injury.
The disadvantages of direct laryngoscopy are its invasive nature, its cost, and the inability to
observe laryngeal function. Prior to the relatively recent explosion of other imaging techniques,
direct laryngoscopy was sometimes necessary as the only means to examine the larynx in persons
for whom indirect laryngoscopy was unsuccessful.

Flexible Fiberoptic Laryngoscopy

The advent of fiberoptic technology has opened much of the human body to view in ways
never before possible. Fiberscopes are used in many branches of medicine as diagnostic tools. A
fiberscope, in simple terms, is a bundle of flexible fibers, some carrying light to the object to be
examined and others carrying the image back to the viewer. The flexible laryngeal fiberscope
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FIGURE 8.1. Schematic of instrumentation used in a fiberoptic examination of the larynx. The
procedure used during the examination is listed.

was introduced in the late l960s (Sawashima & Hirose, 1981). In order to examine the larynx,
the fiberscope is passed through the nasal cavity, over the soft palate, and into the oropharynx
and the hypopharynx, as shown diagrammatically in Figure 8.1. Its moveable lens tip can be
angled (the degree depending on the particular instrument), and the fiber bundle can be rotated
to view the full larynx. The tip of the scope is usually positioned vertically, slightly above the
epiglottis, but can be moved closer to the vocal folds for more detailed visualization. One of
the benefits of this instrument is the flexibility possible in the positioning of the scope in the
vertical dimension so as to allow visualization not only of the larynx but also of supraglottal
structures and even of the velopharyngeal mechanism. Within the larynx, it is usually possible
to view the anterior commissure, which is difficult to do with a mirror exam. The use of wide
angle and zoom lenses also adds to visualization capabilities. The zoom lens allows for a closer
look at specific laryngeal structures without discomfort to the patient, whereas the wide angle
lens permits visualization of the entire larynx and supraglottal structures as well (depending on
the vertical placement of the scope within the vocal tract). An example of a fiberoptic view of
the vocal folds during respiration is seen in Figure 8.2, and Figure 8.3 shows the same larynx
during phonation.
There are many advantages to this examination method. Although it may be characterized
as invasive because the scope is introduced into the body, it causes only minimal discomfort
as the scope is passed through the narrowest part of the nose. As the diameter of the scope
has decreased in size (and will perhaps continue to do so), discomfort to the patient has
decreased. The fiberscope can be used to successfully visualize laryngeal structure and function
in all but a relatively few patients. It is used with all age groups including infants, and it
allows visualization of the larynx in persons with hyperactive gag reflexes and those in whom
the anatomic relationships are only minimally distorted. It is possible to have the instrument
coupled to a video camera, thereby allowing for visualization of an enlarged image on a television
monitor during the examination and for videotaping the examination for careful subsequent
review. The image can be observed simultaneously by a number of people and has been used by
some as a feedback tool during therapeutic intervention (Bastian, 1987). Recording the exam
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226 Understanding Voice Problems

FIGURE 8.2. A normal larynx during respi-

ration. See color plate.

provides the addition of visual documentation to the traditional verbal description and can make
comparison of laryngeal conditions over time, or over a course of treatment, much more reliable.
A method for computer-assisted measurement of fiberoptic images has been described by
Conture et al. (1981) and was demonstrated to be useful in measuring and documenting actual
intrasubject change in laryngeal physiology accompanying the use of therapeutic techniques
(Casper, Brewer, & Conture, 1981). Digital acquisition of flexible fiberoptic images now permits
the use of digital manipulation and analysis techniques on these images (Colton, Casper,
Brewer, & Conture, 1989). Kay Pentax offers a stroboscope that features software to perform
measurements of vocal fold amplitude, glottal area, and lesion size. A major advantage of
fiberoptic laryngeal examination is that the patient is able to speak, sing, whistle, play a wind
instrument, or simply to sit at rest, with minimal interference created by the presence of the
fiberscope. This makes it possible for the patient’s phonatory and nonphonatory laryngeal
and supraglottal behavior to be observed. Speech tasks tend to move the scope because of

FIGURE 8.3. A normal larynx during

phonation. See color plate.
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the movements of the soft palate, and occasionally structures in the larynx may displace the
instrument. Rarely does the presence of the endoscope result in excessive nasality.
The quality of the fiberoptic examination will be influenced by the quality of the equipment
used. With traditional nasopharyngoscopes, a camera is attached to the proximal end of the
scope, and light is then directed through the scope to illuminate the image visualized. Casper,
Brewer, and Colton (1987b) cautioned that, with this type of scope, imaging of laryngeal
structures will be affected by factors inherent in the equipment, such as the wide angle lens
distortion effect, particularly at the periphery of the image, and distortions created by the
angling of the scope tip. Although these effects are not of sufficient degree to deny the overall
effectiveness of the instrument, they must be taken into account when interpreting observed
structural or behavioral deviations. Hibi, Bless, Hirano, and Yoshida (1988) have described
the distortions as systematic and have suggested a mathematical procedure that corrects for the
distortions. Newer technology utilizes a camera chip located in the tip of the scope, so that the
image to be visualized and the camera are much closer to each other, minimizing these kinds of
distortion and allowing more light available for illumination. These new generation endoscopes
are often referred to as videoscopes, or “chip in the tip” scopes. In addition to knowledge of
the capabilities of the equipment and the skill of the examiner in handling the endoscope, it
is important to consider the sample of laryngeal and supralaryngeal behavior elicited from the
patient. One of the primary advantages of this technique is that it allows such a diversity of
behaviors to be explored. In examining singers who are having difficulty in a particular portion
of their range or in some aspect of their singing technique relative to phonatory behavior,
it is possible to watch the larynx and vocal tract as they “perform.” For examination of the
voice-disordered patient, a complete protocol of speech and nonspeech activities, designed to
elicit habitual speech behavior, flexibility of pitch adjustments, adductory nonspeech behavior,
resting state, and any other behaviors of interest, must be well thought out. In order to obtain the
best visualization of the larynx during speech, stimulus sentences should be heavily loaded with
the /ee/ and /oo/ vowel sounds. Whistling, a nonphonatory activity, frequently provides the
opportunity to observe abductory-adductory vocal fold behavior at a slower rate than is possible
in speech. In short, vocal behaviors typically sampled in a conventional voice evaluation can be
elicited while the examiner both listens to the voice and observes the structures producing it. We
refer to this technique as a “phonoscopic exam.” A suggested examination protocol can be found
in the appendix. This protocol may serve only as a starting point, after which activities designed
to elicit a particular behavior of interest or to attempt to change a laryngeal gesture may be added.
The person who performs this aspect of the fiberoptic examination must be skilled in “reading”
the image, in understanding the physiology, and in knowing the types of vocal maneuvers that
might elicit the desired changes in behavior. That person is frequently the speech-language
pathologist skilled in diagnosis of phonatory function. In some states, the use of endoscopes to
perform the phonoscopic evaluation requires an addition to the professional license required to
practice speech pathology. This may require mentoring by an otolaryngologist, documentation
of experience, or other evidence of competency in the use of the endoscope.
One of the limitations of endoscopic techniques using a continuous light source is that
vibratory behavior of the vocal folds cannot be seen. The technique does not alter the speed
of movement of the structures beyond what is visible with the human eye. Thus, in a certain
sense, fiberoptic examination provides a relatively gross look at phonatory behavior at the vocal
fold level. It can be used to assess the valving function of the vocal folds and, of course, to
visualize any pathology. It can be also used to assess vibration if it is used in conjunction with
a stroboscopic light source (as described below).
Who should perform fiberoptic endoscopy? Naturally, any ENT physician should have
the necessary training and experience to perform this procedure and to be able to handle
any potential problems that might arise. As noted, speech-language pathologists in increasing
numbers are receiving the training necessary to perform these procedures. ASHA has issued
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228 Understanding Voice Problems

guidelines to be followed by speech-language pathologists who are engaged in the use of this
and other imaging techniques (American Speech-Language-Hearing Association, 1992). It
is incumbent on the practitioner to receive adequate training and gain supervised experience
before performing this or any other procedure for the examination of the larynx. The individual
clinician is also responsible for knowing and adhering to any state licensure requirements
governing the use of endoscopes.

Stroboscopy
Stroboscopy is a procedure that has been used to examine the larynx, since the late 1800s. It is
now the primary technique used to view the behavior of the vocal folds in most clinics, hospitals,
and doctor’s offices in many European countries, Japan, and the United States. During the past
10 years or so, sophisticated and easy-to-use equipment has become available. Hirano (1981b)
states that “stroboscopic examination, as a routine clinical test, is the most practical technique
for examination of the vibratory pattern of the vocal folds.” Stroboscopy, indeed, permits vi-
sualization of vibratory behavior in a way otherwise not possible with the human eye and, in
so doing, enhances understanding of the physiological basis of voice disorders. Kitzing (1985)
further points out the benefits of the stroboscopic technique for early detection of neoplasms
and for differential diagnosis of laryngeal paresis and its outcome. Stroboscopy has been helpful
in differentiating between functional voice problems and those caused by subtle structural ab-
normalities of the larynx (Bless & Brandenburg, 1983; Woo, Colton, Casper, & Brewer, 1991).
The stroboscopic light emits rapid pulses at a rate that can be set by the examiner or
controlled by the fundamental frequency of the vocalization. If the frequency of the light pulse
is the same as the vocal frequency, the resulting image will appear to be static and the vocal
folds will seem to be at a standstill. At a frequency slightly less or greater than the frequency of
vocal fold vibration (often between 1 and 2 Hz), the image is, in effect, sampled at different
points in the vibratory cycle and, over several successive cycles, takes on the appearance of
slow-motion movement of the vocal folds. Each pulse of light illuminates a different point of
the vibratory cycle, as schematized in Figure 8.4. These fragmented sections become fused due
to the phenomenon of Talbot’s law, that is, the persistence of an image on the human retina
for 0.2 seconds after exposure.

FIGURE 8.4. Basic principle of stroboscopy. When a rapidly moving object (represented by the high-
frequency waveform) is strobed by flashes at a lower frequency (curve with open circles), the rapidly
moving object appears to move more slowly.
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Thus, stroboscopy differs from ultra-high-speed photography in that it creates an optical

illusion of slow motion and does not show details of each vibratory cycle, whereas high-speed
photography captures parts of each vibratory cycle at a very rapid rate, which appears as slow
motion when the film is projected at a normal rate of 24 frames per second.
The clearest images are obtained by using a rigid endoscope, a straight tube in which the
light-carrying and image-carrying fibers are encased. At the end of the scope is a prism that
directs light and receives the image at various angles depending on the specific endoscope in use.
Common angles are 90 degree and 70 degree. The flexible endoscope can also be used with the
stroboscopic unit. Recent developments by some equipment manufacturers have dramatically
improved the clarity and brightness of the images obtained with flexible fiberoptic endoscopy.
Another development made by manufacturers is the introduction of digital technology to
record and store the stroboscopic images. Digital storage of these recordings allows greater ease
of retrieval and side-by-side viewing of two different recordings. Digital recording techniques
also allow for greater ease of editing recordings for teaching purposes and the analysis of the
recordings using digital image-processing techniques.
At the start of the examination with the rigid endoscope, the patient is asked to protrude
his or her tongue, which is held by the examiner outside the oral cavity with a gauze pad. The
endoscope is then inserted into the mouth until its end is in the pharynx (but not touching
the velum or posterior pharyngeal wall, which may cause gagging). The exact position of the
endoscope needs to be altered slightly as the examination progresses to bring the vocal folds
into view. The technique is not difficult and can be learned rather quickly. Possible dangers are
gagging, bruising (if the endoscope is pushed hard against the delicate mucosa), or chipping of
the teeth. Practice can increase the skill of the examiner in obtaining good examinations even
with wide variations of anatomy and patient cooperation.
It is possible to carry out a stroboscopic examination using a rigid endoscope, a flexible
fiberoptic laryngoscope, or both. Kitzing (1985) also describes the use of stroboscopic light in
the operating microscope, combining good magnification and “superb optic resolution” while
providing stereoscopic evaluation of the mucosal wave.
The method for obtaining stroboscopic images is not difficult. A microphone is placed or
held on the patient’s neck along the lateral aspect of the thyroid lamina in order to record the
voice signal from which the fundamental frequency is extracted and used to control the rate of
firing of the stroboscopic light. The rigid or flexible scope is introduced, the stroboscopic light
is switched on (usually by a foot pedal), and the patient is asked to sustain phonation of the
vowel /ee/. The patient needs to produce a sufficiently long sample to permit the stroboscopic
unit to track the phonation and produce reliable stroboscopic light pulses. Because vocal fold
vibratory behavior will vary with frequency and loudness, it is important to obtain samples
of phonation produced in various ways. The following conditions should be a part of the
examination: (a) a minimum of 2 seconds (4 seconds is better) of sustained vowel phonation
at the patient’s habitual pitch and loudness level, (b) another phonation at a higher pitch, (c)
another phonation produced at a pitch lower than the habitual pitch level, (d) production
of sound at habitual pitch but at a level much louder than habitual loudness level, and (e)
phonation on inhalation. Often patients will initially produce a vowel at a level higher than
their habitual pitch or loudness level. With coaching and practice, they will be able to produce
a phonation more typical of their habitual pitch and loudness. Sometimes, additional samples
of phonation may be requested such as a string of the vowel /ee/ with intervening silences, or
a pitch glide. Samples of speech are not appropriate for stroboscopic examination.

Interpretation of the Stroboscopic Image

The stroboscopic image provides information about the following areas: symmetry of movement
of the vocal folds, regularity or periodicity of successive vibrations, glottal closure, amplitude
(horizontal excursion) of the vocal folds, presence and adequacy of the mucosal wave, phase
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230 Understanding Voice Problems

closure (open/closed phase), presence of any nonvibrating portions of the vocal folds, and addi-
tional observations relative to the presence of lesions and their apparent effect on the vibratory
behavior. Although all of these parameters can be systematically rated, most clinicians place con-
siderable importance on glottal closure, the mucosal wave, and the presence of any nonvibrating
segments. Observations of the stroboscopic image must be based on a thorough understanding
of laryngeal anatomy and physiology as well as of the changes in the mechanical characteristics
of the vocal folds that result from variations in frequency and intensity. Interpretation of the
observations requires understanding and knowledge of laryngeal pathologies.

Symmetry of Vocal Fold Vibration

The judgment of symmetry refers to the timing of the opening and closing of the folds relative
to each other, as well as to the extent of lateral excursion of the folds. If the folds are functioning
equally, they are said to be symmetric and are mirror images of each other. When there is phase
asymmetry, one fold may appear to move out of phase or the vocal folds may appear to be
following one another. It is important to remember that if one fold is abducting, the other fold
should be abducting also. Furthermore, in order to be symmetric in movement, they should be
abducting at about the same speed.

Aperiodicity
As noted previously, when the stroboscopic light flashes are synchronous with the fundamen-
tal frequency, the image appears to be static. Under this synchronous condition, any visible
movement is evidence of irregularity of successive vocal fold vibratory cycles, or aperiodicity.
Aperiodicity may be present always or the vibration of the folds may be intermittently irregular,
in which case the image appears static part of the time, moving at other times. It is not necessary
to stop the stroboscopic light at a specific part of the cycle in order to judge aperiodicity. The
judgment can be made from the typical stroboscopic image by using the slow-motion feature
of the playback and observing the clarity of the image. If the image is clear, the vocal folds are
reasonably periodic; if the image is fuzzy or unclear, even momentarily, the frequency of phona-
tion is more variable. Hoarseness is usually associated with periodicity of vibratory behavior.
When aperiodicity is constantly present it may not be possible to obtain a stroboscopic image;
even if obtained it would be difficult to interpret the image.

Glottal Closure Configuration

Judgments about glottal closure (the extent to which the vocal folds approximate each other)
and glottal configuration during the closed phase are made during observation of phonations
of normal pitch and intensity level, that is, at the patient’s normal or comfortable pitch level.
Bless, Hirano, and Feder (1987) have described seven categories of glottal closure that seem to
encompass the possible variations (complete, anterior chink, irregular, bowed, posterior chink,
hourglass, incomplete). Complete closure occurs when the vocal folds close completely during
each vibratory cycle. Anterior chink or gap is a noticeable opening in the anterior portion of
the vocal folds. “Irregular” refers to the appearance of several points of contact with openings
in between and along the length of the vocal folds. Bowing refers to a pattern in which the
folds close anteriorly and posteriorly but not in the midsection. It is possible for one cord to
be bowed and the other straight. Posterior chink or gap, as described by Bless et al. (1987),
is an opening at the posterior area of the folds. We have observed variations in the size and
configuration of this chink. In some it appears as a Y formation with a relatively small gap at the
vocal processes. In others, it has the appearance of a V with the opening or chink tapering down
as far anteriorly as two-thirds of the length of the vocal folds. Hourglass closure pattern looks
just like an hourglass, a noticeable narrowing of opening at about the midpoint of the vocal
folds. Incomplete closure is when no portion of the vocal folds touch each other. Although
the primary judgment of closure is made during the speaking pitch and comfortable loudness
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CHAPTER 8 I The Voice History, Examination, and Testing 231

FIGURE 8.5. Schematic of the larynx to illustrate

rating horizontal excursion of the vocal folds. The
solid line between the folds illustrates no horizon-
tal movement; the first mark along the dotted line
illustrates normal horizontal excursion, whereas the
second mark outside of the dotted line illustrates
greater movement.

condition, it is also advisable to note any changes that occur during the other conditions of
voicing, particularly loud voice.

Horizontal Excursion of the Vocal Folds

Amplitude is defined as the extent of horizontal (lateromedial) excursion of the vocal folds
during vibration. Each vocal fold is rated independently for this parameter. The absolute
amplitude is contingent on the size of the vocal folds; thus, it tends to be larger for adults.
The amplitude of the horizontal excursion is approximately one-third the width of the visible
part of the vocal fold in normal persons (Fig. 8.5). During abnormal vibration, the amplitude
of movement may be less than normal or greater than normal. We rate amplitude as normal,
slightly, moderately, or severely decreased or increased, or absent. It is important to remember
that with increased loudness there will be greater lateral excursion, and with high pitch lateral
excursion will be reduced. Therefore, when interpreting stroboscopic examinations, judgments
of amplitude should be made during the habitual pitch, habitual loudness condition.

Horizontal Excursion of the Mucosal Wave

The mucosal wave, a ripple-like wave of mucosa, originates in the subglottal area and follows
the contour of the vocal fold. With stroboscopy, we see, and thus rate, only the horizontal
excursion across the superior surface of the fold. It often appears as a ripple along the surface
much like the ripple on the surface of a body of water. Sometimes it can be visually tracked as
a light reflection traveling along the upper surface.
“Normal” refers to the range and size of the mucosal wave for phonation produced at
habitual pitch and loudness levels. The extent of the wave varies, but it normally traverses at
least a third of the width of the visible part of the vocal fold. If a wave is visible on only part of
the fold, the rating should be based on the overall impression of the wave travel.

Vocal Fold Edge

This judgment pertains to the straightness and smoothness of the edge of each vocal fold
individually. This is rated on a 4-point scale where 1 is smooth and 4 is extremely rough. This
rating can be affected by the particular point in the cycle chosen for making the judgment. If
the tape is advanced frame by frame through a cycle it is possible to see an edge that appears
smooth on full abduction, whereas, on partial adduction, a lesion may clearly be present. With
this understanding it may be important to routinely make the judgment at a given point in the
cycle. This parameter refers to the smoothness of the medial edge and should not be confused
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232 Understanding Voice Problems

with the appearance of a bowed vocal fold that, despite the convexity of shape, nevertheless has
a smooth edge.

Phase Closure
Phase closure refers to the approximate proportion of time the vocal folds are open. On a
5-point scale, 3 refers to normal phase closure with an open phase of about 40% to 60% of the
total cycle. A rating of 1 refers to a wide open phase as one might find during a whisper, whereas 5
indicates hyperadduction or a condition in which the closed phase predominates. Phase closure
will depend on the loudness, effort, and pitch, as well as mode of phonation. It is important
that this rating be made on a phonation that is appropriate. Phase closure can be estimated by
counting the number of video frames during the open phase and the number for the entire
cycle and computing an approximate open quotient. Because there can be much cycle-to-cycle
variability, it is necessary to sample more than a single cycle. Ten to 12 open frames out of a 20-
frame cycle is considered normal. Ratings made using this slow-motion or stop-frame counting
procedure may differ from those based on an overall gestalt using regular-tape playback speed.

Vibratory Behavior
This is a judgment of whether or not the entire vocal fold is seen to vibrate. We rate vibratory
behavior independently for each fold. It is sometimes difficult to distinguish between mucosal
wave and vibratory behavior. Indeed, we probably judge vibratory behavior by the presence of
mucosal wave. For a complete rating of all phonatory conditions, a 5-point rating scale can be
used, that is, 1 is always fully present, 2 is partial absence sometimes, 3 is partial absence always, 4
is complete absence sometimes, and 5 is complete absence always (totally immobile fold).
Based on our experience with judging stroboscopic images, we are aware of a number of
unresolved questions with respect to this process. Among them are the following:

What criteria should be used in selecting the sample for judging?

Should judgments be made on the overall gestalt without attention to a specific sample?
Is it better to use slow motion to rate mucosal wave, amplitude, and phase symmetry, or is
viewing at regular speed adequate?
How much of the length of the vocal fold must be visible to judge glottal closure, mucosal
wave, vibratory behavior, and amplitude?
Which of the parameters that we are rating actually make a difference clinically? There is
redundancy in the information obtained. What information is most valuable?
On the last point, we have found that a subset of signs could be used to adequately describe
the major characteristics of a stroboscopic examination (Kelly, Colton, Casper, Paseman, &
Brewer, 2010). The two most important aspects of the stroboscopic exam appear to be an
evaluation of the vibratory behavior of the vocal folds (as manifested in the signs of mucosal
wave, amplitude, vibratory behavior) and the straightness and smoothness of the vocal fold edge.

Diagnostic Probing during Stroboscopic Examination

The rigid scope limits but does not totally eliminate the use of diagnostic probes. Indeed,
such probing may yield the most important information of the examination. Patients can be
instructed to vary or manipulate pitch and/or loudness of the vowel being produced. Pro-
ducing the vowel (ee) on inhalation provides interesting information that can be helpful in
differentiating among nodules, cysts, polyps, and other benign lesions (Behlau et al., 1999).

Ultra-High-Speed Photography
This technique was developed by scientists at the Bell Telephone Laboratories in 1937, and since
that time many scientists have modified and used the technique to observe vocal fold vibratory
events in both normal and pathological larynges (Baer, Löfqvist, & McGarr, 1983a, 1983b;
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CHAPTER 8 I The Voice History, Examination, and Testing 233

Childers, Naik, Larar, Krishnamurthy, & Moore, 1983; Hirano, Kakita, Kawasaki, Gould, &
Lambiase, 1981; Hirano, Yoshida, & Matsushita, 1974; Hirose, Kiritani, & Imagawa, 1991a;
Metz, Whitehead, & Peterson, 1980; Moore, 1975; Moore, White, & von Leden, 1962; Rubin
& LeCover, 1960; Timcke, von Leden, & Moore, 1958, 1959; von Leden, LeCover, Ringel,
& Isshiki, 1966; von Leden & Moore, 1961; von Leden, Moore, & Timcke, 1960). Although
this technique is capable of providing excellent information about the vibratory behavior of the
vocal folds, it has not found widespread acceptance clinically for a number of reasons. It requires
an expensive array of equipment, the technical expertise to operate it, and the expenditure of
much time both in the examination procedure and in subsequent analysis of the films; it also
involves a procedure that is difficult, if not impossible, for many patients.
The primary piece of equipment is a camera capable of taking pictures at a rate of 3,000
frames per second or more. When films taken at these high speeds are viewed at a regular speed
of 24 frames per second, the recorded events are seen in ultra-slow motion. The technique for
obtaining high-speed films (Hirano, 1981b) requires that the patient be able to position him or
herself onto a fixed laryngeal mirror. The mirror must be positioned in such a way as to permit
visualization of the vocal folds. The laryngeal mirror is used in a manner similar to indirect
laryngoscopy, with the difference being that the patient must be capable of moving forward
onto a fixed mirror rather than the mirror being moved into a stationary patient. An example
of a high-speed motion-film sequence is shown in Figure 8.6.
The information obtained from high-speed films is glottal area over time. That is, we can
determine the amount of opening of the vocal folds during the vibratory cycle. It is also possible
to determine the vibratory movement of each vocal fold as well as the pattern of their opening.

High-Speed Videoendoscopy of the Vocal Folds

Hirose and his colleagues (Hirose, 1988; Hirose et al., 1987, 1988, 1991a, 1991b) have de-
scribed a variant of high-speed photography technique. Instead of recording the high-speed
image on film, it is captured using a digital image array that is sampled and stored in the
computer. Up to 1,000 images per second can be obtained, and the image sequence can be
displayed immediately after capture. Images obtained are digital, and digital techniques are used
to track desired aspects of vibration almost in real time. The technological problems discussed
previously remain the same for this technique.

FIGURE 8.6. Example of a high-speed motion-picture sequence. This plate is a single cycle of vibration
produced by a female speaker sustaining the vowel /ee/ at about 275 Hz. The film was exposed at a rate
of 4,000 frames per second.
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234 Understanding Voice Problems

FIGURE 8.7. Example of a sequence of frames taken from a high-speed video. Video courtesy of Dimitar
Deliyski, University of South Carolina, Columbia, SC.

Deliyski (2005, 2010) has reported many studies on the vibratory motion of the vocal
folds using this technique and has also explored some of the limitations of the technique. Newer
cameras are capable of taking pictures in excess of 10,000 frames/sec, although with some loss
of video resolution at the high frame rates (see Fig. 8.7). Deliyski and his colleagues have also
described many of the signs that can be evaluated using this technique (Boniha & Deliyski,
2008; Boniha, Deliyski, & Gerbach, 2008; Boniha, O’Shields, Gerbach, & Deliyski, 2009;
Deliyski, 2005; Shaw & Deliski, 2008). The technique shows considerable promise for use in
the clinic since one can monitor the process in real time and obtain the results immediately.
Recent developments have addressed the huge memory capacity initially required for storing
images as well as the previous limitation of filming only in black and white. The particular appeal
and strength of high-speed videoendoscopy is its reflection of a more detailed picture of actual
vocal fold vibration since, unlike stroboscopic imaging, every cycle of vibration is captured.

Videokymography
Videokymography is a technique for tracking a line from a video image and plotting the intensity
gradient of that line as a function of time. In the United States, video is created by sequentially
scanning an image very rapidly so that the eye fuses the 525 scanned lines into moving pictures.
This scanning process is repeated so that an entire frame is replaced at about 1/30th of a second.
By selecting only one of these scanned lines and plotting its intensity level as a function of time,
one can obtain a trace that shows the variation of intensity as a function of time.
In the case of the vocal folds, the intensity variation may represent the variation of glottal
area as a function of time. The technique was first described and developed by Svec and Schutte
(Schutte, Svec, & Sram, 1998; Svec & Schutte, 1996). To produce a videokymogram, a video
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CHAPTER 8 I The Voice History, Examination, and Testing 235

line is selected from a displayed image of the larynx. As the video is played (or phonation occurs
live), that line is displayed on the video monitor. A typical picture of the spatial image and the
videokymographic image is shown in Figure 8.8.
The videokymography is a valuable addition to the tools use for image acquisition and
analysis. It permits the acquisition of small details as a function of time and, furthermore,
permits the clinician to vary where on the image the desired detailed analysis takes place. With
further work and experience, it should become a valuable tool for use in the voice clinic.

A C

B D

FIGURE 8.8. Example of a Videokymograph tracing. Panels A and B show a frame of the actual video
image whereas panels C and D show the kymogram image taken at the lines labels C and D on panel B.
(From Svec and Schutte, 1996.)
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236 Understanding Voice Problems

The other techniques discussed in this section do not involve direct visualization of the vocal
folds. For excellent detailed discussions of all currently available laryngeal imaging techniques,
see Kendall and Leonard (2010).

Ultrasound
Ultrasound is an imaging technique in which a high-frequency current is passed through a
portion of the body and partially reflected back when it strikes a change in body composition.
Analysis of these reflections can be used to create an image of the part of the body of interest.
It is a relatively safe procedure because the currents and frequencies used are low.
Ultrasound has been little used in the analysis of voice function. A few reports concerned
with the analysis of normal voice function are available (Hamlet, 1981). Few voice clinics
or laboratories possess the costly equipment and have personnel with the expertise to use it
properly.

Laboratory Testing
Acoustic Studies
Fundamental Frequency
Fundamental frequency is an acoustic measure that directly reflects the vibrating rate of the
vocal folds. The term “fundamental frequency” refers to the component in the vocal fold tone
with the lowest frequency or to the frequency spacing between the component frequencies.
The unit of measurement is Hertz (Hz).
Fundamental frequency may be measured in a variety of ways and using any of several
types of speech samples. The phonatory tasks may include sustained vowel phonation, reading,
and conversational speech. The simplest of these is the sustained vowel phonation, in which
the patient is instructed to produce and sustain a vowel (most commonly /ah/ or /ee/) at a com-
fortable, natural pitch and loudness level. The advantages of using a sustained vowel are that it
can usually be sustained in a steady manner and for an adequate period of time. The uncompli-
cated nature of the task makes it possible to obtain accurate measures with relatively simple and
inexpensive equipment. The use of a reading passage or conversational speech as the phonatory
task will usually introduce greater variability of fundamental frequency, thereby making extrac-
tion of fundamental frequency a slightly more complex procedure or one that requires more
expensive instrumentation. There is not full agreement as to whether the speech sample used
has a significant influence on the actual measured fundamental frequency (Hirano, 1981b).
There are a variety of methods available for the measurement of fundamental frequency,
ranging from the very simple to the complex and elaborate. Subjective judgments can be
made through a matching procedure, but such judgments are often quite incorrect. Indeed,
subjective perception of fundamental frequency, particularly in persons with disordered voice,
may be misleading (Murry, 1978). Objective measurement of fundamental frequency from
sustained vowel production can be carried out very simply with the aid of a frequency counter
and a low-pass filter (available for less than US$500). Without the filter, the frequency counter
would attempt to count the many frequencies that a vowel contains. A low-pass filter, when
appropriately set, will remove the higher components of the laryngeal tone, leaving only the
fundamental frequency. The output of this equipment provides objective documentation that
can be used to demonstrate and chart change.
A commercially available and easy-to-use pitch meter or analyzer is available (Visi-Pitch,
Kay Elemetrics Corp.). A sustained vowel or a speaking or reading sample using the patient’s
live voice or a recorded segment is fed into the instrument, and the fundamental frequency
as a function of time is displayed on the screen. It is possible to control the total time to be
displayed and, thus, to obtain a detailed fundamental frequency trace for short periods of time
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CHAPTER 8 I The Voice History, Examination, and Testing 237

FIGURE 8.9. Fundamental fre-

quency during the production of
a sentence produced by a normal
male speaker. The sentence was,
“They have bought a new car.” The
average fundamental frequency of
the sentence was 120.45 Hz with a
standard deviation of 12.28 Hz. The
minimum fundamental frequency was
81.79 Hz, the maximum 153.32 Hz.
Total time of the sentence was 1.3
seconds. Analysis was made using
Praat.

or a less detailed trace of fundamental frequency over longer periods of time. This instrument
can provide measures of other voice and speech parameters as well.
Computer programs, such as Computerized Speech Lab (CSL, Kay Elemetrics Corp.),
Cspeech (a windows version of this program called TF32 is also available), EZ Voice, and
Dr. Speech (Tiger Electronics), which run on personal computers (IBM), extract fundamental
frequency from sustained vowels or longer speech samples. A very good freeware program
that can extract fundamental frequency, Praat, is also available. For the Macintosh computer,
SoundScope (GW Instruments Inc., Somerville, MA) and Praat can be used. These programs
can perform many more measurements than simple frequency measurements and are relatively
simple to use. An example of a fundamental frequency analysis using the Praat program is
presented in Figure 8.9.
Three summary statistics of frequency data that are useful for comparing patients to normal
speakers or to themselves over a course of treatment are mean fundamental frequency, the
standard deviation of fundamental frequency (pitch sigma), and frequency range. Clinically,
these measures are helpful diagnostically and as documentation of pre- and post-treatment
status. Mean fundamental frequency is useful to estimate the appropriateness of frequency level
for the patient’s age and sex. The other two statistics help to assess and document variation of
fundamental frequency during speech or lack thereof. Speakers who are judged to be monotonic
would be expected to have small standard deviations and small ranges of speaking fundamental
frequency.

Phonational Range
Another useful measure of the frequency characteristics of a patient’s voice is phonational range,
that range of frequencies from the highest to the lowest that a patient can produce. The highest
and lowest frequencies are defined as the absolute limits of frequency that a patient can produce
usually of short duration (approximately 1 second), without regard to intensity level or voice
quality. Phonational range is said to reflect the physiological limits of the patient’s voice. It is
expressed in either Hertz or semitones and can be measured using any of the instrumentation
discussed in the preceding section and also by using the phonetogram.
The absolute limits of frequency may be obtained by asking patients to produce the
highest and then the lowest sounds they can, or by using a singing scale progressing upward
and downward in a stepwise fashion. Whichever technique is used, it is usually necessary to
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238 Understanding Voice Problems

FIGURE 8.10. Mean phonational range of 35 male speakers. The modal register refers
to that range of frequencies used most often during speech. Falsetto is a voice quality
usually produced at high fundamental frequencies.

practice this task, encouraging the person to keep extending the range in both directions.
The lowest and highest frequencies produced can be plotted, as shown in Figure 8.10. Kent,
Kent, and Rosenbek (1987) have noted that intra- and inter-subject variability on maximum
performance tasks is large and may be affected by practice, motivation, or instructions. These
caveats hold true for measurement of phonational range.

Voice Range Profile (Phonetogram)

The voice range profile is an extension of the idea behind phonational and dynamic range.
A patient phonates at frequencies from the lowest to the highest frequency he or she can
produce. At each frequency, the patient produces his or her loudest and softest phonation.
These extremes are plotted on a graph that is often referred to as a phonetogram. When done
by hand, the task is very laborious and time consuming. There are a number of software
programs that substantially reduce the time and labor needed (see the Kay Voice Range Profile
program, WEVOSYS lingWAVES, or the Dr. Speech Phonetogram program). An example of
a phonetogram using lingWaves (WEVOSYS) is shown in Figure 8.11.
The voice range profile has been investigated in a number of different populations and
has been shown to yield useful information (Coleman, 1993; Damste, 1970; Giger, 1984;
Gramming, 1988; Gramming & Akerland, 1988; Heylen, Wuyts, Mertens, & Pattyn, 1996;
Pabon, 1991). With the advent of automated computer programs, the use of the VRP may be
useful for routine clinical use.

Vocal Intensity
Measurement of vocal intensity is useful in documenting the dynamics of the voice. Mean
intensity correlates with the perception of vocal loudness, and the variability of intensity would
presumably correlate with a patient’s loudness variations.
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CHAPTER 8 I The Voice History, Examination, and Testing 239

FIGURE 8.11. An example of a voice range profile (VRP). The BRP was produced using lingWaves. Courtesy of
WEVOSYS, Forchheim Germany.

Clinically, the mean intensity level of a patient’s voice is usually a more meaningful measure
than the absolute limits of intensity. However, the intensity range, frequently referred to as
dynamic range, may be diagnostically important and helpful in documenting change. Patients
whose mean intensity level is lower than expected for his or her age (see Chapter 15 for some
normative data on vocal intensity) and whose vocal intensity range is markedly reduced need
very careful and complete examination, including, of course, audiological assessment. The
procedure for establishing intensity or dynamic range requires that the person produce the very
softest /ah/ possible and, at the other extreme, the very loudest /ah/. Patients should be asked to
produce both of these sounds at a natural and comfortable frequency because frequency level
will have an influence on intensity level (Coleman, Mabis, & Hinson, 1977; Colton, 1973).
An example of plotting the highest and lowest sustainable intensity is shown in Figure 8.12.
Intensity can be measured from sustained vowels or connected speech. A simple intensity
measurement device can be found on most tape recorders (e.g., the VU volume unit meter).
However, this provides a very rough measure because these meters usually lack calibration in
traditional intensity units (dB sound pressure level). A sound-level meter that is so calibrated can
be purchased at reasonable cost (Radio Shack). A digital version is also available at slightly higher
cost. The patient is asked to sustain a vowel at a normal loudness level with the microphone of the
sound-level meter held at a given distance from the mouth, and the intensity of the phonation
in decibels is read from the meter. This device is of little use, however, for measurement of vocal
intensity during connected speech.
The Visi-Pitch can be used to measure and to visually display vocal intensity during
connected speech. CSL, Cspeech, EZ Voice, Dr. Speech, and Praat will display the intensity
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240 Understanding Voice Problems

FIGURE 8.12. Example of

intensity range measurement
and portrayal. These data
were collected on a sample
of 35 older men (mean age =
56.17 years) and 27 women
(mean age = 57.48 years)
while they were phonating
the vowel /ah/ at 40% of
their modal register frequency
range.

of speech production over time. It is also possible to obtain summary statistics such as average
intensity level and standard deviation from these instruments and programs. It is important
that the microphone used be capable of responding to all of the frequencies present in the tone
whose intensity is to be measured. All sound-level meters have microphones that can respond to
those frequencies expected in the speech signal, as does the Visi-Pitch. In computer programs,
the sampling rate of the speech signal determines the frequencies present in the waveform and
should be high enough to accurately reproduce frequencies of at least 5000 Hz (i.e., a sampling
rate of 10,000 samples per second).
Another consideration when measuring vocal intensity is the distance between the speaker’s
lips and the microphone. The actual distance is not as important as that it be documented and
consistent. Remember, sound intensity will be reduced by the square of the distance. That
means a doubling of the distance will produce an intensity difference of 6 dB. The noise level
of the room in which phonation is measured must also be taken into account. It is not necessary
to have a sound-isolated room, although that would be ideal. It is important to have a reasonably
quiet room and to know its noise characteristics. Most rooms will have a considerable amount of
ambient noise below 60 Hz. Because most speech exhibits frequencies above 100 Hz, the use of
a simple high-pass filter will attenuate the energy below 100 Hz and permit valid measurements
to be made. Many sound-level meters possess a weighting function that, in effect, carries out
this filtering process. The presence of heavy drapes and floor carpeting helps to reduce noise
and yield usable recordings.
Once again, it must be noted that the variability of maximum performance measures may
be large. Thus, caution must be used in the interpretation of measures obtained.

Perturbation
Perturbation refers to the small, rapid, cycle-to-cycle changes of period and amplitude that occur
during phonation. These changes reflect the slight differences of mass, tension, and biomechan-
ical characteristics of the vocal folds as well as the slight variations in their neural control (Baer,
1979). Perturbation correlates with perceived roughness or hoarseness in the voice (Wendahl,
1963, 1966) so that patients with voice problems manifesting roughness or hoarseness would
be expected to show a large amount of both frequency and amplitude perturbation.
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CHAPTER 8 I The Voice History, Examination, and Testing 241

FIGURE 8.13. Example of frequency and amplitude perturbation in a sustained vowel produced by a
normal (left panel) and a hoarse voice (right panel). These waveforms were produced using CSpeech.

Perturbation must be measured from sustained vowel phonation in which the patient is
instructed to produce a steady pitch level. Connected speech confounds the measure because
linguistically produced frequency variations cannot be separated from frequency variations
produced by the biomechanical characteristics of the vocal folds.
An example of frequency perturbation within a sustained vowel /ah/ is shown in Figure
8.13; an example of normal, sustained phonation is shown in the left panel. The acoustic
waveform is shown in the upper portion of this panel and the results of a CSpeech analysis of
fundamental frequency is shown in the lower portion of the panel. The average fundamental
frequency is 133.02 Hz with a standard deviation of 1.0 Hz. The frequency did not vary more
than 4 Hz. The percent jitter value was 0.30 and percent shimmer was 2.11. In contrast, an
example of hoarse voice is shown in the panel on the right. Note the greater irregularity both in
the period of the raw acoustic waveform shown at the top of the panel and in the amplitude of
the phonation. The lower frequency track shows large swings of fundamental frequency in what
is supposed to be a steady-state sustained vowel. The mean fundamental frequency is 132.67 Hz
with a standard deviation of 17.67 Hz. The largest frequency variation was about 76 Hz. The
percent jitter value was 3.335, and percent shimmer was 11.82. The differences of perturbation
between the normal and hoarse voice is very striking, suggesting that frequency and amplitude
perturbation should be an important acoustic measurement to make on pathological voices.
Frequency perturbation, also called jitter, is obtained by measuring the period of each cycle
of vibration, subtracting it from the previous or succeeding period, averaging the differences,
and dividing by the average period. If the result is multiplied by 100, jitter can be expressed
as a percent change of period relative to the average period. That measure is referred to as the
jitter factor. There are several other formulations for computing frequency perturbation, which
make comparison of data somewhat difficult (Casper, 1983). Titze (1995) recommends the use
of some form of ratio measurement of jitter.
Frequency perturbation can be measured by the Visi-Pitch, which reports it as a ratio
measurement. These measures are helpful for comparison of intra- or inter-subject data when
the same measure is being used for that comparison. The computer programs CSL, CSpeech
(TF32), and Praat calculate frequency perturbation and report results in a variety of ways.
For example, CSpeech reports jitter results both as the average absolute change of period in
milliseconds and as percent change of frequency.
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242 Understanding Voice Problems

Amplitude perturbation, or shimmer, refers to the small cycle-to-cycle changes of the am-
plitude of the vocal fold signal. As was the case for the measurement of frequency perturbation,
the amplitude of each glottal cycle is measured, subtracted from the previous or following
period, and averaged over all differences. Shimmer is most often expressed in average change in
decibels, although percentage and ratio measurements may be reported and may be preferred
(Titze, 1995).
Amplitude perturbation can be obtained directly from the CSpeech program, CSL, and
Praat, as well as from a number of other software programs. The measure of amplitude perturba-
tion from the speech signal emitted at the lips is determined not only by the vocal folds but also by
the resonance characteristics of the vocal tract. Thus, a measure of amplitude perturbation prob-
ably reflects the effect of the vocal tract on the speech signal as well as the effect of the vocal folds.

Spectrograms
Spectrograms reflect the properties of the source of sound (the vibratory characteristics of the
vocal folds) and the resonator (the vocal tract). In order to compare spectral characteristics
of a given phonation, it is important to use the same vowel. It is also necessary to have a
good working knowledge of the acoustic characteristics of normal speech to properly interpret
spectrograms obtained from voice patients.
Spectrograms are useful for analyzing and showing changes in the spectral characteristics
of the vocal fold sound. Noise and weak sounds will exhibit characteristics that can easily be
studied from a spectrogram. As shown in Figure 8.14, the spectrum of a hoarse voice (right
panel) has considerable noise energy in the higher frequencies, whereas the normal voice on the
left has little high-frequency noise energy but strong low-frequency periodic energy. Amplitude
sections can be taken at selected points and a detailed analysis made of the spectral characteristics
of the sound. Spectrograms can be stored in the patient’s record for analysis and comparison
with later phonatory samples.
One useful measure that can be obtained from spectrograms is harmonics-to-noise ratio
(also called signal-to-noise ratio). This is a measure of the energy in the harmonics of the voice
signal (i.e., the frequencies produced by the vibrating vocal folds) and the noise energy in the
signal. Abnormal voices will exhibit greater noise either directly (i.e., produced at the vocal
folds) or indirectly as greater perturbation (Klingholz & Martin, 1985). On a spectrogram of
an abnormal voice, there would be greater noise and less energy in the harmonics of the sound.
The harmonics-to-noise ratio is a convenient measure to express this relationship. For example,
the normal sustained vowel shown in Figure 8.14 had a signal-to-noise ratio of 22.4 dB, whereas

FIGURE 8.14. Spectrogram of a normal voice (left panel) and a hoarse voice (right panel).
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CHAPTER 8 I The Voice History, Examination, and Testing 243

the signal-to-noise ratio for the hoarse voice was 11.61 dB. After treatment, the spectrogram
of a voice patient would exhibit greater harmonics-to-noise ratio because greater energy in the
harmonic components of the sound would be expected, along with less noise energy.
There are several computer software programs that produce acceptable spectrograms (CSL,
Kay Pentax, Lincoln Park, NJ; Cspeech (Windows version is called TF32), Paul Milenkovic,
Madison WI; Dr. Speech, Tiger DRS Inc, Seattle WA; Praat, (Bosma and Weenik, Amsterdam,
the Netherlands); SoundScope (Mac), GW Instruments, Somerville, MA). The use of these
programs makes it possible to obtain spectrograms routinely on voice patients and greatly
speeds the process of measurement. It is also possible to compute a harmonics-to-noise ratio
via computer analysis (Kitajima, 1981; Kojima, Gould, & Lambiase, 1979; Kojima, Gould,
Lambiase, & Isshiki, 1980).

Acoustic Spectrum
Acoustic spectrum is a plot of the energy in each of the frequencies present in a complex
tone. The amplitude section from a spectrograph is an example of acoustic spectrum. It is
possible to determine acoustic spectrum directly from the speech signal using special-purpose
spectrum analyzers or appropriate computer programs. Special-purpose spectrum analyzers are
very expensive, but several computer programs are available that are not only less expensive but
also more practical for clinical application. An example of a spectrum analysis produced by the
CSpeech software program is shown in Figure 8.15. Such spectral profiles can be printed out for
inclusion in a patient’s file. Of course, it is important that the patient produce the same vowel
or sound under similar conditions for each profile to properly interpret any spectral changes
that might be obtained.
Another variant of spectrum analysis is computation of the one-third octave spectrum of
the speech sample. One advantage of the one-third octave spectral analysis is that it produces
a small, manageable number of distinct frequency bands. In normal speech, one expects to

FIGURE 8.15. Spectral plot

of a vowel produced by a nor-
mal speaker. These data were
produced using CSpeech. A
Fourier analysis produces a plot
of all of the frequencies present
in the phonation. An LPC anal-
ysis is used to compute the for-
mant frequencies of the utter-
ance.
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244 Understanding Voice Problems

find energy in frequencies from 100 to 5000 Hz. In a one-third octave display, the spectrum is
analyzed into 10 to 20 different frequency bands, depending on the frequency range desired.
Furthermore, there is a well-documented and internationally accepted body of data concerning
standardization of the one-third octave spectra and the characteristics of the filters. Another
advantage of the one-third octave analysis is that it is similar, although not identical to, the way
in which the ear analyzes sound. In view of this, the results of the one-third octave analysis may
correlate best with perceptual measurements of voice. Unfortunately, there are few data available
on this relationship. In our judgment, the one-third octave or some variant seems to be the best
choice at this time for analyzing the spectral characteristics of normal and abnormal voices.
There are several expensive one-third octave spectrum analyzers available for performing
these measurements. It is also possible to extract one-third octave information from a computer-
generated spectrum.

Physiological Studies
Electroglottography
Electroglottography (EGG) is a technique for the measurement of vocal fold–contact area
based on the principle that tissue conducts current. A high-frequency, low-current signal is
passed between the vocal folds via electrodes located on the external neck over the thyroid
lamina. When the vocal folds touch, greater current flows than when they are open. There is a
proportional variation of current when the vocal folds are less than maximally open or closed.
Electroglottographic recordings can be used to determine when the vocal folds are closed and
how fast they are closing. If carefully interpreted, it is possible to determine characteristics of
the opening of the vocal folds from an electroglottographic recording.
Devices to record the electroglottographic signal are readily available. Currently these
include the Voiscope and Laryngograph (Laryngograph, Ltd.), the single channel SC1 or the
EG2-Standard or EG2-PCX (Glottal Enterprises), and the unit from FJ Electronics. For a
full discussion of the measurement technique, see Baken (1987). The electrical output of the
electroglottograph can easily be converted to hard copy using an oscillograph or similar graphic
recording device, or from a computer-generated display.
The literature on EGG is primarily qualitative in nature, based on interpretation of the
waveform.
Several studies have related the shape of the EGG waveform to the underlying physiol-
ogy of vocal fold vibration (Childers et al., 1983; Dromey, Stathopoulos, & Sapienza, 1992;
Hicks, Larar, Moore, & Childers, 1985; Houben, Buekers, & Kingma, 1992; Kiritani, Ima-
gawa, & Hirose, 1986; Painter, 1988; Rothenberg, 1981; Titze, 1984, 1990; Titze & Talkin,
1981). Information has also been reported on characteristic waveforms in patients with vocal
pathology (Berry, Epstein, Fourcin, Freeman, & MacCurtain, 1982; Berry, Epstein, Freeman,
MacCurtain, & Noscoe, 1982; Borden, Baer, & Kenney, 1985; Chevrie-Muller, Arabia-Guidet,
& Pfauwadel, 1987; Childers, Alsaka, Hicks, & Moore, 1986; Colton, Brewer, & Rothenberg,
1983; Dejonckere & Lebacq, 1985; Gerratt & Hanson, 1987; Haji, Horiguchi, Baer, & Gould,
1986; Hanson, Gerratt, Karin, & Berke, 1988; Jentzsch, Unger, & Sasama, 1981; Karnell, Li,
& Panje, 1991; Kaszniak, Garron, Fox, Bergen, & Huckman, 1979; Kitzing & Löfqvist, 1978;
Sataloff, Spiegel, Carroll, Darby, & Rulnik, 1987; Scherer & Titze, 1987; Sorin, McClean,
Ezerzer, & Meissner-Fishbein, 1987; Swenson, Zwirner, Murry, & Woodson, 1992; Trapp &
Berke, 1988; Ward, 1990; Wechsler, 1976; Wirz & Anthony, 1979). There have been many
attempts to quantify the electroglottograph signal (Brodie, Colton, & Swisher, 1988; Higgins
& Saxman, 1993; Karnell et al., 1991; MacCurtain & Fourcin, 1982; Moore & Childers, 1984;
Rasinger, Neuwirth-Riedi, & Kment, 1986; Rothenberg & Mahshie, 1988; Scherer & Titze,
1987; Singh & Ainsworth, 1992; Titze & Talkin, 1981; Wendler & Köppen, 1988; Wendler,
Köppen, & Fischer, 1986).
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CHAPTER 8 I The Voice History, Examination, and Testing 245

EGG reflects the state of the vocal folds in a way that can be easily demonstrated and
interpreted to patients. However, a limitation of the technique is that it cannot be used with
all patients. Because the technique depends on vocal fold contact, the signal is considerably
diminished or even absent in patients with lack of good contact, such as those with unilateral
paralysis, or aphonia. It may also be difficult to obtain a clear waveform in the presence of severe
hoarseness. The thick or large necks of some patients hinder transduction of the current and
result in a poor EGG tracing. Manufacturers of EGGs have greatly enhanced its clinical value.
For example, both EGG models made by Glottal Enterprises uses two identical circuits and
two sets of electrodes. The output of each electrode pair is compared and displayed on a meter.
When the meter reading is 0, the output of the two channels is identical and the vocal folds are
centered between the two electrode pairs. This simple monitoring device helps to ensure the
proper placement of the electrodes and an optimal EGG signal.

Photoglottography
Photoglottography is a technique designed to obtain estimates of variations of glottal area
during phonation. Light is directed from above, usually from a fiberoptic light source passed
through the nose. The light passes through the glottis and is detected by a light-sensitive device
usually positioned over the skin of the trachea immediately beneath the vocal folds. As the
vocal folds vibrate, their area of opening will vary and so will the amount of light passing
through the glottis. It is a simple, relatively noninvasive device that yields a good, but not
exact, approximation of glottal area. The photoglottographic technique is complementary to
the EGG signal (Baer et al., 1983a, 1983b).
There are several measurements that can be made from photoglottographic recordings. The
first, speed quotient (SQ), is the speed of the opening phase of the vocal folds divided by the speed
of their closing phase. The second, open quotient (OQ), is the time of the open phase of the vocal
folds divided by the total period of vibration. This term is somewhat analogous to the term “duty
cycle” used in engineering. Open quotient and speed quotient reflects efficient vocalizations,
although it is unclear which values are produced with maximally efficient phonations. Titze
concluded that an OQ around .50 resulted in efficient vocalization (1994).
There have been a few studies relating photoglottographic results to different kinds of
speech and voice production (Gerratt, Hanson, & Berke, 1988; Gerratt, Hanson, Berke, &
Precoda, 1991; Gerratt, Hanson, Hunt, & Karin, 1985; Hanson, Gerratt, & Ward, 1983; Han-
son, Ward, Gerratt, Berci, & Berke, 1989; Sonnesson, 1959; Vallancien, Gautheron, Pasternak,
Guisez, & Paley, 1971).
There is some concern that the waveform obtained from this technique is not an entirely
accurate representation of the actual glottal area waveform (Wendahl & Coleman, 1967).
However, it may be useful for extracting measures such as speed or open quotient, which are
known to be affected by disorders of the vocal folds (von Leden et al., 1960).

Inverse Filtering
In the inverse-filtering procedure, the voice signal emitted at the lips is analyzed to remove
the resonant effects of the vocal tract, producing an estimate of the waveform produced at the
vocal folds. According to the acoustic theory of speech production (Fant, 1970; Stevens &
House, 1961), speech is the product of a sound source and a filter. That is, the sound output
of the vocal folds is modified by the resonant characteristics of the vocal tract. If the resonant
characteristics of the vocal tract are known, it should be possible to retrieve the characteristics
of the output of the vocal folds from the orally emitted speech signal.
Inverse filtering has been performed on the acoustic sound pressure waveform (Hillman
& Weinberg, 1981; Miller & Mathews, 1963; Sondi, 1975), and on the airflow waveform
(Rothenberg, 1973, 1977, 1981). We have used the airflow waveform for inverse filtering of
normal and voice-disordered persons (Brodie et al., 1988; Casper, Colton, & Brewer, 1985;
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246 Understanding Voice Problems

FIGURE 8.16. Acoustic waveform

(top trace), inverse-filtered airflow
(middle trace), and electroglottograph
waveform (bottom trace) of a normal
speaker. In this plot, vocal fold contact
is indicated by a downward deflection
in the electroglottogram waveform.

Colton & Brewer, 1985; Colton et al., 1983). We routinely record the EGG signal simul-
taneously with the inverse-filtered airflow signal to extract information about the vibratory
characteristics of the vocal folds during the complete cycle. The techniques complement each
other in that airflow will often not be present during the closed phase of the vocal folds, but
the EGG provides information about vibratory characteristics of the vocal folds during that
phase. Thus, with both techniques, we are able to obtain a more complete picture of vocal fold
vibratory characteristics during speech.
The result of inverse filtering the oral airflow waveform is called a flow glottogram, and an
example is shown in Figure 8.16. Four channels are collected directly into the computer using
CSpeech. These are (a) acoustic waveform, (b) raw oral airflow waveform, (c) EGG waveform,
and (d) intraoral air pressure pulses associated with the stop plosives in the utterance (not shown
in Fig. 8.16 but see Fig. 8.17). The oral airflow waveform is inverse filtered using CGlott, a
computer program separate from but complementary to CSpeech. The result is the inverse-
filtered or flow glottogram shown in Figure 8.16. Similar traces may be obtained by using the
windows version of CSpeech called TF32, also available from Milenkovic (Madison Ws). An
explanation of the analysis of the intraoral air pressure traces may be found in the next section.
Collection of electroglottographic and inverse-filtered airflow waveforms is routine in our
clinic. The following measures are obtained from computer-assisted analysis of the waveform:
(a) each cycle’s minimum (or leakage) and ac airflows, (b) the ratio of the time of the airflow
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CHAPTER 8 I The Voice History, Examination, and Testing 247

FIGURE 8.17. Air pressure

traces during the production of
the syllable /bœp/. The line
drawn between each peak rep-
resents an estimate of the sub-
glottal air pressure during the
production of the vowel.

pulse relative to the total period (airflow duty cycle), (c) the ratio of the closing and opening
slopes of the airflow pulse (airflow speed quotient), (d) the ratio of the open time to the total
period of the electroglottographic waveform (abduction quotient), (e) the closing time of the
electroglottogram waveform, and (f ) lung pressure (described below). Each cycle’s measure-
ments are added to the other cycles in the data and averaged. Patient data are thus available for
comparison with data collected on a small group of normal speakers.

Subglottal (Lung) Air Pressure

Proper interpretation of the airflow rates through the vocal folds requires knowledge about
the driving pressure beneath the vocal folds, often called subglottal pressure (and sometimes
by a variety of other names such as lung pressure, tracheal pressure, etc.) There are various
techniques for the measurement of the air pressure beneath the vocal folds, including the
esophageal balloon technique and intratracheal puncture.
In the esophageal balloon technique, a small, latex balloon attached to a catheter is swal-
lowed and positioned in the esophagus immediately behind the trachea and inferior to the
cricoid cartilage. The posterior wall of the trachea is composed of smooth muscle, and any
pressures in the trachea will be reflected through this muscle wall into the esophagus. The
balloon will reflect these pressure changes, which will be converted to a recordable voltage by
a pressure transducer at the other end of the catheter. There are several potential problems
and pitfalls in the use of this technique (Kunze, 1964) but, with care, reliable and accurate
measurements can be made (Schutte, 1980).
The second technique used to measure subglottal pressure is a tracheal puncture. A small
needle attached to a catheter is inserted through the skin/tissue between a tracheal ring, usually
the second or third ring. The pressure in the trachea is recorded using a pressure transducer.
With both techniques, appropriate calibration maneuvers are performed to be able to relate
pressure magnitude to the level of the electrical signal.
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248 Understanding Voice Problems

A third way of measuring subglottal pressure is by recording the intraoral air pressure
variations as a speaker produces stop plosives (e.g., /b/, /p/). The theory is that the pressures
produced behind the oral constrictions are the same as the pressures in the rest of the respiratory
tract since the tract is a closed system. Thus, the intraoral pressure magnitudes will be similar
to the subglottal air pressure magnitudes, at least during the production of the consonant.
During the actual production of the vowel following the consonant, intraoral pressure will
drop markedly; however, there will still be subglottal pressure since now the constriction is at
the vocal folds. However, the intraoral pressures will be good estimates of the subglottal pressure
during the vowel (Hixon & Smitheran, 1982; Rothenberg, 1982; Smitheran & Hixon, 1981).
An illustration of the technique for obtaining subglottal air pressure estimates from intraoral
air pressure traces is shown in Figure 8.17. In our system, the peak pressures before and after
the vowel are measured, averaged, and used to estimate the subglottal or lung pressures.

Electromyography
Electromyography (EMG), a technique in which electrodes are inserted into specific muscles
to measure their electrical activity, is used routinely by neurologists for the study of peripheral
muscle function in various neuromuscular and neurological diseases. EMG is invasive and
requires expertise; precautions must be taken to safeguard the patient’s well-being. For these
reasons, EMG has enjoyed limited use in the diagnosis and management of voice disorders.
EMG of the vocal muscles requires detailed knowledge of head and neck anatomy, along
with considerable experience in manipulating needles or needle carriers within the pharynx
and larynx. The muscles involved in phonation are not readily accessible. Electromyographic
recording equipment is available from a variety of manufacturers and has been engineered to
be medically safe. The output of the equipment, an electromyogram, is a detailed tracing of
muscle activity. An example of an electromyogram is shown in Figure 8.18.
Interpretation of electromyographic recordings requires experience and practice. Onset or
offset of muscle activity, the pattern of muscle activity, and the overall amplitude of muscle

FIGURE 8.18. Electromyogram of the cricothyroid muscle in an elderly speaker during

sustained vowel production (upper trace) and consonant–vowel syllable production (lower
trace).
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CHAPTER 8 I The Voice History, Examination, and Testing 249

activity are the parameters that provide the most valuable information. Electromyographic pat-
terns of neurologically disordered patients will show greater- or lesser-than-normal amplitudes
of muscle activity, extraneous bursts of muscle activity, and slower- or faster-than-normal mus-
cle activation. Laryngeal electromyograms may be helpful in those patients with voice problems
of suspected neurological or neuromuscular etiology. Another use for EMG is to verify excessive
muscle activity prior to injection of BOTOX for symptom relief of spasmodic dysphonia. The
needle used to inject the BOTOX is used as an electrode whose electrical activity is monitored
aurally to assist in the placement of the toxin in muscle. An EMG study can be helpful in
differentiating vocal fold paralysis from arytenoid ankylosis.

Respiratory Studies
Air Volumes and Capacities
Many clinicians advocate the analysis of a patient’s respiratory function, including studies of lung
volumes, vital capacity, residual capacity, and phonation volume. Others doubt the necessity for
obtaining these data and question their value provided the patient is able to maintain adequate
air volumes and airflows needed for speech. There is no controversy concerning the helpfulness
of this information when dealing with professional voice users, particularly singers and actors.
There are, of course, research issues for which such information is important.
The wet spirometer is the most common instrument used for the analysis of respiratory
volumes. This device consists of an upper and a lower canister, each with an open end. The
lower canister is filled with water. The open end of the upper canister fits into the mouth of the
lower so that an airtight seal is produced. The two canisters are now effectively sealed, partially
filled with known volumes of air and of water. A pipe, into which the patient breathes, connects
to the air within the sealed canisters. When the patient exhales, air is forced into the sealed
lower canister, the upper portion of which is allowed to move to accommodate the increased air
volume. A pen or other marker attached to the vertically moving drum records the movement of
the drum in response to the patient’s breathing. Since the relationship between the air-volume
change and the movement of the pen is known, it is possible to obtain the volume of air used
by the patient. Common measurements obtained from voice patients include tidal volume (the
volume of air in an average breath), vital capacity (the volume of air that can be maximally
exhaled after maximum inhalation), and total lung capacity (the total volume of air in the
lungs). Other volumes that may be measured are inspiratory reserve volume (the amount of
air that can be inspired from the end-expiratory level of a tidal breath) and expiratory reserve
volume (the amount of air that can be expired from the end-expiratory level of a tidal breath).
Respiratory physiologists are also concerned with reserve volume and gas exchange, but such
measurements are not performed routinely for voice patients.
A certain amount of air volume, flow, and pressure is required for speech. The respiratory
system, however, can provide considerably more volume, flow, or pressure than is required for
speech or even for singing. Only a small portion of the total available volume is normally used
in speaking. Thus, it would seem unnecessary, and perhaps unproductive, to spend inordinate
amounts of time gathering information about lung volumes for most voice patients. Information
that may be more valuable is that concerning the control of the respiratory system during speech.
It is necessary and vitally important that informed decisions be made concerning the relative
contributions of respiratory versus laryngeal function to the presenting voice problem.

Respiratory Movements
It may be important to assess control of respiratory movements in some voice patients. As-
sessment of the movement of the thorax and abdomen during speech may provide important
information about the control exerted by a voice patient. Analysis of these movements is possible
using a variety of tools, including mercury-filled strain gauges (Baken, 1987), the respiratory
inductive plethysmograph (Bless, Hunker, & Weismer, 1981; Sackner, 1980; Watson, 1979),
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250 Understanding Voice Problems

FIGURE 8.19. Examples of traces ob-

tained with an inductive plethysmograph.
The top trace is the acoustic signal, the
middle trace reflects the circumferential
changes occurring in the chest wall, and the
bottom trace shows changes occurring in
the abdomen. The speaker was a man who
inhaled normally and produced a sustained
vowel /œ/. Since we were only interested
in time events, the rib cage and abdomen
traces reflect voltage changes and not vol-
ume changes.

and magnetometers (Hixon, 1987). Bless et al. (1981) provide a comparison of these tech-
niques. Although their methods vary, all of these tools are able to monitor the movements
of the chest and abdominal walls using noninvasive external devices. All are available from
commercial manufacturers; there is some variation in the expertise required for their operation.
A typical recording of the movements of the chest wall and abdomen is shown in Figure
8.19. Note that the rib cage (upper trace) shows a steady decrease of circumference as exhalation
progresses, with irregular but decreasing changes noted in the abdominal channel. These curves
can be calibrated to produce estimates of lung volume.

Noninstrumental Testing
Critical Listening and Description
Although we have presented the voice history as a separate section, in practice there can be no
separation between history taking and the voice evaluation. The initial interview, during which
the history is elicited, is the point at which the evaluation begins. It affords the clinician the
opportunity to listen critically not only to the content of the message but also to the vocal output.
Because patients are referred for voice therapy from various sources following laryngological
examination, it is essential for the speech-language pathologist to always have this question in
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mind: Are the vocal symptoms consistent with the referral diagnosis? The voice clinician’s ears
must always be turned on and tuned in. It is not unusual to pick up very significant clues about
the presenting problem before the patient is aware that the examination is in progress.

Case Study
A 35-year-old woman who complained of having lost her voice several weeks previously was
answering all questions put to her in an aphonic whisper. During her aphonic explanation of
the effect of this problem on her work, she cleared her throat. The clinician noted the entirely
normal sound of the throat clearing. What information did this present?

While listening critically, the clinician should make observations about the consistency or
variability in the sound of the voice and about its stability. When the voice exhibits variability
or instability, it is important to be aware of the nature or pattern of that variability. For example,
is the voice clear and strong initially, with gradual worsening over time? Does this happen with
each sentence or two or over a more extended period of time? What is changing: quality, pitch,
or loudness?
It is appropriate to make a perceptual judgment of vocal pitch, but such judgments must be
made with caution and later verified with objective data. Perhaps the most important perceptual
judgment to be made relative to pitch is whether or not its level is appropriate for the age and
sex of the speaker. Perceptual impressions of fundamental frequency in the presence of laryngeal
pathology tend to suggest lower-than-expected pitch levels; however, it has been shown (Murry,
1978) that the fundamental frequency of some voice problems does not differ systematically
from the norm, with the exception of reduction in phonational range in laryngeal paralysis.
Another aspect of pitch to which the clinician must attend is its variability. Variations in pitch are
used linguistically to mark the meaning of utterances. In the English language, pitch is expected
to fall at the end of a declarative sentence and to rise to mark a question. Voices that show pitch
variability are generally thought to be more “interesting” and less apt to lull the listener.

Case Study
While taking the history from a 65-year-old man, the clinician was struck by an absence of inflec-
tion and a monotonic, flat, and unvarying delivery. Questions and statements were undifferenti-
ated by the usual pitch changes. This observation, combined with noticeable slurring of speech,
alerted the clinician to look for additional signs of neurological involvement. What would this
absence of pitch variability suggest to you and what other signs might you expect to find?

The loudness level of the patient’s voice during assessment in presumably quiet surround-
ings should be another focus of the clinician’s critical listening. The salient judgments to be made
are whether the voice is too loud, too soft, or out of control. The consistency and variability of
the loudness level are also important to note.
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Case Study
Another observation made about our 65-year-old patient mentioned above was the tendency for
the loudness level of his voice to remain constant, with some decay at the end of an utterance.
When asked to count and to alternate loud and soft voice for each successive number, the
patient was able to comply with only the first three numbers, after which the loudness level
became constant. Is this consistent with our previous observation, and why?

Descriptions of voice quality are most difficult to make. Many adjectives are used to describe
voice quality, but they are difficult to quantify, and there is no widespread agreement on the
meanings of voice-quality terms. Some perceptions of quality can be checked against objective
measures. For example, in the presence of hoarseness, there is the expectation of increased
frequency perturbation (Coleman & Wendahl, 1967). Scaling of perceptions is perhaps the
most valid approach to assigning a degree of objectivity to subjective judgments. Various types
of scales will be discussed later in this chapter.
Those aspects of speech referred to as suprasegmentals may hold information about voice
production or may add to other findings in the search for the diagnosis. The rate of speech
is one such aspect. Excessively fast or laboriously slow rates may be suggestive of neurological
involvement or may simply be a reflection of personality. Persons who tend to talk very rapidly
often tend also to stretch vocalization to the last bit of air they can squeeze out. This style
of speech is often characterized by increased tension in the respiratory and laryngeal systems.
Prosody of speech may be disturbed by vocal behavior, as is the case with spasmodic dysphonia.
If the clinician is aware of a disturbance of prosody, it is important to determine the nature of
that disturbance and to describe it as accurately as possible.
Attention must be paid to any unusual vocal characteristics, such as stridor, grunts, and
vocal tics. Of particular importance is the observation of stridor, inspiratory, and/or expira-
tory noise. The presence of stridor suggests obstruction somewhere in the airway, subglottally,
glottally, or supraglottally. It may be a sign of a laryngeal web, an obstructing lesion, severe
inflammation, or abductor vocal fold paralysis. In infants inspiratory stridor is usually symp-
tomatic of laryngomalacia. Yet another cause of stridor may be fixation or ankylosis of the
cricoarytenoid joints as a consequence of rheumatoid arthritis.

Case Study
J. W., a 41-year-old nurse, presented for a voice evaluation with a 10-year history of vocal
difficulty and shortness of breath. She denied concern about her voice quality, which she
claimed was unchanged. She believed that her vocal pitch was perhaps slightly higher than it
had been but not significantly enough to be of concern. Perceptually, we were in agreement with
these judgments. Her main vocal complaint was the inability to complete a whole sentence on
one breath. J. W. has continued to work during this 10-year period but admitted to shortness of
breath in climbing stairs or during other physical exertion. Throughout this history taking, the
examiner was aware not only of her obvious shortness of breath and the disruption in the prosody
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of speech caused by frequent interruptions in order to renew breath supply but also of her
characteristic thrusting forward of the mandible during inspiration and of audible inspiratory
stridor. J. W. was immediately referred for laryngological examination, which revealed abductor
vocal fold paralysis, probably as a consequence of a viral infection.

Vocal tics are characterized by sudden, unexpected, and involuntary vocalizations. They are
usually thought to be a symptom of a neurological disorder. Other unusual vocal manifestations
that may suggest a neurological etiology include grunts, barking sounds, and echolalia.

Critical Observations and Descriptions

It is very important that the clinician maintains eye contact with the patient and be in visual
contact so as to be able to make observations of behavior that may not be audible. This
requires that note taking be kept to a minimum, freeing the clinician to take full advantage
of all diagnostic clues. After completion of the examination, the clinician should describe all
observations made.
Watch facial expression and body language. Do they match the words being spoken? How
do they change in response to questions? Is the person comfortable, anxious, tense, fidgety?
Is eye contact made and maintained? Are there extraneous facial or body movements? Is there
tremor of the head, the hands, and the jaw? Can you observe signs of neck, face, or laryngeal
tension or strain? What is the emotional affect being projected? Does the person make adequate
use of mouth opening and lip movement?
We suggest that observations of respiratory behavior be made during the period of eliciting
the history and prior to asking the patient to engage in any specific vocal or respiratory tasks.
It is important to observe respiratory behavior both during speech and at rest. Does the person
have sufficient air supply to complete sentences? Does the person habitually speak until the air
supply is exhausted? Does the person release exhalation prior to voice onset, or do you observe
a holding of the breath in anticipation of speaking with an abrupt, sharp voice onset? Where
do you observe the greatest amount of respiratory activity when the person is speaking, and
when at rest? Is it clavicular, midthoracic, or abdominal/diaphragmatic?

Diagnostic Testing Probes

The procedures used in this part of the evaluation cannot be rigidly specified because they
often depend on the symptoms presented by the patient and the observations made by the
clinician up to this point. The objectives of this part of the evaluation are to explore the
patient’s response to different ways of producing voice; to attempt to elicit an improved voice;
to test the patient’s ability to manipulate parameters such as pitch, loudness, and resonance;
and to test the limits of the voice. Sometimes this involves making sounds and noises that create
some self-consciousness. Patients with psychogenic voice disorders often appear frightened and
threatened when asked to produce “different” sounds, perhaps because they are uncertain of
their ability to maintain control over such phonations. Each step of this process must be carried
out with sensitivity and encouragement. It is also essential that the clinician demonstrate the
task being required of the patient. If the patient is being asked to produce a grunt, it will ease
self-consciousness if the clinician models the grunt as the patient is to do it.
The following are some diagnostic testing tasks that might be useful.

Production of Reflexive Sounds

These include coughing, laughing, clearing the throat, and the vocalized pause “uh-huh.” The
clinician’s ears should have been tuned in to hear these sounds if they occurred spontaneously
during the interview. It is interesting then to compare the quality of the sound produced
spontaneously with that elicited during this task. The rationale for using this task is to determine
the quality of the phonation produced in a nonspeech task. It is most important to judge whether
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this elicited quality differs from the voice heard in speech in quality, pitch, or loudness. It is
often necessary to work with the patient on these tasks until you are satisfied that the best sound
that person is capable of, or is willing to produce, has been heard.

Altering Pitch
Before attempting to obtain a phonational range, it is helpful to work with patients on the
concept and on their ability to change pitch upward and downward. Some patients are unable
to succeed on this task for reasons having to do with the nature of their problem. Others
seem unable to carry it out due to difficulty in discriminating pitch changes and difficulty in
matching pitches. It is important to try, during this diagnostic therapy period, to determine
which of these is operative. It is helpful to engage in this activity as a practice for the actual
testing of phonational range that may be carried out later. When patients exhibit difficulty in
either matching a pitch or spontaneously altering pitch, we have found it useful to have them
imitate animal sounds, such as the high-pitched meow of a kitten, the squeal of a mouse, or
the howl of a wolf. Once again it is important to emphasize that such activities often create
feelings of self-consciousness, which must be allayed by the clinician. One of the most effective
methods of accomplishing this is through humor as the clinician models the desired sounds.
The rationale for this activity is to test one of the limits of the voice, to explore whether the
patient is capable of copying a model presented by the clinician, and to determine whether
there is an overall improvement in the clarity of the sound at any point in the range. (Caution:
This is not a search for an optimal pitch, which we do not believe is a viable concept, but rather
an attempt to understand the physiology responsible for the vocal behavior.)

Sustaining Steady, Prolonged Phonation

As in the previous activity, it is helpful to allow the patient some practice on this task prior to
the taking of measurements. An increased level of tension is often generated in patients when
they know an activity is being timed, and it is not unusual to find that they perform better in
a more relaxed activity. The vowel of choice is usually /ah/. It is important for the clinician to
observe carefully how the patient prepares to carry out this task and how natural or strained the
phonation is as well as noting the steadiness and length of the phonation. The rationale for this
activity is to observe the patient’s ability to control phonation and respiration. Vocal tremor,
if present, will become more obvious on this task than during connected speech. The patient
may be asked to produce such a phonation at various pitch levels as a means of continuing to
explore vocal capacity.

Altering Vocal Loudness

It is usually not difficult to elicit a very quiet sound, but people are often quite reticent to produce
the loudest phonation of which they are capable while seated in a quiet office. Therefore, it may
be necessary to pursue increments of loudness in steps, with the clinician providing the model.
Clearly, if the patient has been referred with the diagnosis of a vocal fold lesion, inflammation,
or edema, this activity should not be carried out. Some persons who have habituated very loud
voice use find it difficult to lower the loudness level and ask with incredulity whether they can
be heard. The rationale for this activity is to further test the limits of voice production and
explore the patient’s ability to manipulate isolated vocal parameters and match a model.

Phonation with Effortful Glottal Closure

It is essential that this activity be used wisely and only with those patients for whom the
activity itself will not be harmful. There are a variety of techniques that elicit effortful closure
of the glottis: grunting, isometric pushing together of the palms, while keeping hands at chest
height; isometric pulling-apart of linked hands held chest height; lifting a very heavy object;
and attempting to raise a chair while seated on it. The person is required to phonate while
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tension is maintained during the activity. The rationale for the use of such a stressful phonatory
act is to attempt to force vocal fold adduction and elicit a nonspeech sound that is difficult
to control voluntarily. It is an activity that we have found helpful in eliciting a lowered pitch
level in young boys who present with puberphonia and an improved voice in some patients
with psychogenic dysphonias. Use of this procedure in therapy is discussed in Chapter 10. The
intent here is to use the technique as an exploratory measure as part of the total assessment.

“Placing the Voice”

This is often referred to as placing the voice in the mask, or voice focus. As a diagnostic task,
it constitutes one of the methods used in the search for the best voice a patient can produce.
This technique is discussed more completely in Chapter 10.

Noninstrumental Objective Measurements

Maximum Phonation Time
An individual’s ability to sustain phonation provides some information about the control
of respiratory function, glottal efficiency, and laryngeal control. When respiratory function is
compromised, there will be either reduction in the amount of air available to support phonation
or a problem in the control of the airflow. If the problem is at the laryngeal level, glottal resistance
to airflow may be reduced due to inadequate glottal closure, or increased due to obstruction
or hyperadduction. Certain problems affecting motor control of phonation may not inhibit
or restrict maximum phonation time but may affect the quality of the phonation. The task is
designed to test the limits of function and as such may uncover weaknesses that are not apparent
at lower levels of function. Thus, for example, in the case of an individual with essential tremor,
a vocal tremor may become increasingly obvious as phonation is sustained, although it may
have escaped notice during speech.
The patient should be instructed to take a deep breath and sustain the vowel /ah/ for as
long as possible. This should be done at pitch and loudness levels that are comfortable for
the patient. A stopwatch should be used to obtain the measure, and patients should be asked
to repeat the task at least 3 times (Hirano, 1981b), with the greatest duration being adopted
as the maximum phonation time. Kent et al. (1987) caution, however, that the database for
this, as well as many other maximum performance measures of speech production, may not be
adequate for confident clinical use. Although Stone (1983) and others (Finnegan, 1984, 1985;
Lewis, Casteel, & McMahon, 1982; Neiman & Edeson, 1981) have reported instability of the
maximum phonation time measure over as many as 15 trials, Bless and Hirano (1982) found
that three trials were adequate if participants were given adequate instruction and practice in
the task. Corroboration of this can be found in the report that coaching and instruction led to
a mean increase in maximum phonation time of 5.2 seconds for a group of girls studying in
their third grade (Reich, Mason, & Polen, 1986). The available normative values for sustained
phonation may be found in Chapter 15.
The ability to sustain phonation is developmental and increases from childhood to adult-
hood. It is logical that this should be the case in view of the physical growth of the body and
increased lung capacity. Significant differences in maximum phonation time exist between the
sexes, but that difference does not begin to appear until puberty, when growth spurts between
the sexes differ in degree (Hirano, 1981b). There is an overall reduction of pulmonary func-
tion with aging, as well as a lessening of laryngeal efficiency (Kent et al., 1987), resulting in a
decrement in maximum phonation time in the geriatric population.

S/Z Ratio
As noted previously, both respiratory and laryngeal factors play some role in determining max-
imum phonation time. However, the measure of maximum phonation time does not provide
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256 Understanding Voice Problems

sufficient information to differentiate between deficits in respiratory support versus laryngeal

inefficiency. Boone (1977) introduced the s/z ratio as an expansion on the measurement of
maximum phonation time. The underlying theoretical construct suggests that individuals with
normal larynges should be able to sustain vocalization (i.e., /z/) for a period of time equal to
that of sustained expiratory airflow without vocalization (i.e., /s/), resulting in a ratio that ap-
proximates 1. If the respiratory system is compromised and the laryngeal system is intact, there
should be an equal reduction in expiratory airflow for the voiceless /s/ and the voiced /z/ compo-
nents of the task, which again would yield a ratio approximating 1. However, reduced vibratory
efficiency of the abnormal larynx should result in air wastage, with reduction in the ability to
sustain phonation but without a reduction in duration of expiratory airflow in the absence of
phonation. Thus, the s/z ratio would be greater than 1 in the presence of laryngeal abnormality.
Eckel and Boone (1981), in a study of dysphonic adults with and without laryngeal pathol-
ogy, obtained results that support this notion. In all, 95% of patients with vocal fold–margin
pathology studied by Eckel and Boone had s/z ratios above 1.4, whereas the ratios for both the
normal control group and those patients with dysphonia without pathology approximated 1.
Two studies have been reported investigating the use of the s/z ratio with children, and
the results have not supported the previous research. In a study of 16 children with vocal
nodules, Rastatter and Hyman (1982) report s/z ratios of 1, similar to expectations in the
normal population. Similar findings are reported by Hufnagle and Hufnagle (1988) in a larger
study of 123 dysphonic children, of whom 69 had vocal fold nodules. Based on the results of
these studies, it would appear that the s/z ratio is not sensitive to the presence of vocal fold
pathology in children, nor does it separate dysphonic children (with or without pathology)
from children with normal voices. Although the reason for the difference between adults and
children on this measure is not entirely clear, it is theorized that the size and stiffness of the
pathology may have been greater in the adult participants than in children, all of whom in
the Hufnagle and Hufnagle study were reported to have had small- to moderate-size nodules
that were soft in consistency. Measures of maximum duration of production of both /s/ and
/z/ have been reported by Tait, Michel, and Carpenter (1980) for 53 children aged 5, 7, and
9 years with normal voices. Their results are shown in Figure 8.20. As one might expect, the

FIGURE 8.20. Maximum duration of phonation in sustained vowels produced by male and female children
aged 5, 7, and 9 years.
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older children had longer maximum phonations than the younger children, reflecting perhaps
greater lung capacity or greater phonatory control. The maximum duration times for both
/s/ and /z/ reported by Rastatter and Hyman (1982) and by Hufnagle and Hufnagle for their
participants who had vocal fold nodules or were dysphonic were lower than those reported by
Tait et al. for their participants with normal voice.
The procedure for measuring the s/z ratio is very straightforward. The patient is instructed
to take a deep breath and then sustain an /s/ for as long as possible. The examiner should
model the task, although it is not necessary to sustain the model maximally. The task should
be repeated at least twice by the patient, with the longest duration taken as the score. The same
procedure is carried out for sustaining the /z/. It is best to use a stopwatch in obtaining these
measures. The ratio is obtained by dividing the maximal /s/ value by the maximal /z/ value.
Available normative s/z ratio data are presented in Chapter 15.
Although this measure has been demonstrated to have some validity for adults, the cautions
discussed relative to maximum phonation time measures also apply here. The s/z ratio should
be used primarily as a screening measure or as one test among many others. A diagnosis of
pathology should never be made based on the result of this procedure alone. However, it may
alert a clinician to the need for medical examination, if that has not been done, or conversely,
it may raise questions about a diagnosis of pathology if the results are not consistent. The
validity of this measure for children is still open to question, and thus it should be used in that
population with even greater caution.
The apparent simplicity of this measure may be somewhat deceiving. Clinically, we have
found that it is necessary to teach this task to patients and to allow them adequate practice
before taking formal measures (Chapter 15).

Scaling
Perceptual judgments of various aspects of voice, quality in particular, are usually described as
being subjective and with the implication that such judgments are not valid. However, percep-
tions can be quantified using well-established techniques of psychophysics and the procedure
of scaling. The simplest type of quantification of qualitative or categorical variables is at the
level of the nominal scale. The fundamental principle of nominal scales is equivalence; that is,
all observations placed within the same category are considered to be equal. For example, voice
qualities can be assigned names such as harsh, breathy, hoarse, or strident, which constitute
categories. The perceptual judgment task may be to place voice samples within categories along
that scale. No judgments are made or implied as to quantity or severity of the quality perceived.
This is simply, as the name of the scale implies, a naming task.
However, we are usually interested in more than naming. Perhaps we want to make judg-
ments about the degree of a quality that is present. Using our group of participants who were
nominally scaled as having hoarse voice quality, we can now engage in rank ordering them
according to severity, using an ordinal scale. In this scale, numbers are used to express order
of magnitude of the perception. The rank order means that higher numbers have a greater
amount of a feature than lower numbers. Thus, the voice quality given a rank order of 1 has
been judged to have less hoarseness than that with a rank order of 15. Ranks do not tell us
how much of a feature is present or how much difference there is between ranks or even if the
difference between ranks are equal. The only information we have is that at a given rank there
is less or more of a feature than at the ranks above or below.
Interval scales are very common in voice-quality scaling because we can use them to
determine how much of a feature is present in one quality compared to another. The refinement
over an ordinal scale is that the distance between adjacent points on the scale has meaning, and
a given interval between measures has the same meaning anywhere along the scale. Common
examples of this type of scale are degrees of temperature and calendar years. In the latter
we know that as much time elapsed between 1790 and 1800 as between 1970 and 1980. The
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258 Understanding Voice Problems

interval scale thus has a defined unit of measure. However, it does not necessarily have a defined
beginning or a meaningful zero point.
The ratio scale has all the properties of the interval scale, with the added benefit of an
absolute zero. Such a scale makes it possible to talk meaningfully about ratios. Examples of this
type of scale are measures of length.
A visual analog scale simply presents a continuum between two anchor points, such as
an undifferentiated 5-inch line scale along which a mark is made representing the quantity of
a feature judged to be present. Such a scale does not use any verbal descriptors along it and
is reported by some to produce more reliable and valid judgments because it permits finer
discriminations to be made (Kempster, 1984). For scoring purposes, the 5-inch line in the
example above could be converted into a 100-point rating scale.
The most complex scaling method is referred to as multidimensional scaling, a method
for identifying the perceptual attributes of complex stimuli such as voice quality (Kempster,
1984; Schiffman, Reynolds, & Young, 1981). Algorithms of multidimensional scales represent
stimuli as points on a spatial map. The difference between points is then a reflection of the
judged similarity or dissimilarity of the stimuli. The closer the points, the greater the similarity
of the feature being judged.

CAPE-V Perceptual Rating Form

The Consensus Auditory-Perceptual Evaluation of Voice (CAPE-V) system was developed at a
consensus meeting in 2002 sponsored by Division 3, Voice and Voice Disorders, of ASHA and
the University of Pittsburgh. Speech-language pathologists, voice scientists, and other scientists
interested in sound perception met to discuss the current state of the art for the perceptual
rating of voice and to create a system that could be used for the routine perceptual rating of
disordered voices. The intent was to develop a standardized procedure for rating, define the basic
qualities of the voice that should be rated, and to recommend the development of a standardized
training system. The CAPE-V was the outcome of that meeting (Kempster, Gerratt, Verdonlini,
Karkmeier-Kraemer, & Hillman 2009) and is currently in its testing and evaluation stage. The
latest approved version of the form along with instructions is available from the ASHA Web
site (ww.ahsa.org; see form in Appendix XX).
The scale identifies six core perceptual attributes of the voice, that is, overall severity,
roughness, breathiness, strain, pitch, and loudness. The degree of each attribute is indicated on
a 100-mm line where the left end indicates normal or a very mild severity, whereas the extreme
right end indicates severe amount of the attribute. The rater may also indicate whether the
attribute is consistent or intermittent in the voice sample rated. For pitch and loudness, the
rater is to indicate the nature of the abnormality as well as the rating. There is also space for two
additional but unnamed attributes to be added by the clinician and rated. There is also space
for comments about resonance as well as any other perceptual features observed in the sample.
The ratings are to be made after the completion of several tasks, including sustained vowels,
sentences, and spontaneous speech. The clinician marks the amount of the deviancy on the
100-mm line and, after completion of the ratings, measures the distance from the left end of the
line to the mark and writes the value in the column labeled ???/100. For example, if the distance
of the line for overall severity is 57, then the notation 57/100 would appear. The clinician may
also use descriptive words such as mildly deviant, moderately deviant, or severely deviant.
The consensus group expects that there will be modifications to the basic reporting form
as more clinicians begin using the form and further experience is gained.

Scaling of Pitch
Perceptual judgments of voice quality are often confounded by other perceptual attributes of
the voice sample and may not always be related to a simple acoustic correlate. For example,
let us examine the perception of pitch. Wolfe and Ratusnik (1988) have shown that listeners
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will rate the pitch of rough vowels much lower than the pitch of normally produced vowels.
Consequently, vowels produced by a patient with a hoarse voice may be expected to be perceived
as lower in pitch than their measured fundamental frequencies would predict. Furthermore,
Wolfe and Ratusnik reported that the pitch matches they obtained were related to the acoustic
measures of noise energy level and jitter ratio rather than to fundamental frequency. Thus, it
appears that with respect to pitch, other abnormal perceptual (e.g., roughness, hoarseness) or
acoustic (e.g., jitter, noise level, spectrum) attributes may result in inaccurate judgment. This
may account for some of the discrepancies that have been noted between perceptual pitch
judgments of abnormal voices and the measured acoustic correlate of fundamental frequency.
Wilson, Wellen, and Kimbarow (1983) suspect that there is a skill in discriminating pitch
differences in the speaking voice that is not easily developed. Their judges, described as trained
and untrained, performed at chance level on a pitch discrimination task until there was at least
a 20- to 29-Hz difference present between paired voice samples.
Another factor affecting the reliability and validity of perceptual judgments is the experience
of the listener. Many studies in which perceptual judgments were reported used experienced
listeners or listeners with extensive exposure to normal and abnormal voice qualities. How
much experience is needed to produce reliable judgments is somewhat unclear. Bassich and
Ludlow (1986) conducted a study using 4 judges who required 16 half-hour training sessions
before reaching 80% agreement with one another. Perhaps the lack of training or experience
may account for the lack of difference between groups of trained and untrained listeners in
distinguishing pitch differences between pairs of children’s voices in the Wilson et al. (1983)
study. The trained group consisted of 10 graduate students in speech-language pathology, of
which only 4 had had previous experience in working with patients with voice disorders.
It would seem highly unlikely that graduate students with only a brief exposure to voice
disorders (usually a single academic course and perhaps an actual patient in clinic) would be
able to reliably and accurately rate attributes of the voice such as pitch, loudness, and tremor.
In a study reported by Colton and Estill (1981) concerned with the identification of four
distinct voice qualities, the group of 6 speech-language pathologists performed slightly worse
than the group of 15 “naive” listeners (66% vs. 68%). Singers and individuals who played a
musical instrument performed somewhat better than these two groups (73% for singers, 75%
for instrumentalists). Although the differences between the groups were not large, these results
suggest that experience in music may help a listener to make judgments concerned with voice-
quality attributes. At the very least, musicians may attend better to the nonlinguistic aspects of
the speaker’s utterance.
It is clear that perceptual judgments of vocal pitch are sufficiently unreliable to cast doubt on
their use in planning treatment strategies. Determinations of the appropriateness of pitch level
should be made on the measurement of its acoustic correlate, fundamental frequency, for which
normative values appropriate for age and sex are available for comparison. Whenever measurable
acoustic correlates of vocal attributes are available, their use is encouraged in preference to
reliance on the perceptual feature.

Scaling Vocal Effort

The effort a patient makes to vocalize may be important to assess in the exploration of a voice
problem. Many patients report that at the end of a day of prolonged talking, they feel vocally
fatigued. They may also report that they need to expend more energy in talking than they did
prior to onset of their vocal problem. It is difficult for the clinician to know how to assess such
reports and what value to give them. However, there is a way for such “feelings” to be measured,
and such measures can be helpful therapeutically and in assessing the efficacy of treatment and
of specific treatment techniques.
How does the clinician quantify the vocal effort a patient uses during phonation? Simply
by asking the patient to produce a vocalization and afterward asking that patient to assign
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FIGURE 8.21. Vocal effort/sound pressure level and vocal effort/fundamental frequency relationships
for five normal speakers.

it a number that represents the amount of effort used. It has been shown that patients can
scale their own effort levels with this simple procedure (Colton & Brown, 1973; Irwin &
Mills, 1965; Lane, Catania, & Stevens, 1961; Wright & Colton, 1972a, 1972b). Wright and
Colton (1972a, 1972b) asked speakers to produce the vowel /ah/ at their minimum, most
comfortable, and maximum effort levels. The fundamental frequency and the sound pressure
level of each phonation were measured during each vocalization. The patients were then asked
to assign a number that represented the amount of effort used. They could use any number
they wished, with the understanding that greater effort levels would be associated with higher
numbers. This procedure is often referred to in the psychophysical literature as the method of
magnitude estimation. Median results for the group are shown in Figure 8.21. The left panel
shows vocal effort in assigned numbers versus SPL in decibels. In the right panel, vocal effort
is compared to fundamental frequency. The solid lines connect minimum, most comfortable,
and maximum effort levels. The data points between these three effort levels (squares) were
generated by asking the patient to produce a phonation whose effort was halfway between
minimum and most comfortable or most comfortable and maximum. Each of these intervals
then was bisected again to produce the estimates of vocal effort shown in this figure. Note how
consistent the participants were in producing and rating their effort levels, especially for effort
versus SPL. The data points for magnitude production (shown by circles) were obtained by
providing a number to the patient and asking him or her to produce a phonation with an effort
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level representative of the number supplied. These data are very similar to the data obtained
in the magnitude estimate phase of the experiment. The vocal effort/fundamental frequency
data show somewhat more variability between magnitude production and estimation than the
vocal effort/SPL data. It is abundantly clear, however, that individuals can rate the effort they
use to produce voice and that variations of vocal effort are manifested acoustically by variation
of SPL and fundamental frequency.
The data of Figure 8.21 clearly show that an increase of vocal effort is accompanied by an
increase of both intensity and frequency. Colton and Brown (1973) have shown that speakers
also exhibit systematic increases of intraoral air pressure with an increase of vocal effort. In
simple consonant-vowel syllables, intraoral air pressure can be a good estimate of the pressures
driving the vocal folds (Hixon & Smitheran, 1982; Rothenberg, 1982; Smitheran & Hixon,
1981). Thus, it is not unreasonable to suspect that the magnitude of subglottal air pressure,
accompanied by the consequent tension of the vocal folds, contributes to the judgments of
vocal effort.
Verdolini-Marston and her colleagues (Verdolini-Marston, Burke, Lessac, Glaze, & Cald-
well, 1995) reported using vocal effort scaling in their study of the effectiveness of two kinds
of therapy for vocal nodules. Prior to therapy, five participants who received the confidential
voice therapy protocol have a mean rated effort level of 115 (a judgment of comfortable level of
effort while talking was assigned the number 100), whereas the three participants who received
the resonant voice therapy protocol have a mean rated effort level of 142. After a 2-week,
concentrated period of voice therapy, the confidential therapy group reported a mean effort
level of 90 and the resonant therapy group an effort level of 105. These measures were obtained
2 weeks after therapy had ended, and both therapy groups had a mean effort level of 97. These
results suggest that monitoring vocal effort may reflect the physiological changes that occur as
a result of therapy and may monitor the vocal usage by patients with voice disorders.
Listeners can also rate vocal effort from recorded samples of speech (Brandt, Ruder, &
Shipp, 1969; Lane et al., 1961; Moll & Peterson, 1969; Warren, 1962), but the ratings are not
simply ratings of the vocal loudness (Brandt et al., 1969). Listeners apparently use the increase
of energy in the higher frequencies as cues for their judgments of vocal effort as well as the
greater sound pressure levels that accompany increased effort levels. They may also internalize
what they hear and relate their judgments to their own perceived efforts. It is important to
understand that increased tension in the adducted vocal folds results in greater subglottal air
pressure and also results in the production of increased energy in the higher frequencies. Thus,
listeners and speakers appear to use similar cues; only the speaker has access to the significant
physiological variable, air pressure, whereas the listener must depend solely on its acoustic
manifestation, increased high-frequency energy.
The concept of vocal effort, as well as its measurement, have implications for the manage-
ment of voice problems, monitoring progress, and assessing treatment efficacy (see Chapter 10).

Voice Sample Recording

One of the easiest and simplest ways of testing a person is to obtain a voice recording. Even
if no further analysis of the recording is performed, the recording itself can be invaluable.
Recording makes repeated listening possible, allowing the voice clinician further opportunities
to learn about the person’s voice characteristics. A voice recording during the initial assessment
provides a baseline record of the voice prior to intervention. This documentation can be helpful
for demonstrating progress or change as a result of treatment and for judging the efficacy
of treatment. A baseline recording is highly important when medical-legal issues arise. It is
surprising, therefore, that so little attention is generally given to the techniques and equipment
needed for producing good-quality recordings. The material presented in the following sections
is based both on personal experience and on discussions by Izdebski (1981, 1983).
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Audio Recorders
There are several kinds of voice recorders that can be used to make audio recordings of patient
vocalizations: (a) reel-to-reel, (b) cassette, (c) video tape recorders, (d) DAT recorders, (e)
minidisc recorders, (f ) Direct-to-CD recorders and digital recorders. The reel-to-reel models
have an excellent frequency response and a wide dynamic range but are not often found in
most voice clinics. Manufacturers of reel-to-reel units include Nagra, Ampex, and Revox.
Cassette recorders are much more popular and offer the conveniences of portability and use
of cassette tapes. Although inexpensive cassette recorders are available, they rarely have good
frequency response or adequate dynamic range, do not produce good recordings, have high tape
instability (wow and flutter), and are prone to breakdown. These inexpensive recorders are not
recommended for clinical use. There are many cassette recorders costing US$200 to US%600
that have good to excellent characteristics and are easy to use. We include videotape recorders
in this category because many of the medium-priced models, as well as the higher-priced ones,
have excellent frequency and dynamic ranges in the audio range, very low tape instability, and
can store considerable data. Furthermore, many can record and reproduce in stereo.
Two additional recording devices may be available although their availability appears to be
more problematic with the advent of other digital recording systems. The DAT recorder is very
similar to a cassette recorder except that the analog voice signal is digitized and recorded on
tape. The cassette is about the size of a microcassette (the kind used in dictating equipment),
but, depending on the tape quantity and the recording speed, up to 4 hours of high-quality
signal can be recorded. At the fastest speed presently available, the quality rivals that heard on
compact discs (CDs). DAT recorders are made by Sony, JVC, and Aiwa, among others.
Minidisc recorders use a small disc about the size of the 31/2 disc used in many computer
systems. The recorder can record about 60 to 70 minutes of vocalization with CD quality. Sony
makes a minidisc recorder that is about the size of a Walkman. Although perceptually the record-
ings sound excellent, the frequency response may be limited because of circuitry used to pack
the samples on the small disc. Thus, a minidisc recorder may not be suitable for critical clinical
applications but is suitable if the intent is only to collect audio recordings for listening purposes.
Beware of minidisc players that can play prerecorded minidiscs but have no record capability.
Several manufacturers (e.g., Marantz) produce direct-to-CD recorders. With these units,
it is possible to record audio samples direct to a CD with very high quality. New recordings can
be added at any time and when the CD is full and finalized, it can be played in any computer
system. Individual recordings can be identified on the CD and quickly retrieved for listening
or analysis.
There are a variety of digital recorders that record direct to a compact flash disk, a secure
digital disk, or a memory stick. For example, Tascam (Teac Professional, www.tascam.com)
makes several disk recorders that record standard WAV-type files. This recording format is
lossless unlike the common but lossy mp3 format that is found in many sound recorders
available for popular use. To obtain full fidelity recordings, the clinician should use a WAV-
type format (or similar) and not mp3 or similar lossy formats. Marantz (www.marantz.com)
also produces solid-state digital recorder. High-capacity storage cards permit the recording of
considerable length and like the CD allow for random retrieval of the audio material.
If the clinician decides to use standard tape recorders, it is also important to use high-
quality recording tape. High-quality tape has a number of advantages: (a) It is strong enough
to withstand the starting and stopping required when many speech samples are recorded and
played back, and (b) less of the oxide particles in the tape will rub off to affect the recording and
playback heads and interfere with the motor and wheels that transport the tape. Cassette tapes
are available in 30- to 120-minute lengths. It is best to avoid the 120-minute tapes because the
tape is very thin and can break easily. Cassette tapes made by TDK, Maxell, Sony, Nakamichi,
3M, or similar manufacturers are of good quality. Tapes may also differ in type, for example,
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standard tape, chromium dioxide tape (a high-bias tape), or metal tape (also a high-bias tape).
Most tape recorders are able to play back all of these types of tape. Metal tape tends to have the
best response characteristics, but at considerably greater cost. Many of the good to excellent
cassette recorders will have metal tape recording/reproducing capability.
Microphones
Microphones should be selected on the basis of low distortion, low sensitivity, wide frequency
response (50–16,000 Hz), directionality, stability, and cost. Good-quality microphones can
be purchased for relatively low cost (US$50—US%100). A good source for microphones is
Radio Shack. Many new microphones are of the electret type, which contain a small battery
and pickup element that has very good frequency and dynamic response characteristics. There
are also condenser and dynamic microphones that have excellent characteristics at moderate
cost. A pressure-zone microphone, a relatively new type of microphone that permits recording
large groups with good fidelity, is also worthy of consideration.
For voice work, a microphone attached to an earphone band works very well. It maintains
a constant mike-to-mouth distance and, since it is very close to the source, can produce good
recording levels even with a very quiet voice. However, the mike should be placed at an angle
and to the side of the lips to avoid transient noises due to the air flows produced during speech.
Environment
Recordings should be made in a quiet room, away from noisy corridors and windows that face
onto busy streets. The room need not be completely sound proof, however. Carpeted floors
and walls and windows hung with fabric coverings serve to reduce noise level significantly. Of
course, special acoustic absorbing panels can be installed, which will produce a very quiet room.
The clinician should measure the noise levels within the room to make sure they are acceptable
(less than 50 dB at the low frequencies) and periodically check these levels to ensure that the
noise present is predominantly low frequency.
Tasks
It is important to chose a variety of tasks for the patient to carry out that will sample the full
range of the patient’s vocal capabilities. Sustained vowels are useful for subsequent measurement
of fundamental frequency, perturbation, and spectra. Syllables and sentences should be used
to sample the patient’s voice under more speech-like conditions and yet yield data that can be
compared at different time periods. Testing of vocal limits, that is, phonational (frequency)
range and dynamic (intensity) range, can also be recorded. We usually include a standard
reading passage, the Rainbow Passage (Fairbanks, 1960), and a sample of conversational speech
as part of our recording protocol. Of course, it is important to also record any special or unusual
characteristics of a patient’s vocal behavior. The speech tasks from the protocol for fiberoptic
examination in the appendix may be used for any audio recording. One could also use the
speech tasks recommended by the CAPE-V consensus group (Kempster, Gerratt, Verdolini,
Barkmeier-Kraemer, & Hillman, 2009; see Appendix XX).

Quality-of-Life Evaluation
Voice evaluation has traditionally involved the use of perceptual, acoustic, aerodynamic, and
other physiological measures. The intent of these tools is to allow the clinician to describe
the voice, compare it to normal, document changes with time or treatment, and estimate the
severity of the dysphonia present. Despite the extensive use of these instruments, however,
many questions regarding their reliability and validity, as well as how they are obtained and
interpreted, are unresolved (Gerratt & Kreiman, 2001; Karnell, 1991; Karnell, Hall, & Landahl,
1995; Karnell, Scherer, & Fischer, 1991; Kent et al., 1987; Kreiman & Gerratt, 2000). In recent
years, increasing attention has been given to the patient’s own assessment of the dysphonia, and
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its impact on his or her life. The development of patient-view instruments, for many disorders,
has been motivated by a number of factors.
With rising health care costs, and increasing competition for limited available funds, it has
become more critical to assess outcomes of treatment(s). Though health care providers have
always been interested in the effects of their interventions, the ability to document these in
meaningful and objective ways has become imperative. Institutions that manage health care
services, insurers, and other funding sources scrutinize the relative effectiveness of treatments
in an effort to determine the best use of resources and to establish standard-of-care guidelines.
With the intense focus on outcomes research, there has been a growing realization that subjective
information regarding the effects of disability on the individual patient represents an important
addition to assessment batteries. Insights into the effects of a disorder on a patient’s emotional
and social well-being and on his or her ability to function in real-world situations, such as in a
work setting, are revealed in a manner not possible with clinician-view measures.
The impact of disability on “quality-of-life” issues is reflected in a number of tools designed
specifically for patients with voice disorders. Typically, these instruments take the form of a
set of questions, or statements, which require a response from the patient. Though simplistic
in form, good quality-of-life instruments reflect the same rigorous development that is key to
establishing the validity and reliability required of any assessment tool (see Hogikyan & Rosen,
2002, for a review of subjective assessment).
The Voice Handicap Index (VHI; Jacobson et al., 1997) is one of the first, and perhaps
most frequently used, quality-of-life instruments specific to voice disorders. In its original form,
the VHI included 85 items taken from patients’ reports of the impact of their voice disorder on
various aspects of their lives. These were then administered to 65 patients with voice disorders
and the results subjected to tests for internal consistency and reliability. This testing identifies
items that best represent the scale’s content and contribute to its overall reliability. Through
this process the original 85 items were reduced to 30. These 30 items were found to reflect
3 domains in equal proportions, that is, a 10-item functional subscale, a 10-item emotional
subscale, and a 10-item physical subscale. The items are expressed in first person, for example, “I
use the phone less often than I would like.” Patients respond to each item using a 5-point scale
from “0,” indicating that the particular item was “never felt” to “5,” indicating that the item
was “always felt.” Scores are determined for each domain, and for the total VHI. The higher
the score, the more severe the dysphonia and its impact are perceived to be by the patient.
Differences in VHI scores before and after treatment reflects the “amount” of improvement,
or lack thereof, the patient has experienced as a result of treatment. The VHI has proved useful
not only in comparing patients’ perceptions of disability before and after treatment but also
in comparing patients with different pathologies. Benninger, Ahuga, Gardner, and Grywalski
(1998) reported results of VHI testing on patients with different vocal pathologies as well as on
patients with chronic, non–voice-related diseases. The authors found that patients with vocal
fold paralysis had the highest level of pretreatment disability, as compared to patients with
masses or edema. Interestingly, the authors also used another tool for assessing general (not
specific to a particular disorder) quality of life and found that dysphonia represented a significant
disability even when compared to sinusitis, sciatica, mental health, and angina pectoris. Rosen
and Murry (2000) compared performances on the VHI across patients representing three types
of disorders, including muscular tension dysphonias, benign vocal fold lesions, and unilateral
vocal fold paralysis. Consistent with the Benninger et al.’s study, these authors found that, both
before and after treatment (surgery, voice therapy, or both), patients with paralysis demonstrated
the highest self-perception of handicap whereas patients with benign lesions demonstrated the
lowest perceptions of handicap severity.
Murry and Rosen (2000) described the possible utility of voice-specific outcome measures
in treatment planning. For example, a patient with a low score on the VHI and benign laryngeal
pathology may be best served by voice therapy or conservative treatment, whereas a patient
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with similar pathology but a higher self-perception of handicap may be more quickly directed
to surgical intervention. These authors (1999) investigated relative self-perceptions of severity
of handicap in a group of patients who shared a diagnosis of vocal fold paralysis. One group
included working professionals; the second group was comprised of individuals who were
retired. Results indicated that the working professionals demonstrated greater self-perceptions
of handicap than did the individuals who were retired. Although this result might be anticipated
when looking at group evidence, it should not be taken to suggest that voice is not important
to retired persons. Rather, the findings lend support to the value of individual assessment and
quality-of-life testing in treatment planning.
In another study, Rosen and Murry (2000) compared scores on the VHI in singers and
nonsingers who demonstrated various types of laryngeal pathologies. Interestingly, the profes-
sional singers appeared to view their dysphonia as a less severe handicap than did the recreational
singers. The authors suggested several reasons for the findings, including the possibility that the
VHI may not reflect the unique features of dysphonia in a singer, such as a diminished pitch
range, or inability to control voice while singing softly at high pitches. It may also have been
the case that singers sought treatment very early on in their dysphonia, whereas nonsingers may
have waited until the dysphonia had reached a handicap level. The authors caution that results
of the VHI must be considered in the context of the particular population with which it is used.
Since its introduction, the VHI has been used in a number of studies and has been adapted
to many other languages (Amir et al., 2006; Attieh et al., 2008; Behlau, ves Dos Santos, &
Oliveira, 2010; Bouwers & Dikkers, 2009; Hakkesteegt et al., 2006; Hsiun, Kang, & Wang,
2003; Malki et al., 2010; Ohlsson & Dotevall, 2009; Schindler et al., 2010; Verdonck et al.,
2008; Woisard, Bodin, & Puech, 2004). It has proved to be a valuable tool for the evaluation of
the voice of persons with vocal problems (Bovo, Galceran, Petruccelli, & Hatzopoulos, 2007;
Cohen, Dupont, & Courey, 2006; D’Alatri et al., 2008; Dogan, Eryukel, Kocak, Celkel, &
Sehtoglu, 2007; Evans, Carding, & Drinnan, 2009; Martinez, Remacle, & Lawson, 2010;
Welham, Dailey, Ford, & Bless, 2007; Zur et al., 2007). It is one of the tools one could use to
demonstrate the effectiveness (or lack thereof ) of treatment and should be part of the routine
evaluation of patients.
The Voice-Related Quality of Life (V-RQOL) is another instrument designed specifically
to assess quality of life in patients with vocal handicaps (Hogikyan & Sethuraman, 1999).
The instrument tests three domains, including social-emotional, physical, and general. Patients
are required to consider 10 statements, for example, “I have trouble speaking loudly or being
heard in noisy environments,” and “I avoid going out socially because of my voice.” Items
were reportedly based on interviews with patients and with the authors’ clinical experience.
Responses are on a 5-point scale where “1” indicates no problem, and “5” indicates that
the problem is as “bad as it can be.” Both domain and overall scores are easily manipulated
to form 0 to 100 scales, with “0” indicative of poor V-RQOL, and “100,” an excellent V-
RQOL. As a part of the development of this instrument, the scale was administered to patients
reflecting a wide variety of voice disorders, and reliability, construct validity (ability of the
instrument to identify significant differences in populations with regard to predetermined a
priori hypotheses), and responsiveness to change and burden (related to how “burdensome”
the instrument is to potential responders) were investigated. The authors concluded that the
V-RQOL met appropriate standards of validity and reliability, was sensitive to change, and did
not, in its administration, represent an undue burden to patients.
The V-RQOL instrument has been used to assess patients with vocal fold paralysis and
patients with spasmodic dysphonia. In one investigation, patients with untreated vocal fold
paralysis were compared to patients with paralysis who had undergone thyroplasty (Hogikyan,
Wodchis, Terrell, Bradford, & Esclamado, 2000). Differences between the two groups were sig-
nificant, with the treated patients generating scores significantly higher than untreated patients.
In the second study, (Hogikyan, Wodchis, Spak, & Kileny, 2001) 27 new patients diagnosed
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with adductor spasmodic dysphonia completed the V-RQOL before, and 6 to 8 weeks after,
administration of BOTOX injections. Mean scores improved from 30 to more than 80 between
assessments. The authors concluded that the instrument is capable of documenting and differen-
tiating the effects of voice disorders and their treatments and continued to investigate its utility.
One other instrument that should be mentioned is the Voice Outcome Survey (VOS;
Gliklich, Glovsky, & Montgomery, 1999). The VOS includes 5 items, one of which is related
to a general appraisal of the speaking voice, and 4 others that address specific effects of the
voice disorder, for example, “To what extent does your voice now limit your ability to be
understood in a noisy area?” In developing the VOS, the authors investigated 56 patients with
uncompensated vocal fold paralysis. Patients underwent testing before, and 6 months after,
treatment for their paralyses. They also underwent tests of objective voice measures, including
maximum phonation time and average intensity. The authors reported that the VOS was
more sensitive to changes associated with treatment than other measures administered and
recommend the VOS not only because of its sensitivity but also because, in their opinion, it
meets appropriate standards of validity, reliability, is quickly and easily administered, and is
highly sensitive to change. This scale may be limited in applicability to patients with unilateral
vocal fold paralysis. However, it does set a model for development of disorder-specific scales by
using fewer items, but ones that may be unique to or typical of a particular disorder.
Hartnick (2002) used a modified version of the VOS to assess the impact of voice disorder
in children who either had a tracheotomy or who had achieved surgical decannulation. In this
study, parents and caregivers of children responded to items on the assessment instrument.
Following analyses of the construct validity and reliability of the instrument, one item on the
scale related to swallowing, for example, “How often do you have trouble with food or liquids
going ‘down the wrong pipe’ when you eat, or find yourself coughing after eating or drinking?,”
was removed. On the resulting 4-item scale, the instrument demonstrated good ability to assess
voice-related quality of life in children, at least as perceived by a parent or caregiver. It was able to
discriminate between two subpopulations, that is, children who had undergone decannulation
were perceived by their parents (or caregivers) as less vocally handicapped than children who
had tracheotomies, and the authors suggested that the parent-proxy tool may play a valuable
role in assessing the effect of pediatric voice disturbances on the child’s overall quality of life.
We might question whether a 4-item scale would be sufficient to differentiate a wide range of
pediatric dysphonias from each other; for the specific problem and populations investigated by
these authors, however, the small number of items was apparently appropriate.
Yet another voice-specific rating tool recently described is the Voice Symptom Scale (VoiSS;
Deary, Wilson, Carding, & MacKenzie, 2003). In the first phase of this instrument’s develop-
ment, 133 consecutive patients reflecting a variety of disorders were asked to list all of their
voice-related problems. A total of 467 responses were subsequently classified by WHO (World
Health Organization) criteria into 24 impairments, 15 disabilities, and 15 handicaps. One
item (reported by only one patient) was removed, and the remaining 53 items comprised the
pilot scale. Each item had two 5-point response scales, the first dealing with frequency of the
complaint, that is, all the time, occasionally, and the second dealing with the severity of the
complaint, that is, unbearable, slight.
The pilot scale was then administered to a large number of patients reflecting, again, a
variety of voice disorders, excluding those related to malignancy or surgical causes for dysphonia.
A principal components analysis performed on the results indicated that not all the items were
independent, and the scale was revised in order to eliminate redundant items. Based on the large
number of incomplete responses to the questionnaire, in particular to the severity scale, the
authors also felt the scale needed to be shortened. Modified with these findings and concerns
in mind, the final questionnaire was comprised of 43 items that appeared best able to capture
information pertinent to patients’ voice-related perceptions of handicap. The 5 components of
the scale consider the impact of dysphonia according to “communication problems,” “throat
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infections,” “psychosocial distress,” “voice sound and variability,” and “phlegm,” respectively.
These components are of particular interest since, as noted, they were derived from complaints
expressed by a large number of patients with voice disorders. The authors of VoiSS note that
further empirical exploration may produce further changes in the scale. Though longer than the
other scales described, the development of the instrument to date is impressive in its attention
to the reality of patient complaints, and in its exposure to a large number of participants.
Other patient-view scales have been developed, or are in various stages of development,
which are at least in part directed to the impact of voice disorders on an individual’s workplace
performance. Smith et al. (1998), for example, investigated work-related effects of spasmodic
dysphonia and vocal fold paralysis. Their results provide interesting insights into both the
perceived and real liabilities associated with vocal disability and success in the workplace.
Difficulty performing required work and keeping a job, or having to change jobs, were reported
significantly more often in individuals with spasmodic dysphonia and vocal fold paralysis than
in individuals who had no vocal impairment. In addition, these individuals viewed their vocal
disability as having a significant potential to adversely affect future career options. In another
study, Smith, Gray, Dove, Kirchner, and Heras (1997) found that teachers had experienced more
missed days of work than did other occupation groups for problems related to voice. Perceptions
that voice problems would adversely affect their career options in the future were also more
common to teachers than to individuals in other occupations. Our understanding of the impact
of a voice disorder on an individual’s ability to work is rudimentary and, in fact, there is little
information available regarding the prevalence of vocal disability among various occupational
groups. Obviously, such data and instruments that can elaborate these issues are needed.
Assessing the impact of a voice disorder on an individual patient is important not only
to determining treatment outcomes, or to determining the degree of disability associated with
various types of pathologies, but also to establishing the relative worth of vocal disability. In
this country, annual claims for workmen’s compensation and occupational disability involve
huge amounts of money. As one example, in 1998, the California Workmans’ Compensation
System spent a total of US$6.4 billion on disability claims. By 2003, the overall cost of the
worker’s compensation system in California was estimated to approximate US$29 billion. The
consequences of such costs spiraling out of control have broad-reaching implications, including
increasing costs of insurance that are generally absorbed by employers.
The need for instruments that can provide realistic insights into the determination of
vocal disability is particularly acute. Although work-related claims involving voice or speech
are less common than other types of claims—such as those for back or hand injuries or noise-
induced hearing loss—vocal function disability appears to be on the increase as well. Cellular
telephones, voice-activated computer systems, open-office designs that add to ambient noise
levels, and buildings that create hostile breathing environments may be contributing factors.
Major differences exist between many other injuries and voice injuries. Voice injuries are less
well known and are poorly understood; they are invisible and often do not involve physical pain.
And, in some instances, they may vary in severity as they are affected by amount and type of voice
use. Not surprisingly, another major difference between vocal injuries and many other injuries
is the lack of well-established guidelines for determining vocal disability. There is in fact little
information available to help a physician or voice clinician determine or elaborate a worker’s
level of impairment or to formulate appropriate restrictions and limitations on voice use.
Many states use guidelines that have been developed by the American Medical Association
(AMA) for this purpose. For speech impairment, this organization recommends three criterion
measures for determining disability—audibility, intelligibility, and functional efficiency. For
each, there are five levels of disability, depending on severity. In terms of audibility, for example,
a Class 1 impairment implies that the patient can produce speech of sufficient intensity for most
everyday needs, although this may occasionally require effort and occasionally may be beyond
the patient’s capacity. A Class 5 impairment in audibility implies that the patient can produce
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268 Understanding Voice Problems

speech of intensity sufficient for none of the needs of everyday speech communication. The de-
termination is made on the basis of observing the patient, reports from others, and on the results
of selected tasks. Interestingly, a patient classified as demonstrating maximum disability on all
3 criteria, according to the AMA, would have only a 35% impairment of the “whole person.”
State guidelines may be even less delineated and may vary from state to state. Again using
California as an example, the California Labor Code (California Labor Code, State of California)
defines permanent disability as a “medical or mental condition that results in an inability or
reduced ability to compete in the open labor market.” Both subjective and objective measures are
considered in determining disability. Objective factors are defined as “those findings on physical
examination that can be directly measured, observed or demonstrated, and are not in the control
of the patient.” Unfortunately, there are currently no objective criteria for determining voice
or speech disability, and there are only 2 levels of disability that can be assessed—“difficulty
speaking,” which is rated as a 10% disability, and “complete loss of speech,” rated as a 50%
disability. Beyond this, the determination can be made by an otolaryngologist, or a general
practitioner, neither of whom is required to have any background in voice or speech.
In short, commonly used guidelines for determining occupational disability related to
voice (and speech) are inadequate, in particular, for those individuals whose occupations rely
heavily on voice use. Objective measures of voice, including perceptual and acoustic, have not
been particularly helpful in resolving this situation. There is no wide agreement on a particular
set of measures that should be used for this purpose, and the selection of almost any particular
measure available could be argued in terms of its relevance to voice use in a work setting.
Quality-of-life measures that address this issue from the patient’s perspective have the potential
to play a valuable role in determining the impact of vocal disability on this very specific matter,
that is, how handicapped is an individual, and to what extent does this affect the ability to
maintain or resume his or her usual occupation.
As noted, years of attention to objective acoustic, perceptual, and physiological measures,
although beneficial to other purposes, have not yet yielded robust measures that are universally
used to provide objective indices of vocal disability, differentiate vocal impairment across types
of voice disorders, or document treatment effects in individual patients. Such data are necessary
to demonstrate the benefit of voice therapy to third-party payers and others, to help establish
meaningful guidelines for determining vocal disability, and for many other purposes. QOL
measures seem uniquely able to demonstrate significant differences, are easily and quickly
administered, and are easy for both patients and professionals to understand. They are a relevant
and excellent inclusion in the voice clinician’s evaluation battery and should be administered
to each patient prior to, and at the termination of, treatment. At this point in time, the VHI
and V-RQOL scales are probably the most commonly used.

Special Testing
Psychiatric
The link between personality and voice cannot be overemphasized. It is expressed in a multitude
of ways by all speakers. Second only to our appearance, the voice serves as our identity, as a means
of identification even in the absence of the visual presence. It serves as our emotional escape
valve as we laugh, cry, scream in fear, or shout in rage. It speaks of our well-being, of our energy
level, of our emotional state. We use it to cajole, to seduce, to energize, to subdue, to question,
to arouse, to soothe, to scorn, to demand, to plead, and, in short, to give special meaning to our
words. And we are called upon to use our voices to impart information; to express opinions;
to defend our property, our rights, ourselves; to intercede for others; to influence others; and
simply to interact with others. Our voices are a road between people, the road on which the
words we speak travel. Is it any wonder, then, that the road is sometimes subject to bumps and
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irregularities, that it becomes altered due to excessive tensions and stresses? In some cases these
changes are minor, requiring only that someone understand the situation and arrive at a way
to resolve it. However, other problems require extensive repairs and require specific types of
expertise if they are to be attended to properly.
The analogies are obvious. For some people, excess tensions are felt most keenly in the
laryngeal area. The effect of these tensions may take time to gradually become apparent and
bothersome, or they may reach a significant level rather quickly. There is a continuum of effect,
from the very mild hoarseness that tends to come on at the end of the day to the constant and
all-pervasive lack of voice. However, that continuum should not be equated with the depth
of the problem. The degree of the dysphonic symptoms is not necessarily correlated with the
“severity” of the problem.
Clinically, patients with voice disorders of psychological origin constitute a fascinating
group of people, for many of whom almost magical return of voice is not infrequent. Skill,
understanding, and patience are required, but the reward for the speech-language pathologist, in
the form of immediate success, comes rarely in the practice of the profession. Specific procedures
for the treatment of these kinds of problems will be discussed in Chapter 10.
For a significant number of patients, however, the basic problems are much deeper. The
patient is unable to give up the symptom, or unable to do so permanently. In such cases, there
is a clear need for referral for psychiatric or psychological consult or counseling. Indeed, such a
referral is also often necessary and helpful for those persons who, with our help, may be able to
abandon their symptoms, but for whom there continue to be problems that need attention.

Case Study
R. W., an overweight and not very attractive 16-year-old, was referred for voice therapy with
a diagnosis of dysphonia in the presence of a normal-appearing larynx. It was very difficult to
engage R. W. in conversation. He responded to all questions in as few words as possible. He
made only fleeting eye contact. The dysphonia was in its third month, and he had been out
of school for that entire period on doctor’s orders. Prior to this referral, he had already been
on a regimen of voice rest and through several courses of pharmacological treatment, with no
change in symptoms. R. W.’s voice sounded very strained and tense. Hoarseness was present.
Working very slowly, with constant encouragement and praise, we were able to elicit a normal
voice quality. R. W. refused to recognize this change at first, but slowly became willing to use
the good voice more frequently. Within a few therapy sessions R. W. had full return of normal
voice and was ready to return to school.
During the therapy sessions the need for R. W. to see a psychiatrist or psychologist was
raised both with him and his mother. With return of normal voice a direct referral for such
additional treatment was made. A month later R. W. returned. His voice had worsened, with a
full recurrence of earlier symptoms. Our referral for psychiatric follow-up had not been carried
out. R. W. was seen again for several sessions of voice therapy, during which he continued to be
very closed in all respects. Once again voice was restored and once again referral for psychiatric
consultation was made even more strongly. Two months later R. W.’s mother wished to schedule
another appointment as once again the symptoms had recurred. She was advised that it was not
appropriate to continue voice treatment, because it was clear that numerous other problems
were present and particularly in view of the lack of follow-up on our referral for psychiatric
consultation.
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It is often necessary to move slowly when referral for counseling or psychiatric examination
is being considered. A sense of trust must be built between the clinician and the patient. The
clinician must be sufficiently attuned to the patient’s needs to be able to approach the referral in
the manner that will be most likely to be accepted. Referrals made too abruptly may be totally
rejected by the patient, who may also reject the person making the referral. When that occurs,
the patient may be lost to follow-up or treatment of any kind for some period of time. This is
what we were hoping to avoid in R. W.’s case. Unfortunately, even our best efforts sometimes
do not bring about the desired result.
It is vitally important to consider all possible etiologies of a presenting problem before
adopting the diagnosis of psychogenic voice disorder. There are a number of neurological dis-
ease processes whose early symptoms may be very similar to those presented by patients with
emotionally based problems. Furthermore, the presenting symptoms and signs of psychogenic
dysphonia sometimes may be similar to those of spasmodic dysphonia or musculoskeletal ten-
sion/hyperfunctional dysphonia. These patients present with minimal visible laryngeal changes,
if any, and with symptoms that may be mystifying and histories that may be confounding.

Neurological

Case Study
J. R., a 37-year-old woman with intermittent dysphonia, had been examined and treated by
several otolaryngologists over a period of several months with no change in her vocal status.
She was then referred for a trial of voice therapy. J. R. reported a rather troubled social history
involving a very difficult recent divorce preceded by a number of years in an abusive marriage
during which she had suffered attempted strangulation and blows to the neck. She and her
7-year-old son were now living with a friend as she was trying to put her life in order. Her voice
symptoms began during the course of the divorce process. She described a “gravelly” quality
that came on gradually with any extended period of talking but that cleared when she was able
to rest and be silent for a while. She denied any other physical symptoms.

The history thus far seemed to suggest a classic voice disorder of psychological etiology.
During the initial evaluation, however, the clinician was impressed with this patient’s attitude,
forthrightness, and overall affect. Furthermore, we noted the gradual worsening of voice as the
evaluation progressed, which J. R. attributed in part to having engaged in much conversation
during a lengthy car trip from her home to our office. Trials of diagnostic therapy procedures
were totally ineffective in eliciting improved voice quality. J. R. was subsequently referred for
neurological examination and a diagnosis of myasthenia gravis was made.
Referral for neurological examination is usually well accepted by patients. It should be
considered when laryngeal findings are either negative or suggestive of disordered coordination
of laryngeal function, when the voice symptoms are neither consistent with nor explained by the
history, when changes in vocal output cannot be altered by behavioral approaches, and whenever
there is a family history of neurological problems. Similarly, patients usually respond well when
referred for further medical examinations, as might be indicated when gastroesophageal reflux
is suspected as a key factor in the voice problem.
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CHAPTER 8 I The Voice History, Examination, and Testing 271

Imaging
The past decade has seen major growth and development of increasingly sophisticated imaging
technology: computed axial tomography (CT scan), ultrasound, magnetic resonance imaging
(MRI), and positive emission tomography (PET), to name a few. Although these techniques are
being widely used to determine the location and extent of disease, data relevant to phonatory
behavior are only beginning to appear. Baer and others (Baer, Gore, Boyce, & Nye, 1987;
Baer, Gore, Gracco, & Nye, 1991; Lufkin & Hanafee, 1985; Stark, Moss, Gamsu, Clark, &
Gooding, 1984) have applied the technique of MRI to the study of normal neck anatomy and
the physiology of the vocal tract during speech acts. Leboldus and his colleagues (Leboldus,
Savoury, Carr, & Nicholson, 1986) showed how MRI imaging could be applied to the diagnosis
and treatment of ENT problems. Others (Shaefer, Freeman, Finitzo, Close, & Cannito, 1985;
Swenson et al., 1992) have used MRI to study brain dysfunction in patients with spasmodic
dysphonia. There is considerable promise of MRI and CAT images to the study of normal and
disordered speech and voice. At this time the primary use of these techniques for the study
of laryngeal function is in the realm of research. Clinical use is more limited, due in part to
limitations of the equipment, limited equipment availability, and the cost of the procedure.

Summary
The voice history is a critical part of the diagnostic process not only for the information obtained
but also because of the relationship that is established between the clinician and the patient
during the information gathering. The first section of this chapter was devoted to a discussion
of the skill involved in the interview process. The content of the interview was presented in
some detail and included the following sections: the problem and its effects, the developmental
history of the problem, its onset and duration, the variable or consistent nature of the problem
and associated symptoms, the patient’s health history, and vocational, social, and recreational
histories.
The array of techniques used in the examination and testing of the voice have been de-
scribed in the second and third sections of this chapter. Examination of the larynx can be
carried out through both direct and indirect methods. Technological advances have substan-
tially increased our ability to visualize not only the structure of the larynx and supraglottal
vocal tract but also the dynamic physiology of both phonatory and nonphonatory behav-
ior. The examination procedures described include indirect laryngoscopy, direct laryngoscopy,
flexible fiberoptic laryngoscopy, stroboscopy, ultra-high-speed photography, and ultrasound.
Advantages and disadvantages of each are discussed.
Laboratory testing procedures provide documentable and measurable evidence of vocal
function. These techniques sometimes provide indirect evidence about the functional status
of the larynx. They include acoustic measures of fundamental frequency and its variability,
functional limits of the voice relative to frequency and intensity, periodicity and stability of the
voice as evidenced by measures of perturbation, and visual evidence of the acoustic compo-
nents of the voice as displayed in a spectrogram or an acoustic spectrum. Physiological studies
provide further evidence and information about the larynx and the voice. These include elec-
troglottography, photoglottography, inverse filtering of airflow, and electromyography. Testing
of respiratory function is another aspect of physiological function that can add to the total data
pool in selected cases.
We have also included various forms of noninstrumental evaluation of the voice, usually
carried out by the speech-language pathologist, but useful to all who examine and work with
the voice-disordered patient. These noninstrumental methods include critical listening, ob-
servation, and description. Formalization of the kinds of observations that should be made,
both auditory and visual, will help to focus the examiner’s careful attention to the variety of
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272 Understanding Voice Problems

clues that can be obtained about vocal function through this approach. The clinical trial in-
volved in a diagnostic therapy approach allows the examiner to test hypotheses and extend the
observations.
Objective measurements that can be made without the benefit of any equipment more
sophisticated than a stopwatch are also discussed. Although fairly simple to obtain, these
measurements can be extremely useful in establishing baseline measures of vocal function and
subsequently to chart progress or assess the results of treatment. Within this section we have also
discussed the need for suitable audio recordings and the types of equipment that are appropriate
to address this need.
The final section of this chapter deals briefly with the need for referral for additional testing.
Such testing may include psychiatric or psychological consultation, neurological examination,
medical assessment for associated problems, and special imaging techniques.

SUGGESTED READINGS
Bernstein, L., & Bernstein, R. S. (1985). Interviewing, a guide for health professionals (4th ed.). Norwalk, CT: Appleton-
Century-Crofts.
Hersen, M., & Turner, S. M. (1985). Diagnostic interviewing. New York: Plenum Press.
Levinson, D. (1987). A guide to the clinical interview. Philadelphia: WB Saunders.
Maple, F. F. (1985). Dynamic interviewing, an introduction to counseling. Beverly Hills, CA: Sage Publications.
Kempster, G. B., Gerratt, B. R., Verdolini, A. K., Barkmeier-Kramer, J., & Hillman, R. E. (2009). Consensus auditory-
perceptual evaluation of voice: Development of a standardized protocol. American Journal of Speech-Language Pathol-
ogy, 18, 124–132.
Kendall K. A., & Leonard, R. (2010). Indirect laryngoscopy to high-speed digital imaging. New York: Thieme Medical
Publishers.
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CHAPTER

9
Surgical and Medical Management
of Voice Disorders
Keywords
surgery, endoscope, microphonosurgery, laryngoscope, instrumentation, microscopes,
laser, reflux, nodules, polyps, Reinke’s edema, mucoceles, pseudocysts, intracordal
cyst, sulcus vocalis, granuloma, dysplasia, papilloma, carcinoma, medialization,
injection, implantation, thyroplasty, adduction, lateralization, arytenoidectomy,
cordotomy, anterior commissure, anastomosis, spasmodic dysphonia, webs, stenosis,
infection, systemic disease, allergy, tremor, Parkinson’s disease, Myasthenia gravis

There are three general approaches to the management of voice problems; none of which necessarily
excludes the others. These approaches are (a) surgical, (b) medical, and (c) behavioral.
The first two approaches will be discussed in this chapter; the behavioral approach will be discussed in
Chapter 10. Although these approaches are being presented separately, often the ideal treatment requires
the use of combined treatment modalities. For example, the patient who has sustained traumatic laryngeal
damage in an automobile accident may first be a surgical candidate. However, after surgery and healing,
this patient may well benefit from vocal rehabilitation to reestablish the best possible voice production.
Many patients who present with vocal fold lesions also have reflux disease and poor vocal hygiene. All
three modalities of treatment are required: surgically remove the lesion, medically control the reflux, and
behaviorally correct vocal misuse.
Surgery is considered the more radical treatment approach because of the need to cut into tissues
to remove body parts or abnormal growths, or to physically alter or augment the shape or position of
structures. A review of surgical techniques that are being used in the management of laryngeal problems
with a phonatory component is presented in the first section of the chapter. The medical approach to
the treatment of voice disorders refers to the techniques that are not as invasive or do not involve surgical
ablation, reconstruction, or alteration; these will be discussed in the second section.

Surgical Management
Introduction
Surgical management of the larynx is a broad topic by virtue of the multitude of pathologies that can
affect the larynx. The main premise for whatever procedure is performed is that the function of the larynx
be preserved or improved. For example, in a patient who has a poor voice due to a unilateral polyp,
surgical removal should yield an improvement in the voice and possibly respiratory airway if the polyp
is very large. A patient with a unilateral immobile vocal fold who undergoes a medialization procedure
should have improved voice and be able to swallow without aspiration.
Over the past 40 years, there have been tremendous changes and advances in all aspects of vocal
fold surgery. Indeed, in the past it was not unlikely for vocal fold lesions to be “plucked” or “stripped”

273
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using cupped forceps either by direct or indirect non-magnified laryngoscopy. Scarring of the
vocal fold with subsequent dysphonia was not an uncommon result. Hirano (1981) helped usher
in the modern age of vocal fold surgery by detailing the structure of the vocal folds in his “cover-
body” theory. The concept that a delicate mucosa moves on a cushion of ground substance
over a rigid ligament and muscle hundreds of times per second leads to the appreciation of the
needed precision required in preserving this vibrating tissue.
Advances have been made in binocular microscopes, laryngoscopes, micro-
instrumentation, surgical techniques, and lasers. Complementing these surgical improvements,
there have also been advances in complementary medical and behavioral care of the larynx.
Surgical treatment is often combined with medical and behavioral treatments to yield the
best possible functional outcome for a patient. Certainly any laryngologist will attest to the
importance of perioperative voice care to surgical outcome. Such care should include train-
ing in proper vocal hygiene and medical control of reflux disease, asthma, or other causes of
inflammation.
The goals of surgical management are to conserve, reconstruct, and improve laryngeal
functions—phonation, swallowing, and respiration.
There are four major groups of surgery:
1. Endoscopic removal of pathological tissue (microphonosurgery)
2. Surgical correction of the position, shape, and/or tension of the vocal fold(s) by endo-
scopic or external approach
3. Surgery directed at neuromuscular function of the vocal folds
4. Surgical repair or reconstruction for partial loss and/or deformity of the larynx. These
abnormalities can arise from blunt or penetrating trauma, congenital abnormalities,
acute or chronic diseases, or exposures.

History
The earliest laryngeal examinations and procedures done in the mid 1800s were performed
indirectly by way of mirror visualization. The first direct laryngeal examinations were carried out
in 1852 and 1895. Kirstein laid out the advantages to this approach (Zeitels, 1999). During
the next half century, advances included the introduction of suspension laryngoscopy; the
Jackson laryngoscope with a sliding, removable blade; and the use of the microscope, although
still with monocular vision. Surgical procedures consisted of removal of lesions and vocal fold
injections for paralyzed vocal folds. In the 1960s, binocular visualization was possible due
to wider laryngoscopes commercially produced by Pillings and Storz. von Leden (1991) first
published the term “phonosurgery,” indicating the desire to have vocal fold surgery address a
major function of the larynx, that is, phonation.
Over the next two decades, better understanding of laryngeal anatomy and physiology led
to a greater appreciation of vocal fold function and the need for newer techniques to address
this expanded knowledge base. At the same time, technological advances in illumination led to
better visualization and increased precision of surgery. The operative microscope was combined
with the CO2 laser (Jako, 1972), resulting in a potent new tool. Consistent improvement in
voice results was continually sought.
In the 1990s, laryngology blossomed as a field with advances in all aspects from the basic
science of histology, wound healing, and pathophysiology to evaluation using stroboscopy
to surgical refinements. Endoscopic visualization, development of fine micro-instrument sets,
precision laser micromanipulators, and newer materials for implantation all occurred. These
advances have clearly resulted in improved surgical techniques and thereby also improved
surgical outcomes. Quality of life scales and outcome studies have validated that voice disorders
have a negative impact on an individual’s functional, emotional, physical, and vocational life,
all of which are significantly improved by intervention (Murry & Rosen, 2000).
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CHAPTER 9 I Surgical and Medical Management of Voice Disorders 275

Removal of Pathological Tissue: Microphonosurgery

Principles
The basis for operative technique stems from an understanding of the gross and fine structure of
the larynx. Hirano (1981) first described the “cover-body” anatomy of the vocal fold, and this
led to modeling of how this structure oscillates. Gray and his colleagues (Chan, Gray, & Titze,
2001; Gray, Titze, Alipour, & Hammond, 1999a, 1999b; Gray, Titze, Chan, & Hammond,
1999) are responsible for further delineating many of the vocal fold components (elastin,
collagens, laminin, hyaluronic acid), their location within the lamina, as well as their properties
within the layered structure of the vocal fold. The complex detail of the epithelial attachment
to the superficial lamina was described, as well as the effects of aging, vocal and surgical trauma,
and pathology. This work has impacted on the practice of surgical excision and on the goals
of research, specifically tissue regeneration. Current research is focused on understanding vocal
fold wound healing and ways to enhance or even regenerate the microenvironment of the
vibrating lamina. Perhaps someday a material can be placed in the vocal fold after the surgery
to allow for quick healing, minimal scar, and restoration of a vibrating surface.

Instrumentation
To perform precise microlaryngeal surgery, state-of-the-art instrumentation is needed. Because
of its anatomic location and differences in individual anatomic features, direct imaging of
the larynx has historically presented a challenge. Several generations of laryngoscopes have
been designed, each with the goal of giving the best view of the larynx. Anatomic factors that
influence which particular scope may fit best include neck thickness, neck mobility, tongue
size, mandibular arch dimensions, dentition, and mandibular mobility. Benefits of the later
generation of laryngoscopes are the ability to adjust the dimensions of the scope in situ, the
incorporation of suction channels, fiberoptic light carriers, and placement of these channels
in such a manner as to reduce interference with passage of instruments through the scope.
An example of a newer laryngoscope features a triangular end to conform to the shape of the
glottic introitus. This Zeitels glottiscope features a lateral recessed area near the mouth for
easier instrument entry (Fig. 9.1). It further provides the ability to slide out the floor of the
scope, if intubation through the scope is needed, and permits interchangeable blades. It also
can be used with a suspension gallows attached to the operative table, giving true suspension
of the larynx so that the surgeon can use both hands for instruments rather than holding the
laryngoscope (Fig. 9.2). Most laryngoscopes are retained on a Mayo stand or the patient’s chest
by a torsion–fulcrum method (Figs. 9.3 and 9.4).
Microscopes have evolved with fingertip adjustable focusing and zoom magnification in
addition to digital video outputs for archiving and enhanced display (Fig. 9.5).
Instrument sets have also been refined over the past decade (Fig. 9.6). The Ossoff-Pilling
microlaryngeal set features a variety of picks, spatulas, scissors, and forceps. Other compa-
nies including Medtronic (Xomed/Microfrance) and Storz, in cooperation with other leading
phonosurgeons such as Sataloff, Bouchayer, and Kleinsasser, have designed instrument sets.
Instruments that can be attached to a cautery unit have also aided in pushing the limits of
endoscopic resection of larger tumors. Powered tissue shavers have a suction channel that draws
the soft tissue into the tip of the rotating instrument and slices it off (Fig. 9.7). The main
role for shavers is currently for papilloma removal or debulking tissue. Ongoing refinements in
increasingly fine scissors, tissue-grasping forceps, and dissecting picks continue to be seen. To
dissect out or excise relatively small lesions such as an intracordal cyst or a polyp, with minimal
mucosal disruption, the array of fine instruments is essential. Accessory instruments such as
disposable blades and injectors are also now available.
Lasers have been used for over 40 years to remove laryngeal tissue. These are machines
that generate collimated, monochromatic emission of energy directed at a target. Each type of
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276 Understanding Voice Problems

FIGURE 9.1. The Zeitels glottis-

cope. Different size blades can easily
be exchanged depending on the pa-
tient’s anatomy.
B

laser generates energy of a specific wavelength that has a different effect on tissue. The CO2
laser was the first and still often used laser for laryngeal surgery because its energy can be passed
in a straight beam to the larynx. The wavelength of energy is absorbed by the water-rich vocal
folds and can be used to incise, vaporize, and coagulate tissue.
Newer lasers have been developed, which have different characteristics from the CO2 laser.
Potassium titanyl phosphate (KTP) and pulsed dye laser (PDL) lasers emit energy absorbed
by the “red wavelength” and thus are particularly useful for ablating vascular lesions or in

FIGURE 9.2. The glottiscope is sus-

pended on a gallows attached to the bed.
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CHAPTER 9 I Surgical and Medical Management of Voice Disorders 277

FIGURE 9.3. Laryngoscope placement for surgery. (From Kleinsasser, O. [1990]. Microlaryngoscopy and
endolaryngeal microsurgery [3rd ed]. Philadelphia: Hanley & Belfus, Inc.)

facilitating tumor removal in the larynx. These also differ in their delivery. Their laser energy
exits through the tip of the long fiber that can be placed in proximity to the lesion (Fig. 9.8).
Special safety precautions including eye protection and special airway tubes are needed during
laser use for both the personnel in the operating room (OR) and the patient. The fiber can be
passed through a flexible laryngoscope and used with the patient awake in the office setting.
The primary concern with laser use has been that thermal injury may extend beyond
the target area and damage adjacent tissue. Full knowledge of the concept of power density

FIGURE 9.4. Patient with the laryngo-

scope perched on a stand; another com-
mon way to “suspend” a patient so that the
surgeon has both hands free for surgery.
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278 Understanding Voice Problems

FIGURE 9.5. The Zeiss microscope has

powered focus and zoom buttons on the
handpiece and a center micromanipulator
for aiming the CO2 laser if attached.

is mandatory for a surgeon using a laser. Some advocate using iced saline on the vocal folds
prior to using the laser. Another concern has been the belief by some that healing time is
longer following laser surgery than “cold knife” techniques. Benninger (2000) and Hormann,
Baker-Schreyer, Keilmann, and Biermann (1999) reported studies in which results of laser
versus “cold-knife” excisions were compared. There were no significant differences between the
outcomes. Abitbol (2000) has demonstrated that a laser, in the proper hands, is equivalent to
“cold-knife” excision.

FIGURE 9.6. A typical phonosurgery instru-

ment set.
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CHAPTER 9 I Surgical and Medical Management of Voice Disorders 279

FIGURE 9.7. The “shaver” or skimmer

blade for removal of exophytic lesions
(Medtronic Xomed, Jacksonville, FL).

Surgical Course of Treatment

Once medical and behavioral therapies have been exhausted and benign appearing lesions
remain and are causing the patient bothersome dysphonia, surgery can be offered. Sataloff offers
a nice general algorithm stressing the importance of preoperative care and conservative approach
for offering surgery. It is important to note that although laryngeal cancer or malignancy is
a small percentage of overall laryngeal pathology, early diagnosis by biopsy correlates with
survival. If malignancy is suspected given the clinical picture and laryngeal examination, the
recommendation for biopsy supersedes all others. Most lesions are removed under anesthesia in
the OR as an outpatient surgery. Occasionally, these can be removed or biopsied in the office,
whereas other lesions such as granulomas and papilloma can be treated by injection. What
follows is focused on surgical treatment in the operative setting.
Preoperative considerations include accurate diagnosis, the patient’s general health status,
the patient’s desire and need for improved voice, timing that takes into account postoperative
needs for proper care and optimal healing, and informed consent. A recommendation for surgery
comes only after thorough examination, consideration being given to appropriate conservative
approaches, and the diagnosis being as definitively confirmed as possible.
Once a decision is made to proceed with surgery, a time is scheduled. Most phonomicro-
surgeries are performed in an outpatient setting. After patients are anesthetized, they are often

FIGURE 9.8. A KTP laser fiber can be

directed precisely to ablate tissue or “seal”
blood vessels.
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FIGURE 9.9. The patient is intubated

and in suspension for phonosurgery. The
surgeon examines and palpates the vocal
folds. A monitor allows others to simulta-
neously watch the procedure.

intubated with a small endotracheal tube to provide ventilation. Occasionally, other techniques
of ventilation are employed, but that is beyond the scope of this chapter. After placing the
larynx in suspension, the vocal folds are inspected and probed for any other abnormalities that
are not appreciated by stroboscopy (Fig. 9.9). Concurrent subglottic scars, infra-lesion or lateral
small sulci, epithelial bridges, or micro-webs are often found (Figs. 9.10 and 9.11). Infusion of

FIGURE 9.10. A micro-web found at the

anterior commissure.
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FIGURE 9.11. In this patient, palpation of

the vocal folds uncovered bilateral mucosal
bridges.

saline is very useful to inflate the epithelium from the ligament. This not only gives information
about the depth of adherence of a lesion, such as a sulcus, but also provides additional buffer
margin for dissection (Fig. 9.12). With laser use, this additional volume can serve to dissipate
the laser-generated heat. Care must be taken to visualize exactly where the incisions are to
be made prior to any distortion from injection. Intraoperative goals include minimal normal
tissue disruption, maximum preservation of the lamina layered structure, and promotion of
rapid healing. These goals can be met by utilizing state-of-the-art knowledge and techniques
of laryngeal visualization, incision placement, dissection, and wound healing.
Creating a straight edge and preservation of the subepithelial stroma are needed to prevent
tethering of the new epithelium to the fibrous ligament and allow for mucosal wave motion.
Postoperative care is extremely vital to the final surgical outcome. Medications such as an-
tireflux medication (proton pump inhibitor), mucolytics, cough suppressants, and infrequently,
antibiotics and steroids may be prescribed for a short postoperative period according to the
surgeon’s practice. Although there is general agreement concerning the need for some period
of voice rest, the duration is still debated. Some advocate no need for any period of voice rest,
others advocate fairly lengthy periods of silence, but the majority of laryngologists recommends
3 to 5 days. Our approach is individualized and adapted to the patient. It is based on the exten-
siveness of the surgery, knowledge of the patient’s typical presurgical voice use patterns, and the
patient’s ability to comply with instructions. Most typically, patients are instructed to maintain
complete voice rest for a period of 4 days. Furthermore, all patients are instructed to avoid
laughing, crying, coughing, and throat clearing. We see the patient for repeat stroboscopy 4 to
5 days postoperatively prior to allowing voice use. Depending on our findings upon visualization
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FIGURE 9.12. Prior to injection, a sulcus

was noted on the right vocal fold. Injec-
tion of saline into the superficial lamina
elevated the surrounding epithelium and
made the extent of the tethered surface
more obvious.

of the surgical site, we determine how much talking the patient should be instructed to do.
The patient is instructed in a gradual return to normal voice use, using a modified vocal rest
approach. Care after surgery for professional voice users is a particularly important and difficult
time. Once again, very specific and firm instructions have to be given but must be adapted
to the individual. Cooperation between the otolaryngologist and the voice clinician is vital in
both the preoperative and postoperative care of the surgical patient. Adherence by the patient
to the pre- and postoperative instructions should result in a voice restored to normal function.
That is the ultimate goal.

Vocal Fold Nodules (Midmembranous Lesions)

Vocal nodules are not typically treated by surgery. The initial treatment of choice is voice
therapy. In fact, if the nodular-appearing lesions do not regress with behavioral care, the clinical
diagnosis should be reconsidered. Almost all nodules in children disappear spontaneously by
the end of adolescence. Surgery is indicated only in extreme cases in which the effects of the
voice abnormality are serious and voice therapy has not been effective. In cases of long-standing
poor vocal hygiene, there may be a more mature fibrous component of the nodule and surgical
removal may be needed, but again only when voice therapy has not been effective.
In adherence to the concepts previously mentioned, when nodules are surgically removed,
only the excessive tissue should be ablated. The postsurgical result should be a vocal fold with
a minimal surgical wound. Forceps are used to grasp just the nodule, and then the vocal fold is
trimmed using scissors (Figs. 9.13 and 9.14). The wound will be small with superficial lamina
exposed, but new epithelium will grow and cover this defect. If deeper structures are exposed or
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A B C

D E

FIGURE 9.13. Surgery for vocal fold nodules.

excessive tissue removed, healing will be slower and scar tissue may develop that will interfere
with normal vocal fold vibration.

Vocal Fold Polyps/Reinke’s Edema

Small unilateral polyps usually do not respond to medical or behavioral treatments and require
surgical removal. Again, only excessive mass should be removed; care should be taken not to
excise healthy tissue. Small polyps are removed by incision, dissection, and trimming with
scissors. The result should be a normal contour of the vocal fold (Figs. 9.15 and 9.16) with
minimal epithelial defect.
In the case of polypoid degeneration or Reinke’s edema, after an incision is made in the
upper margin of the vocal fold edge, the mucosa is retracted medially to expose the myxoid
stroma. Gentle teasing of this jelly-like material to remove excess is performed. Suctioning of
the material may lead to excessive loss of lamina volume and subsequent scarring or tethering to
the ligament. The mucosal edge is redraped onto the superior surface, and the excess mucosa is
conservatively trimmed. The edges of mucosa may be left to rest together, or be “spot welded”
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FIGURE 9.14. This patient has bilateral nodules. The right one was gently grasped and trimmed off,
leaving a straight edge with minimal tissue loss.

with laser or fibrin glue, or sutured to try to get better primary closure and quicker healing (Woo,
Casper, Griffin, Colton, & Brewer, 1995). Steroids may be infiltrated into the wound (Fig. 9.17).
Removal of polyps may be done with laser, but the power density should be kept at a
minimum. Excessive energy or an unfocused laser can lead to thermal injury to the lamina
propria and vocal scarring. Abitbol (2000) advocates using iced-saline gauze on the vocal folds
to minimize these heat effects (Fig. 9.18). Hemorrhagic polyps are more vascular and may be
removed with the use of laser or by “cold dissection” (Fig. 9.19).
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D E

FIGURE 9.15. Surgery for vocal fold polyps.

Mucoceles and Pseudocysts

These are exophytic fluid-filled lesions, typically small in size and found along the medial margin
of the vocal fold. Removal is the treatment of choice. The technique is similar to removal of
polyps with maintenance of an adequate amount of lamina and mucosal cover. These are not
true cysts, and therefore minimal tissue removal is needed (Fig. 9.20).

Intracordal Cysts
A true cyst within the vocal fold requires complete surgical removal. In dissecting the cyst wall,
care must be taken to observe and remove any tracts that may connect the cyst to the surface
epithelium. The incision, in general, should be as small as possible to allow cyst removal. Lateral
incisions preserve the vibrating edge of the vocal fold as the dissection is within the lamina. The
mucosal incision may also be made over the cyst if it is located medially. The cyst is carefully
elevated from the underlying structures and removed. The mucosal edges are re-opposed and
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FIGURE 9.16. A right vocal fold polyp

was removed, preserving some of the in-
ferior epithelium, thus leaving no gap along
the edge.

may be left to heal or be sutured. Injection of steroid is recommended by some in an attempt

to reduce scar formation (Figs. 9.21 and 9.22).

Sulcus Vocalis
Vocal fold sulcus is a depression along the margin of the vocal fold, which may result in poor
vibratory capability (decreased mucosal wave or glottic closure). This depression can vary on
depth and can extend to the vocal ligament. Preoperative stroboscopic examination can be
suggestive of the degree of the sulcus, but intraoperative examination allows for definitive
diagnosis. If a shallow sulcus is found, medialization of the folds can be performed. This
may allow for better glottic closure and voice improvement. Surgical repair of a deeper sulcus
presents a difficult challenge for the surgeon. The depressed mucosa must be dissected to “free
it” from the deeper attachments, which then exposes the deep layer of the lamina propria or
vocal ligament. Several surgical techniques, described later, have been proposed, and each has
its proponents, but none are certain of success. Scarring and re-adherence of mucosal tissue to
the underlying layers are both possible sequelae of surgery, resulting in stiffness of the vocal
fold and dysphonia. In some instances, there may be a need for a second procedure.
Sulcusectomy (Hirano, 1975) involves making a mucosal incision along the upper edge of
the sulcus. The stiff tissue around the sulcus is elevated from the underlying normal tissue and
removed (Fig. 9.23). The mucosal edges are then approximated and held in place by means of
fibrin glue or suturing (Fig. 9.24).
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FIGURE 9.17. In this series of pictures of a patient with polypoid chorditis, the right vocal fold was
grasped, incised along the margin, debulked of myxoid material, trimmed of excess tissue, and then closed
with sutures to prevent secondary healing or excessive scar.

Pontes (1993) described a novel approach to this difficult problem. The “mucosal slicing
technique” is based on the idea of scar rearrangement. The tissue involving the sulcus is elevated
from the deeper vocal ligament and then vertically sliced at several locations and for differing
lengths. The wound is then left to heal secondarily. The postoperative rehabilitation may take
months and involves aggressive vocal therapy.
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FIGURE 9.18. This patient had bilateral

hemorrhagic polyps. The CO2 laser is aimed
using a red laser beam. When activated by
a pedal, the site of the red spot vaporizes.
Here the lesion was being removed in the
posterior to anterior direction.

FIGURE 9.19. This patient appeared to

have a unilateral left hemorrhagic polyp.
After incision, an unusually well-defined
vascular lesion was dissected free and re-
moved without a laser.

288
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FIGURE 9.20. In removing this pseudo-

cyst, the epithelium was trimmed and the
lamina inspected. No cyst wall is found.

Granuloma
These lesions most often arise at the vocal process and can be bilateral. The etiologies include
gastroesophageal reflux disease, intubation, and poor vocal hygiene. Unless causing airway
obstruction, granuloma should first be treated aggressively with vocal hygiene programs and
antireflux therapy over several months. Proton-pump inhibitor use is very effective in yielding
the resolution of a majority of granuloma (Fig. 9.25). For cases that recur or do not respond to
medical and behavioral management, a steroid or BOTOX injection (to weaken the adductor
force at the level of the vocal process) can be offered. Granuloma can be vaporized with lasers
that use a fiber in the office under local anesthesia.
When these modalities do not prove to be effective, granuloma can be surgically excised
under general anesthesia. The granuloma is removed with the use of scissors and forceps, leaving
the perichondrium covered—a “cold” technique. Steroid can be injected into this base. Several
types of lasers have been used as well, but there is a risk of thermal injury to the perichondrium,
which may lead to a recurring lesion.

Epithelial Hyperplasia and Dysplasia

Thickened epithelium can occur due to repeated physical, chemical, or even thermal trauma.
Chronic vocal misuse, smoking, and chronic inhalant chemical exposure can all cause epithe-
lial pathology. Only microscopic examination by a pathologist can determine whether diseased
tissue is benign thickening, pre-cancerous, or cancer. The indications for surgical removal of
diseased tissue are to reestablish a vibrating, straight vocal fold margin and provide a specimen
to the pathologist to see if any additional treatment is needed. Removal of the causative agents
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A B C

D E

FIGURE 9.21. Surgery for epidermoid cyst of the vocal fold.

may occasionally result in a reduction or even disappearance of hyperplastic and dysplastic

epithelium. To provide a clean, complete specimen, infusion followed by “cold” removal tech-
nique is ideal. Inclusion of the basement membrane in the specimen is essential for correct
diagnosis. CO2 laser, PDL, or KTP laser can be used for “planing” down exophytic lesions, but
again, care must be taken to not cause thermal injury (Figs. 9.26 and 9.27).

Laryngeal Papilloma
The most frequently occurring benign neoplasm of the larynx is papilloma. Papillomas are
caused by the Human Papilloma Virus (HPV). There are many “types” of virus. Some have a
higher risk of transformation of benign growths becoming cancerous growths over time. Most
papilloma in the larynx are from “low-risk” HPV. Both adults and children can be affected
and require numerous surgical procedures due to the high recurrence rate. The juvenile form
is more aggressive in growth (until adolescence) and more often affects the airway due to the
dimensions of the pediatric airway. Rarely, the papilloma can extend below the larynx to the
trachea where obstruction can occur and surgical excision is more complex.
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FIGURE 9.22. A left cysts was dissected

and removed. The edges of the incision
were reapproximated.

FIGURE 9.23. Histological picture of sulcus vocalis.

291
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FIGURE 9.24. A right vocal fold sulcus was found and then excised. After advancing the edges, a suture was placed
to close the defect.

Surgery consists of removal of these lesions. The CO2 laser vaporization of papilloma
was widely accepted and is still often used. “Cold-knife” removal is also possible and has been
aided by use of the infiltration technique noted earlier and advancements in the design of
surgical instruments. Proponents of this technique cite its benefits as: more control of the
depth of injury, quicker postoperative healing, and less time expense. The recent introduction
of laryngeal “shavers” offers a “cold” technique with more rapid removal of lesions. An inner
rotating blade trims the tissue that is drawn into the tip of the outer sheath and suctioned up
the blade and into the tubing (Fig. 9.28).
Scarring of the vocal folds is a potential sequelae of the multiple surgical excisions that are
often required. Anterior true vocal fold webs and false–true vocal fold webs may also occur and
are difficult to treat (Fig. 9.29). Prevention of these complications is paramount. Staging the
removal of extensive and bilateral papilloma to avoid webbing is encouraged.
As with any disease that is difficult to treat, nonsurgical therapies have also been tried but
have not been proven universally effective including indole-3-carbinol, ribavirin, alfa-interferon,
and photodynamic therapies. Injection of Cidofovir into the papilloma may significantly sup-
press its growth and reduce the frequency of surgeries. The use of Cidofovir is somewhat
controversial though, as it has the potential of transforming the viral lesions into a malignancy.
Studies with human clinical use over 10 years, however, have shown no increased rate of cancer
from papilloma. More recent research supports possible mechanisms that implicate cidofovir
to malignant transformation.

FIGURE 9.25. A left vocal process granuloma resolved after aggressive medical and behavioral treatment. If there
had not been improvement after weeks of conservative care, surgical excision and steroid injection would have been
offered.
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A B C

D E

FIGURE 9.26. Surgery for epithelial hyperplasia and dysplasia.

FIGURE 9.27. The left vocal fold lesion was removed, sparing the vocal ligament.
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FIGURE 9.28. Papillomas were removed using a “shaver.” A laser could also be used. Lesions often recur regardless
of the method of removal.

Other lasers (KTP and PDL) are used to remove papilloma, sometimes in the office setting.
The most recent trials involve using KTP laser to remove papilloma and then injection with
Avastin, a chemotherapy agent that blocks blood vessel regrowth, a hallmark characteristic of
papilloma (Maturo, 2010; Zeitels, 2009).

Complex Lesions
Not all lesions found in the larynx fall neatly into one category and thus require some creativity
and planning on the part of the surgeon. Polyps are often found with a sulcus on the same vocal
fold. Tissue from the polyp can be used to resurface the defect from an elevated sulcus. Anterior
webs can be found in patients with papillomas who have previously had surgery. Ectasias or
vascular lesions are often found with polyps and can be treated at the same time (Fig. 9.30).

Glottal Carcinoma
Laryngeal cancer occurs in 12,000 Americans per year and is much less common than benign
vocal fold lesions. In general, the cancer invades normal tissue and can spread to neck lymph
nodes and distant sites in the body such as the lung, liver, and bone. Details of tumor staging,
survival rates, and specific pathologies of glottic carcinoma are beyond the scope of this chapter.

FIGURE 9.29. This patient previously

had multiple surgeries before presenting
with an elevated pitch and rough voice due
to papilloma and an anterior web.
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FIGURE 9.30. The patient had a hemor-

rhagic polyp and prominent blood vessel in
the left vocal fold. KTP laser ablated the
vessel, the lesion was excised “cold,” and
the vocal fold redraped.

Risk factors for developing laryngeal cancer include smoking, alcohol abuse, chronic irritation
from reflux, genetics, and HPV.
In general, smaller cancers of the true vocal folds can be surgically excised with low
morbidity and preservation of good function, whereas larger cancers are more often treated
with radiation and chemotherapy. If these fail, laryngectomy is performed. Cancer tissue has
to be completely excised with “negative” margins determined by a pathologist. The location
and the extent of glottal carcinoma dictate what degree of surgery is needed.
Cancers confined to the membranous vocal fold may be completely removed with the aid
of laser for cutting and hemostasis (Figs. 9.31 and 9.32). Excellent exposure is needed, and
careful mapping of the extent of disease particularly below the vocal fold, anteriorly, and in the
ventricle is also required. Use of rigid angled telescopes in addition to a microscope provides this
capability. Infusion technique also provides information about the depth of the lesion and vocal
ligament involvement. More extensive tumors may be removed endoscopically, depending on
surgeon’s skill, experience, and ability to expose the region.
Once the excision has begun, maintaining orientation of the specimen is needed so that
margins can be determined. To obtain a margin around the tumor, part and sometimes all of
the thyroarytenoid (TA) muscle must be taken. In this case, cancer removal takes priority over
vocal result. With large tissue loss, incomplete closure or areas of nonvibrating tissue can result.
Additional surgeries can be offered to rehabilitate the voice, and some of these techniques will
be discussed later in this chapter.
Some glottic carcinoma can also be successfully treated with radiation therapy alone.
Voice outcomes for patients treated by surgery versus radiotherapy have been studied and are
comparable.
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A B C D

FIGURE 9.31. Surgery for early glottal carcinoma.

FIGURE 9.32. After intraoperative pathological confirmation, an early glottic cancer was excised and the surrounding
tissue lased with KTP energy. The vocal ligament was exposed. Again, intraoperative pathology was needed to confirm
adequate resection of all cancerous tissue.
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Surgeries to Modify Vocal Fold Position, Shape, and/or Tension

Vocal Fold Medialization
Medialization is desired when a glottic gap exists and laryngeal function is compromised. One
or both vocal folds may be medialized, depending on the need. Indications include unilateral
vocal fold immobility, vocal fold atrophy, or bowing due to aging, scarring, or neurological
disease. The two main classes of techniques for membranous vocal fold medialization are
(a) injection of material into the vocal fold and (b) implantation of material into the larynx
by an external approach. Movement of the membranous fold to close the glottis often yields
improvement. Additional manipulation by arytenoid rotation and position adjustment in the
immobile arytenoid may provide even greater benefit by closing a posterior glottic gap. In
a survey by Rosen (1998), 70% of respondents only performed medialization thyroplasty.
Although it is technically more difficult to perform, arytenoid adduction may be needed to
achieve the best functional result.

Injection
Injection of material into the membranous vocal fold is often done to correct an incompetent
glottis (i.e., the inability to close the glottis) (Fig. 9.33). There are two general techniques:
transoral and transcutaneous (through the thyrohyoid membrane from above the vocal folds
or through the cricothyroid membrane from below the vocal folds). With either approach, the
goal is to place material into the middle or lateral vocal fold to “plump up” or medialize the
fold edge and thus close a glottic gap, thereby improving vocal strength and often reduce the
risk of aspiration.

FIGURE 9.33. This patient with right vo-

cal fold paralysis was aphonic. The top two
pictures were prior to medialization injec-
tion (respiration and phonation) and the
bottom two after transhyoid injection of
Restylane (respiration and phonation).
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Materials
Numerous materials have been used in the attempt to “plump up” a paralyzed or atrophic,
thinned vocal fold. Teflon, autologous fat, collagens (Zyderm, Zyplast/Collagen Corp., Palo
Alto, CA), acellular dermis (Cymetra/LifeCell, Branchburg, NJ), fascia, and more recently,
hydroxyapatite (Radisese, VoiceGel /Bioform, San Mateo, CA) and hyaluronates (Restylane/
Medicis, Juvederm/Allergan, Scottsdale, AZ) have been used for medialization. Overwhelming
evidence of long-term granuloma formation and substance migration associated with Teflon has
placed that substance in disfavor and disuse. Although a good viscosity and vibratory potential
match for vocal folds, fat survival is unpredictable even with different methods of preparation
with less traumatic harvesting, washing, and gentler delivery of the fat.
The clinical situation determines which material is most appropriate. When a patient
is thought to have a temporary vocal fold immobility following a neck surgery and “needs” a
medialization for a few months until the nerve recovers and motion is restored, materials such as
collagen, fat, Cymetra, or Voice Gel have been shown to have volume loss within 2 to 6 months
in animal studies or by clinical follow-up. When an immobility or glottic gap is thought to be
permanent, Radiesse may be preferable since it is FDA approved and may last longer. Hyaluronic
acid has been shown to last beyond a year in animal models (Hertegard, 2004).
The ideal goal is to inject a nonresorbing substance with viscosity similar to that found in
the normal vocal fold that would theoretically not only fill space but would also allow “normal”
vibratory behavior.

Techniques
“In-office” techniques include vocal fold injection by transoral injection using indirect laryngeal
exposure with a rigid telescope using a monitor or by transcutaneous injections either through
the cricothyroid space or through the thyrohyoid membrane (Amin, 2006).
When injection is done in the office by an indirect method, the mucosa of the pharynx and
larynx is anesthetized with a topical solution. The internal branches of the bilateral superior
laryngeal nerves may also be anesthetized using a nerve block. The trachea can be instilled with
lidocaine. Transoral injection is performed while the patient sits with the mouth open and the
tongue pulled forward. A curved laryngeal needle is used to administer the substance into the
fold, and its effect is monitored visually and auditorily as the injection proceeds (Fig. 9.34).
For transcutaneous injection, the nasal, pharyngeal, and laryngeal mucosa is anesthetized
with lidocaine. A fiberscope is inserted through the nose to expose the larynx. It is coupled to a
video camera, and the fiberscopic image of the larynx is viewed on a television monitor screen.
Local anesthesia is administered through the cervical skin at the thyrohyoid or cricothyroid

FIGURE 9.34. A left transoral injection

with a needle placed in the posterior third
of the vocal fold.
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FIGURE 9.35. A right transthyrohyoid injection performed while monitoring the larynx
using a fiberoptic scope.

space. The needle for intrafold injection is inserted into the larynx through these spaces, and its
location is monitored by direct visualization (thyrohyoid) or moving it back and forth medially
(cricothyroid). The effect of injection is again monitored visually and auditorily during the
procedure (Fig. 9.35).
“Operative” technique is by direct laryngoscopy under general anesthesia in the OR.
This allows for very precise placement of material but at a higher cost and potential risk
of general anesthesia. With the patient anesthetized, the larynx is exposed with the use of a
laryngoscope and can be viewed with an operating microscope. Injection is performed by means
of a specially designed injection set such as the Arnold-Bruening (Pierre, SD) syringe (useful
for fat) or through a butterfly needle held by a forcep, or by long injection needles for less
viscous materials (Fig. 9.36). With this technique, only visual appearance of the vocal fold is
possible. For some materials that are known to resorb, such as fat, over-injection is performed.

FIGURE 9.36. Transoral injection under anesthesia allows for easier placement of material in the same location as
an in-office injection but without immediate feedback of voicing. Here the left vocal fold is injected with Cymetra.
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FIGURE 9.37. Coronal (left) and axial (right) views of the final implant placement. (From
Ossoff, R. [2003]. The larynx [p. 292]. Baltimore, MD: Lippincott Williams & Wilkins.)

The target location and volume for the injected material depends on the material. Radiesse
for medialization should be injected lateral to the TA muscle. Fat, dermis, Cymetra, and
collagen for medialization should be placed into the body of the TA muscle. Collagen, fat, and
hyaluronate for scar elevation and superficial lamina reconstitution should be injected into the
deep lamina.

Implantation
The most common laryngeal framework surgery is vocal fold medialization or augmentation by
implantation. The basic principle is to insert material medial to or within the thyroid cartilage
at the level of the vocal folds, thus pushing the vocal folds medially (Fig. 9.37). This is often
referred to as type I thyroplasty, referring to Isshiki’s classification of framework procedures.

Materials
A silicone block (Silastic/Dow, Midland, MI) is commonly employed as the augmentation
material. This was popularized by Netterville (1993), who described how to individually carve
the block into the ideal dimensions for medialization. Of all the implant materials, this is the
least expensive (estimate $10) but does require skill and experience to get the best shape. Car-
tilage autograft from the upper part of the thyroid cartilage or nasal septum or rib cartilage can
also be used. Another popular choice for implant material is GORE-TEX (Gore, Newark, DE)
(McCulloch & Hoffman, 1998). Advocates state that no carving is needed and the ribbon of ma-
terial can be layered into the glottis and placement adjusted as needed to give better voice quality.
Commercially available kits without the need to carve or adjust the shape are available. The
Montgomery Thyroplasty Set (Boston Medical Products, Westborough, MA) with polymer
implant and the VoCom hydroxyapatite Implant sets (Gyrus ENT, Bartlett, TN) are each
designed for ease of placement. The Montgomery comes with a series of shim sizes for the male
and female larynges. The VoCom set also has a series of available sizes as well as locking shims to
adjust the location within the created window. These premade kits offer some advantages such
as the ability to try various implant sizes and perhaps save time; they are relatively expensive
and limit the versatility of the custom-carved or placed materials.
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FIGURE 9.38. Placement of the thyroplasty window is critical for proper placement of a shim or implant. This
implant has an unusually large posterior portion for pushing the arytenoid to get better posterior glottic closure. It
will be placed through the window seen in the thyroid cartilage.

Techniques
Thyroplasty
The surgery is performed under local anesthesia with sedation. A shoulder roll may be used to
help extend the neck. After infiltrating with local anesthetic and prepping the neck, a horizontal
skin incision is made over the lower aspect of the thyroid cartilage and extended to the side
in need of correction. The strap muscles are divided in the midline and the thyroid cartilage
exposed (Fig. 9.38). A 4 × 10 mm window is created by removal of a block of cartilage. A
drill may need to be used in cases of cartilage ossification often seen in older patients. The
upper surface of the vocal fold is normally situated at the midlevel of the anterior angle of the
thyroid cartilage. The posterior end of the membranous vocal fold is usually located at the
anteroposterior midpoint of the thyroid lamina. Therefore, the augmentation material should
be placed in the lower and anterior quadrant of the thyroid lamina. The inner perichondrium
is then exposed.
Some advocate preservation of the inner perichondrium to prevent the prosthesis from
working its way into the glottis or to prevent significant muscle atrophy or scarring. Others feel
that without incising the perichondrium, the medialization will be more limited. The size and
location of the material are adjusted by auditorily monitoring the patient’s voice during the
procedure. Simultaneous visual monitoring with the use of a fiberscope attached to a monitor
is also useful. Once the material is located in the right place, it can be sutured to the thyroid
cartilage to prevent postsurgical migration.
There can be individual variances in vocal fold location relative to the external cartilage
landmarks. If the created window in the thyroid cartilage is just superior or not level to the
desired level of the vocal fold, a carved shim can be made offset to still be oriented to the
level of the vocal fold. If needed, a larger carved posterior shim may push the arytenoid and
close a posterior gap. In such instances, the premade shims would not be able to be ideally
situated.

Mini-Thyroidotomy
Similar to the thyroplasty technique previously described, this procedure entails exposing the
thyroid cartilage and creating smaller and more medial “windows” through the anterior cartilage
at the level of the vocal fold. The vocal fold is exposed and viewed with a camera monitor. After
sharp dissection to elevate the vocal fold surface through this window, materials can now be
placed into this “pocket” to augment the medial edge of the fold (Fig. 9.39).
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FIGURE 9.39. The minithyroidotomy opening is small but allows for soft material to be placed superficially in the
vocal fold. This patient had a sulcus on the right vocal fold and after elevation of the surface, autologous fat was
placed. Excess fat is used since some will resorb within a few months.

Fixation
Arytenoid Adduction
The basic principle of this technique (Fig. 9.40) is to rotate the arytenoid cartilage by traction
of the muscular process in the direction of the adductor muscles, thus adducting the tip of the
vocal process to the midline and medializing the vocal fold (Isshiki, Tanabe, Ishizaka, & Board,

B C

FIGURE 9.40. Schematic presentation of the principle of rotation of the arytenoids

cartilage, as developed by Isshiki (1977). A: The suture pulls and rotates the arytenoid
cartilage so the vocal process is medialized. B,C: To access the arytenoid for suture
placement, a posterior window is made in the thyroid cartilage.
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1977). Arytenoid adduction is often done at the same time as placement of a medialization
implant.
The surgery is conducted under local anesthesia with sedation, and patient positioning
and exposure of the larynx are the same as the thyroplasty technique previously discussed. The
posterior edge of the thyroid lamina is exposed on the affected side by removal of the inferior
constrictor. The muscular process of the arytenoid cartilage is exposed by either dislocating the
cricothyroid joint and removing the inferior thyroid cornu or by removing a 1-cm window of
the posterior ala without disturbing the joint. A Prolene suture (Ethicon, Piscataway, NJ) is
placed through the muscular process and the attachment verified by a pull while simultaneously
watching the glottis through a flexible scope on a monitor. The desired vector of retraction is
parallel to the pull of the lateral cricoarytenoid (LCA), thus rotating the vocal process medially.
Holes are made in the anterior inferior thyroid ala just off the midline, and the sutures pass
anteriorly, through these holes. When the best voice is obtained by pulling and rotating the
vocal process, the thread is tied. As with the implant placement, the surgeon must continually
assess whether the desired glottic configuration has been achieved and be willing to make
adjustments. Additional sutures with other pull vectors may be needed.
A second method of medializing the arytenoid is by placement of a large silastic prosthesis
through the thyroplasty cartilage window into the paraglottic space (Hong, Kim, & Kim, 2001).
Theoretical potential downsides to this technique are TA muscular atrophy and interference
with nerve regeneration.

Cricoarytenoid Fixation
In addition to rotation of the arytenoids with suture fixation, direct fixation of the arytenoid
cartilage may provide more precise height changes to the vocal fold and help reestablish more
comparable tension. During the surgery, the arytenoid is approached in a similar fashion to
the adduction procedure. The cricoarytenoid joint is opened, and the arytenoid is fixed in the
optimal location.

Vocal Fold Lateralization

Vocal fold lateralization is indicated for a patient with difficulty breathing due to bilateral vocal
fold immobility from bilateral paralysis or ankylosis of the cricoarytenoid joints. Generally,
these patients have a narrow glottic gap resulting in a good voice but poor airway. Not every
patient with these conditions will require surgery, but it is indicated for patients with dyspnea.
The purpose is to improve the airway often at the expense of making the voice worse. Some
may elect for a tracheotomy tube placement to bypass the narrowing and preserve the voice.
However, when conservation of voice is part of the surgical plan, a phonosurgical approach can
often help to minimize effects on the voice.
There are several techniques to lateralize the vocal fold.

External “Open” Approach

One of the earlier techniques was the lateral fixation by external approach. This is done under
general anesthesia. A suture is placed in the arytenoid cartilage and is drawn laterally as the
glottis is inspected. Postoperative aspiration, breathy dysphonia, and infection are risks. With
the introduction of the CO2 laser arytenoidectomy, the lateral fixation technique has fallen out
of favor.

Arytenoidectomy
Ossoff et al. (1984) using a CO2 laser removed one arytenoid cartilage and the attachment to
the vocal ligament and found that the airway was improved with acceptable voice and swallow
results. The principle of arytenoidectomy is to remove one arytenoid cartilage and widen the
posterior glottis (Fig. 9.41). Initially, there is a large posterior chink due to the absence of
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FIGURE 9.41. Schematic presentation

of the principle of arytenoidectomy.

the arytenoid. With wound healing, however, this space does diminish to where the voice is
generally good and no aspiration occurs.

Cordotomy
Kashima (1991) has advocated a lateral cordotomy with the laser. In this technique, the false
vocal fold is removed and then the posterior vocal fold in incised to a depth of the ipsilateral
perichondrium. Although this sounds as though the voice result would be disabling, he reports
on airway improvement and maintenance of good voice in a majority of patients.

Modifications
Partial removal of the anterior arytenoid and vocal process, leaving the majority of the arytenoid
and vocal fold, works well but may need to be repeated if wound healing results in an inadequate
airway. Others have modified these techniques. Linder (1992) used fibrin glue to seal the
vocal mucosal flap to lateralize it. Ejnell (1993) used an endoscopically guided, transcutaneous
suture to hold the vocal fold laterally. BOTOX has also been used in the post-resection period to
prevent muscle contracture and a scarred, closed glottis. TA myectomy constitutes a lateralizing
procedure and has also been described for the treatment of SD. This can be done endoscopically
with a laser or by a thyroplasty approach.

Vocal Fold Lengthening/Increase Tension

Data regarding the long-term functional results of vocal fold tensing, lengthening, or shortening
are not available. We have included descriptions of these surgeries, although it appears that they
have not met with resounding success and are perhaps little used at this time.

Lengthening Vocal Folds/Increasing Tension

The major purpose of vocal fold tensing surgery is to raise the vocal pitch. Indications for such
surgery may include (a) excessively low pitch in females caused by an androgen or pregnancy;
(b) the low vocal pitch of the “sex-transferred” female; and (c) senile, flaccid vocal folds. Surgical
techniques to tense the vocal folds have been developed by Isshiki (1977); LeJeune, Guice, and
Samuels (1983); and Tucker (1985). There are two major surgical techniques to accomplish
vocal fold tensing:
Cricothyroid Approximation. The basic principle of cricothyroid approximation is to
create a permanent approximation of the cricoid arch to the thyroid cartilage anteriorly (Fig.
9.42), simulating the function of the cricothyroid muscle (Isshiki et al., 1977). Recall that
contraction of the cricothyroid muscle results in the approximation of the cartilages and that
in so doing the vocal folds are lengthened and tensed. Both the decreased mass of the folds
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FIGURE 9.42. Schematic presentation of the

principle of cricothyroid approximation, as devel-
oped by Isshiki.

and the increased tension under which they are held result in a faster vibratory rate, and thus
a higher pitch is produced. Zeitels (1999) has advocated performing this on the paralytic side
when a patient undergoes medialization thyroplasty. This provides additional tension and may
enhance voice results. The surgery is best conducted under local anesthesia so that the pitch
of the voice can be monitored during the procedure. However, if the patient is unable to
tolerate the procedure, general anesthesia is given. Following horizontal cervical skin incision,
the thyroid and cricoid cartilages are exposed. They are approximated anteriorly by means of
non-resorbable sutures. Stretching of the vocal fold can be visually monitored with the use of
a fiberscope.
Anterior Commissure Advancement. The basic principle of anterior commissure ad-
vancement is to stretch the vocal folds by advancing the anterior commissure anteriorly relative
to the arytenoid cartilages (LeJeune, Guice, & Samuels, 1983). The surgery may best be per-
formed under local anesthesia, but general anesthesia is employed when the patient cannot
tolerate the procedure. Following a horizontal cervical skin incision, the thyroid cartilage is
exposed. A vertical cartilage flap is made in the midportion of the thyroid cartilage. The flap
may be inferiorly based, superiorly based, or sectioned both superiorly and inferiorly. The flap
is advanced and stabilized in place by inserting a shim posterior to the flap (Fig. 9.43). When
local anesthesia is employed, changes in vocal pitch are auditorily monitored during surgery.
Vocal fold stretching can be visually monitored by means of a fiberscope.

Shortening Vocal Folds/Reducing Tension

The major purpose of vocal fold slackening surgery is to reduce the tension of the vocal folds
(Isshiki et al., 1977). Vocal pitch can be lowered as tension is reduced. This is a desired result
in transgender (female to male) surgery. This procedure has also been tried in patients with

FIGURE 9.43. Schematic presentation of the principle of anterior commissure advancement, as developed
by LeJeune, Guice, and Samuels (1983) and Tucker (1985).
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FIGURE 9.44. Schematic presentation of the principle of anterior

commissure pushback, as developed by Isshiki (1977).

adductor SD as a means of reducing tension (Isshiki, Haji, Yamamoto, & Mahieu, 2001;
Tucker, 1989).
In this surgery, the anterior commissure is moved closer to the arytenoid cartilage. The
surgery can be performed under local anesthesia, so auditory monitoring of voice change is
available. A vertical cartilage flap is made in the midportion of the thyroid cartilage and pushed
back and secured (Fig. 9.44). The anterior commissure is thus moved closer to the arytenoid
cartilage.

Surgery to Alter Laryngeal Neuromuscular Function

Recurrent Laryngeal Nerve Anastomosis for Vocal Fold Paralysis
While medialization injection or implantation move the impaired vocal fold to improve glottic
closure, thus voice and swallowing ability, this procedure attempts to have the nerve regen-
erate and thus medialize the vocal fold through increased reinnervated muscle bulk or actual
adductory movement.
The ideal treatment for vocal fold paralysis would be to restore normal innervation of
all laryngeal muscles. This is, however, not possible in cases of axonotmesis and neurotmesis.
That the recurrent laryngeal nerve (RLN) contains both adductor and abductor fibers creates
one of the major problems in the neurosurgical treatment of vocal fold paralysis. Simple nerve
anastomosis or nerve graft of the RLN causes misdirected reinnervation. Some neurons that
originally innervated one of the adductor muscles now may innervate the abductor muscles,
whereas some neurons that were originally for abductor innervation now act to innervate the
adductor muscles. This is called synkinesis and results in a lack of gross vocal fold mobility
(Hiroto, Hirano, & Tomita, 1968; Siribodhi, Sundmaker, Atkins, & Bonner, 1963).
Experimental and clinical attempts have been made to avoid the problems resulting from
misdirection of regenerated nerve fibers. The nerve–muscle pedicle procedure wherein a muscle
pedicle (along with its nerve) obtained from the ansa hypoglossi nerve that innervates the
omohyoid, sternothyroid muscles (Tucker, 1978; Tucker & Rusnov, 1981) is chosen as the
donor. In cases of bilateral abductor paralysis in which the vocal folds are fixed near the midline,
causing dyspnea, the nerve–muscle pedicle is implanted into the LCA muscle. This technique
has not met with wide acceptance or success.
Other surgical approaches for bilateral paralysis have been reported and include anasto-
mosis of the split phrenic nerve to the posterior cricoarytenoid (PCA) or to the nerve branch
innervating the PCA muscle (Crumley, 1983) and anastomosis of the split vagus nerve to the
nerve branch of the PCA (Miehlke & Arnold, 1982).

Recurrent Laryngeal Nerve Surgery for Adductor Spasmodic Dysphonia

Dedo (1976) first reported unilateral section of the RLN for SD. The procedure and its various
modifications were then carried out by many laryngologists. The immediate postsurgical results
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were reported to be highly successful and appreciated by many patients (Dedo, 1976). However,
the long-term results were conflicting, with many reports of symptom recurrence (Aronson &
DeSanto, 1981, 1983). In 1991, Netterville (1996) modified the procedure with a more distal
lysis and, in a follow-up report, noted that a vast majority were without spasms but with breathy
dysphonia. Although some few surgeons continue to perform the procedure today, most have
abandoned it due to the too-frequent return of symptoms despite continued paralysis of the
vocal fold caused by the sectioning procedure. Selective bilateral denervation of the TA muscles
for adductor dysphonia has been reported by Berke (Hong et al., 1998). The distal nerve
ends are microsutured to the ansa cervicalis to prevent aberrant reinnervation by the recurrent
nerve. Long-term results appear good (Chhetri, 2006). However, with the introduction and
effectiveness of BOTOX injection as a treatment modality, albeit not a cure, the RLN surgeries
are not common. (See discussion later in this chapter under “Medical Management.”)

Surgical Reconstruction for Partial Loss and/or Deformity of Larynx

Surgical removal of lesions and medialization surgery to correct the glottis with an immobile
vocal fold are the most common laryngeal surgeries. Less frequent and often much more
complicated surgeries involve surgical correction of tissue loss and deformity. These laryngeal
problems can be congenital or acquired through surgical or other trauma. Creativity and careful
planning are essential in reaching the optimal result. Several stages may be necessary, such as
tissue transfer or stent placement and removal. A surgical treatment plan must be individualized,
but a few examples will be covered.

Anterior Glottic Webs, Stenosis

Anterior glottal web can be a rare congenital malformation or is caused by trauma, including
surgical trauma. The web can be thin or thick, small or involving most of the membranous
vocal edge. There are two major surgical techniques for its removal: endolaryngeal surgery
and external approach thyrotomy. There has been a trend toward endoscopic treatment as
instrumentation has improved.
With the vocal folds exposed by direct laryngoscopy under general anesthesia, the web is
sectioned at the midline or partly removed. A CO2 laser may be used for this purpose (Fig.
9.45), but “cold” scissor division can also be done. After removal of the web, a silastic plate is
placed in the glottis to prevent postsurgical reunion of the vocal folds. To do this, suture is passed
through a rounded, trimmed piece of silastic sheeting. A 14-g needle is passed transcutaneously
into the larynx. One end of the thread is passed down the laryngoscope and out the needle to
the skin. The needle is withdrawn and reintroduced into the larynx, and the second limb of

FIGURE 9.45. Endolaryngeal surgery for anterior glottal web.

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the thread passed through the glottiscope and out through the needle. Both ends are tied over
a soft piece of silastic or plastic on the anterior neck skin.
Lichtenberger (2002) has made a specialized endolaryngeal needle. This allows transcuta-
neous sutures to be placed from the lumen side toward the skin.
The silicone plate is removed endolaryngeally 1 to 2 weeks after surgery. This can be done
by cutting the external suture and retrieving the plate with a flexible bronchoscope or curved
indirect laryngoscopy forceps.
The silastic sheet can also be sewn in place within the larynx using Prolene suture. To
prevent reforming of the web, the silastic can be placed along the length of one of the vocal
folds. The silastic, however, does need to be retrieved under general anesthesia, but this affords
another opportunity to inspect the glottis and remove any granulation that may have grown
around the implant.

Posterior Glottic Stenosis

Posterior glottic stenosis may be due to a web or scar typically between the arytenoid cartilages.
Prolonged intubation in the intensive care unit setting may lead to arytenoid fibrosis, inter-
arytenoid scarring, or webbing. A laser can be used to divide the web, but mucosa should be
preserved as much as possible. Microflaps of mucosa are lifted, the submucosal scar removed,
and the mucosa returned in place. Stents can also be placed, but a second procedure is needed
for removal. Additional procedures to establish an adequate airway include the lateralization
procedures described earlier.
An external approach can be used for thick and more extensive webs. A midline cervical
incision is made followed by splitting the strap muscles to expose the thyroid cartilage. The
midline is then divided. Endoscopic monitoring is desired to insure that upon entering the
larynx, the web is divided evenly and in the center. The attachment of the vocal fold to the
cartilage is rechecked and, if not secure, can be sutured to the cartilage. The wound is sutured
closed in layers.
More difficult-to-treat problems involve greater tissue loss of the larynx due to burns,
cancer surgery, or trauma.
Surgical ingenuity is important. Mucosa from the surrounding laryngeal region can be
rotated or advanced into place. Oral mucosal grafts can also be sutured into place to replace an
absent vocal fold with success. Rib cartilage grafts in addition to Silastic or GORE-TEX shims
can be useful for medializing the thickened, scarred hemilarynx.

Medical Management
Although certain disease states of the larynx result in conditions that are irreversible and need to
be addressed surgically, the majority of people who have voice problems are managed without
surgery. Medical management plays a large role in the treatment of many conditions. This
section will address those disease states that typically require the medical and pharmacological
expertise of the otolaryngologist.

Infection
Viral laryngitis is the most common type of laryngeal infection. The disease is self-limited
but may last 5 to 10 days. Patients note vocal difficulty due to laryngeal edema, inflammation,
thickened mucus, and decreased vibratory behavior of the vocal folds. Coughing due to laryngeal
irritation is also often a symptom. Vocal rest, analgesics, mucolytics, and remedies such as tea
with honey often comfort the patient. Antibiotics are not indicated for viral infections, and
bacterial infections of the larynx are uncommon.
Laryngitis, though, may be due to bacterial infections elsewhere in the head and neck region
such as sinusitis. Antibiotics are frequently prescribed for patients who present with upper
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respiratory symptoms. Bacterial epiglottitis has become exceedingly rare, but supraglottitis
still occurs and presents as sore throat and voice changes. Depending on the clinical picture,
admission for airway observation or intubation and intravenous antibiotics may be needed.
Tracheotomy is rarely needed.
Fungal laryngitis also occurs particularly in the setting of the asthmatic, diabetic, or im-
munocompromised patient. Chronic steroid inhaler use can cause fungal infections. On exami-
nation, the larynx has whitish material along the margin. The pharynx may also be involved and
have whitish-yellow patches. These are best treated with the oral antifungal agents (Nystatin,
Mycelex, Diflucan, Pfizer, New York, NY) for up to 3 weeks. The pulmonologist should be
informed of the infection to see whether the medication or the delivery of the medication can be
changed. Fungal infections can recur and may require repeated or longer courses of treatment.

Systemic Disease
There are numerous systemic diseases that may have effects on the voice. These may be from
the disease itself or from the treatment or medications for that disease. For example, cardiac
disease may lead to voice problems due to medications that reduce body water volume. Although
frustrating for the patient, they must be reminded of the importance of taking these medications
unless another is available that does not have the same side effects.
Sarcoidosis, amyloidosis, and Wegner’s granulomatosis can all have diffuse involvement
with thickening of the laryngeal tissue in characteristic patterns. Sarcoidosis is usually diagnosed
by chest x-ray and known prior to involvement in the larynx. Wegner’s granulomatosis usually
involves the subglottis, and patients may initially present with stridor. Similarly, amyloidosis in
the larynx causes dysphonia and may be the first sign of the disease. A high level of suspicion
for these diseases is needed to alert the pathologist to perform special testing of the biopsied
tissue to make the diagnosis. The voice may improve as systemic treatment is instituted or when
diseased tissue is removed or debulked.
Metastatic neoplastic disease may also involve the larynx, including breast or renal cell
carcinoma or lymphomas. These are uncommon lesions.
Arthritis is a systemic disease that can also affect the cricoarytenoid joints, causing ankylosis
and immobility. Rheumatoid nodules can occur in the membranous vocal folds causing voice
problems. Once again, steroid use as an anti-inflammatory often reduces symptoms, although
the subepithelial nodules can be surgically removed. A well-known endocrine abnormality that
can, but rarely does, affect the voice is hypothyroidism. Water retention accompanies this con-
dition, the vocal folds may become edematous, and the pitch of the voice may lower with the
increased mass. Diabetes is a disease that can affect the larynx in several ways. Wound healing is
impaired, and diabetic patients are more susceptible to glottic scarring from intubation. Dehy-
dration or water loss may contribute to voice problems. Sjogren syndrome, lupus, pemphigoid,
and other autoimmune disorders may have dysphonia as a symptom.

Allergy
Patients often comment that their voice problem is “allergy-related.” However, there are few
studies looking at the direct organ effect of allergy. It is not clear how much immunoglobulin
E–mediated histamine release occurs in the larynx. Likely, the effect on voice is secondary to
other organs being affected by allergies, such as the nose and lower airways. Prior to prescribing
medications, an extensive exploration should be done to try to determine what in the patient’s
environment may be the cause. Some of the most common allergens are year-round such as
molds, animal dander, and dust mite. Allergy testing is warranted to determine the triggers
and aid in deciding a medical treatment plan. Antihistamines may help the voice by improving
the health of the other organs, may help the larynx itself, but may harm the larynx by causing
dryness. Topical nasal steroids and immunotherapy, however, are very effective for allergic
rhinitis and do not adversely affect the vocal folds. As noted earlier, many patients with allergies
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also take numerous medications including inhaled steroids. It has been documented that long-
term use of these inhalants can cause laryngeal and voice problems.

Laryngopharyngeal Reflux (LPR)

Over the past two decades, this disease has received much attention as a very frequent cause
of laryngeal disease. Less than half of the patients will have symptoms of “heartburn.” Lesions
associated with reflux include epithelial growths, generalized inflammation of the folds, and
laryngeal cancer. On endoscopy, the posterior larynx can be erythematous and edematous,
whereas thick mucus is considered a hallmark finding.
Diagnostic testing is not always mandatory, and empiric treatment is reasonable in most
circumstances. Barium swallow, upper gastrointestinal series, and esophagogastroduodenoscopy
often cannot detect reflux disease that affects the upper aerodigestive tract. Koufman (1996)
has promoted the term “laryngopharyngeal” rather than “gastroesophageal” to reflect that the
two are different clinical entities. Dual pH probe monitoring is the current “gold standard” to
detect reflux occurring at the level of the posterior larynx but is uncomfortable. Newer probes
to determine reflux at the level of the larynx employ probes that are situated though the nose
and rest in the nasopharynx (Sun, 2009).
It is also possible that nonacidic and enzymatic reflux occurs causing inflammation. Pepsin,
a gastric enzyme, is found in the posterior larynx in patients with LPR (Johnston, 2006).
Treatment of LPR entails behavioral management as well as proper medication use.
Behavioral changes such as wearing loose-fitting clothing, eating frequent small meals, not
eating 2 to 3 hours before bedtime, and elevating the headboard 6 are all recommended.
Dietary restrictions such as avoidance of alcohol, caffeine avoidance, and spicy foods are rec-
ommended. When obesity is present, dietary restriction for weight loss is important.
Over-the-counter medications include antacids that are taken after meals to neutralize
acids and acid suppressants including H-2 blockers such as cimetidine, famotidine, nizatidine,
or ranitidine. Antacids are brief acting and are often insufficient.
Proton pump inhibitors (PPIs) are a far more effective class of medications (omeprazole,
lansoprazole, rabeprazole, and others). These are best taken 30 to 60 minutes before breakfast
and typically only once daily. Medication is often prescribed particularly around the time of any
surgical intervention. Patients that have a granuloma often require PPIs twice daily for several
months. Prokinetic agents (metoclopramide) that increase gastric emptying and increase lower
esophageal pressures can be used for shorter periods of time (weeks). Surgery for “tightening”
the lower esophageal region can be performed in patients that are not medically controlled,
usually by a general surgeon.

Noxious Inhalants
Smoking of tobacco or illegal substances is irritating to the exposed mucosa. Smoking cessation
is very difficult and has been most successful when attempts are coupled with support groups and
taking medications such as Chantix (Pfizer), Zyban (GlaxoSmithKline, Research Triangle Park,
NC), or Wellbutrin (GlaxoSmithKline). Nicotine gum and patches have not helped a majority
of smokers to stop. Nonsmokers who are exposed to tobacco smoke have eye and respiratory tract
irritation (U.S. Department of Health and Human Services, 1986) and increased risk of cancer.

Neurological Conditions
Spasmodic Dysphonia
SD is a neurological condition affecting the larynx. The etiology is not known. Most patients
have a strained, strangled, and choppy voice quality. Extensive studies have been performed
on this condition, including electromyogram (EMG), confirming this as a form of focal dys-
tonia. There are two types: adductor and abductor (Aronson, Brown, Litin, & Pearson, 1968),
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although some patients may have both. The adductor type is marked by irregular hyperadduc-
tion of the vocal folds, which disrupts voicing and is much more common (>75%). Abductor
dysphonia is characterized by whispered segments typically following the production of an
unvoiced consonant. Indeed, it has been described as a disruption in the ability of the vocal
folds to close.
Treatment consists of periodic injections of botulinum toxin (BTX) into the affected
muscle group(s). BTX is thought to act by blocking neurotransmitter release at the neuromus-
cular junction, thus causing muscle weakness/paralysis. The most common type of BTX is “A”
(BOTOX-A, Dysport), but many other subtypes have been described. Resistance due to anti-
body formation to the toxin has been shown in relatively few individuals. BTX B (Myobloc-B,
Myobloc, Solstice Neurosciences, Inc., Malvern, PA), however, can then be used. The thera-
peutic amount is individualized and is based on the historical duration of benefit and degree
of side effects. The technique of BTX injection is the same as described earlier. Teflon-coated
needles are typically used so that an EMG can be done to confirm placement. Transoral or
transcutaneous methods can be used. After injection, there is a 1- to 3-day delay in the clin-
ical effect that at first is breathiness. After 7 to 14 days, the voice strength returns without
the spasms. The usual duration of benefit is 3 to 4 months until symptoms return as neural
sprouting occurs and new neuromuscular junctions are formed. Over time, as a patient receives
many injections, fibrosis occurs, making needle insertion more difficult.
For adductor SD, the BTX is injected into the thyroarytenoid or lateral cricoarytenoid
muscle. Most injections are given bilaterally in dosages of 0.75 to 2.0 units per side as a starting
point. The amount may be reduced in future injections if the breathy period is prolonged or
any significant aspiration occurs.
Treatment of patients with abductor SD with BTX injection is more difficult. The PCA
muscle is approached either transcutaneously by rotating the thyroid cartilage or by passing the
needle from anterior to posterior through the thyroid lamina. The latter is more difficult due
to ossification of the cartilage. Placement is verified by having the patient sniff while recording
the EMG.

Vocal Tremor
Tremor is characterized by a rhythmic oscillation of the voice. It is not uncommon to note the
presence of some tremor associated with SD. However, there are patients who present only with
tremor. Medications may be helpful and include propranolol and primidone. However, their
effectiveness may be reduced by 50% within a year, and side effects of the medication can occur.
Although BTX treatment for tremor is not as effective as it is for SD, many find the injection
of BTX to be helpful (Warrick, 2000). They experience a reduction in severity of tremor, an
improvement in intelligibility, and less effort involved in speaking. They tend to follow a similar
pattern of return of symptoms within a number of months as do the SD patients.

Parkinson’s Disease
This is a well-known, progressively deteriorating neurological disease marked by tremor, rigidity,
and bradykinesia. The voice may be an early site of deterioration with decreased intensity and
a muffled quality. A more complete discussion of this disease is found elsewhere in this chapter
as is the behavioral speech treatment. Although the clinical status of the patient as seen in
movement characteristics is often improved with a variety of medications, these drugs have no
beneficial effects on voice or speech (Larson, Ramig, & Scherer, 1994).

Myasthenia Gravis
Pyridostigmine (Mestinon) is used to control the symptoms of muscle weakness in myasthenia
gravis (Ravits, 1988). There are numerous other drugs used in similar ways in the treatment
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312 Understanding Voice Problems

of many progressively debilitating neurological diseases, but their effects on voice and speech
have not been noted to be marked, although they have not been well studied.

Summary
In the first section of this chapter, a review of phonosurgical techniques currently in use for
the treatment of voice problems was presented. Phonosurgical techniques are divided into four
categories: (a) removal of pathological tissue; (b) correction of the position, shape, and/or tension
of the vocal folds; (c) surgery to restore laryngeal neuromuscular function; and (d) reconstruction
for a partial loss or deformity of the larynx. A brief description of the techniques currently
used by otolaryngologists was given to aid the reader in understanding the advantages and
disadvantages of the techniques.
In the second section of this chapter, some of the techniques used in the medical manage-
ment of voice problems were reviewed. Many of these techniques involve the use of drugs for
the relief of symptoms as well as for treating the original cause(s) of the voice problem. Allergies,
asthma, and the drugs used in their treatment are often implicated as a cause of voice prob-
lems. Other medical techniques include counseling and behavioral modification techniques to
encourage the patient to change habits (smoking, drinking), lifestyle, or the environment.
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CHAPTER

10
Vocal Rehabilitation

Keywords
benign tissue pathology, birth control pill, botox, chewing, confidential voice, contact
ulcer, coughing, diagnosis, digital manipulation, effort, falsetto, goal, granuloma, hum,
hypothyroidism, imagery, isometrics, laughing, malpractice, massage, neuromuscular,
nodules, normal, paradoxical vocal fold motion, paralysis, Parkinson’s disease,
phonoscopic approach, pitch, polyps, presbyphonia, prevention, prognosis, PVFM,
relaxation, resonant voice, REST, semiocclusion, sign, spasmodic dysphonia,
transsexual, tremor, trill, virilization, vocal function exercises, voice therapy,
whispering, yawn/sigh

Goal of Voice Therapy

The details of voice therapy vary from patient to patient. But the goal of therapy for every patient is to
restore the best voice possible, a voice that will be functional for purposes of employment and general
communication. The patient must be the final arbiter of what constitutes acceptable voice. But it is
important for both the patient and the clinician to recognize that restoring voice to the way it previously
sounded, or to some idealized goal, may not be possible. When irreversible alterations have occurred in
laryngeal structure or physiology, the former voice may never be restored. This realization is particularly
traumatic for persons who have relied heavily on their vocal skills for their livelihood, or as their primary
source of pleasure. The intent of this chapter is to review current concepts and practices in vocal
rehabilitation.

Concept of Normal Voice

A single definition of normal voice does not exist. There are no established standards, and no boundaries
of accepted norms have been set. Attempting to set such standards might be likened to defining what
constitutes normal appearance. Cultural, environmental, and individual factors contribute to the deter-
mination of what is designated normal. And voice, again like appearance, does not remain constant. It
changes across the lifespan; it changes in reaction to emotion; it changes in response to environment;
it reflects the state of health of the body and of the mind. Normal is not a single point, but rather,
ranges along several continua. Whether voice is judged as “normal,” or not, will vary depending on the
listener, and on the unique characteristics of the speaker, as well as on the specific features of the voice
produced. Objective measures of voice (see Chapter 13) are affected similarly by these factors. That is,
our concepts of “normal” are based on values associated with voices generally perceived by listeners as
normal. The start and end points of these ranges can fluctuate, and investigators remind us that both
intra- and inter-subject variability may be very large (Kent, Kent, & Rosenbek, pp. 367–387).
It is perhaps easier to attempt to define the abnormal. For example, voices that are so soft that
most people have difficulty hearing them, or produced at extremely high or low pitches, or sufficiently
313
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dysphonic that they interfere with intelligibility, are likely to be judged as abnormal by most
listeners. The lack of a definition of normal voice can create problems in setting therapeutic
goals and in describing abnormality and its degree of severity. There is no complete, objective
template against which to measure and compare it. In fact, a major complication in research
in this area is the identification of both subjective and objective measures that meet acceptable
criteria of validity and reliability in documenting degree of dysphonia. Such confounding
may also be reflected in a lack of agreement between clinician and patient regarding just how
dysphonic a voice is, or how much it has improved, or failed to improve. Ultimately, however,
it is the patient who has sought treatment, and change, and it is this individual whose opinion
must be considered a priority.

Normal Anatomy and Physiology

If the concept of “normal voice” is complex, it is nonetheless true that voice therapy must be
rooted in and derived from an understanding of normal laryngeal anatomy and phonatory
physiology as well as a detailed understanding of what’s “broken” in a particular voice. The
greater the clinician’s understanding of both, the greater the likelihood the disordered voice can
be repaired in an efficient, effective manner. Modeling disordered voice from the perspective
of normal production allows the clinician to specify and describe particular deficits and to
develop strategies appropriate for their modification. As with any specialty area, clinicians who
choose to work with this patient population are obliged to be as prepared as possible in their
understanding of normal and abnormal.

Diagnosis
Accurate diagnosis is of course a critical component of treatment planning for voice therapy.
Most patients who arrive in the voice clinician’s office have been referred for therapy by a physi-
cian, usually an otolaryngologist. This physician will have examined the larynx and provided
a diagnosis. Some referring physicians will offer considerable detail, for example, a description
of pathology present and of how the patient appears to be producing voice. In other cases, a
diagnosis may be as perfunctory as “vocal nodules,” or “functional dysphonia.”
Increasingly, speech-language pathologists who work with voice patients in selected set-
tings are performing their own laryngeal imaging studies. The intent of this exam is not to
diagnose tissue pathology, which is the responsibility of the physician, but rather, to elaborate
“vocal” pathology. We have referred to this exam as a “phonoscopic” exam because it permits the
clinician to visualize specific laryngeal behaviors and associate them with the voice produced by
these behaviors (Leonard & Kendall, 2002, 2005). The phonoscopic study not only elaborates
the effects of tissue pathology (if present) on voice but also specific aberrant laryngeal and vocal
behaviors and the circumstances under which they occur, that is, consistently, at the onset of
phonation, when pulmonary support is compromised. In our experience, there is not a one-to-
one relationship between laryngeal behavior and voice resulting from it; thus, these kinds of in-
sights are difficult to discern unless one is observing as well as listening. Treatment probing with
imaging also allows the clinician to assess the effects of various maneuvers designed to minimize
further exacerbation of pathology and/or to alter aberrant vocal behaviors that are identified.
Combined with other assessment information, the imaging study provides a foundation
for both understanding the problem and for developing a specific approach to its treatment. In
our opinion, clinicians who are treating dysphonic patients must make every attempt to acquire
this kind of detail. Clinician imaging is ideal, but if this is not a realistic option, then the speech
pathologist needs to go back to the referring physician and request appropriate information.
Settling for a one- or two-word diagnosis or description is in no one’s best interest. And, once
referring physicians know what kinds of information may be useful to the voice clinician,
they are likely to be pleased to comply. Ideally, an accurate diagnosis will allow the clinician
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to determine whether, and how, voice therapy will help an individual patient and provide
insights into specific treatment goals and strategies likely to be both effective and efficient. If
the patient is not responding to therapy in an expected manner, the clinician should return
to the referring physician with this report. Possibly, the initial diagnosis was not accurate and
needs to be reconsidered. In some cases, resolving edema or inflammation, for example, may
allow for more accurate diagnosis of underlying pathology. It is not appropriate for the clinician
to continue to see patients in therapy when little or no progress is being demonstrated.

Prognosis
Many factors enter into the consideration of a prognosis. Because voice therapy requires full
patient participation, it is often difficult to predict its anticipated outcome. In determining
whether a patient is an appropriate candidate for a voice therapy approach and arriving at a
prognosis, the clinician should consider the following factors. First, the patient must recognize
that there is a problem. People possess internal references about how they should feel, what is
normal for them, and how they should sound. A voice that sounds abnormal to us may not
sound particularly deviant to the person with the voice. Similarly, although the patient is aware
that the voice is not normal, he or she may not find it objectionable or in need of “fixing.” Sec-
ond, the patient must be willing to follow a therapy plan, including regular practice periods as
required. This is difficult for those seeking the quick cure for which they do not have to assume
responsibility. Third, there must be a willingness to give up vocally traumatic habits and to alter
or eliminate some voice use, at least temporarily. This is easier said than done for most people.
Changing manner and amount of talking involves changes in lifestyle, in everyday habits, and
even, it may seem, in personality. Fourth, psychiatric problems, if present, may interfere with
the ability to modify vocal behavior. A voice problem may be a manifestation of a psychiatric
problem. Amelioration of the voice problem may be possible temporarily, but it will not deal
with the larger, underlying problem (recall the case of R. W. in Chapter 7). Fifth, the patient’s
voice disorder must be amenable to change through a voice therapy approach. For some voice
problems, surgical or medical management may be the first or sole step. For other patients,
the nature of the disorder may preclude any real possibility of success through voice therapy.
The patient and the speech-language pathologist must be able to recognize the limitations
of voice therapy. Sixth, appropriateness of the patient’s expectations must be considered. If a
person has an essentially normal voice but wishes to sound like a favorite role model or celebrity,
voice therapy is not indicated. Seventh, it is necessary to give full consideration to the patient’s
laryngeal condition and general health status. Some patients are insistent upon attaining full
return of premorbid voice. The nature of the disorder and the resultant laryngeal changes may
be such that this expectation is unrealistic. Patients may have other health problems that may
limit their ability to participate in voice therapy or may place constraints on their ability to con-
trol phonatory behavior. Finally, prognosis is dependent on the speech-language pathologist.
The clinician’s understanding of the problem, and competence in dealing with it, including
an ability to relate well to the patient, will contribute to the success or failure of therapy.

Voice Therapy
Voice therapy can assume many forms. In some cases, it may be the only intervention needed
to resolve a problem. In others, it may be prescribed in an attempt to reduce benign pathology,
so that a more accurate diagnosis can be made, or in the hopes of minimizing any necessary
surgical intervention. Postsurgery, therapy may be important in helping a patient develop
optimal voice use and prevent additional difficulty. Dysphonia that is related to a medical
condition, for example, laryngopharyngeal reflux, or thyroid disease, may need to accompany
other treatment in order to optimize vocal function. Nonorganic disorders may similarly benefit
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from multiple therapies that address etiological and exacerbating factors. Basic components
of most therapies, however, will include patient education and modification of voice use.
Patient education typically involves some instruction of the patient in how normal voice is
produced, identification of factors that are likely contributing to the disorder, and nondirect
strategies, for example, voice conservation and improved vocal hygiene, which will improve
vocal function. The particular and unique domain of the voice clinician, however, is the use of
therapy techniques to modify how voice is being produced.
Consider that normal voice is comprised of a vocal “space,” that is, a set of variables
(pitch, loudness, airflow, pressure, vocal fold contact patterns, etc.), each with a range (high to
low, soft to loud, incomplete to complete, etc.) within which voice is produced. In a normal
speaker, these ranges across various vocal production parameters can be visualized as a space
of a given size. The visual display of a phonetogram or vocal range profile may be analogous,
if only for frequency and intensity. The visual display represented in the KayPentax Multi-
Dimensional Voice Program, which can present ranges for multiple variables simultaneously, is
also illustrative of this concept of vocal “space.” In the dysphonic patient, one or more of these
ranges, perhaps all, have been reduced, altered, and perhaps even eliminated. Voice therapy
involves first identifying, or mapping, the existing space, and then implementing an optimal
vocal space for a patient, that is, ranges of vocal parameters within which voice is produced in the
most efficient, economical, and least aversive manner possible. Some of the variables mapped
lend themselves to manipulation, and these are what the clinician hopes to change. Initially, a
more normalized space may be small, perhaps present only on a single sound or syllable. Once
appropriate, or more normal, voice is identified, in whatever context, the clinician will work
to expand it across phonatory variables, phonetic contexts, and speaking situations, with the
ultimate goal of normal, or optimal, vocal function. In the next sections of this chapter, voice
therapy associated with specific disorders will be described, including the particular roles of
adjunct treatments, patient education, and modification of vocal behaviors.

Voice Therapy Associated with Benign Tissue Pathology

Depending on type, extent, and chronicity of laryngeal pathology, voice therapy may be the
only treatment required or may accompany other intervention. Certainly, if voice use is a factor
in the development or maintenance of pathology, education of the patient regarding these
factors is indicated, even if the eventual resolution of pathology will require other intervention.
A discussion of how voice is normally produced, and how the patient’s behavior may differ from
this, is particularly useful. If available, the patient’s imaging study can be compared to a normal
study, and specific aberrant or excessive behaviors typical of the patient can be explained. In
our clinic, patients with this type of pathology are encouraged to monitor the voice from a.m.
to p.m., paying particular attention to how the voice sounds and how effortful it is to produce.
The goal is to get through the day without deleterious changes in quality or increases in effort.
Clinically, this is referred to as avoidance of “vocal fatigue.” Once patients begin to monitor
voice use, specific practices that “use up” vocal resources more quickly are often identified. In
addition, particular patterns, for example, how voice changes or remains stable on particular
days, or with particular activities, may be revealed. Information pertinent to hydration, effects of
medications, laryngeal function in vegetative behaviors, or other stimuli that may have aversive
effects on vocal fold tissues is also addressed.
Specific voice therapy techniques are directed to reducing contact forces at the site of
pathology, by reducing loudness, minimizing behaviors that involve forceful contact between
the vocal folds, including coughing and abrupt onsets of voicing, and, possibly, altering vocal
fold–contact patterns to modify sites of greatest collision. Other strategies address maladaptive
behaviors that may represent a consequence of tissue pathology. For example, patients who
lose air more quickly because of incomplete closure of the vocal folds may continue to speak
even when pulmonary support is markedly compromised. If this behavior is accompanied
by supraglottic constriction or medialization, then these inappropriate behaviors need to be
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identified and minimized or eliminated. The intent is to achieve balance between pulmonary
support and vibratory forces.

Vocal Fold Nodules

There is wide agreement across specialists in the fields of both otolaryngology and speech-
language pathology that voice therapy is appropriate for vocal nodules (Aronson, 1990; Bastian
1965–1987; Boone & McFarlane, 1988; Gould, 1987, pp. 327–332; Sataloff, 1987, pp. 92–
104, 191–201, 283–292; Vaughan, 1982, pp. 863–866) (see also Chapter 8 of this book). Some
authorities make a distinction between early nodules, which appear to be soft and reddish, and
nodules that have been present for months or years and are large, hard, and white. Voice therapy
as the initial treatment is recommended for the former, and surgical removal followed by a period
of voice therapy is most commonly recommended for the latter (Arnold, 1980, pp. 2470–2488;
Boone & McFarlane, 1988; Case, 1984). Sataloff (1987, pp. 191–201) states that even nodules
that are large and fibrotic may disappear, regress, or become asymptomatic through a course of
voice therapy. And if there is partial regression of pathology, any surgery required may be less
extensive. Since there is also wide agreement that vocal nodules are associated with excessive or
hyperfunctional vocal practices, voice therapy is indicated for prevention of future difficulty.
Improvement or resolution of pathology, improvement that leads to more accurate diagnosis,
and patient education/modification of vocal practices are all reasonable goals.
In our own experience with adults, etiologies may appear relatively more speaker specific, or
more situation specific. In the first case, the speaker, regardless of context or situation, demon-
strates vocal behaviors that are hyperfunctional. The impression is that this patient has, perhaps
since childhood, demonstrated aggressive vocal behaviors, that is, is inappropriately loud, has a
ballistic speaking style, and is a self-described “talker.” Careful questioning may further reveal
a life-long history of frequent episodes of hoarseness, likely related to voice use. DeBodt et al.
(2007) recently reported on a group of 91 adults who had been diagnosed with vocal nodules
in childhood; 21% of the group continued to have voice complaints, and 34% of this group
had vocal nodules. The authors reported that gender, degree of dysphonia, and presence of
allergens appeared to be predictive of persistent dysphonia, with women who experienced the
greatest dysphonia and were affected by allergens most at risk for continued difficulty.
In contrast, another group of patients demonstrate few individual behaviors that could be
considered predictive of vocal nodules. Rather, it appears to be the particular vocal demands of
the current situation, that is, work or home environment, which are relatively more implicated
in nodule development. Often, this patient describes no previous history of voice problem
and only began having difficulty in a new situation, that is change in work responsibilities
and transfer to new environment. Clinically, the former patient may require more intensive or
prolonged conservative treatment focused on vocal behaviors reflective of personality, whereas
the latter may benefit greatly, and expediently, from strategies designed to modify situational
factors associated with vocal behaviors.
Holmberg et al. (2001) reported on 11 women with chronic vocal nodules who underwent
voice therapy comprised of vocal hygiene counseling, respiratory retraining, direct facilitation,
and carryover strategies. Pretherapy voice samples were compared to samples following each
phase of therapy, and the authors found significant improvements on perceptual measures of
voice quality following direct facilitation and respiration portions of treatment. Nodules had
decreased in size, and edema was reduced; however, in no case were the nodules completely
resolved, as evidenced on laryngeal imaging. Holmberg et al. (2003) subsequently evaluated
the relative benefits of selected acoustic and aeromechanical measures in assessing treatment
outcomes in this same group of patients. The authors concluded that aeromechanical measures
were more sensitive to changes than the particular acoustic measures investigated.
Recently, Behrman et al. (2008) compared the effects of a direct therapy approach, involv-
ing modification of voice production, to an approach involving only vocal hygiene education.
A total of 62 women with benign, phonotraumatic pathology were randomly assigned to one
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318 Understanding Voice Problems

or the other of the treatment groups, and both groups underwent 6 weeks of therapy. Patient
self-assessment was the outcome measure. Though both groups demonstrated improvement,
results were significantly better in patients who underwent direct therapy. Evidence of tissue
change was not available.
Other authors have compared the results of different treatment strategies in patients with
vocal nodules. Murry and Woodson (1992), investigating 59 patients, reported that patients
who were treated with an integrated approach involving both a speech pathologist and oto-
laryngologist demonstrated greater progress than patients who underwent therapy after surgery,
and patients who underwent therapy only. However, all patients demonstrated progress. The
authors also speculated that patients with longer-standing pathology were possibly referred for
surgery more often than patients with more acute pathology, who may have been referred more
often for voice therapy only.
More recently, Chernobelsky (2007) followed 28 classical singers over periods up to
24 years to investigate the effects of nonsurgical treatment. Specific intervention varied de-
pending on the maturity of the pathology, with soft thickenings treated by voice rest only, and
more fibrous thickenings, with voice rest followed by ultrasound therapy. Of particular interest
in the study was the author’s report that nodules rarely resolved completely in any patient, even
with major alterations in voice training and singing technique.

Vocal Polyps
Vocal fold polyps are often thought to be the result of vocal trauma, sometimes caused by a single
or intense period of trauma during which small blood vessels rupture. They are also thought by
some to be amenable to a voice therapy approach, particularly the sessile, or broad-based, polyps.
As with vocal nodules, opinions about the preferred mode of treatment are mixed; however,
as is the case with nodules, little is lost when a period of voice therapy is the initial treatment
provided. Therapy goals and strategies are similar to those described for vocal nodules.

Contact Ulcers and Granuloma

Contact ulcers and granulomas were once thought to result from a specific type of vocally abusive
phonation. More recently, a number of investigators have identified an association between this
type of pathology and laryngopharyngeal (LPR), or extraesophageal, reflux (Belafsky, 2003;
Cherry & Margulies, 1968, pp. 1937–1940; Chodosh, 1977, pp. 1418–1427; Delahunty,
1972, pp. 335–342; Delahunty & Cherry, 1968, pp. 1941–1947; Koufman, Belafsky, Bach,
Daniel, & Postma, 2002; Ward et al., 1980, pp. 262–269). This type of reflux represents
the backflow of stomach contents out of the esophagus into the pharynx and larynx. Vagal
mediation of acid content in the lower esophagus may be an additional contributing factor.
Granulomatous lesions typically occur on the posterior, cartilaginous vocal processes. These
structures are close to the upper esophageal sphincter and, thus, a likely site for irritation
from refluxed material. In the late 1980s, investigators identified drops in the pH levels of the
pharynx in patients with LPR symptoms (Wiener, Koufman, & Wu, 1987; Wiener, Koufman,
Wu, Cooper, Richter et al., 1989); “pH” is a measure of the alkalinity or acidity of a solution, and
drops in pH levels (below “7”) indicate an environment becoming more acidic. Though reflux
of this type is thought to occur to some extent in many individuals, there is increasing evidence
that mucosal airway injury may result from even an isolated reflux event (Little et al., 1985).
The vocal processes also adduct forcefully during selected reflexive or vegetative behaviors.
According to Ward and Berci (1982) it is the initial irritation, and the patient’s subsequent
responses to it, including coughing and throat clearing, that contribute to contact ulcer and
granuloma formation. In fact, nonacidic reflux that elicits coughing may be traumatizing to
tissues. Chronic nonspecific laryngitis, pharyngitis, and pachydermia laryngis (irritated tissue
in the interarytenoid region that appears similar to the folds of an elephant’s trunk) are included
in the family of problems with this underlying pathophysiology.
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Koufman et al. emphasize the potentially destructive nature of gastroesophageal reflux

disease (GERD) on the larynx, leading to problems that may be very serious, including cancer
(Koufman, 1995, pp. 161–175; Koufman et al., 1988, pp. 78–89). In our experience, most
physicians regard evidence of reflux irritation of the larynx as serious and may recommend fur-
ther evaluation with reflux-specific instruments, such as pH testing or fluoroscopic evaluation of
the esophagus. Behavioral changes, including alcohol and tobacco avoidance, and medications
designed to suppress acid production (proton-pump inhibitors or H2-receptor antagonists), are
also frequently prescribed. Surgery, on the other hand, is typically attempted as a “last resort”
because lesions often recur, sometimes very quickly, after excision. This may also be related to
the location of the lesion site on the vocal processes, that is, an area that is extremely difficult to
secure from adduction forces associated with swallowing, voicing, coughing, and throat clearing.
Voice therapy is appropriate as one part of the treatment regimen in particular, to eliminate
vocal and laryngeal behaviors most likely to be exacerbating pathology. We have also found it
useful, in a small group of patients, to modify contact between the vocal folds during voicing
(Leonard & Kendall, 2005). Patients who appear to effect closure between the vocal processes
(as opposed to those who typically have a small posterior gap) may be particularly susceptible
to reflux effects. If this pattern is identified, it may be possible to alter vocal fold contact for
voicing in a way that reduces posterior contact, while retaining or even improving contact
between the membranous vocal folds. An example of this treatment is presented on the DVD
accompanying this book.

Polypoid Changes
Polypoid changes of the vocal folds (Reinke’s edema) are highly related to long-term, excessive
smoking and to age (Hirano, Kurita, Matsuo, & Nagata, 1980). Although a component of
vocal misuse may also be present and may aggravate the condition, these lesions are generally
not caused by abuse and not responsive to voice therapy. However, many patients will benefit
from a course of voice therapy following surgical excision of the lesion.

Other Pathology
There are numerous other laryngeal lesions that are not caused by vocal trauma and that require
medical and surgical intervention. However, vocally harmful habits may result as the patient
attempts to compensate for a poorly functioning mechanism. Those habits may persist beyond
resolution of the pathology, and a period of voice therapy may be required. A specific group of
patients that would be included in this category are those with papilloma, requiring frequent
surgical removal over a period of years. The condition of the mucosal cover of the vocal folds
following numerous surgeries will be an important factor in determining the quality of voice
that will be possible.

Voice Therapy Associated with Neurological Problems

Neurologic problems affecting voice may be specific to the vocal folds or be a component of
a much broader problem. They may improve or be associated with progressive deterioration
of neural control. Depending on the nature of the disorder, the voice clinician’s role, as well
as specific therapy goals, will vary. In some cases, direct work on voice may be indicated. In
others, focus may be on tactics to improve speech intelligibility, or even to identify appro-
priate alternative means of communication. In some cases, attention may be usefully directed
to suprasegmental factors such as breath groups, prosody, rate, and marking for stress and
inflection. The potential effects of feedback modification techniques with selected neurologic
disorders have been reported by a number of authors. Hanson and Mettler (1980) described
the use of a small, wearable, delayed auditory feedback (DAF) device in the treatment of a
patient with progressive supranuclear palsy and severe hypokinetic dysarthria. The patient,
who was noted to have weak vocal intensity, demonstrated an increase of vocal intensity with
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the introduction of 100 milliseconds of DAF in both reading and counting aloud conditions,
and this increase was maintained during the follow-up testing after a 3-month period of daily
use of the device. More recently, Coutinho, Diaferia, Oliveira, and Behlau (2009) used DAF,
masking noise and amplification, respectively, with Parkinson patients and found immediate
improvements in voice and speech with masking but not with DAF or amplification.
Voice therapy can offer no cures when neuromotor disability is involved. However, through
voice therapy, patients may be able to learn to produce the best voice possible and to exert a
degree of voluntary control over the production of voice that may allow them to remain
communicatively functional in occupational and social settings for longer than expected (Ramig
et al., 1994; Rosenfield, 1987). The speech-language pathologist can also be helpful in assessing
the effects of medications on the patient’s voice and speech production. If functional verbal
communication is not a viable option, direct voice therapy becomes inappropriate, and the
goal then must be to provide the patient with a means of nonverbal communication.
The therapeutic process may be difficult for neurologically impaired patients with pro-
gressive disorders and also for their voice clinicians because of the constraints of the underlying
disorder and the gradual but inexorable deterioration in the patient’s condition. It is incumbent
on the clinician to recognize the limitations of the therapeutic approach and not to promise
what cannot be delivered but to make every effort to help the patient arrive at the best means
of communication possible for as long as possible.

Neuromuscular Disorders
Voice problems are but one of the dysarthric components of disability that may accompany
certain neuromuscular disorders. It is possible that the earliest symptoms of a neurological
condition may be exhibited in changes or aberrations of phonation. However, in progressively
debilitating neuromuscular diseases, the worsening of motor behavior and increased limitations
in many areas of function may become relatively more handicapping to the person. The speech-
language pathologist may be involved with these patients in working on not only phonatory
problems but also on other comorbid disorders such as dysarthria (articulation and resonation),
apraxia, aphasia, and dysphagia. One therapy protocol focusing on the voice has been developed
and shown to be effective for patients with Parkinson’s disease and the Parkinson plus syndrome
(Countryman, Ramig, & Pawlas, 1994; Ramig, Bonitati, Lemke, & Horii, 1994; Ramig &
Scherer, 1992; see “Voice Therapy Techniques” later in this chapter for further discussion).

Isolated Paralysis/Paresis of the Vocal Folds

Lesions or injury that affect CN X, or the recurrent or superior laryngeal nerves, will typically
have consequences for voice. In particular, the more abducted the position of the involved fold,
or the greater a glottal gap during voicing, the more affected voice is likely to be. Interestingly,
however, knowing the exact site of injury may not necessarily predict voice. It is also important to
note that lack of observed movement in a vocal fold is not equivalent to a lack of innervation.
In fact, some authors suggest that a truly “denervated” vocal fold is rare, whereas residual
innervation is often dysfunctional (Sulica & Myssiorek, 2004). It is also important to remember
that observed movement of the vocal folds does not rule out a neurological injury. For example,
if the superior laryngeal nerve is involved, patients may complain primarily about loss of pitch.
Questioned carefully, these individuals may also describe more frequent coughing or choking
when drinking liquids. Vocal fold movement and closure may appear appropriate in these
individuals, though stroboscopic imaging is likely to reveal vibratory asymmetries that have
implications for vibratory closed phases.
Data to support the efficacy of vocal rehabilitation are limited. When the etiology of the
paralysis is idiopathic, the literature suggests that either spontaneous recovery or increased
compensatory movement of the healthy fold occurs (Tucker, 1980). The major portion of such
recovery is believed to take place within 6 months of onset, although there are reports of recovery
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for up to a year postonset (Ward & Berci, 1982a). When voice therapy is undertaken during
that time period, and improvement occurs, separating the effects of therapy and spontaneous
recovery may be difficult. Several phonosurgical approaches designed to improve vocal function
are available. In general, these procedures are designed to either augment or position the
paralyzed fold in such a manner that the intact fold can achieve contact with it during phonation,
thereby minimizing air loss and improving vocal volume. However, if the involved vocal fold
is unable to contract, or to create resistance to subglottal pressure required for increasing vocal
intensity, loudness will likely be compromised even if closure between the folds is improved.
Our own studies comparing surgical and voice therapy treatment of patients with a unilat-
eral vocal fold paralysis have shown that both approaches can be effective in improving the voice.
Thirty-nine patients were studied, all with unilateral vocal fold paralysis or paresis. Twenty-one
patients received surgical treatment, and 18 received voice therapy as their major treatment.
Patients in both treatment groups showed improvement in voice quality and changes in several
measures of vocal fold function. These measurements are shown in Figure 10.1. Note that
the surgery patients tended to have higher pretreatment mean, peak, and leakage airflow rates,
suggesting greater severity of glottal incompetence than the therapy group. Leakage flow reflects
glottal incompetence, and both treatment approaches reduced the magnitude of leakage flow.
Not shown in the figure are open quotient data for both groups. For patients in the surgery
group, the open quotient was much greater prior to treatment than after treatment (0.67 vs.

FIGURE 10.1. Z scores for a group of patients with unilateral vocal fold paralysis on selected voice
measurements made before and after treatment. There were 15 men and 6 women in the surgery group
and 6 men and 12 women in the therapy group. The dotted line represents the critical value of Z to exceed
normal limits at the 0.05 level. Normal data were obtained from Holmberg, Hillman, and Perkell (1988) for
25 men and 20 women producing phonations at normal loudness and frequency levels.
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322 Understanding Voice Problems

0.54, men and women pooled). For patients in the therapy group, the open quotient was also
greater prior to treatment than after treatment (0.61 vs. 0.56). These results mean that the vocal
folds were open a greater proportion of the time during the vibratory cycles prior to treatment
for both groups but that those who underwent surgery had preoperative open quotients larger
than those patients who received therapy. After surgery, the open quotient decreased, suggesting
greater vocal fold adduction. Heuer et al. compared patient satisfaction in patients treated with
voice therapy alone or surgery; 80% of patients (21/26) felt their voices improved following,
on average, 3 sessions of therapy; 88% of patients (16/18) reported improvements in voice with
surgery. Objective assessments, that is, stroboscopic, acoustic, and aerodynamic assessments,
were not available for posttreatment, precluding more direct comparisons of surgery and therapy.

Spasmodic Dysphonia
Spasmodic dysphonia (SD), today considered a neurogenic disorder, is generally thought to be
relatively unaffected by voice therapy. The primary treatment modality at this time is Botox,
which weakens muscles involved and, in many patients, permits more fluent and less effortful
speech. Controversy continues about the etiology of this puzzling condition as well as about its
treatment. Historically, the strain/struggle voice of the patient with spasmodic dysphonia was
thought to be entirely psychologically based (Arnold, 1959). More recently, research points to
SD as being a disorder of central nervous system origin, and as a focal dystonia. The need for very
thorough differential diagnosis is well accepted in order to differentiate spasmodic dysphonia
from other neurogenically based disorders, as well as from those of psychogenic origin. A trial of
voice therapy is often recommended to determine whether relief can be obtained through that
approach. A trial of voice therapy is often diagnostically useful as well. Although voice therapy
is generally not an effective treatment modality for significantly modifying the symptoms of
true spasmodic dysphonia, it has been shown to increase the interval between Botox injections
(Murry & Woodson, 1995). Furthermore, voice therapy can be helpful in educating patients
about the disorder: What they can expect, and how to manage the variable vocal function they
will experience. Other surgical techniques used to treat spasmodic dysphonia, including selective
deinnervation–reinnervation procedures and procedures designed to physically separate the
vocal folds with a Type II thyroplasty (Chhetri, Mendelsohn, Blumin, & Berke, 2006; Sanuki,
Yumoto, Minoda, & Kodama, 2010), are not widely used at this time but may offer new
potential, in particular for patients who have not achieved satisfactory responses with botox.

Vocal and Laryngeal Tremor

Vocal and laryngeal tremor can occur independently, in association with other focal tremors
or progressive neurologic diseases or with spasmodic dysphonia. In some cases, tremor may be
perceptible primarily in certain speaking contexts, as on sustained vowel productions. In other
patients, inappropriate separation of the vocal folds during voicing may seriously compromise
speech. Patients’ attempts to compensate for tremor can also lead to apparent adaptive behaviors
that mimic the hyperadduction observed in adductor spasmodic dysphonia, making differential
diagnosis difficult. Based on anecdotal reports of reduced tremor in some patients undergoing
Botox treatment for spasmodic dysphonia, the drug is sometimes used in patients with tremor,
only. We have reported mixed but somewhat favorable results of botox delivered to the inter-
arytenoid and thyroarytenoid muscles in patients with both tremor and spasmodic dysphonia
(Kendall & Leonard, 2010). Barkmeier and colleagues (2010) have experienced success with
voice therapy designed to reduce syllable duration in a manner that reduces perceived tremor.

Therapy for Special Voice Problems

A number of voice problems that do not readily fit the above categories but that may appro-
priately require a period of vocal rehabilitation will be covered in this section.
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The Transsexual Voice

“It is important for the clinician to acquire an understanding of the life experiences of trans-
gendered clients in order to provide thoughtful, effective therapy” (Freidenberg, 2002, p. 1).
Freidenberg presents a complete tutorial on working with this population of patients, including
much information on therapeutic approaches.
The voice problem most immediately associated with a gender reassignment is that of
inappropriate pitch. In the case of change from a female to male, this problem is usually
resolved through the use of male hormones, which cause an increase in laryngeal mass and thus
lower fundamental frequency. However, no drugs are available to reduce the mass of the vocal
folds, so that a male to female change is not accompanied by elevation of pitch secondary to
hormone therapy. The incongruity of a masculine voice in a woman can present a significant
psychological barrier. Therapeutic attempts to elevate speaking fundamental frequency should
be undertaken with care, recognizing the physiological limits of the larynx. The use of breathy
phonation can be helpful in giving the illusion of a higher pitch without the risk of inviting
laryngeal trauma.
However, in addition to differences in pitch between the male and female voice, there are
differences in other speech patterns, habits, and mannerisms. This has been demonstrated ex-
perimentally by Coleman (1971, 1973, 1976) who found that female voices are still recognized
as female even when the pitch difference between male and female voice is removed. Some of
the difference between male and female voice lies in vowel quality in that the relative sizes of the
oral and pharyngeal cavities are different in the two sexes. Other differences include those of
stress, inflection, timing, and even choice and use of words and conversational style. Changes in
these areas will go far in feminizing a voice even in the presence of a low speaking fundamental
frequency. The actress Lauren Bacall presents a good model of someone whose voice is low in
pitch and yet whose style is entirely feminine. A program of voice therapy designed to make
the male-to-female change should include careful study of this and other models of feminine
low-pitched speech. The goal of therapy should be to make those changes that will be effective
in changing the overall image rather than to work on artificial changes, such as pitch change,
which may never become natural and may in fact court laryngeal problems.
The pitch of the voice is only one of many aspects of communication that differentiates
and distinguishes the sexes. Because we do not advocate artificial elevation of pitch that can be
potentially damaging, we recommend that some of the following areas be targeted for change:
1. Slight increase in breathiness of voice;
2. Using the concept of vocal effort, a lighter and softer voice may be encouraged by
reducing vocal effort;
3. Increased use of pitch variability rather than loudness to mark inflection, stress, and
alter rhythm of speech;
4. Target nonphonatory areas, such as conversational topics, conversational style, prag-
matic aspects of communication. In some instances, listening to other voices may pro-
vide the patient with insights into particular vocal characteristics that are more or less
appealing.

Voice Problems Due to Endocrine Disorders or Hormone Imbalance

Hypothyroidism
Hypothyroidism is a condition that can occur at any age. The symptoms may develop gradually
over a lengthy period of time. As a result, their effect may not be recognized until a critical
level of symptomatology has been reached. Change in the voice may be one such symptom.
Typically, the voice of the patient with hypothyroidism is hoarse and has gradually lowered
pitch due to increased mass (edema) of the vocal folds. Therefore, the diagnostician must be
alert to this as a possible diagnosis when vocal fold edema is noted and does not appear to be
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related to factors of vocal abuse. Referral back to the physical for appropriate testing should be
pursued, and voice therapy is not indicated.
Virilization
This term is used to refer to the increase in size and mass of the vocal folds that occurs in
women as the result of excessive secretion of the androgenic hormones or due to ingestion
of androgen-containing hormones in treatment of menopausal symptoms or other problems.
Damste (1967) described these changes and also showed them to be generally irreversible. Voice
therapy is contraindicated.
Menstruation, Pregnancy, and Birth Control Pill Use
Most of the voice-related negative effects of hormonal changes associated with the menstrual
cycle occur in the pre- or early-menstrual days. Excess loading of the vocal folds with fluid
changes their mass and thus may affect vibratory behavior. This is usually not problematic
for the average speaker but may present a problem for the professional singer. Submucosal
hemorrhages in the larynx are not uncommon. Diuretics should be avoided because they do
not free the protein-bound submucosal fluid (Sataloff, 1987b) and may have irritating drying
effects on airway tissues. Voice therapy should be limited to counseling/information/vocal
hygiene instruction. The clinician should be aware of the possibility of some subtle voice
changes in female patients during these time periods.
Pregnancy may also result in change in the voice. During pregnancy the woman’s en-
docrinological state undergoes great change. If a change in voice occurs, it is usually irreversible
(Sataloff, 1987b). There are no drugs available to counteract the normal physiological effects
of either the menstrual period or pregnancy, and voice therapy is of no value in these cases.
Voice clinicians must be aware, however, that such changes may be reported by patients.
A very small number of women appear to experience changes in the voice as a result of the
use of birth-control pills (Simkin, 1964). The quality and range of the voice may show these
effects. Once again, they are usually not noted by the average speaker but may create problems
for the singer. These voice changes are reversible when use of the pills is terminated.

Paradoxical Vocal Fold Motion or Vocal Fold (Cord) Dysfunction

This is a disability that can easily be mistaken for asthma and treated accordingly, even to
the point of tracheostomy. Whether due to improved diagnosis or an increased prevalence
of patients with difficulty, these patients are a rapidly growing segment of our own and other
reported clinical populations (Hicks, Brugman, & Katial, 2008; Murry & Sapienza, 2010). The
primary characteristic of paradoxical vocal fold motion disorder (PVFM) is not voice change,
but rather, obstruction of the airway with vocal fold closure throughout the respiratory cycle,
including inspiration. Because patients often present with some degree of respiratory distress
and its hallmarks, for example, inspiratory stridor, apparent inability to inhale, sometimes
momentary loss of consciousness, they are often seen in emergency rooms and immediately
treated symptomatically before a diagnosis is made. The symptoms mirror those of an asthma
attack or laryngospasm. Laryngospasms that wake the patient from sleep and are accompanied
by a burning sensation in the throat are now usually recognized to be caused by gastroesophageal
reflux and generally abate within a short time. However, they can be initially exceedingly
frightening, create a panic reaction, and may result in emergency medical attention.
PVFM has been referred to historically by as many as 35 names, which attests to the
confusing nature and presentation of the disorder (Gallivan & Andrianopoulos, 2004). A 1983
study by Christopher et al. described 5 patients 14 to 68 years of age, of whom 4 were men
and one woman, who presented with paroxysms of wheezing and dyspnea and had initially
been diagnosed as severe, uncontrollable asthmatics. However, the patients failed to respond
to standard therapy for asthma and, indeed, did not test positively for the expected symptoms
of asthma. All patients had a chronic history of repeated “attacks,” ranging from 1 to 13 years.
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One patient had undergone eight tracheotomy procedures. Laryngological examination during
the spasm revealed adduction of both true and ventricular folds during the full respiratory
cycle, and patients exhibited both inspiratory and expiratory stridor. Laryngeal function was
normal during asymptomatic periods. Inhalation of a mixture of helium (80%) and oxygen
(20%) was found to be effective in relieving at least the acute symptoms and frequently re-
sulted in symptom reduction even after cessation of the treatment. All patients were found to
have psychological problems, and all were referred for both speech therapy and psychological
counseling. Follow-up ranged from 3 to 21 months, and no patient had recurrence of the
symptoms. A variation of this type of PVFM, in which the primary abnormality is adduction
of the vocal folds during deep inspiration, and at least slight abduction on expiration, has also
been reported (Kellman & Leopold, 1982; Rogers & Stell, 1978). Patients described in these
studies demonstrated significant improvement in response to various interventions, including
speech therapy, intravenous injection of diazepam or of a placebo, hypnosis, and verbal support.
In 1995, Bless and Swift suggested a broader definition of PVFM as a “symptom with
multiple determinants.” According to these authors, etiology may include (a) hyperreactivity of
the airway, (b) neurogenic etiology of either central or peripheral origin, (c) psychological (has
not been ruled out), (d) pharmacological, or (e) other unspecified medical problems. Murry
et al. (2006) described a high prevalence of laryngopharyngeal reflux and reduced laryngeal
sensation in patients treated for PVFM. Vertigan et al. (2007) noted a strong association between
PVFM and chronic cough. Koufman and Block (2009) reported that most patients do have a
specific etiology for their symptoms, either inflammatory, neurological, neoplastic, iatrogenic,
or psychological, making accurate diagnosis critical to treatment success. Gracco et al. (1995)
reported another variant of the disorder induced by exercise. PVFM also occurs in children and
is perhaps increasing in this population segment (Sandage & Zelazny, 2004).
Consistent with this broadened view of etiology, current approaches to PVFM involve
thorough assessment and, often, a combination of medical, behavioral, and psychological ap-
proaches. Although voice symptoms ranging from aphonia to weak or hoarse voice may be
present, our own experience suggests that, in many, perhaps most, instances, voice is not com-
promised. Restoring the airway and eliminating recurrence of the symptoms are of primary
importance. Therapy, if not directly related to voice, can nonetheless be helpful in teaching
these patients specific breathing techniques that can minimize or resolve symptoms. Psycho-
logical treatment may also be indicated in some cases. Specific behavioral approaches will be
discussed in the next section of this chapter.

Voice Therapy Techniques: Associated Physiology and Indications for Use

It is important to recognize that the manner in which a therapeutic technique is used will vary
from clinician to clinician. Furthermore, with experience each clinician will develop and perfect
those techniques found to be most useful and effective. Clinicians bring their own personalities
and approaches to the clinical process, and the techniques that fit that style and produce a level
of comfort and confidence are the ones that are most likely to be adopted and well used.
It is the philosophy of this book that an understanding of laryngeal anatomy and phonatory
physiology is basic to being a skilled voice clinician. Therapeutic techniques are only valid when
they are used knowledgeably. The clinician must develop the knowledge base and the skill to
determine what therapeutic approaches make sense for the individual patient. Indeed, a skilled
clinician may develop a technique never tried before but something that makes sense for a given
person, and for which there is an underlying rationale. Examples of the application of specific
strategies in three patients are provided on the DVD accompanying this text. A description of
therapy in each case is included in the appendix for this chapter.
There are few techniques that are specific to a single voice disorder because there is so
much similarity in laryngeal physiology across many disorders. For example, patients who
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misuse their voices and those who traumatize them to the point of creating mucosal changes
may be engaging in the same inappropriate vocal behaviors from a physiological perspective.
Thus, many of the same therapeutic techniques may be appropriate for both. The specific type
of misuse or abuse (i.e., talking too much vs. talking too loudly) will differ from patient to
patient, and that issue must be addressed individually. However, the means of changing those
patterns may be similar across patients.
A major lack in voice research has been documentation of the efficacy of therapeutic tech-
niques and outcome data. This lack, although decried by many (Johnson, 1985; Ludlow, 1981;
Moore, 1977; Perkins, 1985; Reed, 1980), is not easily corrected. Problems of terminology,
of definition, of qualitative and quantitative assessment procedures, and of well-established
normative standards (as discussed previously) plague the researcher who wishes to address the
issue. Not surprisingly, wide variety is found in outcome measures used to assess treatment
effects. Brewer and McCall (1974) used endoscopy to demonstrate visible changes in laryngeal
physiology as patients were instructed in a therapeutic technique. Casper, Brewer, and Conture
(1981) reported on computer-assisted measurement of specific intrasubject changes in laryn-
geal physiology, visible on fiberoptic images, which were felt to be the result of therapeutic
intervention. The procedure, although workable, was fairly time consuming, and the results
could be interpreted only relative to each individual’s performance. Recently, Narayana et al.
(2010) described neural changes associated with the effects of the Lee Silverman voice therapy
approach in Parkinson patients. Increasingly, tools such as the Voice Handicap Index and the
Voice Related Quality-of-Life scale are being used to assess patients’ own estimates of change
associated with voice therapy (Berg, Hapner, Klein, & John, 2008; MacKenzie, Millar, Wilson,
Sellars, & Deary, 2001). Voerman et al. (2009) used patient and professional assessments of
therapy effects in patients undergoing treatment for nonorganic voice disorders. Using these
criteria, 80% (100/116) of patients demonstrated improvement or cure, most with only one
session of therapy. Cohen and Garrett (2007) reported results of voice therapy in patients with
polyps or cysts. The outcome measures were symptom resolution, or persistence of symptoms
that eventually led to surgery. Reportedly, 49.1% of a total of 57 patients achieved resolution
with therapy alone. Of further interest, patients with translucent polyps responded with greater
success than patients with hemorrhagic, fibrotic, or hyaline polyps.
Specific vocal parameters, that is, acoustic, perceptual, and aerodynamic, which would
objectively reflect improvement of voice have been proposed or examined; however, wide
generalization of any set of measures has been elusive (Maryn, Roy, De Bodt, Van Cauwenberge,
& Corthais, 2009; Mehta & Hillman, 2008; Kempster, Gerratt, Verdolini Abbott, Barkmeier-
Kraemer, & Hillman, 2009). In the remainder of this chapter, a number of therapy techniques in
current use will be described. For each, a description of how the technique is performed, as well
as at least a theoretical rationale of why it may work, is included. The authors want to caution
again that any technique is only as good as the clinician who is making use of it. Clinicians are
obligated to apply any technique as appropriately as possible and to continue to question its
efficacy and search for ways to demonstrate it. It is not the intent of the authors to suggest that
a single technique need be selected in any given circumstance. Quite the opposite is often the
case, and several techniques may be used concurrently or at different points in a therapy plan.
There is no particular meaning to be assigned to the order in which these techniques are
presented. There is also no intent to make this an all-inclusive list. Indeed, most clinicians adapt
procedures to fit their personal styles and develop unique ones, as do most voice coaches. Voice
therapy that is approached as a recipe, that is, by just following a series of steps as indicated by
the directions, is likely to be ineffective and, frankly, unsatisfying for both clinician and patient.
The challenge is to be able to think through a problem in such a way that the clinician can
select, modify, or devise techniques based on an understanding of the type of vocal behavior
desired and behaviors currently in use. No single technique will be equally effective with all
individuals.
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Breathy Phonation: The Confidential Voice

We have found this technique to be widely appropriate and easy for patients, for example,
those who demonstrate excessive loudness as a component of their disorder, to learn and to
use, and it has resulted in clinical success. Producing voice is a holistic activity that is usually
accomplished without conscious attention to pitch, loudness, variability, or other aspects of
voice production. In light of this it seems reasonable to think that a therapy technique that can
function in a holistic manner to accomplish its goals should be beneficial and easy for patients
to adopt. The use of breathy phonation is such a technique (Casper, 1993). The patient has
only to concentrate on making the voice very breathy, and, in so doing, he or she accomplishes
a number of other desirable goals. These include reduction of loudness, reduction of rate (no
more than 5–6 syllables per breath), reduction of hyperfunction, and a beginning awareness of
allowing the expiratory airflow do the work of producing sound.
It is important to stress at the outset that breathy voice is being recommended here as
a technique to be used for a circumscribed period of time during therapy and not as the end
product of therapy. The voice is described to patients as being the softest intensity they can
produce, much like the voice one would use to exchange a confidence with a friend when one
does not wish others nearby to hear. It is a confidential voice. It differs from whisper in that
some voicing is present. The very breathy quality of the voice is its hallmark and differentiates
it from a voice just reduced in intensity.
Instruction to talk in a confidential voice and the model of that voice presented by the
clinician are often all that is necessary for the patient to understand and to be able to produce
the voice. However, when that is not sufficient, it is often helpful to start vocalization activities
with other techniques such as the sigh and the yawn/sigh. In both of these the focus is on
producing easy, unimpeded airflow and breathy voicing without stress.
There are several undesirable behaviors that may accompany a patient’s use of breathy
phonation that are very easily resolved if the clinician is alert. It is not enough for the voice
just to be lowered in intensity; it must be breathy. The breathiness must be marked by ease of
airflow without evidence of pushing or forcing air. The phonation that is produced must be
“well focused” in that pitch should not be lowered, nor should mouth opening be reduced. It
will not and, indeed, cannot be a resonant voice at this stage.
The patient is instructed to use this voice for all speaking and is forewarned that it will be
inaudible in any noisy environment. All loud talking is thus eliminated temporarily. It is also
important to instruct the patient that fewer words per breath will be possible because of the
increased expenditure of air. Furthermore, because one effect of the increased airflow may be a
drying of the mucosa, we suggest that the patient increase fluid intake. This technique is appro-
priate for patients who need to eliminate vocal abuse or misuse. It is helpful as part of a vocal
hygiene program whenever a period of modified voice rest or reduction of voice use is indicated.
Verdolini-Marston and her colleagues (Verdolini-Marston, Burke, Lessac, Glaze, & Cald-
well, 1995) investigated the efficacy of the confidential voice therapy technique with five female
patients with vocal fold nodules. The therapy was provided by 2 clinicians over a 2-week pe-
riod. Pre- and post-treatment measurements of phonatory effort, auditory perceptual ratings of
voice disorder severity, and visual ratings of vocal fold characteristics seen in videostroboscopic
recordings were obtained. An additional five patients with nodules comprised the control group.
Many patients showed improvement after the 2-week therapy period, whereas there was little
improvement of voice production in the control group. Most therapy patients had a decrease
of phonatory effort and a decrease in the rated severity of dysphonia. Four of the five patients
in the therapy group showed visible changes of the vocal folds. These data suggest that the
confidential voice therapy approach can be effective in reducing vocal trauma and result in
better voice production.
Another interesting finding from this study was the report that continued use of the
therapeutic techniques after therapy had ended contributed to improved voice performance.
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Patient compliance and willingness to use the new form of voice production in routine voice
usage appear to be predictive of long-term voice improvement.
Rationale: We have observed laryngeal physiology endoscopically as we have asked patients
and normal speakers to use this confidential voice and have noted the desired effect (Casper, Colton,
Brewer, & Woo, 1989). The glottis remains very slightly open, thus reducing the force of contact
and of medial compression of the vocal folds. The larynx seems to remain vertically at about the
resting level. There is an absence of any appearance of laryngeal tightness or squeezing, and the closed
phase of the glottal cycle is reduced. In some patients there may be a tendency to produce breathiness
with a posterior glottal chink and “Y” appearance more characteristic of whisper. This is not as
desirable as incomplete glottal closure along the full length of the folds and may be indicative of
a greater-than-necessary degree of tension or strain in producing the phonation. In such cases, the
use of visual biofeedback with the flexible endoscope in place can be very effective. Thus, with one
maneuver the patient is provided with a type of voice production that eliminates trauma yet allows
continued voice use, albeit different and reduced. It is a holistic approach that does not require that
the act of speaking be broken down into its component parts, with each addressed separately and
then put back together. We have also found it rather simple for patients to move gradually from the
breathy, confidential voice to increased voicing without returning to previous habits.
After approximately 4 to 6 sessions most patients are ready to begin reducing vocal breathiness and
increasing intensity. The previous vocal hoarseness should not be present. Full voicing is reintroduced
gradually for certain situations or certain amounts of time. During this time it is appropriate to
introduce the concepts of vocal resonance and vocal focus. If the clear vocal quality is maintained for
the next 2 weeks, therapy can be terminated or reduced in terms of frequency. Revisualization of the
larynx and other posttherapy testing (i.e., QOL) should be completed.

Sigh, Aspirate Initiation, Easy Initiation of Phonation

These three techniques are combined under one heading because they are variations on a theme
sharing a common rationale. For the sigh, the patient is instructed to produce the most relaxed,
effortless, natural sigh possible. Whether or not voicing is present does not matter initially,
but as this is practiced it is hoped that some voicing emerges naturally and easily. In a natural,
spontaneous sigh it is not uncommon to release some air audibly before the actual voicing
begins, then to produce just minimal voicing in terms of loudness and duration, and to finish
the sigh with audible expiration of the rest of the breath supply. It is important that the patient
not hold the breath after the inspiration. There must be a continuous flow from inhalation
through exhalation; otherwise, there is a tendency to close the glottis tightly as the breath is
held.
From the sigh it is easy to have the patient practice aspirate initiation of voicing, using
words that begin with an /h/. This should be done in a slightly exaggerated manner so that the
/h/ is held and the voicing is initiated much as in the sigh and with a breathy quality. As the
patient becomes adept at this maneuver, it is possible to omit the actual production of the /h/
yet continue the effortless gliding into easy initiation of phonation.
Rationale: These techniques reduce laryngeal and vocal tract tensions, reduce the force of vocal
fold contact and of medial compression, teach easy coordination of airflow and phonation, counteract
traumatic habits of tension and hard glottal attack, and foster resting level laryngeal posture. They
may be very helpful for patients who have difficulty in learning to use a breathy voice for general
conversation and appear to need more direct step-by-step work to learn to reduce tensions. In a
fiberoptic and stroboscopic study of aspirate initiation of phonation, Casper et al. (1989) observed
the expected physiological characteristics described previously.

Yawn/Sigh
The patient is instructed to simulate a real yawn, or if possible, to actually trigger a real yawn.
The yawn is completed with a sigh, making sure to allow air to be released in a relaxed way.
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This is not always easy for patients to do. We tend to be socialized into hiding and stifling
public yawns. It is sometimes helpful to instruct the patient to open the mouth very wide, pull
the tongue back, and inhale long and deeply. Initiation of voicing should be carried out with
this same oral posture, with a gradual closing of the mouth as the yawn and sigh progress. It is
well to suggest that patients become aware of natural yawns and try to concentrate on how they
feel when they occur spontaneously. As the patient learns the technique and can identify the
tension reduction, a gradual shaping of the yawn/sigh into production of words, then phrases,
and finally sentences should proceed slowly. The yawn should be gradually eliminated.
Rationale: In a true vegetative yawn, the larynx lowers dramatically (Casper et al., 1989). This
change can be observed fiberoptically. The physiology of a yawn is incompatible with the excessive
laryngeal tensions that many patients exhibit. Easy, natural airflow and phonation are fostered.
The intent is to eliminate tight initiation and maintenance of phonation and to reduce laryngeal
tensions. Individuals who have adopted hyperfunctional habits of voice production tend to have a
high laryngeal posture. They often complain of pain in the extrinsic laryngeal muscles. The yawn/sigh
maneuver, which lowers laryngeal posture, serves to “stretch” those muscles, providing relief from the
tightness. This is a further benefit of the technique.

Post Botox Injectoin Therapy (Spasmodic Dysphonia)

Following successful injection, patients often experience a brief period of breathy voice. During
that time there is a natural desire to “push” the voice so as to get the most voicing possible. The
thrust of voice treatment, which should be restricted to three or four sessions, is to counter-
act this tendency. Easy onset of phonation is taught using techniques described earlier. The
patient must be taught to concentrate on the airflow, specifically the initiation and gentle
maintenance of that flow. Pushing for increased loudness is discouraged. Indeed, we encourage
the patient to “give in” to the soft voice and learn from it. The aspects of voicing on which they
can focus are the ease of producing it (albeit quietly), the slowed rate of speech, the shorter
phrase groups. The fact that the voice will get louder with time and without any effort on their
part is stressed. However, we also urge them to maintain some of the new voice behaviors they
have learned during the breathy period.

Trill
The trill is a sound made by the tongue tip making contact with the alveolar ridge and oscillating
rapidly as sound is produced. The sound can be described as the trilled /r/ heard in many
languages, including Spanish. The trill can also be made using the lips and allowing them to
oscillate rapidly as voice is produced. Both of these trills can also be produced in a voiceless
manner but are not beneficial to voice production that way. When used as a vocal exercise the
sound is essential and the patient is asked to sustain the trill. This is an exercise used by many
singers to “warm up” the voice. Very rapid and strong laryngeal vibrations can be felt if the
fingers are placed on the larynx during production of the trill.
We have found the trill to be very useful and productive with a variety of disordered
voices. We began using it with patients whose vocal folds were scarred postoperatively. The
results seemed to be much better than any we had obtained with this population using other
techniques. Subsequently, we have used it with patients who present with a variety of disorders,
particularly of the hypofunctional type.
Patients are first instructed in production of the sustained trill at a comfortable pitch and
loudness. Pitch variation is then introduced by sustaining the trilled sound at various pitches
and then by gliding the trill through a range of pitches in both descending and ascending glides.
We find it helpful as therapy progresses to extend the trilled sound into voicing without trill.
This is done by instructing the patient to start the trill and smoothly transition into a prolonged
vowel with no break in phonation or change in pitch. This can be done with a variety of vowel
sounds and at various pitches as well. And finally, the sound is shaped into speech. Although
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we extend practice beyond the trill itself, we also instruct patients to continue practice of the
trill as such and to use it as a warm-up exercise at the start of the day and prior to any extended
speaking. During therapy, patients are instructed to practice the trill for short periods of time
as often as possible throughout the day. This is particularly important for patients with scarred,
stiff vocal folds and may be required over a lengthy time period. These exercise protocols may
be done with either the lip or tongue trill. Some individuals are incapable of producing the
tongue trill, and it does not warrant the use of valuable therapy time to try to teach that. It has
also been our experience that some older patients may have difficulty with this task.
Rationale: The trill appears to “jump start” the vibratory behavior of the vocal folds. It is claimed
that production of the trill balances resonance, fosters normal laryngeal tension by equalizing the aero-
dynamic and the myoelastic forces, and enhances coordination of respiration/phonation/articulation
(Behlau & Pontes, 1990). McGowan (1992) described some work on modeling the tongue tip trill
based on physiological data and modeling experiments. Basically, the tongue tip acts like a springed
trap door that creates pressure differences between the outside air and the cavity behind the tip con-
striction. These pressure differences oscillate to produce the desired effect. What happens in the cavity
behind the constriction is dynamic with oscillatory changes of air pressure and air-volume velocity.
There appear to be oscillations on the pharyngeal walls creating small-volume velocity changes of
the air passing through them. These pharyngeal-wall variations may be important also for vocal
fold oscillation because they could create a greater pressure difference across the vocal folds producing
oscillation. McGowan also suggests that the subglottal air pressures during the production of tongue
trills may be greater than during normal phonation, again creating a greater force for vocal fold
oscillation. There are little research data to substantiate these claims, but clinical experience suggests
that the technique is a very useful one that is capable of eliciting improved voice in many patients. In
the patient with postoperative scarring of the vocal folds, the increased stiffness of the cover interferes
with vibratory behavior. The trill appears to have the potential to reduce the effect of the stiffness
probably because of the forceful but healthy vibratory behavior.

Range Expansion and Stabilization Techniques (REST) and Exercises

These exercises, in our experience, are useful in situations where a patient’s vocal space, as
described earlier in this chapter, has been significantly reduced, for one or a number of reasons.
For example, these exercises may be appropriate when the clinician is attempting to eliminate
maladaptive behaviors and implement more appropriate behaviors in an individual patient.
They may be equally helpful in efforts to optimize vocal function following surgery, or when
a physical limitation interferes with vocal function, for example, paresis, scarring, and glottic
incompetence. We typically characterize the exercises to patients as “physical therapy” for the
voice. Preparatory to implementing the exercise protocol, voice produced in the most optimal
manner possible must be identified and produced consistently by the patient. Often, this voice
is only possible over a very limited range of frequencies or intensities, perhaps only for a
single sustained sound. The exercises are designed to expand the optimal production over an
increasingly larger range, including both vocal parameters and phonetic contexts, eventually
providing a basis for conversational situations.
Three specific tasks comprise the exercise protocol. First, frequency glides are introduced.
The patient is asked, on a vowel sound, to glide from a comfortable pitch to a pitch approxi-
mately one-third of an octave higher, hold the higher tone briefly, and then relax down to the
starting tone. Having exhaled to resting expiratory level, the patient is asked to pause for 1 to
2 seconds and to then repeat the task 2 to 3 more times. Emphasis is on gliding, not jumping
or skipping, from the lower pitch to the higher and back, and is described to the patient as a
“stretching” exercise. If endoscopic feedback is available, the stretching maneuver can be ob-
served by the patient. Once completed for the small interval, the patient can (as possible) glide
from the lower tone over one-fifth of an octave and then over an octave interval.
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The second exercise, referred to as “swell tones,” requires the patient to again start at the
optimal pitch (best voice identified). This time, the idea is to stay at this pitch (to the extent
possible) and go from soft to loud, holding the tone only 3 to 4 seconds, and then relaxing
to resting expiratory level. Once the patient is able to increase loudness while maintaining the
same pitch level, focus is on increasing loudness by simply exhaling/relaxing. That is, loudness
is not increased by straining, forcing, or using structures other than the vocal folds, but simply,
by increasing resistance in the true vocal folds. Endoscopic information is useful in ensuring, to
both patient and clinician, that the task is being performed correctly. The exercise is described as
a “resistance” exercise. This task can be difficult for some patients to learn, but in our experience,
is worth the effort. Finally, patients are asked simply to select 3 to 4 pitches that are comfortable
for them (possibly only one, at first) and to control expiratory flow carefully in an attempt to
sustain the sound for as long as possible. This exercise is described as an “endurance” task.
Rationale: REST exercises, as noted, are described to patients as stretching, resistance, and
endurance exercises, and as a kind of physical therapy for the voice. The maneuvers involved require
the vocal folds, in a very structured manner, to engage in behaviors basic to voice production, that
is, pitch change, loudness change, and integration of airflow with phonation. If an “optimal” voice
production can be elicited or identified, even on a single sound produced at a single intensity or
frequency level, it can serve as a basis for systematically expanding vocal space, hopefully, to one that
is consistent with normal voice use.

Chewing
The act of chewing as a therapy technique was described by Froeschels in 1952. The technique
requires that the patient practice the motions of chewing in an exaggerated manner and then
sequentially, over time, add voicing, random sounds, words, phrases, sentences, and conver-
sation while gradually reducing the degree of exaggeration of the mouth movements. As the
technique is described, it is very important to help the patient imitate the chewing act quite
exactly. This must involve constant movement of the tongue. Exaggeration of the act requires
that the mouth be open while chewing. The resulting sounds produced when the activity is
carried out correctly should be very variable. If the sound produced tends to be a repetitive,
unchanging “yam yam,” the chewing is being done with inadequate tongue movement. It has
been our experience that it is often difficult for patients to learn to do this chewing motion
correctly. As with yawning, we have been socialized into chewing as unobtrusively as possible
and certainly with the mouth closed. If this technique is to be used, the clinician must be adept
at, and comfortable with, modeling it for the patient. It is often helpful for the clinician to do
the activity along with the patient, thereby reducing self-consciousness. The use of chewable
substances can help the patient identify the components of the chewing act. It then becomes
somewhat easier to carry out that activity based on recall and imagery and without the actual
substance in the mouth. (It is not a good idea for the clinician to provide chewable material.
Instead, the clinician should suggest that the patient bring crackers, gum, or other chewable
foods to the therapy session.) Each step of chewing as a therapy approach must be mastered
before the next level is introduced. Thus, the patient must learn to chew in the most exaggerated
manner while producing voicing and random sounds before being asked to practice words. It
is important to realize that articulatory clarity will be reduced in the early stages of using this
technique as the focus remains on the chewing motion. Use of words and phrases that begin
with vowels may be the easiest to begin practice. As the patient progresses and longer utterances
are introduced, the chewing motions are almost eliminated, but excess tensions associated with
phonation should not be evident.
Rationale: In adopting this technique, Froeschels sought a natural vegetative movement onto
which phonation could be added without changing the totality of the act and without adding tensions
or other negative behaviors the patient had habituated into the speaking act. The chewing motion
has a tendency to release excess tensions in the vocal tract and laryngeal area and, when done correctly,
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encourages mouth opening and reduction of mandibular tensions. These behaviors in turn foster easy
onset of phonation without making that a specific focus of attention.

Chant Talk
The name of this technique describes a manner of speaking that is a cross between speaking
and singing or, from the singer’s point of view, a form of singing that is a cross between singing
and speaking. We tend to think of it as having limited frequency variability while retaining the
flow of song. It can be used as a therapeutic technique in a number of different ways. Most
simply, the patient can be asked to chant an utterance rather than speak it. If this is effective in
eliciting effortless phonation of a good quality, the technique can be extended in practice with
gradual reduction of the sing-song quality of the chant. If a particular “voice placement” or
“focus” is sought, this chanting can be one of a variety of ways of finding that focus. For example,
using Cooper’s “um-hum” technique (1973; see also the “um-hum” therapy technique described
later), the patient may be asked to sustain that sound and chant the counting of numbers, or
series of words or a sentence. It may be helpful for some patients to locate and identify the
desired vocal sound through this chanting approach. When the sound can be produced at
will, therapy moves on through chanting of syllables, words, sentences. When that is mastered,
practice turns to reducing the chanting quality while maintaining the vocal focus. This process
may require several sessions.
Rationale: The chanting of an utterance encourages an easy flow of phonation, reducing
the tendency toward hard glottal attack and increased force of vocal fold contact. Voicing flows
continuously rather than the start/stop characteristic of connected speech. There may be some increased
proprioceptive feedback as vibrations are felt through the nose and cheek areas, thus helping the patient
to reduce focus on the larynx. It is also felt that if the voice is produced in this manner, there is usually
a reduction in laryngeal and vocal tract tensions. Because chanting differs from talking and is usually
a new way for patients to produce voice, it may be easier for them to alter voice production through
this activity than to attempt to do so in speaking, wherein the habits are entrenched.

Hum and Nasal Consonants

This is another technique designed to teach easy voice production through a “natural” approach.
The patient is asked to produce a hum and to be able to feel the resonance of that hum in
the nose and cheeks. The pitch of the voice is generally not of direct concern, although it may
seem to change as the patient searches for an easily produced, fully resonant sound. The hum
is sustained, and the patient practices this until the target sound is produced without difficulty.
It is often instructive to then ask the patient to fully lower and then elevate the mandible,
keeping the lips closed while sustaining the hum. This results in an almost palpable forward
movement of the focus of the voice, with a tickling sensation often being reported around the
lips and along the alveolar ridge of the palate. One of the authors was instructed by a voice
coach to “hook” the sound in the back of the throat in order to master this kind of voice
quality. The sound used for practice was the /ng/. Bear in mind that the sound being sought
is not a nasal sound but rather a sound that might best be described as the “twang” that is
typical of Country Western singing (Colton & Estill, 1981). Gradually the production of these
sounds is shaped into speech by first using nonsense syllables and words heavily loaded with
the nasal consonants. Although the early practice of this technique may result in greater nasal
resonance than is desirable, the nasality is temporary and normalizes as speech is introduced.
This technique can easily be combined with the chant-talk technique.
Rationale: As described in the rationale for chant-talk, the act of humming is different from
speaking and, thus, may not be encumbered with undesirable habituated behaviors. A hum encourages
easy initiation of phonation and provides proprioceptive feedback of nasal and facial vibration, thus
refocusing the patient’s preoccupation with the laryngeal area. The continuant nasal consonant
promotes ease of sustained phonation by reducing the pressure required for phonation initiation
(inclusion of the nasal cavity to the vocal tract is associated with a pressure drop in the supraglottic
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airway). It can easily be coordinated with the idea of smooth airflow from inhalation through
exhalation. The “twang” sound also elicits a mode of vocal fold vibration that produces a greater
number of harmonics and, thus, a richer sound (Colton & Estill, 1981). Another positive feature
of the nasal consonant “m” is that the patient can focus on the “buzz” or vibration present in the
lips when it is produced appropriately. In our experience, this can serve to shift the focus away from
what’s happening at the larynx and can also serve as a “carrier” for a following vowel sound. That is,
for example, the patient is asked to sustain “m” and, when he hears the sound and feels the vibration
in the lips or nose, it transitions into a vowel sound, that is, “mmmmmme” or “mmmmmma.”

Vocal Tract Semiocclusion and Elongation (Impedance Matching)

A number of voice therapies, including many described here, specify the use of particular vowel
and consonant sounds as facilitators for “easy, economical, effortless, resonant” voice quality.
Bilateral plosives, anterior fricatives and semivowels, trills, humming and nasals are fre-
quently described as being particularly useful. Resonant voice therapy emphasizes the sensory
feedback available from sounds with an “anterior focus.” Tubes, referred to as “resonance tubes”
and straws have been used to elongate the vocal tract during phonatory tasks, and again, have
been reported to be beneficial in producing easy, effortless phonation (Bele, 2005). The use of
these stimuli and devices is not a coincidence, but has come about because clinicians and voice
coaches, as well as patients and students, have found from experience that they are beneficial.
As investigators have become increasingly interested in the topic, models and experiments have
provided greater insights into why constrictions in the vocal tract at strategic points, for exam-
ple, at the lips or with the tongue positioned for an anterior fricative, and in the area just above
the vocal folds, can contribute to greater economy in voice production. Typically, these tasks
require individuals to sustain phonation of selected stimuli, and to focus on coordination of
respiration and phonation, ease of production and of sensations associated with these produc-
tions. The strategies have been termed “impedance matching,” referring to the optimization of
impedance in the vocal tract with impedance of the vibratory source.
Rationale: We think about articulatory postures, or vocal tract shape, as important for accurate
speech production and perception. Constrictions in the vocal tract determine resonance characteristics
of the tract that are manifest in formant locations of the tract’s output. As tract shape changes,
resonance locations and formants also change, allowing for differentiation of speech sounds. For
example, a speaker can maintain the same fundamental frequency, or even whisper, and say ‘ee’, ‘oo’
or ‘ah’. The vowels are perceived accurately as long as the vocal tract resonances unique to each shape
produce a unique set of formant frequencies appropriate for each vowel. But there are also interesting
relationships between formants, determined primarily by vocal tract shape, and the fundamental
frequency and its harmonics, determined primarily by the vibratory source. For example, when the
fundamental frequency (F0 ), and its first or second harmonics (2F0 and 3F0 ), are below the first,
or lowest formant frequency (F1 ), the amplitude of vocal vibration, and amount of glottal flow, will
increase, leading to an increase in the overall power radiated at the mouth opening (Titze, 2004).
Voicing tasks that permit this circumstance are likely to be sustained sounds with a low F1, or sounds
produced with an elongated tract that shift all formants to lower frequencies. Elongation of the tract
with a tube may actually lower formants to such an extent that F0 and perhaps the first or second
harmonic may be just below F2 , rather than F1 , but with similar benefit.
A number of investigators have defined the process of optimizing these interactions as
“impedance matching” between the vocal tract and vibratory source (Story, Laukkanen and
Titze, 2000; Titze and Story, 1997; Bele, 2005). Acoustic impedance is defined as the ratio
between pressure and flow. When the supraglottal vocal tract is more constricted, both the mean
supraglottal pressure and the mean intraglottal pressure increase. This causes the vocal folds to
be displaced slightly laterally, cushioning the impact stress when they contact each other during
vibration (Laukannanen, Titze, Hoffman and Finnegan, 2008). Situations in which the vocal
tract is elongated, as with a tube or straw, or constricted in other ways that lower formants,
have been shown to produce other beneficial results, including a lowering of the larynx and
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relaxation of both laryngeal and pharyngeal musculature (Bele, 2005). Some authors have
reported favorable changes in thyroarytenoid muscle (TA) activity associated with impedance
matching (Laukkanen, Titze, Hoffman and Finnegan, 2008). That is, as intraglottal pressure
increases, relatively more thryoarytneoid muscle (TA) activity compared to cricothyroid muscle
(CT) activity occurs (lateral cricoarytenoid muscle held constant). Increased TA activity causes
the glottis to become more rectangular in shape, and thickens the vocal folds, both of which can
lower the phonation threshold pressure, i.e. minimum pressure required to initiate and maintain
phonation. The ratio of oral radiated power to aerodynamic power, which defines glottal
economy and efficiency, also increases in this circumstance. Titze (2004) has demonstrated
increases in peak glottal area and flow, and maximum flow declination rate with impedance
matching, i.e. F0 and first one or two harmonics less than F1. According to Titze, such changes
can account for an increase in acoustic power radiated at the mouth opening of several dB.
Resulting vibration in facial tissues is likely to be pronounced, providing valuable sensation
to the speaker striving for optimal vocal output. Rothenberg (1981) notes that increasing
maximum flow declination rate, which involves slower opening of the vocal folds and more
rapid closing within a vibratory cycle, adds to the amount of high frequency energy generated
at the instant of vocal fold closure.
Acoustic impedance describes both the resistance and reactance of wave motion, in the
case of voice production, in the air. The resistance component uses up energy, that is, if flow is
impeded, some energy is lost. The reactance component is more difficult to conceptualize, but
refers to energy that is not lost, but stored due to inertia in the system. If the reactance is positive,
referred to as “inertance,” the acoustic load of voicing, and thus vibration, is made easier. Titze
(2004) notes that the benefits of impedance matching occur under this circumstance, i.e. an
inertive vocal tract. Strategies that seek to lower F1, by either constricting or lengthening the
vocal tract, and to keep F0 , 2F0 and perhaps 3F0 just under F1, are used routinely by some
vocal pedagogists, and elements of impedance matching are common to many voice therapies.
Their utility, however, has not been demonstrated in a large variety of patient groups.

Vocal Function Exercise Program

Stemple, Glaze, and Gerdeman (1995) propose a specific program of exercises that are reported
to be efficacious in the treatment of various voice disorders. Specifically, patients are instructed
in four exercises and required to practice them several times a day: (a) sustaining the vowel /ee/
on the note F above middle C for women and below middle C for men softly and for as long
as the person is capable of sustaining the voiceless /s/; (b) producing the word “knoll” starting
on a high pitch and allowing the pitch to glide down while still holding on to the word; (c) the
same as (b) but in reverse, starting low and gliding high; and (d) sustaining the vowel /o/ softly
on the following notes: C, D, E, F, and G beginning on middle C for women and an octave
lower for men.
Rationale: The authors state that many etiological factors may be responsible for weakening,
straining, and creating imbalance of the laryngeal mechanism. These exercises are felt to address these
areas and provide a systematic exercise program to restore balance, strength, and ease of phonation.

Digital Manipulation, Pressure, and Massage

Aronson (1985) has described a technique that involves direct physical manipulation and
massage of the laryngeal area. The clinician must identify the tips of the hyoid bone and exert
light pressure in a circular motion in that area. The clinician then moves the fingers into the
thyrohyoid space and carries out the circular motion massage, moving posteriorly from the
thyroid notch area. The massage is then done on the posterior borders of the thyroid cartilage.
With the fingers along the superior border of the thyroid cartilage, the clinician begins to gently
exert pressure in a downward manner in order to move the larynx down. There should be an
increase in the thyrohyoid space. During these maneuvers the patient is asked to phonate vowels.
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When a positive change in the voice is noted (clearer quality and lowered pitch), the focus shifts
to the production of that voice with, and then without, the manipulation. This entire activity
needs to be carried out with care and with recognition that some pain might result. Patients
must be reassured that the pain is temporary and is like any muscular pain associated with
excessive tension and its reduction through direct manipulation and massage. According to
Aronson, this technique may be effective in eliciting normal voice in a single therapy session
in cases of dysphonia due to increased musculoskeletal tensions. However, when the condition
has been long standing, a longer course of treatment using this technique may be necessary.
Roy has described extensively the use of this technique and its efficacy (Roy, 1994; Roy &
Leeper, 1993; Roy, Nissen, Dromey, & Sapir, 2009; Roy, Tasko, & Harvey, 1995; Tasko, Roy, &
Harvey, 1994) and confirms the finding that many patients are able to achieve normal voice in a
single therapy session. The diagnoses of the patients so treated fall primarily into two categories,
that is, musculoskeletal tension and functional or psychogenic disorder. He states that 88%
of the patients in his study population reported pain on palpation of the laryngeal area often
radiating to the ear. His description of the technique begins with palpation of the laryngeal
area to determine the degree and location of tension and pain, the mobility of the larynx in
the vertical dimension, and the extent of laryngeal elevation. The technique is otherwise as
described earlier.
Rationale: This technique is based on the need to reduce “cramping” in the extrinsic and
intrinsic laryngeal muscles, which is believed to be the cause of dysphonia in many patients. The
massaging of muscles induces relaxation, and the technique promotes a lowered laryngeal position,
permitting ease of phonation, and relieves pain of muscle tension. In using this technique, it is
particularly important that the clinician understand and be able to identify the specific disturbance
of phonatory physiology exhibited by a patient. Many but not all voice patients who are classified as
having a hyperfunctional voice disorder speak with the larynx in an elevated posture. Care must be
taken not to exert undue effort in pushing the larynx lower than is comfortable for the patient.
Boone (1983) has described a method of digital pressure that is very different in both intent
and technique from that described earlier. Boone suggests that digital pressure be applied as
a gentle inward push on the anterior aspect of the thyroid cartilage while a patient sustains a
vowel. This pressure should result in lowered fundamental frequency and can be used to elicit
and then habituate this lowered pitch, when that is a therapeutic goal. In our own experience,
this technique has been particularly useful in eliciting more appropriate voice in patients who
are speaking habitually in falsetto. In some cases, simply tapping on the thyroid cartilage is
sufficient to produce voice at a lower, more appropriate, pitch level.
Rationale: Applying pressure as described tilts the thyroid cartilage posteriorly and in so doing
shortens vocal fold length and increases mass. This then results in a lowered fundamental frequency
of vibration, perceived as lowered pitch. Once elicited in this manner, the lowered pitch becomes the
target to be practiced and produced voluntarily.

Easy Production of Falsetto or High-Pitched Sounds

This technique is yet another one that tends to shift the patient away from habituated patterns
of voice use. It is especially helpful for patients who demonstrate anteroposterior laryngeal
squeezing and for some who are found to be using ventricular phonation. It may require trial
and error and much suggestion on the part of the clinician to facilitate the patient’s ability to
produce a high-pitched sound. The use of imagery can be very helpful (see “Imagery” below) as
can the use of animal sounds, such as the meow of a kitten or a wolf ’s howl. It is important to
observe that there is a continuous flow of air from inhalation through exhalation, as the patient
may have the tendency to increase tension and hold the breath prior to initiation of voicing.
When the patient learns to easily produce the high-pitched vowels at will, that sound can be
sustained and the pitch gradually lowered in a glissando to the comfortable speaking level,
without a change in voice quality. The patient is then asked to produce a sustained vowel at
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336 Understanding Voice Problems

that targeted speaking pitch, maintaining the improved quality. As this is established, it can be
shaped into speech. There is no attempt to specify a pitch level beyond that which is identified
by the patient as comfortable and normal sounding.
Rationale: Easy production of the upper frequency range is most commonly produced by a
lengthening of the vocal folds, decreasing their mass. It cannot be done using ventricular phonation,
for example. Therefore, if a high-pitched sound is elicited from a patient who has been using
ventricular phonation, the technique has successfully shifted the patient out of that phonatory mode.
The same rationale may be applied to patients who tend to constrict the larynx in the anteroposterior
dimension or to those whose aberrant voice production behaviors are psychologically based. Patients
with psychogenic voice problems have “learned” a particular manner of phonation that produces
their aberrant sound. If they are asked to produce sound in some novel way, they often must abandon
their “learned” method, and in so doing normal voice may be elicited. Thus, the change in laryngeal
physiology from their particular behavior to that required for the production of the upper frequency
range, if successful, may be sufficient to restore normal phonatory function, which can then be
maintained as pitch is normalized.

Imagery
The use of imagery can be very helpful in describing how a particular type of sound should be
produced. For example, statements of imagery such as “Make it feel as if your voice is floating
effortlessly out of your throat and up into your head” can describe to the patient a way that
effortless voicing might feel. Patients should be encouraged to provide their own imagery as
they release tensions and change their manner of initiating phonation. The use of imagery can
be combined with many of the other techniques, as it can help patients keep in mind what they
are attempting to do. Imagery is often used in those techniques designated by some as “placing
the voice” or finding a “focus” for the voice. It has been reported that professional singers and
actors use imagery concerning their breathing, which although often in contradiction to known
physiological fact, works well for them (Hixon, 1987; Watson, Hixon, & Maher, 1987).
Rationale: The physiology of imagery is receiving increasing attention as its use grows in the
training of athletes and in fighting disease (Keaton, 1983; Ungerleider, 1986). It has been used
in singing pedagogy for many years, and its effectiveness is perhaps attested to by legions of superb
performers. We use it in voice therapy to help a patient understand something about how to produce
voice or what quality to attempt to produce, when other types of explanations are either not possible
or have not been effective. Imagery, although perhaps not physiologically correct, can describe what
seems to happen in a very subjective, sensory way. There is no doubt that a patient will remember
an image used to describe the feeling of producing a certain sound long after the muscles involved
are long forgotten.

Pushing, Pulling, and Isometrics

These techniques are placed together because they are used interchangeably to produce the
same end result. Pushing refers to any of the many ways that patients may be encouraged to
push against a wall, push down on a chair, and so on, whereas pulling refers to the opposite
maneuvers of pulling up on a very heavy desk, pulling up on the chair one is sitting in, and the
like. Isometric forms of these activities include placing the palms of the hands together at chest
height and pressing them together or locking the fingers of the hands together at chest height
and pulling them apart. Whichever method is used, the patient is instructed to phonate at the
point of maximum pull or push. The sound produced will be a forceful grunt and should be
demonstrated by the clinician. All of the varieties of these techniques are designed to force effort
closure of the glottis, a form of hyperfunction of the mechanism. They can often be used with
surprising success in eliciting a low-pitched phonation in cases of puberphonia and in eliciting
voicing in patients who present with psychogenic aphonia. Once the patient has learned to
carry out the push or pull, the same effect can be obtained by holding the breath, bearing down,
and grunting. As the desired voicing is produced, the patient is instructed to sustain that sound
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as the force of the maneuver is gradually released. In a gradual stepwise fashion, the targeted
sound is practiced with less and less need for the forceful push or pull activity.
Because these activities enforce a certain behavior on the larynx, patients with psychogenic
problems also may have difficulty holding on to their typical mode of voice production. Thus
through the use of push, pull, or isometric activities these patients may find an acceptable way
to abandon their symptom and produce voice in a more typical fashion.
Rationale: These maneuvers are designed to create effort closure of the glottis with the larynx
in a lowered position. As such they are the opposite of hypofunction. Furthermore, the posture of the
laryngeal mechanism is determined by the activity and dictates a particular type of vocalization.
This shifts the individual from the usual manner of vocal production and introduces a behavior
difficult to counteract. If tension is released prior to phonation, then the technique will be ineffective.
As noted earlier, we have found these techniques to be effective in eliciting a low-pitched voice
from patients with puberphonia. The vocal fold and laryngeal postures that naturally occur in the
use of these techniques are incompatible with anything but a low-pitched voice, if they are being
done correctly.
Although these techniques are potentially useful, there is a caveat. By their nature they induce
hyperfunction and, thus, are potentially abusive. They should, therefore, be used judiciously. We have
found that their effectiveness will be noted fairly quickly, if indeed they are going to be effective.
Thus, it is usually not necessary to prolong their use. When assigned for home practice, the amount
of time involved should be clearly specified. These effort closure techniques should be used cautiously
and sparingly in recognition of their potentially abusive nature.
These procedures have been recommended by some authors for treatment of unilateral vocal
fold paralysis believing that the effort closure forces a crossing of the midline of the unaffected vocal
fold to approximate the paralyzed fold. We, on the other hand, caution against the use of effort
closure techniques with patients who demonstrate unilateral vocal fold paralysis. It has been our
experience that the result of practicing these push–pull techniques appears to fatigue the mechanism.
Endoscopically, patients often utilize other structures, including the false vocal folds, during pushing
exercises. Patients have also reported increased hoarseness and reduced volume, almost close to aphonia,
after a period of such practice. Further discussion of this topic will be found later in this chapter
under “Unresolved Issues and Myths.”

Laughing, Coughing, Throat Clearing, Gargling, and Other Reflexive Acts

In the attempt to elicit voice from the aphonic patient who appears to have a normally func-
tioning larynx, or to find a normal voice for the dysphonic patient when there are no positive
laryngologic findings, the use of any of the above nonspeech vocalizations can be extremely
effective. Indeed, it is important for the clinician to listen for spontaneous laughing, coughing,
vocalized pauses, or throat clearing during general conversation with the patient. Patients may
not be aware that these reflexive laryngeal behaviors are produced by the same mechanism used
for producing the speaking voice. Thus, such sounds may be heard during conversation or even
when the patient is asked to produce them. The skilled clinician can make use of that sound
by shaping it into speech in a gradual manner. This technique may occasionally be startlingly
effective. However, it may also be ineffective with patients who will continue to use dysphonic
voice, or no voice, in response to a direct request to repeat the vocalization even though they
may have produced such sounds spontaneously. Again, it takes the skill of the clinician to utilize
all instances of good voicing to reestablish normal voice.
Rationale: These behaviors are so automatic that the patient may perform them unaware that
voice is being produced. This is not to suggest that patients are voluntarily producing abnormal voice
but, rather, that some voice disorders may have more to do with speech, or communication, than
with the actual physical status of voice-producing structures. That is, because vegetative or reflexive
behaviors are not “speech behaviors,” their production may be free of habituated but undesirable
phonatory speech behaviors. The inability to elicit an improved voice using these behaviors also may
be a meaningful finding. It may suggest that the patient is somewhat resistant to “giving up” the bad
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voice, or perhaps there is a problem present that has not been identified. In fact, we have experienced
the situation where a patient has been diagnosed with a “functional dysphonia” because voice on
cough was relatively intact, but significantly breathy during speech. It should be remembered that
coughing typically involves greater compressive pressures than voicing. Patients who have a vocal fold
paresis may produce cough that sounds reasonably appropriate but be unable to produce voice for
speech in a normal manner. Further exploration may reveal ways to elicit voice and/or an etiology
of the problem that was not previously identified. Although throat clearing and coughing can be
abusive to the laryngeal mechanism and, thus, are not recommended for extensive therapeutic use,
they can be used judiciously and often effectively in the search for normal voicing.

“Um-Hum”
In this technique, the patient is instructed to say “um-hum”—something of a variant on the use
of nasals previously described—the vocalized utterance used by a listener to indicate agreement
with the speaker, in a naturally spontaneous and sincere manner. There is a deceptive simplicity
to this technique, and the clinician must be sure to elicit a very natural production of “um
hum.” This is difficult for some persons to do when it becomes a conscious and voluntary
utterance. When it is captured in a natural manner, the production is then shaped by adding
single words, as in “um-hum one.” Gradually this is extended through the use of increasingly
longer utterances until the patient is able to produce the targeted voice without needing the
starting “um-hum.”
Rationale: According to Cooper (1984) this simple utterance, if said as naturally as possible,
results in producing a voice at the appropriate pitch level and with the correct focus for the individual.
Vibration should be perceptible along the bridge and sides of the nose and down to the lips. This
technique, similar to the preceding one, capitalizes on a phonatory act that is almost reflexive in
nature. The fact that a nasal component is present in the consonant /m/ adds to the appropriate
focusing of the voice.

Whispering
Whispering is the act of moving the articulators to form words in the presence of rapid airflow
but the absence of phonation. Very little instruction is usually required to elicit whispering.
A quiet, unforced whisper can be used when vocal rest or minimal voice use is part of the
treatment plan. It is sometimes instructive to ask patients who habitually use excessive loudness
to limit themselves to a quiet whisper for part (or parts) of each day. The pronounced contrast
between the whisper and the habitual loudness level may help to focus the patient’s awareness
and to make reducing loudness to an acceptable level easier to accomplish.
Rationale: Despite many caveats in the literature that whispering is harmful, there is no
experimental evidence to support that notion. Indeed, there is evidence that suggests otherwise. This
issue is addressed more completely in the section “Unresolved Issues and Myths.” An unforced whisper
by definition is an absence of phonation. This suggests that the vocal folds are not fully adducting
and thus collision forces are reduced. Gentle airflow is present, and there should be an absence of
tensions. Caution is taken to ensure that the whisper doesn’t become excessive and strained, which is
counter to the reduction of tension sought in the first place. In fact, the bad “advertising” associated
with whisper likely results from the fact that, used in a truly gentle, unstrained fashion, whisper is
difficult to hear or understand for many listeners. Difficulty arises when soft, gentle whisper turns
into a stage whisper that is much more effortful and, likely, excessive.

Respiratory Facilitation of Phonation, or Respiratory-Phonatory Matching

In our own clinical experience, respiration is as much a focus as phonation in much of voice
therapy. Respiration is, after all, the power source for voicing, and voice can not only be com-
promised by reduced pulmonary capabilities but also facilitated by attention to the matching
of respiratory with phonatory capabilities. In our hands, this often involves first implementing
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a typical tidal breathing pattern in patients. Perhaps the greatest difficulty in achieving this pat-
tern, which is perfectly normal and natural in its typical autonomic state, is getting the patient to
focus on it without also changing it in some way. The terms “tidal,” “rest,” or “vegetative” breath-
ing all imply that this type of breathing is efficient, and relatively effortless, requiring minimal
volitional control. This is quite different from breathing that typically supports speech. Remem-
ber that the diaphragm is a muscle of inhalation and is active during inspiration (Fig. 10.2).
But at high lung volumes it may be necessary to contract the diaphragm in order to prevent
the rapid, unwanted descent of the rib cage, that is, to impose the “checking” action of several
muscle groups that ensures a controlled descent (see Fig. 10.2) and more uniform subglottal
pressures. Though this is a common feature of human speech, the need to control respiratory
forces to this extent would seem to make the task of speaking, or voicing, more complex.

FIGURE 10.2. In the upper por-

tion of this figure are shown the
lung volume–muscle pressure re-
lationships during the production
of a sustained vowel. At high lung
volumes, a large amount of inspi-
ratory muscle pressure is needed
to counteract the large lung pres-
sures that are created. As lung
volume decreases, less inspira-
tory effort is needed, until rest-
ing lung volume is reached (the
point where the curve crosses
the vertical line in the middle of the
graph). At still lower lung volumes,
expiratory muscle effort is needed
to produce the necessary subglot-
tal pressures for speech. In the
panel below, a schematic of mus-
cle activity in the diaphragm, ex-
ternal intercostals, internal inter-
costals, rectus abdominis, exter-
nal oblique, and latissimus dorsi is
shown in relationship to the pres-
sure relationships shown above.
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Producing voice, or speech, on a tidal respiratory cycle, minimizes this complexity. That is,
tidal breathing involves inhaling to about 30% to 50% of one’s vital capacity, then exhaling
to resting expiratory level simply by relaxing the active forces that allowed inspiration, that
is, with no attempt to control the rate of descent of the lungs. In addition, no active expira-
tory forces that compress the lungs below resting expiratory level are used. After pausing for
2 to 3 seconds, the next respiratory cycle is begun. In a tidal breathing cycle, the inspiratory
phase requires as much time as the expiratory phase—again, very different from the shortened
inspiration (10%) and markedly lengthened expiration (90%), typical of normal speech pro-
duction. Once the tidal pattern is observed and can be comfortably implemented and sustained
by a patient, a small amount of voicing, usually a single vowel sound, or perhaps 1 to 2 syllables,
is superimposed on the expiratory portion of the cycle. If, in this situation, voice is produced
and maintained in a more optimal, adaptive manner, then both respiratory and phonatory
behaviors can expand to accommodate longer utterances. As the patient is able, the pattern can
move from tidal breathing to a pattern more typical of connected speech.
This focus on breathing can also be effectively paired with other techniques, that is, the
yawn-sigh, aspirate initiation of phonation, and so on. A nasal or humming sound produced on
tidal exhalation may also be possible. Again, it is important initially to simulate tidal breathing
as closely as possible, with pauses between breath groups, and an emphasis on exhalation
associated with relaxation. The clinician must remember that average conversational utterances
on one continuous respiration tend to be very short, about 5 seconds (Boone & McFarlane,
1988) and that, therefore, nonprofessional voice users do not need to inhale as deeply as do
professional voice users in singing, acting, or public speaking. In our hands, this matching of
respiratory and phonatory capabilities has often been a basic element in identifying, for an
individual patient, optimal voice production, and then “growing,” or expanding this into a
vocal space consistent with functional speech.
Rationale: The respiratory system is the power source for the voice. The systems involved in
phonation are closely intertwined, and tensions in one system cannot easily be isolated from the
rest. Thus, reducing respiratory tensions and assuring continuous airflow from inspiration through
expiration assists in reducing laryngeal tensions and avoiding closure of the glottis prior to the
initiation of phonation. Tidal breathing represents perhaps the least effortful, most economical
breathing available to us. Using it to support vocalization, even if limited, can help reduce the
overall effort level associated with voice production, and facilitate elicitation of normal voice. This is
not to say, however, that respiration is somehow disturbed in dysphonic speakers. Most patients, with
the exception of those who have chronic respiratory problems, chronic obstructive lung disease, or
neuromotor impairment of the control of respiration, tend to have normal respiration and adequate
air supply for speech. This topic will be discussed later in “Unresolved Issues and Myths.” Singers,
actors, and other professional voice users may have demands placed on voice use that require greater
control of increased volumes of air. This group of voice users will need more extended training in the
management of breath support and breath control than the average speaker.

Relaxation
A variety of techniques are used to teach generalized relaxation. These include progressive
relaxation in which the patient is instructed to concentrate on specific parts of the body one
at a time and then through imagery and suggestion to release the tensions present (Jacobson,
1938). Another part of the technique involves purposefully tensing a specific body area, followed
by a release of that tension. Imagery is often used in teaching relaxation, and deep breathing
exercises are frequently incorporated as well. The shoulders, upper back, and neck are very
vulnerable to muscle tightening in tense individuals (Nagler, 1987). A popular activity for
relaxation of these tensions has been the head roll, in which the patient is instructed to very,
very slowly allow the head to be rotated 360 degrees. However, it has been suggested that
circular rotation of any part of the spine may not be helpful to the intervertebral disks, and the
following exercises are recommended instead (Nagler, 1987):
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1. While holding the left elbow in the right hand, pull it over to the right side, hold, then
relax. Do the same with the other arm, and repeat the sequence three times for each
arm. Maintain a normal breathing pattern.
2. Place the hands, palms in, on the upper chest, with elbows out to the sides. Circle the
elbows in one direction and then reverse. Repeat 3 times. Maintain a normal breathing
pattern.
3. Raise shoulders up as high as possible, hold, then slowly release. Repeat 3 times while
maintaining a normal breathing pattern.
Rationale: The rationale for engaging in relaxation therapy as one segment of a vocal rehabil-
itation program is primarily to release excess tensions in systems involved with phonation. However,
it must be recognized that most of our talking is done in states other than complete relaxation. Thus,
it is important to use these techniques in specific ways and then to incorporate them into healthy
patterns of phonation. Patients should be instructed in these techniques and then asked to practice
them at home. In view of the restrictions placed by third-party payers on the number of voice therapy
sessions that will be covered, it is typically not possible to spend much therapy time on such practice.
This is also applicable to practice on breathing.

Phonating on Inhalation
The technique for creating voice in this way is just as described by the title. The patient is
instructed and shown how to make sound in the reverse of the normal pattern, that is, as air is
being drawn into the lungs. This is usually a fairly simple sound for most people to make. The
technique has been described by many authors as useful in reversing ventricular phonation.
This author has rarely found that to be true but has used the technique for other purposes. The
patient is instructed to switch directly from voice produced on inhalation into voice produced
on exhalation. If this technique is successful in eliciting an improved voice quality in the
exhalatory phase, it can then be gradually shaped into speech with a gradual reduction of the
need to start with phonation on inhalation. It is also another manner in which to force change
in an habituated but maladaptive phonatory pattern. We have found it useful occasionally in
eliciting phonation from an otherwise aphonic or dysphonic patient who presents with normal
laryngeal examination.
Another use of inspiratory speech has been described by Harrison et al. (1992) in a patient
with spasmodic dysphonia. The technique of speaking on inhalation differs from that described
previously in that there is no attempt to transfer from the phonation produced on inhalation to
similar phonation on exhalation. Rather, the focus here is on learning to use inspiratory speech
to replace expiratory speech, to establish the inspiratory speech as the habitual pattern. Harrison
et al. (1992) describe a patient with adductor spasmodic dysphonia who had discovered that he
could produce speech during inhalation in a much more fluent and less effortful manner than
his typical spasmodic speech. He adopted the inspiratory form of speech, which was judged
to be perceptually somewhat rough but intelligible and more acceptable to listeners than the
strain/struggle–interrupted spasmodic speech. One of the authors of the Harrison et al.’s paper
was able to learn the inhalatory form of speech with relative ease although the authors recognize
that may not be the case for all patients. Nevertheless, it is offered as an alternative to other
methods of treatment for patients with spasmodic dysphonia. Others have described use of this
type of phonation for spasmodic dysphonia (Freeman & Shulman, personal communication).
It is a noninvasive form of treatment, which, if successfully learned, may offer consistent voice
to the patient.
Rationale: Voice produced on inhalation is produced by the true vocal folds with a pulling
away (abduction) of the ventricular folds (Lehmann, 1965; Williams, Farquharson, & Anthony,
1975). In our experience, this observation has been frequently confirmed by endoscopic visualization
of patients engaging in this task. Thus, in patients who are using ventricular fold phonation or those
who are improperly using the vocal folds, it is theorized that this technique will stimulate more
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342 Understanding Voice Problems

appropriate physiology. In the pattern of inspiratory speech described by Harrison et al. (1992), the
vocal folds were not fully approximated, and the authors believe that a posterior gap was present
although not fully visible. Clearly this laryngeal posture differs from the abducted folds that we expect
to see on inhalation without phonation. The authors suggest that contraction of the cricothyroid
muscle, which begins along with the diaphragm, is an involuntary action that is not likely to be
accessible to voluntary control, may serve as a counter to the adductory forces of the laryngeal muscles,
thereby reducing the force of vocal fold approximation and allowing for fluent speech. A second
explanation offered by the authors has to do with the respiratory reflexes of the larynx, which may be
abnormal in persons with spasmodic dysphonia.

Vocal Hygiene
This category will include techniques that should be incorporated into most voice therapy
programs. Instruction in vocal hygiene may occasionally constitute the entire rehabilitation
program, but it is typically at least one part of the program. In most instances of misuse of the
voice, it should be a routine part of the program, and training in vocal hygiene as a preventive
measure should be the final stage of voice therapy after a successful outcome has been attained
(Fig. 10.3). Morrison and Rammage (1994) provide a useful listing of dos and don’ts and
helpful hints about vocal hygiene. The following are components of vocal hygiene instruction.

Reducing the Amount of Talking

Patients who are excessive talkers, those who have a tendency toward traumatic voice use or
vocal fatigue, those who have undergone laryngeal surgery, and certainly those involved in
voice therapy for conditions associated with misuse with or without tissue change, should
be counseled about the need to significantly curtail their voice use. This restriction may be
necessary for perhaps only a specified period of time. This is sometimes referred to as modified
vocal rest. Instructions should be as detailed as needed and should include all restrictions on
voice use. As noted earlier in this chapter, one technique we have found particularly helpful is
to have patients monitor the voice throughout the day for evidence of vocal “fatigue,” explained
to them as evidence of either deterioration in vocal quality, or increase in effort required to

FIGURE 10.3. Vocal hygiene.

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produce voice. Simple tasks, that is, counting, singing a song, are repeated the same way at
various times throughout the day. For at least the first and last voice “checks,” the patient is
asked to rate these parameters and note them, as on a calendar. The goal is to get through
the day with no fatigue. That is, even if the voice is not normal early in the day, at least, it
should not deteriorate over time. An analogy that we frequently use is to liken the amount of
available “voice” to fuel in a gas tank. If the available amount is exceeded, trouble is ahead.
Useful insights, for example, days where the goal is more easily accomplished, activities that
“use up” the voice more quickly, are typically forthcoming. The topic of complete voice rest
will be discussed in greater detail in “Unresolved Issues and Myths.”

Reducing Loudness
This may involve eliminating all use of the voice when the ambient noise level requires a vocal
intensity level above that permitted by a soft breathy voice. Such a restriction will not allow
yelling for the dog or for children playing outside or upstairs; it will not allow talking in a
car, above a television or radio, above machinery or other noise in an employment setting, at
a cocktail party, or in a bar with loud music playing, and so on. Such reduction of loudness is
necessary when there have been mucosal changes, whether evidenced by inflammation, edema,
or vocal nodules.
There are some patients who routinely use excessive loudness. Modification of this habit-
uated behavior often requires intensive effort and is not an easy pattern to alter. We all have a
vocal image in our minds, which includes a loudness level. Patients who are excessively loud
often do not believe that listeners will be able to hear them if they speak more softly. They must
be willing to test whether this is the case by engaging in intensity reduction activities. Devices
that provide visual or auditory feedback can be extremely helpful in establishing an acceptable
level of loudness. A useful device known as the Voice Intensity Controller (VIC, Behavioral
Controls, Inc.) is small enough to be worn by the patient and preset to beep when a specific
loudness level has been exceeded. Visual feedback of loudness can also be provided with the
use of the Visi-Pitch (Kay Elemetrics Corp.), the Vocal Loudness Indicator (LinguiSystems),
or a number of computerized programs that permit online visualization of the voice signal.

Identifying and Reducing or Eliminating Vocal Misuse

All vocal behaviors potentially detrimental to laryngeal health should be identified and elimi-
nated if possible, or at least reduced to a minimum. Exploration of such behaviors needs to be
very broad and thorough. Aversive behaviors include smoking of legal or illegal substances; use
of certain drugs; spending large amounts of time in dry, dusty, or smoke-filled environments;
exposure to airborne irritants; frequent habitual throat clearing; constant cough; excessive
drinking of alcoholic beverages; as well as the traumatic behaviors of excessive talking, excessive
loudness, and excessive strain discussed elsewhere. All identified behaviors need to be discussed,
and specific plans need to be made as to how they will be reduced or eliminated. Patients should
be required to monitor their performance on the agreed-upon plan.

Environmental Manipulation
When appropriate, changes can be made in the environment to help patients function with
reduced voice use or to make the environment itself more hospitable. For example, humidifi-
cation can be increased by the use of room humidifiers, amplification can be used when there
are demands on vocal loudness, whistles or bells can be adopted by teachers to obtain attention
in place of typically loud voice use, the television volume can be muted when it is necessary
to talk, and so on. Creativity is sometimes required in order to plan environmental changes.
People may be resistant to changing their habitual modes of functioning. It is often necessary
for both clinician and patient to work through this resistance and for the clinician to find ways
to encourage patients to adopt the plans and give them a fair trial.
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The need for adequate moisturization and humidification of the upper respiratory tract
should also be discussed as part of a vocal hygiene program. Conditions that may deter and
interfere with good levels of environmental humidity should be explored. These might include
the use of wood stoves for home heating, a work environment that is extremely dry or dust-filled
(e.g., old school buildings, theaters), extensive airplane travel, and others. When such conditions
exist it becomes the individual’s responsibility to take whatever remedial or compensatory
actions possible, such as using room humidifiers or increasing liquid intake.
At the successful conclusion of a therapy program, with voice restored to its normal state,
patients should be advised about monitoring their vocal health. Because hoarseness may accom-
pany an upper respiratory infection or may result from an evening’s overuse, patients need to
understand that it need not signal a recurrence of the initial problem. However, they should be
advised to immediately restrict voice use and loudness and increase liquid intake when experi-
encing symptoms of a condition with implications for voice. They, of course, should follow any
additional course of treatment prescribed by their physician for the condition, as well. If such
hoarseness persists for more than a week, or if it persists beyond the resolution of other symptoms
of upper respiratory infection, it would be advisable to return for laryngological examination.
Rationale: The rationale for all of the above is to help patients engage in those activities and
behaviors that foster laryngeal and vocal health. Several of them serve to reduce either the force or the
amount of vocal fold contact, or both. In so doing, they potentially eliminate irritation of the mucosa
and change. Others have to do with maintaining the healthiest possible conditions for the mechanism
to work well. Prevention of recurrence is certainly a major reason for using these vocal hygiene
procedures. The history of vocal hygiene as a therapeutic technique and the meanings associated with
it are discussed more fully in the MIT Encyclopedia of Communication Disorders (Casper, 2003).

Energizing the Voice

This technique is a difficult one to describe because of the abstractness of the concept. It is
perhaps analogous to the car engine that is chugging along on only three spark plugs rather
than all six. It is akin to the desire to “set a match” under someone who is too low keyed, too
subdued, and laid back. It is appropriate for use with patients who are known to have normal
metabolic states and a normal ear, nose, and throat examination and who are not psychiatrically
depressed. It includes (a) the use of adequate mouth opening and movement of the articulators,
(b) the use of more inflection or variability of pitch, (c) the use of adequate loudness level and
increased variability of loudness as appropriate to mark meaning, and (d) the use of a “well-
placed” and well-supported (respiration) voice. Many methods can be used to accomplish this
energization of the voice. They will vary depending on the age, personality, and speaking needs
of the patient. The use of scripted material from plays or other sources can be helpful, as can
exercises such as practicing the role of a drill sergeant, calling out cadences, practicing in a large
room, moving and using the whole body while counting, and so on. Care must be taken so that
the patient does not simply begin to shout. Whatever exercise or material is used, the patient
must have specific goals that have been explained and practiced at lower levels of difficulty first.
Many of these activities are often better carried out with the patient and the clinician standing
some distance away from each other. It is useful to explain to patients that voice originating
at the level of the larynx can be enhanced by opening up the “flared,” or mouth end of the
vocal tract, which allows for easier transmission of sound. On the other hand, for the same
amount of vocal effort, closing down the oral cavity during speech results in a less efficient
transmission of sound. In other cases, asking the patient to imagine that he or she is speaking
to someone who has a hearing problem and needs, not greater loudness, but more visual cues
in order to better read the speaker’s lips, may produce the desired result. Variability in pitch
and loudness can be aided by the use of instruments that provide visual feedback (Visi-Pitch,
computer programs, etc.) until such time the patient has improved auditory sensitivity to and
discrimination of these parameters.
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Rationale: Some patients complain about having “weak” voices that do not carry, that do not
convey the desired image, and that seem to fatigue as the day goes by. In the absence of hormonal
imbalance, serious psychiatric problems, laryngeal abnormality, or other organic problems, it is most
likely that the problem lies in the way in which the person has learned to speak. These are behaviors that
should be accessible to change. The activities described above address the types of speech patterns often
seen in patients with these complaints and are designed to introduce changes in those patterns. It is
clear that personality factors may be heavily involved, and the clinician must always keep this in mind.

Vocal Effort
The concept and technique of measuring vocal effort was described in Chapter 7. It is a simple
concept that can be adapted for use as a therapy technique. It requires that the patient assign
a number to represent the amount of effort being expended in habitual speech. (The only
stipulation is that the numbers used increase with an increase of effort.) In order to obtain a
comparative scale for that patient, have him produce phonations at a minimum effort level, a
comfortable effort level, and a maximum effort level. For example, if a patient complains of
feeling that it is a strain to talk and assigns the number 17 to the degree of effort involved, but
phonation with minimum effort is produced at a number 5, suggest that he talk with a degree
of effort corresponding to a number 8 or 10. Patients can learn to internally monitor their effort
levels and modify their behavior accordingly, thereby achieving an increased measure of control
over phonation. They are able to experiment with how they produce sound in order to achieve a
more efficient and vocally less tiring, and likely less traumatic, mode of phonation. Yet another
benefit of this technique is the ease with which progress can be tracked. After a period of use
of either reduced or increased effort (whichever was the goal), patients can again be asked to
assign a number to their habitual phonations. This can be compared to the previous judgment.
Rationale: Because it has been determined that patients are able to estimate vocal effort and
that their estimates are manifested acoustically by variation in sound pressure level and fundamental
frequency (Colton & Brown, 1973; Wright & Colton, 1972a, 1972b), using that ability in a thera-
peutic manner is quite appropriate. This approach accomplishes its desired goals in a holistic manner
without fragmenting the various components of producing voice. It is also a technique that is easy for
patients to understand and to retain in memory, thereby increasing the likelihood that they will be able
to put it to use. It does not require extensive practice and provides almost immediate reinforcement
both through a sense of accomplishment and control and awareness of the reduction in strain.

The Resonant Voice

Resonant voice therapy is based on techniques used to improve voice production in actors
and singers (Cooper, 1973; Lessac, 1987). It is a form of sound production that is based on
“sensations on the alveolar ridge and other facial plates during phonation.” It appears to result
from a tuning of the first formant to individual components of the glottal tone (Raphael &
Scherer, 1987; Smith, Finnegan, & Karnell, 2005) or to a change in the source spectrum. It
is produced with a slightly abducted vocal fold posture; thus, it should not be harmful. There
are a variety of exercises that can be used to teach the technique, although some patients may
require a period of time to learn the desired sound.
Verdoloni-Abbott (2004) has proposed a structured therapy program that is designed
to teach the resonant voice, Lessac Madsen Resonant Voice Therapy (LMRVT), for patients
with hyper or hypoadducted voice disorders. Since its inception, a number of investigators
have described the use of LMRVT with various populations (Barrichelo-Lindstrom & Behlau,
2009; Chen, Hsiao, Hsiao, Chung, & Chiang, 2007; Grillo & Verdolini, 2008).
Tone placement and “flow phonation” are the main tools of the resonant therapy program
(Lessac, 1987). Patients with dysphonic voices often report feeling the voice vibrating in the
throat. In the resonant therapy program, sensory processing is also stressed as the patient is
taught to produce a more forward placement so that the sensations of voice production can be
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felt in the palate, tongue, and lips. The configuration of the vocal folds is noted to be in a barely
separated posture. This configuration is said to maximize the ratio of voice output intensity to
the intensity of vocal fold impact pressure (Berry et al., 2001). In other words, it results in the
production of the most voice with the least effort. The structured program involves 8 sessions
over an 8-week period.
Verdolini-Marston et al. (1995) compared the resonant therapy technique to the confi-
dential voice therapy technique described earlier in this chapter. Measures of phonatory effort,
auditory-perceptual ratings of severity of dysphonia, and visual impressions of the appearance
of the vocal folds were obtained from 13 patients with vocal fold nodules. Three patients com-
prised the resonant therapy group, whereas 5 patients were part of the confidential therapy
group. In addition, five patients received no therapy (control group). The results showed that
both therapy programs improved the voice. Phonatory effort was reduced in both groups with
little change in the control group. Two of the five patients in the confidential therapy group
showed improvement on ratings of the severity of dysphonia, whereas all three patients showed
improvement in the resonant therapy group. Four of the five patients in the confidential therapy
group showed visual changes in appearance of the nodule as viewed stroboscopically, whereas
two of the three patients in the resonant therapy groups showed similar changes. There were
few changes on any of the measures studied for patients in the control group.
The authors of this study also reported that patient compliance was predictive of voice
improvement, more so than the type of therapy program. Although preliminary, these results
suggest that the resonant voice therapy approach is viable for the treatment of vocal fold nodules
and perhaps similar lesions.
Rationale: It has been reported (Verdolini-Marston et al., 1995; Verdolini & Titze, 1995)
that this type of phonation results in limited vocal fold adduction as compared to “pressed voice.” It is
theorized, therefore, that the impact forces of the vocal folds as they adduct are also reduced. Such an
effect is desirable when attempting to change hyperfunctional voice behaviors. Despite the reduced
adductory forces the voice remains strong.

Neuromuscular Stimulation
Transcutaneous electrical stimulation has long been used to enhance muscular activity in limb
musculature, by preventing atrophy of paretic muscles and facilitating regeneration. In the
last few years, electrical stimulation has been used in the anterior neck and submental area
for patients with dysphagia of various types. In general, these therapies have been directed
to increasing hyoid and laryngeal elevation in an attempt to improve airway protection and
swallow function. There have been mixed reports of the success of stimulation, used alone or in
combination with more traditional treatments (Ludlow, 2010). Recently, some clinicians have
investigated the potential of electrical stimulation in patients with voice disorders. Ptok and
Strack (2008) compared outcomes of electrical stimulation with vocal exercise to a traditional
vocal exercise program in patients with unilateral vocal fold paralysis. A starting stimulation
level was determined by evidence of a twitch in the affected vocal fold, and no patient’s pare-
sis was related to resection of the recurrent laryngeal nerve. Dependent variables included
maximum phonation duration and irregularity of vibration. Patients undergoing electrostim-
ulation with vocal exercise showed a slight, but not significant, advantage, as compared to
patients undergoing traditional therapy. In another recent study, LaGorio, Carnaby-Mann and
Crary (2010) described results of neuromuscular stimulation combined with traditional voice
therapy in patients with vocal fold bowing. Significant improvement in maximum phonation
time, and nonsignificant improvements in the Voice Handicap Index were noted. Of interest,
improvements were still apparent at 3 months post-treatment. No control group was included.
The use of electrical stimulation is in its infancy in the treatment of voice disorders, and
there is currently little available evidence to suggest its benefit over existing therapies. With
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systematic investigation into its use, in particular, with specific types of delivery, specific types
of patients, and in comparison to other therapies, its potential, or lack thereof, should be
forthcoming.
Rationale: Transcutaneous electrical stimulation involves the application of electrical current
to muscles. Two electrodes are placed on the skin overlying particular muscles. Current then passes
between the electrodes. The distance between the electrodes, as well as the strength and particular
type or shape of impulse delivered, can be varied. Typically, the strength of the stimulus is increased
according to patients’ tolerance, and most therapies have massed trials over a few days or weeks. Other
uses of electrical stimulation involve direct stimulation, in which stimuli are delivered via needle
electrodes; the use of these in laryngeal muscles in humans is not well-documented.

Voice Therapy for Patients with Parkinson’s Disease

Traditional speech therapy has been provided for patients with Parkinson’s disease for many
years and with less than resounding success. That therapy focused on rate of speech and on
the dysarthric components as they affect articulation. However, several authors have reported
therapeutic success by targeting phonation (Johnson & Pring, 1990; Ramig et al., 1988; Robert-
son & Thompson, 1984; Scott & Caird, 1983). Building on these beginnings, Ramig and her
colleagues have developed and shown the efficacy of a very specific therapy protocol (Ramig,
1995; Ramig et al., 1994; Ramig & Scherer, 1992; Smith et al., 1994) called the Lee Silver-
man Voice Treatment program (LSVT). Although this program focuses entirely on phonation,
improvement in clarity of articulation, rate, and overall intelligibility has also been documented.
Countryman et al. (1994) studied the efficacy of this program with three patients diagnosed
with Parkinson’s plus syndromes. Patients so diagnosed often have more severely debilitating
symptomatology and more rapidly progressive decline of function than those with idiopathic
parkinsonism. Nevertheless, all three patients demonstrated improvement in overall speech
intelligibility, functional communication, and voice deficits. All 3 patients maintained some
carryover above pretreatment levels at 6 months posttreatment.
The LSVT is designed as an intensive program of 4 individual sessions per week for 1 month
during which loudness, maximum phonatory effort, high therapeutic effort, and voice awareness
are targeted. The methods used include some of the techniques already described in this chapter,
as well as others, as follows: maximum duration sustained loud phonation, maximum frequency
range (sustained highest and lowest pitches), posture, and maximal loudness. Patient’s receive
immediate reinforcement from their productions. The method is simple, making it possible for
patients to practice at home and to remember to incorporate the new learning into all speech
events. Patients are advised to “think loud, think shout.”
Rationale: Vocal fold bowing and incomplete glottal closure are characteristic of the phona-
tory behavior of parkinsonian patients as is reduction in respiratory support. Some of the exercises
are designed to increase vocal fold adduction. The high effort and stress on “maximum” perfor-
mance are necessary to override the rigidity and hypokinesia of Parkinson’s disease. The intensity of
the therapy maintains consistency of the high effort over the course of a month. It is reinforcing for
the patient as progress is seen thereby motivating him to continue to put forth the effort maximizing
habituation and generalization of the improved voice and speech.. The single primary focus on loud
voice is maintained to make it easier for these neurologically compromised patients to hold that
thought in memory and operationalize it. This “recalibration,” or alteration in patient’s perceptions
of vocal loudness, has been increasingly recognized as a key element of the therapy. In recent years,
LSVT has been reported to benefit patients with other types of dysarthria and has been associated
with improvements not only in voice but also in articulation, facial expression, and swallowing (Fox
et al., 2006). As described earlier, recent investigations of neural changes associated with LSVT
suggest that improvements noted with the technique may represent a shift in cortical control to the
right hemisphere (Narayana et al., 2010). The kind of systematic inquiry evidenced for LSVT over
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the past 10 to 15 years represents the kind of sustained investigative process likely to elaborate and
validate the clinical utility of any therapeutic process.

Voice Therapy for Patients with Paradoxical Vocal Fold Movement (PVFM; Vocal
Cord Dysfunction [VCD])
Treatment for this condition was first described in the 1970s and 1980s. It is generally agreed that
the condition often requires the teamwork of otolaryngologists, pulmonologists, psychologists,
and speech-language pathologists. The latter are primarily responsible for treatment. It has been
our experience that an explanation to the patient, parent, or significant other, of the nature of
the problem is one of the most important initial therapeutic steps. It is otherwise difficult for
them to understand or accept the need to see a speech-language pathologist. This explanation
should include the way in which the vocal folds work in coordination with breathing.
As described by Florence Blager (Martin, Blager, Gay, & Wood, 1987) a therapy protocol
that has been found to be effective with many patients who display PVFM involves the following
steps:
1. Inhalation through the nose with lips closed
2. Relaxed tongue posture
3. Prolonged audible exhalation through pursed lips or on the production of sustained /s/
4. Diaphragmatic breathing with emphasis on exhalation.
In our clinic, endoscopic feedback is typically provided to patients during a variety of
tasks, that is, sniffing, deep inspiration, producing voice on inspiration (stridor), to illustrate
strategies for maximizing airway opening and, conversely, behaviors that are inconsistent with
easy inspiration. In patients whose symptoms appear to be triggered by environmental stimuli,
or during sustained exercise (running), practice with breathing strategies often quickly leads
to resolution or marked reduction in symptoms. In patients whose symptoms are triggered by
particular athletic activities, for example, soccer, which requires intense bursts of exercise that are
somewhat unpredictable, simulation of symptoms in a clinical setting, as well as the application
of techniques for airway opening, may be more difficult. We have sometimes performed botox
injections of the vocal folds in few such patients (typically premiere female athletes), which
appears to minimize their symptoms and/or allow them to utilize behavioral strategies more
effectively.
Sapienza and her colleagues have described benefits of respiratory muscle strength training
in patients with PVFM (Murry & Sapienza, 2010; Murry, Tabaee, & Aviv, 2004; Sapienza,
2008), as well as with abductor paralyses of the vocal folds. In essence, these techniques uti-
lize small, hand-held breathing devices that impose increased resistance to breathing (either
inspiration, expiration, or both). Presented to PVFM patients in a structured manner over a
sustained period of 3–4 weeks, therapy is focused on inspiratory training requiring continued
airway maintenance in the presence of increased resistance on inspiratory airflow; improved or
resolved symptoms were reported posttherapy.
Rationale: These activities focus the patient’s attention on a breathing technique, thus reducing
the tendency to panic and increase tension. The patient is taught a technique over which he or she has
control, which replaces the panic of feeling out of control. Nasal rather than oral inhalation increases
full glottal abduction, and attention to exhalation helps relax the system. The various steps must be
practiced many times so as to be almost automatically brought into play at the first sign of difficulty.
If the patient is able to trigger the “attack” it is desirable to do that in practice and immediately
reverse it through the use of these techniques. Because these “attacks” are often brought on by stress
or exercise, it is important to have the patient move fairly slowly at first through the process of (a).
awareness of early symptoms, (b). cessation of ongoing activity, (c). initiation of breathing exercise,
and (d) restoration of normal breathing. Several minutes of rest are then helpful before resuming
the activity or getting the stress under control. The goal of therapy is to be able to abort the “attack”
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without the need for the cessation of the activity and finally to eliminate the symptom. A number of
variations of the therapeutic scheme have been reported (see Gallivan & Andrianopoulos, 2004).

Voice Therapy for the Patient with Presbyphonia

These are treatment approaches for those often described as older adults, people usually 65 years
of age who are in generally good health (in that they are not suffering from any progressive
neurological problems), do not have severe emphysema or significant hearing loss, can partic-
ipate in general physical conditioning activities, and have no laryngeal pathology. A relatively
common clinical situation is an older adult female whose voice is not as “strong” as previously,
whose spouse (and likely, a number of friends) whose hearing has deteriorated. Collectively,
the deficits, even if minor, can affect quality of life.
The approaches to treatment with these patients can be similar to the therapy program
described for parkinsonian patients but adapted to the needs of this population. Therapy need
not be intensive, although patient practice and involvement in the treatment requires full effort.
The concept of vocal effort can be incorporated into the therapy as can other techniques that
“push” the system and are effective for hypofunctional voice disorders. Posture is an important
consideration, and respiratory support may need some attention. It has also been our experience
that encouraging these individuals to become involved in a program of fitness conditioning
or regular exercise, including some aerobic activities, is beneficial to the voice. We have also
experienced good effects with the REST exercise program described earlier. Interestingly, an
increasing number of older adults are familiar with the Internet and go “online” with relative
ease. There are a number of readily available software tools that can facilitate the home exercise
protocol. For example, a number of online keyboards are available that permit patients to
practice pitch glides and swell tones (www.apronus.com; www.play-piano.org).
Rationale: Biological aging is different from chronological aging. Some individuals who are
aged 65 or older are healthy, active, and seem younger than their years, whereas others of the same age
may show very obvious signs of aging. These differences are also revealed in the voice (Ramig & Ringel,
1983). The voice described as presbyphonic is usually lacking in stability, as evidenced by increased
aperiodicity and pitch breaks, reduced intensity, and a “muffled” quality lacking in resonance.
The laryngeal or stroboscopic findings usually reveal glottic incompetence (often a bowed pattern),
reduced amplitude of excursion, and reduced mucosal wave. All of the activities described above
should potentially “push” the system to greater performance, thereby increasing glottal competence
and improving all other functions. Surgical approaches to the treatment of this condition were
described in the previous chapter.

Phonoscopic Approach to Treatment Probing and Treatment

Over the past several years, increasing numbers of voice clinicians have been able to take
advantage of endoscopic instruments in their assessment and treatment of dysphonic patients.
The goal is to observe the structures of the larynx at the same time voice is being produced, hence
the term, “phonoscopic exam,” , i.e. observation of phonation. Aspects of such an examination,
the need for voice clinicians to be proficient in the use of endoscopic tools and to be skilled
in the interpretation of laryngeal images, diagnostic probing, and wide sampling of phonatory
behavior, are all discussed in greater detail in the chapters on examination and testing earlier in
this text. During treatment, visual information, in addition to the sound and “feel” of voicing,
becomes part of the feedback to patients regarding the appropriateness, or lack thereof, of
various behaviors. Not surprisingly, the capability to combine visual and auditory information
in these ways represents a significant inclusion to our clinical toolbox. Leonard and Kendall
(2002) have described in detail a rationale for, and the utility of, the “phonoscopic” approach
to both evaluation and treatment in voice disorders. It is applicable to most dysphonic patients,
regardless of pathology, and adds both precision and economy to our treatment efforts.
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Criteria for Termination of Therapy

When undertaking any treatment plan it is necessary to consider possible outcomes and how
they are to be handled. In the current climate of accountability and stress on outcomes of
treatment, documentation of the therapy process, beginning with the evaluation and all test
data, is essential in helping to determine and to support the decision to continue or to terminate
therapy. If comparison of the data reveals positive changes that can logically be attributed to the
therapy although the desired endpoint has not been reached, it is possible to make a good case for
continuation of the treatment plan. Furthermore, awareness of such progress can be effectively
used to motivate the patient and inspire an added measure of confidence—confidence the
patient has in the clinician and self-confidence the patient gains based on the progress made.
If the data are negative, revealing essentially no change, the door is opened for discussion of
possible reasons, and support is lent to the need for additional testing, examination, or in some
instances, termination of therapy. The following sections will set forth some criteria for the
termination of therapy.

Elimination or Reduction of Vocally Asymptomatic Tissue Changes

For some patients, a significant reduction in the size, extent, or severity of mucosal pathology
may lead to essentially normal voice. We have known of patients who, although totally asymp-
tomatic for voice problems, were found (during routine ear, nose, and throat examination) to
have vocal fold nodules. These patients were not only vocally asymptomatic at the time of the
examination but denied experiencing any change in voice in the past. It appears that certain
small lesions may be so situated as to have minimal effect on glottal closure or on mucosal
vibratory behavior, leaving the voice perceptually unchanged. This then may also be the case
with a patient who has reached a stage in therapy where the voice is normal-sounding and
a complete vocal range has been restored despite the continued presence of some mucosal
pathology. In the first example, voice therapy may take the form of a single session in which
vocal hygiene concepts are taught. In the second example vocal hygiene should be taught prior
to termination of treatment in order to prevent a recurrence or worsening of the laryngeal
condition. The patient who experiences full resolution and elimination of signs of pathology
and return of good voice is obviously also a candidate for termination of voice therapy.

Improved Voice of a Quality Acceptable to Patient

In clinical practice, a patient may experience a degree of improvement that is looked upon
by the clinician as only a point along the road to the “best” voice but that is accepted by the
patient as being totally adequate. This may be a form of resistance to therapy, or it may be
related to the expense incurred in continuation of the therapy, or it may reflect the patient’s
view and expectation quite precisely. At some point it is important for the clinician to raise the
self-directed question, “Whose needs am I interested in fulfilling, mine or this patient’s?”
There are also many situations in which restoration of normal voice is not a realistic goal.
For those patients, the attainment of an acceptable voice should signal the consideration of
termination of therapy.

Elimination of Physical Symptoms of Pain, Discomfort, and Fatigue

Patients sometimes complain of pain, discomfort, and fatigue associated with voice production
more vigorously than they do of voice symptoms such as hoarseness and pitch breaks. Indeed,
the voice symptoms may be fairly minimal perceptually. Thus, for such patients, the relief of
pain, discomfort, and fatigue associated with phonation is the goal, and attainment of that goal
may be the proper time to terminate therapy. Incidentally, when these symptoms are relieved,
patients have usually changed phonatory behavior in ways that are also reflected in improved
voice production.
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Habituation of Changed Vocal Behaviors with No Return of Symptoms

When a patient has fully adopted the desired vocal behaviors and no longer complains of any
of the initial phonatory problems that brought him or her to treatment, therapy should be
terminated.

Lack of Improvement after an Appropriate Therapy Trial

Voice therapy is generally not a long-term process. Some improvement should be perceptually
discernible with most voice patients after a month of therapy, assuming at least one session
per week and a patient who complies with the therapeutic protocol. If that is not the case, the
clinician should review the case thoroughly. Every attempt should be made to resist adopting
the facile excuse that the patient is resistant to therapy and is not practicing. Indeed, that may
sometimes be the case, but it is incumbent upon the clinician to fully explore all other possi-
bilities as well. These may include an erroneous initial diagnosis, an inappropriate therapeutic
approach, the presence of psychological factors that do not allow the patient to abandon a
symptom, environmental or medical factors helping to maintain a problem that have not been
identified or dealt with, or the presence of a condition that is not responsive to a voice therapy
approach. Possible actions to be taken would include consultation with the referring physician,
referral to a voice laboratory for additional testing, reassessment and alteration of the therapy
approach, and referral for additional consultations (neurological, psychiatric, etc.). It may well
be that after all of the appropriate steps have been taken, a decision to terminate therapy may
be the correct one.

Unresolved Issues and Myths

Clavicular Breathing: The Cause of Voice Problems?
After many years of experience in examining and working with voice-disordered patients, we
are struck by the absence of clavicular breathing as a symptom or a sign. This is especially so
in view of the frequent mention of this breathing pattern in many texts. Moreover, despite the
claims, there is an absence of data to support this notion.
Clavicular breathing may be present in patients whose respiratory function is compromised
as a result of chronic obstructive airway disease, other disease states, or neurological impairment.
It may also be apparent in persons who are anxious and extremely tense. It is difficult to
understand what the nature of the pathophysiology would be for an otherwise healthy individual
to develop true clavicular breathing. On the other hand, it is important for the voice clinician
to be aware of respiratory factors that might affect voice. For example, Powers, Kavazis, and
Livine (2009) report changes in both structure and function of the diaphragm associated with
prolonged mechanical ventilation. Changes described, including both diaphragmatic atrophy
and contraction dysfunction, occurred with a minimum of 18 hours of ventilation. Patients
with chronic obstructive pulmonary disease and reduced ventilatory capacity may experience
limitations in respiratory support for speech as well, though possibly not apparent on typical
speaking tasks.
It is often the case, and indeed it happens almost universally, that when people are asked to
take a deep breath during examination, they will lift the shoulders and give a good example of
clavicular breathing. However, if the patient’s breathing pattern is carefully observed (without
comment) during general conversation and at rest, we would submit that clavicular breathing
will rarely be seen. That is not to say that a patient’s manner of voice production does not affect
respiratory function or is not affected by it. It is difficult to isolate excess tension only to the
larynx and supraglottal vocal tract. Increased generalized thoracic tensions, thus, might be a part
of the total voice production behavior, disrupting effective respiratory support for phonation.
This should not be interpreted, however, as a basic respiratory problem or abnormality.
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Talking from the Diaphragm

“Talking from the diaphragm” seems to have become a phrase known to all whether or not
any understanding of its meaning is attached to its utterance. It no doubt stems from singing
pedagogy and early elocution training. If taken literally, it is physiologically impossible. How-
ever, it seems to be understood to mean that exhalation may be controlled in some way by the
diaphragm. Physiologically, we know that the diaphragm is the primary muscle of inspiration,
acting to enlarge the thoracic cavity in the vertical dimension. It is not an active muscle of ex-
piration. When it is important to fully enlarge the thoracic cavity in order to be able to fill the
lungs, then it would seem to be of value to spend time working on “diaphragmatic breathing.”
In addition, it has been shown that the diaphragm is active during the initial expiratory phase
of respiration when phonation is begun on high lung volumes (Hixon, 1987). There is no
doubt that professional voice users should be well trained in respiratory control. However, the
average speaker is rarely called upon to have that degree of control. The normal speaker adjusts
inspiration (speed and amount) and expiration (rate) to the demands of the utterance (Bless &
Miller, 1972). Daniloff, Schuckers, and Feth (1980) state that speakers tend to breathe deeper
when the utterance ahead is a long one, and less deeply when the anticipated utterance is short.
In soft speech, the average duration of expiratory airflow is reported to be 2.4 to 3.5 seconds,
as compared with the well-trained singer’s ability to phonate loudly for more than 15 to 20
seconds (Daniloff et al., 1980). It is at high (or low) lung volumes that greater muscular control
of respiration needs to be exercised. However, for normal speech activity, great diaphragmatic
breaths are not required.
It is our impression that a great deal more emphasis has been placed on “teaching” or
“correcting” breathing than is usually necessary in working with the voice-disordered patient
who is not a professional voice user. As noted several times in this chapter, attention to easy
and relaxed breathing can be helpful in reducing effort, facilitating voicing and diverting focus
from the larynx. But this is not to suggest that something is “wrong” with respiration. We
would suggest that, in general, more therapy attention should be paid to the ways in which the
speaker uses the air supply.
For example, does the person release a lot of the available air supply before initiating
phonation? Or does the person keep talking after the easily available air supply has been
exhausted, and in so doing increase tension? Or does the person tend to stop in mid-sentence
without releasing the air supply or replenishing it before starting up again? Is there a tendency
to hold the breath before starting to talk? Direct work on such behaviors will help to indirectly
change respiratory behavior and improve smooth respiratory/phonatory coordination.

Ventricular Phonation: Diagnosis or Description?

The term “dysphonia plica ventricularis,” or dysphonia resulting from ventricular fold phona-
tion, was very often given as the diagnosis of a voice disorder, in particular, before the wide
availability of laryngeal imaging. We suggest that ventricular phonation is really a description
based on visual observation, through indirect, flexible fiberoptic or stroboscopic laryngoscopy,
of greater-than-expected approximation of the ventricular folds during phonation. The de-
scriptive term does not reveal the underlying etiology of the behavior. The name given to this
problem implies that the ventricular folds are the actual source of sound, which would suggest
that the true vocal folds are not fully adducting. However, we have observed full true vocal fold
adduction in the presence of compression of the ventricular folds, suggesting perhaps that the
ventricular folds, rather than being the source of sound, may produce a damping effect on
the sound emitted at the true vocal fold level or a restraining effect on the vibratory behavior of
the true vocal folds. We have also observed ventricular fold vibratory behavior in some instances.
Often the medialization of the ventricular folds obscures visualization of the true vocal folds,
making it difficult to determine their movement characteristics. When it can be seen that the true
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vocal folds are not adducting, it appears that the ventricular fold activity is a compensatory be-
havior and may actually result in the best voice a person is capable of producing. It is important,
however, to attempt to determine the reason for the impairment of true vocal fold adduction.
Much is yet to be learned about the physiology, acoustics, and etiology of ventricular
phonation. When the observation of excessive ventricular fold activity is made, it is necessary
to continue the process of differential diagnosis in an attempt to uncover its etiology. Therapeu-
tically we have found that ventricular phonation as a maladaptive, hyperfunctional laryngeal
gesture often associated with psychogenic etiology is rather easily reversed. However, when the
true vocal folds are incapable of adduction, ventricular phonation may well be an adaptive
mechanism resistant to change through behavioral therapy.

Unilateral Vocal Fold Paralysis: Does It Cross the Midline?

It has been stated for many years that the compensatory behavior involved in the restoration of
good voice in the presence of unilateral vocal fold paralysis is a crossing beyond the midline of
the uninvolved fold to make contact with the paralyzed fold. As a result, the goal of therapeutic
procedures espoused for use with this population has been a strengthening of the normal vocal
fold through activities of forceful effort closure of the glottis. There have been scant data to
support the crossover effect in the presence of unilateral vocal fold paralysis. The question
must also be raised as to whether return of voice has been in some instances inappropriately
credited to the therapy program when the patient has, in fact, experienced spontaneous return
of function (as is often the case with an idiopathic paralysis). Or perhaps the therapy hastened
or assisted the return of function. Answers to these speculations are unavailable. And, indeed,
there are those patients who, despite continued paralysis, have experienced return of good voice.
How? What makes the difference between those who experience return of voice in the presence
of paralysis and those whose voices continue to be aberrant?
Although the notion of the crossover effect is an appealing one, we have been impressed by
the lack of its occurrence in many patients we have examined using flexible fiberoptic endoscopy
(Casper, Colton, & Brewer, 1985), whether or not they exhibited return of voice. We explored
whether the crossover could be elicited through various voice therapy maneuvers and failed
to observe its occurrence in the few patients we studied. Schematic representations based on
information obtained from high-speed films of the behavior of the vocal folds in the presence
of unilateral paralysis have shown that the glottis remains open, with the normal vocal fold
approaching the midline but not crossing it, whereas the affected fold has a motion described
as being like a “flag flapping in the wind” (Hirano, Kakita, Kawasaki, & Matsushita, 1977).
More recently, using the rigid stroboscope, which permits an enlarged image, we have become
aware of instances that appeared to show a crossover effect of the intact vocal fold. Further
investigation of this effect is needed to determine whether in fact the vocal fold crosses the
midline, whether there is a shifting of the entire larynx, how this is accomplished and learned
by some individuals but apparently unavailable to others, and many other questions.
Paralysis of the vocal fold not only results in its inability to be moved by contraction of
the affected muscle(s) but also in changes of its level and shape. These parameters—the level,
tension, thickness, and eventual position relative to midline—of a paralyzed vocal fold will be
determined by a variety of factors, including muscle fibrosis and contractures (Ballenger, 1985).
These effects must be better understood in order to be factored into an understanding of the
variability of vocal performance in the presence of paralysis.. It should also be noted that though
the term “paralysis” may refer to a condition in which there is known or suspected injury to a
laryngeal nerve, it is also used frequently to describe a vocal fold that may be fixed due to other
factors, such as scarring from an intubation injury. In some cases, innervation to the fold may
remain intact. Possible differences in fold position and function between an immobile fold and
one that is paralyzed due to a nerve injury have not been thoroughly elaborated. Similarly, we
do not fully understand the effects of residual electrical activity in a fold that is paralyzed. Even
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if the fold is not moving, different degrees of residual electrical activity could possibly influence
its function or position.
Some authors (Yamaguchi et al., 1993) report good success with pushing exercises to
achieve greater glottal closure. In our own experience, we have not been impressed by the
results obtained in voice therapy using effort closure techniques. Indeed, many patients have
reported such exercises to be fatiguing to the voice and seeming to result in poorer vocal
performance for a period of time during and after their execution. In view of these many
concerns, we feel constrained not to recommend the routine use of such exercises in these
cases. Other techniques have been incidentally reported to be effective in producing clearer and
less breathy voice. Among these is the use of a high pitch. When the superior branch of the
recurrent laryngeal nerve is intact and functional, stretching and thinning of the affected vocal
fold will still occur due to the action of the cricothyroid muscle. This action has a component
of adduction and results in greater approximation of the folds and increased tension in the
lax paralyzed fold. The problem with this technique is that the effect and the improved voice
quality that it allows is not transferable to a modal register phonation at an acceptable frequency
level for general communication.
Often patients with unilateral paralysis attempt to compensate for the loss of the ability to
increase loudness level by increasing subglottic pressure and phonatory effort. The effect that
this particular compensatory behavior has is to worsen the voice and make the patient fatigued
with the effort of talking. In such instances, therapy designed to reduce effort and increase
tension and pressures can result in improved phonation. Methods of treating unilateral vocal
fold paralysis through the use of phonosurgical techniques were described in Chapter 9.

The Myth of Optimum Pitch

The concept of an optimum pitch dates back to at least 1940, when it was described by Fairbanks
(1940). It has been defined variously as (a) that pitch at which the voice has good quality and
maximum intensity with the least effort, (b) that pitch at which there is a “vocal swell,” and
(c) a biologically determined ideal pitch for an individual, determined by the anatomical and
physiological characteristics of individual larynges. The methods for its determination have
also varied somewhat, and include the following:
1. Listening for that pitch at which the quality of the voice is best and intensity is the
greatest;
2. Counting the number of musical notes in a person’s full range (optimum pitch will be
that which is 25% of the way up from the bottom of the range);
3. Using the same technique as in (2) above and going up one-third of the way from the
bottom of the range;
4. Having the patient say “um-hum” naturally, with the lips closed and a rising inflection,
while feeling the oronasopharyngeal surfaces for the most resonant frequency;
5. Finding the pitch at which the sustained phonation of the vowel /ah/ is the longest and
loudest;
6. Finding the lowest pitch a person can produce and counting at least four notes up the
scale;
7. Listening for the pitch of the sigh of a yawn-sigh maneuver, which is said to represent
a person’s optimal pitch.
Experimental attempts have been made to explore the claims made about optimum pitch.
In 1958 Thurman measured intensity at the various frequencies as participants hummed a scale.
Only 11% of the highest intensity levels occurred within the range of frequencies that might
be considered to be appropriate for an adult’s optimum pitch. A number of other investigators
have examined frequency–intensity relationships (Coleman, Mabis, & Hinson, 1977; Damste,
1970; Komiyama, Watanabe, & Ryu, 1984) and have reported maximum intensity occurring
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about 70% up from the participant’s lowest sustainable frequency (not the 25%–30% claimed
for optimum pitch). Vocal efficiency, another tenet of optimum pitch, can be measured as
the ratio of the total output (acoustic) power over the total input (aerodynamic) power at
the glottis. Van den Berg (1956), using a catheter between the vocal folds to obtain a direct
measure of subglottal pressure and an esophageal catheter for an indirect measure, found a
positive relationship between subglottal pressure and sound pressure level (SPL). He converted
the SPL into speech power in watts to measure laryngeal efficiency at various frequencies and
intensities. If optimum pitch exists, the expectation would be that an increased output power
would be obtained for the same level of input power at a given frequency. This did not occur.
Using slightly different methodology, Isshiki (1964) reported results similar to van den Berg’s.
House (1959) demonstrated an important contribution of the vocal tract when he reported
that a perceptible change in overall intensity occurred when a vocal harmonic coincided with
the center of a vocal tract resonance. The so-called “vocal swell” thus does not appear to be
related to the concept of laryngeal efficiency. Another line of questioning was pursued by Stone
(1983) when he questioned the perceptibility of the intensity change that was claimed to mark
the optimum pitch. He found that the intensity changes between 100 and 200 Hz, the range
in which optimum pitch would be expected to fall for adult males, were very minimal and
thus imperceptible. Similar to previous reports, Stone also found greatest intensity for half of
his participants to occur at frequencies well above the level at which optimum pitch would
be anticipated. And still further, using the Fairbanks method for measuring optimum pitch,
Stone reported that in 23 of 30 trials (N 5 10 3 3 trials each), the “optimal pitch” fell above
the speaker’s modal pitch. Minifie (1984) reported that the efficiency of the power conversion
increased with intensity rather than with frequency. This author could find no evidence to
support the concept of an optimal pitch as being most efficient.
All of the studies cited thus far used normal-speaking participants. However, Ludlow,
Connor, and Coulter (1984) explored the viability of the optimum pitch concept in patients
with laryngeal pathology. Their results suggested that vocal function is best at the frequencies
in the upper 50% of the speaking range for normal speakers, but not for those with laryngeal
pathology. They interpreted their findings to mean that a set of lawful relationships exists
between several measures of phonatory function and frequency in normal speakers, which are
disturbed in the presence of pathology. Pathology compromises phonatory function, limiting
it to a particular range in frequencies. Thus, in pathological states it is the disturbance of the
lawful relationships that is meaningful rather than the existence of a particular fundamental
frequency range at which phonation can be expected with least effort.
These data all seem to substantially reject the notion of an optimum pitch, at least as cur-
rently defined. Finally, it is important to be wary of subjective perceptions of pitch level. Murry
(1978) demonstrated that judgments of pitch in dysphonic voices may be confounded by other
voice signal parameters, such as loudness, effort, and voice quality. He found a reduction in
phonational range in patients with laryngeal paralysis but did not find speaking fundamental
frequency in dysphonic patients to be significantly lower than in the normal-speaking pop-
ulation. In Chapter 5 it was reported that a prominent perceptual characteristic of voice in
Huntington’s chorea was low pitch. However, actual measurements of fundamental frequency
in this population showed it to be within the normal range. Wilson, Wellen, and Kimbarow
(1983) demonstrated that trained listeners were not better than untrained listeners in judg-
ments of perceived fundamental frequency (pitch) of children’s voices and that neither group
could identify differences of less than 20 Hz at better than chance level. It is also important
to recognize that raising pitch level may appear to reduce breathiness or hoarseness but that
this happens at the expense of, not for the benefit of, the larynx. The extra effort put forth
by the patient may serve to override some of the vocal symptoms. Reduction of loudness is
physiologically a much sounder approach. It seems quite logical that even an optimum pitch,
if there were one, could be used in improper, abusive ways.
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It is the philosophical approach of this book that if phonatory physiology is normalized,

the voice that emerges will be at an appropriate pitch level for that individual. Therefore,
approaching the rehabilitation of disordered voice by attempting to impose an arbitrary pitch
level seems inappropriate, perhaps incorrect, and often unproductive.

Whispering: Is It Harmful?
Some authors believe that whispering should be avoided during periods of voice rest or as a
therapeutic technique because they claim that it results in vocal fold adduction that is unde-
sirable, or that extreme glottal friction characterizes the whisper, which is also undesirable. Are
there available experimental data to support these contentions? There have been a number of
investigations of laryngeal configurations during whisper (Hamlet, 1972; Monoson & Zemlin,
1984; Pressman, 1942; Pressman & Kelemen, 1955; Solomon, McCall, Trosset, & Gray, 1989;
Zemlin, 1988), describing a variety of configurations, including (a) lack of complete adduction
along the full length of the glottis, (b) an inverted V shape, (c) a bowed appearance, (d) a Y shape
with a posterior chink, (e) a bimodal (anterior and posterior) chink, (f ) a parallel configuration
with some adduction, and (g) toeing in of the vocal processes. Various reasons have been sug-
gested for these differences in glottal configuration. Some have suggested that the glottal shape
is a function of the effort involved in the whisper, others suggest it has to do with the type of
whisper (quiet vs. forceful whisper), and yet others claim a relationship to the phonetic context.
Monoson and Zemlin (1984) compared laryngeal appearance (high-speed films), elec-
tromyograms, acoustic, and airflow data for four conditions: quiet whisper, forced whisper,
breathy phonation, and conversational phonation. Glottal configurations varied to some ex-
tent among the conditions and were believed to be at least partially determined by the effort
level involved. Vibratory behavior was absent in both whisper conditions and present in both
breathy and conversational phonation. Airflow was greatest in forced whispering, which was
felt to be due in part to an increase in activity of the expiratory muscles in that condition. These
data do not support the thesis that whispering is an abusive behavior. However, the increases
in expiratory muscle activity and in airflow attributed to the forced whisper suggest an increase
in effort and perhaps in tension.
Solomon et al. (1989) reported on a study of laryngeal configurations for two types of
whispering (high effort and low effort) in 10 speakers using consonant–vowel units and running
speech. The laryngeal configurations were visualized via a fiberoptic bronchoscope and video-
taped for analysis. Significant individual variability was reported. Intrasubject inconsistency was
also noted, although most participants exhibited a preferred configuration. A medium-sized
glottal opening was described for most participants, with a large glottal size occurring more fre-
quently in the high-effort whisper than in the low-effort whisper. Although some constriction
of supraglottal structures was reported, it apparently occurred less than half of the time, even
in high-effort whispering. The glottal configurations described by these authors were primarily
of two types: a straight-edge, parallel configuration, or a toeing-in of the vocal processes.
It is still not clear how such approximation of the vocal folds occurs during whisper,
although these authors report observation of more contact during running speech than in the
production of consonant–vowel units. Four of the 10 participants displayed the straight margin
configuration of the glottis, and these same participants did not approximate the vocal folds.
These authors suggest that the determination regarding the use of whisper as a therapeutic
technique or during periods of vocal rest should be made on an individual basis, depending on
the type of glottal configuration assumed for whisper by that patient. The efficacy of whispering
as a therapeutic approach was not addressed in this study. Hufnagle and Hufnagle (1988)
reported that patients demonstrated improved voice quality following a period of whispering,
suggesting, therefore, that the behavior is not harmful and, indeed, may be helpful.
Recently, Rubin, Praneetvatakul, Gherson, Moyer, and Sataloff (2006) described endo-
scopic findings in 100 patients evaluated for voice disorders. Tasks included counting from 1
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to 10 in a typical voice, and then repeating the task in whisper. The authors reported increased
supraglottic activity in whisper for 69% of patients. The remaining 31% demonstrated no
change or reduced supraglottic activity. The authors do not note whether whisper effort or
intensity were controlled, but the impression is that whisper may involve greater supraglottic
constriction than typical voicing in many dysphonic patients.
There is not yet sufficient evidence available to state unequivocally that whispering is not
harmful. However, our clinical intuition suggests that it may be helpful for some patients, with
a few caveats. Because the high-effort forced whisper tends to suggest increased tension and
effort somewhere in the system and because tension and force are precisely the behaviors that
most patients need to reduce or eliminate, it seems to us that the use of the forced whisper could
be counterproductive. It is also important that the patient recognize that whispering may have
a drying effect on the mucosa of the vocal folds, which should be counteracted by an increase
of fluid intake.
In short, the available evidence about whisper is not nearly as frightening as some of the
strongly stated admonitions against its use. However, much remains to be learned about the
mechanism of whispering. The amount of force in medial compression of the folds when
they appear to make contact during whispering has not been addressed and remains an open
question, as does the degree of expiratory muscle effort involved.

Prevention of Voice Problems

We can discuss the prevention of voice problems by addressing both primary prevention—
preventing the occurrence of the problem in the first place—or secondary prevention—
preventing the recurrence of a problem. In the category of primary prevention, an understanding
of the deleterious effects of cigarette smoking has been effective in convincing many people to
change their habits and eliminate smoking. Throughout American society, steps have been taken
to minimize the spread of the effects of inhaling environmental cigarette smoke by establishing
prohibitions against smoking in theaters, planes, certain sections of restaurants, and other places
of public gathering. Much more needs to be done, however, as it appears that, in absolute num-
bers, the population of smokers has not decreased significantly. The evidence linking smoking
with laryngeal cancer, heart disease, and numerous other medical problems is impressive.
Greater strides need to be made in recognizing the aversive effects on the airway of certain
noxious gases. However, in the absence of widespread information, it behooves professionals to
suggest safeguards that individuals may take when knowingly exposed to a variety of potentially
harmful agents. Such safeguards include wearing appropriate protective masks, avoidance of
unnecessary exposure, introducing air-purifying systems, or improved ventilation.
Education is the primary need in decreasing vocal misuse. We know that cheerleading
constitutes a very stressful, abusive use of the voice that often results in mucosal damage.
However, this knowledge seems not to have penetrated the cheerleading world so that training
in voice use and voice conservation might be provided. There are other abusive activities that
could be similarly identified. Some, such as rock singing in the presence of highly amplified
sound, may not be amenable to change. Despite, or perhaps due to, laryngeal pathology such as
nodules or polyps, some rock singers have a “sound” uniquely theirs that would not be possible
without abuse.
Another group of people who would benefit from increased education about the voice
are choir singers. Many have untrained voices and abuse them with regularity but without
awareness. Choir directors frequently have limited backgrounds in vocal pedagogy and are
thus ill-equipped to train their choirs in healthy habits of singing and voice use. This becomes
increasingly critical when the choir is composed of or includes prepubertal children.
Primary prevention through education needs to be increased in the public schools so
that children learn to recognize beginning signs of vocal problems and are trained in voice
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358 Understanding Voice Problems

conservation. In addition to education of the children, all school personnel should have a
greater understanding of vocal misuse, its harmful effects, and ways to avoid or eliminate it.
Such education not only would be helpful to them in managing their own voice production but
also would make them more capable of identifying the problem in children. Such a program,
which had impressive results, is described by Nilson and Schneiderman (1983). Their program
was directed at second- and third-grade students and their teachers and included discussion
of the vocal mechanism and voice production, voice qualities both normal and abnormal, and
learning to identify vocal abuse. Both the children and the teachers were found to have gained
and retained significant knowledge about the voice, and when the children who had been part
of the program were retested for voice, no new cases of dysphonia were identified. A primary
prevention plan has been proposed by Flynn (1983), and Marge (1984) has addressed prevention
of voice disorders as one area under the broader topic of prevention of communication disorders.
Secondary prevention, for those who have experienced even a single episode of vocal
disturbance that required treatment, is essential. It is incumbent upon laryngologists who
successfully treat a patient with a preventable problem that they either take the time to clearly
instruct the patient in a program of vocal hygiene or refer that patient to a speech-language
pathologist for such education and counseling. Indeed, failure to do so might leave the door
open for medical-legal problems.

Malpractice
In the current litigious climate, it is important that all those who treat patients with voice
problems, including speech-language pathologists, recognize how they may be vulnerable to
malpractice actions and take appropriate steps to safeguard themselves. Instances of persons
with voice problems bringing suit against otolaryngologists or speech-language pathologists
and of speech-language pathologists being called upon to testify as “expert witnesses” in suits
brought against others have already occurred. During the years 1980 to 1985, there was a 10%
increase in claims against speech-language pathologists (Kooper & Sullivan, 1986).
Prime candidates to bring such suits are persons who claim that the treatment provided,
surgical or otherwise, created or resulted in a permanent condition no better or worse than the
original problem and that they had not been advised of the possibility of that outcome. Others
might claim damages for a missed diagnosis that resulted in unnecessary treatment and/or
delayed initiation of appropriate treatment. The extent of liability for a disabling condition
appears to be directly related to the severity of the injury as measured by its duration (Kooper
& Sullivan, 1986). Thus, if a voice disorder is present and is not expected to abate or change
over the person’s lifespan, its severity will be judged to be greater if the patient is 25 years old
than if he or she is 85. The extent of liability will be related to the perception of the degree of
severity of the problem.
It is of utmost importance that very complete, dated records be maintained on each patient.
Such records should contain the results of all testing and examination, case history material,
statements of diagnosis or a listing of the differential diagnosis if full exploration has not been
completed, a treatment plan, statements of prognosis specific to planned treatment modalities,
and a record of all contacts with the patient or about the patient. Furthermore, whenever
surgical intervention is planned, a recorded sample of the patient’s voice should be a part of the
record. A second recording should be made postoperatively, with additional recordings made
periodically as changes in voice occur. The speech-language pathologist should make audio
recordings of the patient’s voice at the time of the initial visit and periodically after that.
Those who work with voice-disordered patients, when called upon to testify in court as
an expert witness, must establish their expertise. They must be knowledgeable and articulate
about phonatory physiology as well as about testing and treatment procedures, the nature of
voice disorders, and the emotional ramifications of disturbed communication skills or loss of
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the source of a livelihood. The primary question to which they will be expected to respond deals
with the acceptability of the treatment that was provided in the case. This does not require that
the witness agree with the course of treatment, as long as it is an accepted form of treatment
for the problem.

Summary
Vocal rehabilitation in its broadest sense is discussed in this chapter. Concepts, principles, and
guidelines basic to vocal rehabilitation receive attention, and specific therapeutic techniques are
presented. The role of voice therapy in the treatment of voice disorders, the appropriate goals of
such treatment, and the nature of the therapeutic process is proposed for the various categories
of voice disorders, such as those associated with mucosal changes, those involving misuse and
abuse, and those with neurological involvement. A section is devoted to discussion of some
special voice problems that do not fit into these categories. The discussion of specific therapeutic
techniques includes a description of how they are done, with suggestions and cautions gained
from clinical practice. A rationale is presented for each technique that relates its physiological
implications to the disturbed physiology typical of the voice disorders to which it is applicable.
The considerations that must be taken into account in developing a prognostic statement are dis-
cussed, and some criteria for termination of therapy are suggested. The authors raise some issues
in vocal rehabilitation that are based on unresolved questions and for which no substantiating
data are available and question the continued use of optimum pitch as a viable concept. Dis-
cussions of the prevention of voice disorders and of malpractice concerns complete the chapter.
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CHAPTER

11
Voice and Laryngectomy

Keywords
alaryngeal, botulinum, cancer, cordectomy, electrolarynx, esophageal,
hemilaryngectomy, laryngectomy, laser, metastasis, myotomy, PES, prosthesis,
resection, TEP, TNM staging, tracheoesophageal

This chapter is concerned with voice and voice therapy when all or a portion of the larynx has been
ablated. When the larynx is completely removed, referred to as a total laryngectomy, an alternative voice
source is required. If a portion of the larynx is removed, that is, partial laryngectomy, voice therapy may
be indicated. The most common reason for laryngeal ablation is cancer of the larynx, which is diagnosed
in more than 12,000 new patients in the United States each year (National Cancer Institute, 2009).
The most frequent type of cancer in the larynx is squamous cell. Across age and race, the incidence of
laryngeal cancer is 6.1 per 100,000 in men; 1.3 per 100,000 in women. The National Cancer Institute
reports further that more than 3,000 patients die from their disease each year. Unfortunately, 5-year
survival rates, based on all types of laryngeal cancer, have not improved substantially in several years and
is currently at about 61% in the United States. Survival rates are improved dramatically when disease is
localized to the larynx, and diminished if there is involvement of lymph nodes, or more distant structures.

Classification of Laryngeal Cancer

For epidemiological purposes, head and neck cancers are described by general location, as of the lip,
tongue, mouth, pharynx, or larynx. Further specification in the medical/surgical literature may localize
cancers to the tonsil, soft palate, floor of mouth, various parts of the tongue (base, tip, lateral), mandible,
maxilla, pharynx, and other structures. In the larynx, it is classified as affecting the supraglottis or false
vocal folds, the glottis, or true vocal folds, and the subglottis. Cancers may also be classified according
to a staging system proposed by the American Joint Committee on Cancer (2002) based on both the
site and extent of a lesion. In this schema, for example, a tumor limited to one or both vocal folds (both
mobile) is designated “T1”; a “T4” classification would denote a tumor with deep invasion of other
structures, for example, the laryngeal cartilages, trachea, esophagus. Tumor staging is also elaborated
separately for cancers affecting supra- or sub-glottal tissues. Additional staging involves the regional
lymph nodes. For example, “N0” indicates no regional lymph node metastasis. Staging according to the
presence, extent, or absence of distant metastasis, that is, disease originates in one location and travels
to another, is designated with “M,” as MO (no distant metastasis), M1 (distant metastasis), or MX,
indicating metastasis cannot be assessed. A patient with T1NOMO lesion would thus have a lesion
confined to one vocal fold (mobile) with no extension to the lymphatic system or distant metastasis.
Other staging addresses histological characteristics of the tumor, invasion of the lymphatic system (not
just a node), and venous invasion, respectively. Tumor staging is a part of the physician’s pretreatment
diagnostic evaluation of a patient. A more definitive classification may emerge as treatment is actually
360
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CHAPTER 11 I Voice and Laryngectomy 361

undertaken. It is important for the voice clinician to recognize that a cancer described as
originating in the larynx may also have extension to other head and neck, or more distant,
structures. A careful review of treatment records, comprehensive clinical examination, and
consultation with physicians involved in the patient’s care may all be required in order to
understand the extent of a patient’s deficit, the specific type and intent of any reconstructive
procedure utilized, and the functional status of remaining tissues.

Implications of Laryngeal Resection for Voice and Speech

As surgical and medical management of laryngeal cancer has improved, conservation treat-
ments that restore or preserve laryngeal structures have been introduced. Though the emphasis
rightfully continues to be on eradication of disease, these new approaches have expanded the
possibilities for voice restoration in many laryngeal cancer patients. At the same time, it has
become clear that preservation of laryngeal tissue does not always translate into improvements
in all laryngeal functions. This is in part a reflection of the diverse roles of the larynx in airway
protection and maintenance, and phonation. That is, what may suffice as a voicing source may
not work equally well as an airway protector.
There is a tendency for us to think of “ablation” as associated with steel instruments that cut
away diseased tissue, and certainly surgery with conventional instruments continues to be used
in the management of laryngeal cancer. However, other ablative tools are available and widely
utilized in contemporary treatments of laryngeal cancer. Lasers, in particular, C02 lasers, but
some others as well, have become increasingly popular in the treatment of early glottic lesions
restricted to the vocal folds (Zeitels, Burns, Lopex-Guerra, Anderson, & Hillman, 2008). In
transoral laser endoscopy, the laser is introduced through the oral cavity, precluding the need
for access to the tumor site through an “open” procedure that requires cutting through other,
healthy tissues. Patients do not need a tracheotomy and may be able to speak and swallow
very quickly after surgery. Other treatment modalities include radiotherapy and chemotherapy.
Continued improvements in radiotherapy permit greater precision and delivery to involved
tissues, and it is sometimes used independently, or in combination with other treatments. For
some lesions, either radiotherapy or surgery may offer comparable survival rates, affording
an individual patient realistic alternatives to treatment. However, prolonged and worsening
fibrosis of vocal fold tissues associated with radiation, as well as mucositis and atrophy, can
seriously interfere with a patient’s voicing potential. Chemotherapy currently appears to be
used primarily in the treatment of advanced laryngeal cancer, most often in conjunction with
radiotherapy (Jacobi, van der Molen, & Huiskens, 2010). Independent effects of chemotherapy
on voice are thus difficult to determine.
Ablative procedures of the larynx can be generally divided into partial and total laryn-
gectomies. Total laryngectomy involves removal of the entire larynx and is typically indicated
in large lesions. Carcinoma in situ (confined to the site of origin) and microinvasive disease
involve only the vocal fold cover and are often managed by endoscopic excision. Partial or total
cordectomy, in which only one true vocal fold is involved, is indicated for T1–T2 lesions and is
typically treated with either radiotherapy or conservation surgery. Other partial laryngectomy
procedures include “vertical,” which may be either a standard or extended hemilaryngectomy,
and “horizontal,” also referred to as a supraglottic laryngectomy, standard or extended. Subto-
tal or near-total laryngectomy implies greater extent of disease and resection, and typically a
neoglottic reconstruction with some type of tissue flap utilizing spared nontumor tissue. In the
next section, the specific effects on voice and speech associated with each type of resection, as
well as rehabilitation strategies unique to each, will be discussed.

Total Laryngectomy and Speech Rehabilitation

Total laryngectomy affects more than speech, and the voice clinician needs to be aware of just
how extensive the consequences can be. The trachea is now dissociated from the upper airway,
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362 Understanding Voice Problems

requiring a permanent tracheostoma and tracheostomy tube for breathing. Changes, including
lack of humidification of inhaled air, and diminished smell and taste, are dramatic. The
esophagus is intimately related to the airway, and removal of the larynx may also affect swallow
function. Life-style activities previously taken for granted, like taking a shower or coughing,
are complicated. One goal for the voice clinician is to provide the patient with functional
communication, as quickly as possible. Pretreatment counseling, if only to get acquainted
with a patient and plan for the immediate postoperative period, for example, ensuring that
the patient can write or otherwise make his needs known right after surgery, is well advised.

Implications for Speech

If the larynx is completely resected, voice produced by the true vocal folds is lost, and the
patient is unable to produce vowel sounds and all voiced consonant sounds. Even with the
airway diverted to the neck, most individuals can quickly learn to use residual air in the oral
and pharyngeal cavities to produce voiceless speech sounds (p, wh, f, t, s, sh, ch, k). One
exception to this is the sound /h/, which is articulated by the vocal folds. Articulation of other
speech sounds, and the speaker’s ability to effect resonance changes in the vocal tract, typically
remain intact.
The history of voicing alternatives in alaryngeal speech is fascinating and extensive (Kear-
ney, 2004; Leonard, 2010), illustrating both human ingenuity and the power of the need and de-
sire to communicate orally. Currently, however, there are three primary options for the alaryngeal
speaker, including electronic devices, otherwise referred to electrolarynges, esophageal speech.
and tracheoesophageal speech. In keeping with both the contemporary popularity and preva-
lence of these rehabilitation strategies, our discussion here will address only these alternatives.

Electrolarynx
The “electrolarynx” is one of the most enduring voice options for speakers with total laryngec-
tomy. These battery-powered instruments produce sound electronically and then transmit this
sound into the upper airway. If sound energy sufficient to excite this column of air is delivered,
the speaker should be able to articulate voiced speech sounds. There are two major types of
these instruments, a neck type and an intraoral type. The neck or throat device is placed on
tissues of the neck (or perhaps cheek) and sound is transmitted through transcervical tissues
of the body into the airway (Fig. 11.1). An intraoral device transmits sound directly from the
electronic source into the oral cavity through a plastic tube that the speaker holds in the corner
of the mouth (Fig. 11.2). Some neck-type electrolarynges can be fitted with an attachment that
permits them to be used as an intraoral device. These instruments may be indicated in patients

B
A

FIGURE 11.1. Neck-type electrolarynx

(Servox) is shown. At right in figure, at-
tachment for using a mouth placement is C
shown.
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CHAPTER 11 I Voice and Laryngectomy 363

FIGURE 11.2. Intraoral electrolarynx

(Cooper-Rand).

with thick or fibrotic neck tissues that preclude use of a neck-type electrolarynx. A second type
of intraoral device can be encased in a specially fitted palatal prosthesis and attached to the
palate. Sound is then introduced into the oral cavity and pharynx for articulation. A hand-held
control permits turning the instrument on or off and making adjustments of pitch and volume.
The devices are designed to prevent damage from saliva or food.
The advantages of electrolarynges include their applicability, availability, and ease of use.
Many alaryngeal speakers are candidates for these instruments, have access to them, and can
quickly learn to use them shortly after surgery. Though newer instruments are small and
compact, they do require the use of one hand, and generally preclude talking and engaging
in complex manual activities at the same time. With some intraoral devices, a placement
that doesn’t interfere with articulation can be difficult, and the tube may collect saliva. If a
patient has trismus, or restricted jaw opening, placement of a palatal prosthesis containing
an instrument may not be possible. The sound produced by most electronic devices does not
closely approximate human vocal quality. A related problem is that, unlike natural speech, which
includes both voiced and unvoiced sounds, all speech sounds produced with the electrolarynx
are voiced. Other differences may not necessarily be detrimental. For example, there is evidence
that the association between speech and breathing in normal speakers may be altered in some
alaryngeal speakers using electrolarynges (Bohnenkamp et al., 2010; Liu et al., 2004; Stepp,
Heaton, & Hillman, 2008). Usui (1979) reported that speakers accustomed to long and lone
use of an electrolarynx demonstrated difficulty with other methods of alaryngeal speech that
required more usual respiratory patterns.
Newer developments in electrolarynx technology have focused on greater intensity gener-
ation and pitch variability, increased ease of use, and decreased radiated noise, but electronic
devices that permit speech that sounds more natural, or is unique to the speaker, are generally
not available at this time. Investigation of a “hands-free” electrolarynx has been an ongoing
project for one group of researchers in the past few years (Goldstein, Heaton, Kobler, Stanley,
& Hillman, 2004; Goldstein, Heaton, Stepp, & Hillman, 2007; Saikachi, Stevens, & Hillman,
2009). The intent of this device is to allow a speaker to control an electrolarynx (attached to the
submental neck) using electromyographic (EMG) activity from intact strap muscles. Real-time
feedback from surface EMG is used to teach patients how to control various aspects of voice
production, including onsets and offsets, and pitch. Preservation of strap muscle innervation
on one side is currently required, though the investigators suggest that other muscles may also
be appropriate control sites. This device is to our knowledge not yet commercially available, but
may provide an attractive alternative to some alaryngeal speakers. Sharifzadeh, McLoughlin,
and Admadi (2010) have described a potential technique in which the speaker whispers into
an external device that then recreates and outputs natural-sounding speech. The technique
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364 Understanding Voice Problems

uses linear prediction processing to analyze formant and other characteristics of the patient’s
own whispered speech and to then reconstruct the missing voiced elements so that the output
sounds more like normal speech. To date, the authors report good reproductions of vowels and
diphthongs but less success in regenerating complete sentences. If continued development leads
to continued improvement, this type of device may one day offer significant new potential for
alaryngeal speakers.

Voice Therapy and Electrolarynges

As noted, one appeal of an electrolarynx is its wide applicability across patients. Nonetheless, the
voice clinician’s input can be vital. Assessing the patient’s candidacy for any particular alaryngeal
speech alternative, and educating the patient about these possibilities, is a first step. If it is decided
that an electrolarynx is appropriate, the clinician needs to assess the patient’s potential for a
neck- or, possibly, intraoral-type device and manual skills appropriate for their respective use.
The clinician can also assist with identifying an optimal placement for the vibratory source,
one that is not painful and provides maximum transfer of energy into the vocal tract. Features
important to care of the device, that is, changing batteries, cleaning, and so on, should also be
discussed. Many learners will exhale forcefully through the stoma when first using the device
for speech, which adds noise to the output that can interfere with intelligibility. Learning to
time onsets and offsets of the device with speech can be difficult for some patients, with some
activating it before, and others after, they begin speaking. Work on precise articulation of speech
sounds is also important to improving intelligibility with a voicing source that is continually
“on.” Typically, most therapy goals can be accomplished in s few sessions.

Esophageal Speech
Reports of alternative tissues, including the pharynx, tongue, and esophagus, used as vibratory
sources for speech date to the 1800s (Luchsinger & Arnold, 1965). Esophageal speech refers
to the use of the upper esophageal sphincter (UES), also referred to as the pharyngoesophageal
(PES) segment, as a vibratory sound source. To speak in this fashion, speakers must learn to
inject and/or inhale air into the esophagus and to then direct this back over the PES. Injection
requires using the tongue as a sort of pump to elevate supraglottal pressure (as in production
of a plosive consonant) and force air into the esophagus. Inhalation involves relaxing the PES
during inspiration so that air can enter the esophagus. Even in the best esophageal speakers,
voice production is lower in frequency than normal, on the order of 60 to 70 Hz, even in
women, and is limited in variability. The air capacity of the esophagus (80–100cc) is less than
the lungs (5–6 liters), so that fewer syllables can be produced per air expulsion, and overall
speaking rate is reduced (Snidecor & Isshiki, 1965). But, produced by the speaker’s own tissues,
utilizing intact vocal tract modulators, it does have the advantage of being unique to the speaker
(and distinct from other speakers), requires no batteries or free hands, and represents a viable
alternative for those individuals who are able to learn it.
There are a number of characteristics of the structure of the PES that can influence its
ability to produce sound. For example, hypertonicity or spasm of the PES, as well as excessive
flaccidity, can interfere with sound quality. Dilation, pharyngeal neurectomy, myotomy, and
botulinum toxin have all been used in the treatment of PES hypertonicity (Zormeier et al.,
1999). The application of compression to the neck in the area of the PES, either by hand
or with a neck band, can sometimes be effective in patients with a flaccid segment. Izdebski
et al. (1988) reported that patients who developed esophageal, or tracheoesophageal, speech
following laryngectomy, but prior to radiotherapy, experienced deleterious changes in voice and
speech during radiotherapy. The authors attributed this to changes in the impaired mobility
and vibratory capability of the esophageal wall and mucosa, to fibrosis of the submandibular
region, and to trismus. Speech and voice function was generally restored to preradiotherapy
levels within weeks of the end of radiation, however.
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Voice Therapy and Esophageal Speech

One of the intriguing questions regarding voice therapy for an esophageal speaker is whether
proficiency in esophageal speech is necessary for the voice clinician. In our own experience,
the ability to at least demonstrate esophageal sound production, with individual sounds and
possibly short utterances, is helpful. It is also true that alaryngeal speakers who are proficient
in esophageal speech are also sometimes excellent teachers. The International Association of
Laryngectomees (IAL) and the American Cancer Society (ACS) are resources for identifying
such individuals. A number of texts and other materials are also available that focus on teaching
esophageal speech (Lauder, 1998; Shanks, 1994). The voice clinician can certainly be helpful
in determining a patient’s candidacy for esophageal speech. Perhaps the first issue to consider is
the motivation and learning capability of the patient, since esophageal speech requires learning
that can sometimes be intensive. Beyond this, the integrity of the PES to produce sound needs
to be determined. If a patient is having difficulty swallowing, for example, the status of the PES
may be questionable. A fluoroscopic swallow study can be combined with an insufflation test,
that is, inserting a catheter into the esophagus, below the PES, and injecting air into it (from
an external source or by having the patient blow into it gently) to assess the potential of the
segment to produce voice. The progression of therapy is generally from producing esophageal
sound consistently and easily on vowels or voiced syllables, to longer utterances. Additional
goals will include variability in pitch, optimal loudness, reduction of excessive stomal noise that
masks speech, maintaining or improving articulatory precision, and increasing speaking rate.
Again, this process may be daunting for some patients, an acceptable challenge for others. If
progress is elusive, effective and immediate troubleshooting is required, and the voice clinician
can be instrumental in the process.
In the mid-1900s, esophageal speech was an attractive alternative to the patient whose
other choices might be limited to an electrolarynx. However, available reports indicate that as
many as one-third of patients failed to become proficient in its use (Goode, 1975). Interestingly,
there are contemporary reports suggesting that some patients who first become proficient with
a tracheoesophageal prosthesis are able eventually to use “nonprosthetic” esophageal speech,
suggesting that the experience of using the PES as a vibratory source, regardless of where the
air to power it comes from, may facilitate its acquisition (Iwai, Shimano, & Omae, 2006).

Tracheoesophageal Speech
The third primary alternative for alaryngeal speakers is tracheoesophageal speech, popularly
referred to as TE speech or TEP speech. This method is based on a series of historical attempts
to surgically establish a route for air from the trachea to the cervical esophagus. In 1979,
Blom and Singer described a surgically created fistula from the posterior wall of the trachea
into the cervical esophagus through which a one-way silicon valve, that is, tracheoesophageal
prosthesis, could be placed. In order to produce voice, the speaker occluded the stoma and
exhaled, allowing air to be diverted into a small inferior port in the tracheal portion of the
prosthesis and then through the valve into the esophagus. When air pressure under the PES
was adequate, esophageal sound could be produced and used to support speech (Fig. 11.3). A
major advantage of this method, as compared to traditional esophageal speech, is in the number
of syllables that can be produced on one exhalation. As noted, the esophagus can deliver only
a small amount of air (80–100cc) to power the PES, as compared to the much greater amount
of pulmonary air typically available. At least two studies have characterized sub-pseudoglottic
pressures required for speech in TE speakers as greater than normal, and airflows as lower than
normal, but the differences identified were not excessive, suggesting relative ease of initiating
and maintaining PES sound (Kotby, Hegazi, & Gamal, 2009; Schutte & Nieboer, 2002).
Other advantages of TE speech over esophageal speech may include a higher fundamental
frequency. Factors that adversely affect a patient’s ability to use a tracheoesophageal prosthesis
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366 Understanding Voice Problems

FIGURE 11.3. Tracheoesophageal pros- A

thesis (Blom-Singer, from In-Health). Pha- C
lange shown at (A) is taped outside the
stoma. (B) shows portion or prosthesis, a
“one-way valve,” which is placed between B
esophagus and trachea. In (C), tool used for
insertion of device is shown.

include stoma size, manual skills, and the integrity of the PES as a sound generator. A video clip
illustrating the surgical creation of the tracheoesophageal fistula is in the disk accompanying
this text (Tracheoesophageal fistula creation).
Since its introduction, TE speech has become widely accepted and utilized. The proce-
dure was first described as a secondary procedure to laryngectomy, but can also be performed
at the time of laryngectomy. A number of studies have reported no difference in speech quality
whether the TE surgery is done as a primary or secondary procedure (Izdebski, Reed, & Ross,
1994; Kao, Moore, & Kimmel, 1994; Maniglia, Lundy, & Casiano, 1989; Wenig, Mulooly,
& Levy, 1989). Prior radiation therapy does not typically affect the complication rate of the
TE surgical procedure, or speech outcome, though some patients may experience greater diffi-
culty with leakage and, possibly, necrosis of the fistula tract related to radiation (Artazkoz del
Toro, Lopez, & Martinez, 1997; LaBruna, Klatsky, & Huo, 1995; Trudeau, Schuller, & Hall,
1989). Another advantage of TE speech is that it may be used effectively in patients who have
undergone pharyngectomy and laryngectomy and have then been reconstructed with radial
forearm or jejunum flaps (Deschler, Doherty, & Reed, 1994; McCauliffe, Ward, & Bassett,
2000). However, quality of speech is likely to be significantly poorer in these patients than in
patients with total laryngectomy only (Simpson, Postma, & Stone, 1997).
In the 30 plus years since their introduction, tracheoesophageal prostheses have under-
gone a number of modifications. These include increases in the diameter of the valve and
modifications of the esophageal port to achieve lower resistances (and greater ease in sound
generation), variations in design of the esophageal portion of the prosthesis to prevent flow
of material from the esophagus into the airway, and alterations designed to minimize fungal
colonization (Eerenstein, Grolman, & Schouwenburg, 1999; Izdebski, Ross, & Lee, 1987) and
improve airway humidification. In addition, a prosthetic valve that automatically occludes in
response to certain levels of tracheal air pressure, eliminating the need for digital occlusion, and
“indwelling” prostheses designed to eliminate the need for frequent removal and cleaning of the
device have been introduced (Fig. 11.4; Cavalot, Magnano, & Nazionale, 1997; Graville, Gross,
& Andersen, 1999; Leder & Erskine, 1997). Available prostheses come in a variety of lengths
and can be further customized with a standard laryngectomy intraluminal button modified
to accommodate individual tracheostoma characteristics (Lewin, Montgomery, & Hutcheson,
2009). Several devices are available, for example, Blom-Singer (In-Health), Provox, Groningen,
Voice Master, Nijdam, and a few investigations have compared speech characteristics between
or among prostheses (Chung, Patel, & Ter Keurs, 1998; Delsupehe, Zink, & Lejaegere, 1998;
van den Hoogen, Van den Berg, & Oudes, 1998). The devices are relatively inexpensive, with
current prices in this country ranging from less than US$50 to $200 or more (Lombard &
Popovich, 2008). They are widely available in some parts of the world but can be expensive
and difficult to obtain in some locations.
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FIGURE 11.4. (A) Indwelling prosthesis

A (Provox 2, from Atos), and (B) brush used
for cleaning prosthesis. Remaining imple-
ments are used for placement of prosthe-
sis, typically by a trained professional. In-
dwelling prostheses may last for several
months but will require eventual replace-
B ment.

In our own experience, even with newer devices, some patients may not prefer prostheses
with automatic valves, in particular, if they are capable of a wide range of exercise levels that have
differing respiratory requirements. We have also noted a direct relationship between increased
diameters of valves and degree of leaking around the prosthesis and have attempted to strive for
the least resistance possible without also incurring excessive leakage. Use of the laryngectomy
buttons previously noted can be very helpful to this purpose. Our own philosophy has been to
ensure that patients are proficient at both maintaining, that is, removing, cleaning, inserting,
and using TEPs prior to dismissal from therapy, in part because many of our patients live far
away from our center and have few resources for expedient help should they experience diffi-
culty. The first indwelling devices required physician insertion and replacement, and minimal
patient involvement. Newer materials and insertion techniques have made some of these more
“user friendly” for patients and voice clinicians, and they have become increasingly popular.
Nonetheless, all tracheoesophageal prostheses are vulnerable to breakdown over time and will
require replacement.

Voice Therapy with TEP

The voice clinician’s role in patients with tracheoesophageal prostheses often extends well
beyond voice improvement. In fact, the American Speech-Language-Hearing Association has
published an extensive document regarding knowledge and skills necessary for voice clinicians
interested in evaluating and treating patients with TEPs (www.asha.org) . Many clinicians are
actively involved in selecting and fitting the prosthesis, and in helping patients manage its
ongoing use and care. As noted, any prosthesis is subject to deterioration over time. Leakage
through the prosthesis suggesting microbial colonization is a first sign of the need to replace
it. If leakage around the prosthesis is persistent, replacement with a shorter prosthesis, or
even removal of the prosthesis to allow the fistula to shrink, may be indicated. In some cases,
injections of materials such as collagen, fat, or other substances around the insertion site in the
trachea may be used to reduce fistula size. The voice clinician’s ability to troubleshoot and assist
patients with this issue and many others related to use and maintenance of the prosthesis can
be a critical factor in its success.
Available data regarding the relative use of electrolarynges, esophageal speech, and tra-
cheoesophageal speech in this country often present disparate conclusions. For example, artifi-
cial larynx use among alaryngeal speakers has been reported at rates ranging from 5% to 66%
(Hillman, Walsh, & Wolf, 1998). The prevalence of traditional esophageal speech is similarly
in doubt but is undoubtedly less now than prior to the emergence of the TE prosthesis. Use of
TEP speech has been reported to range from 30% to 93% (Hillman et al., 1998). Two surveys
among head and neck surgeons reported the acquisition rate of TEP speech as between 30%
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368 Understanding Voice Problems

to 38%, the rate of esophageal speech acquisition between 38% and 49%, and artificial larynx
(including electrolarynx) use between 21% and 48% (Gates, Ryan, & Cooper, 1982; Pawar,
Sayed, & Kazi, 2008). In a survey of 151 experienced speech-language pathologists, TEP speech
was reported to be their “preferred” rehabilitation alternative, and the electrolarynx, their least
preferred method. However, the electrolarynx was reportedly the most frequently used method
(Culton & Gerwin, 1998). As much as 50% of the speech-language pathologists surveyed re-
ported that fewer than 6 therapy sessions were required for patients to become competent with
TEPs; 20% reported the need for 10 or more therapy sessions. Hillman et al. (1998) described
functional outcomes, including voice and speech, in patients who received either surgery and
radiation, or radiation and induction chemotherapy, for treatment of T3 and T4 laryngeal
squamous cell carcinoma. Of 166 patients who underwent total laryngectomy followed by
radiation therapy, 6% developed esophageal speech or remained nonvocal (8%), 55% used an
electrolarynx, and 31% successfully used tracheoesophageal prostheses.

Nontotal, Partial Laryngectomies

Carcinoma In Situ/Microinvasion
Lesions that are minimally invasive and amenable to either surgical, often with a transoral
endoscopic approach, or radiation therapy may nonetheless have consequences for voice. The
epithelial layer of the vocal fold affected is the outer layer of the fold’s vibratory margin, and
voice quality following treatment is likely to be influenced by how much mucosa is excised as
well as the straightness of the edge of the fold. A number of authors have reported good results
for postoperative voice using the C02 laser. Zeitels et al. (2008) described excellent health and
voice outcomes in patients treated with an angiolytic laser (KTP), which destroys the tumor’s
blood supply and cancer cells while sparing healthy tissues. Other authors have reported good
results with careful microdissection using “cold” phonomicrosurgical techniques.

Cordectomy
For lesions (typically T1 or T2) that involve one vocal fold, partial cordectomy is achieved
with surgical or radiation therapy. Voice posttreatment is likely to be affected by the amount of
tissue loss, the degree of contact between both true vocal folds on voicing, and the condition of
the mucosa. If treated with laser excision, scar tissue eventually replaces the missing tissue and
is covered by mucosa. However, the underlying stiffness of the fold at this site may be revealed
by the lack of a mucosal wave on stroboscopic imaging and may contribute to poorer voice
quality. Well-known effects of radiation include necrosis, mucositis, edema, xerostomia, and
fibrosis, all of which may affect the vibratory source and resulting voice quality posttreatment.
In total cordectomy the entire vocal fold, from the vocal process of the arytenoid to the anterior
commissure, is involved.
Collective review of studies investigating effects on voice of cordectomy appears to demon-
strate clearly only that poorer voice is associated with partial laryngectomy than with radio-
therapy or laser microsection and that voice may not return to normal regardless of treatment
modality (Colton, Sagerman, & Chung, 1978; Hoyt, Lettinga, & Leopold, 1992; Murry, Bone,
& Von Essen, 1974; Stoicheff, 1976; Tsunoda, Soda, & Tojima, 1970). Although the weight of
the available evidence may suggest more benign effects of radiotherapy than laser microsurgery,
there is at least some evidence that voice results may not differ significantly between these two
modalities. It should also be noted that procedural problems with much of the available research
make findings problematic in some cases, and comparisons difficult. A lack of pretreatment
comparisons across patients, insufficient control over lesion type and extent, some patients
receipt of multiple treatment modalities, variability in time of evaluation posttreatment, and
variability in voicing measures obtained are a few of the factors contributing to this dilemma.
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CHAPTER 11 I Voice and Laryngectomy 369

FIGURE 11.5. Shown at left is an anterior view of structures involved

in an extended hemilaryngectomy. In a standard hemilaryngectomy the
dashed lines on the left side of the larynx would extend through the
midline, not involving the opposite side. On the right is a superior view of
the same larynx. Dashed line illustrates structures involved in resection.
Lesion is illustrated on left at arrow; note extension across midline at
anterior commissure. (Figure courtesy of Donald, P. The Difficult Case
in Head and Neck Cancer Surgery.)

Hemilaryngectomy
Hemilaryngectomy refers to a partial laryngectomy, either vertical or horizontal. The horizontal
partial laryngectomy is also called a “supraglottic” laryngectomy and will be discussed next.
In a vertical partial laryngectomy, the true vocal fold, false vocal fold, ventricle, and anterior
thyroid cartilage are removed. The epiglottis remains intact. In an extended hemilaryngec-
tomy (Fig. 11.5), the ipsilateral arytenoid cartilage and part of the contralateral true fold are
involved as well. Voice is obviously affected by such procedures, and numerous strategies for
reconstructing the excised side have been described, including muscle flaps from distant areas,
epiglottic laryngoplasty, corniculate-cuneiform flaps, and several types of local flaps (as from
pyriform sinus, platysma, false vocal fold, or aryepiglottic fold). Mandell, Woo, and Behin
(1999) examined 42 patients who had undergone vertical partial laryngectomy with various
types of reconstruction. These authors found that the contralateral false vocal fold was the most
common site of vibration, followed by contralateral arytenoid mucosa and then contralateral
true vocal fold. No differences were found in quality of voice with respect to site of vibration,
and voice quality was judged similar for pyriform mucosa flap reconstructions and other types
of reconstruction. Voice outcomes associated with various reconstruction techniques have been
reported (Blaugrund, Gould, & Haji, 1984; Hirano, 1987; Luna-Ortiz, Campos-Ramos, &
Villavicancio-Valencia, 2010; Salam, el-Kahky, & el-Mehiry, 1992). However, questions regard-
ing the best alternative for reconstruction in these patients are complicated by wide variability
in both treatment modalities and reconstruction options and the generally small numbers of
participants within each group available for study.

Supraglottic Laryngectomy
This procedure involves excision of the epiglottis and preepiglottic space, aryepiglottic folds,
false vocal folds, upper third of the thyroid cartilage, a radical neck dissection, and possibly the
hyoid bone (Fig. 11.6). The true vocal folds are left intact, and voice is typically good to excellent
following treatment. If poor, factors to consider are edema, radiation fibrosis, aspiration effects,
and impaired mobility of residual structures.
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FIGURE 11.6. Supraglottic laryngec-

tomy. Shown are anterior views of lar-
ynx with dashed line illustrating structures
involved in resection. (Figure courtesy of A
Donald, P. The Difficult Case in Head and
Neck Cancer Surgery.) B

Other Nontotal Laryngectomies

If the lesion crosses the anterior commissure of the larynx, invading the anterior portions
of both true vocal folds, an anterior frontal laryngectomy may be indicated. A frontolateral
laryngectomy (Fig. 11.7) is similar, but an entire fold is removed on one side. Other structures
may be removed as well, depending on extent of disease. Approaches to treatment include
resection by endoscopy or through a surgical incision. Flaps of tissue from various sites, for
example, the platysma or nasal septum, may be used to reconstruct glottal defects and permit
voicing (Dedivitis et al., 2008; Szmega & Leszczynska, 1999).
Procedures that remove most laryngeal structures are often referred to as subtotal, or near-
total laryngectomies. For example, in supracricoid partial laryngectomies, the thyroid cartilage
and true and false vocal folds are removed, and reconstruction utilizes the hyoid, epiglottis, and
cricoid cartilage. In a more extensive procedure, the epiglottis is also removed. The goal of these
procedures is to remove disease but permit postoperative voice and, if at all possible, breathing
without a tracheostomy tube. Voice outcomes with these procedures have not been reported
in great numbers. In most cases, both the potential voicing source and its sound-producing
characteristics are likely to differ significantly from normal voice; thus, “functional” voice is
often a realistic goal.

FIGURE 11.7. Frontolateral laryngec-

tomy. On left, anterior view of larynx with
dashed lines outlining structures involved
in resection. At right, posterior view with
arytenoids retracted illustrates lesion on
right true vocal fold. (Figure courtesy of
Donald, P. The Difficult Case in Head and
Neck Cancer Surgery.)
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In 1980, Pearson et al. described a near total laryngectomy in which the larynx is entirely
removed except for retained portions of the subglottis and segments of true vocal fold and
arytenoid cartilage. These remnants are surgically formed into a tissue shunt that allows air to
enter it with the stoma occluded. The interaction of air and tissue produces sound that, in some
patients, supports speech. Hoasjoe, Martin, and Doyle (1992) described great variability in voice
production across patients who had undergone this procedure, a finding that appeared related
to small tissue differences resulting from resection and/or reconstruction. High fundamental
frequencies and significant noise in the voicing signal as well as hyperfunctional behaviors
were also characteristic of speakers investigated. Maamoun, Amira, and Younis (2004) reported
“intelligible” speech in 31 of 45 patients reconstructed with a tunneled mucosa shunt.

Voice Therapy in Nontotal Laryngectomy

As previously noted, patients who have undergone ablative procedures will experience changes
in tissues and functional status for days, or perhaps weeks, following initial resection. Therapy
is thus a continuing process that considers an individual’s particular needs at each stage of
recovery. Initially, a patient’s ability to write legibly or to use a communication board may be
priorities. With additional healing, other treatment goals may be implemented. These will be
determined to a large extent by the nature of the patient’s resection and the integrity of residual
structures. But it is equally important to assess those aspects of the individual that are likely to
influence his or her treatment progress, for example, the ability and motivation to learn new
skills. In every case, a patient’s specific needs, desires, and capabilities must be determined and
then matched to the most optimal treatment alternative available.
Specific objectives for voice therapy in nontotal laryngectomy patients will be determined
by the ablative treatment(s) undergone. The clinician’s understanding of normal function, and
careful review of available treatment records, are imperative. Unfortunately, there are scant
available data describing particular treatment protocols for any group of these patients or
effectiveness or efficacy of treatment. If the vocal folds remain intact, as in a supraglottic
procedure, voice may be excellent. With limited resections, perhaps affecting only one vocal
fold, the primary problem is likely to be voice quality related to alterations in the composition
of the vibratory source. Stretching exercises, that is, going from high to low in fundamental
frequency in sweep or stair-step fashion, or vocal trills, may be useful in increasing compliance
and elasticity of residual tissue. Our usual practice is to recommend that patients perform
such exercises several times a day, but for only a few minutes each session. We also encourage
vocal hygiene measures, such as keeping well-hydrated, practicing at least conservative reflux
precautions, and avoiding vocal hyperfunction.
In more extensive resections, such as cordectomy, vertical partial laryngectomy, or subtotal
procedures, voice therapy may be focused on involving residual or reconstructed tissues in
sound generation. We have found the use of the flexible endoscope quite useful to this purpose,
both for the clinician attempting to maximize voicing potential and as a feedback tool for
patients who are learning to use a neoglottis. Vocal hygiene measures and the avoidance of
vocal hyperfunction are also considered. Amplification may be helpful both in improving
intelligibility and in preventing aversive adaptations. Interestingly, if healthy tissue is available,
and is positioned in such a way that air can be directed over it to produce vibration, voice
may be quite functional. Secondary procedures that can augment existing tissues may also be
considered. In our own clinic, we have had patients with extensive partial laryngectomies who
developed voice that was in many ways improved over patients with scarring of one vocal fold
but an otherwise intact larynx. Tissue engineering techniques may one day offer improved
alternatives in both situations (Ringel et al., 2006). If adequate sound is possible, then attempts
to increase duration and perhaps achieve some variability in pitch or loudness may be explored.
Prevention of hyperfunctional behaviors is also a realistic objective. In short, the clinician’s task
is to consider each patient individually, both in terms of treatment details, and of patient needs,
through and beyond medical and surgical treatments.
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CHAPTER

12
Anatomy of the Voice Production
Mechanism
Keywords
muscles, extrinsic, intrinsic, suprahyoid, infrahyoid, cartilage, thyroid, cricoid, arytenoid,
cunieform, corniculate, epiglottis, body-cover, folds, cavities, laryngoscopy

In the human body, structure determines function. That is, the shape and form of a structure determine
the manner in which the structure will operate. Understanding structure is thus critical to understanding
function. The larynx has several important functions. Primarily it is a respiratory organ controlling the
flow of air into and out of the lower respiratory tract. Another of its functions is to protect the lower
airway from access by anything other than air, and in that regard, it also has a role in deglutition. A
third but overlayed function is producing the sound source for speech. Because the focus of this book
is phonation, we will focus primarily on the role of the larynx as the primary sound generator. When
laryngeal function for voice is compromised in some way, however, behaviors more typical of other
functions, for example, supraglottic or false fold constriction associated with airway protection, may be
observed during phonation.
A brief review of the anatomy of the larynx will be presented in this chapter. The focus will be on
functional anatomy, that is, the determination of how a structure functions based on its anatomy. It is
not the intent of this chapter to present full anatomical details of structures, their articulation with other
structures, and their blood and nerve supply. Such details may be found in many complete anatomy
texts (Cubertson, Cotton, & Tanner, 2006; Dickson & Dickson, 1982; Fink & Demarest, 1978; Moore
& Dalley, 2006; Zemlin, 1998). Rather, it is our purpose to present those details needed to understand
the structure and how it functions in voice production. This information is presented so that clinicians
can rapidly review a segment of anatomy and use that information to better understand a given voice
problem. It is hoped that this section will be actively used during the process of differential diagnosis and
in the management plan. Anatomy need not be memorized if it is understood and if reference materials
are consulted in a meaningful manner.
We will begin our discussion of laryngeal anatomy from the outside and proceed to the inside; that
is, we will first consider the extrinsic muscles of the larynx, then move inward to the cartilages of the
larynx and the intrinsic muscles. A brief overview of the internal structures and cavities of the larynx will
follow, and, finally, we will consider the body cover model of vocal fold structure and laryngeal anatomy
as viewed through a flexible laryngoscope.

Extrinsic Muscles of the Larynx

The extrinsic muscles of the larynx are those that are attached at one end to a structure within the larynx
and have one or more attachments to a structure outside the larynx. It is necessary to understand that the
hyoid bone, which is a distinct anatomical structure, is considered here to be part of the larynx. Some of its
features are shown in the upper panel of Figure 12.1. All extrinsic muscles have their laryngeal attachments
372
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CHAPTER 12 I Anatomy of the Voice Production Mechanism 373

FIGURE 12.1. Schematic representation of the hyoid bone and the extrinsic mus-
cles of the larynx. Part of the extrinsic muscle group forms a sling to support the hyoid
bone and larynx from above. These muscles can move the hyoid and larynx upward,
forward, or backward. The other group of extrinsic muscles can pull the hyoid and
larynx down.

on the hyoid bone. The attachments outside of the larynx include many different structures,
such as the mandible, the mastoid, and structures in the thorax. Recall that in anatomy the
origin of a muscle refers to its least moveable attachment, whereas the insertion refers to its
more moveable attachment.
There are eight extrinsic muscles, four that lie below the hyoid bone and four that lie
above it. For those reasons, they are divided into the suprahyoid and infrahyoid groups. The
muscles that comprise these two groups are listed in Table 12.1 and shown in Figure 12.1. The
morphological characteristics of these muscles and the intrinsic laryngeal muscles are presented
in useful tables by Kahane (2004, p. 16).
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TABLE 12.1 Extrinsic muscles of the larynx

Suprahyoid Muscles
Digastric A two-part muscle consisting of a posterior belly and an anterior belly.
Origin Anterior belly: originates on the lower border of the mandible near the
mandibular symphysis.
Posterior belly: originates on the mastoid process.
Insertion Anterior belly: intermediate tendon.
Posterior belly: intermediate tendon connecting to the hyoid bone.
Function Anterior belly: pulls hyoid bone anteriorly and slightly upward.
Mylohyoid A thin muscle forming the floor of the mouth.
Origin Along the mylohyoid line on the inner surface of the mandible.
Insertion Most fibers meet with fibers of the opposite side at the midline raphe.
Function Pulls hyoid bone anteriorly and slightly upward.
Geniohyoid A cylindrical muscle located above the Mylohyoid muscle.
Origin On the mental spine at the mental symphysis of the mandible.
Insertion Anterior surface of the corpus of the hyoid bone.
Function Pulls hyoid bone anteriorly and slightly upward.
Stylohyoid A long slender muscle located superficially to the posterior belly of the digastric.
Origin On the styloid process of the temporal bone.
Insertion On the body of the hyoid bone.
Function Pulls hyoid bone posteriorly and upward.
Infrahyoid Muscles
Thyrohyoid A thin muscle that lies deep to the omohyoid.
Origin From the oblique line on the thyroid lamina.
Insertion On the lower border of the greater horn of the hyoid bone.
Function Decreases distance between thyroid and hyoid, especially anteriorly.
Sternothyroid A long, thin muscle on the anterior side of the neck.
Origin Posterior surface of the manubrium of the sternum and the first costal cartilage.
Insertion On the oblique line of the thyroid.
Function Pulls down on the thyroid cartilage.
Sternohyoid A thin muscle lying on anterior side of the neck.
Origin On the posterior surface of the manubrium of the sternum and end of the
clavicle.
Insertion On the lower border of the body of the hyoid bone.
Function Pulls down on the hyoid bone.
(continued )
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CHAPTER 12 I Anatomy of the Voice Production Mechanism 375

TABLE 12.1 Extrinsic muscles of the larynx (continued )

Omohyoid A long, narrow, two-part muscle on the anterior and lateral surfaces of the neck.
Origin Inferior belly: along the upper surface of the scapula.
Superior belly: intermediate tendon.
Insertion Inferior belly: intermediate tendon.
Superior belly: the border of the great horn of the hyoid bone.
Function Both divisions pull down on the hyoid, although the superior belly has a more
pronounced effect in this direction than the inferior belly.

Suprahyoid Group
In Figure 12.1, note how the suprahyoid group forms a sling supporting the hyoid bone and,
secondarily, the larynx. The anterior part of the sling is formed by a part of the digastric (anterior
belly), the geniohyoid, and the mylohyoid muscles. When contracted, this group of muscles pull
the hyoid bone (and thus the larynx) forward. These muscles are active during the production
of a front vowel or a consonant that requires a high front-tongue position. The posterior belly of
the digastric and the stylohyoid form the rear part of the sling. Their contraction pulls the hyoid
posteriorly. Note that the angle of pull is steep for this muscle group, whereas the angle of pull of
the anterior muscle group is shallow. Thus, the action of the posterior group is expected to pull up
on the larynx, whereas the anterior muscle group is expected to exert pull on the hyoid bone that
is more forward than upward. In fact, if the jaw is lowered, it is possible that the anterior group
could lower the larynx slightly. Keep in mind that muscles used for voicing are also used for other
laryngeal functions. The anterior and superior movements of the larynx, for example, are critical
to airway protection and opening a relaxed upper esophageal sphincter during swallowing.

Infrahyoid
This group is made up of four muscles: the thyrohyoid, sternohyoid, omohyoid, and sternothy-
roid. With the exception of the thyrohyoid, the other muscles in this group have attachments
from the hyoid to structures below the larynx. As a result, their contraction has the effect of
pulling the larynx downward. The lowered laryngeal position results in a lengthening of the
vocal tract, which affects vocal resonance characteristics. A more direct effect on the voice may
result from the restriction of thyroid cartilage movement that is caused by contraction of this
muscle group. This restriction of movement is related directly to vocal fold length, mass, and
tension and thereby affects vocal pitch regulation. Other muscles are also involved in pitch
regulation, and they will be discussed later.
The course of the thyrohyoid muscle is between the hyoid bone and thyroid cartilage, and
its action contributes to determining the angle of the thyroid with respect to the cricoid cartilage.
If the thyroid cartilage is fixed (by other muscles) so that it cannot move, then contraction of
the thyrohyoid would contribute to pulling the hyoid bone down. If, however, the hyoid bone
is fixed (by contraction of muscles above it), then contraction of the thyrohyoid would pull
upward on the thyroid, increasing the distance between it and the cricoid cartilage (especially
anteriorly). Thus, most of the effect of the thyrohyoid muscle is to pull the thyroid cartilage
upward and in so doing to potentially alter length, mass, and tension of the vocal folds, thereby
affecting the pitch of the voice.
Positioning of the larynx in the vertical dimension during speaking is primarily related
to vowel or consonant production. There is some variation of position in singing, and good
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376 Understanding Voice Problems

singers may vary the vertical position of the larynx considerably, depending on their style of
singing and the music (Shipp, 1975; Shipp & Izdebski, 1975; Sundberg, 1987). Speakers with
voice problems may have a tendency to maintain higher-than-normal laryngeal position. This
may be indicative of excessive muscle tension (Aronson, 1985; Morrison, Rammage, Belisle,
Pullan, & Nichol, 1983; Roy, 1996, 2003) in the extrinsic muscles of the larynx.

Cartilages of the Larynx

The framework of the larynx is composed of hyaline cartilage. Cartilage is softer and more
flexible than bone, though it becomes more ossified with aging. Hyaline refers to the type of
cells that make up the cartilage.
The cartilages of the larynx are presented in Figure 12.2. The major cartilages are the
thyroid, cricoid, and arytenoid. The other cartilages are much smaller and form parts of other
structures. For example, the corniculates are small cartilages attached to the arytenoid at their

FIGURE 12.2. Schematic of the cartilages of the larynx.

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CHAPTER 12 I Anatomy of the Voice Production Mechanism 377

apices. The cuneiforms are small cartilages embedded in the muscle tissue that connects the
arytenoids to the epiglottis

Thyroid Cartilage
The thyroid cartilage is the largest cartilage of the larynx. The most anterior angle of this
cartilage, commonly referred to as the “Adam’s apple,” is a very prominent feature in some
men. It is shaped like a shield and can be thought of as shielding the structures inside. The
thyroid is actually composed of two plates of cartilage, called lamina, joined at the midline to
form an angle that is more acute in men than women (Zemlin, 1988). The more acute angle
of the thyroid together with laryngeal size accounts for the more pronounced outline of the
larynx in the male neck.
Posteriorly, the thyroid cartilage has two horns or cornua. The superior horn connects
the thyroid to the hyoid bone, and the inferior horn connects it to the cricoid cartilage below.
Along the lateral surface of the thyroid lamina is a ridge identified as the oblique line. It is here
that the thyrohyoid and sternothyroid muscles attach.

Cricoid Cartilage
The second largest laryngeal cartilage is the cricoid, which completely surrounds the trachea.
Sometimes it is referred to as the uppermost tracheal ring, but it is quite different in configura-
tion from the other tracheal rings. It is larger and higher posteriorly, while anteriorly it tapers and
lowers to the cricoid arch. The thyroid cartilage articulates with the cricoid on its posterolateral
surface. Two kinds of movements of the thyroid on the cricoid cartilage are permitted, as illus-
trated in Figure 12.3. The arytenoids articulate with the cricoid on its posterosuperior surface.
The details of this articulation are important and will be discussed further in the next section.

Arytenoid Cartilages
There are two arytenoid cartilages, each positioned on either side of the midline on the supra-
posterior surface of the cricoid cartilage. The arytenoids are roughly pyramidal in shape and have
four surfaces, three angles at the base, and, of course, a single point at the apex. The basal surface
is important to consider because essential intrinsic musculature attaches at two of its angles.

FIGURE 12.3. Movements permitted by the articulation of the thyroid and cricoid cartilages. A rocking
motion of the thyroid on the cricoid is the major movement permitted (left panel). In addition, a slight
anteroposterior movement is possible (right panel).
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378 Understanding Voice Problems

FIGURE 12.4. Type of movements permitted by the cricoarytenoid joint.

The most anterior angle of the base of the arytenoid is referred to as the vocal process. It is
here that the true vocal folds attach. The more lateral angle, referred to as the muscle process, is
the point of attachment for the posterior cricoarytenoid and the lateral cricoarytenoid muscles.
The surface of the arytenoid that articulates with the cricoid cartilage is concave in ap-
pearance. The surface of the cricoid that meets the arytenoid is convex. These surfaces help
to determine how the arytenoid will move on the surface of the cricoid. Because of the shape
of these surfaces, a rotating motion is not permitted, but a rocking motion can occur (Broad,
1973; von Leden & Moore, 1961). Broad has described the permitted motions by comparing
them to the movement of two matching cylinders, as shown in Figure 12.4. Two kinds of
motion are permitted, a gliding motion along an anteroposterior plane and a rocking motion
in a mediolateral direction. When these two motions occur together, there is the appearance of
a rocking motion either medially and anteriorly directed (if the arytenoids are moving in) or
posteriorly (if the arytenoids are moving out). Depending on the speed of medial movement
relative to anterior movement of the arytenoids, it is possible for the vocal processes to be the
first point of contact during adduction of the vocal folds.

Epiglottis
The epiglottis is a leaf-shaped cartilage attached on the mesial surface of the thyroid cartilage
at the juncture of the two thyroid plates. The anterior surface of the epiglottis attaches to the
hyoid bone via a ligament.
Inversion of the epiglottis during swallowing assists in protecting the airway and directing
food and liquids into the esophagus. During phonation, it is usually out of the way of the
egressive airstream. However, it moves considerably during the production of different vowels
and consonants. In some cases, it will obscure the view of the vocal folds. However, tongue
position in the production of vowels like /ee/ and /oo/ usually results in forward movement of
the epiglottis, thereby allowing a good view of the vocal folds. There is no evidence to support
the contention that the shape of the epiglottis will alter the voice. Pulling the epiglottis over
the laryngeal opening may affect sound transmission and reduce intensity level.
The epiglottis can vary considerably in shape and curvature. Usually it is slightly concave
when viewed via a laryngeal mirror or endoscope. Sometimes it may have a very pronounced
omega shape. The so-called omega-shaped epiglottis appears to be found most often in immature
larynges or children’s larynges. However, it may also be simply a variation of normal human
laryngeal anatomy.

Other Cartilages
The remaining cartilages are the corniculate and the cuneiform cartilages. The corniculates are
small, cone-shaped cartilages that form the apex of the arytenoid. The cuneiforms are small,
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CHAPTER 12 I Anatomy of the Voice Production Mechanism 379

rod-shaped cartilages found within the aryepiglottic fold, a fold of tissue and muscle coursing
from the arytenoids to the epiglottis.

Intrinsic Muscles of the Larynx

Muscles that have both of their attachments to structures within the larynx are called intrinsic
laryngeal muscles. The five muscles, along with their origins and insertions, are shown in Table
12.2. In this review they will be discussed approximately in order of their activation when a
person produces voice.

Arytenoideus
The arytenoideus or interarytenoid muscle is a two-part muscle lying between the two arytenoid
cartilages. One part consists of muscle fibers that course in a horizontal direction. The effect of
these fibers is to pull the bases of the two arytenoids toward each other, thus adducting the vocal
folds. The other part consists of fibers that course from the base of one arytenoid to the apex
of the other arytenoid. The effect of these fibers is to pull the tips of the arytenoids together.
Together, the two parts adduct the arytenoids and close off the extreme posterior airway.
Although the time when these muscles are activated depends on the speech task, in general,
activity in the arytenoideus occurs anywhere from 0.5 to 0.3 seconds before sound is produced.

Lateral Cricoarytenoid
The lateral cricoarytenoid muscle is a paired muscle coursing from the sides and upper surface
of the cricoid cartilage to the muscle process of the arytenoid. The effect of this muscle is to
pull the muscle process anteriorly, rocking the arytenoid medially and adducting the vocal folds
themselves. Time of activation may be about 0.1 second after activity in the arytenoideus.
These two muscles (arytenoideus and lateral cricoarytenoid) function together to adduct
the vocal folds. It is not necessary to completely adduct the folds for phonation to commence.
Rather, there need only be sufficient adduction to impose an obstruction to the flow of air
coming from the lungs.

Posterior Cricoarytenoid
This is the only intrinsic muscle that abducts the vocal folds. From its origin on the posterior
lamina of the cricoid, the muscle fibers converge to insert on the muscle process. Contraction
of the muscle will pull the muscle process posteriorly, thus opening the vocal folds.
The posterior cricoarytenoid is active at the end of phonation in order to open the folds
(Hirose, 1976). Moreover, it is also active during speech since there are many speech sounds that
require an absence of vocal fold vibration (e.g., the stop consonants /p/, /t/, and /k/; the fricative
consonants /s/ and /sh/, etc.). Thus, a short burst of activity in the posterior cricoarytenoid
quickly abducts the vocal folds enough to stop their vibration.

Cricothyroid
The origin of the cricothyroid muscle is along the upper surface of the sides of the cricoid
cartilage. Its insertion is along the lower border of the thyroid cartilage. It is considered to
be the main muscle for pitch control and its major function is to raise vocal pitch. It does so
by rocking the cricoid cartilage upward or the thyroid cartilage downward, thereby increasing
the distance between the thyroid cartilage and the vocal processes of the arytenoids, which are
situated on the rear surface of the cricoid. The vocal folds, which are attached anteriorly on the
inner surface of the thyroid cartilage and posteriorly on the vocal processes of the arytenoids,
are stretched and elongated by either of these actions. Stretching the vocal folds decreases their
cross-sectional area and subjects the folds to greater longitudinal tension. The decrease of area
and increase of tension permit the vocal folds to vibrate at higher frequencies and thus produce
the perception of higher pitch.
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TABLE 12.2 Intrinsic muscles of the larynx

An unpaired muscle consisting of fibers oriented in two directions,
Arytenoideus oblique and transverse.
Origin Oblique fibers originate at the base of one arytenoid and course to the apex
of the other arytenoid. Transverse fibers originate along the lateral margin
of one arytenoid and course to the lateral margin of the other arytenoid.
Insertion Arytenoid of opposite side.
Function Adducts arytenoids, thus closing the cartilaginous glottis
Lateral A fan-shaped muscle lying along the upper surface of the cricoid cartilage.
cricoarytenoid
Origin On the upper border of the cricoid.
Insertion Anterior surface of the muscular process of the arytenoid.
Function Adducts the vocal processes of the arytenoids, thus closing the
membranous glottis.
Posterior A fan-shaped muscle located on the posterior surface of the cricoid.
cricoarytenoid
Origin On the posterior lamina of the cricoid.
Insertion Posterior surface of the muscular process of the arytenoid.
Function Abducts the arytenoids, thus opening the glottis.
Cricothyroid A fan-shaped muscle located between the cricoid and thyroid cartilages,
consisting of two divisions, pars oblique and pars recta. These divisions
refer to the different orientation of the fibers.
Origin Arch of the cricoid.
Insertion Inner inferior margin of the thyroid.
Function Decreases the space between the thyroid and cricoid, thus increasing the
distance between the thyroid and arytenoid cartilages; increasing the
length of the vocal folds, decreasing their mass and increasing their
tension; and increasing vocal pitch.
Thyroarytenoid A bundle of muscle fibers making up the true vocal folds.
Origin Anteriorly, from the posterior surface of the thyroid. Insertion along the
lateral base of an arytenoid from the vocal process to the muscle process.
Insertion Along the lateral base of an arytenoid from the vocal process to the muscle
process.
Function Decreases the distance between the thyroid and arytenoid cartilages,
shortening the vocal folds, increasing their mass, and decreasing their
tension, and decreasing vocal pitch.
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CHAPTER 12 I Anatomy of the Voice Production Mechanism 381

Decreasing the level of activity in the cricothyroid will result in a decrease of tension,
resulting in a slower vibratory rate and a decrease of fundamental frequency. However, the rate
of decay of muscle activity in the cricothyroid may be too slow for speech purposes. That is, it
may be necessary, for linguistic purposes, to lower pitch more rapidly than would be possible
by waiting for the decay of cricothyroid activity. Thus, other physiological mechanisms of
frequency change may be operating to actively lower vocal pitch during speech.

Thyroarytenoid
The thyroarytenoid muscle comprises the bulk of the vocal folds. Its contraction decreases
the length of the vocal folds, increases their cross-sectional area, and decreases longitudinal
tension. The action of this muscle represents one way to actively lower vocal pitch. Of course,
contraction of this muscle also changes the configuration of the vocal folds themselves, thereby
affecting how they will move within the vibratory cycle.
The thyroarytenoid may be divided into two muscle groups. The medial portion of the
muscle is called the thyrovocalis muscle, and the more lateral portion is referred to as the
thyromuscularis muscle. There is some controversy about whether or not the two parts are
anatomically distinct (Dickson et al., 1982). From a functional point of view, the medial
portion of the thyroarytenoid (or thyrovocalis) is most active during the vibratory activity
of the vocal folds and, therefore, may have a significant effect on phonation. The lateral (or
thyromuscularis) portion may exhibit little movement during vibration, and thus its action
may have minimal effect on the vibratory characteristics of the vocal folds.
The shortening action of the thyroarytenoid opposing the stretching effect of the cricothy-
roid appears to be responsible for most of the length change possible in the vocal folds (Titze,
1994). However, the interaction of the thyroarytenoid and cricothyroid is complex and likely
depends on the particular pitch level of the phonation (Titze & Sundberg, 1992). At pitches
typical of speech, the foregoing discussion describes the basic action of these two muscles.

Detailed Anatomy of the Vocal Folds: The Body Cover Model

Hirano (1974, 1981) proposed a model of the vocal folds that has considerable merit in
explaining the variation of human voice production. Simply stated, the vocal folds consist of
three layers: (a) the outer cover, consisting of epithelium; (b) a middle layer, the lamina propria;
and (c) the body. A schematic diagram of the three layers is shown in Figure 12.5.
The cover of the vocal folds is composed of squamous cell epithelium. Mechanically,
epithelium is very stiff, making this layer much stiffer than its neighbor, the lamina propria
(Kakita, Hirano, Kawasaki, & Matsushita, 1976). It is this difference of stiffness that determines
the manner in which the layers will respond to deformation during vibration. In some modes of
vibration, the degree of coupling between the epithelium and the lamina propria is very small
(as in low-frequency speech activities). In other modes of vibration, the degree of coupling
between the cover, the lamina propria, and the body may be very great (as may be the case
in falsetto voice). Thus, the combination of the mechanical characteristics of the three layers
will ultimately determine the mode of vocal fold vibration (see Fujimura, 1981, for a good
discussion of the relationships between biomechanical characteristics of the vocal folds and
sound production).
The lamina propria is actually a three-layered area of connective tissue lying between the
cover and the body. Its superficial layer is very pliable, consisting of loose, fibrous components.
The intermediate layer consists primarily of elastic fibers. The deepest layer consists of collage-
nous fibers. Mechanically, each layer will exhibit different characteristics, and variation in the
composition of each of the three layers of the lamina propria will alter the manner of vocal fold
vibration.
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382 Understanding Voice Problems

FIGURE 12.5. Schematic

representation of the vocal
folds as a body and cover. A.
Cross-sectional representation.
B. The kinds of fibers present
in each layer.
B
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CHAPTER 12 I Anatomy of the Voice Production Mechanism 383

FIGURE 12.6. Cross-sectional representation of the larynx.

The body of the vocal fold is the vocalis muscle, or thyrovocalis. Although muscle cells are
the primary components of muscle, blood cells, collagen cells, and inorganic material are also
present. Muscle fibers themselves exhibit different mechanical characteristics when they are in
the process of contracting than when they are contracted or at rest (Colton, 1988). Thus, there
can be considerable variation in the mechanical characteristics of the body, depending on the
amount of muscle activation, the amount of collagenous or elastic fibers present, the amount
of heat generated (Cooper & Titze, 1985; Hill, 1938; Titze, 1981), and other variations due
to blood flow, oxygen consumption, and the like.

Folds and Cavities of the Larynx

Folds
The folds and cavities of the larynx—sagittal and coronal cross-sections—are shown in Figure
12.6. The major folds of interest are the true vocal folds. Superior and lateral to the true vocal
folds are the false or ventricular folds. The false vocal folds do not usually vibrate in normal voice
production, except perhaps at very low fundamental frequencies (50 Hz or less). They have few
muscle fibers, and it is very difficult to regulate their tension, mass, and length. Nonetheless, in
some patients they are seen to adduct partially, or almost completely, even obscuring the true
vocal folds. Vibration of the ventricular folds is observed infrequently and usually in association
with some kind of vocal problem.
The aryepiglottic folds comprise a ring of muscle and connective tissue extending from the
tips of the arytenoids to the epiglottis. In effect, they form a sphincter enclosing the entrance
to the larynx. During swallowing and protective acts, the aryepiglottic folds (as well as true and
false vocal folds) contract to reduce the diameter of the laryngeal entrance and thus protect
the airway. Sphincteric movements of these folds can sometimes be observed during phonatory
attempts in vocally disordered patients.
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384 Understanding Voice Problems

FIGURE 12.7. Laryngoscopic view of the larynx. This is a view typically seen during
indirect mirror, fiberoptic, or stroboscopic examination of the larynx.

Cavities
The major cavities of the larynx are (a) the supraglottal cavity, (b) the subglottal cavity, and (c)
the ventricles.
The supraglottal cavity lies above the glottis or the opening between the vocal folds. Its
superior boundary is the aryepiglottic sphincter. This cavity could potentially act as a resonator
of the sound produced by the vibrating vocal folds, although it is usually considered to be part
of the entire vocal tract acoustically.
The subglottal cavity lies beneath the true vocal folds. Its lower boundary is the first tracheal
ring. It is in this cavity that pressure increases beneath the closed vocal folds until it becomes
sufficient to force the vocal folds open and begin phonation.
The ventricles, often referred to as the ventricles of Morgagni, are paired cavities lying
above and slightly lateral to the true vocal folds. The opening of these cavities is usually very
small, and thus they seem to have little effect on the sound produced at the vocal folds.
However, in some conditions encountered in singing, the opening may be sufficient to permit
meaningful resonance and thus add to the glottal tone. Sundberg (1974) has shown that under
certain conditions, they could resonate frequencies in the vicinity of 2800 Hz. In most speech
conditions, however, their resonant effect on sound would be minimal.

Laryngoscopic View of the Larynx

Figure 12.7 presents a schematic view of the larynx typically seen when observing the larynx
either through a laryngeal mirror or a laryngeal endoscope (flexible or rigid). It is a view
commonly chosen by most otolaryngologists and to speech-language pathologists and voice
scientists. The various structures that can be viewed are identified in this figure. It is essential to
know these landmarks to properly interpret images of the larynx. A good knowledge of normal
anatomy and its variations is needed in order to correctly identify laryngeal pathology. It is
important to recognize that there is much variability in normal anatomic structures. Examples of
this variability as seen fiberscopically were discussed by Casper, Brewer, and Colton (1987) and
recently by Kendall and Leonard (2010). According to Casper et al., the most marked structural
variability occurred in the configuration of the “arytenoid complex” (arytenoids, cuneiforms,
corniculates). There were obvious movement differences among the participants in this area.
Some participants exhibited symmetrical movement, whereas in others the movements were
asymmetrical. There was also asymmetry in the apparent length of the true vocal folds. Notably,
the marked anteroposterior movement and twisting of the larynx, often seen in patients with
voice disorders, were not observed in normal speakers. “Normal” can span a broad range of
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CHAPTER 12 I Anatomy of the Voice Production Mechanism 385

differences in both structure and function. Asymmetry is not necessarily a sign of an abnormal
larynx.

Summary
A brief review of the anatomy of the larynx and the vocal folds is presented. The extrinsic muscles
of the larynx help to support and adjust the position of the larynx. The intrinsic muscles of
the larynx attach to the various cartilages of the larynx (thyroid, cricoid, arytenoid) and serve
to adjust the length, tension, and mass of the vocal folds, as well as to adduct them. A brief
discussion of the cavities and folds of the larynx is presented, concluding with a presentation
of the laryngoscopic view of laryngeal anatomy.
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CHAPTER

13
Phonatory Physiology

Keywords
physiology, initiaition, Bernoulli, fundamental frequency, tension, loudness, subglottal,
air pressure, airflow, resistance, qualaity, timbre

The vibrating vocal folds are the major source of periodic sound for speech. There are other periodic
sound sources (e.g., flapping lips), but these are minor compared to the sound produced from the vocal
folds. In addition, there are aperiodic sound sources such as those used for the production of voiceless
consonants. The vocal folds may be involved in the production of aperiodic sound, as, for example, in
the consonant /h/.
In this chapter, we will review the basic concepts of phonatory physiology. First, the conditions that
must exist before sound can be produced will be presented, followed by discussion of the mechanisms
necessary for initiating and sustaining sound. The third and fourth sections will be brief discussions of the
physiological mechanisms for control of vocal pitch and intensity control by the vocal folds, respectively.
Finally, a review of some of the mechanisms for control of voice quality will be presented. The reader
interested in further information on these topics is referred to the excellent text by Titze (1994).

Glottal Tone Initiation

Before sound can be produced from the vocal folds, several conditions must be established. First, the
vocal folds must be approximated or almost approximated in the phonatory position. This position,
in comparison to the inspiratory position of the vocal folds (Fig. 13.1A), is shown in Figure 13.1B.
Phonation may also be initiated after completely closing the vocal folds.
It is also necessary to properly tense and elongate the vocal folds prior to actually producing sound.
Length and tension are important determinants of the fundamental vibrating rate of the vocal folds, in
ways that will be discussed later under “Mechanisms of Vocal Frequency Change.”
Finally, there must be airflow from the lungs. In order to be able to produce the required flow of
air from the lungs, there must be a sufficient quantity of air in the lungs. Typically, we inhale before we
begin producing sound for an utterance.
Once these initial conditions have been established, phonation can start. When the vocal folds are
in the phonatory position, it is necessary to close them in order to start vibration. If one starts with the
vocal folds fully closed, the egressive air stream will open them to start vibration. Whatever the starting
point, the process thereafter is similar and is simply described as a series of alternate openings and closings
of the vocal folds. The opening and closing is regulated by the degree of tension in the vocal folds and
two aerodynamic events.
The aerodynamic event important for closing the vocal folds is called the Bernoulli effect, named
after a famous 18th-century Swiss physicist. Bernoulli was most interested in fluid flows, but his principles
hold for gas flows as well. Simply stated, Bernoulli’s second law of fluid mechanics states that the sum
386
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CHAPTER 13 I Phonatory Physiology 387

FIGURE 13.1. Schematic representation of the stages of vocal fold adduc-

tion. A. During inspiration. B. At start of phonation.
B

of the static pressures and the kinetic pressures in a gas is always equal to a constant. The constant
may vary according to the temperature, pressure, or molecular structure of the gas. But within
these conditions, when motion of the molecules changes, there is a change in the static pressure
exerted by the molecules. Stating the principle another way, when there is increased motion of
gas molecules, there will be decreased pressure.
The Bernoulli effect is often evoked to explain how airplanes rise in the air. The under-
surface of the wing of an airplane is rather flat, whereas the upper surface is more convex in
shape. This curvature on the upper wing surface means that the air molecules passing over the
top of the wing have a greater distance to travel to pass over the wing than those molecules
that pass under the wing. The velocity of the molecules traveling along the surface of the upper
wing must increase in order to travel the distance in the same time as the molecules traveling
under the wing. In short, their kinetic “pressure” has been increased. According to Bernoulli’s
principle, when the kinetic pressure increases, the static pressure must decrease. Thus, there is
less pressure along the upper surface of the wing. By the same token, there is greater pressure
below the wing, and this greater pressure will lift the wing (and the airplane) into the sky.
The same principle holds for the vocal folds. The vocal folds impose a partial obstruction
to the flow of air. The molecules traveling along the sides of the trachea, when meeting the
vocal folds, must travel a greater distance around the fold to meet the molecules traveling up
the center of the trachea. The molecules along the surface of the vocal folds must increase their
velocity and kinetic pressure. Again, static pressure on the surface of the vocal folds will be
decreased. The vocal folds, being pliable and movable, will begin to move toward the center of
the trachea because of this pressure differential. Eventually, the two vocal folds will meet at the
midline, and airflow will cease.
The trick that needs to be performed to produce vibration is to create the Bernoulli effect
when you wish to close the vocal folds and a positive pressure when you wish to open them
(Titze, 1994). When the vocal folds close, there is a sudden decrease of airflow (Fig. 13.2B).
When the vocal folds open, there is a momentary delay in the start of airflow due to this
inertia. This explains the characteristic shape of the airflow pulse through the glottis where
the rising airflow phase is slower than the opening of the vocal folds (Fig. 13.2A and B).
Air particle velocities through the glottis also show asymmetry (Fig. 13.2C). Generally, these
velocities increase as the vocal folds open and change direction when the airflow pulse shuts off
at closure. Intraglottal air pressure is solely dependent on air particle velocity (Titze, 1994). The
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388 Understanding Voice Problems

FIGURE 13.2. Relationships be-

tween displacement and velocity of
the vocal folds, airflow, air particle
velocity, and intraglottal air pressures.

classic Bernoulli equation states that as kinetic energy increases, static “energy” must decrease as
both sum to a constant. Thus, as air particle velocity increases, intraglottal pressure decreases.
Air particle directional change results in an abrupt negative change of intraglottal pressure (Fig.
13.2C and D)—just when we need it to produce vocal fold closure. Positive pressure below the
vocal folds forces them open.
The tension and mass of the vocal folds create a resistance to vibration. Consequently,
there is a minimum pressure required to force the folds into vibration. Titze (1992) calls this
pressure phonation threshold pressure (PTP). PTP is dependent on the frequency of phonation
and may be slightly different for men and women (and probably for children as well). PTP is
also dependent on hydration levels of vocal fold tissues (Verdolini-Marston, Titze, & Druker,
1990). Intensity control is also related to PTP (Titze & Sundberg, 1992).

Mechanisms of Vocal Frequency Change

The human vocal mechanism is capable of producing a wide range of frequencies, sometimes
in excess of three octaves. In this section, we will review some of the physiological mechanisms
that determine the fundamental vibrating rate of the vocal folds.
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CHAPTER 13 I Phonatory Physiology 389

Early in the study of phonation, individuals compared the vocal folds to vibrating strings.
After all, both the vocal folds and strings had a length and a mass and were under tension.
Furthermore, much was known about the determinants of frequency in strings, and the analogy
was thought to be a good one. As research on voice physiology progressed, evidence accumulated
that prompted a reevaluation of the analogy between the mechanism of frequency variation by
the vocal folds and by a string.
Recent evidence has confirmed that the physical properties that determine the frequency
of a vibrating string also determine the vibrating frequency of the vocal folds..
The vibratory frequency of a string and of the vocal folds is determined by its length,
tension, and mass. Actually, in the case of the vocal folds, it is not their total mass that is
significant but rather the mass that is set into vibration. The amount of mass set into vibration
will depend on fundamental frequency, intensity, and mode of vibration. Furthermore, the
amount of mass varies as a function of the length of the string or vocal fold. The relationship
of vocal fold thickness to length is similar to that observed in a rubber band. As the band is
stretched, the thickness of the band decreases.

Vocal Fold Length and Fundamental Frequency

A convenient way of understanding the relationships between length, mass, and tension in a
string and in the vocal folds is by graphing the parameters as a function of frequency. A plot
of fundamental frequency as a function of vocal fold length is shown in Figure 13.3. In the
modal register (the range of frequencies used most often during speaking), as vocal fold length
increases, frequency increases. This relationship is clearly opposite to that predicted by the
classic equation for determining the frequency of a vibrating string. However, when phonation
is produced in the falsetto or upper register, fundamental frequency appears to decrease as vocal
fold length is increased. Subsequent research has shown that the length of the vibrating portion
of the vocal folds decreases as frequency is increased (Hollien & Colton, 1969). These opposite
effects, at least for modal register phonation, is why the string analogy was thought by some to
be inappropriate for the control of fundamental frequency by the vocal folds. But length is not
the sole mechanism for control of fundamental frequency either in strings or the vocal folds.

FIGURE 13.3. The relationship be-

tween fundamental frequency and vocal
fold length.
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390 Understanding Voice Problems

FIGURE 13.4. The relationship be-

tween fundamental frequency and vo-
cal fold thickness.

Vocal Fold Mass and Fundamental Frequency

The mass of the vocal folds may also play a role in frequency control. Figure 13.4 shows the
relationship between thickness of the vocal folds and frequency. Note that, for the vocal folds,
vocal frequency decreases as mass increases, a relationship similar to that for a vibrating string.

Vocal Fold Tension and Fundamental Frequency

Tension affects the vibrating frequency of a string and the vocal folds. The relationship between
tension and frequency of the vocal folds is shown in Figure 13.5. As tension increases, so too
does frequency. In general, the effect of tension on the vocal folds produces changes of frequency
much like in a string.
It is very difficult to measure tension directly in the living human vocal fold. Indirect
evidence must be obtained from recordings of muscle activity or measurements made on dog
or excised human larynges (Perlman & Titze, 1984, 1988; Perlman, Titze, & Cooper, 1984).
Moreover, the variations of tension produced by muscle contraction must also be considered
(Colton, 1987) when trying to understand how tension determines the fundamental frequency
of phonation.
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CHAPTER 13 I Phonatory Physiology 391

FIGURE 13.5. The relationship between

fundamental frequency and vocal fold ten-
sion.

Tension becomes more important in the determination of fundamental frequency at certain

areas of an individual’s total phonational range. Van den Berg and Tan (1959) have shown that
the largest variation of tension occurs at upper frequencies, most often produced in the falsetto
register. A small amount of tension variation occurs at frequencies typically heard in speech.
Thus, although tension is an important determinant of fundamental frequency variation, it is
not the only determinant. As has been shown, the mass of the vocal folds (or more accurately,
their mass per unit length) has a pronounced influence on the fundamental frequency of the
vibration.
It is clear that there may be several mechanisms determining fundamental frequency in
the human voice. At some frequencies (usually in the modal register), overall mass may be the
most important determinant (Allen & Hollien, 1973), whereas at other frequencies (usually in
the falsetto register), tension may be the dominant factor. It is the combination of these factors
that ultimately determines the fundamental frequency of vocal fold vibration.
The data from van den Berg and Tan also show that the relationship between tension
and fundamental frequency differs as airflow rates differ (Fig. 13.5). Thus, airflow appears to
be another contributing factor in the physiological mechanisms of vocal frequency control. In
some cases, airflow may be the major determinant of frequency, much as it is for tones whose
frequency of vibration is controlled by the rate of airflow. You may have walked through an
open field in which telephone or electrical wires passed overhead and heard the sound the
wind makes when striking the wires. This is an example of an aeolian tone whose frequency is
determined by the speed of the airflow rushing across the wire. In many patients with phonatory
disorders, there is excessive airflow. Although the speed of the airflow may not directly affect
the fundamental frequency of the vocal folds as in an aeolian tone, it may be a sign of an
inefficient mechanism being used for the variation of vocal pitch. Or it may be that the patient
is using a combination of tension, mass, and airflow that causes or contributes to the voice
problem. These possibilities point to the need for information about all of these parameters
with voice patients. The availability of such information may help in understanding the bases
for the patient’s vocal problem.
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392 Understanding Voice Problems

As in a string, the fundamental frequency of the vocal folds is determined by a complex

interaction between length, mass, and tension. There may be various combinations of these
parameters that produce the same fundamental frequency. However, not all combinations of
length, mass, and tension may be efficient for the production of voice.

Mechanisms of Loudness Change

The human voice is capable of producing a wide range of vocal intensities, sometimes exceeding
60dB. Additional changes of intensity result from variation in the size and shape of the vocal
tract, which acts as a resonator of sound. The mechanisms for the control of vocal intensity, much
as those of pitch control, involve muscular activity in combination with airflows and pressures.
Vocal intensity is usually reported in decibels (dB) of sound pressure level. Since sound
is basically a pressure disturbance, we would expect that increased pressures beneath the vocal
folds, when released by the folds, would produce a greater intensity, and indeed, experimental
evidence supports this expectation (Ladefoged & McKinney, 1963). As shown in Figure 13.6,
when the subglottal air pressure increases, intensity increases, although the exact relationship
will vary for different vowels and voice qualities.
However, the controlling mechanism of vocal intensity is not solely due to subglottal air
pressure. Rather, the controlling mechanism is the degree and time of closure of the vocal folds
themselves. That is, by maintaining closure of the vocal folds, there is more time to build up
pressure beneath them. More intense sound results when the subglottal air pressure is sufficient
to overcome the resistance of the vocal folds. Resistance is the important factor in intensity
control. The more vocal fold resistance there is to opening, the greater the pressure disturbance
when the resistance is overcome and the folds are forced to open. Thus, intensity is most often
controlled by the vocal folds through variations of glottal resistance. Glottal resistance is defined
as the ratio of the pressure divided by the flow. Measuring these two quantities will allow the
calculation of resistance.

FIGURE 13.6. Relationship between

sound pressure level and subglottal air
pressure.
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CHAPTER 13 I Phonatory Physiology 393

FIGURE 13.7. Sound pressure levels

and maximum rate of declination of the
airflow pulse (or the slope of the closing
portion of the airflow pulse) as derived
from inverse filtering.

Isshiki (1959, 1964, 1965) has shown that glottal resistance is a major controlling mech-
anism of vocal intensities for low fundamental frequencies, that is, fundamental frequencies
produced in the lower part of an individual’s phonational range or in the modal register. At
higher frequencies, especially frequencies produced in falsetto, glottal resistance is no longer the
major factor. Rather, it appears that airflow becomes the dominant variable in intensity varia-
tion at these high fundamental frequencies. Furthermore, the range of intensities an individual
can produce in the falsetto register is much smaller than can be produced in the modal register
(Colton, 1973). This finding would suggest, or at least be in consonance with, the existence of
a different controlling mechanism for intensity control in falsetto.
Another mechanism of intensity control has been described (Sundberg, Titze, & Scherer,
1993; Titze, 1994). The vocal folds produce sound when they close. The intensity (and spectra)
of the sound is dependent on the velocity of closure of the vocal folds. Glottal power is directly
related to the rate of change of the airflow pulse at the moment of closure (Titze & Sundberg,
1992). This rate of change of airflow at closure is often referred to as maximum declination
rate or simply airflow closing slope. The relationship between the airflow closing slope of the
airflow pulse and intensity is shown in Figure 13.7. Therefore, intensity control by the vocal
folds may be dependent on at least two factors, glottal resistance and the rate of airflow change
at the moment of closure.
For a variety of reasons, some patients have difficulty in completely closing their vocal
folds. In an attempt to speak at a normal vocal intensity, these patients increase air pressure by
increasing the expiratory force from the thorax-abdomen system. The patient may also attempt
to increase glottal closure in an effort to increase glottal resistance and to maintain an adequate
level of tension in the vocal folds. As a result of this effortful vocal behavior, greater-than-normal
subglottal pressures are developed, and there is increased tension in the vocal folds. Because
greater-than-normal muscle activity is involved, these conditions may create vocal fatigue as
well as excessive air rushing across the vocal folds. The latter creates greater noise levels in the
voice. A vicious cycle ensues, as the vocal fatigue may result in even poorer vocal fold adduction
and the need for even greater effort on the patient’s part, leading cyclically to poorer voice.
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394 Understanding Voice Problems

There is another factor that will affect the sound pressure level (SPL) of phonation. That
factor is the spectral characteristics of the tone produced by the vocal folds. It is well known that
variation of the frequency composition of a tone will vary its intensity (and vice versa). Adding
frequencies or varying the amplitude of the components of the tone will affect the intensity of
the complex tone. Similarly, the spectrum of the vocal folds can be varied within limits and thus
alter the overall intensity of the vocal fold tone. Consequently, the vocal folds can affect the
intensity of the tone by variation of the frequency components in the tone. Speed of closure of
the vocal folds will affect the spectral features of the glottal tone (Löfqvist, 1993; Titze, 2006).
In some patients with phonatory disorders, the spectral characteristics of the tone produced
are markedly different from normal. Usually, but not always, the number of frequency com-
ponents in the pathological voice is much smaller than in the normal voice. When that is the
case, then lower intensities would be expected. In order to compensate for the different spectral
characteristics and their effect on intensity, a patient may try to increase subglottal pressures or
adductory forces, resulting in increased strain and subsequent abuse of the vocal folds.
Loudness is the perceptual correlate of intensity, but intensity is not the only physical
factor that affects loudness. The pitch of the voice and its spectral composition may also affect
its perceived loudness. Of course, factors such as the distance from the speaker, room acoustics,
diffraction, and interference may also affect the loudness of a voice as perceived by a listener.

Mechanisms of Quality Variation

Voice quality is an important attribute of normal and abnormal voices. Voice quality identifies
the individual and sets him or her apart from another. A change of voice quality may signal
the presence of a benign problem or one that could be life threatening. But defining voice
quality can be difficult and imprecise (Krieman et al., 1993; Kreiman & Gerratt, 1998, 2000;
Kreiman, Gerratt, & Berke, 1994).
Many adjectives are used to describe voice quality: pleasant and unpleasant, normal, and
pathological. Singers, actors, professional speakers, and those who work with the voice use
jargon to describe the variation of normal voice quality. Quantification of these terms either
acoustically or physiologically has proven to be very difficult.
Acoustically, the important parameter concerned with voice quality is spectrum. Spectrum
refers to the number and amplitude of the frequencies present in a complex tone, such as the
vocal fold tone. Figure 13.8 presents the spectrum of a typical vocal fold tone produced during
speech. However, the vocal folds can produce many different voice qualities, each with its own
spectral characteristics (Fig. 13.9).

FIGURE 13.8. Inverse filtered airflow waveform of the vocal folds

(top panel) and its corresponding frequency spectrum (bottom panel)
from a phonation produced by a male participant.
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FIGURE 13.9. Some spectra of different voice qualities. Mode 1 refers to a quality typically heard during speech, mode 2 to a quality of a
sound heard during sobbing or during the singing of a lullaby, mode 3 to a quality typically heard in Country Western singing, and mode 4 to

395
a quality heard in operatic singing.
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Other factors may be important in describing a voice quality acoustically. Although pitch
would be expected to be one such factor, it is interesting to note that it apparently is not used
in distinguishing one voice quality from another (Colton, 1987). This finding is similar to
the influence of pitch in the perception of nonphonatory sounds like complex sounds (Plomp,
1976) and noise bands (Chipman & Carey, 1975). Varying the pitch level may alter some of
the details of a voice, but not its basic voice quality.
Voice quality is not solely determined by the vibratory characteristics of the vocal folds. The
shape and configuration of the vocal tract are also determinants of voice quality. For example,
women have slightly different vocal tract configurations than men do, and as a result, female
voices can still be recognized as female even when the obvious pitch difference is removed
(Coleman, 1971, 1973, 1976). The overall characteristics of an individual’s vocal tract, such
as the length, cross-sectional area, ratio of oral to pharyngeal cavity size, and so on, would also
determine that individual’s voice quality.
Physiological change in laryngeal and vocal tract configurations and characteristics have
been observed in individuals as they produced various voice qualities (Colton & Estill, 1981;
Painter, 1986, 1991). For example, in some voice qualities, the size of the pharyngeal cavity is
much larger than in other voice qualities. Many of these differences appear to occur in the larynx
itself as well as in the pharynx. We have little information about the vocal tract characteristics
of patients with voice disorders (although there is some recent evidence suggesting that the
vocal tract length changes in some patients with functional voice disorders, for example see
Roy, Nissen, Dromey, & Sapir, 2009).

Summary
In this chapter, a brief review of the mechanisms for voice production, frequency control,
intensity variation, and the generation of voice quality have been reviewed. The tone produced
by the vocal folds results from the complex interaction of airflow, air pressure, and muscular
activity, which regulate the length, mass, and tension of the vocal folds. Variation in these
parameters will affect the fundamental frequency of the voice as well as its intensity and voice
quality. Measurement of these acoustic parameters of the voice will assist in the quantification
of the vocal behavior and help to determine the nature of the problem. Accurate measurement
of these acoustic, perceptual, or physiological parameters can play a part in understanding and
treatment planning.
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CHAPTER

14
Neuroanatomy of the Vocal
Mechanism
Keywords
neuroanatomy, cortical, phonatory control, subcortical, midbrain, PAG, brainstem,
cerebellum, vagus, recurrent, superior laryngeal

Volitional control of the muscles of the larynx resides in the brain. However, there are many connecting
points or stations within the brain, including the cortex, subcortical areas, midbrain, and medulla, that
play an important role in the ultimate control of phonation. Thus, saying that phonation is controlled
by the brain is much too simplistic and underemphasizes the roles various structures play in integrating
information and coordinating the activity of the muscles active in phonation. In this chapter, a brief
review of the neuroanatomy and neurophysiology of phonation will be presented. A further and more
detailed review of brain mechanisms controlling vocalization may be found in Larson (1988).

Cortical Mechanisms of Phonatory Control

The cerebral cortex is that portion of the brain responsible for the conceptualization, planning, and
execution of the speech act, including phonation. Some areas of the cortex may be responsible for
creating the act, others for its linguistic characteristics, and still others for the emotionality of the act.
Penfield and Roberts (1959) have identified three major areas of the cortex directly responsible for
vocalization. These are, in decreasing order of importance, (a) the precentral and postcentral gyrus
(Rolandic area), (b) the anterior (or Broca’s) area, and (c) the supplementary motor area. These areas
are shown in Figure 14.1. Experiments have demonstrated that vocalization occurs when certain spots
within these areas are stimulated in both the dominant and nondominant hemispheres (Fig. 14.2).
Within these areas, depending on the specific areas stimulated, it has been shown that vocalization can
be initiated or stopped and speech can be slurred or distorted. These behaviors occur as the result of
stimulation in either the dominant or the nondominant hemisphere. Speech and phonation are complex
motor acts involving simultaneous activation and control of many muscles. Although the control of
these motor acts occurs primarily in the cortex, control of individual muscles seems to occur at a much
lower level in the brain. There is no evidence to suggest that cortical stimulation produces a response in
a single solitary muscle. Higher brain function is concerned with idealization of the event, integration of
sensory information, feedback control, and coordination of various muscles required for the motor act.
In the last few years, a number of brain imaging techniques, including functional magnetic reso-
nance imaging, positron emission tomography scans, and transcranial stimulation, have been applied
to investigations of vocal control, in both animals and humans. These techniques are particularly valu-
able since they permit relatively noninvasive ways of examining relationships between voice and speech,
and activity in many parts of the brain. These promise to elaborate our understanding of neural con-
trol for voice production in both normal and abnormal conditions, as well as task-specific functional
differences. For example, Simonyan et al. (2009) have described lateralization differences in the laryngeal
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398 Understanding Voice Problems

FIGURE 14.1. Cortical areas involved

in speech movement control. Area 4
(primary motor cortex), areas 3, 1, and 2
(somatosensory cortex), area 44 (Broca’s
area), and area 6 (premotor cortex and
supplementary motor area).

motor cortex associated with voice production and breathing. In short, a syllable repetition task
demonstrated lateralization to the left hemisphere, whereas voluntary, controlled breathing,
essential to voice production, showed bilateral representation.

Subcortical Mechanisms of Phonatory Control

The motor cortex has numerous connections to the thalamus, a major portion of the dien-
cephalon or interbrain. Other parts of the diencephalon include the hypothalamus, metathala-
mus, epithalamus, and subthalamus (Riklan & Levita, 1969). The third ventricle is also part of
the diencephalon (Gardner, 1963). The thalamus has major pathways to the motor cortex and
Broca’s area (Penfield & Roberts, 1959). In addition, the thalamus has numerous connections
to the cerebellum, midbrain, and other structures in the diencephalon (Fig. 14.3). There are
various nuclei in the thalamus that project to parts of the cerebral cortex. These are shown in
Figure 14.4. Note that the motor area (precentral gyrus) located anterior to the central sulcus
receives much of its projection from the ventral lateral nucleus of the thalamus. Botez and
Barbeau (1971) concluded that the ventrolateral nucleus was responsible for the initiation of
speech movements as well as control of loudness, pitch, rate, and articulation. Broca’s area

FIGURE 14.2. Areas on the left and right hemispheres that produce vocalization when stimulated.
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CHAPTER 14 I Neuroanatomy of the Vocal Mechanism 399

FIGURE 14.3. Diagrammatic representation of the brain stem.

receives connections from the dorsal median and centromedian nuclei of the thalamus. (The
centromedian nuclei help form the massa intermedia shown in Figure 14.4.)
The thalamus is a most fascinating structure in the diencephalon since it appears to act
both as a relay for impulses occurring in lower areas of the brain and as an integrator of
information (Riklan et al., 1969). Furthermore, the thalamus is involved in the maintenance of
consciousness, alertness, and attention and may also integrate emotion into a complex motor
act. The major role of the thalamus appears to be the control and integration of the motor
systems. Some of the thalamic nuclei are nonspecific and project to many areas on the cortex
(Fig. 14.5). Thus, insofar as speech and voice are concerned, the thalamus plays a major role in
integrating incoming sensory information, coordinating outgoing information from the cortex
and other areas of the brain, and, perhaps, adding emotionality to speech and voice.

Midbrain Structures
The midbrain or mesencephalon lies beneath the thalamus (House & Pansky, 1967). On the
anterior surface of the midbrain are the cerebral peduncles that connect the cerebrum with the
brain stem and spinal cord. On its posterior surface, there are four rounded areas called the
colliculi. The superior colliculi are concerned with visual function, whereas the inferior colliculi
are concerned with audition. Within the midbrain there is a cavity called the cerebral aqueduct
of Sylvius, which is surrounded by a thick zone of gray matter. An important area of this gray
matter, dorsal to the aqueduct, is called the periaqueductal gray (PAG).
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FIGURE 14.4. The major thalamic nuclei and their projections.

Several investigators have shown that stimulation of the dorsal and ventrolateral areas of
the PAG produces activity in some laryngeal muscles (Larson, 1985; Larson & Kistler, 1986;
Ortega, DeRosier, Park, & Larson, 1988). Larson (1985) has reported that some cells in the
ventrolateral area stimulate muscle activity, whereas other cells suppress muscle activity. He
suggested that the PAG may be an intermediate area between the recognition of a stimulus or
event and the subsequent production of the motor act. Other areas, such as the hypothalamus,
amygdala, and anterior cingulate gyrus, are responsible for vocalizations but of a kind that
Larson (1985) notes are species specific. Botez and Barbeau (1971) also implicated the PAG in
disorders involving mutism.
Lesions in the PAG and adjacent areas have produced mutism (Adametz & O’Leary, 1959;
Randall, 1964). Moreover, electrical stimulation of the PAG has produced natural sounding
vocalizations in a variety of species (Jürgens & Pratt, 1979; Kelly, Beaton, & Magoun, 1946;
Yajima, Hayashi, & Yoshii, 1982). Chemical stimulation of the PAG has elicited two kinds of
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CHAPTER 14 I Neuroanatomy of the Vocal Mechanism 401

FIGURE 14.5. The connections between

the pulvinar nuclei of the thalamus and the
posterior speech area of the cortex. The
figure also shows the pathway between the
thalamus and the superior speech cortex
(supplementary motor area).

vocalizations in cats (Zhang, Davis, Bandler, & Carrive, 1994). One vocalization type (Type A)
consisted of meows, howls, and growls remarkably similar to normal feline vocalizations. The
other vocalization type (Type B) was described as a hiss, also found in normal feline repertoire.
Type A vocalizations were all voiced with a fundamental frequency and strong harmonics. It
involved activity in the cricothyroid, genioglossus, and internal oblique muscles. Type B has
no voicing and no activity in the cricothyroid muscles but normal activity in the genioglossus
and internal oblique muscles. Zhang and his colleagues point out that these vocalization types
are very similar to voiced and unvoiced sounds produced by humans.
Zhang et al. (1994) found strong evidence for the PAG to be involved in the control of
patterns of muscle activity involving muscles of respiration and vocalization and in the orofacial
area. They specifically pointed out that no PAG sites were found that activated individual
muscles. They concluded that the PAG contains neurons involved in the control of at least
two kinds of vocalization. In 1996, Davis et al. elaborated on these findings with evidence
that the PAG generates specific respiratory and laryngeal motor patterns essential for human
speech and song. Recently, Schulz et al. (2005) used positron emission tomography to investigate
differences in PAG activity between voiced and unvoiced speech utterances. Voiced productions
were associated with increased activity in midline structures, as well as in other cortical and
subcortical areas. Interestingly, areas in the temporal lobe and cerebellum were noted to be
active during voicing but not during production of voiceless utterances.

Brain Stem
The major bilateral structures in the brain stem implicated in the neural control of phonation
include the nucleus ambiguus, nucleus tractus solitarii, and nucleus parabrachialis. Yoshida,
Mitsumasu, Hirano, Morimoto, and Kanaseki (1987) performed an elegant study in which
they traced the connections among these structures. When they injected a tracer chemical into
one nucleus ambiguus, they found evidence of the tracer throughout the contralateral nuclei,
in the nuclei tractus solitarii bilaterally, in the nuclei parabrachialis, and bilaterally in the lateral
and ventrolateral parts of the PAG area, with a predominance ipsilaterally. Injection of a tracer
into the nucleus tractus solitarii resulted in labeled cells throughout the nucleus itself, as well
as in the dorsal motor nucleus of the vagus, part of the hypoglossal nucleus, the medial portion
of the nucleus gracilis, and the dorsal part of the reticular formation. Clearly, there are many
interconnections bilaterally among the nucleus ambiguus, nucleus tractus solitarii, reticular
formation around the nucleus ambiguus, motor roots of the vagus, and PAG area.
Zhang, Davis, Carrive, and Bandler (1992) have also implicated the nucleus retroam-
bigualis in the control of vocalization. This “structure” is actually the caudal one third of the
ventral respiratory group located in the ventrolateral medulla. Neurons in this area have been
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402 Understanding Voice Problems

long implicated in the control of respiration (von Euler, 1986), but it has been shown that they
also have an important role in the control of laryngeal muscles and vocalization.

Cerebellum
The cerebellum, a structure lying immediately posterior to the midbrain area, is strongly
implicated in the control of movement. Its location is shown in Figure 14.6A. Figure 14.6B
shows the cerebellum from a dorsal view after the cerebrum has been removed. The three main
portions of the cerebellum seen in this figure are the vermis (V), the pars intermedia (PI), and
the hemispheres (H). The cerebellum consists of many transverse folia, shown in Figure 14.6C,
whose complex infolding vastly increases the surface area of the cerebellum in much the same
way as is seen in the cerebrum. The fissura prima (FP) is a deep fissure separating the anterior
and posterior lobes.
Two major areas of the cerebellum are instrumental in the control of movement (von Euler,
1986). The first, the pars intermedia, has many direct connections via the midbrain nuclei with
the cerebrum (Fig. 14.7A). Impulses from the motor cortex are quickly relayed from the
pyramidal tracts (PT) to the pars intermedia via the nuclei pontis, lateral reticular nucleus, and
inferior olive. The pars intermedia analyzes the movement patterns and quickly returns the
results of its analysis to the cerebral cortex via connections through the interpositus nucleus,
the ventral lateral nuclei of the thalamus, and the red nucleus. As such, the pars intermedia acts
like a computer controlling a missile. It may not have given the original command to fire, but
it constantly monitors the missile, taking small corrective actions whenever the missile deviates
from its intended flight plan (Eccles, 1977).
The role of the cerebellar hemispheres in movement control seems to be one of planning
the stages of a movement pattern. As shown in Figure 14.7B, there are few direct connections to
tracts that lead to lower motoneurons, as was the case for the connections between the cerebrum
and the pars intermedia of the cerebellum. Rather, the connections from the motor cortex pass
through the nuclei pontis and inferior olive directly to cells within the cerebellar hemispheres,
and impulses from the cerebellar hemispheres pass through the nucleus dentatus to the ventral
lateral nuclei of the thalamus and red nucleus back to the cerebral hemispheres, where movement
is initiated. It appears that the command center, after drafting a movement plan, sends it on to
the cerebellar hemispheres for revision and refinement before adopting it. According to Eccles

A C
FIGURE 14.6. A. Human cerebrum and cerebellum. B. The cerebellum from its dorsal aspect. C. Midline
view after sagittal section. H, hemispheres; V, vermis; PI, the pars intermedia; FP, fissura prima.
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CHAPTER 14 I Neuroanatomy of the Vocal Mechanism 403

A B
FIGURE 14.7. Cerebrocerebellar circuits in motor control. A. The main circuit starts in the motor cortex
(4) and travels down the pyramidal tract (PT) to the spinal cord, with side branches via the pars intermedia
(PI) to the cerebellum. Impulses from Purkinje cells (PC) in the cerebellum communicate with the motor
cortex and down to the spinal cord. B. Circuits from area 6 in the cerebrum to the cerebellar hemispheres
(H). A return circuit from the Purkinje cells (PC) back to areas 4 and 6 is shown. Also shown is a circuit
from area 6 to the basal ganglia (BG) and its return to the cerebrum. Spinal centers (SpC) are indicated.
Evolving movement refers to the desired movement pattern of a structure.

(1977), the cerebellar hemispheres are concerned with anticipatory planning based on learning,
experience, and sensory information they receive from other brain centers.
The importance of the cerebellum in the control of speech movement cannot be emphasized
enough. Kornhuber (1977) believes that without it (and other midbrain areas) the cerebral cor-
tex could not function and would be ineffective in the generation of movements. The cerebellum
acts to regulate motor movement continuously and quickly, requiring some degree of prepro-
gramming and adjustment by learning. Certainly, coordination of muscles within the larynx is
necessary for phonation, as is coordination with other systems involved in speech production.

Peripheral Connections: The Vagus Nerve

The vagus nerve is the major nerve that supplies the larynx (and other parts of the body as well).
The vagus provides sensory fibers within the larynx, as well as fibers that control all the muscles
of the larynx. The cell bodies of the vagus are located in the nucleus ambiguus. Laryngeal
muscles are controlled by cells in the more caudal portions of the nucleus. The vagus emerges
from the surface of the medulla between the cerebellar peduncle and the inferior olives in the
midbrain. It exits the skull through the jugular foramen.
After exiting the skull, the vagus divides into many branches that serve the head, neck,
thorax, and abdomen. These are shown schematically in Figure 14.8. Shortly after exiting the
jugular foramen, a small filament (the meningeal filament) exits the nerve to serve the dura
mater on the posterior fossa of the base of the skull. The auricular branch provides sensory
fibers to the skin behind the pinna and to the posterior part of the external auditory meatus.
The pharyngeal branch provides motor fibers to the muscles of the pharynx and soft palate.
The major portions of the vagus serving the larynx are the superior laryngeal and the
recurrent laryngeal nerves. The superior laryngeal is the primary sensory nerve for the larynx. It
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FIGURE 14.8. The vagus nerve.

arises from the inferior ganglion of the vagus and descends along the side of the pharynx behind
the internal carotid artery, where it sends off two branches. The external branch descends along
the side of the larynx to serve the cricothyroid muscle. The internal branch descends to an
opening in the thyrohyoid membrane and enters the larynx to serve the mucous membrane
of the larynx down to the true vocal folds. The recurrent laryngeal nerve follows a different
course on either side of the body. On the right side, the recurrent laryngeal nerve descends
in the neck to loop around the subclavian artery (just below the clavicle) and then ascends
alongside the trachea to serve the remaining intrinsic muscles of the larynx. On the left side,
the recurrent laryngeal nerve takes a much more circuitous route, descending into the thorax,
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CHAPTER 14 I Neuroanatomy of the Vocal Mechanism 405

TABLE 14.1 Branches of the vagus (10th cranial nerve)

In the Jugular Fossa
Meningeal Serves dura mater in posterior fossa at the base of the skull
Auricular Serves skin on back of outer ear (auricle) and posterior part of the external
auditory meatus
Pharyngeal Joins with glossopharyngeal, sympathetic, and exter-nal laryngeal nerves to
form pharyngeal plexus, which serves the muscles and membranes of the
phar-ynx and muscles of the soft palate, with the excep-tion of the tensor
In the Neck
Superior laryngeal
External Supplies cricothyroid
Internal Pierces the hyothyroid membrane to supply the mucous membrane of the
larynx down to the true vocal folds
Recurrent
Right side Arises in front of the subclavian artery to travel upward along the trachea
Left side Arises on the left side of the arch of the aorta
Both Enter the larynx behind the articulation of the inferior cornu of the thyroid
with the cricoid
Serve all intrinsic muscles with the exception of the cricothyroid
Superior cardiac Serves cardiac plexus
Inferior cardiac Serves cardiac plexus
In the Thorax
Anterior bronchial Sensory to the lung
Posterior bronchial Sensory to the lung
Esophageal Sensory to the esophagus
In the Abdomen
Gastric Sensory to the stomach
Celiac Sensory to the pancreas, spleen, kidneys, suprarenal bodies, and intestine
Hepatic Sensory to the liver

looping around the aorta, and then ascending alongside the trachea until it reaches the larynx.
It also provides motor fibers to the remaining intrinsic laryngeal muscles.
There are other branches of the vagus nerve in the neck, thorax, and abdomen that provide
sensory innervation to various structures within these areas. These branches of the vagus are
shown in Table 14.1.
The extrinsic laryngeal muscles are innervated by several nerves. The anterior belly of the
digastric muscle receives its innervation from the mylohyoid branch of the inferior alveolar
nerve, whereas the posterior belly is innervated by the seventh cranial nerve (the facial). The
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406 Understanding Voice Problems

mylohyoid muscle is innervated by the mylohyoid branch of the inferior alveolar nerve, and
the geniohyoid, sternohyoid, sternothyroid, and omohyoid muscles by the ansa cervicalis (C1).
The thyrohyoid is innervated by ansa cervicalis (C1) via the hypoglossal nerve.
There are numerous protective mechanisms within the respiratory tract, but the most
vigorous exist in the larynx. Some are mechanical and act to close off the airway; others are
expulsive and serve to force foreign substances from the airway. All are reflexive and operate
under involuntary control.
There are many sensory endings within the larynx that collect information about the
state of the larynx and respiratory tract and transmit this information via several reflex arcs
as well as directly to the central nervous system. Wyke (1967, 1997) has written extensively
about these reflex control mechanisms. The complexity of these control systems and their
interactions with the respiratory and other body systems make this a fascinating area of study.
For example, sensory endings exist in the mucosa or lining of the larynx that respond to
mechanical forces or air pressure changes within the tract. These nerve endings are capable of
sending information to the central nervous system about the mechanical state of the lining of
the respiratory tract. Furthermore, reflex endings exist within the joints of the various cartilages
of the larynx that discharge when these joints are moved. These discharges have been shown to
affect the ongoing electrical activity of some intrinsic laryngeal muscles (Wyke, 1967). Finally,
the intrinsic laryngeal muscles contain specialized stretch receptors that discharge when the
muscle is stretched or contracted (Wyke, 1969). The various levels of reflex mechanisms within
the larynx suggest that elaborate precautions are in place to protect the airway and maintain life.
From our perspective in voice pathology and its treatment, they are important to consider when
trying to understand the physiology of normal and aberrant human phonation and laryngeal
behavior. Wyke (1969) hypothesizes that some types of stuttering may be related to disorders
of the various reflex mechanisms within the larynx.

Summary
Proper control of the muscles of the larynx is critical in the production of voice. The levels of
control within the central nervous system are multiple and complex. Lesions in some parts of
the system, especially in the cortex and thalamus (and related structures), would be expected
to have profound effects on speech and voice production. However, the fact that cortical and
some subcortical controls are present bilaterally provides some measure of safety when lesions
are unilateral. Indeed, cases have been reported wherein portions of the cerebral cortex were
surgically removed with little lasting effect on speech and phonation. Lesions farther down
in the brain might be expected to have a more singular effect on a specific muscle or set of
muscles. However, innervation is still bilateral and redundant in some lower level brain areas,
thus affording considerable protection of the systems involved in speech production. Once the
nerves exit the skull, lesions of a nerve will have more specific effects involving, perhaps, a single
muscle or small number of muscles bilaterally or unilaterally.
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CHAPTER

15
Some Normative Data on the Voice

Keywords
normative, data, fundamental frequency, perturbation, jitter, shimmer, intensity, s/z ratio,
duration, airflow, vibratory airflow, air pressure, <FDR

In this chapter, some normative data on the voice are presented. Our purpose is not to present all the
available data, much of which is incomplete and confusing, but rather to provide the most meaningful
data against which patient data may be compared clinically. The data reported here were gathered from
a variety of sources, all of which are referenced for those seeking further information. An invaluable
source for more complete data is the Baken and Orlikoff book, Clinical Measurement of Speech and Voice
(Baken & Orlikoff, 2000). The sources of the data in the tables in this chapter are indicated by numbers
in the body of the table, keyed to references below the table. The full citation for these sources appears
in the reference list at the end of the book. Additional information about these measures and how they
are obtained can be found in Chapter 8.

Fundamental Frequency
The measure of fundamental frequency, reflecting the vibratory rate of the vocal folds, is useful for com-
paring intra- and inter-subject pitch levels. Fundamental frequency can be measured during production
of sustained vowels or during a reading passage. Note, however, that fundamental frequency will vary de-
pending on the type of speech material used. Considerable data are available on fundamental frequency,
covering ages from birth to death. At many ages, however, fundamental frequency plateaus and may not
change for many years. The data in Table 15.1 represent a summary of fundamental frequencies. Several
studies have reported fundamental frequency at certain ages or within certain age ranges. The data in
Table 15.1 represent the average of these studies. Table 15.2 presents summary data for untrained and
trained speakers.

Fundamental Frequency Variation

The standard deviations of fundamental frequency, often referred to as the variability of fundamen-
tal frequency or pitch sigma, are also shown in Table 15.1. Variability is much smaller for sustained
vowels than for reading passages. Fundamental frequency variability or lack thereof may be a physi-
cal measure that relates to the perception of voice monotone, a perceptual sign noted in some voice
disorders.

Frequency Perturbation
Frequency perturbation or jitter refers to the variation of fundamental frequency present in all speakers
to some degree and detected when the subject is attempting to produce a steady, sustained vowel. The
407
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408 Understanding Voice Problems

TABLE 15.1 Fundamental frequencies

Age Range Mean F0 SDa Range Referenceb
Males reading
7 294 2.2 1
8 297 2.0 1
10 270 2.4 1
11 227 1.5 192–268 2
14 242 3.4 1
19 117 2.1 85–155 3
Adult 132 3.3 4
20–29 120 5
30–39 112 5
40–49 107 5
50–59 118 5
60–69 112 5
70–79 132 5
80–89 146 5
Females reading
7 281 2.0 6
8 288 2.8 6
11 238 1.51 98–271 2
19 217 1.71 65–255 3
20–29 224 3.8 192–275 7
30–40 196 2.5 171–222 8
40–50 189 2.8 168–208 8
60–69 200 4.3 143–235 7
70+ 202 4.7 170–249 7
80–94 200 2.7 183–225 9

a
Standard deviation (SD) is expressed in semitones.
b
Reference key: (1) Fairbanks, Wiley, and Lassman (1949); (2) Horii (1983); (3) Fitch and Holbrook (1970); (4) Snidecor (1943);
(5) Hollien and Shipp (1972) and Shipp and Hollien (1969); (6) Fairbanks, Herbert, and Hammond (1949); (7) Stoicheff (1981);
(8) Saxman and Burk (1967); and (9) McGlone and Hollien (1963).

frequency variations are the result of instability of the vocal folds during vibration. As such,
perturbation reflects the biomechanical characteristics of the vocal folds, as well as variations
of neuromuscular control. Normal speakers have a small amount of frequency perturbation,
which may vary according to age, physical condition, and in some cases, sex. These variables
are included in Table 15.3, obtained from data reported by Casper (1983).
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CHAPTER 15 I Some Normative Data on the Voice 409

TABLE 15.2 Mean speaking fundamental frequencies for various age groups
20–35 40–55 65–85
Age Groups Mean SD Mean SD Mean SD
Females
naı̈ve 192.00 2.00 195.00 3.40 175.00 2.40
Trained 217.00 3.60 205.00 4.10 201.00 5.20
Males
naı̈ve 118.00 2.60 100.00 2.60 127.00 3.10
Trained 131.00 3.10 126.00 3.90 125.00 4.00

Maximum Phonational Range

Maximum phonational range refers to the range of frequencies, from lowest to highest, which
an individual can produce. The intensity of the tone is usually not controlled, and the person
may be asked to sustain the tone for approximately 1 second. Placing further demands on the
production of the sound (i.e., production at a specific intensity or for a longer duration) may
be expected to alter the magnitude of the range obtained. The data reported in Table 15.4 were
obtained from many sources and represent the means of several studies. Note that there are no
data for children.

TABLE 15.3 Frequency perturbation data

Directional Pitch Perturbation
Jitter Factor Perturbation Factor Quotient
Age Range Measure /ee/ /oo/ /ee/ /oo/ /ee/ /oo/
Males
20–29 Mean 0.78 0.72 70.73 69.48 0.65 0.57
SD 0.4 0.36 11.25 14.87 0.3 0.26
40–49 Mean 0.99 0.87 74.37 72.49 0.77 0.7
SD 0.61 0.51 10.86 14.84 0.38 0.32
60–69 Mean 0.91 0.87 67.77 69.43 0.77 0.74
SD 0.63 0.56 15.46 14.55 0.5 0.43
Females
20–29 Mean 0.55 0.56 46.3 47.83 0.56 0.57
SD 0.41 0.41 19.67 19.68 0.39 0.37
40–49 Mean 0.63 0.61 53.06 51.67 0.65 0.61
SD 0.4 0.42 16.57 19.76 0.41 0.4
60–69 Mean 0.66 0.7 49.91 48.88 0.65 0.69
SD 0.52 0.59 19.1 18.64 0.49 0.56
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410 Understanding Voice Problems

TABLE 15.4 Maximum phonational range

Age Range Low Frequency High Frequency Range Referencea
Males
17–26 80 764 39.06 1
18–36 80 675 36.92 2
35–75 80 260 20.4 3
40–65 83 443 28.99 5
68–89 85 394 26.55 4
Females
18–38 140 1,122 36.03 2
66–93 134 571 25.09 4
35–70 136 803 30.75 5

a
Reference key: (1) Hollien and Jackson (1973); (2) Hollien, Dew, and Phillips (1971); (3) Canter (1965); (4) Ptacek, Sander,
Maloney, and Jackson (1966); and (5) Colton and Hollien (1972).

Vocal Intensity
The intensity of phonation observed during speech is dependent on several factors. These
include the intensity produced at the glottis, the shape of the vocal tract, the amount of lip
opening, and the distance of the microphone from the lips of the speaker. Physical and emotional
characteristics of the speaker also may affect vocal intensity. Thus, the data presented in Table
15.5 should be used with caution. They may be useful as an indicator of expected approximate
intensity levels, but be sure to check the specific vowel/syllable used and the lip–microphone
distance.

Amplitude Perturbation
During sustained vibration, the vocal folds exhibit slight variation of amplitude from one cycle
to the next. This is called amplitude perturbation or shimmer. Normal speakers present a small
amount of shimmer, which depends both on the vowel used and the sex of the person. Some
typical shimmer values are shown in Table 15.6.

Maximum Intensity Level

Patients may vary considerably in their ability to produce loud tones. This may be a helpful
diagnostic sign or a measure of change following treatment. Thus, measuring maximum-
intensity output may prove useful. Normal speakers usually can produce maximum outputs in
excess of 110 dB; this is somewhat dependent on sex, age, the frequency at which the phonation
is produced, and the measurement procedure. Table 15.7 presents a summary of maximum
intensity levels for different ages and both sexes.

S/Z Ratio
The s/z ratio is a simple measure designed to examine the effect of pathological conditions on
phonation. Although there is some variation among normal speakers, generally ratios greater
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TABLE 15.5 Vocal intensity in monosyllables and reading passage

Utterance Type Loudness Level N Age Mean dB SD (dB) Referencea
Females
/pa/
Soft 10 20–30 65.35 1.84 1
Comfortable 10 20–30 70.44 1.88 1
Loud 10 20–30 76.75 3.38 1
/pœ/
Soft 20 18–36 83.30b 3.20 2
Comfortable 20 18–36 76.40 4.00 2
Loud 20 18–36 71.50 4.90 2
Rainbow Passage 20–30 68.15 3
Males
/pa/
Soft 10 20–30 70.42 3.19 1
Comfortable 10 20–30 74.69 3.08 1
Loud 10 20–30 80.72 3.51 1
/pœ/
Soft 25 17–30 75.00 2.50 2
Comfortable 25 17–30 79.50 3.30 2
Loud 25 17–30 86.00 4.30 2
Rainbow Passage 20–30 70.42 3

a
Reference key: (1) Stathopoulos and Sapienza (1993). SPL was measured from a pressure transducer placed in a circumferen-
tially exhausted face mask. Therefore, distance of the microphone to the lips of the speaker is estimated to be about 1 inch;
(2) Holmberg, Hillman, and Perkell (1988); (3) Ryan and Gelfer (1993).
b
Averaged over 15 syllable repetitions.

TABLE 15.6 Amplitude perturbation data

Vowel Mean SD
Males
/ah/ 0.47 0.34
/ee/ 0.37 0.28
/oo/ 0.33 0.31
Mean 0.33 0.31
Females
/ah/ 0.33 0.22
/ee/ 0.23 0.08
/oo/ 0.19 0.04
Mean 0.25 0.11

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412 Understanding Voice Problems

TABLE 15.7 Maximum intensity levels

Age Mean SD Range Referencea
Males
18–39 106 5.1 92–116 1
45–65 110 7.1 99–129 2
68–89 101 5.9 88–110 1
Females
18–38 106 3 99–112 1
40–70 101 18.2 93–115 2
66–93 99 4.5 90–104 1

a
Reference key: (1) Ptacek, Sander, Maloney, and Jackson (1966); (2) Colton, Reed, Sagerman, and Chung (1982).

than 1.4 are considered abnormal. Ratios close to 1 are normal and expected for both children
and adults of different ages (Table 15.8). The clinician is cautioned to use this measure as one
of a battery of measures rather than as a single definitive measure. Numerous authors (Case,
1991; Hufnagle & Hufnagle, 1988; Mueller, Larson, & Summers, 1993; Sorensen & Parker,
1993) have raised concerns about the validity of the measure.

Maximum Phonation Duration

Maximum phonation duration is the maximum time a person can sustain a tone on one con-
tinuous expiratory breath. It supposedly is a measure of phonatory control and respiratory

TABLE 15.8 S/Z ratios

Age Mean Range Referencea
Males
5 0.92 0.82–1.08 1
7 0.7 0.52–0.97 1
9 0.92 0.66–1.5 1
Females
5 0.83 0.50–1.14 1
7 0.78 0.51–1.10 1
9 0.91 0.75–1.26 1
Adults 0.99 0.41–2.67 2
Aged 0.76 3
0.82 3

a
Reference key: (1) Tait, Michek, and Carpenter (1980); (2) Eckel and Boone (1981); (3) Young, Bless, McNeil, and Braun (1983).
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CHAPTER 15 I Some Normative Data on the Voice 413

TABLE 15.9 Maximum phonation duration

Group Ages Mean (sec) SD
Males
Young children 3–4 8.95 2.16
Children 5–12 17.74 4.14
Adults 13–65 25.89 7.41
Aged 65+ 14.68 6.25
Females
Young children 3–4 7.5 1.8
Children 5–12 14.97 3.87
Adults 13–65 21.34 5.66
Aged 65+ 13.55 5.7

“support.” As Kent, Kent, and Rosenbek (1987) have pointed out, maximum phonation du-
ration can be influenced by variables that have little to do with phonatory control. Important
variables include age, sex, and, of course, the physical characteristics of the respiratory system.
Table 15.9 presents a summary of the data reported on maximum phonation duration from

TABLE 15.10 Average flow rates (mL/sec)

Age Task Mean Range N Referencea
Males
7 /ah/ 96 51–128 10 3
Adult /ah/ 119 96–141 5–36 1
/ee/ 144 89–136 30 4
Reading 177 141–218 4 2
Adult /pah/
Soft 130 10 5
Comfortable 120 10 5
Loud 140 10 5
Females
7 /ah/ 72 45–115 10 3
Adult /ah/ 112 89–136 5–36 1
/ee/ 177 30 4
Reading 191 152–170 4 2

a
Reference key: (1) Based on data presented in table 3.1 of Hirano (1981a); (2) Horii and Cooke (1978); (3) Beckett, Thoelke,
and Cowan (1971); (4) Woo, Colton, and Shangold (1987); (5) Stathopoulos and Sapienza (1993).
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414 Understanding Voice Problems

many studies. This measure should be used with care because of uncertainty about its validity
and stability on repeat trials (Kent et al., 1987).

Airflow
Average Airflow Rates
Measurements of physiological parameters such as airflow and air pressure have some
face validity in that vocal pathological conditions will affect their magnitude. Both air-
flow and air pressure are dependent on a number of factors, however, including respira-
tory drive, vocal fold valving, frequency, and intensity. Thus, the conditions under which
these measurements are obtained must be understood and controlled to be properly inter-
preted.
Average airflow measures are shown in Table 15.10. Average airflow is reported in cubic
centimeters per second or milliliters per second. Many researchers and clinicians have re-
ported data on airflow for both normal speakers and those with vocal pathological conditions.
Some of the data for normal-speaking participants are reported in Table 15.10. There is some
variation depending on the task the participant performs, and there is some suggestion that
children have much smaller flows than adults. Women tend to have slightly lower flows than
men do.

TABLE 15.11 Vibratory airflows based on inverse filtering of oral airflow data
(mL/sec)
Age Range N Conditiona AC Flow DC Flow Referenceb
Males
17–30 25 Normal 260 120 1
25 Soft 220 180 1
25 Loud 490 110 1
21–30 8 Normal 2
20–31 10 Comfortable 3
69+ 10 Comfortable 3
Females
17–30 20 Normal 140 90 1
20 Soft 110 120 1
20 Loud 180 90 1
21–30 8 Normal 189 75 2
20–31 10 Comfortable 140 3
69+ 10 Comfortable 150 3

a
Normal, soft, and loud refer to the loudness level at which the speakers were asked to produce the phonation.
b
Reference key: (1) Holmberg, Hillman, and Perkell (1988, tables AI–AVI); (2) Brodie, Colton, and Swisher (1988); (3) Higgins
and Saxman (1993); phonation was a series of /bcep/s.
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CHAPTER 15 I Some Normative Data on the Voice 415

Vibratory Airflow
Vibratory airflow refers to the variations of airflow during a cycle of vibration. Two major
aspects of vibratory flow have been measured and are reported in Table 15.11. The first, AC
flow, refers to the peak airflow during vibration. The second, minimum or DC flow, refers to
any airflow that occurs when the vocal folds are supposedly closed. Both appear to be correlated
with breathiness in the voice. AC flow varies both as a function of sex and of the intensity level
at which the phonation is produced. Women have much lower AC flows than men do, and
there is a tendency for minimum or DC flow to be lower for female speakers also. As intensity
levels increase, so too does airflow.

Air Pressure
The amount of air pressure used in producing phonation will, in large measure, determine the
intensity of the voice. In normal speakers, air pressure ranges between 4 and 5 cm H2 O for
normal conversational- or moderate-level phonations (Table 15.12). Air pressure also affects
the magnitude of airflow; thus, one must know at what pressures airflow measures have been
collected. These data were derived from measurement of intraoral air pressure according to
techniques described by Rothenberg (1968), Smitheran and Hixon (1981), and Rothenberg
(1982). In some current literature, pressure is reported in kiloPascals (kPa). To convert pressure
in cm H2 O to kPa, multiply by 10.197.

TABLE 15.12 Air pressure measurements based on intraoral pressure

estimates (cm H2 O)
Age Range N Conditiona Pressureb SD Referencec
Males
17–30 25 Normal 5.91 1
25 Soft 4.79 1
25 Loud 8.39 1
2–130 8 Normal 4.12 1 2
20–31 10 Comfortable 5.81 1.4 3
69+ 10 Comfortable 7.99 2.73 3
Females
17–32 25 Normal 6.09 1
25 Soft 4.79 1
25 Loud 8.46 1
21–30 8 Normal 4.28 0.88 2
20–31 10 Comfortable 6.51 0.8 3
69+ 10 Comfortable 6.35 1.71 3

a
Loudness level at which the phonation was produced. All used the indirect intraoral air pressure method for estimating lung
pressure (Smitheran & Hixon, 1981).
b
To convert cm H2 O to kPa, multiply cm H2 O by 10.197.
c
Reference key: (1) Holmberg, Hillman, and Perkell (1988); (2) Brodie, Colton, and Swisher (1988); (3) Higgins and Saxman
(1993).
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416 Understanding Voice Problems

TABLE 15.13 Maximum flow declination rates (or closing slope of the inverse
filtered airflow waveform pulse) for normal speakers
Syllable N Age Mean SD Referencea
Males
/pœ/
Soft 25 17–30 171.1 71.30 1
Comfortable 25 279.6 90.40 1
Loud 25 481.1 162.60 1
/pa/
Soft 10 20–30 218.43 100.03 2
Comfortable 10 367.78 130.20 2
Loud 10 573.16 186.22 2
Females
/pœ/
Soft 20 18–36 117.2 57.80 1
Comfortable 20 164.00 57.50 1
Loud 20 248.90 84.00 1
/pa/
Soft 10 10–20 148.05 70.62 2
Comfortable 10 248.42 87.20 2
Loud 10 397.21 168.56 2

a
Reference key: (1) Holmberg, Hillman, and Perkell (1988); (2) Stathopoulos and Sapienza (1993).

Maximum Flow Declination Rate (Closing Slope)

Maximum Flow Declination Rate (MFDR) or the closing slope of the inverse-filtered airflow
waveform reflects the closing rate of the vocal folds. The faster the closing rate, the greater the
amplitude in the higher frequencies. Thus, MFDR is related to vocal intensity production by
the vocal folds and their spectrum. Table 15.13 presents some data from normal speakers at
three intensity levels.
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APPENDIX

Forms Used in
Voice Evaluation:
Clinic and Laboratory

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Appendix 419
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Appendix 421
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422 Understanding Voice Problems

 LWBK726-APX
P1: KWW/KKL

NATIONAL SPASMODIC DYSPHONIA ASSOCIATION

Botulinum Toxin Injection Information and Tracking Chart
This sheet is designed to better track the progression of your treatment with botulinum toxin injections. Use a new sheet for each injection.
P2: KWW/KWR

Name: Doctor: Date: Injection #:

LWBK726-Colton-v1

Days Weeks after botulinum toxin injection

Before
Rating Scale
BTX 1 2 3 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 20 22
Normal 1
2
QC: KWW/FLX

Mild 3
4
Moderate 5
T1: KWW

6
Severe 7

Comments and Notes:

Voice spasms: Tense sudden stoppages X Voice Breathiness: The “airy or breathy” Form of Spasmodic Dysphonia:
(either an opening “abductor” or closing “adductor” quality of your voice that usually appears at the ___ Abductor ___ Adductor ___ Mixed
spasm. Mark a circle in the box that indicates your botulinum toxin injection weakens your vocal muscles.
own judgment of the severity of your voice spasms. Mark an X in the box that indicates your judgment of Other Symptoms:
the severity of your voice breathiness. ___ Vocal Tremor ___ MTD

Right Left Right Posterior Left Posterior Lateral Interaryteniod

Muscle Injected Thyroaryteniod (TA) Thyroaryteniod (TA) Cricoaryteniod (PCA) Cricoaryteniod (PCA) Cricoaryteniod (LCA) (IA)
Appendix

Amount

This sheet was adapted from various sources including William Beaumont Hospital. The NSDA only provides this as a resource and is not recommending or promoting any treatment for spasmodic dysphonia.
423
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Appendix 425
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426 Understanding Voice Problems

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Appendix 427
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Appendix 429
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Appendix 431
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Appendix 433
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Figure 5.17. Aronson, A. E., Brown, J. R., Litin, E. M., & Pearson, J. S. (1968). Spastic
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(1988). Glottal airflow and transglottal air pressure measurements for male and female speakers
in soft, normal and loud voice. Journal of the Acoustical Society of America, 84, 511–529 (Tables
AI–AVI).
Figure 13.9. Based on data from Colton, R. H., Estill, J., & Gerstman, L. (1981). Identification
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Figure 14.2. Based on data from Penfield, W., & Roberts, L. (1959). Speech and brain mecha-
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Tables
Table 5.2. Adapted from Hoehn, M. M., & Yahr, M. D. (1967). Parkinsonism: onset, pro-
gression and mortality. Neurology, 17, 427–442.
Table 5.4. Adapted from Ballenger, J. J. (1985). Neurologic diseases of the larynx. In J. J.
Ballenger (Ed.), Diseases of the nose, throat, ear, head, and neck (pp. 513–548). Philadelphia:
Lea & Febiger.
Table 5.5. Adapted from Ballenger, J. J. (1985). Neurologic diseases of the larynx. In J. J.
Ballenger (Ed.), Diseases of the nose, throat, ear, head, and neck (pp. 513–548). Philadelphia:
Lea & Febiger.
Table 5.6. Adapted from Hirano, M., Feder, R., & Bless, D. M. (1983). Clinical evaluation
of patients with voice disorders: stroboscopic evaluation. Paper presented at the convention of
the American Speech-Language-Hearing Association, Cincinnati, OH.
Table 5.7. Adapted from Carpenter, R. J., McDonald, T. J., & Howard, F. M. (1988). The
otolaryngologic presentation of amyotrophic lateral sclerosis. Otolaryngology, 86, 479–484.
Table 5.8. Adapted from Carrow, E., Mauldin, M., & Shamblin, L. (1974). Deviant speech
characteristics in motor neuron disease. Archives of Otolaryngology, 100, 212–218.
Table 5.10. Adapted from Jarema, A. D., Kennedy, J. L., & Shoulson, I. (1985). Acoustic and
aerodynamic measurements of hyperkinetic dysarthria in Huntington’s disease. Paper presented at
the convention of the American Speech-Language-Hearing Association, Washington, DC.
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Dysarthria in multiple sclerosis. Journal of Speech and Hearing Research, 15, 229–245.
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descriptive and methodological study. Unpublished doctoral dissertation, Syracuse University,
Syracuse, NY.
Table 15.6. Adapted from Baken, R. J. (1987). Clinical measurement of speech and voice. San
Diego: College Hill Press, p. 117.
Table 15.9. Adapted from Table 2 in Kent, R. D., Kent, J., & Rosenbek, J. (1987). Maximum
performance tests of speech production. Journal of Speech and Hearing Research, 52, 367–387.
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INDEX

Page numbers followed by “f denote” figures; those followed by a “t” denote tables.

Abuse, 86–89 and airflow, 415, 415t

breathy phonation for, 327–328 normal versus pathologic, 27–28
coughing, 87–88 in spasmodic dysphonia, 139, 142
elimination of habitual, 327 Air volumes and capacities, 249
excessive, prolonged loudness, 86 Airflow
identification and reduction of, 342 air pressure and, 415, 415t
misuse versus, 85–86 average rates of, 413t, 414
of screamer and noise maker, 88 drugs affecting, 92
sigh, aspirate, easy initiation of phonation for, 328 maximum flow declination rate of, 416, 416t
by sports/exercise enthusiast, 88–89 with nodules, 100
strained, excessive use during swelling/ normal versus pathologic, 27
inflammation, 87 normative data for, 407–416
throat clearing, 87–88 in spasmodic dysphonia, 142
Acoustic signs, 19–26, 20t in unilateral vocal fold paralysis, 133, 134f
amplitude, 21f, 22–24 vibratory, 415, 414t
frequency breaks, 20t, 26 Airflow waveforms (see also Inverse filtering )
fundamental frequency, 20–22, 20t, 21f, 23f inverse filtering of, 245
normal acoustics, 26 Alcohol
phonation time, 20t, 25, 47t, 48t carcinoma from, 180
signal-to-noise ratio, 24 voice quality and, 4
tremor, 25, 26f Allergic reaction
vocal rise or fall time, 24–25 effect on voice, 309–310
voice stoppages, 25–26 medical management of, 309
Acoustic spectrum ALS (see Amyotrophic lateral sclerosis [ALS])
definition of, 243 Alternative therapies, herbal preparations and, 94–95,
one-third octave analysis of, 243–244 96t, 97t
spectrum analysis and software for, 243 American Medical Association (AMA), 267
Acoustic studies, 236–244 Amino glycoside antibiotics, ototoxicity of, 94
acoustic spectrum analysis in, 243, 243f Amplitude, 22–24
of fundamental frequency, 236–237 dynamic range of, 23, 24f
of perturbation, 240–242 sound pressure level in, 21f, 23, 24f
of phonational range, 237–238, 238f variability of, 23
spectrograms in, 242–243 Amplitude perturbation, 23–24, 241f, 242, 410, 411t
of vocal intensity, 238–240 in amyotrophic lateral sclerosis, 152t, 153
Acoustics measurement of, 242
in aging voice, 4 with nodules, 100
normal, 26 in Parkinson’s disease, 123, 124t
Actors, voice, 2 in vocal fold paralysis, 132
Adam’s apple, 377 Amyotrophic lateral sclerosis (ALS), 150–162
Age and gender differences, in lamina propria, 68 acoustic signs in, 150
Aged voice (see Geriatric voice) description and etiology of, 150, 153
Aging (see also Geriatric voice) pathophysiology of, 153
acoustics in, 5 perceptual voice signs and symptoms in, 150, 154f
essential tremor and, 153–156, 155f physiological signs of, 153
theories of, 203–204 speech signs in, 150, 151t
voice in, 4 symptoms of, 150, 152f
Air pressure (see also Subglottal (lung) air Anatomical malformations, laryngoscopic view of, 32t,
pressure) 33

475
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476 INDEX

Anatomy Babinski-Nageotte syndrome, etiology and effect of,

of larynx, 372–381 130t
of vocal folds, 381–383, 382f Basement membrane zone, histology of, 66, 67f
Androgen-containing hormones, adverse effect of, Behavior therapy, 311–312
324 Benign lesion(s), 65, 70–74
Androgens, effect on vocal structure, 94 ankylosis of cricoarytenoid joint, 173
Ankylosis of the cricoarytenoid joint, 173 contact ulcer, 168–170
versus vocal fold paralysis, 173 cysts, 71
Ansa cervicalis nerve, 406 edema, 106–108, 106f
Anterior commissure advancement, 305, 305f granuloma, 73, 167–168, 168–170
Anterior commissure pushback, for vocal fold keratosis, 165–166
slackening, 305, 305f laryngeal web, 176
Anterior glottal web leukoplakia, 165–166
cause of, 307 nodules, 70, 72f
endolaryngeal surgery for, 307–308, 307f pachydermia laryngis, 170–171
thyrotomy for, 307 papilloma, 171–172
Antidepressants, mucosal drying from, 93, 96t polyps, 70–71
Antihistamines Reinke’s edema, 72–73, 106f
effect on voice, 309 trauma, 177–179
mucosal drying from, 93, 96t vascular disorders, 174
Antihypertensives, mucosal drying from, 94 varix and ectasia, 175
Antipsychotics, mucosal drying from, 93 Bernoulli effect, 386–387
Antitussives, mucosal drying from, 93 Bernoulli’s second law of fluid mechanics, 386
Aphonia Beta blockers, effect on voice, 95, 97
in differential diagnosis, 14, 16t, 19, 55 Biglycan, in vocal fold ECM, 64
case study of, 55–56 Biological drug response, variability of, 89–90
consistent, 19 Birth control pills, voice change from, 324
episodic, 19 Blood supply, aging and, 204
as perceptual sign, 14, 39t, 43t, 46t Blunt trauma, effects of, 177, 177f
psychological, 82–83 Botox injection
signs associated with, 46t for granuloma, 289
Apraxia, phonatory, 34 for spasmodic dysphonia, 311, 322
Arnold-Chiari malformation voice therapy following, 322, 346
description of, 163 Body cover model, 381–383, 382f
types of, 163 Body language
vocal fold paralysis in, 163 during clinical interview, 214
Articular cartilages, aging of, 204 during voice evaluation, 263
Articulation error, in Parkinson’s disease, 122 Bonnier’s syndrome, etiology and effect of, 130t
Aryepiglottic folds, function of, 1, 383 Brainstem, in phonation, 401–402
Arytenoid adduction (see Arytenoid cartilages, rotation Breathiness
of ) in differential diagnosis, 14, 18, 38
Arytenoid cartilages, 377–378, 378f case study of, 51–53, 52f–54f
excision (arytenoidectomy), 304, 304f as symptom, 18
in medialization surgery, 302–303 with nodules, 99
cricoarytenoid fixation, 303 signs associated with, 43t–44t
rotation of, 302–303, 302f Breathing exercises in relaxation, 339
Arytenoid complex, 384 Breathing training, 339
Arytenoidectomy, 304, 304f Breathy phonation (confidential voice), 327–328
Arytenoideus muscle, origin, insertion, function of, Broca’s area, in speech movement control, 398–399,
379, 380t 398f
Aspirate initiation of phonation, 328 Bronchoconstrictors, effect on airflow, 92
Aspirin, effect on voice, 95
Ataxic dysarthria, in cerebellar ataxia, 158–159, 159f
Augmentation California Labor Code, 268
for unilateral vocal fold paralysis, 196 CAPE-V Perceptual Rating Form, 258–261
of vocal fold, 301, 302f Carcinoma and tumors
Avellis’ syndrome, etiology and effect of, acoustic signs of, 180–182, 184f
130t description and etiology of, 180, 181f, 182t, 183f
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INDEX 477

glottal tumors in, 186

classification of, 180, 182t vocal fold paralysis in, 131, 131f
excision of, 294, 292f, 296f voice use history of, 220
pathophysiology of, 185 Clavicular breathing, 349–350
perceptual signs and symptoms of, 180 Clergy, voice use history of, 220
physiological signs of Clinical interview
measurable, 182 patient-practitioner interaction in, 214
observable, 184–185 practitioner in
TNM systems classification of, 180, 182t responsibilities, 214
treatment of, 185 skills of, 213–214
of vocal folds, 180, 181f, 181, 182t CO2 laser
Cartilage in endolaryngeal surgery for anterior glottal web, 307,
articular, 204 307f
arytenoid, 168, 302, 302f, 369, 370f, 377–378, in excisional surgery, 290, 292f
378f Coaches of voice and singing on voice team, 7
corniculate, 376, 378 Collagen, in vocal fold ECM, 64, 65t, 66
cricoid, 377f, 377, 380t Collet-Sicard syndrome, laryngeal paralysis in, 135t
cuneiform, 378 Computed axial tomography (CT scan), 271
epiglottic, 378 Computerized Speech Lab (CSL)
thyroid, 204, 301, 302f, 377, 377f program in amplitude perturbation measurement,
Central nervous system depressants, effect of, 90 241
Central nervous system stimulants, effect of, 91, 91t in frequency perturbation measurement, 241
Cerebellar ataxia, 158–159 in fundamental frequency study, 241
acoustic signs of, 158–159 in vocal intensity study, 238–240
description and etiology of, 158 Confidential voice, 327–328
pathophysiology of, 159 Congenital anomalies
perceptual voice signs and symptoms of, 158, 159f in children, 193–194
physiological signs of, 159 on laryngoscopy, 33
Cerebellar disorder(s) Congenital cysts, 194
Arnold-Chiari malformation, 163 Congenital webs, 193–194
cerebellar ataxia, 158–159 Consensus Auditory-Perceptual Evaluation of Voice
Cerebellum, 402f (CAPE-V) system, 258
hemispheres of, 402–403 Consonants, nasal and hum, in therapy, 332–333
in motor control, 402, 403f Contact ulcer
in speech movement control, 403 acoustic signs of, 169
Cerebral cortex, in phonatory control, 397, 398f combination voice therapy and medical treatment of,
Cerebrum, 402f 319
Cestan-Chenais syndrome, etiology and effect of, 130t comparison with granulomas, 318–319
Chant-talk therapy, 332 description and etiology of, 168
Chemotherapy, cancer, ototoxicity of, 94 pathophysiology of, 170
Chewing technique, 331–332 perceptual signs and symptoms of, 169
Children physiological signs of
childhood voice of, 3–4 (see also Pediatric voice) measurable, 170
epiglottis in, 378 observable, 170
Gilles de la Tourette syndrome, 163 Contact ulcer diathesis, 170
hoarseness in, 88 Conversational speech in fundamental frequency study,
laryngeal webs in, 176 236
nodules in, 195–196 Coordination, and proprioception, drug effect on,
cause of, 88, 99 90–92
excision of, 283 Corniculate cartilages, 378–379
voice therapy trial vs. surgery for, 317 Cortex
papilloma in, 171, 194 hemispheres of, 397, 398f
excision of, 290 lesions of, in loss of phonation, 115
prevention of voice problems in, 355–356 Corticosteroid inhalants, effect on voice, 93
s/z ratio in, 192, 255–256, 256f Coughing
as screamers and noise makers, 88 as abusive behavior, 87–88
speech-language pathologist treatment of, 320 effect on voice, 309
steam inhalation trauma in, 178 therapeutic, 336
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

478 INDEX

Cover-body theory of phonation, 274 Diuretics

Coworkers, voice problem effect on, 217 effect on mucosal fluid balance, 90, 92
Cricoarytenoid joint effect on voice, 222
ankylosis of, 173 ototoxicity of, 94
versus vocal fold paralysis, 173 Dosage versus efficacy of drug, 90
movements of, 378, 378f Dose-response relationship on drug effect, 90
Cricoarytenoid muscle(s) Dr. Speech Science forWindows, in fundamental
lateral, origin, insertion, function of, 378, 379, 380t frequency study, 237, 238
in neuromuscular surgery, 306 Drug therapy
posterior for Gilles de la Tourette syndrome, 163
origin, insertion, function of, 379, 380t for multiple sclerosis, 160–162
in Parkinson’s disease, 123 for myasthenia gravis, 121
Cricoid cartilage, 377f, 377, 380t Drugs
Cricothyroid approximation, 304–305 effects of, 91t
Cricothyroid muscle, origin, insertion, function of, on airflow, 92
379–381, 380t on children, 210
Cricothyroid space, in intrafold injection surgery, 299, on coordination and proprioception, 90–92
298f on fluid balance, 92–93
Critical listening and description, 250–253 on hearing, 94
for loudness level, 251, 252 laryngeal by class, 91t
for quality, 252 on secretions of upper respiratory tract,
for rate of speech, 252 93–94
for variability or instability, 251 on vocal fold mucosa, 94
for vocal characteristics, 252 on vocal fold structure, 94
Crying, voice and, 3 voice-related, 89–97
CSpeech program ototoxic, 94
in amplitude perturbation measurement, 241–242 pharmacologic principles of, 90
in frequency perturbation measurement, 241 response in elderly, 90
in fundamental frequency study, 241 Dry air, effect on voice, 93
in vocal intensity study, 239, 240 Dynamic range, 20t, 23, 24f (see also Intensity)
Cuneiform cartilages, 377–378 Dysarthria
Cysts (see also Intracordal cysts) from cerebellar lesions, 115, 158
in children, 194 in pseudobulbar palsy, 148
congenital, 194 in Shy-Drager syndrome, 127
histology of, 71 Dyskeratosis (see Keratosis)
Dysphonia (see also Spasmodic dysphonia)
in children, 187, 199–201
Decibel (dB), 392 psychological, 82–83
Decongestants, effect on mucosal fluid balance, 90, spastic, diazepam effect on, 91
92 Dysphonia plica ventricularis (see Ventricular
Decorin, in vocal fold ECM, 64, 65t, 69 phonation)
Delayed auditory feedback (DAF) device, for
supranuclear palsy, 319
Diagnostic therapy task(s), 253–255 ECM (extracellular matrix) (see Extracellular matrix
loudness alteration, 254–255 [ECM, vocal fold])
phonation with effortful glottal closure, 254–255 Ectasia
pitch alteration, 254 definition of, 175
“placing the voice,” 255 pathophysiology of, 176
production of reflexive sounds, 253 physiology signs of, 175
sustaining prolonged phonation, 254 Edema, 106–107 (see also Reinke’s edema)
Diaphragm, talking from, 350 acoustic signs of, 107
Diazepam (Valium), effect on voice, 91 causes and medical management of, 309
Diencephalon, 398, 399f description of, 106
Digastric muscle, origin, insertion, function of, 374t, etiology of, 106, 106f
375 pathophysiology of, 107
Diplophonia, 16t, 19 perceptual signs and symptoms of, 107
Disinfection (see Universal precautions) physiological signs of, 107
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
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INDEX 479

Effort Expectations, patient, 315

scaling of, 259, 260f–261f Extracellular matrix (ECM), vocal
therapeutic measurement of, 350 fold, 64–66
EGG (see Electroglottography [EGG]) age and gender differences in, 68–69
Elastin, in vocal fold ECM, 64, 65t, 67–68 biology of, 64–70
Elderly ECM components, 65
drug response in, 90 ECM constituents, 66, 65f, 68
presbyphonia in voice therapy for, 347 epithelium, 65–66, 66f
Electrical stimulation 346–347 histology, 63–64
Electroglottography (EGG), 28 lamina propria, 65t, 66–68, 66f, 67f
advantages and limitations of, 244–245 Extrapyramidal system, 115, 116, 117f
in children, 193 EZ Voice forWindows, in fundamental frequency study,
description of, 245, 121f, 134f 237
literature on, 244
recording devices for, 244
in unilateral vocal fold paralysis, 129, 133f Face masks, disinfection of, 224
Electrolarynx 362, 362f Facial expressions
Electromyography (EMG) during clinical interview, 214
application of, 28 during voice evaluation, 253
description of, 248–249, 248f Facial nerve (7th cranial), 40, 93
uses of, 134, 248 False vocal fold (see Ventricular fold [false vocal fold])
EMG (see Electromyography [EMG]) Falsetto register (see also Puberphonia)
Emotion, voice and, 2 easy production of, 334
Emotional problems, referral for, 270, 324 fundamental frequency in, 391, 391f
Endolaryngeal surgery, for anterior glottal web, tension effect on, 390–391
307–308, 307f Falsetto-like voice, in women, 80
Endoscope Family
disinfection of, 223 effect on, 222
in stroboscopy, 228, 229 voice effect on, 217
Endotracheal intubation, granulomas from, 168 Fatigue
Energizing the voice, 343 in differential diagnosis, 13
Environment case study of, 42t, 45–51
effect on voice, 220 energizing the voice for, 343
manipulation of, 342–343 signs associated with, 42t
for voice recording, 263 termination of therapy and, 348–349
Environmental irritants, effect on airflow, 92 Feedback, during voice therapy, 319
Environmental pollutants Fiberoptic examination, 225f, 227 (see also
carcinoma from, 180 Laryngoscopy, flexible fiberoptic)
keratosis from, 165 Fiberscope, laryngeal, 224–225
Epidermoid cyst, 104–105, 194 Fibrillar proteins, vocal fold ECM
excision of, 290f composition and, 64
Epiglottis, 378 Fibromodulin, in vocal fold ECM, 64, 65t, 68
Epiglottitis, bacterial, 309 Fibronectin, in vocal fold ECM, 64, 65t, 68, 70
Epithelial hyperplasia and dysplasia, 289–2290 Flow glottogram, 28, 246, 246f
excision of, 290f Fluid balance, mucosal drugs affecting, 92–93
specimen collection in, 295 Frequency perturbation (see Perturbation, of
Essential tremor, 153–156 fundamental frequency)
acoustic signs of, 154, 155f Fundamental frequency, 22, 22t, 261
classification of, 153 in abductor SD, 141f, 142
description and etiology of, 153–154 acoustic studies of, 236–237
pathophysiology of, 156 computer programs for, 237, 237f
perceptual voice signs and symptoms of, 15, 154f equipment for, 236
physiological signs of, 156 phonatory tasks for, 236
Exercise summary statistics in, 237
relaxation, 339 in adulthood, 4
vocal abuse during, 88–89 breaks in, 26
Exercise program for vocal function, 333 changes with aging, 208–209
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

480 INDEX

Fundamental frequency (Contd.) configuration of stroboscopic information on, 135,

in children, 190 230–231
definition of, 236–237 with nodules, 100, 101
in Huntington’s chorea, 145f, 146 in Parkinson’s disease, 125, 125f
interaction of length, mass, tension in, 392 phonation with effortful, 254–255
maximum phonational range in, 409, 410t with polyps, 103
mean or average, 20–22, 20t, 21f on stroboscopy, 30
nodule effect on, 100 Glottal fry, in misuse, 80–81
normative data on, 407–409 Glottal incompetence, 125, 321, 347
summaries of, 407, 408t, 409t, 410t Glottal resistance, in loudness change, 392–393
in Parkinson’s disease, 123, 124t Glottal tone initiation
perturbation of, 22, 23f, 407–408, 408t aerodynamics in, 386
phonational range in, 20, 22 conditions for, 386, 387
versus pitch, 21–22 phonation threshold pressure in, 388
in pseudobulbar palsy, 147 physiological process of, 386–388, 387f, 388f
in spasmodic dysphonia, 156 vocal fold adduction in, 387, 387f
variability of, 22, 407, 408t Glottis
vocal fold length and, 389, 389f surgery of
vocal fold mass and, 390, 390f for carcinoma, 294, 296f
in vocal fold paralysis, 130, 132 for stenosis, 308
vocal fold tension and, 390–392, 391f for widening, 303
Glottiscope, 275, 276f
Gloving, for laryngeal examination, 223
Gag reflex, 1 Glycoproteins, vocal fold ECM composition and, 64
Gard-Gignoux syndrome, laryngeal paralysis in, 135t Glycosaminoglycans (GAG), vocal fold ECM
Gargling, therapeutic, 336 composition and, 63
Gastroesophageal reflux disease (GERD) Granuloma
combination voice therapy and medical treatment, Bo-Tox injection for, 289
319 combination voice therapy and medical treatment of,
contact ulcers from, 168–170 318
coughing in, 87 contact ulcers and, 318–319
effect on voice, 319 description and etiology of, 167–168, 167f,
keratosis from, 165–166 168–169
mucosal irritation from drug-related, 87 laryngeal, 167–173
in pediatric upper airway disorders, 196 nonspecific, 318
problem variability with, 219 characteristics of, 73
Gender and age differences, in lamina propria, 68 histology of, 73
Geniohyoid muscle, origin, insertion, function of, 374t, perceptual signs and symptoms of, 168
3783 physiological signs of, 168, 170
GERD (see Gastroesophageal reflux disease [GERD]) vocal fold, 73
Geriatric voice, 202–212 vocal process, 168–170, 292f
acoustic signs of, 207–209 Guillain-Barré syndrome, vocal fold paralysis in, 137
anatomical and physiological changes in, 204,
205t–206t
lifestyle and, 202, 203 Hard glottal attack
pathophysiology of, 210–212, 208t, 210f chant-talk therapy for, 332
perpetual signs of, 207, 208t strain from, 77, 86t
physiological signs, observable, 209–210 Harmonics-to-noise ratio, 24
stroboscopic features of, 209–210 Health history, 221–222
Gilles de la Tourette syndrome, 163 drug use in, 221, 222
Gland(s) previous status, 221
mucus, 93 of surgery, 221
salivary, 93 Hearing loss, drug-related, 94
Glottal attack, hard, 77 Hemorrhage
Glottal cancers, classification of, 193, 182t description and etiology of, 174
Glottal closure pathophysiology of, 174
in aging voice, 209 perceptual signs and symptoms of, 174
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

INDEX 481

physiological signs of, 174 Infant

submucosal during menstruation, 324 vocal fold ECM biology in, 64
Herbal preparations, and alternative therapies, 94–95, voice of, 3
96t–97t Infection control (see Universal precautions)
Heredity Infection, laryngeal, 308–309
essential tremor and, 153 Inferior alveolar nerve, 405, 406
in Huntington’s chorea, 144 Inflammation, 309
High-speed videography, 32 excessive use during, 87
History (see Voice history) Infrahyoid muscles, origin, insertion, function of, 375t,
Hoarseness, 6 375–376
in children, 88 Inhalants
differential diagnosis of, 13, 14t, 17 effect on voice, 309
case study of, 36–45, 39t–41t, 53f, 76t preventive protection from, 355–356
etiology, 12 Inhalation phonation, 340
as symptom, 13, 14t Inhalation and thermal trauma, 178–179
with nodules, 98–101 case study of, 179–180
signs associated with, 35 chemical damage from, 178
Horizontal excursion symptoms of, 178
of mucosal wave, 231 Inhaled substances, laryngeal effect of, 88
of vocal fold, 231, 231f Intensity (see also Loudness)
Hospitalization, history of patient, 221 in aging, 220
Hughlings-Jackson syndrome, etiology and effect of, amplitude perturbation and, 410, 411t
130t in amyotrophic lateral sclerosis, 153
Hum and nasal consonants, 332–333 dynamic range of, 23
Humidification, 342 in Huntington’s chorea, 144, 145f, 144–145
Huntington’s chorea, 144–147 maximum level of, 410, 412t
acoustic signs of, 144–146, 146f maximum phonation duration and, 412–414, 413t
description and etiology of, 144 mean level of, 238–239
pathophysiology of, 147 measurement and portrayal of, 239, 240f
perceptual voice signs and symptoms of, 144, 145f normative data on, 410, 411t, 412t, 415, 417
physiological signs of, 147 s/z ratio in, 410, 412t
Hyaluronan, in vocal fold ECM, 64 software for, 242–243
Hydrophilic proteins, 64 in spasmodic dysphonia, 156, 157f
Hydrophobic proteins, 64 in vocal fold paralysis, 132
Hygiene techniques, 340–345, 341f Interarytenoid muscle, in Parkinson’s disease, 123
Hyoid bone, 372, 373–375, 370f, 373f, 377 Interpersonal interaction, during history taking, 214
Hyper adduction, 34, 119t, 138, 142 Interval scale, 257
Hyperkeratosis (see also Keratosis) of vocal folds, 166f Intracordal cysts
Hypofunction acoustic signs, 108
pitch extension exercises for, 335 description, 104–105, 105f
trill for, 329 etiology, description, 104–105
Hypothyroidism, voice in, 323–324 pathophysiology, 106
perceptual signs and symptoms, 105
physiological signs
Imagery measurable, 105
for high-pitched sounds, 334 observable, 105–106
physiology of, 335 Intrafold injection
in relaxation training, 339 materials for, 299, 299f
as therapeutic technique, 335 techniques in, 304, 306f
Imaging transcutaneous, through cricothyroid space, 298, 299,
application of, 271 298f
studies of, 271 transoral
Improvement, termination of therapy and, 348 with laryngeal mirror, 298, 298f
Inappropriate pitch, 15, 79 under direct laryngoscope, 299f
lack of variability in, 81 Intubation
persistent glottal fry, 80–81 endotracheal, granulomas from, 168
puberphonia, 79–80 injury in children, 194
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

482 INDEX

Inverse filtering Laryngoscopic observations, 32–34, 32t

application of, 245–246 Laryngoscopy
computer-assisted analysis of, 246 anatomy of larynx on, 383f, 384–385,
description of, 245 384f
flow glottogram from, 246f, 264 direct, 224
Involuntary laryngeal activity, 34 flexible fiberoptic, 224–228
Irritation, 318 advantages of, 225–226
drug-related, 91, 91t limitations of, 227
procedure in, 225f, 226f, 227
quality of, 227
Jitter (see Perturbation, of fundamental frequency) schematic of, 225f
Keratosis training and experience for, 227
acoustic signs of, 166 indirect
description and etiology of, 165–166, 166f limitations of, 224
pathophysiology, 166 procedure in, 224
physiological signs of, 166 Larynx (see also Vocal fold)
Klinkert syndrome, laryngeal paralysis in, 135t anatomy of, 372–381
anteroposterior
dimensions of, 33
Laboratory testing squeezing of, 78
acoustic studies, 236–244 biological importance of, 1–2
physiological, 244–249 cancer of (see also Carcinoma and tumors)
respiratory, 249–250 incidence of, 180
Lamina propria, 384, 385f cartilages of, 376, 376f
age and gender differences in, 68–69 arytenoid, 377–378, 378f
in animals, 69–70 corniculate, 376–378
aging of, 217 cricoid, 377, 377f
histology of, 66–68, 66f, 67f, 69f cuneiform, 377–378
of vocal fold, 64–65, 65t epiglottis, 378
Laminin, in vocal fold ECM, 64 thyroid, 377, 377f
Laryngeal web, 176f cavities of, 383–384, 383f
acoustic signs of, 176 condition of, prognosis of therapy and, 315
description and etiology of, 176 congenital anomalies in children, 193–194
pathophysiology of, 177 cross-sectional schematic of, 383f
perceptual signs and symptoms of, 176 examination of, 223–236
physiological signs of, 176–177 laryngoscopy in, 224–228
Laryngectomy, 360–362, 369 procedures for, 223–224
Laryngitis, 6, 12, 85 stroboscopy in, 228
acoustic signs of, 108–109 ultra-high-speed photography in, 232–233
acute, 108, 109 ultrasound in, 236
bacterial, 309 video kymography in, 234–235
chronic, 108, 108f, 109 folds of, 383, 383f
description and etiology of, 108, 108f aryepiglottic, 383
excessive use during true, 383
swelling/inflammation, 87 ventricular (false), 383
fungal, 309 growths and lesions of, 223
pathophysiology of, 109 hyoid bone of, 372–373, 373f
perceptual signs and symptoms of, 108 infection of, 308–309
physiological signs of involuntary activity of, 34
measurable, 109 laryngoscopic view of, 36, 384–385, 384f
observable, 109 medical management of, 307–308
reflux, 108 muscles of, 373f, 374t, 380t
viral, 308 extrinsic, 372–376, 373f, 374t
Laryngitis sicca, 109 intrinsic, 379, 380t, 381
Laryngologist, on voice team, 7, 8 normal in fiberoptic view, 224, 225f, 226f
Laryngomalacia, 33, 193 paralysis in Arnold-Chiari malformation,
Laryngopharyngeal reflux in children, 196 163
medical management of, 309–310 physiology of therapy and, 314
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

INDEX 483

position, in children, 187–188 Mackenzie syndrome, etiology and effect of, 130t
protective mechanisms in, 383 Macrophages, in vocal fold ECM, 67
reconstruction of, 307–308 (see also Anterior glottal Magnetic resonance imaging (MRI), studies of,
web) 271
reflex arcs in, 406 Malpractice
reflex mechanisms in, 1–2 expert witness and, 356–357
rehabilitation (see Therapy) prevention of, 356–357
strain from high position of, 76 risk of, 356
structures in, 1 Manipulation, pressure, massage of, laryngeal area,
surgical management of, 273–274 333–334
voice and, 2–3 Matrix metalloproteinases (MMPs), vocal fold ECM
voice therapy for, 315–319 composition and, 64
Lateral fixation, of vocal fold, 304 Maximum flow declination rate (closing slope),
Lateralization, 303 normative data for, 416, 416t
arytenoidectomy in, 304, 304f Maximum phonation duration, 412–414, 413t
Laughing in children, 191
therapeutic, 336 Maximum phonation time, 25
voice and laughter, 2 in children, 191
Lawyers, voice use history of, 220 in voice evaluation, 266
Lee Silverman Voice Treatment program, 345 Maximum phonational range, 409, 410t
Lessac Madsen Resonant Voice Therapy (LMRVT), Medialization, 297
344 augmentation
Leukoplakia 165–166; procedure in, 300
Lifestyle intrafold injection (see also Intrafold injection)
effect on voice, 217, 220 technique in, 299, 298f
geriatric voice and, 210 rotation of arytenoid cartilage
Listening (see also Critical listening and description) procedure in, 302–303
during evaluation process, 250–251 schematic of, 302f
during interview process, 215–216 Medication
Local anesthetics, over stressing voice with, 92 adverse effect on larynx, 319
Loft (falsetto) register, 80 adverse effect on larynx and speech, 320
Long-term average spectrum (LTAS), in spasmodic Menstruation, voice change in, 324
dysphonia, 140, 141f Microphone
Loop diuretics, ototoxicity of, 94 in vocal intensity study, 240
Lou Gehrig’s disease (see Amyotrophic lateral sclerosis for voice recording, 263
[ALS]) Microphonosurgery
Loudness concepts of, 297
in aging voice, 4 instrumentation, 275, 276f, 277f, 278f, 279f
change mechanisms in, 392–394 Midbrain (mesencephalon), 399–401
degree and time of vocal fold closure, Mirror, laryngeal, 233, 233f
392 Misuse, 75–85, 76t (see also Inappropriate pitch)
glottal resistance, 392 abuse versus, 85–86
spectral characteristics of tone in, 394 aphonia and dysphonia, 83–85, 86t
velocity of vocal fold closure, 393, 393f characteristics of, 76t
contact ulcer formation in, 169, 170 description of, 75
critical listening and description of, 251 excessive talking, 81–82
development of, 4 inappropriate pitch, 79–81, 86t
diagnostic alteration in, 254 onset of voice problems with, 218
excessive, prolonged, 86, 86t strain, 76–78
whispering for, 337 therapy for
monoloudness, 17 goal of, 325, 342
as perceptual sign, 16t therapeutic intervention for, 326
reduced range of, 17 voice alone, 326
reduction of, 354 ventricular phonation, 82
variation in, 17 vocal, identifying, 342
LTAS (see Long-term average spectrum Modal register, 80, 238f
[LTAS]) Monoloudness, 17
Lumican, in vocal fold ECM, 64 Monotone voice, 2
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

484 INDEX

Mucoceles, 285 Nervous system (see also Nervous system disorder[s])

Mucosa afferent, 115
cysts, 71 in body function control, 113, 114
epidermoid cyst, 104 brainstem and medulla, 117
epithelium, 65–66, 66f central, 113
extracellular matrix (ECM), 63–64 cerebellum, 115
biology, 64–70, 65t in control of speech, 114–115
granuloma, 73 in coordination of function, 113–114
irritation of, drug-related, 94 cortex and pyramidal tracts, 115
lamina propria, 66–70, 66f, 67f, 69f efferent, 115
nodules, 70, 72f extrapyramidal system of, 116, 116f
nonspecific granuloma, 73 function and dysfunction of, 114
polyps, 70–71, 72f laryngeal nerves and, 117–118
Reinke’s edema, 72–73 organization of and voice pathology, 116–118, 116f,
scarring, 74 117f
sulcus vocalis, 74 peripheral, 129
tissue changes in, 32t, 33 in phonation and speech, 114–115
Mucosal wave in reception and integration of sensory information,
horizontal excursion of, 231 114
stroboscopic information on, 30 role of, 113
Mucus glands, drug-induced drying of, 93 Nervous system disorder(s)
Multidimensional scaling, 258 amyotrophic lateral sclerosis, 150–156
Multiple sclerosis, 160–162 Arnold-Chiari malformation, 163
acoustic signs in, 162 essential tremor, 153–156
description and etiology of, 160–161, 161t extrapyramidal, 115, 116, 117f
neurological signs in, 161t Gilles de la Tourette syndrome, 163
pathophysiology of, 162 Huntington’s chorea, 144–147
perceptual voice signs and symptoms in, 161 lower motor neuron, 117, 150
physiological signs in, 162 miscellaneous syndromes, 163
speech deviations in, 161t multiple sclerosis, 160–162
Muscle(s) of muscle and myoneural junction
activity measurements of, 27t, 28–29 myasthenia gravis, 118–121, 121f
arytenoideus, 379, 380t peripheral nerve lesions, 129–136
cricoarytenoid, 128, 379, 380t vocal fold paralysis, unusual case of, 137–138
cricothyroid, 135, 379–381, 380t Parkinsonism, 121–126
infrahyoid, 374t, 375–376 pseudobulbar palsy, 147–149, 148f
suprahyoid, 373, 374t, 375 Shy-Drager syndrome, 127–129
thyroarytenoid, 380t, 381 spasmodic dysphonia, 138–144
thyromuscularis, 381 versus other dysphonias, 143–144
thyrovocalis, 381 supra- or pseudobulbar palsy, 147–149
vocalis, 383 upper motor neuron (cortical and pyramidal), 115
Muscle Tension Dysphonia (MTD), 83 Neuroanatomy of vocal mechanism, 397–406
Music, voice in, 2 brainstem in, 401–402
Mutism, from anterior cingulated cortex lesions, cerebellum in, 402–403, 402f, 403f
115 cerebral cortex in, 397, 398f
Myasthenia gravis cortical, 397, 398f
acoustic signs of, 120 midbrain (mesencephalon) in, 399–401
description and etiology of, 118–120 motor cortex in, 398, 398f
pathophysiology of, 121 subcortical, 398–399, 399f, 400f
perceptual voice signs and symptoms of, 120 vagus nerve in, 403–406, 404f, 405t
physiological signs of Neurolaryngologist, on voice team, 7
measurable, 120, 121f Neurological conditions, medical management of,
observable, 120–121 310–312
treatment of, 120, 311–312 Neurological disease, onset of voice problems with, 218
Mylohyoid muscle, origin, insertion, function of, 374t, Neurological evaluation, 270
375 referral for, 270
Myofibrils, in vocal fold ECM, 67 Neuromuscular development, pediatric, 189
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

INDEX 485

Nodule excision of, 290

acoustic signs of, 99–100 voice therapy following, 319
acute, 99–100 pathophysiology of, 171–172
in children, 198 perceptual signs and symptoms of, 171
chronic, 98 physiological signs of
description of, 98–99, measurable, 171
etiology of, 98 observable, 171, 172f
histology of, 70, 72f Paradoxical vocal fold motion (PVFM)
pathophysiology of, 101 versus asthma, 324
perceptual signs and symptoms, 99 etiology of, 325
physiological signs of psychotherapy for, 325
measurable, 100 treatment of, 325, 346–347
observable, 101 voice therapy for, 324–325, 346–347
versus polyps, 102 Paralysis (see Vocal fold paralysis)
voice therapy trial for, 322 Parkinsonism, 121–126
Noise acoustic signs of, 123–130, 124
noise-to-harmonics ratio, in children, 198 description of, 121–122
signal-to-noise ratio, 24 etiology of, 121–122, 122t
in amyotrophic lateral sclerosis (ALS), 153 fundamental frequency levels of, 123, 124t
in Parkinson’s disease, 123, 124t pathophysiology of, 125–126
Nominal scale, 257 perceptual voice signs and symptoms of, 122, 123f
Normal voice physiological signs of
abnormal vs., 313–314 measurable, 123–124
concept of, 313–314 observable, 124–125, 126f
pre-therapy, 314 staging of, 122–123, 122t
therapeutic goals and, 314 Parkinson’s disease
Note taking, during clinical interview, 215 idiopathic, 122
Lee Silverman Voice Treatment program for, 345
neurological conditions, 311
Occupational disability guidelines, related to voice, 268
strobe signs in, 125, 126f
Omohyoid muscle, origin, insertion, function of, 375t,
voice therapy for, 345–346
375
Pars intermedia of cerebellum, in motor control, 402
Open-ended questions, during clinical interview, 216
Partial laryngectomy 361, 369
Optimum pitch
Passive smoking, effect on voice, 310
concept of, 352
Patient
determination of, 352
expectations of, 315
as myth, 352–354
perception of, 267, 345
Ordinal scale, 257
prognostic considerations and, 315
Otolaryngologist, 6
Patient history
malpractice and, 356
health in, 221–222
on voice team, 6, 7
psychological, 222–223
Over-the-counter preparations, in patient history,
recreational, 222
222
social, 222
vocational, 222
Pachydermia laryngis voice use in, 220–222
acoustic signs, 170 Patient-practitioner interaction, 223
description and etiology of, 170–171 Pediatric voice, 187
perceptual signs and symptoms, 170 acquired laryngeal disorders
physiological signs acoustic signs of, 197–198
measurable, 170 perceptual signs and symptoms of, 197
observable, 171 physiological signs of, 198–199
Pain, 14 aerodynamic characteristics, 191
case study of, 60–61v case study of, 199–201, 201f
termination of therapy and, 348–349 congenital anomalies, 193–194
Papilloma, 171–172, 294f congenital laryngeal disorders, signs and symptoms
in children, 194 of, 194–195
description and etiology of, 171 EGG characteristics, 193
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

486 INDEX

Pediatric voice (Contd.) Phonation on inhalation technique, 340

fundamental frequency characteristics, 190–191 Phonation threshold pressure (PTP)
intubation injury, 194 description of, 28
laryngeal and vocal development, 187 in glottal tone initiation, 388
anatomical changes, 189–190 Phonation time, maximum, 25, 191–192, 255
larynx position, 187–188 Phonational range
neuromuscular development, 189 acoustic study technique for, 237–238, 238f
vocal fold histology, 188–189 definition of, 20, 22, 237
voice physiology, 190–193 maximum, 409, 410t
laryngopharyngeal reflux, 196 with nodules, 100
maximum phonation times/durations, 191–192 reduced
nodules, 195–196, 198 case study of, 38, 45t
pharmaceutical causes of, 197 signs associated with, 45t
vocal fold paralysis, 196 reduction of, 14t, 17
voice range profile characteristics, 192, 198 Phonatory apraxia, 34
Penetrating trauma, effects of, 177–178, 177f Phonatory physiology, 386–396
Perceptual judgment of pitch, 257–258 of frequency change, 388–392, 389f–391f
reliability and validity of experience and, 259 glottal tone initiation in, 386–388, 387f–388f
Perceptual signs, 15–26, 16t of loudness change, 392–394, 392f–393f
aphonia, 14, 16t of quality variation, 394, 394f–395f, 396
loudness, 16t, 17 Phonetogram, 192, 238, 239f
pitch, 15–17 Phonoscopic approach 349
quality, 17–19 Phonosurgery
Periaqueductal gray (PAG) concept of, 274
laryngeal muscles and, 400 microphonosurgery
lesions and mutism, 400 concepts of, 275, 279–282
Periodicity, of vocal folds, 31 instrumentation, 275, 278f–279f
Peripheral nerve lesions, 129–131 (see also Vocal fold for vocal fold paralysis, 321
paralysis) Phonotrauma
Person-voice relationship, importance in therapy, 315 abuse, 86–89
Personality vocal misuse, 76–85, 76t
type A, 168 Photoglottography, 28
voice and, 2, 216 description of, 245
Perturbation measurements from, 245
of amplitude, 23–24, 411t studies of, 245
measurement of, 241 Physical development, voice in, 3
with nodules, 102 Physical state, voice in, 3
definition of, 240–241 Physiological studies, 244–249
frequency, 241, 409t electroglottography, 244–245
of fundamental frequency, 22, 23f electromyography, 248–249
in aging, 209 inverse filtering, 245–247
example of, 240, 241f photoglottography, 245
measurement of, 241 subglottal air pressure, 247–248
Phase closure Pitch (see also Inappropriate pitch)
in Parkinson’s disease, 125, 126f in aging voice, 4
on stroboscopy, 30, 232 breaks in, 14, 16–17, 56–57
of vocal folds, 30 development of, 4
Phase symmetry, of vocal folds, stroboscopic, 30–31 diagnostic alteration of, 254
Phonation in differential diagnosis, 14
cover-body theory of, 65 extension exercises, in therapy, 330
with effortful glottal closure, 254 frequency and, 21–22
maximum duration of, 255–256, 256f, 412–414, 413t high, easy production of, 334
maximum range of, 409, 410t inappropriate, 15–16
phonoscopic approach to treatment of, 347–348 monopitch and, 15
physiology of, 6–7 optimum as myth, 352–354
sustained, prolonged, 254 in Parkinson’s disease, 121
ventricular, 82, 350–351 as perceptual sign, 16t
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

INDEX 487

reduced range in, 14 Pseudocysts, 285

scaling of, 258–259 Psychiatric evaluation, referral for, 269–270
sex differences in, 323 Psychogenic dysphonia
in vocal fold paralysis, 132 manipulation, pressure, massage therapy for, 333–334
Pitch breaks or falsetto onset of, 218
case study of, 56–57 pushing, pulling isometric therapy for, 335–336
in differential diagnosis, 14 Psychological factors, effect on voice, 222–223
signs associated with, 47t Psychotherapist, on voice team, 7
Pitch sigma, 132 PTP (see phonation threshold pressure [PTP])
Placebo effect of drugs, 90 Puberphonia
Placing the voice, 255 definition of, 79
Plasmapheresis, for Guillain-Barré syndrome, 137 in female, 80
Plethysmograph, inductive, of respiratory movements, psychosocial factors in, 80, 85
249, 250f pushing, pulling isometric therapy for, 335
Polyp Pulse register (see Glottal fry)
acoustic signs of, 103 Pushing, pulling isometric therapy, 335–336
description of, 101–103 abuse potential of, 336
etiology of, 101–103, 102f PVFM (see Paradoxical vocal fold motion [PVFM])
hemorrhagic, 101–102, 295f Pyriform sinus, changes in, 33
histology of, 70
nodules versus, 98–99, 101
pathophysiology of, 104 Quality
perceptual signs and symptoms of, 103 critical listening and description of, 250
physiological signs of as perceptual sign, 16t
measurable, 103 termination of therapy and, 348
observable, 104 variation of
sessile, 102f, 104 spectral characteristics of tone in, 394, 395f
vocal fold, 102f vocal fold shape in, 396
voice therapy for, 318 Quality of life issues, 263–268
Polypoid degeneration Questionnaires, preappointment, 216
combination excision/voice therapy for, 319 Questions
nodules versus, 99 directed, 215
Positive emission tomography (PET), 271 open-ended questions, 216
Pregnancy, voice change in, 324
Presbyphonia
in geriatric voice, 202 Radiologist, on voice team, 7
trill for, 329–330 Rate of speech, critical listening and description of, 252
voice therapy for, 347 Ratio scale, 258
Prescription drugs, in patient history, 222 Reading, in fundamental frequency study, 236, 408t
Prevention of voice problems, 355–356 Recreational activities, effect on voice, 222
education in, 355 Recurrent laryngeal nerve (RLN)
posttreatment vocal hygiene in, 356 injury to and speech, 118
smoking cessation in, 355 lesion of, 129
Primary care physicians, on voice team, 6 section of, for spasmodic dysphonia, 307
Problem in vocal fold paralysis, 129, 196
effect of, 217 Referral diagnosis, patient’s understanding of, 251
patient understanding of, 217 Reflex arcs, 406
Professional voice user, history of, 220 Reflex mechanisms, laryngeal, 1
Proteins, fibrillar, vocal fold ECM Reflexive acts, therapeutic, 336
composition and, 63–64 Reflexive sound production, 253–254
Proteoglycans, vocal fold ECM composition and, 63–65 Rehabilitation (see Therapy)
Pseudobulbar palsy, 147–149 Reinke’s edema
acoustic signs of, 148 characteristics of, 72–73
description and etiology of, 147–148 description of, 102, 106f
pathophysiology of, 149 histology of, 72–73
perceptual voice signs and symptoms of, 148, 148f physiological signs of, 107
physiological signs in, 149 Reinke’s space, polyps in, 67, 99, 103, 106
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

488 INDEX

Relaxation exercises, 339 in Parkinson’s disease, 123, 124t

Reliability, of perceptual judgment of pitch, 258–259 spectrogram of, 242
Resonant voice therapy, 344–345 Sign(s), 15–36 (see also Acoustic signs; Perceptual signs)
Respiration acoustic, 19–26, 20t
during voice evaluation, 255, 256 definition of, 13
in normal speech, 338 measurable
Respiratory movements, 249–250, 25f aerodynamic, 27–29
Respiratory studies, 249–250 muscle activity, 27t, 28–29
of air volumes and capacities, 249 physiological signs, 27, 27t
of respiratory movements, 249–250, 250f vibratory behaviors, 28
RLN (see Recurrent laryngeal nerve [RLN]) observable
laryngoscopic, 32–34, 32t
physiological signs, 29–34, 29t, 32t
S/z ratio stroboscopic, 29–32, 29t
with children, 192, 256, 256f perceptual, 15–19, 16t
in differential diagnosis, 25, 38 symptoms versus, 12–13
measurement of, 255–257, 256f Silence, during clinical interview, 215
normative data for, 410–411, 412t Singers, voice use history of, 220
use of, 256 Slicing mucosa, for sulcus vocalis, 287
Salivary glands, drug-induced drying of, 94 SLN (see Superior laryngeal nerve [SLN])
Scaling Smoking
instruments for, 257–258 carcinoma from, 180
of pitch, 258–259 effect on voice, 310–312
of vocal effort, 259–261, 260f keratosis from, 165
by listener, 261 laryngeal effect of, 97
by patient, 259–261, 260f noxious inhalants, 310
Scarring Reinke’s edema and, 106
characteristics of, 74, 286 voice quality and, 4
pitch extension exercises for, 329–331 Smoking cessation
trill therapy for, 330 for epithelial hyperplasia, 289
vocal fold, histology of, 74 noxious inhalants, 310
Schmidt’s syndrome, etiology and effect of, 130t for pachydermia larynges, 170
Screamer and noise maker, 88 for voice problem prevention, 355
Screamer’s nodes, 88 Sound pressure level (SPL), 21f, 23, 393f
Secretions, upper respiratory tract, drug effect on, 93–94 Spasmodic dysphonia
Semiocclusion 333 abductor (opening), 156–158, 310
Sensations, voice problem-related, 219–220 acoustic signs of, 156–157
Sensory endings, laryngeal, 1 pathophysiology of, 158
Sensory information, reception and integration of, 114 perceptual voice signs and symptoms in, 156
Sex differences physiological signs of, 158
in lamina propria, 68–70 vocal intensity of, 156, 157f
in multiple sclerosis, 160 acoustic signs of, 140–141, 141f
in voice, 323 adductor (closing), 139–140, 310
Shimmer (see Amplitude perturbation) Bo-Tox injection for, 307, 311, 322
Shy-Drager syndrome (Parkinson’s plus syndrome), brainstem abnormalities in, 143
127, 117–129 description of, 138–139
acoustic signs of, 128 differential diagnosis of, 139
description and etiology of, 127–129 as dystonia, 138–139, 143
pathophysiology of, 128–129 etiology of, 138–139
perceptual voice signs fundamental frequency levels of, 140
and symptoms in, 127–128 versus hyperfunctional, 143–144
severity rating of, 128f long-term average spectrum of, 140–141, 141f
physiological signs in, 128 medical management of, 310
voice therapy for, 345 neurological, 138, 143, 310
Sigh, aspirate/easy initiation of phonation, 328 pathophysiology of, 142
Signal-to-noise ratio, 24 perceptual voice signs and symptoms of, 139–140,
in amyotrophic lateral sclerosis (ALS), 152t, 153 140f
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

INDEX 489

phonation on inhalation technique for, 340 Stylohyoid muscle, origin, insertion, function of, 374t,
physiological signs of 375
measurable, 142 Subglottal cavity, 384
observable, 142 Subglottal (lung) air pressure
versus psychogenic, 138, 143 in children, 191–192
psychological, 138 esophageal balloon technique, 247
recurrent laryngeal nerve section for, 307 intraoral air pressure trace, 247f, 248
treatment resistance of, 139 measures, 247
voice therapy for, 322 pressure transducer, 247
Spastic dysphonia (see Spasmodic dysphonia) tracheal puncture, 247
Spectrogram Subglottal pressures, in vocal fold paralysis,
description of, 242–243, 242f 133
software for, 243 Subglottal stenosis, 33
Spectrum (see Acoustic spectrum) in children, 196
Speech Substance use
nervous system control of, 114–115 inhalant, 310
production of, 1 in patient history, 221
systems in, 117 Sulcus vocalis, 110
Speech-language pathologist acoustic signs of, 110–111
and intubation injury, 194 coronal cross-section of, 110, 110f
malpractice and, 356–357 description and etiology of, 110
prognosis of therapy and, 315 histology of, 74, 286, 291f
and traumatic injuries, 177 mucosa slicing of, 287
and treatment of children, 314 pathophysiology of, 111
on voice team, 6–7 perceptual signs and symptoms of, 110
Spirometer in respiratory volume analysis, 249 physiological signs of, 111
SPL (see Sound pressure level [SPL]) vergeture, 111
Sports, vocal abuse during, 88–89, 91t Superior laryngeal nerve (SLN)
Squeezing, anterior laryngeal, 78 injury to and speech, 118
Sternohyoid muscle, origin, insertion, function of, 374t, vocal fold paralysis from lesion in, 129
375 Supraglottal cavity, 384
Strain Supraglottitis, 309
anteroposterior laryngeal squeezing in, 78 Suprahyoid muscles, origin, insertion, function of, 373,
description of, 76–77 373f, 374t, 375
excessive use during swelling/inflammation, Supranuclear bulbar palsy (see Pseudobulbar palsy)
87 Surgery, 273–308
hard glottal attack in, 77, 86t for anterior glottal web
high laryngeal position in, 77–78 endolaryngeal, 307–308, 307f
Strain/struggle thyrotomy, 307
in differential diagnosis, 14, 16t, 18 corrective
case study of, 57–58 vocal fold lateralization, 303, 304f
as symptom, 14 vocal fold medialization, 297
in Parkinson’s disease, 125 excisional
in Shy-Drager syndrome, 127–128 for benign neoplasms, 290
signs associated with, 48t for epidermoid cyst, 290f
in spasmodic dysphonia, 310–311 for epithelial hyperplasia and dysplasia, 289–290,
Stridor, 19 290f
critical listening and description of, 252 for glottal carcinoma, 294, 295, 296f
Stroboscopy, 228–232 for laryngeal papilloma, 290, 294f
advantages of, 228 for mucoceles and pseudocysts, 285, 289f
description of, 31–32, 228–229, 228f for nodules, 282, 283f–284f
development of, 229 for nonspecific granuloma, 301
diagnostic probes during, 232 for polyps, 298–299, 297f
image interpretation, 229–230 history, 274
measurements in, 32–33, 32t laryngeal neuromuscular
procedure in, 228 recurrent laryngeal section, 306
versus ultra-high speed photography, 232–233 for vocal fold paralysis, 306
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

490 INDEX

Surgery (Contd.) endocrine and hormone disorders and, 323–324

microphonosurgery goal of
concepts of, 275–278 general, 313
instrumentation, 275, 277f–279f in laryngeal tissue or structure changes, 319
for posterior glottic stenosis, 308 in misuse/abuse problems, 326
reconstructive laryngeal, 307 in neurological problems, 319
for slackening of vocal fold, 305, 305f guidelines for
for sulcus vocalis feedback, 319
histology of, 286, 291f instrumentation and, 275
intrafold injection technique (see Medialization) patient compliance and, 327–328
removal of, 287 for patient perception, 267, 345
slicing mucosa techniques, 287 progression and, 365
surgical management, 273–274 tape recording and, 261–262
for tensing of vocal fold, 305 hypothyroidism and, 323
anterior commissure advancement in, 305, 306f for laryngeal tissue or structure
cricothyroid approximation in, 305, 305f changes, 315
indications for, 305 combination therapy for, 316–319
Surgical history of patient, 220 goals of, 319
Swelling, excessive use during, 87 therapeutic intervention for, 325
Symptoms, 12–15, 14t, 219–220 voice therapy alone, 322
associated with voice problem, 231 malpractice and, 356–357
signs versus, 13 menstruation and, 324
Systemic disease, voice and, 309 for misuse/abuse problems, 325–326, 342, 355–356
goals of, 326
therapeutic intervention for, 326
Talking voice therapy alone, 326
excessive, 81–82 myths and unresolved issues in, 349–355
reduction of, 341 clavicular breathing, 349–350
Tape recordings optimum pitch, 352–354
equipment, 262–263 talking from diaphragm, 350
tape, 262 unilateral vocal fold paralysis, 351–352
Tapia’s syndrome, laryngeal paralysis in, 135t ventricular phonation, 350–351
Task(s) whispering as harmful, 354–355
diagnostic, 255 nature of, 319
for voice recording, 263 for neurological problems, 319–322, 321f
Teachers goals of, 319
voice disorders in, 267 therapeutic intervention for, 320
of voice and singing on voice team, 7 normal voice and, 313–314
voice use history of, 220 outcome data for, 326
Teflon injection, for unilateral vocal fold paralysis, 311 for paradoxical motion or dysfunction of vocal fold,
Tension (see also Strain) 324–325, 346–347 (see also Paradoxical vocal
chant-talk therapy for, 332 fold motion (PVFM))
chewing technique for, 331 phonoscopic approach to, 347–348
digital manipulation, pressure, massage for, 333–334 pregnancy and, 324
effect on falsetto register, 391 for presbyphonia, 347
fundamental frequency and, 390–392, 391f prognostic considerations, 315
with misuse, 75–76 for spasmodic dysphonia, 322
musculoskeletal manipulation, pressure, massage for special voice problems, 322–325
therapy for, 333–334 techniques in, 325–348
as symptom, 15 aspirate initiation of phonation, 328
yawn/sigh for, 328–329 breathing, 346
Thalamus breathy phonation, 327–328
motor cortex connection to, 398–399, 400f–401f chant-talk, 332
in speech and voice production, 399 chewing, 331–332
Therapy digital manipulation, pressure, massage,
anatomic and physiological bases of, 314, 325–326 333–334
birth control pills and, 324 easy initiation of phonation, 328
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

INDEX 491

easy production of falsetto, 334 aging of, 204

efficacy of, 35, 90 augmentation of, 300, 301f
energizing the voice, 343 massage of, 333
environmental manipulation, 342–343 Thyromuscularis muscle, 381
falsetto or high pitched sound production, 334 Thyroplasty (see also Medialization) for unilateral vocal
hum and nasal consonants, 332–333 fold paralysis, 300, 301f, 322
hygiene techniques, 340, 341f Thyrotomy for anterior glottal web, 307, 307f
imagery, 334–335 Thyrovocalis muscle, 381
individualized, 311 Tissue inhibitors of MMPs (TIMPs), vocal fold ECM
isometrics, pushing/pulling, 335–336 composition and, 64
loudness reduction, 341–342 Tobacco, laryngeal effect of, 97
massage, 333–334 Torsion–fulcrum method, 275, 277f
for Parkinson’s disease, 345–346 Tracheobronchitis, chemical, 178
phonation on inhalation, 340 Tracheoesophageal prosthesis 365, 366f
pitch extension exercises, 330–331 Transsexual voice, 323
post Botox injection therapy, 329 voice therapy for female to male, 323
range expansion and stabilization techniques male to female, 323
(REST), 330–331 Trauma
reflexive acts, 336 blunt or penetrating, 177–178, 177f
relaxation, 339 inhalation and thermal effects of, 178–179
resonant voice production, 344–345 patient history and, 221
respiratory-phonatory matching, 337–339 Tremor
sigh, 328–329 as acoustic sign, 25, 26f
talking reduction, 341 in differential diagnosis, 14
trill, 329–330 case study of, 58–60
“um-hum,” 336–337 as symptom, 18
vocal effort monitoring, 343–344 essential
vocal function exercise program, 333 acoustic signs, 154, 155f
vocal hygiene, 340–345, 341f classification of, 153
whispering, 337 description and etiology, 153–154
yawn/sigh, 328–329 pathophysiology, 156
termination criteria in, 348–349 perceptual voice signs and symptoms, 154, 154f
asymptomatic mucosal pathology, 348 physiological signs, 156
elimination of physical symptoms, 348–349 medical management of, 310–311
habituation of changed vocal behaviors, 349 in Parkinson’s disease, 311
lack of improvement after appropriate trial, 349 signs associated with, 49t
patient acceptance of improvement, 348 voice, 25, 26f, 159f
therapeutic intervention Trill, 329–330
in misuse/abuse problems, 326–327 Tumor, node, metastasis (TNM) classification, of glottal
for neurological problems, 319–320 cancers, 180, 182t
for transsexual voice, 323 Tumors, laryngeal, 180
for unilateral vocal fold paralysis, 321, 321f, 351 Ultra-high speed photography
virilization and, 324 digital image array variant of, 232
Thermal trauma, 178–179 disadvantages of, 233
Throat clearing information from, 233f, 233
as abusive behavior, 87–88 stroboscopy vs., 229
in differential diagnosis, 38 Ultrasound, 236, 271
excessive, 19 “Um-hum” therapy, 336–337
therapeutic, 336 Universal precautions
Thyroarytenoid muscle of endoscopes, 223
origin, insertion, function of, 380t, 381 of face masks, 223
thyroid vocalis, 381 of laryngeal examination, 224
thyromuscularis, 381
Thyrocricoid articulation, 377, 377f
Thyrohyoid muscle, origin, insertion, function of, 374t, Vagus nerve (10th cranial) 403
375 branches of, 403–405, 403f, 405t
Thyroid cartilage, 377, 377f components and function of, 403, 404f
P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

492 INDEX

recurrent laryngeal nerve branch, 403–404, extracellular matrix biology, 64–70, 65t
405t epithelium, 65–66
superior laryngeal nerve branch, 403, 405t lamina propria, 66–70, 66f, 67f, 69f
Valium (diazepam), effect on voice, 92 function of, 1
Variability in fundamental frequency change
of biological response to drug, 89–90 length of, 389, 389f
of fundamental frequency, 22, 407, 408t tension of, 390–392, 391f
listening for, 251 thickness of, 390, 390f
of voice production, 219 hemorrhage of, 95
Varix histology, in children, 188
acoustic signs, 175 on laryngoscopy
description and etiology of, 175 approximation, 32
pathophysiology of, 176 lengthening of, 34
physiology signs of, 175, 175f movement of, 33
Vascular disorder(s) lateralization of, 303
contact ulcer, 168–170 lengthening of on laryngoscopy, 34, 304
ectasia, 175–176 medialization of (see Intrafold injection;
hemorrhage, 174 Medialization)
varix, 175–176 movement in acoustic studies, 19–20
Ventricles, 384 mucosa of (see Mucosa)
Ventricles of Morgagni, 384 paralysis of (see Vocal fold paralysis)
Ventricular fold (false vocal fold) periodicity of, 31
anatomy of, 383, 383f slackening of, surgical, 305, 305f
on laryngoscopy, 33 stroboscopic information on
Ventricular phonation aperiodicity of vibratory cycles, 230
description and diagnosis of, 82 edge straightness and smoothness, 231–232
issue: diagnosis or description, 350–351 horizontal excursion, 231, 231f
rehabilitation in, 340 phase closure, 30, 232
Vernet’s syndrome, laryngeal paralysis in, 135t symmetry of vibration, 230
Vertical laryngeal position, on laryngoscopy, 34 vertical level of, 30
Vertical level, of vocal folds, 30 vibratory amplitude, 30
Vibratory behavior vibratory behavior of, 232
measurements of, 28 structure of, androgen effect on, 94
stroboscopic, 30, 232 tensing of, surgical, 305
Vibratory frequency vibratory behavior of
with nodules, 101 on stroboscopy, 232
of string compared with vocal folds, 389 on ultrahigh speed photography, 232–233,
Video kymography, 234–235, 235f 233f
Videotaping, of fiberoptic endoscopy, 225 Vocal fold paralysis
Villaret’s syndrome, laryngeal paralysis in, 135t acoustic signs of, 132
Virilization, 324 airflow and electroglottogram of, 133, 134f
Visi-pitch program, 20 ankylosis of the cricoarytenoid joint versus, 173
in frequency perturbation measurement, 241 in Arnold-Chiari malformation, 163, 193
in vocal intensity study, 239–240 bilateral, 128–129, 131f, 196
Visual analog scale, 258 in children, 131, 131f, 193
Vocal fold etiology of, 136
adduction of, 120, 162, 379, 387f in adults, 136–138, 138f, 130, 130t, 131f
anatomy of, 383, 384f in children, 131, 131f
benign lesions, 70–74 in Guillain-Barré syndrome, 137
body cover model of, 381, 382f, 383 intrafold injection for, 299, 298f
body of, 381, 382f, 383 muscles in, 136
carcinoma, 180, 181f, 181, 182t neuromuscular surgery for, 306
closure of anastomosis of the split phrenic nerve in,
Bernoulli effect in, 387–388 307
loudness control and, 392, 392f nerve-muscle pedicle procedure in, 307
congenital webs, 193–194 pathophysiology of, 136
cover of, 381, 382f, 383 peripheral syndromes in, 135t
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LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

INDEX 493

physiological signs of associated symptoms and sensations and, 219–220

measurable, 133–135, 133f–134f development of, 217
observable, 135–136 duration of, 218–219
recurrent laryngeal nerve in, 130 effect of, 217
stroboscopic signs in, 135–136, 136t onset of, 217–218
superior laryngeal nerve in, 136 problem definition in, 216–217
unilateral variability vs. consistency of, 219
augmentation approach to, 196, 300 patient history in health, 221–222
comparative study of surgery/voice therapy for, psychological, 222–223
321–322, 321f recreational, 222
description of, 129–131, 131f, 134f social, 222
etiology of, 130, 130t, 131f, 133f vocational, 222
myths and unresolved issues in, 349–355 voice use, 220–222
phonosurgery for, 275, 278f, 280f as process: interview, 213–216
speed quotient measurements of, 123, 133, 134f listening in, 215–216
unusual case of, 137–138 patient personal history in, 214
Vocal fold paresis, in Shy-Drager syndrome, 128 professional personal history in, 214–215
Vocal hygiene, 340–345, 341f questionnaires, preappointment, 216
Vocal intensity (see Intensity) responsibilities of professional and, 214
Vocal jitter, 22 Voice Intensity Controller, for monitoring therapy, 342
Vocal process diathesis, 170 Voice Outcome Survey (VOS), 266
Vocal process granuloma (contact ulcer) (see Contact Voice problems, 11
ulcer) from benign lesions, 165–173
Vocal rise or fall time, 24–25 from carcinoma, 180–186
Vocal shimmer, 22 differential diagnosis of
Vocal swell, 352–353 in aphonia, 19, 46t, 55–56
Vocal tics, critical listening and description of, 252, 253 in breathiness, 14, 18, 43t–44t, 51–53
Vocalis muscle, 381, 383 case studies of, 36–61
Vocalization in hoarseness, 17, 36–45, 39t
cerebral cortex in, 397, 398f in pain, 14, 60–61
nucleus retroambigualis in, 401 in pitch breaks or falsetto, 14, 16–17, 47t, 56
periaqueductal gray in, 399 in reduced phonational range, 22, 38, 45t
Vocational status, effect on voice, 222 in strain/struggle, 54, 55t, 5614, 18, 48t–49t,
Voice (see also Abuse; Drugs; Misuse) 57–58
abuse of, 86–89, 108 in tremor, 18, 25, 26f, 49t, 58–60
misuse versus, 85–86, 86t in vocal fatigue, 13, 42t, 45
adult, 4 etiology of, 12
aged, 4–5 geriatric voice, 202–212
childhood, 3–4 prevention of, 355–356
drug effects on, 89–97, 112 signs of, 12
examination of (see Larynx, examination of; Voice acoustic, 19–26, 20t
testing) interrelatedness of, 34–35
forms used in voice evaluation, 422–441 laryngoscopic, 32–34, 32t
infant, 3–4 measurable physiologic, 27, 27t
larynx and, 2–3 observable physiologic, 29–32, 29t
misuse of, 75–85, 76t, 112 perceptual, 15–19, 16t
versus abuse, 85–86 versus symptoms and, 13
normative data on, 407–416 symptoms of, 12–15, 14t
pathologies secondary to abuse/misuse, 98–111 therapy for (see Therapy)
production of, 5–6 from trauma, 178–179
rehabilitation of (see Therapy) from vascular disorders, 174–180
sex differences in, 323 Voice Range Profile Index for Children (VRPIc), 192,
systemic disease on, 309 198
“Voice box” (see Larynx) Voice registers, normal, 80
Voice Handicap Index (VHI), 264 Voice-Related Quality of Life (V-RQOL) instrument,
Voice history, 213–235 265
as content: problem, 216–219 Voice sample recording, 261–263
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LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59

494 INDEX

Voice scientists, on voice team, 7 scaling in, 257–258

Voice stoppages, 25 special, 2865–271
Voice Symptom Scale (VoiSS), 266 tasks in, 263
Voice team usefulness of, 237
approaches of, 6–10 voice sample recording in, 261–263
laryngologist and speech-pathologist, 7–8 Voice use
separate meetings with individual specialists, 6–7 in patient history, 220–222
separate, same day meeting with, 8 stress-related, 223
team-patient interaction at video Voicing, sudden interruption of, 18
laryngostroboscopic examination, 9, 9f Vowel
members of, 6–8 sex differences in quality, 323
Voice testing sustained, in fundamental frequency study, 236
acoustic studies in, 236–244
critical listening in, 250–253
critical observations in, 253 Wallenberg’s syndrome, etiology and effect of, 130t
diagnostic therapy in, 253–255 Weak voice, energizing the voice for, 343
environment for, 263 Webs, congenital, 193–194
equipment for, 236, 248–249, 248f Whispering
imaging in, 271 harmful, 354–355
laboratory, 236–250 therapeutic, 337, 354–355
maximum phonation time in, 255 Workplace, effect on voice, 217, 222
neurological evaluation in, 270 World Health Organization (WHO), 266
noninstrumental, 255–261
objective noninstrumental measurements in,
255–261 Yawn/sigh therapy, 328–329
physiological, 244–249
psychiatric, 268–270
s/z ratio in, 255–257 Zeitels glottiscope, 275, 276f
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LWBK726-Index LWBK726-Colton-v1 November 19, 2010 19:59
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 4.1. FIGURE 4.2.

FIGURE 4.3. FIGURE 4.4.

FIGURE 4.5.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 4.6. FIGURE 4.7.

FIGURE 6.1. FIGURE 6.2.

FIGURE 6.3.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 6.4.

FIGURE 6.5. FIGURE 6.6.

FIGURE 6.7.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 6.8. FIGURE 6.9.

FIGURE 8.2. FIGURE 8.3.

************

FIGURE 8.7.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.10.

FIGURE 9.11.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.12.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.14.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.16.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.17.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.18.

FIGURE 9.19.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.20.

FIGURE 9.22.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.24.

FIGURE 9.25.

FIGURE 9.27.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.28.

FIGURE 9.29.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.30.

FIGURE 9.32.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.33.

FIGURE 9.34.
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LWBK726-Color˙Plate LWBK726-Colton-v1 November 9, 2010 17:56

FIGURE 9.36.

FIGURE 9.38.

FIGURE 9.39.